AMC MCQ (CAT) cardiology questions

ST elevation in leads II, III and aVF indicates an inferior myocardial infarction, which is most commonly caused by occlusion of the right coronary artery (supplying the inferior wall in most people). The reciprocal ST depression in leads I and aVL (the lateral leads) is characteristic of inferior STEMI and supports this localisation. The right coronary artery also frequently supplies the atrioventricular node, so inferior STEMI carries a risk of bradyarrhythmia and heart block. Right-sided leads (V4R) should be checked to assess for right ventricular involvement, which affects management such as avoiding nitrates.

• B. Left anterior descending occlusion typically causes ST elevation in the anterior leads V1-V4, not the inferior leads.
• C. Septal perforator occlusion would affect the septal leads V1-V2, not the inferior leads.
• D. Left circumflex occlusion typically causes ST elevation in the lateral leads I, aVL, V5-V6.
• E. Left main occlusion typically causes widespread ST elevation in aVR with diffuse ST depression, not isolated inferior changes.

A single normal troponin at presentation cannot exclude myocardial infarction, particularly if the pain onset was recent, because troponin takes time to rise after myocardial injury. Current guidelines recommend a repeat high-sensitivity troponin measurement at 1-3 hours (depending on the assay) to assess for a significant delta change, combined with clinical risk scores such as the HEART score, before a diagnosis of ACS can be safely excluded. This patient has a moderate-risk score and risk factors, so early discharge without a repeat troponin is unsafe. Serial troponin testing with risk stratification tools is the standard accelerated diagnostic pathway in Australian emergency departments.

• A. A single negative troponin is insufficient to exclude myocardial infarction, especially this early after symptom onset, so discharge is unsafe.
• B. Invasive angiography is not indicated until non-invasive risk stratification confirms a diagnosis of ACS.
• D. Outpatient stress testing a week later is inappropriate when the patient may still be having an evolving acute coronary syndrome.
• E. Empirical anticoagulation is not indicated before a diagnosis of ACS is confirmed and risk is further stratified.

When primary PCI cannot be delivered within 90-120 minutes of STEMI diagnosis, as is typical in rural and remote Australia, fibrinolytic therapy should be administered immediately (door-to-needle time under 30 minutes) unless contraindicated, followed by transfer to a PCI-capable centre for early angiography. Delaying treatment to wait for transport when PCI delay exceeds the guideline-recommended window increases infarct size and mortality. This pharmaco-invasive strategy balances rapid reperfusion with definitive revascularisation. Dual antiplatelet therapy alone without reperfusion therapy is inadequate for STEMI, and GTN infusion does not achieve reperfusion.

• A. GTN infusion relieves pain and may reduce preload but does not achieve coronary reperfusion in STEMI.
• C. Antiplatelet therapy alone without a reperfusion strategy does not restore coronary blood flow in STEMI.
• D. Waiting for retrieval when transport delay exceeds the guideline-recommended time to PCI unacceptably delays reperfusion.
• E. A 4-hour road transfer exceeds the time window within which primary PCI remains superior to immediate fibrinolysis.

Following acute coronary syndrome with drug-eluting stent insertion, current Therapeutic Guidelines recommend dual antiplatelet therapy with aspirin plus a P2Y12 inhibitor (ticagrelor or prasugrel preferred over clopidogrel in ACS) for 12 months in patients without a high bleeding risk, to reduce the risk of stent thrombosis and recurrent ischaemic events. After this period, most patients transition to lifelong single antiplatelet therapy, usually aspirin alone. Shorter durations of 1-3 months may be considered in patients at high bleeding risk, but 12 months remains the standard duration for ACS-related stenting. Indefinite dual therapy is not routinely recommended due to increasing bleeding risk without added ischaemic benefit beyond 12 months in most patients.

• A. One month is appropriate only for selected high-bleeding-risk patients, not the standard recommendation after ACS.
• B. Three months may be used in high bleeding risk patients but is not the standard duration after ACS with stenting.
• C. Indefinite dual antiplatelet therapy increases bleeding risk without additional benefit beyond 12 months in most patients.
• D. Two weeks is far shorter than the evidence-based duration needed to reduce stent thrombosis risk after ACS.

A new pansystolic murmur loudest at the lower left sternal border with a palpable thrill, occurring 3-5 days post-MI with haemodynamic compromise, is classic for ventricular septal rupture, confirmed here by echocardiographic demonstration of a left-to-right shunt across the septum. This complication results from necrosis and rupture of the infarcted interventricular septum and is more common after anterior STEMI. Papillary muscle rupture causes acute mitral regurgitation with a murmur radiating to the axilla, not a left-to-right shunt. Both VSD and papillary muscle rupture present similarly with sudden haemodynamic deterioration days after MI, making echocardiography essential to distinguish them and guide urgent surgical referral.

• A. Acute mitral regurgitation from papillary muscle rupture causes a murmur radiating to the axilla and mitral regurgitation on echo, not a septal shunt.
• B. Aortic regurgitation is not a recognised mechanical complication of myocardial infarction and would show a diastolic murmur.
• C. Right ventricular infarction causing tricuspid regurgitation typically occurs with inferior MI and does not produce a septal shunt on echocardiogram.
• E. Free wall rupture typically causes sudden cardiac tamponade and electromechanical dissociation, not a pansystolic murmur with a demonstrable shunt.

Cocaine causes sympathetic overdrive through blockade of catecholamine reuptake, producing coronary vasospasm, tachycardia and hypertension. Beta-blockers (including labetalol and esmolol, which retain beta activity) leave alpha-mediated vasoconstriction unopposed, worsening coronary spasm and hypertension. Benzodiazepines reduce central sympathetic outflow, lowering heart rate and blood pressure while easing agitation, and are the recommended first-line agent in cocaine-associated chest pain. Nitrates and calcium channel blockers can be added for ongoing hypertension or suspected spasm, but benzodiazepines are the initial step.

• A. Labetalol has beta-blocking activity and carries the same risk of unopposed alpha stimulation.
• B. Nifedipine is not first-line; benzodiazepines are given first to reduce sympathetic drive before considering a calcium channel blocker.
• C. Esmolol is a pure beta-blocker and risks the same unopposed alpha-mediated vasospasm.
• E. Beta-blockade leaves alpha-adrenergic vasoconstriction unopposed, worsening coronary vasospasm.

Acute pulmonary oedema should be managed with the patient sitting upright to reduce venous return and improve ventilation, supplemental oxygen to correct hypoxaemia, and sublingual or intravenous glyceryl trinitrate, which rapidly reduces preload and afterload through venodilation and arterial dilation. Intravenous frusemide is also given but acts more slowly through diuresis and venodilation, so nitrates are prioritised for immediate symptomatic relief. Beta-blockers are avoided in the acute decompensated phase as they can worsen cardiac output. Supine positioning worsens pulmonary congestion and dyspnoea.

• B. Beta-blockers are avoided in the acute phase of decompensated heart failure as they can further reduce cardiac output.
• C. Supine positioning worsens venous return to the lungs and increases breathlessness.
• D. Salbutamol is not indicated as there is no wheeze or bronchospasm, and supine positioning is harmful.
• E. Heparin is not part of first-line management of acute pulmonary oedema; the priority is positioning, oxygen and vasodilation.

The four pillars of disease-modifying therapy for HFrEF are an ACE inhibitor or ARNI, a beta-blocker, a mineralocorticoid receptor antagonist (such as spironolactone or eplerenone), and an SGLT2 inhibitor. Mineralocorticoid receptor antagonists block aldosterone-mediated sodium retention, myocardial fibrosis and remodelling, and have been shown in randomised trials to reduce mortality and hospitalisation when added to ACE inhibitor and beta-blocker therapy. His preserved renal function and normal potassium make this a safe addition with monitoring. Loop diuretics improve symptoms but do not alter mortality, and calcium channel blockers and alpha-blockers have no proven mortality benefit in HFrEF.

• A. Non-selective alpha-blockers have no established role and are not part of the four pillars of HFrEF therapy.
• B. Loop diuretics relieve congestive symptoms but have not been shown to reduce mortality in HFrEF.
• C. Centrally acting alpha-2 agonists are not part of guideline-directed therapy for HFrEF.
• E. Dihydropyridine calcium channel blockers have no mortality benefit in HFrEF and are not part of standard therapy.

Heart failure with preserved ejection fraction (HFpEF) is defined by clinical signs and symptoms of heart failure, an ejection fraction of 50% or greater, elevated natriuretic peptides, and structural or functional evidence of diastolic dysfunction such as left atrial enlargement or impaired relaxation. This patient's ejection fraction of 58% with diastolic impairment and raised NT-proBNP fits this definition. HFrEF requires an ejection fraction below 40%, and heart failure with mildly reduced ejection fraction refers to an ejection fraction of 41-49%. There is no finding here to suggest isolated right heart failure or a high-output state.

• B. Mildly reduced ejection fraction refers to a range of 41-49%, not 58%.
• C. There is no finding to suggest isolated right-sided failure such as cor pulmonale or tricuspid pathology.
• D. HFrEF requires an ejection fraction below 40%, which is inconsistent with her result of 58%.
• E. There is no evidence of a high-output state such as anaemia, thyrotoxicosis or arteriovenous shunting.

In general practice, when the diagnosis of heart failure is uncertain after history and examination, measurement of a natriuretic peptide such as NT-proBNP is recommended as an initial test because of its high negative predictive value. A normal result makes heart failure unlikely and avoids unnecessary echocardiography referral, while an elevated result supports referral for echocardiography to confirm the diagnosis and determine the type of heart failure. Chest X-ray can show congestive changes but is less sensitive for excluding heart failure. Echocardiography is the confirmatory test but is reserved for patients with a positive or inconclusive natriuretic peptide result to use resources appropriately.

• A. Echocardiography is the confirmatory investigation but is used after natriuretic peptide testing to triage referrals appropriately.
• B. Chest X-ray may support a diagnosis but is less sensitive than natriuretic peptide testing for excluding heart failure.
• C. Exercise stress testing is used to investigate ischaemia, not to establish a diagnosis of heart failure.
• E. Holter monitoring is used to investigate arrhythmia, not as an initial test for suspected heart failure.

Non-steroidal anti-inflammatory drugs inhibit renal prostaglandin synthesis, which normally maintains afferent arteriolar vasodilation and promotes natriuresis. This inhibition causes renal vasoconstriction, reduced glomerular filtration, and increased sodium and water retention, precipitating fluid overload in patients with underlying heart failure. NSAIDs can also blunt the diuretic effect of frusemide, compounding fluid retention. They do not cause direct myocardial toxicity, arrhythmia induction, accelerated atherosclerosis, or suppression of natriuretic peptides as their mechanism of decompensation.

• B. NSAIDs do not have a direct cardiotoxic effect on myocardial contractility.
• C. NSAID-induced decompensation occurs through fluid retention, not through accelerated atherosclerosis over this timeframe.
• D. NSAIDs do not suppress natriuretic peptide secretion; the mechanism is renal sodium and water retention.
• E. There is no indication of arrhythmia on the history or examination given.

Cardiorenal syndrome involves a bidirectional interaction where venous congestion and reduced cardiac output impair renal perfusion, and aggressive diuresis can further compromise renal function through intravascular volume depletion. When creatinine rises during diuresis, the diuretic dose should be reduced and the patient reassessed clinically for persisting congestion versus over-diuresis, since the patient remains overloaded on examination despite rising creatinine, a modest dose reduction with close monitoring is preferred over stopping diuretics or fluid resuscitation, which would worsen congestion. Sequential nephron blockade is used for diuretic resistance with persistent congestion, not when renal function is actively declining. Increasing ACE inhibitor dose acutely would further reduce glomerular filtration pressure and worsen renal function in this setting.

• A. Adding a thiazide for sequential blockade is used for diuretic resistance with ongoing congestion, not appropriate while renal function is worsening.
• B. Continuing the same dose without adjustment risks further renal deterioration given the significant creatinine rise and falling urine output.
• C. Stopping the diuretic and giving fluids risks worsening pulmonary congestion, as the patient remains volume overloaded on examination.
• D. Increasing ACE inhibitor dose acutely would further reduce glomerular filtration pressure, worsening renal function.

Complete (third-degree) AV block is characterised by complete dissociation between P waves and QRS complexes, with the atria and ventricles each beating at their own regular rate. The ventricular rate is slower than the atrial rate, and QRS width depends on the level of the block (wide if infranodal, as here). Variable intensity of heart sounds and intermittent large 'a' waves reflect varying timing of atrial and ventricular contraction. This rhythm is an indication for permanent pacemaker insertion regardless of symptoms once reversible causes are excluded.

• B. Mobitz II shows a constant PR interval with intermittently dropped QRS complexes, not independent atrial and ventricular rates.
• C. Atrial fibrillation shows an irregular rhythm with no discrete P waves, not a regular atrial rate with dissociated regular QRS complexes.
• D. Mobitz I shows progressive PR prolongation before a dropped beat, not complete dissociation of P waves and QRS complexes.
• E. First-degree block shows a prolonged but constant PR interval with every P wave followed by a QRS, which is not seen here.

This patient has Wolff-Parkinson-White syndrome with pre-excited atrial fibrillation conducting rapidly down the accessory pathway, producing an irregular broad-complex tachycardia with varying QRS morphology. AV nodal blocking agents such as verapamil, diltiazem, beta-blockers, digoxin and adenosine can preferentially block the AV node while sparing the accessory pathway, allowing even faster conduction to the ventricles and precipitating ventricular fibrillation. Haemodynamically unstable patients should undergo synchronised DC cardioversion; stable patients can be treated with a drug that slows conduction through the accessory pathway, such as flecainide or procainamide, under specialist guidance.

• B. Flecainide slows conduction through the accessory pathway and is an appropriate treatment option in pre-excited AF.
• C. Synchronised cardioversion is the treatment of choice in a haemodynamically unstable patient with pre-excited AF.
• D. Procainamide slows accessory pathway conduction and is a recognised treatment for pre-excited AF.
• E. Amiodarone is an acceptable option in pre-excited AF as it affects both the AV node and the accessory pathway.

The combination of exertional angina, syncope and dyspnoea with a harsh ejection systolic murmur radiating to the carotids, slow-rising pulse and soft, delayed A2 is classic for severe aortic stenosis. Transthoracic echocardiography is the investigation of choice to confirm the diagnosis, assess valve area and gradient, quantify left ventricular function, and guide the decision for valve replacement. Exercise testing is contraindicated in symptomatic severe aortic stenosis due to the risk of syncope or sudden death. Coronary angiography is performed later as part of pre-operative work-up, not as the initial diagnostic test.

• A. Coronary angiography is used for pre-operative assessment once aortic stenosis severity has been established by echocardiography, not as the initial test.
• C. Exercise stress testing is contraindicated in a patient with symptomatic aortic stenosis and syncope due to risk of haemodynamic collapse.
• D. Chest X-ray may show cardiomegaly or valve calcification but cannot quantify stenosis severity or guide management.
• E. Holter monitoring assesses rhythm over time and does not characterise valvular structure or severity.

A pansystolic murmur at the apex radiating to the axilla, with a soft S1 and laterally displaced apex beat, is characteristic of mitral regurgitation. In a patient with prior myocardial infarction, ischaemic papillary muscle or chordal dysfunction causing incomplete mitral leaflet coaptation is a common and important cause of chronic mitral regurgitation. Other causes include myxomatous degeneration, rheumatic disease and infective endocarditis, but the history of prior infarction points specifically to ischaemic papillary muscle dysfunction here.

• A. Rheumatic mitral stenosis produces a mid-diastolic murmur with an opening snap, not a pansystolic murmur.
• B. Hypertrophic cardiomyopathy produces a systolic ejection murmur that increases with Valsalva, not a typical axilla-radiating pansystolic murmur.
• C. Aortic valve calcification causes aortic stenosis with an ejection systolic murmur radiating to the carotids, not a pansystolic apical murmur.
• D. Atrial septal defect produces a pulmonary flow murmur and fixed splitting of the second heart sound, not a pansystolic apical murmur.

The modified Duke criteria classify a case as definite infective endocarditis when two major criteria are met, or one major plus three minor, or five minor criteria. Here there are two major criteria: typical organism (Staphylococcus aureus) in two separate blood cultures, and echocardiographic evidence of a vegetation on the tricuspid valve. The fever and injecting drug use additionally serve as minor criteria, but two major criteria alone are sufficient to classify this as definite endocarditis. Osler's nodes (tender pulp nodules) are a further minor criterion, reinforcing the diagnosis.

• A. The criteria here are more than sufficient; two major criteria alone meet the threshold for a definite diagnosis.
• B. Rejected endocarditis applies when an alternative diagnosis explains the findings or criteria resolve rapidly with antibiotics, which does not apply here.
• D. Possible endocarditis applies when findings fall short of definite criteria, which is not the case here given two major criteria are met.
• E. There is no category of 'excluded requiring alternative diagnosis' in the Duke criteria, and the findings strongly support endocarditis rather than refute it.

Patients with prosthetic heart valves, including bioprosthetic valves, are in the highest-risk category for infective endocarditis and are recommended antibiotic prophylaxis before dental procedures involving manipulation of the gingival tissue or periapical region, such as extractions. Therapeutic Guidelines recommend a single oral dose of amoxycillin 2 g given 1 hour before the procedure for patients who can take oral medication and have no penicillin allergy. Clindamycin is reserved as the alternative for patients with a penicillin allergy. Multi-day courses are not used for dental prophylaxis.

• B. Cephalexin is not the first-line recommended agent, and prophylaxis must be given before, not after, the procedure to achieve adequate tissue levels.
• C. This patient has a prosthetic valve, a high-risk condition for which prophylaxis before invasive dental procedures is specifically recommended.
• D. Clindamycin is the appropriate alternative only in patients with penicillin hypersensitivity; this patient has no stated allergy.
• E. Prophylaxis for dental procedures is a single pre-procedure dose, not a multi-day course.

This patient has rheumatic heart disease with mitral stenosis, most likely following unrecognised acute rheumatic fever, a condition with disproportionately high incidence among Aboriginal and Torres Strait Islander people, particularly in remote communities. Secondary prophylaxis with regular intramuscular benzathine penicillin G every 4 weeks (3-4 weekly depending on risk) is recommended to prevent recurrent group A streptococcal infection and further valve damage, and should continue for a minimum duration based on age and disease severity, often into adulthood. Oral penicillin is less effective due to adherence issues and is only used when intramuscular therapy is refused or contraindicated.

• A. Aspirin has no role in preventing recurrent rheumatic fever or progression of valve disease.
• B. Prophylaxis must be continuous year-round, not seasonal, to prevent recurrent streptococcal infection.
• C. Continuous oral amoxycillin is not the recommended regimen; adherence is poor and intramuscular benzathine penicillin is preferred for secondary prophylaxis.
• D. Anticoagulation may be needed if atrial fibrillation or thromboembolism develops, but it does not prevent recurrent rheumatic fever or valve progression.

Mechanical heart valves require lifelong vitamin K antagonist therapy (warfarin) because direct oral anticoagulants have been shown in trials to increase the risk of valve thrombosis and thromboembolic events compared with warfarin. Target INR depends on valve type and position (generally 2.5-3.5 for mechanical aortic valves with additional risk factors, or 2.0-3.0 for low-risk bileaflet aortic valves). Warfarin's reversibility and established dosing predictability through INR monitoring make it the only validated option for mechanical prostheses. Aspirin may be added for additional antiplatelet effect but does not replace anticoagulation.

• A. DOACs are contraindicated in mechanical valves due to increased thrombotic risk shown in trials (e.g. RE-ALIGN with dabigatran).
• C. Dabigatran was associated with increased thromboembolic and bleeding events in mechanical valve patients and is contraindicated.
• D. Rivaroxaban has no proven efficacy and is not recommended for mechanical prosthetic valves.
• E. Aspirin alone is insufficient to prevent valve thrombosis in mechanical prostheses.

Office blood pressure of 140/90 mmHg or higher combined with a normal ambulatory daytime average (below 135/85 mmHg) defines white coat hypertension. Ambulatory blood pressure monitoring is the reference standard for confirming a diagnosis of hypertension because it reduces misclassification from the white coat effect and provides a better predictor of cardiovascular risk than isolated clinic readings. Patients with confirmed white coat hypertension do not require pharmacological treatment but should have periodic blood pressure review and cardiovascular risk assessment, as some progress to sustained hypertension. Lifestyle advice is still appropriate.

• A. Masked hypertension is the opposite pattern: normal clinic readings with elevated ambulatory readings.
• B. Ambulatory monitoring is the more reliable, guideline-recommended confirmatory test, not the clinic reading.
• D. There is no indication of secondary hypertension; the ambulatory result demonstrates a white coat effect rather than true hypertension.
• E. Sustained hypertension would require an elevated ambulatory average as well as elevated clinic readings; her ambulatory average is normal.

In patients with diabetes and microalbuminuria or proteinuria, an ACE inhibitor (or ARB if intolerant) is the preferred first-line agent because it reduces intraglomerular pressure and slows progression of diabetic nephropathy independent of its blood pressure-lowering effect. This renoprotective benefit is additional to blood pressure control and is specifically recommended by the RACGP Red Book and eTG for hypertensive patients with diabetic kidney disease. Calcium channel blockers and thiazide-like diuretics are reasonable alternatives but lack the specific antiproteinuric effect of renin-angiotensin system blockade.

• A. Amlodipine is a reasonable add-on agent but does not provide the specific renoprotective effect needed with microalbuminuria.
• C. Indapamide is an appropriate first-line option in uncomplicated hypertension but is not preferred over an ACE inhibitor when microalbuminuria is present.
• D. Beta-blockers are not first-line for uncomplicated hypertension and have no specific renoprotective benefit here.
• E. Spironolactone is reserved for resistant hypertension, not first-line therapy, and risks hyperkalaemia in diabetic nephropathy.

Paroxysmal hypertension accompanied by the classic triad of headache, palpitations and diaphoresis, especially when episodic and triggered by abdominal pressure (such as straining), is highly suggestive of phaeochromocytoma. Plasma free metanephrines (or 24-hour urinary fractionated metanephrines) have high sensitivity for catecholamine-secreting tumours and are the recommended first-line biochemical screening test. Renal artery imaging would be appropriate if the clinical picture suggested renovascular disease, such as resistant hypertension with an abdominal bruit or flash pulmonary oedema, which is not described here.

• B. Thyrotoxicosis can cause palpitations but does not produce this pattern of paroxysmal severe hypertension with headache and diaphoresis.
• C. Cushing syndrome classically presents with weight gain, striae and other features of cortisol excess, not paroxysmal catecholamine symptoms.
• D. Renal artery stenosis typically causes sustained rather than episodic hypertension and would not explain the paroxysmal catecholamine-type symptoms described.
• E. Primary hyperaldosteronism causes sustained hypertension, often with hypokalaemia, rather than episodic symptomatic surges.

This patient has severely elevated blood pressure without evidence of acute target organ damage (no encephalopathy, papilloedema, acute kidney injury, acute coronary syndrome, or pulmonary oedema), consistent with hypertensive urgency rather than emergency. Hypertensive urgency is managed with oral antihypertensive therapy and close outpatient follow-up over days rather than rapid intravenous blood pressure reduction, which risks hypoperfusion injury. Hypertensive emergency, defined by acute end-organ damage, requires controlled intravenous therapy with a target reduction of blood pressure by around 25% within the first hour. Rapid uncontrolled lowering, as with sublingual nifedipine, is contraindicated due to the risk of precipitating ischaemic stroke or myocardial infarction.

• A. Severely elevated blood pressure of this degree still requires treatment and prompt follow-up, not deferral for a month.
• B. Sublingual nifedipine causes uncontrolled rapid blood pressure drops and is contraindicated due to risk of cerebral or myocardial ischaemia.
• C. The 25% within one hour reduction target applies to hypertensive emergency with target organ damage, not urgency.
• E. Intravenous nitroprusside and ICU admission are reserved for hypertensive emergency with end-organ damage, which is absent here.

A persistent dry cough developing after starting an ACE inhibitor is a recognised class effect caused by accumulation of bradykinin and substance P in the respiratory tract due to inhibited ACE-mediated breakdown. The cough typically resolves within days to a few weeks of stopping the drug. Angiotensin receptor blockers act on the same renin-angiotensin pathway for blood pressure control and renal protection but do not inhibit bradykinin breakdown, so they rarely cause this cough, making them the preferred substitute rather than switching to an unrelated drug class.

• A. Dose reduction does not reliably resolve ACE inhibitor-induced cough, which is not clearly dose-dependent.
• C. The cough is a drug-induced class effect that will persist while the ACE inhibitor is continued; symptomatic treatment does not address the cause.
• D. Symptomatic cough suppression does not address the underlying bradykinin-mediated cause and the patient should not remain on a poorly tolerated drug when an equally effective alternative exists.
• E. A calcium channel blocker is a reasonable antihypertensive but is not the preferred replacement, since an ARB maintains the same pathway benefits (e.g. renal protection) without causing the cough.

True resistant hypertension, defined as blood pressure above target despite three antihypertensive agents at optimal doses including a diuretic, with confirmed adherence, warrants screening for secondary causes before escalating therapy. Primary hyperaldosteronism is the most common identifiable secondary cause in this setting and is screened for using the plasma aldosterone-to-renin ratio, alongside checking electrolytes for unexplained hypokalaemia. Identifying a secondary cause can change management significantly, such as targeted therapy with a mineralocorticoid receptor antagonist or adrenalectomy, rather than simply layering on empirical fourth-line agents.

• B. Clonidine is a later-line agent and should not be added before secondary causes are excluded.
• C. Renal artery intervention should only follow confirmatory imaging and functional assessment, not be performed empirically.
• D. Spironolactone is an appropriate fourth-line agent in confirmed resistant hypertension but secondary causes should be screened for first, as the result may change management.
• E. Exceeding the recommended maximum dose of a thiazide-like diuretic increases adverse effects without proportional benefit and does not address a possible secondary cause.

Statin-associated muscle symptoms warrant a baseline creatine kinase (CK) measurement to exclude significant myopathy before deciding on dose adjustment or cessation. If CK is normal or only mildly elevated (less than 4 times the upper limit of normal) and symptoms are tolerable, the statin can usually be continued or trialled at a lower dose. Markedly elevated CK (more than 10 times the upper limit of normal) or severe symptoms warrants cessation and investigation for rhabdomyolysis. Checking CK first guides safe decision-making rather than reflex cessation or reassurance without data.

• A. Immediate permanent cessation without biochemical assessment is premature when symptoms are mild and CK status is unknown.
• B. Electromyography is not indicated for straightforward statin-associated myalgia without neurological signs.
• D. Switching to a fibrate empirically is not appropriate before confirming the diagnosis and the fibrate class carries its own myopathy risk, especially in combination with statins.
• E. Reassurance without checking CK risks missing a clinically significant myopathy.

Tendon xanthomata, markedly elevated LDL-cholesterol, and a family history of premature coronary disease strongly suggest familial hypercholesterolaemia (FH), an autosomal dominant condition usually caused by LDL-receptor gene mutations. Once FH is clinically suspected or confirmed, cascade testing (sequential screening of first-degree relatives using lipid levels and, where available, genetic testing) is recommended to identify affected relatives early, as per Australian FH guidelines. Early identification allows statin therapy to begin before significant atherosclerosis develops. Diet alone is inadequate for the markedly elevated LDL levels seen in FH.

• A. FH carries a high lifetime risk of premature coronary disease and requires active management even in asymptomatic patients.
• B. Tendon xanthomata are a specific clinical sign of FH, not a normal ageing change.
• C. Coronary angiography is not a prerequisite for starting lipid-lowering therapy in suspected FH without anginal symptoms.
• E. Diet modification alone is insufficient for the severity of LDL elevation typical of FH; statin therapy is required.

In genuine statin intolerance confirmed by trial of at least two or three different statins, ezetimibe is the recommended next pharmacological step as it lowers LDL-cholesterol by inhibiting intestinal cholesterol absorption and has a low rate of muscle-related adverse effects. PCSK9 inhibitors (such as evolocumab) are reserved for patients with inadequate LDL control on maximally tolerated statin plus ezetimibe, or genuine statin intolerance with persistently high LDL despite ezetimibe, and require specialist initiation and PBS criteria. Fibrates and niacin are not first-line for LDL-lowering in this context, and bile acid sequestrants are poorly tolerated and less effective.

• A. PCSK9 inhibitors are reserved for patients who have not achieved target LDL on ezetimibe or have specific PBS-defined criteria, not as an immediate first-line step.
• B. Bile acid sequestrants are poorly tolerated and less effective than ezetimibe for LDL reduction.
• C. Fibrates primarily lower triglycerides and have modest LDL-lowering effect; they are not first-line after statin intolerance.
• D. Niacin has a poor adverse effect profile and is not first-line LDL-lowering therapy.

This presentation with positional chest pain, pericardial friction rub, diffuse ST elevation with PR depression, and recent viral prodrome is classic for acute pericarditis. First-line treatment is a nonsteroidal anti-inflammatory drug such as ibuprofen combined with colchicine, which reduces symptom duration and the risk of recurrence. Corticosteroids are reserved for cases with contraindications to NSAIDs, autoimmune aetiology, or recurrent pericarditis refractory to NSAIDs/colchicine, as early steroid use increases recurrence risk. Anticoagulation is avoided due to the risk of haemorrhagic transformation into tamponade in the presence of pericardial inflammation.

• A. Beta-blockers have no established role in uncomplicated acute pericarditis management.
• B. The clinical and ECG findings are typical of pericarditis rather than acute coronary syndrome, and urgent angiography is not indicated.
• C. Corticosteroids are not first-line as they increase the risk of recurrent pericarditis; they are reserved for refractory or contraindicated cases.
• E. Anticoagulation is avoided in pericarditis as it increases the risk of haemorrhagic pericardial effusion and tamponade.

This patient has Beck's triad (hypotension, elevated jugular venous pressure, and muffled heart sounds) along with pulsus paradoxus greater than 10 mmHg, consistent with cardiac tamponade, likely from malignant pericardial effusion. Tamponade is a medical emergency requiring urgent pericardiocentesis to relieve the pressure on the heart and restore cardiac output. While bedside echocardiography should be performed urgently to confirm the diagnosis and guide drainage, it should not delay life-saving intervention in a haemodynamically unstable patient. Diuretics and anticoagulation are contraindicated as they can worsen haemodynamic compromise or precipitate bleeding into the pericardial space.

• A. Waiting for a routine echocardiogram delays life-saving treatment in a haemodynamically unstable patient.
• C. Corticosteroids have no role in the emergency management of cardiac tamponade.
• D. Diuretics reduce preload and can worsen hypotension in tamponade, where adequate filling pressure is needed to maintain cardiac output.
• E. Anticoagulation risks worsening a haemorrhagic pericardial effusion and is contraindicated in tamponade.

This presentation, a viral prodrome followed by arrhythmia, heart failure symptoms, elevated troponin and a normal coronary angiogram, is characteristic of acute myocarditis. Cardiac magnetic resonance imaging is the investigation of choice as it can identify myocardial oedema, hyperaemia and late gadolinium enhancement using Lake Louise criteria, confirming the diagnosis non-invasively. Endomyocardial biopsy remains the gold standard in selected severe or ambiguous cases but is more invasive and reserved for when MRI findings are inconclusive or fulminant myocarditis is suspected. Exercise testing is inappropriate and potentially dangerous in suspected acute myocarditis due to arrhythmia risk.

• A. A ventilation-perfusion scan assesses for pulmonary embolism and does not address the suspected myocardial pathology.
• C. Right heart catheterisation is not the investigation of choice for diagnosing myocarditis; it assesses haemodynamics rather than myocardial tissue characteristics.
• D. Exercise stress testing is contraindicated in suspected acute myocarditis due to the risk of inducing malignant arrhythmia.
• E. Thyroid dysfunction would not explain the troponin elevation or the clinical picture following a viral illness.

Peripartum cardiomyopathy typically presents with heart failure symptoms, dyspnoea, orthopnoea, and oedema, developing in the last month of pregnancy to five months postpartum in a woman without prior cardiac disease. The presence of an S3 gallop, elevated jugular venous pressure, and bibasal crackles indicates true left ventricular dysfunction rather than the mild physiological dyspnoea expected from pregnancy-related haemodynamic changes, which resolves rather than worsens postpartum. Echocardiography confirming a reduced left ventricular ejection fraction (typically below 45%) establishes the diagnosis. Early recognition is important as it is a leading cause of pregnancy-associated cardiovascular morbidity and mortality.

• A. Pulmonary embolism typically presents with pleuritic chest pain and tachycardia without the gallop rhythm and bilateral crackles pattern seen here, though it remains a differential; the combined signs point more specifically to heart failure.
• B. Postpartum pre-eclampsia is associated with hypertension and proteinuria, which are absent here.
• D. Anaemia can cause dyspnoea and tachycardia but does not account for the S3 gallop and elevated jugular venous pressure indicating fluid overload and ventricular dysfunction.
• E. Normal physiological dyspnoea does not cause an S3 gallop, elevated jugular venous pressure, or crackles, and would be expected to improve rather than worsen after delivery.

A fixed, widely split S2 that does not change with respiration is the classical auscultatory finding of an atrial septal defect (ASD), caused by chronic right ventricular volume overload from left-to-right shunting, which equalises filling times of both ventricles regardless of the respiratory cycle. The associated systolic flow murmur reflects increased flow across the right ventricular outflow tract and pulmonary valve, not the shunt itself. Many ASDs are first diagnosed in adulthood because they are often asymptomatic in childhood, with symptoms such as dyspnoea and atrial arrhythmias emerging in the third or fourth decade. Right axis deviation and incomplete RBBB on ECG reflect right ventricular volume overload, supporting this diagnosis.

• B. VSD typically causes a harsh pansystolic murmur at the lower left sternal border, and S2 splitting is usually normal or narrowly split.
• C. Mitral valve prolapse causes a mid-systolic click and late systolic murmur at the apex, not a fixed split S2.
• D. Pulmonary stenosis causes an ejection systolic murmur with a widely split S2 that still varies with respiration.
• E. PDA classically causes a continuous 'machinery' murmur, not an isolated systolic murmur with fixed split S2.

Coarctation of the aorta classically presents with hypertension in the upper limbs and reduced, delayed blood pressure and pulses in the lower limbs, because the narrowing is usually located just distal to the left subclavian artery near the ductus arteriosus. The interscapular systolic murmur arises from turbulent flow across the coarctation site and through dilated collateral intercostal arteries. This combination of radio-femoral delay and an arm-leg blood pressure gradient of more than 10-20 mmHg is diagnostic and warrants echocardiography and CT or MR angiography to confirm the site and severity. Early recognition is important because untreated coarctation leads to left ventricular hypertrophy, aortic dissection and premature cardiovascular disease.

• A. Takayasu arteritis can cause limb pulse discrepancies but typically presents in young women with systemic inflammatory features and arm-arm, not predominantly arm-leg, differences.
• B. PDA causes a continuous machinery murmur and does not typically cause this pattern of upper-limb hypertension with reduced leg pulses.
• C. Renal artery stenosis causes hypertension but does not cause radio-femoral delay or an interscapular murmur.
• D. Essential hypertension would not cause a femoral pulse delay or a leg blood pressure lower than the arm.

In a haemodynamically stable patient with a clinical picture suggesting acute aortic dissection, contrast-enhanced CT angiography of the chest, abdomen and pelvis is the investigation of choice because it rapidly and accurately defines the extent of dissection, involvement of branch vessels, and presence of complications such as rupture, and is widely available. The blood pressure discrepancy between arms and asymmetric pulses reflect involvement of the aortic arch branches, strongly supporting this diagnosis. Transthoracic echocardiography can detect proximal dissection but has lower sensitivity for the descending aorta, making it inferior to CT for full anatomical assessment. D-dimer may be used to help exclude dissection in low-probability cases but is not definitive and does not replace imaging when the clinical suspicion is high.

• B. D-dimer has a role in excluding dissection in low-risk patients but cannot confirm the diagnosis in a high pre-test probability scenario like this.
• C. Transthoracic echocardiography has limited sensitivity, particularly for the descending aorta, so it is not the most appropriate confirmatory test when CT is available.
• D. An exercise stress test is contraindicated and irrelevant in suspected acute aortic dissection.
• E. Chest X-ray may show a widened mediastinum but lacks the sensitivity and specificity to confirm or exclude dissection.

Perioperative risk assessment combines estimated surgical risk with functional capacity, expressed in metabolic equivalents (METs). A patient able to climb two flights of stairs or walk briskly without symptoms has a functional capacity of at least 4 METs, which is considered good and is associated with low perioperative cardiac risk regardless of a moderate-risk procedure. Current guidelines recommend proceeding directly to surgery in patients with good functional capacity (≥4 METs) without further non-invasive cardiac testing, as such testing rarely changes management and delays surgery. Stress testing or angiography is reserved for patients with poor or unknown functional capacity and additional clinical risk factors undergoing higher-risk surgery.

• A. Exercise ECG testing is not required when functional capacity can already be reliably estimated as good from history.
• B. Stress echocardiography is unnecessary in a patient with good functional capacity and stable symptoms; it would only be considered if functional capacity were poor or unknown with additional risk factors.
• D. Routine biomarker testing is not part of standard preoperative assessment when functional capacity is good and the patient is clinically stable.
• E. Angiography is not indicated for routine preoperative risk stratification in a patient with stable, mild coronary disease and good functional capacity.

After drug-eluting stent placement, dual antiplatelet therapy is typically continued for at least six to twelve months to reduce the risk of stent thrombosis. For elective, non-cardiac, non-urgent surgery with a bleeding risk, clopidogrel is usually withheld for five days preoperatively to allow platelet function to recover, while aspirin is continued perioperatively to provide some ongoing protection against stent thrombosis, unless the bleeding risk of the specific procedure (such as neurosurgery) is prohibitive. Clopidogrel is then restarted as soon as safely possible after surgery. Elective surgery should ideally be delayed until at least six months after drug-eluting stent insertion if clinically feasible, but by eight months this patient is past that minimum window, so proceeding with this bridging strategy is appropriate rather than further delay.

• A. Stopping both agents significantly increases the risk of stent thrombosis and is not standard practice for inguinal hernia repair.
• C. The minimum six-month period after drug-eluting stent placement has already passed, so further delay to twelve months is not required.
• D. Aspirin should generally be continued, not stopped, as it carries lower bleeding risk and helps protect against stent thrombosis; clopidogrel is the agent usually withheld.
• E. Continuing both agents unchanged increases perioperative bleeding risk unnecessarily for a procedure where this can be mitigated.

Cardiac rehabilitation programs, which combine supervised exercise training, risk factor modification, education and psychosocial support, have strong evidence for reducing cardiovascular mortality and hospital readmission after myocardial infarction and are recommended for all patients following an acute coronary event. Referral should occur before or shortly after discharge, and programs can be delivered via telehealth or community-based models for patients in rural or remote areas to improve access. There is no indication here for routine serial echocardiography alone as the sole additional step, pacemaker assessment, an additional rate-limiting agent without a specific indication such as ongoing angina or arrhythmia, or a blanket recommendation to avoid physical activity, which is counterproductive to recovery.

• A. Prolonged avoidance of physical activity is not recommended and contradicts the exercise-based recovery supported by cardiac rehabilitation.
• B. There is no indication of conduction disease or bradyarrhythmia requiring pacemaker assessment in this patient.
• C. There is no specific indication, such as refractory angina, for adding a calcium channel blocker to his current regimen.
• D. Routine echocardiography alone does not address secondary prevention and is not a substitute for a structured rehabilitation program.

Vasovagal syncope is suggested by a clear situational trigger such as prolonged standing, heat and a crowded environment, together with a prodrome of nausea, diaphoresis and light-headedness, and rapid, complete recovery of consciousness. Brief myoclonic jerks lasting only a few seconds can occur during convulsive syncope due to transient cerebral hypoperfusion and do not indicate epilepsy, which would be expected to cause a more prolonged seizure with a slower, confused post-ictal recovery. Cardiac syncope typically occurs abruptly without a prodrome, may happen during exertion or while supine, and would be expected to show ECG abnormalities, none of which are present here. Normal orthostatic blood pressure measurements exclude orthostatic hypotension as the cause.

• A. The brief myoclonic jerks and rapid, non-confused recovery are consistent with convulsive syncope rather than a true epileptic seizure, which would show a more prolonged ictal and post-ictal phase.
• B. There is no history of exertional onset or known structural heart disease to suggest hypertrophic cardiomyopathy.
• C. Cardiac syncope due to arrhythmia usually has little or no prodrome and often occurs without positional triggers; this patient had a classic vasovagal prodrome and trigger.
• E. Lying and standing blood pressure measurements were normal, excluding orthostatic hypotension.

Validated chest pain risk stratification tools such as the HEART score combine history, ECG findings, age, risk factors and troponin results to identify patients at low risk of a major adverse cardiac event who can be safely managed without invasive early investigation. Even in a low-risk category, current practice requires a second troponin measurement several hours after symptom onset, in line with the diagnostic protocol being used, to confidently exclude myocardial infarction before considering discharge, because a single normal troponin very early after symptom onset may not have had time to rise. Immediate discharge without any repeat testing risks missing early myocardial infarction, while angiography, thrombolysis or direct catheterisation laboratory transfer are not indicated for a patient already classified as low risk with a normal ECG.

• B. Inpatient angiography is not indicated for a patient stratified as low risk with a normal ECG and normal initial troponin.
• C. A single early troponin result alone is insufficient to exclude myocardial infarction; a repeat troponin after an appropriate interval is required even in low-risk patients.
• D. There is no ECG evidence of ST elevation or other indication for thrombolysis.
• E. Direct transfer to the catheterisation laboratory is reserved for high-risk presentations such as STEMI, not a low-risk chest pain presentation.

Costochondritis is characterised by sharp, localised chest wall pain that is reproducible on direct palpation of the costal cartilages, typically worsened by movement or deep breathing, occurring in a patient with a normal ECG and no systemic or cardiovascular red flags. This reproducibility of pain on palpation is a key clinical feature distinguishing musculoskeletal chest pain from cardiac or other serious intrathoracic causes, which are not typically reproduced by chest wall pressure. Unstable angina presents with exertional or rest pain without a clear chest wall trigger, usually in patients with cardiovascular risk factors, and would not be reproduced by palpation. Pulmonary embolism and pneumothorax typically present with dyspnoea, hypoxia or pleuritic pain without a clearly reproducible tender point, and pericarditis usually causes positional pain with classic ECG changes such as diffuse ST elevation and PR depression, none of which are present here.

• A. Pulmonary embolism typically presents with dyspnoea or hypoxia and pleuritic pain, not pain reproducible by chest wall palpation, and this patient has normal oxygen saturation and no risk factors.
• B. Acute pericarditis usually causes positional chest pain with characteristic diffuse ECG changes, which are absent here.
• C. Spontaneous pneumothorax typically causes sudden dyspnoea and reduced oxygen saturation, neither of which is present in this patient.
• D. Unstable angina would not typically be reproduced by direct chest wall palpation and usually occurs with exertion or cardiovascular risk factors.

His CHA2DS2-VASc score is 2 (hypertension = 1, age 65–74 = 1), which meets the threshold for recommending oral anticoagulation in non-valvular AF according to Therapeutic Guidelines. A direct oral anticoagulant is preferred over warfarin in most patients with non-valvular AF because of comparable or superior efficacy, lower intracranial bleeding risk and no need for routine monitoring. Aspirin alone is no longer recommended for stroke prevention in AF because it is inferior to anticoagulation and carries a similar bleeding risk. Aboriginal and Torres Strait Islander people have higher cardiovascular risk and should not be undertreated; a CHA2DS2-VASc score of 2 or more in men warrants anticoagulation regardless of ethnicity.

• A. A CHA2DS2-VASc score of 2 warrants anticoagulation, not simple observation.
• B. Aspirin monotherapy is not recommended for stroke prevention in AF as it is inferior to anticoagulation.
• C. There is no haemodynamic instability or indication for urgent cardioversion.
• D. Echocardiography is not required to decide on anticoagulation, which is based on clinical risk scoring.

This patient has new-onset AF with adverse features of haemodynamic compromise, including hypotension, pulmonary oedema and altered mental state, which is an indication for immediate synchronised cardioversion. Delaying cardioversion to trial rate- or rhythm-controlling drugs risks further deterioration in a patient who is already unstable. Synchronisation avoids delivering the shock during the vulnerable period of the T wave, reducing the risk of inducing ventricular fibrillation. Rate-controlling drugs such as beta-blockers or digoxin may worsen hypotension and are not appropriate first-line therapy in this unstable setting.

• A. Amiodarone infusion acts too slowly for a haemodynamically unstable patient requiring immediate intervention.
• B. Flecainide is contraindicated in a haemodynamically unstable patient and in those with possible structural or ischaemic heart disease.
• C. Digoxin has a slow onset of action and does not address the acute instability.
• E. Beta-blockers can worsen hypotension and heart failure and do not address the need for immediate rhythm restoration in an unstable patient.

In persistent AF, a rate control strategy is generally preferred as first-line management when ventricular rate is adequately controlled and symptoms are mild, as rhythm control has not been shown to improve survival over rate control in most patients. This man has well-controlled heart rate, minimal symptoms, preserved ejection fraction and good functional status, so continuing current therapy with regular review is appropriate. Rhythm control strategies, such as cardioversion or antiarrhythmic drugs, are reserved for patients with significant symptoms, young age, first episode, or if rate control fails to relieve symptoms. AV node ablation with pacing is a last resort for refractory rate control, not first-line therapy.

• B. Elective cardioversion is not necessary given good rate control and minimal symptoms; rhythm control confers no mortality benefit over rate control in this context.
• C. Digoxin is not indicated when rate is already well controlled with a beta-blocker and would add toxicity risk without symptomatic benefit.
• D. Amiodarone has significant long-term toxicity and is not indicated when the patient is minimally symptomatic on a rate control strategy.
• E. AV node ablation and pacing is reserved for refractory cases unresponsive to pharmacological rate control, not appropriate here.

Direct oral anticoagulants are contraindicated in patients with mechanical heart valves because trials have shown increased rates of thromboembolism and valve thrombosis compared with warfarin, which remains the standard of care in this setting. Warfarin's vitamin K antagonism provides anticoagulation that has been specifically validated for mechanical valve prostheses, unlike DOACs, which target factor Xa or thrombin and have not demonstrated equivalent protection against valve thrombosis. This contraindication applies regardless of renal function or bleeding risk. She should continue warfarin with regular INR monitoring to maintain her target therapeutic range.

• A. DOACs are contraindicated with mechanical valves; combining with INR monitoring does not make this safe.
• B. Dabigatran is a direct thrombin inhibitor and is specifically contraindicated with mechanical heart valves due to increased thromboembolic events.
• C. Rivaroxaban, like other DOACs, is contraindicated with mechanical heart valves irrespective of dose.
• D. Adding aspirin to a DOAC does not overcome the contraindication to DOAC use with a mechanical valve and increases bleeding risk.

After failed vagal manoeuvres in a haemodynamically stable patient with regular narrow-complex SVT, intravenous adenosine is the treatment of choice. Adenosine transiently blocks conduction through the AV node, interrupting the re-entrant circuit responsible for most SVTs, and has a very short half-life of under 10 seconds, requiring rapid bolus administration followed immediately by a saline flush to ensure it reaches the heart before being metabolised. If the initial 6 mg dose fails, a larger 12 mg dose can be given. Electrical cardioversion is reserved for haemodynamically unstable patients or when pharmacological measures fail, while oral agents act too slowly for acute termination.

• A. Oral metoprolol has too slow an onset for acute termination of this tachycardia.
• B. Cardioversion is reserved for unstable patients or failure of pharmacological therapy, not as the immediate next step here.
• C. Digoxin has a slow onset of action and is not appropriate for acute termination of SVT in the emergency setting.
• D. Amiodarone is not first-line for acute termination of stable SVT after failed vagal manoeuvres; adenosine is preferred for its rapid onset and short duration of action.

This ECG shows classic features of ventricular tachycardia: a very broad QRS of 160 ms, atrioventricular dissociation with capture beats, and negative precordial concordance, where all precordial leads show a predominantly negative QRS. These findings, especially AV dissociation and precordial concordance, are highly specific for a ventricular origin rather than a supraventricular rhythm with aberrant conduction. His history of prior myocardial infarction further raises pre-test probability for VT, since scarred myocardium is a common substrate for re-entrant ventricular arrhythmias. SVT with aberrancy typically shows a regular relationship between P waves and QRS complexes rather than AV dissociation.

• A. AV dissociation and precordial concordance are not features of aberrant conduction and strongly favour a ventricular origin.
• B. Multifocal atrial tachycardia shows an irregular rhythm with varying P wave morphology, not AV dissociation with capture beats.
• C. The rhythm is regular, without the irregularity typical of atrial fibrillation, and there is no evidence described of an accessory pathway.
• E. AV dissociation and concordance point to ventricular origin rather than aberrant supraventricular conduction.