Cardiology Practice Questions

Q: All of the following are true about Atrial Septal Defect (ASD) except?

Left atrial hypertrophy. ### Explanation In an **Atrial Septal Defect (ASD)**, the primary pathophysiology involves a **left-to-right shunt** due to the pressure gradient between the atria. Because the right ventricle (RV) is more compliant than the left ventricle (LV), blood flows from the left atrium (LA) into the right atrium (RA) [1]. **Why Left Atrial Hypertrophy is the Correct Answer (The Exception):** In ASD, the left atrium does not undergo hypertrophy or significant enlargement. This is because the LA effectively "decompresses" itself into the RA through the defect. There is no pressure or volume overload localized to the LA; instead, the excess volume is immediately shunted to the right side of the heart. **Analysis of Incorrect Options:** * **Right Atrial Hypertrophy (A):** The RA receives both the normal systemic venous return and the shunted blood from the LA, leading to volume and eventually pressure overload, causing RA enlargement/hypertrophy. * **Right Ventricular Hypertrophy (C):** The RV handles the increased stroke volume (volume overload). Over time, increased pulmonary blood flow leads to structural changes and hypertrophy. * **Pulmonary Hypertension (D):** Chronic high-volume flow into the pulmonary circulation causes remodeling of the pulmonary vasculature, eventually leading to increased pulmonary vascular resistance and pulmonary hypertension (which can lead to Eisenmenger syndrome). **NEET-PG High-Yield Pearls:** * **Most common type:** Ostium Secundum (located in the region of the fossa ovalis) [1]. * **Auscultation:** Characterized by a **fixed, wide splitting of S2** and a mid-systolic flow murmur at the pulmonary area. * **ECG Findings:** RBBB (Right Bundle Branch Block) and Right Axis Deviation (in Secundum) or Left Axis Deviation (in Primum). * **Paradoxical Embolism:** A unique complication where a systemic venous thrombus crosses the ASD to cause a stroke.

Q: A 50-year-old female patient on losartan and spironolactone therapy for hypertension developed hypotension and bradycardia. The ECG taken is as shown. What is the effective treatment for her condition?

IV calcium gluconate followed by IV sodium bicarbonate. ***IV calcium gluconate followed by IV sodium bicarbonate*** - **Calcium gluconate** provides immediate **membrane stabilization** and cardioprotection against hyperkalemic cardiac toxicity, while **sodium bicarbonate** shifts potassium intracellularly. - This combination addresses both the immediate cardiac danger and begins potassium correction in **hyperkalemia** caused by the **losartan-spironolactone** combination. *Temporary pacing via the right femoral vein* - Pacing will not address the underlying **hyperkalemia** and may be ineffective in severe potassium elevation with **wide QRS complexes**. - The bradycardia here is secondary to **hyperkalemic cardiotoxicity**, not a primary conduction defect requiring pacing. *Intravenous noradrenaline or phenylephrine* - These **vasopressors** address hypotension but do not treat the underlying **hyperkalemia** causing the cardiac conduction abnormalities. - May worsen cardiac arrhythmias in the setting of **severe hyperkalemia** without membrane stabilization. *300 J DC shock* - **Defibrillation** is indicated for **ventricular fibrillation** or **pulseless ventricular tachycardia**, not for bradycardia with hyperkalemia. - Electrical cardioversion without addressing **hyperkalemia** first may precipitate **ventricular fibrillation** or **asystole**.

Q: Which of the following is NOT true about Hypertrophic Obstructive Cardiomyopathy?

Beta agonists are useful.. **Explanation:** Hypertrophic Obstructive Cardiomyopathy (HOCM) is characterized by a hyperdynamic left ventricle and dynamic outflow obstruction. The correct answer is **A** because **Beta-agonists are contraindicated**, not useful, in HOCM. **1. Why Option A is the correct answer (False statement):** Beta-agonists (like Dobutamine or Isoproterenom) increase myocardial contractility (inotropy) and heart rate (chronotropy). In HOCM, increased contractility worsens the narrowing of the outflow tract, while increased heart rate reduces diastolic filling time. This exacerbates the dynamic obstruction and decreases cardiac output. Conversely, **Beta-blockers** are the first-line treatment as they slow the heart rate and reduce contractility, allowing for better ventricular filling. **2. Analysis of other options:** * **Option B:** Asymmetrical Septal Hypertrophy (ASH) is the hallmark of HOCM, where the interventricular septum is significantly thicker than the posterior wall (Ratio >1.3:1). * **Option C:** Obstruction is "dynamic" because it varies with loading conditions. It is caused by the thickened septum and the **Systolic Anterior Motion (SAM)** of the mitral valve. * **Option D:** A double apical impulse (or "triple" in some cases) occurs due to a forceful atrial contraction against a stiff ventricle (S4) followed by the sustained ventricular apex beat. **Clinical Pearls for NEET-PG:** * **Murmur Dynamics:** The systolic murmur of HOCM **increases** with maneuvers that decrease preload (Valsalva, standing) and **decreases** with maneuvers that increase preload or afterload (Squatting, Handgrip). * **Drug of Choice:** Beta-blockers (Propranolol/Atenolol). Verapamil is an alternative. * **Avoid:** Nitrates, Diuretics, and Digitalis (these worsen the obstruction). * **Genetic Basis:** Most commonly due to mutations in the **Beta-myosin heavy chain** or Myosin-binding protein C [1].

Q: Which of the following drugs should not be used empirically in the management of isolated systolic hypertension in the elderly?

Prazosin. **Explanation:** **Isolated Systolic Hypertension (ISH)**, defined as SBP ≥140 mmHg with DBP <90 mmHg, is common in the elderly due to age-related arterial stiffness. The primary goal of treatment is to reduce stroke and cardiovascular events without causing significant orthostatic hypotension. **Why Prazosin is the correct answer:** Prazosin is a selective **Alpha-1 blocker**. It is not recommended as first-line empirical therapy for ISH because it is associated with a high risk of **orthostatic (postural) hypotension** and "first-dose phenomenon." In elderly patients, whose baroreceptor reflexes are already blunted, this significantly increases the risk of syncope, falls, and fractures. Furthermore, the ALLHAT trial demonstrated that alpha-blockers are less effective than diuretics in preventing heart failure. **Why the other options are incorrect:** * **Chlorthalidone (Thiazide-like Diuretic):** Historically the "gold standard" for ISH. Large trials (SHEP trial) proved that low-dose thiazides significantly reduce stroke risk in the elderly. * **Amlodipine (Calcium Channel Blocker):** Long-acting DHP-CCBs are highly effective in ISH because they directly reduce peripheral vascular resistance and arterial stiffness. * **Enalapril (ACE Inhibitor):** ACE inhibitors (or ARBs) are preferred first-line agents, especially if the patient has co-morbidities like diabetes mellitus or chronic kidney disease. **High-Yield Clinical Pearls for NEET-PG:** * **First-line for ISH:** Thiazide diuretics (Chlorthalidone/Indapamide) or Long-acting DHP-CCBs (Amlodipine). * **Prazosin Indication:** Primarily used for Benign Prostatic Hyperplasia (BPH) or as add-on therapy in resistant hypertension. * **Side Effect Profile:** Always warn elderly patients about the risk of "first-dose syncope" with Alpha-blockers; advise taking the medication at bedtime.

Q: The most common cause of tricuspid regurgitation is secondary to:

Dilatation of the right ventricle. Tricuspid Regurgitation (TR) is classified into two types: **Primary (Organic)** and **Secondary (Functional)**. **Why Option B is correct:** The most common cause of TR is **Secondary (Functional) TR**, accounting for over 80% of cases [1]. It occurs not due to a primary valve defect, but because of **dilatation of the right ventricle (RV)** and the tricuspid annulus [1]. This is typically a consequence of pulmonary hypertension (secondary to left-sided heart disease), RV infarction, or cardiomyopathy [1]. The enlargement of the RV causes tethering of the valve leaflets, preventing proper coaptation. **Why other options are incorrect:** * **Option A (Rheumatic Heart Disease):** While a common cause of *primary* TR in developing countries, it rarely occurs in isolation and is almost always associated with mitral or aortic valve involvement [1]. * **Option C (Coronary Artery Disease):** While CAD can cause mitral regurgitation (via papillary muscle dysfunction), it is an uncommon cause of TR unless it leads to significant RV infarction or chronic left-sided heart failure. * **Option D (Endocarditis):** IV drug abuse is the most common cause of *isolated primary* TR, but it is far less frequent than functional TR caused by RV dilatation. **High-Yield Clinical Pearls for NEET-PG:** * **Physical Exam:** Look for a holosystolic murmur at the left lower sternal border that increases with inspiration (**Carvallo’s sign**) [1]. * **Jugular Venous Pulse (JVP):** Characterized by a prominent **'v' wave** and a steep 'y' descent [1]. * **Pulsatile Liver:** Severe TR often presents with a tender, pulsatile liver (congestive hepatomegaly) [1].

Q: A 36-year-old man presents with the sensation of a racing heart. His blood pressure is 110/70, respiratory rate 14/min, and O2 saturation 98%. ECG is shown. Carotid massage and Valsalva maneuver do not improve the heart rate. Which of the following is the initial therapy of choice?

Adenosine 6-mg rapid IV bolus. ***Adenosine 6-mg rapid IV bolus*** - **Adenosine** is the **first-line pharmacologic treatment** for supraventricular tachycardia (SVT) after failed vagal maneuvers due to its rapid onset and short half-life. - It works by blocking **AV node conduction** temporarily, breaking the re-entrant circuit in **AVNRT** or **AVRT** within seconds of administration. *Verapamil 2.5 to 5 mg IV over 1 to 2 minutes* - While **verapamil** is effective for SVT, it has a **longer half-life** and slower onset compared to adenosine, making it a second-line option. - Risk of **hypotension** and **negative inotropic effects** make it less preferred as initial therapy in hemodynamically stable patients. *Diltiazem 0.25-mg/kg IV over 2 minutes* - **Diltiazem** is another **calcium channel blocker** that can terminate SVT but has slower onset than adenosine. - Like verapamil, it carries risk of **hypotension** and **bradycardia**, making it less ideal as first-line treatment. *Digoxin 0.5 mg IV slowly* - **Digoxin** has a very **slow onset** (hours) and is not appropriate for acute SVT termination. - Its mechanism involves **vagal stimulation** and **AV node depression**, but the delayed effect makes it unsuitable for emergency SVT management.

Q: A 68-year-old male admitted to the ICU for acute exacerbation of COPD develops sudden onset of palpitations. The ECG shows irregular rhythm with varying P wave morphology and varying PR intervals. What is the most likely diagnosis?

Multifocal atrial tachycardia. ### Explanation **Multifocal Atrial Tachycardia (MAT)** is the correct diagnosis based on the classic triad of clinical and ECG findings presented: 1. **Clinical Context:** MAT is most commonly associated with severe underlying pulmonary disease, particularly **Acute Exacerbation of COPD**. It is often triggered by hypoxia, hypercapnia, or the use of theophylline/beta-agonists. 2. **ECG Criteria:** The diagnosis requires: * An irregular rhythm (irregularly irregular). * At least **three distinct P-wave morphologies** in the same lead. * Varying PR and PP intervals. * Atrial rate typically >100 bpm. #### Analysis of Incorrect Options: * **A. Atrial Fibrillation:** While also "regularly irregular," AF is characterized by the **absence of discernible P waves** (replaced by fibrillatory waves) [1]. This patient has distinct, albeit varying, P waves. * **B. Ventricular Tachycardia:** This presents as a wide-complex, regular tachycardia. The presence of P waves and an irregular rhythm makes this diagnosis unlikely. * **C. Acute Myocardial Infarction:** While MI can trigger arrhythmias, it typically presents with ST-segment and T-wave changes rather than the specific P-wave morphology variations described. #### NEET-PG High-Yield Pearls: * **Treatment Priority:** The primary treatment for MAT is **treating the underlying cause** (e.g., correcting hypoxia/COPD exacerbation). * **Pharmacotherapy:** If rate control is needed, **Verapamil (Calcium Channel Blocker)** is the drug of choice. * **Contraindication:** **Beta-blockers are generally avoided** in these patients due to the risk of worsening bronchospasm in the setting of COPD. * **Wandering Atrial Pacemaker (WAP):** If the heart rate is <100 bpm with the same P-wave criteria, the diagnosis is WAP.

Q: Which of the following statements regarding a patient with atrial fibrillation is false?

Brain imaging is not done. ### Explanation In the clinical management of a patient presenting with **Atrial Fibrillation (AF)**, the primary goals are hemodynamic stabilization, rate/リズム control, and thromboembolic risk assessment. **1. Why "Brain imaging is not done" is the correct (False) statement:** Atrial fibrillation is the leading cause of cardioembolic strokes. While not every stable AF patient requires immediate neuroimaging, it is **routinely indicated** if there is any suspicion of a Transient Ischemic Attack (TIA) or acute stroke [1]. Furthermore, in the context of initiating anticoagulation, a baseline CT/MRI may be necessary to rule out intracranial hemorrhage [1]. Therefore, stating that brain imaging is "not done" is clinically incorrect. **2. Analysis of other options:** * **Troponin I is sent:** This is a standard part of the initial workup. AF can be triggered by an acute myocardial infarction (MI), or conversely, the rapid ventricular rate in AF can cause "demand ischemia," leading to elevated Troponin levels. * **Echocardiogram is done:** This is a **mandatory** investigation [2]. A Transthoracic Echo (TTE) assesses chamber size, valvular morphology (e.g., Mitral Stenosis), and left ventricular function. A Transesophageal Echo (TEE) is the gold standard to rule out a left atrial appendage (LAA) thrombus before cardioversion [1]. **Clinical Pearls for NEET-PG:** * **CHADS₂-VASc Score:** Used to determine the need for long-term anticoagulation in non-valvular AF. * **Holiday Heart Syndrome:** AF triggered by excessive alcohol consumption. * **Treatment of Choice:** For hemodynamically unstable AF, the immediate treatment is **Synchronized DC Cardioversion**. * **Ashman Phenomenon:** A long R-R interval followed by a short R-R interval resulting in an aberrantly conducted QRS complex (usually RBBB morphology).

Question 1

Reperfusion is useful for which of the following types of myocardium?

Accepted Answer

Hibernating myocardium

Answer

Stunted myocardium

Answer

Non-ischemic viable myocardium

Answer

Mixed ischemic myocardium

Question 2

All of the following are true about Atrial Septal Defect (ASD) except?

Accepted Answer

Left atrial hypertrophy

Answer

Right atrial hypertrophy

Answer

Right ventricular hypertrophy

Answer

Pulmonary hypertension

Question 3

A 50-year-old female patient on losartan and spironolactone therapy for hypertension developed hypotension and bradycardia. The ECG taken is as shown. What is the effective treatment for her condition?

Accepted Answer

IV calcium gluconate followed by IV sodium bicarbonate

Answer

Temporary pacing via the right femoral vein

Answer

Intravenous noradrenaline or phenylephrine

Answer

300 J DC shock

Question 4

Which of the following is NOT true about Hypertrophic Obstructive Cardiomyopathy?

Accepted Answer

Beta agonists are useful.

Answer

Asymmetrical hypertrophy of the septum.

Answer

Dynamic left ventricular outflow obstruction.

Answer

Double apical impulse.

Question 5

Which of the following drugs should not be used empirically in the management of isolated systolic hypertension in the elderly?

Accepted Answer

Prazosin

Answer

Enalapril

Answer

Amlodipine

Answer

Chlorthalidone

Question 6

The most common cause of tricuspid regurgitation is secondary to:

Accepted Answer

Dilatation of the right ventricle

Answer

Rheumatic heart disease

Answer

Coronary artery disease

Answer

Endocarditis due to intravenous drug abuse

Question 7

A 36-year-old man presents with the sensation of a racing heart. His blood pressure is 110/70, respiratory rate 14/min, and O2 saturation 98%. ECG is shown. Carotid massage and Valsalva maneuver do not improve the heart rate. Which of the following is the initial therapy of choice?

Accepted Answer

Adenosine 6-mg rapid IV bolus

Answer

Verapamil 2.5 to 5 mg IV over 1 to 2 minutes

Answer

Diltiazem 0.25-mg/kg IV over 2 minutes

Answer

Digoxin 0.5 mg IV slowly

Question 8

A 68-year-old male admitted to the ICU for acute exacerbation of COPD develops sudden onset of palpitations. The ECG shows irregular rhythm with varying P wave morphology and varying PR intervals. What is the most likely diagnosis?

Accepted Answer

Multifocal atrial tachycardia

Answer

Atrial fibrillation

Answer

Ventricular tachycardia

Answer

Acute myocardial infarction

Question 9

A 16-year-old girl presents with chest pain and respiratory distress. On physical examination, she is short of breath, wheezing, and gasping for air. Cardiac auscultation reveals a prominent pansystolic murmur and a prominent third heart sound. Chest X-ray shows marked enlargement of the heart. The patient expired despite intensive supportive measures. Microscopic examination of the myocardium at autopsy discloses aggregates of mononuclear cells arranged around centrally located deposits of eosinophilic collagen. What is the appropriate diagnosis?

Accepted Answer

Rheumatic heart disease

Answer

Acute bacterial endocarditis

Answer

Subacute bacterial endocarditis

Answer

Viral myocarditis

Question 10

Which of the following statements regarding a patient with atrial fibrillation is false?

Accepted Answer

Brain imaging is not done

Answer

Troponin I is sent

Answer

Echocardiogram is done

Answer

All of the above

Cardiology — MCQs

Cardiology — MCQs

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