Cardiology — MCQs

Cardiology Indian Medical PG Practice Questions and MCQs

Question 581: Bundle of Kent is seen in which of the following conditions?

A. Brugada syndrome
B. Romano-Ward syndrome
C. Wolff-Parkinson-White syndrome (Correct Answer)
D. Jervell and Lange-Nielsen syndrome

Explanation: **Explanation:** The **Bundle of Kent** is an abnormal accessory conduction pathway between the atria and the ventricles [1]. In **Wolff-Parkinson-White (WPW) syndrome**, this bypass tract allows electrical impulses to circumvent the AV node, leading to "pre-excitation" of the ventricles [1], [3]. **Why Option C is Correct:** In WPW syndrome, the Bundle of Kent conducts impulses faster than the AV node [1]. This results in the classic ECG triad: 1. **Short PR interval** (<0.12s) due to rapid bypass of the AV node [1]. 2. **Delta wave** (slurred upstroke of the QRS) representing early ventricular activation [1]. 3. **Widened QRS complex** due to the fusion of the accessory and normal conduction pathways [1]. **Why Other Options are Incorrect:** * **Brugada Syndrome (Option A):** A genetic sodium channelopathy (SCN5A mutation) characterized by RBBB pattern and ST-elevation in V1–V3. It does not involve accessory pathways. * **Romano-Ward Syndrome (Option B):** The most common form of **Congenital Long QT Syndrome (LQTS)**. It is autosomal dominant and involves only cardiac symptoms (no deafness). * **Jervell and Lange-Nielsen Syndrome (Option D):** An autosomal recessive form of **Congenital LQTS** associated with **sensorineural deafness** [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Treatment of Choice:** Radiofrequency ablation of the accessory pathway (Bundle of Kent). * **Acute Management:** Procainamide or Ibutilide are preferred. * **Contraindication:** Avoid **ABCD** drugs (**A**denosine, **B**eta-blockers, **C**alcium channel blockers, **D**igoxin) in WPW with Atrial Fibrillation, as they block the AV node and may force all impulses through the Bundle of Kent, leading to Ventricular Fibrillation [3].

Question 582: Which type of myocardial infarction is most likely to cause fatal arrhythmias?

A. Posterior
B. Inferior (Correct Answer)
C. Anterolateral
D. Subendocardial

Explanation: **Explanation:** **Why Inferior MI is the Correct Answer:** Inferior wall myocardial infarction (MI) is most frequently associated with fatal arrhythmias, particularly **bradyarrhythmias and heart blocks**. This is due to the blood supply anatomy: in approximately 80-90% of individuals (Right Dominant circulation), the **Right Coronary Artery (RCA)** supplies the SA node (60%) and the AV node (90%). Ischemia to the RCA leads to increased vagal tone and direct nodal ischemia, resulting in sinus bradycardia, Mobitz Type I (Wenckebach) block [2], or complete heart block [3]. Additionally, inferior MIs often involve the Right Ventricle (RV infarction), which can lead to profound hypotension and life-threatening cardiogenic shock. **Analysis of Incorrect Options:** * **Posterior MI:** While it can cause arrhythmias, it is often an extension of an inferior or lateral MI. Isolated posterior MI is less common and less frequently associated with the high-grade heart blocks seen in RCA-related inferior MIs [1]. * **Anterolateral MI:** These are typically caused by LAD or LCX occlusion. While they can cause Ventricular Tachycardia (VT) or Ventricular Fibrillation (VF) due to large-scale muscle damage, they are less classically associated with the primary conduction system failures (bradyarrhythmias) that characterize the acute phase of inferior MI. * **Subendocardial MI (NSTEMI):** This involves partial-thickness ischemia [1]. While serious, the risk of immediate, fatal transmural electrical instability is generally lower compared to acute STEMIs [1]. **NEET-PG High-Yield Pearls:** * **Bezold-Jarisch Reflex:** This triad of bradycardia, hypotension, and apnea is specifically associated with Inferior MI due to the stimulation of vagal afferents in the left ventricular wall. * **Treatment Tip:** Bradycardia in Inferior MI often responds well to **Atropine** [3], whereas heart blocks in Anterior MI usually require a pacemaker. * **ECG Leads:** Look for ST-elevation in leads **II, III, and aVF**. Always check right-sided leads (V4R) to rule out concurrent RV infarction.

Question 583: A young man, previously diagnosed with congenital heart disease with a left-to-right shunt, has a very loud pansystolic murmur at the left sternal edge without any hemodynamic disturbance. What is the most likely diagnosis?

A. Atrial septal defect
B. Large ventricular septal defect (Correct Answer)
C. Small ventricular septal defect
D. Eisenmenger's syndrome

Explanation: ### Explanation The correct answer is **Large ventricular septal defect (VSD)**. **1. Why Large VSD is Correct:** A pansystolic (holosystolic) murmur at the left sternal edge is the classic auscultatory finding for a VSD. The loudness of the murmur in VSD is determined by the pressure gradient between the left and right ventricles [1]. In a **Large VSD**, there is a significant volume of blood shunting from left to right, creating a loud, turbulent murmur. While a small VSD (Roger’s disease) often produces a very loud, harsh murmur, the question specifies a "previously diagnosed" case with "no hemodynamic disturbance" in a young man, which clinically aligns with a large defect that hasn't yet progressed to pulmonary hypertension [1]. **2. Why the Other Options are Wrong:** * **Atrial Septal Defect (ASD):** ASDs do not produce a pansystolic murmur [2]. They typically present with a **fixed split S2** and a mid-systolic flow murmur over the pulmonary area due to increased stroke volume across the pulmonary valve [2]. * **Small Ventricular Septal Defect:** While these produce very loud (Maladie de Roger) pansystolic murmurs, they are usually asymptomatic and often close spontaneously. However, in the context of NEET-PG patterns, a "very loud" murmur in a known CHD patient is the hallmark of VSD turbulence. * **Eisenmenger’s Syndrome:** This occurs when pulmonary pressures exceed systemic pressures, reversing the shunt (right-to-left) [1]. As pressures equalize, the **murmur actually disappears** or softens significantly because the pressure gradient across the defect is lost [1]. **3. NEET-PG High-Yield Pearls:** * **VSD Murmur:** The smaller the hole, the louder the murmur (inverse relationship) until the defect becomes so large that pressures equalize. * **Eisenmenger Sign:** Disappearance of a previously loud murmur + Cyanosis + Loud P2. * **Most Common CHD:** VSD is the most common congenital heart disease overall. * **Location:** Most VSDs are **membranous** (70-80%) [1].

Question 584: All of the following are signs of pulmonary hypertension, except?

A. Right parasternal heave (Correct Answer)
B. Raised JVP
C. Palpable P2
D. Low volume pulse

Explanation: **Explanation:** The clinical signs of Pulmonary Hypertension (PH) are primarily derived from the effects of increased pressure in the pulmonary circuit and the subsequent strain on the right side of the heart [1]. **Why "Right Parasternal Heave" is the correct (except) option:** While a parasternal heave is a classic sign of right ventricular hypertrophy (RVH) associated with PH [1], it is technically a **left parasternal heave** [2]. The right ventricle is an anterior structure; when it hypertrophies, it lifts the left sternal border. A "right" parasternal heave is not a standard clinical finding in PH and is therefore the "except" in this list. **Analysis of other options:** * **Raised JVP:** As PH progresses, it leads to right heart failure. This causes back-pressure into the systemic venous system, manifesting as a raised Jugular Venous Pressure (JVP), often with a prominent 'a' wave due to forceful atrial contraction against a stiff RV [1]. * **Palpable P2:** High pressure in the pulmonary artery causes the pulmonary valve to close forcefully. This is felt as a palpable second heart sound (P2) in the left second intercostal space [2]. * **Low Volume Pulse:** Severe PH leads to reduced right ventricular output, which in turn decreases left-side filling (preload). This results in a low stroke volume and a low-volume peripheral pulse. **High-Yield Clinical Pearls for NEET-PG:** * **Auscultation:** Look for a loud P2 (most common sign), an ejection click, and a Graham Steell murmur (early diastolic murmur of pulmonary regurgitation). * **ECG Findings:** Right axis deviation, 'P pulmonale' (tall peaked P waves), and RVH patterns (R/S ratio >1 in V1) [1]. * **Gold Standard Investigation:** Right heart catheterization (Mean Pulmonary Artery Pressure >20 mmHg at rest).

Question 585: Renal artery stenosis may occur in all of the following except?

A. Atherosclerosis
B. Fibromuscular dysplasia
C. Takayasu's arteritis
D. Pelvic inflammatory disease (Correct Answer)

Explanation: Renal Artery Stenosis (RAS) is a condition characterized by the narrowing of one or both renal arteries, leading to secondary hypertension (Renovascular Hypertension) and potentially chronic kidney disease. **Why Option D is Correct:** **Pelvic Inflammatory Disease (PID)** is an infection of the female upper reproductive tract (uterus, fallopian tubes, and ovaries), typically caused by *Chlamydia trachomatis* or *Neisseria gonorrhoeae*. It is a localized inflammatory process within the pelvic cavity and has no anatomical or pathological association with the renal arteries. **Why Other Options are Incorrect:** * **A. Atherosclerosis:** This is the **most common cause** of RAS (approx. 90%), typically affecting the ostium or proximal third of the renal artery. It is most common in elderly males with cardiovascular risk factors. * **B. Fibromuscular Dysplasia (FMD):** This is the second most common cause, typically seen in **young females**. It involves non-inflammatory, non-atherosclerotic thickening of the arterial wall, often presenting with a "string of beads" appearance on angiography. * **C. Takayasu’s Arteritis:** Also known as "Pulseless Disease," this is a large-vessel vasculitis that commonly involves the aorta and its primary branches, including the renal arteries, leading to stenosis. **NEET-PG High-Yield Pearls:** * **Clinical Clue:** Suspect RAS if there is a sudden worsening of hypertension or an **unexplained rise in serum creatinine (>30%)** after starting an ACE inhibitor or ARB. [1] * **Gold Standard Investigation:** Digital Subtraction Angiography (DSA). * **Screening Test of Choice:** Duplex Doppler Ultrasound or CT/MR Angiography. [1] * **Auscultation:** A systolic-diastolic epigastric bruit is highly suggestive of RAS.

Question 586: The Stanford classification is used to represent which of the following?

A. Aortic rupture
B. Aortic dissection (Correct Answer)
C. Intramural hematoma
D. Penetrating atherosclerotic ulcer

Explanation: **Explanation:** The **Stanford classification** is the most widely used system for categorizing **Aortic Dissection**, based on the anatomical involvement of the aorta [1]. It is crucial for determining management strategies: * **Stanford Type A:** Involves the **ascending aorta** (regardless of where the original tear started). These are surgical emergencies due to the risk of complications like aortic regurgitation, cardiac tamponade, or coronary artery occlusion [1]. * **Stanford Type B:** Involves only the **descending aorta** (distal to the left subclavian artery). These are typically managed medically with aggressive blood pressure control (e.g., IV Labetalol) unless complications arise [1], [2]. **Analysis of Incorrect Options:** * **Aortic Rupture (A):** This is a catastrophic complication of an aneurysm or trauma where all layers of the aortic wall are breached. It is not classified by the Stanford system [1]. * **Intramural Hematoma (C) & Penetrating Atherosclerotic Ulcer (D):** Along with aortic dissection, these are part of the **Acute Aortic Syndrome** spectrum. While they may be managed similarly to dissections, the Stanford classification specifically describes the longitudinal cleavage of the aortic media (dissection). **High-Yield Clinical Pearls for NEET-PG:** * **DeBakey Classification:** Another system for dissection. **Type I** (Ascending + Descending), **Type II** (Ascending only), and **Type III** (Descending only). * **Gold Standard Investigation:** CT Angiography (CTA) is the investigation of choice [2]. * **Classic Presentation:** Sudden onset "tearing" or "ripping" chest pain radiating to the back [1]. * **Physical Exam:** Look for pulse deficit or blood pressure discrepancy between arms.

Question 587: Reperfusion is useful for which of the following types of myocardium?

A. Stunted myocardium
B. Hibernating myocardium (Correct Answer)
C. Non-ischemic viable myocardium
D. Mixed ischemic myocardium

Explanation: ### Explanation The correct answer is **Hibernating Myocardium**. **1. Why Hibernating Myocardium is correct:** Hibernating myocardium refers to a state of **chronic but reversible** left ventricular dysfunction due to persistent reduced coronary blood flow (chronic ischemia). In this state, the myocytes remain viable but "downregulate" their contractility to match the low oxygen supply, preventing irreversible necrosis [1]. Because the tissue is viable but under-perfused, **revascularization (reperfusion)** via PCI or CABG restores blood flow, allowing the myocardium to recover its contractile function over weeks to months [2]. **2. Why the other options are incorrect:** * **Stunned Myocardium:** This is a state of temporary contractile dysfunction that persists *after* blood flow has already been restored (e.g., after a successful thrombolysis or exercise-induced ischemia). Since the tissue is already reperfused, "further" reperfusion is not the treatment; it simply requires time to recover. * **Non-ischemic viable myocardium:** This refers to healthy, normal heart muscle. While it is viable, it does not have a perfusion deficit, so reperfusion therapy offers no therapeutic benefit to its function. * **Mixed ischemic myocardium:** This is a non-specific clinical term. While it may contain areas of hibernation, the standard physiological definition for recovery post-reperfusion specifically targets hibernating tissue. **Clinical Pearls for NEET-PG:** * **Gold Standard for Detection:** PET scan (showing F-18 FDG uptake) is the gold standard to detect myocardial viability. * **Stunned vs. Hibernating:** Remember, **Stunned** = Flow is normal, function is low (post-ischemic). **Hibernating** = Flow is low, function is low (chronic ischemia). * **Contractile Reserve:** Both stunned and hibernating myocardium show improvement in contraction with low-dose **Dobutamine** (Dobutamine Stress Echocardiography). **Reperfusion therapy:** Reperfusion therapy is used to restore the patency of coronary arteries following thrombosis, and if administered early enough (before irreversible damage), it can significantly reduce mortality from myocardial damage [2].

Question 588: All of the following are true about Atrial Septal Defect (ASD) except?

A. Right atrial hypertrophy
B. Left atrial hypertrophy (Correct Answer)
C. Right ventricular hypertrophy
D. Pulmonary hypertension

Explanation: ### 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.

Question 589: 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?

A. Temporary pacing via the right femoral vein
B. Intravenous noradrenaline or phenylephrine
C. IV calcium gluconate followed by IV sodium bicarbonate (Correct Answer)
D. 300 J DC shock

Explanation: ***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**.

Question 590: Pulsus alternans is seen in which of the following conditions?

A. Severe ventricular dysfunction (Correct Answer)
B. Hypertrophic obstructive cardiomyopathy (HOCM)
C. Aortic stenosis (AS)
D. Coarctation of the aorta (CoA)

Explanation: **Explanation:** **Pulsus alternans** is a clinical sign characterized by a regular rhythm but with alternating strong and weak pulses. This occurs due to an alternation in stroke volume during each cardiac cycle. **1. Why Severe Ventricular Dysfunction is Correct:** The underlying mechanism is a beat-to-beat variation in the left ventricular (LV) end-diastolic volume and contractility [1]. In a failing heart (**Severe LV Dysfunction/Congestive Heart Failure**), a weak contraction leads to a higher residual volume left in the ventricle [2]. This increased "preload" for the next beat, combined with a longer recovery time for the myocytes (Frank-Starling mechanism), results in a stronger subsequent contraction. This cycle repeats, creating the alternating pulse strength. **2. Analysis of Incorrect Options:** * **HOCM (B):** Typically associated with **Pulsus Bisferiens** (a double-peaked systolic pulse). * **Aortic Stenosis (C):** Characterized by **Pulsus Parvus et Tardus** (a small-amplitude, slow-rising pulse). * **Coarctation of the Aorta (D):** Characterized by **Radio-femoral delay** and diminished pulses in the lower extremities compared to the upper extremities. **3. High-Yield Clinical Pearls for NEET-PG:** * **Best way to detect:** Pulsus alternans is best elicited by applying light pressure on the peripheral arteries (e.g., radial or femoral) or by using a sphygmomanometer (noting a 10–20 mmHg difference in systolic pressure between beats). * **Differentiating Factor:** Unlike *Pulsus Bigeminus* (which also has alternating strengths), Pulsus alternans has a **regular rhythm**. * **Clinical Significance:** It is a grave prognostic sign indicating advanced myocardial failure [2]. * **Electrical Alternans:** If seen on an ECG (alternating QRS amplitude), it is a classic sign of **Cardiac Tamponade** [3].

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Cardiology — MCQs

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