Cardiology — MCQs
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A 61-year-old man presents with progressive dyspnea and fatigue. Echocardiogram shows severe aortic stenosis with valve area $0.5\mathrm{cm}^2$. He develops syncope during exercise testing. What is the most appropriate management?
A 57-year-old diabetic man presents with a non-healing foot ulcer for 3 months. Ankle-brachial pressure index is 0.3. What does this indicate?
A 55-year-old woman presents with progressive dyspnea and fatigue. Echocardiogram shows severe aortic regurgitation with LV end-systolic dimension 58mm and EF 48%. She is asymptomatic at rest. What is the most appropriate management?
A 53-year-old woman presents with progressive dyspnea and fatigue. Echocardiogram shows severe mitral regurgitation with flail posterior leaflet. LV function is normal but LV end-systolic dimension is 45mm. What is the most appropriate management?
A 46-year-old man presents with progressive dyspnea and fatigue. Echocardiogram shows severe mitral stenosis with valve area 0.7 cm². He is in atrial fibrillation with rapid ventricular response. What is the most appropriate initial management?
A 61-year-old woman presents with progressive dyspnea and bilateral ankle swelling. Echocardiogram shows severe tricuspid regurgitation. Right heart catheterization shows mean PAP 50 mmHg. What is the most likely diagnosis?
A 67-year-old man presents with progressive dyspnea and orthopnea. Chest X-ray shows cardiomegaly and Kerley B lines. BNP is 1800 pg/mL. What does BNP level indicate?
A 58-year-old man presents with progressive dyspnea and bilateral ankle swelling. JVP is elevated and there's a third heart sound. Chest X-ray shows pulmonary edema. What is the most likely cause of the third heart sound?
A 67-year-old man presents with progressive dyspnea and fatigue. Echocardiogram shows concentric LVH with EF 55% but impaired diastolic function. What is the most likely diagnosis?
A 62-year-old woman presents with progressive dyspnea and bilateral ankle swelling. Chest X-ray shows cardiomegaly. BNP is 2800 pg/mL. Echocardiogram shows EF 30%. What is the most appropriate first-line medication?
Cardiology UK Medical PG Practice Questions and MCQs
Question 1: A 61-year-old man presents with progressive dyspnea and fatigue. Echocardiogram shows severe aortic stenosis with valve area $0.5\mathrm{cm}^2$. He develops syncope during exercise testing. What is the most appropriate management?
- A. Medical management
- B. Balloon aortic valvuloplasty
- C. Urgent aortic valve replacement (Correct Answer)
- D. Heart transplantation
- E. ICD insertion
Explanation: ***Urgent aortic valve replacement*** - The patient has **severe aortic stenosis** (valve area $0.5\mathrm{cm}^2$) and is highly symptomatic, indicated by **syncope during exercise**, which significantly increases the risk of sudden cardiac death. - **Aortic valve replacement (AVR)** or TAVR is the definitive and urgent treatment required for symptomatic severe AS to alleviate symptoms and improve survival. *Medical management* - Medical therapy does not treat the underlying **fixed mechanical obstruction** of the aortic valve, making it ineffective for severe symptomatic AS. - Relying solely on medical management in this scenario leads to a very poor prognosis due to the high risk of **sudden cardiac death**. *Balloon aortic valvuloplasty* - BAV is primarily a temporary measure, often used as a **bridge to AVR/TAVR** or in hemodynamically unstable patients, due to its high rate of restenosis. - Given the patient is likely a surgical candidate, BAV is not considered the **definitive long-term solution** for severe AS. *Heart transplantation* - Heart transplantation is reserved for **end-stage heart failure** that is refractory to other medical and surgical options. - The primary pathology (severe AS) is surgically addressable via AVR, making transplantation an **inappropriate** initial therapy. *ICD insertion* - Syncope in severe AS is typically due to **flow limitation** and **exertional hypotension** caused by the fixed obstruction, rather than primary ventricular tachyarrhythmias. - Treating the underlying mechanical pathology with AVR resolves the cause of the syncope and the high risk of sudden death; therefore, an **ICD is not indicated**.
Question 2: A 57-year-old diabetic man presents with a non-healing foot ulcer for 3 months. Ankle-brachial pressure index is 0.3. What does this indicate?
- A. Normal arterial supply
- B. Mild arterial disease
- C. Moderate arterial disease
- D. Severe arterial disease (Correct Answer)
- E. Venous disease
Explanation: ***Severe arterial disease*** - An **Ankle-Brachial Pressure Index (ABPI)** of **0.3** indicates severely reduced blood flow to the lower extremities. - This severe reduction in arterial supply is consistent with the patient's **non-healing foot ulcer** and diabetes, a major risk factor for peripheral arterial disease. *Normal arterial supply* - **Normal ABPI** values typically range from **0.90 to 1.30**, which is significantly higher than the given 0.3. - An ABPI of 0.3 suggests profound compromise, far from normal blood flow required for tissue healing. *Mild arterial disease* - **Mild arterial disease** is generally indicated by an **ABPI between 0.70 and 0.90**. - An ABPI of 0.3 is well below this range, signifying much more severe impairment of arterial flow. *Moderate arterial disease* - **Moderate arterial disease** corresponds to an **ABPI between 0.40 and 0.69**. - The patient's ABPI of 0.3 is lower than this range, indicating a more critical level of arterial obstruction. *Venous disease* - The **ABPI** is a diagnostic tool primarily used to assess **arterial insufficiency**, not venous disease. - While venous disease can cause ulcers, an ABPI of 0.3 specifically points to significant **peripheral arterial disease** as the underlying cause.
Question 3: A 55-year-old woman presents with progressive dyspnea and fatigue. Echocardiogram shows severe aortic regurgitation with LV end-systolic dimension 58mm and EF 48%. She is asymptomatic at rest. What is the most appropriate management?
- A. Medical management
- B. Aortic valve replacement (Correct Answer)
- C. ACE inhibitors and monitoring
- D. Exercise stress testing
- E. Cardiac catheterization
Explanation: ***Aortic valve replacement*** - The patient presents with **severe aortic regurgitation** and objective evidence of **left ventricular (LV) dysfunction** (EF 48% < 50%) and **LV dilatation** (end-systolic dimension 58mm > 50-55mm). These findings are Class I indications for **aortic valve replacement**, even in an asymptomatic patient. - Surgical intervention is crucial to prevent irreversible myocardial damage and improve long-term outcomes in chronic **severe aortic regurgitation** once these thresholds for LV impairment are met. *Medical management* - Medical management is typically reserved for patients with **mild to moderate aortic regurgitation** or those with severe AR but **preserved LV function** and no significant LV dilatation who are asymptomatic. - It does not address the underlying mechanical defect of the **aortic valve** and will not reverse the progressive LV remodeling and dysfunction. *ACE inhibitors and monitoring* - While ACE inhibitors can be considered for management of hypertension or symptomatic heart failure in some AR patients, they are not the definitive treatment for **severe aortic regurgitation** with established LV dysfunction. - **Monitoring alone** is inappropriate given the significant LV remodeling and dysfunction, which necessitate surgical intervention to prevent further irreversible damage. *Exercise stress testing* - Exercise stress testing is primarily used to unmask symptoms in **asymptomatic patients** with severe valve disease (e.g., aortic stenosis or regurgitation) and **preserved LV function** to assess their functional capacity and guide surgical timing. - In this case, the patient already has clear echocardiographic evidence of **LV dysfunction** (EF 48%) and significant **LV dilatation** (ESD 58mm), which are direct indications for surgery, rendering stress testing unnecessary for decision-making. *Cardiac catheterization* - **Cardiac catheterization** is primarily a diagnostic procedure performed to assess for **coronary artery disease** (CAD) in patients undergoing cardiac surgery, especially in older individuals or those with CAD risk factors. - It is not the definitive management for **aortic regurgitation** itself but may be a pre-operative step. The primary treatment remains valve replacement.
Question 4: A 53-year-old woman presents with progressive dyspnea and fatigue. Echocardiogram shows severe mitral regurgitation with flail posterior leaflet. LV function is normal but LV end-systolic dimension is 45mm. What is the most appropriate management?
- A. Medical management
- B. Mitral valve replacement
- C. Mitral valve repair (Correct Answer)
- D. Heart transplantation
- E. Balloon valvuloplasty
Explanation: ***Mitral valve repair***- Repair is the preferred management for **severe primary mitral regurgitation (MR)**, especially when the mechanism is degenerative (like a **flail leaflet**), as it provides better long-term survival and preserves native annular-ventricular continuity.- Surgery is mandated because the patient is **symptomatic** (dyspnea and fatigue) and meets criteria for severe MR (along with an **LVESD of 45 mm**, which is an independent indication for surgery even in asymptomatic patients with preserved LVEF).*Medical management*- Medical management (e.g., ACE inhibitors/beta-blockers) is appropriate only for **asymptomatic patients** who do not meet surgical LV dimensional or functional thresholds.- It is **insufficient** to halt the progression or reduce mortality in symptomatic severe primary MR, which requires definitive surgical correction.*Mitral valve replacement*- Replacement is reserved for valves deemed **unrepairable** due to extensive destruction, calcification, or complex pathology.- Repair is favored because it avoids the risks associated with prosthetic valves, such as lifelong **anticoagulation** (for mechanical valves) and prosthetic valve dysfunction.*Heart transplantation*- This procedure is reserved for **end-stage heart failure** (NYHA Class III/IV symptoms) that is refractory to all other medical and surgical therapies.- The patient has **normal LV function** (preserved LVEF), making transplantation completely unnecessary and inappropriate.*Balloon valvuloplasty*- This intervention is the primary treatment for severe, pliable **mitral stenosis**, most commonly due to rheumatic disease.- It is **contraindicated** in severe MR, particularly MR secondary to leaflet prolapse or flail, as it would worsen the severity of the regurgitation.
Question 5: A 46-year-old man presents with progressive dyspnea and fatigue. Echocardiogram shows severe mitral stenosis with valve area 0.7 cm². He is in atrial fibrillation with rapid ventricular response. What is the most appropriate initial management?
- A. Rate control with digoxin (Correct Answer)
- B. Immediate cardioversion
- C. Balloon mitral valvuloplasty
- D. Mitral valve replacement
- E. Anticoagulation alone
Explanation: ***Rate control with digoxin***- Rapid ventricular rate in **atrial fibrillation** significantly reduces **diastolic filling time**, which is crucial for adequate **left ventricular filling** in severe **mitral stenosis (MS)**.- Rate control (e.g., with rate-limiting calcium channel blockers, beta-blockers, or **digoxin** in the setting of MS, especially if associated with heart failure) is the immediate priority to alleviate acute symptoms of heart failure.*Immediate cardioversion*- Cardioversion is generally postponed until the patient is properly **anticoagulated** (due to high risk of systemic **thromboembolism**) unless the patient is **hemodynamically unstable** (e.g., shock/hypotension).- In severe MS, AF often recurs due to chronic **left atrial enlargement** and high pressure, making rate control the preferred strategy over rhythm control initially.*Balloon mitral valvuloplasty*- This is the preferred definitive treatment for symptomatic severe MS but is an invasive procedure and is not appropriate as the *initial* acute management for **AF with RVR**.- A stable patient requires rate control and anticoagulation first before determining the timing of the **structural intervention** (BMV).*Mitral valve replacement*- **Mitral valve replacement (MVR)** is a major surgical procedure reserved for patients with MS who fail percutaneous **balloon mitral valvuloplasty (BMV)** or have unfavorable valve morphology.- This is not indicated as the *initial* non-invasive step to manage acute **rate complications** in a symptomatic patient.*Anticoagulation alone*- Anticoagulation is essential management for MS complicated by AF (high **thromboembolism** risk) but does not address the acute physiological cause of **dyspnea and fatigue** (the rapid heart rate).- Ignoring the **rapid ventricular response** would leave the patient vulnerable to acute circulatory deterioration and continued pulmonary congestion.
Question 6: A 61-year-old woman presents with progressive dyspnea and bilateral ankle swelling. Echocardiogram shows severe tricuspid regurgitation. Right heart catheterization shows mean PAP 50 mmHg. What is the most likely diagnosis?
- A. Left heart failure
- B. Pulmonary hypertension (Correct Answer)
- C. COPD
- D. Pulmonary embolism
- E. Tricuspid valve disease
Explanation: ***Pulmonary hypertension*** - The **mean pulmonary artery pressure (PAP) of 50 mmHg** measured by right heart catheterization is the definitive diagnostic criterion for **pulmonary hypertension**, which is defined as a mean PAP > 20 mmHg at rest. - The **progressive dyspnea** and **bilateral ankle swelling** (signs of right heart failure) along with **severe tricuspid regurgitation** (a common consequence of right ventricular pressure overload due to PH) are direct clinical manifestations of elevated pulmonary pressures. *Left heart failure* - While **left heart failure (LHF)** is the most common cause of **Group 2 pulmonary hypertension**, the right heart catheterization explicitly confirms the *presence* of pulmonary hypertension, making it the most direct diagnosis based on the provided hemodynamic data. - LHF primarily causes elevated **pulmonary capillary wedge pressure (PCWP)** due to back pressure from the left side of the heart, which would be the more specific diagnostic finding for LHF as the *primary* problem. *COPD* - **COPD** can lead to **Group 3 pulmonary hypertension** due to chronic hypoxia and vasoconstriction, but the question primarily focuses on the hemodynamic findings of severe PH and its consequences rather than specific lung disease features like smoking history or spirometry results. - The clinical presentation emphasizes the cardiac manifestations of high pulmonary pressures (dyspnea, ankle swelling, severe tricuspid regurgitation) rather than primary respiratory symptoms typical of advanced COPD. *Pulmonary embolism* - An acute massive **pulmonary embolism** typically presents with sudden or subacute onset of dyspnea and often chest pain, which is less consistent with the patient's history of **progressive dyspnea**. - While **chronic thromboembolic pulmonary hypertension (CTEPH)** is a form of pulmonary hypertension, the question asks for the *most likely diagnosis* given the direct finding of elevated PAP, which is pulmonary hypertension itself. *Tricuspid valve disease* - The **severe tricuspid regurgitation (TR)** observed is most likely *secondary* or functional, resulting from the severe right ventricular dilation and remodeling caused by the chronic pressure overload from **pulmonary hypertension**. - Primary tricuspid valve disease would typically be the *cause* of the TR, but it would not directly explain the high **mean PAP of 50 mmHg** as the primary pathology unless it led to PH (which is less common as a primary mechanism).
Question 7: A 67-year-old man presents with progressive dyspnea and orthopnea. Chest X-ray shows cardiomegaly and Kerley B lines. BNP is 1800 pg/mL. What does BNP level indicate?
- A. Mild heart failure
- B. Moderate heart failure (Correct Answer)
- C. Severe heart failure
- D. Acute coronary syndrome
- E. Pulmonary embolism
Explanation: ***Moderate heart failure***- A **BNP level of 1800 pg/mL** is highly elevated and confirms the diagnosis of acute decompensated heart failure; based on common clinical stratification, this level falls into the **moderate** severity range (often 900–1800 pg/mL).- This elevated level reflects significant **ventricular wall stress** and stretching due to volume overload, correlating strongly with the patient's clinical status (dyspnea, orthopnea, Kerley B lines).*Mild heart failure*- Mild heart failure is typically associated with BNP concentrations significantly lower than 1800 pg/mL, usually ranging between **100 to 500 pg/mL**.- Patients showing features of acute volume overload, such as **Kerley B lines** and pronounced orthopnea, rarely have BNP levels in the mild range.*Severe heart failure*- While 1800 pg/mL is very high, **severe heart failure** or decompensated end-stage disease is typically associated with BNP levels exceeding **2000 to 4000 pg/mL**, depending on the threshold used.- This threshold indicates profound biventricular dysfunction and is usually reserved for the most critical or shock states, which are higher than the patient's current measurement.*Acute coronary syndrome*- While acute myocardial infarction (a subset of ACS) can cause a secondary rise in BNP due to resulting acute heart failure, BNP's primary use is to aid in the diagnosis and staging of **heart failure**, not to diagnose ACS directly.- ACS findings are usually based on ECG changes or **troponin elevation**, whereas this clinical presentation is dominatingly characterized by signs of fluid overload.*Pulmonary embolism*- Large pulmonary embolisms can cause right heart strain and elevate BNP, but the levels are often **less predictable** and usually lower than 1800 pg/mL compared to severe biventricular failure.- The X-ray findings of **cardiomegaly** and **Kerley B lines** are highly specific indicators of pulmonary venous congestion due to left-sided heart failure, making PE an unlikely primary cause of this specific constellation of findings.
Question 8: A 58-year-old man presents with progressive dyspnea and bilateral ankle swelling. JVP is elevated and there's a third heart sound. Chest X-ray shows pulmonary edema. What is the most likely cause of the third heart sound?
- A. S3 gallop (Correct Answer)
- B. S4 gallop
- C. Opening snap
- D. Ejection click
- E. Pericardial knock
Explanation: ***S3 gallop*** - The presence of **dyspnea**, **bilateral ankle swelling**, **elevated JVP**, and **pulmonary edema** indicates severe **congestive heart failure (CHF)** and **volume overload**. - An **S3 gallop** is a low-frequency sound in early diastole, indicative of **ventricular volume overload** or **systolic heart failure**, resulting from rapid ventricular filling into a dilated, non-compliant ventricle. *S4 gallop* - An **S4 gallop** is a presystolic sound heard in late diastole, typically associated with **diastolic dysfunction** (e.g., in **hypertension**, **aortic stenosis**) due to atrial contraction into a stiff ventricle. - This patient's presentation with significant **pulmonary edema** and **volume overload** points more towards systolic dysfunction and an S3 rather than isolated diastolic dysfunction. *Opening snap* - An **opening snap** is a high-pitched diastolic sound characteristic of **mitral stenosis**, caused by the sudden opening of a stenotic mitral valve. - The clinical picture does not suggest primary valvular stenosis but rather global heart failure. *Ejection click* - An **ejection click** is a high-pitched systolic sound occurring shortly after S1, often related to the opening of a **stenotic semilunar valve** or a dilated great artery. - This is a systolic event, not the diastolic third heart sound described in the question. *Pericardial knock* - A **pericardial knock** is a loud, early diastolic sound heard shortly after S2, characteristic of **constrictive pericarditis**. - While associated with elevated JVP and edema, constrictive pericarditis often presents with less prominent **pulmonary edema** and may feature **Kussmaul sign**, which is not mentioned.
Question 9: A 67-year-old man presents with progressive dyspnea and fatigue. Echocardiogram shows concentric LVH with EF 55% but impaired diastolic function. What is the most likely diagnosis?
- A. Dilated cardiomyopathy
- B. Heart failure with preserved ejection fraction (Correct Answer)
- C. Hypertrophic cardiomyopathy
- D. Restrictive cardiomyopathy
- E. Ischemic cardiomyopathy
Explanation: ***Heart failure with preserved ejection fraction*** - The combination of progressive dyspnea and fatigue, **concentric LVH** with a **preserved ejection fraction (EF 55%)**, and **impaired diastolic function** are the hallmark diagnostic criteria for **HFpEF**. - This condition is characterized by stiff, non-compliant ventricles that impair ventricular filling (diastolic function) rather than myocardial contractility (systolic function).*Dilated cardiomyopathy* - This condition is defined by ventricular chamber enlargement and globally reduced myocardial contractility, leading to a significantly **reduced ejection fraction (HFrEF)**, typically less than 40%. - The echocardiogram findings of **concentric LVH** and preserved EF contradict the features of DCM, which usually presents with thin ventricular walls.*Hypertrophic cardiomyopathy* - While HCM causes **diastolic dysfunction** and can have a preserved EF, it is primarily a genetic structural heart disease characterized by often **asymmetric hypertrophy** and sometimes dynamic left ventricular outflow tract obstruction. - The general presentation of HF with preserved EF due to concentric hypertrophy is more broadly classified as **HFpEF**, rather than a specific hypertrophic cardiomyopathy unless further diagnostic details (e.g., specific genetic mutation, severe asymmetric septal hypertrophy) are provided.*Restrictive cardiomyopathy* - This is a structural diagnosis primarily caused by infiltrative processes like **amyloidosis** or sarcoidosis, characterized by rigid ventricular walls leading to severe diastolic dysfunction and often **biatrial enlargement**. - Although a cause of HFpEF, restrictive cardiomyopathy typically presents with distinct restrictive filling patterns and often normal or slightly increased ventricular wall thicknesses, making HFpEF the broader and most direct diagnosis given the information.*Ischemic cardiomyopathy* - This condition results from myocardial damage due to coronary artery disease, typically leading to widespread **systolic dysfunction** and ventricular remodeling, causing **heart failure with reduced ejection fraction** (HFrEF). - The presence of a **preserved EF (55%)** in this patient directly contradicts the definition of ischemic cardiomyopathy, which is characterized by a reduced EF due to regional wall motion abnormalities.
Question 10: A 62-year-old woman presents with progressive dyspnea and bilateral ankle swelling. Chest X-ray shows cardiomegaly. BNP is 2800 pg/mL. Echocardiogram shows EF 30%. What is the most appropriate first-line medication?
- A. Furosemide
- B. ACE inhibitor (Correct Answer)
- C. Beta-blocker
- D. Spironolactone
- E. Digoxin
Explanation: ***ACE inhibitor*** - **ACE inhibitors** (or ARBs/ARNIs) are the cornerstone of **Guideline-Directed Medical Therapy (GDMT)** for **Heart Failure with reduced Ejection Fraction (HFrEF)**, demonstrating significant reduction in morbidity and mortality. - They work by blocking the **Renin-Angiotensin-Aldosterone System (RAAS)**, leading to reduced afterload and preload, and reversing detrimental cardiac remodeling. *Furosemide* - Although vital for managing the patient's acute **volume overload** (dyspnea, ankle swelling) by inducing diuresis, it is a symptomatic treatment and is not considered the first-line medication to improve long-term survival in HFrEF. - Diuretics like Furosemide must be used in conjunction with foundational **GDMT** agents (ACEi/BB/MRA) but are not the initial mortality-reducing treatment. *Beta-blocker* - Beta-blockers are a mandatory class of first-line agents in HFrEF (along with RAAS inhibitors) that reduce mortality by blocking sympathetic overactivity. - However, they are often initiated or up-titrated *after* the patient is stabilized and on an ACE inhibitor because they can worsen symptoms during acute decompensation if not dosed carefully. *Spironolactone* - This agent is a **Mineralocorticoid Receptor Antagonist (MRA)**, which confers additional mortality benefit when added to a regimen of an ACE inhibitor (or ARB/ARNI) and a beta-blocker. - It is used as part of **triple therapy** and is not the appropriate *first* medication to initiate RAAS inhibition, especially due to risks like **hyperkalemia**. *Digoxin* - Digoxin is primarily used to control symptoms (reducing hospitalizations) in patients with severe HFrEF who remain symptomatic despite optimal **GDMT**, or for rate control in coexisting **atrial fibrillation**. - It does not improve overall survival and is therefore not a first-line choice for mortality benefit in HFrEF.
Practice by Chapter
Acute coronary syndromes
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Atrial fibrillation and anticoagulation
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Cardiovascular risk assessment (QRISK)
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Heart failure (HFrEF, HFpEF)
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Hypertension diagnosis and management
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Stable angina
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Valvular heart disease
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