Cardiology Practice Questions

Q: A 50-year-old patient complains of dizziness and palpitations. What does the ECG show?

Bradycardia-tachycardia syndrome. ***Bradycardia-tachycardia syndrome*** - Demonstrates **alternating periods** of bradycardia and tachycardia on ECG, characteristic of **sick sinus syndrome** in older patients. - Symptoms of **dizziness and palpitations** correlate with the fluctuating heart rates, requiring **pacemaker therapy** for management. *Mobitz I block* - Shows **progressive PR interval prolongation** followed by a dropped QRS complex in a **Wenckebach pattern**. - Typically **asymptomatic** and does not cause the alternating bradycardia-tachycardia pattern seen in this patient. *Mobitz II block* - Characterized by **sudden dropped QRS complexes** without prior PR interval prolongation, with **constant PR intervals**. - Usually presents with **consistent bradycardia** rather than alternating heart rate patterns with palpitations. *Complete heart block* - Shows **complete AV dissociation** with independent atrial and ventricular rhythms, resulting in **severe bradycardia**. - Presents with **persistent slow heart rate** and does not explain the palpitations from tachycardic episodes.

Q: Which of the following is true regarding neurocardiogenic syncope?

Vasodilation and bradycardia. Explanation: Neurocardiogenic syncope (Vasovagal syncope) is the most common cause of fainting. It is mediated by the **Bezold-Jarisch reflex**, a cardio-inhibitory reflex [1]. **1. Why Option A is correct:** The pathophysiology involves a sudden surge in sympathetic activity followed by a paradoxical, overwhelming parasympathetic (vagal) response [1]. This leads to two primary effects: * **Vasodilation:** Due to sympathetic withdrawal (vasodepressor response), leading to hypotension [1]. * **Bradycardia:** Due to increased vagal tone (cardio-inhibitory response) [1]. The combination of low blood pressure and low heart rate results in cerebral hypoperfusion and loss of consciousness [1][2]. **2. Why other options are incorrect:** * **Option B & C:** The reflex is initiated in the **inferoposterior wall of the left ventricle**. It is triggered by **vigorous/forceful contractions** of a relatively **underfilled (empty) ventricle** (e.g., due to prolonged standing or dehydration) [1]. This stimulates mechanoreceptors (C-fibers) that falsely signal the brain that the heart is overloaded, triggering the reflex. * **Option D:** The reflex occurs when the heart chambers are **depleted of blood** (low preload), not filled [1]. **Clinical Pearls for NEET-PG:** * **Triggers:** Prolonged standing, emotional stress, pain, or sight of blood [1][2]. * **Prodrome:** Characterized by nausea, pallor, diaphoresis (sweating), and blurred vision [2]. * **Diagnosis:** Primarily clinical; **Head-up Tilt Table Test (HUTT)** is the gold standard for confirmation. * **Management:** Reassurance, increasing fluid/salt intake, and physical counter-pressure maneuvers (e.g., leg crossing, handgrip). Midodrine can be used in refractory cases.

Q: What is the earliest feature of pulmonary venous hypertension?

Upper lobar vessel dilatation. **Explanation:** Pulmonary venous hypertension (PVH) occurs when the left heart fails to pump blood efficiently, leading to increased pressure in the pulmonary veins. This process follows a predictable radiological sequence on a chest X-ray: **1. Why "Upper lobar vessel dilatation" is correct:** This is the earliest sign of PVH (Grade 1). Normally, in an upright position, gravity causes the lower lobe vessels to be larger than the upper lobe vessels. When pulmonary venous pressure rises (12–18 mmHg), it triggers reactive vasoconstriction in the lower lobes. Blood is then shunted to the upper lobes, causing the upper lobe vessels to dilate. This phenomenon is known as **Cephalization** or **Antler Sign**. **2. Why the other options are incorrect:** * **Kerley B lines:** These represent interstitial edema (Grade 2) and occur when pressures reach 18–25 mmHg. They are horizontal lines at the lung bases representing thickened interlobular septa. They appear *after* cephalization. * **Left atrial enlargement:** While often present in chronic conditions like mitral stenosis, it is a structural cause/consequence rather than a specific radiological feature of the pulmonary vasculature sequence. * **Pleural effusion:** This represents a more advanced stage of heart failure (Grade 3/Alveolar edema) where fluid spills into the pleural space. **Clinical Pearls for NEET-PG:** * **Staging of PVH on CXR:** * **Grade 1 (12-18 mmHg):** Cephalization (Upper lobe diversion). * **Grade 2 (18-25 mmHg):** Interstitial edema (Kerley B lines, peribronchial cuffing). * **Grade 3 (>25 mmHg):** Alveolar edema (Bat-wing appearance, Pleural effusion). * **PCWP Correlation:** Pulmonary Capillary Wedge Pressure (PCWP) is the gold standard for measuring these pressures clinically.

Q: Which of the following agents should NOT be used for oral anticoagulation in high-risk patients with atrial fibrillation?

Clopidogrel. **Explanation:** The core concept in managing atrial fibrillation (AF) is the prevention of **thromboembolic strokes**. In AF, the stasis of blood in the left atrium leads to the formation of **red thrombi** (fibrin-rich), which are best prevented by **anticoagulants**, not antiplatelets. [1] **Why Clopidogrel is the Correct Answer:** Clopidogrel is an **antiplatelet agent** (P2Y12 inhibitor). While it is effective in preventing arterial thrombosis (white thrombi) in conditions like Myocardial Infarction or Stroke, clinical trials (like ACTIVE-W) have proven that antiplatelets are significantly less effective than anticoagulants in preventing strokes in high-risk AF patients. Therefore, it is NOT recommended as a primary oral anticoagulant for AF. **Analysis of Incorrect Options:** * **Warfarin (Option A):** A Vitamin K Antagonist (VKA). It has been the gold standard for decades for stroke prevention in both valvular and non-valvular AF. [1] * **Dabigatran (Option B):** A Direct Thrombin Inhibitor (DTI). It is a NOAC (Non-vitamin K Oral Anticoagulant) approved for non-valvular AF. * **Rivaroxaban (Option C):** A Direct Factor Xa inhibitor. Like Dabigatran, it is a NOAC preferred over Warfarin in non-valvular AF due to a lower risk of intelligence hemorrhage and no need for INR monitoring. **High-Yield Clinical Pearls for NEET-PG:** * **CHADS₂ / CHA₂DS₂-VASc Score:** Used to stratify stroke risk in AF and decide when to start anticoagulation. [1] * **Valvular AF:** Defined as AF in the presence of moderate-to-severe mitral stenosis or a mechanical heart valve. **Warfarin** is the only indicated agent; NOACs are contraindicated. * **Reversal Agents:** Idarucizumab (for Dabigatran) and Andexanet alfa (for Rivaroxaban/Apixaban).

Q: Three weeks after surgery to implant a mechanical aortic valve, a 70-year-old man develops chest pain, fever, and leukocytosis. On examination, the JVP is increased, there is a mechanical S2 sound, and a pericardial friction rub. Which of the following is the most likely diagnosis?

Post pericardiotomy syndrome. **Explanation:** The clinical presentation of fever, chest pain, leukocytosis, and a pericardial friction rub occurring 1–6 weeks after cardiac surgery is classic for **Post-pericardiotomy Syndrome (PPS)**. **1. Why Post-pericardiotomy Syndrome is Correct:** PPS is an immune-mediated pleuropericarditis triggered by damage to the pericardium and the presence of blood in the pericardial space. The 3-week timeline is the "sweet spot" for this delayed hypersensitivity reaction. Key diagnostic features seen in this patient include: * **Pericardial Friction Rub:** Pathognomonic for pericarditis. * **Increased JVP:** Suggests pericardial effusion or tamponade physiology. * **Systemic Inflammation:** Fever and leukocytosis. **2. Why Other Options are Incorrect:** * **Infection in the aortic valve (Endocarditis):** While fever and leukocytosis occur, the presence of a **mechanical S2** indicates the valve is functioning normally. Endocarditis usually presents with a new murmur (regurgitation) rather than a friction rub. * **CMV Infection:** Known as "Post-perfusion syndrome" (due to bypass/transfusions), it presents with fever and atypical lymphocytosis but does not cause a pericardial friction rub or signs of pericarditis. * **Pulmonary Embolism:** While it causes chest pain and tachycardia, it would not typically cause a pericardial friction rub or a high-grade fever 3 weeks post-op without other localizing signs. **Clinical Pearls for NEET-PG:** * **Treatment:** The first-line treatment for PPS is **NSAIDs (Aspirin)** and **Colchicine**. Steroids are reserved for refractory cases. * **Triad of PPS:** Fever, pleuritic chest pain, and pericardial/pleural effusion. * **Differentiation:** Unlike early postoperative pericarditis (which occurs within 48–72 hours due to surgical trauma), PPS is a delayed immunological phenomenon.

Q: Which of the following conditions causes a wide pulse pressure?

Aortic regurgitation. **Explanation:** **Pulse pressure** is the difference between systolic blood pressure (SBP) and diastolic blood pressure (DBP). A **wide pulse pressure** occurs when there is either an increase in stroke volume or a decrease in peripheral vascular resistance/arterial compliance [1]. **Why Aortic Regurgitation (AR) is the Correct Answer:** In AR, blood flows back from the aorta into the left ventricle during diastole [3]. This leads to: 1. **Increased SBP:** The left ventricle handles an increased stroke volume (normal venous return + regurgitant volume), ejecting more blood into the aorta [1]. 2. **Decreased DBP:** The rapid "runoff" of blood back into the ventricle and into the peripheral circulation causes a significant drop in diastolic pressure. The combination of high SBP and low DBP results in a characteristically wide pulse pressure. **Why Other Options are Incorrect:** * **Aortic Stenosis (AS):** Causes a **narrow pulse pressure** (*pulsus parvus et tardus*). The obstructed outflow reduces stroke volume, leading to a low systolic pressure [2]. * **Mitral Stenosis (MS) & Tricuspid Stenosis (TS):** These conditions limit ventricular filling, which reduces stroke volume and cardiac output, typically resulting in a narrow or normal pulse pressure [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Water-hammer pulse (Corrigan’s pulse):** A rapid upstroke and collapse of the carotid pulse, pathognomonic for AR [1]. * **Traube’s sign:** "Pistol shot" sounds heard over the femoral arteries. * **Duroziez’s sign:** A systolic and diastolic murmur heard over the femoral artery when compressed. * **Other causes of wide pulse pressure:** Thyrotoxicosis, Patent Ductus Arteriosus (PDA), Anemia, Beriberi, and Atherosclerosis (due to stiffened arteries).

Q: Which of the following findings is NOT seen in primary pulmonary hypertension?

Right parasternal heave. In primary pulmonary hypertension (now classified under Pulmonary Arterial Hypertension), the core pathophysiology involves increased resistance in the pulmonary vasculature, leading to **Right Ventricular (RV) hypertrophy and dilatation.** [1] **Why "Right parasternal heave" is the correct answer (the finding NOT seen):** This is a classic "trick" question regarding bedside physical examination. A heave (precordial lift) caused by right ventricular enlargement is felt at the **Left Parasternal** border (3rd/4th intercostal space) [3]. There is no such clinical entity as a "Right parasternal heave" in the context of pulmonary hypertension; the heart is situated in the left hemithorax, and RV enlargement displaces the impulse toward the left sternal border, not the right. **Analysis of Incorrect Options:** * **Left parasternal heave:** This is a hallmark sign of RV hypertrophy/enlargement, which occurs as the right ventricle pumps against high pulmonary pressures [3]. * **Single S2:** In severe pulmonary hypertension, the pulmonary component (P2) becomes very loud and occurs earlier, often merging with the aortic component (A2), resulting in a single, loud S2 [1]. * **Pulmonary ejection click:** This is caused by the sudden opening of the pulmonary valve into a dilated pulmonary artery under high pressure. It is typically heard at the left upper sternal border. **High-Yield Clinical Pearls for NEET-PG:** * **P2 Intensity:** A loud P2 (palpable in the 2nd left intercostal space) is the most sensitive physical sign of pulmonary hypertension [3]. * **Graham Steell Murmur:** A high-pitched, decrescendo diastolic murmur of pulmonary regurgitation may be heard. * **ECG Findings:** Look for "P pulmonale" (tall, peaked P waves) and Right Axis Deviation [2].

Question 1

A 50-year-old patient complains of dizziness and palpitations. What does the ECG show?

Accepted Answer

Bradycardia-tachycardia syndrome

Answer

Mobitz I block

Answer

Mobitz II block

Answer

Complete heart block

Question 2

Which of the following is true regarding neurocardiogenic syncope?

Accepted Answer

Vasodilation and bradycardia

Answer

Initiated at the left ventricle

Answer

Associated with forceful contraction of the heart

Answer

Occurs when heart chambers are filled with blood

Question 3

What is the earliest feature of pulmonary venous hypertension?

Accepted Answer

Upper lobar vessel dilatation

Answer

Kerley B lines

Answer

Left atrial enlargement

Answer

Pleural effusion

Question 4

Which of the following agents should NOT be used for oral anticoagulation in high-risk patients with atrial fibrillation?

Accepted Answer

Clopidogrel

Answer

Warfarin

Answer

Dabigatran

Answer

Rivaroxaban

Question 5

A 35-year-old athlete with a height of 184 cm, arm span of 194 cm, pulse rate of 64/min, and BP of 148/64 mm Hg presents with a long diastolic murmur heard over the right second intercostal space on routine chest auscultation. What is the probable diagnosis?

Accepted Answer

Aortic regurgitation

Answer

Atrial septal defect

Answer

Ebstein anomaly

Answer

Coarctation of the aorta

Question 6

Which of the following conditions is associated with a QRS duration greater than 0.16 seconds?

Accepted Answer

Bundle branch block

Answer

Sick sinus syndrome

Answer

Mobitz type 1 heart block

Answer

Mobitz type 2 heart block

Question 7

Three weeks after surgery to implant a mechanical aortic valve, a 70-year-old man develops chest pain, fever, and leukocytosis. On examination, the JVP is increased, there is a mechanical S2 sound, and a pericardial friction rub. Which of the following is the most likely diagnosis?

Accepted Answer

Post pericardiotomy syndrome

Answer

Infection in the aortic valve

Answer

Cytomegalovirus (CMV) infection

Answer

Pulmonary embolism

Question 8

Which of the following conditions causes a wide pulse pressure?

Accepted Answer

Aortic regurgitation

Answer

Aortic stenosis

Answer

Mitral stenosis

Answer

Tricuspid stenosis

Question 9

An 18-year-old man is admitted to the hospital with acute onset of substernal chest pain that began abruptly 30 minutes ago. The pain radiates to his neck and right arm. He has otherwise been in good health. On physical examination, he is diaphoretic and tachypnoeic. His BP is 102/48 mmHg and heart rate is 112 bpm, with a regular rhythm but is tachycardiac. A 2/6 holosystolic murmur is heard best at the apex and radiates to the axilla. His lungs have bilateral rales at the bases. The ECG demonstrates 4 mm of ST elevation in the anterior leads. In the past, he was hospitalized for some problem with his heart when he was 4 years old. His mother, who accompanies him, reports that he received aspirin and gamma globulin as treatment. Since that time, he has required intermittent follow-up with echocardiography. What is the most likely cause of this patient's acute coronary syndrome?

Accepted Answer

Thrombosis of a coronary artery aneurysm

Answer

Dissection of the aortic root and left coronary ostia

Answer

Presence of a myocardial bridge overlying the left anterior descending artery

Answer

Vasospasm following cocaine ingestion

Question 10

Which of the following findings is NOT seen in primary pulmonary hypertension?

Accepted Answer

Right parasternal heave

Answer

Left parasternal heave

Answer

Single S2

Answer

Pulmonary ejection click

Cardiology — MCQs

Cardiology — MCQs

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