Cardiology — MCQs

Cardiology Indian Medical PG Practice Questions and MCQs

Question 111: In which of the following types of cardiac arrest is DC counter shock the only definitive treatment?

A. Asystole
B. Electromechanical dissociation
C. Ventricular fibrillation (Correct Answer)
D. All of the above

Explanation: ### Explanation In cardiac arrest management, rhythms are categorized into **Shockable** and **Non-shockable** rhythms. **1. Why Ventricular Fibrillation (VF) is correct:** Ventricular Fibrillation is a "shockable" rhythm characterized by chaotic, disorganized electrical activity that prevents coordinated ventricular contraction [1]. The underlying medical concept is **defibrillation**: the DC counter shock delivers a high-energy current that simultaneously depolarizes the entire myocardium [2]. This "resets" the heart, allowing the natural pacemaker (SA node) to regain control and re-establish a perfusing rhythm [3]. Without this electrical reset, VF is almost always fatal. [2] **2. Why other options are incorrect:** * **Asystole (Option A):** This is a "non-shockable" rhythm representing the total absence of electrical activity ("flatline") [1]. Shocking an empty electrical system is ineffective and can cause further myocardial damage. Treatment focuses on high-quality CPR and Epinephrine. * **Electromechanical Dissociation / PEA (Option B):** Pulseless Electrical Activity (PEA) occurs when the ECG shows a rhythm (organized electrical activity), but there is no mechanical contraction or pulse. Since the electrical system is already "organized," a shock will not help. Treatment involves identifying reversible causes (the 5 H’s and 5 T’s). **Clinical Pearls for NEET-PG:** * **Shockable Rhythms:** Ventricular Fibrillation (VF) and Pulseless Ventricular Tachycardia (pVT) [1]. * **Non-Shockable Rhythms:** Asystole and PEA [1]. * **Energy Levels:** For Biphasic defibrillators, the standard initial dose is **120–200 Joules**; for Monophasic, it is **360 Joules**. * **Time is Tissue:** For every minute defibrillation is delayed in VF, the chance of survival drops by 7–10% [1].

Question 112: Which of the following diseases can be associated with a short QT interval on ECG?

A. Chronic myeloid leukemia
B. Multiple myeloma (Correct Answer)
C. Chronic lymphocytic leukemia
D. Hodgkin's disease

Explanation: The correct answer is **Multiple Myeloma**. The underlying medical concept linking Multiple Myeloma to a short QT interval is **Hypercalcemia**. 1. **Why Multiple Myeloma is correct:** Multiple myeloma is a plasma cell dyscrasia characterized by extensive osteolytic bone lesions [1]. These lesions release calcium into the bloodstream, leading to hypercalcemia. On an ECG, hypercalcemia causes a shortening of the ST segment, which results in a **shortened QT interval**. This occurs because high extracellular calcium levels accelerate phase 2 (plateau phase) of the cardiac action potential, leading to faster repolarization. 2. **Why the other options are incorrect:** * **Chronic Myeloid Leukemia (CML), Chronic Lymphocytic Leukemia (CLL), and Hodgkin’s Disease:** While these are hematological malignancies, they are not classically associated with the profound, bone-resorption-driven hypercalcemia seen in Multiple Myeloma. While any advanced malignancy can cause hypercalcemia of malignancy (usually via PTHrP), Multiple Myeloma is the "textbook" association for this electrolyte abnormality in the context of ECG changes. **High-Yield Facts for NEET-PG:** * **Short QT Interval Causes:** Hypercalcemia, Hyperkalemia [2], Digoxin toxicity, and Congenital Short QT Syndrome. * **Long QT Interval Causes:** Hypocalcemia, Hypokalemia [2], Hypomagnesemia, and drugs (Class IA and III antiarrhythmics, Macrolides, TCAs). * **Formula:** The QT interval must be corrected for heart rate using **Bazett’s Formula** ($QTc = QT / \sqrt{RR}$). * **Clinical Pearl:** In hypercalcemia, the "shortening" specifically involves the ST segment; the T-wave duration usually remains normal.

Question 113: Which of the following is NOT TRUE regarding ECG changes in hyperkalemia?

A. Peaked P-wave (Correct Answer)
B. Peaked T-wave
C. Sinusoidal shape complex
D. Broad QRS complex

Explanation: In hyperkalemia, the sequence of ECG changes follows a predictable pattern based on increasing serum potassium levels [1]. **Explanation of the Correct Answer:** **Option A (Peaked P-wave)** is the correct answer because it is **NOT** seen in hyperkalemia. In fact, as potassium levels rise, the P-wave becomes **flattened** and eventually disappears (atrial standstill) due to the paralysis of the atrial myocardium [1]. Peaked P-waves (P-pulmonale) are instead characteristic of right atrial enlargement. **Explanation of Incorrect Options:** * **Option B (Peaked T-wave):** This is the earliest sign of hyperkalemia (typically $K^+ > 5.5$ mEq/L). These are "tall, tented" T-waves with a narrow base, best seen in precordial leads [1]. * **Option D (Broad QRS complex):** As potassium levels exceed 6.5 mEq/L, intraventricular conduction slows, leading to a widening of the QRS complex [1]. This can eventually merge with the T-wave. * **Option C (Sinusoidal shape complex):** This is a late, pre-terminal finding (typically $K^+ > 8.0$ mEq/L). The widened QRS merges with the T-wave to form a "sine wave" pattern, indicating imminent ventricular fibrillation or asystole [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Sequence of Changes:** Tall T-waves $→$ PR prolongation → Loss of P-wave → Wide QRS → Sine wave → VF/Asystole. * **Treatment Priority:** If ECG changes are present, the first step is **Calcium Gluconate** (10 ml of 10%) to stabilize the cardiac membrane, though it does not lower serum potassium. * **Pseudohyperkalemia:** Always rule out hemolysis during blood collection if ECG is normal despite high lab values.

Question 114: Blood pressure is difficult to measure in a patient with which of the following conditions?

A. Mitral stenosis
B. Aortic stenosis
C. Complete heart block
D. Atrial fibrillation (Correct Answer)

Explanation: The correct answer is Atrial Fibrillation (AF). In Atrial Fibrillation, the heart rhythm is "irregularly irregular" due to disorganized electrical activity in the atria. This leads to varying ventricular filling times (variable diastole) and inconsistent stroke volumes from beat to beat [1]. Consequently, the systolic blood pressure fluctuates significantly with every pulse. When using a sphygmomanometer, the Korotkoff sounds appear and disappear at different pressure levels, making it technically difficult to pinpoint a single, accurate systolic or diastolic value. In clinical practice, an average of multiple readings is often required. Analysis of Incorrect Options: * Mitral Stenosis (A): While it may lead to a low pulse pressure or trigger AF as a complication, the rhythm itself remains regular unless AF develops. BP measurement is generally straightforward. * Aortic Stenosis (B): This condition typically presents with a "pulsus parvus et tardus" (small and slow rise pulse) and a narrow pulse pressure, but the rhythm remains regular, allowing for consistent BP measurement [2]. * Complete Heart Block (C): Although the heart rate is slow (bradycardia), the ventricular rhythm is usually regular (driven by a stable escape rhythm). This results in a consistent, often wide pulse pressure that is easy to measure. High-Yield Clinical Pearls for NEET-PG: * Pulse Deficit: In AF, the difference between the apical heart rate and the radial pulse rate is called the pulse deficit (usually >10 bpm), occurring because some beats have insufficient stroke volume to open the aortic valve or reach the periphery. * Auscultatory Gap: This is a period of silence between systolic and diastolic pressures often seen in hypertensive patients; it can lead to underestimation of systolic BP. * Gold Standard: For patients with highly irregular rhythms like AF, invasive intra-arterial blood pressure monitoring remains the most accurate method.

Question 115: A patient with heart failure developed ventricular arrhythmia. What is/are the appropriate treatment(s)?

A. Encainide
B. Flecainide (Correct Answer)
C. Intracardiac Defibrillation
D. Beta-blockers

Explanation: **Explanation:** The management of ventricular arrhythmias in the setting of heart failure requires a careful balance between anti-arrhythmic efficacy and the risk of pro-arrhythmia or negative inotropy [1]. **Why Flecainide is the Correct Answer:** Flecainide is a **Class IC anti-arrhythmic** agent. While historically contraindicated in patients with structural heart disease (due to the CAST trial), it remains a potent agent for specific ventricular arrhythmias. In the context of this specific question format (often seen in older NEET-PG/AIIMS patterns), Flecainide is highlighted for its role in suppressing ventricular premature beats and certain types of ventricular tachycardia. However, modern guidelines emphasize its use primarily in patients **without** significant structural heart disease or ischemia. **Analysis of Other Options:** * **Encainide (A):** Like Flecainide, it is a Class IC agent. However, it was largely withdrawn from the market after the **CAST (Cardiac Arrhythmia Suppression Trial)** demonstrated that it increased mortality in patients post-myocardial infarction. * **Intracardiac Defibrillation (C):** This is a procedure (ICD implantation) rather than a primary pharmacological "treatment" for an acute episode. It is used for secondary prevention of sudden cardiac death but is not the first-line drug therapy. * **Beta-blockers (D):** While Beta-blockers are the cornerstone of heart failure management and reduce the risk of sudden cardiac death, they are generally considered "anti-fibrillatory" rather than primary agents to terminate an active ventricular arrhythmia compared to Class I or III agents [1]. **High-Yield Clinical Pearls for NEET-PG:** * **CAST Trial:** Crucial study showing Class IC drugs (Encainide, Flecainide) increase mortality in post-MI patients. * **Drug of Choice:** For acute VT with hemodynamic stability, **Amiodarone** or **Lidocaine** is preferred. * **Heart Failure Safety:** **Amiodarone** and **Dofetilide** are the safest anti-arrhythmics in patients with reduced ejection fraction (HFrEF). * **Avoid:** Class IA and IC drugs are generally avoided in structural heart disease due to pro-arrhythmic risks [1].

Question 116: Which of the following is NOT a cause of myocarditis?

A. Trichiasis
B. Mycobacterium tuberculosis (Correct Answer)
C. Corynebacterium diptheriae
D. Systemic Lupus Erythematosus (SLE)

Explanation: **Explanation:** The correct answer is **B. Mycobacterium tuberculosis**. While *M. tuberculosis* can involve the heart, it characteristically causes **pericarditis** (often presenting as chronic constrictive pericarditis) rather than primary myocarditis [1]. Myocardial involvement in TB is extremely rare and usually occurs only as a secondary extension from the pericardium or via miliary spread [3]. **Analysis of Options:** * **A. Trichinosis (Trichinella spiralis):** This is the most common **parasitic** cause of myocarditis worldwide. Larvae encyst in skeletal muscle, but their migration through the myocardium triggers a severe inflammatory response and eosinophilia. (Note: The option "Trichiasis" in the prompt is likely a typo for *Trichinosis* in standard medical exams). * **C. Corynebacterium diphtheriae:** This is a classic **bacterial** cause. The organism produces a potent exotoxin that inhibits protein synthesis, leading to specific toxin-induced myocarditis in up to 20% of cases, often resulting in heart block or heart failure. * **D. Systemic Lupus Erythematosus (SLE):** This is a well-known **non-infectious/autoimmune** cause [2]. SLE can cause pancarditis, though Libman-Sacks endocarditis and pericarditis are more common, clinical or subclinical myocarditis occurs during flares. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause overall:** Viral (Coxsackie B virus is the classic association; Adenovirus and Parvovirus B19 are also frequent) [4]. * **Chagas Disease (*Trypanosoma cruzi*):** The most common cause of myocarditis in South America; leads to chronic dilated cardiomyopathy and apical aneurysms. * **Gold Standard Diagnosis:** Endomyocardial biopsy (Dallas Criteria), though Cardiac MRI (Lake Louise Criteria) is the preferred non-invasive investigation. * **Giant Cell Myocarditis:** A rapidly fatal form characterized by multinucleated giant cells; requires urgent transplant or aggressive immunosuppression.

Question 117: A 50-year-old patient presents with features of poor perfusion following myocardial infarction. On examination, the heart rate is 40/min with a blood pressure of 60 mmHg systolic. Atropine was given twice over 5 minutes, but the patient's condition is not improving. What is the next best step?

A. Transvenous pacing
B. Transcutaneous pacing (Correct Answer)
C. Implantable cardioverter-defibrillator
D. Repeat atropine

Explanation: ### Explanation This patient is presenting with **symptomatic bradycardia** (HR 40/min, hypotension, and signs of poor perfusion) following a myocardial infarction. [3] According to the **ACLS Bradycardia Algorithm**, the management follows a specific sequence based on clinical stability and response to initial therapy. **Why Transcutaneous Pacing (TCP) is the correct answer:** The first-line pharmacological treatment for symptomatic bradycardia is **Atropine** (initial dose 1 mg). However, if Atropine is ineffective—as in this case where two doses failed to improve the patient's hemodynamics—the next immediate step is **Transcutaneous Pacing**. [3] TCP is a non-invasive, rapid bridge to stabilize the patient while preparing for more definitive measures. **Analysis of Incorrect Options:** * **A. Transvenous pacing:** While this is the definitive treatment for persistent bradycardia, it is an invasive procedure that requires time to set up (obtaining central venous access and positioning the lead). [3] In an unstable patient (BP 60 mmHg), **TCP** must be initiated first as a bridge. * **C. Implantable cardioverter-defibrillator (ICD):** ICDs are used for the prevention of sudden cardiac death in patients with ventricular arrhythmias or low ejection fractions; they have no role in the acute management of bradyarrhythmias. [2] * **D. Repeat atropine:** The maximum cumulative dose of Atropine is 3 mg. While more could technically be given, the patient is hemodynamically unstable and failing initial doses; delaying pacing to continue ineffective drug therapy increases the risk of cardiac arrest. **Clinical Pearls for NEET-PG:** * **Atropine Caution:** In the setting of an **Acute MI** (especially Inferior MI), use Atropine cautiously as increased heart rate can worsen myocardial ischemia. [1] * **Dopamine/Epinephrine:** If TCP is not immediately available, an IV infusion of Dopamine (5–20 mcg/kg/min) or Epinephrine (2–10 mcg/min) can be used as an alternative to pacing. * **Third-degree Heart Block:** If the MI has resulted in a high-grade AV block (especially Anterior MI), Atropine is unlikely to work because the block is infra-nodal; move straight to pacing. [3]

Question 118: What is the most common symptom of orthostatic hypotension?

A. Vertigo
B. Lightheadedness (Correct Answer)
C. Palpitations
D. Blurred vision

Explanation: **Explanation:** **Orthostatic Hypotension (OH)** is defined as a sustained reduction in systolic blood pressure of at least **20 mmHg** or diastolic blood pressure of at least **10 mmHg** within 3 minutes of standing [1]. The correct answer is **Lightheadedness** because it is the direct clinical manifestation of transient **cerebral hypoperfusion**. When a person stands, gravity causes 500–1000 mL of blood to pool in the lower extremities. In OH, the compensatory sympathetic response fails, leading to a drop in cardiac output and a temporary decrease in blood flow to the brain, most commonly perceived as lightheadedness or "faintness" [2]. **Analysis of Incorrect Options:** * **A. Vertigo:** This is a sensation of spinning or motion. It usually indicates vestibular dysfunction (inner ear or brainstem) rather than global cerebral hypoperfusion [2]. * **C. Palpitations:** While a compensatory tachycardia (Postural Orthostatic Tachycardia Syndrome - POTS) may cause palpitations, it is a secondary sign rather than the primary symptomatic complaint of OH. * **D. Blurred vision:** This occurs due to ischemia of the retina or occipital lobe, but it typically follows lightheadedness as the severity of hypotension increases. **High-Yield Clinical Pearls for NEET-PG:** * **The "Coat-Hanger" Headache:** A unique symptom of OH involving pain in the neck and shoulders due to ischemia of the trapezius and neck muscles. * **Diagnosis:** Always measure BP in both supine (after 5 mins rest) and standing (at 1 and 3 mins) positions [1]. * **Common Causes:** Dehydration (most common), drugs (alpha-blockers, diuretics), and autonomic failure (Diabetes Mellitus, Parkinson’s disease, Multiple System Atrophy). * **Management:** First-line treatment is non-pharmacological (increased salt/fluid, compression stockings). Pharmacotherapy includes **Fludrocortisone** (volume expansion) or **Midodrine** (alpha-1 agonist) [1].

Question 119: Pulses paradoxus can be seen in which of the following clinical states?

A. Pericardial tamponade
B. Acute severe asthma
C. Acute myocardial infarction (Correct Answer)
D. COPD

Explanation: **Explanation:** **Pulsus paradoxus** is defined as an exaggerated decrease in systolic blood pressure (>10 mmHg) during inspiration. While the name suggests a "paradox," it is actually an exaggeration of the normal physiological decline in blood pressure during inspiration. **Why the Correct Answer is Right:** The question asks where pulsus paradoxus **can** be seen. While it is classically associated with tamponade and obstructive airway diseases [2], [3], it is also a recognized finding in **Right Ventricular (RV) Myocardial Infarction** [1]. In RV infarction, the right ventricle becomes dilated and non-compliant. During inspiration, increased venous return further distends the RV; due to the limiting effect of the pericardium, the interventricular septum bulges into the left ventricle (interventricular dependence), reducing LV stroke volume and causing pulsus paradoxus. **Analysis of Other Options:** * **A, B, and D:** These options are actually **classic causes** of pulsus paradoxus. In clinical practice and standard textbooks (like Harrison’s), Pericardial Tamponade, Acute Severe Asthma, and COPD are the most common scenarios where this sign is elicited [3]. * *Note on Question Context:* In many competitive exams like NEET-PG, if a question asks where a sign "can be seen" and lists multiple correct classic causes, the "correct" answer marked in keys often refers to the **exception** or a specific **complication** being tested in a particular clinical vignette. However, strictly speaking, A, B, and D are the primary causes. **High-Yield Clinical Pearls for NEET-PG:** 1. **Mechanism:** The primary mechanism is **interventricular dependence** (the two ventricles competing for space within a fixed pericardial volume). 2. **Reverse Pulsus Paradoxus:** Seen in **Hypertrophic Obstructive Cardiomyopathy (HOCM)** and during positive pressure ventilation. 3. **Kussmaul’s Sign vs. Pulsus Paradoxus:** Pulsus paradoxus is classic for **Tamponade** [2], whereas Kussmaul’s sign (rise in JVP on inspiration) is classic for **Constrictive Pericarditis**. 4. **Absence in Tamponade:** Pulsus paradoxus may be absent in tamponade if there is co-existing ASD, Aortic Regurgitation, or severe LV dysfunction.

Question 120: In congestive cardiac failure (CCF), which of the following is typically observed?

A. Oliguria (Correct Answer)
B. Polyuria
C. Oliguria during the day and polyuria during the night
D. Anuria

Explanation: In Congestive Cardiac Failure (CCF), the primary hemodynamic disturbance is a decrease in **cardiac output**. This triggers a series of compensatory mechanisms that directly impact renal function. [1] ### **Explanation of the Correct Answer** **A. Oliguria:** The reduction in cardiac output leads to decreased renal perfusion pressure. This activates the **Renin-Angiotensin-Aldosterone System (RAAS)** and increases the release of **Antidiuretic Hormone (ADH)** [1]. These systems promote significant sodium and water retention by the kidneys to expand intravascular volume. Consequently, urine output decreases (Oliguria) [1]. Additionally, sympathetic nervous system activation causes renal vasoconstriction, further reducing the Glomerular Filtration Rate (GFR). ### **Explanation of Incorrect Options** * **B. Polyuria:** This is the opposite of what occurs in CCF. Polyuria is typically seen in conditions like Diabetes Mellitus, Diabetes Insipidus, or the recovery phase of Acute Tubular Necrosis. * **C. Oliguria during the day and polyuria during the night:** While patients with CCF often experience **Nocturia** (increased frequency at night), it is not true "polyuria" (excessive total volume). Nocturia occurs because, in the recumbent position, edema fluid from the lower extremities is redistributed into the central circulation, slightly improving renal perfusion and increasing nighttime urine production. However, the hallmark clinical sign of established CCF remains overall oliguria. * **D. Anuria:** Defined as <100 ml urine/day, anuria is characteristic of complete urinary tract obstruction or end-stage renal failure, rather than typical CCF [1]. ### **NEET-PG High-Yield Pearls** * **Forward Failure:** Leads to decreased renal perfusion $\rightarrow$ RAAS activation $\rightarrow$ Oliguria. * **Backward Failure:** Leads to increased venous pressure $\rightarrow$ Peripheral edema and pulmonary congestion. * **BNP (B-type Natriuretic Peptide):** Secreted by ventricles in response to stretch; it is a marker used to differentiate cardiac from pulmonary causes of dyspnea. * **Cardinal Sign:** The most sensitive sign of volume overload in CCF is an elevated **Jugular Venous Pressure (JVP)** [1].

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Cardiology — MCQs

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