Cardiology — MCQs
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Reversible myocardial stunning with ECG changes of acute myocardial infarction is seen in which of the following conditions?
ECG changes in atrial fibrillation do not include which of the following?
A 35-year-old lady presents with a skin lesion and repeated episodes of syncope on sudden change of position. What does the ECG show?
A 72-year-old man has had poorly controlled hypertension for the past 20 years. Over the past day he has had a severe headache with nausea, followed by confusion, then convulsions. On examination he is afebrile, but his blood pressure is now 260/150 mm Hg. There is bilateral papilledema. Which of the following pathologic lesions is most likely to have developed in his brain during the past day?
What is the most common valvular lesion in carcinoid syndrome?
A 60-year-old man presents with dizziness, nausea, and shortness of breath of several months' duration. Physical examination shows hepatomegaly, ascites, and anasarca. His blood pressure is 200/115 mm Hg. A chest X-ray demonstrates cardiomegaly and mild pulmonary edema. Although different mechanisms may have contributed to the pathogenesis of hypertension in this patient, what is the common end result for all of them?
All are features of the given ECG except:
Which of the following is NOT a feature of atrial septal defect?
A 55-year-old man presents with gradually increasing shortness of breath and leg swelling over the past month. He has orthopnea and paroxysmal nocturnal dyspnea. His medical history includes hypercholesterolemia treated with simvastatin and hypertension treated with hydrochlorothiazide. Current blood pressure is 140/90 mm Hg. Physical examination reveals mild jugular venous distension, bibasilar crackles, an S3 gallop, and minimal pedal edema. Echocardiography shows a left ventricular ejection fraction (LVEF) of 40% without segmental wall-motion abnormality. The patient wishes to minimize his medication regimen. What change in his management would you recommend?
Intermittent claudication is characterized by which of the following?
Cardiology Indian Medical PG Practice Questions and MCQs
Question 901: Reversible myocardial stunning with ECG changes of acute myocardial infarction is seen in which of the following conditions?
- A. Restrictive cardiomyopathy
- B. Hypertrophic cardiomyopathy
- C. Takotsubo cardiomyopathy (Correct Answer)
- D. Dilated cardiomyopathy
Explanation: **Explanation:** **Takotsubo Cardiomyopathy** (also known as "Broken Heart Syndrome" or "Apical Ballooning Syndrome") is the correct answer. It is characterized by transient, **reversible left ventricular (LV) systolic dysfunction** that typically follows a period of intense physical or emotional stress. * **Pathophysiology:** The condition is thought to be caused by a "catecholamine surge" leading to microvascular spasm or direct myocardial toxicity. This results in **myocardial stunning**, where the heart muscle is alive but temporarily non-functional. * **Clinical Presentation:** Patients present with symptoms identical to an Acute Coronary Syndrome (ACS)—chest pain and dyspnea. * **ECG & Labs:** ECG often shows ST-segment elevation or T-wave inversions, and cardiac enzymes (Troponin) are frequently elevated, mimicking an **Acute Myocardial Infarction (AMI)**. However, coronary angiography reveals **no obstructive coronary artery disease** [1]. **Why other options are incorrect:** * **Restrictive Cardiomyopathy:** Characterized by stiff ventricular walls and impaired diastolic filling; it does not typically present as reversible stunning mimicking an AMI. * **Hypertrophic Cardiomyopathy (HCM):** A genetic disorder causing asymmetrical septal hypertrophy. While it can cause ECG changes (LVH, deep Q waves), it is a chronic structural disease, not a reversible stunning event. * **Dilated Cardiomyopathy (DCM):** Involves progressive enlargement and thinning of the LV. While it causes systolic heart failure, it is generally chronic and irreversible, unlike the transient nature of Takotsubo. **High-Yield Pearls for NEET-PG:** 1. **Classic Imaging Finding:** "Apical ballooning" on ventriculography (resembling a Japanese octopus trap, or *Takotsubo*). 2. **Demographics:** Most common in **postmenopausal women**. 3. **Prognosis:** Excellent; LV function usually returns to normal within 1–4 weeks with supportive care.
Question 902: ECG changes in atrial fibrillation do not include which of the following?
- A. Absence of P waves
- B. Irregularity of R-R interval
- C. Tall P waves (Correct Answer)
- D. None of the above
Explanation: Atrial Fibrillation (AF) is characterized by rapid, disorganized electrical activity in the atria (350–600 bpm), leading to a lack of effective atrial contraction. [1] **Why "Tall P waves" is the correct answer:** In AF, there is no coordinated atrial depolarization. Instead of distinct P waves, the baseline shows fine or coarse "f-waves" (fibrillatory waves). Therefore, **Tall P waves** (typically seen in Right Atrial Enlargement or *P-pulmonale*) cannot exist in AF because the organized P wave itself is absent. **Analysis of other options:** * **Absence of P waves:** This is a hallmark of AF. Because the sinoatrial (SA) node is overridden by multiple re-entrant circuits, normal P waves disappear and are replaced by an oscillating baseline. [1] * **Irregularity of R-R interval:** This is the most characteristic feature of AF, often described as **"irregularly irregular"** rhythm. The AV node is bombarded by rapid impulses and conducts them unpredictably, leading to inconsistent timing between ventricular contractions (QRS complexes). [1] **High-Yield Clinical Pearls for NEET-PG:** * **ECG Triad of AF:** 1. Absence of P waves; 2. Presence of fibrillatory (f) waves; 3. Irregularly irregular R-R intervals. * **Pulse Deficit:** In AF, the apical heart rate is higher than the radial pulse rate (Pulse deficit >10 bpm) due to some beats having insufficient stroke volume to open the aortic valve. * **Common Causes:** Mitral stenosis (most common valvular cause), Thyrotoxicosis, Hypertension, and "Holiday Heart Syndrome" (alcohol-induced). * **Management:** Focuses on **Rate control** (Beta-blockers/CCBs), **Rhythm control** (Amiodarone/DC cardioversion), and **Anticoagulation** (based on CHA₂DS₂-VASc score) to prevent embolic stroke. [1]
Question 903: A 35-year-old lady presents with a skin lesion and repeated episodes of syncope on sudden change of position. What does the ECG show?
- A. Complete heart block (Correct Answer)
- B. First-degree heart block
- C. Second-degree heart block
- D. 2:1 heart block
Explanation: ***Complete heart block*** - **Positional syncope** in a young patient with skin lesions suggests **cardiac sarcoidosis** or **Lyme carditis**, both commonly causing complete heart block with **Stokes-Adams attacks**. - ECG shows **complete AV dissociation** with independent atrial and ventricular rhythms, causing hemodynamic instability and syncope on position changes. *First-degree heart block* - Characterized by **prolonged PR interval** (>200ms) but all P waves are conducted to ventricles. - Patients remain **asymptomatic** and do not experience syncope as ventricular rate is maintained. *Second-degree heart block* - **Mobitz Type I** shows progressive PR prolongation with dropped beats, while **Mobitz Type II** has fixed PR intervals with intermittent dropped beats. - Usually **asymptomatic** or causes mild symptoms, not severe positional syncope requiring emergency intervention. *2:1 heart block* - Shows **every second P wave** conducted to ventricles with a regular pattern of dropped beats. - While it can cause symptoms, the **regular ventricular response** typically doesn't cause severe positional syncope seen in complete heart block.
Question 904: A 72-year-old man has had poorly controlled hypertension for the past 20 years. Over the past day he has had a severe headache with nausea, followed by confusion, then convulsions. On examination he is afebrile, but his blood pressure is now 260/150 mm Hg. There is bilateral papilledema. Which of the following pathologic lesions is most likely to have developed in his brain during the past day?
- A. Arteriolar fibrinoid necrosis (Correct Answer)
- B. Cortical telangiectasia
- C. Lacunar infarction
- D. Putaminal hematoma
Explanation: ### Explanation **Correct Option: A. Arteriolar fibrinoid necrosis** This patient presents with a **Hypertensive Emergency** (specifically **Hypertensive Encephalopathy**), characterized by a systolic BP >180 mmHg or diastolic BP >120 mmHg along with acute end-organ damage (papilledema, confusion, seizures). The underlying pathophysiology involves a sudden, severe rise in blood pressure that exceeds the limits of cerebral autoregulation. This leads to endothelial injury and increased vascular permeability. Plasma proteins leak into the vessel wall, and the subsequent activation of the coagulation cascade results in **fibrinoid necrosis** of the arterioles [1]. This process causes the "onion-skin" appearance of vessels and localized cerebral edema, leading to the clinical symptoms of encephalopathy. **Analysis of Incorrect Options:** * **B. Cortical telangiectasia:** These are small, dilated capillary-like vessels (vascular malformations) that are usually congenital and incidental; they are not caused by acute hypertensive crises. * **C. Lacunar infarction:** These are small ( <15 mm) strokes caused by **hyaline arteriolosclerosis** (chronic hypertension) [1]. While common in hypertensive patients, they represent chronic ischemic damage rather than the acute, necrotizing changes seen in an encephalopathic crisis. * **D. Putaminal hematoma:** While hypertension is the leading cause of intraparenchymal hemorrhage (most commonly in the putamen), the clinical triad of headache, papilledema, and global encephalopathy in the setting of extreme BP elevation specifically points toward the diffuse vascular damage of fibrinoid necrosis. **High-Yield Clinical Pearls for NEET-PG:** * **Hypertensive Urgency:** High BP without end-organ damage; treat with oral medications over 24–48 hours. * **Hypertensive Emergency:** High BP with end-organ damage; treat with IV medications (e.g., Labetalol, Nicardipine, Nitroprusside). * **Target BP Reduction:** Reduce Mean Arterial Pressure (MAP) by no more than **25% within the first hour** to prevent cerebral ischemia (exception: Aortic dissection). * **Histology:** Chronic HTN leads to *Hyaline* arteriolosclerosis; Malignant HTN leads to *Fibrinoid* necrosis and *Hyperplastic* (onion-skin) arteriolosclerosis [1].
Question 905: What is the most common valvular lesion in carcinoid syndrome?
- A. Aortic stenosis
- B. Tricuspid regurgitation (Correct Answer)
- C. Mitral stenosis
- D. Aortic regurgitation
Explanation: **Explanation:** Carcinoid heart disease occurs in approximately 50% of patients with carcinoid syndrome, typically associated with metastatic neuroendocrine tumors of the midgut. [1] **Why Tricuspid Regurgitation is correct:** The pathophysiology involves the release of vasoactive substances, primarily **serotonin (5-HT)**, into the systemic circulation. [1] These substances cause fibrous plaque-like endocardial thickening. Because these mediators are inactivated by the lungs (via monoamine oxidase), the **right side of the heart** is predominantly affected. The plaques lead to retraction and fixation of the valve leaflets. The most common manifestation is **Tricuspid Regurgitation (TR)**, often accompanied by pulmonary stenosis. [2] **Why other options are incorrect:** * **Aortic Stenosis (A) & Aortic Regurgitation (D):** Left-sided lesions are rare because the lungs act as a metabolic filter, neutralizing serotonin before it reaches the left atrium. Left-sided involvement only occurs in the presence of a right-to-left shunt (e.g., Patent Foramen Ovale) or primary bronchial carcinoid. * **Mitral Stenosis (C):** Similar to aortic lesions, the mitral valve is protected by pulmonary metabolism. While mitral regurgitation can occur in rare cases, it is never the "most common" lesion. **High-Yield Clinical Pearls for NEET-PG:** * **Pathognomonic finding:** Glistening, white, pearly fibrous plaques on the endocardium. * **Biomarker:** Elevated urinary **5-HIAA** (5-Hydroxyindoleacetic acid) is used for diagnosis. * **Management:** Somatostatin analogues (Octreotide) reduce symptoms; definitive treatment for severe valve heart failure is surgical valve replacement. * **Triad of Carcinoid Syndrome:** Flushing, Diarrhea, and Right-sided heart failure.
Question 906: A 60-year-old man presents with dizziness, nausea, and shortness of breath of several months' duration. Physical examination shows hepatomegaly, ascites, and anasarca. His blood pressure is 200/115 mm Hg. A chest X-ray demonstrates cardiomegaly and mild pulmonary edema. Although different mechanisms may have contributed to the pathogenesis of hypertension in this patient, what is the common end result for all of them?
- A. Aerial cystic medial necrosis
- B. Decreased plasma oncotic pressure
- C. Generalized vasodilation
- D. Increased peripheral vascular resistance (Correct Answer)
Explanation: ### Explanation **1. Why the Correct Answer is Right:** The patient presents with signs of **congestive heart failure (CHF)** secondary to long-standing, severe hypertension (BP 200/115 mm Hg) [3]. In the pathophysiology of systemic hypertension, regardless of the initiating trigger (e.g., renin-angiotensin-aldosterone system activation, sympathetic overactivity, or endothelial dysfunction), the **common final pathway is an increase in Total Peripheral Resistance (TPR)**. [1] According to the hemodynamic equation **Mean Arterial Pressure (MAP) = Cardiac Output (CO) × TPR**, a sustained elevation in blood pressure must be driven by either an increase in CO or TPR. In chronic hypertension, CO often remains normal or decreases (as seen in this patient’s heart failure), meaning the primary driver maintaining the high pressure is the constriction and structural remodeling of small arteries and arterioles, leading to increased TPR [1], [2]. **2. Why Incorrect Options are Wrong:** * **A. Arterial cystic medial necrosis:** This is a pathological feature of the aorta, typically associated with Marfan syndrome or aortic dissection; it is not the universal mechanism for hypertension. [1] * **B. Decreased plasma oncotic pressure:** This occurs in nephrotic syndrome or liver failure. While this patient has edema, his edema is "cardiogenic" (increased hydrostatic pressure) due to heart failure, not low protein. * **C. Generalized vasodilation:** Vasodilation would *lower* blood pressure. Hypertension is characterized by vasoconstriction. [2] **3. NEET-PG High-Yield Pearls:** * **Resistance Vessels:** The **arterioles** are the primary site of peripheral resistance. * **Poiseuille’s Law:** Resistance is inversely proportional to the fourth power of the radius ($R \propto 1/r^4$). Even minor narrowing of the vessel lumen significantly spikes the BP. * **Hypertensive Emergency vs. Urgency:** This patient has symptoms of end-organ damage (pulmonary edema), classifying this as a **Hypertensive Emergency**, requiring parenteral antihypertensives (e.g., Labetalol or Nitroglycerin). [3]
Question 907: All are features of the given ECG except:
- A. Wide QRS complexes
- B. Absent P wave
- C. Complete compensatory pause
- D. Prolonged PR interval (Correct Answer)
Explanation: ***Prolonged PR interval*** - **PR interval** represents atrial to ventricular conduction time and is **not applicable** in PVCs since they originate from the **ventricles**, bypassing the normal AV conduction system. - PVCs arise from **ectopic ventricular foci**, making PR interval measurement irrelevant as there is no preceding **P wave** from sinus node activation. *Wide QRS complexes* - PVCs originate from **ventricular myocardium** rather than the normal **His-Purkinje system**, causing slow cell-to-cell conduction. - This abnormal conduction pathway results in **QRS duration >120 ms**, creating the characteristic wide, bizarre morphology. *Absent P wave* - PVCs are **ectopic beats** originating from ventricular tissue, independent of **sinus node** activity. - The **atrial depolarization** (P wave) may be hidden within the wide QRS complex or completely absent due to **retrograde conduction** block. *Complete compensatory pause* - The **sinus node** continues its regular rhythm uninterrupted, creating a pause after the PVC where **two normal R-R intervals** equal the time from the beat before PVC to the beat after. - This occurs because the PVC does **not reset** the sinus node timing, unlike premature atrial contractions which cause incomplete compensatory pauses.
Question 908: Which of the following is NOT a feature of atrial septal defect?
- A. Fixed S2 split
- B. Mid diastolic murmur
- C. Ejection systolic murmur
- D. Paradoxical pulse (Correct Answer)
Explanation: **Explanation:** In an Atrial Septal Defect (ASD), the primary pathophysiology involves a left-to-right shunt, leading to volume overload of the right atrium and right ventricle [1]. **Why Paradoxical Pulse is the Correct Answer:** **Pulsus paradoxus** (an exaggerated drop in systolic blood pressure >10 mmHg during inspiration) is typically seen in conditions involving cardiac tamponade, severe asthma, or constrictive pericarditis. It is **not** a feature of ASD. In fact, because the right and left atria communicate in ASD, the normal respiratory variations in stroke volume are dampened, which is why the S2 split remains "fixed." **Analysis of Incorrect Options:** * **Fixed S2 Split:** This is the hallmark of ASD. The split is "wide" due to delayed closure of the pulmonary valve (increased RV volume) and "fixed" because the shunt equalizes the respiratory pressure changes between the two atria. * **Ejection Systolic Murmur (ESM):** This occurs due to **increased flow** across the pulmonary valve (functional pulmonary stenosis). It is heard best at the left upper sternal border. * **Mid-Diastolic Murmur:** This occurs due to **increased flow** across the tricuspid valve (functional tricuspid stenosis) during ventricular filling. It is heard best at the lower left sternal border. **High-Yield Clinical Pearls for NEET-PG:** * **Most common type:** Ostium secundum (located in the region of the fossa ovalis) [1]. * **ECG findings:** Right Axis Deviation and RSR' pattern in V1 (Partial RBBB) are classic for Secundum ASD. * **Chest X-ray:** Shows cardiomegaly, prominent pulmonary artery, and increased pulmonary vascular markings (plethora). * **Contraindication:** ASD closure is contraindicated if Eisenmenger syndrome (reversal of shunt) has developed.
Question 909: A 55-year-old man presents with gradually increasing shortness of breath and leg swelling over the past month. He has orthopnea and paroxysmal nocturnal dyspnea. His medical history includes hypercholesterolemia treated with simvastatin and hypertension treated with hydrochlorothiazide. Current blood pressure is 140/90 mm Hg. Physical examination reveals mild jugular venous distension, bibasilar crackles, an S3 gallop, and minimal pedal edema. Echocardiography shows a left ventricular ejection fraction (LVEF) of 40% without segmental wall-motion abnormality. The patient wishes to minimize his medication regimen. What change in his management would you recommend?
- A. Add spironolactone
- B. Add an ACE inhibitor and a beta-blocker (Correct Answer)
- C. Add digoxin
- D. Add a calcium-channel blocker
Explanation: ### Explanation This patient presents with classic signs and symptoms of **Heart Failure with reduced Ejection Fraction (HFrEF)**, characterized by an LVEF of 40%, orthopnea, PND, S3 gallop, and pulmonary congestion [1]. **1. Why Option B is Correct:** The cornerstone of HFrEF management is **Guideline-Directed Medical Therapy (GDMT)**. ACE inhibitors (or ARBs/ARNIs) and Beta-blockers are the first-line agents proven to **reduce mortality and morbidity** in patients with HFrEF [1]. * **ACE Inhibitors:** Reduce afterload and prevent cardiac remodeling by inhibiting the renin-angiotensin-aldosterone system (RAAS) [1]. * **Beta-blockers:** (specifically Carvedilol, Metoprolol succinate, or Bisoprolol) reduce sympathetic overactivity, prevent arrhythmias, and improve long-term LVEF [1]. **2. Why Other Options are Incorrect:** * **Option A (Spironolactone):** While Mineralocorticoid Receptor Antagonists (MRAs) reduce mortality, they are typically added *after* the patient is stabilized on an ACE inhibitor and Beta-blocker if symptoms persist (NYHA Class II-IV). * **Option C (Digoxin):** Digoxin may reduce hospitalizations and improve symptoms but has **no mortality benefit** [1]. It is reserved for patients who remain symptomatic despite optimal GDMT or those with concomitant atrial fibrillation. * **Option D (Calcium-channel blocker):** Non-dihydropyridines (Verapamil/Diltiazem) are **contraindicated** in HFrEF due to their negative inotropic effects, which can worsen heart failure. **Clinical Pearls for NEET-PG:** * **Mortality-reducing drugs in HFrEF:** ACE inhibitors, ARBs, ARNIs, Beta-blockers, MRAs (Spironolactone/Eplerenone), and SGLT2 inhibitors (Dapagliflozin/Empagliflozin) [1]. * **S3 Gallop:** A highly specific sign of ventricular filling into a dilated, compliant left ventricle (hallmark of systolic HF). * **Diuretics (e.g., Furosemide):** Excellent for symptom relief (congestion) but do **not** improve survival.
Question 910: Intermittent claudication is characterized by which of the following?
- A. Most common in the calf region (Correct Answer)
- B. Occurs at rest
- C. The claudication distance is not consistent for an individual
- D. Pain is positional
Explanation: **Explanation:** Intermittent claudication is the hallmark symptom of **Peripheral Arterial Disease (PAD)**, resulting from exercise-induced muscle ischemia due to fixed arterial stenosis [1]. **1. Why Option A is Correct:** The pain of claudication typically occurs in the muscle group **distal** to the site of arterial occlusion [1]. Since the **superficial femoral artery** is the most common site of atherosclerotic involvement in PAD, the **calf muscles** (gastrocnemius) are the most frequently affected site [1]. **2. Why the Other Options are Incorrect:** * **Option B (Occurs at rest):** By definition, claudication is induced by exercise and relieved by rest (usually within 10 minutes) [1]. Pain at rest indicates **Critical Limb Ischemia (CLI)**, a more advanced stage of PAD (Fontaine Stage III/IV) [2]. * **Option C (Inconsistent distance):** True claudication is characterized by a **fixed/consistent claudication distance**. The patient can typically predict exactly how far they can walk before the pain starts. Inconsistency suggests "Pseudoclaudication" (e.g., Lumbar Canal Stenosis). * **Option D (Pain is positional):** Claudication pain is related to **metabolic demand (exertion)**, not posture. Positional relief (like leaning forward) is characteristic of neurogenic claudication, not vascular claudication. **High-Yield Clinical Pearls for NEET-PG:** * **Fontaine Classification:** Stage I (Asymptomatic), Stage II (Claudication), Stage III (Rest pain), Stage IV (Ulcer/Gangrene). * **Leriche Syndrome:** Triad of claudication (hip/buttock), impotence, and absent femoral pulses (due to Aorto-iliac occlusion). * **Ankle-Brachial Index (ABI):** The best initial diagnostic test. ABI < 0.9 is diagnostic of PAD; < 0.4 indicates severe disease/rest pain. * **Management:** Smoking cessation is the most important modifiable risk factor. **Cilostazol** (PDE-3 inhibitor) is the drug of choice for symptomatic relief.
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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