Cardiac
Valvular disease, arrhythmias, ischemic heart disease, CPB, vasoactive drugs, pacemakers, congenital heart disease. ← All topics
Q1. WPW with atrial fibrillation
A patient with Wolff-Parkinson-White presents with atrial fibrillation with rapid ventricular response (HR 220). Which of the following is the most appropriate IV agent?
A. Verapamil, which slows AV nodal conduction and stabilizes ventricular rate
B. Digoxin, which increases vagal tone and controls ventricular response rate
C. Diltiazem, which blocks calcium channels and decreases AV nodal conduction
D. Procainamide, which prolongs the refractory period of the accessory pathway
E. Adenosine, which transiently blocks AV node and terminates reentrant rhythms
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Answer: D. In Wolff-Parkinson-White syndrome with atrial fibrillation, AV nodal blocking agents (verapamil, diltiazem, digoxin, adenosine) are contraindicated because they preferentially block conduction through the AV node while allowing unopposed rapid conduction down the accessory pathway, which can precipitate ventricular fibrillation. Procainamide is the appropriate choice because it prolongs the refractory period of the accessory pathway, preventing rapid ventricular rates. Ibutilide is an alternative agent with similar mechanism. If the patient is hemodynamically unstable, immediate synchronized cardioversion is indicated.
Q2. Protamine catastrophic reaction
Five minutes after weaning from CPB, a patient becomes acutely hypotensive (MAP 38) with pulmonary artery pressures rising from 25/12 to 65/40 immediately after slow protamine administration. The most likely mechanism is:
A. Anaphylactic IgE-mediated mast cell degranulation causing systemic vasodilation and bronchospasm
B. Direct myocardial depression by protamine causing biventricular failure and reduced cardiac output
C. Thromboxane A₂-mediated pulmonary vasoconstriction causing acute right ventricular afterload increase
D. Heparin rebound causing recurrent anticoagulation with bleeding and hypovolemic shock
E. Histamine release from rapid central line administration causing systemic vasodilation and hypotension
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Answer: C. Catastrophic pulmonary hypertension after protamine is mediated by thromboxane A₂ release, which causes severe pulmonary vasoconstriction leading to acute right ventricular failure. The dramatic rise in pulmonary artery pressures (from 25/12 to 65/40) with systemic hypotension is the classic presentation. Risk factors include prior NPH insulin exposure, fish allergy, vasectomy, and prior protamine exposure. Treatment includes pulmonary vasodilators such as PGE₁ infusion and inhaled nitric oxide, along with vasopressors for systemic support. Always administer protamine slowly via a peripheral line to minimize this risk. Type I anaphylactic reactions present differently with bronchospasm and diffuse vasodilation. Direct myocardial depression would not selectively elevate pulmonary pressures. Heparin rebound occurs hours later. Histamine release from rapid administration causes systemic hypotension without isolated pulmonary hypertension.
Q3. Aortic stenosis hemodynamic goals
For a patient with critical aortic stenosis undergoing non-cardiac surgery, ideal hemodynamic management includes:
A. Maintain SVR, avoid tachycardia, maintain sinus rhythm, maintain preload
B. Decrease SVR, allow tachycardia, maintain sinus rhythm, maintain preload
C. Decrease SVR, avoid tachycardia, accept atrial fibrillation, decrease preload
D. Maintain SVR, allow tachycardia, accept atrial fibrillation, decrease preload
E. Decrease SVR, decrease contractility, maintain sinus rhythm, maintain preload
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Answer: A. Severe aortic stenosis hemodynamic management is remembered as "full, slow, tight, and in sinus." Patients require maintained preload (full) because the hypertrophied, non-compliant left ventricle depends heavily on adequate diastolic filling and atrial kick for cardiac output. Tachycardia must be avoided (slow) to preserve diastolic filling time. SVR must be maintained (tight) because coronary perfusion pressure depends on aortic diastolic pressure; decreasing SVR drops coronary perfusion pressure and risks myocardial ischemia in an already hypertrophied ventricle with high oxygen demand. Sinus rhythm must be preserved because loss of atrial kick or development of atrial fibrillation can lead to catastrophic hemodynamic collapse in these patients. The combination of maintained preload, normal to slow heart rate, maintained SVR, and sinus rhythm optimizes forward flow across the stenotic valve while preserving coronary perfusion and ventricular filling.
Q4. Aortic regurgitation hemodynamics
In severe aortic regurgitation, the ideal hemodynamic management is:
A. Bradycardia with increased systemic vascular resistance
B. Tachycardia with decreased systemic vascular resistance
C. Bradycardia with increased preload and contractility
D. Normal heart rate with increased afterload
E. Increased contractility with normal vascular resistance
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Answer: B. The ideal hemodynamic management for severe aortic regurgitation is often remembered as "fast and loose." Tachycardia shortens diastolic time, which reduces the duration available for regurgitant flow back into the left ventricle. Afterload reduction (decreased SVR) reduces the regurgitant fraction by lowering the pressure gradient favoring retrograde flow. Bradycardia should be avoided because it prolongs diastole and worsens regurgitation. High SVR should also be avoided as it increases the regurgitant gradient. Pure alpha-agonists like phenylephrine and vasopressin can worsen hemodynamics by increasing afterload without beneficial chronotropic effects.
Q5. Mitral stenosis hemodynamics
In severe mitral stenosis with new-onset atrial fibrillation, immediate priorities include:
A. Maintain rapid heart rate to optimize cardiac output and diastolic filling time
B. Rate control to allow adequate diastolic filling time across the stenotic valve
C. Vasodilation with nitroprusside to reduce elevated pulmonary vascular pressures acutely
D. Inotropic support with milrinone to augment left ventricular contractile function
E. Liberalize preload with crystalloid boluses to maintain forward cardiac output
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Answer: B. In severe mitral stenosis, rate control is the immediate priority when atrial fibrillation develops. The stenotic mitral valve requires a prolonged diastolic filling period to allow adequate left ventricular filling across the narrowed orifice. New-onset atrial fibrillation causes two problems: loss of atrial kick (which normally contributes significantly to ventricular filling) and tachycardia (which shortens diastole). Together, these can precipitate acute pulmonary edema. If the patient is hemodynamically unstable, prompt cardioversion is indicated. Tachycardia worsens the situation by further reducing diastolic filling time. Pulmonary vasodilators should be avoided as they may unmask right ventricular dysfunction. Hypotension and large volume shifts should also be avoided, as patients with mitral stenosis are preload-dependent but cannot tolerate volume overload due to fixed obstruction to left ventricular inflow.
Q6. HOCM management
A 32-year-old with hypertrophic obstructive cardiomyopathy develops hypotension during induction. Most appropriate vasoactive is:
A. Ephedrine, because mixed alpha and beta agonism restores preload and maintains cardiac output
B. Dobutamine, because beta-1 agonism improves cardiac output and reduces outflow tract gradient
C. Milrinone, because phosphodiesterase inhibition improves contractility and reduces afterload appropriately
D. Phenylephrine, because pure alpha agonism increases SVR and restores preload without worsening obstruction
E. Isoproterenol, because pure beta agonism increases heart rate and improves forward flow
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Answer: D. HOCM behaves like dynamic LVOT obstruction, similar to a more dynamic form of aortic stenosis. The key is to avoid worsening the outflow obstruction. Pure alpha-agonists such as phenylephrine or vasopressin are ideal because they increase systemic vascular resistance (SVR), which restores preload and maintains afterload, without increasing contractility or heart rate. Inotropes and chronotropes (ephedrine, dobutamine, milrinone, isoproterenol) worsen outflow obstruction by increasing contractility, heart rate, or both, which narrows the LVOT further and exacerbates the dynamic obstruction. Phenylephrine's pure alpha-agonism makes it the most appropriate choice for hypotension in HOCM.
Q7. Cardiac tamponade physiology
A patient with cardiac tamponade has:
A. Increased preload with elevated afterload and augmented venous return to both ventricles
B. Equalization of right and left heart filling pressures with pulsus paradoxus and decreased stroke volume
C. Decreased central venous pressure with increased pulmonary capillary wedge pressure and reduced cardiac output
D. Increased systemic vascular resistance with decreased venous return and preserved left ventricular filling
E. High cardiac output state with elevated stroke volume and increased systemic oxygen delivery
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Answer: B. Cardiac tamponade causes equalization of intracardiac pressures, with RA pressure equal to RV diastolic pressure equal to PCWP, typically around 20 mmHg. Pulsus paradoxus (a drop in systolic blood pressure greater than 10 mmHg with inspiration) is a classic finding. Stroke volume and cardiac output are decreased due to impaired ventricular filling. Hemodynamic goals for anesthetic management include maintaining preload (full), heart rate (fast), contractility (tight), and spontaneous ventilation. Induction with ketamine is preferred, and positive pressure ventilation should be avoided until the pericardium is decompressed, as it further reduces venous return and can precipitate cardiovascular collapse.
Q8. Brugada syndrome anesthesia
A 28-year-old with type 1 Brugada pattern undergoes anesthesia. Which agent is best avoided?
A. Propofol bolus for induction of anesthesia
B. Prolonged propofol infusion for maintenance of anesthesia
C. Etomidate bolus for induction of anesthesia
D. Sevoflurane inhalation for maintenance of anesthesia
E. Sugammadex bolus for reversal of neuromuscular blockade
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Answer: B. Brugada syndrome results from sodium channel mutations and presents with pseudo-RBBB pattern plus ST elevations in leads V1–V3, carrying risk of polymorphic ventricular tachycardia and sudden cardiac death. Prolonged propofol infusion should be avoided in these patients as it can precipitate arrhythmias, whereas short propofol boluses for induction are generally considered safe. Other agents to avoid include Class 1C antiarrhythmics, bupivacaine, and tricyclic antidepressants. During anesthesia, a defibrillator should be immediately available. Refractory arrhythmias may be treated with isoproterenol or quinidine. Optimize electrolytes and avoid hyperthermia and hyperkalemia, as these can trigger arrhythmias.
Q9. Pacemaker codes
A pacemaker labeled "DDD" indicates:
A. Single-chamber atrial pacing and sensing with inhibited response to sensed atrial activity
B. Dual-chamber pacing and sensing with both triggered and inhibited response to sensed activity
C. Dual-chamber asynchronous pacing without sensing or response to any underlying cardiac activity
D. Single-chamber ventricular demand pacing with rate modulation based on physiologic sensor input
E. Biventricular pacing with defibrillation capability and single-chamber sensing for cardiac resynchronization therapy
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Answer: B. The NASPE/BPEG generic pacemaker code uses five positions: I=chamber paced, II=chamber sensed, III=response to sensing, IV=rate modulation, V=multisite pacing. In DDD mode, both atria and ventricles are paced (first D), both chambers are sensed (second D), and the response is dual—both inhibited and triggered (third D). This allows physiologic AV sequential pacing. Asynchronous modes such as D00, V00, or A00 are used in pacemaker-dependent patients during electrocautery to prevent electromagnetic interference from inhibiting pacing; applying a magnet over the pacemaker converts it to asynchronous mode temporarily.
Q10. Magnet over ICD
Placing a magnet over a combined pacemaker/ICD will:
A. Convert pacing to asynchronous mode and inhibit antitachycardia therapy
B. Disable pacing function temporarily and suspend all tachyarrhythmia detection
C. Trigger immediate defibrillation and convert pacing to demand mode
D. Erase device programming and require complete interrogation before use
E. Inhibit antitachycardia therapy but preserve the current pacing mode
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Answer: E. Placing a magnet over a combined pacemaker/ICD inhibits antitachycardia therapy (including cardioversion and defibrillation) but does NOT typically change the pacing mode in most modern combined devices. This differs from a stand-alone pacemaker, where magnet application converts pacing to asynchronous (VOO/DOO) mode. The magnet effect is temporary and reversible upon removal. Device behavior can vary by manufacturer and model, so always check the specific device. Best practice for pacemaker-dependent patients undergoing procedures with electrocautery above the umbilicus is to have the device interrogated and reprogrammed beforehand to avoid electromagnetic interference.
Q11. Torsades de pointes treatment
A patient with QTc 540 ms develops polymorphic VT. He is awake and stable. The most appropriate immediate therapy is:
A. Amiodarone 300 mg IV bolus over 10 minutes
B. Lidocaine 1.5 mg/kg IV bolus over 2 minutes
C. Magnesium sulfate 2 g IV bolus over 5 minutes
D. Synchronized cardioversion at 100 joules biphasic energy
E. Calcium chloride 1 g IV bolus over 5 minutes
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Answer: C. Torsades de pointes in a stable patient is treated with magnesium sulfate 1–2 g IV bolus, which can be repeated in 5–15 minutes if the arrhythmia persists. If the patient becomes unstable, immediate unsynchronized defibrillation is required. Drugs that cause or worsen torsades include class IA antiarrhythmics (sodium channel blockers that prolong QT), class III antiarrhythmics (potassium channel blockers that prolong QT), methadone, ondansetron, droperidol, and haloperidol. Correct any underlying hypokalemia and hypomagnesemia. Amiodarone is a class III agent that prolongs the QT interval and could worsen torsades. Lidocaine does not treat torsades effectively. Synchronized cardioversion is inappropriate for polymorphic VT. Calcium chloride has no role in torsades treatment.
Q12. Coronary perfusion pressure
Coronary perfusion pressure for the left ventricle is best estimated by:
A. Mean arterial pressure minus central venous pressure
B. Aortic diastolic pressure minus left ventricular end-diastolic pressure
C. Mean arterial pressure minus intracranial pressure
D. Mean pulmonary artery pressure minus pulmonary capillary wedge pressure
E. Aortic systolic pressure minus right ventricular systolic pressure
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Answer: B. Left ventricular coronary perfusion occurs primarily during diastole because LV intramural pressure exceeds aortic pressure during systole, compressing the coronary vessels. Therefore, coronary perfusion pressure for the left ventricle is best estimated by aortic diastolic pressure minus left ventricular end-diastolic pressure (LVEDP). This relationship is particularly important in clinical scenarios such as critical aortic stenosis or LV dysfunction, where the goal is to maintain coronary perfusion pressure above 50 mmHg. Choice A represents cerebral perfusion pressure, choice C represents a modified cerebral perfusion pressure calculation, choice D represents transpulmonary gradient, and choice E does not represent a physiologically meaningful pressure gradient for coronary perfusion.
Q13. Anesthetic preconditioning
Volatile-induced preconditioning is mediated primarily through:
A. β₁-adrenergic receptor stimulation leading to increased myocardial contractility and oxygen demand
B. Opening of mitochondrial K-ATP channels leading to preservation of mitochondrial function during ischemia
C. NMDA receptor antagonism leading to reduced excitotoxic calcium influx in cardiac myocytes
D. Inhibition of nitric oxide synthase leading to decreased production of reactive nitrogen species
E. Adenosine A₂ receptor blockade leading to reduced inflammatory cytokine release and tissue injury
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Answer: B. Mitochondrial K-ATP channel opening is the primary mechanism underlying volatile-induced preconditioning and cardioprotection. This mechanism limits infarct size if ischemia occurs by preserving mitochondrial function and reducing cellular injury. The protective benefit appears 1–2 hours after volatile anesthetic exposure, then dissipates, and reappears 24 hours later for up to 3 days (the delayed or second window of protection). Clinically, continuous sevoflurane administration throughout cardiac surgery reduces postoperative myocardial infarction compared to administration only before and after bypass or compared to propofol-based anesthesia. The other options represent mechanisms that are not primarily responsible for volatile-induced preconditioning, though some may play minor contributory roles in anesthetic effects on the myocardium.
Q14. DAPT timing for elective surgery
A patient had a drug-eluting stent placed 4 months ago for stable angina. He needs elective hernia repair. The recommended approach is:
A. Continue aspirin and clopidogrel perioperatively, proceed with surgery now
B. Defer surgery until 6 months from stent placement, continue aspirin perioperatively
C. Stop both antiplatelets immediately, bridge perioperatively with unfractionated heparin
D. Stop clopidogrel only, continue aspirin alone, proceed after 5 days
E. Switch clopidogrel to ticagrelor, continue aspirin, proceed after loading dose
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Answer: B. Current ACC guidelines recommend minimum dual antiplatelet therapy (DAPT) duration after drug-eluting stent (DES) placement of 6 months for stable ischemic heart disease, 1 month after bare-metal stent (BMS), and 12 months after acute coronary syndrome (ACS). Elective noncardiac surgery should be deferred until the minimum DAPT duration is complete. Aspirin should be continued perioperatively when possible, as the bleeding risk is generally outweighed by the thrombotic risk. Premature discontinuation of DAPT significantly increases the risk of stent thrombosis, which carries approximately 50% mortality. Heparin bridging does not prevent stent thrombosis and is not recommended. Switching P2Y12 inhibitors or stopping clopidogrel early while continuing aspirin alone does not provide adequate protection during the critical 6-month period after DES placement for stable disease.
Q15. ST elevation lead correspondence
ST elevation in leads II, III, and aVF most likely reflects ischemia in which territory?
A. Anterior left ventricle supplied by the left anterior descending artery
B. Lateral left ventricle supplied by the left circumflex artery
C. Inferior left ventricle and right ventricle supplied by the right coronary artery
D. Posterior left ventricle supplied by the posterior descending artery
E. Interventricular septum supplied by septal branches of the left anterior descending
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Answer: C. Leads II, III, and aVF are the inferior leads and reflect the right coronary artery (RCA) territory in approximately 80% of patients. When inferior ST elevation is present, right-sided leads (particularly V4R) should be checked to evaluate for right ventricular infarction, which occurs in up to 50% of inferior MIs. Right ventricular infarction is preload-dependent, so nitrates and aggressive diuresis should be avoided to maintain adequate preload. The anterior wall (leads V1–V4) corresponds to the left anterior descending artery. The lateral wall (leads I, aVL, V5–V6) corresponds to the left circumflex artery.
Q16. Carotid baroreceptor afferent
Carotid sinus baroreceptors send afferent signals via:
A. Hering's branch of the glossopharyngeal nerve (CN IX) to the nucleus tractus solitarius
B. Recurrent laryngeal branch of the vagus nerve (CN X) to the nucleus ambiguus
C. Vagus nerve (CN X) from the aortic arch to the nucleus tractus solitarius
D. Superior laryngeal branch of the vagus nerve (CN X) to the nucleus ambiguus
E. Hypoglossal nerve (CN XII) descending branch to the cervical sympathetic ganglion
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Answer: A. Carotid sinus baroreceptor afferents travel via Hering's nerve (also called the carotid sinus nerve), which is a branch of the glossopharyngeal nerve (CN IX). These afferents project to the nucleus tractus solitarius (NTS) in the medulla, which then activates the caudal ventrolateral medulla (CVLM). The CVLM inhibits the rostral ventrolateral medulla (RVLM), resulting in decreased sympathetic outflow, and simultaneously activates vagal nuclei to increase parasympathetic outflow. In contrast, aortic arch baroreceptors send afferents via the vagus nerve (CN X). Carotid baroreceptors are most sensitive between mean arterial pressures of 80–160 mmHg; chronic hypertension dulls this baroreceptor response through resetting of the sensitivity curve.
Q17. Pulmonary artery catheter waveforms
The "v wave" on a CVP tracing represents:
A. Atrial contraction during ventricular diastole
B. Tricuspid valve closure during ventricular systole
C. Passive atrial filling against a closed tricuspid valve
D. Ventricular relaxation following tricuspid valve opening
E. Rapid ventricular ejection during early systole
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Answer: C. The v wave on a CVP tracing represents passive atrial filling against a closed tricuspid valve during ventricular systole. The complete CVP waveform consists of: a wave (atrial contraction), c wave (tricuspid valve closure), x descent (atrial relaxation), v wave (atrial filling against closed tricuspid valve), and y descent (tricuspid valve opening). Large v waves are seen in tricuspid regurgitation. Cannon a waves occur with AV dissociation. Absent a waves are characteristic of atrial fibrillation.
Q18. Cardiogenic shock pressors
The 2018 SCAI/AHA expert consensus for cardiogenic shock recommends first-line vasopressor:
A. Dopamine
B. Norepinephrine
C. Phenylephrine
D. Vasopressin
E. Epinephrine
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Answer: B. Norepinephrine is the preferred first-line vasopressor for cardiogenic shock according to the 2018 SCAI/AHA expert consensus statement. It is favored over dopamine due to lower arrhythmia rates and reduced 28-day mortality as demonstrated in the SOAP-II trial. Dopamine, while previously used more commonly, is associated with higher rates of tachyarrhythmias and increased mortality. If additional inotropic support is needed beyond vasopressor therapy, dobutamine or milrinone can be added. For refractory cardiogenic shock that does not respond to pharmacologic management, mechanical circulatory support devices such as intra-aortic balloon pump (IABP), Impella, or veno-arterial extracorporeal membrane oxygenation (VA-ECMO) should be considered.
Q19. Norepinephrine receptor profile
Norepinephrine acts predominantly on:
A. α₁ > β₁, minimal β₂
B. β₁ > α₁, minimal β₂
C. β₂ > β₁, minimal α₁
D. α₂ > α₁, minimal β₁
E. D₁ > D₂, minimal α₁
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Answer: A. Norepinephrine has a receptor profile of α₁ ≥ β₁ >> β₂, producing strong vasoconstriction via α₁ receptors with some positive inotropic effect via β₁ receptors, and minimal β₂-mediated vasodilation. This contrasts with epinephrine, which has more balanced alpha and beta effects (with β₂ activity prominent at lower doses). Pure vasoconstrictors like phenylephrine and vasopressin lack any inotropic effects. The predominant α₁ activity explains norepinephrine's primary use as a vasopressor to increase systemic vascular resistance and blood pressure.
Q20. Adenosine mechanism
Adenosine terminates supraventricular tachycardia by:
A. Activating A₁ receptors to increase potassium outflow at the AV node
B. Blocking L-type calcium channels to decrease conduction through the AV node
C. Antagonizing β₁ receptors to reduce sympathetic tone at the AV node
D. Increasing vagal tone via cranial nerve X to slow AV nodal conduction
E. Antagonizing ryanodine receptors to reduce calcium release from sarcoplasmic reticulum
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Answer: A. Adenosine acts at A₁ receptors on AV nodal cells, which activates IK,ACh channels (potassium channels). The resulting increase in potassium outflow hyperpolarizes the cell membrane and produces transient AV block lasting approximately 10 seconds, terminating the reentrant circuit of supraventricular tachycardia. Important cautions include severe bronchospasm in asthmatic patients and transient asystole. Heart transplant recipients are supersensitive to adenosine due to denervation and upregulation of adenosine receptors, so lower doses should be used. Theophylline and caffeine are methylxanthines that competitively antagonize adenosine receptors and may reduce its effectiveness.
Q21. PVC criteria for treatment
Premature ventricular contractions warrant treatment with IV lidocaine 1–2 mg/kg when:
A. Frequency >6/min, multifocal origin, salvos of ≥3 beats, or R-on-T phenomenon
B. Any single isolated PVC regardless of frequency, morphology, or clinical context
C. Bigeminy pattern alone without other high-risk features or hemodynamic compromise
D. PVCs visible only in lead II without manifestation in other ECG leads
E. Any PVC occurring in a patient currently receiving β-blocker therapy
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Answer: A. Indications for treatment of PVCs with IV lidocaine 1–2 mg/kg include frequent PVCs (>6 per minute), multifocal origin, salvos of 3 or more consecutive beats, or R-on-T phenomenon. R-on-T occurs when a PVC falls on the relative refractory period of the T wave, which can trigger polymorphic ventricular tachycardia. Single isolated PVCs, bigeminy alone without other concerning features, PVCs in only one lead, and PVCs in patients on β-blockers do not by themselves warrant lidocaine treatment. Always search for and treat underlying causes including ischemia, hypoxia, hypokalemia, hypomagnesemia, and mechanical irritation from catheters or other devices.
Q22. Carotid endarterectomy ischemia monitoring
The most reliable intraoperative monitor for cerebral ischemia during awake CEA is:
A. Cerebral oximetry with bilateral frontal lobe near-infrared spectroscopy monitoring
B. Electroencephalography with continuous bilateral hemispheric activity analysis
C. Somatosensory evoked potentials with median nerve stimulation and cortical recording
D. Awake neurologic exam with contralateral hand grip strength and speech testing
E. Transcranial Doppler with middle cerebral artery flow velocity measurement
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Answer: D. Awake neurologic exam during carotid endarterectomy performed under regional anesthesia is the gold standard for detecting cerebral ischemia intraoperatively. It allows direct, real-time assessment of neurologic function including contralateral hand grip strength and speech, which are sensitive indicators of hemispheric perfusion. Under general anesthesia, awake exam is not possible, so clinicians must rely on surrogate monitors including EEG, somatosensory evoked potentials, cerebral oximetry, and transcranial Doppler. While these modalities provide useful information, none matches the directness and clinical relevance of testing actual neurologic function. The GALA trial demonstrated no significant difference in stroke, myocardial infarction, or death rates between general and regional anesthesia techniques for CEA.
Q23. Stellate ganglion location
The stellate ganglion lies:
A. Posterior to the C2 transverse process, superior to the middle cervical ganglion
B. Anterior to the C7/T1 vertebral bodies, just inferior to the C6 transverse process
C. At the level of the cricoid cartilage, lateral to the trachea and thyroid
D. At the T4 paravertebral space, posterior to the sympathetic chain and pleura
E. Within the brachial plexus sheath, between the anterior and middle scalene muscles
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Answer: B. The stellate ganglion is formed by fusion of the inferior cervical and first thoracic sympathetic ganglia. It lies anterolateral to the C7 vertebral body and just inferior to the C6 transverse process. The C6 transverse process (Chassaignac's tubercle) serves as the key anatomic landmark for stellate ganglion block. The block technique involves placing a needle at the C6 tubercle, then withdrawing slightly and redirecting caudally and medially. Horner's syndrome (ptosis, miosis, anhidrosis) is an early sign of successful block, while temperature rise in the ipsilateral upper extremity is the most reliable indicator of sympathetic blockade. Complications include pneumothorax, recurrent laryngeal nerve block, intrathecal injection, and seizure from inadvertent vertebral artery injection.
Q24. Bivalirudin in HIT for CPB
Bivalirudin is preferred over argatroban for cardiopulmonary bypass in HIT because:
A. Bivalirudin undergoes primarily renal clearance with minimal hepatic metabolism
B. Bivalirudin anticoagulation can be reversed effectively with protamine sulfate
C. Bivalirudin has a 25-minute half-life via non-organ-dependent thrombin cleavage
D. Argatroban is absolutely contraindicated in all cardiac surgical procedures
E. Bivalirudin directly reverses and eliminates circulating HIT antibody complexes
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Answer: C. Bivalirudin is preferred over argatroban for cardiopulmonary bypass in HIT because of its short 25-minute half-life achieved through thrombin-mediated proteolytic cleavage, which is non-organ-dependent (with only 20% renal clearance). In contrast, argatroban and hirudin bind thrombin irreversibly and have much longer half-lives, making them less ideal when predictable offset at the end of bypass is needed. Bivalirudin is not reversed by protamine; instead, stagnant circuit portions should be flushed every 15-20 minutes to prevent clotting. The short, predictable half-life allows for more controlled anticoagulation management during cardiac surgery.
Q25. ACT for CPB
The standard activated clotting time goal for safe initiation of cardiopulmonary bypass is:
A. Greater than 200 seconds
B. Greater than 300 seconds
C. Greater than 400 seconds
D. Greater than 600 seconds
E. Greater than 800 seconds
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Answer: C. The standard activated clotting time (ACT) goal for safe initiation of cardiopulmonary bypass is greater than 400 seconds, with some institutions targeting 400–480 seconds for full CPB. Normal baseline ACT is approximately 107 seconds. Heparin is administered as a loading dose of 300–400 units/kg to achieve this target. ACT is preferred over aPTT for monitoring anticoagulation during CPB because it is less affected by hemodilution and hypothermia, and it demonstrates a linear response to heparin concentrations between 1–5 units/mL.
Q26. Alpha-stat vs pH-stat during DHCA
During deep hypothermic circulatory arrest in an adult, the preferred acid-base management is:
A. pH-stat, adding CO₂ to maintain pH 7.4 corrected to the patient's hypothermic core temperature
B. Alpha-stat, managing based on uncorrected ABG values measured at 37°C without temperature correction
C. Either alpha-stat or pH-stat, as both strategies produce equivalent clinical outcomes in adults
D. Hypocapnia-stat, targeting PaCO₂ below 30 mmHg to reduce cerebral metabolic oxygen demand
E. Lactate-stat, adjusting ventilation based on serial lactate measurements to optimize tissue perfusion
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Answer: B. Alpha-stat is the preferred acid-base management strategy for adults undergoing deep hypothermic circulatory arrest. With alpha-stat, blood gas values are measured at 37°C and not corrected for the patient's actual hypothermic temperature. This approach preserves cerebral autoregulation and maintains physiologic intracellular enzyme function. In contrast, pH-stat (adding CO₂ to maintain pH 7.4 when corrected to core temperature) is preferred in pediatric patients because it improves cerebral perfusion during cooling. However, pH-stat causes cerebral vasodilation and increases microembolic load, making it less desirable in adults. As a reference point, PaCO₂ falls approximately 2 mmHg for every 1°C drop in body temperature during hypothermia.
Q27. Post-bypass coagulopathy workup
A patient is bleeding diffusely 30 min after separating from CPB. ACT is 130 (normalized post-protamine), platelets 90, fibrinogen 110, INR 1.9, PTT mildly prolonged, TEG shows decreased MA and prolonged K time. The most targeted intervention is:
A. Additional protamine to reverse residual heparin effect and normalize the ACT further
B. Cryoprecipitate to raise fibrinogen and platelets to correct thrombocytopenia and dysfunction
C. Tranexamic acid to inhibit fibrinolysis and stabilize clot formation at surgical sites
D. Recombinant factor VIIa to bypass intrinsic pathway defects and promote thrombin generation
E. Whole blood to replace all coagulation factors, platelets, and red cells simultaneously
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Answer: B. The TEG findings are key to targeted therapy. MA (maximum amplitude) reflects platelet function and fibrinogen-mediated clot strength, while K time reflects the speed of fibrin cross-linking, which depends heavily on fibrinogen levels. This patient has low fibrinogen (110 mg/dL, normal 200-400) and thrombocytopenia (90,000), with TEG confirming both deficits (decreased MA and prolonged K time). Cryoprecipitate is the most concentrated source of fibrinogen and also contains factor VIII, von Willebrand factor, and factor XIII. Platelets address both the quantitative deficiency and the qualitative platelet dysfunction induced by cardiopulmonary bypass. The ACT is already normalized at 130 seconds, making additional protamine unnecessary. Tranexamic acid treats fibrinolysis, which is not evident here. Factor VIIa is reserved for refractory bleeding after multiple rounds of massive transfusion protocol when conventional factor replacement has failed. Whole blood provides dilute replacement of all components but is less targeted than specific factor and platelet repletion.
Q28. Endocarditis prophylaxis indications
Per AHA, antibiotic prophylaxis for infective endocarditis is indicated in which scenario?
A. Mitral valve prolapse with regurgitation undergoing routine dental cleaning with gingival manipulation
B. Bicuspid aortic valve without prior endocarditis undergoing colonoscopy with mucosal biopsy
C. Prosthetic heart valve undergoing dental procedure with manipulation of gingival tissue
D. Hypertrophic cardiomyopathy without obstruction undergoing transesophageal echocardiography with probe insertion
E. Prior coronary artery bypass grafting undergoing dental extraction with perforation of oral mucosa
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Answer: C. Current AHA guidelines recommend antibiotic prophylaxis for infective endocarditis only in the highest-risk cardiac conditions: prosthetic valve material, prior infective endocarditis, unrepaired cyanotic congenital heart disease, congenital heart disease with residual defect at a prosthetic patch site, completely repaired congenital heart disease within 6 months of repair, or cardiac transplant with structural valve abnormality. Prophylaxis is indicated only for specific procedures: dental procedures involving gingival manipulation or perforation of the oral mucosa, respiratory tract procedures involving incision or biopsy of mucosa, or procedures on infected skin or musculoskeletal tissue. Mitral valve prolapse, bicuspid aortic valve, hypertrophic cardiomyopathy, and prior CABG are not indications for prophylaxis. Colonoscopy and transesophageal echocardiography do not require prophylaxis. The standard regimen is amoxicillin 2 g orally 1 hour before the procedure; vancomycin is used for penicillin allergy or when staphylococcal coverage is needed.
Q29. Revised cardiac risk index
A 72-year-old with diabetes on insulin, prior CVA, and Cr 1.8 is undergoing infrarenal aortic surgery. Per RCRI, his cardiac risk class is:
A. Class I (low risk, 0 points on RCRI, <0.5% cardiac event rate)
B. Class II (1 point on RCRI, 0.5–1% cardiac event rate)
C. Class III (2 points on RCRI, 1.5–4% cardiac event rate)
D. Class IV (3 points on RCRI, ≥6.6% cardiac event rate)
E. Cannot be calculated without echocardiography to assess ventricular function
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Answer: D. The Revised Cardiac Risk Index (RCRI) assigns 1 point each for: (1) ischemic heart disease, (2) heart failure, (3) cerebrovascular disease, (4) insulin-treated diabetes mellitus, (5) creatinine ≥2 mg/dL, and (6) high-risk surgery (suprainguinal vascular, intrathoracic, or intra-abdominal). This patient has cerebrovascular disease (prior CVA), insulin-treated diabetes, and high-risk surgery (infrarenal aortic surgery is suprainguinal vascular), totaling 3 points. Note that the creatinine of 1.8 does not meet the threshold of ≥2.0. Three points corresponds to Class IV with a major adverse cardiac event (MACE) rate of ≥6.6%. With ≥2 RCRI points and poor functional capacity (<4 METs), pharmacologic stress testing is reasonable if it would change management.
Q30. ECMO V-A vs V-V
A patient with severe ARDS who is hemodynamically stable should be considered for which type of ECMO?
A. VA-ECMO with femoral cannulation for combined cardiopulmonary support
B. VV-ECMO for isolated respiratory support without cardiac assistance
C. VAV-ECMO with hybrid configuration for biventricular cardiac support
D. Central VA-ECMO with direct aortic cannulation for cardiac support
E. ECMO is contraindicated in isolated pulmonary failure without shock
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Answer: B. Hemodynamically stable ARDS with refractory hypoxemia is the indication for VV-ECMO, which provides lung support only without cardiac assistance. VA-ECMO is reserved for patients requiring both cardiac and respiratory support, but it requires arterial cannulation and increases left ventricular afterload, which can lead to complications such as Harlequin syndrome (also called north-south syndrome) with peripheral VA-ECMO configurations. VAV-ECMO is a hybrid configuration used in select cases. The EOLIA trial demonstrated mortality benefit of VV-ECMO in severe ARDS by Bayesian post hoc analysis. In hemodynamically stable patients with isolated respiratory failure, VV-ECMO is the appropriate choice because it avoids the cardiac complications associated with arterial cannulation while providing adequate gas exchange support.
Q31. Lead extraction risks
A 60-year-old man requires removal of leads placed 8 years ago. The greatest perioperative risk is:
A. Pneumothorax requiring chest tube placement and delayed extubation
B. Cardiac or great vessel perforation requiring emergent thoracotomy or sternotomy
C. New atrial fibrillation with rapid ventricular response requiring cardioversion
D. Thromboembolic stroke from dislodged vegetation or lead-adherent thrombus
E. Esophageal injury from posterior left ventricular lead extraction attempts
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Answer: B. Lead extraction (versus simple explant within 1 year of placement) carries a 1–2% risk of catastrophic vascular or cardiac perforation, which is the most serious perioperative complication. Risk factors include female sex, BMI less than 25, ICD leads, and oldest lead greater than 5 years in situ. Because of this risk, lead extraction requires meticulous preparation: establish central venous access for potential balloon tamponade, have cardiac surgery on standby in the operating room or immediately available, use transesophageal echocardiography for monitoring, and have blood products in the room. While pneumothorax, new atrial fibrillation, thromboembolic stroke, and esophageal injury can occur, they are less common and generally less immediately life-threatening than cardiac or great vessel perforation.
Q32. Ventricular tachycardia stable
A patient with monomorphic VT and a blood pressure of 110/70 is alert. The most appropriate next step is:
A. Synchronized cardioversion at 100 J biphasic energy level
B. Amiodarone 150 mg IV bolus over 10 minutes
C. Defibrillation at 200 J biphasic energy level
D. Lidocaine 1 mg/kg IV bolus push over 2 minutes
E. Adenosine 6 mg IV rapid push followed by flush
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Answer: B. Stable monomorphic ventricular tachycardia is treated with antiarrhythmic medications rather than immediate cardioversion. First-line options include amiodarone 150 mg IV over 10 minutes, procainamide, or lidocaine 1 to 1.5 mg/kg IV bolus. Amiodarone is preferred in most guidelines. Synchronized cardioversion is reserved for hemodynamically unstable VT (hypotension with poor perfusion, altered mental status, chest pain, or acute heart failure). Unsynchronized defibrillation is used for pulseless VT or ventricular fibrillation. Adenosine is effective for supraventricular tachycardia, not ventricular tachycardia. After stabilizing the rhythm, clinicians should investigate underlying causes including myocardial ischemia, electrolyte abnormalities (hypokalemia, hypomagnesemia), hypoxia, and mechanical irritation from central lines or pacing wires.