Cardiology — MCQs

Cardiology Indian Medical PG Practice Questions and MCQs

Question 331: Left ventricular hypertrophy is caused by all of the following conditions except?

A. Mitral stenosis (Correct Answer)
B. Mitral regurgitation
C. Aortic stenosis
D. Aortic regurgitation

Explanation: The core concept in determining ventricular hypertrophy is identifying which conditions impose a **pressure or volume load** on the Left Ventricle (LV) [3]. **Why Mitral Stenosis (MS) is the correct answer:** In Mitral Stenosis, there is a mechanical obstruction between the Left Atrium (LA) and the Left Ventricle. This leads to increased LA pressure and pulmonary venous congestion [1]. Crucially, the LV is "protected" from this high pressure; in fact, the LV often remains small or even underfilled in isolated MS. Therefore, MS causes **Left Atrial Enlargement (LAE)** and **Right Ventricular Hypertrophy (RVH)** (due to pulmonary hypertension) [1][3], but **never** Left Ventricular Hypertrophy (LVH). **Why the other options are incorrect:** * **Aortic Stenosis (AS):** Creates a pressure overload on the LV as it must pump against a narrowed orifice [3]. This leads to **concentric LVH** [4]. * **Aortic Regurgitation (AR):** Causes volume overload because the LV receives blood from both the LA and the leaking aorta [3]. This leads to **eccentric LVH** (dilatation and hypertrophy) [4]. * **Mitral Regurgitation (MR):** Similar to AR, this creates a volume overload state [3]. The ECG and imaging show both Left Atrial and Left Ventricular hypertrophy [2]. The LV must pump an increased stroke volume to compensate for the blood leaking back into the atrium, leading to **eccentric LVH**. **High-Yield Clinical Pearls for NEET-PG:** 1. **Concentric Hypertrophy:** Caused by pressure overload (e.g., Hypertension, Aortic Stenosis) [3]. Wall thickness increases without cavity dilatation [4]. 2. **Eccentric Hypertrophy:** Caused by volume overload (e.g., AR, MR, Dilated Cardiomyopathy). The ventricular cavity dilates [4]. 3. **MS Paradox:** MS is the only left-sided valvular lesion that does not cause LVH. If a patient with MS has LVH, look for a co-existing condition like Hypertension or Aortic Valve disease.

Question 332: Which condition is characterized by a reduced PR interval?

A. Wenckebach phenomenon
B. Wolff-Parkinson-White syndrome (Correct Answer)
C. Hypothyroidism
D. Complete heart block

Explanation: ### Explanation **Correct Answer: B. Wolff-Parkinson-White (WPW) syndrome** **Why it is correct:** The PR interval represents the time taken for electrical impulses to travel from the atria to the ventricles. In a normal heart, this impulse is delayed at the AV node. In **WPW syndrome**, an accessory pathway (the **Bundle of Kent**) bypasses the AV node, conducting the impulse faster than normal [1]. This "pre-excitation" results in a **shortened PR interval (<0.12 seconds)** [1]. Other classic ECG findings in WPW include a widened QRS complex and a **Delta wave** (slurred upstroke of the QRS) [1, 3]. **Why the other options are incorrect:** * **A. Wenckebach phenomenon (Mobitz Type I):** This is characterized by progressive **prolongation** of the PR interval until a QRS complex is dropped [2]. * **C. Hypothyroidism:** This typically causes bradycardia and may lead to a **prolonged** PR interval (First-degree heart block) due to slowed conduction, along with low-voltage complexes. * **D. Complete heart block (Third-degree):** There is no relationship between P waves and QRS complexes (AV dissociation). The PR interval is **variable**, not consistently reduced. **High-Yield Clinical Pearls for NEET-PG:** * **Short PR Interval Differential:** WPW syndrome, Lown-Ganong-Levine (LGL) syndrome, and Duchenne Muscular Dystrophy [1]. * **Prolonged PR Interval (>0.20s):** Seen in First-degree AV block, Rheumatic fever (Jones criteria), Hyperkalemia, and Digoxin toxicity [2]. * **WPW Treatment:** Hemodynamically unstable patients require DC cardioversion. Definitive treatment is **Radiofrequency Ablation** of the accessory pathway. * **Contraindication:** Avoid AV nodal blockers (ABCD: **A**denosine, **B**eta-blockers, **C**alcium channel blockers, **D**igoxin) in WPW with Atrial Fibrillation, as they can promote conduction through the accessory pathway, leading to Ventricular Fibrillation [3].

Question 333: Hypocalcemia is associated with which of the following?

A. Metabolic acidosis
B. QT prolongation (Correct Answer)
C. Hypomagnesemia
D. Myocardial irritability

Explanation: **Explanation:** **Correct Option: B. QT prolongation** The hallmark ECG finding in hypocalcemia is **QT interval prolongation** [2], specifically due to the lengthening of the **ST segment**. Physiologically, extracellular calcium is essential for the plateau phase (Phase 2) of the cardiac action potential. Low serum calcium levels delay the influx of calcium through L-type channels, thereby prolonging Phase 2. Since the T-wave (ventricular repolarization) remains relatively unchanged, the overall QT interval increases [2]. This is a high-yield distinction from other electrolyte imbalances, as hypocalcemia rarely causes T-wave changes or arrhythmias unless severe [3]. **Incorrect Options:** * **A. Metabolic acidosis:** Acidosis actually increases the fraction of **ionized calcium** (the physiologically active form) by displacing calcium from albumin [2]. Therefore, alkalosis, not acidosis, is associated with symptomatic hypocalcemia [2]. * **C. Hypomagnesemia:** While hypomagnesemia can *cause* hypocalcemia (by inducing PTH resistance), it is a separate electrolyte abnormality [2]. The question asks what hypocalcemia is associated with/manifests as, rather than its etiology. * **D. Myocardial irritability:** This is a feature of **hypercalcemia** [1] or hypokalemia. Hypocalcemia generally results in decreased myocardial contractility (negative inotropy) and heart failure in extreme cases, rather than irritability. **NEET-PG High-Yield Pearls:** * **ECG in Hypocalcemia:** Prolonged ST segment → Prolonged QT interval [2]. * **ECG in Hypercalcemia:** Shortened ST segment → Shortened QT interval (Osborn waves may also be seen). * **Clinical Signs:** Trousseau’s sign (carpal spasm with BP cuff) and Chvostek’s sign (facial twitching) are classic indicators of neuromuscular irritability in hypocalcemia. * **Correction:** Always check the **Albumin** level [2]; for every 1 g/dL drop in albumin, serum calcium drops by 0.8 mg/dL, but ionized calcium remains normal [2].

Question 334: Which of the following ECG findings would indicate a posterior wall myocardial infarction?

A. ST elevation in V1-V3 leads (Correct Answer)
B. Tall and broad R waves
C. Tall T waves
D. Significant R waves

Explanation: ### Explanation **Correct Answer: A. ST elevation in V1-V3 leads** In clinical practice, a **Posterior Wall Myocardial Infarction (PWMI)** is often diagnosed using a standard 12-lead ECG by looking for **reciprocal changes** in the anterior leads (V1-V3) [1]. Because the posterior wall is opposite to the anterior leads, the typical "STEMI" findings are "flipped": * ST-segment depression (instead of elevation) * Tall, broad R waves (instead of Q waves) * Upright, tall T waves (instead of T-wave inversion) [1] **Note on the Question:** While the standard ECG finding for PWMI is ST-depression in V1-V3, the diagnosis is **confirmed** by placing posterior leads (**V7-V9**). In these specific leads, the finding that indicates infarction is **ST-elevation** [3]. Therefore, in the context of posterior-specific leads, ST-elevation is the definitive finding. #### Analysis of Incorrect Options: * **B & D (Tall/Significant R waves):** These are indeed features of PWMI on a standard ECG (representing the "inverted" Q wave of the posterior wall). However, they are secondary diagnostic criteria compared to ST-segment changes. * **C (Tall T waves):** While tall, symmetric T waves in V1-V3 are seen in PWMI, they are non-specific and can also be seen in hyperkalemia or early de Winter’s T-waves. #### NEET-PG High-Yield Pearls: * **Artery Involved:** Most commonly the **Right Coronary Artery (RCA)** or the Left Circumflex (LCx). * **The "Mirror Test":** If you flip a standard ECG upside down and look at it through the back of the paper, the V1-V3 leads in a PWMI will look like a classic STEMI. * **Associated Infarcts:** PWMI rarely occurs in isolation; it is frequently associated with **Inferior Wall MI** (leads II, III, aVF) [2]. Always check posterior leads if you see ST-depression in V1-V3 that is not explained by ischemia.

Question 335: What is the cut-off for severe hypertension?

A. >140 mm Hg
B. >150 mm Hg
C. >160 mm Hg
D. >170 mm Hg (Correct Answer)

Explanation: **Explanation:** In clinical cardiology and hypertension management, the classification of blood pressure is essential for determining the urgency of treatment. While standard guidelines (like JNC 8 or AHA/ACC) focus on Stage 1 and Stage 2 hypertension, the term **"Severe Hypertension"** specifically refers to a threshold where the risk of acute target organ damage increases significantly. **Why Option D is Correct:** According to standard clinical definitions used in emergency medicine and cardiology, **Severe Hypertension** is defined as a Systolic Blood Pressure (SBP) **>170 mm Hg** or a Diastolic Blood Pressure (DBP) **>110 mm Hg**. When BP exceeds these levels, it is often categorized as a "Hypertensive Urgency" (if asymptomatic) or "Hypertensive Emergency" (if signs of organ damage like encephalopathy or acute kidney injury are present). **Analysis of Incorrect Options:** * **Option A (>140 mm Hg):** This is the threshold for **Stage 1 Hypertension** (per JNC 8) or the general definition of hypertension. It is not considered "severe." * **Option B (>150 mm Hg):** This was previously a target threshold for initiating therapy in patients over 60 years old (JNC 8), but it does not define a severity grade. * **Option C (>160 mm Hg):** This is the threshold for **Stage 2 Hypertension** (per JNC 8). While significant, it falls below the "severe" classification used for hypertensive crises. **High-Yield Clinical Pearls for NEET-PG:** 1. **Hypertensive Urgency:** BP >180/120 mm Hg without acute target organ damage. 2. **Hypertensive Emergency:** BP >180/120 mm Hg WITH acute target organ damage. 3. **Malignant Hypertension:** Characterized by severe BP elevation with **Grade III/IV hypertensive retinopathy** (papilledema). 4. **Drug of Choice:** For most hypertensive emergencies, **IV Labetalol** or **Nicardipine** is preferred; however, **IV Sodium Nitroprusside** is used for rapid titration (though rarely first-line now due to toxicity).

Question 336: Which valve is most commonly affected in subacute bacterial endocarditis?

A. Mitral (Correct Answer)
B. Tricuspid
C. Pulmonary
D. None of the above

Explanation: In subacute bacterial endocarditis (SABE), the **Mitral valve** is the most commonly affected valve. This is because SABE typically occurs on valves that have pre-existing structural abnormalities, such as mitral valve prolapse (the most common underlying condition in developed countries) or chronic rheumatic heart disease (common in developing countries) [1]. The high-pressure gradient across the mitral valve creates turbulent blood flow, leading to endothelial damage and the formation of sterile fibrin-platelet vegetations (Non-Bacterial Thrombotic Endocarditis), which then become seeded by low-virulence organisms like *Streptococcus viridans* [1]. **Analysis of Options:** * **Mitral Valve (Correct):** It is the most frequent site of involvement overall. If the question specifies both Mitral and Aortic involvement, the combination is also very common, but individually, the Mitral valve leads. * **Tricuspid Valve (Incorrect):** This is the most common valve affected in **Intravenous Drug Users (IVDUs)**, typically associated with *Staphylococcus aureus* [1]. In the general population, right-sided involvement is much less common than left-sided. * **Pulmonary Valve (Incorrect):** This is the least commonly affected valve in infective endocarditis. **High-Yield Clinical Pearls for NEET-PG:** * **Most common organism (SABE):** *Streptococcus viridans* (low virulence, follows dental procedures) [1]. * **Most common organism (Acute IE):** *Staphylococcus aureus* (high virulence, affects normal valves) [1]. * **IVDU classic triad:** *S. aureus*, Tricuspid valve involvement, and multiple septic pulmonary emboli [1]. * **Prosthetic Valve Endocarditis:** *Staphylococcus epidermidis* is the most common cause within the first year of surgery. * **Culture-negative IE:** Most commonly due to prior antibiotic use or HACEK group organisms.

Question 337: Which physical sign characterizes mitral stenosis?

A. Loud first heart sound (Correct Answer)
B. Soft single second heart sound
C. Third heart sound
D. Pulsatile liver

Explanation: **Explanation** In **Mitral Stenosis (MS)**, the **loud first heart sound (S1)** is a hallmark finding [1]. This occurs because the elevated left atrial pressure keeps the mitral valve leaflets wide apart until the very end of diastole. When ventricular systole begins, the leaflets must travel a greater distance to close, slamming shut with increased force. Additionally, the leaflets remain pliable enough in early stages to vibrate intensely, creating the characteristic "tapping" apex beat. **Analysis of Options:** * **A. Loud S1 (Correct):** As explained, the wide excursion of leaflets leads to a loud S1 [1]. Note: S1 becomes soft only in late-stage MS if the valve becomes heavily calcified and immobile. * **B. Soft single S2:** This is characteristic of **Aortic Stenosis**, where the aortic component (A2) is delayed or diminished. In MS, S2 is usually normal or shows a loud P2 if pulmonary hypertension develops. * **C. Third heart sound (S3):** S3 is a sign of rapid ventricular filling, typically seen in **Mitral Regurgitation** or Heart Failure [3]. It is notably **absent** in MS because the stenotic valve restricts rapid filling. * **D. Pulsatile liver:** This is a classic sign of **Tricuspid Regurgitation**, caused by the backflow of blood into the venous system during systole. **NEET-PG High-Yield Pearls:** * **Auscultatory Triad of MS:** Loud S1, Opening Snap (OS), and Mid-diastolic rumbling murmur (MDM) [1], [2]. * **Severity Marker:** The shorter the **A2-OS interval**, the more severe the MS (indicating higher left atrial pressure) [2]. * **The "Tapping" Apex:** In MS, the palpable S1 at the apex is often mistaken for a forceful impulse; it is actually just the vibration of the loud S1. * **Common Complication:** Atrial Fibrillation (loss of 'a' wave in JVP and disappearance of the presystolic accentuation of the murmur) [1], [4].

Question 338: Which of the following conditions presents with an ECG pattern that mimics myocardial infarction, often referred to as 'myocardial stunning'?

A. Takotsubo cardiomyopathy (Correct Answer)
B. Restrictive cardiomyopathy
C. Brugada Syndrome
D. Pericardial effusion

Explanation: **Explanation:** **Takotsubo Cardiomyopathy** (also known as "Broken Heart Syndrome" or "Stress-induced Cardiomyopathy") is the correct answer. It is characterized by transient left ventricular apical ballooning, typically triggered by intense emotional or physical stress. 1. **Why it is correct:** The pathophysiology involves a massive surge of catecholamines leading to microvascular dysfunction or direct catecholamine toxicity, resulting in **"myocardial stunning."** On ECG, it frequently presents with ST-segment elevation and T-wave inversions, closely mimicking an Acute Coronary Syndrome (ACS). However, coronary angiography reveals **no obstructive coronary artery disease.** 2. **Why the other options are incorrect:** * **Restrictive Cardiomyopathy:** Typically presents with low-voltage QRS complexes and signs of diastolic heart failure, not an MI-mimicking pattern. * **Brugada Syndrome:** Shows a characteristic "coved" ST-elevation in V1-V3 followed by a negative T-wave (Type 1 pattern). It is a sodium channelopathy associated with sudden cardiac death, not myocardial stunning. * **Pericardial Effusion:** Classically presents with low-voltage complexes and **electrical alternans** [1] (beat-to-beat variation in QRS amplitude). **High-Yield Pearls for NEET-PG:** * **Demographics:** Most common in post-menopausal women. * **Echocardiography:** Shows apical ballooning with hypercontractile basal segments (resembling a Japanese octopus trap, or *Takotsubo*). * **Cardiac Biomarkers:** Troponins are often mildly elevated, but the rise is disproportionately low compared to the extent of wall motion abnormalities. * **Prognosis:** Generally excellent, with ventricular function returning to normal within weeks.

Question 339: Pulsus alternans is seen in:

A. Mitral stenosis with mitral regurgitation
B. Aortic stenosis with aortic regurgitation
C. Left ventricular failure (Correct Answer)
D. Digitalis poisoning

Explanation: **Explanation:** **Pulsus alternans** is a clinical sign characterized by a regular heart rhythm but with an alternating beat-to-beat variation in the strength (amplitude) of the arterial pulse [1]. **Why Left Ventricular Failure (LVF) is correct:** The underlying mechanism is the **Frank-Starling law** [2]. In a failing left ventricle, the stroke volume is reduced. A weak contraction leads to a higher end-systolic volume remaining in the ventricle. This increased volume (preload) stretches the myocardial fibers for the subsequent beat, resulting in a stronger contraction [2]. This cycle of a weak beat followed by a strong beat repeats, making it a hallmark sign of **severe left ventricular systolic dysfunction** [1]. **Analysis of Incorrect Options:** * **A & B (Valvular Heart Disease):** While chronic AS or AR can eventually lead to LVF, pulsus alternans is not a direct feature of the valvular lesion itself. Aortic regurgitation is typically associated with **Pulsus Bisferiens** (double-peaked pulse) [1]. * **D (Digitalis Poisoning):** Digitalis toxicity commonly causes arrhythmias like atrial tachycardia with block or **Ventricular Bigeminy**. While bigeminy can mimic the "strong-weak" pattern, it is characterized by an irregular rhythm (premature beats), whereas pulsus alternans occurs in a strictly **regular rhythm**. **High-Yield Clinical Pearls for NEET-PG:** * **Best site to palpate:** The femoral or radial artery. It is often easier to detect while inflating a BP cuff (the Korotkoff sounds will alternate in intensity). * **Pulsus Paradoxus:** An exaggerated drop in systolic BP (>10 mmHg) during inspiration [3]; seen in Cardiac Tamponade [3]. * **Pulsus Bisferiens:** Seen in AR, AS+AR, and HOCM. * **Pulsus Parvus et Tardus:** Small volume, slow-rising pulse seen in Aortic Stenosis.

Question 340: The ECG in hyperkalemia classically shows:

A. Increased QRS duration (Correct Answer)
B. Shortened PR interval
C. Prominent U waves
D. Increased R wave amplitude

Explanation: **Explanation:** Hyperkalemia is a life-threatening electrolyte abnormality that significantly alters cardiac conduction. As serum potassium levels rise, the resting membrane potential of myocytes becomes less negative (partially depolarized), which decreases the velocity of the upstroke of the action potential (Phase 0) [1]. This results in **slowed intraventricular conduction**, which manifests on the ECG as an **increased QRS duration** (widening) [1]. If untreated, this can progress to a "sine wave" pattern and eventually ventricular fibrillation or asystole. **Analysis of Options:** * **B. Shortened PR interval:** Incorrect. Hyperkalemia actually causes **prolongation of the PR interval** due to slowed AV conduction [1]. Eventually, P waves may disappear entirely (atrial standstill) [1]. * **C. Prominent U waves:** Incorrect. Prominent U waves are a classic hallmark of **hypokalemia**, not hyperkalemia. * **D. Increased R wave amplitude:** Incorrect. In hyperkalemia, the R wave amplitude typically **decreases**, and the S wave depth increases as the QRS widens. **NEET-PG High-Yield Pearls:** * **Sequential ECG Changes:** 1. Tall, "tented" or peaked T waves (earliest sign, usually K+ >5.5 mEq/L) [1]. 2. PR prolongation and P wave flattening [1]. 3. QRS widening (K+ >6.5 mEq/L) [1]. 4. Sine wave pattern (K+ >8.0 mEq/L). * **Treatment Priority:** The first step in managing hyperkalemia with ECG changes is **Intravenous Calcium Gluconate** to stabilize the cardiac membrane, followed by insulin/dextrose to shift potassium intracellularly [2].

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Cardiology — MCQs

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