Case Discussions

Session 1 — long stem

Aortic valve replacement for bicuspid valve with chronic severe aortic regurgitation

A 56 y.o., 82 kg, 5'10" man with a bicuspid aortic valve and chronic severe aortic regurgitation is scheduled for aortic valve replacement, with possible aortic root replacement.

HPIProgressive exertional dyspnea and declining exercise tolerance over the past two years, now winded after one flight of stairs, with occasional orthopnea and bounding pulsations he feels in his neck at rest. No chest pain, no syncope.

PMHBicuspid aortic valve with chronic severe aortic regurgitation. Long-standing hypertension. A dilated aortic root noted on prior imaging. No prior cardiac surgery.

MEDSLisinopril, amlodipine, atorvastatin, furosemide as needed for swelling.

PHYS EXAMHR 58; BP 158/52; RR 16; SpO2 97% on room air; T 36.8°C. Wide pulse pressure with a bounding, collapsing peripheral pulse. Apex displaced laterally; a high-pitched early diastolic murmur at the left sternal border and a soft systolic flow murmur.

ECGSinus rhythm at 58. Left ventricular hypertrophy with a strain pattern. First-degree AV block (PR 218 ms). Occasional PVCs.

ECHOBicuspid aortic valve with severe aortic regurgitation, wide regurgitant jet with holodiastolic flow reversal in the descending aorta. Dilated LV (LVEDD 68 mm) with declining systolic function, LVEF now 40–45%, down from 55% a year ago. Aortic root dilated to 46 mm. Mild functional MR. Estimated PA systolic pressure 40 mmHg.

LABSHgb 13.6 g/dL; platelets 205 K/uL; INR 1.0; K+ 4.1 mEq/L; creatinine 1.2 mg/dL; BNP elevated; glucose 108 mg/dL.

OR ARRIVALAwake radial arterial line placed; line traces a wide pulse pressure with a low diastolic. Two large-bore peripheral IVs. External defibrillator/pacing pads on. Consent includes possible root replacement.

A. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Hemodynamic goals for chronic severe AR at induction — keeping forward flow in a regurgitant, volume-loaded ventricle; the costs of bradycardia and rising afterload; protecting a dilated, eccentrically hypertrophied LV going onto bypass; and separating a volume-loaded, dysfunctional ventricle from CPB.

1. Induction and hemodynamic goals in AR

Induction agents and doses? Goals for rate, rhythm, preload, afterload here? Why? Despite a measured induction, BP falls to 88/38 and HR drifts to 48. Of concern? Why in this lesion? Rx? Would you give phenylephrine here? Why/why not? Glycopyrrolate, ephedrine, volume — which, and to what end point? Bearing of bradycardia on the regurgitant fraction? If instead the pressure were driven by a rising afterload, bearing on forward flow? Would your approach change if he became tachycardic at 115?

Considerations and pitfalls

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Induction goals. full, fast, and forward — maintain preload, keep a faster heart rate to shorten diastole and limit regurgitant time, and reduce afterload to favor forward output. A plan built around slowing the rate or supporting pressure with pure alpha-agonism runs against this lesion.
BP falls with bradycardia. bradycardia lengthens diastole and worsens the regurgitant fraction, so a low diastolic pressure plus a slow rate is doubly bad here; want recognition that the slow rate is part of the problem, not just the number on the cuff.
Phenylephrine — why/why not. raising SVR with phenylephrine increases the pressure gradient driving regurgitation and the reflex bradycardia it brings worsens it further; reaching for phenylephrine as the first move in AR deserves a probe.
Preferred moves / end point. chronotropy and preload — ephedrine or glycopyrrolate to bring the rate up, judicious volume, afterload kept low; looking for a concrete target (restore a forward-favoring rate and an adequate diastolic), not 'fix the pressure.'
Regurgitant fraction and rate. a faster rate shortens diastole and reduces the regurgitant volume per beat; this is why bradycardia is poorly tolerated and why a slightly faster rate is the goal.
Rising afterload / tachycardia at 115. rising SVR worsens regurgitation and forward flow; a modestly faster rate is favorable, but frank tachycardia at 115 compromises filling and perfusion of the hypertrophied wall and demands reassessment rather than reassurance.

2. Going onto bypass with a dilated LV

As bypass is initiated the surgeon places the aortic cross-clamp and begins antegrade cardioplegia. Concerns specific to this ventricle going onto CPB? Why does a dilated, regurgitant LV distend here? Bearing on myocardial protection and oxygen demand? Antegrade vs retrograde cardioplegia — which, and why in this valve? With an incompetent aortic valve, what happens to antegrade delivery? The team notes LV distension on TEE during arrest. Of concern? Rx? How do you protect this ventricle while the surgeon works?

Considerations and pitfalls

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Concerns going onto CPB. an incompetent aortic valve lets the heart fill from the root during diastole and during cardioplegia delivery, and a dilated, eccentrically hypertrophied LV is prone to distension once it is no longer ejecting; distension raises wall tension and myocardial oxygen demand and impairs protection.
Why it distends. with AR the ventricle has no competent valve to stop retrograde filling; on bypass it can distend from bronchial/aortic return and from regurgitant flow, especially if antegrade cardioplegia is given into a root with an incompetent valve.
Antegrade vs retrograde. antegrade cardioplegia into the aortic root is unreliable with a regurgitant valve because much of it crosses the valve and distends the LV rather than perfusing the coronaries; retrograde (coronary sinus) delivery, or direct ostial delivery once the aorta is open, protects this myocardium better. A candidate who defaults to root antegrade in severe AR deserves a probe.
LV distension on TEE during arrest. distension is harmful — it stretches the protected myocardium and worsens demand; communicate with the surgeon, decompress with an LV vent, and reconsider the cardioplegia route.
Myocardial protection. vent the LV, deliver cardioplegia by a route that actually reaches the coronaries (retrograde or ostial), keep the heart decompressed and the temperature managed; the dilated eccentrically hypertrophied wall is at particular risk if protection is incomplete.

3. Separation from bypass

AVR complete, root preserved; attempting to wean. TEE shows a well-seated valve, no paravalvular leak, but a dilated, hypocontractile, volume-loaded LV. BP 84/46, CI 1.6 on low-dose epinephrine. Of concern? DDx for failure to separate in this ventricle? Volume — more or less here? Why? Inotrope — epinephrine, milrinone, or both? Why/why not in a dilated, afterload-sensitive LV? End point you are titrating to? He still won't wean; the LV looks distended. Bearing? IABP — indicated? Why/why not?

Considerations and pitfalls

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DDx for failure to separate. the chronically dilated, eccentrically hypertrophied LV with declining function may be stunned and unable to handle the volume it now must eject through a competent valve; consider residual ischemia, inadequate or excessive preload, incomplete myocardial protection, RV dysfunction, vasoplegia, or a surgical problem (TEE helps exclude).
Volume — more or less. unlike the stiff small AS ventricle, this dilated ventricle is already volume-loaded and over-distension worsens wall tension and function; cautious afterload reduction and avoiding further volume loading are often the right instinct, with filling guided by TEE rather than reflex bolusing.
Inotrope choice. milrinone improves contractility and unloads a dilated, afterload-sensitive ventricle but vasodilates; epinephrine adds contractility and some tone; a defended choice tied to this dilated, afterload-sensitive LV is what is wanted, not a list. Pure alpha-agonism to chase pressure works against forward flow here.
End point. a concrete hemodynamic target (CI, perfusion pressure, a decompressed LV on TEE) titrated to, not simply 'more epi.'
Persistent distension. the dilated ventricle is failing to unload — reduce afterload, optimize rate and rhythm, decompress, and reassess protection; escalating inotrope into a distending ventricle without unloading is the trap.
IABP. afterload reduction and diastolic coronary augmentation suit a dilated, afterload-sensitive, LV-predominant low-output state; a defensible commit if tied to mechanically unloading this ventricle, not reached for reflexively.

4. Conduction block and pacing

On separation the rhythm is complete heart block with a junctional escape at 40. Immediate management? Why is this valve, and this patient, set up for surgical block? Epicardial pacing — which leads, which mode? AV-sequential vs ventricular alone — which, and why in this ventricle? You pace at 90 with good capture, then lose ventricular capture. DDx? Checks? Capture threshold climbs over the next hour — concern? What determines whether he needs a permanent device before discharge?

Considerations and pitfalls

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Immediate management. support rate and pressure, place and confirm epicardial pacing; recognize that the aortic annulus sits next to the conduction system and that pre-existing first-degree block primes this patient for surgical high-grade block.
Mode — AV-sequential vs ventricular. this dilated, dysfunctional ventricle still benefits from a coordinated atrial contribution and a forward-favoring rate; AV-sequential pacing preserves filling and lets you keep the rate up, where VVI sacrifices the atrial kick. Settling for ventricular-only pacing here deserves a probe.
Loss of capture / DDx. lead dislodgement or poor contact, rising threshold, generator settings, electrolyte shifts; a systematic check of connections, output, and sensing.
Rising threshold. edema or ischemia at the lead site; ensure an adequate output margin and a reliable backup before relying on the system.
Permanent device. persistence of high-grade block beyond the expected recovery window drives the decision; want judgment about observation versus committing to a permanent pacemaker, not a recited criterion.

B. POST-OPERATIVE CARE

Teaching focus. Owning the consequences of a dilated, volume-loaded ventricle into the ICU: post-CPB LV failure and inotrope selection; recognizing new atrial fibrillation and RV strain on top of LV dysfunction; managing pacing dependence; and disclosing an unexpected course to the family.

1. Post-CPB LV failure

First hours in the ICU on epinephrine and milrinone: BP 88/50, CI 1.7, mixed venous low, rising lactate, cool peripheries. Of concern? Why is this dilated ventricle struggling now that the valve is competent? Add an agent or change strategy — which, and why? Vasopressin for the milrinone-driven vasodilation — reasonable? End point you are titrating to? Echo at the bedside — what are you looking for? He stays low-output despite escalation. Mechanical support — IABP, Impella, ECMO — which, and why?

Considerations and pitfalls

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Why struggling now. the chronically volume-loaded ventricle adapted to ejecting a large total stroke volume with a leaky valve; with a competent valve and lost preload reserve it must generate forward flow it is no longer conditioned for, and its declining function is unmasked. Recognizing this as expected physiology, not a surprise, is the judgment.
Add/change strategy. optimize rate, rhythm, and afterload reduction before piling on inotrope; milrinone unloads but vasodilates, so pairing it with a vasoconstrictor to hold perfusion pressure is often the move.
Vasopressin. reasonable to hold perfusion pressure against milrinone-induced vasodilation without adding the chronotropy/arrhythmia burden of more catecholamine; want it tied to maintaining coronary perfusion while keeping the ventricle unloaded.
End point. a concrete target — CI, mixed venous, lactate clearance, perfusion pressure — titrated to, not 'more support.'
Mechanical support. for refractory LV-predominant low output, IABP or Impella unloads and augments; ECMO if biventricular or refractory. Want the choice tied to which ventricle is failing and to unloading this dilated LV, not a reflex.

2. New atrial fibrillation and RV strain

Overnight he develops atrial fibrillation at 150 with BP 82/48 and worsening output; the CVP climbs and the RV looks distended and hypokinetic on echo with PA pressures 58/32. DDx for the deterioration? Bearing of new AF on this dilated, dysfunctional LV? First moves — rate or rhythm control? Synchronized cardioversion, when and at what energy? Bearing of the distended RV — what is driving it, and Rx? Inhaled pulmonary vasodilator — indicated? How do you avoid worsening PVR? He stays unstable. Now what?

Considerations and pitfalls

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DDx for deterioration. new AF with loss of atrial contribution on an already low-output LV, evolving RV failure with pulmonary hypertension, tamponade, ischemia, or volume/electrolyte derangement; the combination of AF and a distending RV is the pattern to recognize.
AF on this ventricle. the dilated, dysfunctional LV depends on rate control and the atrial contribution to maintain forward flow; a fast, disorganized rhythm collapses an already marginal output. Treating this as routine post-op AF is a flag.
Rate vs rhythm / cardioversion. hemodynamic instability favors prompt synchronized cardioversion over titrated rate control; commit to a synchronized shock and a reasonable starting energy and address triggers (electrolytes, ischemia, distension).
Distended RV. rising PA pressure and a distended, hypokinetic RV signal RV failure — optimize rhythm and preload, avoid acidosis/hypoxia/hypercarbia that raise PVR, support RV contractility, and consider an inhaled pulmonary vasodilator.
Inhaled pulmonary vasodilator. inhaled nitric oxide or epoprostenol selectively lowers PVR and offloads the RV without systemic hypotension; want it tied to unloading the failing RV while protecting systemic pressure.
Persistent instability. escalate — mechanical support if biventricular failure, surgical re-look if tamponade suspected; do not keep titrating drugs into a deteriorating patient.

3. Pacing dependence and anticoagulation

He remains in complete heart block, now pacing-dependent, and persists in atrial fibrillation despite cardioversion. Bearing of AF under complete block on his filling and your pacing? How does that change your pacing mode and settings? Anticoagulation — when do you start it given the fresh sternotomy and chest tubes? Heparin bridge, warfarin, or a DOAC? Why? With a mechanical valve, does that change the agent? Threshold and workup for a permanent pacemaker before discharge? What must you confirm before relying on the system?

Considerations and pitfalls

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AF under complete block. with fibrillating atria and complete block, the atrial contribution is already gone, so rate, volume, and perfusion pressure carry the dilated ventricle's output; want recognition that there is no kick to preserve and the ventricular rate is what you control.
Pacing mode / settings. with fibrillating atria, atrial pacing accomplishes nothing — ventricular or rate-responsive ventricular pacing at a forward-favoring rate is what he needs; keeping him on AV-sequential pacing into AF deserves a probe.
When to start anticoagulation. balance fresh surgical bleeding, the chest tubes, and a fresh sternotomy against AF and prosthetic-valve stroke risk; typically delay until hemostasis is secure, then start, often with a titratable heparin bridge first.
Agent / mechanical valve. a mechanical valve mandates warfarin, not a DOAC, and AF on top reinforces that; if a bioprosthesis was placed the agent choice is broader. A titratable heparin bridge allows quick reversal if bleeding recurs.
Permanent pacemaker. persistent high-grade block beyond the recovery window; confirm capture thresholds, sensing, and an adequate safety margin before discharge dependence.

4. Failure to wean from the ventilator

By the next day hemodynamics are improving on weaning support, but he fails a spontaneous breathing trial with rising work of breathing and a borderline gas. Of concern? In this patient, what is driving the failure? Cardiac vs pulmonary contribution — how do you sort it out? Diuresis in a dilated, recently failing ventricle — reasonable? End point? He becomes hypoxemic and the CVP and PA pressures rise during the trial. Bearing? Rx? Extubate, continue weaning, or reintubate — which, and what must be true?

Considerations and pitfalls

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Of concern / driver. weaning loads the heart — the negative-pressure effort and increased venous return stress a dilated, recently failing LV, so weaning failure here is often cardiac, not purely pulmonary; recognizing the cardiopulmonary interaction is the judgment.
Sort cardiac vs pulmonary. look for pulmonary edema, rising filling pressures during the trial, gas-exchange trend, and echo; rising CVP/PA pressures and edema during the trial point cardiac, where a primary pulmonary problem would behave differently.
Diuresis. reasonable if he is volume-overloaded and the failure is cardiac/edematous, with a concrete end point (filling pressures, oxygenation, weight/balance); over-diuresing a preload-dependent dilated ventricle into low output is the opposite trap.
Hypoxemia with rising pressures. weaning-induced LV loading and pulmonary edema — support the ventricle, reduce afterload, treat the edema rather than simply pushing the wean.
Extubate vs reintubate. do not extubate into cardiac failure; stabilize the heart, optimize fluid balance, and wean again, reintubating or continuing support if the trial keeps failing. Either continued support or a planned re-wean is defensible if the cardiac cause is addressed.

5. Disclosure of an unexpected course

He is stabilizing but remains pacing-dependent on low-dose support, still intubated, with a longer ICU course than planned. The family arrives expecting a routine recovery and asks why he isn't off the breathing machine and what the heart block means. What will you tell them? What do you say about why he is still on the ventilator? How do you frame the pacing dependence honestly without over-promising? They ask whether the surgery caused the heart block — what will you tell them? How do you coordinate that message with the surgical team? He remains pacing-dependent — what must they understand before discharge planning?

Considerations and pitfalls

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Telling the family. a plain, honest account — the valve was replaced, the heart's electrical system was affected and he now depends on a pacemaker, and the recovery is slower than hoped — without overpromising or assigning blame, with room for questions.
Framing pacing dependence. explain in lay terms that his own rhythm is unreliable, that the pacemaker is doing the work, and that this likely means a permanent device, while being honest about uncertainty.
Coordinate with surgery. a single, consistent message agreed with the surgical team so the family is not given conflicting accounts of the course and prognosis.
Before discharge planning. they need to understand the likely permanent pacemaker, what dependence means for monitoring, anticoagulation if it applies, and follow-up.

C. ADDITIONAL TOPICS

Teaching focus. Unrelated by design: an operating-room fire during MAC, a pediatric laryngospasm on emergence, and an obstetric postdural puncture headache. Rapid pivot across domains.

1. Operating-room fire during MAC

During MAC with nasal-cannula oxygen for an excision on the face, the surgeon uses electrocautery and a flash fire ignites at the drapes. Immediate actions? Sequence of priorities? How does the fire triad apply here? How could this have been prevented? Once the fire is out, your assessment of the patient?

Considerations and pitfalls

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Immediate actions. stop the procedure, stop the supplemental oxygen and remove the airway source, remove the burning drapes and material, extinguish.
Priority sequence. protect the patient and remove the fuel and oxidizer first, then extinguish, then attend to the patient — the order matters.
Fire triad. oxidizer (supplemental O2 pooling under drapes), ignition (cautery), fuel (drapes, prep, hair) — a high-risk head-and-neck MAC setup.
Prevention. minimize or avoid open high-flow O2 near cautery, secure the airway or use blended air, let the prep dry, tent the drapes to avoid oxygen pooling.
Post-fire assessment. evaluate the airway and any skin or airway burns, confirm ventilation, plan airway management if inhalation injury is suspected.

2. Laryngospasm on emergence in a child with recent URI

A 3 y.o. with a runny nose for the past week undergoes bilateral myringotomy under mask anesthesia. During emergence the child develops stridor, then no air movement, and SpO2 falls to 80%. Diagnosis? Contributing factors in this child? Immediate maneuvers and their sequence? SpO2 now 70% with bradycardia to 60 — Rx? If laryngospasm persists, agent and dose? Once recovered, what will you tell the parents about the risk and your decision to proceed?

Considerations and pitfalls

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Diagnosis. laryngospasm — stridor progressing to complete glottic closure, classically on light emergence.
Contributing factors. recent URI, light plane of anesthesia, airway secretions, young age.
Maneuvers and sequence. remove the stimulus, 100% oxygen, jaw thrust with continuous positive airway pressure (Larson maneuver); escalate if it fails.
Bradycardia with desaturation. deepen anesthesia (propofol) or give succinylcholine; treat hypoxic bradycardia and be ready to ventilate or intubate; an answer that gives succinylcholine without addressing oxygenation deserves a probe.
Succinylcholine. a small IV dose breaks refractory laryngospasm; IM is an option without IV access; have atropine available in the young child.
Counseling parents. a plain explanation of what happened, that it was recognized and treated, and the implications for timing future elective anesthesia after a URI.

3. Recognized wet tap, POD 1 positional headache

A 28 y.o. woman, 24 hours after a labor epidural complicated by a recognized wet tap, has a positional fronto-occipital headache that is relieved by lying flat. Diagnosis and supporting features? What else must you exclude? Conservative measures? She cannot care for her newborn — definitive treatment and how it works? Risks of that procedure?

Considerations and pitfalls

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Diagnosis. postdural puncture headache — postural, following a known dural puncture.
Must exclude. other serious causes of postpartum headache (preeclampsia, cortical vein thrombosis, meningitis, subdural hematoma) before anchoring on PDPH.
Conservative measures. time, analgesia, hydration, caffeine; evidence is limited, and overstating their efficacy is worth a probe.
Definitive treatment. epidural blood patch, which works by tamponade and by sealing the dural leak.
Risks. repeat dural puncture, back pain, infection, rare neurologic complications.

Session 1 — long stem

Surgical aortic valve replacement for severe aortic stenosis

A 78 y.o., 68 kg, 5'4" woman is scheduled for surgical aortic valve replacement for severe aortic stenosis.

HPIProgressive dyspnea on exertion over the past year, now limited after half a flight of stairs, with one pre-syncopal episode while gardening last month. Occasional exertional chest tightness that resolves with rest.

PMHSevere calcific aortic stenosis. Long-standing hypertension. Paroxysmal atrial fibrillation. Type 2 diabetes. Chronic kidney disease, stage 3.

MEDSApixaban (last dose 36 hours ago), metoprolol, lisinopril (held), amlodipine, atorvastatin, metformin (held).

PHYS EXAMHR 62; BP 160/88; RR 16; SpO2 96% on room air; T 36.7°C. Late-peaking systolic ejection murmur radiating to the carotids; soft, single S2.

ECGSinus rhythm, left ventricular hypertrophy with a strain pattern, first-degree AV block (PR 224 ms), occasional PACs.

ECHOAVA 0.7 cm²; mean gradient 48 mmHg; peak velocity 4.5 m/s. Severe concentric LVH. LVEF 55% with grade II diastolic dysfunction. Mild MR. Estimated PA systolic pressure 44 mmHg.

LABSHgb 11.8 g/dL; platelets 180 K/uL; INR 1.3; K+ 3.4 mEq/L; creatinine 1.6 mg/dL (eGFR 38); glucose 184 mg/dL.

OR ARRIVALAwake radial arterial line placed. Two 18 g peripheral IVs. External defibrillator/pacing pads on. Apixaban held 36 hours; INR 1.3.

A. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Hemodynamic goals and coronary perfusion in severe AS at induction; the cost of losing sinus rhythm in a hypertrophied, stiff ventricle; separating a non-compliant LV from bypass; and managing post-valve conduction block with epicardial pacing.

1. Induction and coronary perfusion

Induction agents and doses? Goals for rate, rhythm, preload, afterload here? Why? Despite a measured induction, BP falls to 78/44 and the inferolateral ST segments depress further. Of concern? Why? Rx? Phenylephrine? Volume? To what end point? Bearing on coronary perfusion? HR drifts to 108. Bearing? Would your approach change if PA pressures rose to 70/40?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Induction goals. maintain preload and afterload, preserve sinus rhythm, avoid tachycardia; a fixed obstruction tolerates neither hypotension nor a fast, poorly filled ventricle. A plan that drops SVR with a generous propofol bolus is worth challenging.
BP falls, ST depresses. subendocardial ischemia of a hypertrophied LV; restore diastolic pressure promptly. Want recognition that this ventricle is supply-dependent, not just a number to chase.
Phenylephrine vs volume. early alpha-agonism restores aortic diastolic pressure and coronary driving pressure; volume helps a preload-dependent stiff LV. Reaching for an inotrope or chronotrope first is a red flag here.
End point. looking for a concrete target (e.g., restore diastolic BP toward baseline), not a vague 'improve the pressure.'
Threat to coronary perfusion. low aortic diastolic pressure against a high LV end-diastolic pressure from LVH and diastolic dysfunction narrows the perfusion gradient; tachycardia shortens diastole further.
HR to 108 / rising PA pressures. tachycardia is doubly harmful (demand up, diastolic filling and perfusion down); rising PA pressure signals the stiff LV is failing to accept volume. Should prompt rate control and reassessment, not more fluid alone.

2. Atrial fibrillation before bypass

Before cannulation she converts to atrial fibrillation at 142 with BP 84/50. Of concern? Why this patient, this lesion? First moves? Rate or rhythm control? Which, and why? Synchronized cardioversion — when, and at what energy? If instead you rate-control pharmacologically — agent? Cost in this ventricle? She remains at 130 and hypotensive. Now what?

Considerations and pitfalls

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Of concern / why here. a hypertrophied, non-compliant LV depends heavily on the atrial contribution to filling; losing it at a fast rate collapses stroke volume and coronary perfusion. Treating this as routine AF is a flag.
First moves. call it early, restore pressure, look for and correct triggers (electrolytes, ischemia, light anesthesia), prepare to cardiovert.
Rate vs rhythm. an unstable, hemodynamically significant rhythm in this lesion favors prompt restoration of sinus rhythm over titrated rate control.
Synchronized cardioversion. indicated when unstable; commit to synchronized shock and a reasonable starting energy rather than hedging.
Pharmacologic agent / cost. rate-controlling agents (beta-blocker, calcium-channel blocker, amiodarone) all carry negative inotropy or vasodilation poorly tolerated here; the hemodynamic cost is the issue, not which drug is named.
Persistent instability. escalate to cardioversion; do not keep titrating drugs into a deteriorating patient.

3. Separation from bypass

AVR complete; attempting to wean from bypass. TEE shows a well-seated valve, no paravalvular leak, but a hypocontractile, underfilled LV. BP 80/45, CI 1.6 on low-dose epinephrine. Of concern? DDx for failure to separate here? Volume? Inotrope — which? Epinephrine, milrinone, or calcium? Why/why not in this ventricle? End point you are titrating to? The RV now looks distended with PA pressures 60/35 — bearing? She still won't wean despite escalating inotropes. IABP — indicated? Why/why not?

Considerations and pitfalls

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DDx for failure to separate. stunned hypertrophied LV, inadequate preload, residual ischemia or air in the grafts/coronaries, RV dysfunction, vasoplegia, valve or surgical problem (TEE helps exclude).
Volume / preload. a stiff, hypertrophied LV is preload-dependent; cautious filling is often needed, but over-distension of a failing ventricle is the opposite trap.
Inotrope choice. epinephrine for contractility, milrinone improves lusitropy and unloads but vasodilates a patient who may already be soft; calcium transiently. Want a defended choice tied to this ventricle, not a list.
End point. a concrete hemodynamic target (CI, perfusion pressure) titrated to, not simply 'more epi.'
RV distension / high PA pressure. evolving RV failure; consider inhaled pulmonary vasodilator, optimize rhythm and preload, avoid acidosis/hypoxia/hypercarbia that raise PVR.
IABP. reduces afterload and augments diastolic coronary perfusion — attractive for LV-predominant low output. But this patient's evolving RV distension and pulmonary hypertension are not addressed by an IABP; a candidate who recognizes the failure is becoming RV-predominant and reaches for an RV strategy (inhaled pulmonary vasodilator, mechanical RV support/ECMO) rather than an IABP is reasoning well. Either commit is defensible if tied to which ventricle is failing.

4. Conduction block and pacing

On separation the rhythm is complete heart block with a junctional escape at 42. Immediate management? Epicardial pacing — which leads, which mode? AV-sequential vs ventricular alone — which, and why? You pace at 90 with good capture, then lose ventricular capture. DDx? Checks? Capture threshold climbs over the next hour — concern? What determines whether she needs a permanent device before discharge?

Considerations and pitfalls

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Immediate management. support rate and pressure, place/confirm epicardial pacing; recognize the valve annulus and prior first-degree block set this patient up for surgical heart block.
Mode — AV-sequential vs ventricular. this hypertrophied, diastolic-dysfunction ventricle depends on the atrial kick; AV-sequential pacing preserves filling that VVI would sacrifice. Settling for ventricular-only pacing here deserves a probe.
Loss of capture / DDx. lead dislodgement or poor contact, rising threshold, generator settings, electrolyte shifts; systematic check of connections, output, sensing.
Rising threshold. edema/ischemia at the lead site; ensure adequate output margin and a reliable backup before relying on the system.
Permanent device. persistence of high-grade block beyond the expected recovery window drives the decision; want judgment about observation versus committing to a permanent pacemaker, not a recited criterion.

B. POST-OPERATIVE CARE

Teaching focus. Distinguishing surgical from medical bleeding after bypass and treating it on a held-anticoagulant background; recognizing tamponade in a postsurgical chest; managing pacing dependence and when to re-anticoagulate; and an embolic deficit after a calcific valve, including honest disclosure.

1. Post-bypass bleeding

First hour in the ICU: chest-tube output 250 mL/hr of bright blood. Of concern? Surgical vs medical bleeding — how do you distinguish? Residual heparin after protamine — how would you know? Which tests guide you? On TEG/ROTEM with fibrinogen 120 and platelets 90, what do you give, and in what order? Bearing of the held apixaban? When does she go back to the OR?

Considerations and pitfalls

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Of concern. rate and character suggest significant ongoing loss; act before she becomes coagulopathic and unstable.
Surgical vs medical. brisk, sustained, bright bleeding with a normalizing coagulation profile points surgical; diffuse oozing with abnormal studies points medical. The distinction drives OR re-exploration vs product correction.
Residual heparin. heparin–protamine mismatch or heparin rebound; assess with ACT/anti-Xa or TEG with heparinase comparison; redose protamine if confirmed.
Targeted products. fibrinogen 120 favors cryoprecipitate/fibrinogen concentrate; platelets 90 with bypass dysfunction favors platelets; correct the specific deficit rather than blind FFP.
Held apixaban. last dosed 36 h ago with eGFR 38 — roughly 2.5–3 half-lives, so residual effect is modest and not the likely driver of brisk surgical bleeding; recognizing that is part of the judgment. It is a factor Xa inhibitor, not reversed by FFP; andexanet alfa or PCC if reversal is truly needed, with awareness that andexanet can complicate heparin anticoagulation around bypass.
Return to OR. persistent high-volume bleeding despite corrected coagulation, tamponade physiology, or instability mandates re-exploration; endless transfusion without surgical control is the trap.

2. Sudden hemodynamic collapse

Three hours later the chest-tube output abruptly drops to near zero. CVP 20, PA 42/24, CI 1.4, BP 86/52, oliguric. DDx? Diagnostic studies — which, and how fast? TEE is equivocal for a discrete effusion in a postsurgical chest — bearing? Your immediate priorities? Is a diuretic indicated for the oliguria? Why/why not? How will you maintain output until the OR? Induction priorities here? Agents?

Considerations and pitfalls

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DDx. tamponade (localized clot) given equalizing pressures and a chest tube that stopped, RV failure, hypovolemia, valve/graft problem, pneumothorax; the stopped tube plus rising filling pressures is the pattern to recognize without being told.
Diagnostics / equivocal TEE. echo is first-line but localized postsurgical clot can be missed; a high index of suspicion and surgical communication outweigh a negative study.
Priorities. maintain preload and rate, support pressure, avoid anything that drops venous return, mobilize surgery for re-exploration.
Diuretic. contraindicated — the oliguria is from low forward flow, not volume overload; diuresing a tamponading patient worsens filling. A reflexive diuretic order is a red flag.
Maintain CO until OR. keep full, fast, and tight: preserve preload and chronotropy, pressor support, possibly open the chest at bedside if arresting.
Induction for re-exploration. preserve preload/afterload/rate, anticipate decompensation on relief of tamponade, surgeon prepped and scrubbed before induction.

3. Pacing dependence and anticoagulation

Overnight she reverts to atrial fibrillation; she remains in complete heart block and pacing-dependent. Bearing of AF under complete block on her filling and your management? How does that change your pacing mode and settings? Anticoagulation — when do you restart it after last night's bleeding? Apixaban, warfarin, or a heparin bridge? Why? Threshold and workup for a permanent pacemaker before discharge? What must you confirm before relying on the system?

Considerations and pitfalls

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AF under complete block. the atrial kick was already lost when she went into AF; this stiff ventricle has no organized atrial filling, so rate, volume, and perfusion pressure carry the output. Want the candidate to recognize the kick is already gone, not 'about to be lost.'
Pacing mode / settings. with fibrillating atria, atrial pacing accomplishes nothing — ventricular (or rate-responsive ventricular) pacing is what she needs; a candidate who keeps her on AV-sequential pacing into AF deserves a probe.
Restart anticoagulation. balance fresh surgical bleeding and the chest tube against AF stroke risk; typically delay full anticoagulation until hemostasis is secure, then resume.
Agent choice. a titratable heparin bridge allows quick reversal if bleeding recurs; apixaban/warfarin once stable. Restarting full-dose anticoagulation the morning after heavy bleeding is worth challenging.
Permanent pacemaker. persistent high-grade block beyond the recovery window; confirm capture thresholds, sensing, and an adequate safety margin before discharge dependence.

4. Delayed awakening

Sedation is off, but at 6 hours she does not follow commands and the right side is weak. DDx? Most concerning here, given the valve she had? Why is this lesion a setup for it? Workup — what, and how urgently? Imaging shows an acute left MCA infarct. Bearing on the anticoagulation decision you just made? Whom do you involve? What can you still offer this patient?

Considerations and pitfalls

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DDx. residual sedation/metabolic causes, embolic stroke, hypoperfusion/watershed injury, seizure, intracranial bleed; a focal deficit shifts suspicion toward a structural cause.
Most concerning / why this lesion. calcific aortic valve surgery and intracardiac air/manipulation embolize debris; a heavily calcified valve and AF make embolic stroke a recognized risk.
Workup urgency. urgent neuro exam and CT/imaging; time-sensitive because it changes both prognosis and the anticoagulation plan.
Bearing on anticoagulation. a fresh large infarct raises hemorrhagic-conversion risk and complicates the AF anticoagulation timing already in tension with surgical bleeding.
Involve / offer. neurology and surgery; supportive neuroprotective ICU care, shared decisions on anticoagulation, honest prognostication.

5. Extubation and disclosure

She is now awake but with a residual right-sided deficit, still intubated, stable on low-dose epinephrine and ventricular pacing. Extubate now? Why/why not? What must be true first? The family arrives and asks why she isn't waking up normally and whether the operation caused it. What will you tell them? How do you coordinate that message with the surgical team? She remains pacing-dependent — what must they understand before discharge planning?

Considerations and pitfalls

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Extubate or not. a residual neurologic deficit raises airway-protection and aspiration concerns; weigh against the harms of prolonged intubation. Either is defensible if the airway and gas exchange are addressed.
Before extubation. adequate mental status to protect the airway, stable hemodynamics off escalating support, gas exchange, reliable pacing.
Telling the family. a plain, honest account of the stroke, that it was recognized, the uncertainty of recovery, without overpromising or assigning blame; room for questions.
Coordinate with surgery. a single, consistent message agreed with the surgical team so the family is not given conflicting accounts.
Pacing dependence. they need to understand the likely permanent pacemaker and what dependence means for monitoring and discharge.

C. ADDITIONAL TOPICS

Teaching focus. Unrelated by design: a regional-anesthesia crisis after an eye block, a pediatric airway emergency on emergence, and an obstetric postdural puncture headache. Rapid pivot across domains.

1. Retrobulbar block complication

A 72 y.o. man undergoing cataract surgery becomes acutely bradycardic, then within minutes confused, dysarthric, and apneic shortly after a retrobulbar block. Possible causes? Most concerning? Mechanism of brainstem anesthesia after a retrobulbar block? Immediate management? How would your differential change if instead he developed sudden proptosis and a tense globe right after the injection? How could the original event have been reduced?

Considerations and pitfalls

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Possible causes. brainstem anesthesia from intrathecal spread, oculocardiac reflex, intravascular local-anesthetic injection, and a primary cardiac or neurologic event.
Most concerning. brainstem anesthesia causing apnea and depressed consciousness, immediately life-threatening.
Mechanism. spread of local anesthetic along the optic nerve sheath into the subarachnoid space, producing central effects including respiratory arrest.
Management. support ventilation, airway, and circulation until the block recedes; usually transient with prompt respiratory support, and failing to ventilate is the danger.
Proptosis / tense globe. suggests retrobulbar hemorrhage with rising orbital pressure threatening the optic nerve — urgent ophthalmology and possible canthotomy rather than central support.
Risk reduction. meticulous technique, appropriate needle choice and depth, aspiration before injection, consideration of less invasive blocks.

2. Laryngospasm on emergence in a child

A 3 y.o. with a runny nose for the past week undergoes bilateral myringotomy under mask anesthesia. During emergence the child develops stridor, then no air movement, and SpO2 falls to 80%. Diagnosis? Contributing factors in this child? Immediate maneuvers and their sequence? SpO2 now 70% with bradycardia to 60 — Rx? If laryngospasm persists, agent and dose? Once recovered, what will you tell the parents about the risk and your decision to proceed?

Considerations and pitfalls

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Diagnosis. laryngospasm — stridor progressing to complete glottic closure, classically on light emergence.
Contributing factors. recent URI, light plane of anesthesia, airway secretions, young age.
Maneuvers and sequence. remove the stimulus, 100% oxygen, jaw thrust with continuous positive airway pressure (Larson maneuver); escalate if it fails.
Bradycardia with desaturation. deepen anesthesia (propofol) or give succinylcholine; treat hypoxic bradycardia and be ready to ventilate or intubate; giving succinylcholine without addressing oxygenation deserves a probe.
Succinylcholine. a small IV dose breaks refractory laryngospasm; IM is an option without IV access; have atropine available in the young child.
Counseling parents. a plain explanation of what happened, that it was recognized and treated, and implications for timing future elective anesthesia after a URI.

3. Postdural puncture headache

A 28 y.o. woman, 24 hours after a labor epidural complicated by a recognized wet tap, has a positional fronto-occipital headache relieved by lying flat. Diagnosis and supporting features? What else must you exclude? Conservative measures? She cannot care for her newborn — definitive treatment and how it works? Risks of that procedure?

Considerations and pitfalls

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Diagnosis. postdural puncture headache — postural, following a known dural puncture.
Must exclude. other serious postpartum headache: preeclampsia, cortical vein thrombosis, meningitis, subdural hematoma.
Conservative measures. time, analgesia, hydration, caffeine; evidence is limited, and overstating efficacy is worth a probe.
Definitive treatment. epidural blood patch — tamponade and sealing of the dural leak.
Risks. repeat dural puncture, back pain, infection, rare neurologic complications.

Session 1 — long stem

Urgent CABG for left main / three-vessel disease with failure to separate from bypass

A 64 y.o., 92 kg, 5'9" man is scheduled for urgent coronary artery bypass grafting for left main plus three-vessel disease.

HPIAdmitted four days ago with an NSTEMI; troponin peaked and has plateaued. Cardiac catheterization showed a 90% left main stenosis with severe disease in the LAD, circumflex, and right coronary arteries. Recurrent rest angina on the floor despite a heparin infusion and nitrates; cardiology and surgery have called the case urgent.

PMHLeft main plus three-vessel coronary artery disease. Recent NSTEMI. Ischemic cardiomyopathy. Insulin-requiring type 2 diabetes. Chronic kidney disease, stage 3.

MEDSAspirin (continued) and ticagrelor (last dose this morning), heparin infusion, metoprolol, atorvastatin, lisinopril (held), insulin glargine and sliding-scale insulin.

PHYS EXAMHR 78; BP 104/68; RR 18; SpO2 95% on 2 L nasal cannula; T 36.6°C. Jugular venous distension to the angle of the jaw, bibasilar crackles, a soft S3, trace pedal edema.

ECGSinus rhythm with deep T-wave inversions and 1–2 mm ST depressions across the anterolateral leads; first-degree AV block (PR 218 ms).

ECHOLVEF approximately 35%. Anterolateral and inferior hypokinesis. Moderate functional mitral regurgitation. Mildly dilated, mildly hypokinetic RV. Estimated PA systolic pressure 48 mmHg. No significant valvular stenosis.

LABSHgb 10.6 g/dL; platelets 165 K/uL; INR 1.2; PTT therapeutic on heparin; K+ 4.1 mEq/L; creatinine 1.7 mg/dL (eGFR 44); glucose 212 mg/dL.

OR ARRIVALAwake radial arterial line placed. Two large-bore peripheral IVs. External defibrillator/pacing pads on. He reports ongoing chest pressure on arrival; the heparin infusion is running and the surgeon is scrubbing.

A. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Protecting a fixed-coronary, poorly compressed circulation through induction and maintaining coronary perfusion pressure; anticoagulating for bypass against heparin resistance; and separating a low-output, ischemic ventricle from CPB with rational inotrope, vasopressor, and mechanical-support choices.

1. Induction in a fixed-coronary circulation

Induction agents and doses for this patient? Goals for rate, rhythm, preload, and afterload at induction? Why? Despite a measured induction, BP falls to 76/42 and the anterolateral ST depressions deepen. Of concern? Why? Rx? Phenylephrine? Volume? To what end point? Bearing on coronary perfusion pressure here? HR climbs to 104 — bearing? Would your approach change if PA pressures rose to 64/34?

Considerations and pitfalls

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Induction goals. maintain diastolic pressure and SVR, preserve sinus rhythm, avoid tachycardia and hypotension; a critical left main lesion makes the whole myocardium supply-dependent. A generous propofol bolus that drops SVR is worth challenging in this patient.
BP falls, ST deepens. worsening subendocardial ischemia in a circulation that cannot recruit collateral flow past a fixed obstruction; restore perfusion pressure immediately rather than chase the number. Want recognition that this is an ischemic emergency, not transient induction hypotension.
Phenylephrine vs volume. alpha-agonism restores aortic diastolic and coronary driving pressure quickly; modest volume helps a soft, preload-dependent ventricle, but a failing LVEF-35 heart tolerates over-filling poorly. Reaching first for an inotrope or chronotrope in active ischemia is a red flag.
End point. looking for a concrete target — restore diastolic/perfusion pressure toward baseline and resolve the ST change — not a vague 'bring the pressure up.'
Coronary perfusion pressure. CPP is aortic diastolic minus LVEDP; hypotension lowers the numerator while an ischemic, failing LV raises filling pressure, narrowing the gradient. The left main means there is no downstream reserve to make up the difference.
HR to 104 / rising PA pressures. tachycardia raises demand and shortens diastolic perfusion time simultaneously — doubly harmful here; rising PA pressure signals the ischemic LV is failing to accept volume. Should drive rate control and reassessment, not more fluid.

2. Anticoagulation for bypass and heparin resistance

Surgeon is ready to cannulate. Goal for ACT before bypass? You give your weight-based heparin dose and the ACT returns 360, short of target and barely changed from a repeat dose. Of concern? Why does this matter before cannulation? DDx for an inadequate ACT response here? Bearing of the heparin infusion he has been on for days? Next steps? How would you correct it — product, and which? Would you proceed onto bypass on an ACT you cannot bring to target? Why/why not?

Considerations and pitfalls

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ACT goal. want a specific target for full CPB anticoagulation (commonly >480 s) rather than a vague 'high enough'; the number protects against clot in the circuit and consumptive coagulopathy.
Of concern / why before cannulation. cannulating and initiating bypass without adequate anticoagulation risks circuit thrombosis, DIC, and a catastrophic clotting event; this must be resolved before going on pump.
DDx for poor ACT response. heparin resistance, most often antithrombin deficiency or depletion from prolonged preoperative heparin exposure; also high factor VIII/fibrinogen states, thrombocytosis, or a lab/technique issue.
Bearing of days of heparin. prolonged heparin infusion depletes antithrombin, the recognized setup for acquired heparin resistance — the candidate should connect his preop course to the blunted response rather than just redose heparin endlessly.
Next steps / antithrombin. additional heparin first, then restore antithrombin — antithrombin concentrate where available, or FFP as a source; recheck ACT to confirm response before committing to bypass.
Proceed on a subtarget ACT. should not initiate CPB until adequate anticoagulation is confirmed; commit to correcting the deficit and re-measuring rather than gambling the circuit. Going on pump on an unexplained low ACT is the trap.

3. Failure to separate from bypass

Grafts complete; attempting to wean from CPB. TEE shows a globally hypokinetic, dilated LV with persistent anterolateral hypokinesis; BP 78/46, cardiac index 1.5 on low-dose epinephrine. Of concern? DDx for failure to separate here? Volume? Inotrope — which? Epinephrine, milrinone, or calcium? Why/why not in this ventricle? End point you are titrating to? The RV now distends with PA pressures 58/32 — bearing? He still won't wean despite escalating inotropes. IABP — indicated? Why/why not, and what does it do for this patient?

Considerations and pitfalls

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DDx for failure to separate. stunned/ischemic LV after recent infarct and cross-clamp, incomplete revascularization or graft problem, residual ischemia or air in a graft, RV dysfunction, vasoplegia, inadequate preload; TEE helps localize.
Volume / preload. a dilated, failing LV needs enough preload to eject but tolerates over-distension poorly; cautious, TEE-guided filling rather than reflexive volume loading.
Inotrope choice. epinephrine for contractility, milrinone improves contractility and lusitropy and unloads the RV but vasodilates a soft patient, calcium transiently; want a defended choice tied to this low-output, post-ischemic ventricle, not a list.
End point. a concrete hemodynamic target — CI and perfusion pressure — titrated to, not simply 'more epinephrine.'
RV distension / high PA pressure. evolving RV failure superimposed on the LV problem; consider inhaled pulmonary vasodilator, optimize rhythm and preload, avoid hypoxia/hypercarbia/acidosis that raise PVR.
IABP. augments diastolic coronary perfusion and reduces LV afterload — well matched to an ischemic, LV-predominant low-output state and a fresh revascularization. But it does little for the failing RV; a candidate who recognizes the picture is becoming RV-predominant and reaches for an RV strategy (inhaled pulmonary vasodilator, RV mechanical support) reasons well. Either commit is defensible if tied to which ventricle is failing. Recall the IABP needs a rhythm to time to and is contraindicated with significant AR or aortic disease.

4. Post-bypass low output and pressor selection

On the IABP at 1:1 with epinephrine and milrinone, CI improves to 2.0 but BP is 82/40 with SVR low. Of concern? DDx for the low SVR here? Vasopressor — norepinephrine, vasopressin, or phenylephrine? Which, and why in this patient? Bearing of an inotrope-driven vasodilation on your choice? End point for perfusion pressure? Methylene blue — when would you consider it? Lactate is rising and urine output is low despite an adequate CI — bearing? Priorities before leaving the OR?

Considerations and pitfalls

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Of concern / low SVR DDx. post-CPB vasoplegia (SIRS from the circuit, prior ACE-inhibitor use, milrinone-driven vasodilation), residual anesthetic, or under-recognized ongoing low output; distinguish a vasodilated adequate-CI state from a still-failing pump.
Vasopressor choice. norepinephrine restores SVR with some inotropy; vasopressin is useful for catecholamine-refractory vasoplegia and spares the pulmonary circulation in RV dysfunction; phenylephrine raises afterload on an already struggling LV. Want a defended choice tied to this physiology.
Inotrope-driven vasodilation. milrinone's vasodilation often demands a concurrent vasoconstrictor to hold perfusion pressure; recognizing that pairing is the judgment being tested.
End point. a concrete MAP/perfusion-pressure target adequate for coronaries, brain, and kidneys in a CKD patient — not just 'a better blood pressure.'
Methylene blue. an option for refractory vasoplegia unresponsive to catecholamines and vasopressin; not a first move, and a candidate who jumps there before standard pressors deserves a probe.
Rising lactate, low UO despite CI 2.0. global or regional malperfusion, ongoing ischemia, or a CI still inadequate for this patient's demand; reassess output, perfusion pressure, and the IABP rather than accept the number. Priorities: secure perfusion pressure, confirm pacing/rhythm, optimize the IABP, and hand off a clear hemodynamic plan.

B. POST-OPERATIVE CARE

Teaching focus. Owning the consequences of the intra-op course: distinguishing surgical from medical bleeding on a recent-ticagrelor background and treating it by targeted product; separating tamponade from RV failure in a postsurgical chest; managing new atrial fibrillation in a pacing-vulnerable, low-output patient; and extubation judgment with an honest family disclosure.

1. Post-bypass bleeding on a DAPT background

First hour in the ICU: chest-tube output 300 mL/hr of bright blood. Of concern? Surgical vs medical bleeding — how do you distinguish? Bearing of his ticagrelor dosed this morning? Residual heparin after protamine — how would you know? TEG/ROTEM — which tracings tell you what here? With R time prolonged, fibrinogen 130, and a low MA despite a platelet count of 110, what do you give, and in what order? Why platelets when the count is 110? When does he go back to the OR?

Considerations and pitfalls

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Of concern. rate and bright character suggest significant ongoing loss; act before he becomes coagulopathic and unstable.
Surgical vs medical. brisk, sustained, bright bleeding with a normalizing coagulation profile points surgical and toward re-exploration; diffuse ooze with abnormal viscoelastic studies points medical and toward targeted products.
Ticagrelor this morning. a potent, recently dosed P2Y12 inhibitor produces a real platelet defect that the count does not capture; this is the likely driver of platelet-type bleeding and argues for platelet transfusion despite an adequate count. Ticagrelor is not dialyzable and is not reversed by stopping it acutely.
Residual heparin. heparin-protamine mismatch or rebound; assess with ACT or a TEG/ROTEM heparinase comparison (CK vs CKH); redose protamine if confirmed.
Targeted products. prolonged R time — factor deficiency — favors FFP or PCC (PCC spares volume in a patient with RV dysfunction); fibrinogen 130 favors cryoprecipitate or fibrinogen concentrate; low MA with a normal count points to the antiplatelet effect and favors platelets. Correct the specific deficit rather than blind product.
Return to OR. persistent high-volume bleeding despite corrected coagulation, tamponade physiology, or instability mandates re-exploration; endless transfusion without surgical control is the trap.

2. Tamponade versus RV failure

Three hours later the chest-tube output abruptly drops to near zero. CVP 22, PA 44/26, CI 1.3, BP 84/50, oliguric. DDx? How do you separate tamponade from RV failure here, and how fast? TEE is equivocal for a discrete effusion in a postsurgical chest — bearing? Your immediate priorities? Is a diuretic indicated for the oliguria? Why/why not? How will you maintain output until the OR? Induction priorities for re-exploration? Agents?

Considerations and pitfalls

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DDx. localized tamponade from clot given the abruptly stopped tube and equalizing filling pressures, versus RV failure (already mildly dysfunctional and recently strained), hypovolemia, graft problem, or pneumothorax; the stopped tube plus rising filling pressures is the pattern to recognize unprompted.
Tamponade vs RV failure. echo and surgical communication, looking for localized compression versus a dilated hypokinetic RV; localized postsurgical clot is easily missed, so a high index of suspicion and willingness to re-explore outweigh an equivocal study.
Equivocal TEE. a negative or equivocal study does not exclude localized clot in a postsurgical chest; do not let it falsely reassure.
Priorities. maintain preload and rate, support perfusion pressure, avoid anything that drops venous return, mobilize surgery for re-exploration.
Diuretic. contraindicated — the oliguria reflects low forward output, not volume overload; diuresing a tamponading or RV-failing patient worsens filling and output. A reflexive diuretic order is a red flag.
Maintain CO / induction. keep full, fast, and tight with pressor and inotrope support; surgeon prepped and scrubbed before induction; anticipate decompensation on relief of tamponade; choose agents that preserve preload/afterload/rate.

3. New atrial fibrillation in a low-output patient

Overnight, hemostasis now secure, he goes into atrial fibrillation at 150 with BP 88/52 and a falling CI. Of concern in this ventricle, this early postop? First moves? Rate or rhythm control — which, and why? Synchronized cardioversion — when, and at what energy? If you rate-control pharmacologically instead — agent, and its cost in this low-EF heart? He stays at 140 and hypotensive — now what? When do you restart anticoagulation given last night's bleeding, and with what?

Considerations and pitfalls

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Of concern / why here. a dilated, low-EF ventricle on inotropes loses the atrial contribution and the diastolic filling time at a fast rate, collapsing an already marginal output; new postop AF is common but is not benign in this patient.
First moves. call it early, restore perfusion pressure, look for and correct triggers (electrolytes, ischemia, light sedation, catecholamine excess, volume), prepare to cardiovert if unstable.
Rate vs rhythm. hemodynamic instability in this physiology favors prompt restoration of sinus rhythm over titrated rate control.
Synchronized cardioversion. indicated when unstable; commit to a synchronized shock and a reasonable starting energy rather than hedging; recall the post-cardiac-surgery thromboembolic considerations.
Pharmacologic agent / cost. beta-blockers and calcium-channel blockers carry negative inotropy poorly tolerated here; amiodarone is often preferred for rate/rhythm control with less hemodynamic penalty but is not free. The cost in a low-EF heart is the issue, not naming the drug.
Restart anticoagulation. balance fresh surgical bleeding against AF stroke risk; typically delay until hemostasis is durably secure, then favor a titratable heparin bridge that can be reversed if bleeding recurs over immediately restarting full oral anticoagulation.

4. Glycemic and renal management

By morning he is stable on a low-dose epinephrine infusion; glucose runs 240–280 on his sliding scale and creatinine has risen to 2.3 with urine output 0.3 mL/kg/hr. Of concern? Target glucose range in this postop cardiac patient, and how do you achieve it? Why does tight control matter here? Bearing of the epinephrine infusion on his glucose? DDx for the rising creatinine? Bearing of the contrast cath, the CPB run, and his pressure history? Nephrotoxins to stop? When would you involve nephrology or consider renal replacement?

Considerations and pitfalls

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Of concern. sustained hyperglycemia and worsening renal function after CPB; both are linked to worse outcomes and demand active management rather than observation.
Glucose target / how. a moderate target (commonly ~140–180 mg/dL) via an insulin infusion with frequent monitoring; avoid both hyperglycemia and hypoglycemia. Want a defended range and a method, not just 'control the sugar.'
Why control matters. hyperglycemia in cardiac surgery is associated with infection, poor wound healing, and worse outcomes; a diabetic on catecholamines needs a deliberate plan.
Epinephrine and glucose. epinephrine drives gluconeogenesis and insulin resistance, raising glucose and complicating control; recognizing the infusion as a contributor is the judgment tested.
Rising creatinine DDx. cardiac-surgery-associated AKI — multifactorial from the contrast load, CPB (nonpulsatile flow, hemolysis, inflammation), perioperative hypotension/low output, and nephrotoxins on a CKD baseline.
Manage AKI. optimize perfusion pressure and cardiac output, stop nephrotoxins, avoid further contrast, dose-adjust drugs; involve nephrology and consider RRT for refractory volume overload, hyperkalemia, or acidosis rather than a fixed creatinine number.

5. Extubation and disclosure

He is now awake and following commands, hemodynamics stable on low-dose epinephrine, but the overnight course included a prolonged low-output period and he remains marginal. Extubate now? Why/why not? What must be true first? The family arrives, anxious, and asks whether the surgery went as planned and why he needed so much support. What will you tell them? How do you coordinate that message with the surgical team? He may need ongoing inotropic support — what must they understand about the days ahead?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Extubate or not. weigh adequate mental status, gas exchange, and hemodynamic stability off escalating support against the harms of prolonged intubation in a marginal, recently low-output patient; either is defensible if airway, oxygenation, and hemodynamics are explicitly addressed.
Before extubation. following commands and protecting the airway, acceptable gas exchange and respiratory mechanics, stable hemodynamics not on escalating support, controlled bleeding, and a stable rhythm.
Telling the family. a plain, honest account that the bypass was completed but the heart was weak afterward and needed medication and support, with realistic uncertainty about the days ahead, without overpromising or assigning blame; room for questions.
Coordinate with surgery. a single, consistent message agreed with the surgical team so the family is not given conflicting accounts of the course.
Days ahead. they need to understand the possibility of continued inotropic support, a slow wean, and the monitoring that implies for ICU course and discharge planning.

C. ADDITIONAL TOPICS

Teaching focus. Unrelated by design: a regional-anesthesia systemic-toxicity crisis after a brachial plexus block, a pediatric airway emergency on emergence, and an obstetric postdural puncture headache. Rapid pivot across domains.

1. LAST after interscalene block

A 60 y.o. woman receives an interscalene block for shoulder surgery. Two minutes after injection she becomes agitated and then has a generalized seizure. Most likely cause? Immediate priorities? She loses her pulse with a wide-complex rhythm. How does management differ from standard ACLS? Principle and role of lipid emulsion? What would have reduced the risk?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Most likely cause. local anesthetic systemic toxicity from intravascular injection or rapid systemic absorption.
Immediate priorities. stop injecting, call for help, secure airway and oxygenation, control the seizure, obtain lipid emulsion.
ACLS modifications. give lipid emulsion, reduce epinephrine dosing relative to standard ACLS, avoid certain antiarrhythmics, anticipate prolonged resuscitation, consider cardiopulmonary bypass for refractory arrest.
Lipid emulsion. bolus followed by infusion per the published protocol; a specific therapy, not an afterthought.
Prevention. incremental injection with aspiration, ultrasound guidance, a test dose, lowest effective dose.

2. Laryngospasm on emergence in a child with recent URI

A 3 y.o. with a runny nose for the past week undergoes bilateral myringotomy under mask anesthesia. During emergence the child develops stridor, then no air movement, and SpO2 falls to 80%. Diagnosis? Contributing factors in this child? Immediate maneuvers and their sequence? SpO2 now 70% with bradycardia to 60 — Rx? If laryngospasm persists, agent and dose? Once recovered, what will you tell the parents about the risk and your decision to proceed?

Considerations and pitfalls

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Diagnosis. laryngospasm — stridor progressing to complete glottic closure, classically on light emergence.
Contributing factors. recent URI, light plane of anesthesia, airway secretions, young age.
Maneuvers and sequence. remove the stimulus, 100% oxygen, jaw thrust with continuous positive airway pressure (Larson maneuver); escalate if it fails.
Bradycardia with desaturation. deepen anesthesia (propofol) or give succinylcholine; treat hypoxic bradycardia and be ready to ventilate or intubate; an answer that gives succinylcholine without addressing oxygenation deserves a probe.
Succinylcholine. a small IV dose breaks refractory laryngospasm; IM is an option without IV access; have atropine available in the young child.
Counseling parents. a plain explanation of what happened, that it was recognized and treated, and the implications for timing future elective anesthesia after a URI.

3. Postdural puncture headache

A 28 y.o. woman, 24 hours after a labor epidural complicated by a recognized wet tap, has a positional fronto-occipital headache that is relieved by lying flat. Diagnosis and supporting features? What else must you exclude? Conservative measures? She cannot care for her newborn — definitive treatment and how it works? Risks of that procedure?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Diagnosis. postdural puncture headache — postural, following a known dural puncture.
Must exclude. other serious causes of postpartum headache (preeclampsia, cortical vein thrombosis, meningitis, subdural hematoma) before anchoring on PDPH.
Conservative measures. time, analgesia, hydration, caffeine; evidence is limited, and overstating their efficacy is worth a probe.
Definitive treatment. epidural blood patch, which works by tamponade and by sealing the dural leak.
Risks. repeat dural puncture, back pain, infection, rare neurologic complications.

Session 1 — long stem

Cardiogenic shock and mechanical circulatory support after a large anterior MI

A 64 y.o., 88 kg, 5'9" man with ischemic cardiomyopathy is in the cardiac ICU in decompensated cardiogenic shock after a large anterior MI, and the team is deciding on and placing mechanical circulatory support.

HPIAnterolateral STEMI five days ago, late-presenting, with a culprit proximal LAD lesion stented but a large infarct territory. Progressive low-output failure since, now cool and mottled with worsening confusion over the last several hours. Urine output has fallen to 10 mL/hr.

PMHIschemic cardiomyopathy with prior MIs. Hypertension. Type 2 diabetes. Prior tobacco use with claudication on long walks. No prior valve surgery.

MEDSNorepinephrine 0.3 mcg/kg/min, epinephrine 0.1 mcg/kg/min, dobutamine 5 mcg/kg/min, all escalating over the last 12 hours. Aspirin and ticagrelor (post-stent). Heparin infusion.

PHYS EXAMHR 118; BP 78/58 (MAP 64) on the above support; RR 26; SpO2 92% on high-flow nasal cannula; T 35.9°C. Cool extremities, faint pedal pulses bilaterally, rising lactate. Soft S3, no diastolic murmur.

ECGSinus tachycardia, anterior Q waves with persistent ST elevation, frequent PVCs and short runs of nonsustained VT.

ECHOLVEF ~15%, akinetic anteroapical wall, severely dilated LV. No LV thrombus seen. Trileaflet aortic valve, no significant AS or AR. Moderately depressed RV function. Estimated PA systolic pressure 52 mmHg. No pericardial effusion.

LABSHgb 9.6 g/dL; platelets 140 K/uL; INR 1.4; lactate 6.2 mmol/L; creatinine 2.1 mg/dL; AST and ALT rising; ABG 7.28 / 32 / 78 on high-flow.

CURRENT STATEFemoral access obtained. The interventional and surgical teams are at bedside debating device selection; pressor and inotrope requirements continue to climb and lactate is not clearing.

A. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Device selection under shock for a failing LV and the contraindications that actually decide it; hemodynamic support around cannulation in a patient with no reserve; the afterload and venting consequences once VA-ECMO is running; and differential hypoxia when native lung disease meets retrograde ECMO flow.

1. Device selection under shock

The team is choosing among IABP, Impella, and VA-ECMO for this patient. What does each do for this particular ventricle? Which do you favor here? Why? What in his echo and exam decides it? If the echo had read moderate AR instead — bearing on each option? If the aortic valve had been mechanical? If the echo had shown an LV thrombus? His access risk — bearing on device and approach? Commit to a device and defend it against the next-best option.

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

What each does for THIS LV. IABP modestly augments coronary perfusion and unloads afterload (~20% CO bump) but does little for a near-akinetic LV in profound shock; Impella actively pumps LV to aorta, generating flow and venting the LV; VA-ECMO replaces both heart and lung output but does not unload the LV and adds afterload. The candidate should match output need to device, not recite a list.
Which here / why. with EF ~15%, rising lactate, and failing perfusion on escalating triple support, a modest IABP is likely inadequate; an Impella or VA-ECMO is the real debate. RV dysfunction and a falling SpO2 push toward ECMO; isolated LV failure with adequate oxygenation favors Impella. Want the choice tied to which ventricle is failing and whether oxygenation is threatened.
AR contraindication. moderate-or-worse AR is a contraindication to both IABP (worsens LV distension on inflation) and Impella/VA-ECMO (regurgitant flow distends the LV); recognizing AR reshapes the whole decision is the point.
Mechanical AVR / LV thrombus. a mechanical aortic valve precludes crossing it with an Impella and raises clotting risk on ECMO; an LV thrombus contraindicates the Impella (risk of embolizing or ingesting clot). These are the device-deciding findings, not trivia — the candidate should know why each forecloses an option.
PAD / access. faint pulses and claudication signal peripheral vascular disease — limb-ischemia and access-failure risk for any large femoral cannula; may favor a smaller device, alternative access, or upfront distal perfusion planning. A candidate who ignores the legs deserves a probe.
Commit. looking for a defended commitment to one device tied to this patient's physiology and contraindications, not a hedge across all three.

2. Induction and support around cannulation

He needs sedation and airway control for cannulation and has essentially no reserve. Induction agents and doses? Goals here? Why? Hemodynamic support you have ready before you push anything? On induction BP falls to 60/40 and the rhythm degenerates toward VT. Rx? Vasopressor? Which, and to what end point? Would you proceed to cannulation during the instability or pause? He arrests on the table before the device is running. Now what? How does an imminent device change your resuscitation?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Induction goals / agents. preserve preload, afterload, contractility, and rate in a patient with no reserve; a careful, low-dose, hemodynamically neutral induction (e.g., etomidate or ketamine with minimal opioid) over a propofol bolus that will drop SVR and cause arrest. Naming a generous propofol induction here is a red flag.
Support ready first. pressors/inotropes already running and titratable, push-dose vasopressor drawn up, pads on, surgical and perfusion teams prepped to cannulate emergently; do not induce a shock patient without rescue in hand.
Hypotension / VT on induction. restore perfusion pressure promptly with vasopressor, treat the rhythm, and recognize the induction itself unmasked the lack of reserve. Want a concrete pressor choice and end point (restore MAP toward baseline), not a vague 'support the pressure.'
Proceed vs pause. the device is the definitive treatment for the shock; expediting cannulation may be the resuscitation rather than a reason to delay — judgment about pressing forward versus stabilizing first is the test.
Arrest before device running. ACLS with high-quality compressions, but the failing pump is the problem the device fixes — emergent cannulation onto VA-ECMO during CPR (ECPR) is the escalation; chest compressions over a femoral Impella also have specific concerns. Want recognition that the device is the exit from the arrest.
Mechanism of the collapse. fixed low-output state plus anesthetic vasodilation and loss of sympathetic tone; reasoning about why THIS patient crashed on induction, not a generic answer.

3. LV distension on VA-ECMO and venting

He is now on peripheral VA-ECMO at full flow with a MAP of 70. Within an hour the arterial waveform flattens, PA diastolic and LA pressures climb, and the chest film shows new pulmonary edema. Of concern? Why is this happening on ECMO? Mechanism? Bearing of his aortic valve barely opening? Immediate moves? Reduce flow, add inotrope, vent the LV — which, and why? If you vent, how? IABP, Impella, or surgical vent — trade-offs here? He has frequent VT — bearing on LV filling and your venting decision?

Considerations and pitfalls

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Of concern / why on ECMO. retrograde ECMO flow raises aortic root afterload; a near-akinetic LV cannot eject against it, so the LV distends — rising LVEDP and LA pressure back up into the lungs. The candidate should recognize ECMO is not resting this LV, it is loading it.
Mechanism / flat waveform. loss of pulsatility means the aortic valve is failing to open against the ECMO afterload; LVOT/LV stasis risks thrombus (worse with any valve), and rising LA pressure drives pulmonary edema. Flat arterial line is the tell, not a number to chase.
Immediate moves. do not simply crank flow; options are reducing ECMO flow to allow ejection, adding an inotrope to help the LV eject, and actively venting the LV. Want these tied to relieving distension, not a list.
How to vent. Impella (ECpella) actively unloads the LV; IABP is a weak vent; surgical/apical or pulmonary-vein vent is most definitive. Inotropes alone partially help but defeat 'resting' the heart — which is why inotropes are often kept on. A defended choice tied to severity is the target.
Aortic valve barely opening. an unopening valve plus stasis is a clot setup even when heparinized; this urgency drives the venting decision and is what the flat waveform is warning about.
VT and filling. VT compromises organized LV filling and ejection, worsens stasis and distension, and argues for rhythm control and active venting rather than tolerating it on support.

4. Differential hypoxia on VA-ECMO

His native lungs are now wet and his heart begins to recover some ejection. The right radial ABG returns PaO2 of 55 while the femoral arterial PaO2 is over 300. Of concern? What is this telling you about where his blood is coming from? Mechanism? Which territory is at risk? How do you confirm it? How would you fix it? Optimize the vent, move the return, go to VAV — trade-offs of each? End point you are aiming for in the upper-body oxygenation? If instead BOTH sites read low, bearing?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Of concern / interpretation. a low right-radial PaO2 with a high femoral PaO2 is differential hypoxia (Harlequin / north-south): the recovering LV is ejecting poorly oxygenated blood from diseased lungs up the innominate to the brain and coronaries, while retrograde ECMO blood perfuses the lower body. The candidate should read the split sampling, not be told the diagnosis.
Mechanism / mixing cloud. as native ejection recovers, the mixing cloud moves distal in the arch; if the lungs cannot oxygenate the LV output, the head and right arm see hypoxemic blood. Right-radial sampling exists precisely to catch this.
Territory at risk. cerebral and coronary perfusion via the innominate/aortic root — the highest-stakes territory — which is what makes upper-body hypoxia urgent.
Confirm. compare right-radial (preductal-equivalent) to femoral PaO2; pulse ox differential between right hand and lower body supports it.
Fix / trade-offs. optimize the ventilator (raise FiO2, PEEP, recruit) to oxygenate native ejection; if lungs are too damaged, convert to VAV-ECMO to deliver oxygenated blood to the RA and through the lungs. VAV shares total flow, reducing arterial flow. Want a defended escalation, not just 'increase the FiO2.'
Both sites low. global oxygenation failure (oxygenator problem, recirculation, or inadequate sweep/FdO2) rather than differential hypoxia — a different fix; recognizing the distinction is the judgment.

B. POST-OPERATIVE CARE

Teaching focus. The ICU course on support: anticoagulation and bleeding while the device runs, recognizing and acting on a suction event and hemolysis, managing limb ischemia from the cannula, the weaning-versus-escalation decision, and an honest family conversation about bridge-to-what.

1. Anticoagulation and bleeding on support

He is on the device with a heparin infusion and remains on aspirin and ticagrelor from his stent. Overnight he oozes from the cannula site and the access wound, Hgb drifting down. Of concern? How do you balance device thrombosis against bleeding here? What guides your anticoagulation target on this device? Tests? You suspect HITT — bearing, and what now? Bearing of the recent stent on whether you can simply stop his antiplatelets? When do you transfuse, and to what? When does the bleeding force a change in support strategy?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Of concern. ongoing blood loss in an already anemic shock patient who must stay anticoagulated to keep the circuit and device from clotting; act before he becomes unstable or the device thromboses.
Balance thrombosis vs bleeding. the foreign surface and (for Impella) the purge demand anticoagulation; bleeding pushes to lower it. The judgment is titrating to a target rather than swinging between full anticoagulation and none. Recognizing both failure modes is the point.
Target / tests. device-specific anticoagulation (ECMO typically PTT-guided, lower ACT than CPB; Impella runs a heparinized purge that contributes systemic heparin); monitor PTT/anti-Xa, ACT, fibrinogen, platelets, and hemolytic indices. A candidate who targets CPB-level ACT is off.
HITT. suspected HITT forces stopping heparin and switching to a non-heparin agent (e.g., bivalirudin) and, for an Impella, a bicarbonate-based purge instead of heparin; missing this is a real harm.
Recent stent / antiplatelets. a fresh proximal-LAD stent on dual antiplatelet therapy makes simply stopping antiplatelets a stent-thrombosis risk — the bleeding-versus-stent tension is the judgment, not a reflex to hold everything.
Transfuse / change strategy. transfuse to a sensible threshold for an actively bleeding, ischemic patient; persistent uncontrolled bleeding may force reducing anticoagulation, surgical control, or reconsidering the device. Endless transfusion without addressing the source is the trap.

2. Suction event and hemolysis

On an Impella the console alarms with a drop in flow and the placement signal looks wrong; the same shift his plasma turns pink and LDH climbs. DDx for the flow drop? Suction event — why does it happen in this patient? Before you bolus volume, what do you check? Echo, pulsatility, device position — in what order? How do you fix a suction event? Now the hemolysis — possible causes on this device? Mechanism? What confirms it, and what do you do? If reducing speed fixes the suction but his output falls, now what?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

DDx for flow drop. suction event from device malposition or inadequate LV preload, RV failure starving the LV, pump thrombosis, or changing LV geometry; the alarm plus a wrong-looking placement signal points to position/preload before reflexive volume.
Why suction here. a small, underfilled, or RV-compromised LV lets the inlet draw against the wall; in this patient RV dysfunction and hypovolemia are live drivers. Recognizing the cause sets the fix.
Check before bolusing. assess arterial pulsatility, get echo (TTE/TEE) for device position and LV filling, and consider reducing speed to let the LV fill — do not blindly bolus a heart-failure patient. The order matters.
Fix suction. reposition under imaging if malpositioned, reduce P-level to bring the wall off the inlet, and give volume only for confirmed preload deficit or incessant suction.
Hemolysis cause/mechanism. turbulent high-speed flow and shear, inlet/outlet near LV wall or valve apparatus, or pump thrombosis chewing RBCs; high P-levels and held anticoagulation predispose. Reasoning about this device and this event, not a definition.
Confirm / act. trend LDH, bilirubin, free Hgb, haptoglobin; check anticoagulation; reposition or reduce speed, and consider reimplantation if thrombosis. If lowering speed costs output, escalate support (add inotrope, reconsider ECMO) rather than accept inadequate flow.

3. Limb ischemia from the cannula

The cannulated leg is now cool, mottled, and pulseless distal to the access. Of concern? Why is this patient set up for it? How do you confirm? Immediate priorities? Distal perfusion cannula — place it now? Why/why not? He develops a tense, painful calf — bearing, and what now? If the limb is unsalvageable against his overall trajectory, how does that weigh on continuing this support? What surveillance prevents the next one?

Considerations and pitfalls

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Of concern / setup. a large arterial femoral cannula can obstruct distal flow; his baseline PAD and claudication make limb ischemia especially likely. Recognizing the predisposing vasculature is part of the judgment.
Confirm. exam (pulses, color, temperature, cap refill), Doppler/NIRS on the limb, compare to the contralateral leg; act on a clear deficit rather than waiting.
Immediate priorities / distal perfusion. restore distal flow — place or confirm a distal perfusion cannula, involve vascular surgery; a distal perfusion catheter is the standard mitigation and is often placed at cannulation. A candidate who just watches it is off.
Compartment syndrome. a tense, painful calf signals reperfusion/compartment syndrome — urgent surgical evaluation for fasciotomy; this is a limb- and life-threatening escalation.
Bearing on support. an unsalvageable limb against a poor overall trajectory becomes part of the goals-of-care and bridge-to-what calculus, not an isolated decision; want integration, not tunnel vision.
Surveillance. scheduled limb perfusion checks (exam, Doppler, NIRS) and early distal perfusion are how the next ischemic limb is prevented.

4. Weaning versus escalation

Over two days his lactate clears and pressors come down; the team raises weaning the device. What tells you he is ready to wean? Echo, pulsatility, filling pressures, inotrope need — what are you watching, and which way is reassuring? How do you actually wean this device? He tolerates a flow reduction poorly — ejection drops and lactate ticks up. Now what? If he simply will not recover function, what are the options? Bridge to LVAD or transplant — what makes him a candidate or not here? Bearing of his renal function on that?

Considerations and pitfalls

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Readiness to wean. improving/sustained LV function on echo, rising arterial pulsatility, stable or falling filling pressures, and falling vasopressor/inotrope need; worsening function or rapidly rising filling pressures as flow comes down means not ready.
How to wean. stepwise reduction of support (ECMO flow or Impella P-level) over hours to days with echo and hemodynamics at each step, full anticoagulation maintained during ramp-down to prevent thrombus; plan decannulation only after a low-support trial is tolerated.
Fails the wean. do not force it — return to fuller support and treat the underlying failure; a failed wean is information, not a reason to push to decannulation. Want recognition that the heart isn't ready.
Won't recover. the honest fork is bridge to durable LVAD, bridge to transplant, or withdrawal — 'LVAD vs OHT vs comfort care' — depending on candidacy. The candidate should name that this is now the decision.
Candidacy. irreversibility, end-organ recovery, frailty, and comorbidity drive durable-support/transplant candidacy; his renal dysfunction, if it persists, threatens transplant/VAD eligibility and reframes whether support is bridging to something. Want this weighed, not skipped.
Integration. the weaning decision is inseparable from the bridge-to-what question and from the family conversation that follows.

5. Family conversation and bridge to what

His function has not recovered, his kidneys are failing, and he is not a transplant or durable-LVAD candidate. The family arrives and asks whether the device will get him better and what happens next. What will you tell them? How do you frame what the device is and is not doing for him? How do you coordinate that message with the cardiac surgery and heart-failure teams? They ask whether you can 'just keep the machine going' — how do you respond? What decisions do you put before them now?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

What to tell them. a plain, honest account: the device is supporting his circulation but his heart has not recovered and he is not a candidate for the next step (transplant/durable LVAD); avoid false reassurance and avoid foreclosing too bluntly. Room for questions.
Frame the device. it is a bridge, and the bridge needs a destination; without recovery or candidacy for durable support, it is sustaining him without a path forward. Honest framing of bridge-to-what is the skill being tested.
Coordinate the message. a single consistent message agreed with cardiac surgery and heart-failure/transplant so the family is not given conflicting accounts; conflicting stories from teams is a real harm.
'Keep the machine going'. acknowledge the wish, explain the burdens and limits of indefinite support without a destination, and move toward goals of care rather than reflexively continuing or stopping. Tests communication and limits, not a script.
Decisions before them. shared goals-of-care decision about continued support versus transition to comfort, given no recovery and no bridge target; the candidate should name this clearly and humanely.

C. ADDITIONAL TOPICS

Teaching focus. Unrelated by design: a regional-anesthesia crisis after an eye block, a pediatric airway emergency on emergence, and an obstetric postdural puncture headache. Rapid pivot across domains.

1. Retrobulbar block complication

A 72 y.o. man undergoing cataract surgery becomes acutely bradycardic, then within minutes confused, dysarthric, and apneic shortly after a retrobulbar block. Possible causes? Most concerning? Mechanism of brainstem anesthesia after a retrobulbar block? Immediate management? How would your differential change if instead he developed sudden proptosis and a tense globe right after the injection? How could the original event have been reduced?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Possible causes. brainstem anesthesia from intrathecal spread of local anesthetic, oculocardiac reflex, intravascular local-anesthetic injection, and a primary cardiac or neurologic event.
Most concerning. brainstem anesthesia causing apnea and depressed consciousness, which is immediately life-threatening.
Mechanism. spread of local anesthetic along the optic nerve sheath into the subarachnoid space, producing central effects including respiratory arrest.
Management. support ventilation and the airway and circulation until the block recedes; the event is usually transient with prompt respiratory support, and failing to ventilate is the danger.
Proptosis and tense globe. that picture suggests retrobulbar hemorrhage with rising orbital pressure threatening the optic nerve, prompting urgent ophthalmology assessment and possible canthotomy rather than central support.
Risk reduction. meticulous technique with appropriate needle choice and depth, aspiration before injection, and consideration of less invasive blocks; relying on technique alone without monitoring is worth a probe.

2. Postdural puncture headache

A 28 y.o. woman, 24 hours after a labor epidural complicated by a recognized wet tap, has a positional fronto-occipital headache that is relieved by lying flat. Diagnosis and supporting features? What else must you exclude? Conservative measures? She cannot care for her newborn — definitive treatment and how it works? Risks of that procedure?

Considerations and pitfalls

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Diagnosis. postdural puncture headache — postural, following a known dural puncture.
Must exclude. other serious causes of postpartum headache (preeclampsia, cortical vein thrombosis, meningitis, subdural hematoma) before anchoring on PDPH.
Conservative measures. time, analgesia, hydration, caffeine; evidence is limited, and overstating their efficacy is worth a probe.
Definitive treatment. epidural blood patch, which works by tamponade and by sealing the dural leak.
Risks. repeat dural puncture, back pain, infection, rare neurologic complications.

3. Laryngospasm on emergence in a child

A 3 y.o. with a runny nose for the past week undergoes bilateral myringotomy under mask anesthesia. During emergence the child develops stridor, then no air movement, and SpO2 falls to 80%. Diagnosis? Contributing factors in this child? Immediate maneuvers and their sequence? SpO2 now 70% with bradycardia to 60 — Rx? If laryngospasm persists, agent and dose? Once recovered, what will you tell the parents about the risk and your decision to proceed?

Considerations and pitfalls

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Diagnosis. laryngospasm — stridor progressing to complete glottic closure, classically on light emergence.
Contributing factors. recent URI, light plane of anesthesia, airway secretions, young age.
Maneuvers and sequence. remove the stimulus, 100% oxygen, jaw thrust with continuous positive airway pressure (Larson maneuver); escalate if it fails.
Bradycardia with desaturation. deepen anesthesia (propofol) or give succinylcholine; treat hypoxic bradycardia and be ready to ventilate or intubate; an answer that gives succinylcholine without addressing oxygenation deserves a probe.
Succinylcholine. a small IV dose breaks refractory laryngospasm; IM is an option without IV access; have atropine available in the young child.
Counseling parents. a plain explanation of what happened, that it was recognized and treated, and the implications for timing future elective anesthesia after a URI.

Session 1 — long stem

Mitral valve repair for severe degenerative mitral regurgitation

A 64 y.o., 82 kg, 5'10" man is scheduled for mitral valve repair for severe degenerative mitral regurgitation.

HPIProgressive dyspnea on exertion over the past eight months, now breathless climbing one flight, with two episodes of paroxysmal nocturnal dyspnea this month. Reduced exercise tolerance and fatigue; no chest pain. Referred after a murmur was worked up.

PMHSevere primary mitral regurgitation from a flail posterior leaflet with ruptured chordae. Hypertension. Hyperlipidemia. Remote tobacco use. No prior cardiac surgery.

MEDSLisinopril (held morning of surgery), metoprolol, furosemide, atorvastatin, aspirin (continued).

PHYS EXAMHR 78; BP 134/72; RR 18; SpO2 95% on room air; T 36.6°C. Laterally displaced apex; holosystolic murmur at the apex radiating to the axilla; bibasilar crackles; trace pedal edema.

ECGSinus rhythm at 80, left atrial enlargement, left axis deviation, occasional PACs, no acute ST changes.

ECHOFlail posterior mitral leaflet with an eccentric anteriorly directed regurgitant jet; severe MR by quantitative criteria. LV dilated, LVEDD 64 mm, LVESD 44 mm; LVEF 56%. Dilated left atrium. Estimated PA systolic pressure 52 mmHg; mildly dilated RV with preserved function.

LABSHgb 13.9 g/dL; platelets 205 K/uL; INR 1.0; K+ 4.0 mEq/L; creatinine 1.1 mg/dL; BNP elevated; type and screen sent.

OR ARRIVALAwake radial arterial line placed; large-bore peripheral access; pulmonary artery catheter and TEE planned. External pads on. Patient anxious but cooperative.

A. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Hemodynamic goals in severe regurgitation — forward versus regurgitant fraction, and why bradycardia and high afterload are the enemy; a measured induction that protects forward flow; the masked true ventricle revealed once the low-impedance leak is repaired; and the counterintuitive recognition and management of systolic anterior motion after repair.

1. Induction and hemodynamic goals

Induction agents and doses? Goals for rate, rhythm, preload, afterload here? Why? Rate target — to what end, and why not slower? After induction BP falls to 82/40 and the PA pressures climb. Of concern? Rx? Phenylephrine? Volume? Ephedrine? Which, and why? Bearing on forward versus regurgitant fraction? HR drifts to 52. Bearing here? Would your approach change if the patient were instead tachycardic at 120?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Induction goals. maintain preload, keep the rate normal-to-slightly-fast, and keep afterload low to favor forward flow over the regurgitant jet; avoid myocardial depression. A plan that lets the heart slow or drives up SVR is the wrong direction and worth challenging.
Rate target / why not slower. a slower rate prolongs diastole and the regurgitant filling time and lets the dilated ventricle distend; want recognition that bradycardia worsens the regurgitant fraction, not a generic 'keep it stable.'
BP falls, PA pressures climb. falling forward output with rising pulmonary pressures; restore perfusion without clamping down SVR and worsening the leak. Recognition that pure alpha-agonism is double-edged here is the point.
Phenylephrine vs volume vs ephedrine. pure phenylephrine raises afterload and can increase the regurgitant fraction; a small dose may be needed for coronary perfusion but ephedrine or a touch of inotropy/chronotropy that supports forward flow is often better-suited. Reaching reflexively for phenylephrine alone deserves a probe.
Forward vs regurgitant fraction. the EF overstates true forward performance because a large fraction ejects backward into a low-pressure atrium; lowering afterload and keeping the rate up shift the balance forward.
HR to 52. bradycardia is harmful — it lengthens diastole, distends the LV, and increases regurgitant volume; should prompt chronotropy, not tolerance. Tachycardia at 120 is comparatively better tolerated in this lesion, which is the teaching contrast.

2. Pulmonary hypertension and PA catheter

On floating the PA catheter, PA pressures are 58/30 with a large v wave on the wedge tracing. Bearing of the v wave here? After sternotomy and before bypass, PA pressures rise further to 70/38 with falling systemic pressure. Of concern? Why this ventricle, this circulation? First moves? Goals for PVR — how do you lower it? Ventilation? Agents? An inhaled pulmonary vasodilator — when, and to what end point? If the RV begins to distend on TEE, bearing? Now what?

Considerations and pitfalls

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Large v wave. reflects the regurgitant volume filling a left atrium against which the wedge is read; recognition that the v wave tracks the leak rather than simple volume overload is the point. Want the candidate to read it as a marker of regurgitant severity, not just a number.
Rising PA pressure / of concern. the volume-loaded left heart and chronic regurgitation have produced pulmonary hypertension; acute rises threaten the RV and forward flow. Treating this as benign is a flag.
First moves / PVR goals. avoid hypoxia, hypercarbia, acidosis, and high airway pressures that raise PVR; optimize oxygenation and depth, correct anything driving the rise.
Inhaled pulmonary vasodilator. inhaled nitric oxide or inhaled prostacyclin selectively lowers PVR without dropping systemic pressure; commit to an agent and a hemodynamic end point rather than naming a list.
RV distension. evolving RV strain or failure from the pulmonary hypertension; support RV preload judiciously, maintain coronary perfusion pressure to the RV, lower PVR, consider inotropy. Over-filling a distending RV is the opposite trap.
Now what. escalate pulmonary vasodilation and RV support, communicate with the surgeon about going on bypass; do not keep volume-loading a failing RV.

3. Separation from bypass and the unmasked ventricle

Repair complete with an annuloplasty ring; TEE shows no residual MR. Attempting to wean, the LV is hypocontractile and dilated, BP 84/46, CI 1.7 on low-dose epinephrine. Of concern? Why might the ventricle look worse now than before repair? DDx for failure to separate here? Volume? Inotrope — epinephrine, milrinone, or both? Why/why not in this ventricle? End point you are titrating to? The lateral wall now looks hypokinetic on TEE — bearing, and what must be excluded? He still won't wean despite escalating support. Next step?

Considerations and pitfalls

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Why worse after repair. the regurgitation was a pop-off into a low-pressure atrium; closing it removes the low-impedance escape and now the true, often depressed, contractile state of a chronically volume-overloaded LV is unmasked against full afterload. Want explicit recognition that the EF flattered the ventricle before repair.
DDx for failure to separate. unmasked LV dysfunction, inadequate preload, residual ischemia or air, RV dysfunction from the pulmonary hypertension, vasoplegia, or a surgical/valve problem (TEE helps exclude).
Inotrope choice. epinephrine for contractility; milrinone improves lusitropy and unloads but vasodilates an already-soft patient; a combined, defended strategy tied to this unmasked ventricle beats reciting a list.
End point. a concrete hemodynamic target — CI and perfusion pressure — titrated to, not simply 'more epi.'
Lateral-wall hypokinesis. post-repair the circumflex runs near the mitral annulus and ring sutures can kink or occlude it; new lateral hypokinesis must raise circumflex compromise, communicated to the surgeon, not attributed to stunning alone.
Persistent failure. escalate inotropy and address the specific cause; consider mechanical support (IABP or VA-ECMO) and return-to-bypass with the surgeon rather than titrating endlessly into a deteriorating patient.

4. Systolic anterior motion after repair

Off bypass, the patient becomes acutely hypotensive at 70/40; TEE now shows turbulent flow in the LVOT and the anterior mitral leaflet drawn toward the septum during systole, with new MR. Of concern? Mechanism here? Rx? Inotrope and vasodilator running — keep them? Volume? Afterload — raise or lower? Rate — faster or slower? Why does each move help or hurt? It persists despite medical measures — what does that tell the surgeon, and what is the next step?

Considerations and pitfalls

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Mechanism. systolic anterior motion of the anterior leaflet with dynamic LVOT obstruction — an underfilled, hypercontractile, vasodilated ventricle with a small cavity draws the leaflet into the outflow tract, classically after annuloplasty. Want the candidate to name the obstruction, not chase the low pressure with more inotrope.
The wrong instinct. the reflex to treat hypotension with inotropes, vasodilators, and the head-down empty ventricle makes SAM worse; recognizing that the usual moves are exactly backward is the heart of this probe.
Stop inotrope / vasodilator. discontinue inotropes and vasodilators — both worsen dynamic obstruction by emptying and overdriving the ventricle.
Volume and afterload. give volume to fill and enlarge the cavity, and raise afterload with an alpha-agonist (phenylephrine) to open the outflow tract — the opposite of standard MR management and the counterintuitive crux.
Rate. slow the heart to lengthen diastolic filling and reduce contractility; a beta-blocker may be appropriate once volume and afterload are addressed.
Persistent SAM. failure of medical management raises a structural cause and the question of surgical revision of the repair; communicate to the surgeon that this is not simple low output.

B. POST-OPERATIVE CARE

Teaching focus. Owning the consequences of the case in the ICU: distinguishing surgical from medical bleeding after bypass; recognizing right-heart failure from persistent pulmonary hypertension; managing new post-operative atrial fibrillation in a fresh repair; an embolic deficit and its bearing on anticoagulation; and honest disclosure to the family.

1. Post-bypass bleeding

First hour in the ICU: chest-tube output 300 mL/hr of bright blood. Of concern? Surgical versus medical bleeding — how do you distinguish? Residual heparin after protamine — how would you know? Which tests guide you? On TEG/ROTEM with fibrinogen 110 and platelets 95, what do you give, and in what order? Bearing of the aspirin he continued to surgery? When does he go back to the OR?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Of concern. the rate and bright character suggest significant ongoing loss; act before he becomes coagulopathic and unstable.
Surgical vs medical. brisk, sustained, bright bleeding with a normalizing coagulation profile points surgical; diffuse oozing with abnormal studies points medical — the distinction drives re-exploration versus product correction.
Residual heparin. heparin–protamine mismatch or heparin rebound; assess with ACT or a heparinase TEG comparison; redose protamine if confirmed.
Targeted products. fibrinogen 110 favors cryoprecipitate/fibrinogen concentrate; platelets 95 with bypass platelet dysfunction favors platelets; correct the specific deficit rather than reflexive FFP.
Continued aspirin. platelet inhibition from aspirin contributes to a qualitative platelet defect after bypass and lowers the threshold to transfuse platelets; recognizing it as a real but modifiable contributor is the judgment, not a reason to withhold surgical control.
Return to OR. persistent high-volume bleeding despite corrected coagulation, tamponade physiology, or instability mandates re-exploration; endless transfusion without surgical control is the trap.

2. Right-heart failure

Overnight, CVP climbs to 18 while the wedge stays low; CI 1.6, BP 88/54, rising lactate and oliguria, PA pressures 64/34. DDx? Why does this patient's physiology point one way? TEE shows a dilated, poorly contractile RV and a small underfilled LV — bearing? Your priorities? Volume — give or withhold? Why? Inotrope and pulmonary vasodilator — which, and to what end point? Ventilator settings here — what do you avoid and why? He is not improving — next escalation?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

DDx / why this patient. the chronic pulmonary hypertension and an RV that was already mildly dilated set him up for post-operative RV failure; high CVP with a low wedge and a distended RV on TEE is the pattern to recognize without being told.
RV dilated, LV underfilled. the failing RV cannot deliver preload to the LV and septal bowing impairs LV filling — the low output is right-sided, and managing it as LV failure with more fluid is the trap.
Volume. the over-distended RV usually needs less volume, not more; cautious management of preload to avoid worsening RV distension and septal shift.
Inotrope / pulmonary vasodilator. an inodilator (milrinone) or epinephrine for RV contractility plus inhaled nitric oxide or prostacyclin to lower PVR; commit to an end point in RV function and perfusion pressure.
Ventilator. avoid hypoxia, hypercarbia, acidosis, and high mean airway pressures/PEEP that raise PVR and further load the RV.
Escalation. mechanical RV support or VA-ECMO if maximal medical therapy fails; involve the surgeon early rather than escalating pressors indefinitely.

3. New atrial fibrillation

On post-operative day two he goes into atrial fibrillation at 150 with BP 92/56 and worsening dyspnea. Of concern in a fresh mitral repair? Why this patient? First moves? Rate or rhythm control — which, and why? If unstable, synchronized cardioversion — when and at what energy? If pharmacologic, agent and its cost in this heart? Bearing on anticoagulation given his post-operative bleeding? When and with what do you anticoagulate?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Of concern / why here. post-cardiac-surgery AF is common, but in a fresh repair with a stiff, recovering LV and pulmonary hypertension the loss of atrial kick and the fast rate drop output and raise left atrial and pulmonary pressures. Treating it as benign post-op AF is a flag.
First moves. restore pressure, correct triggers (electrolytes — magnesium and potassium, hypoxia, pain, ischemia), and decide on rate versus rhythm by stability.
Rate vs rhythm / cardioversion. hemodynamic instability favors prompt synchronized cardioversion; commit to a synchronized shock and a reasonable starting energy rather than hedging.
Pharmacologic agent / cost. amiodarone is commonly chosen; beta-blockers and calcium-channel blockers carry negative inotropy and vasodilation poorly tolerated in a recovering ventricle — the hemodynamic cost is the issue, not the name.
Anticoagulation. balance fresh surgical bleeding and chest-tube output against the stroke risk of new AF after a left-sided repair; typically delay full anticoagulation until hemostasis is secure, then resume — a titratable agent first if bleeding risk is live.
Trap. restarting full-dose anticoagulation the day after heavy bleeding, or ignoring AF stroke risk entirely, are both worth challenging.

4. Delayed awakening and embolic deficit

Sedation is off, but at six hours he does not follow commands and the right side is weak. DDx? Most concerning here, given the operation he had? Why is mitral surgery a setup for it? Workup — what, and how urgently? Imaging shows an acute left MCA infarct. Bearing on the anticoagulation decision you just made for his AF? Whom do you involve? What can you still offer this patient?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

DDx. residual sedation/metabolic causes, embolic stroke, hypoperfusion/watershed injury, seizure, intracranial bleed; a focal deficit shifts suspicion toward a structural cause.
Most concerning / why this operation. left-heart manipulation, intracardiac air, atrial thrombus dislodged in new AF, and the left atrial work of a mitral repair all make embolic stroke a recognized risk; want this tied to the procedure, not generic.
Workup urgency. urgent neuro exam and CT/imaging; time-sensitive because it changes both prognosis and the anticoagulation plan.
Bearing on anticoagulation. a fresh large infarct raises hemorrhagic-conversion risk and directly collides with the AF anticoagulation timing already in tension with surgical bleeding — the candidate must hold all three against each other.
Involve / offer. neurology and surgery; supportive neuroprotective ICU care, shared decisions on anticoagulation timing, honest prognostication.

5. Extubation and disclosure

He is now awake but with a residual right-sided deficit, still intubated, off inotropes, in rate-controlled atrial fibrillation. Extubate now? Why/why not? What must be true first? The family arrives and asks why he isn't moving his right side and whether the heart operation caused the stroke. What will you tell them? How do you coordinate that message with the surgical team? Given his deficit and AF, what must they understand about the plan going forward?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Extubate or not. a residual neurologic deficit raises airway-protection and aspiration concerns; weigh against the harms of prolonged intubation — either is defensible if the airway and gas exchange are addressed.
Before extubation. adequate mental status to protect the airway, stable hemodynamics off escalating support, acceptable gas exchange, controlled rhythm.
Telling the family. a plain, honest account of the stroke, that it was recognized, the uncertainty of recovery, without overpromising or assigning blame; room for questions.
Coordinate with surgery. a single, consistent message agreed with the surgical team so the family is not given conflicting accounts.
Going forward. they need to understand the rehabilitation course, the AF and its anticoagulation balance against the fresh stroke, and the uncertainty in neurologic recovery.

C. ADDITIONAL TOPICS

Teaching focus. Unrelated by design: refractory hypoxemia in ARDS, a bleeding pediatric airway emergency, and an operating-room fire. Rapid pivot across domains.

1. ARDS with refractory hypoxemia

A 55 y.o. man with severe pneumonia is intubated in the ICU. On volume control with FiO2 1.0 and PEEP 12, the PaO2 is 58, the PaO2/FiO2 ratio is 90, and the plateau pressure is 32 cm H2O. Of concern? Interpretation of these numbers? Tidal-volume target and why? Plateau-pressure goal? He stays hypoxemic — higher PEEP, recruitment, or prone positioning? Defend. Role of neuromuscular blockade? When would you consider ECMO? BP falls to 80/50 as you raise PEEP — DDx and Rx?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Diagnosis. ARDS — acute, bilateral infiltrates not fully explained by cardiac failure, with a PaO2/FiO2 of 90 placing it in the severe range.
Tidal volume. low tidal volume (~6 mL/kg predicted body weight) lung-protective ventilation; an answer that ventilates to a normal CO2 at the cost of high volumes is worth challenging.
Plateau pressure. keep plateau ≤ ~30 cm H2O; 32 is above target and the candidate should respond to it.
Higher PEEP vs recruitment vs prone. each is defensible if reasoned; proning has the strongest outcome signal in severe ARDS. Look for a committed, justified escalation rather than a list.
Neuromuscular blockade. may be considered for severe dyssynchrony or refractory hypoxemia; not a default for every ARDS patient.
Hypotension on raising PEEP. reduced venous return vs pneumothorax vs sepsis; lower PEEP or give volume/pressor, and exclude pneumothorax before simply pushing fluids.

2. Post-tonsillectomy hemorrhage in a child

A 4 y.o. returns to the ED six hours after tonsillectomy, swallowing repeatedly and now vomiting bright blood, tachycardic and pale. Concerns? Why is this airway and resuscitation challenging? Pre-induction priorities? Your induction and intubation plan — full stomach, hypovolemia, possibly difficult view from blood? He desaturates during laryngoscopy with blood obscuring the view — actions? What do you tell the surgeon and the family about urgency?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Concerns. a bleeding, hypovolemic child with a contaminated airway and a swallowed blood load; the visible bleeding underestimates the true loss.
Why challenging. aspiration risk, a blood-obscured view, hypovolemia that propofol or volatile can unmask as collapse, and a child's limited reserve.
Pre-induction. obtain IV access and resuscitate volume, type and cross, prepare two suctions and multiple tube sizes and a skilled assistant, have the surgeon present.
Induction plan. a rapid-sequence approach with cricoid as judged, reduced induction-agent dose for hypovolemia, head-down or lateral positioning to manage blood, readiness for a difficult view; over-dosing the induction agent in a hypovolemic child is a flag.
Lost view on laryngoscopy. large-bore suction, optimize position and external manipulation, consider a smaller styletted tube or video laryngoscopy, call for help early; have a surgical-airway backup in mind.
Communication. convey the emergent nature plainly to surgeon and family and align on the plan and risks.

3. Operating-room fire during MAC

During MAC with nasal-cannula oxygen for an excision on the face, the surgeon uses electrocautery and a flash fire ignites at the drapes. Immediate actions? Sequence of priorities? How does the fire triad apply here? How could this have been prevented? Once the fire is out, your assessment of the patient?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Immediate actions. stop the procedure, stop the supplemental oxygen and remove the airway source, remove the burning drapes and material, extinguish.
Priority sequence. protect the patient and remove the fuel and oxidizer first, then extinguish, then attend to the patient — the order matters.
Fire triad. oxidizer (supplemental O2 pooling under drapes), ignition (cautery), fuel (drapes, prep, hair) — a high-risk head-and-neck MAC setup.
Prevention. minimize or avoid open high-flow O2 near cautery, secure the airway or use blended air, let the prep dry, tent the drapes to avoid oxygen pooling.
Post-fire assessment. evaluate the airway and any skin or airway burns, confirm ventilation, plan airway management if inhalation injury is suspected.

Session 1 — long stem

Mitral valve replacement for severe rheumatic mitral stenosis

A 54 y.o., 60 kg, 5'3" woman is scheduled for mitral valve replacement for severe rheumatic mitral stenosis.

HPIProgressive dyspnea over the past year, now after walking one block, with two recent nights of orthopnea. Last week she coughed up a small amount of blood-streaked sputum. Palpitations for several months. Emigrated from a high-prevalence region as a young adult; childhood febrile illness with joint pains.

PMHSevere rheumatic mitral stenosis. Atrial fibrillation. Pulmonary hypertension. Two prior episodes of pulmonary edema requiring admission.

MEDSWarfarin (held; bridged), metoprolol, digoxin, furosemide. Penicillin prophylaxis as a child.

PHYS EXAMHR 88, irregularly irregular; BP 112/74; RR 20; SpO2 93% on room air; T 36.8°C. Loud S1, opening snap, low-pitched diastolic rumble at the apex. Bibasilar crackles. JVD with prominent waves; trace pedal edema.

ECGAtrial fibrillation, controlled ventricular response. Right axis deviation. Right ventricular hypertrophy with right atrial enlargement pattern. No acute ST changes.

ECHOMVA 0.9 cm²; mean transmitral gradient 12 mmHg. Dilated left atrium with spontaneous echo contrast; doming “hockey-stick” anterior leaflet, fused commissures, thickened subvalvular apparatus. LVEF 60% with an underfilled, small LV. Dilated, mildly hypokinetic RV. Estimated PA systolic pressure 68 mmHg. Moderate tricuspid regurgitation.

LABSHgb 11.2 g/dL; platelets 168 K/uL; INR 1.4 on bridge; K+ 3.6 mEq/L; creatinine 1.1 mg/dL; BNP elevated.

OR ARRIVALAwake radial arterial line placed. Two large-bore peripheral IVs and an introducer. External defibrillator pads on. Heparin infusion stopped per protocol; INR 1.4. Anxious, breathing 24, SpO2 92% on 2 L nasal cannula.

A. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Protecting a fixed transmitral obstruction at induction — preload, rate, rhythm, and SVR all at once; the cost of rapid atrial fibrillation across a stenotic valve; the right ventricle and pulmonary hypertension under acidosis and hypoxia; and pulmonary edema/hemoptysis before bypass.

1. Induction across a fixed obstruction

Induction agents and doses? Goals for rate, rhythm, preload, afterload here? Why? She is anxious and tachypneic on arrival — premedicate? With what, and what is the risk? After induction HR climbs to 120 and BP falls to 80/46. Of concern? Why this lesion? Rx? Phenylephrine? Volume? Esmolol? To what end point? Would your approach change if SpO2 fell to 85% as you treated this?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Induction goals. maintain preload, hold SVR, keep the rate slow, preserve a low-stress rhythm; a fixed orifice tolerates neither hypovolemia, tachycardia, nor a drop in SVR. A propofol-heavy bolus that vasodilates and a ketamine choice that drives rate both deserve a probe.
Premedication. anxiolysis blunts tachycardia from anxiety, but oversedation risks hypercarbia and hypoxemia that raise PVR and threaten the RV; want a balanced, defended choice, not a reflexive benzodiazepine or a refusal to treat the anxiety.
Tachycardia of concern / why here. diastole is when an obstructed LV fills; a fast rate shortens filling time across the stenotic valve, collapses stroke volume, and raises LA and pulmonary pressures. Treating the number rather than the filling problem is the trap.
Phenylephrine vs volume vs esmolol. phenylephrine restores SVR/coronary pressure without driving rate; cautious volume supports a preload-dependent obstruction; rate control (esmolol) directly buys diastolic filling. Reaching for an inotrope or chronotrope first is a red flag in MS.
End point. looking for a concrete target — control the rate toward baseline and restore perfusion pressure — not a vague 'fix the pressure.'
Desaturation while treating. rising LA pressure floods the lungs and the hypoxia raises PVR and threatens the RV; the candidate must integrate oxygenation, rate, and RV protection rather than chase BP alone.

2. Rapid atrial fibrillation and rate control

Despite rate control she accelerates to atrial fibrillation at 150 with BP 78/48 before cannulation. Of concern? Why does this rate hurt this valve specifically? First moves? Rate or rhythm control — which, and why? Synchronized cardioversion — when? Bearing of the dilated left atrium and the echo contrast on cardioverting her? If you rate-control pharmacologically instead — agent? Cost in this patient? She stays at 140 and hypotensive. Now what?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Of concern / why this valve. a fast ventricular rate shortens diastole, the only window for filling across a fixed stenosis, so output and LA decompression both fail; this is the classic decompensation in MS, not routine AF.
First moves. call it early, restore perfusion pressure, look for and correct triggers (light anesthesia, electrolytes, hypoxia/hypercarbia, volume), prepare to cardiovert.
Rate vs rhythm. unstable, hemodynamically significant AF favors prompt synchronized cardioversion; if stable, slow the rate to lengthen diastole. Commit, do not hedge.
Cardioversion / LA thrombus risk. the dilated LA with spontaneous echo contrast raises clot/embolic concern, but hemodynamic instability still mandates restoring rhythm; the candidate should name the embolic risk and proceed anyway when she is unstable.
Pharmacologic agent / cost. rate-controlling agents (beta-blocker, non-dihydropyridine calcium-channel blocker, amiodarone, digoxin) all carry negative inotropy, vasodilation, or slow onset poorly suited to a deteriorating, RV-strained patient; the hemodynamic cost is the point, not the drug name.
Persistent instability. escalate to synchronized cardioversion; do not keep titrating drugs into a failing patient.

3. Right ventricle and pulmonary hypertension

As you reposition for cannulation, SpO2 drifts to 86%, ETCO2 rises, and the CVP climbs with a distending RV on TEE. Of concern? Bearing of her PA pressures? What raises PVR right now that you control? Optimal PaCO2 here? Ventilator and oxygenation strategy? PA pressures rise to 75/40 and the RV dilates further. Rx? Inhaled pulmonary vasodilator — indicated? Why/why not? Inotrope for the RV — which, and why? End point?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Of concern. an already pressure-loaded, hypokinetic RV is being pushed by rising PVR and may fail; the rising CVP and distending RV are the warning, not a number to chase.
Controllable PVR drivers. hypoxia, hypercarbia, acidosis, hypothermia, light anesthesia/sympathetic surges, lung derecruitment — all raise PVR and all are at least partly in the anesthesiologist's hands. Naming and correcting these is the core of RV protection in MS.
PaCO2 / ventilation target. want a specific goal — normocarbia to mild hypocarbia, adequate oxygenation, avoid high mean airway pressures that impede RV output; not a vague 'ventilate well.'
Inhaled pulmonary vasodilator. inhaled nitric oxide or prostacyclin selectively lowers PVR and unloads the RV without dropping SVR; well-suited here. The candidate should tie it to the RV, not reach for a systemic vasodilator that would drop SVR.
RV inotrope. epinephrine or milrinone for RV contractility — milrinone helps PVR but vasodilates; pair with a pressor to hold SVR. Want a defended choice tied to this RV, not a list.
End point. a concrete target — lower PA pressures, a less distended/better-contracting RV, restored perfusion pressure — titrated to, not simply 'more drug.'

4. Hemoptysis and pulmonary edema before bypass

Pink frothy fluid appears in the ETT and SpO2 falls to 84% before you can go on bypass. DDx? Most likely here, given her valve? Mechanism in MS? Immediate priorities? PEEP — helpful or harmful here? Why? Diuretic now — indicated? Why/why not? She is coughing frank blood into the circuit and desaturating further. How do you maintain oxygenation until cannulation? Bearing on how urgently she goes on bypass?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

DDx / most likely. cardiogenic pulmonary edema from the obstructed LA emptying, with possible rupture of bronchial/pulmonary vessels causing hemoptysis; far less likely TRALI/aspiration. The valve and the high LA pressure make pulmonary edema the lead.
Mechanism in MS. the fixed stenosis keeps LA and pulmonary venous pressure high; tachycardia and volume tip it into frank edema, and chronically engorged bronchial veins can bleed — reasoning about this patient's physiology, not a recited list.
Priorities. oxygenation and airway, lower LA/pulmonary pressure by slowing the rate and avoiding overload, support perfusion pressure, and move toward bypass.
PEEP. modest PEEP can recruit and reduce edema/oxygenation deficit, but excessive PEEP impedes RV output and venous return in a pressure-loaded RV; a defended, titrated answer beats a reflexive high-PEEP or none-at-all.
Diuretic. reasonable to reduce pulmonary congestion if she is volume-overloaded, but the obstruction is fixed and she may be preload-dependent — aggressive diuresis can underfill the LV; want recognition of that tension, not a reflexive dose.
Maintain oxygenation / bypass urgency. escalate FiO2 and airway support, accept that definitive relief is mechanical, and recognize that worsening edema/hemoptysis argues for expediting cannulation and bypass rather than prolonged medical temporizing.

B. POST-OPERATIVE CARE

Teaching focus. Separating a chronically pressure-loaded RV from bypass with an inhaled pulmonary vasodilator; post-bypass RV failure and arrhythmia; bleeding on a held-anticoagulant, mechanical-valve background and when to re-anticoagulate; pulmonary hypertensive crisis in the ICU; and an honest family conversation about a hard course.

1. Separation from bypass with RV failure

MVR complete; attempting to wean. TEE shows a well-seated prosthesis, no paravalvular leak, a now-decompressed LA, but a dilated, poorly contracting RV with septal bowing. BP 84/50, CI 1.7. Of concern? DDx for failure to separate here? Volume — give it or not, and why? Inotrope — epinephrine, milrinone, or both? Why in this RV? Inhaled nitric oxide — start it? Rationale? End point you titrate to? She still won't wean and the RV distends further. Mechanical support — which, and why not an IABP?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

DDx for failure to separate. RV failure from chronic pulmonary hypertension now unmasked, residual high PVR, air or ischemia, inadequate or excess preload, arrhythmia, residual valve/surgical issue (TEE helps exclude). The septal bowing points RV-predominant.
Volume judgment. the RV is volume-intolerant when failing — over-filling worsens septal bowing and LV filling; cautious, TEE-guided preload, not reflexive volume loading.
Inotrope choice. epinephrine for RV contractility and perfusion; milrinone improves contractility and lowers PVR but vasodilates — often paired with a pressor; want a defended choice tied to the RV, not a list.
Inhaled nitric oxide. selectively lowers PVR and unloads the RV without dropping SVR — a logical first-line pulmonary vasodilator here; the candidate should connect it to RV afterload reduction.
End point. a concrete target — a less distended, better-contracting RV, acceptable CI and perfusion pressure, lower PA pressures — not simply 'more epi.'
Mechanical support / why not IABP. an IABP unloads the LV and augments coronary perfusion but does little for an RV-predominant failure; an RV assist device or VA-ECMO addresses the failing RV. A candidate who recognizes the failure is RV-predominant and reaches for RV-appropriate support rather than an IABP is reasoning well.

2. Post-bypass bleeding and anticoagulation

First hour in the ICU: chest-tube output 300 mL/hr of bright blood. Of concern? Surgical vs medical bleeding — how do you distinguish? Residual heparin after protamine — how would you know? Which tests guide you? On TEG with fibrinogen 130 and platelets 95, what do you give and in what order? Bearing of her held warfarin and INR 1.4? She has a mechanical valve — when and how do you restart anticoagulation against this bleeding? When does she go back to the OR?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Of concern. rate and bright character suggest significant ongoing loss; act before she becomes coagulopathic and unstable.
Surgical vs medical. brisk, sustained, bright bleeding with a normalizing coagulation profile points surgical and toward re-exploration; diffuse oozing with abnormal studies points medical and toward product correction.
Residual heparin. heparin–protamine mismatch or heparin rebound; assess with ACT/anti-Xa or TEG with a heparinase comparison; redose protamine if confirmed.
Targeted products. fibrinogen 130 favors cryoprecipitate/fibrinogen concentrate; platelets 95 after bypass favors platelets; correct the specific deficit rather than blind FFP. Her INR 1.4 reflects the held warfarin, not the acute surgical bleeding.
Mechanical valve / restart anticoagulation. a new mechanical mitral prosthesis carries real thrombotic risk, but restarting full anticoagulation into heavy fresh bleeding invites disaster; want a staged plan — secure hemostasis, then a titratable heparin bridge — not full-dose anticoagulation the same hour she is bleeding.
Return to OR. persistent high-volume bleeding despite corrected coagulation, tamponade physiology, or instability mandates re-exploration; endless transfusion without surgical control is the trap.

3. Pulmonary hypertensive crisis in the ICU

Overnight, on weaning the inhaled nitric oxide, her PA pressures spike, SpO2 falls, CVP rises, and BP drops. Of concern? What just happened mechanistically? Triggers you look for? Restart the inhaled agent — and how do you wean it differently this time? Ventilator and sedation adjustments to lower PVR? Pressor vs inotrope for the failing RV now — which, and why? End point? If she arrests — what is different about resuscitating acute RV failure?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Of concern / mechanism. rebound pulmonary hypertension on withdrawal of the inhaled vasodilator, raising RV afterload and tipping the chronically loaded RV into acute failure with falling LV preload and output; recognizing the rebound without being told is the point.
Triggers. hypoxia, hypercarbia, acidosis, pain/agitation, light sedation, hypothermia, abrupt weaning of the inhaled agent — all correctable PVR drivers.
Restart and re-wean. resume the inhaled vasodilator and wean slowly with adjuncts (e.g., sildenafil) to prevent rebound; a candidate who simply turns it back to full and stops there misses the weaning problem.
Vent / sedation. optimize oxygenation and normocarbia, deepen sedation to blunt sympathetic surges, avoid high mean airway pressures — concrete moves that lower PVR.
Pressor vs inotrope. maintain SVR/coronary perfusion to the RV with a pressor (e.g., vasopressin, which spares PVR) while supporting contractility with an inotrope; want the RV-perfusion logic, not a reflexive single agent.
RV arrest. treat the cause (afterload, hypoxia, acidosis), maintain coronary perfusion to the RV, consider mechanical support/ECMO early; standard chest compressions alone will not relieve an obstructed RV.

4. Postoperative arrhythmia and pacing

On day one she is again in atrial fibrillation with a rapid response and her pressure sags. Bearing of AF now, with the mitral obstruction relieved but a stiff RV and pulmonary hypertension? First moves? Rate or rhythm control here — which, and why now? Bearing on her anticoagulation timing? She then develops a junctional rhythm at 45 — epicardial pacing, which mode and why? AV-sequential vs ventricular — which, and why? End point for rate?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

AF now / bearing. the valve is fixed but the RV is still pressure-loaded and rate-sensitive; a fast rate worsens RV filling and output and the loss of organized atrial filling still costs her. Recognizing she remains rate-sensitive after MVR is the judgment.
First moves / rate vs rhythm. restore perfusion pressure, correct triggers, then rate-control if stable or cardiovert if unstable; commit rather than hedge, with attention to her recent surgery and bleeding.
Anticoagulation timing. the new AF plus mechanical valve raises embolic stakes, but fresh post-op bleeding constrains timing; tie the rhythm decision to the staged anticoagulation plan rather than treating them separately.
Epicardial pacing mode. for the slow junctional rhythm, pace to restore rate and perfusion; AV-sequential restores AV synchrony and the atrial contribution only if the atrium can capture, so in a patient with chronic/recurrent AF the atrial lead may be futile and ventricular (or DDD that will track/pace appropriately) is what reliably delivers rate. A candidate who reflexively leaves AV-sequential running through an episode of AF, expecting an atrial kick that cannot occur, deserves a probe.
End point. a concrete rate/perfusion target that protects the RV — controlled ventricular rate, adequate filling and pressure — not simply 'pace her.'

5. Family disclosure on a hard course

By day two she is stable but still intubated on an inhaled pulmonary vasodilator, with a prolonged, complicated course ahead. The family arrives and asks why she is so much sicker than they expected and whether something went wrong. What will you tell them? What do they most need to understand first? How do you frame the pulmonary hypertension and RV problem without false reassurance or blame? How do you coordinate that message with the surgical and ICU teams? What must they understand about the road ahead and her anticoagulation?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Telling the family. a plain, honest account of the severe pulmonary hypertension and right-heart strain that predated and complicated surgery, the difficult but expected course, and the uncertainty — without overpromising or assigning blame.
Framing without false reassurance. convey seriousness and uncertainty honestly while leaving room for hope and questions; neither catastrophizing nor falsely reassuring.
Coordinate with the teams. a single consistent message agreed with surgery and intensive care so the family is not given conflicting accounts.
Road ahead / anticoagulation. they should understand the prolonged weaning, the mechanical valve and lifelong anticoagulation, and what RV recovery and pulmonary hypertension mean for her trajectory.

C. ADDITIONAL TOPICS

Teaching focus. Unrelated by design: a retrobulbar block complication, local anesthetic systemic toxicity after an interscalene block, and a suspected amniotic fluid embolism at delivery. Rapid pivot across domains.

1. Retrobulbar block complication

A 72 y.o. man undergoing cataract surgery becomes acutely bradycardic, then within minutes confused, dysarthric, and apneic shortly after a retrobulbar block. Possible causes? Most concerning? Mechanism of brainstem anesthesia after a retrobulbar block? Immediate management? How would your differential change if instead he developed sudden proptosis and a tense globe right after the injection? How could the original event have been reduced?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Possible causes. brainstem anesthesia from intrathecal spread of local anesthetic, oculocardiac reflex, intravascular local-anesthetic injection, and a primary cardiac or neurologic event.
Most concerning. brainstem anesthesia causing apnea and depressed consciousness, which is immediately life-threatening.
Mechanism. spread of local anesthetic along the optic nerve sheath into the subarachnoid space, producing central effects including respiratory arrest.
Management. support ventilation and the airway and circulation until the block recedes; the event is usually transient with prompt respiratory support, and failing to ventilate is the danger.
Proptosis and tense globe. that picture suggests retrobulbar hemorrhage with rising orbital pressure threatening the optic nerve, prompting urgent ophthalmology assessment and possible canthotomy rather than central support.
Risk reduction. meticulous technique with appropriate needle choice and depth, aspiration before injection, and consideration of less invasive blocks; relying on technique alone without monitoring is worth a probe.

2. LAST after interscalene block

A 60 y.o. woman receives an interscalene block for shoulder surgery. Two minutes after injection she becomes agitated and then has a generalized seizure. Most likely cause? Immediate priorities? She loses her pulse with a wide-complex rhythm. How does management differ from standard ACLS? Principle and role of lipid emulsion? What would have reduced the risk?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Most likely cause. local anesthetic systemic toxicity from intravascular injection or rapid systemic absorption.
Immediate priorities. stop injecting, call for help, secure airway and oxygenation, control the seizure, obtain lipid emulsion.
ACLS modifications. give lipid emulsion, reduce epinephrine dosing relative to standard ACLS, avoid certain antiarrhythmics, anticipate prolonged resuscitation, consider cardiopulmonary bypass for refractory arrest.
Lipid emulsion. bolus followed by infusion per the published protocol; a specific therapy, not an afterthought.
Prevention. incremental injection with aspiration, ultrasound guidance, a test dose, lowest effective dose.

3. Suspected amniotic fluid embolism at delivery

A 31 y.o. woman at term has just delivered vaginally under a labor epidural. Moments after delivery she becomes acutely dyspneic and agitated, SpO2 falls to 78%, BP is 70/40, and oozing is noted from her IV sites. DDx? Leading diagnosis and why? Immediate priorities? She arrests with PEA — how is resuscitation in late pregnancy modified? Role of perimortem cesarean delivery and its timing? She is resuscitated but now diffusely bleeding — interpretation and management?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

DDx. amniotic fluid embolism, eclampsia, high/total spinal, local anesthetic systemic toxicity, pulmonary embolism, hemorrhage with hypovolemia, anaphylaxis.
Leading diagnosis. amniotic fluid embolism — abrupt cardiorespiratory collapse plus coagulopathy around delivery; a clinical diagnosis of exclusion.
Immediate priorities. call for help, secure the airway, support oxygenation and circulation, left uterine displacement, large-bore access, activate massive transfusion.
Resuscitation in late pregnancy. manual left uterine displacement or tilt, no change to drug doses or defibrillation energy, anticipate difficult airway and rapid desaturation.
Perimortem cesarean. consider delivery within about 4 minutes of arrest to aid maternal resuscitation; an answer that delays it indefinitely is worth probing.
Coagulopathy. DIC is common with AFE; treat with goal-directed product replacement and fibrinogen; reassess with point-of-care testing.

Session 1 — long stem

Post-CPB coagulopathy and massive transfusion after redo aortic root/ascending replacement under DHCA

A 66 y.o., 92 kg, 5'10" man is undergoing a redo aortic root and ascending aortic replacement for an expanding root aneurysm at the site of a prior bioprosthetic aortic valve.

HPIBioprosthetic AVR eleven years ago for a bicuspid valve. Surveillance imaging over the past year shows a 5.6 cm root and ascending aneurysm. Reoperative sternotomy with extensive mediastinal adhesions was anticipated.

PMHBicuspid aortic valve, prior bioprosthetic AVR. Hypertension. Hyperlipidemia. Mild chronic kidney disease. Remote tobacco use. No prior bleeding disorder.

MEDSAspirin 81 mg (continued through surgery), metoprolol, losartan (held), atorvastatin, rosuvastatin discontinued.

INTRAOP COURSEReoperative dissection of dense adhesions was slow and bloody. Cardiopulmonary bypass time is now 4 hours and 20 minutes, with a 26-minute interval of deep hypothermic circulatory arrest at 18°C during the open distal anastomosis. Rewarming is underway. Cell-salvage and homologous transfusion have been ongoing throughout the case.

PHYS EXAM / HEMODYNAMICSRewarming through 33°C. On separation attempts: BP 92/54 on low-dose norepinephrine and epinephrine, CVP 12, PA 36/20, CI 2.2 by TEE. Diffuse oozing is visible from every suture line, cannulation sites, and raw mediastinal surfaces as the surgeon tries to close.

LABS / POCPre-protamine: Hgb 8.1 g/dL; platelets 88 K/uL; fibrinogen 110 mg/dL; INR 1.9; ACT 540 s; ionized Ca 0.94 mmol/L; K+ 5.6 mEq/L; pH 7.24; base deficit -8; lactate 4.8; temp 33°C.

CURRENT STATEThe aortic and root grafts are in and the surgeon reports the suture lines look surgically intact, but the field will not dry. Protamine is being given as you prepare to separate definitively and close. The surgeon is asking for product.

A. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Anticipating coagulopathy in a redo, long-bypass, DHCA patient; confirming heparin neutralization after protamine and recognizing rebound; distinguishing surgical from medical bleeding at the field; and driving point-of-care–guided, targeted product therapy rather than blind transfusion while separating from bypass.

1. Anticipating the coagulopathy on separation

As you rewarm and prepare to separate, the field is oozing diffusely. Of concern? What about this case sets him up for it? Which of those contributors can you act on right now, and how? Target temperature before you rely on his clotting? Bearing of his current acidosis and ionized calcium on the bleeding? You correct what you can and oozing persists. Surgical vs medical bleeding — how do you tell them apart here? Which way does this picture point, and why?

Considerations and pitfalls

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Of concern / setup. redo sternotomy with raw adhesed surfaces, 4+ hour bypass, and DHCA together produce a multifactorial coagulopathy; consumptive activation, hemodilution, platelet dysfunction, hypothermia, acidosis, and fibrinolysis all stack. Treating diffuse field ooze in this exact patient as routine is the flag.
Modifiable now. rewarm fully, correct acidosis and ionized calcium, ensure adequate platelets and fibrinogen, confirm heparin is neutralized; want concrete moves, not a recited list of CPB coagulopathy causes.
Temperature target. looking for a concrete endpoint (core toward 36–37°C) before trusting the coagulation cascade; enzyme kinetics and platelet function are temperature-dependent.
Acidosis and ionized calcium. acidosis impairs the coagulation enzymes and worsens with hypoperfusion; ionized calcium 0.94 is low for a bleeding cardiac patient and impairs clot formation and myocardial function — a candidate who ignores the calcium deserves a probe.
Surgical vs medical. diffuse oozing from every raw surface with abnormal point-of-care studies points medical; brisk, sustained, localized bright bleeding with a normalizing profile points surgical. The distinction is what governs whether product or the surgeon fixes it.
Which way here. the universal ooze plus deranged labs points medical/coagulopathic; recognizing that this field is medical bleeding to be corrected with targeted product, not chased back to a single suture line, is the judgment being tested.

2. Heparin neutralization and rebound

Protamine is in at a full reversal dose, yet the ACT remains 480. Interpretation? Possible reasons it is still prolonged? How do you confirm residual heparin specifically rather than another cause? Say you have a heparinase-modified channel against the native — what comparison confirms it? It confirms residual heparin. Now what, and how much? An hour later, after the ACT had normalized, the field worsens again and the ACT climbs. What is this? How do you treat it? Risk of overdosing protamine — bearing?

Considerations and pitfalls

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ACT 480 after full protamine. incomplete neutralization, under-dosing relative to circulating heparin, heparin redistribution, or a non-heparin coagulopathy also prolonging the ACT — the ACT is not heparin-specific.
Confirm heparin specifically. compare a heparinase-modified TEG/ROTEM against the native channel, or an anti-Xa/heparin level; the point is that ACT alone cannot separate residual heparin from coagulopathy.
TEG with/without heparinase. a native R time that is prolonged but corrects (normalizes) on the heparinase channel localizes the problem to residual heparin; if both channels are equally abnormal, the defect is not heparin. Want recognition of the comparison, not the raw R-time numbers.
Redose protamine. give additional protamine titrated to the residual heparin rather than a reflexive large empiric dose; reassess the ACT/TEG after.
Rebound. heparin rebound — redistribution of tissue-bound heparin after protamine has cleared; recognize it as a recurrence, not a new surgical bleed, and re-treat with incremental protamine guided by testing.
Protamine overdose. excess protamine itself is an anticoagulant and impairs platelet function and the cascade, plus its hypotension and pulmonary hypertension/anaphylactoid risk; titrating to evidence of residual heparin, not piling it in, is the judgment.

3. Point-of-care–guided targeted therapy

Heparin is now neutralized but he keeps oozing. TEG: prolonged R, K prolonged with low angle, functional-fibrinogen MA low, and a citrated-kaolin MA of 42 with a platelet count of 90. Interpretation, channel by channel? What do you give, and in what order? Fibrinogen 110 — cryoprecipitate or fibrinogen concentrate? Why one over the other here? Why is the platelet function poor despite a count of 90? An antifibrinolytic — do you start or continue one? Why? You have given two rounds of targeted product and he is still diffusely bleeding with a dry surgical field. rFVIIa or PCC — would you, and why or why not?

Considerations and pitfalls

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Channel-by-channel interpretation. prolonged R = clotting-factor deficiency (FFP or PCC); low K/angle and low functional-fibrinogen MA = fibrinogen deficit (cryo/fibrinogen concentrate); citrated-kaolin MA 42 with count 90 = a platelet-function rather than purely number problem. Reading the channels to a targeted plan is the skill.
Order of products. correct the specific deficits the TEG shows — fibrinogen and platelets drive clot strength and are usually first when MA is the problem; factors via FFP/PCC for the prolonged R. Blind FFP-for-everything is the trap.
Cryo vs fibrinogen concentrate. both raise fibrinogen; fibrinogen concentrate is low-volume, pathogen-reduced, and fast to dose by weight, attractive when volume or RV function matters; cryo is the alternative when concentrate is unavailable. Want a defended choice tied to this patient, not a list.
Platelet dysfunction despite count 90. CPB acquires platelet dysfunction from extracorporeal contact, activation/desensitization, hypothermia, and aspirin on board; the count overstates function, so transfuse platelets for the dysfunction, not just the number.
Antifibrinolytic. long bypass and DHCA drive fibrinolysis; continue/start tranexamic acid (or aminocaproic acid) as part of correcting medical bleeding — recognizing fibrinolysis as a contributor is the point.
rFVIIa / PCC as last resort. after targeted correction of fibrinogen, platelets, factors, calcium, temperature, and a confirmed dry surgical field, low-dose factor concentrate or rFVIIa may be considered for refractory microvascular bleeding — with explicit awareness of thrombotic risk, especially with fresh grafts and possible ECMO. Reaching for rFVIIa before correcting the substrate or excluding surgical bleeding is a red flag.

4. Separation, calcium, and potassium

You are transfusing briskly to keep up. Ionized calcium drops to 0.82 and the pressure sags with each unit. Mechanism? Rx, and to what end point? Meanwhile K+ is now 6.4 with peaked T waves on the monitor. Bearing during separation from bypass? Immediate Rx? Which agents, and why these? He separates but remains soft on rising pressor. As you weigh more product against his hemodynamics, what determines whether you keep correcting in the OR versus pack and come back? What must be true to leave the chest open?

Considerations and pitfalls

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Ionized calcium 0.82 mechanism. citrate load from rapid blood-product transfusion chelates calcium faster than the liver clears it, compounded by hypothermia and hypoperfusion; the hypocalcemia impairs both contractility and coagulation.
Calcium Rx / endpoint. give IV calcium (chloride centrally) titrated to a concrete ionized-calcium target and to restored contractility, not a fixed dose; reassess after.
K+ 6.4 with peaked T waves. hyperkalemia from transfused/cardioplegia load and acidosis, dangerous during separation when an unstable rhythm is least tolerated; recognize the ECG change as a forcing function.
Hyperkalemia Rx. calcium to stabilize the membrane (also fixes the hypocalcemia), then insulin/glucose and correction of acidosis/ventilation to shift potassium; diuresis/dialysis if it persists. Want the membrane-stabilize-then-shift logic, not a single drug.
Stay vs pack and return. if targeted correction is being outrun by ongoing loss, the surgical field is dry, and the patient is becoming unstable, damage-control with an open packed chest and planned re-exploration beats endless transfusion in a deteriorating patient.
Open chest criteria. myocardial edema preventing closure, hemodynamic intolerance of closure, or the need to keep re-exploring — a defended decision to leave the sternum open and return, not closing into tamponade.

B. POST-OPERATIVE CARE

Teaching focus. Carrying the coagulopathy into the ICU: ongoing point-of-care–guided correction and the limits of transfusion; recognizing surgical re-bleeding and tamponade in a postsurgical chest; the complications of massive transfusion (TRALI/TACO, dilutional, citrate, hyperkalemia); deciding when to re-explore; and an honest family disclosure.

1. Ongoing ICU coagulopathy

Chest closed, in the ICU now: chest-tube output 200 mL/hr of dark blood, still oozing from line sites. Of concern? Repeat TEG: R improving, MA still low, functional fibrinogen low; fibrinogen 130, platelets 95, temp now 36.2, pH 7.32. What do you give, and what do you no longer need to give? When does continued transfusion stop being the answer? He has now had 14 units of PRBC, 6 of FFP, two pools of platelets, and cryo. What new problems does that volume of transfusion itself create? How will you watch for them?

Considerations and pitfalls

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Of concern. sustained 200 mL/hr with persistent oozing means the coagulopathy is not yet corrected and re-bleeding is on the table; act before he destabilizes.
Targeted, de-escalating. the improving R means factors are catching up — stop blind FFP; the persistently low MA/functional fibrinogen still needs platelets and fibrinogen. Correcting to the current TEG, including stopping what is no longer indicated, is the judgment.
Limits of transfusion. once temperature, pH, calcium, fibrinogen, platelets, and heparin are corrected and bleeding continues, the problem is surgical until proven otherwise — transfusion is not the endpoint.
Massive transfusion complications. dilutional coagulopathy and thrombocytopenia, citrate-induced hypocalcemia, hyperkalemia, hypothermia, acid-base shifts, TRALI and TACO, and transfusion reactions — want the candidate to name the syndrome of massive transfusion, not one item.
Monitoring. serial ionized calcium and potassium, temperature, repeat point-of-care coagulation, oxygenation and filling pressures to separate TACO from TRALI, and vigilance for ongoing surgical loss.

2. Re-bleeding versus tamponade

Two hours later the chest-tube output abruptly falls to near zero. CVP rises to 22, PA 40/26, CI 1.5, BP 88/52, oliguric, pulsus on the arterial line. DDx? Which is most concerning given his last few hours? Diagnostic studies — which, and how fast? TEE is equivocal for a discrete effusion in this postsurgical chest — bearing? Your immediate priorities? Is a diuretic indicated for the oliguria? Why/why not? How do you maintain output until the chest is open? He is decompensating fast — bedside sternotomy in the ICU, yes or no?

Considerations and pitfalls

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DDx. localized clot causing tamponade given the suddenly-stopped tube and equalizing/rising filling pressures, ongoing surgical hemorrhage, RV failure, hypovolemia, pneumothorax; the stopped tube plus rising pressures is the pattern to recognize unprompted.
Most concerning. tamponade from a retained clot — in a chest that was bleeding then suddenly drains nothing, with rising CVP and pulsus, suspect it even with an equivocal echo.
Equivocal TEE. localized postsurgical clot is easily missed; a high index of suspicion and direct surgical communication outweigh a negative study — do not let a clean echo falsely reassure.
Priorities. keep full, fast, and tight — preserve preload and rate, support pressure, avoid anything that drops venous return, and mobilize the surgeon for re-exploration.
Diuretic. contraindicated — the oliguria is low forward flow from impaired filling, not volume overload; diuresing a tamponading patient worsens it. A reflexive diuretic is a red flag.
Bedside sternotomy. if he is arresting or peri-arrest from tamponade, emergent chest reopening in the ICU is life-saving and the right call; a defended yes, with how he will support hemodynamics through it, is what is sought.

3. Transfusion-related lung injury

After re-exploration and more product, he is back in the ICU and over the next two hours desaturates to 86% on FiO2 1.0 with pink frothy secretions and diffuse bilateral infiltrates; the bleeding has finally stopped. DDx? How do you distinguish TRALI from TACO here? What at the bedside helps you tell them apart? Bearing of his filling pressures and his transfusion volume on that distinction? Management if you think TRALI? Ventilator strategy — settings and targets? Does this change what you transfuse for any residual bleeding?

Considerations and pitfalls

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DDx. TRALI, TACO, cardiogenic pulmonary edema, aspiration, evolving ARDS from the long pump run and shock — a focal-in-time desaturation after heavy transfusion raises the transfusion-related causes.
TRALI vs TACO. TRALI is non-cardiogenic, normal-to-low filling pressures, often within ~6 hours of transfusion, no response to diuresis; TACO is hydrostatic with elevated filling pressures and improves with diuresis. The massive volume he received makes both plausible — use the filling pressures to separate them.
Bedside distinction. filling pressures/echo, response to diuresis, character of the edema fluid, and timing relative to transfusion; want the candidate to reason from data, not flip a coin.
TRALI management. supportive — lung-protective ventilation, oxygenation, hemodynamic support; it is not volume overload, so diuresis is not the treatment and report the suspected unit.
Ventilator strategy. low tidal volume (~6 mL/kg ideal body weight), plateau-pressure limit, PEEP titrated to oxygenation, permissive hypercapnia as needed — concrete settings and targets, not 'lung protective.'
Bearing on transfusion. minimize further transfusion, give only TEG-targeted product for true residual bleeding, and avoid volume-heavy blind FFP that worsens the lungs.

4. When to return to the OR

Bleeding slowed but never fully stopped: chest tube settles around 120 mL/hr through the evening, point-of-care studies are now corrected, calcium and temperature normal, heparin long gone. Interpretation now that the coagulopathy is fixed? What does persistent bleeding with a corrected profile tell you? Threshold to re-explore — what numbers or trends push you there? Whom do you involve, and how fast? He drops a pressure with a tense, full chest — decision? What must be ready before he goes back?

Considerations and pitfalls

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Interpretation. a corrected coagulation profile with ongoing bleeding reclassifies this as surgical bleeding — the earlier medical coagulopathy has been treated and is no longer the explanation.
Persistent bleeding, corrected labs. this is the cardinal pivot: once the medical contributors are fixed and he still bleeds, the surgeon owns it; continuing to transfuse into a surgical bleed is the trap.
Re-exploration threshold. sustained high-volume output (e.g., persistent >200 mL/hr, or a large total over a few hours), an acute increase, tamponade physiology, or hemodynamic instability — a defended threshold and trend, not an exact recited number.
Involve / urgency. early, explicit communication with the surgical team and OR/perfusion; do not sit on a surgical bleed waiting for it to stop.
Tense full chest. tamponade/re-accumulation — emergent return to the OR (or bedside opening if arresting); a clear decision, not more observation.
Before return. blood products checked and available, access and monitoring secured, hemodynamic support and the team briefed, anticipating decompensation on relief of tamponade.

5. Disclosure to the family

He is stabilizing after the second washout, still intubated and sedated, transfused heavily through the night. The family arrives and asks why he needed so much blood, whether the bleeding was a complication, and whether all those transfusions could hurt him. What will you tell them? How do you describe the bleeding without alarming or assigning blame? How do you coordinate that message with the surgical team? They ask what the transfusions could still cause — what do you say? What do they need to understand about the days ahead?

Considerations and pitfalls

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What to tell them. a plain, honest account — a difficult reoperation with significant bleeding that required many blood products and a return to the OR, recognized and treated, with the current status and remaining uncertainty.
Without alarm or blame. frame the bleeding as a known risk of a complex redo on long bypass that the team managed actively; avoid both false reassurance and assigning fault.
Coordinate with surgery. one consistent message agreed with the surgical team so the family does not hear conflicting accounts.
Transfusion risks. acknowledge honestly — lung injury, fluid overload, electrolyte disturbance, reactions, and infection risk — framed as monitored-for and largely outweighed by the need to treat life-threatening bleeding.
The days ahead. ongoing ICU support, the possibility of further bleeding or complications, and that recovery from this magnitude of operation and transfusion takes time; leave room for questions.

C. ADDITIONAL TOPICS

Teaching focus. Unrelated by design: an obstetric collapse at delivery, a regional-anesthesia systemic-toxicity crisis, and an eye-block complication. Rapid pivot across domains.

1. Suspected amniotic fluid embolism at delivery

A 31 y.o. woman at term has just delivered vaginally under a labor epidural. Moments after delivery she becomes acutely dyspneic and agitated, SpO2 falls to 78%, BP is 70/40, and oozing is noted from her IV sites. DDx? Leading diagnosis and why? Immediate priorities? She arrests with PEA — how is resuscitation in late pregnancy modified? Role of perimortem cesarean delivery and its timing? She is resuscitated but now diffusely bleeding — interpretation and management?

Considerations and pitfalls

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DDx. amniotic fluid embolism, eclampsia, high/total spinal, local anesthetic systemic toxicity, pulmonary embolism, hemorrhage with hypovolemia, anaphylaxis.
Leading diagnosis. amniotic fluid embolism — abrupt cardiorespiratory collapse plus coagulopathy around delivery; a clinical diagnosis of exclusion.
Immediate priorities. call for help, secure the airway, support oxygenation and circulation, left uterine displacement, large-bore access, activate massive transfusion.
Resuscitation in late pregnancy. manual left uterine displacement or tilt, no change to drug doses or defibrillation energy, anticipate difficult airway and rapid desaturation.
Perimortem cesarean. consider delivery within about 4 minutes of arrest to aid maternal resuscitation; an answer that delays it indefinitely is worth probing.
Coagulopathy. DIC is common with AFE; treat with goal-directed product replacement and fibrinogen; reassess with point-of-care testing.

2. LAST after interscalene block

A 60 y.o. woman receives an interscalene block for shoulder surgery. Two minutes after injection she becomes agitated and then has a generalized seizure. Most likely cause? Immediate priorities? She loses her pulse with a wide-complex rhythm. How does management differ from standard ACLS? Principle and role of lipid emulsion? What would have reduced the risk?

Considerations and pitfalls

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Most likely cause. local anesthetic systemic toxicity from intravascular injection or rapid systemic absorption.
Immediate priorities. stop injecting, call for help, secure airway and oxygenation, control the seizure, obtain lipid emulsion.
ACLS modifications. give lipid emulsion, reduce epinephrine dosing relative to standard ACLS, avoid certain antiarrhythmics, anticipate prolonged resuscitation, consider cardiopulmonary bypass for refractory arrest.
Lipid emulsion. bolus followed by infusion per the published protocol; a specific therapy, not an afterthought.
Prevention. incremental injection with aspiration, ultrasound guidance, a test dose, lowest effective dose.

3. Retrobulbar block complication

A 72 y.o. man undergoing cataract surgery becomes acutely bradycardic, then within minutes confused, dysarthric, and apneic shortly after a retrobulbar block. Possible causes? Most concerning? Mechanism of brainstem anesthesia after a retrobulbar block? Immediate management? How would your differential change if instead he developed sudden proptosis and a tense globe right after the injection? How could the original event have been reduced?

Considerations and pitfalls

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Possible causes. brainstem anesthesia from intrathecal spread of local anesthetic, oculocardiac reflex, intravascular local-anesthetic injection, and a primary cardiac or neurologic event.
Most concerning. brainstem anesthesia causing apnea and depressed consciousness, which is immediately life-threatening.
Mechanism. spread of local anesthetic along the optic nerve sheath into the subarachnoid space, producing central effects including respiratory arrest.
Management. support ventilation and the airway and circulation until the block recedes; the event is usually transient with prompt respiratory support, and failing to ventilate is the danger.
Proptosis and tense globe. that picture suggests retrobulbar hemorrhage with rising orbital pressure threatening the optic nerve, prompting urgent ophthalmology assessment and possible canthotomy rather than central support.
Risk reduction. meticulous technique with appropriate needle choice and depth, aspiration before injection, and consideration of less invasive blocks; relying on technique alone without monitoring is worth a probe.

Session 1 — long stem

Open repair of acute Stanford Type A aortic dissection

A 58 y.o., 92 kg, 5'11" man is brought emergently to the OR for open repair of an acute Stanford Type A aortic dissection.

HPISudden, severe tearing chest and interscapular back pain two hours ago while at work, with diaphoresis and a brief near-syncopal episode. Pain has migrated and remains unrelenting. Now reports a cold, mottled right leg.

PMHLong-standing poorly controlled hypertension. Hyperlipidemia. Former smoker. No prior cardiac surgery.

MEDSAmlodipine, hydrochlorothiazide, atorvastatin; admits to inconsistent adherence. Took a full aspirin in the ED.

PHYS EXAMHR 112; right-arm BP 178/96, left-arm BP 142/80; RR 22; SpO2 95% on 4 L nasal cannula; T 36.4°C. Diaphoretic and anxious. A new early diastolic murmur at the left sternal border. Diminished right femoral pulse with a cool, mottled right foot.

ECGSinus tachycardia, left ventricular hypertrophy, ST-segment depression in the inferior leads. No ST elevation.

IMAGING (CT / TEE)Outside CTA: intimal flap extending from the aortic root through the arch into the descending thoracic aorta, with the dissection reaching the right common iliac. A moderate pericardial effusion is noted. Post-induction TEE planned to confirm the diagnosis, grade aortic regurgitation, interrogate the coronary ostia and regional wall motion, and assess for tamponade and true-lumen wire position.

LABSHgb 12.6 g/dL; platelets 210 K/uL; INR 1.1; creatinine 1.5 mg/dL; lactate 3.2 mmol/L; troponin mildly elevated; type and crossmatch in progress.

OR ARRIVALAwake, in severe pain, hypertensive and tachycardic. One 18 g peripheral IV. No arterial line yet. External defibrillator pads on. Surgeon scrubbing; perfusion setting up for possible deep hypothermic circulatory arrest. Blood products being mobilized.

A. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Anti-impulse hemodynamic control before and through induction in an unrepaired Type A dissection; arterial-line site and large-bore access decisions driven by the dissection anatomy and malperfusion; the collision of acute aortic regurgitation, tamponade, and induction; and cerebral protection for deep hypothermic circulatory arrest.

1. Anti-impulse control and access before induction

Before any drug, hemodynamic goals here? Why? Targets for HR and BP? Agent first — beta-blocker or vasodilator? Why that order? First move? Esmolol? Then nicardipine or nitroprusside? Where do you place the arterial line, and why this site over the alternatives? Which arm — right or left? Why? Access — what large-bore lines and monitors do you want in before induction, and which can wait?

Considerations and pitfalls

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Hemodynamic goals. anti-impulse therapy — lower aortic wall shear stress by controlling rate of rise of pressure (dP/dt) and heart rate, not just the number; an unrepaired dissection can rupture or extend with a hypertensive, tachycardic, high-impulse aorta. Treating this as ordinary hypertension is a flag.
HR and BP targets. want concrete targets — HR ~60, SBP ~100-120 while preserving vital-organ and (here) limb perfusion; named numbers, not 'lower it.'
Beta-blocker before vasodilator / why order. rate control first so a vasodilator does not provoke reflex tachycardia and a rise in dP/dt that worsens the dissection; giving nitroprusside alone first is the classic error to probe.
First agent / titration. titratable beta-blockade (esmolol) to bring HR down, then add a vasodilator (nicardipine, nitroprusside) if SBP remains high with adequate rate control. Caution: with significant acute AR, beta-blockade blunts the compensatory tachycardia and can worsen forward flow — want that recognized.
Arterial line site. the dissection and the right-arm/left-arm pressure differential plus a possible axillary cannulation strategy drive the site; right radial detects innominate compromise but is unreliable if right axillary antegrade perfusion is used, in which case left radial is needed; femoral line senses distal aortic perfusion. Want a defended choice, often bilateral radial plus femoral, tied to the surgical plan.
Right vs left arm. the higher (true-lumen) pressure and which great vessel may be malperfused govern which side reads a real central pressure; a single arbitrary radial line is the trap.
Large-bore access / sequence. large-bore IV access and rapid-transfusion capability and central access for vasoactives and CVP/PA monitoring before a case that may need massive transfusion and circulatory arrest; an awake arterial line and adequate access should precede induction in this unstable aorta.

2. Induction with acute aortic regurgitation and effusion

Induction agents and doses here, and why? Goals for rate, rhythm, preload, afterload with the new diastolic murmur? Why? Despite a controlled induction, BP falls to 74/40 and the rhythm slows to 50. Of concern? Why in this patient? Rx? Phenylephrine? Ephedrine? Volume? To what end point? Post-induction TEE shows severe aortic regurgitation and a growing pericardial effusion with early diastolic RV collapse. Bearing? Does this change how fast the chest must be opened? The surgeon asks to open the pericardium now — your hemodynamic concern as tamponade is relieved?

Considerations and pitfalls

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Induction agents / goals. a smooth induction that avoids hypertensive surges (extension/rupture) and avoids hypotension (coronary and now limb/visceral malperfusion); preserve afterload and a controlled rate. Want preparedness for both directions, with anti-impulse control maintained.
Goals with acute AR. acute AR favors a relatively faster rate to shorten diastolic regurgitant time and avoid LV overdistension, adequate preload, and avoidance of high afterload that worsens the regurgitant fraction — directly in tension with the anti-impulse aim of slowing the heart; the candidate should name and resolve that conflict.
Hypotension and bradycardia. in acute AR a slow rate lengthens diastole and the regurgitant volume, dropping forward output and coronary perfusion of a hypertrophied LV; bradycardia is poorly tolerated. Reflexively treating like ordinary hypotension is a flag.
Phenylephrine vs ephedrine vs volume / end point. pure alpha-agonism raises afterload and can worsen AR regurgitant fraction; some chronotropy and preload support may serve acute AR better; want a defended agent and a concrete pressure/perfusion end point, not 'improve the BP.'
TEE — severe AR + effusion with RV collapse. tamponade physiology superimposed on acute AR; early diastolic RV collapse signals hemodynamically significant effusion and accelerates the timeline to sternotomy and bypass. Want recognition of tamponade without being told.
Pericardial decompression hazard. relief of tamponade can be followed by abrupt hypertension and aortic rupture; anticipate the surge, have anti-impulse agents and pressors ready, and coordinate femoral cannulation and CPB readiness before opening. Opening without that preparation is the trap.

3. Malperfusion across territories

You now have several malperfused beds at once. Which territories are at risk in this anatomy, and how would each declare itself? The right leg is cold and the femoral pulse is gone — bearing on cannulation strategy and on what you monitor? The TEE shows a new regional wall-motion abnormality of the inferior wall — interpretation? Bearing on your plan? Cerebral oximetry on the right drops 20 points after the surgeon begins right axillary perfusion — DDx? Checks? Rising lactate and a falling urine output — significance? What can the surgeon do about visceral and limb malperfusion, and when?

Considerations and pitfalls

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Territories at risk. coronary (ostial involvement — ischemia/wall-motion change), cerebral (carotid/innominate — stroke, asymmetric oximetry), visceral (mesenteric/renal — rising lactate, oliguria), and limb (iliac/femoral — pulse deficit, cold mottled leg). Want the candidate to enumerate by anatomy, not be handed them.
Limb malperfusion / cannulation. a lost femoral pulse argues against femoral arterial cannulation into a malperfused/false-lumen iliac; axillary or central true-lumen cannulation is favored, and TEE must confirm wire in the true lumen. Want the access decision tied to the malperfusion.
New inferior wall-motion abnormality. coronary ostial dissection (often right coronary) causing ischemia; bears on cannulation, on the need for concomitant CABG, and on inotropic support; not simply 'an old ECG change.'
Cerebral oximetry drop with axillary perfusion. malperfusion of the antegrade cerebral circuit — cannula malposition, dissection of the perfused vessel, line/flow problem, or a true-lumen issue; systematic check of flow, position, pressure, and TEE before accepting a falling brain saturation.
Rising lactate / falling UO. visceral and renal malperfusion; a marker that organ ischemia is ongoing and time-critical, informing urgency of restoring true-lumen flow and post-op renal vigilance.
Surgical options / timing. restoring true-lumen flow with the central repair often resolves downstream malperfusion; persistent limb or visceral ischemia may need a separate revascularization or fenestration. Want judgment on sequence, not a recited list.

4. Deep hypothermic circulatory arrest and cerebral protection

The arch must be opened, requiring circulatory arrest. Goals before arrest — temperature, and how do you confirm you are there? Other measures to protect the brain? Antegrade or retrograde cerebral perfusion — compare, and your preference here, with the right axillary already cannulated? Why? What do you monitor during arrest? Cooling and rewarming — your targets and the hazards of each? Rewarming too fast — concern? As you come off arrest, glucose is 240 — bearing on the brain, and target?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Temperature target / confirmation. deep hypothermia lowers cerebral metabolic rate to tolerate arrest; want a named target (e.g., ~18 C for unprotected DHCA, warmer with adjunctive cerebral perfusion) confirmed by site-specific (e.g., nasopharyngeal/tympanic) temperature and EEG silence where available, not 'cool the patient.'
Adjunctive neuroprotection. antegrade or retrograde cerebral perfusion to extend safe arrest time, topical cooling, glucose and acid-base management, possibly pharmacologic adjuncts; hypothermia plus cerebral perfusion is the spine of protection.
Antegrade vs retrograde. antegrade (via right axillary or selective great-vessel) delivers oxygenated flow and supports longer repairs; retrograde via SVC flushes debris and provides some cooling but less reliable substrate; with the axillary cannulated, antegrade is the natural choice — want a defended preference, not a definition.
Monitoring during arrest. cerebral oximetry, processed EEG/temperature, ensuring symmetric cerebral perfusion; asymmetry should prompt a check of the antegrade circuit.
Cooling/rewarming hazards. inadequate cooling risks ischemic injury; aggressive rewarming risks cerebral hyperthermia and worse neurologic outcome; want gradient and temperature-cap discipline.
Hyperglycemia and the brain. hyperglycemia worsens ischemic neurologic injury around arrest; want a moderate glucose target and treatment, recognizing the at-risk brain rather than ignoring the number.

B. POST-OPERATIVE CARE

Teaching focus. Coagulopathy and massive transfusion after a long circulatory-arrest run; tamponade in the fresh postsurgical chest; a post-op neurologic deficit after arch repair and arrest; acute kidney injury layered on intra-op malperfusion; and an honest family disclosure that coordinates with the surgical team.

1. Coagulopathy and massive transfusion off a long arrest

Off bypass after a long arrest, the field is diffusely oozing and chest-tube output is 300 mL/hr. Of concern? Surgical vs medical bleeding — how do you distinguish here? Why does this particular case predispose to coagulopathy? Residual heparin after protamine — how would you know? Which tests guide you? TEG/ROTEM shows low fibrinogen at 110 and a long clotting time; platelets 80. What do you give, and in what order? Bearing of the aspirin he took in the ED? Targets you are resuscitating to — temperature, calcium, pH? When does he go back for re-exploration?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Of concern. rate and diffuse character signal a developing coagulopathy on top of possible surgical bleeding; act before he becomes unstable. The combination is dangerous.
Surgical vs medical. brisk, sustained, bright bleeding with a normalizing profile points surgical; diffuse oozing with abnormal studies points medical — the distinction drives re-exploration versus product correction; both can coexist here.
Why this case predisposes. long deep-hypothermic circulatory arrest, prolonged bypass, hemodilution, hypothermia-induced platelet and enzyme dysfunction, fibrinolysis, and consumption — a recognized recipe for post-arrest coagulopathy. Want this reasoned, not a generic 'they bleed.'
Residual heparin. heparin-protamine mismatch or rebound; assess with ACT/anti-Xa or heparinase TEG comparison and redose protamine if confirmed.
Targeted products / order. fibrinogen 110 favors cryoprecipitate/fibrinogen concentrate; long clotting time favors plasma/factors; platelets 80 with bypass and aspirin dysfunction favor platelets; correct the specific deficit and consider antifibrinolytic rather than blind product.
Aspirin / metabolic targets. the ED aspirin adds platelet dysfunction favoring transfused platelets; resuscitate the lethal triad — normothermia, ionized calcium, correct acidosis — without which products will not clot. Ignoring temperature/calcium is the trap.
Return to OR. persistent high-volume bleeding despite corrected coagulation, tamponade physiology, or instability mandates re-exploration; endless transfusion without surgical control is the error.

2. Postoperative tamponade

Four hours into the ICU, chest-tube output abruptly drops to near zero. CVP 21, PA 40/23, CI 1.5, BP 84/50, oliguric. DDx? Diagnostic studies — which, and how fast? TEE is equivocal for a discrete effusion in a fresh postsurgical chest — bearing? Your immediate priorities? Is a diuretic indicated for the oliguria? Why/why not? How will you maintain output until the OR? Induction priorities for re-exploration here? Agents?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

DDx. tamponade from localized clot given equalizing pressures and a tube that stopped, RV failure, hypovolemia, graft/suture-line bleeding, pneumothorax; the stopped tube plus rising filling pressures is the pattern to recognize unprompted.
Diagnostics / equivocal TEE. echo is first-line but localized postsurgical clot is easily missed; a high index of suspicion and direct surgical communication outweigh a negative study.
Priorities. maintain preload and rate, support pressure, avoid anything that drops venous return, mobilize surgery for re-exploration.
Diuretic. contraindicated — the oliguria is from low forward flow, not volume overload; diuresing a tamponading patient worsens filling. A reflexive diuretic order is a red flag.
Maintain CO until OR. keep full, fast, and tight — preserve preload and chronotropy, pressor support, prepared to open the chest at bedside if arresting.
Induction for re-exploration. preserve preload/afterload/rate, anticipate decompensation on relief of tamponade, surgeon prepped and scrubbed before induction.

3. Postoperative neurologic deficit

Sedation is off, but at 6 hours he does not follow commands and the left side is weak. DDx? Most concerning here, given the operation he had? Why is an arch repair with circulatory arrest a setup for it? Workup — what, and how urgently? Imaging shows an acute right MCA territory infarct. Bearing on prognosis and on what you do now? Whom do you involve? What can you still offer this patient?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

DDx. residual sedation/metabolic causes, embolic or hypoperfusion stroke, watershed injury from the arrest, seizure, intracranial hemorrhage; a focal deficit shifts suspicion toward a structural cause.
Most concerning / why this operation. arch manipulation, atheroembolism, air, and the circulatory-arrest period itself make embolic and hypoperfusion stroke a recognized risk after Type A repair; want this tied to the procedure, not generic.
Workup urgency. urgent neuro exam and CT/imaging; time-sensitive because it changes prognosis, anticoagulation, and goals of care.
Bearing now. a large fresh infarct constrains any anticoagulation, raises hemorrhagic-conversion concern, and reframes the recovery trajectory; informs blood-pressure and supportive targets.
Involve / offer. neurology and surgery; supportive neuroprotective ICU care — perfusion, glucose, temperature — and honest, shared prognostication rather than nihilism or false hope.

4. Renal injury and ongoing instability

By the next morning creatinine has risen to 3.0 and he is making 10 mL/hr of urine despite an adequate pressure. DDx for the renal injury in this specific patient? Bearing of the intra-op course? Is a fluid challenge or a diuretic the right next step? Why/why not? How do you protect what kidney function remains? He becomes hyperkalemic at 6.4 with peaked T waves — immediate Rx? Indications for renal replacement here, and how does it interact with his bleeding and anticoagulation?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

DDx in this patient. ischemic ATN from intra-op visceral/renal malperfusion and the arrest, low forward output, nephrotoxins/contrast from the CTA, pigment from transfusion/hemolysis; want it tied to his specific course, not a textbook list.
Bearing of intra-op course. documented malperfusion, hypotension, bypass, and circulatory arrest make ischemic injury the leading mechanism — recognizing that guides expectations and management.
Fluid vs diuretic. assess volume and forward flow first; he is likely not volume-deplete and reflexive diuresis or fluid-loading without that assessment is the trap — optimize perfusion pressure and output instead.
Renal protection. maintain perfusion pressure and output, avoid further nephrotoxins, manage acid-base and potassium; no agent reliably 'rescues' established ATN.
Hyperkalemia Rx. membrane stabilization with calcium, shift with insulin/glucose and beta-agonist, and removal — with peaked T waves this is an emergency; want the sequence and urgency.
RRT indications / interaction. refractory hyperkalemia, acidosis, volume overload, uremia; in a freshly bleeding, possibly anticoagulation-restricted patient, favor a circuit/strategy that minimizes anticoagulation (e.g., regional citrate or no-heparin CRRT). Want awareness of the bleeding interaction.

5. Family disclosure

He is now awake but with a residual left-sided deficit, extubated and hemodynamically stable. The family arrives and asks why he isn't moving his left side normally and whether the operation caused it. What will you tell them? How much do you disclose now versus defer? How do you coordinate that message with the surgical team? They ask whether this could have been prevented — how do you respond? What must they understand about his kidney injury and recovery before discharge planning?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Telling the family. a plain, honest account of the stroke, that it was recognized and is being treated, the genuine uncertainty of recovery, without overpromising or assigning blame; leave room for questions.
How much / when. disclose what is known plainly and promptly; acknowledge uncertainty rather than guessing at prognosis or cause before the picture is clear; defer specifics you do not yet have rather than speculate.
Coordinate with surgery. a single, consistent message agreed with the surgical team so the family is not given conflicting accounts of cause or prognosis.
'Could it have been prevented'. frame stroke as a recognized, sometimes unavoidable risk of emergency Type A repair and circulatory arrest, honestly and without defensiveness or false guarantees; avoid both blame and dismissiveness.
Kidney injury / recovery. they should understand the AKI, the possibility of temporary dialysis, and the multi-organ recovery course this kind of emergency carries, so discharge expectations are realistic.

C. ADDITIONAL TOPICS

Teaching focus. Unrelated by design: a regional-anesthesia crisis after an eye block, an obstetric collapse at delivery, and refractory hypoxemia in the ICU. Rapid pivot across domains.

1. Retrobulbar block complication

A 72 y.o. man undergoing cataract surgery becomes acutely bradycardic, then within minutes confused, dysarthric, and apneic shortly after a retrobulbar block. Possible causes? Most concerning? Mechanism of brainstem anesthesia after a retrobulbar block? Immediate management? How would your differential change if instead he developed sudden proptosis and a tense globe right after the injection? How could the original event have been reduced?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Possible causes. brainstem anesthesia from intrathecal spread of local anesthetic, oculocardiac reflex, intravascular local-anesthetic injection, and a primary cardiac or neurologic event.
Most concerning. brainstem anesthesia causing apnea and depressed consciousness, which is immediately life-threatening.
Mechanism. spread of local anesthetic along the optic nerve sheath into the subarachnoid space, producing central effects including respiratory arrest.
Management. support ventilation and the airway and circulation until the block recedes; the event is usually transient with prompt respiratory support, and failing to ventilate is the danger.
Proptosis and tense globe. that picture suggests retrobulbar hemorrhage with rising orbital pressure threatening the optic nerve, prompting urgent ophthalmology assessment and possible canthotomy rather than central support.
Risk reduction. meticulous technique with appropriate needle choice and depth, aspiration before injection, and consideration of less invasive blocks; relying on technique alone without monitoring is worth a probe.

2. Suspected amniotic fluid embolism at delivery

A 31 y.o. woman at term has just delivered vaginally under a labor epidural. Moments after delivery she becomes acutely dyspneic and agitated, SpO2 falls to 78%, BP is 70/40, and oozing is noted from her IV sites. DDx? Leading diagnosis and why? Immediate priorities? She arrests with PEA — how is resuscitation in late pregnancy modified? Role of perimortem cesarean delivery and its timing? She is resuscitated but now diffusely bleeding — interpretation and management?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

DDx. amniotic fluid embolism, eclampsia, high/total spinal, local anesthetic systemic toxicity, pulmonary embolism, hemorrhage with hypovolemia, anaphylaxis.
Leading diagnosis. amniotic fluid embolism — abrupt cardiorespiratory collapse plus coagulopathy around delivery; a clinical diagnosis of exclusion.
Immediate priorities. call for help, secure the airway, support oxygenation and circulation, left uterine displacement, large-bore access, activate massive transfusion.
Resuscitation in late pregnancy. manual left uterine displacement or tilt, no change to drug doses or defibrillation energy, anticipate difficult airway and rapid desaturation.
Perimortem cesarean. consider delivery within about 4 minutes of arrest to aid maternal resuscitation; an answer that delays it indefinitely is worth probing.
Coagulopathy. DIC is common with AFE; treat with goal-directed product replacement and fibrinogen; reassess with point-of-care testing.

3. ARDS with refractory hypoxemia

A 55 y.o. man with severe pneumonia is intubated in the ICU. On volume control with FiO2 1.0 and PEEP 12, the PaO2 is 58, the PaO2/FiO2 ratio is 90, and the plateau pressure is 32 cm H2O. Of concern? Interpretation of these numbers? Tidal-volume target and why? Plateau-pressure goal? He stays hypoxemic — higher PEEP, recruitment, or prone positioning? Defend. Role of neuromuscular blockade? When would you consider ECMO? BP falls to 80/50 as you raise PEEP — DDx and Rx?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Diagnosis. ARDS — acute, bilateral infiltrates not fully explained by cardiac failure, with a PaO2/FiO2 of 90 placing it in the severe range.
Tidal volume. low tidal volume (~6 mL/kg predicted body weight) lung-protective ventilation; an answer that ventilates to a normal CO2 at the cost of high volumes is worth challenging.
Plateau pressure. keep plateau ≤ ~30 cm H2O; 32 is above target and the candidate should respond to it.
Higher PEEP vs recruitment vs prone. each is defensible if reasoned; proning has the strongest outcome signal in severe ARDS. Look for a committed, justified escalation rather than a list.
Neuromuscular blockade. may be considered for severe dyssynchrony or refractory hypoxemia; not a default for every ARDS patient.
Hypotension on raising PEEP. reduced venous return vs pneumothorax vs sepsis; lower PEEP or give volume/pressor, and exclude pneumothorax before simply pushing fluids.

Session 2 — short stem

Pacemaker-dependent ICD patient for noncardiac surgery with EMI

A 79 y.o., 88 kg man with an implantable cardioverter-defibrillator placed for nonischemic cardiomyopathy and an episode of monomorphic VT is scheduled for an elective laparoscopic sigmoid colectomy. He is pacemaker-dependent, in permanent atrial fibrillation after an AV-nodal ablation, and his last device interrogation was 11 months ago. The surgical team plans extensive monopolar electrocautery, and the patient will be in steep Trendelenburg with the device generator on the left upper chest. He has an LVEF of 25% and chronic kidney disease; he takes carvedilol, sacubitril-valsartan, furosemide, and apixaban. He tells you he 'gets the device checked sometimes' and once 'felt a big jolt' a year ago, and he has brought no card or printout. P 70 (paced); BP 142/80; SpO2 95% on room air; K+ 5.1 mEq/l.

A. PRE-OPERATIVE EVALUATION

Teaching focus. What you must know about a CIED before an EMI-heavy case, and how to get it: device type, indication, pacing dependence, tachytherapy status, and currency of interrogation; building the EMI and reprogramming plan from those facts rather than reflexively reaching for a magnet.

1. Device information you need and how to get it

What must you know about this device before proceeding? Why each? He has no card and cannot give you the settings — how do you obtain them? Is his last interrogation current enough for this case? Why/why not? What is your threshold to interrogate before the OR? Is the underlying rhythm something you can read off the monitor, or must the device tell you? Does his 'big jolt' bear on what you order? Whom do you call, and what do you ask them to do?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

What you must know. device type (pacemaker vs ICD vs combined), manufacturer, indication, pacing dependence and underlying rhythm, current mode and rates, tachytherapy on/off, battery status, last interrogation. Pacing dependence is the single most important fact; reciting NBG letters instead of asking these is a flag.
No card, vague history. obtain a recent interrogation report from the managing EP/cardiology service, query the manufacturer, or get a perioperative device interrogation; do not proceed on the patient's recollection.
11-month interrogation. outside typical pre-op windows for an ICD/combined device (commonly interrogated within ~3 months); too stale here given dependence and planned EMI. Want recognition that this needs a fresh interrogation, not a recited number.
Underlying rhythm. in a paced, AV-node-ablated patient the monitor shows paced beats; the intrinsic escape (or absence of one) comes from interrogation. Assuming the monitored rhythm is the underlying rhythm is the trap.
The 'big jolt'. suggests a prior ICD shock — confirms tachytherapy capability and raises the stakes for disabling it during cautery; drives the interrogation and reprogramming plan.
Who to call. the perioperative device/EP service to interrogate, document dependence and settings, and plan reprogramming; a clear ask, not a vague 'cardiology consult.'

2. Pacing dependence and underlying rhythm

Interrogation confirms he is 100% ventricularly paced with no escape below 30. Bearing on your intra-op plan? What specifically worries you about EMI in a dependent patient? Does his AV-nodal ablation change how you think about this versus a patient with sinus node disease? If the device inhibits during cautery, what does this patient do? How does dependence shape your choice between a magnet and reprogramming? What backup for pacing do you want available in the room before incision?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

100% paced, no escape. EMI-induced oversensing can inhibit pacing output; with no underlying escape this means asystole, not just a dropped beat. The candidate should connect dependence directly to the asynchronous-pacing decision.
Why EMI worries you here. monopolar cautery can be oversensed as intrinsic activity and inhibit the pacemaker; in a dependent patient that is life-threatening.
AV-nodal ablation. an ablated node means no reliable conduction or escape — this is what makes him truly dependent; contrast with sinus node disease where some intrinsic rhythm may persist.
Inhibition consequence. asystole until the EMI stops; recognizing the catastrophic, not nuisance, nature is the point.
Magnet vs reprogram. dependence pushes toward securing asynchronous pacing (VOO here) so cautery cannot inhibit output. Because the device is an ICD, a magnet will not deliver asynchronous pacing — it only suspends shocks — so reprogramming is the route here, not a magnet.
Backup. external pacing/defibrillation pads applied and connected, drugs and a plan for transcutaneous pacing; do not rely on the device alone in a dependent patient during EMI.

3. Tachytherapy and the ICD before this case

His device is also an ICD with tachytherapy on. Of concern given the planned cautery? Why? What do you want done with the tachytherapy function, and when? If it is disabled, what must be true in the room from that moment on? Above or below the umbilicus — does the surgical site change your EMI risk assessment here? Does his positioning and the generator's location bear on that risk? Reprogram the ICD off versus use a magnet — which do you choose for this patient, and why?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Tachytherapy on during cautery. monopolar EMI can be misread as VT/VF and trigger an inappropriate shock intra-op; this is the central ICD-specific hazard. Want this surfaced, not the EMI risk treated generically.
What and when. disable antitachycardia therapy for the cautery portion, arranged with the device team, ideally just before incision and reactivated post-op.
Once disabled. external defibrillator pads on and connected and a defibrillator in the room from the moment therapy is off, with continuous monitoring; the device can no longer rescue a real arrhythmia.
Surgical site. abdominal/below-umbilicus cautery carries lower clinically meaningful EMI than thoracic/above-umbilicus, but this is a hedge, not a pass — laparoscopic colectomy still involves substantial cautery and the generator is in the upper chest.
Trendelenburg, generator near field. proximity of the active electrode and return path to the generator/leads raises EMI risk; reinforces disabling tachytherapy and optimizing cautery technique.
Reprogram vs magnet for the ICD. in a dependent patient a magnet over an ICD suspends shocks but does NOT make the pacemaker asynchronous — so it solves inappropriate shocks but not inhibition. Reprogramming addresses both. Choosing a magnet alone for a dependent ICD patient deserves a hard probe.

4. Optimization and the EMI plan

Of concern about his potassium and his medication regimen before a case where you may need to pace and defibrillate? Rx? How do you want the cautery run — bipolar vs monopolar, and if monopolar, what do you ask of the surgeon? Where do you want the dispersive pad, and why? Does his anticoagulation bear on placing external pads or a central line, and on the case itself? What is your one-line plan you hand off to the team before incision?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

K+ 5.1 before pacing/defibrillation. hyperkalemia raises pacing thresholds and arrhythmia risk and degrades defibrillation in a patient you may depend on both for; correct toward normal before proceeding. Ignoring it in a dependent ICD patient is a flag.
Rx. treat hyperkalemia (shift and remove), recheck, and confirm thresholds are reliable; tie it to the dependence, not a generic potassium answer.
Bipolar vs monopolar. bipolar avoids the EMI entirely and is preferred where feasible; if monopolar, ask for short intermittent bursts at lowest effective power and to avoid cautery directly over the generator/leads.
Dispersive pad. place so the current path between active tip and pad arcs away from the generator and leads — keep the heart out of the arc; with whole-table pads assume some current near the device and plan accordingly.
Apixaban. bearing on neuraxial/central access timing and bleeding; external defibrillation pads are noninvasive and unaffected, but a planned line or any rescue procedure must account for residual anticoagulation and renal clearance.
One-line handoff. a crisp pre-incision plan: dependent ICD patient, tachytherapy off, pacing asynchronous, pads on and connected, bipolar/short-burst cautery, K+ corrected, device team to reactivate post-op.

B. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Executing and adapting the EMI plan: securing asynchronous pacing and disabling tachytherapy, recognizing and responding to oversensing/inhibition and inappropriate shocks in real time, managing loss of capture, and the hazards of asynchronous pacing itself in this failing ventricle.

1. Securing the device for cautery

You are ready to induce. How and when do you put the pacemaker into asynchronous mode and the ICD's tachytherapy off? Magnet or reprogramming for this patient — commit and defend. If you use a magnet, what does it do to the pacing function of this device? Is that what you need here? What rate will asynchronous pacing run, and is that adequate for a steep-Trendelenburg laparoscopic case in a patient with his ventricular function? What must be confirmed before the surgeon starts cautery?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

How and when. arrange device-team reprogramming to asynchronous pacing and tachytherapy off, completed and confirmed before cautery begins; full monitoring and pads from that point.
Magnet vs reprogram, commit. for a dependent ICD patient, reprogramming is the cleaner commit — it makes pacing asynchronous (VOO) AND disables shocks. A magnet over an ICD disables shocks but does NOT make the pacing asynchronous, so a dependent patient could still be inhibited. Want a defended choice that reflects this.
What a magnet does here. over an ICD it suspends tachytherapy only, with no effect on pacing mode; relying on it to prevent inhibition in a dependent patient is the misconception to catch.
Asynchronous rate adequacy. fixed-rate VOO at a default may underserve a low-EF patient under pneumoperitoneum and Trendelenburg; consider a higher programmed rate to support output. A candidate who ignores the hemodynamic adequacy of the set rate deserves a probe.
Before cautery. confirm asynchronous capture on the monitor, tachytherapy off, pads on and connected, defibrillator in room; only then clear the surgeon.

2. Oversensing and inhibition

Despite preparation, early in the case you see the paced rhythm drop out whenever the surgeon activates cautery, with pauses on the monitor. Interpretation? Immediate actions, in order? What do you tell the surgeon right now? If this device were NOT yet asynchronous, what would these pauses mean in this patient? How does a magnet help or not help in this moment? Pauses persist despite stopping cautery — now what? What is your endpoint before you let cautery resume?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Interpretation. EMI oversensing inhibiting pacing output — the device reads cautery as intrinsic activity and withholds the spike. In a dependent patient these pauses are asystole, recognized without prompting.
Immediate actions. tell the surgeon to stop cautery, confirm/establish asynchronous pacing via the device team, ensure pads on and connected, support circulation; recognize that over an ICD a magnet will not fix the inhibition (it only suspends shocks), so reprogramming is what secures pacing here.
Tell the surgeon. stop cautery now; coordinate short bursts only once the device is secured.
If not yet asynchronous. the pauses are EMI-induced asystole — life-threatening in a dependent patient — and the reason asynchronous pacing was the plan.
Magnet now. over this ICD a magnet suspends tachytherapy but leaves the pacing mode in demand — it does NOT stop the EMI inhibition, so it does not rescue these pauses. The fix is reprogramming to asynchronous pacing; a candidate who reaches for the magnet expecting it to solve inhibition has the core misconception.
Persistent pauses / endpoint. if pauses continue, pace externally via the pads, escalate, and do not resume cautery until reliable asynchronous capture is confirmed.

3. Inappropriate shock and arrhythmia

Suppose the team had NOT disabled tachytherapy. Mid-case the device delivers a shock and the patient's pressure drops. Of concern? What likely happened? Immediate management? Now consider the opposite: tachytherapy is correctly off and the patient genuinely goes into VF on the monitor. What protects him now, and what do you do? How fast do you defibrillate, and with what? Once stable, what must happen to the device before you continue?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Shock with tachytherapy on. EMI misread as VT/VF triggering an inappropriate shock; concern for the shock itself, induced arrhythmia, and hemodynamic compromise in a 25% EF. Recognize this as the predicted hazard of leaving therapy on.
Immediate management. stop cautery, place a magnet to suspend further shocks if not reprogrammed, assess rhythm and hemodynamics, support as needed, get the device team.
Tachytherapy off and real VF. with ICD therapy disabled the device will NOT rescue him — external defibrillation via the pads is the safety net, which is exactly why pads were placed and connected.
How fast / with what. immediate external defibrillation through the applied pads at appropriate energy, ACLS, treat reversible causes; speed is the point because the device is intentionally disarmed.
Device before continuing. reinterrogate, reactivate tachytherapy appropriately, confirm pacing and sensing before relying on it again.

4. Loss of capture

Later you note pacing spikes on the monitor but the rate and blood pressure don't match — narrow complexes between spikes, hypotension. Interpretation? Does a pacing spike guarantee capture? How do you confirm? DDx for loss of capture here? Bearing of his K+ and any lead issue? How do you restore capture — what do you adjust, and what is your backup if the device won't capture? Pneumoperitoneum and Trendelenburg are on — do they bear on any of this?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Spikes without matching rate/BP. loss of capture — the spike is delivered but not depolarizing the myocardium; the surface spike is not proof the heart responded.
Spike ≠ capture. telemetry shows the spike, not the myocardial response; confirm with paced morphology (RV pacing gives an LBBB-pattern wide complex) and a matching pulse/pressure, not the spike alone.
DDx. rising threshold from hyperkalemia, ischemia, or lead problem; lead dislodgement or fracture; inadequate output; metabolic derangement.
K+ and leads. hyperkalemia raises capture threshold — his K+ matters; also consider lead integrity, especially with positioning and a stale interrogation.
Restore capture / backup. increase output, correct K+, check connections and settings; if the device cannot capture, pace externally through the pads and get the device team — do not keep delivering uncaptured spikes.
Position effects. pneumoperitoneum and Trendelenburg shift physiology and can stress a borderline lead and a failing ventricle; relevant to both capture and hemodynamics.

5. Hazards of asynchronous pacing

He is being paced VOO at a fixed rate while cautery runs. What is the specific danger of asynchronous pacing if intrinsic ventricular activity returns? Mechanism? In whom and when is that risk highest? The surgeon finishes the cautery portion and you have a quiet field — do you keep him asynchronous, and why or why not? As you near emergence and transport, what mode do you want, and what must you never do on the way to the PACU? How do you confirm the device is doing what you think before you move him?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Danger of asynchronous pacing. a fixed-rate spike can land on a returning intrinsic beat's vulnerable period — R-on-T — and precipitate VF. The candidate should name this as the cost of asynchronous mode, not treat it as free.
Mechanism / when highest. asynchronous pacing ignores intrinsic activity; risk is highest when an underlying rhythm returns and competes — relevant once EMI stops and demand pacing could safely resume.
Keep asynchronous after cautery?. once cautery is done, returning to demand pacing avoids competition and R-on-T; staying VOO with no EMI source needlessly carries that risk.
Emergence/transport mode. restore appropriate demand pacing (and plan tachytherapy reactivation) before transport; never travel in asynchronous mode unless explicitly intended and discussed.
Confirm before moving. verify mode, capture, and that tachytherapy status is what you intend, on full monitors, before leaving the OR; reinterrogation by the device team closes the loop.

C. ADDITIONAL TOPICS

Teaching focus. Unrelated by design: a pediatric airway emergency on emergence, an obstetric postdural puncture headache, and an operating-room fire. Rapid pivot across domains.

1. Laryngospasm on emergence in a child

A 3 y.o. with a runny nose for the past week undergoes bilateral myringotomy under mask anesthesia. During emergence the child develops stridor, then no air movement, and SpO2 falls to 80%. Diagnosis? Contributing factors in this child? Immediate maneuvers and their sequence? SpO2 now 70% with bradycardia to 60 — Rx? If laryngospasm persists, agent and dose? Once recovered, what will you tell the parents about the risk and your decision to proceed?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Diagnosis. laryngospasm — stridor progressing to complete glottic closure, classically on light emergence.
Contributing factors. recent URI, light plane of anesthesia, airway secretions, young age.
Maneuvers and sequence. remove the stimulus, 100% oxygen, jaw thrust with continuous positive airway pressure (Larson maneuver); escalate if it fails.
Bradycardia with desaturation. deepen anesthesia (propofol) or give succinylcholine; treat hypoxic bradycardia and be ready to ventilate or intubate; an answer that gives succinylcholine without addressing oxygenation deserves a probe.
Succinylcholine. a small IV dose breaks refractory laryngospasm; IM is an option without IV access; have atropine available in the young child.
Counseling parents. a plain explanation of what happened, that it was recognized and treated, and the implications for timing future elective anesthesia after a URI.

2. Postdural puncture headache

A 28 y.o. woman, 24 hours after a labor epidural complicated by a recognized wet tap, has a positional fronto-occipital headache that is relieved by lying flat. Diagnosis and supporting features? What else must you exclude? Conservative measures? She cannot care for her newborn — definitive treatment and how it works? Risks of that procedure?

Considerations and pitfalls

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Diagnosis. postdural puncture headache — postural, following a known dural puncture.
Must exclude. other serious causes of postpartum headache (preeclampsia, cortical vein thrombosis, meningitis, subdural hematoma) before anchoring on PDPH.
Conservative measures. time, analgesia, hydration, caffeine; evidence is limited, and overstating their efficacy is worth a probe.
Definitive treatment. epidural blood patch, which works by tamponade and by sealing the dural leak.
Risks. repeat dural puncture, back pain, infection, rare neurologic complications.

3. Operating-room fire during MAC

During MAC with nasal-cannula oxygen for an excision on the face, the surgeon uses electrocautery and a flash fire ignites at the drapes. Immediate actions? Sequence of priorities? How does the fire triad apply here? How could this have been prevented? Once the fire is out, your assessment of the patient?

Considerations and pitfalls

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Immediate actions. stop the procedure, stop the supplemental oxygen and remove the airway source, remove the burning drapes and material, extinguish.
Priority sequence. protect the patient and remove the fuel and oxidizer first, then extinguish, then attend to the patient — the order matters.
Fire triad. oxidizer (supplemental O2 pooling under drapes), ignition (cautery), fuel (drapes, prep, hair) — a high-risk head-and-neck MAC setup.
Prevention. minimize or avoid open high-flow O2 near cautery, secure the airway or use blended air, let the prep dry, tent the drapes to avoid oxygen pooling.
Post-fire assessment. evaluate the airway and any skin or airway burns, confirm ventilation, plan airway management if inhalation injury is suspected.

Session 2 — short stem

Myasthenia gravis for abdominal hysterectomy

A 40 y.o., 50 kg, 5'2" woman is scheduled for abdominal hysterectomy for menorrhagia. History of myasthenia gravis and hiatal hernia with esophageal reflux. Medications: pyridostigmine (Mestinon) 360 mg/day, prednisone 15 mg/day, antacids. Vital signs: HR 80; BP 120/80; RR 18; T 37°C. Hgb 9.3 g/dL.

A. PRE-OPERATIVE EVALUATION

Teaching focus. Assessing adequacy of MG therapy and predicting postop ventilatory risk; transfusion decision-making in chronic anemia; aspiration risk from hiatal hernia with reflux; stress-dose steroids in the chronically treated patient.

1. Myasthenia gravis

Anesthetic concerns with myasthenia? How assess adequacy of therapy? How manage her meds preop? PFTs preop — yes? Which? Why? What do you expect if therapy adequate? Bearing on your plan for NMB?

Considerations and pitfalls

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Concerns. resistance to sux, sensitivity to NDMR, bulbar weakness and aspiration risk, postoperative respiratory failure, steroid-related HPA suppression.
Adequacy. ptosis, diplopia, dysphagia, proximal weakness; bedside FVC, NIF, single-breath count; medication compliance and prior hospitalization history.
Meds. continue pyridostigmine (some hold the morning dose to limit sux interaction and secretions — controversial); continue steroids with a stress dose.
PFTs. yes if bulbar or severe symptoms — FVC, NIF; predicts postoperative ventilation need.
Adequate therapy. FVC >50% predicted, NIF more negative than -25, no bulbar symptoms.
NMB plan. anticipate exaggerated NDMR effect; use sugammadex-reversible roc at reduced dose if NMB required; consider techniques that avoid NMB.

2. Anemia

Surprised she's anemic? Etiologies? Transfuse preop — yes/no? Why? Acute vs chronic anemia — does it change your threshold? Why? Target Hgb? Bearing on her case if she bleeds intraop?

Considerations and pitfalls

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Surprised. no — menorrhagia explains chronic blood loss.
Etiologies. chronic blood loss/iron deficiency; rule out chronic disease, hemolysis, marrow issues.
Transfuse preop. no — stable, asymptomatic; optimize with iron, defer elective surgery if needed.
Acute vs chronic. chronic better tolerated (2,3-DPG up, compensated); acute drops threshold.
Target. 7-8 in healthy patients, 8-10 with cardiac disease or active bleeding.
Bearing. low starting reserve means earlier escalation if she bleeds intraop.

3. Hiatal hernia and aspiration

Importance of hiatal hernia with reflux? Does severity of reflux affect aspiration risk? How determine severity? Preop measures to reduce aspiration risk? Does this mandate RSI? Why? Cricoid — yes/no? Awake intubation — when?

Considerations and pitfalls

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Importance. increased aspiration risk on induction and emergence.
Severity. yes — frequency, nocturnal symptoms, regurgitation volume, response to PPI inform the risk.
Determine. history, PPI response, EGD if needed.
Preop measures. NPO, H2 blocker, PPI, non-particulate antacid (sodium citrate), metoclopramide.
RSI. yes for symptomatic GERD plus hiatal hernia; cricoid as judged; awake intubation if airway concerns.
Awake intubation trigger. anticipated difficult airway plus active reflux argues for awake.

4. Steroid therapy

Does chronic steroid affect your management? How? Is 15 mg/day prednisone sufficient for surgery? Why? Stress dose plan? How recognize adrenal insufficiency under GA? Risks of high-dose hydrocortisone (100 mg) preop?

Considerations and pitfalls

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Affects management. HPA suppression, infection risk, hyperglycemia, fragile skin, delayed healing.
15 mg sufficient. no for major surgery — stress dose.
Stress dose. hydrocortisone 100 mg pre-induction, then 50 mg q8h × 24 h, taper.
Recognize AI under GA. refractory hypotension despite fluids/pressors, hypoglycemia, hyperkalemia, hyponatremia.
High-dose risks. hyperglycemia, infection, fluid retention, impaired healing; minimal for a single dose; benefits outweigh.

B. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Monitor selection in MG; regional vs GA when bulbar weakness limits both; muscle-relaxant choice and the sux-pyridostigmine interaction; transfusion and red-urine DDx during pelvic dissection; extubation readiness in the patient who cannot afford residual block.

1. Monitor selection

TOF reliable in myasthenia? Why? Indicates need for relaxant? Anemia — bearing on SpO2 monitoring? Why? ETCO2 — yes? Waveform vs value alone — which? Why?

Considerations and pitfalls

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TOF reliable. yes — baseline often shows fade; essential for NDMR titration.
Indicate need for relaxant. no — TOF assesses neuromuscular function, not surgical need for relaxation.
Anemia + SpO2. reliable until severe (<5 g/dL); measures % of available Hgb saturated; needs pulsatile flow.
ETCO2. standard plus hypoventilation risk in MG.
Waveform vs value. waveform confirms airway, detects bronchospasm, rebreathing, leak, disconnect.

2. Anesthetic technique

Regional acceptable? Why/why not? Advantages and disadvantages? Patient consents to regional — spinal or epidural? Why? Level you want for hysterectomy? How achieve? What if block is too high?

Considerations and pitfalls

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Regional acceptable. yes — avoids airway manipulation and NMB.
Advantages. spares NMB, better postoperative pulmonary function, postoperative analgesia.
Disadvantages. high block compromises ventilation given baseline weakness, full stomach risk, anxiety, T4 level needed for hysterectomy.
Spinal vs epidural. epidural — slower titratable level, lower max block, catheter for postop.
Level. T4 for hysterectomy; achieve slowly.
Too-high block. support ventilation, support BP, reassure, do not deepen sedation reflexively.

3. Induction, sux, NDMR choice

She prefers to be asleep — your response? How induce GA? Rationale? Sux — avoid? Why? NDMR — which, dose? Why? Inhalation-favored vs opioid-favored maintenance — pick. Defend. Sugammadex available — bearing on choice?

Considerations and pitfalls

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She wants asleep. discuss risks/benefits; GA acceptable with careful plan; consider combined GA + epidural for postop.
Induction. propofol + opioid + RSI for full stomach; avoid sux if possible.
Sux concerns. resistance (need ~2x dose); pyridostigmine reduces pseudocholinesterase activity — prolonged block; prefer low-dose roc with sugammadex.
NDMR. 1/10 to 1/2 normal dose, titrate to TOF; rocuronium with sugammadex available is the favored pairing.
Inhalation vs opioid. inhalation-favored — provides relaxation, reduces NMB need, faster offset; minimize opioid (respiratory depression).
Sugammadex. definitive reversal for steroidal NDMR; reduces postop weakness risk.

4. Bleeding and red urine

During pelvic dissection she bleeds heavily. When transfuse? After 2 units, she keeps bleeding. BP 80/40, HR 105. No blood available. Now? FFP — indicated? Why? Her urine turns red. DDx? Evaluation? Methylene blue was given to assess ureters — bearing on your SpO2 reading? Management?

Considerations and pitfalls

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When transfuse. ongoing loss, hemodynamic instability, Hgb <7-8 (or <10 with cardiac disease or active bleeding).
No blood available. emergency-release O-neg, activate MTP, crystalloid/colloid bolus, pressors, surgical hemostasis, cell saver, TXA, communicate with surgeon.
FFP. yes if coagulopathy (PT/PTT >1.5x); after ~4-6 units PRBC start 1:1:1.
Red urine DDx. hemolytic transfusion reaction, myoglobinuria, free Hgb from cell saver/dilution, surgical injury to bladder/ureter.
Evaluation. stop transfusion, recheck pretransfusion sample and T&C, plasma color, DAT, haptoglobin, LDH, bilirubin, K, coags, urinalysis.
Methylene blue and SpO2. false low SpO2 — absorbs near red wavelength; transient (1-5 min); confirm with ABG before chasing.
Management. supportive — IVF, maintain UOP >1 mL/kg/h, alkalinize urine (bicarbonate), treat hyperkalemia, pressors as needed.

5. Extubation

Case done. Criteria for extubation in this patient? If you used NDMR — reverse? How? Why? Sugammadex vs neostigmine here? Pyridostigmine postop — when, what dose? Disposition — floor or step-down? Why?

Considerations and pitfalls

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Criteria. awake, follows commands, FVC >15 mL/kg, NIF more negative than -25, sustained head lift >5 s, TOF >0.9, adequate gas exchange, hemodynamically stable, normothermic.
Reverse. yes — sugammadex preferred (rocuronium/vecuronium); avoids cholinergic crisis risk with neostigmine + pyridostigmine.
Sugammadex vs neostigmine. sugammadex cleaner here; neostigmine + glyco acceptable if no sugammadex but additive to pyridostigmine.
Pyridostigmine postop. resume at reduced dose; titrate based on exam.
Disposition. step-down or ICU given respiratory risk; floor only if exam clearly back to baseline and continuous monitoring available.

C. ADDITIONAL TOPICS

Teaching focus. Pediatric cleft palate repair with postop hemoptysis; airway and fluids in the burn patient; regional anesthesia decisions in severe COPD with respiratory distress after a spinal.

1. Pediatric cleft palate repair

Healthy 18-month-old, 15 kg, for cleft palate repair. Venous access preinduction — mandatory? Why? How induce? Adult circle system acceptable? Why? If mechanically ventilated, vent settings? Compare Ve and Vt vs adult — different? Why? PACU: respiratory distress and coughing up blood. Evaluation? Mgmt?

Considerations and pitfalls

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IV preinduction. no — healthy child, mask induction standard; place IV after induction.
Induce. inhalational sevoflurane + N2O/O2.
Adult circle. yes — modern circles fine for >10 kg; low compliance, heated humidified.
Vent. PCV preferred, Vt 6-8 mL/kg, RR 20-30, PIP <20, PEEP 4-5, I:E 1:2.
Ve/Vt vs adult. higher Ve per kg (higher RR), Vt/kg similar; higher metabolic rate and O2 consumption.
PACU distress + hemoptysis. bleeding at surgical site, retained throat pack, airway edema, laryngospasm.
Mgmt. O2, careful suction (suture line), call surgeon, return to OR for hemostasis, secure airway, head down.

2. Burned patient

Called to ED for a patient with burns to arms, chest, and face. Concerns? Intubate — when? Airway management approach? Fluid plan? Endpoints? Burn surface area drives what? Inhalation injury — workup?

Considerations and pitfalls

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Concerns. airway edema (face burn), inhalation injury, CO/cyanide toxicity, hypovolemia, associated trauma, hypothermia, rhabdo, compartment syndrome.
Intubate when. stridor, hoarseness, singed nasal hair, soot, facial/oropharyngeal edema, increased work of breathing, deep neck/face burns, large %TBSA, decreased LOC, planned long transport — when in doubt, intubate early.
Airway. large ETT (≥7.5) for bronch; awake fiberoptic if stable, RSI if rapidly worsening; anticipate progressive edema.
Fluids. Parkland — 4 mL/kg × %TBSA LR over 24 h, half in first 8 h from time of burn; titrate.
Endpoints. UOP 0.5 mL/kg/h adult (1 mL/kg/h peds, 1-2 if myoglobinuria), MAP >65, lactate clearance, mental status.
TBSA drives. fluid total, ICU vs burn center transfer, prognosis.
Inhalation workup. bronchoscopy, carboxyhemoglobin, ABG, CXR.

3. Regional in severe COPD

A 50 y.o. man with COPD and productive cough is scheduled for emergency exploration for probable testicular torsion. PFTs 3 months ago: FVC 3.0 L, FEV1 1.0 L, no improvement with bronchodilators, room-air PaO2 65, PaCO2 48, pH 7.40. Interpretation? Repeat PFTs — yes? Patient asks if regional is safest. Your response? Proceed with regional — how? Ten min post-spinal he reports dyspnea. DDx? Rx? T4 level — does it contribute? Mgmt?

Considerations and pitfalls

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PFTs interpretation. severe obstructive (FEV1/FVC 0.33), no reversibility, chronic compensated CO2 retention, hypoxemia at rest.
Repeat. no — emergency, recent stable PFTs; optimize with bronchodilators, treat productive cough.
Regional safest. not necessarily — high block compromises expiratory muscles that COPD patients depend on; CO2 retention risk, anxiety.
Proceed with regional. low spinal (saddle/T10 max) or epidural to titrate; avoid heavy sedation; supplemental O2; have airway gear ready.
Post-spinal dyspnea DDx. high block, bronchospasm, anxiety, mucus plug, PE, MI, pneumothorax.
Rx. O2, reassure, support BP and HR, bronchodilators, prepare to intubate.
T4 contributes. yes — loss of intercostals and abdominal muscles reduces expiratory reserve and impairs cough; phrenic spared but accessory muscles are required in COPD.
Mgmt. O2, support ventilation (NIV if cooperative), pressors, intubate if hypoxemic or CO2 climbing; treat bronchospasm; reassess as block recedes.

Session 1 — long stem

Adult polytrauma with TBI for emergent craniotomy

A 35 y.o., 82 kg, 5'8" man is brought to the operating room for emergent left frontotemporal craniotomy and evacuation of an acute subdural hematoma.

HPIUnrestrained driver ejected from a motor vehicle collision approximately 90 minutes ago. EMS found him unresponsive at the scene and intubated him in the field with succinylcholine and etomidate. Brought to MGH ED where ATLS resuscitation was initiated. Two large-bore peripheral IVs in place. One unit of PRBC began infusing in the ED. CT scans completed. Now arriving in OR.

PMHMyocardial infarction 3 years ago, treated with two drug-eluting stents to the LAD. No anginal symptoms since. Hypertension. Hyperlipidemia. No prior surgeries.

MEDSAspirin 81 mg daily, atorvastatin 40 mg daily, lisinopril 20 mg daily. Last meal 5 hours prior to MVC.

PHYS EXAMHR 115; BP 95/55; assist control ventilation, FiO2 1.0; T 36.0°C; SpO2 92%. GCS 8T (E2, M4, intubated off sedation). Pupils: left 5 mm sluggish, right 3 mm reactive. Cervical collar in place. Chest auscultation: decreased breath sounds on the right. Abdomen soft. Right thigh and pubic region tender. Foley catheter in place.

CT HEADLarge left frontotemporal acute subdural hematoma with 8 mm midline shift. Effacement of the left lateral ventricle. No contralateral hemorrhage. No skull fracture.

CT C-SPINEUnstable C5-C6 ligamentous injury without fracture.

CT CHESTRight pulmonary contusion; small right pneumothorax, no chest tube; three right-sided rib fractures (4th, 5th, 6th).

CT PELVISRight superior and inferior pubic ramus fracture without retroperitoneal hematoma.

LABSHgb 9.8 gm/dL; platelets 198 K/uL; INR 1.3; K+ 3.2 mEq/L; glucose 220 mg/dL; lactate 5.2 mmol/L; creatinine 1.1 mg/dL. ABG on FiO2 1.0: pH 7.30; PaO2 88; PaCO2 38.

OR ARRIVALPatient is intubated and sedated on propofol 30 mcg/kg/min. Two 16 g peripheral IVs functioning. Arterial line not yet placed. Type and crossmatch sent; 4 units PRBC available in the OR. Surgeon is scrubbed and ready to incise.

A. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Induction in polytrauma TBI under C-spine and ICP constraints; CPP/ICP tradeoff during ongoing hemorrhage; hyperosmolar choice when hypotensive; recognizing tension pneumothorax during an open-cranium case.

1. Initial OR management and anesthetic plan

Pt intubated on propofol 30 mcg/kg/min. Surgeon wants to incise now given midline shift. First priorities? Confirm ETT placement — how? Maintenance — TIVA vs volatile? Why? Arterial line before incision — yes/no? Why? End point? Surgeon objects to any delay. How proceed? Other access needed? Why?

Considerations and pitfalls

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First priorities. secure airway and ventilation verified, hemodynamic targets set (CPP), confirm products available, set monitors and access before incision; communicate with surgeon on minimum safe prep.
Confirm ETT. EtCO2, bilateral breath sounds, fiberoptic confirmation if any doubt with a field-intubated patient; misplaced ETT after field intubation is real.
TIVA vs volatile. either defensible; TIVA preserves CO2 reactivity and avoids volatile-related ICP rise; volatile at low MAC also acceptable. Candidate should commit and defend.
Arterial line. yes before incision if it does not delay decompression; beat-to-beat BP critical for CPP. Defensible to place during induction or immediately after.
Surgeon objection. communicate the why; minute or two for arterial line is a worthwhile trade for beat-to-beat BP.
Other access. central line and second large-bore IV for vasopressors and ongoing resuscitation; consider placing as case proceeds.

2. Induction and hemodynamic management

After remifentanil load and propofol bolus to deepen anesthesia, BP falls to 75/40. Of concern? Why? Rx? Phenylephrine? Norepinephrine? Volume? End point? BP responds but is persistently 90-100 systolic on infusion. DDx? Hgb 8.2 after 1 L crystalloid. Continue resuscitation? Activate MTP? Threshold for PRBC in TBI? Why? Goal MAP for this pt? Why?

Considerations and pitfalls

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Concern. hypotension reduces CPP and worsens secondary brain injury; severe in this pt.
Rx. vasopressor support with volume; norepinephrine often preferred; phenylephrine reasonable; reflex large volume bolus without considering coronary disease is a flag.
Persistent borderline BP. ongoing hemorrhage (chest, pelvis, occult), under-resuscitation, anesthetic depth, coronary ischemia from prior MI.
MTP. trigger on instability with falling Hgb in polytrauma.
PRBC threshold in TBI. higher than baseline; many target Hgb ≥8 to protect oxygen delivery to injured brain.
MAP goal. MAP ≥80 (CPP ≥60) typical for TBI; the candidate should reason from CPP.

3. Hyperosmolar therapy and ICP management

Bone flap removed; surgeon reports tense dura and requests hyperosmolar therapy. Mannitol vs hypertonic saline? Why? Pt remains hypotensive on phenylephrine. Mannitol still appropriate? Concerns? You choose hypertonic saline: 3% bolus vs 23.4% bolus? Why? Through what access? Risks of 23.4% peripheral? Hyperventilation — PaCO2 target? Why? Risks? Head position 30° head up — concerns with hypotension?

Considerations and pitfalls

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Mannitol vs HTS. mannitol diuresis worsens hypovolemia and hypotension; HTS expands volume while reducing brain water; HTS often preferred in the hemodynamically unstable TBI.
Mannitol with hypotension. concerning; risk of further BP drop from osmotic diuresis.
3% vs 23.4%. 23.4% is faster and lower volume; requires central access; 3% requires more volume and acceptable peripherally.
23.4% peripheral. extravasation causes severe tissue injury; standard is central line.
Hyperventilation target. PaCO2 30-35 as a bridge; pCO2 <30 risks cerebral ischemia and is reserved for impending herniation.
Head position. 30° head up improves cerebral venous drainage; balance against BP — keep CPP.

4. Intraoperative tension pneumothorax

45 min into craniotomy, dura still open. PIP rises from 24 to 38 cm H2O over 1 minute. SpO2 92 to 84%. BP 80/45. ETCO2 falls from 32 to 22. DDx? Auscultation: absent breath sounds on right, hyperresonance, trachea midline. Tension PTX suspected. Immediate Rx? Can you safely needle-decompress with the cranium open? Why? Where: anterior 2nd intercostal vs 4th-5th lateral? After decompression, BP recovers and SpO2 91%. Chest tube — now or after craniotomy? Could this have been prevented?

Considerations and pitfalls

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DDx. tension pneumothorax expanding under positive pressure, mucus plug, mainstem migration, severe bronchospasm, equipment failure.
Immediate Rx. needle decompression and prepare for chest tube; communicate with surgeon — falling EtCO2 with hypotension and rising PIP is the picture.
Needle with open cranium. yes, do not delay; tension pneumothorax kills faster than ICP swings; expect intracranial pressure transient with decompression.
Site. 4th-5th intercostal anterior axillary line increasingly favored; 2nd ICS midclavicular traditional but lower yield in adults.
Chest tube timing. immediately after decompression — needle is a temporizing measure.
Prevention. recognize chest CT findings, share with surgeon, consider chest tube preop if positive-pressure case anticipated.

B. POST-OPERATIVE CARE

Teaching focus. Sedation balanced with hourly neuro checks; tiered escalation of ICP control; differentiating DI from osmotic diuresis; ARDS-PEEP-ICP tradeoff in TBI; prognostic disclosure under uncertainty.

1. ICU ventilation and sedation strategy

Case complete. Pt arrives in NeuroICU intubated. Extubate? Why/why not? Sedation choice: propofol vs dexmedetomidine vs midazolam? Why? Hourly neuro checks needed. Approach to permit accurate exam? Bolus interruptions? Switch agents for exam window? Pt on propofol 40 mcg/kg/min. Concerns at 24-48 hours? Paralytics — role? Why/why not?

Considerations and pitfalls

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Extubate. no — GCS 8T, polytrauma, need for ICP control, ongoing instability. Defensible only as a hypothetical.
Sedation choice. propofol allows quick on/off for exam windows; dexmedetomidine permits exam but slower titration; midazolam accumulates and impairs exam — usually avoided.
Hourly neuro exam. scheduled sedation interruption or pulse-down to allow exam; coordinate with bedside team.
Propofol 24-48 h concerns. propofol infusion syndrome with prolonged high doses; metabolic acidosis, rhabdomyolysis, cardiac dysfunction.
Paralytics. for severe ICP refractory to sedation, or vent dyssynchrony with worsening hypoxia; not routine; obscure exam.

2. ICP elevation at 8 hours

ICP monitor reads 28 mmHg sustained. DDx? Repeat CT shows no new hemorrhage, diffuse brain edema. Tiered approach. First step? Specific options: deepen sedation? CSF drainage from EVD? Hyperosmolar bolus? Hyperventilation? Paralytics? Barbiturate coma? Sequence? Why? Current Na 152. Continue HTS infusion? Goal sodium? Why? ICP responds to a 23.4% NaCl bolus but creeps back to 28 within 2 hours. Next step? When decompressive craniectomy?

Considerations and pitfalls

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DDx of rising ICP. edema, expanding hematoma, hydrocephalus, hypoventilation, fever, seizure, agitation, venous outflow obstruction.
Tiered approach. head up and neutral, deepen sedation, CSF drainage if EVD, HTS bolus, hyperventilation transiently, paralytics, barbiturate coma, decompressive craniectomy.
Sequence. less invasive first; coordinate with neurosurgery throughout.
HTS continuation and Na goal. continue with target Na 150-160; over-rapid correction risk; monitor.
Refractory ICP. after maximal medical therapy with rising ICP and clinical deterioration, decompressive craniectomy considered with neurosurgery.

3. Sodium derangement and DI

POD 1. Serum Na 158. Urine output 450 mL/hr over the past 2 hours. DDx? Urine osm 200 mOsm/kg; urine Na 30. Interpretation? DI vs osmotic diuresis from prior mannitol — how distinguish? DI confirmed. Rx? Desmopressin dose and route? Fluid replacement strategy: D5W vs 0.45% NaCl? Why? Why is DI particularly dangerous in a TBI patient?

Considerations and pitfalls

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DDx. diabetes insipidus (central from injury), osmotic diuresis from mannitol or HTS, hyperglycemia, intentional negative balance.
Distinguishing. DI: dilute urine despite high serum osm; osmotic: high urine osm. Urine osm 200 with high serum Na fits DI.
Rx. vasopressin or desmopressin (DDAVP); replace free water deficit; monitor electrolytes closely.
DDAVP dose. 1-4 mcg IV or SC; titrate to UOP and Na.
Fluid replacement. match insensible plus losses; D5W for free water with attention to glucose; 0.45% NaCl an alternative.
DI in TBI. rapid Na shifts cause brain edema or osmotic demyelination; correcting too fast or too slow both harm.

4. Worsening oxygenation on POD 2

POD 2. PaO2/FiO2 falls to 180. CXR shows bilateral patchy infiltrates. DDx? Pulmonary contusion progression vs ARDS vs neurogenic pulmonary edema vs aspiration vs transfusion-related? How distinguish? ARDS most likely. Ventilation strategy in TBI with ARDS: low Vt? PEEP level? Concerns with high PEEP? Why? Acceptable PaCO2 ceiling in TBI with ARDS? Prone positioning — pros and cons in TBI with elevated ICP?

Considerations and pitfalls

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DDx. contusion progression, ARDS (multiple insults), neurogenic pulmonary edema (early after injury), aspiration, TACO vs TRALI.
Distinguishing. timing, transfusion history, fluid balance, BNP, echo for cardiogenic etiology.
Vent in TBI + ARDS. lung-protective with the lowest PEEP that supports oxygenation; high PEEP raises ICP through reduced venous return and increased intrathoracic pressure.
PaCO2 ceiling. permissive hypercapnia raises ICP; balance — accept some rise if needed for protective ventilation but watch ICP.
Prone. improves oxygenation but raises ICP and complicates neuro exam; reserved for severe ARDS when other measures insufficient, with neurosurgery aware.

5. Family communication and prognostic disclosure

POD 3. Pt in barbiturate coma. ICP controlled but neurologic prognosis uncertain. Family asks if he will wake up. What will you tell them? Father asks: 'Did the anesthesiologist do something wrong during surgery? He was fine before.' Response? Family wants to discuss withdrawal of care. Your role in that conversation? Brother arrives wanting to discuss organ donation. Timing of brain death evaluation? How assess brain death in a patient on barbiturates?

Considerations and pitfalls

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Will he wake up. plain honest uncertainty; describe what is known and unknown; do not promise either way.
Anesthesiology question. explain what happened plainly; redirect from blame to mechanism; do not become defensive.
Withdrawal of care. neurosurgery and intensivist primary; anesthesia supports the conversation by sharing what happened in the OR.
Organ donation timing. organ donation discussions led by transplant coordinators; not the time during active resuscitation.
Brain death on barbiturates. barbiturates confound the exam; cannot diagnose brain death until levels are sub-therapeutic; ancillary tests (EEG, cerebral blood flow studies) used if pharmacologic confounders persist.

C. ADDITIONAL TOPICS

Teaching focus. Severe preeclampsia with HELLP requiring emergent cesarean; pediatric foreign body aspiration; post-herpetic neuralgia in a diabetic patient.

1. Severe preeclampsia with HELLP

A 32 y.o. G2P1 at 34 weeks gestation is admitted with severe preeclampsia: BP 180/110, headache, RUQ pain. Platelets 65K; AST 240; LDH 800; Hgb 8.5. MgSO4 infusion running. FHR shows recurrent late decels. Emergent C-section. Concerns? Plt 65K — regional acceptable? Why/why not? Pt prefers regional. Spinal vs epidural? Defend. Surgeon insists no time; GA chosen. RSI agent? Sux concerns with MgSO4? Mgmt of hypertensive response to laryngoscopy (BP 195/115)? After delivery, atony EBL 1500 mL. Mgmt? Effect of MgSO4 on uterine tone?

Considerations and pitfalls

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Concerns. airway in pregnancy and preeclampsia, thrombocytopenia, magnesium effect on NMB, BP control, hemorrhage risk.
Plt 65K. below most thresholds; trajectory and clinical bleeding signs matter; defensible to choose GA; choosing regional requires explicit reasoning.
Spinal vs epidural. if going regional, spinal often chosen for time; depends on clinical picture.
RSI under mag. sux works but mag potentiates non-depolarizers; reduce roc dose; clinical strength assessment more useful than train of four alone.
BP on laryngoscopy. pretreat with opioid, labetalol, or remifentanil; target controlled response.
Atony with mag. mag tocolyzes uterus; need higher uterotonic doses; oxytocin, methergine cautious in HTN, misoprostol, mechanical.

2. Pediatric foreign body aspiration

A 2 y.o., 13 kg girl is brought urgently after sudden choking while eating peanuts. Biphasic stridor and intermittent cyanosis. SpO2 88% RA. CXR: hyperinflation of right lung. Rigid bronchoscopy planned. Concerns? Induction: IV vs inhalational? Why? Pt agitated and no IV. Mask induction with sevoflurane: spontaneous vs controlled? Why? IV obtained. Muscle relaxant? Why/why not? Anesthetic depth for rigid bronchoscopy? Object retrieved. Wheezing, SpO2 90%. DDx? Rx?

Considerations and pitfalls

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Concerns. complete obstruction with positive pressure, severe hypoxemia, agitation worsening obstruction, shared airway.
Induction. inhalational often preferred to preserve spontaneous ventilation; IV reasonable if access available.
Mask induction. spontaneous ventilation maintained; positive pressure can push the FB distally and worsen obstruction.
Muscle relaxant. controversial; surgeon preference; many proceed without paralysis to preserve spontaneous ventilation.
Depth. deep enough to tolerate scope without coughing or laryngospasm.
Post-retrieval wheeze. bronchospasm, residual debris, airway edema; bronchodilator, steroids, supportive care.

3. Post-herpetic neuralgia

A 72 y.o. woman with type 2 diabetes presents with severe burning pain in a T5 dermatomal distribution 4 months after a shingles outbreak. Pain unresponsive to gabapentin 600 mg TID and oxycodone 5 mg q6h. Pain score 8/10. Evaluation? Mechanism of post-herpetic neuralgia? Why might oxycodone be ineffective? Next-line: TCA, SNRI, lidocaine patch, capsaicin? Defend choices. Does diabetes affect your choice? Why? Interventional therapy: thoracic epidural, intercostal block, intrathecal pump, spinal cord stimulator? When would you consider each?

Considerations and pitfalls

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Evaluation. characterize pain quality, prior treatments, function, sleep, mood, comorbidities; rule out alternative diagnoses.
Mechanism. neuropathic from sensitization and remodeling after viral neuronal injury.
Oxycodone ineffective. opioid responsiveness in neuropathic pain is limited; tolerance and side effects often dominate.
Next-line. TCA (nortriptyline preferred over amitriptyline in elderly), SNRI (duloxetine), lidocaine patch (well-tolerated, local), capsaicin (high-concentration patch — option).
Diabetes. TCAs cautious with orthostasis and arrhythmia risk; SNRIs reasonable; lidocaine patch safe.
Interventional. thoracic epidural or paravertebral for refractory acute pain; SCS for chronic neuropathic refractory pain; intrathecal pump rare for PHN.

Session 1 — long stem

Morbid obesity, OSA, prior failed neuraxial, repeat cesarean with placenta accreta

A 36 y.o. G3P2 at 39 weeks gestation, 152 kg, 5'4" (BMI 58), is scheduled for repeat cesarean delivery, her third. Obstetric ultrasound raises concern for placenta accreta over the prior cesarean scar.

HPIFirst cesarean under uncomplicated spinal at an outside hospital. Second cesarean at age 31: 90 minutes of attempted epidural placement, ultimately converted to general anesthesia after surgical incision under inadequate block; required two attempts at intubation. She recalls feeling pulling during the second cesarean but reports no nightmares or avoidance. On home CPAP at 14 cm H2O for severe OSA (AHI 65), uses it nightly. Has been doing prenatal pool exercise. BMI was 48 prior to pregnancy.

PMHClass III obesity. Severe OSA on CPAP. Gestational diabetes on insulin. Chronic hypertension on labetalol. Mild iron-deficiency anemia. GERD on PPI.

MEDSLabetalol 200 mg PO BID; insulin lispro sliding scale; omeprazole 40 mg PO daily; low-dose aspirin 81 mg; prenatal vitamins.

PHYS EXAMHR 88; BP 142/88; RR 18; SpO2 94% on room air; T 37.0°C. Neck circumference 47 cm. Mallampati IV, restricted neck extension, mouth opening 3 fingerbreadths, thyromental distance 4 cm. Bilateral end-expiratory wheezes. Redundant soft tissue over the lumbar back; bony landmarks not palpable on exam.

LABSHgb 10.5 g/dL; platelets 195 K/uL; INR 1.0; glucose 110 mg/dL; creatinine 0.7 mg/dL. Type and screen positive antibody (anti-E); four units crossmatched.

IMAGINGObstetric ultrasound suggestive of placenta accreta spectrum (lower segment, prior scar adherence). MRI confirms placenta increta with bladder involvement. Cardiology TTE: LV hypertrophy, mild diastolic dysfunction, EF 65%, RVSP 38 mmHg.

FETALEstimated fetal weight 4200 g. FHR baseline 140 with appropriate variability.

OR ARRIVALBariatric OR table with ramp pillows in place. After multiple attempts a single 18 g IV in the right forearm. Right radial arterial line attempted twice unsuccessfully. Ultrasound brought into the room. NICU and gynecologic oncology team notified for the accreta. IR notified for possible postpartum embolization.

A. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Modality choice when neuraxial is technically hard and GA airway is hard too; ultrasound-guided block in the morbidly obese; awake fiberoptic intubation versus optimized RSI; physiology of ventilation and position in the patient with BMI nearly 60; managing accreta hemorrhage with massive transfusion.

1. Modality decision

Concerns? Modality for this case? Spinal — yes/no? Why? Slow epidural vs CSE — pick. Defend. Ultrasound for neuraxial in this patient — useful? Why? Anticipated time to block — bearing? OB pushing to start given accreta risk and bleeding. Adjust? GA — what makes it the bigger risk? She tells you she does not want to go to sleep again. How respond?

Considerations and pitfalls

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Concerns. OSA, obesity-related ventilation issues, anticipated difficult airway, anticipated difficult neuraxial, accreta with high bleeding risk, prior failed regional and recall.
Modality. neuraxial preferred for delivery and avoiding airway, but technically challenging; commit and defend the plan.
Spinal vs slow epidural vs CSE. CSE allows immediate surgical anesthesia plus prolonged catheter for accreta course; spinal alone may be too brief if accreta dissection extends; commit.
Ultrasound. very useful in obesity to identify midline, depth, and interspace; reduces attempts and time.
Time to block. engage OB on timing; communicate the expected duration of placement; pre-position before delivery if possible.
GA risk. difficult airway plus prior recall plus aspiration plus desaturation rate.
Patient preference. honor her concern, explain the plan to mitigate recall, share the safety reasoning.

2. Backup airway plan

You decide on CSE but prepare for GA. Backup airway plan — articulate. Awake fiberoptic — what setup? Local plan? Sedation choices and limits in OSA? Video laryngoscopy as first attempt under GA — defensible? Why? You complete a CSE, surgical anesthesia at T4. As OB enters, BP 80/45 and SpO2 90% on 4 L NC. DDx? Rx? Position changes — what?

Considerations and pitfalls

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Backup plan. named awake plan, named asleep plan with VL and fiberoptic ready, surgical airway available, named decision points.
Awake fiberoptic. atomized topicalization, nerve blocks if comfortable, light sedation only; commit to the topicalization sequence.
Sedation in OSA. minimal short-acting, dexmedetomidine often preferred over opioids/benzodiazepines.
VL first under GA. defensible given the predicted view; awake remains backup.
BP fall + SpO2 90%. sympathectomy plus obesity-induced atelectasis with supine position; left tilt aggressive, reverse Trendelenburg, raise SVR, deepen oxygenation.

3. Ventilation, position, accreta finding

OB confirms increta with bladder involvement. Surgical plan: cesarean hysterectomy. Position issues now — what? Ventilation strategy if you must convert to GA? PEEP — start where, why? Tidal volume by what weight? Plateau goal? Pressors and inotropes — what's available, in hand? Blood is set up — products in room? OB says: she's bleeding briskly. Now?

Considerations and pitfalls

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Position. ramp, head-up, aggressive left tilt; tidal volumes drop with abdominal mass and bleeding.
Ventilation if GA. low tidal volume by predicted (not actual) body weight; modest PEEP 8-10; plateau ≤30; rate to PaCO2.
Pressors/inotropes. multiple agents drawn up and labeled, calcium ready, norepinephrine running, vasopressin available.
Blood ready. PRBC, FFP, platelets, cryo or fibrinogen in room; calcium and TXA at hand.
Brisk bleeding. activate MTP, communicate, large-bore access if not yet, consider rapid transfuser, pace resuscitation with surgery.

4. Massive transfusion and coagulopathy

EBL 4 L, climbing. BP 75/40 on norepi 0.3, vasopressin 0.04. Plan? Volume and product ratios? Calcium — how often? Cryo or fibrinogen concentrate — pick, why? TXA — yes/no, when? She becomes restless, then unresponsive under what was a regional. Now what? GA — induction agent? Dose? Awareness mitigation in a patient with prior recall?

Considerations and pitfalls

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Plan. ongoing resuscitation, goal-directed products, communicate with surgery on pace, escalate help.
Products. 1:1:1 default, fibrinogen replacement specific, calcium frequent, lactate trending.
TXA. early in obstetric hemorrhage; within 3 hours.
Conversion to GA. needed for awareness and airway control; named induction agent reduced for hypovolemia (ketamine or low-dose etomidate), full RSI dose paralytic, secure airway.
Awareness mitigation. named hypnotic dose, midazolam early, processed EEG if available, document; address her history before induction.

B. POST-OPERATIVE CARE

Teaching focus. Extubation judgment in the BMI-60 OSA patient after massive transfusion; postop respiratory failure and noninvasive support; multimodal analgesia that respects OSA; VTE prophylaxis in the high-risk postpartum; disclosure when the patient had a prior bad anesthetic and another hard course.

1. Extubation

Case done, hysterectomy completed, EBL 5 L, products 10 PRBC, 8 FFP, 2 platelets, 10 cryo, TXA given. BP 100/60 on norepi 0.05. Extubate in the OR? Why/why not? Criteria? Position for extubation? CPAP available in PACU? Why? She extubates and SpO2 falls to 85% on 6 L within 20 min. DDx? Rx? Reintubate threshold? Disposition?

Considerations and pitfalls

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Extubate or not. many would leave intubated after a 5 L blood loss with morbid obesity and OSA; defensible either way if criteria named.
Criteria. gas exchange, reversal confirmed, normothermia, hemodynamic stability, hemostasis.
Position. head-up, ramped, CPAP applied within minutes of extubation if OSA severe.
Post-extubation hypoxemia DDx. obesity-induced atelectasis, residual block, opioid, pulmonary edema (TRALI, TACO), aspiration; reach for the most likely while scanning the rest.
Rx. CPAP/BiPAP, position, recruit, treat the specific cause.
Disposition. ICU.

2. Postoperative respiratory failure

POD 1: hypoxic on CPAP, RR 30, P/F 180, climbing PaCO2. DDx? Most likely here? NIV trial — settings? When does NIV fail? Reintubate — threshold? Bronchoscopy — when? She becomes obtunded. Now what? Airway plan a second time?

Considerations and pitfalls

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DDx. atelectasis from positioning and obesity, plugging, pulmonary edema, aspiration, opioid-induced hypoventilation.
Most likely. atelectasis with obesity hypoventilation contribution.
NIV settings. BiPAP with higher EPAP than at home (e.g., 8-10), titrate IPAP to volumes and CO2.
NIV failure. worsening gas exchange, rising CO2, declining mental status.
Reintubation. do not delay in obtunded patient with rising CO2; her airway is hard and a crash induction on the floor is the danger.
Bronchoscopy. for suspected plugging or aspiration assessment.

3. Multimodal analgesia in OSA

Pain plan? Opioid-sparing — what? IV opioid for breakthrough — agent, dose, considerations? PCA in this patient — concerns? Acetaminophen, NSAID, gabapentinoid — yes/no on each? Why? Truncal block — TAP or QL? Pick. Defend. CPAP through the night — bearing? OB asks why no PCA. What say?

Considerations and pitfalls

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Plan. multimodal with regional truncal block, scheduled non-opioids, opioid-sparing as default.
Opioid-sparing. acetaminophen scheduled, NSAID if renal/bleeding ok, regional block.
PCA in OSA. high risk for respiratory depression; not a default; if used, monitored setting with capnography.
Gabapentinoid. controversial in OSA; sedation risk; modest analgesic benefit; not a default.
Block choice. TAP or quadratus lumborum — either reasonable; QL may give better visceral coverage.
CPAP. essential overnight; recognize that hospital BiPAP/CPAP settings may differ from home.

4. VTE prophylaxis

POD 1: hemostasis good, drains low. VTE prophylaxis — when start? Agent? Dose? Mechanical compression in the meantime — why important here? She develops new unilateral leg swelling on POD 2. Concerns? Workup? Anticoagulation if confirmed — concerns given recent surgery and accreta course?

Considerations and pitfalls

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When start. as bleeding risk allows, typically within 12-24 h postpartum in cesarean hysterectomy; named plan with OB.
Agent. enoxaparin commonly; dose adjusted for obesity.
Mechanical compression. essential; reduces VTE in the high-risk patient with delayed pharmacologic prophylaxis.
New leg swelling DDx. DVT primary concern; cellulitis, hematoma.
Workup. ultrasound; D-dimer of limited utility postpartum.
Therapeutic anticoagulation. weigh against re-bleeding risk; IVC filter considered in rare scenarios; multidisciplinary call.

5. Disclosure and follow-up

POD 3. She asks: what went differently this time, and why did I have to be put to sleep? What say? She asks about future surgeries. What say? OB has shared the hysterectomy decision plainly with her. Bearing on what you say about anesthesia? Family asks about discharge timing — your input? What anesthesia summary do you want her to carry?

Considerations and pitfalls

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What changed. honest account of the airway difficulty, the bleeding, why GA, what was done to prevent recall.
Future surgeries. her airway and history will be a meaningful factor; emphasize awake intubation considerations, ICU bed planning, multimodal analgesia.
OB framing. align with OB; don't contradict; focus your portion on anesthesia.
Discharge timing. defer to OB; ICU course and respiratory status drive it.
Summary letter. portable anesthesia record with intubation history, products received, complications, recommendations.

C. ADDITIONAL TOPICS

Teaching focus. Three unrelated vignettes: ARDS with refractory hypoxemia, LAST after interscalene block, and PDPH after a recognized wet tap.

1. ARDS with refractory hypoxemia

A 55 y.o. man with severe pneumonia is intubated in the ICU. On volume control, FiO2 1.0, PEEP 12: PaO2 58, P/F 90, plateau 32. Interpretation? Tidal-volume target and why? Plateau goal? Hypoxemic still — higher PEEP, recruitment, or prone? Defend. NMB role? When ECMO? BP falls to 80/50 on raising PEEP. DDx and Rx?

Considerations and pitfalls

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Interpretation. severe ARDS by P/F; plateau above target.
TV. ~6 mL/kg PBW.
Plateau. ≤30.
Escalation. prone has the strongest signal.
NMB. for severe dyssynchrony or refractory hypoxemia.
ECMO. refractory hypoxemia despite optimal vent; early referral.
Hypotension on PEEP. reduced venous return, pneumothorax, or sepsis.

2. LAST after interscalene block

A 60 y.o. woman receives an interscalene block for shoulder surgery. Two minutes later she becomes agitated and seizes. Cause? Priorities? She loses her pulse with a wide-complex rhythm. ACLS modifications? Lipid emulsion — principle and dose? Prevention?

Considerations and pitfalls

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Cause. LAST.
Priorities. stop injecting, call for help, airway/oxygenation, control seizure, lipid.
ACLS mod. lipid, reduced epinephrine, avoid certain antiarrhythmics, prolonged resuscitation, bypass for refractory.
Lipid. bolus and infusion per protocol.
Prevention. incremental injection, ultrasound, test dose, lowest dose.

3. PDPH after wet tap

A 28 y.o. woman, 24 hr after a labor epidural with recognized wet tap, has a positional fronto-occipital headache relieved by lying flat. Dx and features? Exclude what? Conservative measures? She can't care for her newborn — Rx? Mechanism? Risks?

Considerations and pitfalls

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Diagnosis. PDPH.
Exclude. preeclampsia, CVST, meningitis, subdural.
Conservative. time, analgesia, hydration, caffeine; limited evidence.
Definitive. epidural blood patch; tamponade, sealing.
Risks. repeat dural puncture, back pain, infection, rare neurologic complications.

Session 1 — long stem

Severe rheumatic mitral stenosis with new AF, planned cesarean

A 33 y.o. G2P1 at 36 weeks gestation, 58 kg, 5'3", is admitted for planned cesarean delivery tomorrow morning for known severe rheumatic mitral stenosis with progressive symptoms.

HPIProgressive exertional dyspnea since week 28, now NYHA class III to IV; orthopnea and paroxysmal nocturnal dyspnea for the past week. Two triage visits in 10 days for shortness of breath. Today walking from the parking lot left her breathless. No chest pain. Immigrated from Vietnam at age 19; first child delivered uneventfully at 24.

PMHChildhood rheumatic fever. Severe rheumatic mitral stenosis with mitral valve area 0.85 cm² and mean gradient 18 mmHg on echo this month. New-onset atrial fibrillation four weeks ago, rate-controlled. Mild gestational hypertension. No prior anesthetics other than uncomplicated spinal for first cesarean.

MEDSMetoprolol 50 mg PO BID; furosemide 20 mg PO daily; therapeutic-dose enoxaparin 1 mg/kg SC BID for AF (last dose 24 hours ago); prenatal vitamins.

PHYS EXAMHR 92 (atrial fibrillation, controlled); BP 118/72; RR 22; SpO2 95% on 2 L NC; T 36.8°C. Loud opening snap, low-pitched mid-diastolic murmur at the apex with presystolic accentuation lost in AF. Bibasilar crackles to the mid-zone. JVP elevated to the angle of the jaw. Mild pitting edema. Airway: Mallampati II, full mouth opening, full neck extension.

ECGAtrial fibrillation at 92 with diffuse repolarization changes; no ischemic features.

LABSHgb 10.2 g/dL; platelets 195 K/uL; INR 1.2; creatinine 0.7 mg/dL; BNP 1240 pg/mL; anti-Xa from yesterday morning 0.5 IU/mL. Type and screen positive for anti-K antibody (notified blood bank, two crossmatched units on hold).

IMAGING / TTE todayMitral valve area 0.85 cm², mean gradient 18 mmHg; estimated RVSP 60 mmHg; RV mildly dilated with preserved function; LV ejection fraction 60%; biatrial enlargement; no thrombus seen. CXR with cephalization and small bilateral pleural effusions.

FETALFHR baseline 140 with appropriate variability and accelerations.

OR ARRIVALTwo 16 g peripheral IVs and a right radial arterial line in. Cardiology and cardiac surgery on standby. NICU team present. Epidural cart in the room. ECMO consult notified the day before.

A. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Hemodynamic goals for fixed mitral stenosis with new AF in late pregnancy; neuraxial choice when slow ascent of level governs the technique; managing the post-delivery autotransfusion in a patient who cannot accept the volume; rate control and pulmonary pressures intraoperatively.

1. Pre-induction goals and monitoring

Hemodynamic goals here? Targets — HR, rhythm, preload, afterload, PVR? Why each? Monitoring — what do you want beyond standard? CVP — useful here? Why/why not? TEE intraop — useful? Bearing on your modality choice? She is anxious on the table, HR jumps to 118 in AF. Now what? Drug choice — esmolol, metoprolol, dexmedetomidine, magnesium? Pick. Why?

Considerations and pitfalls

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Goals. slow HR (maintain ~70-90), maintain sinus when possible (she is in AF, so rate control is the lever), avoid drops in preload and SVR, avoid rises in PVR (no hypoxia, hypercarbia, light anesthesia).
Monitoring. arterial line in place; some advocate PA catheter, others avoid given fixed lesion; TEE intraop has a role if the question is volume and RV function; CVP has limited utility with severe MS and AF.
TEE. useful if available; can guide volume and detect new thrombus or worsening regurgitation.
Anxious tachycardia. treat before induction; addressing anxiety is part of the plan, not a sideshow.
Agent. esmolol or low-dose metoprolol for rate; dexmedetomidine to manage anxiety while preserving rate; magnesium has a role; defend the choice on time course and hemodynamics.

2. Modality decision and neuraxial technique

Modality? Spinal — yes/no? Why? Slow epidural vs CSE vs continuous spinal? Pick. Defend. Last enoxaparin was 24 hours ago at 1 mg/kg BID — bearing? Anti-Xa 0.5 — bearing? Test dose with epinephrine in this patient — concern? Why? Sensory level you want for incision — to what dermatome? How slowly do you climb?

Considerations and pitfalls

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Modality. slow-titration epidural or continuous spinal preferred over single-shot spinal in severe MS; rapid sympathectomy poorly tolerated. A reflexive spinal here is a flag.
Anticoagulation timing. therapeutic LMWH requires 24-hour interval before neuraxial; the timing here is at the boundary. Anti-Xa is helpful but not definitive.
Anti-Xa 0.5. elevated for a patient ostensibly off enoxaparin for 24 hours; consider further delay or change of plan.
Epinephrine test dose. an epinephrine-laced test dose may raise rate in AF and unmask intravascular catheter; isolated tachycardia is harder to interpret. Some omit epinephrine here; defensible.
Target level. T4-T6; achieve slowly to allow compensation, avoid abrupt sympathectomy.

3. Intraoperative rate, rhythm, and BP swings

Level is T5. As surgeon enters the peritoneum, HR jumps to 130 in AF; BP 88/52. DDx? Priorities? Rate control — agent? Why? She is already on metoprolol — bearing? Phenylephrine bolus — concern with severe MS and PHTN? Why? Now: SpO2 87% on 4 L NC, RR 28, faint crackles. DDx? Rx? Diuresis — yes/no? Why?

Considerations and pitfalls

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Tachycardia DDx. anxiety, light block height, surgical stimulus, volume shift, sympathetic response to manipulation.
Rate control. short-acting beta blocker (esmolol) preferred over deep bolus of long-acting agent; address cause as well as rate.
Phenylephrine concerns. raises SVR (preserves coronary perfusion) but can raise PVR; cautious dose.
New hypoxemia. pulmonary congestion from MS and tachycardia, or pulmonary edema, or PE; high suspicion for cardiogenic edema.
Diuresis intraop. small dose of furosemide if volume status supports; aggressive diuresis can drop preload below MS tolerance — judge carefully.

4. Post-delivery autotransfusion and uterotonics

Baby out. Surgeon asks about oxytocin. Your input — bolus or slow? Why? Dose? OB sees atony at 5 minutes. Methergine — yes/no in this picture? Carboprost — yes/no? Misoprostol — yes/no? She becomes acutely dyspneic, SpO2 89%, HR 140 AF, BP 90/55. DDx? Rx? Endpoint? Diuretic now — yes? Cardiology bedside — when?

Considerations and pitfalls

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Oxytocin. slow infusion over minutes, not IV push; push doses cause vasodilation, tachycardia, and pulmonary pressure spikes — poorly tolerated in MS.
Atony agents. methergine raises SVR and PVR, contraindicated; carboprost raises PVR, contraindicated in severe pulmonary HTN; misoprostol or mechanical management preferred.
Post-delivery dyspnea. autotransfusion from uterine contraction overwhelms a fixed MS; pulmonary edema is the expected complication.
Rx. diuresis after delivery, optimize rate, sit up, oxygen, NIV; consider milrinone (caution: vasodilation) for RV support; ICU now.
Cardiology. early bedside; surgical consult if balloon valvuloplasty is on the table; ECMO referral for refractory case.

B. POST-OPERATIVE CARE

Teaching focus. Postpartum hemodynamics in fixed mitral stenosis; resuming anticoagulation in the immediate postpartum period; recognizing when temporizing fails and definitive valve intervention is needed; counseling on future pregnancies after a near-miss.

1. Immediate postpartum ICU course

Arrives ICU on 4 L NC, HR 100 AF, BP 105/65, SpO2 93%, mild crackles. Plan? Diuretic goal — endpoint? Anticoagulation — when restart? Agent? Dose? OB is concerned about uterine bleeding. Bearing on your timing? Beta blocker — IV or PO? Pulmonary edema returns 2 hours in. Now?

Considerations and pitfalls

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Plan. rate and rhythm control, gentle diuresis, oxygen, watch for return of pulmonary edema.
Diuresis endpoint. respiratory comfort, oxygenation improvement, while preserving filling for MS — perfusion endpoints carry weight beyond a daily weight change.
Anticoagulation timing. balance VTE/AF stroke risk against postpartum hemorrhage; typically start with mechanical compression and resume pharmacologic prophylaxis or therapy 12-24 h postpartum if hemostasis.
Agent and dose. heparin infusion (titratable, reversible) often preferred early; LMWH when bleeding risk lower.
Recurrent edema. additional diuresis, NIV, rate control, possibly milrinone with careful pressure support.

2. AF with RVR and hemodynamic decompensation

POD 1: HR 150 AF, BP 78/45, SpO2 88% on NIV, lactate 4. Rx priorities? Rate control agent and dose? Cardioversion — indicated? Settings? Anticoagulation status — bearing? Beta blocker not working — next agent? Amiodarone in fixed MS — yes? Why? Cardiology says she needs balloon mitral valvuloplasty. Your role in transport and procedure planning?

Considerations and pitfalls

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Priorities. stabilize rate and rhythm, support perfusion, treat the failing physiology, prepare for definitive intervention.
Rate control. IV beta blocker or calcium channel blocker; diltiazem an option; dose to effect.
Cardioversion. indicated for hemodynamic instability despite recent onset AF; anticoagulation status increases stroke risk; weigh with cardiology.
Amiodarone. reasonable for rhythm in this setting; watch BP and pulmonary effects long term.
BMV planning. transport with hemodynamic monitoring and rescue meds; anesthesia presence often required in the cath lab; coordinate access and airway plan.

3. Postpartum hemorrhage in the cardiac patient

POD 1 evening: heavy lochia, hemoglobin from 8.4 to 6.8 over 4 hours, BP 95/60, HR 130. Concerns? OB asks for uterotonics. Choice given her cardiac picture? Volume — what, how much, how fast? Pressor choice if BP fails? Transfusion threshold here? Cell saver postpartum — role? Heparin held — implications? Communicate with OB — what?

Considerations and pitfalls

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Concerns. any rapid fluid shift is poorly tolerated in MS; uterotonic choice constrained by hemodynamic profile.
Uterotonic. oxytocin slow, misoprostol; avoid methergine and carboprost; mechanical and surgical options earlier than usual.
Volume. slow, titrated, watch lungs; do not flood.
Pressor. norepinephrine or vasopressin; avoid pure beta agonists.
Transfusion threshold. higher than baseline given limited oxygen-carrying tolerance; specific number depends on context.
Heparin. held for active bleeding; restart when controlled; mechanical compression in interim.

4. Balloon mitral valvuloplasty postpartum

Cardiology proceeds with balloon valvuloplasty. Plan for the cath lab? Anesthetic — sedation vs GA? Why? Monitoring? Anticoagulation during the procedure? Sudden hypotension during balloon inflation — DDx? Rx? Post-procedure echo: residual gradient 6, no significant new MR. Disposition? Implications for breast feeding and her care plan?

Considerations and pitfalls

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Plan. anesthesia presence with full monitoring; rescue meds; clarify backup if hemodynamic collapse.
Sedation vs GA. sedation preferred when tolerated; have a GA plan ready; avoid drops in preload or rises in PVR.
Anticoagulation. heparinization for the procedure; reversal plan if bleeding.
Hypotension during inflation. transient occlusion expected; persistent suggests cardiac tamponade, severe MR, or arrhythmia — quick differential and Rx.
Post-procedure. ICU or step-down with monitoring; counseling on activity, anticoagulation, and breastfeeding compatibility.

5. Counseling and future pregnancy

POD 4. She is asking about going home, breastfeeding, and whether she can have more children. What do you tell her about this episode and what it means? Anticoagulation plan going forward — what do you say at this level? Future pregnancy — what counseling do you support OB and cardiology with? Documentation — what do you ensure goes home with her? Breastfeeding while on her anticoagulant — bearing on her choice? Follow-up with anesthesia — useful, when?

Considerations and pitfalls

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Episode framing. honest account of severity, what was done, and what to watch for; defer specifics to cardiology and OB.
Anticoagulation. ongoing for AF; coordinate with cardiology; explain why.
Future pregnancy. high-risk; preconception cardiology, possible definitive valve intervention; the candidate supports rather than owns this conversation.
Documentation. anesthesia summary, valve intervention details, anticoagulation, recommendations for any future anesthetic; portable letter for the patient.
Breastfeeding. compatibility depends on agent; heparin compatible; warfarin generally compatible; DOACs less data; defer specifics to lactation and cardiology resources.
Anesthesia follow-up. valuable for high-risk patients with a complicated course; a single follow-up visit and a written summary often the right cadence.

C. ADDITIONAL TOPICS

Teaching focus. Three unrelated vignettes: laryngospasm in a child with recent URI, LAST after interscalene block, and amniotic fluid embolism (a different OB physiology than the main stem).

1. Laryngospasm with recent URI

A 3 y.o. with a runny nose for a week undergoes bilateral myringotomy under mask anesthesia. On emergence: stridor, then no air movement, SpO2 80%. Dx? Contributing factors? Maneuvers and sequence? SpO2 70% with bradycardia to 60 — Rx? Persistent — agent and dose? Once recovered, what do you tell the parents?

Considerations and pitfalls

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Diagnosis. laryngospasm — stridor progressing to closure on light emergence.
Contributing factors. recent URI, light plane, secretions, young age.
Maneuvers. remove stimulus, 100% O2, jaw thrust with CPAP (Larson).
Bradycardia + desat. deepen with propofol or succinylcholine; treat hypoxic bradycardia; ready to ventilate or intubate.
Sux dose/route. small IV dose; IM if no IV; have atropine ready.
Counseling parents. plain explanation, what was recognized and treated, timing for future elective anesthesia after URI.

2. LAST after interscalene block

A 60 y.o. woman receives an interscalene block for shoulder surgery. Two minutes after injection she becomes agitated and then has a generalized seizure. Most likely cause? Priorities? She loses her pulse with a wide-complex rhythm. How does Mgmt differ from standard ACLS? Principle and dose of lipid emulsion? Prevention?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Cause. LAST from intravascular injection or rapid absorption.
Priorities. stop injecting, call for help, airway/oxygenation, control seizure, get lipid emulsion.
ACLS modifications. lipid emulsion, reduce epinephrine dosing, avoid certain antiarrhythmics, anticipate prolonged resuscitation, consider bypass.
Lipid emulsion. bolus and infusion per protocol; a specific therapy.
Prevention. incremental injection with aspiration, ultrasound, test dose, lowest effective dose.

3. Amniotic fluid embolism

A 31 y.o. woman at term has just delivered vaginally under a labor epidural. Moments after delivery she becomes acutely dyspneic and agitated, SpO2 falls to 78%, BP 70/40, oozing from IV sites. DDx? Leading diagnosis and why? Immediate priorities? She arrests in PEA — how is resuscitation in late pregnancy modified? Role of perimortem cesarean? She is resuscitated but now diffusely bleeding — interpretation and Mgmt?

Considerations and pitfalls

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DDx. AFE, eclampsia, high spinal, LAST, PE, hemorrhage, anaphylaxis.
Leading dx. AFE — abrupt collapse plus coagulopathy around delivery; clinical diagnosis of exclusion.
Priorities. call for help, airway, oxygenation, circulation, LUD, large-bore access, activate MTP.
Resuscitation in pregnancy. manual LUD or tilt, no change to drug doses or defibrillation energy, anticipate difficult airway and rapid desaturation.
Perimortem cesarean. within ~4 minutes of arrest if undelivered; an answer that delays indefinitely is a flag.
Coagulopathy. DIC is common; goal-directed product replacement and fibrinogen.

Session 1 — long stem

32-week parturient after MVC with hemorrhagic shock and fetal distress

A 27 y.o. G2P1 at 32 weeks gestation, 70 kg, 5'6", is brought to the trauma bay 30 minutes after a head-on motor vehicle collision. Trauma surgery plans emergent exploratory laparotomy for a positive FAST and hemodynamic instability; obstetrics is scrubbed for possible cesarean if fetal status worsens.

HPIRestrained driver, head-on collision at approximately 45 mph, airbag deployed, brief loss of consciousness, complains of left chest and diffuse abdominal pain. Bleeding from a forehead laceration. Last meal was a granola bar and coffee 2 hours ago.

PMHUnremarkable. One prior uncomplicated vaginal delivery three years ago. No prior anesthetics.

MEDSPrenatal vitamins, no other medications.

PHYS EXAMHR 128; BP 92/58; RR 26; SpO2 95% on 4 L NC; T 36.4°C. Cervical collar in place. Airway: Mallampati II, full mouth opening, full neck extension behind collar. Obvious left chest wall ecchymosis with crepitus; decreased breath sounds at the left base. Diffuse abdominal tenderness, gravid uterus tender to palpation. Pelvis stable. 5 cm forehead laceration packed.

ECGSinus tachycardia at 128, no ischemic features.

LABSHgb 9.4 g/dL (12.4 at 26 weeks); platelets 180 K/uL; INR 1.1; fibrinogen 280 mg/dL; lactate 4.2; base deficit minus 7; creatinine 0.8; type and screen with anti-K antibody, two units crossmatched, MTP activated.

IMAGINGFAST positive for free fluid in the right upper quadrant and pelvis. CT not yet performed. Portable CXR: left rib fractures 4-7, small left pneumothorax, no widened mediastinum.

FETALEstimated fetal weight 1900 g. FHR baseline 165 with reduced variability and recurrent late decelerations over the past 20 minutes.

OR ARRIVALTwo large-bore peripheral IVs in upper extremities. No arterial line yet. C-collar maintained. Patient with 15° left tilt on the OR table. Trauma, OB, NICU teams present; cardiothoracic surgeon notified for chest tube and possible thoracotomy.

A. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Trauma resuscitation modified for late pregnancy; airway, ventilation, and lines in the pregnant patient with chest trauma; the intraoperative obstetric decision and how anesthesia supports it; massive transfusion in the bleeding gravid patient.

1. Pre-induction priorities

Priorities? What changes in pregnancy that you must factor? Position — what, why? Airway plan — RSI in this patient — drug, dose? C-collar — bearing? Cricoid — yes/no? Why? Left pneumothorax — needle decompress before induction? Why? Chest tube — when? Arterial line — before or after induction? Why?

Considerations and pitfalls

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Priorities. ABCs simultaneously; address airway and ventilation alongside circulation; coordinate with trauma and OB.
Pregnancy changes. reduced FRC, rapid desaturation, full-stomach physiology, aortocaval compression, expanded plasma volume that masks shock, fetal demand.
Position. left uterine displacement throughout; full supine drops cardiac output sharply.
RSI drugs. induction agent dose-reduced for hypovolemia (ketamine or low-dose etomidate), full RSI dose paralytic; sux 1-1.5 mg/kg or rocuronium 1.2 with sugammadex available.
C-collar. manual in-line stabilization during laryngoscopy; video laryngoscopy first-line.
Cricoid. many programs maintain it for OB; defensible either way.
Pneumothorax pre-induction. small pneumothorax can become tension with positive pressure; have chest tube ready, low threshold for needle decompression.
Arterial line. during induction or immediately after; do not wait so long that it delays the OR.

2. Ventilation, volatile, and uterine relaxation

Induced, intubated first attempt with VL. Tube in. Chest tube placed for pneumothorax. Ventilation strategy now? Tidal volume by predicted body weight or actual? PEEP — how much? Plateau goal? Volatile choice and concentration in pregnancy? Bearing on uterine tone? OB wants to start C/S. Coordinate — who, when?

Considerations and pitfalls

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Ventilation. lung-protective by predicted body weight, modest PEEP (5-8), watch peak/plateau with chest injury.
Volatile. MAC reduced in pregnancy; uterine relaxation at higher MAC complicates atony after delivery; sevoflurane reasonable, kept low if delivery is imminent.
Bearing on uterine tone. high volatile worsens atony; turn down to 0.5 MAC around delivery.
OB coordination. delivery decision is OB's; anesthesia supports timing, communicates hemodynamics and resuscitation pace.

3. Intraoperative C/S decision

Trauma surgeon finds liver laceration with active bleeding. EBL already 1.5 L. Fetal tracing now category III. OB calls for cesarean now. Plan — sequence? Maternal stability before delivery — what target? Uterotonics ready — what, when? Neonatal team in place — what hand-off do you give? Maternal hypoxia — what do you do during fundal pressure? Awareness mitigation when volatile is turned down for atony?

Considerations and pitfalls

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Sequence. OB delivers concurrently with hepatic packing if possible; communicate roles aloud.
Maternal stability before delivery. perfusion endpoints, oxygenation, calcium, ongoing products; do not arrest the mother for the fetus or vice versa — they share physiology.
Uterotonics. oxytocin infusion ready, additional agents drawn up; methergine cautiously (volume status), carboprost if no airway disease.
Neonatal hand-off. gestational age, time of injury, maternal vitals, blood given, anesthesia state, expected condition.
Hypoxia during fundal pressure. respond promptly; FRC further reduced.
Awareness mitigation. midazolam early, opioid, propofol infusion to bridge, processed EEG if available.

4. Massive transfusion and coagulopathy

EBL 3.5 L. BP 75/40 on norepinephrine 0.2. Lactate 7. Plan? Products and ratios? Calcium — frequency? TXA — yes/no, when? Cell saver in pregnancy and trauma — role? Fibrinogen target? Endpoint for resuscitation? Surgical control — what do you communicate to surgery if you are losing the battle? Family in the trauma bay — who talks with them?

Considerations and pitfalls

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Plan. ongoing resuscitation, multidisciplinary communication, escalate help.
Products and ratios. 1:1:1 default, fibrinogen 200+ target, calcium repletion, lactate trending.
TXA. within 3 hours; the trauma indication is strong here.
Cell saver. OK in OB even with amniotic exposure when using leukoreduction filter; OK in trauma.
Endpoint. perfusion (MAP, lactate trend, base deficit), hemostasis.
When losing. name it plainly to the surgical team; ask for control, packing, vascular control.
Family. trauma surgery or social work typically; anesthesia available.

B. POST-OPERATIVE CARE

Teaching focus. ICU management of the postpartum trauma patient; pulmonary contusion evolving to ARDS; analgesia in chest trauma; VTE prophylaxis after trauma and surgery; mental health and psychosocial follow-up after an event with risk for lasting harm.

1. ICU arrival and initial plan

Arrives ICU intubated, hemodynamically improving on norepi 0.05, baby delivered alive to NICU. Initial vent settings? Sedation choice — agent, target? Analgesia plan — what regional or systemic? Bilateral rib fractures — bearing? Magnesium — start? Why? Family at the door — what do you say in the first 5 minutes?

Considerations and pitfalls

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Vent. lung-protective, sized to predicted body weight, PEEP titrated to oxygenation and hemodynamics.
Sedation. infusion-based, light if possible; consider dexmedetomidine for analgesia-sparing.
Analgesia. regional truncal or paravertebral block for ribs; multimodal.
Rib fractures. predict pulmonary toilet difficulty; block earlier rather than later.
Magnesium. not for tocolysis postpartum; consider for analgesia-sparing in some contexts but not a default.
Family. honest, brief, plan-focused; defer prognostic certainty when uncertain.

2. Pulmonary contusion and ARDS

POD 1: P/F 130, plateau 28, bilateral infiltrates with left worse. DDx? Most likely? Vent strategy — what change from current? Prone — when, criteria? NMB — role? Diuresis — yes/no, given recent transfusion? Bronchoscopy — when?

Considerations and pitfalls

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DDx. pulmonary contusion, ARDS, TRALI, aspiration, atelectasis, evolving pneumonia.
Most likely. contusion progressing toward ARDS, with possible TRALI overlap.
Vent. lower tidal volume, optimize PEEP, target plateau ≤30, driving pressure ≤15.
Prone. for severe ARDS (P/F < 150); the candidate should name criteria.
NMB. for severe dyssynchrony or refractory hypoxemia, not routine.
Diuresis. judicious negative balance if volume status permits; correct ongoing losses.
Bronchoscopy. if plugging or aspiration suspected.

3. Pain and regional anesthesia

Pain plan beyond ICU infusion? Regional choice for rib fractures — paravertebral, ESP, intercostal, thoracic epidural? Pick. Defend. Anticoagulation timing — bearing on regional choice? Multimodal — what scheduled? Opioid PCA — appropriate? Why?

Considerations and pitfalls

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Regional choice. thoracic epidural classic but anticoagulation constraints; ESP/PVB/intercostal alternatives; commit and defend.
Anticoagulation timing. neuraxial block earlier (before therapeutic dosing) easier; coordinate with trauma.
Multimodal. acetaminophen scheduled, NSAID if renal/bleeding ok, opioid for breakthrough, ketamine infusion considered.
PCA. appropriate if monitored; CPAP if OSA emerges.

4. VTE prophylaxis after trauma in postpartum

VTE risk — drivers here? Prophylaxis — when start? Agent? Dose for the postpartum patient? Mechanical compression — why important here? She develops new tachycardia and acute hypoxemia on POD 2 — DDx? Workup? Treatment if PE confirmed in this context?

Considerations and pitfalls

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Drivers. trauma, surgery, immobilization, postpartum state, transfusion.
Start. as bleeding risk allows; mechanical compression in the interim.
Agent and dose. enoxaparin; dose-adjusted for body weight.
Compression. essential.
New tachycardia and hypoxemia. PE high; sepsis, evolving ARDS, hemorrhage.
PE treatment. anticoagulation balanced against bleeding; IVC filter consideration in rare scenarios; multidisciplinary.

5. Disclosure and mental health follow-up

She wakes on POD 3 and asks what happened, where her baby is, and whether her partner survived (he was in the same car). What do you say? OB and trauma social work involved — coordinate how? Bearing on her sedation and pain medication choice over the next days? Risk of traumatic stress — your role in flagging? Documentation — what do you ensure travels with her?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

What say. plain, age-appropriate, partial truth as appropriate (defer to social work for major disclosures); avoid extended uncertainty alone.
Coordination. structured family meeting with trauma, OB, social work; aligned messaging.
Medication bearing. avoid heavy sedation if you can; allow her to participate; recognize sleep disruption as part of recovery.
Traumatic stress risk. real; flag to social work and mental health; recommend follow-up plan.
Documentation. anesthesia, trauma, surgical course; recommendations for any future anesthetic; portable letter.

C. ADDITIONAL TOPICS

Teaching focus. Three unrelated vignettes: LAST after interscalene, post-tonsillectomy hemorrhage in a child, and operating-room fire during MAC.

1. LAST after interscalene block

A 60 y.o. woman gets an interscalene block for shoulder surgery. Two minutes later she becomes agitated and seizes. Cause? Priorities? She loses her pulse with a wide-complex rhythm. ACLS modifications? Lipid emulsion — principle and dose? Prevention?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Cause. LAST.
Priorities. stop injecting, call for help, airway/oxygenation, control seizure, lipid.
ACLS mod. lipid, reduced epinephrine, avoid certain antiarrhythmics, prolonged resuscitation, bypass for refractory.
Lipid. bolus and infusion per protocol.
Prevention. incremental injection with aspiration, ultrasound, test dose, lowest effective dose.

2. Post-tonsillectomy hemorrhage

A 4 y.o. returns to the ED six hours after tonsillectomy, swallowing repeatedly and now vomiting bright blood, tachycardic and pale. Concerns? Why challenging? Pre-induction priorities? Induction plan? He desaturates during laryngoscopy with blood obscuring the view — actions? What tell the surgeon and family about urgency?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Concerns. bleeding, hypovolemic child with contaminated airway and swallowed blood; visible bleeding underestimates loss.
Challenges. aspiration, blood-obscured view, hypovolemia unmasked by induction, limited reserve.
Pre-induction. IV access, resuscitate, type and cross, two suctions, multiple tube sizes, surgeon present.
Induction. RSI with reduced dose for hypovolemia, head-down or lateral, ready for difficult view.
Lost view. large-bore suction, optimize position, smaller styletted tube or VL, call for help, surgical airway backup.
Communication. convey emergent nature plainly; align on plan and risks.

3. Operating-room fire

During MAC with nasal-cannula oxygen for an excision on the face, the surgeon uses electrocautery and a flash fire ignites at the drapes. Immediate actions? Sequence? Fire triad here? Once out, assess the patient — how? Prevention?

Considerations and pitfalls

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Immediate. stop the procedure, stop O2 and remove the airway source, remove burning drapes, extinguish.
Sequence. protect the patient and remove fuel and oxidizer first, then extinguish, then care for the patient.
Triad here. oxidizer (open O2 under drapes), ignition (cautery), fuel (drapes, prep, hair).
Post-fire. evaluate airway and burns; plan airway if inhalation injury suspected.
Prevention. minimize open O2 near cautery, secure airway or blend air, let prep dry, tent the drapes.

Session 1 — long stem

Idiopathic pulmonary arterial hypertension in active labor at term

A 26 y.o. G1P0 at 39 weeks gestation, 62 kg, 5'5", presents in active labor at 6 cm cervical dilation. She has known idiopathic pulmonary arterial hypertension and was scheduled for elective cesarean at 37 weeks but presented in spontaneous labor today.

HPIIdiopathic PAH diagnosed at age 22 after presyncope and progressive dyspnea on exertion; right-heart catheterization at that time showed mean PA pressure 56 mmHg, PVR 9 Wood units. Initial improvement on dual oral therapy. Pregnancy proceeded despite counseling; she elected to continue.

PMHIdiopathic PAH (WHO Group 1, functional class II to III). Multidisciplinary plan with cardiology, OB, and anesthesia for delivery at 37 weeks by elective cesarean. No prior surgeries, no prior anesthetics.

MEDSSildenafil 20 mg PO TID; selexipag 1600 mcg PO BID; low-dose aspirin 81 mg daily; prophylactic enoxaparin 40 mg SC daily (last dose 14 hours ago); prenatal vitamins.

PHYS EXAMHR 102, sinus; BP 110/68; RR 22; SpO2 92% on room air; T 37.0°C. Loud P2, parasternal RV heave. JVP elevated to 8 cm. Trace edema. Airway: Mallampati II, full mouth opening, full neck extension.

ECGSinus tachycardia, RV hypertrophy, right-axis deviation, T-wave inversions V1-V3.

LABSHgb 12.4 g/dL; platelets 220 K/uL; INR 1.0; BNP 980 pg/mL; creatinine 0.7 mg/dL; type and screen negative.

TTE (recent)RVSP estimated at 78 mmHg; RV moderately dilated with preserved function; septal flattening; moderate tricuspid regurgitation; reduced RVOT VTI; LV ejection fraction 60%.

IMAGINGCXR with enlarged central pulmonary arteries, no acute infiltrate.

FETALEstimated fetal weight 3500 g. FHR baseline 145 with appropriate variability, no decelerations.

OR ARRIVALAdmitted to L&D 90 minutes ago. Cardiology and adult cardiac anesthesia notified. ECMO team aware. 18 g antecubital IV. No arterial line yet. OB asks whether anesthesia is comfortable with assisted vaginal delivery versus moving to cesarean now.

A. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Labor analgesia and modality choice in fixed pulmonary hypertension; lines and monitoring that earn their cost; RV-protective hemodynamic goals through delivery; recognizing and treating an intrapartum PH crisis.

1. Modality and plan

Concerns? Mode of delivery — your input to OB? Why? Hemodynamic goals here? Targets — HR, rhythm, preload, afterload, PVR? Why each? Monitoring — what beyond standard? Arterial line — where, when? PA catheter — yes/no? Why? Central access — when? TEE — bearing? Enoxaparin last dose 14 hours ago — bearing on regional plan?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Concerns. fixed PH with RV that has to take the autotransfusion, labor catecholamines, possible crisis, postpartum first-24 hour high-risk window.
Delivery mode. assisted vaginal with effective epidural minimizes hemodynamic insult; cesarean has a clearer plan and is the consensus choice in many centers — defensible commit either way.
Goals. avoid rises in PVR (no hypoxia, hypercarbia, light anesthesia, acidosis), maintain SVR and preload, maintain sinus rhythm, support RV.
Monitoring. arterial line before any neuraxial; PA catheter controversial in PH (utility limited, risk real); TEE has a role if PA catheter declined.
Central access. needed for vasoactive titration; place early, before instability.
Enoxaparin timing. prophylactic dose interval 12 h often used; 14 h is reasonable; document and confirm.

2. Neuraxial technique

You plan early epidural for labor or possible C/S. Technique — slow epidural, CSE, or single-shot spinal? Pick. Defend. Local anesthetic choice and concentration? Test dose — agent here? Epinephrine — concern? Why? You place the epidural. After 10 mL bupivacaine 0.0625% with fentanyl, BP 92/58, HR 110. DDx? Rx? Phenylephrine vs norepinephrine in PH — pick. Defend.

Considerations and pitfalls

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Technique. slow epidural or low-dose CSE preferred over single-shot spinal; abrupt sympathectomy poorly tolerated.
LA choice. dilute bupivacaine plus opioid for labor; if escalating to surgical block, slow incremental dosing.
Test dose epinephrine. tachycardia confounds; some omit epinephrine and use other markers; defensible either way.
BP fall on epidural. expected sympathectomy plus baseline volume status; raise SVR, support preload.
Pressor in PH. norepinephrine commonly preferred; phenylephrine raises SVR but can raise PVR at high doses; vasopressin spares PVR and is often a key adjunct.

3. Intrapartum PH crisis

Two hours in. SpO2 falls to 84%, HR 130, BP 82/45, the patient is anxious and short of breath. DDx? Working diagnosis? Rx priorities? Inhaled pulmonary vasodilator — iNO, epoprostenol — which, why? Norepinephrine versus vasopressin — pick. Defend. Milrinone — role? Concern? Intubation — threshold? Bearing on the RV?

Considerations and pitfalls

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DDx. PH crisis with acute RV failure, PE, pulmonary edema, hemorrhage with hypovolemia, evolving infection.
Working diagnosis. acute PH crisis with RV failure given the clinical picture and known disease; the candidate should connect the picture.
Priorities. support coronary perfusion (raise SVR with norepi/vasopressin), reduce PVR (oxygen, treat hypercarbia and acidosis, inhaled vasodilator), support RV (inotrope), call for help.
Inhaled vasodilator. iNO or inhaled epoprostenol selectively lower PVR without systemic drop; either reasonable; epoprostenol may be more available.
Norepinephrine vs vasopressin. norepinephrine for SVR, vasopressin spares PVR; commonly combined; commit and defend.
Milrinone. inodilator; supports RV but drops SVR — pair with vasoconstrictor.
Intubation in PH crisis. double-edged; induction agents drop SVR, positive pressure can drop preload and raise PVR; needed if oxygenation fails, but plan carefully with experienced help.

4. Conversion to C/S and uterotonics

OB decides to proceed with cesarean. You go through the epidural with slow incremental dosing to T4. Stable. Baby out. OB asks about oxytocin. Bolus or infusion? Why? Dose? Atony at 5 minutes — methergine? Carboprost? Misoprostol? Pick. Defend. Now: BP 85/55, HR 130, SpO2 88%, RV looks bad on TEE. Rx? Endpoint? ECMO — when do you call?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Oxytocin. slow infusion; bolus doses cause vasodilation, tachycardia, and pulmonary pressure spikes — high risk in PH.
Atony agents. methergine raises SVR/PVR — contraindicated in severe PH; carboprost raises PVR — contraindicated; misoprostol and mechanical management preferred.
RV decompensation post-delivery. the autotransfusion plus uterotonic stress is the predictable insult; aggressively support RV, reduce PVR, raise SVR; consider mechanical support.
ECMO timing. early call when conventional support is failing; team must be ready before the crash.

B. POST-OPERATIVE CARE

Teaching focus. The first 24-72 hours postpartum carry the highest mortality risk in PH; surveillance and titration of pulmonary vasodilators; resuming targeted PH therapy; postpartum hemorrhage and anticoagulation in the cardiac patient; counseling on lactation and future pregnancy.

1. Immediate postpartum ICU plan

Arrives ICU intubated on norepinephrine 0.15 and vasopressin 0.04, inhaled epoprostenol running. BP 100/65, HR 110 sinus, SpO2 96% on FiO2 0.6, RV looks better on TEE. Plan? Targets for the first 24 hours — BP, HR, SpO2, PaCO2? Sedation — agent, why? Sildenafil and selexipag — when restart? Route? Lactation team paged early — why?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Targets. MAP 65-75 to support coronary perfusion, normal rate, avoid hypoxemia and hypercarbia, SpO2 ≥95%, PaCO2 normal.
Sedation. low-dose propofol or dexmedetomidine to avoid sympathetic surges; opioid for pain.
Targeted therapy. sildenafil and selexipag restart as early as gut function allows; abrupt withdrawal risks rebound.
Lactation. decisions about expressing milk vs not breastfeeding while on selexipag and sildenafil should involve a knowledgeable team early.

2. Wean and extubation

POD 1: stable, weaning to FiO2 0.4, off epoprostenol, on sildenafil PO. Extubation criteria — what? Plan for sedation off, spontaneous breathing trial — what watch for? Reintubation threshold? Cough vs pulmonary toilet support — what? She extubates and HR climbs to 130, RR 32, SpO2 88%. Rx? Trigger to restart inhaled?

Considerations and pitfalls

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Criteria. hemodynamic stability with low pressor support, gas exchange goals met, awake and following commands, no significant ongoing bleeding.
SBT in PH. watch for tachycardia, rising RR, hypoxemia, hypotension — any of which suggests the RV cannot keep up; do not push through.
Reintubation. early rather than late; the cost of a crash on the floor is higher than reintubation in ICU.
Post-extubation deterioration. support oxygenation, restart inhaled vasodilator, reassess RV; consider NIV.

3. Postpartum hemorrhage in PH

POD 1 evening: heavy lochia, Hgb 8.4 to 6.5 in 4 hours, BP 95/55, HR 130. Concerns? Uterotonic choice given PH? Volume — what, how much? Pressor? Blood — threshold? Cell saver — role? Anticoagulation held — implications? Communicate with OB — what?

Considerations and pitfalls

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Concerns. fluid shifts poorly tolerated; uterotonic choice constrained; bleeding worsens RV function.
Uterotonic. oxytocin slow infusion; misoprostol; mechanical and surgical options earlier.
Volume. titrated, watch RV and lungs; transfuse for oxygen-carrying capacity.
Pressor. norepinephrine, vasopressin.
Transfusion threshold. higher than baseline given limited reserve.
Anticoagulation. held for active bleeding; mechanical compression; restart when controlled.

4. Acute crisis on POD 2

POD 2 morning: acute hypotension, hypoxemia, RV severely dilated on TEE, lactate climbing. Possibilities? Working diagnosis? Rx? Mechanical support — VA ECMO or pVAD? Cardiac surgery and ECMO team here — who runs the case? What is your role? Family at bedside — what say?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Possibilities. PE, recurrent PH crisis, recurrent hemorrhage, sepsis, RV failure from cumulative insult.
Working diagnosis. RV failure with crisis physiology, with PE high on the list given postpartum and held anticoagulation.
Mechanical support. VA ECMO for RV failure with hypoxemia; pVAD options limited; early call to ECMO team.
Roles. anesthesia leads airway and perioperative hemodynamic management; ECMO team and cardiology share with surgery; clear shared mental model required.
Family. honest assessment of severity and the plan.

5. Counseling — lactation and future pregnancy

POD 5, off ECMO, extubated, off pressors, back on her oral PH regimen. Family asks if she will have more children. What do you say? Lactation — yes/no on her regimen? Documentation for any future anesthetic — what do you ensure goes home? Anesthesia follow-up — useful? When? What do you tell her about what almost happened?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Future pregnancy. high maternal mortality; strong recommendation against future pregnancy is standard; defer specifics to cardiology and OB; the candidate supports the conversation.
Lactation. depends on agent; selexipag/sildenafil compatibility data limited; defer to specialty resources.
Documentation. anesthesia summary, ECMO course, drug levels, recommendations for future anesthesia; portable letter.
Follow-up. anesthesia follow-up valuable for the patient and the team; one structured visit and a written summary usually right.
What almost happened. honest, plain account; allow her to ask; acknowledge what she went through.

C. ADDITIONAL TOPICS

Teaching focus. Three unrelated vignettes: an anterior mediastinal mass for biopsy, ARDS with refractory hypoxemia, and laryngospasm in a child with recent URI.

1. Anterior mediastinal mass

A 32 y.o. woman has a large anterior mediastinal mass and cannot lie flat for a CT scan. GA needed for sternotomy biopsy. Concerns? Other evaluation needed? Echo shows significant right ventricular and atrial compression. Awake intubation? Pt unable to tolerate fiberoptic. Now what? Mask induction with volatile — appropriate? Controlled vs spontaneous? Why? Indications for CPB?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Concerns. airway compression, great vessel and cardiac compression, hemodynamic collapse on induction, inability to lie flat.
Evaluation. imaging while upright if possible, flow-volume loops, echo.
Awake intubation. preferred when tolerated.
Mask volatile. preserves spontaneous ventilation; reasonable; have surgeon and CPB ready.
Controlled vs spontaneous. spontaneous preserves transpulmonary pressure.
CPB indications. anticipated collapse in critical compression.

2. ARDS with refractory hypoxemia

A 55 y.o. man with severe pneumonia is intubated in the ICU. On volume control, FiO2 1.0, PEEP 12: PaO2 58, P/F 90, plateau 32. Interpretation? Tidal-volume target and why? Plateau goal? Hypoxemic — higher PEEP, recruitment, or prone positioning? Defend. NMB role? When ECMO? BP falls to 80/50 on raising PEEP. DDx and Rx?

Considerations and pitfalls

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Interpretation. severe ARDS by P/F; plateau above target.
Tidal volume. low TV ~6 mL/kg PBW.
Plateau. ≤30.
PEEP vs recruit vs prone. each defensible; prone strongest outcome signal.
NMB. consider for severe dyssynchrony or refractory hypoxemia.
ECMO. refractory hypoxemia despite optimal vent; early referral.
Hypotension on PEEP. reduced venous return vs pneumothorax vs sepsis.

3. Laryngospasm with recent URI

A 3 y.o. with a runny nose for a week undergoes bilateral myringotomy under mask anesthesia. On emergence: stridor, then no air movement, SpO2 80%. Dx? Contributing factors? Maneuvers and sequence? SpO2 70%, bradycardia to 60 — Rx? Persistent — agent, dose? Once recovered, what tell parents?

Considerations and pitfalls

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Diagnosis. laryngospasm.
Factors. recent URI, light plane, secretions, young age.
Maneuvers. remove stimulus, 100% O2, jaw thrust with CPAP (Larson).
Bradycardia + desat. deepen with propofol or sux; treat hypoxic bradycardia.
Sux. small IV dose; IM if no IV; atropine ready.
Parents. plain explanation, timing for future elective anesthesia after URI.

Session 1 — long stem

RUQ pain and abnormal labs in the third trimester (HELLP with hepatic rupture)

A 29 y.o. G1P0 at 33 weeks gestation, 68 kg, 5'4", is admitted to labor and delivery for right upper quadrant pain, malaise, and decreased fetal movement. The obstetricians are asking whether she can go for urgent cesarean delivery.

HPIProgressive RUQ and epigastric pain for 24 hours with nausea and anorexia. Vague headache and brief blurred vision yesterday. Denies fever, contractions, vaginal bleeding. Prenatal visit one week ago: BP 138/86 (baseline 110/70 first trimester), trace proteinuria; she was scheduled for repeat assessment but presented earlier due to symptoms.

PMHUnremarkable. No prior surgeries or anesthetics. No history of viral hepatitis, no recent travel, no alcohol use.

MEDSPrenatal vitamins, no other medications.

PHYS EXAMAppears uncomfortable. HR 104; BP 162/98; RR 20; SpO2 97% on room air; T 37.2°C. Mild scleral icterus. Tender to deep RUQ palpation without rebound. Three-plus pitting edema to the thighs. Brisk reflexes with clonus. Airway: Mallampati II, full mouth opening, full neck extension.

LABSHgb 9.8 g/dL (11.5 one week ago); platelets 92 K/uL (175 one week ago); AST 380, ALT 410; LDH 980; total bilirubin 2.2; INR 1.2; fibrinogen 220 mg/dL; creatinine 1.3 mg/dL; uric acid 8.5 mg/dL; haptoglobin 12; peripheral smear with schistocytes; urine protein 3+. Type and screen sent, no antibodies.

IMAGINGRUQ ultrasound: hepatic capsule irregularity with a small subcapsular fluid collection; gallbladder normal; no biliary dilation. Obstetric ultrasound: estimated fetal weight 1900 g, posterior placenta, no abruption identified.

FETALFHR baseline 130 with reduced variability, no decelerations.

OR ARRIVAL18 g peripheral IV in the antecubital fossa, lactated Ringer's running. No magnesium yet. Obstetric team scrubbed for cesarean; the surgeon asks whether you are ready.

A. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Working a DDx for the parturient with abdominal pain, abnormal labs, and an evolving picture; modality choice when coagulation and hepatic findings constrain neuraxial; recognizing and responding to intraoperative bleeding and hepatic rupture; uterotonic and pressor choice when the patient is already compromised.

1. DDx and workup

Concerns? Working DDx? What ties it together? What argues against cholecystitis or hepatitis? Additional testing — what, and when? Magnesium — start now? Why? OB is pressing to go to the OR. Adjust your plan? You ask about a CT — bearing on timing? Schistocytes on smear — significance?

Considerations and pitfalls

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Concerns. an evolving multi-organ picture in a third-trimester patient with hypertension, hemolysis, low platelets, transaminitis, and imaging findings; don't anchor on one entity before scanning the list.
DDx. HELLP with subcapsular hepatic hematoma, severe preeclampsia, acute fatty liver of pregnancy, TTP, HUS, viral hepatitis, cholecystitis, abruption. Demand a list that goes beyond HELLP.
Tying it together. the combination of hypertension, proteinuria, hemolysis (LDH, haptoglobin, schistocytes), low platelets, transaminitis, and imaging findings is consistent with HELLP; the candidate should reason to it rather than be told.
Against cholecystitis or hepatitis. imaging shows no gallbladder pathology; viral panel pending; transaminase pattern doesn't fit alcoholic; AFLP would more often show ammonia, hypoglycemia, marked coagulopathy.
Additional testing. haptoglobin, LDH, smear (have); add ammonia, glucose, ADAMTS13 if TTP suspected, viral hepatitis panel, INR/fibrinogen trend.
Magnesium. yes, for preeclampsia/HELLP seizure prophylaxis; should not delay delivery if she's deteriorating.
CT. imaging may help characterize hematoma but should not delay delivery in a deteriorating picture; communicate.
Schistocytes. microangiopathic hemolysis; distinguishes from cholestatic disease; supports HELLP or TTP/HUS.

2. Modality decision under coagulopathy

OB wants to proceed. Modality? Spinal — yes/no? Why? Threshold for offering neuraxial in this picture? Other testing — what would change your mind? Magnesium — bearing on NMB? Commit. Defend. Patient asks not to be 'put to sleep.' How respond?

Considerations and pitfalls

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Modality. GA is often the move with platelets 92 trending down, schistocytes, transaminitis, and a possible hepatic hematoma; spinal defensible if reasoned against the trajectory. Anchoring on either without engaging both is a flag.
Threshold. single-number thresholds collapse under trajectory; the candidate should engage trend, fibrinogen, and clinical bleeding signs.
Testing that would change the call. TEG/ROTEM if available; repeat platelets and fibrinogen; bleeding history.
Magnesium on NMB. prolongs and weakens both depolarizing and non-depolarizing block; consider for RSI dosing and reversal.
Patient preference. respect the conversation, explain the safety reasoning, share the plan; an authoritative override without conversation is a flag.

3. Intraoperative bleeding and surgical findings

Induction smooth, intubated first attempt. As OB enters the abdomen they report 800 mL of free blood and identify a ruptured hepatic capsule with active bleeding. BP 88/52, HR 130. Rx now? Volume — what? Pressor — which? Activate MTP — trigger? Call for help — who? Surgical consult intraop — who? Anesthetic management while general surgery scrubs — what's your focus? OB asks about delivering the baby first.

Considerations and pitfalls

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Rx. balanced products, large-bore access (consider rapid transfuser), pressor support, communicate with surgeons; resuscitate while the cause is being addressed.
Volume and products. balanced ratios; calcium repletion; fibrinogen specifically, as HELLP and dilution will drive it down; TXA early.
Pressor. norepinephrine for distributive/hypovolemic shock; phenylephrine bolus while volume runs.
MTP trigger. ongoing surgical bleeding with hemodynamic instability is a clear trigger.
Help. second anesthesiologist or nurse anesthetist, blood bank liaison, general or HPB surgeon, IR if available.
Delivery decision. deliver the baby first to stop uteroplacental demand and let OB tamponade or pack the liver; communicate the order of operations aloud.
Anesthetic focus. maintain perfusion and oxygenation, keep coagulation goal-directed, avoid hypothermia and acidosis, communicate.

4. Post-delivery course and the liver

Baby delivered. General surgery packs the liver. EBL now 4 L; received 8 PRBC, 8 FFP, 2 platelets, 10 cryo. BP 90/55 on norepinephrine 0.15. Lactate 6.2. Now? Goals for the next hour? Disposition — ICU, OR back in 24 hours? What conversation with the family? Magnesium — continue? Anesthetic plan for transport — what do you want with you?

Considerations and pitfalls

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Goals for the next hour. perfusion endpoints (MAP, urine output, lactate trend), correct coagulopathy and calcium, normothermia, ongoing surveillance for rebleed.
Disposition. ICU with critical care and HPB surgery available; staged abdominal closure may keep her packed.
Family conversation. honest account of severity, the surgical state, the plan; involve OB and surgery.
Magnesium. continue for seizure prophylaxis; watch renal clearance with rising creatinine.
Transport. intubated transport with airway adjuncts, vasoactives, blood products en route, point-of-care lactate.

B. POST-OPERATIVE CARE

Teaching focus. ICU management of the postpartum patient with hepatic injury and coagulopathy; recognizing and treating ongoing bleeding when source is hidden; ventilatory support and extubation judgment in a marginal patient; postpartum eclampsia surveillance and disclosure when recovery diverges from the expected course.

1. ICU arrival and initial plan

Arrives ICU intubated, sedated. Open abdomen packed. Lines: arterial line, two large peripherals; you place a central line. Initial vent settings — what? Sedation — agent, target? PEEP — starting point? Magnesium — continue, hold? Family at the door wanting to come in. What say? Goals for the first 6 hours — what do you communicate to ICU team and OB?

Considerations and pitfalls

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Vent settings. lung-protective tidal volume, modest PEEP, FiO2 to target; avoid hyperinflation with hepatic compression.
Sedation. light, infusion-based (propofol, dexmedetomidine if hemodynamics permit), opioid for pain.
PEEP. 5-8 to start; titrate to oxygenation and hemodynamics.
Magnesium. continue for at least 24 h postpartum; adjust for renal function.
Family. brief honest update; involve appropriate team members.
6-hour goals. stabilize hemodynamics, correct coagulopathy, watch hepatic and renal trends, plan re-look in OR with surgery.

2. Ongoing coagulopathy

Six hours in: drains output 800 mL serosanguinous, INR 1.8, fibrinogen 140, platelets 48, hemoglobin stable. Interpretation? Products — what, how much, target? Cryo vs fibrinogen concentrate? Calcium — check how often? Surgical re-exploration — when do you call it? Heparin for VTE prophylaxis — when? Why?

Considerations and pitfalls

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Interpretation. ongoing low-grade bleeding plus consumption; not stable, requires action.
Products. platelets to 50-100K depending on bleeding, fibrinogen to >150-200, FFP to address INR; targets should be reasoned.
Cryo vs fibrinogen concentrate. either works; concentrate is faster, lower volume, less infectious risk; not universally available.
Calcium. frequent monitoring; replace ionized below 1.1.
Re-exploration. if drain output rises, hemoglobin falls, or instability returns; surgical team's call with anesthesia input.
VTE prophylaxis. deferred until bleeding controlled; mechanical compression in the interim; restart in the first 24-48 h with surgeon agreement.

3. Worsening liver function — DDx

POD 1: AST 1200, ALT 1400, bilirubin 4.8, INR climbing despite products, ammonia 95, glucose 62 with low-dose dextrose. Interpretation? DDx now? AFLP — bearing on what you do? Plasma exchange — role and timing? Transplant evaluation — trigger? Who needs to know now?

Considerations and pitfalls

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Interpretation. transaminase rise, hyperammonemia, hypoglycemia, climbing INR after product replacement — the picture has shifted toward acute liver failure, with AFLP back on the table.
DDx. HELLP with hepatic injury, AFLP, ischemic hepatitis from surgical bleeding, drug-induced; the candidate should not anchor on the initial diagnosis.
AFLP bearing. supportive care, glucose, treatment of coagulopathy; expedite delivery already done; some experience with plasma exchange in refractory cases.
Plasma exchange. considered in refractory severe HELLP/AFLP with multi-organ failure; not standard first-line.
Transplant evaluation. rapid hepatology and transplant consult if synthetic function is failing or encephalopathy worsens.
Communication. ICU, hepatology, transplant center, OB, family.

4. Postpartum eclampsia and pulmonary edema

POD 2 morning, sedation lifted briefly for neuro check, she has a tonic-clonic seizure. SpO2 falls to 84% on the ventilator with rising airway pressures. DDx? Priorities? Magnesium — bolus? Dose? Refractory — next? Pulmonary edema — sources here, which most likely? Diuresis — when, what? She develops bilateral coarse crackles. PEEP up or down? Imaging?

Considerations and pitfalls

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DDx of seizure. postpartum eclampsia, intracranial hemorrhage, CVST, metabolic (hypoglycemia, hyponatremia), hepatic encephalopathy.
Priorities. ABCs already secure (intubated); stop seizure, exclude reversible causes, image when stable.
Magnesium. 4-6 g bolus, restart infusion; benzodiazepine if refractory; levetiracetam or phenytoin next.
Pulmonary edema sources. TRALI, TACO, preeclamptic capillary leak, cardiogenic from massive resuscitation; the picture often mixed.
Diuresis. after volume status assessment; furosemide cautious; recognize leaky capillaries don't respond like ordinary CHF.
PEEP and imaging. consider PEEP recruitment for ARDS-like physiology; CXR, lung ultrasound, echo to differentiate.

5. Disclosure and ongoing course

Husband and parents are at bedside, frightened. They ask if she will live. What do you say? They ask why she got so sick. What say? They ask about future pregnancies. What say? OB and surgery have different framings. How coordinate the message? She wakes briefly two days later and asks why her abdomen is open. What say to her then? What do you document for her future obstetric and anesthesia care?

Considerations and pitfalls

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Will she live. honest uncertainty without false reassurance; describe what's working and what's not.
Why so sick. name what the team thinks and where uncertainty remains; do not over-promise a single diagnosis.
Future pregnancies. real recurrence risk; defer specifics to OB once she is stable; emphasize preconception planning.
Coordination. align the message before family conversations; conflicting accounts erode trust.
What she asks when awake. plain explanation of what happened, the surgery, the open abdomen, the plan; appropriate for her current state.
Documentation for the future. a letter she can carry summarizing the HELLP course, hepatic rupture, transfusion exposure, intubation conditions, and recommendations for future obstetric and anesthetic teams.

C. ADDITIONAL TOPICS

Teaching focus. Three unrelated vignettes: anesthesia for an anterior mediastinal mass, a recognized PDPH, and an operating-room fire during MAC.

1. Anterior mediastinal mass

A 32 y.o. woman has a large anterior mediastinal mass and cannot lie flat for a CT scan. GA needed for sternotomy biopsy. Concerns? Other evaluation needed? Echo shows significant right ventricular and atrial compression. Awake intubation? She cannot tolerate fiberoptic attempts. Now what? Mask induction with volatile — appropriate? Controlled vs spontaneous ventilation? Why? Indications for cardiopulmonary bypass?

Considerations and pitfalls

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Concerns. airway compression, great vessel and cardiac compression, hemodynamic collapse on induction, inability to lie flat.
Evaluation. imaging while upright if possible; flow-volume loops; echo for cardiac compression.
Awake intubation. preferred if tolerated; preserves negative-pressure ventilation and patient position.
Mask volatile induction. preserves spontaneous ventilation; reasonable when awake fails; have surgeon and bypass ready.
Controlled vs spontaneous. spontaneous preserves transpulmonary pressure and prevents complete airway collapse.
Bypass indications. anticipated collapse on induction in critical compression.

2. Postdural puncture headache

A 28 y.o. woman, 24 hours after a labor epidural complicated by a recognized wet tap, has a positional fronto-occipital headache relieved by lying flat. Dx? What exclude? Conservative measures? She can't care for her newborn — Rx? Mechanism? Risks?

Considerations and pitfalls

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Diagnosis. PDPH after known wet tap.
Exclude. preeclampsia, CVST, meningitis, subdural.
Conservative. time, analgesia, hydration, caffeine; limited evidence.
Definitive. epidural blood patch; tamponade and seal the leak.
Risks. repeat dural puncture, back pain, infection, rare neurologic complications.

3. Operating-room fire

During MAC with nasal-cannula oxygen for an excision on the face, the surgeon uses electrocautery and a flash fire ignites at the drapes. Immediate actions? Sequence of priorities? Fire triad here? Once out, assess the patient — how? Prevention?

Considerations and pitfalls

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Immediate. stop the procedure, stop the O2 and remove the airway source, remove burning drapes, extinguish.
Sequence. protect the patient and remove fuel and oxidizer first, then extinguish, then care for the patient.
Triad here. oxidizer (open O2 under drapes), ignition (cautery), fuel (drapes, prep, hair) — high-risk head-and-neck MAC.
Post-fire. evaluate the airway and any burns, plan airway if inhalation injury.
Prevention. minimize open O2 near cautery, secure airway or blend air, let prep dry, tent the drapes.

Session 1 — long stem

Severe preeclampsia with thrombocytopenia and morbid obesity, emergent cesarean

A 32 y.o. G2P1 at 35 weeks gestation, 110 kg, 5'5" (BMI 41), is brought from L&D to the OR for stat cesarean delivery for non-reassuring fetal tracing.

HPIAdmitted six hours ago with severe headache, scotomata, and right upper quadrant pain. BPs in the severe range since arrival despite labetalol boluses. Magnesium sulfate running at 2 g/h after a 4 g load. Obstetricians now report category III tracing with persistent late decelerations and minimal variability.

PMHChronic hypertension. Gestational diabetes on insulin. Obstructive sleep apnea on home CPAP, fair adherence. Two prior wet taps with epidurals during her first delivery, ultimately uncomplicated. No prior anesthetic complications she can recall.

MEDSLabetalol 200 mg PO BID, nifedipine ER 60 mg daily, insulin glargine 24 units qHS, magnesium sulfate gtt running, prenatal vitamins.

PHYS EXAMAnxious. HR 108; BP 174/108; RR 22; SpO2 94% on room air; T 37.0°C. Airway: Mallampati IV, thyromental distance 5 cm, neck circumference 44 cm, restricted neck extension from edema. Brisk reflexes with sustained clonus at the ankles. Pitting edema to the thighs and over the hands.

LABSHgb 11.2 g/dL; platelets 78 K/uL (was 142 K/uL one week ago); INR 1.0; fibrinogen 410 mg/dL; AST 112, ALT 138; creatinine 1.1 mg/dL; urine protein 4+; type and screen, no antibodies, two units PRBC on hold.

FETALEstimated fetal weight 2400 g. FHR baseline 95 with recurrent late decelerations and minimal variability over the past 25 minutes.

OR ARRIVAL18 g peripheral IV running LR with magnesium piggyback. Foley draining tea-colored urine. CPAP brought from the floor. Pt positioned with 15° left tilt. Obstetric team scrubbed; surgeon asking how long until incision.

A. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Modality choice under thrombocytopenia and severe-range hypertension; airway plan for the morbidly obese parturient on magnesium; managing BP swings around induction and emergence; recognizing and treating refractory uterine atony when uterotonics interact with the magnesium and the heart.

1. Modality and neuraxial decision

Concerns? Spinal? Why/why not? Threshold for offering neuraxial here? Other testing — what? TEG/ROTEM useful? Why/why not? Surgeon wants to start in five minutes. Bearing on your plan? Commit. Defend. If you go neuraxial, technique — spinal, epidural top-up, or CSE? Why?

Considerations and pitfalls

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Concerns. severe preeclampsia with severe features, falling platelets and rising transaminases (HELLP trajectory), severe-range BP, severe airway, magnesium on board, category III tracing forcing the timeline. Candidate should surface several, not just one.
Spinal — why/why not. the platelet count drives the regional question, but the airway is what makes GA dangerous; a defensible commit either way if reasoned. Reflexive GA without engaging the airway risk is a flag, as is a reflexive spinal without engaging the trajectory of platelets and AST.
Threshold. a defensible institutional threshold for neuraxial in preeclampsia, with explicit attention to trajectory and stability, not a single number quoted from a guideline.
TEG/ROTEM. may help when conventional studies are reassuring but trajectory is concerning; not a substitute for clinical judgment; not universally available.
Timeline pressure. non-reassuring tracing forces a defensible commit now; an answer that delays for further workup at the cost of the fetus should be challenged.
Spinal vs epidural top-up vs CSE. spinal is faster and denser for stat C/S; epidural top-up if one were already in; CSE less suited to a stat indication. Look for a committed, defended choice tied to time, height of block, and stability.

2. GA induction in the obese, preeclamptic, magnesium-loaded parturient

You go to GA. BP 184/112 on the table. Airway plan? Position — ramp, how? Preoxygenation — duration, technique? Drugs and doses for RSI? Sux or roc? Magnesium — bearing on NMB choice and dose? BP swing on laryngoscopy — what do you give and to what target? Cricoid — yes/no? Why? Anticipated change in MAC?

Considerations and pitfalls

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Airway plan. anticipated difficult airway: Mallampati IV, short thyromental, obesity, edema. Video laryngoscopy first-line is reasonable; awake intubation is on the table but the indication is emergent and the patient is uncooperative — a defended commit either way.
Ramp and preoxygenation. ramp to align tragus with sternal notch, head-up, 3-5 min of tight-seal preoxygenation if time permits; explicit attention to FRC and rapid desaturation in this body habitus.
RSI drugs/doses. induction agent dosed to lean body weight with attention to BP; sux 1-1.5 mg/kg total body weight if no contraindication, or rocuronium 1.2 mg/kg with sugammadex available. Magnesium prolongs and potentiates non-depolarizers; a candidate who dose-reduces roc without recognizing the prolongation deserves a probe.
BP on laryngoscopy. anticipate severe hypertensive response; pretreat with labetalol, fentanyl, or remifentanil; target a defensible BP rather than absolute normalization. Reflex nitroprusside is worth challenging.
Cricoid. evidence is mixed; many programs continue to use it for the parturient; a candidate's answer should be considered, not reflexive.
MAC effect. MAC reduced in pregnancy; magnesium adds CNS depression; over-dosing volatile in an already hypotensive picture is a pitfall.

3. Intraoperative BP swings and emergence

Induction smooth, intubated on second look with VL. BP 78/40 after delivery. DDx? Rx? Pressor — which? Why? OB sees uterine atony. Uterotonic sequence? Methergine in this patient — concern? Carboprost — concern? Calcium calcium chloride or gluconate? Now BP 195/118 with light anesthesia near closure. Rx? Antihypertensive of choice? Why? Magnesium — continue, hold, or bolus?

Considerations and pitfalls

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Post-delivery hypotension DDx. loss of aortocaval compression and uterotonic-related vasodilation; hemorrhage from atony; high spinal level not relevant since GA; magnesium effect; residual anesthetic.
Pressor choice. phenylephrine or norepinephrine for SVR-driven drop; reflex epinephrine in the unstable patient is reasonable. Watch for assumptions that phenylephrine is contraindicated in OB; it is not.
Methergine. contraindicated in severe hypertension and preeclampsia — naming it without a flag is a fail.
Carboprost. contraindicated in asthma; reasonable here if no reactive airway, but bronchospasm risk and hypertensive surge to be anticipated.
Calcium. calcium chloride preferred via central access for rapid effect; gluconate via peripheral; either if needed for citrate binding after PRBC.
Hypertensive surge at emergence. labetalol, hydralazine, or short-acting agents (nicardipine, esmolol). Avoid nitroprusside as default.
Magnesium. continue infusion through delivery and into postpartum period; a brief hold without restart misses the eclampsia window.

4. Refractory atony and massive hemorrhage

Atony persists. EBL 2500 mL. BP 70/35, HR 138. Priorities? Volume — what, how much? Activate MTP — trigger? Ratio? Calcium how often? OB asks: Bakri, B-Lynch, IR for uterine artery embolization, or hysterectomy? Your role in that decision? Labs return: fibrinogen 142, INR 1.7, plt 54. Products? TXA — yes/no? When? Patient on magnesium for past 8 hours — bearing? She has bled through 2 L cell saver. Endpoint for resuscitation?

Considerations and pitfalls

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Priorities. call for help, communicate with surgical team, large-bore access, MTP activation, get more hands; resuscitation runs in parallel with treating the cause.
Volume and ratios. balanced products, 1:1:1 in the absence of point-of-care data; whole blood if available.
Surgical options. Bakri, B-Lynch, and IR are uterus-sparing; hysterectomy is definitive; the candidate's role is to inform the decision on whether the patient can tolerate the time and to keep the resuscitation pace. Hand-waving away is a flag.
Coagulopathy products. fibrinogen replacement with cryo or fibrinogen concentrate (target ~200), platelets, FFP. Naming a number target shows judgment.
TXA. give early in obstetric hemorrhage (within 3 hours); a candidate who omits or delays it deserves a probe.
Magnesium interaction. magnesium reduces vascular tone and worsens hypotension; doesn't mean stop it, but recognize it as one piece.
Endpoint. perfusion-based endpoints: MAP, lactate trend, base deficit, urine output once bleeding controlled — not a single Hgb number.

B. POST-OPERATIVE CARE

Teaching focus. Extubation judgment after massive transfusion in an obese parturient on magnesium; recognizing and treating postpartum eclampsia; working up postpartum oliguria when AKI, preeclamptic injury, and ATN compete; the delayed neuraxial decision; honest disclosure when the postpartum course did not match the patient's expectations.

1. Extubation

Case done. EBL 4 L; products 8 PRBC, 6 FFP, 2 platelets, 10 cryo, 1 g TXA. BP 100/60 on norepinephrine 0.04 mcg/kg/min. Magnesium continued at 2 g/h. Extubate in the OR? Why/why not? What must be true? Mag bearing on muscle strength — how assess? Train of four — useful? Why? You extubate. SpO2 88% on 6 L NC after 20 min. DDx? Rx? Reintubate — threshold? Disposition?

Considerations and pitfalls

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Extubate or not. many would leave intubated after massive transfusion with ongoing pressor need; defensible either way if the criteria are named. Reflexive extubation to 'get her to PACU' is a flag.
Criteria. gas exchange, reversal confirmed, normothermia, hemostasis, mental status, hemodynamic stability with low pressor support, no ongoing coagulopathy.
Magnesium and strength. magnesium prolongs and weakens neuromuscular function independent of sugammadex; clinical strength tests (head lift, hand grip) carry weight beyond train-of-four alone.
Postextubation hypoxemia. atelectasis in obesity, pulmonary edema (TRALI, TACO, preeclamptic), residual NMB, narcotic depression, aspiration. Reaching for the most likely without scanning the rest is a flag.
Rx. optimize position, CPAP/BiPAP if appropriate, diuresis if volume overload identified, reintubate if failing trajectory rather than waiting for arrest.
Disposition. ICU for ongoing magnesium, monitoring, possible ventilation.

2. Postpartum seizure

POD 0, 8 hours postop on the floor. Magnesium discontinued by primary team 2 hours ago. Tonic-clonic seizure witnessed. Concerns? DDx? Priorities? Magnesium — bolus or restart gtt? Dose? Refractory at 4 g IV — next? Imaging — when? Airway — secure when? Disposition? Family at bedside — what say?

Considerations and pitfalls

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Concerns. eclampsia is the leading concern; postpartum eclampsia can occur days out, especially when magnesium is stopped early. Other causes (CVST, intracerebral hemorrhage, hyponatremia, drug effect) must remain on the list.
Priorities. ABCs, left lateral position if still pregnant (not here), protect from injury, oxygen, IV access if not present, call for help.
Magnesium dosing. 4-6 g IV bolus, then restart infusion at 1-2 g/h. Stopping mag at 12 hours postpartum is a common error worth probing.
Refractory. consider benzodiazepine, levetiracetam, or phenytoin; investigate non-eclamptic causes — imaging becomes important.
Imaging. non-contrast head CT after stabilization; MRI/MRV if posterior reversible encephalopathy syndrome or CVST suspected.
Airway. secure if airway not protected, recurrent seizures, or hypoxemia; have a low threshold given the airway challenges previously documented.
Family communication. plain explanation of what happened, the plan, the prognosis without false reassurance.

3. Oliguria and rising creatinine

POD 1: UOP 12 mL/h x 4 h. Cr 1.8 (baseline 0.9). BUN 32. BP 112/72 off pressors. DDx? Fluid challenge — yes/no? How much? Magnesium held — bearing? Diuretic — when, why? Lasix or mannitol? Why? Renal consult — trigger? Imaging? She begins to complain of shortness of breath.

Considerations and pitfalls

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DDx. preeclamptic AKI, hypovolemia from blood loss, ATN from hypotension and pigment load, abdominal compartment after massive resuscitation, urinary obstruction. Anchoring on one without scanning the others is a flag.
Fluid challenge. judicious bolus only after volume status assessment; reflexively pushing fluid risks pulmonary edema in a leaky preeclamptic vasculature. Examine before dosing.
Magnesium and renal function. magnesium clears renally; held appropriately if oliguric, but watch for eclampsia recurrence.
Diuretic. after volume optimization, furosemide for volume overload with declining respiratory status; mannitol rarely first-line here.
Renal consult. rising Cr, oliguria refractory to optimization, evolving electrolyte derangement.
New dyspnea. consider pulmonary edema (preeclamptic, TACO, TRALI), and reassess imaging and oxygenation.

4. Delayed neuraxial decision for postpartum procedure

POD 2. OB asks if you can do neuraxial for a planned bilateral tubal ligation she desires. Plt 105, trending up. AST 88, trending down. Will you offer? Why/why not? Threshold today? Platelet transfusion before block — yes/no? Why? Spinal vs epidural? Why? She refuses GA. Now? OB pushes back on delay. Your reasoning to OB?

Considerations and pitfalls

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Offer or not. a defensible commit either way; the trajectory matters as much as the absolute number. A candidate who quotes a single threshold without engaging trajectory is shallow.
Today's threshold. many programs comfortable with neuraxial above 70-80K with stable trend; explicit reasoning matters more than the number.
Platelet transfusion before block. not usually indicated to enable a neuraxial unless the count is very low; transfusing solely to allow a regional is rarely supported.
Spinal vs epidural. spinal for a procedure with a known short duration; either choice defensible if reasoned.
Refusal of GA. respect autonomy; if neuraxial is unsafe and patient refuses GA, the procedure may need to be deferred.
Communicating with OB. patient's safety is the boundary; involve the patient in the conversation; defer the procedure rather than push an unsafe block.

5. Disclosure and counseling

On POD 1 she asks why she ended up in the ICU and why she nearly needed a hysterectomy. What will you tell her? How frame the bleeding? Her husband asks about future pregnancies and recurrence risk. What say? OB has a different framing in mind. Coordinate — how? Anesthesia for a future pregnancy — what would you want her to know? Documentation — what and to whom?

Considerations and pitfalls

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What to tell the patient. a plain, honest account: severe preeclampsia, the bleeding after delivery, why we transfused, why ICU; appropriate for her level of understanding without minimization.
Frame the bleeding. name uterine atony, the role of magnesium, the surgical decisions made and avoided; do not over-personalize beyond your role.
Future pregnancies. real recurrence risk for preeclampsia; preconception planning, aspirin prophylaxis, early prenatal care. The candidate should defer specifics to OB while supporting the patient.
Coordinating with OB. align on the message before talking with the family; conflicting accounts erode trust and have downstream consequences.
Future-pregnancy anesthesia note. an honest account of what worked and didn't this time; what she should ask her future anesthesia team to consider (airway, neuraxial timing, hemorrhage prep).
Documentation. operative and anesthetic record, a letter she can carry, and a clear note for future obstetric and anesthesia teams about preeclampsia course, airway, transfusion, and complications.

C. ADDITIONAL TOPICS

Teaching focus. Three unrelated vignettes: refractory hypoxemia in ARDS, a complication during an eye block, and an operating-room fire during MAC.

1. ARDS with refractory hypoxemia

A 55 y.o. man with severe pneumonia is intubated in the ICU. Volume control, FiO2 1.0, PEEP 12: PaO2 58, P/F 90, plateau 32. Interpretation of these numbers? Tidal-volume target and why? Plateau goal? He stays hypoxemic — higher PEEP, recruitment, or prone positioning? Defend. Role of neuromuscular blockade? When ECMO? BP falls to 80/50 as you raise PEEP. DDx and Rx?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Interpretation. severe ARDS by P/F; plateau is above target; lung-protective ventilation is required.
Tidal volume. low tidal volume (~6 mL/kg predicted body weight); an answer that ventilates to normal CO2 at the cost of high volumes is worth challenging.
Plateau. keep at or below ~30; current 32 demands action.
Higher PEEP vs recruitment vs prone. each defensible; proning has the strongest outcome signal in severe ARDS. Look for a committed, justified escalation rather than a list.
Neuromuscular blockade. consider for severe dyssynchrony or refractory hypoxemia; not a default.
ECMO. refractory hypoxemia despite optimal vent management at experienced center; early referral matters.
Hypotension on raising PEEP. reduced venous return vs pneumothorax vs sepsis; lower PEEP or volume/pressor, exclude pneumothorax before pushing fluids.

2. Retrobulbar block complication

A 72 y.o. man undergoing cataract surgery becomes acutely bradycardic, then within minutes confused, dysarthric, and apneic shortly after a retrobulbar block. Possible causes? Most concerning? Mechanism of brainstem anesthesia after retrobulbar? Immediate Mgmt? Differential change if instead he developed sudden proptosis and a tense globe? Risk reduction?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Possible causes. brainstem anesthesia, oculocardiac reflex, intravascular LA, primary cardiac or neurologic event.
Most concerning. brainstem anesthesia causing apnea and depressed consciousness.
Mechanism. spread of LA along the optic nerve sheath into the subarachnoid space, producing central effects including respiratory arrest.
Management. support ventilation, airway, circulation until block recedes; usually transient. Failing to ventilate is the danger.
Proptosis + tense globe. retrobulbar hemorrhage with rising orbital pressure threatening the optic nerve; urgent ophthalmology, consider lateral canthotomy.
Risk reduction. meticulous technique, appropriate needle, aspiration before injection; consider less invasive blocks where feasible.

3. Operating-room fire during MAC

During MAC with nasal-cannula oxygen for an excision on the face, the surgeon uses electrocautery and a flash fire ignites at the drapes. Immediate actions? Priority sequence? Fire triad here — what feeds it? Once out, assess the patient — how? Prevention?

Considerations and pitfalls

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Immediate. stop the procedure, stop the oxygen and remove the airway source, remove the burning drapes, extinguish.
Sequence. protect the patient and remove fuel and oxidizer first, then extinguish, then care for the patient.
Triad here. oxidizer (open O2 pooling under drapes), ignition (cautery), fuel (drapes, prep, hair) — a high-risk head-and-neck MAC.
Assess after. airway and skin/airway burns, ventilation, plan airway management if inhalation injury suspected.
Prevention. minimize open O2 near cautery, secure airway or blend air, let prep dry, tent the drapes.

Session 2 — short stem

Stat cesarean in laboring parturient with epidural, conversion to general

A 28 y.o. G3P2 at 39 weeks gestation, 5'7", 78 kg, has been in active labor for 11 hours with a continuous lumbar epidural infusion of bupivacaine 0.1% with fentanyl 2 mcg/mL, placed six hours ago without difficulty. She has well-controlled asthma on albuterol prn and mild iron-deficiency anemia (Hgb 10.4). Her last meal was four hours ago, a sandwich and orange juice. Mallampati II at admission; HR 96; BP 128/76; RR 18; SpO2 99% on room air. The obstetric team has managed a prolonged second stage with intermittent variable and late decelerations. She is requesting a top-up because the obstetricians plan a bedside intrauterine pressure catheter and forceps trial.

A. PRE-OPERATIVE EVALUATION

Teaching focus. Assessing a laboring epidural at the bedside; situating a parturient's airway and aspiration risk under labor physiology; reactive airway considerations in pregnancy; anemia and resuscitation preparation when the case may convert.

1. Bedside epidural assessment

Concerns about this epidural? How assess function at bedside? What level of block do you want before forceps? How test? She reports cramping pain over the suprapubic area; legs feel normal. Interpretation? Top-up agent and dose — what do you reach for? Why? Test dose — still needed? Why/why not? OB now wants the catheter and forceps to start in 5 minutes. Adjust your plan?

Considerations and pitfalls

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Concerns. an epidural in for 6 hours can be patchy or migrated; she's now reporting new pain, which may signal block failure or evolving urgency. Don't anchor on top-up before assessment.
Function assessment. review hourly infusion volume and boluses, test sensory level (cold, pinprick, or ethyl chloride), check motor (Bromage), check for unilateral block.
Level for forceps. T10 sensory level typically adequate for low-forceps; higher (T6) needed if cesarean becomes the move.
Cramping suprapubic with normal legs. incomplete sensory level, missed segments, or visceral pain; sometimes a tunneled or partial catheter; redose, reposition, or reconsider.
Top-up agent. lidocaine with bicarbonate and epinephrine for speed if cesarean may be imminent; 2-chloroprocaine if very rapid onset needed; a low-concentration bupi/fentanyl bolus if only forceps coverage; commit and defend.
Test dose. still needed before a higher concentration top-up; catheter position can change.
Time pressure. decide whether to top-up here or move to the OR; commit.

2. NPO and aspiration risk

Time of last meal? Bearing? Pregnant physiology — what changes the risk? She gets a top-up and feels nauseated 10 min later. Significance? Aspiration prophylaxis — what do you give now if you anticipate going to the OR? Why? Particulate vs non-particulate antacid? She has been getting IV ondansetron — bearing? RSI in OB — circumstances when you must be ready?

Considerations and pitfalls

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NPO and pregnancy. decreased LES tone, delayed gastric emptying in labor, opioid effect; effectively full stomach in any laboring patient regardless of stated NPO time.
Nausea after top-up. sympathectomy and BP drop, vagal response to block, or progression of labor; aspiration risk rises with vomiting.
Prophylaxis. non-particulate antacid (sodium citrate) for rapid neutralization, H2 blocker or PPI for sustained effect, metoclopramide for gastric emptying.
Ondansetron. treats nausea but doesn't change aspiration risk.
RSI circumstances. any GA in a parturient, regardless of NPO time; emergent cases especially.

3. Asthma in the parturient

Last albuterol use? Last exacerbation? Currently audible wheeze? Implications for choice of induction agent if you must convert? Ketamine — yes? Why? Propofol — yes? Why? Carboprost contraindication — bearing on a postpartum hemorrhage plan? Beta-2 agonist before induction — yes/no? Why?

Considerations and pitfalls

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History assessment. frequency of rescue inhaler, prior hospitalizations, current symptoms, steroid use.
Induction agent. propofol is bronchodilatory; ketamine bronchodilates and supports BP; either reasonable. Etomidate is neutral.
Carboprost. contraindicated in significant asthma; consider methergine (if no severe HTN) or misoprostol; plan ahead with OB.
Pretreatment. consider albuterol nebulizer pre-induction if wheezing; steroid stress dose only if on chronic high-dose.
Volatile choice. sevoflurane is bronchodilatory and a reasonable choice if GA needed.

4. Anemia and resuscitation prep

Hgb 10.4. Significance? Type and screen — what does she have? Crossmatch — when do you ask for it? Cell saver in OB — role? IV access — what is in, what do you want? Surgeon mentions she had a prior C/S with EBL 1.5 L and a Bakri — bearing? Two large-bore IVs minimum — accept that floor 18 g? Plan if you must go emergently?

Considerations and pitfalls

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Hgb 10.4 in late pregnancy. physiologic dilutional anemia plus iron deficiency; reduces reserve if she bleeds.
Type and screen / crossmatch. T&S on admission for most laboring patients; cross 2 units when risk rises (prior PPH, suspicion of accreta, anticoagulated).
Cell saver. use is supported in OB; concerns about amniotic fluid contamination addressed by leukoreduction filter and washing.
Prior PPH and Bakri. raises baseline risk; pre-arrange products and prepare for repeat hemorrhage.
Access. two large-bore (16 or 18 g) reliable IVs; replace a marginal floor IV before urgent need.

B. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Recognizing block failure under time pressure and committing to conversion; airway and induction in the parturient with a full stomach and a labor airway; troubleshooting hypoxemia and awareness intraoperatively; managing postpartum hemorrhage when uterotonic choice is constrained.

1. Stat C/S call and modality

FHR drops to 60 and stays there. OB calls stat C/S. Epidural is in. Time to incision — what target? Top-up agent for emergent C/S — choice? Dose? Onset? Test dose first — yes/no, given the call? You start lidocaine 2% with bicarb and epi. As you push, BP falls to 80/45 and she becomes tachypneic. DDx? Rx? Continue top-up or stop?

Considerations and pitfalls

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Time to incision. category 1 emergent C/S targets minutes; communicate aloud with the team about what's needed.
Top-up choice. lidocaine with bicarbonate and epinephrine for fastest reliable surgical block via existing catheter; 2-chloroprocaine alternative; bupivacaine too slow.
Test dose under time pressure. many would skip in true category 1; a small initial dose with vigilance is reasonable. Either defensible if reasoned.
BP fall and dyspnea on top-up. high block from rapid epidural extension, or intrathecal injection through migrated catheter, or sympathectomy from baseline volume status. Don't assume LAST without evidence.
Rx. stop top-up, support BP with pressor, position, oxygen, reassess block height and respiratory effort; abandon neuraxial if high spinal evolving.

2. Inadequate block, decision to convert

After full top-up dose, sensory level is patchy at T8 with right-side sparing. OB has the knife in hand. Now? Tell OB — what, and how? Lidocaine ceiling reached — additional agent? Local infiltration — role? Ketamine — bridge? Conversion to GA — when do you call it? Stem — what informs your patience for more block time? She screams as the incision begins.

Considerations and pitfalls

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Inadequate level. patchy unilateral block after full dose suggests catheter problem; redosing rarely fixes; commit a path.
Communicate with surgeon. name the block status and the time you'll give it; align on whether they pause.
Adjuncts. ketamine subdissociative for bridge, local infiltration by surgeon, IV opioid; not a substitute for true block.
Convert to GA. when the patient is in pain and the block won't take or time has run; do not push opioids and ketamine in chase of a failed block while the patient suffers.
Stem. rapidity of fetal deterioration governs how long you have; brittle FHR forces the move.

3. GA conversion

You go to GA. Airway — what changed since admission? Position — labor bed to OR table — what considerations? Preoxygenation — how long given the stem? Drug choice — induction agent and dose? Sux or roc? Cricoid — yes/no? You apply DL: large tongue, edematous oropharynx, anterior view, Cormack-Lehane 3. Next move? Plan B — articulate. SpO2 92% and falling.

Considerations and pitfalls

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Airway change. labor airway: edema, weight gain, supine position; Mallampati can advance by one or two grades over labor.
Position. ramp, head-up, left tilt; check the table can tilt before induction.
Preoxygenation. as long as the FHR permits; 3-5 min by tight mask is ideal but rarely available.
Drugs. induction agent (propofol or ketamine), full RSI dose paralytic; consider reduced thiopental/propofol if hypotensive; sux 1-1.5 mg/kg or roc 1.2 mg/kg with sugammadex available.
Cricoid. many programs maintain it; defensible either way if argued.
CL 3 view. optimize external manipulation, BURP, change blade, video laryngoscopy as first or second attempt; SGA as rescue; commit to the next step before SpO2 collapses.

4. Awareness, hypoxemia, and delivery

Second attempt with VL — Cormack-Lehane 2, tube in. ETCO2 confirms. Surgeon delivers within 2 minutes. Maintenance — agent and dose? Awareness in OB — risk and prevention? After delivery, BP 75/40, HR 140, atony noted by surgeon. Uterotonic choice given her asthma? Methergine — yes/no? Why? OB asks for carboprost. Your reply? Misoprostol — role and route here? Volatile — turn down? To what?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Maintenance. low-dose volatile (e.g., 0.5 MAC sevoflurane) before delivery to reduce uterine relaxation while preventing awareness; supplement with N2O if tolerated and opioids/midazolam after cord clamp.
Awareness risk. elevated in OB-GA, especially with light pre-delivery anesthesia; midazolam after cord clamp, processed EEG if available, document anesthetic plan.
Post-delivery hypotension. atony, sympathectomy effect gone, volatile-induced uterine relaxation; oxytocin needs immediate dosing.
Methergine. ok in this patient (no severe HTN), watch for vasoconstriction.
Carboprost in asthma. contraindicated; communicate clearly; reach for methergine or misoprostol instead.
Misoprostol. rectal or sublingual; slower onset; reasonable adjunct.
Volatile down. reduce or replace with TIVA after delivery to allow uterine tone to recover.

5. Persistent atony and emergence

Despite oxytocin, methergine, and misoprostol, atony persists. EBL 2.0 L, climbing. BP 85/50. OB considers Bakri or hysterectomy. Your input? Resuscitation — products, ratios, calcium? TXA — yes/no? She has been GA, paralyzed, intubated. Extubation criteria after this case — what do you need? She is awake when sux wears off — implications? What will you tell her postop about her airway and the conversion?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Surgical option input. the candidate informs whether the patient can tolerate the time and pace for uterus-sparing; do not abdicate the decision but do not own it.
Resuscitation. balanced products, monitor calcium, fibrinogen target, point-of-care testing if available; TXA early.
Extubation. stable hemodynamics, gas exchange, reversal confirmed, no active bleeding, airway not worsened from baseline; conservative bias after this case.
Awake with sux wearing off. indicates inadequate hypnotic or paralytic; an awake paralyzed patient is a sentinel awareness event.
Postop disclosure. honest account of the airway difficulty, the conversion, why she may have had recall if any; the implications for future anesthesia; document with letter.

C. ADDITIONAL TOPICS

Teaching focus. Three unrelated vignettes: laryngospasm on emergence in a child with recent URI, retrobulbar block complication, and a recognized postdural-puncture headache.

1. Laryngospasm in a child with recent URI

A 3 y.o. with a runny nose for a week undergoes bilateral myringotomy under mask anesthesia. On emergence: stridor, then no air movement, SpO2 80%. Dx? Contributing factors? Maneuvers and sequence? SpO2 70% with bradycardia to 60 — Rx? Persistent — agent and dose? Once recovered, what tell the parents?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Diagnosis. laryngospasm — stridor progressing to closure on light emergence.
Contributing factors. recent URI, light plane, secretions, young age.
Maneuvers. remove stimulus, 100% O2, jaw thrust with CPAP (Larson).
Bradycardia + desat. deepen with propofol or succinylcholine; treat hypoxic bradycardia; ready to ventilate or intubate; sux without addressing oxygenation deserves a probe.
Sux dose/route. small IV dose breaks refractory spasm; IM if no IV; have atropine ready in the young child.
Counseling parents. plain explanation, what was recognized and treated, timing implications for future elective anesthesia after URI.

2. Retrobulbar block complication

A 72 y.o. man undergoing cataract surgery becomes acutely bradycardic, then within minutes confused, dysarthric, and apneic shortly after a retrobulbar block. Possible causes? Most concerning? Mechanism of brainstem anesthesia? Mgmt? Differential change if instead sudden proptosis and tense globe? Risk reduction?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Possible causes. brainstem anesthesia, oculocardiac reflex, intravascular LA, primary event.
Most concerning. brainstem anesthesia with apnea and depressed consciousness.
Mechanism. LA spread along optic nerve sheath into subarachnoid space.
Management. support ventilation, airway, circulation; usually transient. Failure to ventilate is the danger.
Proptosis + tense globe. retrobulbar hemorrhage; urgent ophthalmology, possible canthotomy.
Risk reduction. technique, needle, aspiration, less invasive blocks where feasible.

3. Postdural puncture headache after a wet tap

A 28 y.o. woman, 24 hours after a labor epidural complicated by a recognized wet tap, has a positional fronto-occipital headache relieved by lying flat. Dx and supporting features? What else exclude? Conservative measures? She can't care for her newborn — Rx? Mechanism? Risks?

Considerations and pitfalls

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Diagnosis. PDPH — postural after known dural puncture.
Must exclude. preeclampsia, cortical vein thrombosis, meningitis, subdural hematoma.
Conservative. time, analgesia, hydration, caffeine; evidence limited; overstating efficacy a flag.
Definitive. epidural blood patch; tamponade and sealing the leak.
Risks. repeat dural puncture, back pain, infection, rare neurologic complications.

Session 2 — short stem

Opioid use disorder on buprenorphine in labor

A 30 y.o. G2P1 at 39 weeks gestation, 5'4", 72 kg, presents in active labor at 5 cm cervical dilation. She is on buprenorphine-naloxone 16 mg sublingual daily for opioid use disorder, with two years of stable treatment in recovery. She also takes sertraline for depression and uses cannabis two to three times per week. Smokes five cigarettes daily. Hgb 11.4; platelets 165; vital signs normal; Mallampati II; visible track marks bilaterally on the antecubital fossae.

A. PRE-OPERATIVE EVALUATION

Teaching focus. Pre-op assessment of the parturient in stable opioid recovery; whether to continue buprenorphine through labor and delivery; labor analgesia matched to a partial-agonist baseline; planning for the breakthrough pain that buprenorphine will not cover; IV access in the patient with poor peripheral options.

1. Buprenorphine through labor

Concerns? Continue buprenorphine or hold for labor? Why? Bearing on her labor analgesia plan? Bearing if you must convert to cesarean and need GA? Her addiction provider's input — what do you want? Family in the room — what do you want her to hear from you?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Concerns. stable recovery and the risk of relapse from undertreated peripartum pain, dose-finding on a partial agonist that occupies receptors, perinatal social work needs, neonatal abstinence.
Continue or hold. current practice favors continuing buprenorphine through labor and delivery; holding risks withdrawal, relapse, and worse pain control. A defensible commit to continue is the expected position.
Bearing on labor analgesia. neuraxial is the workhorse; buprenorphine does not preclude it and is essential to maintain through the peripartum period.
Bearing on GA. induction agents work normally; opioid dosing for breakthrough or surgical pain will require higher doses or non-opioid adjuncts because of receptor occupancy.
Addiction provider. current dose, recent stability, plan for postpartum dose adjustment, support resources.
What she should hear. her recovery is respected and supported, the plan is collaborative, pain will be addressed, she has agency in the conversation.

2. Labor analgesia plan

Plan for labor analgesia? Early epidural — yes? Why? Local anesthetic and concentration? Bearing of buprenorphine on epidural opioid choice? Fentanyl in the epidural — bearing? She still reports pain at T8 block. DDx? Rx? Ketamine — role in labor? PCA fentanyl — appropriate here?

Considerations and pitfalls

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Plan. early epidural reduces stress and pain, supports recovery and minimizes systemic opioid.
LA choice. dilute bupivacaine or ropivacaine plus opioid; standard.
Buprenorphine and epidural opioid. partial agonist occupies receptors; fentanyl in epidural still works locally but may be less effective; clonidine or higher local dose can supplement.
Pain despite block. missed segments, patchy block, breakthrough from buprenorphine ceiling, other pain source.
Rx. redose block, assess catheter position, treat the missed segment, consider additional adjuncts.
Ketamine in labor. subdissociative infusion can help refractory pain, particularly when opioids are ineffective.
PCA fentanyl. limited role in the buprenorphine patient; favor neuraxial and non-opioid adjuncts.

3. IV access and resuscitation prep

Access — what do you have, what do you want? Ultrasound — bearing? She has poor peripheral options. Central line — when? Where? PICC — role? Type and screen — what does she need? Her history — bearing on transfusion thresholds? Drug history — bearing on cardiac evaluation?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Access. two reliable large-bore IVs needed; ultrasound essential in track-mark anatomy.
Central line. place early if peripheral access is marginal; do not wait until a code.
PICC. alternative for medication delivery but slower for resuscitation.
Type and screen. standard; sicker patients may need crossmatch.
Transfusion threshold. standard; her recovery does not change blood product use.
Cardiac evaluation. history of IV drug use raises concern for endocarditis and valvular pathology; targeted history and exam at minimum.

4. Plan for conversion

OB warns conversion to C/S may happen. Multimodal pain plan — what scheduled, what regional? Buprenorphine on the day of cesarean — continue or adjust? Why? Opioid for breakthrough — agent and dose, given partial-agonist occupation? Ketamine infusion — role? Neonatal team aware of buprenorphine — yes? Their plan?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Multimodal. acetaminophen scheduled, NSAID if no contraindication, regional truncal block (TAP/QL), ketamine infusion, neuraxial morphine, opioid only as supplement.
Buprenorphine on day of cesarean. continue at usual dose; some programs split into TID dosing peripartum for stable receptor occupancy and analgesia.
Breakthrough opioid. expect 2-3x typical morphine-equivalent dosing because of receptor occupancy; titrate to effect with monitoring.
Ketamine infusion. useful for refractory pain in this physiology.
Neonatal team. aware; plan for NAS monitoring and supportive care; rooming-in often supports both.

B. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Modality choice when GA could cost her recovery; managing breakthrough pain under partial agonist receptor occupancy; postpartum pain plan that respects opioid sparing while controlling pain; transitions to NAS care; discharge planning that protects the recovery she has built.

1. Stat C/S and modality

FHR drops to 70 and stays. OB calls stat C/S. Epidural is in. Top-up agent — pick. Defend. Block height target? Sensory level T4, BP 95/60. OB starts. As surgeon enters peritoneum, she reports sharp pain despite the level. DDx? Rx? Convert to GA — or treat as inadequate visceral coverage? How decide?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Top-up. lidocaine with bicarb and epinephrine for surgical level.
Block height target. T4-T6.
Pain despite level. visceral pain not covered, patchy block, hyperalgesia from chronic opioid use.
Rx. supplement with IV opioid (titrate higher than usual), ketamine bolus, ondansetron and anti-anxiolytic as appropriate; surgeon local.
Convert to GA. if pain cannot be controlled and patient is suffering; reasoned decision.
Decide. patient feedback, vital signs trend, ability to bridge for a few more minutes.

2. Post-delivery pain and uterotonics

Baby out. BP 90/55, HR 110. Atony noted at 5 min. Uterotonic choice in this patient? Pain plan as you proceed? Buprenorphine in PACU — confirm dose? Ketamine — bolus or infusion? Fentanyl — appropriate? Family at recovery room door anxious — what do you say?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Uterotonic. oxytocin slow; methergine if no severe HTN; misoprostol; carboprost if no asthma.
Pain plan. scheduled acetaminophen, regional block, ketamine adjunct, opioid as needed at higher than naive doses, neuraxial morphine if epidural still in.
Buprenorphine confirm. continue home dose; do not skip in the postpartum period.
Ketamine. bolus then infusion for refractory pain; recognize psychotomimetic effects.
Fentanyl. appropriate but may need higher doses; monitor for respiratory depression as opioid is added to her baseline.
Family. plain reassurance, plan for recovery period.

3. Postpartum pain on the floor

POD 1: pain 7/10 despite acetaminophen, ketorolac, scheduled buprenorphine, TAP block, ketamine 0.1 mg/kg/h. Next? Convert ketamine to higher dose? PCA — what settings? Opioid choice? Multidisciplinary input — who? Discharge planning — when? What anticipate?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Next. address the pain plainly; do not pretend it doesn't matter; reassess for other causes (hematoma, infection).
Ketamine. increase to 0.2-0.3 mg/kg/h with vigilance.
PCA. demand-only with hydromorphone or fentanyl at higher than naive doses; capnography monitoring; collaborative with pain team and addiction medicine.
Multidisciplinary. OB, addiction medicine, pain medicine, social work.
Discharge planning. structured plan with addiction provider; safe taper; close follow-up.
Anticipate. she may need higher inpatient opioid doses than naive patients; do not interpret as drug-seeking.

4. Neonatal NAS and breastfeeding

Neonatal team flags possible NAS in the infant. Mother asks if she can breastfeed on buprenorphine. What say? Cannabis use — bearing? Sertraline — bearing? Skin-to-skin and rooming-in — your input? What do you tell her about her own pain medication and her baby?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Breastfeeding on buprenorphine. compatible; small amounts transfer; benefits favor continuation.
Cannabis. active concern; cannabis is excreted in milk and avoided where possible; defer specifics to neonatology.
Sertraline. compatible with breastfeeding.
Skin-to-skin and rooming-in. supports NAS management and bonding; her involvement is part of treatment.
Her medication. honest information about what passes to the infant and what does not; involve neonatology in the message.

5. Discharge planning

POD 2. Pain controlled, neonate stable. Discharge plan — who is involved? Buprenorphine dose adjusted? Opioid prescribed at discharge? Why/why not? Risk of relapse postpartum — what is your role? Documentation she carries — what? Anesthesia follow-up — useful? When?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Discharge plan. OB, addiction medicine, pediatrics, social work, primary care.
Buprenorphine adjusted. may need transient dose increase that tapers postpartum; coordinated with addiction medicine.
Discharge opioid. minimize; if prescribed, small quantities with clear follow-up; coordinate with addiction medicine.
Relapse risk. real; multidisciplinary structured support; the candidate should name the risk and the role of clear plans and follow-up.
Documentation. anesthetic record, multimodal plan, recommendations; portable letter.
Anesthesia follow-up. valuable; one structured visit and a written summary.

C. ADDITIONAL TOPICS

Teaching focus. Three unrelated vignettes: anterior mediastinal mass, laryngospasm with recent URI, and operating-room fire during MAC.

1. Anterior mediastinal mass

A 32 y.o. woman with a large anterior mediastinal mass cannot lie flat for CT. GA needed for sternotomy biopsy. Concerns? Evaluation? Echo shows significant RV and atrial compression. Awake intubation? Patient unable to tolerate fiberoptic. Now what? Mask volatile induction — appropriate? Spontaneous vs controlled? CPB indications?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Concerns. airway/vessel/cardiac compression, collapse on induction, inability to lie flat.
Evaluation. upright imaging, flow-volume loops, echo.
Awake intubation. preferred when tolerated.
Mask volatile. preserves spontaneous ventilation; surgeon and CPB ready.
Spontaneous. preserves transpulmonary pressure.
CPB. anticipated collapse in critical compression.

2. Laryngospasm with recent URI

A 3 y.o. with a runny nose for a week undergoes bilateral myringotomy under mask anesthesia. On emergence: stridor, then no air movement, SpO2 80%. Dx? Contributing factors? Maneuvers and sequence? SpO2 70% with bradycardia to 60 — Rx? Persistent — agent, dose? Once recovered, what tell parents?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Diagnosis. laryngospasm.
Factors. recent URI, light plane, secretions, young age.
Maneuvers. remove stimulus, 100% O2, jaw thrust with CPAP (Larson).
Bradycardia + desat. deepen with propofol or succinylcholine; treat hypoxic bradycardia.
Sux. small IV dose; IM if no IV; atropine ready.
Parents. plain explanation, timing for future elective anesthesia.

3. Operating-room fire

During MAC with nasal-cannula oxygen for an excision on the face, the surgeon uses electrocautery and a flash fire ignites at the drapes. Immediate actions? Sequence? Fire triad here? Once out, assess the patient — how? Prevention?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Immediate. stop the procedure, stop O2 and remove airway source, remove burning drapes, extinguish.
Sequence. protect patient and remove fuel and oxidizer first, then extinguish, then care for patient.
Triad. oxidizer (open O2 under drapes), ignition (cautery), fuel (drapes, prep, hair).
Post-fire. evaluate airway and burns; plan airway if inhalation injury.
Prevention. minimize open O2 near cautery, secure airway or blend air, let prep dry, tent drapes.

Session 2 — short stem

Active asthma flare in labor at term

A 31 y.o. G2P1 at 38 weeks gestation, 5'5", 74 kg, presents in active labor at 5 cm cervical dilation. She has steroid-dependent asthma with two prior ICU admissions and one intubation in the past three years; current peak flow is 60% of her personal best with audible wheezing, and she has been progressively short of breath over the past 24 hours. Aspirin sensitivity and penicillin allergy. Took prednisone 20 mg PO this morning per her chronic regimen. P 108; BP 132/82; RR 24; SpO2 93% on room air; Mallampati II.

A. PRE-OPERATIVE EVALUATION

Teaching focus. Bedside pulmonary assessment in active labor; matching labor analgesia plan to a fragile reactive airway; stress steroid coverage in the chronically treated patient; planning the airway and uterotonic choices that the rest of the case will turn on.

1. Pulmonary assessment

Concerns? Bedside assessment of her pulmonary status now? Peak flow trend — bearing? ABG — yes/no? Why? Wheeze on exam — significance? Treatment now at bedside — what, in order? Steroid stress dose — yes/no? Why? Pulmonologist consult — when?

Considerations and pitfalls

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Concerns. active flare on top of chronic disease, prior intubation, pregnancy physiology reducing reserve, possibility of needing GA.
Bedside assessment. speech in sentences, accessory muscle use, breath sound symmetry, peak flow vs personal best, SpO2, PaCO2 trend if available.
ABG. useful if her status appears worsening; a normal or rising PaCO2 in active flare is a danger sign.
Wheeze significance. moves air; silence is worse; quality and distribution matter.
Bedside treatment. albuterol nebulizer, ipratropium, magnesium IV if severe, systemic steroids, oxygen; address hydration.
Stress steroid. chronic prednisone exposure suggests adrenal suppression risk; stress dose for surgical stress is conservative; many give hydrocortisone.
Pulmonology. early if flaring with active labor.

2. Labor analgesia plan

Plan for labor analgesia? Epidural — when? Why? Local anesthetic and concentration choice — bearing on her asthma? Test dose epinephrine — concern? Why? She gets epidural at T8. Now reports cramping legs and audible wheezing. DDx? Rx? Block height and ventilation — bearing?

Considerations and pitfalls

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Plan. early epidural reduces catecholamines and labor pain that triggers bronchospasm; opioid component supportive.
Timing. as soon as labor is established and she requests.
LA choice. dilute bupivacaine plus fentanyl typical.
Test dose epinephrine. less worry in asthma than in cardiac disease, but BP/HR rise can confound; defensible to omit if she tolerates incremental dosing.
New wheezing after epidural. anxiety, evolving flare, allergic reaction, high block compromising accessory muscles.
Rx. treat as flare while excluding the others; high block needs ventilatory support.
Block and ventilation. T4-T6 block reduces accessory muscle recruitment and can worsen perceived dyspnea; reassure if otherwise stable.

3. Aspirin sensitivity and uterotonic implications

What is the implication of her aspirin sensitivity? Bearing on NSAIDs? Carboprost — yes/no in this patient? Why? Methergine — yes/no? Why? Misoprostol — yes/no? Why? Plan for atony if she delivers and bleeds — what is in your back pocket? Mechanical and surgical options — at what point do you escalate?

Considerations and pitfalls

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Aspirin sensitivity. could be true allergy or NSAID-exacerbated respiratory disease (AERD); the latter contraindicates NSAIDs and aspirin.
NSAIDs. avoid if AERD; acetaminophen and opioid for analgesia.
Carboprost. contraindicated in significant asthma — bronchospasm risk; relative in mild, absolute in severe.
Methergine. ok in asthma if no severe HTN; primary watch is vasoconstrictive effect.
Misoprostol. ok in asthma; reach for it first.
Back pocket. oxytocin infusion, methergine, misoprostol, calcium, fluid, pressors; mechanical and surgical earlier.
Escalation. early when atony is refractory to first two agents.

4. Plan for conversion

OB warns she may need stat C/S. If you go GA — anticipated risks? Induction agent choice — propofol vs ketamine — pick. Defend. Sux vs roc here? Volatile choice and concentration? Steroid stress dose — adjust now? Pre-induction bronchodilator — yes? Family in the room — your conversation?

Considerations and pitfalls

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Risks if GA. bronchospasm on intubation and emergence, high airway pressures, prolonged FiO2, aspiration risk, awareness risk.
Induction. propofol bronchodilatory; ketamine bronchodilatory and supports BP; defensible either way.
Sux vs roc. sux fine; roc reasonable with sugammadex.
Volatile. sevoflurane bronchodilatory; commit and defend.
Steroid. add IV hydrocortisone now.
Pre-induction bronchodilator. albuterol immediately before induction reduces airway reactivity.
Family conversation. honest about plan, possible airway management, what to expect.

B. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Modality choice when GA risk is high; recognizing and treating intraoperative bronchospasm; supporting hemodynamics in a patient with a sympathectomy and a reactive airway; uterotonic and analgesic constraints around delivery; extubation judgment in the asthmatic.

1. Stat C/S decision

FHR drops to 80 and stays. OB calls stat C/S. Epidural is in but block is patchy. Top-up agent — pick. Defend. If top-up fails — GA. Pre-induction albuterol — yes? Induction agents and doses? Sux dose? Cricoid — yes/no? Why? You apply VL and see Cormack-Lehane 2. Tube in. End-tidal up but peak airway pressure 42. DDx? Rx?

Considerations and pitfalls

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Top-up. lidocaine with bicarb and epinephrine; small initial dose vigilantly.
GA decision. if block fails under time pressure; do not push patient through pain.
Pre-induction albuterol. yes; nebulizer or MDI through circuit ready.
Induction. propofol or ketamine, full RSI paralytic.
High peak pressure post-intubation. bronchospasm vs mainstem intubation vs kinked tube vs ventilator issue.
Rx. verify tube position, deepen anesthesia (volatile, propofol bolus), albuterol, anticholinergic, ketamine, magnesium IV, epinephrine if severe.

2. Intraoperative bronchospasm

Despite albuterol and deepening anesthesia, peak pressures 50, SpO2 88%, ETCO2 60. DDx? Now? Volatile — what concentration? Epinephrine — IV, dose? Magnesium — yes? Dose? Heliox — role? Ventilator settings — what change? Tidal volume? PEEP? I:E ratio? Why?

Considerations and pitfalls

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DDx. refractory bronchospasm; reconsider mainstem, ETT obstruction, anaphylaxis.
Volatile. increase sevoflurane to 1-1.5 MAC for bronchodilation while supporting BP.
Epinephrine. IV in escalating doses; or infusion; bronchodilator and pressor.
Magnesium IV. 2 g infusion.
Heliox. limited use intraop but available in some places.
Vent settings. longer expiratory time to avoid breath stacking, reduce respiratory rate, accept permissive hypercapnia, low TV, modest or zero PEEP if dynamic hyperinflation.

3. Post-delivery hypotension and atony

Baby out. BP 75/40, HR 130, SpO2 92%. Atony noted by surgeon. Hypotension DDx? Pressor — pick. Defend. Uterotonic given her asthma — choice and sequence? She still has wheeze, ETCO2 climbing. Volatile — turn up or down? Awareness mitigation as you reduce volatile? Calcium calcium chloride or gluconate?

Considerations and pitfalls

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DDx. uterine relaxation from volatile, sympathectomy gone with delivery, blood loss, ongoing bronchospasm, AFE.
Pressor. norepinephrine or phenylephrine for SVR; epinephrine if bronchospasm prominent.
Uterotonic. oxytocin infusion (slow), misoprostol, methergine if no HTN; avoid carboprost.
Volatile bind. high volatile worsens atony but treats bronchospasm; reduce while bridging with ketamine and propofol and IV bronchodilators.
Awareness mitigation. midazolam, propofol, opioid; processed EEG if available.
Calcium. calcium chloride central, gluconate peripheral.

4. Refractory atony with limited options

Atony continues. EBL 1.8 L, BP 80/45. Bakri vs mechanical compression vs hysterectomy — your input to OB? Resuscitation — products? TXA — yes? Pressor escalation — to what? End point for resuscitation? Asthma flare in parallel — bearing on your fluid plan? Bronchodilator — continued infusion?

Considerations and pitfalls

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Input. candidate informs on whether time and pace allow uterus-sparing; do not own the surgical call.
Resuscitation. balanced products, calcium, fibrinogen, TXA early.
Pressor escalation. norepinephrine + vasopressin; epinephrine for combined bronchospasm and shock.
End point. perfusion endpoints, hemostasis.
Asthma + fluid. watch crystalloid load on a leaky inflamed lung; favor products.
Bronchodilator infusion. epinephrine drip can do both bronchodilator and pressor work.

5. Extubation and pain plan

Case done. EBL 2.5 L, total products 4 PRBC, 4 FFP, 1 platelet, 1 g TXA. Peak pressures down to 22, ETCO2 normal. Extubate in OR? Why/why not? Criteria? Awake or deep extubation? Pain plan in this asthmatic with AERD-suspected aspirin sensitivity? Acetaminophen, opioid, ketamine — what scheduled? PCA — concerns? Continuous bronchodilator on the floor — yes? Until when?

Considerations and pitfalls

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Extubate. defensible if criteria met; cautious bias in asthmatic with recent severe bronchospasm.
Criteria. gas exchange, reversal, awake and protecting airway, stable hemodynamics, no recurrent wheeze.
Awake vs deep. awake usually preferred; deep avoids coughing but risks loss of airway.
Pain plan. acetaminophen scheduled, opioid for breakthrough, regional block (TAP/QL), ketamine infusion; avoid NSAIDs if AERD.
PCA. OK with monitoring; avoid heavy basal infusion in OSA or sedated patient.
Bronchodilator on the floor. continue scheduled nebs, taper steroids per pulmonology, follow-up planned.

C. ADDITIONAL TOPICS

Teaching focus. Three unrelated vignettes: post-tonsillectomy hemorrhage, retrobulbar block complication, and PDPH after a wet tap.

1. Post-tonsillectomy hemorrhage

A 4 y.o. returns to the ED six hours after tonsillectomy, swallowing repeatedly and now vomiting bright blood, tachycardic and pale. Concerns? Why challenging? Pre-induction priorities? Induction plan? He desaturates during laryngoscopy with blood obscuring the view — actions? What tell the surgeon and family about urgency?

Considerations and pitfalls

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Concerns. bleeding, hypovolemic child with contaminated airway.
Challenges. aspiration, blood-obscured view, hypovolemia unmasked by induction.
Pre-induction. IV, resuscitate, type/cross, two suctions, multiple tube sizes.
Induction. RSI reduced dose for hypovolemia.
Lost view. large-bore suction, optimize, smaller tube or VL, surgical airway backup.
Communication. convey urgency plainly.

2. Retrobulbar block complication

A 72 y.o. man undergoing cataract surgery becomes acutely bradycardic, then within minutes confused, dysarthric, and apneic shortly after a retrobulbar block. Possible causes? Most concerning? Mechanism of brainstem anesthesia? Mgmt? Differential change if instead proptosis and tense globe? Risk reduction?

Considerations and pitfalls

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Causes. brainstem anesthesia, oculocardiac reflex, intravascular LA, primary event.
Most concerning. brainstem anesthesia.
Mechanism. LA along optic nerve sheath into subarachnoid space.
Mgmt. support ventilation, airway, circulation.
Proptosis. retrobulbar hemorrhage; ophthalmology, possible canthotomy.
Risk reduction. technique, needle, aspiration, less invasive blocks.

3. PDPH after wet tap

A 28 y.o. woman, 24 hr after a labor epidural with recognized wet tap, has a positional fronto-occipital headache relieved by lying flat. Dx? Exclude what? Conservative? Definitive Rx? Mechanism? Risks?

Considerations and pitfalls

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Diagnosis. PDPH.
Exclude. preeclampsia, CVST, meningitis, subdural.
Conservative. time, analgesia, hydration, caffeine.
Definitive. epidural blood patch.
Mechanism. tamponade, seal.
Risks. repeat dural puncture, back pain, infection, rare neurologic.

Session 2 — short stem

Sickle cell disease in active labor after recent vaso-occlusive crisis

A 24 y.o. G1P0 with hemoglobin SS sickle cell disease at 37 weeks gestation, 5'3", 58 kg, is in active labor at 4 cm dilation. She was discharged five days ago after a vaso-occlusive crisis requiring four days of IV hydromorphone PCA. She has bilateral femoral head avascular necrosis and chronic back pain. Hgb 7.6 g/dL (baseline 8.0), reticulocytes 18%, LDH 920. P 102; BP 118/72; RR 22; SpO2 95% on 2 L NC; mild crackles at bases; Mallampati II.

A. PRE-OPERATIVE EVALUATION

Teaching focus. Sickle cell physiology in late pregnancy and labor; matching labor analgesia to chronic opioid exposure; transfusion thresholds and acute chest surveillance; preparing for conversion when the patient and the system are already running close to the line.

1. Sickle cell in labor

Concerns? Triggers of crisis you must avoid through labor? Hydration plan — how much, what? Oxygen — target SpO2? Why? Hemoglobin and hemolysis labs from this morning — interpretation? Crackles at the bases — significance? Workup at bedside? You ask hematology what they'd add — what do you anticipate?

Considerations and pitfalls

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Concerns. VOC in labor stress, acute chest evolving, anemia and reserve, chronic opioid tolerance, possible postpartum stroke.
Triggers. hypoxia, hypothermia, acidosis, dehydration, pain, infection.
Hydration. isotonic crystalloid with awareness of fluid overload; avoid aggressive D5W boluses.
Oxygen target. SpO2 ≥95%; don't tolerate desats.
Hgb trend. drop from baseline suggests ongoing hemolysis or pregnancy dilution; not at simple transfusion threshold yet.
Retic and LDH. ongoing hemolysis, consistent with disease activity.
Crackles. could be volume status, early acute chest, atelectasis.
Bedside workup. CXR, ABG if symptomatic, lactate, repeat CBC, blood culture if febrile, hematology consult.
Hematology input. transfusion plan, drugs to avoid, antibody profile, prior crisis triggers, exchange threshold.

2. Labor analgesia and opioid tolerance

Plan for labor analgesia? Early epidural — yes? Why? Local anesthetic and concentration? Bupivacaine vs ropivacaine — does it matter in SCD? Why? Chronic opioid use — bearing on her epidural opioid choice? Fentanyl vs hydromorphone in the epidural? Test dose epinephrine — concern? Why? She still reports pain after a good T10 block — DDx?

Considerations and pitfalls

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Plan. early epidural reduces sympathetic surge and pain, supports hydration and rest.
LA choice. dilute bupivacaine or ropivacaine with opioid; ropivacaine slightly less motor block; either reasonable.
Chronic opioid. her usual systemic opioid dose continues for baseline, neuraxial opioid for incremental coverage.
Epidural opioid. fentanyl typical for labor; hydromorphone an option.
Test dose epinephrine. less restrictive than in cardiac disease; reasonable to use.
Pain despite T10 block. evolving acute chest, evolving VOC, bone pain from AVN, missed segments — broaden DDx.

3. Transfusion and acute chest surveillance

Transfusion threshold here? Why? Simple vs exchange — pick. Defend. Crossmatch — special considerations? Antibody phenotype matching — why? She develops mild dyspnea, SpO2 92% on 4 L NC, new infiltrate on CXR. Concern? DDx? Workup? Rx now? Antibiotic — yes? Why?

Considerations and pitfalls

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Threshold. transfuse for symptoms, for evidence of decompensation, for acute chest; specific Hgb numbers vary by program.
Simple vs exchange. simple often first-line; exchange for severe acute chest or stroke; involves hematology.
Crossmatch. extended antigen matching to reduce alloimmunization; sickle patients often have antibodies.
Acute chest concerns. fever, new infiltrate, dyspnea, hypoxia, chest pain; common in sickle and lethal if missed.
Workup. ABG, CXR, cultures, hemolysis labs, hematology.
Rx now. oxygen, hydration, analgesia, transfusion (often exchange), antibiotics, incentive spirometry.
Antibiotic. yes; empirically cover community-acquired pathogens including atypicals.

4. Plan for conversion

OB warns conversion to C/S may be needed. Pre-op communication with hematology — what do you want? Anesthetic choice if you must go to OR? Pressor and uterotonic plan tailored to SCD — what? Avoid what intraoperatively to reduce crisis? Cell saver in SCD — role? Concerns?

Considerations and pitfalls

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Hematology. current transfusion plan, drugs to avoid, known antibodies, prior crisis triggers.
Anesthetic. neuraxial preferred; GA increases atelectasis and post-op pulmonary complications.
Pressor and uterotonic. norepinephrine for SVR; oxytocin slow; methergine for atony if no severe HTN; carboprost cautiously.
Avoid. hypoxia, acidosis, hypothermia, hypovolemia, hypotension.
Cell saver in SCD. controversial because of hemolysis of sickled cells; some centers use carefully; check protocols.

B. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Modality choice when both neuraxial and GA carry sickle-specific risk; recognizing and treating evolving acute chest intraoperatively; managing the opioid-tolerant patient through delivery; postpartum stroke surveillance and pain control discharge planning.

1. Stat C/S and modality

FHR drops to 70 and stays. OB calls stat C/S. Epidural in. Top-up agent — pick. Defend. Block height target? You add lidocaine with bicarb and epinephrine. BP 88/50, HR 130. SpO2 90% on 4 L NC. DDx? Rx? Continue top-up or convert to GA?

Considerations and pitfalls

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Top-up. lidocaine with bicarb and epinephrine for rapid surgical level via existing catheter.
Block height. T4-T6 for cesarean.
BP fall + hypoxia. sympathectomy plus possible evolving acute chest; address both.
Continue or convert. if level is achievable quickly and oxygenation supports, continue; if hypoxia worsening, GA may be needed.
Rx. pressor (norepi), fluids, oxygen, position, supplement block as appropriate.

2. Acute chest evolves

Block to T4 achieved. As OB starts: SpO2 88% on 100% NRB, RR 30, bilateral crackles, fever to 38.6, new infiltrate suspected. Working diagnosis? Priorities? Antibiotic? Exchange transfusion now? Bronchodilator — yes? Why? Continue C/S — or address acute chest first? OB needs to deliver — how do you coordinate?

Considerations and pitfalls

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Working diagnosis. acute chest syndrome during labor.
Priorities. oxygenation, treat the underlying sickling, deliver to reduce maternal demand, antibiotic coverage.
Antibiotic. broad including atypicals.
Exchange transfusion. indicated in severe acute chest; coordinate with blood bank and hematology now.
Bronchodilator. if reactive airway component, yes; mainstay is oxygenation and exchange.
Continue C/S. deliver promptly; maternal status improves with reduced demand; coordinate with OB on speed.

3. Post-delivery hemodynamics and hypoxia

Baby out. SpO2 86% on 100%. BP 80/45. Atony noted. Uterotonic choice in SCD? Volume — what, how much? Pressor choice? Intubation now — yes/no? Plan if GA needed mid-case? Awareness mitigation? Avoid in this patient — what?

Considerations and pitfalls

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Uterotonic. oxytocin slow; methergine if no severe HTN; misoprostol; carboprost if no severe pulmonary disease, though acute chest argues against.
Volume. balanced; products if Hgb falling further; isotonic crystalloid.
Pressor. norepinephrine.
Intubation. low threshold given evolving hypoxemia.
GA mid-case. induction agent dose-reduced for hypovolemia, full RSI paralytic, secure airway.
Awareness mitigation. midazolam, propofol bridge.
Avoid. hypoxia, hypovolemia, acidosis, hypothermia, vasoconstrictors that compromise microcirculation in extremities.

4. Pain in the opioid-tolerant SCD patient

Postop pain plan? Resume her home regimen — when, what? Multimodal — what scheduled? Regional adjunct — what, why? Ketamine infusion — role? Opioid PCA — settings? Discharge planning at this stage — what do you anticipate? Hematology to follow — what handoff?

Considerations and pitfalls

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Resume home opioid. promptly; avoid undertreating baseline; communicate with pain management.
Multimodal. acetaminophen scheduled, opioid for incremental needs, regional block (TAP or QL), ketamine infusion considered.
Regional. TAP/QL or epidural catheter retained for 24-48 h for cesarean.
Ketamine. useful in opioid-tolerant pain crises; low-dose infusion.
PCA. demand-only initially; basal cautiously after stability.
Discharge. anticipate slower discharge for SCD; hematology, OB, pain follow-up.
Handoff. include trigger management, prior crisis triggers, transfusion plan, pain regimen.

5. Postpartum stroke surveillance and counseling

POD 1: she develops mild left-arm weakness. Concerns? DDx? Workup? Communication with hematology and neurology? Stroke prevention plan going forward — what do you support? Future pregnancy counseling — your role? What do you ensure goes home with her?

Considerations and pitfalls

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Concerns. postpartum stroke in SCD is real and missed when subtle.
DDx. ischemic stroke, hemorrhagic stroke, intracranial event from preeclampsia, peripheral neurologic injury.
Workup. imaging (CT then MRI/MRA), labs, neurology, hematology.
Communication. rapid escalation; consider exchange transfusion in confirmed stroke.
Prevention. chronic transfusion or exchange for some patients; hydroxyurea continued; preconception counseling for future pregnancy.
Future pregnancy. high risk; preconception planning; the candidate supports hematology and OB.
Documentation. anesthesia summary, transfusion history, antibody status, prior crisis triggers, pain regimen.

C. ADDITIONAL TOPICS

Teaching focus. Three unrelated vignettes: ARDS with refractory hypoxemia, anterior mediastinal mass, and LAST after interscalene.

1. ARDS with refractory hypoxemia

A 55 y.o. man with severe pneumonia is intubated in the ICU. FiO2 1.0, PEEP 12, PaO2 58, P/F 90, plateau 32. Interpretation? TV target and why? Plateau goal? Hypoxemic — PEEP, recruitment, prone? Defend. NMB role? When ECMO? BP falls to 80/50 on raising PEEP. DDx and Rx?

Considerations and pitfalls

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Interpretation. severe ARDS; plateau above target.
TV. ~6 mL/kg PBW.
Plateau. ≤30.
Escalation. prone strongest signal.
NMB. severe dyssynchrony or refractory hypoxemia.
ECMO. refractory hypoxemia despite optimal vent; early referral.
Hypotension on PEEP. venous return, pneumothorax, sepsis.

2. Anterior mediastinal mass

A 32 y.o. woman with a large anterior mediastinal mass cannot lie flat for CT. GA needed for sternotomy biopsy. Concerns? Evaluation? Echo shows significant RV and atrial compression. Awake intubation? Pt unable to tolerate fiberoptic. Now what? Mask volatile induction — appropriate? Spontaneous vs controlled? Indications for CPB?

Considerations and pitfalls

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Concerns. airway/vessel/cardiac compression, collapse on induction, inability to lie flat.
Evaluation. upright imaging, flow-volume loops, echo.
Awake intubation. preferred when tolerated.
Mask volatile. preserves spontaneous ventilation; surgeon and CPB ready.
Spontaneous. preserves transpulmonary pressure.
CPB. anticipated collapse in critical compression.

3. LAST after interscalene block

A 60 y.o. woman gets an interscalene block for shoulder surgery. Two minutes later she becomes agitated and seizes. Cause? Priorities? Pulse lost with wide complex. ACLS modifications? Lipid emulsion — principle and dose? Prevention?

Considerations and pitfalls

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Cause. LAST.
Priorities. stop injecting, call for help, airway, oxygenation, control seizure, lipid.
ACLS mod. lipid, reduced epinephrine, avoid certain antiarrhythmics, bypass for refractory.
Lipid. bolus and infusion per protocol.
Prevention. incremental injection with aspiration, ultrasound, test dose, lowest dose.

Non-perioperative

SICU postop perforated diverticulitis (Hartmann's), septic shock

A 64 y.o., 92 kg, 5'10" man is admitted directly to the SICU from the OR following emergent exploratory laparotomy with sigmoid resection and end colostomy (Hartmann's procedure) for perforated diverticulitis with feculent peritonitis.

PMHHypertension, type 2 diabetes (HbA1c 8.4%), CKD stage 3 (baseline Cr 1.4), current smoker (30 pack-years), BMI 29. Home meds: lisinopril, metformin, atorvastatin.

INTRA-OPERATIVE COURSE6 hours. EBL 400 mL. 4 L crystalloid, 1 unit PRBC. Norepinephrine started at 0.1 mcg/kg/min during peritoneal washout. Intra-op lactate trended from 2.8 to 4.2. Total UOP 250 mL. Remains intubated and sedated on transfer.

ARRIVAL TO SICUHR 112; BP 95/55 on norepinephrine 0.1 mcg/kg/min; T 38.7°C; SpO2 96% on FiO2 50% / PEEP 8 / Vt 500 / RR 16. Sedated on propofol 30 mcg/kg/min + fentanyl 50 mcg/hr. Piperacillin-tazobactam given intra-op.

LABSWBC 22; Hgb 9.4; platelets 110; Na 138; K 3.1; Cr 2.0; glucose 248; lactate 4.2; ABG pH 7.28 / pCO2 38 / HCO3 18.

A. INITIAL ASSESSMENT ON ADMISSION

Teaching focus. Organized handoff and primary survey in septic shock; recognizing and treating abdominal compartment syndrome; ARDSnet ventilation and escalation paths; oliguria DDx and the RRT decision under refractory hyperkalemia.

1. Handoff and initial priorities

Concerns? First priorities receiving him? Top three in the first hour — what, and why? Primary survey — what do you check at the bedside in the first 10 minutes? Lines and access — what do you want? Antibiotic spectrum — confirm with whom? Mid-handoff, BP drifts to 85/48. How does that change what you do first? The surgeon wants him awake by morning to follow the abdominal exam. Your response — defend.

Considerations and pitfalls

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Organize. structured handoff (course, hemodynamics, vent, labs, drains, abx, anticoag), then primary survey (ETT, breath sounds, perfusion, abdomen, drains, UOP, access).
Top 3. hemodynamic stabilization (septic shock + lactate 4.2), lung-protective ventilation and oxygenation, verify source control and ongoing resuscitation.
First hour. recheck lactate, replace K, blood cultures x 2, confirm antibiotic spectrum, central access if not in place, goal MAP ≥65.
BP drift 85/48. pause handoff, examine — POCUS, ABG/lactate, titrate norepi to MAP ≥65, brief volume assessment before reflex bolus.
Surgeon wants awake. agree in principle (neuro exam matters), defer until perfusion, oxygenation, pain controlled; wean sedation when stable, not on a clock.

2. Hypotension overnight

Hour 4: BP 78/42, HR 124, norepi 0.15, UOP 20 mL/hr. DDx? Sort it bedside — how? Action first — and why? Pressor escalation — to what, and when? No response to a 1 L bolus, then? Steroid stress dose — yes/no? Why? At your next exam abdomen is tense, bladder pressure 28 mmHg. Diagnosis? Mgmt — medical vs surgical? Defend the threshold for decompression.

Considerations and pitfalls

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DDx. distributive (uncontrolled sepsis, adrenal insufficiency), hypovolemic (occult bleed, under-resuscitated, insensible loss), cardiogenic (post-op MI, sepsis cardiomyopathy, arrhythmia), obstructive (PE, tension PTX, abdominal compartment), iatrogenic (sedation).
Sort. exam (JVP, abdomen, drains, perfusion), trend, ECG, POCUS (IVC, cardiac, lung, FAST), sedation review, ABG/Hgb/lactate.
Action. bolus if volume-responsive, norepi to MAP ≥65, lighten propofol, Hgb to rule out bleed, bladder pressure if rigid, ECG, antibiotic timing.
No response. vasopressin 0.03 U/min, hydrocortisone 200 mg/day if refractory, bedside echo, surgical re-eval, second large-bore access.
ACS. bladder pressure 28 with new organ dysfunction = ACS. Medical first: deepen sedation, NMB trial, NG decompression, paracentesis if ascites, avoid more fluid. Surgical decompression for sustained >20 with worsening organ failure despite medical, or any >25.
Defend. ACS is clinical — numbers guide, exam wins. Don't anchor on a single bladder pressure; trend it. Don't wait for arrest.

3. Worsening oxygenation at hour 12

Overnight FiO2 climbs to 70%; morning ABG PaO2 105, pH 7.30, pCO2 42. P/F 150. DDx? Workup? Vent changes from current settings — defend the plan. Target Vt by what weight, and why? Plateau and driving pressure goals? CXR shows new bilateral lower-zone opacities. Diagnosis? Mgmt? Six hours later, paralyzed and proned trial considered, P/F is 90. Now what? When do you escalate, and to where?

Considerations and pitfalls

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DDx. ARDS, atelectasis, mucus plug / ETT malposition, hydrostatic edema from resus, aspiration, early VAP (unlikely <48 hr), PE, TRALI (1 U PRBC within 6 hr), pneumothorax.
Workup. CXR, lung POCUS, suction/ETT inspection, I/O trend, ABG trend, troponin/ECG, transfusion timing.
Vent. P/F 150 = moderate ARDS. ARDSnet: Vt 4-6 mL/kg PBW, plateau ≤30, driving pressure ≤15, PEEP per table, permissive hypercapnia (pH ≥7.20), conservative fluids.
Bilateral opacities + sepsis. non-cardiogenic = ARDS; rule out cardiogenic (echo, BNP, clinical).
Refractory P/F 90. prone (16-hr cycles), adequate paralysis + sedation, recruitment only if responder, inhaled pulmonary vasodilator (iNO, epoprostenol) as bridge — improves oxygenation, no mortality benefit.
ECMO criteria. P/F <80 >6 hr despite optimized vent + prone, plateau >30 at low Vt, pH <7.20 from hypercapnia, single-organ dominant, reversible, transferrable. Refer early — outcomes worsen with delay.

4. Oliguria and rising creatinine

Hour 18: UOP 12 mL/hr × 3 hr, Cr 2.8 (baseline 1.4). DDx? Workup at bedside — what? Reversible drivers — which do you check first? Plan? 8 AM K returns 6.1 with peaked T waves. Now what? Sequence the Rx — and what do you reassess in 1 hr? Despite calcium, insulin/D50, bicarb, the 9 AM K is 6.4. Anuric × 4 hr. Cr 3.5. Initiate RRT now or wait? Defend — what tips you over?

Considerations and pitfalls

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DDx. pseudo-oliguria first (Foley); pre-renal (volume, MAP, intra-abdominal pressure); intrinsic (ATN from septic + hypotensive insult, AIN from antibiotics, pigment); post-renal (ureteral injury from sigmoid resection).
Workup. flush/replace Foley, POCUS IVC, bladder pressure, UA + urine lytes, nephrotoxin review (vanc, contrast, NSAIDs), renal US, surgical communication.
Plan. MAP ≥65, cautious bolus only if responsive, renally dose-adjust meds, hold nephrotoxins, nephrology consult, ACS decompression if confirmed.
K 6.1 + ECG. stabilize (calcium gluconate 1-2 g), shift (insulin/D50, albuterol, bicarb), eliminate (loop, K-binder, RRT if anuric/refractory). Recheck in 1 hr.
RRT triggers (AEIOU). Acidosis refractory, Electrolytes refractory, Intoxication, Overload, Uremia. He hits two — refractory hyperK + anuric AKI with worsening acidosis.
Defend. don't chase another round when you've already failed once and have an evolving second indication. Nephrology, access, start CRRT (continuous, given pressor requirement).

B. ONGOING MANAGEMENT AND COMPLICATIONS

Teaching focus. Source control as the dominant lever in persistent septic shock; ICU agitation and the alcohol-withdrawal carve-out; extubation readiness when cuff leak is the limiting factor; the delirium workup as a syndrome with a driver; goals-of-care and family communication when the course turns long.

1. New fever on POD 2

POD 2: T 39.4, WBC 24, lactate 2.8, still on norepi 0.08 + vaso 0.03. DDx? How does post-op day shape the differential? Workup at bedside — what? Imaging — when, and what? Change antibiotics — yes/no? Pick the spectrum and defend? CT shows a 4 cm rim-enhancing collection near the colostomy stump. Surgeon wants to wait until morning rounds to decide. Your response? Escalation path if surgeon refuses?

Considerations and pitfalls

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DDx (5 Ws). wind (atelectasis, HAP, aspiration), water (UTI), walking (DVT/PE), wound (surgical site, undrained collection, stump leak, line), wonder drugs (drug fever, transfusion); plus translocation, primary BSI.
Day shapes DDx. POD #1-2 atelectasis common, but new spike + persistent pressor + leukocytosis = ongoing source until proven otherwise.
Workup. blood cultures x 2, UA/cx, tracheal aspirate, CXR, line/drain inspection, CT abd/pelvis with contrast, surgical bedside re-eval.
Antibiotics. confirm gut coverage (GNR + anaerobe); pip-tazo or carbapenem for severity; MRSA coverage if hospital exposure or prior abx; echinocandin if persistent shock with risk factors; de-escalate to cultures.
Undrained collection on pressors. not a wait-until-morning problem. Push for IR drainage now (percutaneous if accessible) or OR if not. Frame as patient safety — persistent septic shock + identified undrained source = emergency. Escalate attending-to-attending if needed. Document.
Defend. source control is the dominant lever — antibiotics without it fail. 'What did we miss?' not 'what should we add?'

2. Agitation after lightening sedation

Hour 36, SAT: HR 130, BP 165/95, RASS +3, fighting vent. DDx? How sort it at bedside? Action — defend the order? Pain first or sedation first? Why? Vent asynchrony — what changes? Family arrives, says he drinks ~12 beers/day at home. CIWA at hour 48 is 18. Now what? Benzodiazepine choice and route? Why benzos here when you'd avoid them for delirium?

Considerations and pitfalls

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DDx. pain, delirium, hypoxia/hypercarbia, ETT discomfort, full bladder, withdrawal (ETOH, nicotine, opioid, benzo), hypoglycemia, hypovolemia, drug effect, evolving sepsis, ischemia.
Sort. ABG, vent check, pain score, glucose, tube/Foley, substance history, ECG, abdomen, CAM-ICU after the basics.
Order. (1) treat pain first — fentanyl bolus + adequate background, scheduled IV APAP, no NSAIDs in AKI; (2) fix vent asynchrony; (3) only then deepen/switch sedation; consider dex over propofol; avoid benzos for delirium.
Defend the order. agitation in a vented post-op patient is pain or hypoxia until proven otherwise.
Withdrawal Rx. 12 beers/day + CIWA 18 = alcohol withdrawal. Benzos now first-line — symptom-triggered diazepam or lorazepam by CIWA; phenobarbital if refractory; thiamine before glucose; Mg, folate. Continue dex; avoid haloperidol alone (lowers seizure threshold).
Benzos here vs delirium. in withdrawal, GABA agonism treats the mechanism (chronic ETOH → upregulated NMDA, downregulated GABA → CNS hyperexcitability on stop). In delirium, benzos worsen it. Same drug, opposite role — match pathophysiology.

3. Extubation readiness on POD 3

POD 3: off pressors × 12 hr, FiO2 30% / PEEP 5, afebrile, awake on dex 0.4, following commands. Extubation criteria — what must be true? SBT settings and pass criteria? Pass — but cuff leak is minimal. Now what? Steroids — yes/no? Dose and timing? Five min after extubation, stridor. DDx? Action? He's reintubated. POD 5, same picture. Plan now? When do you call ENT for trach?

Considerations and pitfalls

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Checklist. indication resolved; P/F >200 on FiO2 ≤40%, PEEP ≤5-8; SBT pass (RSBI <105 on PS 5/PEEP 5 × 30 min); hemodynamics; mental status + secretion management; cough; cuff leak; volume status; post-extubation support plan.
Minimal cuff leak. laryngeal edema concern. Steroids (methylprednisolone 20 mg q4h × 4 doses) then extubate, or extubate now with full airway team (videoscope, fiberoptic, smaller ETT, surgical airway plan, attending bedside).
Stridor DDx. laryngeal edema, laryngospasm, vocal cord paresis, secretions/blood, aspiration, anaphylaxis, foreign body.
Action. 100% O2 + jaw thrust + suction, racemic epi nebulizer, IV dex 10 mg, heliox, reintubate early — anticipate difficulty, backup, video first pass, smaller ETT, surgical airway plan stated.
Second attempt POD 5. failed once for the same reason. Re-attempt only with demonstrated resolution — quantitative cuff leak (>110 mL or >12% Vt), pre-extubation steroid course, direct laryngoscopy if equivocal, fully prepped team, attending present.
Trach timing. anticipated prolonged vent (>14 days) or failed extubation × 2 in an otherwise improving patient. Earlier trach (7-10 days) reduces sedation, vent days, ICU LOS — no mortality benefit but quality benefit. After failed extubation × 2 for same cause, have the conversation, not 'wait and see.'

4. Acute confusion on POD 4

POD 4, extubated, step-down. Acute confusion overnight, pulling at Foley and central line, climbing out of bed, talking to people not in the room. CAM-ICU positive. DDx — drivers, not the label? Workup — what at bedside? Non-pharm first — what? Medicate — yes/no? Restrain — yes/no? Defend the order? Despite haloperidol he punches a nurse and tries to climb out. Specific drug, dose, route, monitoring? When do you call for help, what kind?

Considerations and pitfalls

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DDx (drivers, not the label). pain, infection (intra-abdominal, UTI, pneumonia, line, CNS), hypoxia/hypercarbia, electrolyte (Na, glucose, Mg, Ca, phos), medication (opioids, benzos, anticholinergics, steroids), withdrawal (ETOH, nicotine, opioid, benzo), sleep deprivation, retention, stroke, sepsis-associated encephalopathy, non-convulsive status.
Workup. vitals, neuro exam (lateralizing → image), glucose, electrolytes incl Mg/phos, ABG, infection workup, med rec for deliriogenic agents, family for baseline + substances, bladder scan, pain; EEG if not improving.
Non-pharm first. reorient, glasses/hearing aids, day/night cues, family, mobilize, sleep hygiene, treat pain, treat retention, remove unnecessary tubes.
Pharm. only if danger to self/staff or non-pharm failing, while addressing driver. Haloperidol 0.5-1 mg IV or quetiapine 12.5-25 mg PO; QTc monitoring; dex if monitored; avoid benzos unless withdrawal.
Restraints. last resort, time-limited, documented; soft restraints to protect lines while workup proceeds; remove what isn't needed.
Escalation. haloperidol 5 mg IV (or olanzapine 5-10 mg IM if no IV), QTc + continuous monitoring; can repeat q15-30 min × 2 with QTc/BP checks; if still unsafe, dex drip in monitored setting; goal calm, not unconscious. Call attending, security if active threat, consider transfer back to ICU for monitored sedation.
Defend. delirium is a syndrome with a cause. Sedating through it without finding the cause prolongs it and risks missing a treatable problem.

5. Goals of care and family communication

POD 7: still in step-down on dex and a nasal cannula, on every-other-day dialysis, intermittent delirium, slow nutritional progress, two more fevers and one wound infection drained. Family asks if he will get out of this. What say? Adult daughter asks why the team didn't intubate him sooner. What say? Surgical and medical teams have slightly different framings of where things are headed. How coordinate the message? When do you formally raise goals of care? Who leads that conversation? Bearing on his ongoing care — does the framing change anything you do tomorrow?

Considerations and pitfalls

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Will he get out of this. honest, plain account; describe what is improving and what is not; avoid false reassurance and avoid premature certainty in either direction.
Why not earlier intubation. explain the timeline plainly; redirect from blame to decision points; do not become defensive.
Different framings. convene a joint family meeting with both teams; align on the medical facts before the conversation; one voice in front of the family.
When to raise GOC. when prognosis is uncertain and decisions are accumulating (dialysis dependence, prolonged vent risk, repeated infections); the conversation supports decision-making rather than waiting for crisis.
Who leads. the ICU team most often, with surgery present; pre-meet to agree on the message; family decides, the team frames options.

C. ADDITIONAL TOPICS

Teaching focus. Three unrelated vignettes: LAST after interscalene, PDPH after a wet tap, operating-room fire during MAC.

1. LAST after interscalene block

A 60 y.o. woman gets an interscalene block for shoulder surgery. Two minutes later she becomes agitated and seizes. Cause? Priorities? She loses her pulse with a wide-complex rhythm. ACLS modifications? Lipid emulsion — principle and dose? Prevention?

Considerations and pitfalls

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Cause. LAST from intravascular injection or rapid systemic absorption.
Priorities. stop injecting, call for help, airway and oxygenation, control the seizure, lipid emulsion.
ACLS mod. lipid, reduced epinephrine dose, avoid certain antiarrhythmics, prolonged resuscitation, consider bypass for refractory.
Lipid. bolus and infusion per published protocol; a specific therapy.
Prevention. incremental injection with aspiration, ultrasound, test dose, lowest effective dose.

2. Postdural puncture headache

A 28 y.o. woman, 24 hr after a labor epidural complicated by a recognized wet tap, has a positional fronto-occipital headache relieved by lying flat. Dx and features? Exclude what? Conservative? She can't care for her newborn — Rx? Mechanism? Risks?

Considerations and pitfalls

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Diagnosis. PDPH after known dural puncture.
Exclude. preeclampsia, cortical vein thrombosis, meningitis, subdural hematoma.
Conservative. time, analgesia, hydration, caffeine; limited evidence.
Definitive. epidural blood patch; tamponade and sealing of the leak.
Risks. repeat dural puncture, back pain, infection, rare neurologic complications.

3. Operating-room fire

During MAC with nasal-cannula oxygen for an excision on the face, the surgeon uses electrocautery and a flash fire ignites at the drapes. Immediate actions? Sequence of priorities? Fire triad here? Once out, assess the patient — how? Prevention?

Considerations and pitfalls

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Immediate. stop the procedure, stop O2 and remove the airway source, remove burning drapes, extinguish.
Sequence. protect the patient and remove fuel and oxidizer first, then extinguish, then care for the patient.
Triad. oxidizer (open O2 under drapes), ignition (cautery), fuel (drapes, prep, hair).
Post-fire. evaluate airway and burns; plan airway if inhalation injury.
Prevention. minimize open O2 near cautery, secure airway or blend air, let prep dry, tent drapes.

Session 1 — long stem

Cervical mediastinoscopy and biopsy of a large anterior mediastinal mass

A 34 y.o., 60 kg, 5'5" woman is scheduled for cervical mediastinoscopy and biopsy of a large anterior mediastinal mass for tissue diagnosis.

HPISix weeks of cough and progressive dyspnea, now breathless at rest and unable to lie flat; she sleeps upright in a recliner. Two episodes of near-syncope when supine. Facial fullness and a sense of head pressure when she bends forward. No treatment to date; oncology wants tissue before starting therapy.

PMHPreviously healthy. Over the last two weeks she has noticed morning facial puffiness and prominent veins across the upper chest.

MEDSNone. No corticosteroids given to date.

PHYS EXAMHR 104; BP 118/72; RR 22 sitting; SpO2 94% on room air; T 37.1°C. Facial plethora and periorbital edema, distended neck and upper-chest veins, soft stridor audible when she leans back.

IMAGINGCT chest: bulky anterior mediastinal mass, roughly 10 cm, narrowing the tracheal cross-section by about 60% down to the carina, compressing and displacing the SVC, and abutting the main pulmonary artery.

ECHOSmall-to-moderate pericardial effusion with intermittent right atrial and RV inflow compression; preserved LV function.

LABSHgb 12.8 g/dL; platelets 240 K/uL; INR 1.1; K+ 4.0 mEq/L; creatinine 0.8 mg/dL; uric acid mildly elevated; LDH elevated.

OR ARRIVALAwake, sitting at 45°. Two large-bore lower-extremity IVs and a femoral venous introducer sheath placed under local; radial arterial line. Surgeon and perfusion are aware; a rigid bronchoscope is open in the room.

A. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Choosing an anesthetic that preserves the airway and venous return in front of a mass that compresses both; rescuing the predicted induction collapse; reading a damped right-sided arterial trace during mediastinoscopy; managing major mediastinal hemorrhage to a clear end point.

1. Anesthetic plan and ventilation strategy

GA, or can this tissue be obtained another way? Why? Local with sedation feasible? Spontaneous vs controlled ventilation? Why? If spontaneous, agents and technique? Position for induction? Access and monitors sited where, and why there? You begin induction. SpO2 falls to 86% and ventilation becomes difficult. Interpretation? First move?

Considerations and pitfalls

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GA vs alternative tissue. many such biopsies (anterior approach, core, or EBUS) can be done under local with sedation, avoiding the collapse risk of GA; reaching for GA without weighing a less-invasive route under local is worth probing.
Spontaneous vs controlled. maintaining spontaneous ventilation preserves the transpleural gradient and airway patency; positive pressure and paralysis can precipitate dynamic collapse. Committing to early paralysis is a red flag.
Agents/technique. inhalational or carefully titrated IV that keeps the patient breathing; avoid abolishing respiratory drive and muscle tone before the airway is secured distal to the lesion.
Position. induce semi-sitting; map the position that relieves symptoms (often lateral or prone) ahead of time as the rescue position.
Access/monitors. lower-extremity large-bore IV and a femoral sheath because SVC compression makes upper-body access unreliable and pre-stages rescue cannulation.
Desat as spontaneous effort fades. dynamic airway and vascular compression — the predicted event; recognize it as mechanical, not simply light anesthesia.

2. Cardiopulmonary collapse on induction

SpO2 78%, BP 60/40, and you cannot ventilate despite a correctly placed ETT. DDx? Mechanisms here? First maneuver? Reposition — to what? Rigid bronchoscopy — role? Re-establish spontaneous ventilation — how? Still no arterial output — femoral cannulation and bypass? To what end point are you resuscitating, and when do you wake her?

Considerations and pitfalls

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DDx. airway compression distal to the ETT tip, SVC or PA or cardiac compression obstructing venous return and output, tension physiology, tamponade from the effusion.
First maneuver. turn lateral or prone (or sit up) to relieve mechanical compression — the immediate move that addresses the mechanism; chasing pressors alone misses it.
Rigid bronchoscopy. the surgeon passes a rigid scope past the obstruction to stent the airway distal to the lesion — a planned rescue, which is why it is in the room.
Re-establish spontaneous ventilation. lighten and let her breathe; restoring negative-pressure breathing can reopen the airway and venous return.
Femoral CPB. the reason the sheath is in; pre-staged peripheral cannulation for exactly this collapse.
End point / waking. name resuscitation targets; recognize that aborting and waking the patient is a legitimate, sometimes correct, choice.

3. Mediastinoscopy vascular complication

The scope is in; the right radial trace damps and the right-hand pulse oximeter drops. Significance? Cause? What do you tell the surgeon? Brisk bleeding then fills the field and BP is 70/40. Priorities? Transfuse — trigger? Is your access adequate for this injury? To what hemodynamic end point? Surgeon needs to pack and may open the chest — your plan for the next several minutes?

Considerations and pitfalls

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Damped right-sided trace. the scope is compressing the innominate artery; a left-sided or alternate-site monitor reads true pressure. Treating this as true hypotension and escalating pressors is the classic trap.
Tell the surgeon. ask them to release compression; the right-sided monitor is the early-warning system for innominate and cerebral flow.
Bleeding / priorities. major vascular injury (innominate, SVC, azygos); call for help and blood, confirm large-bore access, prepare for sternotomy.
Access for this injury. lower-extremity large-bore matters — fluid given above an SVC injury pools above it; resuscitate from below.
End point. name targets and communicate; anticipate sternotomy or bypass and resource accordingly.

4. Hemodynamics after control

Bleeding controlled. BP 88/52 on low-dose norepinephrine, CVP elevated, repeat echo shows the effusion slightly larger. Of concern? DDx for the hypotension now? How do you distinguish among them? Drain the pericardium — indication? Volume, pressor, or drainage — priorities? Target filling pressure and MAP? Criteria for transporting her intubated to the ICU?

Considerations and pitfalls

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Concern / DDx. persistent hypotension after surgical control: tamponade physiology from an enlarging effusion, RV strain from PA compression, vasoplegia, ongoing occult bleeding.
Distinguish. echo for tamponade and RV function, response to a fluid challenge, the surgical field; do not anchor on one cause.
Pericardial drainage. indicated if tamponade physiology is driving the picture; coordinate with surgery given the open field.
Priorities / targets. support preload and perfusion while identifying the mechanism; name a MAP and filling target rather than treating numbers blindly.
ICU intubated. marginal airway and hemodynamics argue for controlled transport and continued ventilation.

B. POST-OPERATIVE CARE

Teaching focus. Extubation judgment in an airway that already obstructed once; recognizing a post-mediastinoscopy tension pneumothorax; reading new hoarseness and a weak cough; the timing of treatment and tumor lysis; and an honest disclosure when the course goes badly.

1. Extubation decision

Biopsy done, hemodynamically stable. Extubate now? Why/why not? What must be true first? A cuff leak — what does it tell you and what does it not? What changes your threshold here? You extubate and within minutes she has stridor and retractions. Rx? Reintubate — what difficulty do you anticipate? Plan if you cannot?

Considerations and pitfalls

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Extubate or not. the airway that obstructed on induction can obstruct on emergence; keeping her intubated, or extubating only over an exchange catheter with the surgeon present, is defensible. Reflexive extubation is the flag.
Before extubation. fully reversed, awake, sitting, hemodynamically stable, equipment and surgeon at the bedside.
Cuff leak. a leak suggests some patency but does not guarantee the dynamic compression has resolved; absence is more worrying than presence is reassuring.
Post-extubation stridor. residual compression plus edema; reposition, reintubate early with a smaller tube, rigid bronchoscopy and the surgeon as the staged rescue.

2. PACU respiratory distress

One hour later: rising oxygen requirement, RR 30, diminished breath sounds on the right, BP falling. DDx? Most likely here? Confirm — how, and how fast? Needle or tube, and where? Given the operation, what specific injuries fit? SpO2 82% and dropping — act before imaging? To what end point?

Considerations and pitfalls

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DDx. pneumothorax from pleural breach during mediastinoscopy, hemothorax, recurrent airway or cardiac compression, atelectasis.
Most likely / confirm. tension pneumothorax; clinical picture plus ultrasound; do not wait for a portable film in an unstable patient.
Decompress. needle decompression then chest tube on the affected side.
Operation-specific injuries. pleural entry, tracheobronchial injury, vascular injury; keep the procedure in mind when reading the deterioration.

3. New hoarseness and weak cough

Awake but hoarse with a weak, ineffective cough and soft stridor on exertion. DDx? Most concerning? Why? How do you evaluate? She is comfortable at rest but desaturates with effort and after sips of water. Disposition and monitoring? What would make you secure the airway now?

Considerations and pitfalls

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DDx. recurrent laryngeal nerve injury (the left nerve is at risk during mediastinoscopy), laryngeal edema, residual compression, aspiration.
Bilateral involvement. bilateral cord dysfunction can obstruct the airway; unilateral injury is usually tolerated but brings cough weakness and aspiration risk.
Evaluate / disposition. direct or fiberoptic laryngoscopy and ENT; watch for fatigue and aspiration; monitored bed with a low threshold to secure the airway.

4. Treatment timing and tumor lysis

Tissue is obtained; oncology wants to start high-dose steroids and chemotherapy tonight. Your input on timing and monitoring? Why did they wait for tissue first? As the mass shrinks quickly, what happens to her airway and your monitoring? Tumor lysis — what do you watch for and how do you get ahead of it? ICU or floor? Which lines and access do you keep? What end points do you hand off?

Considerations and pitfalls

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Timing / tissue first. steroids before biopsy can obscure a lymphoma diagnosis, which is why tissue came first; with tissue obtained, treatment that shrinks the mass and relieves compression is generally favorable.
Airway as mass shrinks. compression usually improves, but the airway still warrants monitoring during the transition.
Tumor lysis. hyperkalemia, hyperuricemia (note the elevated uric acid and LDH), hyperphosphatemia, AKI; hydration, monitoring, allopurinol or rasburicase.
Disposition. ICU given the airway and metabolic risk; keep reliable access and arterial monitoring; hand off clear targets.

5. Disclosure after a hard course

She required emergency reintubation and is now intubated in the ICU; the family arrives frightened. What will you tell them? How do you explain why this happened? What do you say about what comes next? Coordinate the message with surgery and oncology — how? She is awake enough to write and asks whether she nearly died. Your answer?

Considerations and pitfalls

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Telling the family. a plain, honest account of how the mass compressed her airway and circulation, why support is needed, and that it is often temporary, with room for questions.
Coordinate. a single, specific shared message so the family does not get conflicting accounts from the three teams.
Her question. answer honestly without alarming — acknowledge it was serious, that she was supported through it, and focus on the plan ahead.

C. ADDITIONAL TOPICS

Teaching focus. Malignant hyperthermia; a high spinal during cesarean delivery; venous air embolism in the sitting position. Unrelated by design.

1. Malignant hyperthermia

A 22 y.o. man under sevoflurane for ankle ORIF develops end-tidal CO2 rising to 65, tachycardia, and masseter rigidity 40 minutes in. DDx? Most likely? First actions? What do you stop and what do you start? Dantrolene — dose and how given? Monitoring and labs now? Dark urine and K+ 6.2 appear — Rx? Disposition?

Considerations and pitfalls

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DDx. malignant hyperthermia, thyroid storm, sepsis, inadequate anesthesia or ventilation, pheochromocytoma.
First actions. stop triggering agents, call for help and the MH cart, hyperventilate with 100% oxygen, terminate or expedite the surgery.
Dantrolene. 2.5 mg/kg IV bolus, repeated to effect; know it is the specific therapy, not an afterthought.
Labs/monitoring. ABG, K+, CK, core temperature, urine myoglobin, coagulation; active cooling.
Hyperkalemia / rhabdo. treat hyperkalemia, maintain urine output with fluids; ICU admission and a continued dantrolene plan.

2. High spinal at cesarean delivery

Minutes after a spinal for cesarean, a parturient reports trouble breathing and weak arms, then becomes hypotensive and bradycardic and hard to rouse. Interpretation? Cause? Immediate priorities? Airway — how and when? Pressor for this hypotension with bradycardia — which? The fetus — how does it shape your sequence? After stabilization, when do you proceed with delivery? What will you tell her afterward?

Considerations and pitfalls

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Interpretation / cause. high or total spinal from cephalad spread of local anesthetic.
Priorities / airway. support ventilation and intubate if apneic or obtunded; this comes before chasing the blood pressure alone.
Pressor. ephedrine or epinephrine for combined hypotension and bradycardia, atropine for bradycardia, left uterine displacement and fluids.
Fetus. maternal resuscitation first; expedite delivery if the mother arrests or cannot be stabilized.
Counsel. an honest explanation once she is stable.

3. Venous air embolism, sitting position

During a posterior-fossa craniotomy in the sitting position, the end-tidal CO2 abruptly falls and the patient becomes hypotensive with a new mill-wheel murmur. DDx? Most likely? How confirm? Immediate actions with the surgeon? Aspirate the central line — why was it placed? Position change — to what? If it progresses to arrest, how does management differ? How do you prevent recurrence?

Considerations and pitfalls

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DDx / most likely. venous air embolism given the position and the abrupt end-tidal CO2 fall.
Confirm. precordial Doppler, the capnogram, TEE if available.
Immediate actions. tell the surgeon to flood the field and wax bone edges, jugular compression, 100% oxygen and stop nitrous, aspirate the right-atrial catheter, pressors, lower the head.
Position. left lateral decubitus, head down (Durant).
Prevent. avoid nitrous oxide, maintain venous pressure, monitor with precordial Doppler.

Session 1 — long stem

Right upper lobectomy with one-lung ventilation in severe COPD

A 68 y.o., 70 kg, 5'9" man is scheduled for a right upper lobectomy for a 4 cm non-small-cell lung cancer.

HPIA 50 pack-year smoker who quit two weeks ago. Progressive dyspnea on exertion, now limited to one flight of stairs, with chronic productive cough. An upper respiratory infection three weeks ago has resolved.

PMHSevere COPD. Myocardial infarction four years ago, treated with a drug-eluting stent to the right coronary artery; no angina since. Hypertension, type 2 diabetes, GERD. Echocardiogram shows moderate right ventricular dilation and dysfunction with an estimated PA systolic pressure of 50 mmHg.

MEDSTiotropium, inhaled fluticasone, albuterol prn, aspirin 81 mg, metoprolol, lisinopril, atorvastatin, metformin (held).

PHYS EXAMHR 88; BP 150/85; RR 18; SpO2 92% on room air; T 36.8°C. Barrel chest, prolonged expiratory phase, diminished breath sounds bilaterally with scattered expiratory wheezes.

PFTsFEV1 1.4 L (45% predicted); FEV1/FVC 0.55; DLCO 48% predicted. Estimated postoperative predicted FEV1 ~32%.

ABG (room air)pH 7.36; PaCO2 48 mmHg; PaO2 64 mmHg; HCO3 27 mEq/L.

ECGSinus rhythm with occasional PVCs, right ventricular strain pattern, old inferior Q waves.

IMAGINGCT chest: 4 cm right upper lobe mass without carinal or proximal airway involvement; diffuse hyperinflation; thin-walled bullae in the left upper lobe.

LABSHgb 16.5 g/dL; platelets 210 K/uL; INR 1.0; K+ 3.4 mEq/L; creatinine 1.3 mg/dL; glucose 180 mg/dL.

OR ARRIVALThoracic epidural placed at T6-7 preop; test dose negative, not yet dosed. Left-sided 39 Fr double-lumen tube planned. Radial arterial line and two 18 g peripheral IVs.

A. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Lung isolation choice and confirmation in severe COPD; a ventilator strategy that respects air-trapping; protecting a pressure-loaded RV on one-lung ventilation; recognizing a dependent-lung tension pneumothorax.

1. Lung isolation and induction

DLT or bronchial blocker? Why? Which side? Why? Induction agents and doses? Goals for this RV and this coronary history? Confirm isolation — how? You turn to OLV; peak pressure climbs and BP falls to 88/50. DDx? Rx? Auto-PEEP? How confirm? Disconnect — effect?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

DLT vs blocker. both isolate; a left DLT gives reliable separation and lets you suction and CPAP the operative lung; blocker if the airway is difficult. Want a committed, defended choice, not a list.
Which side. left-sided for a right resection keeps the bronchial cuff clear of the operative bronchus and RUL takeoff; candidate should reason to the side.
Induction goals. avoid tachycardia and hypotension that threaten a fixed coronary lesion and a pressure-loaded RV; support pressure early. Ignoring the RV is a flag.
Confirm isolation. fiberoptic confirmation is standard; auscultation alone is worth challenging.
Pressure up, BP down on OLV. auto-PEEP/breath-stacking, malposition, pneumothorax, RV strain. Reaching for fluid or pressor before a disconnect to let her exhale is worth probing.

2. Hypoxemia on one-lung ventilation

20 min into OLV, SpO2 84% on FiO2 1.0. DDx? Most likely? First move? FOB confirms the tube is correctly placed; SpO2 81%. CPAP to the nondependent lung? PEEP to the dependent lung? Recruitment? Which? Why? Surgeon says CPAP obscures the field. Now what?

Considerations and pitfalls

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DDx. malposition/migration, secretions/plug, shunt through the nondependent lung, dependent atelectasis, bronchospasm, low CO.
Most likely. malposition on a fresh OLV desaturation; secretions and shunt also common here.
First move. FiO2 is already 1.0, so reconfirm position by FOB. Escalating to CPAP/PEEP before confirming isolation is worth probing.
CPAP vs PEEP vs recruit. CPAP to the nondependent lung targets shunt; recruit and modest PEEP to the dependent lung target atelectasis; commit and defend. Red flag: PEEP in severe COPD without noting auto-PEEP.
Surgeon conflict. intermittent two-lung ventilation or brief reinflation; oxygenation over field; communicate.

3. RV strain on OLV

One hour into OLV, chest open: BP 80/45, HR 120, CVP rising, SpO2 90%. DDx? Most concerning here? Rx? Norepinephrine? Vasopressin? Phenylephrine? Which? Why? Inhaled pulmonary vasodilator — role? Surgeon is compressing the mediastinum to expose the hilum. Bearing?

Considerations and pitfalls

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DDx. RV failure from rising PVR, surgical compression of heart/great vessels, dynamic hyperinflation, ischemia or arrhythmia, hemorrhage.
Most concerning. acute decompensation of a chronically pressure-loaded RV; candidate should tie the echo to the picture.
Pressor. norepinephrine and vasopressin commonly favored to preserve RV coronary perfusion; leaning on phenylephrine without noting its potential to raise PVR is worth challenging.
Inhaled pulmonary vasodilator. iNO or epoprostenol selectively lower PVR; reasonable to raise; not a substitute for fixing ventilation and oxygenation.
Surgical compression. don't miss a mechanical cause while chasing drugs; ask for release of retraction.

4. Acute dependent-lung deterioration

Sudden: dependent-lung peak pressure spikes, SpO2 80%, BP 70/40, hard to hand-ventilate. DDx? Most likely? Why here? Immediate Rx? Decompress — where? The chest is open on the right; how does that change recognition? Confirm — how, without losing time?

Considerations and pitfalls

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DDx. tension pneumothorax of the dependent ventilated lung from bulla rupture/barotrauma, DLT migration/obstruction, mucus plug, severe bronchospasm, auto-PEEP.
Most likely / why here. dependent-lung tension pneumothorax from the known left-upper-lobe bullae under positive pressure; candidate should connect to the stem CT.
Immediate Rx. hand-ventilate to assess compliance, drop airway pressure and disconnect to exclude auto-PEEP, call the surgeon, decompress the dependent hemithorax, resuscitate.
Open chest. the operative side can't tension; the danger is the down lung, so recognition rests on airway pressure, hemodynamics, and ultrasound, not the classic exam.

B. POST-OPERATIVE CARE

Teaching focus. Extubation judgment with marginal reserve; postoperative hypoxemia after resection; an air leak and the limits of positive pressure; post-thoracotomy atrial fibrillation; analgesia-dependent pulmonary toilet and honest disclosure.

1. Extubation decision

Case done, stable on low-dose norepinephrine. Extubate in the OR? Why/why not? What must be true first? You extubate; over 30 min RR 30, PaCO2 climbing. Options? NIV after lung resection — concern? Reintubate — threshold?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Extubate or not. early extubation avoids positive pressure on a fresh stump — a reasonable goal; marginal reserve and pressor need argue caution. Either is defensible if committed.
Before extubation. adequate gas exchange, reversal confirmed, normothermia, stable hemodynamics, analgesia for deep breathing.
Tiring, CO2 up. optimize analgesia and toilet, then weigh NIV vs reintubation; delaying a clearly failing patient is a flag.
NIV concern. positive pressure stresses the stump and air leak; not absolute, but uncritical high pressures deserve a probe.

2. Postoperative hypoxemia

6 hr postop in the ICU: P/F 160 on 50%, RR 28, diminished left base. DDx? Studies? Most likely here? Rx priorities? Bronchoscopy — when? Epidural working — bearing on this?

Considerations and pitfalls

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DDx. atelectasis, secretions/plugging, pneumothorax or enlarging space, edema, residual block, aspiration, lobar torsion/herniation.
Studies. CXR, ABG, bronchoscopy if plugging suspected.
Most likely here. secretions and atelectasis in a splinting COPD lung.
Rx priorities. analgesia-enabled toilet, cautious recruitment, bronchoscopy for plugging, treat the specific cause.
Epidural. good analgesia supports cough; a poorly working epidural is a remediable cause.

3. Persistent air leak

POD 1: large continuous chest-tube air leak, lung incompletely expanded. Significance? Bearing on ventilation if she needs support? Surgeon asks to raise suction — your input? Why? When do you suspect a stump problem?

Considerations and pitfalls

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Significance. alveolar or stump leak; a large continuous leak suggests a sizable parenchymal leak or a stump issue.
Ventilation. minimize airway pressure, favor spontaneous/low-pressure modes; high pressures worsen the leak.
Suction level. more suction can increase flow through the leak; balance expansion against leak; coordinate with surgery, don't reflexively raise it.
Stump problem. suspect with a massive leak or signs of dehiscence; isolation of the affected side and surgical involvement become central.

4. Post-thoracotomy atrial fibrillation

POD 1 evening: AF at 150, BP 92/56. Of concern? Why this patient? Triggers to find and correct? Rate or rhythm? Which? Agent? Why? She drops to 78/44. Now what?

Considerations and pitfalls

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Concern. poorly tolerated tachyarrhythmia loses atrial kick and shortens filling on a strained RV with a fixed coronary supply; demand ischemia.
Triggers. electrolytes, hypoxemia, pain, hypovolemia, distension.
Rate vs rhythm. if stable, rate control commonly first while correcting triggers.
Agent. account for negative inotropy and renal function; amiodarone often used; ignoring the agent's hemodynamic effect is a flag.
Unstable. synchronized cardioversion.

5. Analgesia and disclosure

POD 2: the epidural no longer covers the thoracic dermatomes, she is splinting, coughing poorly, PaCO2 climbing. Approach to analgesia? Re-site, replace, or multimodal? Why? If she needs reintubation — what will you tell her and the family? Coordinate the message with the surgeons — how?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Analgesia. re-site or replace the epidural, or move to a multimodal plan that enables cough; respiratory-depressant sedation is the wrong direction.
Telling patient/family. a plain, honest reason for breathing support, the expected course, that it is often temporary, with room for questions.
With the surgeons. a shared, specific message so the family does not get mixed signals.

C. ADDITIONAL TOPICS

Teaching focus. Local anesthetic systemic toxicity after a block; a recognized postdural puncture headache; an operating-room fire. Unrelated by design.

1. Local anesthetic systemic toxicity

A 60 y.o. woman gets an interscalene block for shoulder surgery. 2 min after injection: agitation, then a generalized seizure. Most likely cause? Priorities? She loses her pulse, wide-complex rhythm. How does management differ from standard ACLS? Lipid emulsion — principle and dose? Could you have prevented this?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Cause. LAST from intravascular injection or rapid systemic absorption.
Priorities. stop injecting, call for help, airway and oxygenation, control the seizure, get lipid emulsion.
ACLS mods. lipid emulsion, reduce epinephrine dosing, avoid certain antiarrhythmics, anticipate prolonged resuscitation, consider bypass for refractory arrest.
Lipid emulsion. bolus then infusion per protocol; a specific therapy, not an afterthought.
Prevention. incremental injection with aspiration, ultrasound, a test dose, lowest effective dose.

2. Postdural puncture headache

A 28 y.o. woman, 24 hr after a labor epidural with a recognized wet tap: positional fronto-occipital headache, relieved lying flat. Diagnosis? What must you exclude? Conservative measures? She can't care for her newborn — definitive Rx? How does it work? Risks?

Considerations and pitfalls

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Diagnosis. postdural puncture headache — postural, after a known dural puncture.
Must exclude. other serious postpartum headache: preeclampsia, cortical vein thrombosis, meningitis, subdural.
Conservative. time, analgesia, hydration, caffeine; limited evidence — overstating efficacy is a flag.
Definitive Rx. epidural blood patch; tamponade and sealing the leak.
Risks. repeat dural puncture, back pain, infection, rare neurologic complications.

3. Operating-room fire

MAC with nasal-cannula O2 for a facial excision; the surgeon uses cautery and a flash fire ignites at the drapes. Immediate actions? Sequence — what first? The fire triad here — what feeds it? Once out, assess the patient — how? Could you have prevented this?

Considerations and pitfalls

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Immediate. stop the procedure, stop the O2 and remove the airway source, remove the burning drapes, extinguish.
Sequence. protect the patient and remove the fuel and oxidizer first, then extinguish, then care for the patient.
Triad here. oxidizer (open O2 pooling under drapes), ignition (cautery), fuel (drapes/prep/hair) — a high-risk head-and-neck MAC.
Assess after. airway and skin/airway burns, ventilation, plan airway if inhalation injury is suspected.
Prevention. minimize open O2 near cautery, secure the airway or blend air, let prep dry, tent the drapes.

Session 1 — long stem

Off-site navigational bronchoscopy and transbronchial biopsy in COPD

A 64 y.o., 95 kg, 5'7" man is scheduled for electromagnetic navigational bronchoscopy with transbronchial biopsy and fiducial placement of a peripheral right-lower-lobe nodule, in the off-site interventional pulmonology suite.

HPIA 2.2 cm peripheral RLL nodule found on CT. Moderate COPD with dyspnea on climbing one flight and a chronic cough. No hemoptysis. The case is booked in the bronchoscopy suite, a corridor and an elevator away from the main operating rooms.

PMHModerate COPD. Atrial fibrillation on apixaban, last dose 48 hours ago per instruction. Obstructive sleep apnea on CPAP, obesity (BMI 32), hypertension. Former heavy smoker.

MEDSApixaban (held), metoprolol, tiotropium, inhaled fluticasone-salmeterol, albuterol prn, lisinopril.

PHYS EXAMHR 78 (irregular); BP 142/86; RR 16; SpO2 93% on room air; T 36.7°C. Prolonged expiratory phase with scattered wheeze; short neck, Mallampati III.

PFTsFEV1 1.6 L (60% predicted); FEV1/FVC 0.58; DLCO 60% predicted.

IMAGINGCT chest: 2.2 cm peripheral RLL nodule abutting the pleura; diffuse emphysema with apical bullae.

LABSHgb 15.1 g/dL; platelets 210 K/uL; INR 1.2; K+ 4.0 mEq/L; creatinine 1.0 mg/dL.

SUITEOff-site bronchoscopy suite. Anesthesia machine, standard monitors, suction, and a code cart are present; the difficult-airway cart and blood bank are in the main OR block. The proceduralist plans a shared airway through an endotracheal tube and may use cautery and argon plasma coagulation for hemostasis.

A. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Setting up and choosing an anesthetic for a remote location; sharing the airway and ventilating an obstructed lung during bronchoscopy; managing brisk endobronchial hemorrhage off-site; and an airway fire during endobronchial ablation in an oxygen-rich field.

1. Off-site setup and anesthetic choice

Before you start, what do you confirm about this location? What must be present that you take for granted in the main OR? MAC vs general anesthesia for this procedure? Why? Airway device — natural airway, LMA, or ETT? Why, given navigation and his airway? Maintenance — TIVA or volatile? Why here? Where is your help, blood, and difficult-airway equipment, and how long to reach you?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Confirm about the location. oxygen and backup oxygen, suction, scavenging, adequate monitoring, power, room to work, a clear route for help and for transfer to the OR — the off-site environment is the first hazard.
MAC vs GA. navigation and biopsy generally favor a controlled, often general, anesthetic with a secured airway and managed ventilation for image registration; sedation in an obstructed, obese, OSA patient off-site is worth challenging.
Airway device. an ETT gives a secure shared airway and lets the scope and tools pass while you ventilate; weigh size against the working channel and his airway.
Maintenance. TIVA avoids volatile loss through an open shared airway and operating-room contamination; defend the choice for this setting.
Help / blood / equipment. knowing the time and route to additional hands, blood, and the difficult-airway cart is part of the plan, not an afterthought.

2. Shared airway and ventilation

Scope in the airway, SpO2 drifts to 88% and peak pressures rise. DDx in this patient? How does his obstructive disease shape ventilation around the scope? Auto-PEEP — how do you check and manage it? The proceduralist wants prolonged breath-holds for navigation — how do you support oxygenation? He plans cautery and argon plasma coagulation — your FiO2 then, and why? How do you keep the shared airway coordinated?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

DDx. the scope occupying the airway, breath-stacking and auto-PEEP, bronchospasm, secretions, hypoventilation during instrumentation.
Obstructive ventilation. allow long expiratory times, watch for breath-stacking; a scope in a narrowed airway raises resistance and traps gas.
Auto-PEEP. look at the flow tracing and disconnect to allow full exhalation; reflexively adding PEEP without recognizing trapping is a flag.
Breath-holds / oxygenation. preoxygenate, coordinate apneic periods with the proceduralist, reconnect and recruit between navigation steps.
FiO2 with cautery/APC. lower the FiO2 as far as saturation allows before energy is used in the airway, and avoid nitrous — an oxygen-rich airway plus an ignition source is a fire risk; coordinate energy use with ventilation.

3. Massive endobronchial hemorrhage

During the biopsy, brisk blood wells up the airway and SpO2 falls to 80%. First actions? How do you protect oxygenation? Position him — which way, and why? How do you isolate the bleeding lung, and with what? What do you ask the proceduralist to do through the scope? You are off-site — who do you call and where does he go? Resuscitate to what end point while you arrange it?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

First actions / oxygenate. call for help, 100% oxygen, suction continuously, secure and protect the airway; the immediate killer is asphyxia, not exsanguination.
Position. bleeding side down to protect the healthy lung from soiling, balanced against oxygenation.
Isolate. advance the tube into the nonbleeding main bronchus, or place a blocker or DLT to isolate the bleeding lung; the proceduralist can tamponade or treat through the scope.
Through the scope. iced saline, topical vasoconstrictor, balloon tamponade, or argon plasma coagulation for hemostasis.
Off-site logistics / endpoint. activate help and blood early, plan transfer to the OR or IR; name oxygenation and hemodynamic targets while mobilizing — the remote location is part of the emergency.

4. Airway fire during ablation

During argon plasma coagulation through the scope to control oozing, a flash and flame appear in the airway. Immediate actions? Sequence — what first? What do you do with the tube and the oxygen? Once it is out, how do you assess the airway? What in this setup fed it? You are off-site — what does that change? After assessment, how do you decide whether he goes to the ICU, the OR, or recovery?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Immediate / sequence. stop the energy source, stop ventilation and disconnect the oxygen, remove the burning tube and any material, extinguish with saline, then re-establish a controlled airway and ventilate on the lowest FiO2 that maintains saturation.
Tube and oxygen. a tube fire is fed by the oxygen running through it; cutting the oxidizer and removing the burning tube are central — leaving oxygen flowing is the lethal error.
Assess the airway. bronchoscopy for thermal and inhalational injury — soot, edema, mucosal burn depth; reintubate over a scope as the airway allows, anticipating delayed edema.
What fed it. oxidizer (an oxygen-enriched airway), ignition (argon plasma or cautery), fuel (the tube, tissue, secretions); minimizing FiO2 before energy use is the prevention.
Off-site. limited help and equipment; call for help and the difficult-airway cart early and plan transfer rather than improvising alone.
Disposition. the extent of injury and his stability drive ICU vs OR vs recovery; airway burns warrant admission and observation for evolving edema.

B. POST-OPERATIVE CARE

Teaching focus. Waking and transporting a patient from a remote site; managing a pneumothorax in emphysematous lungs; post-procedure respiratory failure in COPD; recurrent bleeding and the anticoagulation decision; and disclosing an unexpected admission.

1. Emergence and transport off-site

Procedure done. Extubate in the suite or transport intubated? Why? What must be true before you move him? What do you bring for the corridor-and-elevator trip? He desaturates to 86% in the elevator — your kit and your moves? Where does he recover, and what do you hand off? ICU or PACU? What decides it?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Extubate or transport. the remote site, his obstructive disease, and the biopsy risk shape whether to wake him here or move him intubated; commit and justify.
Before moving. stable gas exchange and hemodynamics, oxygen and airway equipment and drugs for the trip, monitoring, a second set of hands.
Desat in transit. the transport kit earns its place here — oxygen, a bag, suction, airway gear, and the ability to stop and treat in the corridor.
Recovery / disposition. match the location to the risk; anticipating an ICU need beats discovering it in the hallway.

2. Pneumothorax in emphysematous lungs

Post-procedure film: a moderate right pneumothorax; he is mildly dyspneic, SpO2 92% on 4 L, hemodynamically stable. Significance? Observe, aspirate, or chest tube? Defend. How do his emphysema and bullae change the decision? If he needs positive pressure later, what is the danger? It enlarges over an hour — now what? Targets that would push you to intervene sooner?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Significance / decision. a stable moderate pneumothorax may be observed or drained depending on size, symptoms, and trajectory; commit and defend rather than reflexively tubing or ignoring it.
Emphysema / bullae. poor reserve and bullae lower the threshold to intervene and complicate distinguishing a bulla from a pneumothorax.
Positive pressure danger. it can enlarge the pneumothorax and tension it; relevant if he needs NIV or reintubation.
Enlarging / targets. an enlarging pneumothorax or worsening gas exchange and hemodynamics warrant a chest tube; name the triggers.

3. Post-procedure respiratory failure

Two hours later: wheezing, RR 30, PaCO2 rising, accessory muscle use. DDx? Most likely here? Rx priorities? Bronchodilators and steroids — role? NIV — is it safe given a recent transpleural biopsy? Why or why not? He tires further — reintubate, and to what threshold? Ventilator settings for severe air-trapping?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

DDx / most likely. COPD exacerbation and bronchospasm, mucus plugging, pneumothorax, residual sedation, fluid; bronchospasm is common after airway instrumentation.
Rx priorities. bronchodilators, steroids, oxygen titrated to target, treat a pneumothorax if present.
NIV after biopsy. weigh the benefit against forcing gas through a fresh pleural breach and worsening a pneumothorax; not automatically contraindicated, but not reflexive.
Reintubation / settings. do not delay a failing patient; long expiratory time, low rate, limit auto-PEEP, accept permissive hypercapnia.

4. Recurrent bleeding and anticoagulation

In recovery he coughs up blood again, a moderate amount, then settles; HR 104, BP stable. Concerns? Workup and monitoring? Restart apixaban — when, and why? What holds you back? If bleeding recurs and he is anticoagulated, reversal — agent and approach? Who do you involve? What is the disposition and what end points do you hand off?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Concerns / workup. recurrent hemoptysis after biopsy in a patient due to resume anticoagulation; monitor airway, serial hemoglobin, and be ready to isolate the lung again.
Restart anticoagulation. balance his atrial fibrillation stroke risk against active bleeding and the fresh biopsy; an individualized, reasoned plan with the proceduralist and cardiology, not a reflex to resume or to hold.
Reversal. if bleeding recurs while anticoagulated, the specific reversal approach for a factor Xa inhibitor; involve the relevant teams.
Disposition. monitored or ICU bed with clear airway and bleeding parameters handed off.

5. Disclosing an unexpected admission

What he expected to be a same-day procedure has become an ICU admission for a pneumothorax and bleeding. He and his family are upset and confused. What will you tell them? How do you explain what happened and why he is being admitted? He asks if this could have been avoided — what do you say? How do you coordinate the message with the proceduralist? He asks whether the biopsy even got an answer — how do you handle that?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Telling them. a plain, honest account of the known complications of the procedure, what happened, and why admission is needed, with room for questions.
Avoidability. honest framing: these are recognized risks of the procedure, not necessarily an error; avoid both false reassurance and unwarranted blame.
Coordinate / his question. a single shared message with the proceduralist; defer the pathology question to the team that will have the result, without guessing.

C. ADDITIONAL TOPICS

Teaching focus. ARDS with refractory hypoxemia; acute pain in an opioid-tolerant patient; an epidural hematoma after neuraxial anesthesia. Unrelated by design.

1. ARDS with refractory hypoxemia

A 55 y.o. man with severe pneumonia is intubated in the ICU. On volume control with FiO2 1.0 and PEEP 12, his PaO2 is 58 and the plateau pressure is 32. Interpretation of these numbers? Tidal-volume target and why? Plateau-pressure goal? He stays hypoxemic — higher PEEP, recruitment, or prone positioning? Defend. Role of neuromuscular blockade? When would you consider ECMO referral? BP falls to 80/50 as you raise PEEP — DDx and Rx?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Interpretation / tidal volume. severe hypoxemic respiratory failure; low tidal volume (~6 mL/kg predicted body weight) lung-protective ventilation; ventilating to a normal CO2 at the cost of high volumes is worth challenging.
Plateau. keep plateau at or below ~30; 32 is above target and should prompt a response.
Escalation. higher PEEP, recruitment, or proning — each defensible if reasoned; proning has the strongest outcome signal in severe disease.
NMB / ECMO. neuromuscular blockade for severe dyssynchrony or refractory hypoxemia; ECMO referral for refractory cases at a capable center.
Hypotension on PEEP. reduced venous return vs pneumothorax vs sepsis; lower PEEP or give volume or pressor and exclude pneumothorax before simply pushing fluids.

2. Acute pain in an opioid-tolerant patient

A 48 y.o. man on high-dose daily opioids for chronic back pain has severe pain after open abdominal surgery, poorly controlled despite escalating opioid boluses. Concerns? How do you think about his baseline requirement? Plan? Role of multimodal and regional techniques? Why is opioid monotherapy failing him? He becomes sedated but still reports 10/10 pain — interpretation and next step? What do you tell him about expectations?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Concerns / baseline. tolerance and hyperalgesia mean his baseline requirement is high; under-dosing relative to baseline and chasing pain with sedating boluses are both traps.
Plan. continue baseline opioid, add multimodal agents and a regional or neuraxial technique where feasible, set realistic targets.
Sedated but in pain. a danger sign of opioid-only escalation; pivot to multimodal and regional rather than more opioid.
Counsel. honest expectations about function over a pain score and a clear plan.

3. Epidural hematoma after neuraxial

A 70 y.o. woman, 18 hours after an epidural for knee arthroplasty, has new severe back pain and progressive leg weakness; the block should have worn off. DDx? Most concerning? What in her history would you look for? Immediate steps? Which imaging, and how urgently? Who do you call, and how fast? What do you tell her?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

DDx / most concerning. epidural hematoma or abscess; a dense or worsening block after it should have resolved is the red flag.
History. anticoagulation and the timing of dosing relative to catheter placement and removal, coagulopathy, traumatic placement.
Steps / imaging. urgent MRI, neurosurgical consultation; do not wait and watch.
Timing / counsel. decompression within hours preserves function; honest, prompt communication about the finding and the plan.

Session 1 — long stem

Right pneumonectomy with borderline pulmonary function and coronary disease

A 66 y.o., 72 kg, 5'10" man is scheduled for a right pneumonectomy for a central non-small-cell lung cancer involving the right main bronchus.

HPIA 45 pack-year smoker who quit at diagnosis. Completed neoadjuvant chemoradiation to the mediastinum six weeks ago. Dyspnea on climbing two flights, with a chronic cough; 6 kg of unintentional weight loss over three months.

PMHCoronary artery disease with a drug-eluting stent to the LAD 18 months ago; clopidogrel stopped two weeks ago on cardiology advice, aspirin continued. Mild COPD. Hypertension. The mediastinal radiation field included the heart.

MEDSAspirin 81 mg, metoprolol, lisinopril, atorvastatin, tiotropium, albuterol prn.

PHYS EXAMHR 82; BP 138/84; RR 16; SpO2 94% on room air; T 36.9°C. Thin, mild expiratory wheeze, no JVD or edema.

PFTsFEV1 1.9 L (58% predicted); FEV1/FVC 0.62; DLCO 50% predicted. Estimated postoperative predicted FEV1 ~30% after right pneumonectomy.

CARDIACEchocardiogram: LVEF 50%, mild RV dilation, estimated PA systolic pressure 42 mmHg. A recent stress study showed no reversible ischemia.

ECGSinus rhythm with frequent atrial premature beats; old anteroseptal Q waves.

IMAGINGCT and PET: right hilar mass involving the right main bronchus, no contralateral disease; post-radiation changes in the mediastinum.

LABSHgb 11.8 g/dL; platelets 190 K/uL; INR 1.1; K+ 3.6 mEq/L; creatinine 1.1 mg/dL; albumin 3.0 g/dL.

OR ARRIVALThoracic epidural placed at T6-7, test dose negative, not yet dosed. Left-sided 39 Fr double-lumen tube planned. Radial arterial line and two large-bore IVs.

A. INTRA-OPERATIVE MANAGEMENT

Teaching focus. Lung isolation and an induction that respects a fixed coronary lesion; recognizing and fixing a malpositioned tube during one-lung-ventilation hypoxemia; reading the right-pulmonary-artery clamp trial; and a fluid strategy that protects the one remaining lung.

1. Isolation and induction

DLT or bronchial blocker for this operation? Why? Which side, and why not the right? Induction agents and doses given the coronary history? Hemodynamic goals? Confirm isolation — how? On turning to one-lung ventilation, peak pressure climbs and BP falls to 90/52. DDx? First move? Auto-PEEP — how do you check?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

DLT vs blocker / side. a left-sided DLT keeps the bronchial cuff clear of the right main bronchus and the planned stump, and lets you manage the dependent lung; a right-sided tube risks the operative bronchus. Want a committed, defended choice.
Induction goals. avoid tachycardia and hypotension that threaten a fixed LAD lesion; support pressure early. Ignoring the coronary history is a flag.
Confirm isolation. fiberoptic confirmation is standard; auscultation alone is worth challenging.
Pressure up, BP down on OLV. breath-stacking and auto-PEEP, malposition, RV strain; disconnect to allow exhalation before reflexively giving fluid or pressor.

2. Hypoxemia and a malpositioned tube

Twenty minutes into one-lung ventilation, SpO2 84% on FiO2 1.0. DDx? First step? Fiberoptic shows the bronchial lumen has ridden up against the carina. Significance? Reposition — how, and what confirms success? SpO2 81% during repositioning. Hand-ventilate the dependent lung or push on? Once the surgeon clamps the right PA, what happens to oxygenation, and why?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

DDx / first step. malposition or migration, secretions, shunt through the nonventilated lung, dependent atelectasis, low cardiac output; FiO2 is already maximal, so reconfirm position by fiberoptic scope.
Malposition significance. a tube riding up obstructs ventilation of the dependent lung and worsens shunt; this is the common, fixable cause early in OLV.
Reposition / confirm. withdraw and reseat under direct vision; confirm dependent-lung ventilation and isolation by fiberoptic scope and chest rise.
PA clamp effect. clamping the right pulmonary artery eliminates shunt through the nonventilated lung, so oxygenation usually improves — a key piece of pneumonectomy physiology.

3. Right PA clamp trial

Before dividing the vessels, the surgeon test-clamps the right pulmonary artery. What are you watching? BP falls to 85/50, HR 120, CVP rising, end-tidal CO2 dropping. Interpretation? Most concerning here? Rx? Norepinephrine? Vasopressin? Phenylephrine? Which, and why? Inhaled pulmonary vasodilator — role? The surgeon asks whether he can safely complete the pneumonectomy. What guides your answer?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Watching. the clamp doubles the load on an already dilated RV; watch RV function, filling, systemic and pulmonary pressures, and gas exchange.
Interpretation / concern. acute RV strain or failure from the abrupt afterload rise on a pressure-loaded ventricle; tie it to the echo and the radiation history.
Pressor. norepinephrine or vasopressin to preserve RV coronary perfusion; leaning on phenylephrine without noting it can raise PVR is worth challenging.
Inhaled pulmonary vasodilator. iNO or epoprostenol selectively lower PVR; reasonable to raise; not a substitute for the clamp-trial decision.
Completing the pneumonectomy. if the RV fails the clamp trial, that is data — the candidate should treat tolerance of clamping as part of the go/no-go, not press on regardless.

4. Fluid and transfusion strategy

Two hours in, EBL 900 mL through friable irradiated tissue, BP 96/58 on low-dose norepinephrine, urine output 20 mL/hr. Fluid approach for a pneumonectomy, and why? Transfuse — trigger in this patient? How do you judge volume without over-resuscitating? Pressor vs fluid for this pressure? What is your hemoglobin and MAP target? He stays oliguric after a small fluid challenge — chase the urine output, or hold? Why?

Considerations and pitfalls

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Fluid approach. pneumonectomy demands a conservative fluid strategy — generous crystalloid is a recognized contributor to post-pneumonectomy pulmonary edema, which is frequently fatal; balance against perfusion.
Transfusion trigger. anemia plus coronary disease raises the threshold for tolerating low hemoglobin; defend a specific trigger rather than a reflex number.
Judging volume. use dynamic indices, response to small challenges, and the surgical field rather than chasing urine output with large boluses.
Targets. name a hemoglobin and MAP target; favor a pressor over flooding the remaining lung.

B. POST-OPERATIVE CARE

Teaching focus. Extubation onto a single lung; recognizing acute cardiac herniation; post-pneumonectomy pulmonary edema; post-thoracotomy atrial fibrillation; and a bronchopleural fistula with honest disclosure.

1. Extubation onto one lung

Case done, stable on low-dose norepinephrine. Extubate in the OR? Why/why not? What must be true first? Why does positive pressure worry you in particular now? You extubate and over 30 minutes he tires, RR 30, PaCO2 climbing. Options? NIV after pneumonectomy — concern? Reintubate — threshold?

Considerations and pitfalls

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Extubate or not. early extubation spares the fresh bronchial stump from positive pressure — a real goal; marginal reserve and pressor need argue caution. Either is defensible if committed and justified.
Before extubation. adequate gas exchange on the single lung, reversal confirmed, normothermia, stable hemodynamics, analgesia that allows deep breathing.
Positive pressure concern. it stresses the bronchial stump and the single remaining lung; this shapes both the extubation decision and any later support.
Tiring patient. optimize analgesia and toilet, weigh NIV against reintubation; uncritical high airway pressures on a fresh stump deserve a probe.

2. Sudden collapse in the PACU

Shortly after a position change in the PACU, he becomes acutely hypotensive with a heart rate of 140 and a sharp fall in SpO2. DDx? Given a right pneumonectomy and a recent position change, what jumps up the list? How confirm, fast? Immediate action with the surgeon? Reposition — which way? He has known coronary disease — how do you keep ischemia on the radar at the same time? End points while you get him to the OR?

Considerations and pitfalls

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DDx. cardiac herniation through a pericardial defect, hemorrhage, mediastinal shift, arrhythmia, myocardial ischemia, pulmonary embolism.
Cardiac herniation. after intrapericardial pneumonectomy a position change can herniate the heart, causing sudden obstruction — a surgical emergency; recognition is the test.
Confirm / action. clinical picture, film if time allows; call surgery immediately, return to the OR.
Reposition. operative side up to relieve herniation while preparing for re-exploration.
Ischemia in parallel. do not tunnel on one cause; the coronary history means ischemia stays on the differential.

3. Post-pneumonectomy pulmonary edema

POD 2: progressive hypoxemia, P/F 150, a new infiltrate in the remaining lung, no clear cardiac cause. DDx? Most likely here? How do you separate it from cardiogenic edema and pneumonia? Ventilator strategy for a single lung? Fluid balance now? He fails to improve on these measures — how far do you escalate, and what are the limits?

Considerations and pitfalls

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DDx / most likely. post-pneumonectomy pulmonary edema in the remaining lung; also cardiogenic edema, pneumonia, aspiration, transfusion-related lung injury.
Separate. echo and filling assessment, the fluid record, the clinical course; post-pneumonectomy edema is a diagnosis that still warrants excluding the others.
Ventilator strategy. lung-protective settings scaled to a single lung — low tidal volume to that lung, limit pressures; this is high-stakes.
Fluid / prognosis. conservative fluids and supportive care; the condition carries high mortality, which shapes honest communication.

4. Post-thoracotomy atrial fibrillation

POD 1 evening: atrial fibrillation at 150, BP 96/58. Of concern? Why this patient in particular? Triggers to find and correct? Rate or rhythm? Which, and why? Agent — accounting for what? He drops to 80/44. Now what? Anticoagulation — what enters the decision given his recent stent and surgery?

Considerations and pitfalls

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Concern. a fast rhythm loses atrial kick and shortens filling on a strained RV with a fixed coronary supply, risking demand ischemia and decompensation.
Triggers. electrolytes (note the K+), hypoxemia, pain, hypovolemia, mediastinal irritation.
Rate vs rhythm / agent. if stable, rate control while correcting triggers is common; account for negative inotropy and renal function — ignoring the agent's hemodynamic effect is a flag.
Unstable. synchronized cardioversion at 80/44.
Anticoagulation. balance stroke risk against fresh surgery and recent stent; a reasoned, individualized plan rather than a reflex.

5. Bronchopleural fistula and disclosure

POD 5: fever, a productive cough of thin fluid, a new air-fluid level change on the film, and rising oxygen need. DDx? Most concerning? Why is positive pressure dangerous now? If he needs intubation, how do you protect the remaining lung? Position him — which way, and why? What will you tell him and the family about what has happened and what comes next?

Considerations and pitfalls

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DDx / most concerning. bronchopleural fistula from stump dehiscence with spillage into the remaining lung; also empyema, pneumonia, recurrent edema.
Positive pressure danger. mask or invasive positive pressure can force gas through the fistula and flood or fail to ventilate the remaining lung.
Protect the lung if intubated. lung isolation (DLT or blocker) to the remaining lung, minimize airway pressure, urgent surgical involvement and drainage.
Position. operative (fistula) side down to protect the healthy lung from soiling, balanced against oxygenation.
Disclosure. a plain, honest account of the complication, the plan, and the seriousness, coordinated with the surgical team.

C. ADDITIONAL TOPICS

Teaching focus. Pediatric post-tonsillectomy hemorrhage; a postdural puncture headache; intraoperative anaphylaxis. Unrelated by design.

1. Pediatric post-tonsillectomy hemorrhage

A 5 y.o. returns to the OR six hours after tonsillectomy bleeding from the surgical bed; he is pale, tachycardic, and has been swallowing repeatedly. Concerns? How do you judge volume status in a child who has been swallowing blood? Resuscitate before induction — to what end point? Induction plan? Airway approach with active bleeding and a full stomach? Equipment and help you want at hand? After control, extubation plan?

Considerations and pitfalls

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Concerns / volume. hypovolemia is routinely underestimated because the blood is swallowed; tachycardia may be the main sign; assess perfusion, not just the visible loss.
Resuscitate first. restore volume before induction; a hypovolemic child can arrest on induction.
Induction / airway. rapid sequence with suction ready, two laryngoscopes and a styletted smaller tube, anticipate a bloody, obscured view; experienced help and the surgeon present.
Extubation. fully awake with the stomach emptied.

2. Postdural puncture headache

A 28 y.o. woman, 24 hours after a labor epidural with a recognized wet tap, has a positional fronto-occipital headache relieved by lying flat. Diagnosis? What must you exclude? Conservative measures? She cannot care for her newborn — definitive Rx? How does it work? Risks? What do you tell her about recurrence?

Considerations and pitfalls

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Diagnosis / exclude. postdural puncture headache — postural, after a known dural puncture; exclude preeclampsia, cortical vein thrombosis, meningitis, subdural.
Conservative. time, analgesia, hydration, caffeine; limited evidence — overstating efficacy is a flag.
Definitive Rx. epidural blood patch; tamponade and sealing of the leak.
Risks / recurrence. repeat dural puncture, back pain, infection, rare neurologic complications; a patch may be repeated if symptoms return.

3. Intraoperative anaphylaxis

Ten minutes after incision and antibiotic dosing, a patient becomes hypotensive with high airway pressures, a rising heart rate, and a new truncal rash. DDx? Most likely? How concerned, and why? Immediate Rx? Epinephrine — dose and route? Triggers to stop? Hypotension refractory to first measures — next? What confirms it later, and when do you draw it? What do you tell the patient afterward?

Considerations and pitfalls

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DDx / most likely. anaphylaxis (antibiotic, neuromuscular blocker, latex, chlorhexidine), also tension pneumothorax, severe bronchospasm, embolism.
Immediate Rx. stop the likely trigger, 100% oxygen, epinephrine, aggressive fluids, call for help.
Epinephrine. titrated IV in this setting; escalate to an infusion for refractory shock; vasopressin as an adjunct.
Confirm later. serial tryptase timed from the event, with later allergy referral and testing.
Counsel. tell the patient clearly, document, and arrange follow-up so the agent is identified.

Session 1 — long stem

Tracheal resection and reconstruction for post-intubation stenosis

A 55 y.o., 98 kg, 5'8" man is scheduled for tracheal resection and end-to-end reconstruction for a post-intubation tracheal stenosis.

HPIProlonged intubation and then a tracheostomy during an ICU stay for ARDS last year; decannulated four months ago. Since then, worsening exertional dyspnea and noisy breathing, now with stridor audible at rest and difficulty clearing secretions; he can climb less than one flight.

PMHObesity (BMI 34), obstructive sleep apnea on CPAP, hypertension, GERD. Former smoker.

MEDSLisinopril, amlodipine, omeprazole, CPAP nightly.

PHYS EXAMHR 92; BP 146/88; RR 20 with biphasic stridor at rest, worse supine; SpO2 95% on room air; T 36.8°C. Short, thick neck; healed tracheostomy scar; Mallampati III.

IMAGINGCT neck and chest: a 1.5 cm segment of mid-tracheal stenosis narrowing the lumen by roughly 70%, beginning about 4 cm below the cords; no distal disease.

FLOW / SCOPEFlow-volume loop with fixed obstruction. Awake nasendoscopy: mobile vocal cords, narrow subglottic-to-mid-tracheal airway.

LABSHgb 14.2 g/dL; platelets 230 K/uL; INR 1.0; K+ 4.1 mEq/L; creatinine 0.9 mg/dL.

OR ARRIVALPlan made jointly with the surgeon. Rigid bronchoscope, an array of small cuffed and armored tubes, sterile cross-field tubing, and a jet ventilator are in the room; perfusion is on standby. Radial arterial line and two large-bore IVs.

A. INTRA-OPERATIVE MANAGEMENT

Teaching focus. An induction that keeps a critically narrowed airway open; sharing the airway with the surgeon during resection; an airway fire in an oxygen-rich field; and rescuing a lost distal airway in the open field.

1. Induction across the stenosis

Awake or asleep? Why? Spontaneous vs controlled ventilation? Why? Inhalational or IV induction here? Where does your initial tube sit relative to the stenosis? Pass a tube through the narrowing, or have the surgeon dilate or rigid-scope first? You attempt to advance past the stenosis and obstruction worsens with desaturation to 85%. Next? Rigid bronchoscopy — role now?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Awake / spontaneous. maintaining spontaneous ventilation through induction keeps a dynamic obstruction open; abolishing drive and giving positive pressure can convert a narrowed airway into a closed one. Early paralysis with a controlled-ventilation plan is a red flag.
Technique. an inhalational or carefully titrated technique that preserves breathing; have the surgeon and rigid scope immediately available, not down the hall.
Tube position. an initial tube above the stenosis with a plan to pass a small tube through it, or to let the surgeon establish the airway, is reasonable; forcing a standard tube blindly through a 70% stenosis is the trap.
Obstruction worsens. rigid bronchoscopy to re-establish and stent the airway past the lesion is the rescue the room is set up for.

2. Ventilation during the open phase

The surgeon divides the trachea distal to the stenosis and is ready to ventilate the distal segment. Options? Cross-field tube vs jet ventilation — choose and defend. Oxygenation during intermittent apnea — how do you support it? CO2 rising during a long apneic period — your target and how you manage it? The field is wet and the cross-field tube keeps fogging — communication plan with the surgeon? How do you keep the shared airway organized between the two of you?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Options. a sterile cross-field tube placed by the surgeon into the distal trachea, or jet ventilation across the stenosis or into the distal segment; commit and defend rather than list.
Cross-field vs jet. a cross-field tube gives a secure cuffed airway but interrupts the field; jet ventilation keeps the field open but risks barotrauma and CO2 accumulation. Either is defensible if reasoned.
Oxygenation / apnea. preoxygenate, use apneic oxygenation and intermittent reconnection, coordinate ventilation around surgical steps.
CO2 target. accept permissive hypercapnia within reason; name a tolerable range rather than chasing normocapnia at the cost of the field.
Communication. explicit, closed-loop handoffs of the airway; a disorganized shared airway is itself the hazard.

3. Airway fire in the field

During dissection the surgeon uses cautery near the open airway while you are running a high FiO2, and a flash fire occurs. Immediate actions? Sequence — what first? What in this setup fed the fire? Once out, how do you assess the airway? Could this have been prevented? How? After assessment, how do you decide whether to proceed with the reconstruction?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Immediate / sequence. stop ventilation and disconnect the oxygen source, remove any burning tube or material, extinguish, then re-establish a controlled airway and ventilate.
What fed it. oxidizer (high FiO2 in an open airway), ignition (cautery), fuel (tube, tissue, drapes) — the open oxygen-rich airway is the dominant risk.
Assess the airway. bronchoscopy for thermal injury to the mucosa and distal airway; look for soot, edema, and the depth of injury.
Prevent. keep FiO2 as low as the saturation allows during cautery, avoid nitrous, coordinate cautery use with ventilation.
Proceed or not. the extent of thermal injury and the patient's stability drive whether to complete the reconstruction now or stage it.

4. Lost distal airway

Mid-resection the cross-field tube dislodges from the distal trachea into the field; SpO2 falls to 82% and you cannot ventilate. First actions? Who does what between you and the surgeon? How do you re-establish the distal airway? Hand the surgeon what? SpO2 75%, HR 130 — how long do you persist before escalating? When does peripheral bypass enter? To what end point do you resuscitate?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

First actions / roles. call it out, 100% oxygen, the surgeon re-secures the distal segment under direct vision while you support oxygenation; clear role assignment prevents two people reaching for the same airway.
Re-establish. the surgeon replaces the cross-field tube into the open distal trachea, or you advance an oral tube past the anastomotic site under vision.
Persistence / escalation. do not persist into arrest; the standby perfusion team is there for exactly an unrecoverable airway.
End point. name oxygenation and hemodynamic targets and the threshold to convert to bypass.

B. POST-OPERATIVE CARE

Teaching focus. Early extubation onto a fresh anastomosis with the neck flexed; post-extubation airway compromise and the danger of blind reintubation; anastomotic dehiscence; balancing sedation against a protected airway; and disclosure when a second operation is needed.

1. Extubation with the neck flexed

Reconstruction complete, a chin-to-chest guardian suture placed. Extubate in the OR? Why/why not? What must be true first? Why is early extubation the goal here? The neck is held flexed — what does that mean for your airway access? You extubate and he is stridorous within minutes. Rx? If he must be reintubated, how do you do it without harming the anastomosis?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Extubate or not. early extubation is generally the goal — it spares the fresh suture line from positive pressure and a cuff sitting on the anastomosis; weigh against airway edema and reserve.
Before extubation. awake, exchanging gas, reversed, hemodynamically stable, with surgeon, fiberoptic scope, and small tubes ready.
Neck flexion. the guardian suture keeps the neck flexed to protect the anastomosis, which makes any reintubation harder — plan for that constraint in advance.
Reintubation safely. fiberoptic-guided, a small tube, the surgeon present, avoiding blind passage that could disrupt or false-passage the anastomosis.

2. Post-extubation airway compromise

Two hours later: increasing stridor, a weak voice, and rising work of breathing. DDx? Most concerning? How do you evaluate without forcing the airway? Heliox or racemic epinephrine — role? He tires and oxygenation falls. Secure the airway — your approach given the anastomosis and the flexed neck? What do you have the surgeon ready to do?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

DDx / most concerning. anastomotic edema, recurrent laryngeal nerve injury, hematoma, secretions, early dehiscence; bilateral cord dysfunction or a tight edematous anastomosis can obstruct.
Evaluate. fiberoptic assessment, gentle and prepared, rather than repeated blind attempts.
Temporizing. heliox and racemic epinephrine may buy time but do not fix a mechanical problem.
Secure the airway. fiberoptic-guided small tube with the surgeon ready for rigid bronchoscopy or a surgical airway; protect the suture line.

3. Anastomotic dehiscence

POD 4: fever, subcutaneous emphysema in the neck, a new air leak, and worsening gas exchange. DDx? Most concerning? Why is positive pressure a problem now? If intubation is unavoidable, where do you want the tube and cuff to sit? How do you involve the surgeon and what is the disposition? End points guiding your support until the OR?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

DDx / most concerning. anastomotic dehiscence with air leak and mediastinal contamination; also wound infection, pneumonia.
Positive pressure. it forces gas through the disruption and worsens the leak and emphysema; minimize airway pressure.
Tube position. the cuff ideally distal to the disruption to bridge the leak, placed with care and imaging or bronchoscopy; this is an urgent surgical problem.
Disposition / endpoints. OR for repair or revision; ICU support; name oxygenation and perfusion targets in the interim.

4. Sedation versus a protected neck

POD 1 in the ICU he is agitated and repeatedly extending his neck against the guardian suture, coughing hard. Concerns? Priorities? Sedation depth — target, and why? Agents you would and would not use, and why? Analgesia plan? Pulmonary toilet without provoking coughing fits — how? What would change your plan toward securing the airway?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Concerns / priorities. neck extension and violent coughing threaten the fresh anastomosis; keep the neck flexed and the patient comfortable without obtunding respiration.
Sedation balance. light, titratable sedation and good analgesia; avoid heavy respiratory depression that pushes toward reintubation.
Agents. favor agents that calm without abolishing drive; justify choices around airway protection and the suture line.
Toilet / escalation. gentle suctioning and humidification; a clear threshold to secure the airway if he deteriorates.

5. Disclosure of a return to the OR

The anastomosis has partially failed and he needs a return to the OR, possibly a tracheostomy. The family is anxious and asks what went wrong. What will you tell them? How do you explain the complication and the plan honestly? What do you say about voice and breathing going forward? How do you coordinate the message with the surgical team? He asks whether he will need a permanent trach — your answer?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Telling the family. a plain account of the dehiscence, why a second operation is needed, and the seriousness, with room for questions.
Voice / breathing. honest about uncertainty rather than false reassurance; defer specifics you cannot yet know.
Coordinate / his question. a single shared message with surgery; answer the tracheostomy question honestly as a possibility, not a certainty, focusing on the immediate plan.

C. ADDITIONAL TOPICS

Teaching focus. Local anesthetic systemic toxicity; the oculocardiac reflex during strabismus surgery; an acute hemolytic transfusion reaction. Unrelated by design.

1. Local anesthetic systemic toxicity

A 60 y.o. woman gets an interscalene block for shoulder surgery. Two minutes after injection she becomes agitated, then has a generalized seizure. Most likely cause? Priorities? She loses her pulse with a wide-complex rhythm. How does management differ from standard ACLS? Lipid emulsion — dose and how given? Could you have prevented this?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

Cause / priorities. LAST from intravascular injection or rapid absorption; stop injecting, call for help, airway and oxygenation, control the seizure, get lipid emulsion.
ACLS modifications. lipid emulsion, reduce epinephrine dosing, avoid certain antiarrhythmics, anticipate a prolonged resuscitation, consider bypass for refractory arrest.
Lipid emulsion. bolus then infusion per protocol — a specific therapy, not an afterthought.
Prevention. incremental injection with aspiration, ultrasound guidance, a test dose, the lowest effective dose.

2. Oculocardiac reflex

During strabismus surgery in a 6 y.o., traction on an extraocular muscle is followed by an abrupt fall in heart rate to 40. DDx? Most likely? First action? What do you ask the surgeon to do? It recurs with each pull — Rx? Atropine — dose and timing? This surgery's PONV risk — plan? When would you worry it is something other than the reflex?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

DDx / most likely. oculocardiac reflex from traction; also hypoxemia, light anesthesia, or a primary arrhythmia.
First action. have the surgeon release traction; confirm oxygenation and ventilation.
Recurrent / atropine. if it recurs or is severe, atropine; deepen anesthesia; persistent traction should pause.
PONV. strabismus surgery is high-risk for PONV; multimodal prophylaxis.
Other causes. if bradycardia persists despite released traction and a treated reflex, look beyond it.

3. Acute hemolytic transfusion reaction

Midway through a red-cell transfusion under general anesthesia, a patient develops fever, hypotension, hemoglobinuria, and oozing from the surgical field. DDx? Most concerning? First actions? Stop what, and send what? How does DIC fit the picture? Maintain renal output — how, and to what target? How would you have prevented this? What do you document and disclose?

Considerations and pitfalls

AI-generated and not yet reviewed by faculty. Verify before teaching from it.

DDx / most concerning. acute hemolytic transfusion reaction, often from ABO incompatibility; also anaphylaxis, TRALI, sepsis, TACO.
First actions. stop the transfusion, maintain the IV with crystalloid, support blood pressure and airway, recheck the unit and patient identifiers, notify the blood bank, send samples.
DIC / renal. hemolysis can trigger DIC and pigment nephropathy; support coagulation as needed, maintain brisk urine output with fluids, name a target.
Prevention / disclosure. rigorous identity checks at every step; document and disclose the error honestly.