Cardiology Practice Questions

Q: Which of the following is NOT associated with coarctation of the aorta?

Renal artery stenosis. Explanation: Coarctation of the aorta is a congenital narrowing of the aortic lumen, typically occurring near the insertion of the ductus arteriosus. **Why Renal Artery Stenosis is the correct answer:** Renal artery stenosis is **not** an associated congenital anomaly of coarctation. While both conditions cause secondary hypertension, they are distinct pathological entities. In coarctation, hypertension occurs due to mechanical obstruction and subsequent activation of the Renin-Angiotensin-Aldosterone System (RAAS) because of reduced renal perfusion *downstream* of the narrowing, not because of a stenosed renal artery itself. **Analysis of incorrect options:** * **Patent Ductus Arteriosus (PDA):** This is frequently associated with the "pre-ductal" (infantile) type of coarctation [1]. * **Bicuspid Aortic Valve:** This is the **most common** associated cardiac anomaly, occurring in up to 50-85% of patients with coarctation. * **Turner’s Syndrome (45, XO):** Approximately 15-20% of females with Turner’s syndrome have coarctation of the aorta [1]. It is a classic association frequently tested in exams. **NEET-PG High-Yield Pearls:** * **Clinical Sign:** Radio-femoral delay and a blood pressure upper limb > lower limb (>20 mmHg difference) [1]. * **X-ray Findings:** "Rib notching" (due to dilated intercostal collaterals) and the "Figure of 3" sign on barium swallow or CXR. * **Associated Risk:** Increased incidence of **Berry aneurysms** (Circle of Willis), which can lead to subarachnoid hemorrhage. Coarctation is also a predisposing factor for aortic dissection [2]. * **Murmur:** Midsystolic murmur heard best over the left back (interscapular area).

Q: Accelerated Idioventricular Rhythm (AIVR) is the most common arrhythmia associated with:

Myocardial Reperfusion. **Explanation:** **Accelerated Idioventricular Rhythm (AIVR)**, also known as "slow ventricular tachycardia," is a ventricular rhythm with a rate typically between 60 and 110 beats per minute. **1. Why Myocardial Reperfusion is Correct:** AIVR is the most characteristic arrhythmia seen following the restoration of blood flow to an ischemic myocardium (reperfusion). It is frequently observed after successful thrombolysis or Primary Percutaneous Coronary Intervention (PCI) in patients with acute MI. The underlying mechanism is increased automaticity of the Purkinje fibers, triggered by free radical release and calcium overload during the reperfusion phase. It is generally considered a **benign, self-limiting sign** of successful reperfusion and rarely requires treatment [1]. **2. Analysis of Incorrect Options:** * **A. Dilated Cardiomyopathy:** While patients with DCM are prone to various arrhythmias (like PVCs, VT, or AFib) due to structural remodeling, AIVR is not the most common or characteristic finding. * **C. Digitalis Intoxication:** Digoxin toxicity typically presents with increased automaticity and decreased conduction. Common arrhythmias include PVCs (most common), Bidirectional VT, and Paroxysmal Atrial Tachycardia with AV block. * **D. Myocarditis:** This usually presents with sinus tachycardia, non-specific ST-T changes, or various degrees of heart block, but AIVR is not the primary association. **3. NEET-PG High-Yield Pearls:** * **Rate:** 60–110 bpm (distinguishes it from Ventricular Escape Rhythm 120 bpm). * **ECG Features:** Wide QRS complexes, regular rhythm, and frequent "fusion beats" or "capture beats" at the onset/offset. * **Clinical Significance:** In the setting of MI, it is a **"Reperfusion Arrhythmia."** [1]. * **Management:** Observation only. Do not suppress with anti-arrhythmics (like Lidocaine), as it may lead to asystole by suppressing the only functioning pacemaker.

Q: Which of the following conditions is associated with a giant 'a' wave in the jugular venous pressure?

Tricuspid stenosis. ### Explanation The **'a' wave** in the jugular venous pulse (JVP) represents **right atrial contraction**. It occurs at the end of diastole, forcing the final volume of blood into the right ventricle. **1. Why Tricuspid Stenosis is Correct:** In **Tricuspid Stenosis**, there is a mechanical obstruction to blood flow from the right atrium (RA) to the right ventricle (RV). To overcome this resistance and fill the ventricle, the RA must contract more forcefully. This increased pressure during atrial systole is reflected back into the jugular vein as a **giant (prominent) 'a' wave**. Other conditions causing giant 'a' waves include Pulmonary Stenosis and Pulmonary Hypertension (due to decreased RV compliance). **2. Analysis of Incorrect Options:** * **Atrial Septal Defect (ASD):** Typically presents with a large 'a' wave only if there is associated pulmonary hypertension. Classically, ASD is associated with a **prominent 'v' wave** or equalized 'a' and 'v' waves due to the large volume shunting into the RA [1]. * **SVC Obstruction:** In this condition, the JVP is **non-pulsatile**. The physical obstruction prevents the transmission of atrial pressure changes to the internal jugular vein. * **Complete Heart Block:** This is associated with **"Cannon" 'a' waves**. These occur sporadically when the RA contracts against a closed tricuspid valve (AV dissociation). Unlike the "giant" 'a' waves of stenosis, cannon waves are intermittent and much more dramatic. **3. High-Yield Clinical Pearls for NEET-PG:** * **Absent 'a' wave:** Atrial Fibrillation (no coordinated atrial contraction). * **Giant 'a' wave:** Tricuspid Stenosis, Pulmonary Stenosis, Right Heart Failure. * **Cannon 'a' wave:** Complete Heart Block, Ventricular Tachycardia, Junctional Rhythms. * **Prominent 'v' wave:** Tricuspid Regurgitation (Lancisi’s sign) [2]. * **Steep 'y' descent:** Constrictive Pericarditis (Friedreich’s sign) and Tricuspid Regurgitation.

Q: A patient presents with a new systolic murmur in the left lower sternum following a myocardial infarction. Which of the following is the LEAST likely cause?

Complete heart block. ### Explanation The correct answer is **A. Complete heart block**. **Why it is the LEAST likely cause:** Complete heart block (CHB) is a conduction abnormality, not a structural mechanical defect. While CHB is a known complication of myocardial infarction (especially inferior wall MI), it typically presents with **bradycardia and cannon 'a' waves** in the jugular venous pulse, rather than a new systolic murmur. A systolic murmur indicates turbulent blood flow during ventricular contraction, which is not a characteristic feature of an isolated conduction block. **Analysis of Incorrect Options:** * **B. Rupture of the interventricular septum (VSD):** This is a classic post-MI mechanical complication (usually 3–5 days post-MI). It produces a harsh, pansystolic murmur loudest at the **left lower sternal border**, often accompanied by a palpable thrill. * **C. Papillary muscle dysfunction:** Ischemia or rupture of the papillary muscles leads to **Mitral Regurgitation (MR)**. This presents as a systolic murmur, typically loudest at the apex but often radiating to the axilla or heard along the left sternal border. * **D. Ischemic cardiomyopathy:** Severe ischemia can lead to ventricular dilatation. This dilatation stretches the mitral valve annulus, resulting in **functional mitral regurgitation**, which manifests as a systolic murmur. **NEET-PG High-Yield Pearls:** * **VSD vs. MR:** Both present with post-MI systolic murmurs. If the murmur is at the **left sternal border with a thrill**, think VSD. If it is at the **apex radiating to the axilla**, think Papillary Muscle Rupture. * **Right Heart Catheterization:** In VSD, there is a **"step-up" in oxygen saturation** from the right atrium to the right ventricle. * **Timing:** Most mechanical complications (Septal rupture, Papillary rupture, Free wall rupture) occur within **3 to 7 days** post-MI.

Q: Carey Coombs murmur is seen in:

Acute rheumatic carditis. ### Explanation **Correct Answer: B. Acute rheumatic carditis** The **Carey Coombs murmur** is a classic clinical sign of **acute rheumatic fever** involving the endocardium (valvulitis) [1]. It is a short, mid-diastolic murmur heard best at the apex. **Pathophysiology:** During the acute phase of rheumatic carditis, the mitral valve leaflets become inflamed and edematous. This swelling, often accompanied by small verrucae along the closure lines, creates a functional narrowing of the mitral orifice [1]. As blood flows from the left atrium to the left ventricle during the rapid filling phase of diastole, the relative stenosis causes turbulence, resulting in the murmur. Unlike permanent mitral stenosis, this murmur is **transient** and disappears as the acute inflammation subsides. **Analysis of Incorrect Options:** * **A. Severe mitral stenosis:** This presents with a long, rumbling mid-diastolic murmur with **presystolic accentuation** and is preceded by an **opening snap**. Carey Coombs lacks both the opening snap and the presystolic accentuation. * **C. Pure aortic regurgitation:** This is associated with the **Austin Flint murmur**, a mid-diastolic murmur caused by the regurgitant jet from the aorta striking the anterior leaflet of the mitral valve, causing it to vibrate and partially obstruct inflow [2]. * **D. Severe pulmonary hypertension:** This is associated with the **Graham Steell murmur**, which is a high-pitched, decrescendo early diastolic murmur heard at the left sternal border due to functional pulmonary regurgitation. **High-Yield Clinical Pearls for NEET-PG:** * **Carey Coombs vs. Mitral Stenosis:** Carey Coombs is soft, lacks an opening snap, and is evanescent (temporary). * **Jones Criteria:** Carditis is a major criterion for the diagnosis of Acute Rheumatic Fever [1]. * **Auscultation Tip:** The murmur is best heard with the bell of the stethoscope at the apex in the left lateral decubitus position.

Q: Cardiac tamponade is characterized by all of the following except:

Irregular pulse. Cardiac tamponade is a life-threatening condition caused by the accumulation of fluid in the pericardial space, leading to increased intrapericardial pressure and impaired diastolic filling of the heart [1]. ### **Explanation of Options** * **A. Irregular pulse (Correct Answer):** Cardiac tamponade typically presents with a **regular tachycardia** as a compensatory mechanism to maintain cardiac output in the face of low stroke volume. An irregular pulse is not a characteristic feature; it is more commonly associated with conditions like atrial fibrillation or premature beats. * **B. Hypotension:** This is a hallmark of tamponade. Increased intrapericardial pressure prevents the heart from filling, leading to decreased stroke volume and a subsequent drop in systemic blood pressure [1]. * **C. Reduced pulse pressure:** As stroke volume falls, the systolic blood pressure drops significantly while diastolic pressure is maintained by compensatory peripheral vasoconstriction, leading to a "narrow" or reduced pulse pressure [2]. * **D. Pulsus paradoxus:** This is a classic sign defined as an exaggerated drop in systolic blood pressure (>10 mmHg) during inspiration. In tamponade, the rigid pericardium causes the interventricular septum to bulge into the left ventricle during inspiration (ventricular interdependence), further reducing left-sided filling and output. ### **High-Yield Clinical Pearls for NEET-PG** * **Beck’s Triad:** Hypotension, Jugular Venous Distension (JVD), and Muffled Heart Sounds. * **ECG Findings:** Low voltage QRS complexes and **Electrical Alternans** (beat-to-beat variation in QRS amplitude due to the heart "swinging" in fluid) [1]. * **JVP Pattern:** Characterized by a **prominent 'x' descent** and an **absent 'y' descent** (due to restricted diastolic filling). * **Treatment:** Immediate **pericardiocentesis** is the definitive management [1].

Q: Which of the following statements is not true about Brugada syndrome?

A pacemaker is considered the treatment of choice.. ### Explanation **Brugada Syndrome** is an autosomal dominant genetic arrhythmia syndrome characterized by a specific ECG pattern and an increased risk of sudden cardiac death (SCD) in the absence of structural heart disease. **Why Option D is the correct (False) statement:** The treatment of choice for symptomatic Brugada syndrome or those at high risk for SCD is an **Implantable Cardioverter Defibrillator (ICD)**, not a pacemaker. While pacemakers manage bradyarrhythmias, they cannot terminate the polymorphic ventricular tachycardia or ventricular fibrillation (VF) that causes death in these patients. **Analysis of other options:** * **Option A:** It is primarily a "sodium channelopathy." Approximately 20–30% of cases are linked to a mutation in the **SCN5A gene**, which encodes the alpha subunit of the cardiac sodium channel. * **Option B:** The syndrome is characterized by a "pseudo-right bundle branch block" and **ST-segment elevation in leads V1–V3**. Many patients remain asymptomatic until a lethal arrhythmic event occurs, often during sleep or fever. * **Option C:** It is a leading cause of **Sudden Cardiac Death** in young males, particularly those of Southeast Asian descent (where it is sometimes called *Lai Tai* or *Bangungut*). **High-Yield Clinical Pearls for NEET-PG:** 1. **ECG Pattern (Type 1):** "Coved-type" ST elevation ≥2mm followed by a negative T-wave in V1-V3. 2. **Triggers:** Fever, alcohol, and certain drugs (e.g., Class IA/IC antiarrhythmics, TCAs) can unmask the ECG pattern. 3. **Provocative Testing:** If the ECG is equivocal, sodium channel blockers like **Ajmaline** or **Procainamide** are used to unmask the pattern. 4. **Pharmacotherapy:** **Quinidine** (an Ito channel blocker) may be used as adjunctive therapy or in patients where an ICD is not feasible.

Q: A 56-year-old female presents with severe chest pain and breathlessness after coming back from cremation grounds due to the death of her husband. ECG shows ST elevation in the precordial leads, most noticeably in V2-V3. Troponin T and BNP are mildly elevated. Invasive coronary angiography shows completely normal coronary arteries. A transthoracic echocardiogram demonstrates apical akinesis and a left ventricular ejection fraction of 40%. What is the most likely diagnosis?

Takotsubo cardiomyopathy. **Explanation:** The clinical presentation is a classic description of **Takotsubo Cardiomyopathy**, also known as "Broken Heart Syndrome" or "Stress-induced Cardiomyopathy." **1. Why Takotsubo Cardiomyopathy is correct:** This condition typically affects postmenopausal women following an intense emotional or physical stressor (e.g., the death of a spouse) [2]. The pathophysiology involves a **catecholamine surge** leading to microvascular dysfunction or direct myocardial toxicity. Key diagnostic features present in this case include: * **ECG changes:** ST-segment elevation (mimicking an anterior MI). * **Biomarkers:** Mild elevation of Troponins and BNP. * **Angiography:** Absence of obstructive coronary artery disease. * **Echocardiography:** Characteristic **apical ballooning** (apical akinesis with basal hyperkinesis), giving the heart the shape of a Japanese octopus trap (*Takotsubo*). **2. Why other options are incorrect:** * **Anxiety:** While the patient is stressed, anxiety alone cannot explain the ST elevation, elevated troponins, or regional wall motion abnormalities [2]. * **Septal Myocardial Infarction:** Although the ECG mimics an MI, the **normal coronary arteries** on angiography rule out obstructive atherosclerotic infarction [1]. * **Coronary Artery Spasm (Prinzmetal Angina):** While it can cause ST elevation and normal coronaries, it typically presents as transient pain at rest and does not characteristically cause the specific apical ballooning pattern seen on echo. **Clinical Pearls for NEET-PG:** * **Demographics:** Most common in postmenopausal females (>90%). * **Diagnosis:** Requires the **Mayo Clinic Diagnostic Criteria**. * **Prognosis:** Generally excellent; LV function usually recovers within 1–4 weeks with supportive care (ACE inhibitors, Beta-blockers). * **Complication:** Left ventricular outflow tract (LVOT) obstruction can occur due to basal hypercontractility.

Question 1

Which of the following is NOT associated with coarctation of the aorta?

Accepted Answer

Renal artery stenosis

Answer

Patent ductus arteriosus

Answer

Bicuspid aortic valve

Answer

Turner's syndrome

Question 2

Which of the following deficiencies does not cause dilated cardiomyopathy?

Accepted Answer

Manganese

Answer

Calcium

Answer

Selenium

Answer

Carnitine

Question 3

True about coarctation of the aorta?

Accepted Answer

Most common site is distal to the origin of the left subclavian artery

Answer

Most common age of presentation is at 15-20 years

Answer

Upper rib notching is due to erosion by dilated collateral vessels

Answer

Right ventricular hypertrophy

Question 4

Accelerated Idioventricular Rhythm (AIVR) is the most common arrhythmia associated with:

Accepted Answer

Myocardial Reperfusion

Answer

Dilated cardiomyopathy

Answer

Digitalis intoxication

Answer

Myocarditis

Question 5

Which of the following conditions is associated with a giant 'a' wave in the jugular venous pressure?

Accepted Answer

Tricuspid stenosis

Answer

Atrial Septal Defect (ASD)

Answer

Superior Vena Cava (SVC) obstruction

Answer

Complete heart block

Question 6

A patient presents with a new systolic murmur in the left lower sternum following a myocardial infarction. Which of the following is the LEAST likely cause?

Accepted Answer

Complete heart block

Answer

Rupture of the interventricular septum

Answer

Papillary muscle dysfunction

Answer

Ischemic cardiomyopathy

Question 7

Carey Coombs murmur is seen in:

Accepted Answer

Acute rheumatic carditis

Answer

Severe mitral stenosis

Answer

Pure aortic regurgitation

Answer

Severe pulmonary hypertension

Question 8

Cardiac tamponade is characterized by all of the following except:

Accepted Answer

Irregular pulse

Answer

Hypotension

Answer

Reduced pulse pressure

Answer

Pulsus paradoxus

Question 9

Which of the following statements is not true about Brugada syndrome?

Accepted Answer

A pacemaker is considered the treatment of choice.

Answer

It is associated with a defect in the SCN5A gene.

Answer

It is characterized by asymptomatic ST segment elevation.

Answer

It can lead to sudden cardiac death.

Question 10

A 56-year-old female presents with severe chest pain and breathlessness after coming back from cremation grounds due to the death of her husband. ECG shows ST elevation in the precordial leads, most noticeably in V2-V3. Troponin T and BNP are mildly elevated. Invasive coronary angiography shows completely normal coronary arteries. A transthoracic echocardiogram demonstrates apical akinesis and a left ventricular ejection fraction of 40%. What is the most likely diagnosis?

Accepted Answer

Takotsubo cardiomyopathy

Answer

Anxiety

Answer

Septal myocardial infarction

Answer

Coronary artery spasm

Cardiology — MCQs

Cardiology — MCQs

On this page

Practice by Chapter

Want unlimited practice?