Cardiac
Valvular disease, arrhythmias, ischemic heart disease, CPB, vasoactive drugs, pacemakers, congenital heart disease. ← Back to Q-Bank
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
B. Digoxin
C. Diltiazem
D. Procainamide
E. Adenosine
Show answer
Answer: D. AV nodal blockers (verapamil, diltiazem, digoxin, adenosine) preferentially block AV nodal conduction and allow rapid conduction down the accessory pathway → VF. Procainamide or ibutilide prolong the refractory period of the accessory pathway. Cardiovert if unstable.
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
B. Direct myocardial depression by protamine
C. Thromboxane A₂-mediated pulmonary vasoconstriction
D. Heparin rebound
E. Histamine release from central line administration
Show answer
Answer: C. Catastrophic pulmonary hypertension after protamine is mediated by thromboxane A₂ release. Risk factors: prior NPH insulin exposure, fish allergy, vasectomy, prior protamine exposure. Treatment includes PGE₁ infusion, inhaled nitric oxide, and vasopressors. Always administer protamine slowly via a peripheral line.
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, accept atrial fibrillation
C. Decrease preload, increase HR, decrease SVR
D. Allow tachycardia, decrease preload, accept arrhythmia
E. Decrease contractility, maintain SVR
Show answer
Answer: A. Severe AS: "full, slow, tight, and in sinus." Coronary perfusion depends on aortic diastolic pressure (decrease SVR → drop in CPP). Loss of sinus rhythm or tachycardia → catastrophic hemodynamic collapse because the hypertrophied LV depends on atrial kick and adequate diastolic filling time.
Q4. Aortic regurgitation hemodynamics
In severe aortic regurgitation, the ideal hemodynamic management is:
A. Bradycardia, increased SVR
B. Tachycardia, decreased SVR
C. Slow HR, increased preload
D. Maintain SVR, decrease HR
E. Increase contractility, maintain SVR
Show answer
Answer: B. "Fast and loose." Tachycardia shortens diastole → less regurgitant time. Afterload reduction reduces regurgitant fraction. Avoid bradycardia (worsens regurgitation) and high SVR. Vasopressin and pure α-agonists can worsen the gradient.
Q5. Mitral stenosis hemodynamics
In severe mitral stenosis with new-onset atrial fibrillation, immediate priorities include:
A. Maintain rapid heart rate to improve diastolic filling
B. Rate control to allow diastolic filling time across the stenotic valve
C. Vasodilation to reduce pulmonary pressures
D. Inotropic support with milrinone
E. Liberalize preload with crystalloid
Show answer
Answer: B. MS: maintain rate control (long diastole needed to fill LV across narrow valve); loss of atrial kick + tachycardia → acute pulmonary edema. Cardiovert promptly if unstable. Avoid pulmonary vasodilators that may unmask RV dysfunction; avoid hypotension/large volume shifts.
Q6. HOCM management
A 32-year-old with hypertrophic obstructive cardiomyopathy develops hypotension during induction. Most appropriate vasoactive is:
A. Ephedrine
B. Dobutamine
C. Milrinone
D. Phenylephrine
E. Isoproterenol
Show answer
Answer: D. HOCM behaves like dynamic LVOT obstruction — like a "more dynamic aortic stenosis." Pure α-agonism (phenylephrine, vasopressin) restores preload via increased SVR without increasing contractility. Inotropes (B, C, E) worsen outflow obstruction by increasing contractility/HR.
Q7. Cardiac tamponade physiology
A patient with cardiac tamponade has:
A. Increased preload, increased afterload
B. Equalization of right and left heart filling pressures, pulsus paradoxus, decreased stroke volume
C. Decreased CVP, increased PCWP
D. Increased SVR, decreased venous return only
E. High cardiac output state
Show answer
Answer: B. Tamponade: equalization of intracardiac pressures (RA = RV = PCWP ≈ 20). Pulsus paradoxus >10 mmHg with inspiration. Hemodynamic goals: "full, fast, tight, and breathing spontaneously" — induction with ketamine, avoid positive pressure ventilation until the pericardium is decompressed.
Q8. Brugada syndrome anesthesia
A 28-year-old with type 1 Brugada pattern undergoes anesthesia. Which agent is best avoided?
A. Propofol bolus
B. Prolonged propofol infusion
C. Etomidate
D. Sevoflurane
E. Sugammadex
Show answer
Answer: B. Brugada (sodium channel mutation; pseudo-RBBB + ST elevations V1–V3; risk of polymorphic VT/SCD). Avoid Class 1C antiarrhythmics, bupivacaine, TCAs, and prolonged propofol infusion. Short propofol bolus generally OK. Keep defibrillator available; isoproterenol or quinidine for refractory arrhythmias. Optimize electrolytes, avoid hyperthermia/hyperkalemia.
Q9. Pacemaker codes
A pacemaker labeled "DDD" indicates:
A. Single-chamber atrial pacing inhibited by sensed atrial activity
B. Dual-chamber pacing, dual-chamber sensing, dual response (triggered/inhibited)
C. Asynchronous dual-chamber pacing
D. Demand pacing with rate response only
E. Defibrillation function with biventricular pacing
Show answer
Answer: B. NASPE/BPEG generic code positions: I=chamber paced, II=chamber sensed, III=response, IV=rate modulation, V=multisite. DDD: both atria/ventricles paced and sensed, both inhibited and triggered. Asynchronous modes (D00, V00, A00) are used in pacemaker-dependent patients during electrocautery to prevent EMI inhibition — apply a magnet to convert.
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
C. Trigger defibrillation
D. Erase device programming
E. Have no effect
Show answer
Answer: A. Magnet over an ICD inhibits antitachycardia therapy but does NOT typically change the pacing mode in a combined device. Magnet over a stand-alone pacemaker converts to asynchronous mode. Always check the specific device — modern devices vary. Best practice for pacemaker-dependent patients with electrocautery above the umbilicus: have the device interrogated and reprogrammed.
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
B. Lidocaine 1.5 mg/kg
C. Magnesium sulfate 2 g IV
D. Synchronized cardioversion
E. Calcium chloride 1 g
Show answer
Answer: C. Torsades: stable → magnesium sulfate 1–2 g IV bolus, repeat in 5–15 min. If unstable → immediate defibrillation. Drugs that cause torsades: class IA (sodium channel blockers, prolong QT), class III (potassium channel blockers, prolong QT), methadone, ondansetron, droperidol, haloperidol. Correct hypokalemia and hypomagnesemia. Amiodarone prolongs QT and could worsen torsades.
Q12. Coronary perfusion pressure
Coronary perfusion pressure for the left ventricle is best estimated by:
A. MAP – CVP
B. Aortic diastolic pressure – LVEDP
C. MAP – ICP
D. Mean PA pressure – PCWP
E. Aortic systolic – RV systolic
Show answer
Answer: B. LV coronary perfusion occurs primarily in diastole because LV intramural pressure exceeds aortic pressure in systole. CPP = aortic diastolic – LVEDP. Goal in critical AS or LV dysfunction: maintain CPP >50 mmHg.
Q13. Anesthetic preconditioning
Volatile-induced preconditioning is mediated primarily through:
A. β₁-adrenergic receptor stimulation
B. Opening of mitochondrial K-ATP channels
C. NMDA receptor antagonism
D. Inhibition of nitric oxide synthase
E. Adenosine A₂ receptor blockade
Show answer
Answer: B. Mitochondrial K-ATP channel opening underlies volatile-induced cardioprotection — limits infarct size if ischemia occurs. Benefit appears 1–2 hr after exposure, dissipates, then reappears 24 hr later for up to 3 days (delayed window). Clinically, full-time sevoflurane in cardiac surgery reduces post-op MI versus pre/post-bypass only or propofol.
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, proceed
B. Defer surgery until 6 months from stent placement, continue aspirin if possible
C. Stop both antiplatelets immediately, bridge with heparin
D. Stop clopidogrel only, proceed in 7 days
E. Switch clopidogrel to ticagrelor
Show answer
Answer: B. Current ACC guidelines: minimum DAPT after DES for stable IHD = 6 months; after BMS = 1 month; after ACS = 12 months. Defer elective surgery until DAPT complete. Continue aspirin perioperatively when possible. Stent thrombosis is catastrophic (~50% mortality).
Q15. ST elevation lead correspondence
ST elevation in leads II, III, and aVF most likely reflects ischemia in which territory?
A. Anterior LV (LAD)
B. Lateral LV (Circumflex)
C. Inferior LV / RV (RCA)
D. Posterior LV
E. Septum
Show answer
Answer: C. II, III, aVF = inferior leads → RCA territory in 80%. Check right-sided leads (V4R) for RV infarct. RV infarct is preload-dependent — avoid nitrates and aggressive diuresis. V1–V4 = anterior (LAD). I, aVL, V5–V6 = lateral (LCx).
Q16. Carotid baroreceptor afferent
Carotid sinus baroreceptors send afferent signals via:
A. Hering's branch of the glossopharyngeal nerve (CN IX)
B. Recurrent laryngeal nerve
C. Vagus nerve from the aortic arch
D. Superior laryngeal nerve
E. Hypoglossal nerve
Show answer
Answer: A. Carotid baroreceptor afferents travel via Hering's nerve → CN IX → NTS in medulla → activates CVLM → inhibits RVLM (decreased sympathetic outflow) + activates vagal nuclei (parasympathetic outflow). Aortic baroreceptors travel via vagus. Carotid baroreceptors are most sensitive between MAP 80–160; chronic HTN dulls the response.
Q17. Pulmonary artery catheter waveforms
The "v wave" on a CVP tracing represents:
A. Atrial contraction
B. Tricuspid valve closure
C. Passive atrial filling against a closed tricuspid valve
D. Ventricular relaxation
E. Rapid ventricular ejection
Show answer
Answer: C. CVP waveform: a wave = atrial contraction; c wave = tricuspid closure; x descent = atrial relaxation; v wave = atrial filling against closed TV; y descent = TV opens. Large v waves: tricuspid regurgitation; cannon a waves: AV dissociation; absent a waves: AFib.
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
Show answer
Answer: B. Norepinephrine is preferred over dopamine in cardiogenic shock — lower arrhythmia rate, lower 28-day mortality (SOAP-II trial). Dobutamine or milrinone added for inotropy if needed. Mechanical support (IABP, Impella, VA-ECMO) for refractory shock.
Q19. Norepinephrine receptor profile
Norepinephrine acts predominantly on:
A. α₁ > β₁, minimal β₂
B. β₁ > α₁, significant β₂
C. β₂ > β₁
D. α₂ predominant
E. D₁ predominant
Show answer
Answer: A. Norepi: α₁ ≥ β₁ >> β₂. Strong vasoconstriction with some inotropic effect; minimal β₂ vasodilation. Epinephrine has more balanced α and β effects (with β₂ at low doses). Vasopressin and phenylephrine are pure vasoconstrictors with no inotropy.
Q20. Adenosine mechanism
Adenosine terminates supraventricular tachycardia by:
A. Activating A₁ receptors → ↑K⁺ outflow at AV node → transient AV block
B. Blocking voltage-gated calcium channels
C. β₁ blockade
D. Increasing vagal tone via CN X
E. Antagonizing the ryanodine receptor
Show answer
Answer: A. Adenosine acts at A₁ receptors → activates IK,ACh channels → AV nodal block for ~10 sec. Caution: severe bronchospasm in asthma; transient asystole. Heart transplant recipients are supersensitive — use lower dose. Theophylline/caffeine antagonize adenosine.
Q21. PVC criteria for treatment
Premature ventricular contractions warrant treatment with IV lidocaine 1–2 mg/kg when:
A. >6 PVCs/min, multifocal, salvos ≥3, or R-on-T phenomenon
B. Any single PVC
C. Bigeminy alone
D. PVCs only in lead II
E. PVCs in a patient on β-blockers
Show answer
Answer: A. Indications for treatment: frequent (>6/min), multifocal, salvos ≥3, R-on-T (PVC on the relative refractory period of the T wave → polymorphic VT). Always search for and treat underlying ischemia, hypoxia, hypokalemia, hypomagnesemia, mechanical irritation.
Q22. Carotid endarterectomy ischemia monitoring
The most reliable intraoperative monitor for cerebral ischemia during awake CEA is:
A. Cerebral oximetry
B. EEG
C. SSEP
D. Awake neurologic exam
E. Transcranial Doppler
Show answer
Answer: D. Awake neurologic exam during CEA (regional anesthesia) is the gold standard — direct testing of contralateral hand grip, speech. Under general anesthesia, EEG + SSEP + cerebral oximetry + TCD are surrogates. The GALA trial showed no difference in stroke/MI/death between general and regional.
Q23. Stellate ganglion location
The stellate ganglion lies:
A. Posterior to C2 transverse process
B. Anterior to C7/T1 vertebral bodies, just inferior to the C6 transverse process
C. At the level of the cricoid cartilage, lateral to trachea
D. At T4 paravertebral space
E. In the brachial plexus sheath
Show answer
Answer: B. Stellate ganglion = fusion of inferior cervical and first thoracic sympathetic ganglia; anterolateral to C7 vertebral body, inferior to C6 transverse process (Chassaignac's tubercle = landmark). Block: needle to C6 tubercle, withdraw and direct caudally-medially. Horner's syndrome = early sign of block; temperature rise is most reliable. Complications: PTX, RLN block, intrathecal injection, seizure from vertebral artery injection.
Q24. Bivalirudin in HIT for CPB
Bivalirudin is preferred over argatroban for cardiopulmonary bypass in HIT because:
A. Bivalirudin is renally cleared
B. Bivalirudin is reversed by protamine
C. Bivalirudin has a 25-minute half-life with non-organ-dependent thrombin cleavage
D. Argatroban is contraindicated in cardiac surgery
E. Bivalirudin reverses HIT antibody production
Show answer
Answer: C. Bivalirudin: half-life 25 min via thrombin proteolysis + 20% renal. Argatroban and hirudin bind thrombin irreversibly and have much longer half-lives — not ideal when reversal at end of bypass is needed. With bivalirudin, no protamine reversal; flush stagnant circuit portions q15–20 min to prevent clotting.
Q25. ACT for CPB
The standard activated clotting time goal for safe initiation of cardiopulmonary bypass is:
A. >200 sec
B. >300 sec
C. >400 sec
D. >600 sec
E. >800 sec
Show answer
Answer: C. ACT >400–480 sec is required for full CPB. Normal ACT ~107 sec. Heparin 300–400 U/kg loading dose. ACT is less affected than aPTT by hemodilution and hypothermia, and has linear response to heparin between 1–5 U/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 (add CO₂ to maintain pH 7.4 at core temperature)
B. Alpha-stat (manage based on ABG at 37°C, ignore temperature correction)
C. Either, with no clinical difference
D. Hypocapnia stat
E. Lactate-stat
Show answer
Answer: B. Adults → alpha-stat (don't add CO₂). Pediatrics → pH-stat (improves cerebral perfusion during cooling). Alpha-stat preserves cerebral autoregulation; pH-stat causes cerebral vasodilation but increases microembolic load. PaCO₂ falls ~2 mmHg per 1°C drop in body temp.
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
B. Cryoprecipitate + platelets
C. Tranexamic acid
D. Factor VIIa
E. Whole blood
Show answer
Answer: B. TEG MA reflects platelet function/fibrinogen-mediated clot strength; K time reflects fibrinogen. Cryo replaces fibrinogen + factor VIII + vWF + XIII. Platelets correct quantitative and CPB-induced qualitative dysfunction. Factor VIIa reserved for refractory bleeding after multiple rounds of MTP.
Q28. Endocarditis prophylaxis indications
Per AHA, antibiotic prophylaxis for infective endocarditis is indicated in which scenario?
A. Mitral valve prolapse with regurgitation, dental cleaning
B. Bicuspid aortic valve, colonoscopy
C. Prosthetic heart valve, dental procedure with gingival manipulation
D. Hypertrophic cardiomyopathy, transesophageal echo
E. Prior CABG, dental extraction
Show answer
Answer: C. AHA prophylaxis indications: prosthetic valve material, prior IE, unrepaired cyanotic CHD, CHD with residual defect at prosthetic patch, completely repaired CHD <6 mo, structural valve abnormality in transplanted heart. Only for gingival manipulation, perforation of oral mucosa, or biopsy of respiratory tract / infected skin. Amoxicillin 2 g PO 1 hr before; vancomycin if penicillin allergic or for staph coverage.
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)
B. Class II
C. Class III
D. Class IV (>5%)
E. Cannot be calculated without echo
Show answer
Answer: D. RCRI: 1 point each for (1) ischemic heart disease, (2) heart failure, (3) cerebrovascular disease, (4) insulin-treated DM, (5) Cr ≥2, (6) suprainguinal vascular/intrathoracic/intra-abdominal surgery. This patient: CVA + insulin DM + vascular surgery = 3 points = Class IV (≥6.6% MACE). 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
B. VV-ECMO
C. VAV-ECMO
D. Central VA-ECMO
E. ECMO is not indicated for ARDS
Show answer
Answer: B. Hemodynamically stable ARDS with refractory hypoxemia → VV-ECMO (lung support only). VA-ECMO adds cardiac support but requires arterial cannulation and increased LV afterload (Harlequin/north-south syndrome with peripheral VA-ECMO). EOLIA trial showed mortality benefit of VV-ECMO in severe ARDS by Bayesian post hoc analysis.
Q31. Lead extraction risks
A 60-year-old man requires removal of leads placed 8 years ago. The greatest perioperative risk is:
A. Pneumothorax
B. Cardiac or great vessel perforation requiring emergent thoracotomy or sternotomy
C. New atrial fibrillation
D. Thromboembolic stroke
E. Esophageal injury
Show answer
Answer: B. Lead extraction (vs. explant within 1 year) carries 1–2% risk of catastrophic vascular or cardiac perforation. Risk factors: female, BMI <25, ICD leads, oldest lead >5 yr. Always have central venous access for balloon tamponade, cardiac surgery on standby, TEE, and blood in the room.
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
B. Amiodarone 150 mg IV bolus over 10 minutes
C. Defibrillation at 200 J
D. Lidocaine 1 mg/kg IV bolus
E. Adenosine 6 mg IV
Show answer
Answer: B. Stable monomorphic VT: amiodarone 150 mg over 10 min, or procainamide, or lidocaine. Cardiovert if hemodynamically unstable. Look for underlying cause (ischemia, hypokalemia/hypomagnesemia, hypoxia, mechanical irritation). Adenosine is for SVT, not VT.