Gray Matter

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• Now, not the afternoon. flail segment plus contusion plus a PaCO2 of 54 in a COPD patient is a respiratory emergency in slow motion; analgesia here is a pulmonary intervention, not comfort care. Triaging this as routine is a flag.
• Bedside measures. respiratory rate and effort, SpO2, serial PaCO2, cough strength and secretion clearance, and an inspiratory or vital-capacity effort; the CO2 trend is the one that predicts intubation.
• Cost of splinting. atelectasis and retained secretions within hours, then hypoxemia and pneumonia; it is a reason to escalate analgesia, not to sedate.
• Both at once. under-analgesed and over-sedated simultaneously is the signature of failing opioid monotherapy. The trap is reading the drowsiness as adequate treatment.
• Trajectory. progressive hypoventilation, hypercarbia, and atelectasis with intubation likely inside a day if he cannot breathe deeply and cough.

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• DDx. pain-limited splinting, contusion shunt, flail mechanics, opioid-induced hypoventilation, and COPD with baseline CO2 retention; several are operating at once.
• Separating them. response to analgesia and to a block, drug timing versus the ABG trend, exam of the flail segment, and serial gases; a CO2 that falls with effective analgesia identifies the pain-limited component.
• NIV now. yes, if he can protect his airway and cooperate; it buys hours while analgesia is established. NIV is a bridge, not the analgesic plan, and using it as a substitute for a block is the error.
• 58 is not success. the direction is right but he is still hypercarbic on support; escalate analgesia and get the block in rather than settle.
• Worsening mentation. delirium threatens airway protection and NIV tolerance; it lowers the threshold for intubation rather than justifying more NIV.
• To the ICU. rising PaCO2 despite support, falling pH, fatigue, failure to clear secretions, or deteriorating mental status.

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• Doubling the opioid. no; more opioid deepens hypoventilation and sedation without reliably covering movement and cough pain. Escalating opioid into a rising CO2 is the central error of this case.
• PCA. PCA requires an awake patient who can self-titrate; drowsiness plus baseline cognitive impairment makes an unmonitored PCA unsafe here. A nurse- or family-controlled substitute is worse.
• Monitoring. sedation score and respiratory rate hourly with continuous pulse oximetry and capnography; sedation precedes respiratory depression, so the sedation score is the early warning.
• RR 9. stimulate, oxygen, support ventilation, hold further opioid, and get the regional plan moving now.
• Naloxone. reserve it for a patient you cannot rouse or ventilate; 40 mcg IV increments titrated to respiration, not to consciousness. A full 400 mcg dose restores his 8/10 pain instantly, drives catecholamines in a 72-year-old, and wears off before the hydromorphone does.
• What carries analgesia. a regional technique plus scheduled non-opioids and ketamine; the plan has to move off systemic opioid, not up the dose.

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• Epidural tonight. no; apixaban dosed roughly 36 hours ago with stage-3 CKD plus prophylactic heparin the same evening puts him inside the interval for a deep neuraxial technique, and epidural hematoma in an anticoagulated 72-year-old is the complication that ends the case.
• Which of the three. erector spinae plane catheter — a superficial, compressible fascial-plane block, the one technique that is defensible tonight. Paravertebral is deep and non-compressible and belongs with the epidural on the no list.
• Intervals. apixaban 72 hours before neuraxial placement in this renal function per ASRA, and 4-6 hours after a prophylactic heparin dose; the point is that the numbers do not line up before tomorrow at the earliest.
• Cost of waiting. two to three more days of splinting is how he earns an intubation; the technique that can be done now beats the better technique that cannot.
• Restarting apixaban. not tonight if you intend to run a catheter and reassess; hold it, use a shorter-acting agent if his stroke risk demands bridging, and time removal of the catheter to trough. Restarting a DOAC with a fresh catheter in place and no plan for removal is the miss.

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• Level and side. right side, transverse process around T5 for fractures of ribs 4-10; a mid-span level lets spread cover the segments above and below.
• Catheter, not single shot. seven fractures need days of analgesia; a single injection buys hours and leaves him splinting again by morning.
• Bolus. 20-30 mL of ropivacaine 0.25-0.5% (or bupivacaine 0.25%); volume is what produces craniocaudal spread in a fascial plane, so do not under-volume it.
• Infusion. ropivacaine 0.2% at 6-10 mL/h, or programmed intermittent boluses of 15-20 mL every 4 hours, which spread better than a continuous trickle.
• Ceiling. keep continuous ropivacaine near or below roughly 0.4-0.5 mg/kg/h and lower it here: age, a 30-hour horizon of accumulation, and stage-3 CKD that clears ropivacaine's active metabolite PPX poorly. The parent drug is hepatically cleared; the metabolite is the renal problem.
• Better at rest, not with cough. expected early - assess spread and dermatomal effect, check the catheter and the volume delivered, and add to the regimen rather than declaring failure. Pulling a working fascial-plane catheter at 30 minutes is the trap.
• Working. keep it, layer the non-opioids on, and hold him at a dose that lets him cough; the endpoint is cough and vital capacity, not the resting pain score.

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• Acetaminophen. 1 g every 6 hours scheduled, capped at 3-4 g/day; a low-risk backbone and it should be scheduled, not PRN.
• Ketorolac. avoid at eGFR in the stage-3 range in a 72-year-old with acute trauma and a hematoma risk; a reflexive NSAID here is a flag. If an NSAID is used at all, it is a short, low-dose course with an explicit risk statement.
• Ketamine. 0.1-0.2 mg/kg/h, opioid-sparing and useful for movement pain; stop or halve it for dysphoria, hallucinations, or worsening delirium in a man with baseline cognitive impairment.
• Gabapentinoid. 300 mg TID is too much too fast for a 72-year-old with CKD and drowsiness; sedation and respiratory depression stack with opioid. If used, a low dose (100 mg at night) and renal adjustment.
• Breakthrough opioid. avoid morphine - the renally-cleared active metabolites M3G and M6G accumulate at his creatinine and cause exactly the delayed sedation you are trying to prevent. Hydromorphone or oxycodone in small doses, monitored.
• Lidocaine plus a catheter. no; systemic lidocaine on top of a continuous ropivacaine infusion stacks amide load toward toxicity with no way to attribute the resulting symptoms. This is the beat that separates additive thinking from arithmetic.

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• Driver. pain is better while CO2 climbs, so this is not analgesic failure - it is residual opioid plus COPD plus fatigue outpacing the benefit, in a man whose flail segment still costs him work of breathing.
• Telling them apart. drug timing against the gas trend, sedation score, block assessment (is he actually covered?), and secretion burden; an effective block with a rising CO2 points away from pain as the cause.
• Rx now. stop systemic opioid, optimize the block, suction and recruit, treat the COPD component, and escalate support while you reassess.
• Intubate. pH 7.24 with obtundation on NIV is a failing trial; intubate rather than watch. Continuing NIV requires an improving pH, a protected airway, and a cooperative patient - he has none of the three.
• Catheter and ketamine. both continue - the catheter reduces sedative and opioid requirement and is what will let you wean him later; stopping regional analgesia because he is intubated is the classic misstep.
• Sedation. dexmedetomidine or propofol with the catheter carrying analgesia; avoid benzodiazepines in a man with baseline cognitive impairment.

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• Dx. local anesthetic systemic toxicity, neurologic prodrome - perioral numbness, metallic taste, and confusion in a man with a running amide infusion.
• Why now. cumulative absorption over 30 hours of continuous infusion. Ropivacaine's parent compound is hepatically cleared, but its active metabolite PPX is renally excreted and accumulates in stage-3 CKD; his acidemia reduces protein binding and lowers the seizure threshold. Blaming a single bolus misses the accumulation.
• Rx now. stop the infusion, 100% oxygen, monitor, get the lipid emulsion to the bedside, and call for help before he progresses.
• Seizure. midazolam 2-4 mg IV (or a small propofol dose only if hemodynamically stable); control ventilation, because hypercarbia and acidosis worsen toxicity.
• Lipid emulsion. give it now, at the seizure - do not wait for cardiovascular collapse. 20% emulsion 1.5 mL/kg (about 100 mL) over 2-3 min, then 0.25 mL/kg/min, redosing the bolus for persistent instability, with a total ceiling around 12 mL/kg.
• Restarting. restart only after symptoms clear, at a lower concentration and a lower hourly dose, with a written cumulative cap that accounts for his renal function; the original miss was dosing him as if he had normal clearance.

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• Order of weaning. overlap effective oral multimodal analgesia first, then remove the catheter, then taper systemic opioid. Pulling the catheter while he is still opioid-dependent for cough is how the rebound happens.
• Oral regimen. scheduled acetaminophen 1 g q6h, low-dose oxycodone 5 mg q4-6h PRN, and a taper plan; no NSAID at his renal function, no morphine, gabapentinoid only if already tolerated.
• Days of opioid. a short, defined course - roughly 3-5 days with no automatic refill - plus a written taper; rib fracture pain lasts weeks but the opioid should not.
• Rebound at two hours. re-treat now: analgesic bolus, reassess whether he needs the catheter replaced, resume incentive spirometry and coughing. A patient who stops coughing is going backward, not simply uncomfortable.
• Sign-off criteria. pain controlled on oral medication, adequate cough and spirometry, stable gas exchange off support, and a documented taper with a threshold to call back.

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• Goals. full, fast, and forward - preserve preload, keep the rate around 80-100 to shorten diastole and cut regurgitant time, and keep SVR low so forward flow wins over the leak. A plan built on slowing him down or squeezing the SVR up runs directly against this lesion.
• BP 88/38 with HR 46. the bradycardia is the problem, not just the number - a long diastole is more time for the ventricle to fill backwards through an incompetent valve. Treat the rate.
• Phenylephrine. no as the reflex first move - raising SVR increases the diastolic gradient driving regurgitation and the reflex bradycardia compounds it. It is not absolutely forbidden, but reaching for it first in AR deserves a probe.
• What instead. ephedrine 5-10 mg or glycopyrrolate 0.2-0.4 mg for chronotropy, epinephrine 10-20 mcg if he needs inotropy with rate, plus volume; target a rate near 90 and an adequate diastolic, not a systolic number.
• 96/42 at 85. better - the rate is doing the work. A low diastolic is expected in severe AR and chasing it with alpha-agonism undoes the gain; judge him by forward flow and rhythm, not by the diastolic alone.
• HR 118 with ST depression. he has overshot - 118 shortens filling and perfusion of a hypertrophied wall with a low diastolic pressure. Deepen anesthesia for the stimulus, back the chronotropy off toward 90, and treat the ischemia; the trade was regurgitant fraction for coronary perfusion time and it has gone too far.

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• Why it distends. an incompetent aortic valve means root pressure fills the LV in diastole; on the arrested heart, antegrade root cardioplegia crosses the valve straight into the ventricle instead of down the coronaries, and bronchial return adds to it.
• What distension costs. wall tension rises, subendocardial perfusion falls, and the cardioplegia never reaches the myocardium - so the ventricle is both stretched and unprotected. In a dilated, eccentrically hypertrophied LV that is the setup for a heart that will not wean.
• Rx now. stop the root dose, vent the LV (aortic root vent or vent via the right superior pulmonary vein), and switch the delivery route; say it to the surgeon immediately rather than watching the TEE.
• Route. retrograde coronary sinus now, direct ostial delivery once the aorta is open; antegrade root delivery in severe AR is the error this probe exists to catch.
• Other protection. keep it decompressed, adequate cooling and repeat doses on schedule, avoid ventricular fibrillation with a distended chamber, watch for aortic insufficiency during rewarming.
• 110-minute clamp. expect a stunned ventricle - have inotrope and pacing ready before the clamp comes off, plan a slow controlled wean with TEE, and anticipate that this LV will need afterload reduction, not just squeeze.

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• DDx. stunned, chronically dilated LV now facing a competent valve; also residual ischemia (coronary air, a compromised ostium after annular work), inadequate protection from the earlier root cardioplegia, RV dysfunction, vasoplegia, or a valve or surgical problem - TEE narrows it.
• More volume. no by reflex - this ventricle has been volume-loaded for years and is already at the flat end of its Starling curve; more preload raises wall tension and worsens function. Fill to TEE, not to a CVP number.
• Inotrope. milrinone 0.25-0.5 mcg/kg/min is well matched here - inodilation unloads an afterload-sensitive dilated ventricle - paired with low-dose epinephrine 0.03-0.06 mcg/kg/min or norepinephrine to hold perfusion pressure against the vasodilation. Pure alpha-agonism to chase the pressure works against forward flow.
• Targets. CI above roughly 2.2 L/min/m2, MAP 65-75, SvO2 above 60%, and a decompressed, better-contracting LV on TEE - a number, not 'more epi'.
• Still distended at MAP 75. he is not unloading - reduce afterload, confirm rate and rhythm (pace to 90 with AV synchrony), vent and decompress, and re-examine the valve and coronaries on TEE. Escalating inotrope into a distending ventricle is the trap.
• IABP. yes, defensible now - diastolic augmentation plus afterload reduction is exactly what this LV-predominant low-output state needs, and the AR that would have contraindicated a balloon has just been replaced. Tie the commit to mechanical unloading, not reflex.

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• First minute. pace - epicardial wires or transcutaneous pads while wires go on; chronotropic drugs (isoproterenol, epinephrine) buy seconds but pacing is the treatment. Perfusion pressure support in parallel.
• Why blocked. the AV node and bundle of His sit immediately beneath the non-coronary and right coronary cusps; annular debridement of a calcified bicuspid valve and suture placement injure them. His pre-existing first-degree block marks conduction that had no reserve.
• Mode and rate. atrial and ventricular wires, DDD pacing at 90 - this dilated, dysfunctional ventricle still needs the atrial contribution and a forward-favoring rate. Settling for VVI here throws away filling he cannot spare.
• Loss of capture. lead dislodgement or poor epicardial contact, rising threshold from edema, output set below threshold, connection or generator problem, hyperkalemia or acidosis, or a drug effect. Check connections and polarity, turn the output up, confirm capture, verify sensing, send a potassium.
• Rising threshold. edema or ischemia at the lead-myocardium interface; keep output at least 2-3 times threshold, keep pads on him, and do not rely on epicardial wires alone for a pacing-dependent patient overnight.

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• Why worse now. for years the LV ejected a huge total stroke volume, most of it regurgitating back at low resistance; the competent prosthesis has abolished that low-impedance escape route, so the ventricle now has to move its whole output forward against systemic afterload. Its declining function is unmasked, not new. Recognizing this as predictable physiology is the judgment.
• Before more epinephrine. optimize rate and rhythm (pace 90, AV synchrony), reduce afterload, correct calcium, potassium, and acidosis, and confirm there is no tamponade or valve problem. Piling catecholamine onto an afterload-sensitive dilated ventricle raises demand and arrhythmia risk without moving forward flow.
• Vasopressin. yes - 1-3 units/h holds perfusion pressure against milrinone-induced vasodilation without adding chronotropy or beta-driven arrhythmia, and it does not raise PVR the way high-dose alpha agents can.
• Targets. MAP 65-75, CI above 2.2, SvO2 above 60%, lactate falling; titrate to those, not to 'more support'.
• TEE finding that changes things. a pericardial collection or RV compression (tamponade), new RV failure, a valve or paravalvular problem, or new regional wall-motion abnormality suggesting a coronary problem - each sends you somewhere different from more inotrope.
• Mechanical support. IABP first for LV-predominant low output - it unloads and augments coronary perfusion, and the prosthetic valve now permits it. Impella if he needs true LV unloading and flow; VA-ECMO if the RV fails too or he arrests. Tie the choice to which ventricle is failing.

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• DDx. new AF with loss of atrial contribution on a marginal LV, evolving RV failure with pulmonary hypertension, tamponade, ischemia, electrolyte or volume derangement. AF plus a rising CVP and a distending RV is the pattern.
• Rate versus rhythm. he is unstable - synchronized cardioversion, not titrated rate control. A dilated LV on inotropes at 150 with no atrial kick has no reserve to negotiate with. Treating this as routine post-op AF is a flag.
• Energy. biphasic synchronized 120-200 J (start at 150-200 for AF), with sedation and pads already on him.
• Amiodarone. 150 mg IV over 10 min, then 1 mg/min for 6 h and 0.5 mg/min for 18 h; correct potassium above 4 and magnesium above 2 first.
• RV after conversion. the RV is the problem now - reduce PVR, avoid over-filling it, keep AV synchrony and a rate near 90, support RV contractility with epinephrine or milrinone, and hold coronary perfusion pressure with vasopressin or norepinephrine so the RV keeps its own supply.
• Inhaled vasodilator. inhaled nitric oxide 10-40 ppm or inhaled epoprostenol 10-50 ng/kg/min - selective pulmonary vasodilation without systemic hypotension; watch for a fall in systemic pressure, methemoglobin with prolonged high-dose NO, and rebound pulmonary hypertension if it is stopped abruptly.
• PaCO2 55. yes, change them - hypercarbia and acidosis raise PVR and load the failing RV. Increase minute ventilation toward a normal or low-normal PaCO2 while keeping plateau pressure and PEEP moderate, since high mean airway pressure also raises RV afterload.

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• Mode. switch to VVI or VVIR at 90 - with fibrillating atria, atrial pacing captures nothing and atrial tracking can drive an erratic ventricular rate. Leaving him in DDD while he fibrillates is the miss.
• Timing. start once hemostasis is durably secure - about 30 mL/h of stable output on POD 1 qualifies. Mechanical aortic valve plus AF plus pacing dependence is a high thrombotic burden and waiting days is its own risk.
• Agent. warfarin is mandatory for a mechanical valve - DOACs are contraindicated (RE-ALIGN showed excess thrombosis and bleeding with dabigatran). Start warfarin now and bridge with an infusion of unfractionated heparin, which is titratable and reversible if he bleeds.
• Heparin. no bolus this soon after sternotomy - start an infusion around 12 units/kg/h and titrate to a PTT roughly 1.5-2 times control (or anti-Xa 0.3-0.7), rechecking Hgb and chest tube output.
• INR target. a bileaflet mechanical aortic valve alone targets 2.5 (range 2.0-3.0); with atrial fibrillation as an added risk factor, target 3.0 (range 2.5-3.5), with low-dose aspirin added.
• Before relying on the wires. capture threshold with an output margin of at least 2-3 times, sensing checked, secure connections, a spare generator and fresh battery at the bedside, transcutaneous pads on him, and a defined escalation plan if capture is lost.

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• Stop the trial. stop it - he is failing, and grinding on adds ischemic and fatigue debt. A failed trial is information, not a defeat.
• Lungs or heart. heart. Spontaneous negative-pressure breathing increases venous return and LV afterload at once; a recently failing dilated LV cannot take that load, so filling pressures and PA pressures rise during the trial. Weaning failure after this operation is cardiac until proven otherwise.
• Bedside proof. the rise in PA and filling pressures timed to the trial, new B-lines or edema, a falling SvO2 during the trial, and echo showing worsening MR or LV function under load - a purely pulmonary failure would not track this way.
• Rx. back to support, keep him unloaded (milrinone, afterload reduction), pace at a rate that helps, and treat the volume.
• Furosemide. 40 mg IV (or an infusion at 5-10 mg/h) targeting net negative 1-2 L/day, with filling pressures, oxygenation, and renal function as the end points - not a fixed weight.
• CI falls after diuresis. he has been taken past his preload sweet spot - give back a modest 250-500 mL, reassess on echo, and diurese more slowly. Over-diuresing a dilated ventricle into low output is the mirror-image trap.
• Next trial. when the CI is stable off escalating support, he is closer to even fluid balance, the rhythm and pacing are reliable, and gas exchange and mechanics are adequate; use pressure support with a low PEEP rather than a bare T-piece in a heart-limited patient.

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• Now or wait. post-surgical high-grade block that persists past about 5-7 days rarely recovers; POD 4 in a pacing-dependent patient is the usual window to commit, and there is little to gain from waiting much longer in someone with no reliable escape rhythm. A defended call either way is what is wanted, not a recited criteria list.
• Device. with permanent AF and complete block, a single-chamber ventricular system (VVIR) is appropriate - an atrial lead has nothing to pace. If he is expected to be pacing nearly all the time with an EF of 40-45%, raise conduction-system or biventricular pacing to avoid pacing-induced cardiomyopathy.
• What you tell the family. plainly and without hedging: the valve was replaced successfully, and the electrical wiring of the heart runs right beside where the valve sits, so replacing it injured that wiring; his heartbeat is now being run by the pacing wires and he will need a permanent pacemaker. Say what is known, say what is uncertain, do not assign blame, and leave room for their questions.
• Anticoagulation for the implant. stop the heparin infusion 4-6 hours before implant; a mechanical valve does not permit a long unprotected window, so restart heparin once hemostasis is confirmed. Do not reverse the warfarin with vitamin K in a mechanical-valve patient for an elective device.
• Before he leaves the ICU. a confirmed permanent pacing plan or a reliable temporary system, thresholds and sensing documented with margin, wires secured and labeled, pads available, anticoagulation plan written, and the team aware he has no escape rhythm.

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• Goals. sinus rhythm, a rate around 60-80, generous preload for a stiff ventricle, and high-normal SVR to hold coronary driving pressure. A fixed obstruction tolerates neither hypotension nor a fast, poorly filled ventricle; a big propofol bolus that drops SVR is worth challenging.
• 78/44 with ST depression. subendocardial ischemia of a hypertrophied LV - restore aortic diastolic pressure now. Phenylephrine 100-200 mcg, or norepinephrine 4-8 mcg, or vasopressin 1-2 units; volume follows, because volume takes minutes and this ischemia is happening now. Reaching first for an inotrope or chronotrope here is a red flag.
• Coronary perfusion. coronary perfusion pressure is aortic diastolic minus LV end-diastolic pressure. LVH and diastolic dysfunction raise the LVEDP, so the gradient is already narrow, and a low diastolic closes it. This ventricle is supply-dependent.
• HR 108. deepen anesthesia for the stimulus, correct hypovolemia, and treat the rate (esmolol 10-20 mg cautiously if she remains hypertensive and tachycardic). Tachycardia raises demand and shortens diastole, cutting both filling of a stiff ventricle and coronary perfusion time - doubly harmful.
• Rising PA pressure and CVP. this is the stiff LV failing to accept the volume it has already been given - more fluid will make it worse. Slow the rate, restore sinus function and perfusion pressure, check for ischemia and MR on TEE, and reassess before another bolus.

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• Why this matters here. a hypertrophied, non-compliant LV takes up to 40% of its filling from atrial contraction; losing the kick at 142 collapses stroke volume and coronary perfusion at once. Treating this as routine AF is a flag.
• Cardioversion. she is unstable in a fixed-obstruction lesion - synchronized cardioversion, not a titrated drug. Rate-controlling agents all cost negative inotropy or vasodilation she cannot afford.
• Energy. biphasic synchronized 150-200 J, with the pads already on her and adequate anesthetic depth.
• Before the second shock. correct what is keeping her in it - potassium, magnesium, oxygenation, depth of anesthesia, perfusion pressure, and any ischemia; shocking repeatedly into a hypokalemic, ischemic, under-perfused heart just fails again.
• Doses. potassium 20-40 mEq via a central line at 10-20 mEq/h with monitoring, magnesium 2 g IV over 10-20 min; amiodarone 150 mg over 10 min to hold sinus once restored.
• Going on pump in AF. acceptable if she is deteriorating and the pump is the fastest route to a decompressed, perfused heart - but restore perfusion pressure first and plan to cardiovert during rewarming or after the clamp comes off. Do not linger unstable in the pre-bypass period simply to chase rhythm.

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• DDx. stunned hypertrophied LV, inadequate preload, residual ischemia or coronary air (classically the right coronary, which sits anterior), RV dysfunction, vasoplegia, incomplete de-airing, or a valve or surgical problem - TEE narrows it quickly.
• Volume. this stiff LV is preload-dependent; give 250 mL at a time from the pump and watch LV end-diastolic area and function on TEE. Stop when filling stops improving contraction, because over-distension of a failing ventricle is the opposite trap.
• Inotrope. epinephrine 0.03-0.06 mcg/kg/min for contractility; milrinone 0.25-0.375 mcg/kg/min improves lusitropy and unloads the RV but vasodilates a soft patient and needs a vasoconstrictor beside it; calcium chloride 500-1000 mg is a brief bridge, not a plan. A defended choice tied to this ventricle is what is wanted, not a list.
• Targets. CI above roughly 2.2 L/min/m2, MAP 70-75 to perfuse a hypertrophied ventricle, SvO2 above 60%, and a filling, contracting LV on TEE.
• RV distension. the failure is shifting to the right - pulmonary hypertension, RV ischemia from coronary air, volume overload, or acidosis and hypercarbia raising PVR. Reduce PVR (inhaled nitric oxide 20-40 ppm or epoprostenol), avoid over-filling the RV, hold coronary perfusion pressure with vasopressin, and support RV contractility.
• IABP versus RV support. an IABP unloads the LV and augments diastolic coronary perfusion, but it does nothing for a distending RV. Recognizing that the failure has become RV-predominant and reaching for an RV strategy is the better reasoning; either commit is defensible if it is tied to which ventricle is failing.

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• First minute. pace - epicardial wires, or transcutaneous pads while the wires go on. Isoproterenol or epinephrine buys seconds; pacing is the treatment, with pressure support in parallel.
• Why blocked. the AV node and bundle of His run immediately below the non-coronary and right coronary cusps; debriding a heavily calcified annulus and placing sutures injures them, and her pre-existing first-degree block marks conduction with no reserve.
• Mode. atrial and ventricular wires, AV-sequential (DDD) at 80-90. A hypertrophied ventricle with grade II diastolic dysfunction depends on the atrial kick; settling for VVI here gives away filling she cannot spare.
• Loss of capture. lead dislodgement or poor epicardial contact, rising threshold from edema, output set too low, connection or generator failure, hyperkalemia or acidosis, drug effect. Check connections and polarity, raise output, confirm capture and sensing, send a potassium.
• Rising threshold. edema or ischemia at the lead-myocardium interface; keep output 2-3 times threshold, keep pads on her, have a spare generator, and do not rely on epicardial wires alone in a pacing-dependent patient.

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• Surgical versus medical. brisk, sustained, bright output with a coagulation profile that is correcting points surgical; diffuse ooze from line sites and suture holes with abnormal viscoelastic studies points medical. The distinction decides re-exploration versus product.
• Heparin excluded. no ACT elevation and no heparinase gap means protamine was adequate and rebound is not the driver - do not keep redosing protamine, which itself impairs platelet function at high doses.
• Next tests. fibrinogen, platelet count, viscoelastic tracing (R time, alpha angle, MA), Hgb, calcium, and temperature - hypothermia and ionized hypocalcemia are correctable causes of coagulopathy that get skipped.
• Targeted product. fibrinogen 120 is the deficit that matters after CPB - cryoprecipitate 10 units or fibrinogen concentrate to get above 150-200 mg/dL; platelets 90 with CPB-induced qualitative dysfunction justifies a pool. A normal R time means she does not need FFP; blind FFP is volume without benefit.
• Apixaban. no. Seventy-two hours is at least five half-lives even with her renal function, so residual effect is negligible and it does not explain brisk bright bleeding. Note it is a factor Xa inhibitor - FFP does not reverse it; andexanet alfa or PCC would be the agents if reversal were truly needed, and andexanet complicates heparin anticoagulation around bypass.
• Back to the OR. now. Sustained 250 mL/hr with corrected coagulation is surgical bleeding, and endless transfusion without surgical control is the trap - it also sets up the tamponade you will see when the tube clots off.

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• DDx. localized tamponade from clot, given a tube that stopped and equalizing filling pressures with low output; also RV failure, hypovolemia, valve or graft problem, pneumothorax. A stopped chest tube plus rising filling pressures is the pattern to recognize unprompted.
• First move. call the surgeon and prepare for re-exploration while you support her - do not spend twenty minutes assembling studies.
• Equivocal TEE. no, it does not reassure. A localized posterior or retro-atrial clot compressing one chamber is easily missed in a postsurgical chest and does not look like a classic circumferential effusion; suspicion beats an equivocal image.
• Furosemide. no - the oliguria is from low forward flow, not volume overload, and diuresing a tamponading patient removes the preload that is still filling her. A reflexive diuretic order here is a red flag.
• Holding her until the OR. full, fast, and tight: volume to maintain filling, keep the paced rate up at 90, norepinephrine 0.05-0.2 mcg/kg/min or epinephrine to hold perfusion pressure, avoid anything that drops venous return - and be prepared to open the chest at the bedside if she arrests.
• Induction. surgeon scrubbed, prepped and draped, chest open kit ready before induction. Ketamine 0.5-1 mg/kg or etomidate 0.1-0.2 mg/kg with a small opioid dose, no propofol bolus, no big positive-pressure breaths - the induction that drops preload or afterload arrests a tamponading patient. Anticipate the swing to hypertension and volume overload the moment the clot is evacuated.

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• Mode. VVI or VVIR at 80-90. With fibrillating atria the atrial output paces nothing and atrial tracking can drive an erratic ventricular response; keeping her in DDD while she fibrillates is the miss. Also recognize that the atrial kick this stiff ventricle depended on is already gone - rate, volume, and perfusion pressure now carry her output.
• Timing. yes, start today - hemostasis is secure after the re-exploration with 25 mL/hr and a stable Hgb, and AF plus a fresh bioprosthesis is real stroke risk. The judgment is not delaying for days out of reflex after yesterday's bleeding.
• Agent. an unfractionated heparin infusion first, without a bolus - titratable and immediately reversible if the chest starts bleeding again. Move to oral anticoagulation once she is stable; a bioprosthesis does not mandate warfarin, so apixaban is an option for the AF, unlike with a mechanical valve.
• Renal function. at creatinine 1.9 with an eGFR near 30, apixaban is dose-reduced to 2.5 mg twice daily only when two of the three criteria are met (age 80+, weight 60 kg or less, creatinine 1.5 or more) - at 78 and 68 kg she meets only the creatinine criterion, so the full 5 mg twice daily dose applies; eGFR near 30 is at the edge of the trial population, which is a reason for caution, not dose reduction. Heparin is monitored by PTT or anti-Xa and is not renally dose-adjusted.
• Before relying on the wires. capture threshold with 2-3 times output margin, sensing verified, connections secure, spare generator and battery at the bedside, pads on her, and a written plan if capture fails - she has no reliable escape rhythm.

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• DDx. residual sedation, metabolic or renal drug accumulation, embolic stroke, watershed hypoperfusion injury, seizure, intracranial hemorrhage on heparin; a lateralizing deficit moves this away from sedation and toward a structural cause.
• Why this operation. surgery on a heavily calcified aortic valve showers calcific and atheromatous debris, and aortic cannulation, cross-clamping, and intracardiac air add to it; her AF compounds the risk. Embolic stroke is a recognized complication of calcific AVR, not a surprise.
• Workup speed. immediate neurologic exam and non-contrast head CT with CT angiography and perfusion imaging, within minutes not hours - it changes the anticoagulation plan and may open a treatment window.
• Heparin after the infarct. hold it. A fresh large infarct carries hemorrhagic conversion risk, especially on systemic anticoagulation the day after a bleeding re-exploration; restarting is a decision made with neurology after repeat imaging, usually days later, and typically balanced against her AF and bioprosthesis risk.
• Thrombectomy. mechanical thrombectomy is not excluded by recent cardiac surgery and is worth pursuing if she has a large-vessel occlusion and salvageable tissue on perfusion imaging, within the extended window up to 24 hours. IV thrombolysis is contraindicated - major surgery within 14 days and a fresh sternotomy.
• BP target. permissive hypertension around a systolic of 140-180 to perfuse the ischemic penumbra while the vessel is occluded; hypotension extends the infarct. Tighten the target after successful reperfusion.

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• Extubate or not. the deficit is the deciding variable - dysarthria and weak cough predict aspiration and reintubation, but prolonged intubation carries its own harms. Either commit is defensible if airway protection, secretion clearance, gas exchange, and hemodynamics are explicitly addressed.
• Before extubation. following commands and protecting the airway, a swallow and cough assessment, acceptable gas exchange and mechanics, stable hemodynamics not on escalating support, controlled bleeding, and a reliable paced rhythm.
• Weak cough with pooling. a bedside swallow evaluation and a defined trial; if she cannot clear secretions after several days, tracheostomy around day 7-10 rather than repeated failed extubations - each failure costs her.
• What you tell the family. plainly: the valve was severely calcified, and operating on that kind of valve can dislodge small pieces of debris that travel to the brain; that appears to be what happened, it was recognized quickly and imaged, and the extent of recovery is uncertain over weeks to months. State what is known, name the uncertainty, do not assign blame, and leave room for questions.
• Before leaving the ICU. the permanent pacemaker decision (high-grade block persisting beyond about 5-7 days rarely recovers), confirmed thresholds and sensing with margin, the anticoagulation plan reconciled between her AF and her fresh infarct, and stroke rehabilitation and swallow follow-up arranged.

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• Goals. sinus rhythm at 60-70, preserved diastolic pressure and SVR, adequate but not excessive preload in a 35% EF ventricle. With a critical left main the whole myocardium is supply-dependent and there is no collateral reserve. A generous propofol bolus that drops SVR in this man is worth challenging - an opioid-based or etomidate induction with a vasopressor drawn up and running is the safer plan.
• 76/42 with deepening ST. this is an ischemic emergency, not transient induction hypotension. Give a vasoconstrictor now - phenylephrine 100-200 mcg or norepinephrine 4-8 mcg, escalating to an infusion - because restoring diastolic pressure is the only thing that reperfuses him in the next 30 seconds. Volume takes minutes and a failing LVEF-35 heart tolerates over-filling poorly.
• CPP terms. aortic diastolic pressure minus LV end-diastolic pressure. Hypotension is lowering the numerator while the ischemic, failing LV raises the LVEDP - the gradient is being squeezed from both ends, and the left main means nothing downstream can compensate.
• HR 104. deepen anesthesia for the stimulus, confirm he is not hypovolemic or ischemic-driven, then treat the rate - esmolol 10-20 mg titrated, given his beta-blocker at home. Tachycardia raises demand and shortens diastolic perfusion time at the same time.
• Nitroglycerin. not as the first move while he is soft - it drops preload and coronary driving pressure and can worsen ischemia in a left-main lesion. Once perfusion pressure is restored, low-dose nitroglycerin for ongoing ischemia is reasonable.
• Large v waves. acute worsening of his functional MR from ischemic papillary muscle and LV dysfunction; the v wave is regurgitant flow into the left atrium, and the rising PA pressures are its consequence. Treat the ischemia - perfusion pressure, rate control, afterload reduction once he tolerates it, inotropic support if the LV is failing - and tell the surgeon, because it changes what the operation may need to include.

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• ACT target. above 480 seconds for full CPB (many centers use 400-480 with heparin concentration monitoring); name the number rather than say 'high enough'. The target protects against circuit thrombosis and consumptive coagulopathy.
• 360 after a full dose. give more heparin first - but a second dose that barely moves the ACT is the signal to stop redosing and find the cause. Cannulating and going on pump on a subtarget ACT risks circuit clot and DIC; it must be resolved before bypass.
• What is going on. heparin resistance, most often antithrombin depletion from four days of continuous preoperative heparin. Heparin works by potentiating antithrombin - with antithrombin consumed, more heparin has nothing to work through. Also consider high factor VIII or fibrinogen states, thrombocytosis, and a lab or sampling artifact.
• Rx. restore antithrombin - antithrombin III concentrate (commonly 500-1000 units, or a dose calculated to the deficit) where available, otherwise 2 units of FFP as a source; then recheck the ACT to confirm the response before committing to bypass.
• 520 - proceed. yes, go on pump, but recheck the ACT frequently, expect a shorter interval before the next dose, and anticipate needing less protamine at the end than the total heparin dose would suggest.
• HIT. keep it on the list - four days of heparin is the classic window and a 50% fall from baseline matters more than an absolute count, so a platelet count of 165 that was 300 on admission is a warning. If HIT is suspected or confirmed, heparin comes off entirely and bypass is run with bivalirudin, which is why the diagnosis has to be raised before cannulation, not after.

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• DDx. stunned and ischemic LV after a recent infarct and cross-clamp, incomplete revascularization or a graft problem (kinked, occluded, or air in a graft - classically the right), residual ischemia, RV dysfunction, vasoplegia, inadequate preload, worsening MR.
• Back to the surgeon. a new or worsened regional wall-motion abnormality in a grafted territory, air in the right coronary distribution, worsening MR, or an unexpected structural finding - a graft problem is fixed at the table, not with more epinephrine.
• Volume. give it in 250 mL increments from the pump with TEE watching LV end-diastolic area; stop when filling no longer improves contraction. A dilated failing LV needs enough preload to eject but over-distension raises wall tension and worsens ischemia.
• Inotrope. epinephrine 0.03-0.08 mcg/kg/min for contractility, milrinone 0.25-0.375 mcg/kg/min for inodilation and RV unloading paired with a vasoconstrictor because it will drop his SVR, calcium chloride 500-1000 mg as a brief bridge only. Defend the choice against this post-ischemic, low-output ventricle rather than listing agents.
• Targets. CI above roughly 2.2 L/min/m2, MAP 70-75 to perfuse fresh grafts, SvO2 above 60%, lactate falling, and improving contraction on TEE.
• RV distension. RV failure superimposed on the LV problem - RV ischemia or air in the right coronary, a rising PVR from hypercarbia, hypoxia, acidosis, or protamine, or simple over-filling. Reduce PVR with inhaled nitric oxide 20-40 ppm or epoprostenol, hold coronary perfusion pressure with vasopressin, support RV contractility, avoid volume loading it further, and keep AV synchrony.
• IABP or something else. an IABP is well matched to an ischemic, LV-predominant low-output state with fresh grafts - it augments diastolic coronary perfusion and cuts LV afterload, and it needs a reasonably regular rhythm to time to. But it does little for a failing RV; if the picture has become RV-predominant, an RV strategy (inhaled vasodilator, RV mechanical support, or VA-ECMO) is the better answer. Either commit is defensible if it is tied to which ventricle is failing.

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• Low SVR DDx. post-CPB vasoplegia from circuit-driven inflammation, his preoperative ACE inhibitor, milrinone-driven vasodilation, residual anesthetic, rewarming; also consider that a low SVR calculated on a low pressure can mask a still-failing pump, and sepsis or adrenal insufficiency in a four-day inpatient.
• Vasopressor. norepinephrine 0.05-0.3 mcg/kg/min is the workhorse - restores SVR with some beta support. Vasopressin 1-3 units/hr is the right partner in vasoplegia with RV dysfunction because it raises SVR without raising PVR. Phenylephrine loads afterload onto a struggling LV with no inotropic offset and is the weakest choice here.
• Target. MAP 70-75 - higher than a routine post-op target because fresh grafts, a hypertrophied ischemic myocardium, and CKD-stage-3 kidneys all need driving pressure; name a number and the reason.
• Methylene blue. reasonable now for catecholamine-refractory vasoplegia at 1-2 mg/kg over 20-30 min - it inhibits guanylate cyclase and restores vascular tone. Not a first move. Risks: serotonin syndrome with serotonergic drugs, hemolysis in G6PD deficiency, transient pulse-oximetry interference, and pulmonary vasoconstriction that a failing RV may not tolerate.
• Lactate up, urine down at CI 2.0. the number is not adequate for this patient's demand, or perfusion pressure and regional flow are inadequate despite it - look for ongoing ischemia, IABP timing errors, tamponade, and a mixed venous saturation to test the assumption. Do not accept the CI as proof of adequacy.
• Before leaving the OR. secure perfusion pressure and a defined hemodynamic plan, confirm rhythm and working pacing wires with margin, verify IABP timing and augmentation, check TEE for a mechanical cause, correct coagulation and temperature, and confirm graft flows with the surgeon.

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• Surgical versus medical. brisk, sustained, bright output with a correcting coagulation profile points surgical and toward re-exploration; diffuse ooze from line sites and suture holes with abnormal viscoelastic studies points medical and toward targeted product. Both can be true after this operation.
• Ticagrelor. a potent, reversibly-binding P2Y12 inhibitor dosed hours before bypass produces a real qualitative platelet defect that the count does not capture at all - a count of 110 tells you nothing about function. It is not dialyzable and stopping it does not help acutely; its half-life is roughly 7-9 hours with an active metabolite.
• Targeted product. prolonged R time means factor deficiency - FFP, or PCC if volume matters in a man with RV dysfunction. Fibrinogen 130 calls for cryoprecipitate or fibrinogen concentrate to get above 150-200. A low MA with an adequate count is qualitative platelet dysfunction from CPB plus ticagrelor - give platelets. Correct the specific defect rather than blind product, and do not forget calcium and temperature.
• MA barely moves. circulating ticagrelor and its active metabolite inhibit the platelets you just transfused - this is the practical consequence of a reversible, high-plasma-level agent, unlike clopidogrel. Expect incomplete correction, redose as the drug clears, and note that standard kaolin MA is relatively insensitive to the P2Y12 effect itself (platelet mapping or ADP aggregometry demonstrates it). Desmopressin has limited benefit here and is not the answer.
• Take him back. yes if the total picture is surgical - a fall to 120 mL/hr after a large product load is not resolution, and the tube that keeps flowing today is the tamponade tomorrow. Persistent high-volume output 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 in a man whose RV was already mildly dysfunctional and recently strained; also hypovolemia, graft occlusion, or pneumothorax. A stopped tube plus rising filling pressures is the pattern to name unprompted.
• First move. call the surgeon and prepare for re-exploration while you support him - a bedside decision, not a workup.
• Equivocal TEE. no. Localized posterior or retro-atrial clot compressing a single chamber is easily missed in a postsurgical chest and does not look like a circumferential effusion; an equivocal study does not exclude it, and suspicion outweighs the image.
• RV failure instead. a dilated, hypokinetic RV with a flattened septum and reduced TAPSE, without a compressing collection, and typically a distended rather than compressed right atrium - the treatments diverge sharply, so the distinction is worth the extra look.
• Furosemide. no - the oliguria reflects low forward output, not volume overload; diuresing either a tamponading or an RV-failing patient strips the preload that is still generating output. A reflexive diuretic order is a red flag.
• Holding him. full, fast, and tight: volume to maintain filling, pace at 90 with AV synchrony, norepinephrine 0.05-0.3 mcg/kg/min or epinephrine for perfusion pressure, avoid anything that drops venous return, be ready to open the chest at the bedside if he arrests.
• Induction. surgeon scrubbed and the chest prepped and draped before induction. Ketamine 0.5-1 mg/kg or etomidate 0.1-0.2 mg/kg with a modest opioid dose; no propofol bolus, gentle positive pressure, preserve preload, afterload, and rate - and anticipate hypertension and sudden volume overload the moment the clot is evacuated.

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• Why this matters here. a dilated 35% EF ventricle on inotropes loses both the atrial contribution and diastolic filling time at 150; new post-op AF is common but in this patient it collapses a marginal output and threatens fresh grafts. Treating it as routine is a flag.
• Cardioversion. he is unstable - synchronized cardioversion rather than titrated rate control. Beta-blockers and calcium-channel blockers carry negative inotropy he cannot afford.
• Energy. biphasic synchronized 150-200 J, adequately sedated, with pads already on him.
• Correct first. potassium above 4.0 and magnesium above 2.0, oxygenation and acid-base, ischemia, volume status, and excess catecholamine from his own infusions - shocking into an uncorrected substrate just fails again.
• Amiodarone. 150 mg IV over 10 min, then 1 mg/min for 6 hours and 0.5 mg/min for 18 hours. It is the least negatively inotropic option, but it is not free - hypotension with rapid loading, bradycardia in a man with first-degree block, and thyroid, pulmonary, and hepatic effects with prolonged use.
• Anticoagulation. AF persisting past 48 hours in a post-cardiac-surgery patient warrants anticoagulation. Start once hemostasis is durably secure - typically 48-72 hours after a bleeding re-exploration - with a titratable unfractionated heparin infusion without a bolus, moving to oral anticoagulation as he stabilizes. A bioprosthesis or grafts do not mandate warfarin, but his renal function shapes any DOAC dose.

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• Target. roughly 140-180 mg/dL. Tighter targets have not improved outcomes in cardiac surgery and cause hypoglycemia; naming a defended range beats saying 'control the sugar'.
• How. a continuous IV insulin infusion with hourly point-of-care glucose until stable, then spacing out; subcutaneous sliding scale on a vasopressor-dependent, edematous patient absorbs unpredictably and is why he is at 280.
• Epinephrine and glucose. epinephrine drives gluconeogenesis, glycogenolysis, and insulin resistance - it is an active cause of his hyperglycemia, so his insulin requirement will fall as the infusion weans, and failing to anticipate that produces hypoglycemia.
• Rising creatinine DDx. cardiac-surgery-associated AKI, multifactorial: contrast from the catheterization four days ago, CPB itself (nonpulsatile flow, hemolysis with free hemoglobin, inflammation), the intraoperative and post-op low-output and hypotensive periods, and nephrotoxins, all on a stage-3 CKD baseline.
• What to stop. the ACE inhibitor stays off, avoid NSAIDs, avoid further contrast, dose-adjust or stop nephrotoxic antibiotics, and revisit the choice of hydroxyethyl starch or high-dose vancomycin if present. Optimize perfusion pressure and cardiac output - that is the treatment that matters more than any drug.
• Hyperkalemia at 6.2. calcium chloride 1 g (or calcium gluconate 3 g) for membrane stabilization, insulin 10 units with dextrose, bicarbonate for the acidosis, a beta-agonist, and a binder if he is making urine - but in an oliguric post-CPB patient this is temporizing.
• Renal replacement. start for refractory hyperkalemia, refractory acidosis, volume overload he cannot diurese, or uremic complications - not at a creatinine number. In a patient this volume-sensitive, earlier continuous renal replacement to control volume is often the right call.

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• Extubate today. a defensible commit either way, but the case has to be made on specifics: following commands and protecting the airway, acceptable gas exchange and respiratory mechanics, hemodynamics stable on non-escalating support, controlled bleeding, a stable rhythm with pacing available, and normothermia.
• P/F 190 and 6 L positive. this is cardiogenic and post-CPB pulmonary edema on top of a marginal heart - extubating into that buys a reintubation. Diurese toward even balance with a furosemide infusion, keep him unloaded, and extubate onto high-flow or non-invasive support once the P/F and fluid balance improve.
• What you tell the family. plainly: the bypass grafts were completed as planned, but his heart was weak after the operation because of the recent heart attack, so it needed medicines and a balloon pump to support it, and he also needed to go back to the operating room for bleeding. He is improving but the next several days are uncertain. State what happened, name the uncertainty, do not overpromise and do not assign blame, and leave room for their questions.
• Days ahead. continued inotropic support means he stays in the ICU with invasive monitoring and a slow, deliberate wean; before he leaves, the inotropes must be off or stably low, the rhythm and pacing plan settled, anticoagulation for his AF decided, renal function trending, glycemic control on a workable regimen, and the goals-of-care conversation had if he is not improving.

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• Which device. IABP gives roughly 0.5–1 L/min of augmentation and afterload reduction — not enough for an EF 15% ventricle on escalating triple support; Impella CP gives 3–3.5 L/min of LV-to-aorta flow and unloads; VA-ECMO gives full flow and oxygenation but loads the LV. Expect a commit to Impella or ECMO, not IABP; reciting all three without picking is the flag.
• SpO2 87% and RV down. an oxygenation problem plus RV dysfunction is what pushes the choice to VA-ECMO: Impella CP needs an RV that can fill it and does nothing for gas exchange. The resident should change the answer when these two facts land.
• Impella CP alone. push back: RV dysfunction starves the inlet (suction), CP flow may not meet his need, and falling SpO2 is not addressed. ECMO first, with Impella later as a vent if needed, is the defended plan. Contraindications the examiner keeps in reserve: moderate-or-worse AR forecloses IABP, Impella, and unvented ECMO; mechanical AVR or LV thrombus forecloses Impella.
• Cannula and the leg. arterial cannula 15–17 Fr, sized to vessel by ultrasound or CT, in a PAD patient; place a 6–8 Fr antegrade distal perfusion cannula at cannulation, not after the foot goes white. Skipping the DPC in a claudicant is the error.
• Lactate, creatinine, ticagrelor. none of these stop cannulation — they are the reasons to cannulate. Ticagrelor and heparin raise bleeding risk at the site; note it and plan, do not delay. Waiting for 'better numbers' in unrelenting shock is the trap.
• Commit. peripheral VA-ECMO, femoral venous and femoral arterial with distal perfusion, initial flow ~60–70 mL/kg/min (about 4–4.5 L/min), sweep to normocarbia, MAP target 65. A defended package, not a hedge.

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• Agent and dose. hemodynamically neutral and small: ketamine 0.25–0.5 mg/kg or etomidate 0.1–0.15 mg/kg, fentanyl 50–100 mcg, rocuronium. A propofol induction or a full-dose anything is the red flag; naming a generous dose is the fail.
• Before you push. pressors on pumps and titratable, push-dose epinephrine 10–20 mcg/mL and vasopressin drawn up, pads on and connected, surgeon scrubbed and perfusion primed. Inducing a shock patient without rescue in hand is the error.
• BP 60/40, VT runs. epinephrine 10–20 mcg boluses or vasopressin 1–2 U while pumps go up; target MAP back above 60–65. Expect a named drug, a dose, and a number, not 'support the pressure.'
• Sustained VT with a pulse, BP 55/30. unstable — synchronized cardioversion 100 J now; amiodarone after, not instead. Drug-first on an unstable rhythm is the flag.
• Cannulate or stabilize. cannulate. The device is the treatment; there is nothing to stabilize him with. Delaying for a better MAP that the drugs cannot deliver is the trap.
• Arrest with ECMO minutes away. high-quality CPR, epinephrine per ACLS, and go straight to cannulation during compressions (ECPR); minimize interruptions, keep the field still for the wire. Recognize the device is the exit from the arrest.
• Heparin bolus. Heparin: full bolus to ACT > 200–250 before cannulation (about 50–100 units/kg on top of the infusion), then confirm the ACT once the circuit is running; skipping the bolus because 'he is already on a drip' is the miss.
• Flow up, no native pulse. stop compressions once the circuit is delivering full flow with an adequate MAP; compressions now risk cannula dislodgement. Continue rhythm management for the LV itself — a fibrillating or standstill heart on ECMO will distend.

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• What is happening. retrograde ECMO flow raises root afterload; an EF 15% LV cannot open the valve against it, so LVEDP and LA pressure climb and the lungs flood. ECMO is loading this ventricle, not resting it.
• Valve not opening, smoke. stasis in the LV and root with thrombus risk — including the coronaries — despite heparin; plus worsening pulmonary edema. This is the urgency behind venting.
• First move. reduce flow modestly and add or increase inotrope to restore ejection while keeping MAP adequate; a small amount of native ejection is the goal. Cranking flow up for the MAP is the wrong direction. Keeping low-dose inotrope running on VA-ECMO to preserve ejection is standard.
• Fails within minutes. medical measures are not enough; the LV needs an active vent. Lactate 5 also says flow reduction cost him perfusion — he needs both flow and a vent.
• Which vent. Impella (ECpella) actively unloads and is the usual choice; IABP is a weak vent; surgical LV/pulmonary-vein vent or atrial septostomy is most definitive but needs the chest or the cath lab. Commit and tie it to severity.
• VT on Impella. VT compromises filling of the Impella inlet and worsens stasis; amiodarone 150 mg then infusion, correct K and Mg, check inlet position (the catheter itself can be ectopic against the septum); shock only if hemodynamically meaningful, and on ECMO the pressure may not tell you. Treating the rhythm rather than tolerating it is the point.
• Anticoagulation. unfractionated heparin to PTT 60–80 s or anti-Xa 0.3–0.5; ACT 180–220 if that is what the unit follows — not CPB-level 400+. Impella purge contributes heparin; count it.

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• What is happening. differential (north–south, Harlequin) hypoxia: the recovering LV is ejecting blood from wet lungs into the arch, and the ECMO mixing point has moved distal; the head and right arm get native, deoxygenated blood while the lower body gets oxygenator blood.
• Who gets the 55. coronaries, brain, right arm — the highest-stakes territory; this is why the right radial line exists.
• Confirm. right-hand versus foot pulse oximetry, right radial versus post-oxygenator and femoral gases, and cerebral NIRS.
• First move. ventilator: raise FiO2, PEEP, recruit — get the lungs to oxygenate what the LV ejects. Raising ECMO flow to push the mixing point proximal is a temporizer with an LV-distension cost.
• Vent fails. the lungs cannot do it; reconfigure to VAV — add a return cannula to the IJ/RA so oxygenated blood goes through the lungs and out the LV.
• Arterial flow on VAV. total pump flow is split; arterial flow falls unless total flow rises and the venous return limb is clamped/restricted to a set ratio. Recognizing the split and managing it (partial clamp on the venous return, raise total flow) is the judgment.
• Target. right radial SpO2 ≥ 90% or PaO2 ≥ 60 — upper-body oxygenation is the endpoint.
• Both sites low. not differential hypoxia — a circuit or oxygenator problem (membrane failure, FdO2 or sweep down, recirculation in the VAV limb) — check the post-oxygenator gas and the blender. Different problem, different fix.

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• Heparin. reduce, do not hold: drop the target to the low end (PTT 50–60 / anti-Xa 0.2–0.3), and rely on the Impella purge for local anticoagulation. Holding heparin on ECpella invites pump and circuit thrombosis; full-target heparin plus DAPT with a falling Hgb is the other failure.
• Send. PTT/anti-Xa, ACT, fibrinogen, platelets, CBC, TEG, plasma-free Hgb/LDH, and a look at the groins for a surgical (cannula-site) source.
• Platelet drop DDx. consumption on the circuit and Impella, HIT, dilution, sepsis, drug effect; a 55% fall on day 5 of heparin with no other explanation puts HIT at the top.
• HIT confirmed. stop all heparin, switch to bivalirudin (start ~0.05–0.1 mg/kg/h, no bolus, titrate to PTT 50–70 or per protocol; start low because bivalirudin is partly renally cleared and his creatinine is 2.1 — argatroban is the alternative if renal failure progresses), and convert the Impella purge to a bicarbonate-based purge. Send the SRA. Missing the purge is a real harm.
• Ticagrelor. hold it if bleeding is life-threatening, but a 5-day-old proximal LAD stent thromboses without DAPT; keep aspirin at minimum and discuss with cardiology — the defensible answer is to hold ticagrelor briefly for active bleeding with a plan to resume, not reflexively stop everything or refuse to touch it.
• Thresholds. Hgb 7–8 on support, higher if oxygen delivery is marginal; platelets > 50 with bleeding, > 20–30 without; fibrinogen > 150. Numbers expected.
• Continued bleeding. stop transfusing into the problem: surgical exploration of the cannula sites, reassess anticoagulation, and reconsider whether the current configuration is sustainable. Endless product is the trap.

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• DDx. suction from underfilling or malposition, RV failure starving the LV, pump thrombosis, VT, tamponade or bleeding dropping preload. Alarm plus a wrong placement signal points to position/preload first.
• Look before volume. arterial pulsatility and CVP, then echo for position and LV filling and RV size, then the purge and motor current. Blind boluses into a heart-failure patient on an RV that is already dilated is the trap.
• Fix. reposition under echo so the inlet sits ~3.5 cm below the valve away from the wall, and lower the P-level; give volume only for a demonstrated preload deficit. Here the RV is the real limit — support it (inotrope, iNO, ECMO flow) so it can fill the LV.
• P6 clears the alarm, CI 1.8. do not accept inadequate flow: add RV support or raise ECMO flow to cover the gap rather than turning the Impella back up into the wall. Escalate support, not P-level.
• Hemolysis cause. shear from high P-level, inlet or outlet against the wall or valve apparatus, or pump thrombus — worse when anticoagulation has been lightened for bleeding.
• Confirm and change. trend plasma-free Hgb, LDH, haptoglobin, bilirubin, urine color; check anticoagulation; reposition and lower speed. Renal protection: urine output, alkalinize if free Hgb is high.
• Still climbing. suspect pump thrombosis; exchange the device or remove it and rely on ECMO with another vent strategy. Persisting hemolysis on a device that is not fixing the problem is the flag.

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• DDx. occluded or kinked distal perfusion cannula, cannula occluding the vessel in a PAD limb, thrombus at the access site, embolus, vasospasm. His claudication is the setup.
• Confirm. exam, Doppler at DP/PT, calf NIRS against the other leg, DPC flow check; treat a clear deficit, do not wait for a confirmatory study.
• Rx now. flush and interrogate the DPC, reposition or replace it, call vascular surgery; if it cannot be restored, move the arterial cannula or add a graft. Watching a pulseless leg is the failure.
• Tense painful calf. reperfusion compartment syndrome; emergent four-compartment fasciotomy, not observation.
• Rhabdomyolysis. aggressive volume within what the RV tolerates, treat the hyperkalemia (calcium, insulin/glucose), consider CRRT early given creatinine 2.6 and the potassium; alkalinization is an option.
• Surveillance. hourly limb checks — color, temperature, Doppler, NIRS — and DPC flow, documented; this is how the next one is caught before it is a fasciotomy.

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• Ready to wean. improving LV function on echo, sustained pulsatility, falling filling pressures, minimal pressor and inotrope, clearing lactate, and lungs that can oxygenate. A number-by-number look, not a gestalt.
• Numbers to go down. LVEF > 20–25%, LVOT VTI > 10–12 cm, TAPSE > 12 mm, at minimal flow, with MAP held and lactate flat; these are the usual wean-trial thresholds.
• Fails at 2 L/min. stop the trial — MAP falling and lactate rising are the answer. A failed wean is information; pushing to decannulation is the error.
• Anticoagulation during the trial. full — low flow through the circuit clots it; give a heparin bolus or raise the target before turning down.
• Options day 8. the fork: bridge to durable LVAD, bridge to transplant, or withdrawal. Name it as the decision now, not 'keep waiting.'
• Candidacy. irreversibility of end-organ injury, frailty, comorbidity, and social support; persistent dialysis dependence is a relative contraindication to LVAD and a barrier to transplant listing. His renal course decides more than his heart.
• Where it goes. no recovery, no destination: support is sustaining him without a path, and the conversation with the family about goals is now due.

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• Healing his heart. no — plainly. The pump replaced his circulation while the team waited for recovery or a next step; his heart has not recovered and he is not a candidate for LVAD or transplant. Honest, without foreclosing questions; agreed in advance with surgery and heart failure so the message is one message.
• Keep it going. acknowledge the wish; explain that support without a destination sustains without a path, carries continuing harms (bleeding, limb, infection, stroke), and that the decision before them is continued support versus comfort — not a negotiation over days.
• Stopping ECMO. opioid and benzodiazepine for comfort before anything else, stop CRRT and pressors, then clamp and stop the circuit; cannulae stay in. A resident who reaches for the clamp before the comfort medications is the flag.
• Expectation. circulatory failure within minutes; tell the family this so they are not surprised.
• Compressions. no — a comfort-focused plan with a DNR order is documented before the clamp goes on.

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• Agent and dose. etomidate 0.2 mg/kg or a small propofol dose (0.5–1 mg/kg) with fentanyl 2–4 mcg/kg and rocuronium, titrated against the arterial line; a full propofol bolus that drops SVR and rate together is the flag. Preload kept, afterload low-normal, contractility preserved.
• Rate. 80–90; slower lengthens diastole, distends the dilated ventricle, and raises regurgitant volume per beat. Want the mechanism, not 'keep it stable.'
• BP 82/40, PA up. forward flow fell and the leak is backing up; pure phenylephrine raises SVR and the regurgitant fraction. Ephedrine (rate plus inotropy) or a small volume bolus is better matched; a small phenylephrine dose for coronary pressure is acceptable if defended. Reflexive phenylephrine alone gets a probe.
• HR 52. bradycardia is the enemy in MR — treat it, do not tolerate it: glycopyrrolate 0.2 mg or ephedrine, or pace if wires were available. Tachycardia to 120 is comparatively well tolerated in this lesion; that contrast lives here, not in the question.
• Nitroglycerin. reasonable at BP 112 — afterload reduction favors forward flow — but not into hypotension; a defended yes with a BP floor, or a defended no because he has just been hypotensive, both pass.
• v wave. regurgitant volume filling the left atrium in systole; its size tracks the leak and LA compliance, not simple volume overload. Read it as a severity marker.

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• First move. ventilate: PaCO2 48 raises PVR — increase minute ventilation, FiO2 1.0, check depth of anesthesia, treat acidosis. Fix the controllable PVR drivers before reaching for a drug.
• PaCO2 target. 30–35, tidal volume 6–8 mL/kg, moderate PEEP 5, avoid high mean airway pressure; a specific goal, not 'ventilate well.'
• iNO. yes — 20 ppm; end point is a falling PA pressure with a stable systemic pressure and a smaller RV on TEE; it lowers PVR without lowering SVR, unlike a systemic vasodilator.
• Volume. no — a dilating RV with TAPSE 12 does not need more preload; overfilling shifts the septum and starves the LV. Cautious, TEE-guided, not reflexive.
• Inotrope. epinephrine 0.03–0.05 or milrinone 0.25–0.375 (with norepinephrine to hold SVR); dobutamine is defensible. Tie it to RV contractility and coronary perfusion pressure.
• Wait or go. go — heparinize and cannulate; bypass unloads everything and 15 more minutes of a failing RV buys nothing. Titrating into a distending RV is the trap.

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• Why worse. the regurgitant orifice was a low-impedance pop-off; closing it makes the chronically volume-loaded ventricle eject the whole stroke volume into the aorta. Pre-repair EF of 56% with LVESD 44 mm was already a flattered number. Want this stated explicitly.
• DDx. unmasked LV dysfunction, preload, ischemia or air, RV failure from his pulmonary hypertension, vasoplegia, a repair problem (TEE excludes).
• Volume. give only if the LV is small on TEE with low filling pressures; a dilated hypocontractile LV does not want more. LVEDA and the wedge decide it.
• Inotrope. epinephrine for contractility; milrinone for lusitropy and unloading — both together is the common defended plan for an unmasked ventricle, with the vasodilation of milrinone anticipated.
• BP 72/40 on milrinone. expected vasodilation; add norepinephrine or vasopressin to restore SVR, do not stop the inotropy that is raising the CI.
• Lateral wall. circumflex compromise from an annuloplasty suture — the circumflex runs behind the posterior annulus. Tell the surgeon it is a new regional wall-motion abnormality in circumflex territory, not stunning; it needs a look (flow probe, angiogram, or release/bypass).
• IABP. reasonable at CI 2.2 on rising epinephrine after an ischemic insult — augments coronary flow and unloads; a defended no (adequate CI, wait and watch) is also acceptable. Endless epinephrine escalation without considering mechanical support is the flag.

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• Dx. systolic anterior motion with dynamic LVOT obstruction — an underfilled, hypercontractile, vasodilated small ventricle after annuloplasty. Naming the obstruction, not chasing the pressure, is the point.
• Inotropes. stop both — they empty and overdrive the ventricle and worsen the obstruction; treating this hypotension with more inotrope is the classic error.
• Volume. 500–1000 mL guided by TEE; enlarging the cavity moves the leaflet out of the outflow tract.
• Pressor. phenylephrine (or norepinephrine) to raise afterload and hold the outflow tract open — MAP 70–80; the reverse of MR management before repair.
• Rate. slow to 70–80 with esmolol 0.5 mg/kg then infusion once filled and afterloaded; longer diastole fills the cavity and beta-blockade lowers contractility.
• Gradient 20. acceptable — mild residual SAM often resolves as the ventricle remodels; continue the strategy and reassess. No further action needed beyond avoiding the triggers.
• Gradient 80 refractory. structural — the repair needs revision (sliding plasty, larger ring, leaflet reduction); tell the surgeon this is SAM, not low output, and go back on bypass.

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• DDx. surgical bleeding at suture or cannulation sites versus medical: residual heparin or rebound, platelet dysfunction, low fibrinogen, fibrinolysis, hypothermia. Bright, brisk, sustained output leans surgical; diffuse ooze with abnormal labs leans medical.
• Send. CBC, fibrinogen, PTT/ACT, TEG or ROTEM with heparinase, ionized calcium, temperature, ABG.
• Native vs heparinase R. R shortens with heparinase — residual heparin or rebound; protamine 25–50 mg titrated, recheck. Both channels equally abnormal would mean a factor problem, not heparin.
• Products. fibrinogen first — cryoprecipitate 10 units or fibrinogen concentrate 2–4 g to > 150–200; platelets one apheresis unit for a count of 95 with MA 42 and aspirin on board; FFP only for a persistently long R. Reflexive FFP-for-everything is the trap.
• Aspirin. yes — qualitative platelet dysfunction on top of bypass; lowers the threshold to give platelets; not a reason to withhold surgical control.
• Back to OR. yes — 300+ mL/hr for two hours with corrected labs is surgical until proven otherwise; transfusing into a surgical bleed is the error. Tamponade physiology or instability makes it emergent.
• Before he goes. blood checked and in the room, products ordered, access and monitoring intact, pressors and the surgeon; anticipate hypotension when the chest opens and tamponade relieves.

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• DDx. RV failure from his pulmonary hypertension, tamponade, RV ischemia (right coronary air or graft issue), volume overload, pneumothorax. High CVP with a low wedge separates it from LV failure and tamponade (which equalizes).
• Dx. RV failure with septal shift starving the LV — the low output is right-sided; treating it as LV failure with fluid is the trap.
• Volume. hold — CVP 18 with a distended RV; more preload worsens septal shift. Consider cautious removal if overloaded.
• Drugs. epinephrine or milrinone (with norepinephrine/vasopressin for SVR) for RV contractility; inhaled NO 20 ppm or inhaled epoprostenol 50 ng/kg/min to lower PVR; end point is a smaller RV, CI > 2.2, MAP 65, lactate clearing. Vasopressin holds SVR with less PVR effect than phenylephrine.
• Ventilator. drop PEEP to 5–8, tidal volume 6 mL/kg, raise the rate to normocarbia, FiO2 up; high mean airway pressure and hypercarbia load the RV.
• Escalation. mechanical RV support — RVAD (Impella RP or ProtekDuo) or VA-ECMO; call the surgeon and perfusion now, not after the third pressor.

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• Why worse here. a fresh repair with a stiff recovering LV and pulmonary hypertension: loss of atrial kick and a rate of 150 drop output and raise LA and PA pressures, loading the RV again. Not routine post-op AF.
• First moves. restore pressure, treat triggers (electrolytes, hypoxia, pain, ischemia), get a 12-lead, decide by stability.
• Electrolytes. KCl to > 4.0, magnesium 2 g IV; magnesium alone converts some.
• Rate vs rhythm. he is symptomatic on an inotrope — rhythm control (amiodarone) is favored; beta-blockers and calcium-channel blockers cost inotropy and pressure in this heart.
• Cardioversion. unstable — synchronized 120–200 J biphasic now, with a small dose of propofol or midazolam; pads are already on.
• Keep him in sinus. amiodarone 150 mg IV then 1 mg/min x6 h, 0.5 mg/min x18 h; correct electrolytes; beta-blocker once hemodynamics allow.
• Anticoagulation. heparin infusion without a bolus once chest-tube output is reliably low (< 50 mL/hr for several hours) — POD 2–3 is typical; a titratable agent first, warfarin later. Restarting full anticoagulation the day after a bleeding re-exploration, or ignoring stroke risk, are both flags.

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• DDx. embolic stroke, residual sedation or metabolic cause, watershed injury from low flow, seizure, intracranial bleed on heparin; a lateralized deficit points structural.
• Next 30 minutes. neuro exam, glucose, stop sedation confounders, stat non-contrast CT with CTA, call neurology; this is a time-critical event.
• Cause. embolism — new AF with a large left atrium, fresh atrial suture line and ring, intracardiac air or debris from the repair; the mitral operation and the AF together are the setup.
• Heparin. hold, do not reverse: hemorrhagic conversion risk in a large fresh infarct versus embolic risk from AF and a fresh repair; typical practice is to hold 3–7 days depending on infarct size, then resume. The resident must hold the three risks (bleeding chest, embolic AF, hemorrhagic conversion) against each other.
• Thrombectomy. possibly — a large-vessel occlusion within the window is a thrombectomy candidate even after cardiac surgery; thrombolysis is contraindicated. Call, do not decide it alone.
• BP. permissive hypertension — leave up to 220/120 untreated without thrombolysis, or ~180/105 after intervention; dropping the pressure into a fresh infarct is the error.

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• Extubate or not. a hemispheric deficit raises airway-protection and aspiration questions, but prolonged intubation has its own harms; either is defensible if the airway assessment is done.
• What must be true. follows commands, protects the airway with a cough and gag, acceptable gas exchange on minimal support, stable rhythm and pressure, no escalating support.
• Extubate or trach. extubate with a speech-swallow evaluation and NPO until cleared; tracheostomy on POD 5 for a single failed criterion is premature.
• Coughing after sips. NPO, aspiration precautions, formal swallow study, chest film; do not let the family feed him.
• Wife's question. honestly: the stroke was an embolic complication, a known risk of mitral surgery and of the atrial fibrillation that followed; it was recognized and imaged promptly; recovery is uncertain and rehabilitation starts now. One message agreed with the surgeon; no blame, no false reassurance.

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• Premedication. midazolam 1 mg IV titrated with oxygen and a pulse oximeter on — anxiety drives the rate, but oversedation brings hypercarbia and hypoxemia that raise PVR in a strained RV. Either extreme (reflexive 2 mg or refusing anxiolysis) gets a probe.
• Induction. etomidate 0.2 mg/kg or propofol in 20 mg increments against the arterial line, fentanyl 3–5 mcg/kg to blunt the rate response, rocuronium; rate target 60–80. A propofol bolus that drops SVR, or ketamine that drives rate, are both flags.
• HR 120, BP 80/46. diastole is the only filling window across a 0.9 cm² valve; the fast rate collapses stroke volume and raises LA pressure. Phenylephrine first to restore SVR and coronary pressure without rate, esmolol to buy diastole, cautious volume only if underfilled. An inotrope or chronotrope first is the red flag.
• More esmolol. yes, toward 70–80, in 10–20 mg increments watching the pressure; digoxin and metoprolol are already on board, so go gently.
• SpO2 85%. rising LA pressure flooding the lungs, plus atelectasis; FiO2 1.0, PEEP 5, slow the rate further, avoid volume; hypoxia raises PVR and threatens the RV — the resident must hold oxygenation, rate, and the RV together.
• Potassium. replace to > 4.0 before bypass — hypokalemia on digoxin invites arrhythmia and AF with rapid rate is her failure mode.

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• Why this rate. diastole shortens; filling across the fixed orifice fails; LA pressure climbs and output falls — the classic MS decompensation, not routine AF.
• First moves. restore pressure (phenylephrine/vasopressin), check depth, electrolytes, oxygenation, and tell the surgeon; prepare to cardiovert.
• Rate vs rhythm. she is unstable — synchronized cardioversion is the ACLS answer; rate control is for the stable patient. Commit.
• Cardioversion with smoke. spontaneous echo contrast raises embolic concern, but she is heparin-bridged (INR 1.4, heparin stopped hours ago) and unstable — name the risk and act anyway; a giant chronically fibrillating rheumatic LA often does not hold sinus, which is the counter-argument.
• Drugs and cost. amiodarone 150 mg over 10 min is the least hemodynamically costly; esmolol and diltiazem drop SVR and contractility in a strained RV; digoxin is too slow. The cost, not the name, is the point.
• Cardiovert or go on. both defensible: synchronized 120–200 J now, or heparinize and expedite bypass, which definitively unloads the valve. Endless drug titration into a failing patient is the trap; want a committed choice with a reason.

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• Controllable PVR drivers. hypercarbia, hypoxia, acidosis, light anesthesia, atelectasis, hypothermia — all correctable now; naming and fixing them is the core of RV protection in MS.
• PaCO2 and vent. 30–35, tidal volume 6–8 mL/kg, moderate PEEP, FiO2 1.0, avoid high mean airway pressure; a number, not 'ventilate well.'
• iNO. yes — 20 ppm; lowers PVR without dropping SVR; a systemic vasodilator here would drop the SVR a fixed-output patient needs.
• Inotrope. epinephrine 0.03–0.05 for RV contractility with coronary pressure preserved; milrinone helps PVR but vasodilates — pair with a pressor. Defend the choice against this RV.
• Pink froth. cardiogenic pulmonary edema from an obstructed LA under a high rate and pressure; hemoptysis from ruptured bronchial veins is the same physiology (the blood-streaked sputum in the HPI); TRALI and aspiration are far behind.
• PEEP. modest increase (8–10) recruits and reduces the oxygenation deficit; excessive PEEP impedes venous return and RV output in a pressure-loaded RV — a titrated answer.
• Furosemide. no — she is preload-dependent behind a fixed obstruction; diuresing now drops output. The fix is mechanical.
• Wait or go. cannulate now — bypass is the only thing that relieves the obstruction; temporizing into worsening edema is the error.

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• DDx. RV failure from chronic pulmonary hypertension now unmasked, residual high PVR, RV ischemia or air down the right coronary, over- or under-filling, rhythm, prosthesis problem (TEE excludes). Septal bowing points RV.
• Volume. no — CVP high and RV distended; more preload worsens the septal shift and starves the LV. TEE-guided, cautious.
• Inotrope. epinephrine for contractility and perfusion pressure; milrinone for PVR and lusitropy with a pressor to hold SVR; both together is the common defended plan.
• Other inhaled. inhaled epoprostenol or milrinone as an adjunct; check for air in the right coronary on TEE.
• Maximal medical failing. this is mechanical support territory; do not titrate a fourth drug into a distending RV.
• IABP. no — it unloads the LV and augments coronary flow but does little for an RV-predominant failure; naming why is the judgment.
• Device. temporary RVAD (RA-to-PA, or a percutaneous ProtekDuo/Impella RP later) or VA-ECMO if oxygenation is also failing; bypass stays in until the device is running; anticoagulation plan for the mechanical valve considered with the device.

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• DDx. surgical (suture lines, cannulation sites, RVAD cannulae) versus residual heparin/rebound, platelet dysfunction, low fibrinogen, fibrinolysis, hypothermia. Bright and brisk leans surgical; diffuse ooze with bad labs leans medical.
• Send. CBC, fibrinogen, PTT/ACT, TEG with heparinase, ionized calcium, temperature, ABG.
• Heparinase corrects R. residual heparin or rebound — protamine 25–50 mg, recheck. Equal abnormality on both channels would mean factors, not heparin.
• Products. fibrinogen first (cryo 10 units or concentrate 2–4 g to > 150–200), then platelets for count 95 with MA 44 after bypass; FFP only for a persistently long R. Blind FFP is the trap.
• INR 1.4. not the cause of this bleeding; do not give FFP or PCC to chase a warfarin-tail INR of 1.4 — PCC in particular is a thrombotic risk with a fresh mechanical valve and a device.
• Heparin timing. staged: secure hemostasis first, then heparin without a bolus at a low target (PTT 50–60) within 24–48 h, higher once dry; the RVAD raises the urgency. Full anticoagulation in the same hour she is bleeding invites disaster; no anticoagulation for days with a mechanical mitral valve and a device is the other failure.
• Back to OR. yes — sustained surgical-rate bleeding with corrected labs and a rising CVP; re-explore before tamponade.

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• Extubate or wait. wait — a respiratory acidosis on pressure support in a pulmonary-hypertensive RV is a set-up: hypercarbia raises PVR and a failed extubation tips the RV. A low threshold to defer is defensible.
• Fix first. diuresis toward euvolemia without underfilling, secretion clearance, sedation off, normocarbia, and RV support optimized.
• Extubate on iNO. yes, with iNO delivered by nasal cannula or a bridging sildenafil dose to prevent rebound; do not stop iNO to extubate.
• What drove it. work of breathing and hypercarbia raised PVR and RV afterload, with residual edema; reason from her physiology, not 'she wasn't ready.'
• Reintubate or BiPAP. reintubate — rising PaCO2 with a strained RV does not tolerate a BiPAP trial that fails an hour later; do not delay into an RV crisis.
• Tracheostomy. comes out when she is off ventilatory support, clearing secretions, tolerating capping, and no longer needs the airway for suctioning; likely weeks.

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• What happened. rebound pulmonary hypertension on abrupt iNO withdrawal; RV afterload spiked and the RV failed, dropping LV preload and output. Recognize the rebound unprompted.
• First move. iNO back on at 20 ppm now, FiO2 1.0.
• Triggers. hypoxia, hypercarbia, acidosis, pain, agitation, light sedation, hypothermia, the abrupt wean itself.
• Vent and sedation. normocarbia to mild hypocarbia, FiO2 up, avoid high mean airway pressure, deepen sedation and analgesia to blunt sympathetic surges.
• Pressor or inotrope. vasopressin for SVR and RV coronary perfusion (spares PVR) plus epinephrine or milrinone for contractility; the RV-perfusion logic, not a single reflexive agent.
• Re-wean. slowly — 1–2 ppm steps over days from 5 ppm downward, with sildenafil 20 mg TID started before the wean.
• RV arrest. compressions do little for an afterload-obstructed RV; treat the cause (iNO, oxygen, ventilation, acidosis), epinephrine, and call for ECMO early.

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• Why still. the RV is still pressure-loaded and rate-sensitive; a fast rate shortens RV filling and drops output, and loss of atrial transport still costs her. She remains rate-sensitive after MVR.
• First moves. restore pressure, magnesium, potassium, oxygenation, rule out tamponade, then rate versus rhythm by stability.
• Rate vs rhythm. amiodarone for rhythm control — beta-blockade and diltiazem drop the contractility her RV needs; cardiovert if she becomes unstable.
• Anticoagulation. she is already therapeutically heparinized for the valve, which covers cardioversion; no change, just confirm the PTT is actually at target.
• Junctional 45. pace — the atrium's state decides the mode; check the atrial wire before choosing.
• Atrial wire check. whether there is organized atrial activity that captures; if she is still fibrillating the atrial lead cannot capture and VVI at 80–90 is what delivers rate.
• Organized and capturing. AV-sequential (DDD or AAI if AV conduction is intact) at 80–90 to restore the atrial kick — valuable in a stiff, pressure-loaded RV. Running DDD through ongoing AF, or dismissing the atrial contribution when she is organized, both get a probe.

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• Something went wrong. no — plainly: her pulmonary hypertension and right-heart strain predated surgery and are why the course has been hard; the bleeding and the arrhythmias were complications that were recognized and treated; recovery will be slow and is uncertain. One message agreed with surgery and the ICU; no blame, no false reassurance.
• Tracheostomy. comes out when she is off ventilatory support, clearing secretions, tolerating capping, and no longer needs the airway for suctioning; likely weeks.
• Anticoagulation. lifelong warfarin for a mechanical mitral valve, INR target 3.0 (2.5–3.5) plus low-dose aspirin; DOACs are contraindicated with a mechanical valve; her atrial fibrillation would require anticoagulation anyway.

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• Why bleeding. redo raw surfaces, 4+ hours of bypass, DHCA, hemodilution, consumption, platelet dysfunction (bypass plus aspirin), fibrinolysis, acidosis, hypocalcemia, and heparin not yet neutralized. Treating this ooze as routine is the flag; the resident should tie the list to this case.
• Fixable now. calcium, acidosis and ventilation, confirm normothermia (done), complete protamine, start targeted product while the TEG runs; concrete moves, not a recited list of CPB coagulopathy causes.
• Calcium. calcium chloride 1 g centrally, repeat to ionized > 1.1–1.2; 0.94 impairs both clot formation and contractility. Ignoring it is a probe.
• Bicarbonate. defensible either way: correct ventilation and perfusion first; bicarbonate 50–100 mEq is reasonable at pH 7.24 with base excess -8 because coagulation enzymes fail below ~7.2, but it raises CO2 and does nothing for the cause.
• Surgical or medical. diffuse ooze from every raw surface with abnormal labs is medical; a localized, brisk, bright bleed with normalizing studies is surgical. Here it is medical until the labs are corrected and it still bleeds.
• Surgeon's demand. partly — product is coming, but it goes by the TEG, not by the surgeon's request; and the field being medical now does not exempt him from a surgical bleed later once the labs are fixed.

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• ACT 180. incomplete neutralization, heparin redistribution, or a non-heparin coagulopathy prolonging the ACT — ACT is not heparin-specific, and with platelets 88 and fibrinogen 110 a residual elevation may not be heparin at all.
• Confirm. heparinase versus native TEG/ROTEM channel, or an anti-Xa/heparin level; ACT alone cannot separate the two.
• R 14 vs 6. R corrects with heparinase — residual heparin is real and is most of the R prolongation; equal channels would have meant factors.
• Rx. protamine 25–50 mg titrated, recheck; not another full empiric dose.
• Recurrent ooze with heparinase-correctable R. heparin rebound — tissue-bound heparin redistributing after protamine has cleared; a recurrence, not a new surgical bleed.
• Rebound Rx. protamine 25–50 mg, guided by the TEG; consider a low-dose infusion if it recurs.
• More protamine. no — with heparin already neutralized on the TEG, excess protamine is itself an anticoagulant and platelet inhibitor, and carries hypotension, pulmonary hypertension, and anaphylactoid risk; titrate to evidence of heparin, not to the ooze.

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• Channels. R 9 = factor deficiency (modest); K/angle and functional-fibrinogen MA 8 = fibrinogen deficit; kaolin MA 42 with count 90 = platelet function and number. Reading the channels into a plan is the skill.
• Order. fibrinogen and platelets first — clot strength is the problem; FFP or PCC for R only if it stays long. FFP-for-everything is the trap.
• Cryo vs concentrate. fibrinogen concentrate 4 g (roughly 50 mg/kg) is low-volume, fast, and pathogen-reduced — attractive when volume matters; cryoprecipitate 10 units is the alternative. Target > 150–200. A defended choice, not a list.
• MA 42 at count 90. bypass acquires platelet dysfunction — extracorporeal contact, activation, hypothermia during DHCA — plus aspirin; the count overstates function. One to two apheresis units.
• TXA redose. yes — long bypass and DHCA drive fibrinolysis; a second 1 g dose or infusion (LY30 on the TEG informs it); seizure risk rises with high total doses and renal impairment, so not unlimited.
• rFVIIa / PCC. with substrate corrected and a dry surgical field, low-dose rFVIIa (20–40 mcg/kg) or 4-factor PCC 15–25 U/kg is a defensible last resort for refractory microvascular bleeding, with explicit thrombotic risk to fresh grafts; reaching for it before substrate correction or before excluding surgical bleeding is the red flag.

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• Calcium 0.82. citrate from rapid product chelates calcium faster than a hypoperfused liver clears it; hypocalcemia costs both contractility and coagulation. Calcium chloride 1 g per 2–4 units of product, titrated to ionized > 1.1 and to the pressure.
• K+ 6.4 with T waves. transfusion load plus cardioplegia plus acidosis; calcium chloride first (stabilizes the membrane and treats the calcium), then insulin 10 units with dextrose 25 g, ventilate to lower CO2, bicarbonate if acidotic; furosemide or CRRT if it persists. Membrane-stabilize-then-shift, not one drug.
• Hgb 6.9. yes — actively bleeding on two pressors after a long pump run: transfuse toward 8–9, not to a stable-patient threshold of 7; each unit brings more citrate and potassium, which is why the calcium and K+ are re-checked with it.
• Close or open. leave open if the field is not dry, the myocardium is edematous, or hemodynamics will not tolerate closure; damage control with packing and planned re-exploration beats closing into tamponade. Pressor requirement and ongoing loss decide it.
• Trial closure fails. reopen — that is tamponade physiology on closure; pack, leave the sternum open with a patch, return in 24–48 h.
• Open chest to the ICU. full sedation with analgesia and usually paralysis (no coughing or bucking against a patched sternum), lung-protective volumes with modest PEEP, and a bedside reopening kit; the handoff carries the product plan by TEG, expected calcium and potassium trends, protamine total and rebound history, pressor doses, and the trigger for emergent reopening.

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• Give and stop. R has corrected — stop FFP; MA and functional fibrinogen still low — fibrinogen and platelets. Correcting to the current TEG, including stopping what is no longer indicated, is the judgment.
• Targets. fibrinogen > 150–200, platelets > 100 with active bleeding after bypass, ionized calcium > 1.1, normothermia.
• Massive transfusion effects. dilutional coagulopathy and thrombocytopenia, citrate hypocalcemia, hyperkalemia, hypothermia, acid-base shifts, TACO and TRALI, immunomodulation and infection; the syndrome, not one item.
• Monitoring. ionized calcium and potassium every hour while transfusing, TEG every 1–2 hours, temperature, filling pressures and oxygenation to separate TACO from TRALI.
• Corrected labs, still bleeding. surgical until proven otherwise — the coagulopathy has been treated and no longer explains it; call the surgeon rather than keep transfusing.

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• Dx. tamponade from retained clot — a bleeding chest that suddenly drains nothing, rising and equalizing pressures, pulsus. Recognize the pattern unprompted.
• Equivocal TEE. no — a localized postsurgical clot is easily missed; a bleeding chest with a stopped tube and this hemodynamic picture is tamponade until the chest is open. A clean echo must not reassure.
• Temporizing. full, fast, tight: volume to keep preload, norepinephrine or epinephrine for pressure, avoid anything that drops venous return or slows the rate; the definitive treatment is opening the chest.
• Furosemide. no — the oliguria is low forward flow from impaired filling; diuresing a tamponading patient is the red flag.
• Bedside sternotomy. yes — peri-arrest tamponade is opened where he lies; a defended yes, with the hemodynamic plan through it (epinephrine ready, blood in the room, surgeon or trained ICU team).
• Clot evacuated. abrupt rise in venous return and pressure, sometimes hypertension and a tachyarrhythmia; be ready to back off pressors and treat the rhythm; then find the bleeder.

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• DDx. TRALI, TACO, cardiogenic edema, aspiration, ARDS from a long pump run and shock — a desaturation within hours of heavy transfusion puts the transfusion causes first.
• TRALI vs TACO. TRALI: non-cardiogenic, normal-to-low filling pressures, within 6 hours, no response to diuresis; TACO: hydrostatic, high filling pressures, improves with diuresis. His numbers say TRALI. Reason from the data.
• Rx. supportive — oxygenation, lung-protective ventilation, hemodynamic support; diuresis is not the treatment; most resolve in 48–96 hours.
• Ventilator. 6 mL/kg PBW (~440 mL for 5'10"), plateau ≤ 30, PEEP 10–14 titrated, permissive hypercapnia; concrete numbers.
• Further product. only TEG-targeted, minimal-volume product (concentrates over FFP); avoid volume-heavy blind transfusion.
• Co-components. no — the blood bank quarantines every component from the implicated donations and evaluates the donor for anti-HLA/HNA antibodies; the case is reported as a suspected TRALI.

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• What it is. surgical — the medical coagulopathy is corrected and no longer explains it; continuing to transfuse into a surgical bleed is the trap.
• Thresholds. > 200 mL/hr for 2 hours, > 150 mL/hr for 4, > 1 L total in a few hours, an acute increase, tamponade physiology, or instability — a defended trend, not a recited number.
• Watch overnight. no — 120 mL/hr for four hours with corrected labs in a chest that has already tamponaded once is a return to the OR tonight; the resident should say so to the surgeon plainly rather than defer.
• Tense chest, hypotension. tamponade again — emergent return to the OR (or bedside opening if he arrests); not more observation.
• Chest opens. relief of tamponade: abrupt rise in venous return and pressure, sometimes hypertension and a tachyarrhythmia; then the bleeder. Blood and products checked in the room, access and monitoring intact, pressors running and drawn up, epinephrine ready to back off.

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• Complication. honestly: bleeding after a difficult reoperation on prolonged bypass with circulatory arrest was a known risk; it was heavy, was treated with blood products and two returns to the operating room, and has stopped; one message agreed with the surgeon, without blame or false reassurance. Name the transfusion risks plainly — the lung injury he is being ventilated for, fluid overload, electrolyte shifts, reactions, small infection risks — framed as monitored for and outweighed by the need to treat life-threatening bleeding.

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• Targets. HR ~60, SBP 100-120 while keeping the mottled leg and the kidneys perfused; want numbers, not 'lower it.' The aim is dP/dt and rate, not the pressure alone — an unrepaired dissection extends or ruptures on a high-impulse aorta.
• Esmolol first. rate control before vasodilation; nicardipine or nitroprusside alone provokes reflex tachycardia and a rise in dP/dt. Vasodilator-first is the classic error.
• Add a vasodilator. nicardipine 5 mg/h titrated, or nitroprusside 0.3-0.5 mcg/kg/min, once rate is controlled. Caution: with the new diastolic murmur (acute AR), heavy beta-blockade removes the compensatory tachycardia; do not chase HR 60 at the cost of forward flow.
• Which arm. the higher pressure is the true-lumen pressure; the 36 mmHg differential means the left subclavian is compromised. A single arbitrary radial is the trap.
• Art line site. right radial reads central pressure now but goes false once right axillary antegrade perfusion starts; left radial is under-reading. Defensible answer: right radial for induction plus a left radial or femoral before bypass, tied to the surgical plan.
• Axillary cannulation. yes — during axillary perfusion the right radial reads pump pressure, so a second site (left radial or femoral) is required.
• Femoral side. left. The dissection reaches the right common iliac and the right femoral pulse is diminished; a right femoral line may read a false-lumen pressure.
• Access sequence. awake art line and a second large-bore IV before induction; central line and rapid infuser immediately after induction; PA catheter or central access for vasoactives before bypass. Inducing on one 18 g is a flag.

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• Agent. etomidate 0.2-0.3 mg/kg or a small propofol dose with generous opioid (fentanyl 5-10 mcg/kg) and esmolol available; goal is no surge on laryngoscopy and no collapse. Either direction is dangerous: surge extends the dissection, hypotension drops coronary and limb perfusion.
• Rate with acute AR. faster is better for AR (shorter diastole, less regurgitant volume, less LV distension); this collides with anti-impulse slowing. Want the conflict named and resolved: HR 70-80, no lower, avoid high afterload.
• 74/40, HR 50. bradycardia is poorly tolerated in acute AR — long diastole, big regurgitant fraction, low forward output, poor coronary perfusion of a hypertrophied LV. Treating as ordinary hypotension is a flag.
• Which pressor. ephedrine or small epinephrine for chronotropy plus modest volume; pure phenylephrine raises afterload and the regurgitant fraction. Defend the choice and name an end point: MAP 65-70 with HR 70-80, not 'better.'
• TEE picture. tamponade physiology on top of acute AR; RV collapse means hemodynamically significant. Accelerates sternotomy and cannulation; want tamponade named unprompted.
• Opening the pericardium. abrupt rise in venous return and pressure as tamponade is relieved — hypertensive surge onto an unrepaired aorta. Nicardipine or nitroprusside and esmolol in hand, cannulation strategy agreed, pump primed before the knife touches pericardium. Opening without that is the trap.
• 196/100 after decompression. nitroprusside 0.5-1 mcg/kg/min or nicardipine 1-2 mg boluses, esmolol 0.5 mg/kg; deepen anesthetic; target SBP 100-120 within a minute or two.

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• Cannulation site. not the right femoral — the right iliac is dissected and the pulse is gone, so a wire there may enter the false lumen. Right axillary (antegrade true-lumen flow, later used for cerebral perfusion) or direct true-lumen aortic cannulation under TEE; left femoral is a fallback.
• True lumen. TEE: wire in the lumen that expands in systole, has the flap moving away from it, and communicates with the LV outflow; false lumen is larger, has spontaneous echo contrast, and expands in diastole.
• Inferior hypokinesis. coronary ostial dissection, usually the right coronary; the stem's inferior ST depression was the early clue. Not an old change.
• Change the operation. the surgeon may need to reimplant or bypass the RCA; ask for a vein graft and plan inotropic support coming off bypass; expect RV dysfunction.
• Right rNIRS drops. antegrade circuit not reaching the right brain: cannula malposition, dissection of the innominate/right carotid by the cannula jet, kinked line, low flow, or compression of the true lumen. Accepting a 20-point fall as 'artifact' is the flag.
• Checks. cannula position and line pressure with perfusion, flow rate, TEE of the arch vessels, radial pressure on the right, then ask for a cannulation change or adjunctive left carotid perfusion.
• Lactate and urine. visceral and renal malperfusion continuing on bypass — ischemia is ongoing and time-critical; keep flow and pressure up (MAP 60-70 on pump), confirm true-lumen perfusion, and warn the surgeon that distal flow is not restored.
• Persistent leg ischemia. restoring true-lumen flow often fixes distal beds, but a leg still pulseless off bypass needs femoral exploration, fem-fem bypass, or fenestration now; also watch for reperfusion hyperkalemia and rhabdomyolysis.

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• Targets. ~18 C nasopharyngeal for unprotected DHCA; 24-28 C (moderate hypothermia) is standard when antegrade cerebral perfusion is used. Want a number with a rationale — CMRO2 falls ~6-7% per degree.
• Site and EEG. nasopharyngeal or tympanic tracks brain temperature; bladder and rectal lag. Electrocerebral silence on EEG (or a fixed cooling time, e.g. 30-45 min) before arrest confirms the brain is actually cold.
• ACP. antegrade via the axillary delivers oxygenated flow and permits longer arrest; retrograde via the SVC gives some cooling and de-airing but unreliable substrate. With the axillary in, ACP is the natural pick — want a committed choice.
• ACP numbers. ~10 mL/kg/min (600-1000 mL/min), pressure 40-70 mmHg measured at the right radial, cold (20-28 C).
• Right rNIRS falls during ACP. the perfused side is under-perfused: cannula or clamp position, innominate flow diverted, flow too low, or a dissected carotid. Check line pressure, flow, and TEE; ask the surgeon to add a left carotid cannula; do not wait for the number to recover on its own.
• Cooling and rewarming. cool over 30+ min with an arterial-venous gradient of 10 C or less; rewarm with a gradient of 10 C or less and arterial inflow capped at 37 C — cerebral hyperthermia after ischemia worsens outcome. Gas solubility and bubble formation are the mechanism behind the gradient limit.
• Glucose 240. insulin infusion to 140-180; hyperglycemia worsens ischemic neurologic injury around arrest. Ignoring the number is the flag; driving it to 100 risks hypoglycemia.
• 37.2 vs 34.1. stop rewarming on the pump. The brain is already at target and the core gradient means afterdrop is coming; the risk now is cerebral hyperthermia, not residual hypothermia. Use forced-air warming and time, not more arterial heat.

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• Surgical vs medical. diffuse ooze from every raw surface with abnormal studies is medical; brisk bright bleeding from one place with normalizing studies is surgical. Both coexist after an arch repair with multiple suture lines.
• ACT 168. modest elevation: residual heparin, heparin rebound, or just coagulopathy and hypothermia. Heparinase-ACT or HEPTEM vs INTEM comparison separates them; if heparin, protamine 25-50 mg. Blind repeat protamine is not harmless.
• First product. fibrinogen — FIBTEM A10 6 mm (fibrinogen ~110) is the deficit that matters most; cryo or fibrinogen concentrate first. Then platelets, then plasma/PCC for the long CT.
• Cryo. 10 units (or 2 pooled) raises fibrinogen ~70-100 mg/dL; target >150-200 mg/dL in ongoing surgical bleeding.
• Platelets. yes — 80 K of aspirin-inhibited, bypass-damaged platelets in a bleeding chest is a transfusion indication; the number alone understates the defect.
• Triad. rewarm to 36 C, ionized calcium >1.1 mmol/L (calcium chloride 1 g increments), correct acidosis with perfusion not bicarbonate. Products will not clot cold and hypocalcemic — ignoring temperature and calcium is the trap.
• TXA. reasonable to redose (e.g., 1 g) if lysis on ROTEM or ongoing ooze; watch seizure risk with high cumulative doses after arrest.
• Corrected but still bleeding. re-exploration. Continued transfusion into a chest that is bleeding with normal studies is the error; also excludes early tamponade.

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• Dx. tamponade from localized clot — a tube that stopped draining plus equalizing pressures and a falling index. Alternatives: RV failure, hypovolemia, suture-line bleeding, pneumothorax; but the stopped tube is the pattern to name unprompted.
• Study. TTE now, at the bedside, within minutes; TEE if TTE is nondiagnostic. Do not send him to CT.
• Negative TTE. no — loculated posterior clot is missed easily in a fresh chest with poor windows. Clinical picture outweighs the study; call the surgeon.
• Furosemide. no. The oliguria is low forward flow; diuresing a tamponading patient collapses filling. A reflexive diuretic order is a red flag.
• Bridge. full, fast, tight: HR 90-100 (avoid bradycardia), small volume boluses to maintain the gradient, norepinephrine or epinephrine; avoid PPV increases and sedation boluses that drop venous return.
• Bedside vs OR. OR if he is holding on the bridge; bedside sternotomy if he arrests or is arresting. Pads on, sternotomy tray at the bedside either way.
• Induce before the surgeon is scrubbed. no — surgeon scrubbed and prepped before induction; induction can collapse a tamponading heart and the only rescue is the knife. Then ketamine 0.5-1 mg/kg or etomidate, minimal positive pressure, pressor running; expect either collapse on induction or a surge on decompression.
• 172/95 after decompression. fresh suture lines on a repaired aorta: nicardipine or nitroprusside to SBP 100-130, deepen anesthetic, rule out pain/light plane.

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• DDx. embolic or hypoperfusion stroke, watershed injury from the arrest, intracranial hemorrhage on coagulopathy, seizure with post-ictal deficit, residual sedation. A lateralizing deficit means structural until proven otherwise.
• Most likely. embolic stroke — arch manipulation, atheroma and air, the dissected innominate/carotid, and the arrest period itself. Want it tied to the operation.
• Next. neuro exam then non-contrast CT (with CTA of the arch vessels) within the hour; stroke neurology called. Waiting to 'let the sedation wear off' is the flag.
• Lysis / thrombectomy. thrombolysis contraindicated (major surgery within hours, recent aortic repair); thrombectomy is possible for a large-vessel occlusion if CTA shows one and the access route is intact — the call belongs to neurointervention with the surgeon.
• BP. permissive but bounded: the fresh aortic repair caps SBP (roughly 120-140 max), while the penumbra needs pressure; avoid hypotension, no aggressive lowering. Name the tension.
• Glucose and fever. insulin to 140-180, acetaminophen and cooling to normothermia; both worsen infarct evolution.
• Wife. plain and honest: he has had a stroke; it is a known risk of emergency repair of a dissection that involves the arch; it was recognized and is being treated; recovery is uncertain and will take time. No blame, no false reassurance, and the same account the surgeon gives.

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• Cause. ischemic ATN from intra-op renal malperfusion, bypass, arrest, and hypotension; contributors: CTA contrast, transfusion pigment load, low output. Want it tied to his course.
• Fluid vs diuretic. neither reflexively — assess volume and forward flow first. A diuretic will not save an ATN kidney and can hide it; a bolus into an overloaded RV worsens congestion.
• Underfilled on echo. volume: 500 mL crystalloid or blood if Hgb is low, reassess; the earlier tamponade and bleeding make hypovolemia plausible. Stated MAP 76 on a pressor with an empty heart is a pressor propping up an empty tank.
• Stop / check. nephrotoxins (NSAIDs, aminoglycosides, contrast), abdominal pressure, Foley patency, CK and hemolysis labs, recheck the malperfused leg.
• K+ 6.4. calcium first (membrane), then insulin 10 units with dextrose 25 g, albuterol nebulized 10-20 mg, bicarbonate if acidotic; then removal — but a 10 mL/h kidney will not remove it, which is the point.
• Calcium. chloride 1 g centrally (three times the elemental calcium of gluconate) or gluconate 3 g peripherally; repeat if T waves persist.
• RRT. yes — hyperkalemia refractory to shift therapy with oliguric AKI; CRRT rather than intermittent HD in a patient on pressors.
• Anticoagulation. regional citrate or a no-anticoagulant circuit; systemic heparin into a chest putting out 90 mL/h is the error. Watch ionized calcium with citrate.

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• SBT. yes — pressor off, modest support, awake; the hemiparesis is not a reason to wait. First: a fluid balance at or below even via CRRT, no active bleeding, electrolytes corrected, and a swallow and secretion assessment, because the left-sided weakness raises aspiration risk.
• Extubate. yes — awake, following commands, adequate tidal volume, no distress. A weak left-sided cough is the stroke, not the lungs; keep him NPO pending a swallow evaluation and aggressive pulmonary toilet. Leaving him intubated for the deficit alone is the flag; heavy secretions he cannot clear would change the answer.
• HR 138 irregular. postoperative AF (peak POD 2-4). First: is he unstable? BP 96/58 is borderline — check K+ and Mg2+, exclude recurrent tamponade, bleeding, and ischemia before treating the rhythm as the whole problem.
• Agent. amiodarone 150 mg IV over 10 min then infusion — rate control without dropping the pressure further; esmolol is titratable but BP 96/58 limits it; synchronized cardioversion if he becomes unstable, and it is safe without anticoagulation this early after onset.
• Anticoagulation. not today — a large fresh MCA infarct carries hemorrhagic-transformation risk that outweighs the embolic risk of new AF in the first days; aspirin now, repeat head CT, and start heparin or a DOAC at roughly 7-14 days from the stroke if imaging shows no hemorrhage, with neurology. A reflexive heparin drip because 'AF plus stroke' is the error; so is an open-ended hold.
• Targets. SBP 100-120, HR <60-70 for the residual dissection; three days out from the stroke the penumbra argument no longer justifies higher pressure. Name the tension and the resolution.
• Oral agents. beta blocker first (metoprolol or carvedilol) — it is the anti-impulse agent; then an ACE inhibitor or ARB (limited by the kidney) or amlodipine. Wean nicardipine as orals take hold, usually over 24-48 h; a beta blocker is never the drug that gets dropped.
• CTA. yes — he is dialysis-dependent so contrast nephropathy is not the constraint; the study defines false-lumen patency, entry tears, branch-vessel perfusion, and the iliac, and sets the surveillance baseline.

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• What you need. device type (pacemaker vs ICD vs CRT), manufacturer, indication, pacing dependence and underlying rhythm, current mode and rate, tachytherapy status, battery and lead status, last interrogation date — and from the interrogation, escape rate, lead impedances and thresholds, and a written plan for reprogramming and reactivation. Reciting NBG letters instead of these facts is a flag.
• Matters most. pacing dependence — it decides whether EMI inhibition means a dropped beat or asystole, and therefore whether asynchronous pacing must be secured.
• Source. a recent interrogation report from the managing EP clinic, the manufacturer registry, or a perioperative interrogation now. Not the patient's recollection.
• 11 months. stale for an ICD — consensus is within ~6 months for ICDs (12 for pacemakers, 3-6 for CRT); with dependence plus planned EMI, this needs a fresh interrogation before the OR, not a recited number.
• Underlying rhythm. no — the monitor shows paced complexes; in an AV-node-ablated patient the escape (or absence of one) is only known by inhibiting the device during interrogation. Assuming the monitored rhythm is the intrinsic rhythm is the trap.
• Big jolt. an ICD shock — confirms tachytherapy is active and that he has had an arrhythmia the device treated; raises the stakes both for disabling therapy during cautery and for what protects him while it is off.

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• Inhibition consequence. asystole, not a dropped beat — the ablated AV node means no conduction and no reliable escape. Recognizing the catastrophic rather than nuisance nature is the point.
• Duration. for as long as the cautery burst lasts; a 10-second burst is 10 seconds of asystole in this patient.
• Magnet vs reprogram. reprogramming. A magnet over an ICD suspends tachytherapy only and does nothing to the pacing mode; it will not prevent inhibition.
• Magnet on the ICD. no effect on pacing — demand mode persists. A learner who expects the magnet to force asynchronous pacing has the core misconception.
• Mode. VOO (asynchronous ventricular) at a set rate; DOO is irrelevant with permanent AF.
• Pads. on and connected to a device that can both pace and defibrillate, with the pacing function tested for connection; pads lying on the chest unattached cost the same minute you cannot afford during asystole.
• Transcutaneous capture. a wide QRS with a T wave after each spike plus a palpable pulse or arterial waveform at the paced rate; the spike alone or pectoral twitching is not capture.

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• What the ICD can do. misread cautery noise as VF and deliver a shock — an inappropriate shock in a 25% EF ventricle can itself provoke VT/VF and hemodynamic collapse. This is the ICD-specific hazard, distinct from pacing inhibition.
• Off / on. off for the cautery portion, programmed just before incision by the device team; reactivated and confirmed in PACU before monitoring is withdrawn. Want timing, not just 'turn it off.'
• While off. continuous ECG monitoring, external pads on and connected, defibrillator in the room, someone watching the rhythm during cautery — the device cannot rescue a real arrhythmia.
• Below the umbilicus. consensus says infra-umbilical surgery with a well-placed pad often needs no reprogramming — but this is a hedge, not a pass: extensive monopolar cautery, a dependent patient, a stale interrogation, and Trendelenburg bringing the field closer to the generator all argue for securing the device. Want the argument engaged both ways and a defended choice.
• Magnet in Trendelenburg. it slips, and tachytherapy is back on with no warning; the first sign may be a shock. In steep Trendelenburg a taped magnet is unreliable; monitoring the magnet is not a plan.
• Commit. reprogram — it secures both asynchronous pacing and tachytherapy off in one step and does not depend on a magnet staying put. Magnet-only for a dependent ICD patient deserves a hard probe.

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• K+ 5.1. no — mild, chronic (CKD plus ARNI), no ECG change; hyperkalemia raises capture threshold, so it matters in a dependent patient, but 5.1 is not a barrier. Demanding shift therapy for a stable 5.1 is overtreatment, not vigilance.
• Would treat. K+ >5.5-6.0, a rising trend, peaked T waves, or loss of capture; recheck the morning of surgery and avoid potassium-containing fluids and acidosis.
• Succinylcholine. avoid — a 0.5 mEq/L rise on 5.1 in a pacing-dependent patient is a threshold problem; rocuronium with sugammadex available.
• Cautery. bipolar where feasible eliminates the EMI; if monopolar, short bursts (<5 s) at lowest effective power, harmonic scalpel for dissection, no cautery over the generator or lead path.
• Dispersive pad. right thigh or buttock so the current path from the pelvis runs away from the left upper chest; the heart and leads must be out of the arc.
• Apixaban. no — hold 48 h for a major surgery with CKD (72 h if CrCl <30); at 36 h he is short, and a laparoscopic colectomy in an anticoagulated CKD patient is a bleeding setup; delay to the 48 h mark unless the surgeon accepts the risk. No neuraxial plan here anyway.
• Central line. reasonable for vasoactives with EF 25%; use the right IJ under ultrasound — the leads run through the left subclavian/SVC and a wire can dislodge or perforate them; a stale interrogation makes lead integrity unknown.
• Before incision. VOO at the programmed rate with capture on the monitor, tachytherapy off and documented, pads on and connected, defibrillator in room, dispersive pad placed, K+ rechecked, device team reachable for reactivation.

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• Mode and rate. VOO; rate 80-90 rather than a nominal 60-70 — fixed stroke volume from a 25% EF ventricle means output is rate-dependent, and pneumoperitoneum plus Trendelenburg cut venous return. A learner who ignores rate adequacy deserves a probe.
• When off. after induction and monitors, immediately before incision, to minimize unprotected time; in holding is acceptable only with pads on and continuous monitoring from that moment.
• Magnet and go. the magnet suspends shocks but leaves pacing in demand mode — a dependent patient can still be inhibited to asystole. It solves half the problem. Proceeding on a magnet alone with extensive monopolar cautery in a dependent patient is the wrong call; wait, or use bipolar/harmonic only until the team arrives.
• Below the umbilicus. the consensus carve-out exists, and the learner should know it; but extensive cautery, dependence, and an upper-chest generator with the field tilted toward it argue for waiting. A defended choice either way; 'always reprogram' without engaging the carve-out is weaker than a reasoned wait.
• Confirm. spikes at the programmed rate with a wide QRS after every spike and an arterial trace matching, tachytherapy status read back, pads connected, defibrillator on.

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• First check. artifact vs true pauses: look at the arterial line or pleth during the burst. ECG noise from cautery mimics dropout.
• Pulsatile through the pauses. artifact — the heart is beating; no action beyond confirming and noting it.
• Flat art line in VOO. true asystole in a device that should not be inhibitable: either loss of capture or an EMI-induced electrical reset to a backup demand mode (VVI at a nominal rate) that cautery can now inhibit. Recognize that a programmed setting can be undone by EMI.
• Actions. surgeon stops cautery; support circulation (chest compressions if no pulse); pads to pace; call the device team back for urgent interrogation; consider epinephrine 10-20 mcg boluses for a paced but hypotensive patient.
• Magnet. no — over an ICD it does not change pacing mode; it is not the rescue for inhibition.
• Persistent pauses. pace externally via the pads now; a device that has reset is not trusted until interrogated.
• Transcutaneous. rate 80-90, output up from 40 mA until electrical and mechanical capture (arterial pulse at the paced rate); expect 60-100 mA; analgesia if awake — not relevant here.
• Endpoint. interrogation confirms mode and settings, reliable capture at the programmed rate, and pads ready; then bipolar or short bursts only.

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• What happened. an inappropriate shock — cautery noise read as VF; concern is the shock itself, a shock-induced arrhythmia, and hemodynamic compromise in a 25% EF. The predicted hazard of therapy being on.
• Actions. stop cautery, assess rhythm and pressure, support with pressor/volume, get the tachytherapy step completed immediately.
• Magnet. yes — now it is the right tool: it suspends further shocks while the team finishes reprogramming, and it costs nothing.
• What protects him in VF. nothing internal — with tachytherapy off the device will not rescue him; the pads and the external defibrillator are the safety net. This is why they were on and connected.
• Energy. 200 J biphasic through the pads already on him; place them anterior-posterior or at least 8 cm from the generator; ACLS between shocks; amiodarone 300 mg if refractory; look for a reversible cause (ischemia, potassium, the shock itself).
• Before continuing. full reinterrogation: confirm mode and capture, lead impedances unchanged (a shock plus a reset can hide lead problems), tachytherapy status intentional, and a decision about when it goes back on.
• Continue?. an elective colectomy after VF with a 25% EF: abort if the arrhythmia was not clearly cautery-provoked, if he is unstable, or if ischemia is suspected; continue only if the cause is understood and the device is secured. Want the judgment, not a reflex either way.

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• Dx. loss of capture — spikes delivered, myocardium not depolarizing; the 34 is whatever is capturing intermittently. Spike frequency is not heart rate.
• Spike vs capture. the spike is the device firing; capture is a wide paced QRS (LBBB morphology from RV pacing) followed by a T wave and a pulse. Confirm on the arterial trace, not the ECG count.
• DDx. acutely raised threshold from hyperkalemia or acidosis, ischemia, lead dislodgement or fracture (positioning plus a stale interrogation), inadequate output after the reset, hypoxia, antiarrhythmic effect.
• Why 6.8 now. CKD plus ARNI baseline, pneumoperitoneum-driven hypercapnic acidosis shifting potassium out of cells, low-output tissue hypoperfusion, and possibly the earlier shocks and compressions. The acute rise from 5.1 is what raises threshold; the baseline 5.1 was never the problem.
• Rx. calcium chloride 1 g (repeat), insulin 10 units with dextrose 25 g, ventilate down the CO2 (pH correction alone lowers K+ and threshold), albuterol 10-20 mg nebulized, bicarbonate 50 mEq given the acidosis, furosemide if making urine. Expect threshold to fall as K+ and pH correct.
• Meanwhile. external pacing through the pads at 80-90 while treating the potassium; do not keep watching uncaptured spikes.
• Capture. wide complex after each pacer artifact plus an arterial waveform at the set rate; skeletal twitching alone is not capture.
• Pneumoperitoneum. release it: it is driving the hypercapnia, cutting venous return, and stressing a failing ventricle; the surgeon pauses until capture is reliable.

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• Leave VOO. no — with no EMI source, asynchronous pacing carries only risk: a fixed-rate spike can land on the vulnerable period of an intrinsic beat (R-on-T) and start VF. VOO is not free.
• PVCs in VOO. this is exactly the competition R-on-T needs — ectopy in a VT-prone cardiomyopathic ventricle after hyperkalemia and shocks; reprogram to demand pacing now, check K+ and ischemia.
• Mode. back to the original demand mode (VVI/VVIR here) before transport; never travel asynchronous unless explicitly intended.
• Tachytherapy. reactivate in the OR once cautery is over and before transport, with pads still on until confirmed; leaving a VT-prone patient unprotected for a PACU handoff is the error.
• Confirm before leaving. interrogation printout: mode, rate, capture threshold and lead impedances unchanged, tachytherapy on; a rhythm strip showing appropriate pacing; pads on for transport.
• PACU. continuous ECG until the device is confirmed in its intended settings and he is rhythmically stable; cardiology/EP follow-up for a full check before discharge given the reset and shocks.

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• Bedside. ptosis, diplopia, dysphagia or nasal speech, neck flexion strength, proximal limb fatigue, single-breath count, cough; recent crises or hospitalizations; adherence to pyridostigmine.
• Evening diplopia only. mild ocular fatigue with no bulbar symptoms and good exercise tolerance — adequately treated; proceed. Cancelling for evening diplopia is over-caution; ignoring dysphagia would be the opposite error.
• FVC 2.1 / NIF -40. FVC 70% predicted, NIF well beyond -25: adequate respiratory reserve; proceed with a plan for post-op monitoring. FVC <50% predicted or NIF weaker than -25 would predict post-op ventilation.
• Pyridostigmine. give the usual morning dose — she is dependent on it and holding invites weakness at emergence; the older practice of holding to limit secretions and succinylcholine interaction is defensible but weaker. Continue the steroid (covered in probe 4).
• Predictors. disease duration >6 years, chronic pulmonary disease, pyridostigmine >750 mg/day, preop FVC <2.9 L, bulbar symptoms; she has none of the strong ones except a dose close to the threshold. Coexisting risk: the abdominal incision itself impairs FVC.
• NMB. use it if the surgeon needs it, but rocuronium at 10-20% of the usual dose (0.1-0.2 mg/kg) titrated to a baseline TOF, with sugammadex on hand; avoid long-acting agents. An epidural for relaxation plus a light GA is the alternative.

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• Cause. chronic blood loss from menorrhagia — iron deficiency; the numbers confirm it. No surprise.
• Transfuse preop. no — chronic, compensated, asymptomatic; red cells fix the number, not the deficit. IV iron is the treatment.
• Delay. a 4-week delay for IV iron raises Hgb by ~1-2 g/dL and reduces transfusion; against it, ongoing monthly loss and a scheduled surgeon. Either is defensible; give iron regardless and proceed if the surgeon will not wait.
• Threshold. 7 g/dL in a healthy 40-year-old with no cardiac disease; higher (8) only if bleeding is ongoing and brisk. A reflex threshold of 10 is the flag.
• T&S vs crossmatch. crossmatch 2 units — she starts low, an abdominal hysterectomy for menorrhagia can bleed, and a fibroid uterus makes it more likely.

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• Risk. high — hiatal hernia with nocturnal regurgitation is symptomatic, poorly treated reflux; add bulbar disease that can impair swallowing and airway protection.
• Prophylaxis. sodium citrate 30 mL within 30 min of induction, famotidine 20 mg IV or a PPI the night before and morning of, metoclopramide 10 mg IV 30 min before (it also has no adverse interaction with myasthenia at this dose). Standard fasting.
• RSI. yes — symptomatic reflux with a hernia; modified RSI with rocuronium at a reduced dose and sugammadex ready, or a full-dose rocuronium RSI accepting a long block and planned sugammadex reversal. See probe B3.
• Cricoid. reasonable to apply and release if the view is poor; evidence is weak either way, and a defended choice is what matters.
• Awake intubation. no — reflux alone does not mandate awake intubation with a reassuring airway; an RSI protects her. Awake fiberoptic is reserved for a difficult airway plus a full stomach; bulbar weakness with dysphagia would tip it, and she has none.
• Morning pill. yes — a sip of water with an essential medication up to 1-2 h before induction is standard.

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• Stress dose. yes — three years on 15 mg/day is HPA-suppressive (>5 mg/day for >3 weeks); a major abdominal surgery is a moderate-to-major stress.
• Dose. hydrocortisone 50-100 mg IV at induction (plus her usual prednisone), then 50 mg q8h for 24 h, then taper to baseline over 1-2 days. The old 100 mg q8h for days is more than needed.
• Hypotension out of proportion. adrenal insufficiency: hypotension out of proportion to blood loss, poor response to volume and phenylephrine, with hyponatremia, hyperkalemia, or hypoglycemia; bleeding would show a falling Hgb, tachycardia, and a field that explains it. Also anaphylaxis, deep anesthetic, high epidural.
• Rx. hydrocortisone 100 mg IV empirically while excluding the others; waiting for a cortisol level is the flag.
• Glucose 240. insulin to keep under 180; hyperglycemia impairs wound healing and infection defense in a steroid patient.
• Week of hydrocortisone. no — hyperglycemia, fluid retention, impaired healing, and infection are dose- and duration-dependent; a 24-48 h course then taper to her home prednisone is enough, and a week buys risk without benefit.

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• Add. quantitative neuromuscular monitor (a baseline and ratio, not tactile TOF); temperature; consider an arterial line only for the bleeding risk, not the myasthenia.
• Baseline TOF. myasthenics can show fade before any relaxant; without a baseline, a TOF of 0.8 after reversal may be her normal or residual block — you cannot tell.
• Baseline 0.82. record it; titrate rocuronium to change from this baseline; recovery target is return to 0.82, not to 0.9; flag that she has measurable baseline weakness and set the post-op monitoring plan accordingly.
• Sloped phase III. expiratory obstruction — bronchospasm, secretions (cholinergic from pyridostigmine), kinked tube, or COPD. Next: suction and listen before treating; glycopyrrolate for secretions, bronchodilator only if wheeze is real.
• Arterial line. not required for the myasthenia; reasonable if brisk bleeding is expected given her starting Hgb, or if an epidural plus GA makes hypotension likely. A defended choice either way.

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• Regional acceptable. yes — it avoids the airway, relaxants, and opioids; the cost is that a T4 block takes intercostal and abdominal muscles she may need, and a full stomach with sedation.
• Level. T4-T6 for peritoneal traction; anything lower will not cover the case.
• Spinal vs epidural. epidural — titratable level, lower peak, a catheter for post-op analgesia that spares opioids; a spinal to T4 in a patient with baseline weakness is a one-shot commitment. Ester local anesthetics (chloroprocaine) may last longer with reduced pseudocholinesterase activity from pyridostigmine; amides are unaffected.
• Options. GA with the epidural used for surgical relaxation and post-op analgesia; or a titrated epidural with light sedation; or GA alone. Her fear is legitimate and a coerced awake patient with a T4 block and a full stomach is a bad combination.
• Epidural plus GA. surgical relaxation without relaxant, less volatile, opioid-sparing post-op analgesia that protects breathing and cough; the biggest lever for a myasthenic laparotomy.
• Epidural with sedation only. a sedated, full-stomach, weak patient with a T4 block who cannot cough — the airway is unprotected exactly when she cannot protect it; the trap answer.

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• Induction. propofol 1.5-2 mg/kg (she is 50 kg: 75-100 mg), fentanyl 1-2 mcg/kg; RSI for the reflux.
• Succinylcholine. usable but awkward: resistance from fewer receptors (needs ~1.5-2 mg/kg, ED95 2.6x normal) and prolonged effect because pyridostigmine inhibits plasma cholinesterase; phase II block possible. Rocuronium with sugammadex is cleaner. Either answer defended is fine; not knowing both effects is the flag.
• Rocuronium. 0.3-0.6 mg/kg for the RSI if the airway looks easy (still adequate conditions in a myasthenic), with sugammadex 16 mg/kg drawn up; full 1 mg/kg accepted if the airway is the bigger risk. Sensitivity is unpredictable — titrate to TOF.
• Maintenance. volatile-heavy: sevoflurane provides relaxation itself (myasthenics are exquisitely sensitive), offsets fast, and spares opioid; opioid-heavy risks respiratory depression at emergence. A TIVA with epidural is also defensible.
• Epidural hypotension. sympathectomy on top of GA with a starting Hgb of 9.3: ephedrine 5-10 mg (rate and pressure), 250-500 mL crystalloid, lighten volatile; glycopyrrolate 0.2 mg if bradycardia persists; smaller epidural increments (3-5 mL) from here.
• More relaxant. TOF count 2 is already deep for her; small increments only (5 mg), or dose the epidural and deepen the volatile instead; keep the epidural doing the work.
• Sugammadex. 2 mg/kg at TOF count 2, 4 mg/kg at post-tetanic count 1-2; target TOF ratio back to her baseline 0.82 or better. Neostigmine on top of 360 mg/day pyridostigmine risks cholinergic weakness and secretions.

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• Transfuse. yes — hemodynamic instability with ongoing loss from a starting Hgb of 9.3; do not wait for a number.
• No blood for 20 min. emergency-release O-negative (or type-specific uncrossmatched), activate MTP, cell saver, TXA 1 g, crystalloid to bridge, vasopressor, surgical pressure or packing, second large-bore line.
• FFP. not at 2 units unless coagulopathy is documented; after 4-6 units or with ongoing massive loss, move to 1:1:1; POC coags or a TEG guide it.
• Red urine. hemolytic transfusion reaction, bladder or ureteral injury during pelvic dissection, hemoglobinuria from cell saver, myoglobin; methylene blue makes urine blue-green, not red.
• Stop. yes, stop the unit; recheck the label and the patient; send the bag, a fresh sample for DAT, plasma free hemoglobin, haptoglobin, LDH, bilirubin, coags, K+, and urinalysis; tell the surgeon to inspect the bladder.
• Methylene blue. false low reading — it absorbs at 660 nm and drags the SpO2 down for 1-5 minutes; confirm with an ABG or co-oximetry before treating; keep FiO2 up meanwhile.
• Hemolytic reaction. acute hemolytic transfusion reaction: stop, support BP, maintain urine output >1-2 mL/kg/h with fluid and mannitol or furosemide, alkalinize if pigment-heavy, treat hyperkalemia, watch for DIC; blood bank recrossmatch before any further units. Steroids and stress-dose cover already given.

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• Criteria. awake and following commands, TOF ratio at or above her 0.82 baseline, FVC >15 mL/kg, NIF stronger than -25, sustained head lift >5 s, normothermic, no residual volatile, hemodynamically stable after the bleed.
• Ratio 0.85. at or above her baseline of 0.82 — adequate as far as the relaxant goes; a second dose will not fix myasthenic weakness. Now the question is her own strength, not the block.
• Neostigmine. additive with 360 mg/day of pyridostigmine: cholinergic crisis (weakness, secretions, bradycardia) is the risk, and it cannot reverse a deep block; acceptable only if sugammadex is unavailable and the block is shallow.
• FVC 11, NIF -18. not yet — below extubation thresholds after a laparotomy and a major bleed; leave the tube in, epidural running for analgesia, sedate lightly, reassess in an hour with the epidural working and volatile gone. Extubating a myasthenic to prove a point is the flag.
• Pyridostigmine. IV neostigmine 1/30 of the oral pyridostigmine dose (roughly 0.5 mg IV q4-6h for 60 mg oral), or IV pyridostigmine 1/30 of oral; restart oral when she can take it; glycopyrrolate for secretions.
• Disposition. step-down or ICU with continuous monitoring and serial FVC/NIF; the floor only when she is clearly at baseline with a monitored bed available.

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• Before the knife. tube confirmed, ventilation set to PaCO2 35-40, blood in the room checked, second unit hanging, MAP target set, art line going in, pupils rechecked; a minute or two of preparation is the trade, not a delay. Incising with an unconfirmed tube and no pressure trace is the flag.
• Confirm ETT. waveform capnography, bilateral breath sounds (already decreased on the right — so chest rise and a quick look at depth), and fiberoptic through the tube if any doubt; field tubes are dislodged or endobronchial more often than one thinks.
• Art line. yes — beat-to-beat pressure is the CPP monitor; place it during positioning and prep without stopping the surgeon; femoral or radial, whichever is fastest. The answer to the surgeon is a specific time, not a standoff.
• Maintenance. either defended: TIVA (propofol plus remifentanil) preserves CO2 reactivity and lowers CMRO2 and ICP; sevoflurane at ≤0.5-1 MAC is acceptable once the dura is open. Above 1 MAC vasodilates and raises ICP.
• Central line. after incision, once the pressure is controlled; right IJ under ultrasound with manual in-line stabilization and the collar front removed, or subclavian; femoral is fast but the pelvic fracture is on the right, so left femoral. Not before decompression.
• Chest tube. yes — a known pneumothorax on positive-pressure ventilation with an open cranium coming is a tension pneumothorax waiting to happen, and you will not have access to the chest under the drapes. Place it now (trauma surgeon, 5 minutes) or immediately after the flap is off; a defended 'after' is acceptable, ignoring it is not.

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• Rx. pressor now plus the second unit of blood; hypotension is the strongest modifiable driver of secondary injury (a single SBP <90 doubles mortality).
• Which pressor. norepinephrine — alpha plus some beta, better cardiac output than phenylephrine in a tachycardic hypovolemic patient with an LAD stent; phenylephrine is acceptable as a bridge. Large crystalloid boluses without considering the coronary disease and the bleeding is a flag.
• MAP. MAP ≥80 until ICP is known (assumes ICP ~20, CPP ≥60); the learner should reason from CPP, not quote a number.
• Persistent borderline. ongoing hemorrhage — pelvis (rami fractures), chest (contusion, ribs), occult abdomen — plus under-resuscitation, anesthetic depth, tension pneumothorax developing, myocardial ischemia.
• Transfuse. yes — Hgb ≥8-9 is the working target in acute TBI to protect oxygen delivery to injured brain; a 7 threshold is for stable non-brain-injured patients.
• MTP. trigger on instability with a falling Hgb and multiple bleeding sources; 1:1:1 with TXA if within 3 h (he is at ~2 h). Waiting for a crossmatch with ongoing loss is the error.
• Fixed pupil. herniation: hyperventilate briefly to PaCO2 30-32, hypertonic saline 3% 250 mL (or 23.4% 30 mL if central), head up, tell the surgeon to hurry the burr hole; keep MAP up — brain that is herniating needs pressure more, not less.

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• Mannitol vs HTS. hypertonic saline — it expands intravascular volume while pulling water from the brain; mannitol's osmotic diuresis worsens hypovolemia and hypotension in a bleeding patient. Mannitol in a hypotensive polytrauma patient is the flag.
• Dose. 3% saline 250 mL (or 5 mL/kg) bolus; 23.4% 30 mL; mannitol would have been 0.5-1 g/kg.
• 3% vs 23.4%. 23.4% is faster and lower volume but needs central access; 3% can go peripherally and gives volume, which he needs. Here 3% peripheral is the right answer until a central line is in.
• 23.4% peripheral. no — extravasation causes tissue necrosis and rapid infusion causes hypotension; central line only, or 3% instead.
• Hyperventilation. PaCO2 30-35 as a bridge for minutes while the surgeon decompresses; below 30 vasoconstricts to the point of ischemia in already injured brain, and the effect wanes in hours. Not a maintenance strategy.
• Head up with hypotension. venous drainage helps ICP but CPP is what matters; 15-20 degrees with a pressor increase rather than flat, and keep the neck neutral in the collar — jugular compression raises ICP more than the tilt lowers it.
• Na 149. yes, continue — the target for hyperosmolar therapy is 145-155 (some go to 160); stop only above 155-160 or with serum osm >320.

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• DDx. tension pneumothorax (known small right PTX on positive pressure), mainstem migration, mucus plug, bronchospasm, circuit obstruction, anaphylaxis; falling ETCO2 with rising PIP and hypotension is the tension picture.
• First check. hand-ventilate to feel compliance while listening to both sides and checking tube depth; then the chest. Seconds, not a chest film.
• Dx / Rx. tension pneumothorax — decompress now; call the trauma surgeon for a tube. Do not wait for imaging.
• Open cranium. yes — tension pneumothorax kills in minutes; ICP swings from a moment of decompression are survivable. Tell the neurosurgeon what is happening and go.
• Site. 4th-5th intercostal space anterior axillary line with a long 14 g catheter (chest-wall thickness beats the 2nd ICS midclavicular in adults); either is acceptable if defended.
• Brain went slack. venous return restored, intrathoracic pressure fell, jugular venous pressure fell — the tension was raising ICP through venous congestion; ETCO2 and BP recovery are the proof.
• Chest tube. now — the needle is temporizing and can re-tension; a trauma surgeon places it at the right chest under the drapes while the craniotomy continues.
• Ventilator until the tube. keep it on but lower Vt and PEEP, avoid high pressures until the tube is in; the leak will persist under positive pressure.

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• Extubate. no — GCS 7T before surgery, pulmonary contusion with a fresh chest tube, ICP to control, ongoing resuscitation. A learner who wants a neuro exam off the tube has the priorities inverted.
• Sedation. propofol — fast on/off for exam windows, lowers CMRO2 and ICP; dexmedetomidine allows exam but is slow to titrate and drops pressure; midazolam accumulates and clouds every exam. Adequate analgesia (fentanyl) underneath.
• Neuro checks. scheduled hold or halving of propofol for 5-10 minutes with the ICP watched; abort the hold if ICP climbs above 20-22; document what returns first.
• Hour 30 labs. propofol infusion syndrome — early, at a dose below the classic threshold (>4 mg/kg/h for >48 h), but the lactate, lipids, CK, and acidosis are the pattern. Stop the propofol now; supportive care; watch for bradycardia and renal failure.
• Switch. midazolam plus fentanyl for the short term with scheduled holds, or dexmedetomidine if pressure allows; ketamine is acceptable as an adjunct with a controlled airway and PaCO2.
• Paralysis. cisatracurium bolus then infusion is reasonable for dyssynchrony driving ICP or hypoxia; not routine — it obscures the exam and seizures; TOF-monitored, with sedation confirmed adequate first.

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• Bedside checks. head position and collar (jugular compression), ETT tie, PaCO2 on the gas, temperature, seizure activity, sedation depth and pain, bladder and abdominal pressure, monitor zero; then CT for a surgical lesion.
• Order. tier 1: head up 30, neutral neck, sedation and analgesia deepened, normothermia, PaCO2 35-40, CSF drainage; tier 2: hyperosmolar bolus, brief hyperventilation to 32-35, paralysis; tier 3: barbiturate coma, decompressive craniectomy, hypothermia as rescue. Less invasive first, neurosurgery involved throughout.
• EVD. yes — open at 10-15 cm H2O or drain 5-10 mL slowly; slit ventricles mean little CSF is available, and over-drainage collapses the ventricle. Not a lever that will carry him.
• Na 152. continue — target 150-155 (up to 160) while ICP is the problem; hold above 160 or serum osm >320; check Na and osm q4-6h; avoid a fall of more than 10 mEq/L per day when weaning.
• Rebound to 28. repeat the bolus (23.4% q4-6h or 3% 250 mL), confirm paralysis and deep sedation, brief hyperventilation to 30-32 as a bridge, and call neurosurgery — this is refractory ICP heading to tier 3.
• PaCO2 30. minutes to an hour at most; a bridge to the next intervention, not a setting; below 30 is reserved for impending herniation.
• Pentobarbital. 10 mg/kg load over 30 min then 5 mg/kg/h for 3 h, then 1-4 mg/kg/h to burst suppression on continuous EEG; expect hypotension needing a pressor and ileus; exam is gone for days.
• Craniectomy. refractory ICP >25 despite tier 2 in a salvageable patient; earlier rather than later — it lowers ICP and mortality but not necessarily disability; a decision made with neurosurgery and the family's understanding of the trade.

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• DDx. central diabetes insipidus from the injury or herniation, osmotic diuresis from hypertonic saline or mannitol, hyperglycemic diuresis, diuretic, over-resuscitation with the kidney unloading it.
• Which. DI — dilute urine (osm 200) in the face of a high serum osm rules out osmotic diuresis (urine osm would be >300); glucose 160 does not explain 450 mL/h. Urine osm is the discriminator; urine Na alone is not.
• DDAVP. 1-2 mcg IV (or SC), repeat q8-12h to urine output and Na; or a vasopressin infusion 0.5-2 units/h if titration is needed. Overshooting is the danger.
• Replacement. D5W or enteral free water to match urine output hourly while DDAVP takes effect; 0.45% saline delivers less free water and is acceptable but slower; watch glucose with D5W. Volume matters as much as tonicity — he is losing circulating volume.
• Rate. no faster than 8-10 mEq/L in 24 h (0.5 mEq/L/h); in an edematous injured brain a fast fall drives water in and raises ICP — the reverse of osmotic demyelination. Both too fast and too slow harm; the ICP monitor is the guide.
• 141 in six hours. 17 mEq/L in 6 hours — far too fast; DDAVP plus free water overshot. Stop the free water, check ICP now, and give hypertonic saline to bring Na back up toward 150; expect ICP to have risen.

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• P/F and DDx. 180 — moderate ARDS range. DDx: contusion progression, ARDS from multiple insults (trauma, transfusion, aspiration), neurogenic pulmonary edema, TACO vs TRALI, aspiration pneumonia, ventilator-associated pneumonia.
• Bedside sort. fluid balance and CVP, echo for LV function and filling, BNP, transfusion timing, secretions and Gram stain, temperature and white count; distinguishes hydrostatic from permeability edema.
• Vt. 6 mL/kg predicted body weight (~450 mL for 5'8"), plateau <30, driving pressure <15 — lung protection still applies in TBI.
• PEEP vs ICP. PEEP that raises ICP more than it raises PaO2 is a bad trade: back to 10-12, head up, ensure PEEP is below ICP (transmission is worst when PEEP exceeds ICP), fix the volume status, treat ICP with sedation and osmotherapy; accept a lower PaO2 (>60-65) rather than a sustained ICP >22.
• CO2. raise the rate first (to 28-30/min watching auto-PEEP); permissive hypercapnia is a direct ICP driver and is not acceptable while ICP is 24; if the rate cannot fix it, prioritize ICP and accept a higher plateau briefly. Name the conflict.
• Prone. not with ICP 24 — proning raises ICP and abdominal pressure, and the collar plus pelvic fracture complicate it; reserved for P/F <100 with ICP controlled and the neurosurgeon in agreement, with the head elevated in reverse Trendelenburg.
• Paralysis. yes if dyssynchrony or persistent hypoxemia; it also helps ICP; short course with TOF and EEG if seizures are a concern.
• ECMO. VV-ECMO is technically possible but anticoagulation into a 2-day-old craniotomy with cerebral edema is the barrier; heparin-free VV runs exist but are exceptional. It is not a realistic offer at P/F 180.

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• Father. plain: he had a severe brain injury from the crash before he ever reached the OR; the surgery removed the clot and the swelling that followed is what the injury does; nothing was done wrong; describe what is being done now; no defensiveness, no blame, no promise either way. (The one counseling beat of the case.)
• Brain death today. no — pentobarbital abolishes the exam and can flatten an EEG; a brain-death exam requires no confounding sedative, normothermia, normal electrolytes, and a stable pressure; he has a working ICP monitor and drug on board.
• Level. a pentobarbital level below the therapeutic range (roughly <5 mg/L) or five half-lives after stopping (days, prolonged by hypothermia and hepatic injury); then the clinical exam and apnea test.
• Ancillary. cerebral blood flow study — nuclear perfusion scan, CT angiography, or transcranial Doppler; EEG is unreliable under barbiturate. Absent flow is diagnostic regardless of the drug.
• ICP 30 on lightening. stop lightening; restore burst suppression; he is not ready for a prognostic exam and the attempt itself is causing injury. The question is when to try again (48-72 h of controlled ICP), not whether to push through. Organ-donation conversations belong to the OPO and the primary team, and only after death or a decision to withdraw — not now.

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• Airway choice. either is defensible; the drivers are longstanding RA (possible atlantoaxial instability, TMJ disease), 3 cm opening with limited extension and Mallampati III, and a stenotic signal-changed cord that tolerates little malposition. Awake fiberoptic keeps the neck neutral and allows a post-intubation neuro check; VL with in-line stabilization is defensible if the view is expected to be workable. Want a committed, defended choice, not both listed.
• Flexion-extension films. voluntary flexion-extension films quantify atlantoaxial instability in RA (ADI >3 mm abnormal; her neutral film is at the margin) and are reasonably safe because the awake patient self-limits. Equally defensible to skip them and simply treat the neck as unstable — the anesthetic plan barely changes. Ordering them without saying what would change is worth probing.
• Succinylcholine. chronic myelopathy with UMN findings carries a theoretical receptor-upregulation hyperkalemia risk; best documented in acute denervation and disuse, uncertain in longstanding CSM. Most avoid it here because nothing forces its use; using it is defensible if defended. Fasciculations jerking a possibly unstable neck is a cited but weak secondary argument.
• Rocuronium and baselines. a single intubating dose abolishes MEPs for roughly 30-60+ minutes; options are timing baselines after spontaneous recovery, sugammadex reversal before baselines, or intubating without relaxant (propofol-remifentanil, or the topicalized awake route). The learner should connect the dose given to when the IONM team can obtain usable baselines.
• Induction and BP. titrated induction with vasopressor drawn up and the arterial line in place; hypotension threatens a chronically compressed cord, and treated hypertension shifts autoregulation rightward. Hold MAP near her baseline (roughly 85-90); blunting the laryngoscopy response without buying a trough is the balance.
• Maintenance. TIVA (propofol-remifentanil) is the default for reliable MEPs; volatile at or below ~0.5 MAC without N2O is sometimes workable but degrades MEP amplitude; no redosing of NMB after intubation. Committing to a technique and tying it to signal fidelity is the expected move.
• Baselines. supine before the flip, then again immediately after — the pre-turn set is the reference that makes a post-turn change interpretable.

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• The turn. neck held neutral by the anesthesiologist until the Mayfield is locked to the table; a coordinated log-roll with lines and ETT guarded. Want the neck-neutral requirement stated, not 'we're careful.'
• First checks. ETT depth, patency, and EtCO2; bilateral breath sounds; all lines and monitors reconnected; eyes free of pressure; face and chin clear of the frame; arms padded (ulnar nerves); breasts and abdomen free; monitoring cables intact.
• Signals after the turn. yes, immediately — positioning itself can injure a stenotic cord; comparing post-turn signals against pre-turn baselines catches a positional insult while it is still reversible by repositioning, before any surgery has happened.
• BP 82/48. venous pooling and reduced venous return from the flip on top of a vasodilating TIVA; also abdominal compression, hypovolemia, anesthetic depth. Rx: vasopressor plus volume and verify the abdomen is truly free. The compressed cord makes this urgent, not routine.
• MAP target. MAP ≥85 (some accept 80) for a compressed, signal-changed cord — perfusion pressure across a stenotic segment with impaired autoregulation; her baseline MAP is ~110, which argues further against settling low. Pushing back on 65 with a stated reason is the point of the beat.
• Eyes, ETT, abdomen. pins spare the face from headrest pressure but the eyes are still checked and documented at intervals (every 15-30 minutes); the ETT is secured against prone secretions and traction with a bite block and circuit support; a free abdomen lowers epidural venous pressure — less field bleeding — and preserves ventilation compliance.

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• Interpretation. a unilateral MEP drop with preserved SSEPs points at the motor tracts / anterior cord — mechanical or perfusion-related from the distraction — rather than a global anesthetic effect, which depresses signals diffusely and bilaterally.
• Systematic response. run anesthetic, physiologic, technical, and surgical causes in parallel, not sequence: confirm no propofol bolus, volatile drift, or NMB; drive MAP up; check temperature, Hgb, and CO2; have the technologist verify electrodes and a control muscle; tell the surgeon immediately.
• MAP. raise promptly to ≥85-90 with vasopressor — the fastest reversible lever on cord perfusion. Watching at 78 to 'see if it recovers' is the flag.
• Temperature. hypothermia depresses evoked potentials, but 35.4 rarely explains a focal unilateral drop; warm her anyway. Blaming temperature and stopping the workup is the pitfall.
• The ask to the surgeon. specific requests: pause, release distraction, inspect the last screw trajectory, irrigate with warm solution, consider imaging the hardware. A vague 'signals are down' with no ask wastes the reversible window.
• Steroids. no solid evidence supports methylprednisolone for intraoperative signal change; NASCIS-based high-dose regimens have fallen from favor with a harm signal. Some centers still give it — defensible either way if reasoned, wrong if presented as mandatory.
• Wake-up test. largely historical: slow, impractical prone in pins with a difficult airway, and MEPs already interrogate the same pathway continuously. Recognizing that it is not realistic here is the answer.
• Signals return. proceed with less correction, hold MAP ≥85, run signals more frequently, keep the anesthetic steady; document the event, timeline, interventions, and recovery contemporaneously.

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• Transfuse at 8.1. with ongoing surgical loss and a cord under active ischemic threat, most would transfuse — restrictive triggers validated in stable populations do not map cleanly onto an at-risk cord plus an elevated MAP goal, and she started at 10.8, so 8.1 is not a plateau. Either commitment is acceptable if the cord appears in the reasoning; a trigger around 8-9 is typical here.
• Ooze DDx. dilution, platelet dysfunction from naproxen taken through yesterday, hypothermia, epidural venous pressure (recheck the abdomen), early consumption; send platelets, coags, fibrinogen, or viscoelastic testing rather than guessing.
• Cell salvage. appropriate in instrumented fusion; keep the salvage sucker off the field while topical hemostatics and bone dust are down, and remember washed cells return no platelets or factors.
• TXA. reduces blood loss in multilevel spine surgery; typical regimen 10-30 mg/kg load then 1-2 mg/kg/h. Seizure risk is a high-dose (cardiac-range) phenomenon; no clear VTE excess at spine doses. Naming a dose is expected.
• Fluid strategy. balanced crystalloid with blood by trigger; prone position degrades dynamic indices, so follow urine output, lactate/base deficit trend, and the arterial trace with that caveat. Over-resuscitation buys facial and airway edema for the extubation decision.
• Emergence plan. TIVA titrated to a prompt wake-up; no NMB since induction but recovery is still confirmed quantitatively; the goal is hands and feet moving to command before leaving the OR, analgesia layered in without burying the exam.

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• What decides it. duration prone, fluid balance, visible face and tongue edema, cuff leak, strength and work of breathing, and her OSA — the decision is a composite; no single test decides it.
• Cuff leak. a present leak is modestly reassuring, not a guarantee of a patent supraglottis; an absent leak after long prone spine surgery predicts post-extubation obstruction and argues for delay with head-up positioning, diuresis toward even balance, and dexmedetomidine or propofol sedation that permits serial exams. Treating the leak as the whole answer, in either direction, is the pitfall.
• How to extubate. over an airway exchange catheter with VL and the difficult-airway cart at hand and the surgeon aware — reintubation now means a fused, immobile neck plus fresh edema, a harder airway than this morning's; do it where rescue is immediate (OR or ICU).
• Disposition. ICU or a monitored unit: edema can still evolve over the next 12-24 hours, she has OSA, and hourly neuro checks are needed after a signal-change event.

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• DDx. epidural hematoma, cord ischemia or reperfusion injury (white cord), residual or new compression from graft or screw, C5 palsy (classically proximal — deltoid/biceps — and typically delayed, so acute bilateral hand weakness fits it poorly), and positioning neuropathy (bilateral ulnar reaches the hands but follows a peripheral pattern).
• Bedside separation. motor pattern by myotome (proximal vs distal, segmental vs level), a sensory level, reflex change, ulnar-territory versus diffuse hand involvement, all against the documented preop exam — a peripheral distribution reads very differently from a new cord level.
• First move. in parallel, not sequence: call the surgeon now, augment MAP, keep her NPO with access in place, expedite imaging.
• MAP. augment to 85-90 with a vasopressor as for acute cord injury — the one mechanism-plausible intervention in the anesthesiologist's hands; leaving MAP at 74 while waiting for the scanner is the flag.
• Imaging. MRI answers both compressive and intrinsic cord causes; modern titanium constructs are MRI-conditional with artifact, not a contraindication; CT shows hardware position only. A rapidly worsening exam can justify return to the OR without any imaging.
• Steroids. high-dose methylprednisolone for perioperative cord injury is not evidence-supported and NASCIS-based practice has receded; some surgeons still request it — the learner should know the evidence is weak whichever way they commit.
• Overnight. ICU with the arterial line kept, MAP ≥85 continued, serial documented exams hourly, normothermia and normoglycemia, mechanical DVT prophylaxis only, and a low threshold to re-image or re-explore if the exam worsens.

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• Concern. an evolving airway after cervical spine surgery — muffled voice and tripod posture are late-phase signs; long prone posterior cases produce pharyngolaryngeal and lingual edema from positioning and venous congestion, and deterioration is nonlinear and fast. A reassuring SpO2 is a lagging indicator. Evaluate at the bedside now — voice, stridor, work of breathing, neck exam — without letting evaluation delay the decision.
• Temporizers. nebulized epinephrine and steroids may shave mucosal edema and heliox lowers work of breathing — bridges that buy transport minutes, none of which change the trajectory; using them as a reason to defer intubation is the pitfall.
• Timing. intubate early and electively, before stridor and desaturation — once she obstructs, the same airway is attempted under the worst possible conditions.
• Technique. an awake, topicalized approach preserves spontaneous ventilation in a patient with a fused immobile neck and distorted anatomy; awake VL is also workable. Do it in the OR with the surgeon scrubbed, a surgical airway set open, and a smaller tube ready.
• Opening the wound. after an anterior approach, bedside wound opening directly decompresses the airway; after a posterior approach the airway threat is positional pharyngolaryngeal edema and venous congestion, so opening the posterior wound rarely rescues the airway — though evacuation may still be indicated for a hematoma itself. Reasoning the anatomy, not reciting the anterior reflex, is the point.
• Tonight. keep her intubated and head-up, treat edema, plan imaging and possible evacuation with the surgical team, and set explicit criteria for any later extubation attempt (returned leak, visibly resolving edema, awake and strong, rescue plan named).

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• DDx. posterior ischemic optic neuropathy (the classic lesion after prone spine surgery), anterior ION, central retinal artery occlusion from globe compression (less likely with Mayfield pins sparing the face), a cortical/occipital event, and corneal abrasion (painful and blurs rather than producing a field defect).
• Exam separators. acuity, fields, relative afferent pupillary defect (present in ION and CRAO), and fundus: pale swollen disc in AION, a normal disc early in PION, cherry-red spot with retinal whitening in CRAO, periocular trauma signs for compression; homonymous field loss with normal eyes points cortical. RAPD with a normal early fundus and no periocular signs is PION.
• Risk factors here. prone over 5 hours, EBL 1.4 L, baseline anemia, hypotensive episodes, and substantial crystalloid — the POVL registry profile — while being honest that prediction is poor and most patients with the same profile see normally.
• Ophthalmology. urgent same-morning consult; for ION there is no proven treatment (correcting anemia and blood pressure is reasonable); CRAO has time-limited maneuvers of marginal benefit. The honest position is limited therapeutic options — overpromising is the flag.
• Will it come back. prompt, plain, factual: this is a recognized complication of prone spine surgery, ophthalmology is engaged, and ION recovery is variable and often incomplete — say so without foreclosing hope; no speculation about cause, no blame, no minimization.
• Next long case. prevention evidence is thin: staging very long cases, head neutral and at or above heart level, no globe pressure, treating severe anemia and hypotension — all reasonable, none proven.

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• Multimodal plan. scheduled acetaminophen, low-dose ketamine as infusion or adjunct, a muscle relaxant used sparingly, and opioid via demand-only PCA; regional options for posterior cervical spine are minimal, so the systemic plan carries the load.
• Ketorolac. the fusion-nonunion concern rests on retrospective and animal data and appears dose- and duration-dependent; a short low-dose course is probably safe — but it is the surgeon's fusion, and many programs avoid NSAIDs for 2-6 weeks. A reasoned conversation is right; a unilateral override is not. Her home naproxen stays held meanwhile.
• Gabapentinoids. sedation and respiratory-depression synergy with opioids in an older OSA patient — if used at all, low dose and reassessed; adding one reflexively to make the plan look multimodal is the flag.
• PCA basal. no basal rate — a background opioid infusion in an opioid-naive OSA patient is the textbook setup for the overnight respiratory arrest.
• Monitoring and CPAP. CPAP whenever asleep with the machine already in the hospital, continuous pulse oximetry at minimum (capnography where available), and a monitored setting for the first floor night; unmonitored q4h vitals are the failure mode.
• Steroids. at 7.5 mg prednisone for 6 years, HPA suppression is plausible; for major surgery, hydrocortisone 50 mg q8h on the day of surgery with a 1-2 day taper back to the home dose, or continuing the home dose with empiric treatment of refractory hypotension, are both defensible — omitting her baseline steroid entirely is the indefensible option.
• Methotrexate. continue — trial evidence and ACR/AAHKS guidance support continuing methotrexate through elective surgery without a wound-healing penalty, while stopping risks a flare; it never needed holding, so she resumes on her usual weekly schedule.

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• Sitting vs park-bench. sitting gives a clean midline field, better venous and CSF drainage, less bleeding; it buys the highest VAE risk (noncollapsible venous channels above heart level), paradoxical embolism, positional hypotension, pneumocephalus, and rare midcervical flexion myelopathy. Park-bench trades some exposure for lower risk. Either is defensible if committed; not weighing the incomplete shunt screen is the flag.
• Bubble study adequacy. no — a negative study at rest does not exclude PFO; right-to-left flow often appears only with Valsalva and release, and roughly a quarter of adults have a probe-patent PFO. The learner should catch the missing provocation; repeating with provocation, or a TEE bubble study after induction before positioning, is the standard fix.
• Proceeding with unknown PFO. a demonstrated PFO is a strong (many say absolute) argument against sitting; leaving it unknown pushes toward completing the screen (intraoperative TEE), choosing park-bench, or accepting sitting only with TEE surveillance and meticulous prevention. A committed, defended position is the point — drifting into sitting by default is the failure.
• Doppler vs TEE. TEE is the most sensitive detector (~0.02 mL/kg) and the only monitor that shows right-to-left passage of air, and it can settle the PFO question in the room; precordial Doppler (right parasternal, 3rd-6th interspaces) is the most sensitive noninvasive monitor and easier to run for hours. EtCO2 fall is less sensitive and hypotension is late. Choosing Doppler alone with the shunt question unresolved is worth challenging.
• Multiorifice catheter tip. at or just below the SVC-right atrial junction for best aspiration yield; confirm with intravascular ECG (tall biphasic P wave), TEE, or radiograph. Placing the line and never confirming the tip is the classic miss.
• PEEP. avoid — PEEP does not reliably prevent entrainment, cuts venous return in a position already fighting preload, and its release can transiently reverse the interatrial gradient and favor paradoxical embolism. Jugular compression at closure is the better maneuver for finding open channels.
• N2O. avoid — it expands intravascular air and any trapped intracranial air.

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• Induction. smooth, pressure-stable IV induction — propofol 1.5-2 mg/kg with opioid, rocuronium for intubation; the single intubating dose will have worn off before facial EMG matters. A morning ACE inhibitor on board predicts exaggerated hypotension later — worth hearing the learner say it.
• Pins. pin application is intensely nociceptive — a hypertensive surge in a man with early obstructive hydrocephalus risks intracranial hypertension. Blunt with deepened anesthetic, opioid bolus (remifentanil 0.5-1 mcg/kg), local infiltration or scalp block at pin sites, +/- esmolol just before application.
• BP 196/108. deepen, opioid, short-acting agent (esmolol 0.5 mg/kg or nicardipine 0.5-1 mg increments); the stimulus is transient — long-acting antihypertensives now compound the positional hypotension coming in minutes.
• Transducer level. zero at the external auditory meatus (circle of Willis). Sitting puts the head 20-25 cm above the heart, so brain-level arterial pressure runs roughly 15-20 mmHg below an arm-referenced number; treating the arm number as CPP overstates cerebral perfusion — the central lesson of sitting-position hemodynamics.
• Hypotension on sitting up. staged elevation, legs flexed at heart level, volume, vasopressor infusion (norepinephrine or phenylephrine); ACE-inhibitor vasoplegia may need vasopressin. Target MAP ≥60-70 at the meatus (CPP ≥60) — the learner should give a number and its reference point, not a vague 'keep it up.'
• Neck flexion. keep at least two fingerbreadths between mentum and sternum: extreme flexion obstructs jugular venous drainage (brain swelling, macroglossia, airway edema), can stretch and compress the cervical cord — midcervical flexion myelopathy, worse if hypotensive — and advances or kinks the ETT. A change in the SSEPs after flexion is the monitor's warning.

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• Dx. an abrupt EtCO2 fall with a Doppler change in a sitting craniotomy is VAE until proven otherwise; circuit disconnect, other embolism, and low cardiac output round out the list, but the paired Doppler change is nearly diagnostic.
• First moves. tell the surgeon — flood the field with saline, wax bone edges, pack; 100% O2; aspirate the multiorifice catheter; bilateral jugular compression to expose the open channel; lower the head toward heart level; support the circulation. Stopping entrainment outranks treating the numbers.
• Aspiration. may retrieve air and supports the diagnosis; yield is often modest — a learner who delays field flooding to aspirate has the order wrong.
• Pressors. norepinephrine boluses (8-16 mcg) or infusion, escalating to epinephrine (10-50 mcg) as severity dictates; a large air lock in the RV outflow behaves like arrest physiology — epinephrine and CPR-style measures if pulseless.
• Jugular compression / head down. compression raises venous pressure at the wound so the surgeon can see and seal the entrainment site; lowering the head shrinks the gravitational gradient driving air in and raises venous pressure at the field.
• ST depressions. with the shunt screen incomplete, think paradoxical air — coronary air embolism, with the same worry for the cerebral circulation; 100% O2, pressure support, and this is where the unfinished bubble study collects its price. A learner who never connects the two has missed the case's spine.
• Continue vs abort. resume only if the source is controlled, hemodynamics are stable, and there is no evidence of ongoing systemic embolism; recurrent or hemodynamically significant VAE argues for repositioning (lateral, head down) or staging. The defended threshold matters more than the specific call.

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• First move. stimulus removal — the reflex arc stops when retraction stops. 'Hands off' beats atropine for a monitored, self-terminating event; atropine given while the stimulus continues treats your monitor, not the patient, and can mask a brainstem warning.
• Recurrent bradycardia. trigeminocardiac-type reflex — trigeminal afferents at the CPA, vagal efferents — or direct traction near the vagal nuclei; the surgeon needs to hear it each time. Options: prophylactic anticholinergic (glycopyrrolate 0.2-0.4 mg gentler, atropine 0.5 mg for abrupt severe events), asking the surgeon to alter retraction, transcutaneous pacing as backup for repeated asystole. Naming the cost — losing a functional brainstem monitor — is the mark of a strong answer.
• Relaxant. facial nerve EMG requires no neuromuscular blockade beyond the intubating dose; immobility comes from anesthetic depth (remifentanil is well suited), not paralysis. Redosing rocuronium mid-case is the error.
• Maintenance. TIVA (propofol + remifentanil) is the common committed answer — stable evoked potentials, no relaxant requirement, rapid predictable emergence for the early neuro exam; low-MAC volatile with opioid is also defensible. Wanting a fast, examinable wake-up after brainstem work should appear in the reasoning.
• PaCO2 target. normocapnia to mild hypocapnia (roughly 30-35 mmHg) for brain relaxation with his early hydrocephalus; aggressive hyperventilation risks cerebral ischemia for little gain.

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• Deep vs awake vs stay intubated. deep extubation is the wrong direction after CPA surgery in a man with preop swallowing trouble — airway protection is exactly what is in question. Awake extubation after demonstrated command-following and strength, versus staying intubated for a formal assessment, are the defensible poles. The preop coughing-on-liquids is the finding the learner must surface unprompted.
• Before extubation. awake and following commands, quantitative confirmation of full reversal, intact cough and gag, normothermia, stable hemodynamics, a reassuring wake-up exam after brainstem-adjacent work.
• Cuff leak. no — a leak speaks to laryngeal edema after a long case with a flexed neck, not to aspiration risk, which is the question in him; knowing what the test does and does not answer is the point.
• Wet voice, pooling. new or unmasked lower cranial nerve (IX/X) dysfunction after CPA retraction — high aspiration risk. Examine palate elevation, gag, volitional cough strength, voice quality; strict NPO.
• Disposition. ICU — hourly neurologic checks and a watched airway after posterior fossa surgery with bulbar signs; PACU-to-floor is indefensible here.

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• DDx. residual anesthetic and opioid, tension pneumocephalus (the sitting position is the classic setup), resection-bed hematoma, acute hydrocephalus, seizure and postictal state, ischemia. Reactive pupils and spontaneous ventilation lean away from catastrophic brainstem compression but exclude nothing.
• Bedside and studies. glucose, temperature, quantitative twitch monitoring, cautious opioid-reversal trial if the exam fits; immediate noncontrast head CT.
• Dx. bilateral frontal air compressing and peaking the frontal lobes (the Mount Fuji picture) is tension pneumocephalus — air under pressure with mass effect — not the near-universal, innocent postoperative pneumocephalus.
• Why him / mechanism. sitting drains CSF and the inverted-soda-bottle effect lets air fill the space; after closure the trapped air warms and expands against a ball-valve dura, compressing the frontal lobes and raising ICP — hence the decline. N2O would have expanded it further.
• Rx. 100% O2 (washing nitrogen from blood steepens the gradient for resorption of the pocket), head positioning, and urgent neurosurgical decompression — burr hole or needle — if there is tension physiology or deterioration; the surgeon sees the CT now, not at rounds.
• Disposition. ICU with hourly neuro checks; improvement on oxygen does not make the fossa safe for the night.

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• DDx. resection-bed hematoma and acute obstructive hydrocephalus lead; hypertension with bradycardia and a crashing GCS is Cushing physiology — brainstem compression until proven otherwise. Edema, seizure, and stroke trail well behind.
• Tempo (for the examiner). a few milliliters matter: the compartment is small and rigid and contains the brainstem and fourth ventricle, so a small clot produces brainstem compression plus CSF obstruction and progresses to apnea and arrest over minutes to a few hours.
• Airway. vomiting with irregular breathing and GCS 8 demands intubation before or en route to imaging; controlled rapid-sequence induction that holds CPP (reduced propofol or etomidate, rocuronium 1.2 mg/kg, pressor drawn up), avoiding both hypotension and a hypertensive surge; hold MAP ≥80.
• CT interpretation. one clot, two problems: direct brainstem compression and obstructive hydrocephalus from the effaced fourth ventricle.
• EVD vs OR. evacuation is definitive; an EVD treats the hydrocephalus and buys minutes but drained alone against a posterior fossa mass risks upward transtentorial herniation — the drain is an adjunct on the way to the OR, not a substitute. Neurosurgical attending, OR desk, and blood bank are called simultaneously; this is measured in minutes.

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• Mechanism. aspiration through impaired glossopharyngeal and vagal function — pharyngeal weakness and an incompletely protected larynx after CPA surgery; the right lower lobe is where it lands in an upright patient. The preop coughing on liquids plus the postop wet voice predicted this; a bedside trial before formal swallow evaluation was the system failure — credit the learner who says so unprompted.
• Rx now. stop intake, sit him up, suction, supplemental O2, chest physiotherapy; bronchoscopy only for large-volume particulate aspiration or lobar collapse.
• Reintubation threshold. escalating oxygen requirement, rising work of breathing, inability to clear secretions, falling mental status — act before frank failure in a man who cannot protect his airway.
• Swallow evaluation. instrumented assessment (FEES at the bedside, or videofluoroscopy) grades the deficit and dictates diet and route; bedside screening alone already failed him once.
• Feeding and antibiotics. NPO with NG (or post-pyloric) feeding until swallowing is demonstrably safe — lower cranial nerve recovery often takes weeks. Aspiration is initially a chemical pneumonitis: supportive care first, antibiotics for evolution toward infection (persistent infiltrate, fever, worsening at 48 h), not reflexively at hour zero.

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• Facial EMG. brisk responses at the end of the case mean the nerve is in continuity — a genuinely hopeful data point; many partial injuries improve over months. Honest uncertainty with defined follow-up, not a promise in either direction.
• Tracheostomy timing. drivers: expected duration of bulbar dysfunction, secretion burden, the aspiration event already on the record, and comfort — early tracheostomy eases secretion clearance and rehabilitation if recovery will take weeks; a defined reassessment interval (e.g., repeat instrumented swallow at 7-10 days) beats an open-ended wait.
• Feeding. NG now; PEG if the instrumented reassessment still shows aspiration at 2-3 weeks; strict NPO until then.
• 'Did something go wrong?'. answer the question actually asked: describe what happened, including the air embolism and the return to the OR, and why these deficits occur with this tumor in this location; no defensiveness, no speculation about blame, one consistent message shared with the surgeon. He is awake and competent — he, not just the family, gets the explanation.

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• Proceed vs delay. proceed — rebleed risk of an unsecured ruptured aneurysm peaks in the first days and dwarfs the cardiac risk; the ECG/troponin/echo picture is neurogenic stress cardiomyopathy, which improves only as the SAH is treated. Delaying for cardiac workup is the flag.
• Cath first. no — modest troponin without a coronary-territory wall-motion pattern (apical dysfunction crossing territories) argues against plaque rupture; cath adds delay, contrast, and arterial access without changing today's plan.
• Mechanism. catecholamine surge from the hemorrhage — neurogenic stunned myocardium / takotsubo physiology; typically reversible over days to weeks.
• Induction. EF 40% narrows the corridor: blunt laryngoscopy without a BP overshoot (rebleed) or a trough (CPP, stunned LV). Slow titrated propofol (1-1.5 mg/kg) or etomidate with generous opioid (remifentanil 1 mcg/kg or fentanyl 2-3 mcg/kg), rocuronium; vasopressor drawn up; ketamine-driven hypertension is the wrong direction.
• Arterial line. before induction — beat-to-beat pressure through laryngoscopy and pinning is the point; the minutes spent are cheap insurance in an unsecured aneurysm.
• BP target. keep her near her running pressure and cap the peaks — commonly SBP <160 with MAP kept above the level that supports her elevated baseline CPP; both the spike and the crash are enemies (transmural pressure = MAP − ICP; a spike raises rupture stress, a trough plus open EVD drops perfusion).
• Pinning spike. pinning is the most stimulating moment before incision; 195/100 threatens rebleed. Esmolol (0.5 mg/kg) or a repeat remifentanil bolus for a brief surge; nicardipine if sustained; deepening propofol works but drips in slowly and overshoots. Pre-treat next time with local at pin sites. Committing and defending matters more than the pick.

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• Reopen and level. reopen once she is settled, at the prescribed height (15-20 cm above the tragus); a clamped drain in a hydrocephalic patient risks ICP creep, but reopening comes with a leveling check — a drain zeroed wrong after position changes silently over- or under-drains.
• 40 mL in ten minutes. overdrainage with the dura closed and the aneurysm unsecured is dangerous: a sudden ICP drop raises transmural pressure across the dome (rebleed risk) and can tear bridging veins. Clamp or raise the drain, tell the surgeon, recheck the level.
• Tight brain options. head up and neutral, confirm venous drainage (tape, ties), deepen anesthesia, modest hypocapnia, CSF drainage via the EVD — the most direct lever here — plus osmotherapy.
• PaCO2. 30-35 mmHg as a temporizing measure; lower buys little more relaxation and risks ischemia in a brain already primed for vasospasm.
• Osmotherapy. mannitol 0.25-0.5 g/kg or hypertonic saline (3% 150-250 mL); either defensible — she is normovolemic, so the hemodynamic argument that dominates in unstable patients is not the issue. Keep the dose modest; the EVD is doing the heavy lifting.
• CSF drainage end point. drain in small aliquots (5-10 mL) against the surgeon's report of the field, not to a number; brisk drainage before the dura is wide open repeats the transmural-pressure error.
• TIVA vs volatile. with MEPs, TIVA (propofol-remifentanil, no relaxant after intubation) preserves signal quality; low-MAC volatile with SSEPs alone is defensible. The learner should tie the choice to the monitoring, not habit.

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• First moves. call for help and blood, large-bore access wide open, keep volume up — the immediate threat is exsanguination plus cerebral hypoperfusion, not ICP. Hypotension here is hemorrhage until proven otherwise.
• Deliberate hypotension. briefly and reluctantly, only if suction cannot clear the field for temporary clipping — profound hypotension in a hypovolemic patient risks global ischemia; modern practice prefers temporary clips over pharmacologic hypotension. If used: short, titrated (MAP no lower than ~50-60), with the pump primed to restore pressure.
• BP after temporary clips. normal-to-high MAP — the distal ACA territories now depend on collaterals, so pressure supports them; the rupture-pressure logic inverts the moment the clips are on.
• Burst suppression. propofol 1-2 mg/kg then infusion titrated to burst suppression on raw/processed EEG — metabolic suppression during temporary occlusion; expect pressor need and treat it rather than lightening.
• Adenosine. 0.3-0.4 mg/kg rapid push through a large proximal or central line gives ~20-40 s of asystole/profound hypotension for a bloodless field. Must be pre-drawn, defibrillator pads on, surgeon and room warned, and the team agreed before it is needed — improvising it mid-crisis is the pitfall.
• Transfusion. yes — active surgical bleeding with Hgb 9.1 and an injured brain; waiting for a lower trigger during ongoing hemorrhage undershoots. In SAH most keep Hgb ≥8-9 and transfuse ahead of losses when bleeding is active.
• 9 minutes of temporary occlusion. within commonly tolerated limits, especially under burst suppression, but not free — ask what the SSEPs/MEPs did during occlusion and whether they recovered; a persistent change alters the emergence plan.

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• Post-clip target. liberalize — the rebleed constraint died with the clip; now perfusion dominates. Avoid hypotension absolutely; most accept SBP up to ~160-180 and treat only extremes. Reciting the pre-clip cap unchanged is the flag.
• Wake vs stay intubated. wake her: preop GCS 13, monitors recovered — the early exam is the most valuable monitor she has. Staying intubated is defensible only with a reason (unrecovered MEP change, long occlusion, swelling, instability).
• Before extubation. reversal confirmed or no relaxant on board, normothermia, normocapnia, hemodynamics controlled, following commands — and a cough/hypertension plan ready.
• Analgesia. scalp block or surgeon's local plus acetaminophen 1 g and judicious short-acting opioid (fentanyl 25-50 mcg increments); loading long-acting sedation that muddies hourly neuro checks is the wrong direction.
• Bucking at closure. treat both the cough and the pressure: remifentanil or IV lidocaine 1-1.5 mg/kg for the reflex, esmolol for the surge. Pure antihypertensive without addressing the cough misses the mechanism.
• ICU orders. a band, not a number — e.g., SBP 110-180, treat outside it, hourly neuro checks, nimodipine continues, daily Na. The floor matters as much as the ceiling: she is entering the vasospasm window with a stunned heart.

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• DDx. acute hydrocephalus from EVD failure, seizure or nonconvulsive status, clip-related ischemia (ACoA perforators), hematoma at the operative site, hyponatremia or CO2 narcosis, oversedation. Early on POD 0, drain failure and seizure sit at the top; vasospasm this early is unlikely.
• Bedside checks. pupils and lateralizing exam, glucose, ABG, review sedation given, and look at the EVD — the fastest reversible causes are checked in two minutes before anyone moves to the scanner.
• Dampened EVD. an occluded or malpositioned catheter — no output plus a flat waveform in a drain-dependent patient means unmeasured rising ICP, not resolution. Escalate to neurosurgery immediately; catheter-side flushing is theirs.
• CT. acute hydrocephalus from drain failure explains the exam; restore drainage (flush, revise, or replace the EVD).
• Persistent drift. focal deficit is not explained by hydrocephalus alone — image the vessels: CTA (and CT perfusion where available) for clip-related occlusion.
• After a clean CTA. nonconvulsive seizure is the remaining common cause of unexplained depressed or fluctuating exam — get EEG; a normal CT/CTA does not exclude it.
• NCSE Rx. benzodiazepine if actively seizing, then load levetiracetam ~60 mg/kg IV (max 4.5 g) — favored over phenytoin for minimal sedation, no drug interactions, and hemodynamic neutrality in a patient whose exam is the monitor.

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• Concern. falling Na lowers seizure threshold and worsens cerebral edema — in a POD 2 SAH patient entering the vasospasm window, hyponatremia plus volume contraction is a direct DCI risk, not a lab curiosity.
• Urine studies and DDx. high urine Na and osm with hyponatremia fit both cerebral salt wasting and SIADH — the urine cannot separate them; the polyuria is the hint that this is salt wasting.
• Bedside separation. volume status: CSW is hypovolemic (negative balance, falling weight/CVP, orthostatic-range tachycardia, high UOP); SIADH is euvolemic with modest output. In SAH, CSW-pattern physiology is common and the default assumption when output is high.
• Fluid restriction. disagree — restriction treats SIADH but in a volume-deplete SAH patient it stacks hypovolemia on a spasm-prone brain; the classic wrong move here. If genuinely uncertain, treat as CSW: replace salt and volume.
• 3% saline. infusion (~0.5-1 mL/kg/hr) titrated to Na, with isotonic volume replacement alongside; reserve 100-150 mL boluses for symptomatic drops. Limit correction to ≤8 mEq/L per 24 h — overcorrection risks osmotic demyelination even from 129.
• Fludrocortisone. 0.1-0.2 mg/day blunts renal sodium loss and shrinks the 3% requirement; reasonable adjunct in SAH salt wasting.
• End point. Na stably ≥135 with matched intake-output and the natriuresis abating — taper rather than stop, and keep daily (or BID) sodium checks through the DCI window.

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• DDx and timing. delayed cerebral ischemia from vasospasm leads on POD 5 — the classic 4-14 day window; also recheck Na, seizure, hydrocephalus, sedation. New focal deficit plus depressed level in the window is DCI until proven otherwise.
• First studies. the exam is the primary monitor; TCDs and CTA/CT perfusion confirm; Na and glucose exclude mimics. Leg-predominant weakness fits ACA territory — exactly the runoff of a clipped ACoA.
• TCD interpretation. mean velocity >200 with a large rise from baseline indicates severe spasm (a high Lindegaard ratio separates spasm from hyperemia) — but TCD is insensitive for the ACA and is not, alone, the trigger; the exam plus vessel/perfusion imaging drives action.
• Rx priorities. induced hypertension on a secured aneurysm, correct volume to euvolemia, keep nimodipine, and involve neurointervention early — in parallel, not sequence.
• Induced hypertension. norepinephrine, stepwise: raise SBP in increments (160 → 180 → 200) titrated to the exam — the deficit reversing is the end point, not a number. Clipping removes the rebleed ceiling; her stunned heart, not the aneurysm, is the practical limit.
• Volume. euvolemia — triple-H is dead; deliberate hypervolemia adds pulmonary edema and cardiac strain (especially with EF 40%) without cerebral benefit.
• Nimodipine hypotension. do not discard the only agent with outcome benefit — split to 30 mg q2h, time doses against pressor titration; hold only if refractory hypotension persists despite that.
• Refractory deficit. endovascular rescue: intra-arterial verapamil/nicardipine for distal or diffuse spasm, balloon angioplasty for proximal segments — six hours of failed medical therapy with a persistent deficit is an indication, not a defeat.

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• Dx and first move. cardiogenic pulmonary edema from the stunned ventricle driven into a SBP-190 afterload; also volume overload, aspiration, flash ischemia. First: oxygenation — sit her up, escalate support — hypoxemia injures the ischemic brain faster than any pressure adjustment helps it.
• TTE. the admission stress cardiomyopathy, now decompensating under forced afterload — the induced-hypertension strategy itself is the precipitant; a treatment complication, not a new disease.
• Norepinephrine. reduce toward the lowest pressure that holds the exam — pure alpha escalation into a failing LV worsens the edema; swapping to a pure inotrope alone abandons the DCI target. Stepwise reduction with the exam watched beat by beat.
• NIV vs intubation. mental status decides — drowsy with DCI, NIV is fragile. Intubation costs the neurologic exam, the one monitor titrating this entire strategy — substitutes are frequent sedation holidays with wake-up assessments, TCDs, imaging, and a low threshold for angio.
• Inotrope. dobutamine — raises CO with modest pressure cost and quick titration; milrinone vasodilates more and lingers (renal clearance), making an unstable pressure target harder to hold. Adding inotropy lets a lower SBP deliver the same cerebral flow.
• New target and end point. the lowest pressure at which the deficit does not worsen — the exam (or its substitutes) is the end point; a fixed 190 is no longer defensible with the heart failing.
• Push back to 190. no — exam unchanged at 168 means the extra 22 mmHg bought nothing and was costing the heart; re-escalate only for a new or worsening deficit.
• Angio suite. yes — when the heart caps induced hypertension, intra-arterial therapy treats the spasm directly and lets the pressure demand come down; the cardiac ceiling is itself an indication for endovascular rescue.

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• First actions. airway and oxygen, lateral position, suction, protect from injury, timed observation — a self-terminating 90-second convulsion needs support and workup, not reflex intubation.
• Recurrence. lorazepam 0.1 mg/kg IV (≈7 mg for her; a single dose is usually capped at 4 mg, repeatable); have a second dose and an airway plan ready.
• What to check. glucose, Na, SpO2, a lateralizing exam, and aspiration — plus a repeat CT for a new structural cause; postictal depression mimics and masks ischemic worsening for hours, and the metabolic surge is bad for a brain with active DCI.
• Na 131 / glucose 128. not the culprit — sodium has been holding on treatment; the seizure is most plausibly cortical irritation from the hemorrhage/ischemia. Do not chase the number with aggressive correction.
• AED choice. levetiracetam load (~60 mg/kg, max 4.5 g) — non-sedating, no interactions, exam-friendly; phenytoin's sedation, hypotension with loading, and interaction profile make it second choice here.
• Will she get back. honest and specific: a seizure after SAH is common and does not itself mean new permanent injury; her real determinants are the DCI course and the recovering heart. Name what is known, what is not, and the months-long timescale — no false reassurance, no foreclosure.

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• Candidate. most likely yes — anxiety is common and modifiable with preparation; his real hooks are procedural anxiety (panic mid-mapping in pins), habitus and snoring (obstruction under sedation with a hard-to-reach airway), and frequent recent seizures (stimulation-triggered seizure during mapping). True barriers are inability to cooperate or communicate, refusal after informed discussion, uncontrollable cough, or severe untreated OSA where sedation is judged unsafe. Want a commit, not a hedge; missing the anxiety or the airway is a flag.
• What cancels it. refusal or panic that preparation cannot settle, inability to lie still semi-lateral for hours, poorly controlled seizures on the day, new deficit making task performance impossible. Reasonable to frame as a joint call with the surgeon.
• 'Will I feel it'. an honest, specific answer beats reassurance: the scalp is blocked and the brain itself has no pain fibers; he will feel pressure, vibration, and sounds, and dural manipulation can briefly hurt and will be treated. Promising he will feel nothing sets up a mid-case crisis of trust. Preparation means walking the timeline (block, sedation, wake-up, tasks, re-sedation), the sounds and positions, and who will be talking to him.
• Rehearsal and stop signal. run the actual language tasks (naming, counting, reading) with the neuropsychologist/speech team preop to establish his baseline — his word-finding pauses make a documented baseline essential; a brief positioning trial is reasonable; an agreed verbal or hand signal for distress that will be honored, not negotiated.
• Midazolam. avoid or minimize — it depresses ventilation on top of dexmedetomidine/opioid in a suspected OSA patient and can degrade task performance during mapping; anxiolysis here comes from preparation and rapport. A small titrated dose before the block is defensible if the learner defends the trade.

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• Bearing on mapping. recent breakthrough seizures mark an irritable cortex: the risk of a stimulation-triggered seizure during mapping is real and elevated. The team may map at lower stimulation currents and use electrocorticography to watch for afterdischarges; the learner should connect the history to intraop risk, not just to home meds.
• Morning levetiracetam. give it — an omitted dose on the morning of a mapping case lowers the threshold on the day it matters most.
• Level. reasonable if adherence or recent titration is in question (his dose was just increased); not mandatory, and normal levels do not guarantee control. Either answer is defensible if reasoned.
• Dexamethasone. peritumoral edema reduction is the usual surgical rationale even in a non-enhancing lesion; for anesthesia it means hyperglycemia — check intraop glucose and treat — and insomnia/agitation that can worsen his anxiety.
• Seizure on the field. iced saline irrigated directly onto the stimulated cortex by the surgeon is the first-line abort — fastest and mapping-sparing; anesthesia owns the systemic backup and the airway. Reaching for a systemic dose first is the flag.
• Rescue doses. small aliquots: midazolam 1-2 mg, propofol in 20-50 mg increments — enough to abort a seizure without costing the airway or the rest of the mapping; suction working, airway rescue equipment sized and checked before the pins go on. Reflexively drawing a full induction dose misses the point of the case.

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• Beyond the standard exam. everything about rescue in position: mask fit, nasal patency for an airway adjunct, neck mobility with the head turned, whether he can lie semi-lateral comfortably, and how much of the airway will be physically reachable once pinned and draped. Treat the snoring as presumptive OSA: nasal airway early, low sedative doses, capnography on the nasal cannula.
• Sleep study first. no — this is oncologic surgery in a patient with breakthrough seizures; weeks of delay for polysomnography that will not change the day-of plan is hard to defend. Manage him presumptively as OSA. A learner who delays surgery for the study should be pressed on what the result would change.
• LMA as primary rescue. yes — with the head fixed in pins and turned away, direct or video laryngoscopy is somewhere between awkward and impossible; an LMA can be seated from almost any position and is the realistic first rescue. The threshold at which the surgeon releases the pins should be stated in advance.
• Aspiration prophylaxis. he is fasted with no reflux history — routine prophylaxis is not indicated, though an H2 blocker is a defensible personal practice for a long sedation without a secured airway. Either way, reasoned, not reflexive.

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• AAA vs sedation throughout. both are practiced; the debate should be built on HIS features. AAA secures the airway during the asleep phases — attractive with suspected OSA — but buys two airway transitions in pins. Monitored sedation keeps spontaneous ventilation and avoids the exchange, but rests everything on titration in an obstruction-prone patient. Either commit is acceptable; ignoring the snoring in the defense is the flag.
• Nerves. six per side for a hemicranium: supraorbital, supratrochlear, zygomaticotemporal, auriculotemporal, greater occipital, lesser occipital (some add greater auricular). The learner should name them, not gesture at 'a scalp block.'
• Agent and concentration. a long-acting agent — ropivacaine 0.375-0.5% or bupivacaine 0.25-0.375%, with epinephrine; the block must outlast hours of surgery.
• Ceiling arithmetic. dose to lean/ideal body weight, not 110 kg: IBW roughly 73-75 kg, so ropivacaine at ~3 mg/kg gives a ceiling near 220-225 mg; 40 mL of 0.5% ropivacaine is 200 mg — near ceiling before the surgeon's pin-site and field infiltration is counted. Do the math and leave headroom (e.g., 30-40 mL of 0.375%); dosing to actual body weight is the classic error.
• Epinephrine. yes — the scalp is vascular; 1:200,000 slows absorption, lowers peak plasma levels, and prolongs the block. Watch for tachycardia/hypertensive response in a hypertensive patient.
• Dexmedetomidine vs propofol-remifentanil. dexmedetomidine preserves respiratory drive and gives arousable sedation — well matched to his airway; its costs are bradycardia/hypotension and slower offset. Propofol-remifentanil titrates fast and wakes clean, but remifentanil plus suspected OSA is an apnea setup. Many combine low-dose strategies; want a committed choice reasoned from his respiratory risk.

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• Before pinning. block working at the pin sites, patient comfortable in the final position with pressure points padded, bladder plan settled, stop signal reconfirmed, rescue drugs and airway equipment at the head — pins convert every later problem into a problem in a fixed head.
• Testing the block. sharp stimulus at each pin and incision site, not just asking if he feels numb; the surgeon supplements pin sites with local infiltration regardless.
• Dexmedetomidine load. 0.5-1 mcg/kg over 10-20 minutes — dosed to lean body weight, and many drop to 0.5 mcg/kg in suspected OSA — then 0.3-0.7 mcg/kg/hr titrated to a rousable patient.
• Remifentanil. low-dose, 0.01-0.05 mcg/kg/min, for pinning and opening; the synergy of opioid plus dexmedetomidine in this airway is exactly the trap — some omit it entirely. Either answer defended is fine.
• Obstruction Rx order. remifentanil off first, verbal stimulation and command to breathe, jaw lift, O2 up, nasal airway if needed, then reduce the dexmedetomidine rate. Reaching for a device before the sedation dial, or bolusing propofol, is the flag.
• Sedation off entirely. usually not — lightening in steps preserves the awake plan; slamming everything off buys an anxious, pinned, uncomfortable patient. Calm narration as he lightens — where he is, all is well, breathe deeply — is a therapeutic tool.
• Pre-draping setup. face and airway accessible under tented, transparent drapes; nasal cannula with capnography; an arm free and visible for signals; airway cart and LMA at the head.

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• Immediate order. announce it — stimulation stops; surgeon irrigates iced saline onto the cortex; support oxygenation; small propofol only if the cortical irrigation does not abort it. Jumping to a large systemic dose first is the flag.
• Propofol. 20-50 mg increments — abort the seizure, keep the airway and the case. An induction-dose bolus costs both.
• Protect in pins. his head cannot move and he cannot fall — the real dangers are hypoxia and limb injury: oxygen, suction ready, guard (not forcibly restrain) the limbs, watch ventilation. A learner reciting the ward-seizure script (lateral position, pad the rails) has not seen the pins.
• Resuming mapping. no — postictal language errors produce false-positive mapping; a site can look eloquent because he is postictal, not because it is. Wait until he is back to his documented baseline on the rehearsed tasks, typically minutes to tens of minutes, and re-run baseline tasks before trusting new data.
• Levetiracetam now. an additional IV dose (500 mg-1 g over 15 min) is reasonable after an intraoperative seizure, coordinated with the surgical team. His month of breakthrough seizures marked him; this was a known risk prepared for, not bad luck.

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• DDx. hypercapnia or hypoxia, full bladder, pain (dural traction is the classic), postictal or evolving seizure activity, anxiety/panic, positional misery after hours still. The learner generates the list; the case then confirms two of them.
• First move. ask him — the awake patient is the monitor; simultaneously check SpO2/EtCO2, glance at the field with the surgeon, and screen pain, bladder, and fear in three questions. Treating agitation as a sedation-dose problem before diagnosing it is the flag.
• EtCO2 52. nasal-cannula capnography under-reads, so the true value is higher — sedation hypoventilation is both agitating him and swelling the brain. Lighten, coach breathing; do not deepen.
• Bladder. if no catheter was placed (a deliberate choice in many awake craniotomies), a urinal or condom catheter at the drapes and easing the fluids; if one is in, check it for kinks. Small, humane, and it works.
• Propofol bolus costs. the language exam (confounded for many minutes), possibly the airway in this habitus, and the surgeon's remaining map; forcible restraint escalates panic in a man whose head is bolted to the table. Treat the causes first — a bolus is the last move, not the first.
• When the awake part ends. when the surgeon has the map complete — or earlier, the moment patient safety or cooperation genuinely fails; the anesthesiologist makes that abort call, and the rehearsed stop signal is honored, not negotiated.

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• Options. induce and seat an LMA — the device least dependent on head position; fiberoptic intubation (through the LMA or nasally); videolaryngoscopy attempted from a compromised angle — possible but the line of approach is wrong, the mouth may face away, and neck movement is zero. Rank them for a fixed, rotated head, not a generic difficult-airway list; the learner betting on VL should be pushed.
• Who unpins, when. the neurosurgeon releases the Mayfield — and the call is made at cannot-ventilate, announced as a threshold in advance, not after desaturation. Knowing the wrench's location and saying the threshold out loud is the mature answer.
• Keep vs exchange. if ventilation and pressures are good and the remaining case is closure, an LMA alone is defensible; exchange to an ETT if airway pressures, brain relaxation, or duration argue for control. Want a commit tied to conditions.
• How exchange. fiberoptic through the LMA with an Aintree catheter is the standard sequence — the airway is never abandoned between devices.
• Full brain DDx. hypercapnia from the fresh conversion is the front-runner; then venous outflow obstruction from the rotated neck, nonconvulsive seizure, expanding hematoma in the cavity, volatile agent depth, head-down drift.
• First three moves. verify ventilation and drive the CO2 down, check head-up and the neck for venous kinking, deepen with propofol (or shift toward TIVA); hyperosmolar therapy after these, and tell the surgeon what you found.
• Ventilation target. PaCO2 roughly 30-35 mmHg as a temporizing bridge, correlated with a gas — sustained aggressive hypocapnia trades brain volume for ischemia.

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• Emergence goals. rapid, smooth return to a testable neurologic exam without coughing, straining, or hypertension driving bleeding into a fresh resection cavity — the exam IS the monitor after this operation.
• Bucking. an LMA is better tolerated at light planes and is a genuine argument for having kept it; with an ETT, opioid titration, IV lidocaine, or deep exchange to an LMA — named, not waved at.
• First language exam. in the PACU within the first hour, as soon as he is awake enough — against the preop baseline tasks; anesthesia's job is to flag residual sedation as a confounder and time the exam honestly.
• Slower naming in PACU. residual sedation and post-mapping fatigue are the benign explanations; resection-cavity hematoma, edema, or ischemia in the opercular region are the ones that matter. Re-examine as sedation clears, tell the surgeon, and a low threshold for CT if it does not improve or anything else appears — attributing a new language change to anesthesia without looking is the flag.
• Disposition. ICU or a dedicated neurosurgical step-down with hourly neuro checks; the intraoperative seizure, suspected OSA plus residual sedation, and the conversion each independently argue for continuous monitoring overnight; a floor bed is wrong for him.
• Overnight monitoring. continuous pulse oximetry, minimized opioids with multimodal analgesia (the scalp block is still working), lateral or head-up positioning, CPAP if he obstructs, and a low threshold to escalate — treat him as the untreated OSA patient he probably is.

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• Proceed at 4 hours. 4 hours post-dose is near peak effect — the worst moment to open the skull uncovered. The tension is a slowly declining exam versus full anticoagulation; the learner should refuse to proceed with neither waiting nor reversing.
• How long to wait. apixaban half-life ~12 h; elective intracranial surgery typically waits 48-72 h off drug. The learner should see that a declining exam makes that window unavailable.
• Creatinine. CrCl here is roughly 40 mL/min — clearance is prolonged, so waiting buys less than the half-life math suggests. Ignoring renal function in the timing estimate is the common miss.
• INR 1.1. proves nothing — PT/INR and aPTT are insensitive to apixaban; a learner reassured by a normal INR has missed the pharmacology.
• Anti-Xa 180. an apixaban-calibrated level quantifies residual effect; 180 ng/mL is a therapeutic-range level, far above the <30-50 ng/mL many labs treat as low. Limits: calibrated assay availability and turnaround, and no validated 'safe' threshold for intracranial surgery.
• Andexanet vs PCC. andexanet alfa is the specific antidote, approved for life-threatening bleeding on apixaban — very expensive, not stocked everywhere, effect wanes after the infusion, thrombotic risk, and not studied as pre-surgical prophylaxis. 4-factor PCC 25-50 units/kg (~1700-3400 units for him; many centers a fixed ~2000 units) is off-label with observational support and is what most centers actually give before urgent surgery. Either is defensible if the tradeoffs are owned; reciting andexanet as 'the answer' without cost/availability/evidence reality is a flag.
• FFP. does not neutralize a direct Xa inhibitor in any useful way, and the volume load is unwelcome in aortic stenosis. 'Give FFP' is the classic wrong reflex carried over from warfarin.
• Declining exam. the exam decides it: reverse (PCC or andexanet per institutional pathway), confirm products and type-and-screen, and go now. Continuing to wait for a lower level while he declines is the failure mode. The learner should think one step past the reversal order — PCC in before incision, PRBC available, hemostasis rechecked with the surgeon.

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• Repeat echo. an echo within about a year with no interval change in symptoms is generally adequate; the real question is whether anything has changed — syncope, angina, worsening dyspnea (hard in a confused patient; ask the daughter). Reflexively re-imaging without asking what it would change is worth probing. Discovering severe AS would tighten hemodynamic discipline and lower the threshold for pre-induction pressors — it would not cancel an urgent evacuation.
• 6-hour delay. waiting 6 hours for an echo while the exam declines is the wrong trade; proceed with AS-appropriate management. Bedside POCUS for a quick gradient/contractility look is a reasonable middle path if immediately available.
• Daughter's history. no syncope or angina is reassuring; reduced walking is nonspecific in a man whose gait is failing from the subdural. Manage as at least moderate AS and treat him as possibly worse.
• HR target. roughly 60-80 and controlled; tachycardia shortens diastole (filling and coronary perfusion of a hypertrophied LV), profound bradycardia drops output across a fixed valve.
• BP floor. his baseline is 158/84 (MAP ~110) — the floor should be set relative to that, not to a textbook 65; most would defend MAP ≥80 and act fast below it. Diastolic pressure is the coronary perfusion pressure that matters here.
• Rhythm. atrial kick is already gone, so rate is everything; the fear is RVR with induction stress or hypotension-triggered catecholamines. Phenylephrine drawn up, esmolol available, pads on and a plan for synchronized cardioversion.
• Arterial line. yes, before induction — beat-to-beat pressure in moderate AS with a reversal-dependent hemostasis plan is cheap insurance; a learner deferring it to 'after we're asleep' should defend that.

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• Can he consent. capacity is decision-specific and assessed at the bedside, not inferred from the MCI label or the repeating — some patients who repeat questions can still consent to this. The learner should go ask him, not adjudicate from the chart.
• What to ask. in conversation: can he say what is wrong (blood pressing on his brain), what is proposed and its main risks, that it applies to him, weigh doing it against not, and hold a consistent choice across the conversation. The four functions (understand, appreciate, reason, express a choice) demonstrated, not recited.
• 'Fix it' enough. no — it expresses a choice but shows no understanding or appreciation. A learner who accepts it because it agrees with the plan is the classic pitfall: agreement is not capacity.
• What would be enough. his own words back: there's a blood collection pressing on his brain, they'll drill and drain it, it could bleed or come back, and without it he'll likely get worse — held onto for more than a minute. He does not need to retain it tomorrow; he needs it for this decision.
• Proxy unclear. he lacks capacity for this consent; verify — chart, PCP office, hospital records — while not letting paperwork stall an urgent case. With a declining exam, an involved daughter with no family disagreement, and surgeon concurrence, proceed per institutional surrogate/two-physician policy; ethics or administration on call if anything conflicts. Document the capacity assessment itself, who consented and on what authority, and the urgency rationale.
• 'Just go'. urgent-not-emergent means there IS time to do this properly — the emergency exception (proceed with no consent at all) is not available while he's conversant and family is present. Neither wait-for-perfect-paperwork nor invoke-emergency is right.

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• The choice. both are done for burr-hole cSDH evacuation; either is defensible if committed and defended against HIS features. For MAC: avoids an induction in moderate AS on a freshly reversed patient, faster return to a followable neuro exam, less delirium exposure. For GA: he repeats questions and reaches — cooperation under drapes is doubtful; a still field; a secured airway you don't have to rescue head-turned under drapes. Wanting the case both ways — 'light GA, sort of' — is the flag.
• Sedation strategy. dexmedetomidine is the best fit for a delirium-prone brain — infusion ~0.2-0.7 mcg/kg/h, load omitted or given very slowly (bradycardia and hypotension both bite in AS). Propofol in small doses risks disinhibition, apnea, and hypotension in exactly this patient. Minimal-to-no sedation with a good scalp block is a legitimate answer.
• Midazolam. avoid — paradoxical agitation and delirium in the elderly, and it clouds the postoperative exam; the learner should produce the why, not just the no.
• Fasting. 5 hours from a light meal in a patient whose exam is declining — the neurologic clock beats the fasting clock; waiting 3 more hours for a guideline interval he nearly meets is the wrong trade. The honest cost: if MAC, sedation depth must respect an imperfectly empty stomach; if GA, this feeds the RSI discussion.
• Airway contingency. decided before draping: head accessible or turnable, airway cart and suction in the room, video laryngoscope ready, induction drugs drawn, and an explicit word with the surgeon that the case stops if you call it. Improvising this at the moment of need is the failure.

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• Monitors. arterial line (AS, reversal-dependent hemostasis), EtCO2 sampling under the drapes for respiratory rate and apnea detection. A learner content with a pulse ox and cycling cuff is under-armed.
• Oxygen and fire. cautery near the head with open oxygen is the OR-fire setup: oxidizer pooling under drapes, ignition source, fuel. Lowest FiO2 that holds saturation — room air or nasal cannula at 1-2 L; not 6 L of open oxygen under a drape.
• Drapes. tented off the face with airway access maintained, suction under the drapes to scavenge oxygen, prep dry before cautery. Concrete requests, not vigilance in the abstract.
• Dexmedetomidine. skip or crawl the load — a standard 1 mcg/kg over 10 min invites bradycardia and hypotension in an elderly man with AS; start the infusion low (~0.3-0.4 mcg/kg/h) and titrate.
• He reaches. first move is verbal — hand on his hand, reorient, warn the surgeon and pause the field. Reaching for a syringe first is the pitfall.
• Next agent. a small titrated increment — dexmedetomidine bolus given slowly or 10-20 mg propofol — accepting that every increment in a disinhibited elderly brain can worsen the disorientation.
• Second reach, stacked propofol. accumulating boluses chase agitation into obstruction, apnea, and hypotension with an unsecured airway under drapes — the classic MAC death spiral.
• What ends MAC. a defined line, decided now: repeated movement threatening the field, obstruction or desaturation, escalating doses without effect. Naming the tripwire in advance is the mark of judgment; drifting deeper is the flag.

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• Induction agent. etomidate 0.15-0.2 mg/kg (~10-14 mg) for hemodynamic stability, or propofol slowly titrated at reduced dose (~0.5-1 mg/kg) with a pressor already running; low-dose ketamine adjunct (~0.5 mg/kg) spares hypnotic dose but watch tachycardia in AS. Any committed, dose-reduced, pressor-supported plan passes; a standard 2 mg/kg propofol push fails him.
• RSI and relaxant. he ate 5 hours ago, is agitated, and just got sedative increments — a modified RSI is reasonable: rocuronium ~1 mg/kg or succinylcholine ~1-1.5 mg/kg (no contraindication here). The learner should connect the fasting history from A4 to the airway plan, not treat this as an elective induction.
• Pressor first. phenylephrine (or norepinephrine) — raises diastolic pressure and coronary perfusion of the hypertrophied LV without tachycardia, and reflex slowing is welcome. Ephedrine is the wrong reflex: tachycardia shortens diastole and raises demand across a fixed valve.
• End point. back toward his own baseline — MAP ≥80, not a generic 65; in AS the cost of running low is subendocardial ischemia, not just a number on the screen.
• Maintenance. either sevoflurane at modest MAC with pressor support or a TIVA is defensible for burr holes; vasodilation from deep volatile is the thing to own either way. Wanting a followable early postoperative exam argues for a light, short-acting technique.

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• Of concern. a diastolic of 45 in a hypertrophied, pressure-loaded LV is a coronary perfusion problem — the LV that most needs diastolic pressure is getting the least. Treating this as routine anesthetic hypotension is the miss.
• Target. anchored to HIS baseline of 158/84 — the learner should reason to 'higher than my usual target' (MAP ≥80, diastolic recovered), not recite MAP 65.
• Lighten vs pressor. 0.7 MAC is already modest, so the bigger lever is vasoconstriction — phenylephrine or norepinephrine infusion; cutting the volatile below amnestic levels to chase pressure trades one problem for another.
• Transient regular 130. likely atrial flutter with conduction or an SVT run — brief, self-terminated, but a warning: this heart tolerates 130 poorly (diastole collapses). Fix pressure, depth, volume, magnesium and potassium, oxygenation first; no beta-blockade on top of hypotension and volatile — negative inotropy at the wrong moment. Reaching for a drug before the triggers is the pitfall.
• Sustained 140 with BP 70/40. unstable — synchronized cardioversion now, 100-200 J biphasic, pads already on from the induction plan; amiodarone 150 mg over 10 min or small titrated esmolol only if he were perfusing.

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• Small levers. allow PaCO2 to drift up to ~45-50 (more cerebral blood volume), level or slightly lower the head, a gentle sustained inspiratory hold to raise venous pressure — all real, all modest. Hyperventilating a brain you want to expand is the active mistake to catch.
• Expectations. a chronically compressed, atrophic 79 y.o. brain re-expands over days, not minutes — the honest answer to the surgeon is 'small levers, mostly time.' Overpromising here is a flag.
• Bradycardia with irrigation. trigeminocardiac/dural traction reflex — the stimulus is the cause, so the first move is 'stop irrigating,' not a syringe. HR recovers when the stimulus stops.
• Atropine. not for a self-resolving reflex with adequate pressure; if recurrent and hemodynamically significant, glycopyrrolate 0.2 mg or atropine 0.4 mg before further irrigation is reasonable, plus warmed irrigant and a gentler hand.
• Back to baseline. defined by the daughter's description — oriented to himself, conversant but repeating questions — not a normal mental status exam he never had. Chasing a crisp exam with more time or stimulation misreads the patient.
• Extubation criteria. the physiologic criteria stand — awake to voice, airway reflexes, regular spontaneous ventilation, full reversal confirmed (TOF ratio ≥0.9), warm, hemodynamically stable — but 'follows commands' is graded against his baseline; a patient at his own confused baseline with intact airway reflexes can be extubated.

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• DDx. bounded to this case: residual sedative sensitivity in a 79 y.o. brain, hypercapnic narcosis, nonconvulsive seizure, reaccumulation or tension pneumocephalus, stroke, and the quick metabolic checks (glucose, sodium, temperature).
• First three actions. look at him (pupils, symmetry, lateralizing signs), support ventilation and get a gas, send glucose and sodium — cheap, fast, and they sort half the list before anyone calls for a scan.
• ABG. PaCO2 61 with pH 7.31 — hypercapnia from residual sedation is at least contributing; stimulate, support ventilation, reassess. The trap is stopping here: hypercapnia found is not the workup finished if he doesn't wake once corrected.
• CT decision. normocapnic and still not waking → CT now; looking for reaccumulation, tension pneumocephalus, and stroke. Waiting another cycle 'to see' on a reversed-anticoagulant fresh subdural is the miss.
• Clean CT. EEG — nonconvulsive seizure after subdural evacuation is real and invisible without it; MRI for stroke if EEG is unrevealing.
• Apixaban restart. not a number to recite — a joint call with neurosurgery and cardiology weighing his AF stroke risk against rebleed into a fresh subdural cavity (and chronic SDH recurs). Typically days to a couple of weeks with imaging stability; interim mechanical prophylaxis and a documented plan. The learner's job is to name the competing risks and the right owners.
• The daughter. plain and honest: he is slower to wake than expected, the likely reason (medications and carbon dioxide in an older brain), what has been checked, what happens next, and when she'll hear more — no false reassurance, no catastrophizing.

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• Two-week story. morning headache with nausea plus a new focal motor sign is the raised-ICP-with-mass-effect cluster; the learner should assemble it and name it themselves. Treating this as a routine elective without engaging the symptoms is the flag.
• Mechanism. a 4 cm mass plus vasogenic edema raises ICP; symptoms worse on waking from recumbency and nocturnal CO2 rise increasing CBF; the drift is focal compression of right motor cortex — an early localizing sign, not just 'clumsiness'.
• What to look for on MRI. degree of midline shift, edema extent, ventricular effacement or trapped ventricle, cisterns, and relationship to the superior sagittal sinus — each changes how much reserve she has under anesthesia.
• Sinus proximity. parasagittal/sinus-abutting meningiomas raise blood-loss and sinus-injury stakes and can obstruct venous outflow; mostly this drives blood availability and tighter hemodynamic discipline, not cancellation.
• Old scan, progressing symptoms. progression since imaging matters more than the calendar date; call the neurosurgeon — the answer may be re-image, move the case up, or steroid adjustment. Silently proceeding on a stale scan with a changing exam is the pitfall.
• Midazolam. either answer is defensible if reasoned: a small titrated dose in a monitored setting for real anxiolysis, versus withholding because sedation-induced hypoventilation raises PaCO2, CBF, and ICP in a patient with reduced compliance. Reflexive premedication without engaging the ICP physiology is the flag.

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• Dexamethasone morning-of. give it. Missing doses risks rebound peritumoral edema on the day you most need a slack brain. Steroids shrink vasogenic (not cytotoxic) edema around the tumor, often improving symptoms within days — it is why her drift may even be better than two weeks ago. Abrupt stop risks rebound edema plus some HPA suppression after a week; many give an additional intraop dose at the surgeon's request.
• Glucose concern. steroid-induced hyperglycemia on top of T2DM; hyperglycemia worsens outcome after brain injury and ischemia, so it is not cosmetic here.
• Target and insulin. roughly 140-180 mg/dL intraop; check in holding, then hourly; IV insulin by small boluses or infusion. Tight control is the opposite error — undetected hypoglycemia under anesthesia is catastrophic for the brain.
• Metformin. hold the morning of surgery per routine; it provides no fasting benefit and simplifies the insulin plan. Lactic acidosis risk is largely historical concern but holding is standard.
• Levetiracetam. give it — she has a cortical supratentorial lesion; an intraop or emergence seizure is exactly what prophylaxis is for.
• Amlodipine. continue. Calcium channel blockers do not cause the refractory induction hypotension associated with ACEi/ARBs, and arriving at 152/88 rather than 190/100 makes the smooth induction easier.

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• RSI for controlled GERD. most would not: asymptomatic on a daily PPI, fasting, normal airway — a standard titrated induction is defensible and avoids trading a controlled induction for a marginal aspiration benefit. RSI is also defensible; the learner must commit and own the tradeoff rather than reflexively RSI everyone with the word 'reflux'. Symptoms, not the diagnosis label, drive the decision — active regurgitation, large hiatal hernia, gastroparesis, recent intake, obstruction.
• Morning vomiting. the wrinkle: her nausea/vomiting is likely ICP-driven, not gastric outlet pathology — but vomiting on the morning of surgery still means a stomach of unknown contents; gastric ultrasound or a pragmatic tilt toward RSI both show good reasoning.
• Prophylaxis. she is already on a PPI; nonparticulate antacid or famotidine add little in a fasting patient but are low-cost; metoclopramide reasonable if gastric concern persists.
• Succinylcholine. acceptable if needed. Its transient ICP rise is clinically minor with an adequate induction, and a two-week mild upper-motor-neuron drift is not a meaningful hyperkalemia risk — but the learner should show they considered both rather than never having heard of either.
• Twitch monitor side. prefer the unaffected (right) arm. A paretic limb upregulates acetylcholine receptors and looks resistant to nondepolarizers, so its twitches overestimate recovery. With a drift this mild the effect is small — the principle, not the panic, is the point.

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• Art line timing. either is defensible for an elective, stable patient. Pre-induction gives beat-to-beat pressure across laryngoscopy — the highest-risk minutes for both spike and trough. Post-induction is quicker and reasonable with frequent NIBP cycling. A committed, defended choice is the point; more shift, labile hypertension, cardiovascular disease, or difficult access tips toward awake placement.
• Central line. not needed for this supine craniotomy — not a sitting-position VAE setup, no expected vasoactive infusions. Placing one 'because craniotomy' is worth challenging.
• PIVs and tucked arms. two IVs, at least one 16-18 g, tested and secured before tucking; after the drapes go up you cannot get to them.
• Neuromonitoring. often none for a frontal meningioma; with her motor findings the team may want MEP/SSEP or motor mapping — ask the surgeon before the plan is set, because MEPs preclude ongoing muscle relaxant and cap volatile depth (favoring a TIVA).
• Type and screen vs crossmatch. meningiomas are vascular tumors, and hers abuts the sagittal sinus — most would crossmatch 2 units rather than screen only. A small convexity lesion far from the sinus is where screen-only is defensible; the learner should tie the answer to the imaging.

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• Goals. the learner should produce both directions themselves: no hypertensive spike (surges CBF into a poorly autoregulating tumor bed — edema, hemorrhage) and no trough (CPP = MAP minus ICP, and her ICP is already up, so 'normal' MAPs buy less perfusion). Naming only one failure mode is the incomplete answer.
• Doses for 80 kg. propofol ~1.5-2.5 mg/kg (120-200 mg) titrated; fentanyl 2-3 mcg/kg (160-240 mcg) or a remifentanil-based technique; either works if deliberately timed against laryngoscopy.
• Relaxant. rocuronium 0.6-1 mg/kg is the usual elective choice; succinylcholine defensible if rapid control were needed (see A3). Want a reason, not a habit.
• Blunting. any committed, dosed choice: fentanyl timed ~3 min before laryngoscopy, esmolol 0.5 mg/kg, lidocaine 1-1.5 mg/kg. Inducing deeply and hoping is the pitfall.
• BP 85/50. yes, of concern — MAP ~62 against an elevated ICP is a real CPP cut, and the injury from hypotension is silent until the postop exam. Treat promptly.
• Rx and target. phenylephrine suits propofol vasodilation with HR 70s; ephedrine if bradycardic; volume runs in the background but is too slow alone. Target near her ward baseline — she lives at 152/88 (MAP ~110), so a MAP in at least the 80s-90s, not a textbook 65.

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• TIVA vs volatile. either is defensible for an elective supratentorial case with a modest ICP picture: volatile at or below ~1 MAC leaves CO2 reactivity and CBF near normal; propofol lowers CMRO2 and CBF and is favored when the brain is tight. Challenge whichever they pick — the reasoning is the target.
• Sevo 1.5 MAC. no — above ~1 MAC, dose-dependent cerebral vasodilation outruns metabolic suppression and autoregulation degrades; exactly the wrong direction for a swollen brain.
• N2O. most avoid it here: a cerebral vasodilator that raises CMRO2, and it expands closed gas spaces — a pneumocephalus concern at and after closure.
• PaCO2. low-normal to mildly hypocapnic (~33-35) as the working target, trimming toward 30 when the surgeon needs a slacker brain with the dura open. Prophylactic aggressive hyperventilation is not a resting state — vasoconstriction has an ischemia price.
• Fluids. isotonic crystalloid (normal saline or a balanced solution). Off the list: anything glucose-containing (she is already 180-240, and hyperglycemia worsens ischemic injury) and hypotonic fluids (free water goes straight to brain water). Large-volume LR is worth a caveat as mildly hypotonic.
• Mannitol. 0.25-1 g/kg; commonly ~0.5 g/kg = 40 g for her, infused over 10-15 min rather than slammed.
• What to watch. a transient rise in intravascular volume as mannitol osmotically pulls water in — increased preload a limited heart would feel, and a rapid infusion can transiently drop BP — then the intended brisk osmotic diuresis; so track volume status and the Foley, and check Na/K and osmolality if dosing repeats. The diuresis you asked for becomes hypovolemia if ignored.

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• First moves. the free, fast physical checks: confirm head-up tilt, neutral head position, no ETT tie or tape compressing the jugulars, no circuit problem stacking pressure, minimal PEEP. Reaching for drugs before checking the table is the classic miss.
• EtCO2 31. not sufficient — EtCO2 underestimates PaCO2 by a variable gradient; send an ABG. A 'hyperventilated' patient by capnograph can be sitting at PaCO2 38.
• Depth and agent. converting from volatile to a propofol-based technique lowers CBF while keeping depth, the one agent change that helps the brain directly; deepen if light, since light anesthesia raises CBF and CMRO2.
• More osmotherapy. either an additional mannitol dose (toward ~1 g/kg total, after checking osmolality/osm gap) or a hypertonic saline bolus is reasonable; want a committed choice with a check-before-redose reflex.
• Dexamethasone now. works on vasogenic edema over hours to days — give it, but it rescues nothing in the next ten minutes; counting it as an acute measure is the flag.
• Telling the surgeon. a plain accounting: what has been done, what is pending (the ABG), what is left — deeper propofol to burst suppression, PaCO2 transiently toward 28-30, more osmotherapy, ventricular drainage from the field, and a surgical conversation about rapid internal decompression of the tumor. No preexisting CSF drain exists to open in this supratentorial crani; the surgeon can drain from the field. The team decides together; silence at the head of the bed is the failure.

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• 400 mL/hr. expected osmotic diuresis after 40 g of mannitol — the timing is the tell. The learner should also surface diabetes insipidus on their own, then argue against it: DI is rare mid-case outside pituitary/hypothalamic surgery, and mannitol diuresis tapers over a few hours while DI is sustained and relentless.
• Bedside sorting. timing relative to mannitol, trajectory (tapering vs escalating), and urine appearance are the no-lab clues; if it persists, send serum Na and urine osmolality — dilute urine against a rising serum Na is DI.
• Replace. partial replacement with isotonic crystalloid guided by hemodynamics. Chasing it 1:1 defeats the purpose of the mannitol; ignoring it entirely buys hypovolemia and hypotension. Middle path, watching the art line.
• Glucose 260. treat — IV insulin in small boluses (e.g., 4-6 units) or an infusion, recheck within the hour, target 140-180. The paired error to name: overshooting into hypoglycemia in an anesthetized patient who cannot declare symptoms.
• Temp 35.2. the mild-hypothermia-for-neuroprotection question is settled — no outcome benefit in aneurysm surgery (IHAST) and none established here, while real costs accrue: coagulopathy in a bleeding field, infection, shivering on emergence raising O2 demand, and a slower wake-up muddying the exam. Maintain normothermia.
• Warming logistics. forced-air over the lower body, fluid warmer, warm the room a notch — all compatible with a pinned head and open cranium.

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• Goals and the collision. the learner should produce the tension themselves: a rapid, clean wake-up so the surgeons get an early neuro exam — against no coughing, bucking, or hypertension on the tube, because venous and arterial spikes bleed into a fresh resection cavity. A slow, smooth wake-up and a fast, violent one each fail a different goal.
• Specific plan. low-dose remifentanil continued through emergence and tapered after the pins are out; lidocaine 1-1.5 mg/kg before suctioning; minimal-stimulation extubation; antihypertensive in hand before the wake-up begins, not fetched after the spike.
• Which antihypertensive. labetalol in 5-10 mg increments or nicardipine (boluses or infusion) — effective without dilating cerebral vessels; esmolol for a rate-dominant picture. Pure vasodilators like nitroprusside/nitroglycerin raise CBF and are the wrong tools.
• Extubation criteria. awake and following commands (the exam is the point of the wake-up), intact airway reflexes, full reversal (TOF ratio ≥0.9), normothermic, adequate gas exchange.
• BP 178/95. treat now — postoperative hematoma clusters in the first hours and tracks with emergence hypertension; most surgeons want SBP held under ~140-160. Labetalol 10 mg IV and re-dose to effect is a reasonable concrete answer.
• Left side slower. residual anesthetic can unmask or exaggerate a pre-existing deficit (differential awakening) — and she started with a drift. But the alternatives are the ones that kill: hematoma, edema, seizure with a postictal (Todd's) paresis. Trajectory over 30-60 min with serial exams decides; any worsening, new deficit beyond baseline, or falling arousal buys an immediate CT rather than more watching. Give the PACU her baseline, the current exam, the BP ceiling, and explicit thresholds for calling and imaging. A vague 'watch her neuro status' is the failed version.

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• Neuraxial vs GA. two defensible paths: neuraxial avoids a predicted difficult airway but is technically challenging in her; many accreta centers plan a controlled GA to avoid a crash conversion mid-hemorrhage (which this case then depicts). The drivers she brings: OSA, obesity ventilation limits, predicted difficult airway AND difficult neuraxial, percreta with high bleeding risk, prior failed regional and recall. Commit and defend either; wanting it both ways is the flag.
• Spinal vs slow epidural vs CSE. CSE allows immediate surgical anesthesia plus a prolonged catheter for a long accreta case; single-shot spinal may be too brief if dissection extends. Commit and own the tradeoff.
• Ultrasound. very useful in obesity to identify midline, depth, and interspace; reduces attempts and time.
• Time pressure. engage OB on timing and pre-position before delivery when possible; the counter-argument is that a long, uncertain placement in a bleeding-risk case argues for a controlled GA from the start. Either is defensible if reasoned.
• GA dangers. difficult airway (MP IV, TMD 4 cm, neck 47 cm, restricted extension, prior 2-attempt intubation), rapid desaturation from reduced FRC, aspiration risk, and prior recall — a full-stomach hard airway in a percreta hemorrhage is the nightmare.

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• Awake vs asleep. with a predicted difficult airway (MP IV, restricted extension, prior 2-attempt intubation, rapid desaturation), an awake technique is the safe default if conversion is elective/semi-elective; asleep VL as first attempt is defensible only if she is already anesthetized and stable with the airway team and fiberoptic ready. Naming decision points is the mark of judgment.
• Awake fiberoptic. atomized topicalization of tongue, oropharynx, and trachea (nebulized/atomized lidocaine, superior laryngeal and transtracheal supplements if comfortable), antisialagogue, patient upright; commit to the sequence.
• Sedation in OSA. minimal, short-acting; dexmedetomidine preferred over stacked opioids/benzodiazepines because it preserves airway tone and drive; over-sedating a difficult airway is the trap.
• BP fall + SpO2 90%. sympathectomy from the CSE plus supine atelectasis and aortocaval compression at BMI 58; aggressive left uterine displacement, phenylephrine or norepinephrine, fluid bolus, FiO2 to 1.0; restore pressure first, then head-up to recruit.

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• Position. ramped, head-up, aggressive left tilt; expect tidal volumes to fall further as the abdomen is packed and she bleeds.
• Pressors/inotropes. multiple agents drawn up and labeled, calcium ready, norepinephrine running or immediately available, vasopressin available.
• Blood ready. PRBC, FFP, platelets, cryo or fibrinogen concentrate in room; calcium and TXA at hand; rapid transfuser primed.
• Brisk bleeding. activate MTP, get a second large-bore line if not already in (she has a single 18 g), start the rapid transfuser, and pace resuscitation with the surgical steps — do not fall behind the loss.

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• Product ratio. 1:1:1 as the default while goal-directed testing catches up; fibrinogen replacement specific and early; calcium repleted frequently; trend lactate and ionized calcium.
• Calcium. recheck ionized calcium every few units — citrate from rapid transfusion chelates calcium, and hypocalcemia both worsens coagulopathy and drops cardiac output. Give calcium chloride/gluconate to keep iCa normal.
• Cryo vs fibrinogen concentrate. either — fibrinogen concentrate delivers a known dose in small volume and fast; cryoprecipitate is the traditional source. Replace to keep fibrinogen above ~150-200 in obstetric hemorrhage; commit.
• TXA. 1 g IV over 10 minutes, ideally within 3 hours of the bleed onset (WOMAN trial); repeat once if bleeding continues. Early, not an afterthought.
• Restless then unresponsive. hemorrhagic shock with cerebral hypoperfusion — she is dying, not lightly anesthetized; secure the airway and control the resuscitation. Reading this as inadequate block alone is the miss.
• Conversion to GA. she needs a secured airway and reliable anesthesia; reduce the induction dose for hypovolemia — ketamine 0.5-1 mg/kg or low-dose etomidate — with a full RSI-dose paralytic (rocuronium 1.2 mg/kg or succinylcholine); pressors up. A standard induction dose here arrests her.
• Ventilator. low tidal volume by predicted (not actual) body weight (~6-8 mL/kg PBW, roughly 300-400 mL for 5'4"); modest PEEP 8-10 to offset the atelectasis of a heavy chest and abdomen; plateau ≤30; rate to PaCO2. Zero PEEP in her collapses dependent lung; sizing volume to 152 kg is the common error.
• Keeping her unaware. the tension the case sets up: a hypovolemic brain tolerates little hypnotic, yet she had prior recall. Use the lowest effective hypnotic plus a benzodiazepine (midazolam) and scopolamine as tolerated, a processed-EEG monitor if available, volatile as pressure allows, and document the plan and her history. Chasing full MAC into arrest, or giving nothing and accepting awareness, are the paired failures.

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• Extubate or not. many would leave her intubated after 5 L blood loss with class III obesity, severe OSA, and a massive transfusion — she is at high risk for post-extubation failure and reintubation would be a hard airway. Defensible either way only if the criteria are named and honestly met.
• Criteria. adequate gas exchange, full reversal confirmed (TOF ≥0.9), normothermia, hemodynamic stability off or on minimal pressor, surgical hemostasis, awake and following commands.
• Position and CPAP. head-up, ramped; apply CPAP within minutes of extubation given severe OSA — do not wait for her to obstruct.
• Post-extubation hypoxemia DDx. obesity atelectasis, residual neuromuscular block, opioid effect, pulmonary edema (TACO or TRALI after massive transfusion), aspiration — reach for the most likely (atelectasis/residual) while scanning for TACO/TRALI given the transfusion volume.
• Rx and reintubation. CPAP/BiPAP, head-up, recruit, treat the specific cause; reintubate for rising CO2 with declining mental status or refractory hypoxemia — do not let a hard airway crash on the ward.
• Disposition. ICU.

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• DDx. atelectasis from positioning and obesity, mucus plugging, pulmonary edema, aspiration, opioid-induced hypoventilation — most likely atelectasis with an obesity-hypoventilation contribution.
• NIV settings. BiPAP with EPAP at or above her home 14 cm H2O to splint the airway, IPAP set higher to augment tidal volume; titrate to exhaled volumes and CO2.
• NIV failure. worsening gas exchange, rising CO2, declining mental status — do not ride a failing trial into an arrest.
• Reintubate. an obtunded patient with a rising CO2 needs the airway now; delaying invites a crash induction on a hard airway. Bring the difficult-airway cart, video laryngoscope and fiberoptic, a second skilled operator, ramp and preoxygenate/apneic-oxygenate, and pick the technique deliberately — this is not a routine floor tube.
• Bronchoscopy. for suspected plugging or to assess aspiration once the airway is secured.

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• Scheduled. multimodal, opioid-sparing by default: acetaminophen scheduled, an NSAID if renal function and hemostasis allow (caution after 5 L loss), plus a truncal block.
• Breakthrough opioid. small, monitored doses only, with continuous pulse oximetry and capnography; every opioid dose stacks on an OSA baseline.
• PCA in OSA. high risk for respiratory depression; not a default — if used at all, only in a monitored setting with capnography and conservative settings. This is the answer to give OB: a basal-rate or generous-demand PCA in severe OSA after this course is how these patients die overnight.
• Gabapentinoid. controversial in OSA — sedation and respiratory-depression risk with modest analgesic benefit; not a routine add here.
• Block choice. TAP or quadratus lumborum — either reasonable; QL may give somewhat better visceral coverage. CPAP whenever she sleeps is part of the analgesic safety plan, not separate from it.

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• When to start. as bleeding risk allows — typically within 12-24 h postpartum after cesarean hysterectomy once hemostasis is secure; a plan agreed with OB. She is very high risk (obesity, cesarean hysterectomy, immobility, postpartum).
• Agent and dose. enoxaparin commonly, dosed for her weight (weight-based or anti-Xa-guided rather than a flat prophylactic dose in class III obesity).
• Mechanical. sequential compression from the start; it is the bridge while pharmacologic prophylaxis is held for bleeding risk, and matters most in exactly this delayed-anticoagulation high-risk patient.
• New leg swelling. DVT is the primary concern; also cellulitis and hematoma. Duplex ultrasound; D-dimer is of limited use postpartum.
• Therapeutic anticoagulation. weigh confirmed DVT against re-bleeding risk days after a percreta hysterectomy; an IVC filter is a bridging option if anticoagulation is truly contraindicated. A multidisciplinary call (OB, hematology, the surgical team), not a unilateral one.

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• Why asleep. an honest account: the bleeding became life-threatening and she lost consciousness from blood loss, so the airway had to be secured and general anesthesia given; what was done to prevent recall this time.
• CPAP off, SpO2 88%. desaturation while asleep off CPAP in severe OSA with opioids on board — CPAP back on whenever she sleeps, continuous oximetry/capnography, review the opioid orders; explain the why rather than simply reordering it.
• Summary letter. a portable anesthesia record: the difficult intubation and technique used, products received, complications, and explicit recommendations for future care.
• Next anesthetic. straight recommendations, not a threat: a predicted difficult airway with an awake intubation option, difficult neuraxial (ultrasound, early placement), an ICU bed, CPAP perioperatively, and a multimodal analgesic plan.

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• Goals. keep HR ~70-90 (diastolic filling time is everything across a fixed valve), maintain rate control in AF, avoid falls in preload and SVR, avoid rises in PVR (no hypoxia, hypercarbia, or light-anesthesia sympathetic surges).
• Monitoring. arterial line already in; TEE intraop has a role if the question becomes volume and RV function; a PA catheter is debated in fixed MS and many avoid it; CVP has limited utility with severe MS and AF (poor surrogate for LV filling).
• Anxious tachycardia at 118. treat it before anything else — the tachycardia collapses diastolic filling and can precipitate pulmonary edema; addressing anxiety is part of the hemodynamic plan, not a sideshow.
• Agent. esmolol (titratable, short) or low-dose metoprolol for rate; dexmedetomidine calms her while preserving rate control; magnesium is an adjunct. Defend on time course and hemodynamics; avoid anything that drops SVR abruptly.

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• Modality. slow-titration epidural or continuous spinal over single-shot spinal in severe MS — a rapid sympathectomy drops preload and SVR that a fixed valve cannot compensate for. A reflexive single-shot spinal here is a flag.
• Anticoagulation timing. therapeutic LMWH wants a 24-hour interval before neuraxial; she is right at that boundary. An anti-Xa of 0.5 IU/mL at ~24 h is higher than expected for a patient truly cleared — it suggests residual effect. Consider a further delay or a modified plan; the number informs but does not by itself license the block.
• Epinephrine test dose. an epinephrine-laced test dose can raise the rate in AF and is hard to interpret as a marker of intravascular placement (baseline rate already irregular); tachycardia is also exactly what you are trying to avoid. Many omit epinephrine and rely on incremental dosing with aspiration; defensible.
• Target level. T4 for cesarean, reached slowly through a titrated catheter so her circulation compensates for each increment; abrupt sympathectomy is the danger.

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• Tachycardia DDx. anxiety, inadequate block for the stimulus, surgical manipulation, volume shift, sympathetic response — and the rate itself is now driving the hypotension.
• Rate vs pressure. rate is the lever in MS: slowing the rate lengthens diastolic filling and usually restores the pressure; pure vasoconstriction without rate control leaves the gradient and filling problem unsolved.
• Rate control. short-acting beta blocker (esmolol) titrated is preferred over a large bolus of a long agent; her home metoprolol does not preclude more, but titrate to effect and treat the trigger too.
• Phenylephrine. raises SVR and coronary perfusion but also raises PVR — use a cautious dose; it supports pressure but does not fix the underlying tachycardia-driven filling failure.
• Pressor vs fluid. with the rate controlled, a modest phenylephrine bolus — she arrived congested (crackles to the mid-zone, JVP at the jaw, BNP 1240), so a 500 mL bolus is the wrong lever and can flash pulmonary edema; volume goes in small, watched aliquots only for measured loss. Reflexive fluid for neuraxial hypotension is the trap in MS.

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• Oxytocin. slow dilute infusion, never an IV push — bolus oxytocin causes vasodilation, reflex tachycardia, and a pulmonary-pressure spike, all poorly tolerated in severe MS with pulmonary hypertension.
• Methylergonovine. avoid — raises SVR and PVR; a hazard with her RVSP 60.
• Carboprost. avoid — raises PVR and can worsen her pulmonary hypertension; relatively contraindicated here.
• Misoprostol. the uterotonic of choice among the drugs here (800-1000 mcg), alongside early mechanical and surgical management, because it spares the pulmonary and systemic vasculature.
• Post-delivery dyspnea. uterine contraction autotransfuses ~500 mL into a circulation with a fixed valve — the preload surge overwhelms the stenosis and flashes pulmonary edema; the tachycardia compounds it. Rx: control the rate, sit up, oxygen/NIV, diurese now that the baby is out (this is the moment diuresis is right), consider milrinone for RV support with caution for its vasodilation. Get cardiology to the bedside early — this is the predicted crisis of the case.

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• Priorities. rate and rhythm control, gentle diuresis, oxygen, and vigilance for recurrent pulmonary edema as fluid mobilizes over the next 24-72 h.
• Diuresis endpoint. respiratory comfort and improving oxygenation while preserving enough filling for the stenotic valve — perfusion and symptom endpoints, not a target weight; over-diuresis drops preload below MS tolerance.
• Anticoagulation timing. balance AF stroke risk against postpartum hemorrhage: mechanical compression immediately, resume pharmacologic anticoagulation ~12-24 h postpartum once hemostasis is secure.
• Agent. a heparin infusion early (titratable and reversible if she bleeds or needs a procedure), transitioning to LMWH once bleeding risk falls.
• Recurrent edema. more diuresis, NIV, tighten rate control, and consider milrinone with careful pressure support if RV function flags.

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• Priorities. she is unstable — hypotension, hypoperfusion, rising lactate from uncontrolled RVR across a fixed valve; immediate synchronized cardioversion is the lead while you support perfusion.
• Cardioversion. synchronized, start ~100-200 J biphasic; instability overrides the usual anticoagulation-before-cardioversion caution — the thromboembolic risk is accepted because she is decompensating now. Decide with cardiology but do not delay for a stable patient's rules.
• Rate control after. only once perfusing, and cautiously in fixed MS: IV beta blocker or diltiazem to effect; nodal agents alone will not rescue an unstable patient — that is what the shock is for.
• Amiodarone. reasonable for rhythm control here; watch BP acutely and pulmonary/thyroid effects over the longer term.
• BMV logistics. transport with full hemodynamic monitoring, rescue drugs drawn, and an anesthesia team present in the cath lab; agree the airway plan and vascular access before moving her.

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• Concerns. she tolerates neither the hypovolemia of the bleed nor the volume of aggressive resuscitation — a fixed valve punishes fluid shifts in both directions; and the tachycardia from hypovolemia itself worsens filling.
• Uterotonic. oxytocin by slow infusion and misoprostol; refuse methylergonovine and carboprost (SVR/PVR effects); escalate to mechanical and surgical control earlier than usual rather than leaning on drugs.
• Volume. slow, titrated, small aliquots with the lungs watched — resuscitate the loss without flooding a fixed valve; blood over crystalloid as she needs replacement.
• Pressor. norepinephrine or vasopressin to support pressure without a big chronotropic hit; avoid pure beta agonists that drive the rate up across the stenosis.
• Transfusion threshold. transfuse at a higher hemoglobin than a healthy postpartum patient — her oxygen delivery is margin-limited by the valve and pulmonary hypertension; the exact number is contextual but err toward earlier replacement.
• Heparin. hold it for active bleeding, keep mechanical compression on, and restart once hemostasis is secure — a reversible agent is exactly why an infusion was chosen early.

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• Sedation vs GA. sedation preferred when she tolerates it — avoids the preload/SVR drop and PVR rise of induction across a fixed valve; keep a GA plan and airway ready for collapse.
• Monitoring. arterial line and full monitoring before instrumentation; rescue drugs drawn; a clear backup plan for hemodynamic collapse.
• Anticoagulation. procedural heparinization with a reversal (protamine) plan if bleeding.
• Hypotension on inflation. transient occlusion of the valve during balloon inflation is expected and brief; a persistent drop suggests tamponade (from transseptal/perforation), acute severe MR from a torn leaflet, or arrhythmia — differentiate fast and treat (pericardiocentesis, support, cardiology).
• Post-procedure. a residual gradient of 6 with no significant MR is a good result; ICU or step-down monitoring; anticoagulation continues for her AF, and both heparin and warfarin are breastfeeding-compatible if she nurses.

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• Future pregnancy. high-risk — pregnancy nearly decompensated her; the message is preconception cardiology, likely definitive valve intervention before another pregnancy, and shared decision-making. The learner supports rather than owns this conversation with cardiology and OB; an honest account of how severe this episode was is part of it.
• Breastfeeding and anticoagulation. her AF is valvular (rheumatic MS), which contraindicates DOACs regardless of lactation — her options are warfarin or heparin/LMWH; both warfarin and heparin are compatible with breastfeeding. Defer dosing specifics to cardiology and lactation resources.
• Documentation. a portable anesthesia summary: the valve disease and RVSP, the intraoperative course and pulmonary edema, the valvuloplasty details, anticoagulation, and explicit recommendations for any future anesthetic.

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• Pneumothorax first. positive pressure turns a small pneumothorax into a tension pneumothorax in a patient already in shock; a chest tube (or at minimum a finger thoracostomy or needle decompression with the tube kit open) goes in before or during induction. Inducing with no plan for the chest is a flag.
• Arterial line. yes if it takes one attempt while the chest tube goes in; it does not delay the incision. Place it after induction if the first attempt fails.
• Induction agent. ketamine 0.5-1 mg/kg or etomidate 0.1-0.2 mg/kg, dose-reduced for hemorrhagic shock; full-dose propofol here is a flag. Expect the pressure to fall regardless once sympathetic tone is removed; have push-dose pressor drawn.
• Paralytic. succinylcholine 1-1.5 mg/kg or rocuronium 1.2 mg/kg; sugammadex 16 mg/kg available if rocuronium.
• Collar. open the front of the collar, an assistant holds manual in-line stabilization, video laryngoscope first pass, bougie ready. MILS worsens the view; expect it and do not lift against it.
• Cricoid. defensible either way; if applied, release it the moment it degrades the view.
• Tilt. left uterine displacement stays. At 32 weeks the supine position can cut cardiac output by a third in a patient who has none to spare. If spine precautions forbid tilting the board, displace the uterus manually.

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• Tidal volume. 6-8 mL/kg predicted body weight; PBW for a 5'6" woman is ~59 kg, so 350-450 mL. Sizing to 70 kg actual weight is the common error.
• PEEP and plateau. PEEP 5-8, plateau ≤30; watch peak pressures with an air leak and fractured ribs.
• Peak 42. right mainstem (the diaphragm is high and the tube migrates), kinked or blocked chest tube with re-accumulating pneumothorax, hemothorax, aspirated blood or gastric contents, bronchospasm. Check depth and breath sounds, suction, look at the chest tube, ultrasound the chest.
• Volatile. sevoflurane at 0.5-0.7 MAC; MAC is reduced ~30% in pregnancy, and she is in shock, so tolerance is low. Above ~1 MAC the uterus relaxes and atony after delivery gets worse. Supplement with ketamine or opioid rather than pushing the vaporizer; awareness risk is real and is addressed in the next probe.
• Deliver now?. the fetus is hypoperfused because the mother is; maternal resuscitation is fetal resuscitation. Delivery is indicated if the tracing does not recover with maternal pressure and oxygenation restored, if the uterus obstructs surgical control of the bleeding, or if the mother is deteriorating and the uterus is a volume sink. A resident who says 'deliver' or 'wait' without naming the tracing, the maternal pressure trend, and hemorrhage control is guessing.

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• Before uterine incision. uterotonics drawn, second suction, blood checked and hanging, calcium in hand, rapid infuser primed; tell the room she will bleed from two places at once.
• Oxytocin. infusion, not a bolus, in a hypotensive patient; a 3-5 IU bolus drops SVR and can crash her. Start ~3 IU over a minute or straight to an infusion of 10-40 IU/L and titrate.
• Second-line agent. carboprost 250 mcg IM or methergine 0.2 mg IM are both acceptable (no asthma, no hypertension); misoprostol is slow and belongs as an adjunct, not the rescue. Commit and give it now; a bimanual uterus from OB at the same time.
• Awareness. midazolam 1-2 mg, ketamine (which also holds pressure), opioid, processed EEG if available; tell her afterward what was done and why. Turning the vaporizer down with nothing in its place is the trap.
• SpO2 88%. packs and retractors push the diaphragm up: FRC falls, the tube can go mainstem. FiO2 1.0, confirm tube depth, ask the surgeon to ease the retractor, recruit, check the chest tube is swinging (recurrent tension is on this list), ultrasound for hemothorax.

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• Ratio. 1:1:1 empirically until viscoelastic data arrive, then goal-directed. Platelets are the component most often forgotten at this volume.
• Calcium. calcium chloride 1 g IV now, roughly 1 g per 2-4 units of citrated product, ionized Ca checked every 30 minutes. Citrate toxicity plus hypothermia plus acidosis is the coagulopathy that products alone cannot fix.
• TXA. yes: 1 g over 10 minutes, then 1 g over 8 hours; within 3 hours of injury, so the trauma indication holds.
• Fibrinogen 120. already dangerously low for a parturient (term normal 350-600; her 280 at arrival was the first signal of consumption). Cryo 10 units (~2 g) or fibrinogen concentrate 4 g; target ≥200 while bleeding. Waiting for a value below 100 is the error.
• Cell saver. amniotic contamination is a theoretical concern that leukoreduction filters address; the real contraindication is bowel injury and gross contamination of the field. If the bowel is intact, use it.
• Anti-K. ~91% of donors are K-negative, so K-negative uncrossmatched units are readily available; ask for them by name and do not wait 40 minutes. Anti-K also matters for the neonate (HDFN); NICU needs to know.
• Temp 34.8. warm every line, forced air on everything not in the field, warm the room; below 35 the clotting cascade slows and platelets stop working regardless of the counts.
• Damage control. when the rate of loss exceeds the rate of replacement and the lactate keeps rising despite products: pack, temporary closure, ICU for rewarming and correction, then IR or a planned re-look. The resident should name lactate trend, base deficit, temp, and ionized calcium as the numbers that call it.

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• Vent. 6 mL/kg PBW, PEEP 8-10 with contusion and a large transfusion, plateau ≤30, driving pressure ≤15.
• Sedation. propofol infusion for a patient who is going back to the OR and has an open abdomen; dexmedetomidine as an adjunct for opioid sparing; avoid benzodiazepine infusions (delirium, prolonged ventilation).
• Block now. early; contused, splinting lungs get worse each hour. Erector spinae plane catheter is the pragmatic choice: superficial, compressible, not constrained by coagulopathy.
• Paravertebral tonight. no. ASRA treats paravertebral like neuraxial; with INR 1.4 and platelets 90 after massive transfusion, wait for correction. Thoracic epidural is also off the table for now.
• Ketorolac. no: fresh massive transfusion, a packed liver, platelets 90, and an undefined creatinine after shock. Acetaminophen scheduled; NSAID later.

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• DDx. pulmonary contusion progressing, ARDS, TRALI, TACO, aspiration at induction, atelectasis, early pneumonia. Contusion plus transfusion is the likeliest combination.
• TACO vs TRALI. TACO: hypertension, raised JVP, positive balance, BNP up, improves with diuresis. TRALI: fever, hypotension, onset within 6 hours of product, no overload, does not respond to diuretics. Both give bilateral infiltrates.
• Vent change. tidal volume to 6 mL/kg PBW (~350 mL), PEEP titrated up with attention to driving pressure, permissive hypercapnia acceptable.
• Prone. P/F <150 on FiO2 ≥0.6 despite optimization meets the criterion; the open abdomen with packs is the real problem and is a relative contraindication. Discuss with trauma; a decision either way must name that trade-off.
• Paralysis. only for dyssynchrony or refractory hypoxemia, not routine.
• Furosemide. yes if she is volume-overloaded (fluid balance, IVC, JVP, echo); no if pressors are climbing or the picture is TRALI. Examine before dosing.
• Peak 50, hypotension. tension pneumothorax with a clotted chest tube until proven otherwise; also mainstem migration or mucus plug. Disconnect from the vent, bag by hand, check the tube, decompress, replace the chest tube.

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• Choice. thoracic epidural or paravertebral catheter gives the best analgesia for four contiguous fractures; ESP catheter is the compromise that sidesteps the anticoagulation timing. Any is defensible if reasoned; intercostal blocks alone are too short-lived.
• Enoxaparin timing. prophylactic dose: neuraxial or paravertebral placement ≥12 hours after the dose (so 1800 or later), next dose ≥12 hours after placement (ASRA), and ≥4 hours after catheter removal. ESP has no such constraint.
• Non-opioids. acetaminophen 1 g q6h scheduled; gabapentinoid optional; lidocaine infusion if no epidural.
• Ketorolac. still no: packed liver 48 hours ago with re-bleed risk, creatinine after shock. Revisit in days.
• PCA. yes, with continuous pulse oximetry and capnography; a patient with rib fractures who is undertreated hypoventilates just as surely as one who is oversedated.
• Ketamine. 0.1-0.2 mg/kg/h.

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• Dose. postpartum plus major trauma plus surgery plus transfusion puts her in the highest-risk group; many trauma protocols use enoxaparin 30 mg BID or 40 mg BID, or weight-based 0.5 mg/kg BID, with anti-Xa monitoring. Once-daily 40 mg under-doses her.
• DDx. PE first, then sepsis, recurrent hemorrhage, tension pneumothorax, progressing ARDS.
• Bedside. point-of-care echo and lung ultrasound, ECG, ABG; a dilated RV with a flat septum and dry lungs in this context is PE until proven otherwise.
• CT. yes if she can be moved with a physician, pressor in hand, and airway equipment; the diagnosis changes the treatment, so it is worth the trip.
• Heparin. yes, unfractionated infusion without a bolus (or a reduced bolus), because it is titratable and reversible; discuss with trauma but do not withhold anticoagulation from a hemodynamically significant PE.
• Lytics. systemic thrombolysis is contraindicated within roughly 10-14 days of major surgery and hemorrhage; hers was 72 hours ago. Catheter-directed therapy, surgical embolectomy, or VA ECMO as a bridge; IVC filter only if anticoagulation truly cannot be given.

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• What happened. plain and honest: the crash, the bleeding, the operation, that her baby was delivered and is alive in the NICU, and that the team will bring the full picture together with OB and trauma. Do not defer the fact that the baby is alive; do not invent prognostic certainty.
• Memories. take it seriously; a structured interview (modified Brice) in a quiet room, no argument about whether it could have happened. Ketamine and low volatile in a shocked patient make awareness plausible.
• Referral. psychiatry or psychology within days, not at discharge; awareness and trauma both carry PTSD risk, and early support changes outcome. Social work alongside for the NICU course.
• Sedation and analgesia. minimize sedatives, keep her lucid enough to participate and see the baby, protect sleep, treat pain with the block and non-opioids so she is not fogged.
• Record. awareness episode and the circumstances, anti-K antibody and transfusion history, massive transfusion, difficult-airway status (not difficult; say so), blocks placed; a letter she carries.

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• Mode of delivery. either is defensible if reasoned. Assisted vaginal delivery under a dense epidural with a shortened second stage avoids surgical stress, blood loss, and a GA she may not tolerate; planned cesarean gives a controlled setting with the full team. She is at 6 cm with a reassuring tracing, so a well-managed vaginal delivery is reasonable; a resident who reflexively chooses cesarean 'because she is sick' should be asked what the cesarean protects her from.
• Enoxaparin. prophylactic dose; ASRA asks for ≥12 hours; 14 hours is fine. Document the time and hold the next dose until ≥4 hours after placement.
• Arterial line. yes, before the block, radial; every hemodynamic decision in the next 24 hours depends on beat-to-beat pressure.
• Central line. before the block, right IJ under ultrasound; she will need titrated vasopressors and possibly inotropes, and placing it during a crisis is the wrong time.
• PA catheter. most PH-experienced teams avoid it: arrhythmia and PA rupture risk in a dilated, hypertensive pulmonary tree with limited decision value; TTE/TEE gives the RV picture. A yes is defensible only with a stated reason.
• Targets. MAP ≥70 (RV coronary perfusion depends on aortic pressure exceeding RV pressure), HR 80-100 in sinus (the dilated RV needs time to fill; loss of atrial kick is catastrophic), SpO2 ≥95%, PaCO2 low-normal for pregnancy (~30-35). Hypoxia, hypercarbia, acidosis, and pain each raise PVR.
• Oxygen. oxygen is a pulmonary vasodilator; at 92% she is on the steep part of the curve where a contraction or a dose of opioid tips her. Start it now.

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• Technique. slow epidural or a CSE with intrathecal opioid only (no intrathecal local); a single-shot spinal produces the abrupt sympathectomy a fixed-PVR patient cannot compensate for. Committing to a spinal here is a flag.
• Test dose. omit the epinephrine: 15 mcg intravascular produces tachycardia that she tolerates badly and that you cannot distinguish from labor. Aspirate, dose incrementally, watch for the block.
• Loading. dilute bupivacaine 0.0625-0.1% with fentanyl in 3-5 mL increments every 5 minutes with the arterial line watched; no 10-15 mL loads.
• Hypotension. expected sympathectomy on top of a preload-dependent RV; treat the pressure before it becomes an RV ischemia spiral. Norepinephrine 4-8 mcg boluses or vasopressin 0.5-1 unit; phenylephrine works but raises PVR at higher doses and produces reflex bradycardia. Any of the three is defensible; the reasoning about PVR is what you are listening for.
• Fluid. 250 mL boluses with reassessment (IVC, JVP, SpO2), not a liter; an over-distended RV pushes the septum into the LV and drops output further.
• Infusion and second stage. standard low-concentration infusion or PIEB; for instrumental delivery, dose the existing catheter in 3-5 mL increments of a stronger solution (lidocaine 2% or bupivacaine 0.25%) with pressor running, aiming for a sacral and perineal block, not a T4 surgical level.

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• DDx. PH crisis with acute RV failure, pulmonary embolism, pulmonary edema, occult hemorrhage, amniotic fluid embolism, sepsis. Bedside echo sorts most of it in two minutes.
• Dx. acute RV failure from a PH crisis: labor catecholamines, pain, hypoxia, and a partially blocked patient add up to a PVR surge the RV cannot overcome.
• Order. oxygen to 100%, restore MAP (norepinephrine first: RV coronary perfusion), inhaled vasodilator, treat pain and anxiety (top up the epidural, small opioid), then inotrope; call cardiac anesthesia and the ECMO team now, not later.
• Inhaled. iNO 20-40 ppm or inhaled epoprostenol 50 ng/kg/min; both are selective pulmonary vasodilators with no systemic drop; whichever the unit can deliver in five minutes.
• Pressor. norepinephrine 0.05-0.2 mcg/kg/min; vasopressin 0.02-0.04 units/min added because it raises SVR without raising PVR. Using both is common.
• Milrinone. inodilator that supports the RV and lowers PVR but drops SVR; start 0.25-0.5 mcg/kg/min without a bolus and only with a pressor already running. Reasonable once MAP is restored; wrong as the first drug.
• Intubation. last resort, when oxygenation or mental status fails despite the above; induction drops SVR and positive pressure raises PVR and cuts preload, and this is where PH patients arrest. Most experienced operator, pressor running, inhaled vasodilator through the circuit, etomidate 0.1-0.2 mg/kg (ketamine acceptable), no propofol bolus.
• Ventilation. 6-8 mL/kg PBW, PEEP 5, plateau low, normocapnia or mild hypocapnia (PaCO2 30-35); hypercapnia and high intrathoracic pressure both push PVR up.

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• Maintenance. sevoflurane ≤0.5-0.7 MAC with opioid (remifentanil infusion or fentanyl) carrying the anesthetic; volatile depresses the RV and lowers SVR, and high MAC relaxes the uterus. Nitrous is out (raises PVR).
• Oxytocin. infusion only, started slowly (for example 1-2 IU over minutes, then a low-rate infusion); a bolus drops SVR, raises HR, and spikes PA pressure. A resident who gives 3-5 IU IV push has not engaged the disease.
• Atony. misoprostol 800-1000 mcg buccal or rectal, TXA 1 g, bimanual compression, early Bakri or surgical measures. Methergine raises PVR and SVR (contraindicated); carboprost is a pulmonary vasoconstrictor and bronchoconstrictor (contraindicated). Naming either without a flag is a fail.
• Autotransfusion. ~500 mL returns from the contracting uterus and caval compression is relieved; the RV takes a preload hit within minutes. Have the diuretic drawn, keep fluid restrictive, watch CVP and the RV on TEE, and do not add volume for the bleeding until the echo says she needs it.
• RV decompensation. raise MAP first (norepinephrine up, vasopressin), increase the inhaled vasodilator, then epinephrine 0.03-0.05 mcg/kg/min for inotropy; milrinone here drops the SVR she is already losing. Correct acidosis and hypercarbia.
• ECMO. call as pressors escalate and the RV keeps dilating; VA ECMO is the support for RV failure with hypoxemia. The team should be cannulating in a controlled setting, not during CPR. Rising lactate, falling SpO2 on maximal support, and progressive RV dilation are the triggers.

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• MAP. 65-75; the RV is perfused during systole only when aortic pressure exceeds RV pressure, so hypotension is RV ischemia.
• PaCO2. 35-40, no hypercarbia; avoid hyperventilation to the point of high airway pressures.
• Sedation. dexmedetomidine or low-dose propofol; the goal is no sympathetic surges (PVR spike) and no hypotension; adequate analgesia matters as much.
• Targeted therapy. restart now via the gastric tube; sildenafil and selexipag have short half-lives, and a gap of 24 hours risks rebound pulmonary hypertension. IV sildenafil exists if the gut is not working.
• Enoxaparin. prophylactic 40 mg daily restarted at 12-24 hours once hemostasis is confirmed; she is at high VTE risk and a PE would be fatal. Mechanical compression until then.
• Diuresis. yes if the RV is distended and she is oxygenating poorly; no if she is pressor-dependent with a small IVC. Echo before the furosemide; the RV is both preload-dependent and preload-intolerant, and the window is narrow.

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• Before the trial. pressor at minimal dose, inhaled vasodilator off for hours without deterioration, oral therapy on board, no bleeding, awake, normal lactate.
• HR 128, RR 28. stop. A rising heart rate and respiratory rate on a trial is the RV failing to keep up; pushing through is how these patients arrest. Rest, and retry in a few hours.
• Extubate to. high-flow nasal oxygen or NIV; some PEEP and a guaranteed FiO2 avoid the desaturation that spikes PVR. Plain nasal cannula is a flag.
• Deterioration. recurrent PH crisis, pulmonary edema after the autotransfusion, PE, atelectasis. Oxygen to 100%, NIV, restart the inhaled vasodilator (epoprostenol nebulized through the NIV or high-flow circuit; iNO via nasal delivery in some units), echo.
• Reintubation. earlier rather than later: rising work of breathing, falling SpO2 on NIV, hypotension, or mental status change. A crash reintubation of a PH patient carries far more risk than an elective one in the ICU with cardiac anesthesia present.

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• Uterotonic. oxytocin infusion at a low rate and misoprostol; methergine and carboprost remain contraindicated; TXA 1 g.
• Volume. blood, not crystalloid: she needs oxygen-carrying capacity without dilution and without volume the RV cannot take. Transfuse unit by unit with echo or CVP between units.
• Target. higher than a healthy parturient, around 8-9 g/dL; a fixed-PVR RV with reduced output depends on oxygen content.
• Pressor. norepinephrine or vasopressin as a bridge to blood, not a substitute for it.
• Enoxaparin. prophylactic dose six hours ago: protamine partially reverses LMWH and is reasonable for life-threatening bleeding, but a single 40 mg dose is rarely the problem; hold the next dose, correct the surgical bleeding.
• Anesthetic for the OR. spinal is the wrong answer (abrupt sympathectomy in a hypovolemic PH patient); GA with a controlled induction and cardiac anesthesia present is the safe default; sedation with paracervical local is possible for a brief exam and balloon but not if the surgeon may need more. Commit and defend.

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• DDx. PE (postpartum, held anticoagulation, immobile), recurrent PH crisis, sepsis, recurrent hemorrhage, tamponade; the echo already excluded effusion.
• PE vs crisis. clot in transit or RV thrombus on echo, McConnell sign, DVT on compression ultrasound of the legs; CTPA only if she can travel. The hemodynamics are identical; the treatment differs.
• Heparin. yes: empiric unfractionated heparin without a bolus if the bleeding has stopped, because a PE in this patient is fatal untreated and UFH is reversible.
• Bridge. MAP first (norepinephrine and vasopressin up), inhaled vasodilator up, epinephrine for RV inotropy, oxygen, intubation only if unavoidable and only with ECMO cannulating.
• VA ECMO. yes; three pressors with MAP 50 and a rising lactate is the definition of failing conventional support. VA ECMO unloads the RV and oxygenates; catheter-directed therapy or surgical embolectomy follows if PE is confirmed.
• LV not opening. LV distension from retrograde VA flow against a stunned LV; reduce ECMO flow slightly, add inotrope, consider an IABP or Impella vent, and keep the lungs ventilated to avoid a hypoxic upper body.

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• Another pregnancy. honest: maternal mortality in PAH pregnancy is roughly 10-25% even in expert centers, and a second pregnancy after RV failure and ECMO is higher; the standing recommendation is against future pregnancy. Say it plainly, say it with cardiology and OB present, and leave room for her to ask. Deferring the whole conversation is a flag; so is delivering it alone at the bedside without her team.
• Contraception. estrogen is contraindicated (thrombosis, fluid retention); progestin-only implant or levonorgestrel IUD, or sterilization when she is ready to decide.
• Lactation. sildenafil transfers minimally and is generally considered compatible; selexipag has no human lactation data and most PH programs advise against breastfeeding on it. Involve the PH pharmacist and lactation team rather than answering off the cuff.
• Enoxaparin. at least 6 weeks postpartum at prophylactic dose; longer, or therapeutic, if the PE was confirmed.
• Letter and follow-up. PH severity and catheterization data, the crisis, the ECMO run, drugs that helped and drugs that are contraindicated (methergine, carboprost, oxytocin bolus, single-shot spinal), airway status, and a contact for any future anesthetic; one clinic visit with anesthesia within weeks.

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• Not ready. she needs blood pressure control, magnesium started, a second large-bore IV, blood in the room, and an arterial line; all of that takes fifteen minutes and none of it should take longer. Saying yes because the surgeon is scrubbed is a flag; so is an hour of workup with a fetus showing reduced variability.
• Dx and DDx. HELLP with a subcapsular hepatic hematoma is the working diagnosis (hypertension, proteinuria, hemolysis by LDH/haptoglobin/schistocytes, platelets halved, transaminitis, capsular finding). The list must include acute fatty liver of pregnancy, TTP, HUS, viral hepatitis, cholecystitis, and abruption. A resident who says only HELLP should be asked what would make it AFLP or TTP.
• BP. labetalol 20 mg IV, doubling every 10 minutes to 80 mg, or hydralazine 5-10 mg IV; target below 160/110 before laryngoscopy or a block, roughly 140/90, not normal. Overshooting drops placental perfusion.
• Magnesium. 4-6 g IV over 20 minutes, then 1 g/h rather than 2 g/h with a creatinine of 1.3; do not delay delivery for the load to finish. It runs through the case.
• CT. no; the ultrasound already shows the capsule and the collection, CT adds transport time and a contrast load to a deteriorating patient, and the treatment (delivery, then surgical control if it ruptures) does not change.
• Access and blood. second 16 g or 14 g IV, arterial line, rapid infuser primed; 4 PRBC, 4 FFP, platelets, and cryo in the room. Fibrinogen 220 is already low for pregnancy and will fall fast if she bleeds.

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• Modality. GA is the expected commit: platelets halved in a week with active hemolysis, a falling fibrinogen, a rising INR, and a hepatic hematoma that may rupture and turn this into a massive hemorrhage under a spinal. A spinal at 92 K is defensible in a stable HELLP; the trajectory is what argues against it. Either answer must engage both the count and the trend.
• Threshold. most accept neuraxial at ≥70-75 K when stable and rising or steady; a count falling this fast has no safe number. What would flip toward spinal: a stable repeat count, normal TEG, no hematoma. What would flip harder toward GA: clinical bleeding, fibrinogen <200, INR >1.5.
• TEG. useful and cheap, but not worth a 15-minute delay in a patient with a hematoma and a non-reassuring fetus; send it and proceed. The answer changes the products, not the modality.
• Induction. propofol 2 mg/kg (she is hypertensive, not hypovolemic yet) with attention to pressure; ketamine raises BP and is the wrong choice here.
• Paralytic. succinylcholine 1.5 mg/kg is not meaningfully potentiated by magnesium and gives the fastest conditions; rocuronium 1.2 mg/kg works but magnesium prolongs and deepens the block, so monitor TOF and expect a long recovery. Sugammadex 16 mg/kg if needed.
• Laryngoscopy. labetalol 20-40 mg IV, plus remifentanil 1 mcg/kg or fentanyl 2 mcg/kg; a hypertensive surge at laryngoscopy in a preeclamptic is a stroke risk. Warn NICU about the opioid.

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• First three. call for help and a second anesthesiologist, activate MTP, open the rapid infuser on the second line; tell the room the diagnosis so OB packs rather than explores.
• MTP and ratio. yes, now; 1:1:1 until viscoelastic data arrive, with fibrinogen replaced early because HELLP consumption plus dilution drives it below 200 quickly.
• Pressor. hemorrhagic shock is treated with blood; norepinephrine 4-8 mcg boluses or phenylephrine 100 mcg as a bridge while the first units run. A resident who titrates a pressor and does not name the products has the priorities inverted.
• Baby or liver first. deliver first: it takes two minutes, removes uteroplacental blood flow demand, lets the uterus contract, and gives OB room to pack the liver with the abdomen open; then pack. Packing first while the fetus is hypoperfused and the uterus is in the way is the wrong order.
• Oxytocin. infusion, no large bolus in a hypotensive patient; 3 IU slowly then an infusion. Methergine is contraindicated in severe hypertension and preeclampsia regardless of the current pressure; naming it without a flag is a fail. Carboprost is acceptable.
• Liver now. pack it with laparotomy pads and hold pressure (Pringle maneuver if the surgeon can); no attempts at repair by OB. Packing buys the 15 minutes.
• Calcium. calcium chloride 1 g IV now, recheck every 30 minutes through the resuscitation.
• TXA. 1 g over 10 minutes, then 1 g over 8 hours; within 3 hours of onset.
• Cell saver. yes, with a leukoreduction filter; amniotic contamination is a theoretical concern. It is the hepatic blood that is worth salvaging.

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• Products. platelets 1 apheresis unit (target ≥50 K, higher if bleeding), cryo 10 units or fibrinogen concentrate 4 g (target ≥200), FFP 2-4 units or PCC for INR ≥1.5 with ongoing bleeding; recheck in 30 minutes.
• Persistent hypotension. ongoing surgical bleeding under the packs, hypocalcemia, hypothermia and acidosis, tension from abdominal packing, transfusion reaction, the magnesium; check ionized calcium, temperature, a TEG, bladder pressure, and ask HPB to look under the packs before you increase the pressor.
• Fascia. leave it open: a packed, coagulopathic, acidotic, edematous abdomen will develop compartment syndrome if closed; temporary closure and a planned re-look at 24-48 hours.
• Magnesium. continue at 1 g/h; creatinine 1.3 and a massive transfusion both reduce clearance; check a level in the ICU and reflexes every hour.
• Transport. intubated and sedated, vasoactives on pumps, blood products and calcium in hand, airway kit, monitor with the arterial line, a second person, the ICU called ahead.
• Back to the OR. rising drain or pack output, a falling hemoglobin after correction, rising pressor requirement with a normal calcium and TEG, or bladder pressure >20; name the numbers, not 'if she gets worse.'

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• Central line. right IJ under ultrasound; a subclavian in a coagulopathic patient is non-compressible; femoral is under the abdominal dressing and dirty.
• Vent. 6-8 mL/kg PBW (PBW ~52 kg, so 350-400 mL), PEEP 5-8 with attention to abdominal pressure transmitted to the chest, plateau ≤30.
• Sedation. propofol infusion for a patient going back to the OR; dexmedetomidine as an adjunct once pressors allow; no midazolam infusion. Opioid for the abdomen; fentanyl, not morphine, with liver and kidney injury.
• Magnesium. 1 g/h, level 4-7 mg/dL, reflexes hourly; hold and check a level if reflexes disappear or RR falls once she is spontaneously breathing. Continue at least 24 hours postpartum, longer if hypertension and neurologic signs persist.
• Transfuse. fibrinogen 180 with an open packed liver: cryo or concentrate now to ≥200; platelets to ≥50 K, so a unit if any bleeding; Hgb 7.9 is acceptable if stable, transfuse if trending down.
• Six-hour goals. MAP ≥65 on falling pressor, lactate halved, temperature ≥36, ionized calcium ≥1.1, fibrinogen ≥200, platelets ≥50 K, INR <1.5, urine output ≥0.5 mL/kg/h, stable hemoglobin, bladder pressure <20.

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• Bleeding or oozing. the volume says bleeding; the hemoglobin holding at 7.8 says the drains may be diluted. Coagulopathy from consumption plus dilution is certain; surgical bleeding is not excluded. Correct the coagulopathy and see whether the output falls.
• Products. cryo 10 units or fibrinogen concentrate 4 g (target ≥200), platelets 1 unit (target ≥50 K, ≥75 K if actively bleeding), FFP 2-4 units (INR <1.5), calcium chloride 1 g. Recheck in 30-60 minutes; empiric repeat dosing without labs is a flag.
• Cryo vs concentrate. concentrate is faster, smaller volume, and dosed precisely (70 mg/kg raises fibrinogen ~100 mg/dL); cryo is cheaper and widely available. Either is right; ask for the dose.
• 400 mL and Hgb 6.5. surgical bleeding until proven otherwise: back to the OR for re-exploration and re-packing, or IR for hepatic artery embolization if she is stable enough to travel and the surgeon prefers it. Waiting with products is the wrong answer once the hemoglobin drops with corrected labs.
• Enoxaparin. not until 24-48 hours after bleeding has clearly stopped and the surgeon agrees; sequential compression until then. Postpartum HELLP with massive transfusion is a high VTE-risk state; starting it too late is also an error.

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• INR through FFP. synthetic failure: the liver is not making factors. This is acute liver failure, not consumption alone; transient correction with FFP followed by drift is the signature.
• DDx. AFLP (hypoglycemia, hyperammonemia, coagulopathy out of proportion to bleeding), HELLP with hepatic infarction or necrosis, ischemic hepatitis from the hemorrhagic shock, drug injury. A resident anchored on HELLP should be asked what the glucose and ammonia mean.
• Glucose. D10 at a higher rate or D20 via the central line, hourly glucose, target >70; hypoglycemia in liver failure is a marker of severity and injures the brain.
• Ammonia. lactulose is safe via the NG tube even with an open abdomen (ileus permitting); rifaximin as an adjunct; avoid sedatives that confound the exam; ammonia >150 raises the intracranial pressure concern.
• NAC. reasonable; non-acetaminophen acute liver failure has a transplant-free survival signal with NAC in early-grade encephalopathy, and the risk is low.
• Plasma exchange. for refractory HELLP/AFLP with multi-organ failure after delivery; not first line, but it is on the table within 24-48 hours if the trajectory continues.
• Candidacy. no uncontrolled sepsis, no irreversible brain injury (ICP management, avoid over-sedation, head up, sodium 145-150 if encephalopathy deepens), hemodynamic support that keeps the other organs alive; early transfer to a transplant center rather than waiting to be sure.

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• First. she is intubated: FiO2 1.0, hand-ventilate if pressures allow, protect the lines and the abdomen, confirm the tube; then treat the seizure.
• Magnesium. 2 g IV over 5 minutes as a re-bolus on top of the running infusion; a full 4-6 g load in a patient with a creatinine of 1.3 already on magnesium risks toxicity. Check a level.
• Refractory. lorazepam 2-4 mg IV or midazolam 2-5 mg; then levetiracetam 1-2 g load; propofol bolus is available since she is intubated. Do not keep pushing magnesium.
• DDx. postpartum eclampsia first, then intracranial hemorrhage (coagulopathic, hypertensive), cerebral venous sinus thrombosis, hypoglycemia, hyponatremia, hepatic encephalopathy, PRES.
• Level 3.2. sub-therapeutic; increase to 2 g/h with hourly reflexes and a repeat level in 4 hours, still watching the creatinine.
• CT. now, once she is stable enough to move: a coagulopathic hypertensive patient with a seizure needs hemorrhage excluded before anything else is assumed; MRI/MRV later for PRES or CVST.
• Pulmonary edema. preeclamptic capillary leak plus volume overload from resuscitation, TACO, TRALI, cardiogenic (peripartum cardiomyopathy is on the list until the echo is read); the echo here says overloaded with a good LV.
• Rx. furosemide 20-40 mg IV and repeat by effect, PEEP up to 10-14 with attention to abdominal and RV pressures, FiO2 1.0, strict restriction, BP controlled; if refractory, paralysis, prone with an open abdomen is nearly impossible, so early ECMO consultation or CRRT for fluid removal.

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• Will she live. honest uncertainty, no false reassurance, no despair: she has survived the bleeding, her liver and kidneys are the question, the transplant team is involved, and the next 48-72 hours will tell. Say what is being done, name who will update him and when. Vagueness and false certainty are both flags.
• Analgesia. fentanyl or hydromorphone in small doses (no morphine with renal failure, no meperidine), ketamine infusion, dexmedetomidine for sedation, regional (TAP catheters) once coagulation allows; avoid NSAIDs (kidney, platelets), avoid benzodiazepines and gabapentinoids that accumulate and cloud the neuro exam.
• Acetaminophen. hold while the liver is failing; when it recovers, ≤2 g/day is acceptable.
• Aspirin. 81-162 mg daily from 12-16 weeks in any future pregnancy; preconception counseling with maternal-fetal medicine.
• Letter. HELLP with hepatic rupture, massive transfusion and any antibodies formed, acute liver failure course, eclampsia, easy airway, the drugs that were held and why, and a request that future anesthetic teams plan early neuraxial with platelet trend in hand.

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• Modality. either is defensible if both risks are engaged. The airway is what makes GA dangerous (Mallampati IV, TMD 5 cm, neck 44 cm, edema, OSA, BMI 41, magnesium); the platelet trajectory is what makes the spinal uncomfortable. With INR 1.0 and fibrinogen 410, a single-pass spinal with a 25 g needle by the most experienced operator is the choice most would make. A reflexive GA without naming the airway, or a reflexive spinal without naming the trend, is a flag.
• Threshold. most accept ≥70-75 K when the count is stable; hers has halved in a week, so the question is whether it is 78 now or 60 by the time the needle goes in. Clinical bleeding, petechiae, a fibrinogen falling, or a repeat count below 70 would push to GA; a stable repeat count reassures.
• TEG. no; a category III tracing does not wait 20 minutes for a test that changes the products more than the modality. Send it and proceed.
• Wet taps. they predict a technically harder back (obesity, edema) and a higher PDPH risk; they are not a contraindication. Ultrasound the spine first; the most experienced hands go first.
• BP. yes, before either: labetalol 20-40 mg IV (she is already on it), or hydralazine 5-10 mg; target <160/110, roughly 140-150/90-100, not normal. A hypertensive surge at laryngoscopy or a hypotensive collapse after a spinal are both worse on an untreated 174/108.
• Spinal dose. hyperbaric bupivacaine 10-12 mg (obesity is not a reason to drop below 10 mg for a cesarean), fentanyl 15 mcg, morphine 100-150 mcg; 25 g pencil-point needle, sitting, ultrasound-marked midline. Phenylephrine or norepinephrine infusion running from the moment she lies down.

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• Ramp. shoulder and head blankets or a commercial ramp to bring the tragus level with the sternal notch, reverse Trendelenburg 20-30°; every minute of ramping is worth it, and it can be done while the surgeon preps.
• Preoxygenation. tight mask, 100% oxygen, head up, CPAP 5-10 or her own CPAP circuit, high-flow nasal oxygen under the mask for apneic oxygenation; go at end-tidal O2 ≥80%, or after 3 minutes if the tracing does not allow more. Expect desaturation in under a minute in this body habitus.
• Induction. propofol 2 mg/kg on lean body weight (~60-65 kg, so 120-150 mg), with the pressure treated first; ketamine is wrong here (hypertensive, headache, scotomata).
• Paralytic. succinylcholine 1-1.5 mg/kg on total body weight (fastest, shortest, minimally affected by magnesium, and the one to choose in a predicted difficult airway); rocuronium 1.2 mg/kg with sugammadex 16 mg/kg ready is acceptable, but magnesium prolongs and deepens it and blunts sugammadex reversal. A resident who dose-reduces rocuronium 'because of the magnesium' has it backwards.
• VL. video laryngoscope first pass: it is the best chance at first-pass success in a Mallampati IV with a short thyromental distance; DL as backup, not the other way round. A second-generation supraglottic and a scalpel on the tray.
• BP 190/115. labetalol 20-40 mg IV plus remifentanil 1 mcg/kg or fentanyl 2 mcg/kg or esmolol 1 mg/kg before laryngoscopy; target below 160/110 for the laryngoscopy; nitroprusside as a first move is a flag. Tell NICU the opioid went in.
• Grade 3 view. bougie under the epiglottis with the VL still in place, external laryngeal manipulation, one more attempt with a different blade or a hyperangulated blade; if that fails, supraglottic airway and ventilate. Repeated laryngoscopy in an edematous preeclamptic airway converts a difficult airway into a lost one.
• Volatile. sevoflurane at 0.5-0.75 MAC until delivery (MAC is reduced in pregnancy, magnesium adds CNS depression, and higher MAC relaxes the uterus); supplement with opioid after the cord is clamped.

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• Post-delivery hypotension. loss of aortocaval compression alone does not do this; oxytocin bolus, bleeding from atony, volatile depth after the sympathetic surge, the magnesium, and residual induction drug. Look at the field before you choose the drug.
• Pressor. phenylephrine 100 mcg or norepinephrine 8 mcg boluses for a vasodilated drop; ephedrine is acceptable but adds tachycardia. Phenylephrine is not contraindicated in obstetrics; a resident who says so should be corrected.
• Oxytocin. infusion rather than a large bolus in a hypotensive patient: 1-3 IU slowly, then 10-40 IU/L infusion. A 5-10 IU IV push here is a flag.
• Methergine. contraindicated in severe hypertension and preeclampsia regardless of the current pressure: it will produce a hypertensive crisis in twenty minutes. Naming it without a flag is a fail.
• Carboprost. no asthma, so it is allowed; give 250 mcg IM, repeat every 15 minutes up to 8 doses, with the caveat that it raises pulmonary and systemic pressure and causes bronchospasm and diarrhea. Misoprostol 800-1000 mcg rectal or buccal alongside; TXA 1 g.
• Hypertensive surge at closing. light anesthesia at 0.5% end-tidal with the incision being closed, pain, hypercarbia, bladder; also preeclampsia itself. Deepen (opioid, propofol), then labetalol 20-40 mg IV or hydralazine 5-10 mg or a nicardipine infusion; target <160/110 before extubation. Nitroprusside as a reflex is a flag.
• Magnesium. continue through emergence and for at least 24 hours postpartum; a brief hold for 'weakness at extubation' without a restart is how postpartum eclampsia happens. Assess strength with the magnesium running, not by stopping it.

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• MTP. yes, now; 1:1:1 until viscoelastic data arrive; a second large-bore line and a rapid infuser; call for a second anesthesiologist.
• Calcium. calcium chloride 1 g IV now, repeat roughly every 2-4 units of citrated product, ionized calcium every 30 minutes.
• Can she go to IR. no: BP 70/35 on no products with an open abdomen is not a patient who travels. Bakri or B-Lynch now with the abdomen open; hysterectomy if those fail. IR is for the stable patient with ongoing bleeding. The resident's job is to say plainly whether she has 40 minutes; hand-waving to the surgeon is a flag.
• Products. cryo 10 units or fibrinogen concentrate 4 g (target ≥200 while bleeding), platelets 1 unit (target ≥50 K, ≥75 K if still bleeding), FFP or PCC for INR ≥1.5; recheck in 30 minutes.
• TXA. 1 g over 10 minutes; a second 1 g if bleeding continues after 30 minutes. If it was not given already, it is late but not too late (within 3 hours).
• Temp 35.1. warm all lines, forced air on the exposed patient, warm the room; hypothermic coagulopathy will not respond to products.
• Magnesium. reduce or briefly hold while she is in hemorrhagic shock; magnesium lowers vascular tone and worsens atony, and clearance falls with hypoperfusion. Restart as soon as she is stable; the eclampsia window does not close. Stopping without a plan to restart is the error.
• Winning. lactate trending down, base deficit closing, MAP ≥65 with falling pressor, urine output returning, ionized calcium ≥1.1, fibrinogen ≥200, a firm uterus; not a single hemoglobin.

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• Extubate or not. leaving her intubated is the safer answer: massive transfusion, a pressor still running, magnesium, a difficult airway, OSA, and a leaky preeclamptic vasculature that will get worse over the next 12 hours. Extubation is defensible only if every criterion is met and the airway team is prepared to reintubate. Extubating to free up the OR is a flag.
• Criteria. awake and following commands, TOF ≥0.9 with sustained head lift, normothermic, pressor off or minimal, no ongoing bleeding, acceptable gas exchange on low FiO2, BP <160/110.
• Magnesium and strength. magnesium weakens the neuromuscular junction independently of the rocuronium and blunts sugammadex reversal; a TOF of 0.95 is reassuring but a 3-second head lift is marginal. A 5-second head lift and a strong grip carry more weight than the monitor here; if in doubt, wait.
• Hypoxemia DDx. pulmonary edema (preeclamptic, TACO, TRALI), atelectasis in obesity, residual weakness, opioid and magnesium respiratory depression, OSA obstruction, aspiration. Bedside echo and lung ultrasound sort most of it.
• Rx. sit her up, CPAP (her own machine is fine if the mask fits and she is awake enough), furosemide 20-40 mg IV, restrict fluids, control BP; TACO and preeclamptic edema both respond, TRALI does not.
• Reintubation. now, before she arrests: falling saturation on CPAP with drowsiness is a failing trajectory. Same ramp, VL first with the bougie in hand, most experienced operator, supraglottic and surgical airway ready, and this time no rush. Waiting for a lower number is the error.

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• First moves. lateral, oxygen, suction, protect her from injury, confirm the IV, call for help; do not force anything into her mouth.
• Magnesium. 2 g IV over 5 minutes, up to 4 g total; she stopped only two hours ago and has residual on board, and her creatinine is 1.1. A full 4-6 g load risks toxicity. Stopping magnesium early postpartum is the error that led here and should be named.
• Refractory. lorazepam 2-4 mg IV or midazolam 2-5 mg; then levetiracetam 1-2 g; be ready to intubate when the benzodiazepine goes in.
• Intubate. a difficult airway, OSA, post-ictal obstruction, and SpO2 90% on a non-rebreather: yes, in a controlled fashion now with the full airway team, rather than after the next seizure or an aspiration. Watchful waiting is defensible only with the airway team at the bedside and improving saturations.
• DDx. postpartum eclampsia first (it occurs up to days out, especially when magnesium is stopped early); intracerebral hemorrhage in a hypertensive thrombocytopenic patient, CVST, PRES, hyponatremia, hypoglycemia (insulin, NPO), local anesthetic is not on the list (no epidural).
• CT. as soon as she is stable enough to move: hemorrhage must be excluded in this patient; MRI/MRV later for PRES or CVST if the CT is negative and the picture does not fit.
• Magnesium after. 1-2 g/h for 24 hours after the seizure, adjusted to creatinine, with hourly reflexes and a level; do not stop it again for a soft reason.

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• DDx. preeclamptic AKI, ATN from hemorrhagic shock and pigment (she had tea-colored urine at the start), hypovolemia from under-resuscitation, abdominal compartment syndrome after massive resuscitation, obstructed Foley, TTP/HUS if platelets fall again. Anchoring on one is a flag.
• First. the Foley, the abdomen (bladder pressure), volume status (IVC, JVP, lung ultrasound, balance), a urine sodium and sediment.
• Fluid. a small bolus (250-500 mL) only if the exam says she is dry (collapsing IVC, dry lungs); a preeclamptic vasculature leaks, and 'a liter for oliguria' produces the pulmonary edema in the next beat. No response to 500 mL means stop giving fluid.
• Furosemide. yes if she is full (IVC plethoric, B-lines) to protect the lungs; it does not treat the AKI, and a dose that produces urine does not mean the kidney is better. 20-40 mg IV.
• Magnesium. renally cleared; at a creatinine of 1.8 reduce to 0.5-1 g/h with a level every 4-6 hours, or hold while the level is checked.
• Reflexes gone, RR 9. magnesium toxicity (loss of reflexes ~10 mEq/L, respiratory depression above ~12); stop the infusion, calcium gluconate 1 g IV over 3 minutes, support ventilation, send a level; dialysis if she is anuric and the level is very high.
• Dyspnea. pulmonary edema (preeclamptic, TACO), magnesium-related hypoventilation, atelectasis, PE; lung ultrasound and echo, then CPAP and diuresis or ventilation as the picture dictates. Renal consultation now for oliguria refractory to optimization, rising potassium, and a possible dialysis need.

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• Stop magnesium. yes — 24 h beyond the seizure with a therapeutic level, no clonus, and a kidney that is clearing it slowly (creatinine 1.5) is the endpoint; continuing indefinitely accumulates toward toxicity, which she has already had once. Persistent severe symptoms (headache, visual change, clonus) would extend it; a BP of 158/98 alone does not.
• BP 168/104. severe-range, treat within 30-60 min: labetalol 20 mg IV (escalating 40, 80), hydralazine 5-10 mg IV, or nifedipine IR 10 mg PO; target 140-150/90-100, not normal — a rapid drop is its own harm.
• Oral regimen. nifedipine ER 30-60 mg daily first (effective postpartum, once daily, compatible with breastfeeding), labetalol 200-400 mg TID added if needed; she was on both before delivery so restart both. Enalapril is breastfeeding-compatible and a good postpartum agent, but with an evolving AKI at creatinine 1.5 hold it until the kidney recovers.
• VTE prophylaxis. yes — cesarean, BMI 41, preeclampsia, massive transfusion, ICU stay: high risk. Platelets >50 and rising with no bleeding and no neuraxial catheter: start now. Enoxaparin weight-based (about 0.5 mg/kg BID, ~60 mg BID at 110 kg) if creatinine clearance is above 30; unfractionated heparin 5000-7500 units TID is the alternative while the creatinine is moving, and it reverses fast if she rebleeds. Withholding prophylaxis for the platelet count is the error.
• Hgb 7.8. no transfusion — asymptomatic, no ongoing bleeding; IV iron (e.g., ferric carboxymaltose or iron sucrose) for a faster recovery than oral; transfuse for symptoms or Hgb <7.
• Glargine. hold or halve — insulin sensitivity returns within hours of delivery and gestational diabetes usually resolves; a full 24 units into a postpartum patient eating poorly produces overnight hypoglycemia. Check fasting glucoses and reassess at the postpartum visit.
• Floor. BP <160/110 on oral agents for 12-24 h, magnesium off with reflexes and mental status normal, off NIV with oxygen requirement stable, urine output improving on a falling creatinine, a VTE plan written, CPAP nightly with continuous oximetry on the floor given OSA and opioids.

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• What to tell her. plain and complete: severe preeclampsia, why the baby had to come out fast, why the spinal failed and she was put to sleep, the bleeding from a uterus that would not contract, the transfusion, that the surgeons used measures to keep her uterus and that a hysterectomy was the next step had they failed, the seizure, the kidney injury. No minimizing, no blame, and the OB and ICU teams told the same account before she hears it. Offering a partial version and referring the rest to OB is a flag.
• Headache DDx. PDPH after two spinal attempts (positional pattern), but preeclampsia is still active at 150/95, and CVST, PRES, and subdural are on the list after eclampsia. Neurologic exam, BP trend, platelets, and a low threshold for MRI/MRV; the positional pattern alone is not enough here.
• Blood patch. not yet: platelets 95 on POD 3 is acceptable for a patch, but with an unexplained seizure three days ago and hypertension, image first and exclude CVST and hemorrhage; a patch into a patient with an intracranial process is the error. Once imaging is clean, a patch at 24-48 hours from symptom onset is reasonable.
• Letter. difficult airway (grade 3 on VL, bougie), failed spinal and the reason, HELLP-range labs, massive transfusion, postpartum eclampsia, magnesium toxicity episode, AKI, OSA; and a recommendation for early neuraxial planning with a platelet trend and an airway team present in any future pregnancy.
• Aspirin. 81-162 mg daily from 12-16 weeks; preconception planning with maternal-fetal medicine, BP optimization, and recurrence risk of preeclampsia around 15-25%, higher with chronic hypertension.
• CPAP. nightly, adherence reinforced; postpartum fluid mobilization and opioids make the first weeks a high-risk window, and a sleep medicine follow-up for retitration after the weight and edema settle.

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• Is it working. T10 to ice bilaterally with new suprapubic and pushing pain is a block losing density and sacral coverage in second stage, not a dead catheter; the flag is reaching for a top-up before checking level, symmetry, motor, and pump history.
• Level for forceps. T10 with dense sacral (S2-4) coverage for low/outlet forceps; a surgical block (T4-T6) only if the plan is cesarean. Something denser than 0.1% bupivacaine either way.
• Top-up agent. bupivacaine 0.25% 8-10 mL for forceps coverage; lidocaine 2% with bicarbonate and epinephrine 8-10 mL if cesarean may follow (fast, extendable); chloroprocaine 3% for the fastest onset. Any is defensible if committed and matched to the likely path.
• Test dose. yes in some form: catheter position changes over six hours of labor; either a formal 3 mL lidocaine 1.5% with epi 1:200,000 or the top-up in 5 mL increments with aspiration and a 3-minute check. Pushing 10 mL in one pass is the error.
• Perineum unchanged. sacral sparing: the large S1-2 roots resist dilute solutions and a catheter that has crept cephalad. Sit her up, larger-volume less-dilute bolus; if a second bolus fails, replace the catheter now rather than discover a non-surgical catheter at a stat cesarean.
• Bedside vs OR. with a marginal block, prior 1.5 L PPH, and a nonreassuring tracing, the OR (trial of forceps with the option to cut) is the stronger answer; bedside forceps is defensible only if she names what she gives up (full monitoring, blood, immediate conversion).

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• Full stomach. yes; labor, pain, and epidural fentanyl slow gastric emptying; the four-hour interval buys nothing. Every laboring patient is a full stomach for induction purposes.
• Nausea with BP 92/58. sympathectomy from the top-up with hypotension; nausea is the symptom of the BP. Treat the BP: LUD, fluid bolus, phenylephrine 100 mcg IV or ephedrine 5-10 mg if HR is low; nausea resolves with the pressure.
• Sodium citrate. 30 mL of 0.3 M within 20-30 minutes of induction; effect lasts about an hour, so redose if the OR is delayed.
• Famotidine. 20 mg IV; onset 30-60 minutes, so it will not help an induction in 10 minutes but does cover a later one and the PACU. Giving it because the case may convert is the point.
• Metoclopramide. 10 mg IV; promotes emptying and raises LES tone; modest effect.
• Vomiting. does not empty the stomach reliably; she remains RSI. Ondansetron 4 mg treats the symptom and changes no aspiration risk.

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• History. rescue frequency, recent URI, night symptoms, prior ED visits, intubations, steroid courses, triggers. Two uses in a week with a URI is mild; a recent steroid course would change the plan.
• Pre-emptive neb. reasonable before GA in any asthmatic with recent symptoms (albuterol 2.5 mg neb or 4-8 puffs MDI); low cost. Not required for a neuraxial case.
• Induction agent. propofol 2-2.5 mg/kg attenuates airway reflexes; ketamine 1-1.5 mg/kg bronchodilates and supports BP; either. Etomidate is neutral and not preferred. Reduce the dose if hypotensive.
• Relaxant. sux 1-1.5 mg/kg; roc 1.2 mg/kg is equivalent for RSI with sugammadex available. No asthma reason to avoid either; avoid histamine-releasing agents.
• Volatile. sevoflurane; desflurane is airway-irritant and increases resistance in reactive airways.
• Carboprost. contraindicated in asthma (bronchospasm); methergine (no severe HTN here) and misoprostol replace it. Say this to OB before the case, not during the hemorrhage.
• Ketorolac. fine unless aspirin-exacerbated respiratory disease; ask about NSAID reactions. Withholding NSAIDs from every asthmatic is a common overcaution.

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• Crossmatch. yes; prior PPH plus prolonged second stage plus possible operative delivery is a hemorrhage risk profile; 2 units crossmatched, blood bank aware. Hgb 10.4 leaves less reserve than the number suggests.
• Access. a positional 18 g is not adequate; two reliable large-bore (16-18 g) IVs before the trial, not after the bleed starts.
• In the room. warmed fluids, rapid infuser available, uterotonics drawn, blood ordered, a plan for OR transfer stated to OB.
• Uterotonics. oxytocin infusion ready (e.g., 30 U/500 mL); methergine 0.2 mg IM; misoprostol 800-1000 mcg; no carboprost (asthma).
• Cell saver. supported in obstetric hemorrhage with a leukoreduction filter; reasonable to have ready given her history; not mandatory for a vaginal trial.
• TXA. 1 g IV within 3 hours of hemorrhage onset once bleeding is established; routine prophylaxis before vaginal delivery is not standard. Either answer needs the reasoning.

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• Target. category 1: delivery as fast as safely possible, commonly quoted as within 30 minutes but the real target is minutes; state aloud what you need.
• Top-up. lidocaine 2% with bicarbonate and epinephrine, 15-20 mL in increments, onset 5-10 min; chloroprocaine 3% is faster but short and antagonizes later neuraxial opioid; bupivacaine 0.5% too slow. Commit.
• Test dose. a formal test dose costs 3 minutes she may not have; incremental 5 mL doses with aspiration and monitoring is the accepted compromise. Either is defensible if reasoned; a single 20 mL push is not.
• BP 80/45, cannot get a full breath. sympathectomy from rapid extension with a nonreassuring tracing on top; high or total spinal from a migrated catheter is the must-exclude. Strong grip, full sentences, and a T4 level make this sympathectomy, not a high spinal. Do not assume LAST without signs.
• Rx. stop injecting, LUD, phenylephrine 100 mcg boluses or norepinephrine, fluid, oxygen; recheck level and respiratory effort.
• Give the rest. no; T4 is the target. More lidocaine buys nothing but a higher block. Proceed to incision.

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• Unilateral block after full dose. a catheter problem (lateral, in a paravertebral gutter); redosing 5 mL rarely fixes a unilateral block after 15 mL and delays the baby. Commit to a path.
• Adjuncts. ketamine 0.25-0.5 mg/kg (20-40 mg), surgeon local, IV fentanyl bridge a patchy block for minutes, not a hemi-block. Naming them as a substitute for a surgical block is the flag.
• Time budget. a persistent FHR of 60 gives essentially no time; state a number (2-3 min) and what forces the move: fetal deterioration and maternal pain.
• She screams. convert to GA now. Chasing a failed block with boluses while she suffers and the baby is bradycardic is the error. Tell OB to stop cutting until she is asleep.

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• Airway change. labor airway: mucosal edema, weight gain, pushing, fluids; Mallampati commonly advances a grade or two over labor. Look again and prepare for a worse airway than admission.
• Position. ramped, head-up 20-30 degrees, left tilt or LUD; check that the table can tilt before induction.
• Preoxygenation. as long as the FHR allows; 3 minutes tidal breathing or 8 vital-capacity breaths on a tight mask; high-flow nasal oxygen during laryngoscopy if available. Pregnant FRC and O2 consumption make her desaturate in about a minute.
• Drugs. propofol 2-2.5 mg/kg (about 150-180 mg; reduce if hypotensive); sux 1-1.5 mg/kg or roc 1.2 mg/kg with sugammadex drawn.
• Cricoid. standard in most OB practice; release if it obstructs the view. Either defensible if argued.
• CL 3. optimize: external laryngeal manipulation, head lift, bougie under the epiglottis; second attempt with video laryngoscopy, not the same blade. Two attempts then SGA; ventilate between attempts.
• SpO2 92% falling. stop looking, mask ventilate with two hands and an oral airway, cricoid on, SGA if mask fails; the sequence is oxygenation, not the tube. Front-of-neck access if cannot ventilate.

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• Maintenance. sevoflurane about 0.7-1 MAC before delivery; enough to prevent awareness, low enough to limit uterine relaxation; N2O 50% can supplement.
• BP 75/40 with a boggy uterus. atony plus volatile-induced relaxation, hemorrhage, and the aortocaval load coming off; amniotic fluid embolism if it does not respond. Oxytocin now.
• Oxytocin. 3 U IV bolus over 30 s (repeat once or twice at 3-minute intervals), then infusion; a 10 U push causes hypotension. Or a 30 U/500 mL infusion run fast.
• Methergine. yes: 0.2 mg IM (or slow IV in some practices); no hypertension here. Repeat at 2-4 h.
• Carboprost. no, asthma; state it plainly and offer misoprostol instead. Bronchospasm in an intubated asthmatic mid-hemorrhage is the trap.
• Misoprostol. 800-1000 mcg rectal or sublingual; slower onset; adjunct.
• Volatile and awareness. drop to 0.5 MAC or convert to propofol infusion; cover with midazolam 2 mg, fentanyl, ketamine; processed EEG if available; document. Volatile at 0.5 MAC alone with no supplement is the awareness setup.

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• Can she tolerate 20 minutes. the anesthesiologist's call to make and state: rate of loss, pressor requirement, product availability, pH/lactate, coagulation. Rising pressor need and loss outpacing replacement means no. Inform the decision without owning the surgical choice.
• Resuscitation. activate massive transfusion; PRBC:FFP:platelets near 1:1:1 until guided by labs; calcium with every 2-4 units (ionized Ca target >1.1); fibrinogen is the first factor to fall in obstetric hemorrhage: cryoprecipitate or concentrate to keep it >200 mg/dL; point-of-care testing if available.
• TXA. 1 g IV over 10 min, repeat once at 30 min if bleeding continues.
• Extubation. hemostasis confirmed, warm (>36), lactate falling, no pressor, reversal confirmed, awake with full strength, airway not worse than at induction (it was CL 3 before edema and fluids). After a difficult airway and 2.8 L, keeping her intubated to a monitored bed is the conservative and defensible answer; extubating over an exchange catheter is a middle path.
• Reported recall. credible awareness: light pre-delivery anesthesia, a difficult airway, and hemorrhage. Tell her it is real and possible, that it was not her imagination, and apologize; do not minimize. Explain why she was put to sleep and what happened with her airway; document, arrange follow-up and psychological support; give her a letter about the difficult airway for future anesthetics.

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• Continue. the expected commit; holding risks withdrawal, relapse, and worse pain control with no offsetting benefit.
• Full-agonist switch. rarely indicated; buprenorphine occupies receptors for days regardless, and the switch destabilizes a stable regimen.
• Her worry about the baby. NAS risk is real on either path; stopping today does not protect the neonate and puts her recovery at risk; the plan is collaborative and she has a voice in it.
• Addiction provider. current dose and timing, recent stability, split-dosing preference, postpartum plan, support resources.
• Neonatology. maternal buprenorphine dose; NAS monitoring and supportive care; rooming-in and breastfeeding are usually supported.

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• Early epidural. yes; reduces stress and systemic opioid exposure; no reason to wait.
• LA. dilute bupivacaine or ropivacaine plus opioid; standard.
• Epidural fentanyl. still works locally but effect is blunted by receptor occupancy; expect less benefit; clonidine or a higher LA concentration can supplement.
• Pain despite T10. missed segment, patchy block, visceral pain, opioid-induced hyperalgesia; assess before redosing.
• Adjuncts. IV fentanyl has little to add on top of buprenorphine; subdissociative ketamine or nitrous are more useful; commit and defend.
• PCA fentanyl. poor choice here; favor neuraxial and non-opioid adjuncts.

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• Access. one marginal 20 g is not adequate for a laboring patient who may bleed; two reliable large-bore lines.
• Ultrasound first. yes; track-mark anatomy makes landmark attempts low-yield.
• Central line. place early rather than during a hemorrhage; internal jugular under ultrasound is the usual pick.
• T&S vs crossmatch. T&S suffices at baseline risk; crossmatch when a risk factor appears.
• Exam. murmur, fever, or stigmata of endocarditis from prior IV drug use; a new murmur warrants an echo before proceeding electively.

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• Scheduled. acetaminophen and NSAID if no contraindication; opioid only as supplement.
• Regional. neuraxial morphine if the catheter is used for the case; TAP or QL as adjunct or if no catheter; either defensible.
• Buprenorphine. continue; many programs split into TID dosing peripartum for steadier analgesia; never hold.
• Breakthrough opioid. expect roughly 2-3x naive morphine-equivalents because of receptor occupancy; titrate with monitoring.
• Ketamine. starting in the OR is reasonable given predictable high requirements; reserving it is defensible if the regional plan is strong.

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• Top-up. lidocaine 2% with bicarbonate and epinephrine, ~15-20 mL incrementally, to T4-T6.
• Pain despite T4. visceral pain not covered, patchy block, opioid-induced hyperalgesia.
• Fentanyl fails. expected in her; escalate to ketamine 0.25-0.5 mg/kg, surgeon local, anxiolysis.
• GA. if pain is uncontrolled and she is suffering, convert; chasing a failed block with repeated boluses is the error. GA in an opioid-tolerant patient is not a relapse risk in itself.

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• Uterotonics. oxytocin infusion first; methergine acceptable (no severe HTN); carboprost acceptable (no asthma); misoprostol adjunct.
• Neuraxial morphine. yes; buprenorphine does not preclude it; standard dose (e.g., 2-3 mg epidural).
• Monitoring. continuous pulse oximetry and capnography for 24 h; opioids stacked on a partial-agonist baseline can still cause delayed hypoventilation.

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• Next. treat the pain; undertreating a tolerant patient risks her recovery. Do not read high requirements as drug-seeking.
• Hydromorphone. titrate in larger increments than naive dosing (roughly 2-3x); monitor.
• Ketamine. bolus 0.25-0.5 mg/kg then 0.1-0.3 mg/kg/h.
• Firm tender incision. exclude hematoma or evolving surgical complication before adding more opioid; call OB.
• Consults. acute pain service and addiction medicine early.

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• Cause. stacked opioid effect (neuraxial morphine plus IV hydromorphone) on a partial-agonist baseline.
• Rx now. stimulate, oxygen, support ventilation, hold further opioid.
• Naloxone. small titrated doses (40 mcg increments); buprenorphine's high receptor affinity makes reversal partial and a full dose can precipitate withdrawal.
• Sweating, vomiting, writhing. precipitated withdrawal; stop naloxone, supportive care, reassess the regimen with addiction medicine; do not restart full-agonist opioid reflexively.
• Monitoring. continuous capnography until reliably awake and ventilating; monitored bed overnight.

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• Buprenorphine tomorrow. home dose confirmed with addiction medicine; splitting into TID doses peripartum gives steadier analgesia; never stopped.
• Monitoring. continuous pulse oximetry and capnography for 24 h after neuraxial morphine and a respiratory-depression event; step down only after a clean interval.
• Naloxone. yes at the bedside, with the 40-80 mcg titration written in the order so the floor does not push 0.4 mg.
• Nurse's question. no; buprenorphine continues alongside full agonists; holding it invites withdrawal and relapse.

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• Treat first. an active flare with a prior intubation in a term parturient; labor pain and catecholamines will worsen it. Treat now, in the L&D room, while the epidural is set up.
• Bedside Rx. oxygen to SpO2 >95%; albuterol 2.5-5 mg neb, repeat q20 min or continuous; ipratropium 0.5 mg neb x3; magnesium 2 g IV over 20 min; hydrocortisone 100 mg IV; continuous SpO2 and fetal monitoring.
• Hydrocortisone. two reasons: her flare needs systemic steroid beyond 20 mg prednisone, and chronic prednisone 20 mg/day suppresses the HPA axis, so labor and possible surgery need stress-dose coverage: hydrocortisone 100 mg then 50 mg q8h for 24 h.
• Magnesium. bronchodilator; it is also a tocolytic and will contribute to atony later; note it and move on.
• ABG. yes: she is tachypneic with SpO2 93% and a history of intubation. A normal PaCO2 of 40 in a laboring pregnant woman whose baseline is 28-32 is relative hypercapnia: fatigue, not reassurance. PaO2 68 on oxygen is poor.
• Where. L&D with continuous SpO2, one-to-one nursing, pulmonology and ICU aware; transfer if she fails to improve or PaCO2 rises. An improving patient does not need the ICU, but the threshold to move is low.

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• Early epidural. yes: pain and hyperventilation drive bronchospasm; an epidural lowers catecholamines and minute ventilation demand and gives a surgical option that is not a GA airway.
• LA. bupivacaine 0.0625-0.1% with fentanyl 2 mcg/mL; keep the level low (T10) to preserve accessory muscles.
• Epinephrine test dose. 15 mcg epinephrine in an asthmatic is not harmful (it bronchodilates); the confounder is her baseline HR of 108. Give it, or dose incrementally with aspiration; either defensible.
• Dyspnea at 20 minutes. worsening flare, high block reducing accessory muscle recruitment, sympathectomy with hypotension and anxiety, allergic reaction, pulmonary edema (magnesium, fluids). Check level and hands first.
• High block. T8 with full grip and no hand numbness is not a high block; the dyspnea is her lungs plus mild sympathectomy. A rising level (T4 or above, weak grip, numb hands) would change the answer to ventilatory support.
• Rx. albuterol, oxygen, phenylephrine for BP, sit her up, continue the flare regimen; reassess PaCO2 if not improving.
• Keep it. yes; the epidural is not the cause and the alternative if she needs a cesarean is a GA airway in an actively flaring asthmatic.

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• History. the reaction (wheeze, flushing, angioedema vs GI upset), timing, which NSAIDs, nasal polyps, chronic rhinosinusitis.
• Dx. aspirin-exacerbated respiratory disease (Samter's triad: asthma, nasal polyps, NSAID reactions); all COX-1 inhibitors are contraindicated, ketorolac included. Not an IgE allergy.
• Acetaminophen. fine at standard doses (high doses have weak COX-1 activity but are tolerated).
• First agent. oxytocin 3 U IV over 30 s or an infusion, repeat once; then infusion.
• Second agent. methergine 0.2 mg IM (BP 132/82 is acceptable) or misoprostol 800-1000 mcg rectal/sublingual; both are asthma-safe. Commit to an order and say why.
• Carboprost. absolute contraindication in severe asthma; life-threatening bronchospasm. Say this to OB before delivery so it is not requested in the moment.
• Refractory. mechanical and surgical early: bimanual compression, Bakri, compression sutures, uterine artery ligation, IR embolization; TXA 1 g; she has one fewer drug than most patients, so escalate sooner.

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• Modality. extend the epidural; GA only for a failed block under time pressure or maternal respiratory failure. Saying so to OB now buys minutes later.
• Albuterol before induction. 4-8 puffs by MDI or a neb in the 15-30 minutes before induction; blunts intubation-triggered bronchospasm.
• Induction. ketamine 1-1.5 mg/kg bronchodilates and holds BP; propofol 2 mg/kg blunts airway reflexes; either, committed. Lidocaine 1.5 mg/kg IV before laryngoscopy is a reasonable add. Avoid desflurane; sevoflurane is the volatile.
• Relaxant. sux 1-1.5 mg/kg or roc 1.2 mg/kg with sugammadex; no asthma reason to avoid either; avoid atracurium/mivacurium (histamine).
• Steroid. she is covered for the day by the 100 mg; continue 50 mg q8h; an additional dose at induction is reasonable. Missing it invites refractory hypotension.
• Cefazolin. yes; childhood hives with penicillin is not a contraindication; cefazolin has a distinct side chain and cross-reactivity is under 1%. Reflexive clindamycin or vancomycin gives worse prophylaxis.
• Husband. the one counseling beat: a plain answer that a ventilator is possible if her lungs fail or if surgery under GA is needed, that everything being done now is aimed at avoiding it, and what she will see if it happens. Not false reassurance.

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• Top-up. lidocaine 2% with bicarbonate and epinephrine, 15-20 mL in 5 mL increments; the asymmetric baseline warns the catheter may not deliver.
• Continue or GA. an asymmetric block still short of T6 after 10 mL with FHR 70: GA. In her, GA is the higher-risk path, but a hemi-block with a bradycardic fetus is not a path at all. Chasing the block is the flag.
• Induction. albuterol 8 puffs via mask before induction; ketamine 1.5 mg/kg (about 110 mg) or propofol 2 mg/kg (150 mg); sux 1.5 mg/kg (110 mg); cricoid per practice; lidocaine 100 mg IV is reasonable.
• Peak pressure 42. bronchospasm vs mainstem intubation vs kinked or obstructed tube vs light anesthesia vs circuit; check depth and breath sounds first.
• Capnogram. shark-fin: expiratory obstruction; bronchospasm.
• Rx. 100% O2, hand-ventilate with long expiration, deepen (sevoflurane up, propofol bolus 50 mg), albuterol 8-10 puffs into the ETT, ketamine 50 mg, epinephrine if not responding; tell OB to proceed.

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• Something else. ETT obstruction or mainstem (pass a suction catheter, auscultate), anaphylaxis (rash, hypotension, edema), pneumothorax, breath-stacking from a fast rate. Free catheter, equal sounds, no rash: refractory bronchospasm.
• Epinephrine. 10-20 mcg IV boluses, escalating; infusion 0.02-0.1 mcg/kg/min if repeated boluses; bronchodilator and pressor in one. Terbutaline 0.25 mg SC is a slower alternative.
• Magnesium. 2 g IV over 10-20 min (second dose today; she had 2 g at admission); it will add to atony after delivery; accept that.
• Ventilator. rate 8-10, tidal volume 6 mL/kg, I:E 1:3-1:4, PEEP 0-5, disconnect briefly to release trapped gas if hypotensive; permissive hypercapnia to PaCO2 60-70 while pH >7.2; fetal acidosis argues for delivery, not high pressures.
• Volatile before delivery. up: bronchospasm is the immediate threat and the uterus can be treated once the baby is out; tell OB that atony is coming and to deliver quickly.

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• DDx. volatile-induced atony with hemorrhage, magnesium, aortocaval load gone, dynamic hyperinflation lowering venous return, ongoing bronchospasm, oxytocin bolus effect, AFE if unresponsive.
• Pressor. epinephrine 10-20 mcg boluses or infusion does both jobs (bronchodilation and pressure); norepinephrine if bronchospasm is improving; phenylephrine is a poor sole choice with HR 130 and bronchospasm.
• Oxytocin. 3 U IV over 30 s, repeat at 3 min, then infusion 30 U/500 mL; not a 10 U push at BP 75/40.
• Carboprost. no, and say why in one sentence; offer methergine and misoprostol. Yielding to the surgeon's request is the trap in the case.
• Methergine. yes: 0.2 mg IM; BP 95/55 is not hypertension. Misoprostol 800-1000 mcg rectal or sublingual as adjunct.
• Volatile. down to 0.5 MAC once bronchospasm is improving (peak 36 from 50); cover bronchodilation with epinephrine infusion, ketamine, magnesium; cover awareness with propofol infusion or midazolam 2 mg plus fentanyl; processed EEG if available.

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• Can she tolerate it. rate of loss vs replacement, pressor trajectory, lactate/pH, coagulation; say yes with a stated stop rule (rising pressor, loss faster than products) rather than defer. Inform the surgical call; do not own it.
• Products. massive transfusion activated; PRBC:FFP:platelets near 1:1:1 until labs guide; warm everything.
• Fibrinogen 150. below the obstetric target of 200: cryoprecipitate 10 units (or fibrinogen concentrate 2-4 g) now; fibrinogen falls first in obstetric hemorrhage.
• TXA and calcium. TXA 1 g IV, repeat once at 30 min; calcium chloride 1 g per 2-4 units or to ionized Ca >1.1; citrate load plus magnesium worsens hypocalcemia and atony.
• Crystalloid. stop at 2 L; inflamed asthmatic lungs plus magnesium and low oncotic pressure invite pulmonary edema; volume comes as products.
• Pressor. escalate epinephrine (it is treating both problems) and add vasopressin 1-2 U bolus or 0.04 U/min for vasoplegia; norepinephrine acceptable. Pressors are a bridge to hemostasis, not a substitute.

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• Extubate. not yet: T 35.4, lactate 2.8, residual wheeze, and a 2.5 L hemorrhage; warm, confirm hemostasis and reversal (TOF), repeat gas; then extubate awake in the OR or ICU. Immediate extubation to prove a point is the flag; so is reflex overnight ventilation in a patient who meets criteria an hour later.
• Awake vs deep. awake with full reversal and a suctioned airway; deep avoids coughing but leaves a full-stomach parturient unprotected; lidocaine IV 1 mg/kg and albuterol before emergence reduce the cough-bronchospasm risk.
• Drawn up. albuterol MDI, epinephrine 10 mcg/mL, ketamine, propofol; a plan to reintubate stated.
• Neuraxial morphine. epidural morphine 2-3 mg before the catheter comes out; respiratory monitoring (continuous SpO2, capnography) 24 h; she is an asthmatic with a fresh flare, so monitoring is not optional.
• Scheduled and out. acetaminophen 1 g q6h, neuraxial morphine, TAP blocks if the neuraxial dose was not given; NO ketorolac or any NSAID (AERD); ketamine infusion 0.1-0.2 mg/kg/h reasonable.
• PCA. demand-only hydromorphone after neuraxial morphine; no basal.
• Disposition and steroid. ICU or high-acuity step-down with continuous SpO2 and scheduled nebs; hydrocortisone 50 mg q8h for 24 h, then her prednisone 20 mg or a flare burst (40-60 mg) per pulmonology.

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• Worried. yes: crackles, oxygen requirement, and tachypnea five days after a VOC is early acute chest syndrome until proven otherwise; also atelectasis, volume overload, pneumonia, PE, peripartum cardiomyopathy.
• Workup. CXR, CBC with retic, type and screen with antibody history, ABG if she worsens, lactate, blood cultures if febrile; hematology called now, not at the cesarean.
• Working Dx. atelectasis with a mild oxygen requirement, but acute chest evolves over hours and the CXR lags; repeat exam, SpO2, and RR every 1-2 h with a low threshold to re-image.
• Fluids. isotonic crystalloid at about 1-1.5x maintenance (100 mL/h) to euvolemia; hypovolemia sickles, but she has crackles and sickle cardiomyopathy is common: no liberal boluses.
• Oxygen and temperature. SpO2 at or above 95%, never tolerate desaturation; normothermia 36.5-37.5 with warmed fluids and a warm room; hypothermia and shivering trigger sickling.
• Labs. Hgb below her baseline with retic 18% and LDH 920 is active hemolysis, not just dilution; reserve is thin and any further loss is poorly tolerated. Not yet a transfusion trigger by number alone.

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• Early epidural. yes: labor pain and catecholamines drive sickling; the epidural lowers oxygen demand, supports rest and hydration, and gives a cesarean option without GA.
• LA and opioid. bupivacaine or ropivacaine 0.0625-0.1% with fentanyl 2 mcg/mL; fentanyl is standard and still adds analgesia in a tolerant patient; hydromorphone is an alternative; opioid-free epidural is defensible but wastes a lever.
• Home oxycodone. continue it: the epidural covers labor, not her AVN pain or her baseline requirement; stopping it invites withdrawal and uncontrolled pain, both crisis triggers.
• Epinephrine test dose. reasonable; no sickle-specific contraindication; baseline HR 102 confounds the read, so watch BP too or dose incrementally.
• Hip and back pain with a good T10 block. not epidural failure: AVN and chronic back pain, an evolving VOC, or bone pain from the labor stress; missed segments if the pattern is dermatomal. Treat systemically; do not redose the epidural for pain the block does not cover.
• Hydromorphone. expect 2-3x naive requirements; 0.5-1 mg IV titrated with SpO2 and RR monitored; hydromorphone PCA (her recent regimen) is reasonable alongside the epidural. Undertreating pain in SCD is the error, not overtreating.

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• Transfuse now. not by the number: Hgb 7.6 near her baseline with no symptoms of anemia; simple transfusion for Hgb below about 7 or a fall of more than 2 g from baseline, symptoms, or evolving acute chest. Prophylactic transfusion in pregnancy is program-dependent; either answer with the reasoning.
• Simple vs exchange. simple for anemia; exchange for severe acute chest, stroke, multiorgan failure, or when raising Hgb without raising viscosity matters (target HbS below 30%, Hgb not above 10). A simple transfusion to Hgb 11-12 raises viscosity and can precipitate crisis.
• Order. 2 units sickle-negative, leukoreduced, antigen-matched for C, E, and Kell at minimum (and antigen-negative for her alloantibodies); crossmatch takes hours with alloantibodies, so order now.
• Emergency. if exsanguinating, uncrossmatched or incompletely matched blood is given and the hemolytic risk accepted; the point is to have matched units ready so that choice is never forced.
• Cell saver. salvaged cells sickle and hemolyze under processing and may be reinfused as sickled cells; most centers avoid it in SS disease or use it only with hematology agreement. Antigen-matched allogeneic blood is the plan.

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• Modality. extend the epidural; GA adds atelectasis, hypoventilation, and postoperative pulmonary complications in a patient already at risk of acute chest. GA only for a failed block or maternal collapse.
• Pressor. norepinephrine or phenylephrine infusion titrated to baseline; ephedrine acceptable for bradycardia; the sickle-specific point is no tolerance of hypotension: hypoperfusion and stasis sickle. SBP within 10-20% of baseline (about 100).
• Uterotonics. oxytocin as an infusion or slow small bolus; a 10 U push drops SVR. Carboprost is not contraindicated by SCD, but with evolving pulmonary findings it raises pulmonary artery pressure and bronchospasm risk; methergine (no HTN) and misoprostol first.
• FiO2 and temperature. supplemental oxygen to SpO2 at or above 95% throughout; warm room, forced air, warmed fluids; a cold OR is a crisis trigger.
• Postop analgesia. neuraxial morphine 100-150 mcg intrathecal or 2-3 mg epidural if the catheter is used, plus TAP blocks as adjunct; multimodal; expect high opioid needs on top.

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• Top-up. lidocaine 2% with bicarbonate and epinephrine 15-20 mL in 5 mL increments to T4-T6.
• BP 88/50 with SpO2 90%. sympathectomy from the rapid extension in a patient with thin reserve; the hypoxemia is the lungs (evolving acute chest, atelectasis) unmasked by the drop in perfusion, or a high block. Check level and hands.
• Rx. LUD, norepinephrine or phenylephrine to SBP near 110 promptly (hypotension sickles), oxygen by non-rebreather, sit head up, modest fluid; recheck level.
• Continue or GA. continue: the block is at T6 and pressure is controlled; SpO2 91% on NRB with a stat fetus is not yet an indication to intubate; state the trigger for GA (SpO2 falling below about 90 on NRB, rising work of breathing, obtundation) and have the airway ready.

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• Working Dx. acute chest syndrome: new hypoxemia, fever, tachypnea, and diffuse crackles in a sickle patient in labor. Also pneumonia, aspiration, pulmonary edema, PE, AFE, transfusion reaction if products have run.
• First move. FiO2 to 1.0 (NRB is already maximal; add high-flow nasal or CPAP if available), sit head up, tell OB the maternal status, call for help and the ICU.
• Intubate or deliver. deliver under the block: the fetus is bradycardic and delivery relieves the maternal load in minutes; intubation of a hypoxemic SCD patient under time pressure adds risk. Intubate if she cannot maintain SpO2 above about 88-90 on maximal oxygen, obtunds, or tires. Either is defensible with a stated trigger.
• Antibiotics. third-generation cephalosporin plus a macrolide (ceftriaxone 1-2 g and azithromycin 500 mg) for typical and atypical organisms; cefazolin surgical prophylaxis is not coverage for acute chest.
• Blood bank and hematology. release the antigen-matched units now; exchange transfusion is the treatment for severe acute chest but is not done in the OR: ask hematology to set up exchange in the ICU immediately after delivery, and give simple transfusion of 1-2 matched units in the OR as a bridge if Hgb falls.
• Albuterol. yes; bronchospasm accompanies acute chest in a substantial fraction and albuterol is low-cost; not a substitute for oxygen, transfusion, and antibiotics.

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• Intubate. yes: SpO2 86% on maximal oxygen with rising work of breathing after delivery is respiratory failure; the delivery did not rescue her. Waiting for arrest is the error.
• Induction. ketamine 0.5-1 mg/kg or etomidate 0.2 mg/kg for a hypotensive hypoxemic patient (propofol only at a reduced dose); sux 1.5 mg/kg or roc 1.2 mg/kg; norepinephrine running; preoxygenation is already maximal, so expect rapid desaturation.
• Uterotonics. oxytocin 3 U slow bolus then infusion; methergine 0.2 mg IM (no HTN); misoprostol; carboprost no: acute chest with hypoxemia is pulmonary vascular disease in the moment and carboprost raises PA pressure and bronchospasm.
• Volume and pressor. matched blood as the volume: Hgb was 7.6 before bleeding began; 1-2 units now, crystalloid modestly, norepinephrine to SBP 100; do not let her sit hypotensive while waiting for products.
• Awareness. she was conscious moments ago; midazolam 2 mg, volatile at 0.5 MAC or propofol infusion once BP allows, fentanyl; processed EEG if available; document.
• Ketamine. helps: hemodynamic support, bronchodilation, and analgesia in an opioid-tolerant patient; 0.5 mg/kg then 0.2 mg/kg/h. The pulmonary vasoconstriction concern is small at these doses.

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• Neuraxial morphine or infusion. epidural morphine 2-3 mg is reasonable even intubated (respiratory depression is monitored); keeping the catheter with bupivacaine 0.1% plus fentanyl for 24-48 h is the better answer for a patient who will need high-dose systemic opioid anyway: it spares opioid and ventilation. Remove with attention to anticoagulation timing.
• Home oxycodone. restart via the OG tube as soon as she can take enteral medication, or sooner as scheduled IV hydromorphone; her baseline 40 mg/day oxycodone must be replaced, not paused.
• Hydromorphone. 0.4-1 mg IV boluses, 2-3x naive requirements; scheduled or PCA once awake; continuous SpO2 and capnography. Undertreatment is a crisis trigger.
• Ketamine. continue 0.1-0.2 mg/kg/h; reduces opioid need and hyperalgesia in SCD crisis pain.
• Ketorolac. no for now: fresh hemorrhage, possible renal injury from hypoperfusion and sickle nephropathy; revisit when stable. NSAIDs are otherwise a mainstay of SCD pain.
• Acetaminophen. 1 g IV q6h.

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• Extubate. yes if she passes a spontaneous breathing trial, cuff leak present, secretions manageable, hemostasis confirmed, and the exchange has done its work; a repeat CXR and gas first. Conservative bias is fine, but keeping a patient who meets criteria intubated for another day adds pneumonia and deconditioning.
• Chest pain after extubation. no: in SCD, chest pain plus a new oxygen requirement is acute chest recurrence, PE, atelectasis, or splinting; repeat CXR, gas, incentive spirometry, oxygen, and analgesia; the patient's label of usual pain does not close the differential.
• Next. incentive spirometry every hour awake (prevents acute chest), oxygen, treat pain fully, hematology for a second exchange if worsening; ICU stay until off oxygen and pain controlled.
• What you tell her. a plain account: her lungs failed during the cesarean, she needed a breathing tube and an exchange transfusion, the baby's status, and what to expect next; answer questions; document; note for future anesthetics that acute chest followed delivery.

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• PMA. 27 + 20 = 47 weeks; under 60 weeks PMA is the postoperative apnea window, and under 50 weeks is the highest-risk group. The resident should compute it, not guess.
• Proceed or postpone. clear rhinorrhea without fever, feeding well, and a hernia that keeps incarcerating: proceed with heightened vigilance is the stronger answer; purulent secretions, fever, or lower-airway signs beyond his baseline wheeze would delay. Reflexive cancellation or reflexive proceeding are both flags; weigh reactivity against incarceration risk.
• Technique. spinal without sedation reduces early postoperative apnea and avoids instrumenting BPD lungs; general with a secured airway gives control if the block fails or the case runs long. Commit to a technique tied to his PMA and lungs.
• Spinal dose. hyperbaric bupivacaine 0.5% about 1 mg/kg (4.5-5 mg, roughly 1 mL) or tetracaine 0.5-1 mg/kg; duration 60-90 min, so the surgeon must be fast. Do not lift the legs after the block (for the cautery pad): a high spinal in an infant shows as apnea, bradycardia, and a limp pale baby, not a complaint.
• Apnea benefit. requires no sedation at all: a swaddled calm infant, a pacifier with sucrose, a warm room; the moment midazolam or ketamine is added, the apnea advantage disappears.
• Block failing at 20 min. sedation converts him to a sedated infant with an unprotected airway and no apnea benefit; dexmedetomidine has the least respiratory effect if the surgeon is minutes from done; a general with a secured airway is the cleaner answer when the block will not last the case. Commit and defend.
• Bronchospasm on mask induction. 100% O2, deepen the sevoflurane, gentle two-handed hand ventilation with long expiration, oral airway; albuterol into the mask; exclude laryngospasm, obstruction, and breath-stacking; a relaxant before deepening is worth a probe. Secure the airway once ventilation is adequate.

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• Airway device. an ETT gives control of pressures and PEEP in BPD lungs with reactive bronchospasm just treated; an LMA reduces stimulation but a short, wheezing, ex-premie under positive pressure argues for the tube. Either with reasoning; a size 3.0-3.5 cuffed (microcuff) or 3.5 uncuffed, leak at 20-25 cm H2O.
• Ventilation. pressure-limited ventilation, PIP as low as gives 6-8 mL/kg (30-35 mL), rate 25-30, PEEP 5, long expiratory time; ETCO2 in the 45-55 range is acceptable (BPD infants live with hypercapnia). Ventilating to a normal CO2 at high pressures is the wrong direction; a rising pressure prompts a search, not more pressure.
• Oxygen. SpO2 91-95%, FiO2 titrated to it, not 1.0; hyperoxia adds oxidative injury in a lung and retina that have already paid for it. Running 100% to be safe should be challenged.
• Fluids. 4 mL/kg/h = about 19 mL/h; a balanced isotonic solution with dextrose 1-2.5% for an ex-premie with limited glycogen; watch the total volume.
• Glucose. check at induction and hourly; 52 in an infant under anesthesia is treated: D10 2 mL/kg (about 10 mL) then a dextrose-containing maintenance; recheck in 30 min. Ignoring glucose is a common miss.
• Temperature. target 36.5-37.5; forced-air warming, room warmed before arrival, warmed fluids, cover the head, measure continuously; his surface-area-to-mass ratio loses heat in minutes.

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• DDx. bronchospasm, mainstem migration (a 1 cm move does it in this trachea), tube kink or plug, secretions, breath-stacking, pneumothorax, circuit problem, light anesthesia.
• First move. hand-ventilate to feel compliance, 100% O2, check tube depth and bilateral sounds, then treat the cause.
• Deepen. sevoflurane up, or propofol 1 mg/kg (5 mg); ketamine 1 mg/kg bronchodilates and holds pressure.
• Albuterol. 8-10 puffs by MDI into the circuit via an adapter, most is lost in the tubing and tube; a single ward-style puff does nothing here.
• HR 90 at SpO2 78. hypoxic bradycardia in an infant: oxygenate and ventilate first; epinephrine 1-10 mcg/kg IV (5-50 mcg) for persistent bradycardia with poor perfusion; atropine does not fix hypoxia.
• HR 55. chest compressions with ventilation when HR stays below 60 with poor perfusion despite oxygenation; epinephrine 10 mcg/kg (50 mcg) IV; the arrest algorithm, not a rhythm chase.
• Still tight. persistence despite deepening and bronchodilator raises tube malposition, plugging, or pneumothorax: pass a suction catheter, reconfirm depth, auscultate and ultrasound the chest, consider tube exchange; epinephrine infusion or IV magnesium 25-50 mg/kg for refractory bronchospasm.

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• Regional vs opioid. a caudal (or ultrasound ilioinguinal block) gives somatic analgesia and spares opioid in an apnea-prone infant; systemic opioid adds apnea and respiratory-depression risk. The opioid cost drives the reasoning.
• Caudal dose. bupivacaine 0.125-0.2% (or ropivacaine 0.2%) at 1 mL/kg = about 5 mL to reach T12-L1; 5 mL of 0.2% = 10 mg. Maximum bupivacaine about 2-2.5 mg/kg = 9-12 mg; the caudal alone is at the ceiling.
• Test dose and intravascular. epinephrine 0.5 mcg/kg (2.5 mcg) in the first 0.1 mL/kg, incremental injection with aspiration; HR rise of 10 or more, T-wave peaking, or BP rise within 60 s means intravascular; injecting the full dose in one pass is a flag.
• Surgeon's infiltration. 5 mL of 0.25% = 12.5 mg on top of 10 mg = 22.5 mg, about 4.8 mg/kg: no. Offer 0.125% or a smaller volume, or reduce the caudal; not counting the surgeon's local is a real miss.
• HR 185 at incision. inadequate block or light anesthesia; deepen first, then supplement with acetaminophen 15 mg/kg IV or PR; fentanyl 0.5-1 mcg/kg (2.5-5 mcg) titrated if needed, accepting that it raises the postoperative apnea risk and mandates monitored observation. A blind 2 mcg/kg is the trap.

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• Deep vs awake. awake with returned reflexes protects a reactive, refluxing airway but coughing can trigger spasm; deep reduces stimulation but leaves an ex-premie with GER unprotected. Either is defensible with stated prerequisites; awake is the more common answer here.
• Before extubation. full reversal (sugammadex or TOF confirmed), regular spontaneous breathing with adequate tidal volumes, eyes open or purposeful movement, suctioned pharynx, warm, glucose known.
• Dx and maneuvers. laryngospasm: remove the stimulus, 100% O2, jaw thrust with CPAP (Larson's), suction; propofol 0.5-1 mg/kg if the IV works.
• HR 80 at SpO2 68. break the spasm now: succinylcholine 1-2 mg/kg IV (5-10 mg) with the IV; without it, 4 mg/kg IM (about 19 mg) or intraosseous; atropine 0.02 mg/kg (0.1 mg) IM with it. Delaying paralysis while he slows is the error.
• Pink froth. negative-pressure pulmonary edema from forceful inspiration against a closed glottis; oxygen and CPAP by mask, usually self-limited over hours; diuretics are not the main treatment.
• Reintubate. not if he oxygenates on CPAP with improving work of breathing; reintubate for persistent SpO2 below about 88 on CPAP, rising CO2, or exhaustion. Either with a trigger stated.

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• Concern and why him. yes: PMA 47 weeks, a general anesthetic, fentanyl, anemia, and BPD all raise postoperative apnea risk; apnea with desaturation in the first hour predicts more.
• Central vs obstructive. central: no chest wall effort; obstructive: effort without airflow, paradoxical chest and abdomen; mixed is the common pattern. The distinction guides airway positioning and CPAP vs respiratory drive (caffeine).
• Workup. glucose, temperature, Hgb, SpO2 trend, residual anesthetic and opioid effect, sepsis if anything else fits; treat the correctable before calling it apnea of prematurity.
• Caffeine. caffeine citrate 20 mg/kg IV load (about 94 mg); maintenance 5 mg/kg/day is reasonable while spells continue; a guessed dose is a flag.
• Spinal alone. reduces early apnea but not late apnea; he would still be admitted and monitored. Claiming a spinal makes monitoring unnecessary is wrong.
• Duration. continuous cardiorespiratory and SpO2 monitoring until at least 12 hours free of events (many programs use 12-24 h); day-surgery discharge is unsafe.

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• Anemia and apnea. anemia is an independent risk factor for postoperative apnea in ex-premies; correcting it can reduce spells, one factor among several.
• Transfuse. a symptomatic anemic ex-premie with recurrent apnea: transfusing is defensible and many would; optimizing caffeine, temperature, and glucose first is also defensible. Tie the decision to his apnea, not a reflex number.
• Threshold. infant and ex-premie thresholds are higher and symptom-driven: commonly Hgb under 10 with symptoms (apnea, poor feeding, tachycardia) or under 7-8 asymptomatic; the adult 7 does not apply.
• Volume and rate. 10-15 mL/kg PRBC (50-70 mL) over 3-4 h; a slow small aliquot, mindful of circulatory overload in BPD.
• Watching for. volume overload (rising RR, crackles, hepatomegaly), hypocalcemia and hyperkalemia with older units, hypoglycemia, temperature drop; reassess spell frequency after.
• If holding. caffeine maintenance, glucose and temperature control, positioning, nasal CPAP for a mixed pattern, continuous monitoring.

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• Now. airway and breathing support, reassess the cause (glucose, temperature, sepsis, aspiration, residual drug), repeat caffeine level or a second dose; a stimulated event with bag-mask marks a high-risk infant.
• Disposition. ICU; a regular floor cannot respond to a bag-mask event and step-down depends on the unit; continuous cardiorespiratory, SpO2, and apnea monitoring with staff able to bag.
• High-flow or CPAP. nasal CPAP 5-6 cm H2O or high-flow 2 L/kg/min (about 8-10 L) splints the airway for mixed or obstructive apnea and unloads BPD lungs; a reasonable step short of reintubation.
• Wheeze. albuterol neb, consider ipratropium; the wheeze raises work of breathing and the apnea picture together.
• pH 7.28, PaCO2 62. a BPD infant's baseline may be 50-55, so read the trend and the work of breathing: escalate CPAP, treat bronchospasm, repeat the gas in 30-60 min; reintubate for a rising CO2 with fatigue, recurrent apnea unresponsive to caffeine and CPAP, or failure to protect gas exchange. A single number does not intubate him.

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• Answer. no; admit and monitor; the recommendation is stated plainly and once, not negotiated.
• What you tell them. the one counseling beat: premature babies can stop breathing for hours after anesthesia, his has done so and needed help, monitors catch it and staff fix it, and it passes; specific, calm, no alarming language.
• Safe to discharge. at least 12 hours (many use 24) apnea-free on room air, off high-flow, feeding normally, caffeine plan settled with pediatrics (it can be continued at home or stopped with a monitored observation period after the last dose).
• Next anesthetic. flag the postoperative apnea and difficult emergence; prefer regional without sedation where possible, plan admission and monitoring for any anesthetic until about 60 weeks PMA (and beyond given this history); treat the BPD and reflux ahead of time.

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• Proceed / baseline. the question is whether he is at his baseline, not whether he is normal: symptom trajectory since the exacerbation, exercise tolerance, sputum, exam against his usual state. Demanding normality from a severe COPD patient, or waving everyone through, both deserve a probe.
• ABG. compensated chronic respiratory acidosis (PaCO2 54, HCO3 31, near-normal pH) with moderate hypoxemia; a retainer with limited reserve. It does not cancel the case; it sets sedation, oxygen, and the cost of any new diaphragmatic insult.
• PFTs. quantify severity but rarely change an elective shoulder decision; want a reason for the test, not a reflex panel. FEV1 well below his prior value would prompt a look for an unresolved exacerbation.
• Wheezes on the day. chronic wheeze at baseline is his normal; new wheeze, more sputum, or a falling saturation argues for treatment or delay. Same as clinic means proceed.
• Preop Rx. usual inhalers that morning plus a nebulized beta-agonist and ipratropium before the block; a fresh steroid burst for a patient at baseline is overtreatment (glucose, healing).
• Another month. postponement only buys something if something will improve: unresolved exacerbation, new infection, reversible bronchospasm. Six weeks out and at baseline, more waiting buys little; a plan built around his fixed limits is the defensible answer.

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• Interscalene yes/no. the standard surgical block for shoulder arthroplasty, and the crux of the case: phrenic (C3-C5) spread at this level produces ipsilateral hemidiaphragmatic paresis in essentially 100% of standard-volume blocks. A flat yes without naming that cost is the flag; a flat no without an alternative is the other.
• Numbers. near 100% paresis at 20 mL; roughly 25-30% loss of vital capacity. In severe COPD with nocturnal oxygen and CO2 retention, that loss may not be tolerable.
• Supraclavicular. phrenic involvement roughly a third to a half at standard volumes, not zero; adds pneumothorax risk in a hyperinflated chest with bullous-prone apices; coverage of the superior shoulder less reliable. Reduces, does not remove, the problem.
• Suprascapular + axillary. phrenic-sparing and good analgesia, but they do not anesthetize the full surgical field (skin over the shoulder cape, deep capsule, glenoid); as the sole anesthetic for an arthroplasty they fail. Claiming they carry the case awake should be challenged.
• 5 mL. low-volume ultrasound-guided injection roughly halves paresis (about 45% in the classic 5 mL vs 20 mL comparison) but is analgesic-grade and risks an inadequate surgical block. A risk modifier, not a fix.
• Committed plan. all three are defensible if the residual risk and rescue path are named: low-volume interscalene with an explicit conversion plan, supraclavicular with pneumothorax vigilance, or conceding that GA with a phrenic-sparing analgesic block is safer than forcing an awake technique on a retainer. What fails is a plan with no named fallback.

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• MAP at the brain. about 0.77 mmHg per cm of vertical height; the external auditory meatus sits 20-25 cm above the heart in a 70-degree chair, so cerebral MAP runs roughly 15-20 mmHg below the arm: MAP 80 at the arm is about 60-65 at the brain. Want the subtraction done out loud.
• Calf cuff. worse; the calf is below the heart, so the reading overestimates cerebral pressure by an even larger margin.
• Target. chronic hypertension right-shifts autoregulation; a normal MAP may be relative hypotension for him. Common framing: stay within 20-30% of his baseline MAP (~117), corrected for the gradient, so arm MAP roughly 85-90 or higher. A target of 65 lifted from the ICU is the trap.
• Arterial line. reasonable: beat-to-beat pressure, hypertension with a wide swing risk, hydrostatic gradient, and a sedation plan that will itself drop pressure. Transducer zeroed at the meatus if used for the cerebral question.
• Cerebral monitoring. under GA there is no direct signal; cerebral oximetry or a tighter pressure target substitutes. Awake, his conversation is the monitor: a real advantage of block-plus-sedation.
• Antihypertensives. hold the ACE inhibitor the morning of surgery (refractory hypotension under anesthesia, in a position that already threatens perfusion); continue the calcium channel blocker. Controlled but not bottomed-out.

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• Agent. dexmedetomidine preserves respiratory drive and arousability and is the reasoned pick, with the caveat that its bradycardia and hypotension compound sitting-position physiology; small ketamine adjunct acceptable. No agent is safe at excessive depth.
• Propofol 50. that rate in an OSA retainer is deep sedation with an unprotected, draped airway; a titrated low-dose infusion is defensible only with the endpoint below kept honest.
• Midazolam + fentanyl. the classic offender combination in OSA; opioids depress the hypercapnic drive he leans on. Opioid-sparing sedation is the point of the block.
• Endpoint. responsive and conversant through the case; that conversation is also the cerebral and airway monitor. Sedation deep enough to obstruct has overshot.
• Oxygen. titrated to SpO2 ~88-92% by nasal cannula; liberal oxygen masks hypoventilation on the oximeter in a retainer.
• Monitoring. capnography under the drapes at minimum; arterial line per A3.
• Obstruction rescue. stop the infusion, verbal and physical stimulation, jaw thrust or nasal airway as access allows, call for drapes down, surgeon pauses, convert to GA if not quickly recoverable. No rehearsed sequence is the flag.
• Still sedation?. rescue difficulty is a genuine argument for GA from the start; light sedation with a rehearsed conversion is the counterargument. Either, if the risk is acknowledged before the drapes go up.

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• Agent / volume. ropivacaine 0.5% is standard; the tension is explicit: 15-20 mL is surgical-grade and near-certain phrenic palsy, 5-8 mL roughly halves paresis but may be non-surgical. Want the resident to own the trade-off chosen in A2 and name the fallback if the block proves inadequate. An unreflective 20-30 mL ignores the preop discussion; an unreflective 5 mL 'surgical' block ignores pharmacology.
• Ceiling. a number in milligrams, on lean or ideal body weight: ropivacaine about 3 mg/kg lean, roughly 200 mg for him, not 3 x 96 = 288. Bupivacaine lower (~2 mg/kg).
• Dexamethasone. perineural 4 mg and IV 8-10 mg both prolong analgesia with a modest perineural edge in meta-analyses; IV avoids off-label perineural use; either if reasoned. Dexmedetomidine also prolongs but adds bradycardia and hypotension, unwelcome in the chair.
• Epinephrine. 2.5-5 mcg/mL as an intravascular marker and to slow uptake; reasonable. Note it can contribute to the vasovagal reflex in the sitting position.
• Injection. the LAST-prevention bundle: needle tip in view, 3-5 mL aliquots, aspirate between each, low injection pressure, stop for any symptom.
• Surgical adequacy. a numb hand is not a numb shoulder. Test sensory loss over the deltoid (axillary), the cape of the shoulder where the incision runs (supraclavicular nerves C3-C4, often needing a superficial cervical plexus supplement), and motor loss of abduction and external rotation. Preserved shrug and abduction at 20 minutes means the block is not surgical; supplement or convert.

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• Dx. prodromal local anesthetic systemic toxicity: tinnitus, metallic taste, agitation are the classic early neurologic signs. Calling it anxiety is the dangerous miss.
• Rx now. stop injecting, call for help and the lipid kit, 100% oxygen, confirm IV, continuous monitoring, benzodiazepine drawn up, ACLS at hand.
• Lipid now. for isolated prodromal symptoms most prepare and watch; any seizure, arrhythmia, or hemodynamic sign triggers it immediately. Aggressive-early or prepared-watchful both fine if the trigger is explicit.
• Lipid dose. 20% lipid: 1.5 mL/kg on lean weight, about 100 mL bolus over 2-3 minutes (ASRA's simplified 100 mL for >70 kg), then 200-250 mL over 15-20 minutes (~0.25 mL/kg/min); repeat bolus for persistent instability; upper limit around 12 mL/kg.
• Seizure. midazolam 2-4 mg (or lorazepam) first; airway and oxygenation; start lipid. Propofol only in small doses with stable hemodynamics; it is not the lipid therapy and depresses the myocardium.
• Arrest drugs. epinephrine in small aliquots (≤1 mcg/kg, ~50-100 mcg) because large doses worsen LAST arrhythmias and blunt lipid efficacy; amiodarone for VT; no lidocaine or other class I agents; no vasopressin; expect prolonged CPR and mobilize ECMO/bypass early.
• Proceed or cancel. genuinely debatable: symptoms resolved, block in, elective case. Proceeding with heightened monitoring is done; cancelling after a systemic toxic event is equally defensible. Want an owned decision with reasons and what the surgeon is told.

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• MAP at the brain. arm MAP ~73 minus 15-20 = mid-50s. Against a baseline MAP near 117, that is a large fractional drop for a chronic hypertensive; marginal at best.
• Rx. vasopressor, modest fluid, lower the chair angle if surgeon allows, lighten sedation; while he is conversant his mentation corroborates. Phenylephrine 50-100 mcg boluses or an infusion; ephedrine 5-10 mg if rate is also soft.
• DDx. vasovagal (Bezold-Jarisch-type) reflex of the sitting position, spreading or high block, oversedation, ischemia, embolic event, anaphylaxis. Abrupt bradycardia with pallor and nausea in a sitting shoulder patient under block points strongly vasovagal.
• Mechanism. venous pooling reduces ventricular filling; sympathetic tone (plus any absorbed epinephrine) drives vigorous contraction of an underfilled ventricle; ventricular mechanoreceptors fire a paradoxical vagal reflex: bradycardia, vasodilation, hypotension. Up to a fifth of sitting shoulder cases under interscalene with sedation.
• Which first. combined bradycardia and hypotension: ephedrine 10 mg addresses both; atropine 0.5 mg for the rate; epinephrine 10-20 mcg for profound or refractory collapse. Any sequenced escalation is fine; fluid alone or waiting is the failure.
• Change for the remainder. vasopressor infusing or at hand, volume topped up, leaner sedation, lower threshold to treat; recurrence is common once the reflex has fired.

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• DDx. hemidiaphragmatic paresis declaring itself, pneumothorax, bronchospasm, oversedation with hypoventilation, aspiration, ischemia or failure. In severe COPD under interscalene, phrenic palsy leads.
• Bedside. auscultation for wheeze and symmetry, sedation depth, capnogram, ultrasound for lung sliding and diaphragm motion: targeted discrimination, not a shotgun.
• Now which. equal breath sounds, no wheeze, sliding present, rising CO2 with shallow fast effort = diaphragmatic paresis with an exhausting accessory-muscle pattern; the anticipated complication.
• Rx. sit more upright if possible, oxygen up with attention to retention, stop sedation contributors, prepare the escalation path. The block will not recede on a useful timescale; NIV is a bridge at best under a head-and-neck field.
• Midazolam. no; sedating an exhausted hypercapnic patient removes the drive keeping him alive and converts compensation into failure.
• Conversion. call for help, surgeon pauses, drapes down for airway access, level or partially recline (laryngoscopy fully sitting without a compelling reason is the flag), preoxygenate as tolerated, induction with hemodynamic care in a preload-reduced patient: etomidate 0.2-0.3 mg/kg or reduced propofol with pressor running, rocuronium 1.2 mg/kg, a cuffed tube rather than a supraglottic in a shoulder case with limited later access and a retainer who will need controlled ventilation.

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• Orders. get ahead of block regression: scheduled acetaminophen, NSAID if renal function and surgeon allow, ice, and a rescue plan timed to the expected overnight recession rather than started after rebound pain.
• Opioid. low-dose short-acting (oxycodone 5 mg or small IV hydromorphone titrated), sedation scoring, continuous oximetry and capnography where available; he combines OSA without CPAP, CO2 retention, and a fresh phrenic hit.
• Disposition. monitored bed: the triad above plus the day's events (LAST prodrome, vasovagal collapse, respiratory failure with conversion). His overnight respiratory risk decides it, not the surgical routine.
• POD 1 discharge. the pathway is for the average patient; anticipate a longer monitored course and tell the surgical team now rather than at dawn.
• His wife. a plain account: early warning signs of local anesthetic toxicity appeared, the injection was stopped, he was treated and monitored, it resolved; what it means for future anesthetics (a documented event, not an allergy). Honest and unhedged without catastrophizing.

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• Spinal yes/no. yes: a documented adequate hold with normal renal function makes neuraxial reasonable. The learner must know the interval rather than react to the word 'apixaban'.
• Interval. 72 hours (ASRA 2018); some guidelines accept 48 hours at standard dosing with normal renal function. Far longer or far shorter needs a justification.
• Reduced clearance. apixaban is ~25% renal; the effect is prolonged with CrCl <30, and the interval lengthens (many extend to 4-5 days) with an anti-Xa level if available.
• Anti-Xa. a calibrated apixaban anti-Xa level can confirm negligible drug; a rising/undetectable result reassures, a measurable level postpones. Not required with a clean 72-hour hold.
• Blocks with residual DOAC. superficial, compressible blocks (adductor canal, IPACK) are acceptable at lower risk; deep, non-compressible blocks (lumbar plexus, paravertebral) carry neuraxial-equivalent bleeding rules; femoral is intermediate and often done with ultrasound. 'Blocks are always fine' deserves a probe.
• Restart. wait until surgical hemostasis is secure and typically 24 hours after a single-shot spinal; with a catheter in place, hold the drug until at least 6 hours after catheter removal (ASRA), or if a dose was given with the catheter in, wait about 5 half-lives (roughly 26-30 hours) before pulling it; her AF stroke risk means it should not be forgotten either.

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• Spinal in moderate AS. acceptable with a controlled dose and vasopressor in hand; the concern is abrupt sympathectomy dropping preload, afterload, and coronary perfusion of a hypertrophied ventricle. Refusing all neuraxial in moderate AS and ignoring the risk are both wrong.
• Rate / rhythm. 60-80, sinus if possible; a stiff hypertrophied LV depends on atrial contribution (up to 30-40% of filling), so AF already costs her preload and any tachycardia shortens diastolic filling and coronary perfusion. Rate control matters.
• Preload. full; hypovolemia in a fixed-output valve is poorly tolerated.
• Dose. a reduced single-shot dose (e.g., hyperbaric bupivacaine 7.5-10 mg rather than 12-15) or a titrated CSE/continuous spinal; a large bolus producing a fast high block is the error.
• Phenylephrine vs ephedrine. phenylephrine: restores afterload and coronary perfusion without tachycardia; ephedrine's chronotropy is unwelcome. Infusion started with the spinal is reasonable.
• Threshold. severe (area <1.0 cm2, mean gradient ≥40, or symptomatic) shifts most toward a carefully controlled GA with invasive monitoring or a slow titrated neuraxial (CSE, continuous spinal); the distinction should change the plan.

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• Sedation. minimal: low-dose dexmedetomidine or small propofol boluses, capnography, no benzodiazepine-opioid stacking; sedatives compound obstruction and blunt arousal. Unmonitored sedation is a flag.
• Opioid-free plan. spinal plus adductor canal and IPACK, periarticular infiltration by the surgeon, scheduled acetaminophen and NSAID/celecoxib; a knee can be nearly opioid-free intraoperatively and well into recovery.
• Airway backup. obesity plus Mallampati III predicts a difficult mask and view: ramped position, preoxygenation with CPAP, video laryngoscope first pass, supraglottic and second-generation rescue ready; a plan made before the spinal, not after it fails.
• CPAP. on in PACU as soon as she is awake enough; continue overnight; residual block and any opioid change her risk, so monitoring continues.
• Disposition. continuous oximetry with capnography at minimum; monitored bed if opioid was needed. OSA plus opioid on an unmonitored floor is the error.

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• Continue tramadol. reasonable: avoids withdrawal and rebound pain; note it implies some opioid tolerance and a serotonergic, seizure-threshold-lowering drug.
• Ondansetron. two issues: both are serotonergic (serotonin syndrome is rare but reported), and 5-HT3 antagonism blunts tramadol's analgesia. Acceptable with awareness; not a reason to skip antiemesis.
• Meperidine. no: serotonergic on top of tramadol (serotonin toxicity), and it adds opioid load in OSA. Warm her, small dexmedetomidine if needed.
• Risk factors. female, non-smoker (assume), prior PONV, likely postoperative opioid: 3-4 Apfel factors, ~60-80% risk. Multimodal prophylaxis with 2-3 agents from different classes, plus regional to cut opioid and avoiding volatile.
• Dexamethasone. 4 mg is effective with a modest, transient glucose rise; acceptable in a controlled diabetic with glucose monitoring; 8 mg and above raise glucose more.
• Scopolamine. avoid in an older patient: anticholinergic delirium, blurred vision, dry mouth.

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• Spinal. hyperbaric bupivacaine 7.5-10 mg, controlled dose for the valve, enough for ninety minutes; isobaric acceptable. An oversized dose producing a fast high sympathectomy is the error.
• Adductor canal vs femoral. adductor canal preserves quadriceps strength for early mobilization and fall prevention while covering the anteromedial knee; femoral is denser but blocks the quadriceps. Adductor canal is the standard TKA answer; commit and defend.
• What you lose. the anterior femoral cutaneous coverage above the knee and some density; supplement with surgeon infiltration.
• IPACK. covers the posterior capsule (genicular branches of the tibial and obturator nerves) that adductor canal misses, without foot drop; reasonable add.
• Volumes / total. adductor canal 15-20 mL of 0.5% (75-100 mg); IPACK 20 mL of 0.25% (50 mg); plus the spinal (~10 mg). Total ~150-160 mg against a ceiling of about 3 mg/kg on ideal weight (~60 kg for an average-height woman), roughly 180-200 mg. Not tallying is a real error.
• Injection. ultrasound with needle tip in view, aspirate, 3-5 mL increments, low pressure, stop for symptoms.

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• Rx. phenylephrine 100-200 mcg boluses then an infusion, legs up, 250-500 mL co-load; treat bradycardia if it persists. Restore afterload first: coronary perfusion of a hypertrophied ventricle depends on diastolic pressure.
• Ephedrine. acceptable for combined bradycardia and hypotension, but its chronotropy shortens diastole; phenylephrine preferred, glycopyrrolate or small ephedrine for rate.
• Refractory. epinephrine 5-10 mcg boluses, escalate to infusion, ECG, consider that the spinal has climbed; TTE if available. Over-aggressive fluid in a stiff ventricle backfires.
• Chest tightness. demand ischemia from hypoperfusion of a hypertrophied LV; fix pressure now, 12-lead, oxygen; this is the failure mode the valve threatened.
• Target. MAP ≥70-75 (near her baseline ~105); she has no reserve, so push early and decisively while avoiding tachycardia and volume overload.

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• Inflation. afterload and BP rise; exsanguination adds a few hundred mL of central volume. Both the afterload and any tachycardia are unwelcome in AS and hypertension; watch for ischemia.
• DDx. tourniquet pain (dull, building after 45-60 minutes, sympathetic rise, through a working block), receding spinal, full bladder, positioning pain.
• Distinguish. check the level: intact sensory block at the knee and a dermatomal level still adequate means tourniquet pain; a falling level means the spinal is receding. Timing and character corroborate.
• Rx. definitive relief is deflation; meanwhile small doses of ketamine (10-20 mg) or dexmedetomidine, cautious given OSA, with capnography; ask the surgeon about tourniquet time; treat pressure with labetalol in small doses if needed (rate-friendly), avoiding a big drop before deflation.
• Deflation. expect a fall in BP from reperfusion, a transient EtCO2 rise, potassium and lactate washout, and a rate rise; have phenylephrine running or in hand, volume topped up, ventilation ready to increase, and the ECG watched. Anticipate rather than react.

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• DDx / most likely. bone cement implantation syndrome (fat/marrow/cement embolism) with cementing and impaction; pulmonary thromboembolism, anaphylaxis, hemorrhage. Timing points to BCIS.
• Rx. 100% oxygen (hypoxemia drives PVR up further and the RV down), vasopressor, fluids as tolerated, tell the surgeon; epinephrine 10-20 mcg boluses or norepinephrine for a failing RV, not phenylephrine alone.
• Difference. the spinal drop was vasodilatory with a normal EtCO2; here EtCO2 falls because pulmonary blood flow has fallen (dead space) and hypoxemia coexists: an obstructive RV problem. Treatment leans on oxygenation and RV support.
• PEA. ACLS with the obstructive cause in mind: epinephrine, high-quality CPR, TEE to see the RV, avoid excessive fluid on a failing RV, consider inhaled pulmonary vasodilator and mechanical support if refractory. Treat the cause, not just the rhythm.

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• Orders. scheduled acetaminophen and an NSAID or celecoxib, the block, limited rescue oxycodone, antiemetics, CPAP, continuous oximetry; tramadol resumed.
• Catheter. extends motor-sparing analgesia and cuts opioid, which helps OSA; against are catheter care, cumulative-dose LAST risk on top of today's ~150 mg, and a restart of apixaban complicated by a catheter. A reasoned weigh-up, not a reflex.
• Infusion math. 8 mL/h of 0.2% = 16 mg/h = ~384 mg/day; within the usual ~28 mg/h ceiling for ropivacaine infusions, but stacked on a large bolus day; know the number.
• Tingling. early LAST until proven otherwise; stop the infusion, oxygen, monitor, lipid at the bedside, benzodiazepine drawn up; dismissing early neurologic symptoms is the danger.
• Lipid. prepared; infuse for any progression (seizure, arrhythmia, hypotension): 100 mL bolus (1.5 mL/kg lean) then 200-250 mL over 15-20 minutes.
• What you tell her. plainly: the numbing medicine may be reaching her bloodstream, the infusion is stopped, she is monitored, treatment is ready, and what symptoms to report; the floor gets the same message.

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• Handoff. a personal bedside check before the OR team leaves: ETT position and breath sounds, perfusion, abdomen and drains, Foley output, line sites, pressor line and rate. While they are there, get the operative findings (stump, contamination, drains), hemodynamic and pressor trajectory, fluids/blood/UOP, airway grade, antibiotic timing.
• Fluid. he has had 4 L and is on a pressor with lactate 4.2; a further bolus only if volume-responsive (POCUS IVC, pulse-pressure variation on the art line, passive leg raise). Reflex liters in a patient headed toward an open abdomen and AKI are the error; so is refusing volume with a collapsing IVC.
• Potassium. central line, 10-20 mEq/h with monitoring; target ≥4.0 given arrhythmia risk on pressors; check Mg.
• Glucose. insulin infusion, target 140-180; hold metformin (AKI, lactate).
• Cultures. two sets before any antibiotic change; confirm intra-op cultures were sent.
• BP 85/48. pause the handoff, look at the patient (bleeding? drains? abdomen?), titrate norepinephrine to MAP ≥65, quick POCUS, repeat Hgb/lactate; do not simply bolus.
• Surgeon's request. agree the exam matters; the timeline is set by perfusion, oxygenation, and analgesia, not the clock. Sedation weaned when he is stable, with a daily SAT; propofol allows a quick exam window if needed.

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• DDx. distributive (uncontrolled sepsis, adrenal insufficiency), hypovolemic (under-resuscitated, occult bleeding, third-spacing), cardiogenic (postoperative MI, septic cardiomyopathy, AF), obstructive (PE, tension pneumothorax, abdominal compartment), sedation.
• First test. POCUS: IVC, LV/RV function, pericardium, lungs; with ECG, Hgb, lactate, ABG, and a look at the drains and abdomen.
• Rx. collapsing IVC with a hyperdynamic LV = volume-responsive distributive shock: 500 mL-1 L crystalloid while titrating norepinephrine to MAP ≥65.
• No response. vasopressin 0.03 U/min once norepinephrine is ~0.25 or rising; hydrocortisone 200 mg/day (50 mg q6h) for ongoing pressor requirement; repeat echo; surgical re-evaluation; second large-bore access.
• Hgb. a 0.5 drop after 5 L of fluid is dilution until proven otherwise; drains, abdomen, and a repeat in two hours decide it. Not a transfusion trigger.
• ACS. bladder pressure >20 with new organ dysfunction (oliguria, rising airway pressures) = abdominal compartment syndrome. Medical first: deepen sedation, neuromuscular blockade, NG decompression, stop further fluid, drain ascites if present, head of bed <20 degrees.
• Decompression. sustained >20 with organ failure worsening despite medical measures, or any pressure >25 with organ failure, is a surgical emergency. The numbers trend the wrong way with a failing kidney and lung; waiting for arrest is the failure. Call now, document, escalate attending-to-attending if refused.

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• P/F. 150: moderate ARDS.
• DDx. ARDS from sepsis, atelectasis, mucus plug or ETT migration, hydrostatic edema after 5+ L, aspiration, TRALI (1 unit within 6 hours), PE, pneumothorax; VAP unlikely under 48 hours.
• Bilateral opacities. ARDS in a septic patient; exclude cardiogenic edema (echo, clinical) and TRALI (timing, transfusion service notified). Recheck ETT depth and suction.
• Vent. PBW for 5'10" male ~73 kg: Vt 6 mL/kg = ~440 mL (4-8 range); plateau ≤30, driving pressure ≤15; PEEP by the ARDSnet table or a decremental trial to best compliance; conservative fluids; 500 mL was ~6.9 mL/kg, and it climbs if compliance falls.
• Permissive hypercapnia. accept pH ≥7.20; 7.22 is fine at 28 breaths rather than raising Vt; bicarbonate or a small rate increase if it drifts lower.
• Refractory P/F 90. prone in 16-hour cycles, adequate paralysis and sedation, recruitment only if a responder, inhaled NO or epoprostenol as a bridge (improves oxygenation, no mortality benefit), fluid removal if tolerated.
• ECMO. EOLIA: P/F <80 for >6 h despite optimized ventilation and prone, P/F <50 for >3 h, or pH <7.25 with pCO2 >=60 for >6 h. At P/F 90 he does not yet meet the P/F threshold; he is close, trending toward it, and early referral/discussion is still right because outcomes worsen with delay. Against: active abdominal sepsis with an open abdomen and anticoagulation, multi-organ failure, age 64; for: reversible cause with source controlled.

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• DDx. pseudo-oliguria (Foley) first; pre-renal (volume, MAP, intra-abdominal pressure); intrinsic (ischemic/septic ATN, AIN from beta-lactams, pigment); post-renal (ureteral injury with sigmoid resection).
• Check first. flush the Foley; then bladder pressure and IVC. Full IVC with a normal bladder pressure excludes the easy reversible causes.
• Now which. intrinsic AKI, septic and ischemic ATN after 20 hours of shock; urine sodium >40, FENa >2%, muddy brown casts.
• Nephrotoxins. hold lisinopril and metformin (already), avoid NSAIDs, no contrast unless needed, dose antibiotics to clearance (pip-tazo dose adjust), avoid vancomycin-pip-tazo combination if MRSA coverage is added.
• Plan. MAP ≥65 (higher, ~70-75, is reasonable in a chronic hypertensive), no further fluid unless responsive, renal dosing, nephrology, daily lytes, watch potassium.
• Hyperkalemia. calcium gluconate 2 g (or chloride 1 g) over 5 minutes for the ECG; insulin 5-10 U with D50 (5 U reasonable in AKI); albuterol 10-20 mg nebulized; bicarbonate 50 mEq given his acidosis; loop diuretic if any UOP; recheck K and glucose at one hour.
• RRT. start now: refractory hyperkalemia after a full shift regimen, anuria, worsening acidosis, and rising creatinine (A, E, and impending O of AEIOU). Another round of shifting buys minutes, not a solution. CRRT because he is on pressors; intermittent HD will drop his pressure. Nephrology and a dialysis catheter now.

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• DDx. the 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 and primary bloodstream infection.
• Most likely. POD 1-2 atelectasis is common, but a new spike with persistent pressors and leukocytosis after feculent peritonitis is an undrained source until proven otherwise.
• Cultures. blood x2 (one from the line), urine, tracheal aspirate, drain fluid; line site inspection; CXR.
• CT. tonight; CT abdomen/pelvis with contrast (renal risk accepted given the stakes, or non-contrast plus ultrasound if creatinine forbids) because the finding changes management now.
• Antibiotics. confirm gut coverage (GNR + anaerobes); escalate pip-tazo to a carbapenem for persistent shock and possible resistant flora after hospital exposure; MRSA coverage (linezolid or vancomycin with renal dosing) if prior colonization or line concern; echinocandin for persistent shock with perforation and TPN/CKD risk factors is reasonable; de-escalate to cultures.
• Collection. source control; antibiotics without it fail. Percutaneous drainage is the answer if reachable; OR if not.
• Tonight vs morning. not a wait-until-morning problem: persistent septic shock plus an identified undrained source is an emergency. Push for IR now, frame it as patient safety, escalate attending-to-attending if refused, and document. 'What did we miss?' not 'what do we add?'

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• DDx. pain, delirium, hypoxia/hypercarbia, ETT discomfort, full bladder, withdrawal (alcohol, nicotine, opioid), hypoglycemia, hypovolemia, evolving sepsis, ischemia.
• Check first. ABG and vent, pain score/grimace, glucose; then tube position, Foley, ECG, abdomen; CAM-ICU after the basics.
• Order. pain first: fentanyl 50-100 mcg bolus and an adequate background; scheduled IV acetaminophen; no NSAIDs in AKI. Agitation in a ventilated postoperative patient is pain or hypoxia until proven otherwise.
• Sedative. dexmedetomidine over propofol for a patient you want to wake and extubate; avoid benzodiazepines for undifferentiated agitation.
• Withdrawal. twelve beers a day with a CIWA of 18 at ~72 hours (propofol masked it) is alcohol withdrawal; seizures and DTs are the risk. Symptom-triggered diazepam 10-20 mg IV or lorazepam 2-4 mg IV by CIWA; phenobarbital if refractory; continue dexmedetomidine as an adjunct, not a substitute.
• Benzos here vs delirium. chronic ethanol upregulates NMDA and downregulates GABA; withdrawal is CNS hyperexcitability, and GABA agonism treats the mechanism. In delirium, benzodiazepines worsen it. Same drug, opposite role; match the pathophysiology.
• Thiamine. 500 mg IV before glucose (Wernicke precipitated by glucose in a deficient patient); magnesium, folate. Haloperidol alone lowers the seizure threshold and treats nothing here.

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• Checklist. cause resolved, P/F >200 on FiO2 ≤40% and PEEP ≤5-8, hemodynamically stable off pressors, mental status adequate, cough and secretions manageable, cuff leak, volume status, a post-extubation plan.
• SBT. PS 5/PEEP 5 or T-piece for 30-120 minutes; pass = RSBI <105, RR <35, SpO2 >90%, no distress or hemodynamic change.
• Cuff leak 40 mL. under 110 mL or 10-12% of Vt predicts post-extubation stridor; with a week of a tube, an open-abdomen fluid course, and a septic patient, laryngeal edema is likely. Extubating on a 40 mL leak without preparation is the flag.
• Steroids. methylprednisolone 20 mg IV q4h x4 starting 12 hours before extubation (or 40 mg once ≥4 hours before); reassess the leak.
• Extubate at 60 mL. borderline; acceptable with the full airway team (video laryngoscope, bougie, smaller ETT, flexible scope, surgical airway plan stated, attending present), or defer another day.
• Stridor. 100% oxygen, sit up, racemic epinephrine 0.5 mL of 2.25% in 3 mL nebulized, dexamethasone 8-10 mg IV, heliox as a bridge; reintubate early rather than late: video laryngoscope first pass, tube a half to full size smaller (7.0), surgical airway ready.
• POD 7. failed once for the same reason; re-attempt only with demonstrated resolution: quantitative leak >110 mL or >12%, a completed steroid course, direct or flexible look at the larynx if equivocal, team present. Same leak, same result.
• Trach. anticipated ventilation >10-14 days or a second failed extubation for the same cause in an otherwise improving patient; earlier trach (7-10 days) reduces sedation and ICU days without a mortality benefit. After a second laryngeal failure, have the conversation, not 'wait and see'.

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• DDx. drivers, not the label: pain, infection (abdomen, UTI, pneumonia, line, CNS), hypoxia/hypercarbia, electrolytes (Na, glucose, Mg, Ca, phos), medications (opioids, benzodiazepines from withdrawal treatment, anticholinergics, steroids), withdrawal (alcohol, nicotine), sleep deprivation, retention, stroke, sepsis-associated encephalopathy, non-convulsive status.
• Check first. vitals, glucose, oxygen, neuro exam for lateralizing signs, bladder scan, pain, medication list; then electrolytes with Mg/phos, infection workup, family for baseline; EEG if no improvement.
• Next. medication reconciliation (opioid dose, any benzodiazepine, anticholinergics), infection screen (cultures, CXR, abdominal exam, line), Mg/phos/Ca, thiamine; nicotine patch.
• Non-pharm. reorient, glasses and hearing aids, day-night cues, family at the bedside, mobilize, sleep, treat pain, remove the central line and Foley if not needed.
• Restraints. last resort, time-limited, documented; soft restraints to protect lines during the workup.
• Pharm. only for danger to self or staff while the driver is addressed: haloperidol 2-5 mg IV for this degree of violence (0.5-1 mg for mild), repeat q15-30 min x2 with QTc and BP checks; olanzapine 5-10 mg IM if no IV; avoid benzodiazepines unless withdrawal has recurred (check CIWA).
• Escalation. haloperidol 2-5 mg; if unsafe after two rounds, dexmedetomidine infusion in a monitored setting (transfer back to ICU); goal calm, not unconscious. Security if active threat.
• QTc 510. stop haloperidol and other QT-prolonging drugs (ondansetron, quinolones), replace K and Mg, switch to dexmedetomidine; QTc >500 is the line. Sedating through delirium without a cause found prolongs it.

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• Daughter. honest and plain: what is better (off pressors, breathing on his own, source drained), what is not (kidneys, brain, repeated infections), that the course is long and the outcome uncertain; no false reassurance, no premature certainty either way. Room for her questions.
• Which is true. nephrology's: dialysis-dependent AKI after septic shock may or may not recover over weeks; a single medical voice is needed before the next meeting, and the ICU team convenes it.
• Palliative care. yes, early, for symptom management and family support; not a signal that treatment stops.
• Tomorrow. nothing withheld; the framing changes the pace of decisions (trach, feeding access, dialysis catheter), not today's care.

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• GA vs alternative. many mediastinal biopsies (anterior Chamberlain, core, or EBUS) go under local with sedation and avoid the collapse risk of GA; reaching for GA without weighing a less-invasive route is worth probing. Here she cannot lie flat, which constrains the awake option and pushes toward the OR plan already staged.
• Spontaneous vs controlled. spontaneous ventilation preserves the transpleural gradient and airway patency and is the conservative default; positive pressure and paralysis can precipitate dynamic collapse. The evidence is softening: with a rigid scope, surgeon, and femoral access standing by, a staged controlled-ventilation technique titrated only after confirming the airway can be maintained is defensible in experienced hands. Early paralysis with no rescue is the red flag.
• Paralyze. not before the airway is secured distal to the lesion and ventilation is proven; loss of tone can close a dynamically compressed airway.
• Agents. inhalational (sevoflurane) or titrated IV (ketamine, low-dose propofol/dexmedetomidine) that keeps her breathing; avoid abolishing drive and tone up front.
• Position. induce semi-sitting; map the symptom-relieving position ahead of time (often lateral or prone) as the rescue.
• Access. SVC compression makes upper-body access unreliable and slow to reach the heart; lower-extremity large-bore and femoral sheaths pre-stage rescue cannulation and resuscitate below the obstruction.
• Desaturation on induction. dynamic airway and vascular compression as spontaneous effort fades: the predicted mechanical event, not simply light anesthesia.

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• DDx. airway compression distal to the ETT tip, SVC/PA/cardiac compression obstructing venous return and output, tension physiology, tamponade from the effusion.
• First maneuver. reposition — lateral, prone, or sitting — to relieve mechanical compression; the immediate move that addresses the mechanism. Chasing pressors alone misses it.
• Rigid bronchoscopy. the surgeon passes the rigid scope past the obstruction to stent the airway distal to the lesion; the planned rescue, which is why it is open in the room.
• No output despite ventilation. the mass is obstructing venous return or the pulmonary artery / heart; ventilation restored but circulation still mechanically obstructed points to CPB.
• Femoral CPB. the reason both femoral sheaths are in; go on bypass for circulatory rescue when repositioning and airway stenting do not restore output.
• End point / waking. resuscitation targets a perfusing rhythm and MAP; if the airway can be maintained by any means, aborting and waking her to breathe spontaneously is a legitimate and sometimes correct choice.

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• Artifact vs real. the scope is compressing the innominate (brachiocephalic) artery; the right radial and right pulse oximeter go flat while the left reads true pressure. Treating this as true hypotension and escalating pressors is the classic trap.
• Tell the surgeon. ask them to release the compression; the right-sided trace is the early-warning monitor for innominate and right cerebral flow.
• Bleeding / priorities. major vascular injury (innominate, SVC, azygos): call for help and blood, activate massive transfusion, confirm large-bore lower-body access, prepare for sternotomy.
• Access for SVC injury. fluid and blood given above an SVC injury pool above the tear; the lower-extremity IVs and femoral sheath let you resuscitate from below, which is why they were placed there.
• Trigger / end point. transfuse to ongoing loss and hemodynamics, not a single number; target a MAP that perfuses while surgical control is achieved; anticipate sternotomy or bypass and resource accordingly.
• Take over ventilation. with the airway still dynamically compressible, keep spontaneous effort if she is oxygenating; take over only if she cannot sustain gas exchange, with the rigid scope ready. Meanwhile products through lower-body access, sternotomy tray and perfusion ready, modest pressure targets until the source is controlled.

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• Why now. persistent hypotension after surgical control: tamponade from the enlarging effusion with RA collapse, RV strain from PA compression, vasoplegia, or ongoing occult bleeding.
• Distinguish. echo for tamponade (RA/RV collapse, respiratory variation) and RV function, response to a fluid challenge, and the surgical field; do not anchor on one cause.
• Drainage. RA collapse with hypotension is tamponade physiology; drain, coordinated with surgery given the open field.
• First. support preload and perfusion (fluid, norepinephrine) while identifying the mechanism, then relieve the tamponade; drainage is definitive if that is the driver.
• Targets. a named MAP (~65-70) and filling target rather than treating the CVP number blindly.
• Transport. marginal airway (the mass and edema) and hemodynamics argue for controlled, intubated transport with 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 and rigid scope present, is defensible. Reflexive extubation is the flag.
• Before extubation. fully reversed, awake, sitting, hemodynamically stable, effusion managed, equipment and surgeon at the bedside.
• Cuff leak. a leak suggests some patency but does not prove the dynamic compression has resolved; its absence is more worrying than its presence is reassuring. Not a green light by itself.
• Exchange catheter. extubate over a catheter so reintubation is guided if she obstructs; the mass has not gone away.
• Post-extubation stridor. residual compression plus laryngeal edema: sit up, 100% oxygen, racemic epinephrine and steroid; keep the exchange catheter until she has been stable for hours and the laryngeal edema is treated (many keep it 1-2 hours minimum, longer with a mass this size); reintubation is hard because the tube must pass the edematous larynx and then the 60% narrowing; rigid bronchoscopy and the surgeon are the staged rescue if the tube will not pass.

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• DDx. tension pneumothorax from a pleural breach during mediastinoscopy, hemothorax, recurrent airway or cardiac compression, atelectasis.
• Most likely / confirm. tension pneumothorax: diminished sounds, tracheal deviation, hypotension; ultrasound (absent lung sliding) at the bedside; do not wait for a portable film in an unstable patient.
• Act before imaging. yes: immediate needle decompression (2nd intercostal space midclavicular or 4th-5th anterior axillary) then a chest tube on the right.
• Injury. pleural entry during the mediastinoscopy; keep tracheobronchial and vascular injury in mind if it does not resolve.
• End point. restored oxygenation, re-expanded lung on the tube, stable hemodynamics; ongoing air leak or bleeding escalates to the surgeon.

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• DDx. recurrent laryngeal nerve injury (the left nerve is at risk during mediastinoscopy), laryngeal edema, residual mass compression, aspiration.
• Most threatening. bilateral cord dysfunction can close the airway; unilateral RLN injury is usually tolerated at rest but brings a weak cough and aspiration risk. Edema on top of either can tip her.
• Evaluate. direct or flexible fiberoptic laryngoscopy and ENT.
• Disposition. monitored bed or ICU: she desaturates with effort and aspirates with sips; watch for fatigue.
• Secure now. rising stridor at rest, progressive desaturation, aspiration, or fatigue — secure the airway before it closes rather than after.

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• Tonight. starting is reasonable given her symptomatic compression: steroids shrink lymphoma fast and relieve airway and SVC compression; the price is tumor lysis, so start with monitoring in place. Tissue came first because steroids before biopsy can obscure the diagnosis.
• Tumor lysis labs. potassium, uric acid, phosphate, calcium, creatinine, LDH every 4-6 hours for the first 24-48 hours; the elevated uric acid and LDH plus a bulky mass flag high risk.
• Fluids. aggressive IV hydration, 2-3 L/m2/day (about 150-200 mL/h in her) targeting UOP >100 mL/h, watching the effusion and RV; no potassium in the fluids.
• Rasburicase vs allopurinol. rasburicase (0.15-0.2 mg/kg, or a single 3-6 mg dose) for high-risk or established TLS with uric acid already up; allopurinol only prevents new urate formation and is for lower risk. Check G6PD if time allows.
• Disposition. ICU for airway and metabolic risk; arterial line and large-bore access stay.
• 0400 labs. hyperkalemia: calcium only if ECG changes or symptomatic, because the calcium-phosphate product is already high and calcium precipitates; insulin/dextrose, albuterol, binders; phosphate binder (sevelamer) and hydration for the phosphate; asymptomatic hypocalcemia is not treated.
• Dialysis. K refractory to medical therapy, rising creatinine or oliguria, phosphate that will not fall, symptomatic hypocalcemia, volume overload; nephrology called early, CRRT if hemodynamics are marginal.

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• Paralyze. only if the tube tip sits distal to the compressed segment and ventilation is proven through it; with a 60% narrowing to the carina a standard tube may sit above the lesion, in which case loss of tone can close the airway distal to the tube. Deepen sedation and keep spontaneous effort if the tip is proximal; rigid bronchoscope at the bedside.
• Tube tip. as far as it will safely go, ideally beyond the narrowest segment, near the carina; confirm by flexible bronchoscopy through the tube, not by depth marking or CXR alone.
• Her mother. the one counseling beat: plain and honest, no blame; tissue was needed before treatment could start, the collapse was a known risk that was planned for with the rigid scope and bypass ready, she was supported through it, and treatment is now under way; room for her questions.

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• DLT vs blocker. left DLT is the expected commit: the bronchial cuff stays clear of the RUL takeoff and the operative bronchus, and the operative lung can be suctioned and given CPAP. A blocker is defensible only with a reason (difficult airway). A right DLT for a right upper lobectomy is a flag.
• Induction. etomidate 0.2-0.3 mg/kg or propofol titrated in 30-50 mg increments with fentanyl 1-2 mcg/kg; rocuronium 0.6-1 mg/kg. Phenylephrine or norepinephrine drawn up before the drug goes in.
• Targets. HR 60-80, MAP within ~20% of baseline (roughly 80-95). Tachycardia and hypotension both threaten the RCA stent territory and RV coronary perfusion. Not naming the RV is a flag.
• Confirm. fiberoptic through the tracheal lumen: bronchial cuff just below the carina in the left main; then through the bronchial lumen to see the LUL/LLL split. Auscultation alone is worth challenging.
• Peak 38, BP 88/50. DDx: breath-stacking/auto-PEEP, tube malposition (bronchial lumen too deep or herniated cuff), tension pneumothorax, RV strain. First move is a disconnect to let him exhale — reaching for pressor or fluid first is the trap.
• BP recovers on disconnect. dynamic hyperinflation was impeding venous return; that is the diagnosis.
• Settings. TV 4-6 mL/kg PBW (~300-400 mL), rate 10-12, I:E 1:3-1:4, PEEP 0-5 (measure intrinsic PEEP before adding extrinsic), accept PaCO2 in the 50s-60s. PEEP 10 in severe COPD without a word about auto-PEEP is a flag.

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• DDx. tube migration/malposition, secretions or plug, shunt through the nonventilated right lung, dependent-lung atelectasis or derecruitment, bronchospasm, low cardiac output.
• Most likely / first move. malposition on a fresh OLV desaturation; FiO2 is already 1.0, so scope first. Escalating to CPAP/PEEP before looking is worth probing.
• Tube confirmed fine. now it is shunt through the up lung plus dependent-lung derecruitment. CPAP 5 cm H2O to the nondependent lung attacks the shunt directly; a dependent-lung recruitment (30 cm H2O for 20-30 s) then PEEP 5 attacks atelectasis. Either is defensible with a number. In severe COPD, PEEP without checking intrinsic PEEP is the flag.
• Still 88%. add the other maneuver; check cardiac output and hemoglobin; consider a brief two-lung reinflation.
• Surgeon conflict. intermittent two-lung ventilation or a brief reinflation coordinated with the surgeon; ask for early ligation of the RUL pulmonary artery branches if the surgeon can; oxygenation wins over the field.

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• DDx. acute RV failure from rising PVR (hypoxemia, hypercapnia, OLV), surgical compression of heart or great vessels, dynamic hyperinflation, ischemia or arrhythmia, hemorrhage.
• Most likely. decompensation of a chronically pressure-loaded RV (echo: RV dysfunction, PASP 50). Rising CVP with falling BP is the RV signature; the learner should tie it to the stem.
• Pressor. norepinephrine 0.05-0.1 mcg/kg/min or vasopressin 0.03-0.04 U/min to restore RV coronary perfusion pressure; vasopressin has the advantage of little pulmonary vasoconstriction. Phenylephrine raises PVR — leaning on it without saying so is worth challenging.
• CVP still 18. the RV needs contractility, not volume: epinephrine 0.03-0.05 mcg/kg/min or dobutamine 2-5 mcg/kg/min; fix PaCO2 and oxygenation.
• Inhaled vasodilator. iNO 20 ppm or inhaled epoprostenol 50 ng/kg/min through the ventilated lumen; selectively drops PVR without systemic hypotension. Not a substitute for fixing ventilation.
• Retraction. a mechanical cause: ask the surgeon to release retraction and pause; reaching for another drug while the heart is compressed is the flag.

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• DDx. tension pneumothorax of the dependent left lung, DLT migration or obstruction, mucus plug, severe bronchospasm, auto-PEEP.
• Most likely / why him. left tension pneumothorax from the thin-walled LUL bullae in the stem, under positive pressure at high peak pressures. Not connecting it to the CT is a miss.
• Disconnect fails. excludes breath-stacking; move to the scope and to decompression in parallel; call for help; 100% O2, hand-ventilate at low pressure.
• Decompress. the down chest is under the drapes: needle or finger thoracostomy at the left 4th-5th intercostal space anterior axillary line reached from the front, or ask the surgeon to open the mediastinal pleura from the right to vent the left hemithorax. Either is defensible; waiting for a film is the flag.
• Open chest. the operative side cannot tension; the danger is the ventilated lung, so recognition rests on airway pressure and hemodynamics, not the classic exam.
• After needle. a left chest tube now, placed by the surgeon; then reassess whether to finish the lobectomy or close.

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• Extubate or not. early extubation spares a fresh stump and a fresh air leak from positive pressure; marginal reserve, RV disease, and pressor need argue caution. Either is defensible if committed and the preconditions are named.
• Preconditions. reversal confirmed by quantitative TOF, normothermia, PaCO2 near his baseline of 48, stable on minimal pressor, and a working epidural before the tube comes out.
• Epidural. yes, dose before emergence: bupivacaine 0.125% or ropivacaine 0.2% with fentanyl 2 mcg/mL, 5-8 mL then 5-6 mL/h; a dense bolus of 0.5% bupivacaine on a pressor is a flag.
• PaCO2 62 awake. splinting, retained secretions, COPD: bronchodilator, toilet, fix the analgesia, then support. NIV is reasonable here despite the fresh stump and a chest tube in place — low pressures (IPAP 10-12, EPAP 4-5); the stump concern is real but not absolute.
• Reintubation threshold. worsening pH below ~7.25, somnolence, inability to clear secretions, hemodynamic instability. Delaying a clearly failing patient is the flag.

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• DDx. atelectasis, secretions/plugging, pneumothorax or enlarging space, edema, residual block, aspiration, lobar torsion.
• Most likely. secretions and atelectasis in a splinting COPD lung with a chronic productive cough.
• Studies. CXR, ABG; bronchoscopy if plugging suspected.
• LLL collapse. sit him up, bronchodilator, chest physio and incentive spirometry once analgesia works; bedside bronchoscopy for a lobar collapse that does not clear within an hour or so — waiting all night is the flag.
• Unilateral epidural. pull the catheter back 1-2 cm and re-bolus; a poorly working epidural is a remediable cause of the whole picture.

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• Continuous leak. a leak through both inspiration and expiration in a spontaneously breathing patient means a sizable parenchymal leak or a stump problem, not a small alveolar leak.
• Suction. more suction increases flow through the leak and can hold it open; balance expansion against leak; reflexively raising it is the error.
• Worse on -40. return to low suction or water seal, reimage, involve the surgeon; consider a second tube if the space is not draining.
• Support. NIV at low pressure is acceptable; if reintubated, low tidal volume, low PEEP, spontaneous mode as soon as possible; a DLT or blocker to isolate the leaking side if the leak steals minute ventilation.
• Stump. a massive leak, new pneumothorax after a period of expansion, fever, fluid in the airway; bronchoscopy shows the dehiscence.

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

• Why it matters. a fast rhythm loses atrial kick and shortens filling on a strained RV with a fixed coronary supply; demand ischemia and RV decompensation.
• Triggers. K+ to >4, Mg to >2, hypoxemia, pain, hypovolemia, mediastinal irritation; magnesium 2 g IV and potassium replacement come before the antiarrhythmic.
• Rate vs rhythm. he is marginal but perfusing: amiodarone 150 mg over 10 min then 1 mg/min is the usual pick because it rate-controls and may convert with modest hemodynamic cost. Diltiazem is a negative inotrope on a failing RV; esmolol or metoprolol in small doses is defensible in a stable patient but not at 92/56.
• Unstable. synchronized cardioversion 120-200 J biphasic under brief sedation.
• Anticoagulation. not on POD 1 with an air leak and a fresh resection; reconsider if AF persists beyond 48 h.

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• Block. re-site the epidural or place a paravertebral catheter if positioning allows; a poorly covered thoracotomy in a COPD lung is a remediable cause of failure; opioid-only escalation is the wrong direction.
• Multimodal. scheduled acetaminophen 1 g q6h, ketorolac 15 mg q6h if creatinine allows (1.3 — cautious), gabapentinoid optional, low-dose opioid, lidocaine or ketamine infusion.
• Ketamine. yes: 0.1-0.2 mg/kg/h, opioid-sparing without respiratory depression.
• PaCO2 70, somnolent. reintubate; NIV has failed and he can no longer protect his airway or clear secretions. Continuing NIV in an obtunded patient is a flag.
• Wife. a plain account: his lungs were marginal to begin with, the pain control failed and he could not clear his secretions, he needs the breathing machine again and it is expected to be temporary; leave room for questions.