Case Discussions

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• Urgent not routine. his flail chest, contusion, rising CO2, and failing cough put him on a path to pneumonia and respiratory failure; analgesia here is a pulmonary intervention, not comfort care.
• Assess pain and breathing. pain at rest and with movement and cough, respiratory rate and effort, oxygenation, cough strength and secretion clearance, and inspiratory effort or vital-capacity effort.
• Bedside numbers. SpO2, respiratory rate, the arterial CO2 trend, and a measure of inspiratory effort; the CO2 trend is central.
• Guarding / won't cough. splinting collapses lung units and retains secretions, driving atelectasis and hypoxemia; it is a reason to escalate analgesia, not to sedate.
• Trajectory as-is. worsening hypoventilation, hypercarbia, atelectasis, and likely intubation within a day if analgesia does not enable breathing and coughing.

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• Of concern. a rising PaCO2 with shallow breathing in a COPD patient signals impending ventilatory failure.
• Why him specifically. limited pulmonary reserve, a flail segment, a contusion, opioids on board, and age and cognition all reduce his margin.
• What is driving it. pain-limited breathing, the contusion's shunt, flail mechanics, and opioid-induced hypoventilation likely all contribute; sort by response to analgesia, exam, and serial ABGs.
• Non-invasive support. NIV or high-flow can support oxygenation and ventilation and buy time while analgesia takes effect, if he can protect his airway and cooperate.
• Toward the ICU. progressive hypercarbia and fatigue, failure of NIV, deteriorating mental status, or an inability to clear secretions.

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• Read on the combination. he is under-analgesed and over-sedated at once — a sign that opioid monotherapy is failing him, not that he needs simply more.
• Problem escalating opioid. more opioid deepens hypoventilation and sedation in a COPD patient with a rising CO2 without reliably relieving movement and cough pain.
• PCA appropriateness. PCA suits an awake, cognitively intact patient who can self-dose; his drowsiness and baseline cognitive impairment make an unmonitored PCA hazardous.
• Monitoring for failure. sedation score, respiratory rate and adequacy, capnography and SpO2, and the CO2 trend, using a sedation-precedes-depression framework.
• Naloxone. reverses opioid depression but can precipitate acute pain and withdrawal and is short-acting; a rescue, not a management plan.

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• Effect on regional plan. apixaban dosed yesterday plus prophylactic heparin makes neuraxial and deep, non-compressible blocks unsafe now; it steers toward superficial fascial-plane options or waiting.
• Off vs on the table. thoracic epidural and, per many, paravertebral are off with current anticoagulation; a superficial erector spinae or serratus plane block is more permissible with caution.
• Hold / wait to open options. an adequate apixaban hold and appropriate heparin timing would reopen neuraxial and paravertebral options; balance that delay against his deteriorating breathing.
• Coordinate with. the trauma and primary team and, as needed, cardiology about atrial-fibrillation stroke risk before holding anticoagulation.
• Urgency of the conversation. soon — his respiratory trajectory means the analgesia decision cannot wait days.

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• Recommendation and why. given anticoagulation and poor reserve, a fascial-plane (erector spinae) catheter is often the pragmatic choice — meaningful analgesia with a lower bleeding risk than neuraxial or paravertebral.
• Epidural vs paravertebral vs ESP. a thoracic epidural gives the best analgesia and pulmonary benefit but is precluded by his anticoagulation; paravertebral is effective but deep and non-compressible; ESP is superficial and more forgiving of coagulation status. The trade-off that decides it here is bleeding risk.
• Single-shot vs catheter. multiple rib fractures need days of analgesia, favoring a catheter and infusion over a single injection.
• Agent and dosing plan. a dilute long-acting local by programmed intermittent bolus or infusion, dosed to stay under cumulative toxic limits given his kidneys.
• Confirmation it works. improved pain with breathing and cough, better inspiratory effort and spirometry, improving oxygenation and CO2, and reduced splinting.

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• Acetaminophen. scheduled acetaminophen is a low-risk backbone; include it unless a specific contraindication.
• NSAID. relative caution or avoidance with stage-3 CKD, age, and trauma/bleeding; defensible either way with an explicit risk statement, but a reflexive NSAID here is a flag.
• Ketamine infusion. low-dose ketamine is a useful opioid-sparing adjunct for rib-fracture pain, run in a low set range while watching for psychotomimetic effects.
• Adjuncts to avoid or limit. renally-cleared drugs and active metabolites (for example morphine), heavy sedatives, and deliriogenic agents given his kidneys, lungs, and cognition.
• Gabapentinoid. may help but adds sedation and respiratory depression, especially with opioids and in the elderly; worth it only with dose caution and monitoring.

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• What is going on. improved pain but rising CO2 and somnolence suggest ventilatory depression or fatigue outpacing the analgesic benefit; the plan is failing on the respiratory axis.
• Your move. reassess ventilation, reduce respiratory depressants, optimize the block, escalate support and monitoring, and prepare for possible intubation.
• Separating causes. opioid effect (sedation-led depression), an inadequate or excessive block contribution, the injury's own course, and CO2 narcosis; use exam, drug timing, block assessment, and ABG.
• NIV vs intubation threshold. trial NIV if he can protect his airway and cooperate; intubate for progressive hypercarbia with obtundation, NIV failure, or secretion and airway compromise.
• If intubated. the regional catheter still reduces sedation needs and aids later weaning; continue opioid-sparing analgesia.

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• Interpretation. early local anesthetic systemic toxicity from cumulative absorption — a neurologic prodrome of perioral numbness, metallic taste, and confusion.
• Most likely cause. accumulation from the continuous infusion, exaggerated in CKD by buildup of active renally-excreted metabolites and by acidosis (which raises the free fraction); the parent amide itself is hepatically cleared.
• Immediate Rx. stop the infusion, oxygen, monitor, manage any seizure and the airway, and prepare lipid emulsion; treat progression early rather than waiting for collapse.
• Lipid emulsion. for evolving neurologic or cardiovascular toxicity, a bolus followed by an infusion per protocol; a specific therapy.
• Infusion setup to avoid this. lower cumulative dosing, a dilute concentration, and a dose cap mindful of his weight, and of CKD's higher free-drug levels and metabolite accumulation; not accounting for CKD is the miss.

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• Wean without rebound. overlap oral multimodal analgesia before removing the catheter and taper opioids; keep breathing and cough protected as regional analgesia is withdrawn.
• Order of weaning. typically wean the block or catheter once oral multimodal analgesia is effective and pulmonary mechanics are stable, then taper systemic opioid.
• Oral regimen for home. an acetaminophen-based multimodal plan with a short, limited opioid course mindful of his lungs, kidneys, age, and cognition; a stewardship-minded plan.
• What to tell him / team. the plan, the signs of regression (worsening pain, poor cough, rising somnolence), and the threshold to re-escalate; align with the trauma team.
• When to sign off. stable pain control on oral medication, adequate breathing and cough, and no need for infusion or advanced support.

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• DDx. anaphylaxis, tension pneumothorax, pulmonary embolism, a primary cardiac event, and severe bronchospasm; the timing after rocuronium and cefazolin with hypotension, bronchospasm, and rash points to anaphylaxis.
• Leading diagnosis. anaphylaxis — abrupt hypotension, bronchospasm with high airway pressure, and rash shortly after drug exposure.
• Immediate priorities. stop the likely trigger, call for help, 100% oxygen and secure the airway, epinephrine, IV fluids, and pause surgery if needed.
• First-line drug. epinephrine, dose and route titrated to severity (IV boluses in the anesthetized, monitored patient, escalating to an infusion); antihistamines and steroids are adjuncts, not first-line.
• Refractory after two doses. escalate epinephrine to an infusion, give aggressive fluids, and consider vasopressin and glucagon (especially if she is on a beta-blocker); get help.
• Confirmatory tests. serial serum tryptase around the event and later allergy or skin testing to identify the culprit; the timing of tryptase matters.
• Culprits and counseling. neuromuscular blockers and antibiotics are common perioperative triggers; document the reaction, identify the agent, and counsel lifelong avoidance and future testing.

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• Diagnosis. laryngospasm — stridor progressing to complete glottic closure, classically on light emergence.
• Contributing factors. recent URI, a light plane of anesthesia, airway secretions, and young age.
• Maneuvers and sequence. remove the stimulus, 100% oxygen, jaw thrust with continuous positive pressure (Larson's maneuver); escalate if it fails.
• Bradycardia with desaturation. deepen anesthesia (propofol) or give succinylcholine, treat the hypoxic bradycardia, and be ready to ventilate or intubate; giving succinylcholine without addressing oxygenation deserves a probe.
• Succinylcholine. a small IV dose breaks refractory spasm; intramuscular is an option without IV access, with 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.

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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, and caffeine; evidence is limited and overstating their efficacy is worth a probe.
• Definitive treatment. an epidural blood patch, which works by tamponade and by sealing the dural leak.
• Risks. repeat dural puncture, back pain, infection, and rare neurologic complications.

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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.

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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 learner 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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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• 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.

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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.

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• DDx for failure to separate. stunned hypertrophied LV, inadequate preload, residual ischemia or air in the coronaries (classically the right), 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 learner 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.

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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.

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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 72 h ago — ≥5 half-lives, so residual effect is negligible and not the 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.

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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.

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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 learner 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 learner 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.

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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.

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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.

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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.

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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.

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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.

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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.

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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 learner 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.

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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 learner 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.

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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 learner 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.

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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 an adequate count signals qualitative platelet dysfunction (CPB plus ticagrelor) and favors platelets — note standard kaolin MA is relatively insensitive to the P2Y12 effect itself (platelet mapping or ADP aggregometry demonstrates it). Circulating ticagrelor partially inhibits transfused platelets, so expect incomplete correction and redose as guided. 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.

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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.

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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.

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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.

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• 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.

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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.

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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.

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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.

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• 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 learner 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 learner 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 learner 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.

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• 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.

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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 learner should recognize ECMO is not resting this LV, it is loading it.
• Flat waveform — interpretation. 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 are a partial fix, but maintaining some ejection prevents root and LV stasis — which is why low-dose inotropes are often kept running on VA-ECMO even though they work against fully 'resting' the heart. 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.

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• 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 learner 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.

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• 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 learner 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.

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• 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.

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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 learner 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.

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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 learner 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.

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• 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 learner should name this clearly and humanely.

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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.

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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.

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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.

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• 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.

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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 learner 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.

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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.

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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 learner 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.

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• 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.

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• 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.

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• 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.

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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 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 learner must hold all three against each other.
• Involve / offer. neurology and surgery; supportive neuroprotective ICU care, shared decisions on anticoagulation timing, honest prognostication.

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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, 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.

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• Diagnosis. ARDS — acute, bilateral infiltrates not fully explained by cardiac failure; the learner should derive the PaO2/FiO2 of 58, 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 learner 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.

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• 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.

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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.

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• 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 learner must integrate oxygenation, rate, and RV protection rather than chase BP alone.

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• 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 learner 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.

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• 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. 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; tie it to the RV, not 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. A defended choice tied to this RV, not a list.
• Pink froth / 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 stenotic valve and high LA pressure make pulmonary edema the lead.
• PEEP / diuresis. modest PEEP can recruit and reduce the oxygenation deficit, but excessive PEEP impedes RV output and venous return in a pressure-loaded RV; a titrated answer beats reflexive high-PEEP or none. Aggressive diuresis is a trap while the obstruction is unrelieved and she may be preload-dependent.
• Priorities / bypass urgency. oxygenation and airway, lower LA/pulmonary pressure by slowing the rate and avoiding overload, support perfusion pressure; recognize that definitive relief is mechanical and that worsening edema/hemoptysis argues for expediting cannulation and bypass rather than prolonged temporizing.

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• 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 learner 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 learner who recognizes the failure is RV-predominant and reaches for RV-appropriate support rather than an IABP is reasoning well.

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• Extubation criteria here. beyond standard readiness (gas exchange, secretions, mentation, hemodynamic stability off high support), this RV tolerates neither hypercarbia nor the work of a failed wean; a low threshold to defer is defensible.
• Pulmonary hypertension / RV bearing. hypercarbia and the work of breathing after a failed extubation raise PVR and can tip the RV; residual pulmonary edema worsens compliance and oxygenation — all argue for a conservative, well-optimized extubation.
• Extubate now or wait. a mild respiratory acidosis on pressure support in a pulmonary-hypertensive patient argues to optimize first (diuresis, secretion clearance, sedation weaning) rather than extubate to marginal reserve; want a defended call, not a reflex.
• Reintubation threshold. rising PaCO2, worsening hypoxemia, fatigue, or hemodynamic deterioration; do not delay reintubation into an RV crisis in this patient.
• What drove the failure. increased work of breathing and hypercarbia raising PVR and RV afterload, plus residual pulmonary edema — reason from her physiology, not a generic 'she wasn't ready.'
• Targets before a second attempt. diuresis toward euvolemia without underfilling, normocarbia, secretion clearance, and RV support; then a planned, unhurried extubation.
• Tracheostomy. persistent failure to wean over days, especially with ongoing RV/pulmonary limitation, makes early tracheostomy reasonable for secretion management and comfortable weaning; repeated reintubation cycles are the trap.

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• 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.

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• 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 learner 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.

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• 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 pacing (VVI) is what reliably delivers rate. A learner 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.'

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• 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.

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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.

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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.

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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.

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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 learner 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.

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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.

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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.

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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.

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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 learner 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.

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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.

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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 learner 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.

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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.

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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.

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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.

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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.

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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.

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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.

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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 learner 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.

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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 learner 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.

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• 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.

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• 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.

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• 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.

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• 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.

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• 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.

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• 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.

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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.

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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.

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• Diagnosis. ARDS — acute, bilateral infiltrates not fully explained by cardiac failure; the learner should derive the PaO2/FiO2 of 58, 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 learner 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.

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• 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 the HRS/ASA consensus windows (ICD within ~6 months, pacemaker ~12, CRT 3–6); at 11 months this ICD is stale, and dependence plus planned EMI make it matter. 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.'

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• 100% paced, no escape. EMI-induced oversensing can inhibit pacing output; with no underlying escape this means asystole, not just a dropped beat. The learner 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.

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• 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.

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• K+ 5.1 before pacing/defibrillation. mild and likely chronic (CKD plus sacubitril-valsartan); relevant because hyperkalemia raises capture thresholds in a patient who may depend on pacing, but 5.1 is not itself a barrier to proceeding. Demanding shift/removal therapy for a stable 5.1 is itself a flag — overtreatment, not vigilance.
• Rx. recheck the morning of surgery, avoid exacerbants (succinylcholine, acidosis, potassium-containing fluids), and treat only if it is rising or there are ECG changes; tie the vigilance to pacing dependence, not a reflex to normalize the number.
• 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+ rechecked and stable, device team to reactivate post-op.

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• 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 learner 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.

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• Interpretation. First distinguish EMI artifact from true pauses — check the arterial line/pleth for continued pulsatility during cautery. In a confirmed-VOO device, oversensing inhibition cannot occur; true pauses should prompt suspicion of loss of capture or an EMI-induced device reset to a backup demand mode, confirmed by urgent interrogation. 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 learner 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.

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• 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.

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• Spikes without QRS following. 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.

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• 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 learner 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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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• TOF reliable. Useful and essential for NDMR titration, but obtain a pre-relaxant baseline — myasthenics may show fade at baseline, so track change from that baseline rather than absolute counts.
• 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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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. Learner 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.

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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 learner should reason from CPP.

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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.

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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.

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• Extubate. no — GCS 7T, 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. PRIS risk low at this dose (classically >4 mg/kg/h for >48 h) but screen — triglycerides, CK, lactate, unexplained acidosis; also lipid caloric load and accumulation clouding the hourly neuro exam.
• Paralytics. for severe ICP refractory to sedation, or vent dyssynchrony with worsening hypoxia; not routine; obscure exam.

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• DDx of rising ICP. edema, expanding hematoma, hydrocephalus, hypoventilation, fever, seizure, agitation, venous outflow obstruction.
• Mgmt. tiered escalation — 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.

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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.

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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.

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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.

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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. oxytocin first; methylergonovine contraindicated in preeclampsia/hypertension; carboprost (caution in asthma); misoprostol; escalate mag-antagonized atony early — mechanical measures, surgical steps.

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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.

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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.

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• Drivers. 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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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• Tachycardia DDx. anxiety, light block height, surgical stimulus, volume shift, sympathetic response to manipulation.
• Rate vs pressure. rate is the lever in MS: slowing rate lengthens diastolic filling and often fixes the pressure; pure vasoconstriction without rate control leaves the gradient problem.
• 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.

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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.

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• Priorities. 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.

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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.

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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.

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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.

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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 learner 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.

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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.

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• 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.

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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.

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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.

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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.

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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.

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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.

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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.

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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 learner 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.

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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.

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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.

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• 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.

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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 with aspiration, ultrasound, test dose, lowest effective dose.

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• 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.

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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.

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• Drivers. 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.

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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.

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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 learner 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.

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• 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.

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• 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.

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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.

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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.

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• 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.

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• Future pregnancy. high maternal mortality; strong recommendation against future pregnancy is standard; defer specifics to cardiology and OB; the learner 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.

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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.
• 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.

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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.

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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.

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• Before saying yes. 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 learner 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.

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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 learner 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. potentiates and prolongs non-depolarizing block (reduce roc dose, monitor reversal — residual weakness risk); succinylcholine is not significantly potentiated.
• Patient preference. respect the conversation, explain the safety reasoning, share the plan; an authoritative override without conversation is a flag.

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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.

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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.

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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.

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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.

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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 learner 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.

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• Priorities. ABCs already secure (intubated); stop seizure, exclude reversible causes, image when stable.
• DDx of seizure. postpartum eclampsia, intracranial hemorrhage, CVST, metabolic (hypoglycemia, hyponatremia), hepatic encephalopathy.
• 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.

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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.

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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.

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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.

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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.

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• Drivers. 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. Learner 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.

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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 learner 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 learner'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.

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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.

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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 learner'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 learner 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.

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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.

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• Priorities. ABCs, left lateral position if still pregnant (not here), protect from injury, oxygen, IV access if not present, call for help.
• DDx. 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.
• 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.

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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.

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• Offer or not. a defensible commit either way; the trajectory matters as much as the absolute number. A learner 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.

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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 learner 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.

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• 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.

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• 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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.
• Time budget. rapidity of fetal deterioration governs how long you have; brittle FHR forces the move.

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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.

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• 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.

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• Surgical option input. the learner 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.

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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 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.

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• 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.

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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.

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• Drivers. 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.

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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.

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• 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.

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• 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.

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• 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.

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• 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.

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• 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.

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• 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.

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• 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 learner 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.

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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.

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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 succinylcholine; treat hypoxic bradycardia.
• Sux. small IV dose; IM if no IV; atropine ready.
• Parents. plain explanation, timing for future elective anesthesia.

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• 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.

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• Drivers. 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.

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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, a rising 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.

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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.

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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.

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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.

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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.

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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.

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• Input. learner 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.

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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.

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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.

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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.

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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.

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• Drivers. 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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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• DDx. ischemic stroke, hemorrhagic stroke, intracranial event from preeclampsia, peripheral neurologic injury.
• Most concerning. postpartum stroke in SCD is real and missed when subtle.
• 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 learner supports hematology and OB.
• Documentation. anesthesia summary, transfusion history, antibody status, prior crisis triggers, pain regimen.

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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.

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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.

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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.

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• Technique choice. spinal or caudal without sedation reduces early postoperative apnea and avoids instrumenting reactive lungs; general with a secured airway gives control if a block fails or the case runs long. Want a committed choice tied to his prematurity and lungs, not a list.
• Spinal, unsedated. the apnea-sparing benefit is lost the moment sedation is added; a swaddled, calm infant and a short case are prerequisites. Adding midazolam 'to keep him still' and still claiming apnea protection is worth challenging.
• Agent, dose, high block. infant spinal uses a weight-based dose of bupivacaine or tetracaine with a short duration; a high or total spinal shows as apnea, bradycardia, or a limp poorly perfused infant rather than a complaint — watch respiration and tone.
• URI, proceed or postpone. copious secretions, fever, or lower-airway signs argue for delay; clear rhinorrhea without fever in a child at incarceration risk may still proceed with heightened vigilance. Reasoning should weigh reactivity against hernia urgency, not reflexively cancel or proceed.
• Bronchospasm on induction. deepen anesthesia, 100% oxygen, hand-ventilate, inhaled beta-agonist; exclude obstruction, breath-stacking, or a mainstem problem. Reaching for a relaxant before deepening is worth a probe.

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• Ventilation targets. gentle lung-protective ventilation with modest tidal volumes and enough expiratory time in obstructive lungs; permissive mild hypercapnia is acceptable. Ventilating to a normal CO2 at high pressures is the wrong direction.
• Peak pressure ceiling. keep pressure as low as gas exchange allows; a rising pressure should prompt a search, not simply more pressure.
• Oxygen target. aim for an SpO2 in the low-to-mid 90s rather than 100%; there is no benefit to hyperoxia and reasons to avoid it. Running 100% 'to be safe' should be challenged to justify.
• Fluid and glucose. a weight-based maintenance rate of a balanced, dextrose-containing solution for an infant this size; check glucose because ex-premies are prone to hypoglycemia. Ignoring glucose is a common miss.
• Temperature. a high surface-area-to-mass ratio means rapid heat loss; forced-air warming, a warm room, warmed fluids, and active monitoring. Name a target, not just 'keep him warm.'

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• DDx. bronchospasm, mainstem migration or tube kink/obstruction, secretions or a plug, breath-stacking/auto-PEEP, laryngospasm around a supraglottic device, pneumothorax, or a circuit problem.
• Most likely. in this reactive-airway infant with worsening wheeze and rising pressures, bronchospasm leads; keep the differential open.
• First moves. hand-ventilate to feel compliance, 100% oxygen, deepen anesthesia, then treat the cause; escalate methodically.
• Albuterol through the circuit. a metered-dose inhaler into the circuit, many puffs, as most drug is lost in the tubing; expecting a normal ward dose to reach the lungs misunderstands circuit delivery.
• Bradycardia in the infant. a heart rate falling toward 90 in this age group is hypoxia until proven otherwise — oxygenate and ventilate first; epinephrine for persistent hypoxic bradycardia, and chest compressions if the rate stays below 60 despite oxygenation. Chasing the rhythm before fixing oxygenation is dangerous.
• Tube as the problem. persistence despite deepening and bronchodilator should raise malposition, kinking, or plugging; pass a suction catheter and reconfirm position.

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• Regional vs opioid. a caudal or ilioinguinal block gives good somatic analgesia and spares opioid in an apnea-prone infant; systemic opioid adds respiratory-depression and apnea risk. The opioid cost should drive the reasoning.
• Caudal agent and volume. a weight-based volume of dilute bupivacaine or ropivacaine reaches the low-thoracic-to-upper-lumbar dermatomes (about T12-L1) needed for the inguinal incision; concentration is chosen for analgesia, not dense motor block.
• Maximum local and staying under. the block plus any surgeon infiltration must stay under the weight-based maximum (each agent has a set mg/kg ceiling); not counting the surgeon's local is a real miss.
• Test dose / intravascular. an epinephrine-containing test dose and incremental injection with aspiration; a rise in heart rate or blood pressure or an ECG change suggests intravascular placement. Injecting the full dose in one pass is worth challenging.
• Patchy block / systemic fallback. supplement with multimodal non-opioid analgesia; if opioid is used, small titrated doses with apnea monitoring and planned postoperative observation.

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• Deep vs awake. awake extubation with returned reflexes protects against aspiration and a reactive airway but coughing can trigger spasm; deep extubation reduces stimulation but leaves the airway unprotected. Either is defensible if the prerequisites are met and stated.
• Before extubation. adequate reversal and spontaneous ventilation, regular respiration, appropriate tone and gas exchange, suctioned airway.
• Laryngospasm recognition. stridor progressing to silence with a still chest is laryngospasm until proven otherwise; also consider obstruction, bronchospasm, and central apnea.
• Maneuvers in order. remove the stimulus, 100% oxygen, jaw thrust with continuous positive pressure (Larson's maneuver), deepen if feasible; escalate if it fails.
• Bradycardia and succinylcholine. a falling heart rate with desaturation demands breaking the spasm — a weight-based IV dose of succinylcholine, or intramuscular/intraosseous without an IV, with atropine ready in the young child. Delaying paralysis while he desaturates and slows is the error.
• Pink froth. negative-pressure (post-obstructive) pulmonary edema after forceful inspiration against a closed glottis; supportive oxygen and positive pressure, usually self-limited. Reflex diuresis is rarely the main treatment.

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• Concern / why him. former prematurity with a low postmenstrual age is the dominant risk factor for postoperative apnea; anemia and a general anesthetic add to it. Recognizing that this baby is high-risk is the point.
• Central/obstructive/mixed. postanesthetic apnea in ex-premies is commonly mixed; the distinction guides whether positioning/airway support or respiratory drive is the lever.
• Workup. look for hypoxemia, hypoglycemia, anemia, temperature instability, and residual anesthetic/opioid effect before attributing it to apnea of prematurity.
• Caffeine. IV caffeine reduces postoperative apnea in at-risk infants and is reasonable; a defensible weight-based dose, not a guess.
• Spinal vs general. an unsedated spinal lowers early apnea risk but does not eliminate late apnea; the infant needs monitoring regardless of technique. Claiming a spinal makes monitoring unnecessary is wrong.
• Monitoring duration. admit and monitor until an adequate apnea-free interval (commonly at least 12 hours free of events); day-surgery discharge is unsafe here.

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• Anemia and apnea. anemia is associated with apnea in ex-premies; correcting it can reduce spells, though it is one factor among several.
• Transfuse or not. a defended decision weighing symptomatic apnea and the hemoglobin against transfusion risk; either transfusing a symptomatic anemic ex-premie or optimizing other factors first can be defensible if reasoned.
• Threshold vs adult trigger. infant and ex-premie thresholds are higher and symptom-driven, not the adult 7 g/dL number; tie the decision to his apnea, not a reflex value.
• Volume and rate. a weight-based aliquot of packed cells given slowly, mindful of circulatory overload in a small infant.
• Watching for. volume overload, electrolyte and glucose shifts, and reaction; reassess apnea frequency afterward.
• If holding off. caffeine, temperature and glucose control, positioning, and continued monitoring.

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• Now what. support airway and breathing, escalate monitoring, and reassess the cause; a spell needing stimulation and bag-mask marks ongoing high risk.
• Disposition. a monitored setting with apnea monitoring and staff able to intervene — step-down or ICU depending on frequency and severity; the regular floor is inadequate after a stimulated event.
• Reintubation threshold. recurrent apnea unresponsive to caffeine and support, rising CO2 with exhaustion, or inability to protect gas exchange.
• Reactive lungs. coexisting wheeze worsens the work of breathing and the apnea picture; bronchodilators and gentle support help.
• High-flow / CPAP. nasal CPAP or high-flow can splint the airway and support mixed or obstructive apnea, a reasonable step short of reintubation.

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• Recommendation and how to put it. admit for monitored observation; explain plainly why an apparently minor operation still needs an overnight stay in this specific baby.
• Conveying risk. honest, calm, and specific — what apnea is, why his history raises the risk, and what monitoring will catch — without alarming language.
• They insist on leaving. keep the child safe first: reiterate the recommendation, involve the surgeon and pediatrician, document, and escalate rather than discharge against a clear safety concern; this is a patient-safety, not a bargaining, matter.
• Safe to discharge. after an adequate apnea-free interval on monitoring, with stable feeding and no events.
• Who else. the surgeon and pediatric or primary team, so the family hears one consistent message.
• Next anesthetic. flag the apnea history and prematurity for future planning — timing, technique, and postoperative monitoring.

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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; 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 considering less invasive blocks.

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• DDx. amniotic fluid embolism, eclampsia, high or 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, unchanged drug doses and defibrillation energy, anticipate a difficult airway and rapid desaturation.
• Perimortem cesarean. consider delivery within about four minutes of arrest to aid maternal resuscitation; indefinitely delaying it is worth probing.
• Coagulopathy. DIC is common with AFE; treat with goal-directed product replacement and fibrinogen, reassessing with point-of-care testing.

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• Interpretation. ARDS physiology — the learner should derive a PaO2/FiO2 of 58, placing it in the severe range, with a plateau above target.
• Tidal volume. 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 pressure. keep plateau at or below ~30 cm H2O; 32 is above target and the learner 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.

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• Driving the options. her anticoagulation, aortic stenosis, OSA, and analgesic goals all bear on neuraxial-versus-general and which blocks; want the salient ones surfaced, not a generic recital.
• Neuraxial on apixaban. with a documented adequate hold and normal renal function, neuraxial is reasonable; the learner must know the interval rather than react to the word 'apixaban.'
• Interval / does three days satisfy. roughly three days (about 72 hours) off apixaban with normal renal function is the commonly cited neuraxial interval; a learner who wants far longer or far shorter should justify it.
• If creatinine were 2.0. impaired clearance prolongs the DOAC effect and lengthens the required hold; recognizing renal dependence is the teaching point.
• If hold inadequate. general anesthesia with peripheral/fascial blocks, or postpone an elective case; proceeding to neuraxial on an inadequate hold is the error.
• Peripheral blocks under residual DOAC. superficial, compressible blocks (adductor canal) are lower-risk; deep, non-compressible blocks carry bleeding risk closer to neuraxial. A blanket 'blocks are always fine' deserves a probe.

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• Single-shot spinal in moderate AS. acceptable with careful titration in moderate stenosis; the concern is an abrupt sympathectomy dropping preload and coronary perfusion. Reflexively refusing all neuraxial in moderate AS, or ignoring the risk, are both worth challenging.
• Hemodynamic goals. maintain preload and afterload, avoid tachycardia, preserve coronary perfusion pressure for the hypertrophied ventricle.
• Preload / rate / rhythm. full, not fast, and in a controlled rhythm; her atrial fibrillation complicates rhythm goals and rate control matters.
• Blunting the sympathectomy. consider an incremental or catheter-based technique, co-loading and vasopressor readiness rather than a large single-shot dose.
• Phenylephrine vs ephedrine. phenylephrine restores afterload and coronary perfusion without tachycardia and is often preferred in AS; ephedrine's chronotropy can be unhelpful. Expect a reasoned choice.
• Severe vs moderate. severe symptomatic AS materially raises single-shot spinal risk and shifts many toward a carefully controlled general or a slow neuraxial; the distinction should change the plan.

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• Which way it pushes. toward opioid-sparing regional and multimodal analgesia to protect a CPAP-dependent, obese airway and respiratory drive.
• Sedation in OSA. sedatives compound obstruction and blunt arousal; minimize and monitor. An unmonitored sedation plan is a flag.
• How far regional gets you. neuraxial plus a peripheral block can make a knee replacement nearly opioid-free intraoperatively and well into recovery.
• Failed block / conversion airway. obesity and Mallampati III predict a potentially difficult mask and intubation; have a plan and positioning ready before converting.
• Postop CPAP. resume her home CPAP early in recovery; opioids and residual block change her risk, so monitoring continues.

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• How they shape the plan. chronic tramadol implies some tolerance and a serotonergic, seizure-threshold-lowering drug; prior severe PONV and opioid sedation argue hard for opioid-sparing and aggressive antiemesis.
• Continue tramadol. reasonable to continue to avoid withdrawal or rebound, while accounting for its interactions; abruptly stopping or ignoring it are both worth discussing.
• Interactions to worry about. serotonergic combinations (other serotonergics, certain antidepressants) risk serotonin toxicity, and tramadol lowers the seizure threshold.
• PONV regimen. multimodal prophylaxis from several drug classes, regional to cut opioid, and avoiding known triggers given a strong prior history.
• Opioid use and blocks. tolerance may raise rescue-opioid needs and strengthens the case for dense regional analgesia; it does not by itself change block safety.

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• Spinal agent / dose in AS. a controlled dose of hyperbaric or isobaric bupivacaine matched to a roughly ninety-minute case; avoid an oversized dose that produces a rapid, high sympathectomy in a stenotic valve.
• Adductor canal vs femoral. adductor canal preserves quadriceps strength for early mobilization while covering the knee; femoral gives denser analgesia but more motor block and fall risk. Commit and defend.
• Motor-sparing. quadriceps strength supports early, safe ambulation and reduces fall risk after TKA — relevant to her recovery.
• IPACK. covers the posterior capsule that an adductor canal block misses, improving analgesia without added motor block.
• Total local under toxic dose. sum spinal plus block local and keep under weight-based maxima, diluting or reducing volumes as needed. Not tallying the total is a real error.
• Aspirate / test. incremental injection with aspiration and ultrasound to avoid intravascular placement and reduce LAST risk.

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• Concern in her particularly. hypotension threatens coronary perfusion of a hypertrophied, stenotic ventricle; she tolerates it poorly.
• Why. the spinal sympathectomy drops afterload and preload while her fixed valve limits compensatory output.
• DDx. sympathectomy from the spinal, hypovolemia, bradycardia-related low output, a vasovagal component, and less likely early ischemia or an embolic event.
• First moves. a vasopressor to restore afterload, fluid as tolerated, leg elevation, and treating bradycardia; keep her full and in rhythm.
• Phenylephrine / fluid sequence. phenylephrine promptly for afterload in AS, with judicious fluid; over-aggressive fluid in a stiff ventricle can backfire.
• AS and how hard to push. restore perfusion pressure early and decisively because she has little reserve, while avoiding tachycardia and volume overload.

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• Hemodynamic change. tourniquet inflation raises afterload and can increase blood pressure; exsanguinating a large limb adds some central volume.
• Bearing on this patient. the added afterload and any tachycardia are unwelcome in AS and hypertension; watch for ischemia.
• Failed block vs tourniquet pain. tourniquet pain is a dull, building discomfort with rising HR and BP after roughly 45 to 60 minutes even with a working surgical block; distinguish it from an inadequate block by timing and character.
• Rx. deepen sedation cautiously given her OSA, treat hypertension, and communicate with the surgeon about tourniquet time; definitive relief is deflation.
• Anticipate deflation. expect a fall in blood pressure, a metabolic washout with a transient rise in EtCO2, potassium, and lactate, and be ready with vasopressor and ventilation.

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• DDx. bone cement implantation syndrome or embolism (fat, marrow, cement), pulmonary embolism, anaphylaxis, and hemorrhage; the timing with cementing and reduction points strongly to embolic BCIS.
• Most likely. bone cement implantation syndrome at cementing/impaction — hypoxia, hypotension, and a falling EtCO2 from an acute rise in dead space and pulmonary vascular resistance.
• Immediate Rx. 100% oxygen, support blood pressure with vasopressors, fluids as tolerated, inform the surgeon, and resuscitate.
• Differs from spinal hypotension. the falling EtCO2 and hypoxemia signal an embolic/obstructive process, not a pure vasodilatory drop; treatment leans harder on oxygenation and right-ventricular support.
• Arrest specifics. consider the obstructive/embolic cause during ACLS — right-ventricular support, and advanced measures in refractory cases; treat the cause, not just the rhythm.

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• Multimodal orders. scheduled acetaminophen and an NSAID if appropriate, the peripheral block or catheter, limited rescue opioid, antiemetics, and continued CPAP with monitoring.
• Catheter for and against. a continuous adductor canal catheter extends motor-sparing analgesia and reduces opioid — helpful in OSA; against are catheter management, LAST vigilance, and cumulative-dose limits. A reasoned weigh-up, not a reflex.
• Circumoral tingling interpretation. early local anesthetic systemic toxicity from cumulative block or infusion dosing until proven otherwise.
• Rx. stop the local, oxygen, monitor, and have lipid emulsion ready; treat progression per protocol. Dismissing early neurologic symptoms is the danger.
• What to tell her / team. name the concern plainly, the monitoring plan, and which symptoms should prompt a call; align the floor team.

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• Concerns. a bleeding, hypovolemic child with a contaminated airway and a swallowed blood load; visible bleeding underestimates true loss.
• Why challenging. aspiration risk, a blood-obscured view, hypovolemia that induction agents 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, a reduced induction-agent dose for hypovolemia, head-down or lateral positioning for blood, readiness for a difficult view; over-dosing the induction agent in a hypovolemic child is a flag.
• Lost view. large-bore suction, optimize position and external manipulation, consider a smaller styletted tube or video laryngoscopy, call for help early, and keep a surgical-airway backup in mind.
• Communication. convey the emergent nature plainly to surgeon and family and align on the plan and risks.

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• DDx. malignant hyperthermia, thyroid storm, sepsis, inadequate anesthesia/analgesia, pheochromocytoma, and rebreathing/hypercapnia; volatile exposure with rigidity and a climbing CO2 points to MH.
• Leading diagnosis. MH — an unexplained rising EtCO2 despite increased ventilation, tachycardia, masseter and generalized rigidity, and hyperthermia after a triggering agent.
• Immediate priorities. stop the trigger, call for help and the MH cart, hyperventilate with 100% oxygen, give dantrolene, and begin cooling; conclude surgery as soon as feasible.
• Dantrolene. a weight-based initial dose repeated until control, reconstituting each vial (the older formulation needs many vials, the newer concentrated form fewer).
• Besides dantrolene. active cooling, treat hyperkalemia and arrhythmias, manage acidosis, promote urine output and watch for rhabdomyolysis, and monitor for recrudescence.
• Hyperkalemia with peaked T waves. calcium to stabilize the membrane, insulin with glucose and a beta-agonist to shift potassium, and further measures; treat promptly as it can be life-threatening.
• Counseling. explain the episode, provide MH documentation and referral for testing, advise trigger avoidance, and note that first-degree relatives may be susceptible.

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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, and plan airway management if inhalation injury is suspected.

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• Handoff. structured handoff before the team leaves (course, hemodynamics, vent, labs, drains, abx, anticoag), then own bedside check (ETT, breath sounds, perfusion, abdomen, drains, UOP, access).
• First priorities. 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.

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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.

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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.

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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).

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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?'

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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.

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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.'

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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.

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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.

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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. small epinephrine boluses (≤1 mcg/kg), avoid vasopressin, avoid lidocaine/procainamide (amiodarone for ventricular arrhythmias), prolonged CPR, early ECMO for refractory arrest.
• Lipid. 20% lipid emulsion 1.5 mL/kg bolus (~100 mL) over 2-3 min, then 0.25 mL/kg/min; repeat bolus and double infusion for persistent instability; cap ~12 mL/kg.
• Prevention. incremental injection with aspiration, ultrasound, test dose, lowest effective dose.

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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.

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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.

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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.

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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 both femoral sheaths are in; pre-staged arterial and venous access for exactly this collapse.
• End point / waking. name resuscitation targets; recognize that aborting and waking the patient is a legitimate, sometimes correct, choice.

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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.

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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.

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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.

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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.

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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.

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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 with hypocalcemia, AKI; hydration, monitoring, allopurinol or rasburicase.
• Disposition. ICU given the airway and metabolic risk; keep reliable access and arterial monitoring; hand off clear targets.

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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.

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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.

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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.

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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.

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• 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; learner 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 him exhale is worth probing.

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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.

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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; learner 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.

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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; learner 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.

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• 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.

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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.

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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.

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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.

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• 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.

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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, get lipid emulsion.
• ACLS mods. lipid emulsion, reduce epinephrine dosing, avoid certain antiarrhythmics, anticipate prolonged resuscitation, consider bypass for refractory arrest.
• Lipid emulsion. 20% lipid emulsion 1.5 mL/kg bolus over ~1 min, then 0.25 mL/kg/min infusion; repeat bolus and double the rate for persistent arrest — a specific therapy, not an afterthought.
• Prevention. incremental injection with aspiration, ultrasound, a test dose, lowest effective dose.

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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.

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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.