Cardiology — MCQs

A 76-year-old woman presents with new-onset syncope and has noticed early fatigue on exertion for the past year. On examination, there is a systolic ejection murmur at the right sternal border that radiates to the carotids. What is the characteristic arterial pulse finding in this patient with suspected aortic stenosis?

Q77Medium

A 56-year-old woman presents with dyspnea, blurry vision, and headaches that began this morning and are worsening. Her past medical history includes hypertension and osteoarthritis. She discontinued her anti-hypertensive medications three months ago due to side effects. On examination, her blood pressure is 210/130 mm Hg, heart rate is 100 beats/min, and oxygen saturation is 95%. Fundoscopy reveals retinal hemorrhages and papilledema. Heart sounds are normal except for an S4, and lung auscultation reveals lower lobe crackles. Which of the following is the most appropriate agent to reduce her blood pressure?

Q78Easy

What is the recommended management for essential hypertension?

Q79Easy

Hyperdynamic circulation is seen in all EXCEPT:

Q80Medium

Which of the following dietary interventions has shown to reduce mortality in patients with coronary heart disease?

Cardiology Indian Medical PG Practice Questions and MCQs

Question 71: Which of the following does NOT increase the chances of Deep Vein Thrombosis?

A. Oral contraceptive pills
B. Hypertension
C. Superficial thrombophlebitis (Correct Answer)
D. Myocardial infarction

Explanation: **Explanation:** Deep Vein Thrombosis (DVT) occurs due to the components of **Virchow’s Triad**: endothelial injury, stasis of blood flow, and hypercoagulability [1]. **Why Superficial Thrombophlebitis is the correct answer:** Superficial thrombophlebitis involves inflammation and thrombosis of the veins near the skin surface (e.g., great saphenous vein). While it causes local pain and redness, it is generally considered a benign, localized condition. Unlike DVT, it does not typically involve the deep venous system and is **not** a major independent risk factor for developing DVT, although the two can occasionally coexist in patients with systemic hypercoagulability. **Analysis of Incorrect Options:** * **Oral Contraceptive Pills (OCPs):** Estrogen increases the hepatic synthesis of clotting factors (VII, X, and fibrinogen) and decreases anticoagulant levels (Protein S), creating a **hypercoagulable state**. * **Hypertension:** Chronic hypertension causes **endothelial dysfunction** and vascular remodeling, which triggers the extrinsic coagulation pathway, increasing the risk of venous thromboembolism (VTE). * **Myocardial Infarction (MI):** MI leads to DVT through **stasis** [1]. Reduced cardiac output (pump failure) and the subsequent period of prolonged bed rest/immobility lead to sluggish venous return in the lower limbs [1]. **NEET-PG High-Yield Pearls:** * **Most common site for DVT:** Calf veins (Soleal sinuses) [1]. * **Most common inherited risk factor for DVT:** Factor V Leiden mutation (activated protein C resistance). * **Strongest clinical risk factor:** Major orthopedic surgery (especially hip and knee arthroplasty) [1]. * **Trousseau’s Sign:** Migratory superficial thrombophlebitis associated with visceral malignancy (most commonly pancreatic cancer).

Question 72: Increased risk of coronary heart disease is seen in which type of hyperlipidemia?

A. Type I hyperlipidemia
B. Type II hyperlipidemia (Correct Answer)
C. Type IV hyperlipidemia
D. Type V hyperlipidemia

Explanation: The risk of **Coronary Heart Disease (CHD)** is most strongly associated with elevated levels of **Low-Density Lipoprotein (LDL)**, which is the primary characteristic of **Type II Hyperlipidemia** (Fredrickson Classification) [1]. 1. **Why Type II is Correct:** * **Type IIa:** Characterized by isolated elevation of LDL due to a deficiency in LDL receptors [1]. * **Type IIb:** Characterized by elevations in both LDL and Very Low-Density Lipoprotein (VLDL). Since LDL is highly atherogenic, it undergoes oxidation within the arterial wall, leading to foam cell formation and plaque buildup. Therefore, Type II carries the highest risk for premature atherosclerosis and myocardial infarction [1]. 2. **Why Other Options are Incorrect:** * **Type I (Hyperchylomicronemia):** Involves an increase in Chylomicrons due to Lipoprotein Lipase (LPL) deficiency. While it causes extremely high triglycerides, it is **not** associated with increased CHD risk. The primary clinical risk here is **acute pancreatitis**. * **Type IV (Hypertriglyceridemia):** Involves elevated VLDL. While high triglycerides are a minor risk factor, they are not as strongly or directly linked to CHD as the LDL elevations seen in Type II. * **Type V:** Involves elevations in both Chylomicrons and VLDL. Like Type I, the predominant clinical concern is pancreatitis rather than accelerated atherosclerosis. **High-Yield Clinical Pearls for NEET-PG:** * **Type IIa** is associated with **Tendon Xanthomas** (especially the Achilles tendon) and Xanthelasma. * **Type III (Dysbetalipoproteinemia)** is associated with **Palmar Xanthomas** and also carries an increased risk of CHD and peripheral vascular disease. * **Mnemonic for Fredrickson:** "1-2-3-4-5" corresponds to "C-L-B-V-M" (Chylomicrons, LDL, Broad-beta, VLDL, Mixed). * **Most common type:** Type IV is the most common in the general population, but Type II is the most significant for CHD [2].

Question 73: A mid-diastolic murmur with presystolic accentuation is typically heard in which condition?

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

Explanation: ### Explanation **1. Why Mitral Stenosis (MS) is Correct:** The classic murmur of Mitral Stenosis is a **low-pitched, mid-diastolic rumbling murmur**, best heard at the apex with the bell of the stethoscope in the left lateral decubitus position [2]. * **Mid-diastolic component:** Caused by turbulent blood flow across the narrowed mitral valve during the passive filling phase of the left ventricle [2]. * **Presystolic accentuation:** This occurs during **atrial systole** (atrial kick), which increases the pressure gradient across the valve just before the first heart sound ($S_1$) [3]. * *Note:* Presystolic accentuation disappears if the patient develops **Atrial Fibrillation**, as there is no coordinated atrial contraction [3]. **2. Why Other Options are Incorrect:** * **Mitral Regurgitation (MR):** Characterized by a **holosystolic (pansystolic) murmur** that radiates to the axilla. It occurs during ventricular systole, not diastole [4]. * **Aortic Stenosis (AS):** Presents as a **crescendo-decrescendo systolic ejection murmur** radiating to the carotids [1]. * **Mitral Valve Prolapse (MVP):** Typically presents with a **mid-systolic click** followed by a late systolic murmur [1]. **3. NEET-PG High-Yield Pearls:** * **Opening Snap (OS):** A high-pitched sound heard after $S_2$ in MS [1]. The shorter the $A_2-OS$ interval, the more severe the stenosis. * **Loud $S_1$:** A hallmark of MS (unless the valve is heavily calcified) [3]. * **Graham Steell Murmur:** An early diastolic decrescendo murmur heard in severe MS due to functional pulmonary regurgitation (secondary to pulmonary hypertension). * **Austin Flint Murmur:** A mid-diastolic murmur heard in **Aortic Regurgitation** that mimics MS but lacks an opening snap.

Question 74: Sinus tachycardia is seen in which of the following conditions?

A. Beta blocker therapy
B. Athletes
C. Hypothyroidism
D. Severe anaemia (Correct Answer)

Explanation: ### Explanation **Correct Option: D (Severe Anaemia)** Sinus tachycardia is a physiological response to maintain adequate tissue oxygenation. In **severe anaemia**, the oxygen-carrying capacity of the blood is significantly reduced. To compensate for this deficit and maintain a stable **Cardiac Output (CO = Stroke Volume × Heart Rate)**, the sympathetic nervous system is activated [1]. This leads to an increase in heart rate (tachycardia) to ensure that the remaining hemoglobin circulates more frequently to meet the metabolic demands of the tissues [2]. **Why the other options are incorrect:** * **A. Beta blocker therapy:** Beta-blockers (e.g., Propranolol, Metoprolol) antagonize the $\beta_1$ receptors in the SA node, leading to a decrease in heart rate (**Bradycardia**). * **B. Athletes:** Well-trained athletes often exhibit **Physiological Bradycardia**. This is due to high vagal tone (parasympathetic dominance) and an increased stroke volume, allowing the heart to maintain cardiac output at a lower rate. * **C. Hypothyroidism:** Low levels of thyroid hormones lead to decreased expression of $\beta$-adrenergic receptors and reduced metabolic demand, typically resulting in **Sinus Bradycardia**. **High-Yield Clinical Pearls for NEET-PG:** * **Definition:** Sinus tachycardia is defined as a sinus rhythm with a rate **>100 beats/minute**. * **Common Causes:** Fever (most common), thyrotoxicosis, hypovolemia, anxiety, exercise, and drugs like caffeine or sympathomimetics [1]. * **Rule of Thumb:** For every 1°F rise in body temperature, the heart rate increases by approximately 10 beats/minute. * **Relative Bradycardia:** If a patient has a high fever but a normal or slow heart rate, consider **Typhoid fever (Faget’s sign)**, Legionnaire’s disease, or Yellow fever.

Question 75: Which of the following is a feature of first-degree AV block?

A. PR interval > 200 ms (Correct Answer)
B. Inversion of T wave
C. Progressive shortening of PR interval
D. Presence of U wave

Explanation: **Explanation:** **First-degree Atrioventricular (AV) Block** is characterized by a delayed conduction through the AV node. The fundamental diagnostic feature is a **prolonged PR interval (>0.20 seconds or >200 ms)** that remains constant from beat to beat [1]. Importantly, every P wave is followed by a QRS complex (1:1 conduction), meaning there are no "dropped" beats. **Analysis of Options:** * **Option A (Correct):** The normal PR interval ranges from 120 to 200 ms. A PR interval exceeding 200 ms (5 small squares on ECG) signifies a conduction delay, defining first-degree AV block [1]. * **Option B (Incorrect):** T wave inversion is a sign of myocardial ischemia, ventricular hypertrophy, or bundle branch blocks, but is not a diagnostic feature of AV blocks. * **Option C (Incorrect):** Progressive *lengthening* (not shortening) of the PR interval until a QRS complex is dropped is the hallmark of **Mobitz Type I (Wenckebach) second-degree AV block** [1]. * **Option D (Incorrect):** U waves are most commonly associated with **hypokalemia**, though they can be seen in bradycardia or with certain drugs (e.g., Digoxin). **High-Yield Clinical Pearls for NEET-PG:** * **Location of Delay:** Usually occurs within the **AV node** itself. * **Clinical Significance:** Usually asymptomatic and benign; often found in athletes or due to increased vagal tone, medications (Beta-blockers, CCBs, Digoxin), or inferior wall MI [1]. * **Management:** No specific treatment is required unless the patient is symptomatic or the block is drug-induced. * **Rule of Thumb:** If the PR interval is long but constant and every P is followed by a QRS, it is 1st-degree block. If the PR interval is long and constant but some P waves are *not* followed by a QRS, it is Mobitz Type II [1].

Question 76: A 76-year-old woman presents with new-onset syncope and has noticed early fatigue on exertion for the past year. On examination, there is a systolic ejection murmur at the right sternal border that radiates to the carotids. What is the characteristic arterial pulse finding in this patient with suspected aortic stenosis?

A. Pulsus tardus (Correct Answer)
B. Pulsus paradoxus
C. Hyperkinetic pulse
D. Bisferiens pulse

Explanation: **Explanation:** The clinical presentation of syncope, exertional fatigue, and a systolic ejection murmur radiating to the carotids is classic for **Aortic Stenosis (AS)**. In severe AS, the narrowed valve orifice creates a mechanical obstruction to left ventricular outflow, leading to a characteristic arterial pulse known as **Pulsus parvus et tardus**. [1] * **Pulsus tardus** refers to a delayed upstroke (slow-rising pulse), while **pulsus parvus** refers to a small/low amplitude. This occurs because the blood is ejected slowly through the stenotic valve, prolonging the time to reach peak pressure. [1] **Analysis of Incorrect Options:** * **Pulsus paradoxus:** Defined as an exaggerated drop in systolic BP (>10 mmHg) during inspiration. It is characteristic of **Cardiac Tamponade**, severe asthma, or COPD, not valvular stenosis. * **Hyperkinetic pulse (Water-hammer pulse):** A rapid, forceful upstroke with sudden collapse. This is seen in **Aortic Regurgitation** or high-output states (e.g., thyrotoxicosis, anemia). [3] * **Bisferiens pulse:** A "double-peaked" systolic pulse. It is typically found in **AR combined with AS** or in **Hypertrophic Obstructive Cardiomyopathy (HOCM)**. **High-Yield Clinical Pearls for NEET-PG:** 1. **Gallavardin Phenomenon:** In AS, the murmur may sound musical and be heard best at the apex, mimicking mitral regurgitation. [1] 2. **S2 Changes:** A paradoxical splitting of S2 or a soft/absent A2 component is a sign of severe AS. [1] 3. **The "SAD" Triad:** Symptoms of AS include **S**yncope, **A**ngina, and **D**yspnea (Heart Failure). [2] Once symptoms appear, the prognosis without valve replacement is poor.

Question 77: A 56-year-old woman presents with dyspnea, blurry vision, and headaches that began this morning and are worsening. Her past medical history includes hypertension and osteoarthritis. She discontinued her anti-hypertensive medications three months ago due to side effects. On examination, her blood pressure is 210/130 mm Hg, heart rate is 100 beats/min, and oxygen saturation is 95%. Fundoscopy reveals retinal hemorrhages and papilledema. Heart sounds are normal except for an S4, and lung auscultation reveals lower lobe crackles. Which of the following is the most appropriate agent to reduce her blood pressure?

A. IV hydralazine
B. IV labetalol
C. Oral methyldopa
D. IV nitroprusside (Correct Answer)

Explanation: ### Explanation **1. Why IV Nitroprusside is Correct:** The patient is presenting with a **Hypertensive Emergency**, defined as severely elevated blood pressure (typically >180/120 mm Hg) associated with **acute target organ damage**. In this case, the presence of papilledema (Grade IV hypertensive retinopathy), headaches, blurry vision, and pulmonary crackles indicates hypertensive encephalopathy and early heart failure. **IV Nitroprusside** is a potent, rapid-acting vasodilator (acting on both arteries and veins) with an immediate onset and short duration of action. It is highly effective for hypertensive emergencies because it allows for precise, minute-to-minute titration of blood pressure, which is critical to avoid cerebral hypoperfusion while rapidly lowering the afterload [1]. **2. Why the Other Options are Incorrect:** * **A. IV Hydralazine:** Its hypotensive response is unpredictable and prolonged, making it difficult to titrate [1]. It is generally reserved for hypertensive emergencies in pregnancy (eclampsia/preeclampsia). * **B. IV Labetalol:** While often used in emergencies [1], it is contraindicated or used with extreme caution in patients with signs of acute heart failure (crackles, S4) due to its beta-blocking effects which can further decrease cardiac contractility [2]. * **C. Oral Methyldopa:** Oral medications have no role in hypertensive emergencies. They have a slow onset of action and cannot be titrated. Furthermore, methyldopa is primarily used in chronic gestational hypertension. **3. Clinical Pearls for NEET-PG:** * **Definition:** Hypertensive Emergency = BP >180/120 + Target Organ Damage (Brain, Heart, Kidney, Retina). * **Management Goal:** Reduce Mean Arterial Pressure (MAP) by no more than **25% within the first hour**, then to 160/100–110 mm Hg over the next 2–6 hours [1]. * **Nitroprusside Toxicity:** Prolonged use can lead to **Cyanide/Thiocyanate toxicity**, especially in patients with renal impairment. * **Drug of Choice for Aortic Dissection:** IV Esmolol or Labetalol (to reduce heart rate and shear stress).

Question 78: What is the recommended management for essential hypertension?

A. No treatment is necessary.
B. Diet modification alone is sufficient.
C. Diet modification and pharmacotherapy are indicated. (Correct Answer)
D. Surgical intervention is the primary treatment.

Explanation: Essential hypertension (primary hypertension) is a chronic medical condition characterized by persistently elevated blood pressure without an identifiable secondary cause [2]. Its management is multifaceted, focusing on reducing cardiovascular morbidity and mortality [1]. **Explanation of the Correct Answer:** **Option C** is correct because the standard of care involves a combination of **lifestyle modifications** (non-pharmacological) and **pharmacotherapy**. Lifestyle changes, such as the DASH diet (Dietary Approaches to Stop Hypertension), sodium restriction (<2.4g/day), and weight loss, can significantly lower systolic BP [3]. However, for most patients with established hypertension (Stage 1 with high CV risk or Stage 2), these are insufficient alone, and antihypertensive drugs (ACE inhibitors, ARBs, Calcium Channel Blockers, or Thiazides) are required to reach target goals (typically <130/80 mmHg) [4]. **Why Other Options are Incorrect:** * **Option A:** Untreated hypertension leads to "target organ damage," including stroke, myocardial infarction, heart failure, and chronic kidney disease [1]. * **Option B:** While diet is crucial, it rarely lowers BP by more than 10-15 mmHg. Most patients require pharmacological intervention to achieve long-term stabilization. * **Option C:** Surgery is reserved for **secondary hypertension** (e.g., renal artery stenosis or pheochromocytoma) and has no role in the primary management of essential hypertension [2]. **NEET-PG High-Yield Pearls:** * **First-line drugs:** For non-black patients, ACEIs, ARBs, CCBs, or Thiazides. For black patients, CCBs or Thiazides are preferred. * **DASH Diet:** High in fruits, vegetables, and low-fat dairy; it is the most effective lifestyle intervention for BP reduction [3]. * **Target BP:** According to ACC/AHA guidelines, the goal for most patients is **<130/80 mmHg** [3]. * **Initial Therapy:** Most patients with Stage 2 hypertension (≥140/90) require **two** antihypertensive agents from different classes.

Question 79: Hyperdynamic circulation is seen in all EXCEPT:

A. Anemia
B. Beriberi
C. Cor pulmonale (Correct Answer)
D. AV fistula

Explanation: **Explanation:** **Hyperdynamic circulation** is a state of increased cardiac output (CO) and decreased systemic vascular resistance (SVR). It is characterized by a "bounding pulse" and increased stroke volume [2]. **Why Cor Pulmonale is the Correct Answer:** Cor pulmonale refers to right ventricular hypertrophy and failure resulting from chronic pulmonary hypertension (usually due to lung disease like COPD) [3]. In this condition, there is **increased pulmonary vascular resistance**, which leads to a **low-output state** rather than a high-output state [1]. The heart struggles to pump blood through the lungs, eventually leading to decreased systemic cardiac output. **Analysis of Incorrect Options:** * **Anemia:** Reduced hemoglobin leads to tissue hypoxia, triggering compensatory vasodilation and increased stroke volume to maintain oxygen delivery. * **Beriberi (Wet):** Thiamine (Vitamin B1) deficiency causes systemic vasodilation and high-output heart failure due to impaired aerobic metabolism. * **AV Fistula:** An abnormal connection between an artery and a vein bypasses the high-resistance capillary bed, significantly reducing SVR and forcing the heart to increase CO to maintain systemic pressure. **NEET-PG High-Yield Pearls:** * **Common causes of Hyperdynamic Circulation:** Pregnancy, Thyrotoxicosis, Fever, Paget’s disease of the bone, Liver Cirrhosis, and Sepsis (early phase). * **Clinical Signs:** Water-hammer pulse (Corrigan’s pulse), wide pulse pressure, and a mid-systolic flow murmur [2]. * **Mnemonic:** Remember **"ABCD P"** for High Output: **A**nemia, **B**eriberi/BMR (Thyrotoxicosis), **C**irrhosis, **D**-AV fistula, **P**regnancy/Paget's.

Question 80: Which of the following dietary interventions has shown to reduce mortality in patients with coronary heart disease?

A. High Fibre diet
B. Stanol Esters
C. Potassium supplements
D. Omega 3 polyunsaturated fatty acids (Correct Answer)

Explanation: **Explanation:** The correct answer is **Omega 3 polyunsaturated fatty acids (PUFAs)**. **Why it is correct:** Omega-3 PUFAs, specifically Eicosapentaenoic acid (EPA) and Docosahexaenoic acid (DHA), have demonstrated significant cardioprotective effects. Large-scale clinical trials (such as the **GISSI-Prevenzione trial**) showed that supplementation with Omega-3 PUFAs significantly reduces the risk of sudden cardiac death and all-cause mortality in patients with a history of myocardial infarction. The underlying mechanisms include stabilization of the myocardial cell membrane (anti-arrhythmic effect), reduction in serum triglycerides, anti-inflammatory properties, and mild anti-platelet activity. Eating oily fish and adopting a diet high in specific polyunsaturated fats are established methods to produce reductions in cardiovascular risk [1], [2]. **Why the other options are incorrect:** * **High Fiber Diet:** While a high-fiber diet (especially soluble fiber) is excellent for lowering LDL cholesterol and improving metabolic health, it has not been definitively proven to reduce *mortality* in established CHD patients to the same extent as Omega-3s in randomized trials. * **Stanol Esters:** Plant sterols and stanols compete with cholesterol for absorption in the gut, effectively lowering LDL levels [3]. However, they are considered an adjunct therapy and lack robust evidence for mortality reduction. * **Potassium Supplements:** While adequate potassium intake is crucial for blood pressure control and preventing arrhythmias, routine supplementation in the absence of deficiency does not reduce mortality in CHD patients and can be dangerous in those with renal impairment or those on ACE inhibitors/ARBs. **NEET-PG High-Yield Pearls:** * **Source:** The primary source of EPA/DHA is oily fish (e.g., salmon, mackerel) [1]. * **Dose:** The AHA recommends approximately 1g/day of EPA+DHA for patients with documented CHD. * **Triglycerides:** High doses (2-4g/day) are used specifically to treat severe hypertriglyceridemia. * **Mediterranean Diet:** Often cited in exams, this diet (rich in alpha-linolenic acid) also shows significant mortality benefits (Lyon Diet Heart Study).

Practice by Chapter

Coronary Artery Disease and Angina

Practice Questions

Acute Coronary Syndromes

Practice Questions

Heart Failure

Practice Questions

Cardiac Arrhythmias

Practice Questions

Valvular Heart Diseases

Practice Questions

Cardiomyopathies

Practice Questions

Pericardial Diseases

Practice Questions

Congenital Heart Disease in Adults

Practice Questions

Hypertension and Hypertensive Emergencies

Practice Questions

Pulmonary Hypertension

Practice Questions

Non-invasive Cardiac Diagnostics

Practice Questions

Preventive Cardiology

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free

Cardiology — MCQs

Cardiology — MCQs

On this page

Practice by Chapter

Want unlimited practice?