Cardiology — MCQs

A 27-year-old male has had hard-to-control hypertension for 2 years. He is taking clonidine, hydrochlorothiazide, verapamil, and lisinopril. His blood pressure is 170/105 mmHg, pulse 90 beats/min, and respirations 16/min. The cardiopulmonary exam is normal. Pedal pulses are intact and there is no edema or misdistribution of fat. Laboratories show potassium of 2.7 mEq/L, BUN 20 mg/dL, creatinine 1.2 mg/dL, bicarbonate 33 mg/dL, and fasting glucose 98 mg/dL. What is the most likely diagnosis?

Q104Easy

Gibson's murmur is a feature of which cardiac condition?

Q105Medium

All of the following cause death in coarctation of the aorta except?

Q106Medium

A 40-year-old woman with a history of rheumatic fever presents with shortness of breath, weight loss, fatigue, and abdominal distension. Physical examination shows rales in the lungs, hepatosplenomegaly, and 2+ pitting edema of the legs. A chest X-ray reveals only left atrial enlargement and pulmonary edema. What is the most likely cause of pulmonary edema in this patient?

Q107Medium

Which of the following is NOT associated with a soft S1 sound?

Q108Easy

What is the causative organism of late prosthetic valve endocarditis?

Q109Easy

All of the following are causes of a pansystolic murmur, EXCEPT?

Q110Medium

Which of the following is NOT true about Dressler's syndrome?

Cardiology Indian Medical PG Practice Questions and MCQs

Question 101: Paroxysmal AV block is associated with which of the following?

A. First degree AV block
B. Type I second degree AV block
C. Type II second degree AV block (Correct Answer)
D. Third degree AV block

Explanation: **Explanation:** **Paroxysmal AV block** is a clinical phenomenon characterized by the sudden, unexpected development of a high-grade or total AV block in a patient with previously stable conduction. It is most strongly associated with **Type II second-degree AV block (Mobitz II).** [1] **1. Why Type II Second-Degree AV Block is Correct:** Mobitz II block occurs due to disease in the **His-Purkinje system** (infra-nodal) [1]. Unlike Mobitz I, where the AV node gradually fatigues, Mobitz II involves an "all-or-nothing" failure of conduction. Because the underlying conduction system is severely diseased, it is highly unstable and prone to sudden, unpredictable failure, leading to paroxysmal complete heart block and Stokes-Adams attacks [1]. **2. Why Other Options are Incorrect:** * **First-degree AV block:** This is merely a delay in conduction (prolonged PR interval) at the AV node [1]. It is usually benign and rarely progresses directly to sudden paroxysmal block. * **Type I second-degree AV block (Wenckebach):** This occurs due to functional fatigue of the AV node. It is typically reversible, often physiological (seen in athletes), and progresses predictably rather than paroxysmally [1]. * **Third-degree AV block:** This is a permanent, established state of complete dissociation. It is not "paroxysmal" because the block is already constant. **Clinical Pearls for NEET-PG:** * **Site of Block:** Mobitz I is usually **Intra-nodal** (AV node); Mobitz II is **Infra-nodal** (Bundle of His) [1]. * **Vagal Maneuvers:** Carotid sinus massage worsens Mobitz II (by increasing AV delay) but may paradoxically improve Mobitz I. * **Management:** Mobitz II is an absolute indication for a **Permanent Pacemaker (PPI)**, even if asymptomatic, due to the high risk of progression to sudden cardiac death [1].

Question 102: All are absolute contraindications for fibrinolysis except?

A. Upper gastrointestinal bleed
B. History of ischemic stroke 6 months prior
C. Systolic blood pressure > 180 mm of Hg at presentation
D. Pregnancy (Correct Answer)

Explanation: **Explanation:** In the management of ST-Elevation Myocardial Infarction (STEMI), distinguishing between absolute and relative contraindications for fibrinolytic therapy is a high-yield topic for NEET-PG. **Why Pregnancy is the Correct Answer:** **Pregnancy** is classified as a **relative contraindication**, not an absolute one. While there is an increased risk of placental abruption or maternal hemorrhage, fibrinolysis can be considered in life-threatening situations where Primary PCI is unavailable. **Analysis of Incorrect Options (Absolute Contraindications):** * **Upper Gastrointestinal Bleed:** Active internal bleeding (excluding menses) or a known structural gastrointestinal vascular malformation/malignancy is an absolute contraindication due to the risk of catastrophic hemorrhage. * **History of Ischemic Stroke 6 months prior:** Any ischemic stroke within the last **3 months** is an absolute contraindication. (Note: A history of any prior intracranial hemorrhage is an absolute contraindication regardless of timing). * **Systolic BP > 180 mmHg:** Severe, uncontrolled hypertension at presentation (SBP >180 mmHg or DBP >110 mmHg) is an absolute contraindication because it significantly increases the risk of hemorrhagic stroke during fibrinolysis. **High-Yield Clinical Pearls for NEET-PG:** * **Absolute Contraindications (The "Never" List):** Prior ICH, known structural cerebrovascular lesion, malignant intracranial neoplasm, ischemic stroke within 3 months, suspected aortic dissection, active bleeding, or significant closed-head/facial trauma within 3 months. * **Relative Contraindications:** Pregnancy, current use of anticoagulants, non-compressible vascular punctures, major surgery (<3 weeks), and poorly controlled chronic hypertension. * **Time Window:** Fibrinolysis is most effective when administered within **12 hours** of symptom onset if Primary PCI cannot be performed within **120 minutes** of first medical contact [1].

Question 103: A 27-year-old male has had hard-to-control hypertension for 2 years. He is taking clonidine, hydrochlorothiazide, verapamil, and lisinopril. His blood pressure is 170/105 mmHg, pulse 90 beats/min, and respirations 16/min. The cardiopulmonary exam is normal. Pedal pulses are intact and there is no edema or misdistribution of fat. Laboratories show potassium of 2.7 mEq/L, BUN 20 mg/dL, creatinine 1.2 mg/dL, bicarbonate 33 mg/dL, and fasting glucose 98 mg/dL. What is the most likely diagnosis?

A. Conn syndrome (Correct Answer)
B. Renal vascular hypertension
C. Cushing syndrome
D. Carcinoid syndrome

Explanation: The clinical presentation of a young patient with **resistant hypertension** (uncontrolled despite ≥3 drugs) and spontaneous **hypokalemia** (2.7 mEq/L) strongly suggests **Primary Hyperaldosteronism (Conn Syndrome)**. **1. Why Conn Syndrome is correct:** In Conn syndrome, an adrenal adenoma or hyperplasia produces excess aldosterone. Aldosterone acts on the principal cells of the renal collecting duct to reabsorb sodium and water (causing hypertension) and secrete potassium and hydrogen ions [1]. This leads to the classic triad seen here: * **Hypertension** (often resistant). * **Hypokalemia** (muscle weakness or asymptomatic). * **Metabolic Alkalosis** (elevated bicarbonate of 33 mg/dL). The absence of edema is due to the "Aldosterone Escape" phenomenon. **2. Why other options are incorrect:** * **Renal Vascular Hypertension:** While it causes resistant hypertension, it usually presents with an abdominal bruit or a significant rise in creatinine after starting an ACE inhibitor (Lisinopril) [3]. * **Cushing Syndrome:** Ruled out by the absence of physical findings like truncal obesity, striae, or "buffalo hump," and the normal fasting glucose (98 mg/dL). * **Carcinoid Syndrome:** Typically presents with flushing, diarrhea, and wheezing, rather than isolated resistant hypertension and hypokalemia. **High-Yield Clinical Pearls for NEET-PG:** * **Screening Test:** Plasma Aldosterone Concentration (PAC) to Plasma Renin Activity (PRA) ratio. A **PAC:PRA ratio > 20-30** is suggestive. * **Confirmatory Test:** Oral/Saline salt loading test (failure to suppress aldosterone) [2]. * **Management:** Surgical excision for Adenoma; Spironolactone/Eplerenone for bilateral hyperplasia [2]. * **Note:** Diuretics like Hydrochlorothiazide can worsen hypokalemia, but the severity here (2.7 mEq/L) in a young hypertensive patient should always trigger a workup for primary aldosteronism.

Question 104: Gibson's murmur is a feature of which cardiac condition?

A. Patent Ductus arteriosus (Correct Answer)
B. Mitral Valve prolapse
C. Pulmonary regurgitation
D. Mitral regurgitation

Explanation: **Explanation:** **Gibson’s murmur** is the classic eponym for a **continuous machinery murmur**. It is the hallmark clinical finding of **Patent Ductus Arteriosus (PDA)** [1]. **Why Patent Ductus Arteriosus is correct:** In PDA, there is a persistent communication between the high-pressure aorta and the lower-pressure pulmonary artery [1]. Because the pressure in the aorta remains higher than in the pulmonary artery during both systole and diastole, blood flows continuously through the ductus [1]. This results in a murmur that begins in systole, peaks at the second heart sound (S2), and continues through diastole, creating the "machinery" quality. It is best heard at the **left infraclavicular area** (Gibson’s area). **Why the other options are incorrect:** * **Mitral Valve Prolapse (MVP):** Characterized by a mid-systolic click followed by a late systolic murmur. * **Pulmonary Regurgitation (PR):** Typically presents as a decrescendo diastolic murmur (Graham Steell murmur if secondary to pulmonary hypertension). * **Mitral Regurgitation (MR):** Presents as a pansystolic (holosystolic) murmur heard best at the apex, radiating to the axilla [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Location:** Best heard in the left 2nd intercostal space, just below the left clavicle. * **Differential for Continuous Murmurs:** Apart from PDA, consider Ruptured Sinus of Valsalva (RSOV), Aortopulmonary window, and Coronary AV fistula. * **Management:** Indomethacin or Ibuprofen (NSAIDs) are used for pharmacological closure in preterm neonates; surgical or device closure is indicated for persistent cases. * **Eisenmenger Syndrome:** If PDA develops right-to-left shunting, it leads to **differential cyanosis** (cyanosis and clubbing in the lower limbs, but not the upper limbs).

Question 105: All of the following cause death in coarctation of the aorta except?

A. Infective endocarditis
B. Congestive cardiac failure (CCF)
C. Intracranial hemorrhage
D. Anterior myocardial infarction (MI) (Correct Answer)

Explanation: Coarctation of the aorta (CoA) is a localized narrowing of the aortic lumen, typically near the ductus arteriosus. While it causes significant hemodynamic stress, **Anterior Myocardial Infarction (MI)** is not a classic or direct cause of death associated with this condition [1]. While long-term hypertension can accelerate atherosclerosis, MI is far less common as a primary cause of mortality compared to the mechanical and vascular complications of the disease. **Why the other options are common causes of death:** * **Congestive Cardiac Failure (CCF):** This is the most common cause of death [2]. The heart must pump against high afterload (proximal to the obstruction), leading to left ventricular hypertrophy and eventual failure. * **Intracranial Hemorrhage:** Approximately 10% of patients with CoA have associated **Berry aneurysms** in the Circle of Willis. The combination of these aneurysms and upper-body hypertension significantly increases the risk of subarachnoid hemorrhage. * **Infective Endocarditis/Endarteritis:** High-velocity turbulent flow at the site of coarctation or associated bicuspid aortic valves predisposes patients to infections, which can lead to sepsis or valvular destruction. * **Aortic Rupture/Dissection:** (Not listed, but important) Chronic hypertension and cystic medial necrosis of the aorta can lead to fatal rupture. **High-Yield Clinical Pearls for NEET-PG:** * **Association:** 50-85% of cases are associated with a **Bicuspid Aortic Valve**. * **Syndrome:** Strongly associated with **Turner Syndrome** (45, XO). * **Clinical Sign:** "Radio-femoral delay" and upper limb hypertension with lower limb hypotension. * **X-ray Findings:** **Figure-of-3 sign** (on barium swallow/chest X-ray) and **Rib notching** (due to collateral flow through intercostal arteries; usually involves 3rd to 8th ribs).

Question 106: A 40-year-old woman with a history of rheumatic fever presents with shortness of breath, weight loss, fatigue, and abdominal distension. Physical examination shows rales in the lungs, hepatosplenomegaly, and 2+ pitting edema of the legs. A chest X-ray reveals only left atrial enlargement and pulmonary edema. What is the most likely cause of pulmonary edema in this patient?

A. Aortic insufficiency
B. Aortic stenosis
C. Mitral stenosis (Correct Answer)
D. Tricuspid insufficiency

Explanation: **Explanation:** The clinical presentation of a patient with a history of rheumatic fever, shortness of breath, and signs of both pulmonary congestion (rales, pulmonary edema) and systemic venous congestion (hepatosplenomegaly, pitting edema) strongly suggests **Mitral Stenosis (MS)**. **Why Mitral Stenosis is Correct:** In MS, the narrowed mitral valve orifice creates a pressure gradient between the left atrium (LA) and the left ventricle (LV). This leads to increased LA pressure, which is transmitted backward into the pulmonary veins and capillaries, causing **pulmonary edema**. Chronic elevation in pulmonary pressure eventually leads to pulmonary hypertension and **right-sided heart failure**, explaining the hepatosplenomegaly and peripheral edema. The chest X-ray finding of isolated LA enlargement without LV enlargement is a classic hallmark of MS. **Why Other Options are Incorrect:** * **Aortic Insufficiency (AI) & Aortic Stenosis (AS):** Both conditions primarily cause **Left Ventricular Hypertrophy/Dilation**. A chest X-ray in these cases would typically show a prominent left ventricular shadow (boot-shaped heart in AS or cardiomegaly in AI), which is absent here. * **Tricuspid Insufficiency (TI):** While TI causes systemic venous congestion (edema, hepatomegaly), it does **not** cause pulmonary edema. In fact, TI often occurs secondary to the pulmonary hypertension caused by MS. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of MS:** Rheumatic Heart Disease (99% of cases). * **Auscultation:** Loud S1, Opening Snap (OS), and a Mid-Diastolic Rumble at the apex. * **ECG/X-ray:** Look for "P-mitrale" (broad, notched P waves) and the "Straightening of the left heart border" on CXR due to LA enlargement. * **Management:** Percutaneous Transvenous Mitral Commissurotomy (PTMC) is the treatment of choice for symptomatic MS with favorable valve morphology.

Question 107: Which of the following is NOT associated with a soft S1 sound?

A. Mitral regurgitation
B. Ventricular septal defect
C. Short PR interval (Correct Answer)
D. Calcific valve

Explanation: ### Explanation The intensity of the first heart sound (S1) is primarily determined by the position of the mitral valve leaflets at the onset of ventricular systole and the mobility of the valve [2]. **Why Option C is the Correct Answer:** A **Short PR interval** is associated with a **Loud S1**, not a soft one. In a short PR interval (e.g., WPW syndrome), ventricular systole begins shortly after atrial contraction [3]. At this moment, the mitral leaflets are still wide open and deep in the ventricular cavity. As they slam shut over a wide distance, they produce a loud sound. Conversely, a long PR interval allows the leaflets to drift back toward a semi-closed position before systole, resulting in a soft S1. **Analysis of Incorrect Options (Causes of Soft S1):** * **Mitral Regurgitation (A):** The leaflets often fail to coapt properly or are structurally damaged, leading to a diminished closing sound. * **Ventricular Septal Defect (B):** Large left-to-right shunts or associated hemodynamic changes can lead to a softening of the S1, often due to the prolonged duration of ventricular contraction or masking by the pansystolic murmur. * **Calcific Valve (D):** If the mitral valve is severely calcified (as in advanced Mitral Stenosis), the leaflets become immobile and "stiff," preventing the sharp closure required to generate a loud S1 [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Loud S1:** Mitral Stenosis (pliable valve), Short PR interval, Tachycardia, High cardiac output states (Anemia, Pregnancy, Thyrotoxicosis). * **Soft S1:** Mitral Regurgitation, Long PR interval (1st-degree heart block), Severe Mitral Stenosis (calcified), Obesity/COPD (muffled sound). * **Variable S1:** Atrial Fibrillation, Complete Heart Block (AV dissociation).

Question 108: What is the causative organism of late prosthetic valve endocarditis?

A. Streptococcus viridans (Correct Answer)
B. Proteus mirabilis
C. Beta hemolytic streptococci
D. Staphylococci

Explanation: **Explanation:** Prosthetic Valve Endocarditis (PVE) is categorized based on the timing of symptom onset following valve replacement. This distinction is critical as it dictates the likely causative pathogen. **1. Why Streptococcus viridans is correct:** **Late PVE** occurs **>12 months** after surgery. At this stage, the prosthetic valve has been endothelialized, making it physiologically similar to a native valve. Consequently, the microbiology mirrors Native Valve Endocarditis (NVE) [1]. **Streptococcus viridans**, a common inhabitant of the oral cavity, is the most frequent cause of late PVE, often introduced via dental procedures or minor oral trauma [1]. **2. Why the other options are incorrect:** * **Staphylococci:** *Staphylococcus epidermidis* (Coagulase-negative) is the most common cause of **Early PVE** (<2 months) and **Intermediate PVE** (2–12 months) due to its ability to form biofilms on prosthetic material during the perioperative period. *Staphylococcus aureus* is a common cause of acute NVE, especially in IV drug users [1]. * **Beta-hemolytic streptococci:** These (e.g., Group A Strep) are more commonly associated with skin infections or acute native valve endocarditis rather than the indolent course typical of late PVE [1]. * **Proteus mirabilis:** Gram-negative bacilli are rare causes of PVE, usually associated with nosocomial urinary tract infections in the early postoperative period. **Clinical Pearls for NEET-PG:** * **Early PVE (<1 year):** Most common organism is **Staphylococcus epidermidis** (CoNS). * **Late PVE (>1 year):** Most common organism is **Streptococcus viridans**. * **Culture-Negative Endocarditis:** Most common cause is prior antibiotic therapy; otherwise, consider **HACEK** organisms or *Coxiella burnetii* [3]. * **Duke’s Criteria:** The gold standard for diagnosing Infective Endocarditis (requires 2 major, 1 major + 3 minor, or 5 minor criteria) [2].

Question 109: All of the following are causes of a pansystolic murmur, EXCEPT?

A. Ventricular Septal Defect (VSD)
B. Tricuspid Regurgitation (TR)
C. Mitral Regurgitation (MR)
D. Atrial Septal Defect (ASD) (Correct Answer)

Explanation: **Explanation:** A **pansystolic (holosystolic) murmur** occurs when there is a pressure gradient between two chambers that persists throughout the entire duration of systole (from $S_1$ to $S_2$) [3]. **Why ASD is the correct answer:** In an **Atrial Septal Defect (ASD)**, the murmur is **not** caused by blood flowing across the defect itself (as the pressure gradient between the atria is too low). Instead, the increased volume in the right heart leads to increased flow across the pulmonary valve, causing a **midsystolic (ejection systolic) murmur**. Additionally, ASD is characterized by a pathognomonic **fixed, wide splitting of $S_2$**. **Why the other options are incorrect:** * **Mitral Regurgitation (MR):** High pressure in the Left Ventricle (LV) compared to the Left Atrium (LA) throughout systole causes a pansystolic murmur, loudest at the apex, radiating to the axilla [1]. * **Tricuspid Regurgitation (TR):** High pressure in the Right Ventricle (RV) compared to the Right Atrium (RA) causes a pansystolic murmur, loudest at the left lower sternal border. It characteristically increases with inspiration (**Carvallo’s sign**). * **Ventricular Septal Defect (VSD):** The significant pressure gradient between the LV and RV throughout systole produces a harsh pansystolic murmur, typically loudest at the left lower sternal border (Erb’s point) [2]. **High-Yield Clinical Pearls for NEET-PG:** 1. **Small VSD (Roger’s Disease):** Produces a louder, more "mal de roussel" murmur than a large VSD [2]. 2. **Dynamic Auscultation:** MR and VSD murmurs increase with **handgrip** (increased afterload), whereas HOCM and Mitral Valve Prolapse murmurs decrease. 3. **ASD Triad:** Fixed wide $S_2$, Ejection Systolic Murmur (pulmonary area), and Mid-diastolic murmur (tricuspid area due to increased flow).

Question 110: Which of the following is NOT true about Dressler's syndrome?

A. It occurs within hours after myocardial infarction. (Correct Answer)
B. It may be due to the early use of anticoagulants.
C. Chest pain is a common symptom.
D. It responds well to salicylates.

Explanation: **Explanation:** Dressler’s syndrome (also known as Post-Myocardial Infarction Syndrome) is an **immune-mediated** delayed pericarditis. **1. Why Option A is the correct answer (False statement):** Dressler’s syndrome typically occurs **2 to 6 weeks** after a myocardial infarction (MI). It is caused by an autoimmune reaction where the body develops antibodies against cardiac antigens released during the necrotic phase of the MI. Because it requires time for the immune system to mount this response, it **cannot** occur within hours. Pericarditis occurring within the first 24–72 hours is instead termed "Peri-infarction Pericarditis," which is due to direct inflammatory extension rather than an immune reaction. **2. Analysis of other options:** * **Option B:** Historically, the early or excessive use of **anticoagulants** post-MI has been associated with an increased risk of hemorrhagic pericardial effusion, which can complicate or mimic Dressler’s syndrome. * **Option C:** **Chest pain** is the hallmark symptom. It is typically pleuritic (worsens with deep inspiration) and positional (relieved by leaning forward). [1] * **Option D:** As an inflammatory condition, it responds excellently to **high-dose Aspirin (salicylates)** or other NSAIDs. [1] Colchicine is often added to prevent recurrence. **High-Yield Clinical Pearls for NEET-PG:** * **Triad:** Fever, pleuritic chest pain, and pericardial effusion. * **Investigation of Choice:** Echocardiography (to detect effusion). * **ECG Findings:** Diffuse ST-segment elevation with PR-segment depression (except in lead aVR). [1] * **Key Distinction:** Do not confuse Dressler’s (weeks later) with early post-infarct pericarditis (days later). Steroids are generally avoided as they may interfere with myocardial scar formation.

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Cardiology — MCQs

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