Cardiology Practice Questions

Q: Reverse splitting of S2 is seen in all except?

LV pacing. **Explanation:** **Reverse (Paradoxical) Splitting of S2** occurs when the aortic valve (A2) closes *after* the pulmonary valve (P2). Normally, A2 precedes P2 [1]. In reverse splitting, the gap narrows during inspiration and widens during expiration. This occurs due to either **delayed LV emptying** or **delayed LV activation**. **Why LV Pacing is the Correct Answer:** In **LV pacing**, the left ventricle is activated first. This leads to early closure of the aortic valve (A2). Since A2 occurs even earlier than usual, it reinforces the normal sequence (A2 followed by P2), making the split wider but **not** reversed. Conversely, **Right Ventricular (RV) pacing** causes delayed LV activation, which *does* cause reverse splitting. **Analysis of Incorrect Options:** * **LBBB (Left Bundle Branch Block):** This is the most common cause. Delayed electrical conduction to the left ventricle delays LV contraction and A2 closure, causing a reverse split. * **WPW Type A:** In Type A, the accessory pathway [3] pre-excites the right ventricle, or there is a relative delay in LV activation compared to the RV, leading to paradoxical splitting. * **Systemic Hypertension:** Severe hypertension or aortic stenosis [2] causes increased resistance to LV emptying (increased afterload), prolonging LV ejection time and delaying A2. **High-Yield Clinical Pearls for NEET-PG:** * **Wide Fixed Split S2:** Pathognomonic for **Atrial Septal Defect (ASD)**. * **Wide Variable Split S2:** Seen in **RBBB**, Pulmonary Stenosis, and MR (conditions delaying P2 or early A2). * **Reverse Split Mnemonic:** "L-A-S-T" (LBBB, AS, Systemic HTN, Type B WPW/RV Pacing). *Note: WPW Type B and RV pacing are classic causes; WPW Type A is less common but can present similarly depending on the bypass tract location.*

Q: What is the treatment of choice for ST-elevation myocardial infarction?

Percutaneous coronary intervention. The primary goal in the management of ST-elevation myocardial infarction (STEMI) is the rapid restoration of coronary blood flow to salvage myocardium. **Why Percutaneous Coronary Intervention (PCI) is the Correct Answer:** Primary PCI is the **gold standard** and treatment of choice for STEMI. Clinical trials have consistently demonstrated that PCI is superior to fibrinolysis in achieving higher rates of vessel patency (TIMI 3 flow), lower rates of re-infarction, and reduced mortality [1]. It is preferred if it can be performed within **120 minutes** of first medical contact. **Analysis of Incorrect Options:** * **A. Thrombolysis with Streptokinase:** While thrombolysis is an alternative, it is only indicated if primary PCI cannot be performed within the recommended 120-minute window [1]. It carries a higher risk of intracranial hemorrhage and is less effective at opening the artery compared to PCI. * **C. Anticoagulate with heparin:** Heparin is an *adjunctive* therapy used during PCI or thrombolysis to prevent further clot propagation; it is not a definitive treatment for mechanical obstruction [2]. * **D. Aspirin and clopidogrel:** Dual Antiplatelet Therapy (DAPT) is a mandatory *supportive* treatment for all STEMI patients to prevent stent thrombosis, but it cannot mechanically open a totally occluded coronary artery. **High-Yield Clinical Pearls for NEET-PG:** * **Door-to-Balloon Time:** Should be <90 minutes (at PCI-capable centers) or <120 minutes (if transfer is required). * **Door-to-Needle Time:** If PCI is unavailable, thrombolysis should be initiated within **30 minutes**. * **Pharmacoinvasive Strategy:** If thrombolysis is performed first, the patient should still be transferred for PCI within 3-24 hours. * **Contraindication:** Remember that Streptokinase is antigenic; it should not be repeated in a patient who has received it previously.

Q: Which of the following drugs should not be used empirically in a patient with severe hypertension, especially in the elderly?

Prazosin. **Explanation:** The correct answer is **Prazosin (Option D)**. **Why Prazosin is avoided empirically:** Prazosin is a selective alpha-1 blocker. Its empirical use in severe hypertension, particularly in the elderly, is discouraged due to the **"First-dose phenomenon."** This refers to sudden, severe orthostatic hypotension and syncope occurring shortly after the initial dose [1]. In elderly patients, baroreceptor sensitivity is already diminished, making them highly susceptible to falls and related injuries (e.g., hip fractures). Furthermore, the **ALLHAT trial** demonstrated that alpha-blockers are less effective than other classes in preventing heart failure and cardiovascular events when used as monotherapy. **Analysis of Incorrect Options:** * **A. Enalapril (ACE Inhibitor):** A first-line agent for hypertension [1]. While it requires monitoring for renal function and potassium, it is a standard empirical choice, especially in patients with diabetes or heart failure. * **B. Amlodipine (Calcium Channel Blocker):** A preferred first-line agent for elderly patients and those of African descent [2]. It is highly effective in reducing systolic blood pressure and has a low risk of metabolic side effects [1]. * **C. Chlorthalidone (Thiazide-like Diuretic):** Often considered the "gold standard" diuretic for hypertension due to its long half-life and proven efficacy in reducing cardiovascular mortality in the elderly (SHEP trial) [2]. **NEET-PG High-Yield Pearls:** * **Drug of Choice (DOC) for Hypertension in Elderly:** Thiazide-like diuretics (Chlorthalidone) or Long-acting CCBs (Amlodipine) [2]. * **Prazosin Indications:** Now primarily used for Benign Prostatic Hyperplasia (BPH) or as add-on therapy in resistant hypertension. * **First-dose phenomenon prevention:** Start with a low dose (0.5–1 mg) and administer at bedtime ("Bedtime dosing").

Q: Angina and syncope in the same patient is a characteristic presentation of which of the following conditions?

Aortic stenosis. **Explanation:** **Aortic Stenosis (AS)** is characterized by the classic clinical triad of **SAD**: **S**yncope, **A**ngina, and **D**yspnea. [1] * **Angina:** Occurs due to an increased myocardial oxygen demand (caused by left ventricular hypertrophy) and decreased supply (due to high filling pressures compressing coronary arteries), even in the absence of coronary artery disease. [2] * **Syncope:** Typically occurs during exertion. The fixed cardiac output cannot meet the demand of peripheral vasodilation during exercise, leading to a drop in cerebral perfusion. [1] **Analysis of Incorrect Options:** * **B. Mitral Valve Prolapse (MVP):** Usually asymptomatic or presents with non-specific chest pain and palpitations (click-murmur syndrome), but syncope is rare unless associated with severe arrhythmias. [3] * **C. Mitral Stenosis (MS):** Primarily presents with dyspnea, hemoptysis, and atrial fibrillation. It does not typically cause angina or syncope unless there is associated pulmonary hypertension or low cardiac output in very late stages. * **D. Aortic Regurgitation (AR):** Presents with features of heart failure and wide pulse pressure (e.g., Water-hammer pulse). While angina can occur (nocturnal angina), syncope is not a classic hallmark of AR. **High-Yield Clinical Pearls for NEET-PG:** * **Murmur of AS:** Harsh crescendo-decrescendo systolic murmur heard best at the right second intercostal space, radiating to the **carotids**. [1] * **Pulse:** *Pulsus parvus et tardus* (slow-rising, low-volume pulse). * **Indication for Surgery:** The onset of symptoms (SAD) is a critical marker; without valve replacement, the average survival is 2 years for Heart Failure, 3 years for Syncope, and 5 years for Angina.

Q: A 50-year-old man had an attack of myocardial infarction and developed ventricular ectopics and a low ejection fraction. Which of the following antiarrhythmic drugs should be given?

Beta-blocker. ### Explanation **Correct Answer: C. Beta-blocker** The management of post-myocardial infarction (MI) arrhythmias focuses on reducing mortality and preventing sudden cardiac death (SCD). **Why Beta-blockers are the drug of choice:** In patients with a history of MI and a low ejection fraction (EF), **Beta-blockers** (e.g., Metoprolol, Carvedilol) are the first-line therapy [1]. They reduce myocardial oxygen demand, decrease sympathetic overactivity, and prevent ventricular remodeling [2]. Most importantly, they are the only class of drugs in this list proven to **reduce mortality** and the risk of arrhythmic death in patients with coronary artery disease and heart failure [1, 2]. **Why other options are incorrect:** * **Flecainide (Class IC):** The landmark **CAST (Cardiac Arrhythmia Suppression Trial)** study proved that Class IC agents increase mortality in post-MI patients due to their pro-arrhythmic effects in scarred myocardium [3]. They are strictly contraindicated in structural heart disease. * **Mexiletine (Class IB):** While it can suppress ventricular ectopics, it has not shown a mortality benefit and is generally reserved as an adjunct therapy for refractory cases. * **Radio-frequency ablation:** This is typically indicated for symptomatic, drug-refractory ventricular tachycardia or specific focal ectopics, but it is not the initial medical management for post-MI ventricular ectopics. **High-Yield Clinical Pearls for NEET-PG:** * **CAST Trial Key Takeaway:** Never use Class IC antiarrhythmics (Flecainide, Propafenone) in patients with prior MI or CAD [3]. * **Low EF + Post-MI:** The most effective intervention to prevent SCD is an **ICD (Implantable Cardioverter Defibrillator)** if the EF remains ≤35% despite optimal medical therapy. * **Amiodarone:** It is "neutral" regarding mortality in post-MI patients; it suppresses arrhythmias but does not improve survival like Beta-blockers do.

Q: A 28-year-old woman presents with symptoms of chest pain that changes with positioning, is worse when lying down, and relieved when sitting up. She also reports increasing dyspnea and edema. On examination, her blood pressure is 85/60 mm Hg with a positive pulsus paradoxus, a low-volume pulse at 110/min, and distant heart sounds. The JVP is at 7 cm with a negative Kussmaul's sign. ECG shows low voltages, and CXR reveals a large cardiac silhouette. What is the most likely diagnosis for a patient presenting with shortness of breath and peripheral edema with these findings?

Cardiac tamponade. The clinical presentation is a classic description of **Cardiac Tamponade**, characterized by the accumulation of fluid in the pericardial space leading to increased intrapericardial pressure and impaired cardiac filling [1]. **Why Cardiac Tamponade is correct:** The patient exhibits **Beck’s Triad**: hypotension (85/60 mm Hg), distant/muffled heart sounds, and elevated JVP. The positional chest pain suggests underlying pericarditis [3]. Key diagnostic features mentioned include: * **Pulsus Paradoxus:** A drop in systolic BP >10 mmHg during inspiration (hallmark of tamponade). * **Negative Kussmaul’s Sign:** In tamponade, the JVP typically falls during inspiration (unlike constrictive pericarditis). * **ECG/CXR:** Low voltage complexes and a "water-bottle" heart silhouette are characteristic [1]. **Why other options are incorrect:** * **Constrictive Pericarditis:** While it shares features like elevated JVP and edema, it is characterized by a **positive Kussmaul’s sign** (paradoxical rise in JVP on inspiration) and a pericardial knock, rather than muffled heart sounds [4]. * **Restrictive Cardiomyopathy:** Presents with heart failure symptoms and a positive Kussmaul’s sign, but usually lacks the acute hypotension and the specific CXR/ECG findings of large pericardial effusion. * **RVMI:** While it causes hypotension and raised JVP, it typically presents with clear lung fields and specific ST-segment elevations in right-sided leads (V4R), not muffled heart sounds or low voltage ECG [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Beck’s Triad:** Hypotension, Muffled Heart Sounds, Raised JVP. * **Pulsus Paradoxus:** Also seen in severe asthma, COPD, and tension pneumothorax. * **JVP Waveform:** In tamponade, there is a **prominent 'x' descent** but an **absent/diminished 'y' descent** (due to restricted diastolic filling). * **Treatment of Choice:** Immediate **Pericardiocentesis**.

Q: What is not true of the "a" wave of venous pulsations in the neck?

Occurs just after the carotid artery pulse. The Jugular Venous Pulse (JVP) reflects pressure changes in the right atrium. Understanding its timing relative to the cardiac cycle is crucial for NEET-PG. ### Why Option C is Correct (The False Statement) The **'a' wave** represents **atrial contraction** [1]. In the cardiac cycle, atrial contraction occurs at the end of diastole, just before the closure of the AV valves [1]. Therefore, the 'a' wave occurs **just before** the first heart sound (S1) and **before** the carotid artery pulse [2]. The carotid pulse corresponds to ventricular systole (specifically the 'c' wave of the JVP). ### Explanation of Other Options * **Option A (Tricuspid Stenosis):** In TS, the right atrium must contract against a narrowed orifice, leading to increased resistance and **giant 'a' waves**. * **Option B (Atrial Fibrillation):** Since the 'a' wave is produced by coordinated atrial contraction, it is characteristically **absent/abolished** in AF, where the atria only quiver. * **Option D (Complete Heart Block):** When the atria contract against a closed tricuspid valve (which happens when the P wave falls between QRS and T waves during AV dissociation), it produces intermittent, very large waves known as **Cannon 'a' waves**. ### High-Yield Clinical Pearls * **'a' wave:** Atrial contraction (absent in AF; giant in TS, PS, and Pulmonary HTN). * **'c' wave:** Carotid impact/Tricuspid bulging during ventricular contraction [2]. * **'x' descent:** Atrial relaxation. * **'v' wave:** Venous filling against a closed tricuspid valve (giant in Tricuspid Regurgitation). * **'y' descent:** Emptying of the atrium into the ventricle (rapid/steep in Constrictive Pericarditis - *Friedreich's sign*).

Question 1

Reverse splitting of S2 is seen in all except?

Accepted Answer

LV pacing

Answer

LBBB

Answer

WPW type A

Answer

Systemic hypertension

Question 2

What is the treatment of choice for ST-elevation myocardial infarction?

Accepted Answer

Percutaneous coronary intervention

Answer

Thrombolysis with Streptokinase

Answer

Anticoagulate with heparin

Answer

Aspirin and clopidogrel

Question 3

A 38-year-old male presents with a two-week history of progressive shortness of breath. He has a past medical history of type II diabetes mellitus. An echocardiogram revealed an ejection fraction (EF) of 25% with anterior, septal, and lateral wall motion defects. He was admitted and stabilized on furosemide, spironolactone, bisoprolol, and ramipril. What would be the next investigation in the course of management?

Accepted Answer

Angiogram

Answer

Endomyocardial biopsy

Answer

Viral titres

Answer

Exercise tolerance test

Question 4

Which of the following drugs should not be used empirically in a patient with severe hypertension, especially in the elderly?

Accepted Answer

Prazosin

Answer

Enalapril

Answer

Amlodipine

Answer

Chlorthalidone

Question 5

Which of the following EKG findings are characteristic of ventricular premature beats?

Accepted Answer

Fusion beat, AV dissociation, Wide QRS complex, Capture beat

Answer

Narrow QRS complex, Wide QRS complex, Capture beat

Answer

Fusion beat, Narrow QRS complex, AV dissociation, Wide QRS complex

Answer

Fusion beat, Narrow QRS complex, Wide QRS complex, Capture beat

Question 6

Angina and syncope in the same patient is a characteristic presentation of which of the following conditions?

Accepted Answer

Aortic stenosis

Answer

Mitral valve prolapse

Answer

Mitral stenosis

Answer

Aortic regurgitation

Question 7

A 50-year-old man had an attack of myocardial infarction and developed ventricular ectopics and a low ejection fraction. Which of the following antiarrhythmic drugs should be given?

Accepted Answer

Beta-blocker

Answer

Flecainide

Answer

Mexiletine

Answer

Radio-frequency ablation technique

Question 8

A 28-year-old woman presents with symptoms of chest pain that changes with positioning, is worse when lying down, and relieved when sitting up. She also reports increasing dyspnea and edema. On examination, her blood pressure is 85/60 mm Hg with a positive pulsus paradoxus, a low-volume pulse at 110/min, and distant heart sounds. The JVP is at 7 cm with a negative Kussmaul's sign. ECG shows low voltages, and CXR reveals a large cardiac silhouette. What is the most likely diagnosis for a patient presenting with shortness of breath and peripheral edema with these findings?

Accepted Answer

Cardiac tamponade

Answer

Constrictive pericarditis

Answer

Restrictive cardiomyopathy

Answer

Right ventricle myocardial infarction (RVMI)

Question 9

What is not true of the "a" wave of venous pulsations in the neck?

Accepted Answer

Occurs just after the carotid artery pulse

Answer

Exaggerated in tricuspid stenosis

Answer

Abolished in atrial fibrillation

Answer

Exaggerated in complete heart block when the P wave falls between the QRS and T waves

Question 10

Presence of a pansystolic murmur of Mitral Regurgitation with left axis deviation in a patient with an Atrial Septal Defect suggests what?

Accepted Answer

Ostium primum with floppy mitral valve

Answer

Transposition of the Great Arteries (TGA)

Answer

Ostium secundum with floppy mitral valve

Answer

Pulmonary Hypertension

Cardiology — MCQs

Cardiology — MCQs

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