USMLE Step 1 Cardiovascular system questions

The Frank-Starling mechanism describes how increased ventricular filling (preload) stretches cardiac sarcomeres toward their optimal length, increasing the number of actin-myosin cross-bridge interactions and increasing the calcium sensitivity of troponin C. This length-dependent activation increases the force of contraction and stroke volume without requiring a change in contractility, heart rate, or neurohormonal input. This intrinsic mechanism allows the heart to match output to venous return beat-to-beat.

• A. Heart rate is not stated to change in this scenario; the mechanism described is preload-dependent, not rate-dependent.
• B. This describes a consequence of the law of Laplace, not the mechanism by which stroke volume increases with preload.
• C. No sympathetic activation is described; the effect is intrinsic to the myocardium, independent of autonomic input.
• D. Afterload refers to resistance against ejection, not the stimulus described, which is increased venous return (preload).

Hemorrhage lowers arterial pressure, reducing stretch on carotid sinus and aortic arch baroreceptors and decreasing their afferent firing rate to the nucleus tractus solitarius. Normally, baroreceptor afferents tonically inhibit the rostral ventrolateral medulla (vasomotor center) and excite the cardioinhibitory (vagal) centers; reduced firing removes this inhibition, so sympathetic outflow increases and vagal tone to the heart decreases. The net effect is tachycardia, increased contractility, and peripheral vasoconstriction to restore blood pressure. This reflex has a short latency and is the primary rapid compensatory mechanism in acute blood loss.

• A. Baroreceptor afferents act centrally on the medulla, not by direct stimulation of the adrenal medulla.
• C. Firing increases, not decreases, inhibition only when pressure rises; this is the opposite of what occurs in hypotension from hemorrhage.
• D. Decreased afferent firing reduces, not increases, vagal efferent output, contributing to tachycardia rather than bradycardia.
• E. Decreased afferent firing decreases parasympathetic tone and increases sympathetic tone, not the reverse.

The Fick principle states that cardiac output equals oxygen consumption divided by the arteriovenous oxygen content difference: CO = VO2 / (CaO2 − CvO2). The AV O2 difference is 20 − 15 = 5 mL O2/dL, which must be converted to mL O2/L of blood (×10) to match the units of VO2, giving 50 mL O2/L. CO = 250 mL/min ÷ 50 mL/L = 5.0 L/min. This method is used clinically to measure cardiac output when thermodilution is unavailable or when shunts are suspected.

• B. This would require an AV O2 difference of 2.5 mL O2/dL, which is not given in the vignette.
• C. This results from failing to convert the AV O2 difference from mL/dL to mL/L before dividing.
• D. This value results from not converting dL to L at all, producing a tenfold overestimate error in the wrong direction.
• E. This results from a unit conversion error that overestimates the AV O2 difference.

The a wave of the jugular venous pulse corresponds to right atrial contraction. In tricuspid stenosis, the right atrium contracts against a fixed, narrowed orifice, generating a markedly elevated resistance and producing a giant a wave. In atrial fibrillation, there is no organized, coordinated atrial contraction, so no a wave is generated at all, regardless of tricuspid valve function. Recognizing these waveform patterns helps localize valvular and rhythm pathology at the bedside without invasive monitoring.

• A. Pulmonic valve closure corresponds to the second heart sound, not a jugular venous waveform component.
• B. The a wave reflects active atrial contraction, not passive filling, and complete heart block produces intermittent giant 'cannon' a waves, not absent a waves.
• C. Rapid ventricular filling corresponds to the y descent, not the a wave, and decreased venous return does not eliminate the a wave.
• E. Isovolumic contraction is a ventricular, not atrial, event and does not correspond to the a wave; tricuspid regurgitation produces a prominent systolic c-v wave, not loss of the a wave specifically from atrial fibrillation.

Pacemaker cells of the sinoatrial node lack a true resting potential and instead exhibit automaticity driven by phase 4 spontaneous depolarization. As the membrane potential becomes maximally negative after repolarization, hyperpolarization-activated cyclic nucleotide-gated (HCN) channels open, producing the funny current (If), a slow mixed Na+/K+ inward current that gradually depolarizes the cell toward threshold. Once threshold is reached, T-type and then L-type calcium channels open to generate the upstroke, since sinoatrial node cells lack significant fast Na+ channel activity. Ventricular myocytes express IK1, which keeps the resting potential stable and prevents spontaneous depolarization, explaining the absence of automaticity in these cells.

• A. The delayed rectifier current mediates repolarization (phase 3), not spontaneous depolarization.
• C. Fast Na+ current drives the rapid upstroke (phase 0) of ventricular action potentials and is largely absent/inactivated in nodal cells; it does not drive diastolic depolarization.
• D. IK1 maintains a stable resting potential in ventricular myocytes and is largely absent in nodal cells, which is why nodal cells, not ventricular cells, show automaticity.
• E. L-type calcium current contributes to the upstroke (phase 0) of the pacemaker action potential after threshold, not the initial slow diastolic depolarization.

Endothelial injury from risk factors such as hypertension and smoking increases permeability to LDL, which accumulates in the intima and becomes oxidized and modified. Macrophages recognize oxidized LDL through scavenger receptors (such as CD36 and SR-A), which, unlike the native LDL receptor, are not subject to negative feedback downregulation as intracellular cholesterol rises. This leads to unregulated lipid uptake, transforming macrophages into cholesterol-laden foam cells, the hallmark of both early fatty streaks and more advanced atherosclerotic plaques. Foam cell death and lipid release contribute to the necrotic lipid core of advanced lesions.

• A. Lipoprotein lipase acts on triglyceride-rich lipoproteins in capillaries for tissue fatty acid delivery, not on macrophage foam cell formation in the arterial intima.
• B. The native LDL receptor pathway is tightly regulated by feedback downregulation and does not lead to the unchecked lipid accumulation seen in foam cells.
• D. Microhemorrhage with erythrophagocytosis can contribute iron and hemoglobin-derived pigment to advanced plaques but is not the primary mechanism of foam cell formation.
• E. Macrophages take up lipid rather than secrete VLDL; VLDL is produced by hepatocytes, not macrophages.

A family history of premature coronary artery disease, defined as myocardial infarction or sudden cardiac death in a first-degree male relative before age 55 (or female relative before age 65), is a major independent risk factor for atherosclerosis that cannot be modified. While elevated LDL, smoking, and hypertension are also major independent risk factors, they are modifiable through lifestyle change or pharmacotherapy. Obesity and sedentary lifestyle are contributory risk factors but are considered less independently predictive and are also modifiable. Recognizing non-modifiable risk factors is important for risk stratification even though clinical management focuses on the modifiable ones.

• A. Elevated LDL is a major independent risk factor but is modifiable with statins and lifestyle changes.
• B. Smoking is a major independent risk factor but is fully modifiable through cessation.
• C. Hypertension is a major independent risk factor but is modifiable with antihypertensive therapy and lifestyle change.
• D. Obesity and sedentary lifestyle are contributory, modifiable risk factors rather than major independent, non-modifiable ones.

Abdominal aortic aneurysms below the renal arteries are most commonly caused by atherosclerosis, which impairs diffusion of oxygen and nutrients from the lumen and compresses the vasa vasorum, causing medial ischemia. This triggers increased matrix metalloproteinase activity from inflammatory cells, degrading elastin and collagen and causing loss of smooth muscle cells, which weakens the media and allows the vessel to dilate. The infrarenal aorta is especially vulnerable because it has fewer vasa vasorum and relies more on luminal diffusion than the thoracic aorta. This mechanism differs from the genetic connective tissue defects seen in Marfan syndrome or the vasculitic mechanisms of autoimmune arteritides.

• A. Immune complex-mediated transmural necrotizing inflammation describes polyarteritis nodosa.
• B. Fibrillin-1 mutations and TGF-beta dysregulation cause Marfan-associated aortic root and ascending aortic disease, not typical infrarenal atherosclerotic AAA.
• D. Granulomatous giant cell destruction describes temporal arteritis, not atherosclerotic AAA.
• E. Bicuspid aortic valve is associated with ascending aortic dilation, not infrarenal abdominal aneurysms.

This patient has classic features of Marfan syndrome (tall stature, arachnodactyly, lens dislocation) caused by a fibrillin-1 mutation, which leads to cystic medial necrosis of the aortic wall through impaired structural support and dysregulated TGF-beta signaling. This predisposes to aortic dissection, presenting as sudden tearing chest pain radiating to the back with a pulse or blood pressure discrepancy between limbs, caused by a tear in the intima allowing blood to dissect through the weakened media and create a false lumen. Diagnosis is confirmed by CT angiography or transesophageal echocardiography showing an intimal flap. Emergency surgical repair is required for ascending (Stanford type A) dissections.

• A. Pulmonary embolism causes pleuritic chest pain and dyspnea, not a tearing quality radiating to the back with an aortic false lumen.
• B. MI typically causes pressure-like substernal pain with ECG changes and troponin elevation, not tearing pain with blood pressure differential between arms.
• D. Esophageal rupture typically follows vomiting and causes mediastinitis, not a false lumen within the aortic wall.
• E. Pericarditis causes sharp pain that worsens with lying down and improves with sitting forward, with a friction rub, not a false lumen on imaging.

Takayasu arteritis is a granulomatous large-vessel vasculitis that classically affects young Asian women, involving the aortic arch and its major branches. It presents with constitutional symptoms, elevated inflammatory markers, and weak or absent pulses in the upper extremities ('pulseless disease'), along with asymmetric blood pressures and bruits. Vessel wall thickening and stenosis are seen on imaging, and histology shows granulomatous inflammation of the media with giant cells. Treatment is with corticosteroids, and surgical bypass may be needed for critical stenosis.

• A. Giant cell arteritis affects the temporal and other cranial branches of the carotid artery in patients over 50 years old, not the aortic arch in young women.
• B. Kawasaki disease is a childhood vasculitis affecting coronary arteries, not the aortic arch in adults.
• C. Polyarteritis nodosa is a medium-vessel vasculitis affecting renal and visceral arteries, not the aortic arch, and typically occurs in middle-aged adults.
• E. Buerger disease affects small and medium distal arteries of the extremities in smokers, causing digital ischemia, not aortic arch involvement.

This patient has giant cell (temporal) arteritis, a granulomatous vasculitis of medium and large arteries, classically the branches of the carotid artery, occurring in patients over 50 years old and associated with polymyalgia rheumatica (proximal muscle stiffness and elevated ESR). Jaw claudication occurs due to ischemia of the masseter muscles. The most feared complication is irreversible monocular blindness due to occlusion of the ophthalmic or posterior ciliary arteries causing ischemic optic neuropathy, which is why high-dose corticosteroids are started immediately on clinical suspicion, even before temporal artery biopsy confirmation.

• A. Digital gangrene is characteristic of Buerger disease or severe Raynaud phenomenon, not giant cell arteritis.
• B. Hemorrhagic stroke is not a characteristic complication of giant cell arteritis, which causes ischemic rather than hemorrhagic vascular events.
• D. Mesenteric ischemia is a feature of polyarteritis nodosa, which affects medium-sized visceral arteries.
• E. Renal artery involvement and hypertension are more characteristic of Takayasu arteritis or polyarteritis nodosa, not giant cell arteritis.

Polyarteritis nodosa is a necrotizing vasculitis of medium-sized muscular arteries that spares the pulmonary circulation and classically presents with constitutional symptoms, renal involvement (hypertension and renal insufficiency from arterial narrowing), mononeuritis multiplex (such as foot drop from vasa nervorum ischemia), livedo reticularis, and subcutaneous nodules. It is associated with chronic hepatitis B infection, with immune complex deposition causing transmural necrotizing inflammation of the arterial wall. Angiography classically shows a 'string of pearls' pattern caused by alternating aneurysmal dilation and stenosis. Treatment involves corticosteroids and cyclophosphamide, with antiviral therapy for HBV-associated cases.

• B. Granulomatosis with polyangiitis involves the upper and lower respiratory tract and kidneys with c-ANCA positivity, not medium-vessel aneurysms associated with hepatitis B.
• C. Kawasaki disease occurs in children and classically affects the coronary arteries, not adult visceral medium-sized arteries.
• D. Microscopic polyangiitis is a small-vessel vasculitis typically associated with p-ANCA and lung involvement, not medium-vessel aneurysms or hepatitis B.
• E. Takayasu arteritis affects the aortic arch and large branches in young women, not medium-sized visceral arteries with a string-of-pearls pattern.

Kawasaki disease is a medium-vessel vasculitis of early childhood presenting with prolonged fever, conjunctivitis, oral mucosal changes, rash, cervical lymphadenopathy, and extremity changes (edema, erythema, and later desquamation), with the most serious complication being coronary artery aneurysm formation. First-line treatment is intravenous immunoglobulin, which reduces systemic inflammation and the risk of coronary artery aneurysms, combined with high-dose aspirin for its anti-inflammatory effect during the acute febrile phase. Aspirin is later continued at a lower, antiplatelet dose until coronary abnormalities resolve. Aspirin use in a child is an exception to the usual contraindication due to the risk of Reye syndrome, because the benefit in Kawasaki disease outweighs this risk.

• A. Oral prednisone and heparin are not standard first-line therapy for Kawasaki disease.
• B. Cyclophosphamide is used for severe systemic vasculitides like granulomatosis with polyangiitis, not Kawasaki disease.
• C. Corticosteroids are not first-line therapy for Kawasaki disease, and warfarin is not standard initial treatment.
• E. Clopidogrel is not the standard antiplatelet agent paired with IVIG in Kawasaki disease; aspirin is used instead.

Thromboangiitis obliterans (Buerger disease) is a segmental, nonatherosclerotic, inflammatory vasculitis of small and medium-sized arteries and veins of the distal extremities, occurring almost exclusively in heavy smokers, typically young to middle-aged men. It presents with distal extremity ischemia, including digital ulceration, cyanosis, and claudication, with normal proximal pulses because the disease spares large vessels. Pathogenesis involves direct endothelial damage and hypersensitivity to tobacco components, causing segmental thrombosing vasculitis with sparing of the vessel wall's internal elastic lamina. Smoking cessation is essential and often leads to improvement.

• A. Systemic sclerosis causes skin thickening and often positive ANA/anti-centromere or anti-Scl-70 antibodies, which are absent here.
• C. Atherosclerotic PAD typically affects older patients with proximal large and medium vessel involvement and risk factors like diabetes and hyperlipidemia, not isolated distal small-vessel disease in a young heavy smoker.
• D. Antiphospholipid syndrome causes recurrent thrombosis and is associated with lupus anticoagulant or anticardiolipin antibodies, not a smoking-related distal vasculitis.
• E. Polyarteritis nodosa affects medium-sized visceral arteries with systemic symptoms and renal involvement, not isolated digital ischemia in a smoker.

Primary Raynaud phenomenon results from exaggerated, reversible vasospasm of the digital arterioles triggered by cold exposure or emotional stress, without any underlying structural vascular disease; it typically occurs in young women and is not associated with tissue damage or abnormal nail-fold capillaries. This contrasts with secondary Raynaud phenomenon, which occurs in the setting of an underlying connective tissue disease such as systemic sclerosis, where structural changes like fibrointimal proliferation of the vessel wall occur and can lead to digital ulceration and abnormal nail-fold capillary findings. The normal examination and capillaries in this patient support a primary, purely functional vasospastic mechanism rather than an underlying structural disease.

• A. Fibrointimal proliferation with vessel wall thickening describes secondary Raynaud phenomenon from an underlying connective tissue disease, not primary Raynaud phenomenon.
• C. Immune complex-mediated necrotizing inflammation describes a vasculitic process, not the reversible vasospasm of Raynaud phenomenon.
• D. Atherosclerotic plaque rupture is not relevant to a young woman with normal vessels and reversible, cold-triggered symptoms.
• E. Irreversible thrombotic occlusion describes Buerger disease, not the reversible, episodic nature of this patient's symptoms.

Fibromuscular dysplasia (FMD) is a nonatherosclerotic, noninflammatory arteriopathy that classically affects the renal arteries of young women, producing alternating areas of medial thinning and fibrous ridges that create the "string of beads" angiographic appearance. Renal artery stenosis from FMD activates the renin-angiotensin-aldosterone system, causing secondary hypertension with hypokalemia from secondary hyperaldosteronism, as seen in this patient. An abdominal bruit in a young, otherwise healthy patient strongly suggests renovascular disease. Atherosclerotic renal artery stenosis typically affects older patients with vascular risk factors and involves the proximal artery, not the characteristic beaded pattern.

• A. Pheochromocytoma presents with episodic headache, palpitations, and diaphoresis, not a renal artery bruit.
• B. Primary aldosteronism causes hypokalemic hypertension but would not produce an abdominal bruit or the beaded renal artery appearance.
• C. Atherosclerotic stenosis typically occurs in older patients with risk factors such as diabetes or smoking, not a young healthy woman.
• E. Essential hypertension would not explain the abdominal bruit or the characteristic imaging finding in a young patient.

ACE (kininase II) normally degrades bradykinin; ACE inhibitors block this degradation, leading to bradykinin accumulation in the respiratory tract, which stimulates sensory nerve fibers and causes a dry, nonproductive cough in up to 10-20% of patients. The same bradykinin accumulation can cause angioedema of the lips, tongue, and face, a more serious adverse effect requiring immediate discontinuation of the drug. This cough typically resolves within days of stopping the ACE inhibitor and does not recur with angiotensin receptor blockers, which do not affect bradykinin metabolism.

• A. Angiotensin I accumulation does not have significant biologic activity causing cough.
• B. ACE inhibitors reduce angiotensin II production; decreased angiotensin II does not cause cough.
• C. The cough is not due to an inflammatory infiltrate but a direct effect of bradykinin on sensory nerves.
• D. Aldosterone levels decrease, not increase, with ACE inhibition, and aldosterone is not linked to cough.

Thiazide diuretics such as chlorthalidone inhibit the Na+/Cl- cotransporter (NCC) in the distal convoluted tubule, reducing sodium reabsorption and producing a mild natriuretic and antihypertensive effect, partly through chronic reduction in plasma volume and peripheral vascular resistance. Thiazides commonly cause hyperglycemia by impairing pancreatic insulin release and reducing insulin sensitivity, and hyperuricemia by competing with uric acid for secretion in the proximal tubule, which can precipitate gout. These metabolic effects are dose-related and are important considerations in patients with diabetes or a history of gout.

• A. This describes the mechanism of potassium-sparing diuretics such as amiloride.
• B. This describes the mechanism of acetazolamide, used for conditions like glaucoma and altitude sickness.
• C. This describes the mechanism of loop diuretics such as furosemide, not thiazides.
• D. This describes the mechanism of aldosterone antagonists such as spironolactone.

Dihydropyridine calcium channel blockers like amlodipine preferentially dilate peripheral arterioles, which increases capillary hydrostatic pressure and promotes fluid transudation into the interstitium, causing peripheral edema that is typically worse in the lower extremities and improves with leg elevation. Because arteriolar dilation lowers blood pressure without a compensatory decrease in venous tone, baroreceptor-mediated reflex sympathetic activation occurs, producing mild tachycardia. Unlike non-dihydropyridine CCBs (verapamil, diltiazem), dihydropyridines have minimal direct cardiac depressant effect, which is why reflex tachycardia rather than bradycardia is observed.

• A. Thiazolidinediones, not CCBs, are classically associated with aldosterone-mediated fluid retention and edema.
• B. The edema results from arteriolar dilation and increased hydrostatic pressure, not venous pooling.
• C. Dihydropyridines have minimal effect on cardiac calcium channels compared to vascular smooth muscle; this would cause bradycardia, not tachycardia.
• E. Amlodipine does not affect hepatic albumin synthesis or plasma oncotic pressure.

Hydralazine, a direct arteriolar vasodilator used for resistant hypertension, is a classic cause of drug-induced lupus, particularly in slow acetylators who metabolize the drug less efficiently via N-acetyltransferase, leading to accumulation of reactive metabolites that trigger an autoimmune response. Drug-induced lupus characteristically produces antihistone antibodies with typically negative anti-double-stranded DNA antibodies, and commonly presents with arthralgia, rash, and fever but rarely causes renal or CNS involvement, distinguishing it from idiopathic SLE. Symptoms generally resolve after discontinuing the offending drug.

• A. The antihistone antibody pattern and absence of anti-dsDNA antibodies point to a drug-induced process rather than idiopathic SLE.
• B. Drug-induced lupus is due to metabolite-driven immune dysregulation, not direct antigenic cross-reactivity.
• D. The mechanism involves immune activation from drug metabolites, not direct complement activation.
• E. Hydralazine-induced lupus rarely involves the kidneys, unlike idiopathic SLE.

Niacin activates GPR109A receptors on epidermal Langerhans cells and dermal macrophages, triggering the release of prostaglandin D2 (and prostaglandin E2) via cyclooxygenase activity, which causes cutaneous vasodilation and the characteristic flushing sensation. Pretreatment with aspirin (or another NSAID) 30 minutes before niacin inhibits cyclooxygenase, reducing prostaglandin synthesis and thereby attenuating the flushing reaction. Niacin's lipid-lowering mechanism itself involves inhibition of hormone-sensitive lipase in adipocytes, reducing free fatty acid release and hepatic VLDL synthesis, which is unrelated to the flushing pathway.

• A. Aspirin does not affect intestinal absorption of niacin.
• B. Aspirin does not act on the GPR109A receptor itself; it acts downstream on cyclooxygenase.
• D. The flushing reaction is prostaglandin-mediated, not histamine-mediated, so antihistamines are not the standard preventive therapy.
• E. Niacin's lipid effects involve inhibition of lipolysis in adipose tissue, not lipoprotein lipase activation, and this is unrelated to flushing.

Familial hypercholesterolemia is an autosomal dominant disorder most commonly caused by mutations in the gene encoding the LDL receptor, impairing hepatic clearance of LDL particles from the circulation and resulting in markedly elevated LDL cholesterol from birth. Heterozygotes present with tendon xanthomas (classically Achilles and extensor tendons), corneal arcus, and premature coronary artery disease, as seen in this child's father who died young of myocardial infarction. Homozygotes have even more severe hypercholesterolemia and can develop coronary disease in childhood. Triglycerides are typically normal, distinguishing this from disorders of triglyceride metabolism.

• A. Familial hypercholesterolemia is autosomal dominant and due to LDL receptor defects, not an X-linked apolipoprotein B deficiency.
• B. Hepatic lipase deficiency is a rare cause of dyslipidemia but is not the mechanism of familial hypercholesterolemia.
• C. ABCA1 mutations cause Tangier disease, characterized by low HDL, not elevated LDL.
• E. Lipoprotein lipase deficiency causes chylomicronemia with markedly elevated triglycerides, not isolated LDL elevation.

Stable angina results from a fixed atherosclerotic stenosis, typically greater than 70% luminal narrowing, that limits the ability of the coronary artery to dilate and augment flow when myocardial oxygen demand rises during exertion. At rest, baseline flow is adequate because distal arteriolar autoregulatory vasodilation compensates, but this reserve is exhausted with increased demand, producing ischemia and pain that resolves with rest. The plaque is stable (not ruptured), distinguishing this from acute coronary syndromes. This supply-demand mismatch is the hallmark pathophysiology of exertional (stable) angina.

• A. Embolic coronary occlusion causes acute, not predictable exertional, symptoms.
• B. Plaque rupture with thrombosis causes unstable angina or myocardial infarction, not a reproducible exertional pattern over months.
• D. Microvascular angina occurs with normal or near-normal epicardial arteries, inconsistent with the 80% fixed stenosis described.
• E. Vasospasm at rest with transient ST elevation describes Prinzmetal angina, not exertional stable angina.

This presentation, rest pain with transient ST elevation that resolves spontaneously, normal troponin, and angiographically normal coronary arteries, is classic for Prinzmetal (variant) angina caused by focal coronary artery vasospasm. Calcium channel blockers such as amlodipine reduce vascular smooth muscle calcium influx, promoting coronary vasodilation and preventing spasm, and are first-line therapy. Nitrates are useful adjuncts for acute relief and prophylaxis but calcium channel blockers are the mainstay of long-term prevention. Beta-blockers can worsen vasospasm by leaving alpha-adrenergic vasoconstriction unopposed and are generally avoided.

• A. Statins treat atherosclerotic disease, which is absent in this patient with angiographically normal arteries.
• B. Beta-blockers may unmask unopposed alpha-mediated vasoconstriction and worsen coronary vasospasm.
• D. Aspirin targets platelet aggregation and atherothrombosis, not vasospasm, and is not the primary preventive therapy here.
• E. Nitrates alone are less effective than calcium channel blockers for long-term prevention of recurrent vasospasm.

Cardiac troponin I rises about 4 hours after myocardial injury, peaks at 24 hours, and remains elevated for 7-10 days, making it highly sensitive but poorly specific for detecting reinfarction occurring within that window because baseline levels are already elevated. CK-MB rises in a similar timeframe but returns to baseline within 48-72 hours, so a new rise in CK-MB after it has normalized is a reliable indicator of reinfarction in a patient whose troponin is still elevated from the index event. This is why CK-MB retains clinical value specifically for detecting reinfarction within 7-10 days of an initial MI.

• A. Myoglobin rises and clears very rapidly but is nonspecific and not routinely used to confirm reinfarction in modern practice.
• B. Lactate dehydrogenase is nonspecific and rises later, offering no advantage for detecting early reinfarction.
• C. Aspartate aminotransferase is nonspecific for myocardial tissue and is not used to assess reinfarction.
• E. B-type natriuretic peptide reflects ventricular wall stress and heart failure, not myocardial necrosis timing.

Between 1 and 3 days after myocardial infarction, the infarcted myocardium shows coagulative necrosis, characterized by anucleate, hypereosinophilic fibers that retain their basic cellular outline, along with a prominent neutrophilic infiltrate responding to the tissue injury. This contrasts with granulation tissue, which appears later at 1-2 weeks and features plump fibroblasts, new capillaries, and loose collagen as the infarct begins to organize. By 2 months, a dense collagenous scar replaces the infarcted region. Recognizing this timeline is essential for correlating histologic findings with the time since infarction.

• A. Macrophage-predominant infiltrate with fibroblast proliferation occurs later, around 1 week, after neutrophils have been cleared.
• B. Dense collagenous scar formation is a feature of the healed infarct at 2 months or later.
• C. Dystrophic calcification is not a characteristic early feature of this timeframe.
• D. Granulation tissue appears later, around 1-2 weeks after infarction, not at 36 hours.

Left ventricular free wall rupture classically occurs 3 to 14 days after myocardial infarction, often at the border of necrotic and viable tissue where the wall is weakest, and presents with sudden hemopericardium leading to cardiac tamponade with hypotension, jugular venous distention, and muffled heart sounds, exactly as seen here with echocardiographic evidence of tamponade. Papillary muscle rupture instead causes acute severe mitral regurgitation with a new holosystolic murmur and pulmonary edema, not tamponade physiology. Dressler syndrome is an autoimmune pericarditis occurring weeks to months after infarction, too late for this timeline.

• A. Papillary muscle rupture causes acute mitral regurgitation with pulmonary edema and a new murmur, not tamponade physiology.
• B. Ventricular septal rupture causes a new harsh holosystolic murmur with a left-to-right shunt and biventricular failure, not isolated tamponade.
• C. Dressler syndrome occurs weeks to months after infarction, not at day 5, and presents as pericarditis rather than acute tamponade.
• E. Chronic ventricular aneurysms develop weeks to months later and typically present with heart failure or arrhythmia, not acute tamponade.

ST-segment elevation in the precordial leads V1 through V4 corresponds to the anteroseptal wall of the left ventricle, which is supplied by the left anterior descending artery. The left anterior descending artery arises from the left main coronary artery and runs along the anterior interventricular groove, supplying the anterior wall, anterior septum, and apex. Reciprocal ST depression in the inferior leads is a common finding with large anterior infarctions and does not indicate separate inferior wall involvement. Recognizing the lead-to-territory correlation allows rapid identification of the culprit vessel before angiography.

• A. Posterior descending artery occlusion is associated with posterior infarction, showing ST depression in V1-V3 with tall R waves, not ST elevation.
• B. Right coronary artery occlusion produces ST elevation in the inferior leads II, III, and aVF, not V1-V4.
• C. Left circumflex artery occlusion produces ST elevation in the lateral leads I, aVL, V5, and V6.
• E. Left main occlusion typically causes widespread ST elevation or depression with hemodynamic collapse, not an isolated anteroseptal pattern.

Reperfusion injury occurs when blood flow is restored to previously ischemic tissue, reintroducing oxygen that is converted into reactive oxygen species by damaged mitochondria and xanthine oxidase, while simultaneous restoration of ion gradients leads to intracellular calcium overload. This calcium overload activates proteases and phospholipases and can trigger mitochondrial permeability transition pore opening, driving additional myocyte death and arrhythmia beyond the injury caused by the ischemia itself. This paradox, where restoring flow causes additional damage, is a well-recognized consequence of thrombolytic or percutaneous reperfusion therapy. Antioxidant and calcium-channel-targeted strategies have been studied to mitigate this injury.

• A. Catecholamine-induced vasospasm is not the primary mechanism of reperfusion injury following thrombolysis.
• B. Thrombus extension would worsen ischemia rather than cause injury specifically tied to the moment of reperfusion.
• C. Microembolization of debris can occur during intervention but does not explain the oxidative and calcium-mediated injury characteristic of reperfusion.
• E. ATP depletion from anaerobic glycolysis characterizes the ischemic phase itself, not the injury that follows reperfusion.

Aspirin irreversibly acetylates a serine residue on cyclooxygenase-1 in platelets, permanently inactivating the enzyme and preventing conversion of arachidonic acid to thromboxane A2, a potent promoter of platelet aggregation and vasoconstriction. Because platelets lack nuclei and cannot synthesize new cyclooxygenase, this inhibition lasts for the entire 7-10 day lifespan of the affected platelets. This antiplatelet effect reduces further thrombus propagation in acute coronary syndrome and has been shown to reduce mortality. The irreversible nature of the inhibition distinguishes aspirin's long duration of action from reversible antiplatelet agents.

• A. Clopidogrel and related agents, not aspirin, act on platelet ADP receptors, and that mechanism is reversible or irreversible depending on the specific drug, not aspirin's mechanism.
• B. Glycoprotein IIb/IIIa inhibitors such as abciximab, not aspirin, block this receptor.
• C. Direct thrombin inhibition describes drugs like dabigatran, not aspirin.
• D. Heparin, not aspirin, potentiates antithrombin III activity.

This patient has heart failure with preserved ejection fraction (HFpEF), driven by long-standing hypertension causing concentric left ventricular hypertrophy. The hypertrophied, stiff myocardium impairs active relaxation and passive compliance during diastole, raising filling pressures despite normal systolic function (EF 60%). This is reflected by the S4 gallop (blood filling a stiff, noncompliant ventricle) and echocardiographic evidence of increased wall thickness with impaired diastolic filling. In contrast, HFrEF results from reduced contractility and ventricular dilation with a low ejection fraction.

• A. This describes systolic dysfunction (HFrEF), which presents with a reduced ejection fraction, not the preserved EF of 60% seen here.
• C. Dilated cardiomyopathy causes eccentric hypertrophy and a reduced EF, the opposite of the findings here.
• D. There is no evidence of aortic stenosis such as a systolic ejection murmur or valve findings on echocardiography.
• E. Constrictive pericarditis is a distinct restrictive process, not suggested by the hypertrophy and wall thickening described.

Chronic left heart failure raises pulmonary capillary hydrostatic pressure, causing chronic pulmonary congestion and microhemorrhages into the alveolar spaces. Alveolar macrophages phagocytose the extravasated erythrocytes and break down hemoglobin into hemosiderin, a golden-brown, iron-containing pigment that stains positive with Prussian blue (Perls') stain. These hemosiderin-laden macrophages are called "heart failure cells" and are a classic histologic marker of chronic pulmonary venous congestion. The resulting brown induration of the lungs is termed "brown induration."

• A. This describes lipid-laden macrophages seen in conditions like exogenous lipoid pneumonia, not Prussian blue-positive pigment.
• B. Carbon pigment (anthracotic pigment) is black and does not stain with Prussian blue; it is seen with pollution or smoking exposure.
• C. Granulomas with mycobacteria would show caseating necrosis and acid-fast organisms, not hemosiderin pigment.
• E. Lipofuscin is a brown "wear-and-tear" pigment but does not stain with Prussian blue and is unrelated to heart failure.

Cor pulmonale is right ventricular failure caused by a primary lung disorder, most commonly COPD. Chronic alveolar hypoxia triggers pulmonary arteriolar vasoconstriction (hypoxic pulmonary vasoconstriction), which over time leads to pulmonary hypertension and increased right ventricular afterload. The right ventricle hypertrophies and eventually fails, producing the classic signs of right heart failure: jugular venous distension, hepatomegaly, and peripheral edema, in the absence of left heart failure findings such as orthopnea or pulmonary edema. This patient's barrel chest, hypoxemia, and hyperresonant lung fields point to COPD as the inciting lung disease.

• A. Protein-losing conditions would not explain the combination of jugular venous distension and heave specific to right ventricular pressure overload.
• B. This describes a cause of left heart failure, but this patient has no orthopnea or signs of pulmonary congestion, and the primary pathology is pulmonary.
• D. Increased capillary permeability would cause pulmonary edema, not the isolated right heart failure pattern seen here.
• E. There is no murmur or history suggesting rheumatic valve disease described in this vignette.

This patient's body habitus (tall stature, long extremities, positive wrist sign) suggests Marfan syndrome, caused by mutations in the fibrillin-1 gene, which is associated with mitral valve prolapse. Mitral valve prolapse results from myxomatous degeneration of the valve leaflets, characterized by excess deposition of proteoglycans and fragmented collagen within the spongiosa layer, causing the leaflets and chordae tendineae to become redundant and floppy. This produces a mid-systolic click (sudden tensing of chordae as the leaflet prolapses into the left atrium) followed by a late systolic murmur from mitral regurgitation, which occurs earlier with maneuvers that decrease left ventricular volume such as standing or Valsalva.

• B. Mitral annular calcification occurs in older adults and restricts rather than produces floppy, prolapsing leaflets.
• C. This describes verrucous vegetations of Libman-Sacks endocarditis seen in systemic lupus erythematosus, not mitral valve prolapse.
• D. This describes the vegetations of nonbacterial thrombotic (marantic) endocarditis, not myxomatous prolapse.
• E. This describes chronic rheumatic mitral stenosis, which produces a diastolic opening snap and murmur, not a systolic click.

Progressive calcific degeneration of a previously normal trileaflet aortic valve is the most common cause of aortic stenosis in elderly patients, producing a crescendo-decrescendo systolic murmur radiating to the carotids with a delayed, weak carotid upstroke (pulsus parvus et tardus). This is distinct from bicuspid valve disease, which typically presents with calcific stenosis at a younger age (50s-60s) due to accelerated mechanical stress on an abnormal two-cusp valve. The patient's age and echocardiographic findings of heavy calcification fit degenerative senile calcific stenosis rather than a congenital bicuspid valve.

• A. Aortic regurgitation produces a diastolic decrescendo murmur, not a crescendo-decrescendo systolic murmur.
• C. Rheumatic mitral stenosis produces a diastolic murmur with an opening snap, not a systolic ejection murmur radiating to the carotids.
• D. Hypertrophic obstructive cardiomyopathy murmur decreases with increased afterload (squatting) rather than depending on leaflet calcification, and carotid upstroke is typically brisk and bifid, not delayed.
• E. Bicuspid aortic valve stenosis classically presents at a younger age (50s-60s), not in a 78-year-old.

The posteromedial papillary muscle receives blood supply solely from the posterior descending artery, making it vulnerable to rupture after an inferior wall myocardial infarction, typically 2-7 days post-infarct. Papillary muscle rupture causes acute, severe mitral regurgitation with a holosystolic murmur radiating to the axilla, pulmonary edema, and cardiogenic shock. The regurgitant jet occurs because the ruptured papillary muscle can no longer tether the chordae tendineae, producing a flail leaflet that fails to coapt during systole. This is a classic mechanical complication of myocardial infarction and a surgical emergency.

• A. Fibrotic fusion of leaflets describes mitral stenosis, which produces a diastolic murmur, not acute holosystolic regurgitation.
• B. Aortic root dilation causes aortic regurgitation, not mitral regurgitation, and does not fit the post-infarct timeline.
• D. Vegetation-induced perforation would suggest infective endocarditis, not an abrupt presentation 2 days after unreported chest pain with markedly elevated troponin.
• E. Myxomatous degeneration causes chronic mitral valve prolapse, not an acute flail valve 2 days after an infarction.

Acute rheumatic fever results from molecular mimicry, in which antibodies generated against the M protein of group A Streptococcus (Streptococcus pyogenes) cross-react with structurally similar self-antigens, including cardiac myosin and valve glycoproteins. This type II hypersensitivity-like mechanism produces inflammation of the myocardium and valves (pancarditis), most commonly affecting the mitral valve. The Jones criteria, including migratory polyarthritis, carditis, erythema marginatum, and subcutaneous nodules, support the diagnosis in the setting of a preceding streptococcal pharyngitis. The disease is an autoimmune, not an infectious, process of the valve itself.

• A. Rheumatic fever is a post-infectious autoimmune phenomenon; the bacteria do not directly invade or infect the valve leaflets.
• C. Superantigen-mediated T cell activation describes toxic shock syndrome, not the pathogenesis of rheumatic carditis.
• D. Sterile fibrin-platelet vegetations describe nonbacterial thrombotic (marantic) endocarditis, not rheumatic valvulitis.
• E. The mechanism is molecular mimicry producing cross-reactive antibodies, not immune complex deposition.

Staphylococcus aureus is the most common cause of infective endocarditis in intravenous drug users and classically affects the tricuspid valve, producing a murmur that increases with inspiration due to increased right-sided venous return. The organism is catalase-positive (distinguishing it from streptococci) and coagulase-positive (distinguishing it from coagulase-negative staphylococci), and it typically grows in clusters on gram stain. S. aureus is also notable for causing acute, rapidly destructive endocarditis even on previously normal valves, unlike viridans streptococci, which typically require a pre-damaged valve.

• A. Streptococcus gallolyticus (bovis) is catalase-negative and associated with colorectal malignancy, not IV drug use.
• B. Enterococcus faecalis is catalase-negative and is more associated with endocarditis following genitourinary procedures.
• C. Streptococcus mutans (a viridans group organism) is catalase-negative and typically causes subacute endocarditis on previously damaged native valves, not acute tricuspid disease in IV drug users.
• D. Candida albicans is a fungus, not a gram-positive coccus, and would not appear in clusters on gram stain.

Osler nodes (tender nodules on finger and toe pads) result from immune complex deposition in small vessels, a type III hypersensitivity reaction. Janeway lesions (non-tender erythematous macules on the palms and soles) result from septic microemboli lodging in cutaneous vessels. Roth spots (retinal hemorrhages with pale centers) are also thought to arise from immune complex-mediated vasculitis causing capillary rupture. Distinguishing tenderness (Osler = immune, tender) from painlessness (Janeway = embolic) is a classic clinical discriminator in infective endocarditis.

• B. This incorrectly assigns platelet-fibrin thrombi to Janeway lesions and immune complex deposition to Roth spots rather than Osler nodes.
• C. This reverses the mechanisms: Osler nodes are immune complex-mediated, not embolic, and Janeway lesions are embolic, not immune complex-mediated.
• D. Osler nodes are not due to platelet-fibrin thrombi, and Roth spots are not due to septic microemboli.
• E. Janeway lesions are not due to platelet-fibrin thrombi deposition; they are embolic phenomena.

Libman-Sacks endocarditis is a sterile, verrucous valvulopathy associated with systemic lupus erythematosus, classically affecting the mitral valve with small vegetations that can form on either surface of the leaflet. It results from immune complex deposition and is associated with antiphospholipid antibodies. The combination of a photosensitive rash, elevated ANA and anti-dsDNA titers, and negative blood cultures in a patient with new valvular vegetations supports a lupus-associated sterile endocarditis rather than an infectious cause.

• A. Carcinoid heart disease typically affects right-sided valves (tricuspid and pulmonic) and is associated with flushing and diarrhea, not a lupus serology profile.
• B. Subacute bacterial endocarditis would typically show positive blood cultures; this patient's cultures are negative.
• C. Rheumatic mitral valvulitis follows streptococcal pharyngitis and is not associated with ANA or anti-dsDNA positivity.
• D. Nonbacterial thrombotic (marantic) endocarditis is associated with malignancy and hypercoagulable states, not with the photosensitive rash and positive dsDNA antibodies seen here.

Hypertrophic cardiomyopathy is most commonly caused by autosomal dominant mutations in genes encoding sarcomere proteins, such as beta-myosin heavy chain or myosin-binding protein C, leading to disorganized hypertrophy of myocardial fibers. The hallmark histologic finding is myocyte disarray, in which hypertrophied fibers branch and align at oblique angles to each other, along with patchy interstitial fibrosis. This produces asymmetric septal hypertrophy that can cause left ventricular outflow obstruction and is a leading cause of sudden cardiac death in young athletes due to ventricular arrhythmias. A family history of sudden death during exertion is classic given the autosomal dominant inheritance pattern.

• A. Mitochondrial DNA mutations cause mitochondrial myopathies, which typically also involve other mitochondria-rich tissues and not primarily this isolated sarcomere disarray pattern.
• C. Desmosomal protein mutations cause arrhythmogenic right ventricular cardiomyopathy, characterized by fibrofatty replacement of the right ventricular myocardium, not septal myocyte disarray.
• D. Autosomal recessive lysosomal enzyme mutations describe a storage disease such as Pompe disease, not the classic sarcomeric hypertrophic cardiomyopathy pattern.
• E. X-linked dystrophin mutations cause Duchenne or Becker muscular dystrophy, which can lead to a dilated, not primarily hypertrophic, cardiomyopathy.

Amyloid deposits bind Congo red dye and, when viewed under polarized light, exhibit characteristic apple-green birefringence due to the beta-pleated sheet structure of the misfolded protein fibrils. This finding is the diagnostic gold standard for confirming amyloid deposition in tissue, including the heart in restrictive cardiomyopathy. The sparkling granular echogenicity on echocardiogram is suggestive but not definitive, making tissue biopsy with polarized Congo red the confirmatory test. Light chain or transthyretin amyloid are the most common cardiac amyloid types in this clinical context.

• A. Electron microscopy can show fibrils but is not the standard confirmatory test and does not define amyloid as specifically as polarized Congo red.
• B. Desmin is a muscle intermediate filament marker, unrelated to amyloid fibril detection.
• D. PAS stains glycogen and is used for glycogen storage diseases, not amyloidosis.
• E. Masson trichrome stains fibrosis, not amyloid protein, and would not confirm the diagnosis.

This patient's presentation of myocarditis following a febrile viral prodrome is most consistent with Coxsackie B virus infection, the most common cause of viral myocarditis in young adults. Biopsy classically shows a lymphocytic infiltrate with associated myocyte necrosis, reflecting direct viral cytopathic injury plus T-cell mediated immune destruction of infected cardiomyocytes. The clinical course of a preceding viral illness followed by heart failure symptoms and elevated troponin supports this diagnosis. Most cases are self-limited, but some progress to dilated cardiomyopathy.

• B. Granulomatous inflammation with giant cells is characteristic of giant cell myocarditis, a rarer and more fulminant entity.
• C. Fibrofatty replacement of the right ventricle describes arrhythmogenic right ventricular cardiomyopathy, a genetic condition.
• D. Non-caseating granulomas with Langhans giant cells suggest cardiac sarcoidosis, not viral myocarditis.
• E. Eosinophilic infiltrate with vasculitis suggests hypersensitivity myocarditis, typically from a drug reaction.

Doxorubicin and other anthracyclines cause dose-dependent cardiotoxicity primarily through generation of free radicals (reactive oxygen species) via iron-mediated redox cycling, leading to lipid peroxidation of cardiomyocyte membranes and progressive dilated cardiomyopathy. Dexrazoxane is an iron-chelating agent that limits free radical formation by preventing iron from participating in redox reactions, thereby reducing cardiotoxicity risk. It is used selectively in patients receiving high cumulative anthracycline doses. Serial echocardiographic monitoring of ejection fraction is standard practice to detect early cardiac dysfunction.

• B. Leucovorin rescues cells from methotrexate toxicity, not anthracycline cardiotoxicity.
• C. Mesna protects against hemorrhagic cystitis from cyclophosphamide/ifosfamide, not cardiotoxicity.
• D. Amifostine protects against cisplatin-induced nephrotoxicity and radiation injury, not cardiotoxicity.
• E. Allopurinol prevents tumor lysis syndrome-associated hyperuricemia, unrelated to cardiac protection.

This patient has constrictive pericarditis, most commonly caused by prior tuberculous pericarditis in endemic regions, in which a fibrotic, often calcified pericardium restricts diastolic filling of the heart. The Kussmaul sign, a paradoxical rise in jugular venous pressure with inspiration, occurs because the rigid pericardium prevents increased venous return from being accommodated by the right heart. The pericardial knock is an early diastolic sound caused by sudden cessation of ventricular filling when the expanding ventricle hits the stiff pericardial shell. Calcified, thickened pericardium on imaging with normal ventricular size and systolic function supports this diagnosis over infiltrative restrictive cardiomyopathy.

• A. Acute rheumatic pancarditis presents with fever, migratory arthritis, and active inflammation, not chronic calcific pericardial thickening.
• B. Cardiac tamponade presents acutely with pulsus paradoxus and a pericardial effusion, not a chronic calcified pericardium with a knock sound.
• C. Restrictive cardiomyopathy involves myocardial infiltration or fibrosis rather than pericardial thickening, and would not typically show a calcified pericardium on imaging.
• E. Hypertrophic cardiomyopathy shows asymmetric septal hypertrophy on echocardiogram, not pericardial thickening or calcification.

This patient has atrial fibrillation, identified by an irregularly irregular rhythm without discrete P waves on ECG, which results from chaotic multiple reentrant wavelets in the atria. Her CHA2DS2-VASc score includes points for age 65-74, hypertension, and diabetes, giving a score of at least 3, which indicates a high annual stroke risk and a guideline-based indication for anticoagulation. A direct oral anticoagulant, such as a factor Xa inhibitor, is preferred over aspirin or warfarin for most patients with non-valvular atrial fibrillation due to better efficacy and safety profile. Rate or rhythm control may be pursued separately for symptom management, but stroke prevention is the most immediately important intervention here.

• A. Aspirin alone is inferior to oral anticoagulation for stroke prevention in patients with a significant CHA2DS2-VASc score.
• B. Urgent cardioversion is not indicated in a hemodynamically stable, asymptomatic patient with unknown duration of atrial fibrillation, due to thromboembolism risk.
• C. Reassurance without anticoagulation would leave her at significant unaddressed stroke risk given her CHA2DS2-VASc score.
• D. Amiodarone addresses rhythm control but does not substitute for anticoagulation in a patient at elevated stroke risk.

This patient has Wolff-Parkinson-White syndrome, indicated by a short PR interval and delta wave (slurred QRS upstroke) from ventricular pre-excitation through an accessory conduction pathway called the bundle of Kent, which bypasses the normal decremental conduction of the AV node. In the setting of atrial fibrillation or flutter with a pre-excitation pathway, AV nodal blocking agents such as verapamil or digoxin suppress conduction through the AV node without affecting the accessory pathway, which lacks the decremental conduction properties of the AV node. This shifts conduction preferentially down the accessory pathway, potentially leading to very rapid ventricular rates and degeneration into ventricular fibrillation. Procainamide or ibutilide, which slow conduction in the accessory pathway itself, are safer choices in this scenario.

• B. Calcium channel blockers do not increase sinoatrial node automaticity; this is not the mechanism of danger in WPW.
• C. QT prolongation and torsades de pointes are not the mechanism by which calcium channel blockers are dangerous in WPW.
• D. Calcium channel blockers do not block fast sodium channels in the accessory pathway; that is a class I antiarrhythmic mechanism.
• E. Calcium channel blockers do not act primarily through vagal tone to affect the accessory pathway; their danger is from differential AV nodal blockade.

Sotalol is a class III antiarrhythmic that blocks the rapid component of the delayed rectifier potassium current (IKr), prolonging the action potential duration and the QT interval. Excessive QT prolongation predisposes to early afterdepolarizations and polymorphic ventricular tachycardia (torsades de pointes), exactly as seen in this patient's ECG. Risk is increased by bradycardia, hypokalemia, and hypomagnesemia, though her electrolytes here are within normal limits, showing this is a direct drug effect. QT-prolonging antiarrhythmics require baseline and follow-up ECG monitoring.

• A. Diltiazem is a calcium channel blocker that slows AV nodal conduction and does not prolong the QT interval.
• B. Flecainide is a class IC agent that slows conduction velocity (widens QRS) but does not significantly prolong the QT interval or cause torsades.
• D. Lidocaine is a class IB agent that shortens the action potential duration and is not associated with QT prolongation or torsades.
• E. Metoprolol is a beta-blocker that slows heart rate and AV conduction but is not associated with QT prolongation or torsades.

Adenosine activates A1 receptors on AV nodal cells, coupling through Gi proteins to open potassium channels (IK,Ado). This increases potassium efflux, hyperpolarizing the cell membrane and slowing conduction through the AV node, which transiently interrupts reentry circuits involving the AV node, such as in AV nodal reentrant tachycardia. Its extremely short half-life (seconds) explains the rapid onset and resolution of adverse effects like flushing and chest tightness. Adenosine is the first-line drug for acute termination of stable reentrant supraventricular tachycardia.

• A. Beta-blockade describes drugs like metoprolol; adenosine does not act on adrenergic receptors.
• B. Sodium channel blockade describes class I antiarrhythmics, not adenosine's mechanism.
• D. Potassium channel blockade prolonging the action potential describes class III antiarrhythmics, which is the opposite of adenosine's effect.
• E. Calcium channel blockade describes the mechanism of verapamil and diltiazem, not adenosine.