Cardiology — MCQs
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A 27-year-old man has a blood pressure of 170/100 mmHg. He has a prominent aortic ejection click and murmurs heard over the ribs on both sides anteriorly and over the back posteriorly. In addition, the pulses in the lower extremities are feeble, and he complains of mild claudication with exertion. What is the most likely diagnosis?
Which of the following is NOT a diagnostic criterion for Infective Endocarditis?
Which of the following is not seen with hyperkalemia?
A young patient presented with a blood pressure of 190/120 mm Hg without any clinical symptoms and a normal fundus examination. What is the treatment of choice?
Inability to perform physical activity with discomfort falls under which NYHA functional classification?
What is indicated by a double apical impulse?
A 62-year-old man presents with symptoms of shortness of breath, worse with exertion and difficulty lying down. He reports no chest pain or palpitations but his feet are swollen. His past medical history includes hypertension and type 2 diabetes, for which he is taking ramipril, amlodipine, and metformin. On physical examination, the blood pressure is 125/84 mm Hg, heart rate is 100/min. The jugular venous pressure is 8 cm above the sternal angle, with a third heart sound, pedal edema, and bibasilar crackles on auscultation of the lungs. Which one of the following may be implicated in fluid retention for this condition?
What is the investigation of choice to confirm hemochromatosis as the cause of cardiomyopathy?
Reperfusion is believed to restore contractile function of which of the following?
Which of the following is a criterion for cardiac shock?
Cardiology Indian Medical PG Practice Questions and MCQs
Question 1031: A 27-year-old man has a blood pressure of 170/100 mmHg. He has a prominent aortic ejection click and murmurs heard over the ribs on both sides anteriorly and over the back posteriorly. In addition, the pulses in the lower extremities are feeble, and he complains of mild claudication with exertion. What is the most likely diagnosis?
- A. Atrial septal defect
- B. Aortic stenosis
- C. Coarctation of the aorta (Correct Answer)
- D. Cardiomyopathy
Explanation: The clinical presentation is a classic description of **Coarctation of the Aorta (CoA)**, a congenital narrowing of the aorta typically occurring distal to the origin of the left subclavian artery [2]. **Why Option C is Correct:** * **Hypertension in a Young Patient:** CoA is a major cause of secondary hypertension. Blood pressure is elevated in the upper extremities but low in the lower extremities. * **Radio-femoral Delay:** The "feeble pulses" in the lower extremities and "claudication" (leg pain on exertion) are due to reduced distal perfusion [2]. * **Collateral Circulation:** The murmurs heard over the ribs and back are caused by dilated intercostal arteries acting as collaterals to bypass the obstruction. * **Aortic Ejection Click:** This is frequently present because CoA is highly associated with a **Bicuspid Aortic Valve** (up to 50-85% of cases). **Why Other Options are Incorrect:** * **A. Atrial Septal Defect (ASD):** Presents with a fixed split S2 and a pulmonary flow murmur, not upper limb hypertension or rib collaterals. * **B. Aortic Stenosis:** While it features an ejection click and systolic murmur, it would cause weak pulses globally (pulsus parvus et tardus), not a differential between upper and lower limbs [1]. * **D. Cardiomyopathy:** Usually presents with signs of heart failure (dyspnea, S3 gallop) rather than localized hypertension and collateral murmurs. **High-Yield Pearls for NEET-PG:** * **X-ray Finding:** "Figure of 3" sign on chest X-ray and **rib notching** (due to pressure erosion by dilated intercostal arteries). * **Associations:** Turner Syndrome and Bicuspid Aortic Valve [2]. * **Gold Standard Diagnosis:** CT Angiography or Cardiac MRI. * **Physical Exam:** Always check for **radio-femoral delay** in any young patient with hypertension [2].
Question 1032: Which of the following is NOT a diagnostic criterion for Infective Endocarditis?
- A. Positive Echocardiogram
- B. Positive Blood culture
- C. Raised ESR (Correct Answer)
- D. Positive Rheumatoid Factor
Explanation: The diagnosis of Infective Endocarditis (IE) is based on the **Modified Duke Criteria**, which categorizes findings into Major and Minor criteria [1]. ### **Why "Raised ESR" is the Correct Answer** While an elevated Erythrocyte Sedimentation Rate (ESR) is a very common finding in patients with IE (occurring in approximately 90% of cases), it is **not** part of the Modified Duke Criteria [2]. ESR is a highly sensitive but non-specific marker of inflammation; it can be raised in various infections, malignancies, and autoimmune conditions, making it unreliable for the specific diagnosis of endocarditis. ### **Analysis of Other Options** * **A. Positive Echocardiogram:** This is a **Major Criterion** [1]. Diagnostic findings include an oscillating intracardiac mass (vegetation), abscess, new partial dehiscence of a prosthetic valve, or new valvular regurgitation. * **B. Positive Blood Culture:** This is a **Major Criterion** [1]. It requires typical microorganisms (e.g., *S. viridans*, *S. aureus*, HACEK group) from two separate blood cultures or persistently positive cultures for other organisms. * **C. Positive Rheumatoid Factor (RF):** This is a **Minor Criterion** [1]. Immunological phenomena, including RF, glomerulonephritis, Osler’s nodes, and Roth spots, are specific components used to satisfy the Duke Criteria. ### **High-Yield Clinical Pearls for NEET-PG** * **Definite IE Diagnosis:** Requires 2 Major OR 1 Major + 3 Minor OR 5 Minor criteria [1]. * **Most Common Cause:** *Staphylococcus aureus* is now the most common cause globally (especially acute IE); *Streptococcus viridans* is common in subacute IE following dental procedures. * **IV Drug Users:** Most commonly affects the **Tricuspid Valve**; the most common organism is *S. aureus*. * **Culture-Negative IE:** Most commonly caused by previous antibiotic use or fastidious organisms like *Coxiella burnetii* (Q fever) and *Bartonella*.
Question 1033: Which of the following is not seen with hyperkalemia?
- A. Sinus bradycardia
- B. Ventricular tachycardia
- C. Slow idioventricular rhythm
- D. Bidirectional tachycardia (Correct Answer)
Explanation: ### Explanation **Correct Answer: D. Bidirectional Tachycardia** **Underlying Medical Concept:** Hyperkalemia acts as a "membrane stabilizer" in a pathological sense; it decreases the resting membrane potential (making it less negative) and slows down the upstroke of the action potential [1]. This leads to generalized depression of the conduction system. **Bidirectional tachycardia**, characterized by a beat-to-beat alternation of the QRS axis, is a classic hallmark of **Digoxin toxicity**. It is also seen in Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) and Aconitine poisoning, but it is **not** a feature of hyperkalemia. **Analysis of Incorrect Options:** * **A. Sinus Bradycardia:** Hyperkalemia depresses the SA node and slows conduction. As potassium levels rise, sinus bradycardia and even sinus arrest (leading to "sine wave" patterns) are common [1]. * **B. Ventricular Tachycardia:** While hyperkalemia typically slows rhythms, the resulting electrical instability and shortened refractory periods can trigger ventricular arrhythmias, including VT and Ventricular Fibrillation, especially in the terminal stages [1]. * **C. Slow Idioventricular Rhythm:** As the serum potassium rises (>7.0 mEq/L), P-waves disappear (atrial standstill) and the QRS widens significantly [1]. This results in a slow, wide-complex "idioventricular-like" rhythm which can eventually evolve into a sine wave. **High-Yield Clinical Pearls for NEET-PG:** 1. **Sequential ECG Changes in Hyperkalemia:** Tall peaked T-waves (earliest) → Prolonged PR interval → Loss of P-wave → Widened QRS → Sine wave pattern → Asystole [1]. 2. **Treatment Priority:** Intravenous **Calcium Gluconate** is the first-line treatment to stabilize the cardiac membrane; it does *not* lower potassium levels. 3. **Bidirectional Tachycardia Triad:** Always think of **Digoxin toxicity**, **CPVT**, or **Hypokalemia** (which predisposes to digoxin toxicity), but never hyperkalemia.
Question 1034: A young patient presented with a blood pressure of 190/120 mm Hg without any clinical symptoms and a normal fundus examination. What is the treatment of choice?
- A. Oral Nitroglycerine
- B. Intravenous Nitroglycerine
- C. Oral Enalapril (Correct Answer)
- D. Sublingual short-acting Nifedipine
Explanation: The clinical scenario describes **Hypertensive Urgency**. This is defined as a severe elevation in blood pressure (typically ≥180/120 mm Hg) **without** evidence of acute target organ damage (e.g., normal fundus, no chest pain, no neurological deficits). [1] **1. Why Oral Enalapril is correct:** In Hypertensive Urgency, the goal is to lower blood pressure gradually over 24 to 48 hours using **oral medications**. [1] Rapidly dropping BP to "normal" levels can lead to cerebral or myocardial ischemia due to altered autoregulation. Oral ACE inhibitors (like Enalapril or Captopril) [1] are preferred as they provide a controlled, predictable decline in BP. **2. Why other options are incorrect:** * **Intravenous Nitroglycerine:** This is indicated for **Hypertensive Emergencies** (BP >180/120 + organ damage like Acute Coronary Syndrome or Pulmonary Edema). Using IV therapy in asymptomatic patients can cause dangerous hypotension. * **Oral Nitroglycerine:** This is primarily an anti-anginal drug and is not the standard of care for managing hypertensive urgency. * **Sublingual short-acting Nifedipine:** This is **蜻contraindicated**. It causes an unpredictable, precipitous drop in BP, which has been associated with fatal strokes and myocardial infarctions. **Clinical Pearls for NEET-PG:** * **Hypertensive Urgency:** High BP + No organ damage → Treat with **Oral** drugs (e.g., Labetalol, Amlodipine, Enalapril). [1] * **Hypertensive Emergency:** High BP + Organ damage (Papilledema, Encephalopathy, AKI) → Treat with **IV** drugs (e.g., Labetalol, Nicardipine, Nitroprusside). [1] * **Goal in Emergency:** Reduce Mean Arterial Pressure (MAP) by no more than 25% within the first hour to prevent ischemic complications.
Question 1035: Inability to perform physical activity with discomfort falls under which NYHA functional classification?
- A. Class I
- B. Class II
- C. Class III
- D. Class IV (Correct Answer)
Explanation: The **New York Heart Association (NYHA) Functional Classification** is a clinical tool used to categorize the severity of heart failure based on the patient’s symptoms and physical activity limitations. ### **Explanation of the Correct Answer** **Class IV** represents the most severe stage of functional impairment. Patients in this class are **unable to carry out any physical activity without discomfort**. Crucially, symptoms of heart failure (such as dyspnea or fatigue) or anginal syndrome may be present **even at rest** [2]. Any attempt at physical activity increases the severity of this discomfort. ### **Analysis of Incorrect Options** * **Class I:** No limitation of physical activity. Ordinary physical activity (e.g., walking or climbing stairs) does not cause undue fatigue, palpitations, or dyspnea. * **Class II:** Slight limitation of physical activity. The patient is comfortable at rest, but **ordinary physical activity** results in fatigue, palpitations, or dyspnea [1]. * **Class III:** Marked limitation of physical activity. The patient is comfortable at rest, but **less than ordinary activity** (e.g., walking short distances or dressing) causes symptoms [1]. ### **High-Yield Clinical Pearls for NEET-PG** * **Dynamic Nature:** Unlike the ACC/AHA Stages (A, B, C, D) which are progressive and irreversible, the NYHA class can change (improve or worsen) based on treatment and clinical status. * **Key Differentiator:** The hallmark of **Class IV** is the presence of symptoms at **rest** or the total inability to perform any activity [2]. * **Prognostic Value:** Higher NYHA classes are strongly associated with increased hospitalization rates and mortality in heart failure patients.
Question 1036: What is indicated by a double apical impulse?
- A. Mitral regurgitation
- B. Aortic regurgitation
- C. Aortic stenosis (Correct Answer)
- D. Mitral stenosis
Explanation: **Explanation:** A **double apical impulse** (also known as a bifid or presystolic impulse) is a classic physical finding in patients with severe **Aortic Stenosis (AS)**. **Why Aortic Stenosis is correct:** In severe AS, the left ventricle (LV) faces high afterload, leading to compensatory **LV hypertrophy** and decreased compliance [1]. To fill this stiff ventricle, the left atrium must contract forcefully. This vigorous atrial contraction (atrial kick) creates a palpable presystolic impulse just before the actual ventricular apex beat. When both the atrial contraction and the ventricular systole are palpable, it results in a "double" impulse. **Why other options are incorrect:** * **Mitral Regurgitation (MR):** Typically presents with a hyperdynamic, displaced apex beat due to volume overload, but it is usually a single, brisk impulse [1]. * **Aortic Regurgitation (AR):** Characterized by a hyperdynamic, "heaving," and laterally displaced apex beat [1]. While severe AR can sometimes cause a "bisferiens pulse" (in the carotids), the apical impulse remains single [2]. * **Mitral Stenosis (MS):** Usually presents with a **tapping apex beat**, which represents a palpable S1 [1]. The LV is typically normal or small in size, so a double impulse is not expected. **NEET-PG High-Yield Pearls:** 1. **Triple Apical Impulse:** Pathognomonic for **Hypertrophic Obstructive Cardiomyopathy (HOCM)**. It consists of a palpable S4 followed by a double systolic peak. 2. **Sustained Apex Beat:** Seen in pressure overload states like AS and Hypertension [1]. 3. **Hyperdynamic Apex Beat:** Seen in volume overload states like AR and MR [1]. 4. **Tapping Apex:** Palpable S1, characteristic of Mitral Stenosis [1].
Question 1037: A 62-year-old man presents with symptoms of shortness of breath, worse with exertion and difficulty lying down. He reports no chest pain or palpitations but his feet are swollen. His past medical history includes hypertension and type 2 diabetes, for which he is taking ramipril, amlodipine, and metformin. On physical examination, the blood pressure is 125/84 mm Hg, heart rate is 100/min. The jugular venous pressure is 8 cm above the sternal angle, with a third heart sound, pedal edema, and bibasilar crackles on auscultation of the lungs. Which one of the following may be implicated in fluid retention for this condition?
- A. Decreased renin
- B. Increased aldosterone (Correct Answer)
- C. Increased estrogen
- D. Increased growth hormone
Explanation: **Explanation:** The clinical presentation of dyspnea, orthopnea, elevated JVP, S3 gallop, pedal edema, and bibasilar crackles [1] is diagnostic of **Congestive Heart Failure (CHF)** [2]. In CHF, the primary driver of fluid retention is the activation of the **Renin-Angiotensin-Aldosterone System (RAAS)** [1]. 1. **Why Option B is Correct:** In heart failure, decreased cardiac output leads to reduced renal perfusion. This triggers the release of Renin, which converts Angiotensinogen to Angiotensin I. Angiotensin-Converting Enzyme (ACE) then produces Angiotensin II, which stimulates the adrenal cortex to secrete **Aldosterone**. Aldosterone acts on the distal tubules and collecting ducts to increase **sodium and water reabsorption**, leading to fluid overload and edema [1]. 2. **Why Other Options are Incorrect:** * **Decreased Renin:** In CHF, renin is significantly **increased** to compensate for low effective arterial blood volume [1]. * **Increased Estrogen:** While estrogen can cause mild sodium retention (e.g., premenstrual bloating), it is not the pathological mechanism behind heart failure-induced edema. * **Increased Growth Hormone:** GH excess (Acromegaly) can cause cardiomyopathy, but it is not the direct mediator of fluid retention in standard CHF. **NEET-PG High-Yield Pearls:** * **S3 Gallop:** The most specific physical sign for heart failure in adults (indicates ventricular filling into a dilated, compliant chamber). * **Spironolactone/Eplerenone:** These Aldosterone antagonists are "disease-modifying" drugs in HFrEF that reduce mortality by preventing myocardial fibrosis and fluid retention. * **BNP (B-type Natriuretic Peptide):** Released from ventricles due to stretch; it acts as a natural antagonist to the RAAS system by promoting natriuresis [1].
Question 1038: What is the investigation of choice to confirm hemochromatosis as the cause of cardiomyopathy?
- A. ECG
- B. Echocardiogram
- C. MRI (Correct Answer)
- D. CT Scan
Explanation: **Explanation:** **Why MRI is the Correct Answer:** Cardiac MRI (specifically **T2* weighted imaging**) is the gold standard and investigation of choice for confirming and quantifying myocardial iron overload in hemochromatosis. Iron is paramagnetic; its deposition in the myocardium causes a shortening of the T2* relaxation time. A T2* value of **<20 ms** indicates iron overload, while **<10 ms** signifies a high risk of developing heart failure. MRI is non-invasive, more sensitive than biopsy (due to the patchy nature of iron deposition), and is used to monitor the efficacy of chelation therapy. In terms of imaging techniques, MRI has high specificity for iron overload [1]. **Why Other Options are Incorrect:** * **ECG:** While it may show non-specific ST-T wave changes, low voltage complexes, or arrhythmias (like supraventricular tachycardia), it cannot confirm the underlying etiology of iron deposition. * **Echocardiogram:** This is the initial screening tool to assess functional status. It typically shows a **restrictive cardiomyopathy** pattern (early stage) or **dilated cardiomyopathy** (late stage), but it cannot differentiate iron overload from other causes of infiltrative cardiomyopathy. * **CT Scan:** CT has poor sensitivity for detecting myocardial iron compared to MRI and involves unnecessary ionizing radiation. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad (Bronze Diabetes):** Cirrhosis, Diabetes Mellitus, and Skin Hyperpigmentation. * **Cardiac Involvement:** Hemochromatosis is a unique cause of "reversible" cardiomyopathy if iron is removed via phlebotomy or chelation. * **Histology:** On biopsy, iron is visualized using **Prussian Blue stain** [1]. * **Screening:** The most sensitive initial lab test is **Transferrin Saturation** (>45%); the most useful screening protein is **Serum Ferritin** [1].
Question 1039: Reperfusion is believed to restore contractile function of which of the following?
- A. Stunned Myocardium
- B. Hibernating Myocardium (Correct Answer)
- C. Ischemic non-bled myocardium
- D. Non ischemic bled myocardium
Explanation: ### Explanation The correct answer is **Hibernating Myocardium**. **1. Why Hibernating Myocardium is Correct:** Hibernating myocardium refers to a state of **chronic** but reversible left ventricular systolic dysfunction due to persistently reduced coronary blood flow (chronic ischemia) [1]. In this state, the myocytes remain viable but "downregulate" their metabolism and contractility to match the low oxygen supply, preventing irreversible necrosis [1]. The hallmark of hibernation is that **contractile function improves or is restored after reperfusion** (e.g., via CABG or PCI), provided intervention occurs before irreversible damage [2]. **2. Why the Other Options are Incorrect:** * **Stunned Myocardium (Option A):** This is a state of temporary contractile dysfunction that persists **after** blood flow has already been restored (post-ischemic dysfunction). Unlike hibernation, the blood flow is already normal, but the muscle takes time to recover. Reperfusion is the *cause* of the recovery process, not the trigger for restoration of function, as the flow is already present. * **Ischemic/Non-ischemic bled myocardium (Options C & D):** These terms are not standard clinical descriptors for reversible myocardial dysfunction. "Bled" (hemorrhagic) myocardium usually implies severe microvascular injury or reperfusion injury, which often leads to permanent damage rather than functional restoration. **3. NEET-PG Clinical Pearls:** * **Gold Standard for Viability:** PET scan (showing FDG uptake) is the gold standard to differentiate hibernating (viable) from infarcted (non-viable) tissue. * **Dobutamine Stress Echo:** Hibernating myocardium shows a **biphasic response** (improvement at low doses, worsening at high doses). * **Key Distinction:** * **Stunning:** Flow is normal; function is low (temporary). * **Hibernation:** Flow is low; function is low (reversible upon revascularization).
Question 1040: Which of the following is a criterion for cardiac shock?
- A. Systolic blood pressure < 90 mm Hg (Correct Answer)
- B. Diastolic blood pressure < 80 mm Hg
- C. Cardiac index < 3.5 L/min/m
- D. Stroke volume 70 ml
Explanation: **Explanation:** **Cardiogenic shock** is a state of end-organ hypoperfusion due to primary cardiac failure, most commonly following a massive myocardial infarction [1]. The diagnosis is based on a combination of clinical and hemodynamic parameters. 1. **Why Option A is Correct:** A **Systolic Blood Pressure (SBP) < 90 mmHg** for at least 30 minutes (or the need for vasopressors to maintain SBP ≥ 90 mmHg) is a hallmark diagnostic criterion. This hypotension reflects the heart's inability to maintain adequate perfusion pressure to vital organs despite adequate intravascular volume [2]. 2. **Why the Other Options are Incorrect:** * **Option B:** Diastolic blood pressure is not a primary diagnostic criterion for shock; the focus remains on SBP and Mean Arterial Pressure (MAP) [2]. * **Option C:** The hemodynamic criterion for cardiogenic shock is a **Cardiac Index (CI) < 2.2 L/min/m²**. A CI of 3.5 L/min/m² is within the normal range (2.5–4.0 L/min/m²). * **Option D:** A stroke volume of 70 ml is considered normal. In cardiogenic shock, stroke volume and cardiac output are significantly reduced. **High-Yield Clinical Pearls for NEET-PG:** * **Hemodynamic Profile:** Low Cardiac Index (< 2.2), **High Pulmonary Capillary Wedge Pressure (PCWP > 15-18 mmHg)**, and increased Systemic Vascular Resistance (SVR). * **Clinical Signs:** Cold/clammy extremities, altered mental status, and oliguria (urine output < 30 ml/hr). * **Management Gold Standard:** Early revascularization (PCI or CABG). Intra-aortic balloon pump (IABP) may be used for stabilization but does not reduce mortality. * **Most Common Cause:** Acute Myocardial Infarction (affecting >40% of the Left Ventricle) [1].
Practice by Chapter
Coronary Artery Disease and Angina
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Acute Coronary Syndromes
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Heart Failure
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Cardiac Arrhythmias
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Valvular Heart Diseases
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Cardiomyopathies
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Pericardial Diseases
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Congenital Heart Disease in Adults
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Hypertension and Hypertensive Emergencies
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Pulmonary Hypertension
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Non-invasive Cardiac Diagnostics
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Preventive Cardiology
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