Cardiology — MCQs

Cardiology Indian Medical PG Practice Questions and MCQs

Question 761: The 'square root sign' is an indication of which of the following conditions?

A. Constrictive pericarditis (Correct Answer)
B. Hypertrophic cardiomyopathy
C. Restrictive cardiomyopathy
D. None of the above

Explanation: ### Explanation The **'Square Root Sign'** (also known as the **dip-and-plateau sign**) is a classic hemodynamic finding seen on ventricular pressure tracings, most characteristically in **Constrictive Pericarditis** [1]. #### Why it occurs: In Constrictive Pericarditis, the pericardium becomes rigid and non-compliant. During early diastole, the ventricles are empty, and blood rushes in rapidly from the atria, causing a sharp **dip** in ventricular pressure. However, because the rigid pericardium limits the total volume the heart can hold, ventricular filling stops abruptly once the cardiac volume hits the limit of the stiff shell. This results in a sudden rise to a high diastolic pressure which then remains stable (**plateau**) until systole [1]. On a pressure-time graph, this rapid descent followed by a flat plateau resembles a square root symbol ($\sqrt{x}$). #### Analysis of Options: * **A. Constrictive Pericarditis (Correct):** This is the classic association [1]. It reflects the abrupt cessation of ventricular filling due to extrinsic rigid constriction. * **B. Hypertrophic Cardiomyopathy (Incorrect):** This is characterized by impaired relaxation (diastolic dysfunction) and outflow obstruction, but it does not typically show the abrupt "dip-and-plateau" filling pattern. * **C. Restrictive Cardiomyopathy (Incorrect):** While Restrictive Cardiomyopathy (RCM) can occasionally show a similar pattern, it is much less common and less pronounced than in Constrictive Pericarditis. In RCM, the pathology is within the myocardium itself, whereas the square root sign is the hallmark of pericardial constraint. #### NEET-PG High-Yield Pearls: * **Kussmaul’s Sign:** Paradoxical rise in JVP on inspiration; seen in Constrictive Pericarditis (but notably absent in Cardiac Tamponade). * **Pericardial Knock:** A high-pitched sound heard in early diastole (due to the same abrupt cessation of filling that causes the square root sign). * **Imaging:** Look for **pericardial calcification** on a lateral chest X-ray as a diagnostic clue for Constrictive Pericarditis [1]. * **Equalization of Pressures:** In Constrictive Pericarditis, the diastolic pressures in all four cardiac chambers typically equalize.

Question 762: The QT interval is shortened in which of the following conditions?

A. Hypocalcemia
B. Hypokalemia
C. Hypercalcemia (Correct Answer)
D. Hyperkalemia

Explanation: The QT interval represents the total time for ventricular depolarization and repolarization. It is primarily determined by the duration of the ventricular action potential. [1] **Why Hypercalcemia is Correct:** In **hypercalcemia**, the increased extracellular calcium concentration shortens the duration of the plateau phase (Phase 2) of the cardiac action potential. This occurs because the increased electrochemical gradient allows calcium to enter the cell more rapidly, leading to earlier activation of outward potassium currents. This results in a **shortened QT interval**, specifically characterized by a shortened ST segment. **Analysis of Incorrect Options:** * **Hypocalcemia (A):** This is the most common cause of a **prolonged QT interval**. Low calcium levels delay the plateau phase of the action potential, lengthening the ST segment. * **Hypokalemia (B):** While it may appear to prolong the QT interval, it actually causes **ST depression, T-wave flattening, and prominent U-waves**. The fusion of the T and U waves often creates a "pseudo-prolonged" QT interval. * **Hyperkalemia (D):** The classic ECG finding is **tall, peaked T-waves**. [1] While it can occasionally shorten the QT interval slightly due to rapid repolarization, hypercalcemia is the classic and more definitive cause of a shortened QT interval tested in exams. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Short QT Interval:** Think "Hyper" (Hypercalcemia, Hyperthermia, Digoxin effect). * **Long QT Interval:** Think "Hypo" (Hypocalcemia, Hypokalemia, Hypomagnesemia) or Drugs (Class IA and III antiarrhythmics, Macrolides, TCAs) which can lead to complications such as Torsades de pointes. [2] * **Osborn Waves (J-waves):** Associated with Hypothermia. * **Digoxin Effect:** Characterized by a "reverse tick" or "sagging" ST-segment depression and a shortened QT interval.

Question 763: A patient presents with normal angiography but exhibits severe hypokinesia of the left ventricular wall. Which of the following is the most likely diagnosis?

A. Hypertrophic Obstructive Cardiomyopathy (HOCM)
B. Restrictive cardiomyopathy
C. Dilated cardiomyopathy (DCM)
D. Takotsubo cardiomyopathy (Correct Answer)

Explanation: The clinical scenario describes a classic presentation of **Takotsubo Cardiomyopathy**, also known as "Stress-induced Cardiomyopathy" or "Broken Heart Syndrome." **1. Why Takotsubo Cardiomyopathy is correct:** The hallmark of this condition is **transient systolic dysfunction** of the apical and/or mid-segments of the left ventricle, leading to a characteristic "ballooning" appearance (resembling a Japanese octopus trap). Crucially, patients present with symptoms mimicking an acute coronary syndrome (chest pain, ECG changes, elevated troponins), but **coronary angiography reveals normal or non-obstructive arteries**. It is typically triggered by intense emotional or physical stress, leading to a "catecholamine surge" that causes myocardial stunning. **2. Why the other options are incorrect:** * **HOCM:** Characterized by asymmetrical septal hypertrophy and dynamic outflow obstruction, not global or wall-specific hypokinesia. Angiography is not the primary diagnostic tool; echocardiography showing a thickened septum is key. * **Restrictive Cardiomyopathy:** Primarily a disorder of **diastolic function** (impaired filling) with relatively preserved systolic function (normal ejection fraction) in early stages. * **Dilated Cardiomyopathy (DCM):** While DCM involves ventricular hypokinesia and dilatation, it is usually a chronic, progressive condition [1]. In a NEET-PG context, the specific mention of "normal angiography" alongside acute severe hypokinesia is the classic "trigger" for a Takotsubo diagnosis. **Clinical Pearls for NEET-PG:** * **Demographics:** Most common in post-menopausal women. * **Echocardiography:** Shows "Apical Ballooning" with basal hyperkinesis. * **Prognosis:** Generally excellent, with ventricular function returning to normal within weeks. * **Key differentiator:** Symptoms of MI + Normal Coronaries + Stress Trigger = Takotsubo.

Question 764: What is the most common feature of essential hypertension?

A. Visual disturbances
B. Headache (Correct Answer)
C. Palpitations
D. Dizziness

Explanation: Essential (primary) hypertension is often referred to as the "silent killer" because it is frequently asymptomatic [1]. However, when symptoms do occur, **headache** is clinically recognized as the most common presenting feature [1]. 1. **Why Headache is Correct:** While many patients with mild-to-moderate hypertension are asymptomatic, those who do experience symptoms most frequently report headaches [1]. Classically, a hypertensive headache is described as occurring in the **early morning**, localized to the **occipital region**, and typically subsiding as the day progresses. It is often a sign of significantly elevated blood pressure. 2. **Analysis of Incorrect Options:** * **Visual disturbances (A):** These are typically signs of **Malignant or Accelerated Hypertension** (Grade IV hypertensive retinopathy with papilledema). They indicate end-organ damage rather than routine essential hypertension. * **Palpitations (C):** While they can occur due to anxiety or associated arrhythmias (like Atrial Fibrillation), they are more characteristic of **Pheochromocytoma** (a secondary cause of hypertension) rather than essential hypertension itself. * **Dizziness (D):** This is a non-specific symptom. While common in the general population, it is less frequently linked specifically to the elevation of blood pressure compared to headaches. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of Hypertension:** Essential Hypertension (95% of cases) [1]. * **Most common cause of Secondary Hypertension:** Renal Parenchymal Disease [1]. * **Most common symptom of Hypertensive Crisis:** Headache, followed by shortness of breath. * **Rule of Thumb:** If a patient presents with a morning occipital headache, always check their blood pressure to rule out essential hypertension.

Question 765: A 23-year-old woman is diagnosed with mitral valve prolapse as seen on echocardiography for evaluation of a systolic murmur. Which of the following is most characteristic of mitral valve prolapse?

A. A pansystolic murmur
B. Usually a benign course (Correct Answer)
C. Sudden death
D. Infective endocarditis

Explanation: **Explanation:** **Mitral Valve Prolapse (MVP)**, also known as Barlow’s syndrome, is the most common valvular heart disease, characterized by the displacement of an abnormally thickened mitral valve leaflet into the left atrium during systole. **1. Why Option B is Correct:** The vast majority of patients with MVP are asymptomatic and follow a **benign clinical course**. Most cases are discovered incidentally during routine physical examination (finding a mid-systolic click [1]) or echocardiography. While complications can occur, they represent the exception rather than the rule for the general population with this condition. **2. Why Other Options are Incorrect:** * **Option A:** The characteristic murmur of MVP is a **late systolic murmur**, typically preceded by a **mid-systolic click [1]**. A pansystolic (holosystolic) murmur is more indicative of chronic, severe mitral regurgitation [2]. * **Option C & D:** While Sudden Cardiac Death (SCD) and Infective Endocarditis (IE) are recognized complications of MVP, they are **rare**. SCD occurs in <1% of cases annually, and the risk of IE is significantly lower than in other valvular pathologies, making these "characteristic" of the complications, but not the disease itself. **High-Yield Clinical Pearls for NEET-PG:** * **Auscultation:** Mid-systolic click [1] followed by a late systolic murmur. * **Dynamic Auscultation:** Maneuvers that decrease preload (Standing, Valsalva) make the click/murmur occur **earlier** in systole and often louder. Maneuvers that increase preload (Squatting) make it occur **later**. * **Association:** Strongly associated with connective tissue disorders like **Marfan syndrome** and Ehlers-Danlos syndrome. * **Pathology:** Characterized by **myxomatous degeneration** of the valve leaflets.

Question 766: Treatment of orthostatic hypotension includes all except:

A. High salt and fluid intake
B. Physical countermaneuvers
C. Dopamine (Correct Answer)
D. Fludrocortisone

Explanation: Explanation: Orthostatic hypotension (OH) is defined as a sustained reduction in systolic blood pressure of at least 20 mmHg or diastolic blood pressure of at least 10 mmHg within 3 minutes of standing. The management strategy focuses on increasing intravascular volume and enhancing peripheral vascular resistance. **Why Dopamine is the Correct Answer (The Exception):** Dopamine is an intravenous inopressor used primarily in acute, hemodynamically unstable states like cardiogenic or septic shock. It is **not** a treatment for chronic orthostatic hypotension because it cannot be administered orally and has a very short half-life. Furthermore, at low doses, dopamine can cause vasodilation (via D1 receptors), which could theoretically worsen hypotension. **Analysis of Other Options:** * **High salt and fluid intake:** This is the first-line non-pharmacological intervention [1]. Increasing sodium (6–10 g/day) and fluid (2–3 L/day) expands the extracellular fluid volume to prevent postural collapse. * **Physical countermaneuvers:** Techniques such as leg crossing, muscle tensing, and squatting increase venous return (preload) to the heart, providing immediate symptomatic relief. * **Fludrocortisone:** This is the first-line pharmacological treatment [1]. It is a potent mineralocorticoid that promotes renal sodium reabsorption, thereby expanding plasma volume and sensitizing alpha-adrenergic receptors. **NEET-PG High-Yield Pearls:** 1. **Midodrine:** A selective alpha-1 agonist; it is the preferred drug when volume expansion alone is insufficient. 2. **Droxidopa:** A synthetic precursor of norepinephrine, recently approved for neurogenic OH. 3. **Pyridostigmine:** An acetylcholinesterase inhibitor that improves ganglionic transmission, helping to increase BP during standing without causing supine hypertension. 4. **Rule out "Reversible Causes":** Always check for drugs (diuretics, alpha-blockers) or dehydration before starting long-term therapy.

Question 767: A 65-year-old man presents with severe chest pain and difficulty in breathing. His ECG showed an S1Q3T3 pattern with sinus tachycardia. What diagnosis does this ECG suggest?

A. Ventricular fibrillation
B. Acute pulmonary embolism (Correct Answer)
C. Second-degree heart block
D. Atrial fibrillation

Explanation: The clinical presentation of sudden onset chest pain and dyspnea, combined with the **S1Q3T3 pattern**, is a classic (though non-specific) indicator of **Acute Pulmonary Embolism (PE)** [1]. **1. Why Acute Pulmonary Embolism is correct:** The S1Q3T3 pattern (McGinn-White sign) reflects **acute right ventricular (RV) strain**. * **S1:** A deep S-wave in Lead I. * **Q3:** A pathological Q-wave in Lead III. [1] * **T3:** T-wave inversion in Lead III. This occurs because a large embolus increases pulmonary vascular resistance, causing the right ventricle to dilate and rotate the heart's electrical axis. While **Sinus Tachycardia** is the most common ECG finding in PE, S1Q3T3 is the most "famous" high-yield sign [1]. **2. Why other options are incorrect:** * **Ventricular Fibrillation:** Characterized by chaotic, irregular electrical activity with no identifiable P, QRS, or T waves; it leads to immediate cardiac arrest. * **Second-degree Heart Block:** Defined by intermittent failure of AV conduction (e.g., progressive PR lengthening in Mobitz I or dropped beats in Mobitz II), not axis shifts or Q-waves. * **Atrial Fibrillation:** Characterized by an "irregularly irregular" rhythm and absence of P-waves. While it can occur due to RV strain in PE, it does not produce the S1Q3T3 morphology. **High-Yield Clinical Pearls for NEET-PG:** * **Most common ECG finding in PE:** Sinus Tachycardia [1]. * **Most specific ECG finding in PE:** T-wave inversions in V1–V4 (precordial T-wave inversion). * **Gold Standard Investigation:** CT Pulmonary Angiography (CTPA). * **Initial screening test of choice:** D-dimer (high negative predictive value).

Question 768: What is Prinzmetal angina?

A. Angina occurring after extreme exertion
B. Caused due to atherosclerotic blockade
C. Caused due to coronary artery spasm (Correct Answer)
D. Calcium channel blockers are not effective

Explanation: **Explanation:** **Prinzmetal Angina** (also known as Variant Angina) is a clinical syndrome characterized by episodes of chest pain at rest, caused by a focal or diffuse **coronary artery spasm**. Unlike stable angina, it is not triggered by exertion but occurs due to transient hyperreactivity of vascular smooth muscle. * **Why Option C is correct:** The hallmark of Prinzmetal angina is an intense vasospasm of a coronary artery (often at the site of a non-obstructive plaque). This leads to transmural ischemia, which manifests as **transient ST-segment elevation** on an ECG during the episode, returning to baseline once the spasm resolves. * **Why Option A is wrong:** Angina after exertion describes *Stable Angina*. Prinzmetal angina typically occurs at **rest**, often in the early morning or at night (circadian variation). * **Why Option B is wrong:** While atherosclerosis may coexist, the primary mechanism is spasm, not a fixed atherosclerotic blockade. It can occur in patients with completely normal coronary arteries. * **Why Option D is wrong:** **Calcium Channel Blockers (CCBs)** and Nitrates are the first-line treatments because they promote vasodilation. Conversely, **Beta-blockers are contraindicated** as they can lead to unopposed alpha-adrenergic activity, worsening the spasm. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Patient:** Often younger, with fewer traditional risk factors, but a strong association with **smoking**, cocaine use, or migraine. * **ECG Finding:** Transient ST-elevation (mimics STEMI, but resolves quickly). * **Gold Standard Diagnosis:** Coronary angiography with provocative testing (e.g., using Ergonovine or Acetylcholine). * **Treatment:** CCBs (e.g., Diltiazem, Amlodipine) are highly effective. Avoid non-selective Beta-blockers (e.g., Propranolol).

Question 769: What is true about Pulsus bisferiens?

A. Has a double peak, one in systole and another in diastole
B. Has a double peak, both occurring in systole (Correct Answer)
C. Is seen in patients with dilated cardiomyopathy
D. Is seen only when aortic stenosis is associated with aortic regurgitation

Explanation: **Explanation:** **Pulsus bisferiens** (from the Latin *bis* meaning twice and *ferire* meaning to beat) is a physical finding characterized by a double systolic peak in the arterial pulse. 1. **Why Option B is Correct:** The pulse waveform in bisferiens consists of two distinct peaks, both occurring during **ventricular systole**. The first peak is the **Percussion wave** (due to rapid early systolic ejection), and the second is the **Tidal wave** (due to reflected waves from the periphery or continued ejection). These peaks are separated by a mid-systolic dip. 2. **Why the other options are Incorrect:** * **Option A:** A pulse with one peak in systole and another in diastole is called a **Dicrotic pulse** (seen in low cardiac output states like severe heart failure or sepsis) [1]. * **Option C:** Dilated cardiomyopathy typically presents with a dicrotic pulse or pulsus alternans, not bisferiens. Bisferiens is characteristic of **Hypertrophic Obstructive Cardiomyopathy (HOCM)**. * **Option D:** While bisferiens is classically seen in **AR associated with AS** (where AR is predominant), it is also seen in **isolated severe AR** [1] and **HOCM**. Therefore, saying it is "only" seen in the combination is incorrect. **NEET-PG High-Yield Pearls:** * **Best site to palpate:** Carotid artery (though it can be felt peripherally in AR) [2]. * **Differential Diagnosis:** 1. **AR + AS** (AR must be the dominant lesion). 2. **Isolated Severe AR** [1]. 3. **HOCM** (The "spike and dome" pattern). * **Mechanism in HOCM:** The first peak is the rapid ejection, the dip is due to mid-systolic obstruction (SAM of mitral valve), and the second peak is the continued ejection.

Question 770: Which of the following drugs is NOT indicated in the management of dilated cardiomyopathy?

A. Beta-blockers
B. Calcium channel blockers (Correct Answer)
C. Spironolactone
D. ACE inhibitors

Explanation: Explanation: Dilated Cardiomyopathy (DCM) is characterized by ventricular dilation and impaired systolic function (reduced ejection fraction). The management strategy focuses on reversing ventricular remodeling and improving cardiac output [2]. Why Calcium Channel Blockers (CCBs) are NOT indicated: Non-dihydropyridine CCBs (like **Verapamil and Diltiazem**) are generally contraindicated in DCM because they possess significant **negative inotropic effects** [1]. In a heart that already has failing contractility, these drugs can further depress systolic function and exacerbate heart failure symptoms. While certain dihydropyridines (like Amlodipine) are safe if needed for hypertension, CCBs are not part of the standard therapeutic regimen for DCM. Why the other options are wrong (Standard Therapy): * **ACE Inhibitors (e.g., Enalapril):** These are first-line agents. They reduce afterload and preload and, most importantly, prevent and reverse **cardiac remodeling**, significantly reducing mortality [3]. * **Beta-blockers (e.g., Carvedilol, Metoprolol succinate):** Once the patient is stable, beta-blockers are essential to counteract the chronic sympathetic overactivity, improve EF over time, and prevent arrhythmias. * **Spironolactone (Aldosterone Antagonist):** Indicated in patients with persistent symptoms (NYHA Class II-IV). It prevents myocardial fibrosis and reduces mortality. High-Yield Clinical Pearls for NEET-PG: * **Mnemonic for Mortality-Reducing Drugs in HFrEF/DCM:** **B-A-S-H** (Beta-blockers, ACE inhibitors/ARBs, Spironolactone, Hydralazine + Nitrates). * **Most common cause of DCM:** Idiopathic (Genetic/Familial in 30% of cases). * **Reversible causes of DCM:** Alcohol (most common toxin), Beriberi (Thiamine deficiency), Tachycardia-induced, and Peripartum cardiomyopathy [2]. * **Drug of Choice for symptomatic relief (but no mortality benefit):** Diuretics and Digoxin.

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Cardiology — MCQs

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