Cardiology — MCQs

A 22-year-old woman with no past medical history is found to have a systolic ejection murmur on routine physical examination. She has no symptoms and feels well. The murmur is heard along the right and left sternal borders and it decreases with handgrip exercises. For the patient with a systolic murmur, what is the most likely diagnosis?

Q807Medium

A patient presents with shortness of breath. On clinical examination, he is found to have a heaving apex and a systolic murmur that intensifies on Valsalva's maneuver. What is the most likely diagnosis?

Q808Easy

Pulsus paradoxus is a characteristic feature of which of the following conditions?

Q809Easy

In atrial septal defect, what is the typical size of the aorta?

Q810Medium

A 59-year-old man complains of recurrent attacks of pain in the region of the left shoulder radiating to the sternum and the pit of the stomach. The attacks of pain occurred at lengthy intervals until the last two days when it became continuous. The physician diagnosed it as angina pectoris. In this case, what pathway carries the pain sensation from the heart?

Cardiology Indian Medical PG Practice Questions and MCQs

Question 801: Antibiotic prophylaxis is recommended to prevent infective endocarditis in all dental procedures in patients having which of the following conditions?

A. Previous coronary bypass surgery
B. Congestive cardiac failure
C. Prosthetic heart valves (Correct Answer)
D. Mitral valve prolapse syndrome

Explanation: **Explanation:** The current guidelines (AHA/ACC and ESC) have significantly narrowed the indications for antibiotic prophylaxis to prevent Infective Endocarditis (IE). Prophylaxis is now reserved only for patients at the **highest risk** of adverse outcomes from IE undergoing procedures involving gingival manipulation or perforation of the oral mucosa [1]. **Why Option C is Correct:** **Prosthetic heart valves** (including mechanical, bioprosthetic, and transcatheter-implanted valves) represent the highest risk category [1]. Other high-risk conditions requiring prophylaxis include: * Prior history of Infective Endocarditis. * Unrepaired cyanotic congenital heart disease (CHD) or repaired CHD with residual shunts/valvular regurgitation at the site of prosthetic material. * Cardiac transplant recipients who develop valvular regurgitation. **Why Other Options are Incorrect:** * **Option A (Coronary Bypass Surgery):** Patients with prior CABG or stents do not have an increased risk of endocarditis compared to the general population. * **Option B (Congestive Cardiac Failure):** CCF is a functional diagnosis of heart pump failure and does not inherently involve the valvular endothelial damage required for vegetation formation. * **Option D (Mitral Valve Prolapse):** While MVP is common, it is now considered a **low-to-moderate risk** condition. Prophylaxis is no longer recommended for MVP, even if associated with mitral regurgitation, to prevent antibiotic resistance [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Amoxicillin (2g orally, 30–60 minutes before the procedure). * **If Penicillin Allergic:** Cephalexin, Clindamycin (though recently discouraged in some guidelines), or Azithromycin/Clarithromycin. * **Procedures NOT requiring prophylaxis:** Routine anesthetic injections, dental X-rays, placement of removable appliances, or shedding of primary teeth [2].

Question 802: Which of the following is NOT true regarding hypertrophic obstructive cardiomyopathy?

A. Systolic dysfunction (Correct Answer)
B. Concentric hypertrophy
C. Diastolic dysfunction
D. Double apical impulse

Explanation: Hypertrophic Obstructive Cardiomyopathy (HOCM) is primarily a disease of **diastolic dysfunction**, not systolic dysfunction. **1. Why "Systolic Dysfunction" is the correct answer (The False Statement):** In HOCM, the ventricular walls are thickened, leading to a hyperdynamic state. The **Ejection Fraction (EF) is typically normal or even supranormal** (>70%). Systolic function remains preserved until the very end-stages of the disease ("burnt-out" phase). Therefore, stating that HOCM is characterized by systolic dysfunction is clinically incorrect. **2. Analysis of Incorrect Options:** * **Concentric Hypertrophy:** While HOCM is classically known for *asymmetric* septal hypertrophy, the overall pathology involves significant thickening of the ventricular walls (concentric-like remodeling) without chamber dilation, making this a characteristic feature. * **Diastolic Dysfunction:** This is the hallmark of HOCM. The thickened, stiff myocardium cannot relax properly during diastole, leading to impaired filling and elevated left ventricular end-diastolic pressure (LVEDP). * **Double Apical Impulse:** This is a classic clinical sign. The first impulse is due to a forceful atrial contraction (S4) against a stiff ventricle (palpable S4), and the second is the actual ventricular apex beat. In some cases, a "triple ripple" may be felt. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Autosomal Dominant (most common mutation: **Beta-myosin heavy chain** or Myosin-binding protein C) [1]. * **Murmur Dynamics:** The systolic murmur of HOCM **increases** with Valsalva and standing (decreased preload) and **decreases** with squatting or handgrip (increased preload/afterload). * **Histology:** Characterized by **myocyte disarray** and interstitial fibrosis [1]. * **Drug of Choice:** Beta-blockers (to increase diastolic filling time). Avoid Nitrates and Diuretics as they worsen the outflow obstruction.

Question 803: Massive hemoptysis is typically seen in which of the following conditions?

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

Explanation: **Explanation** **Mitral Stenosis (MS)** is the most common valvular cause of massive hemoptysis [1]. The underlying mechanism is the obstruction of blood flow from the left atrium to the left ventricle, leading to a chronic increase in left atrial pressure. This pressure is transmitted backward into the pulmonary veins and bronchial veins. The specific cause of "massive" or "explosive" hemoptysis in MS is **Pulmonary Apoplexy**. This occurs when the high pressure causes a sudden rupture of dilated, thin-walled **bronchial submucosal veins** (which act as collateral channels between the pulmonary and systemic venous systems). Other forms of hemoptysis in MS include blood-streaked sputum (due to pulmonary congestion/bronchitis) [1] or pink frothy sputum (due to acute pulmonary edema) [2]. **Why other options are incorrect:** * **Aortic Stenosis (AS) & Aortic Regurgitation (AR):** These left-sided lesions primarily lead to left ventricular failure. While they can cause pulmonary edema and blood-streaked sputum in advanced stages, they do not typically cause the sudden rupture of bronchial veins seen in MS. * **Pulmonary Stenosis (PS):** This is a right-sided lesion that leads to decreased pulmonary blood flow. It does not cause pulmonary venous hypertension; therefore, hemoptysis is not a feature. **Clinical Pearls for NEET-PG:** * **Most common cause of hemoptysis in MS:** Bronchitis or pulmonary congestion [1]. * **Most dramatic/massive cause:** Pulmonary Apoplexy (rupture of bronchial veins). * **Ortner’s Syndrome:** Hoarseness of voice in MS due to compression of the left recurrent laryngeal nerve by a dilated left atrium. * **Auscultation:** MS is characterized by a loud S1, an opening snap [1], and a mid-diastolic rumbling murmur heard best at the apex in the left lateral position [1].

Question 804: Aortic regurgitation may be associated with all of the following conditions except:

A. Ankylosing Spondylitis
B. Marfan's Syndrome
C. Dissection of the aorta
D. Polyarteritis nodosa (Correct Answer)

Explanation: **Explanation:** Aortic Regurgitation (AR) occurs due to either primary disease of the **aortic valve leaflets** or **dilation of the aortic root**. **Why Polyarteritis Nodosa (PAN) is the correct answer:** PAN is a systemic necrotizing vasculitis that primarily affects **medium-sized and small arteries**. It characteristically involves the renal and visceral vessels, leading to microaneurysms and infarctions. Crucially, PAN **spares the large elastic arteries** like the aorta. Therefore, it does not cause aortic root dilation or valvular damage leading to AR. **Analysis of other options:** * **Ankylosing Spondylitis:** This seronegative spondyloarthropathy is a classic cause of **aortitis**. It leads to thickening and shortening of the aortic cusps and dilation of the aortic ring, resulting in AR. * **Marfan’s Syndrome:** This is a connective tissue disorder (FBN1 mutation) leading to **cystic medial necrosis** [1]. It causes progressive aortic root dilation and dissection, making AR a common complication [1]. * **Dissection of the Aorta:** Type A dissections (involving the ascending aorta) can cause AR by widening the aortic root or causing the dissection flap to prolapse through the valve orifice [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Acute AR:** Most commonly caused by Infective Endocarditis or Aortic Dissection [2]. * **Chronic AR:** Most commonly caused by Rheumatic Heart Disease (developing countries) or Aortic Root Dilation/Bicuspid Aortic Valve (developed countries). * **Syphilitic Aortitis:** A classic "textbook" cause of AR due to endarteritis obliterans of the vasa vasorum. * **Physical Sign:** Look for "Water-hammer pulse" (Corrigan’s pulse) and a wide pulse pressure [2].

Question 805: What is the typical pulse pressure in severe aortic regurgitation?

A. 30-45 mmHg
B. 45-60 mmHg
C. 60-75 mmHg
D. 75-90 mmHg (Correct Answer)

Explanation: In **Severe Aortic Regurgitation (AR)**, the pulse pressure is characteristically widened. This occurs due to two simultaneous hemodynamic mechanisms: 1. **Increased Systolic Blood Pressure (SBP):** The large volume of blood leaking back into the left ventricle during diastole leads to an increased stroke volume (Frank-Starling mechanism) during the subsequent systole [1]. 2. **Decreased Diastolic Blood Pressure (DBP):** The rapid "run-off" of blood from the aorta back into the left ventricle and forward into the peripheral circulation during diastole causes the DBP to drop significantly (often <60 mmHg) [2]. The resulting pulse pressure (SBP minus DBP) in severe AR typically exceeds **75–90 mmHg**, reflecting a hyperdynamic circulation. [3] **Analysis of Options:** * **Option A (30-45 mmHg):** This represents a **normal** pulse pressure (approx. 40 mmHg) [3]. * **Option B (45-60 mmHg):** This may be seen in mild AR or other conditions like hypertension, but it does not meet the criteria for "severe" AR. * **Option C (60-75 mmHg):** While elevated, this range is more characteristic of moderate AR. Severe cases consistently push the pressure gradient higher. **NEET-PG High-Yield Pearls:** * **Water-Hammer Pulse (Corrigan’s Pulse):** A rapid upstroke and quick collapse of the pulse, best felt in the radial artery with the arm elevated [1]. * **Duroziez’s Sign:** A systolic and diastolic murmur heard over the femoral artery when compressed. * **Quincke’s Pulse:** Capillary pulsations visible in the nail beds. * **Hill’s Sign:** Popliteal SBP exceeding Brachial SBP by >60 mmHg (the most sensitive indicator of AR severity). * **Austin Flint Murmur:** A mid-diastolic rumble at the apex caused by the regurgitant jet displacing the mitral valve leaflet [2].

Question 806: A 22-year-old woman with no past medical history is found to have a systolic ejection murmur on routine physical examination. She has no symptoms and feels well. The murmur is heard along the right and left sternal borders and it decreases with handgrip exercises. For the patient with a systolic murmur, what is the most likely diagnosis?

A. Aortic stenosis
B. Hypertrophic obstructive cardiomyopathy (HOCM) (Correct Answer)
C. Mitral regurgitation (chronic)
D. Tricuspid regurgitation

Explanation: ### Explanation The correct diagnosis is **Hypertrophic Obstructive Cardiomyopathy (HOCM)**. **1. Why HOCM is correct:** The murmur in HOCM is a **systolic ejection murmur** caused by dynamic left ventricular outflow tract (LVOT) obstruction [1]. The key to this question lies in the response to the **handgrip exercise**. * **Handgrip** increases afterload (systemic vascular resistance). * Increased afterload increases the volume of blood in the left ventricle, which pushes the interventricular septum away from the mitral valve. * This reduces the LVOT obstruction, thereby **decreasing the intensity** of the HOCM murmur [1]. * (Note: HOCM and Mitral Valve Prolapse are the only two murmurs that typically *decrease* with increased afterload/preload maneuvers like squatting or handgrip). **2. Why the other options are incorrect:** * **Aortic Stenosis (AS):** While AS also presents with a systolic ejection murmur, handgrip increases afterload, which typically **increases or maintains** the pressure gradient across the valve, and it does not significantly soften the murmur like it does in HOCM [1]. * **Mitral Regurgitation (MR) & Tricuspid Regurgitation (TR):** These are **holosystolic** (pansystolic) murmurs, not ejection murmurs. Furthermore, handgrip increases the intensity of MR due to increased backpressure from the aorta [2]. **3. NEET-PG High-Yield Pearls:** * **HOCM Murmur Dynamics:** * *Increases with:* Valsalva, Standing (decreased preload/ventricular volume). * *Decreases with:* Squatting, Handgrip, Passive leg raise (increased preload/afterload). * **Genetic Basis:** Most commonly due to mutations in **Beta-myosin heavy chain** or Myosin-binding protein C. * **ECG Finding:** Look for "dagger-like" Q waves in lateral leads (I, aVL, V5-V6). * **Sudden Cardiac Death:** HOCM is the most common cause of SCD in young athletes.

Question 807: A patient presents with shortness of breath. On clinical examination, he is found to have a heaving apex and a systolic murmur that intensifies on Valsalva's maneuver. What is the most likely diagnosis?

A. Valvular aortic stenosis
B. Ventricular septal defect
C. Hypertrophic cardiomyopathy (Correct Answer)
D. Atrial septal defect

Explanation: **Explanation:** The clinical presentation of a **heaving apex** (indicating left ventricular hypertrophy) and a systolic murmur that **intensifies with the Valsalva maneuver** is classic for **Hypertrophic Obstructive Cardiomyopathy (HOCM)**. [1] **1. Why HOCM is correct:** In HOCM, the murmur is caused by dynamic left ventricular outflow tract (LVOT) obstruction. The Valsalva maneuver (strain phase) decreases venous return (preload), leading to a smaller left ventricular volume. This reduction in volume brings the hypertrophied septum and the anterior mitral leaflet closer together, worsening the obstruction and **increasing the intensity** of the murmur. [1] **2. Why the other options are incorrect:** * **Valvular Aortic Stenosis (AS):** While AS also presents with a heaving apex and systolic murmur, the murmur **decreases** in intensity during Valsalva because less blood is flowing across the fixed stenotic valve. [2] * **Ventricular Septal Defect (VSD):** The pansystolic murmur of VSD typically **decreases** with Valsalva due to reduced systemic venous return and reduced shunting. * **Atrial Septal Defect (ASD):** ASD characteristically presents with a mid-systolic flow murmur and a **fixed, wide splitting of the second heart sound (S2)**, which is not mentioned here. **Clinical Pearls for NEET-PG:** * **Dynamic Murmurs:** HOCM and Mitral Valve Prolapse (MVP) are the only two common murmurs that **increase** in intensity with Valsalva or standing (both maneuvers decrease preload). [3] * **Handgrip Exercise:** Increases afterload; this **decreases** the HOCM murmur but **increases** the murmurs of Mitral Regurgitation and VSD. * **Drug of Choice:** Beta-blockers are the first-line medical therapy for symptomatic HOCM to improve diastolic filling.

Question 808: Pulsus paradoxus is a characteristic feature of which of the following conditions?

A. Constrictive pericarditis
B. Cardiac tamponade (Correct Answer)
C. Hypertrophic obstructive cardiomyopathy
D. Restrictive cardiomyopathy

Explanation: **Explanation:** **Pulsus Paradoxus** is defined as an exaggerated fall in systolic blood pressure (>10 mmHg) during inspiration. Under normal physiological conditions, inspiration increases venous return to the right heart, causing the interventricular septum to bulge slightly into the left ventricle (LV). In **Cardiac Tamponade**, the heart is compressed by fluid within a non-compliant pericardial space [1]. This "fixed" total volume forces the ventricles to compete for space. During inspiration, the increased right ventricular filling significantly displaces the septum toward the left, severely reducing LV stroke volume and systolic pressure. **Analysis of Options:** * **Cardiac Tamponade (Correct):** The classic condition associated with pulsus paradoxus due to extreme ventricular interdependence [1]. * **Constrictive Pericarditis:** While it shares features with tamponade, pulsus paradoxus is seen in only about **30%** of cases [2]. The hallmark here is **Kussmaul’s sign** (paradoxical rise in JVP on inspiration), which is typically absent in tamponade. * **HOCM:** Characterized by **Pulsus Bisferiens** (double-peaked pulse). * **Restrictive Cardiomyopathy:** Primarily presents with diastolic dysfunction and Kussmaul’s sign; pulsus paradoxus is rare. **NEET-PG High-Yield Pearls:** 1. **Reverse Pulsus Paradoxus:** Seen in Hypertrophic Obstructive Cardiomyopathy (HOCM) and patients on positive pressure ventilation. 2. **Non-Cardiac Causes:** Severe Asthma and COPD are the most common non-cardiac causes of pulsus paradoxus. 3. **Beck’s Triad (Tamponade):** Hypotension, JVP distension, and muffled heart sounds. 4. **ECG in Tamponade:** Look for **Electrical Alternans** (alternating QRS amplitude) and low voltage complexes [1].

Question 809: In atrial septal defect, what is the typical size of the aorta?

A. Small (Correct Answer)
B. Normal
C. Enlarged
D. Aneurysmal

Explanation: **Explanation:** In **Atrial Septal Defect (ASD)**, the fundamental pathophysiology involves a left-to-right shunt at the atrial level. This leads to a volume overload of the right-sided chambers (Right Atrium and Right Ventricle) and a subsequent increase in pulmonary blood flow [1]. **Why the Aorta is Small:** Because a significant portion of the blood returning to the left atrium is shunted across the defect into the right atrium, there is a **reduction in the volume of blood entering the Left Ventricle (LV)**. This decreased LV stroke volume results in a chronically underfilled systemic circulation. Over time, this leads to a **hypoplastic or "small" aorta** relative to the massively dilated pulmonary artery. On a chest X-ray, this presents as a small or inconspicuous aortic knuckle [2]. **Analysis of Incorrect Options:** * **B. Normal:** The aorta is typically smaller than normal due to the diversion of blood away from the systemic circuit. * **C. Enlarged:** An enlarged aorta is seen in conditions like Aortic Regurgitation, Hypertension, or Patent Ductus Arteriosus (where blood shunts *into* the aorta or its branches). * **D. Aneurysmal:** This suggests structural wall weakness (e.g., Marfan syndrome or syphilis), which is not a feature of ASD. **High-Yield Clinical Pearls for NEET-PG:** * **Chest X-ray Triad in ASD:** 1. Small aortic knuckle, 2. Enlarged pulmonary artery segment, 3. Right ventricular enlargement (Apex tilted upwards) [2]. * **Auscultation:** Characterized by a **wide, fixed split S2** and a mid-systolic flow murmur at the pulmonary area. * **ECG:** Often shows Right Axis Deviation and RSR' pattern in V1 (Incomplete RBBB). Ostium Primum ASD is unique for showing **Left Axis Deviation** [1].

Question 810: A 59-year-old man complains of recurrent attacks of pain in the region of the left shoulder radiating to the sternum and the pit of the stomach. The attacks of pain occurred at lengthy intervals until the last two days when it became continuous. The physician diagnosed it as angina pectoris. In this case, what pathway carries the pain sensation from the heart?

A. Superior cervical cardiac nerve
B. Middle and inferior cervical cardiac nerves
C. Thoracic splanchnic nerves (Correct Answer)
D. Vagus nerve

Explanation: ### Explanation **1. Why "Thoracic splanchnic nerves" is correct:** Cardiac pain (angina) is a visceral sensation triggered by ischemia. The afferent (sensory) fibers responsible for carrying pain from the heart follow the **sympathetic pathway** in a retrograde fashion [1]. These fibers travel from the cardiac plexus through the **thoracic cardiac nerves** to the sympathetic trunk and then via the **white rami communicantes** to the spinal nerves. Specifically, they enter the spinal cord through the dorsal roots of the **T1 to T4/T5 segments** [1]. These pathways are collectively referred to as the thoracic splanchnic (sympathetic) nerves in the context of visceral pain conduction. **2. Why the other options are incorrect:** * **Superior cervical cardiac nerve:** While this nerve contains postganglionic sympathetic fibers going *to* the heart, it typically does not carry sensory afferents back to the CNS. Pain fibers specifically bypass the superior cervical ganglion. * **Middle and inferior cervical cardiac nerves:** Although some afferents may travel through these nerves to the cervical sympathetic chain, they ultimately descend to the upper thoracic spinal segments (T1-T5) to enter the cord. They are not the primary or sole pathway for cardiac pain. * **Vagus nerve:** The vagus nerve (CN X) carries parasympathetic fibers and visceral *reflex* afferents (e.g., baroreceptors, chemoreceptors), but it does **not** carry pain sensations from the heart [1]. **3. Clinical Pearls for NEET-PG:** * **Referred Pain:** Cardiac pain is referred to the T1–T5 dermatomes (precordium and inner aspect of the left arm) because the sensory afferents enter the same spinal cord segments that receive cutaneous supply from these areas [2]. * **Levine’s Sign:** A clenched fist held over the chest to describe ischemic pain—highly suggestive of angina [2]. * **Silent MI:** In diabetic patients, autonomic neuropathy can damage these sympathetic afferent pathways, leading to "painless" or silent myocardial infarction.

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?