CMC Practice Questions (2026) — Free Sample Questions with Answers

Answer: C

Sublingual nitroglycerin to relieve ischemic chest pain: Nitrates reduce preload. In right ventricular infarction they can cause profound hypotension and are avoided.

IV furosemide to reduce the jugular venous distension: Here JVD reflects RV failure, not volume overload. Diuresis would further reduce the preload the failing RV depends on.

IV normal saline bolus to support right ventricular preload: Correct. RV infarction (inferior STEMI with ST elevation in V4R, hypotension, JVD and clear lungs) depends on preload. Cautious IV fluid boluses support output while reperfusion is arranged.

IV metoprolol to slow the heart rate and limit infarct size: Beta-blockers are contraindicated with hypotension and bradycardia. They would worsen cardiac output.

RV infarct triad: hypotension, JVD, clear lungs. Give fluids, avoid nitrates and diuretics, and reperfuse urgently.

Answer: A

Cardiac tamponade from coronary or ventricular perforation: Correct. Hypotension, JVD and muffled heart sounds (Beck's triad) plus pulsus paradoxus over 10 mm Hg after PCI point to tamponade. Expect emergent echocardiography and pericardiocentesis.

Retroperitoneal hemorrhage from the femoral access site: Retroperitoneal bleeding causes hypovolemic hypotension with flat neck veins. It does not cause JVD or muffled heart sounds.

Vasovagal reaction triggered by arterial sheath removal: A vagal reaction causes hypotension with bradycardia, not tachycardia, JVD and pulsus paradoxus.

Acute left ventricular failure caused by early stent thrombosis: LV failure from stent thrombosis would usually cause chest pain, ST changes and pulmonary crackles. Muffled heart sounds and pulsus paradoxus suggest a pericardial process.

Tamponade = Beck's triad (hypotension, JVD, muffled heart sounds) plus pulsus paradoxus over 10 mm Hg. It is a possible complication of PCI, pacing wires and cardiac surgery.

Answer: A

IV magnesium sulfate 2 g, along with potassium replacement: Correct. This is torsades de pointes in the setting of a prolonged QT, hypokalemia and hypomagnesemia. IV magnesium is first-line even when magnesium is normal, and potassium should be corrected to about 4.0 mEq/L or higher.

IV amiodarone 150 mg bolus over 10 minutes for suppression: Amiodarone prolongs the QT interval and can worsen torsades. It is not first-line for this rhythm.

IV procainamide infusion to suppress ventricular ectopy: Procainamide prolongs the QT and is contraindicated in torsades de pointes.

Synchronized cardioversion at 100 joules while sedated: Polymorphic VT cannot be reliably synchronized, and this patient has a pulse between self-terminating runs. If the patient becomes pulseless, defibrillation, not synchronized cardioversion, is indicated.

Torsades de pointes: give IV magnesium, correct potassium, stop QT-prolonging drugs, and consider overdrive pacing or isoproterenol if it recurs. Defibrillate if the patient is pulseless.

Answer: C

Lower the heparin infusion rate and recheck platelets tomorrow: Any continued heparin sustains the immune reaction and the thrombotic risk. All heparin must be stopped.

Switch to enoxaparin and transfuse platelets for the low count: Low-molecular-weight heparin cross-reacts with HIT antibodies. Platelet transfusion is generally avoided because it can fuel thrombosis.

Stop all heparin, including flushes, and begin argatroban: Correct. HIT (a platelet fall over 50% around days 5–10, with thrombosis) requires stopping all heparin, including flushes and coated catheters, and starting a non-heparin anticoagulant such as argatroban or bivalirudin.

Continue heparin and add warfarin to treat the new clot: Starting warfarin during acute HIT can cause venous limb gangrene. It is delayed until platelets recover on a non-heparin agent.

HIT: stop all heparin, start a direct thrombin inhibitor or other non-heparin anticoagulant, avoid platelet transfusion, and delay warfarin until platelets recover.

Answer: C

Early inflation, occurring before the dicrotic notch: Early inflation starts augmentation before aortic valve closure, cutting off ejection. The augmentation then appears before the dicrotic notch.

Late inflation, occurring well after the dicrotic notch: Late inflation shows a visible dicrotic notch before augmentation and reduced diastolic augmentation. It does not raise assisted end-diastolic pressure.

Late deflation, impeding the start of left ventricular ejection: Correct. If the balloon is still inflated as systole begins, the LV ejects against it. Afterload rises, and assisted end-diastolic pressure equals or exceeds unassisted pressure. This is the most dangerous timing error.

Early deflation, causing a sharp drop after augmentation: Early deflation produces a sharp drop after augmentation and a U-shaped end-diastolic dip. Assisted end-diastolic pressure is lower, with possible retrograde coronary flow.

IABP timing: inflate at the dicrotic notch (aortic valve closure) and deflate just before systole. Assisted end-diastolic pressure should be lower than unassisted. If it is equal or higher, suspect late deflation.

Answer: C

Hypovolemic shock: low cardiac index, low PAOP and high SVR: Hypovolemia causes low filling pressures. This patient's PAOP of 28 and CVP of 14 are elevated.

Distributive shock: high cardiac index, low PAOP and low SVR: Distributive (septic) shock typically shows a high cardiac index and low SVR. This patient's CI is 1.5 and SVR is elevated.

Cardiogenic shock: low cardiac index, high PAOP and high SVR: Correct. CI = 3.0 ÷ 2.0 = 1.5 L/min/m2 (low, under 2.2). PAOP 28 is high, and SVR = (68 − 14) ÷ 3.0 × 80 = 1,440 (high, over 1,200). With hypotension after a large MI, this is pump failure.

Neurogenic shock: low SVR with bradycardia and low PAOP: Neurogenic shock causes vasodilation with bradycardia and low filling pressures. This patient is tachycardic and vasoconstricted.

Cardiogenic shock profile: CI under 2.2, PAOP over 18, SVR high and SBP under 90. Calculate CI = CO ÷ BSA and SVR = (MAP − CVP) ÷ CO × 80.