Cardiology — MCQs

Cardiology Indian Medical PG Practice Questions and MCQs

Question 511: All of the following are seen in cardiac arrest except?

A. Electromechanical dissociation
B. Atrial fibrillation (Correct Answer)
C. Ventricular fibrillation
D. Ventricular tachycardia

Explanation: **Explanation:** Cardiac arrest is defined as the sudden cessation of cardiac pump function, resulting in the absence of a palpable pulse and systemic perfusion. To understand this question, one must distinguish between **shockable** and **non-shockable** rhythms that lead to a pulseless state. **Why Atrial Fibrillation (AF) is the correct answer:** Atrial fibrillation is a supraventricular tachyarrhythmia characterized by disorganized atrial activity [4]. While AF can lead to hemodynamic instability or heart failure, it **does not** inherently cause cardiac arrest [5]. In AF, the ventricles still contract (albeit irregularly), maintaining a cardiac output and a palpable pulse. Therefore, AF is not a rhythm of cardiac arrest. **Analysis of Incorrect Options:** * **Ventricular Fibrillation (VF):** This is the most common shockable rhythm in sudden cardiac arrest [1]. The ventricles quiver without effective contraction, leading to zero cardiac output [3]. * **Ventricular Tachycardia (VT):** Specifically, **pulseless VT** is a cardiac arrest rhythm. The rapid rate prevents adequate ventricular filling, resulting in a loss of output [2]. * **Electromechanical Dissociation (EMD):** Now more commonly referred to as **Pulseless Electrical Activity (PEA)**. It is a state where the ECG shows organized electrical activity, but there is no mechanical contraction of the heart muscle to produce a purse. **High-Yield Clinical Pearls for NEET-PG:** * **The Four Rhythms of Cardiac Arrest:** 1. Ventricular Fibrillation, 2. Pulseless Ventricular Tachycardia, 3. Asystole, 4. Pulseless Electrical Activity (PEA) [1]. * **Shockable vs. Non-shockable:** VF and Pulseless VT require immediate defibrillation [1]. Asystole and PEA are managed with high-quality CPR and Epinephrine (defibrillation is not indicated). * **H's and T's:** Always remember the reversible causes of PEA/Asystole (Hypovolemia, Hypoxia, Hydrogen ion/Acidosis, Hypo/Hyperkalemia, Hypothermia; Tension pneumothorax, Tamponade, Toxins, Thrombosis).

Question 512: What is the treatment of choice for a case of congestive failure with hypertension?

A. ACE inhibitors (Correct Answer)
B. Alpha-blockers
C. Calcium channel blockers
D. Nitrates

Explanation: **Explanation:** In patients with Heart Failure with reduced Ejection Fraction (HFrEF) and concomitant hypertension, **ACE Inhibitors (ACEIs)** are the treatment of choice [1]. The underlying medical concept is their ability to counteract the maladaptive activation of the Renin-Angiotensin-Aldosterone System (RAAS) [3]. ACEIs provide a dual benefit: they act as potent vasodilators to reduce systemic vascular resistance (afterload) and, more importantly, they prevent **cardiac remodeling**. Clinical trials (e.g., SOLVD, CONSENSUS) have definitively proven that ACEIs reduce both morbidity and mortality in these patients [1]. **Analysis of Incorrect Options:** * **Alpha-blockers:** These are not first-line agents for heart failure. The ALLHAT trial demonstrated that alpha-blockers (like Doxazosin) actually increase the risk of developing heart failure compared to other antihypertensives. * **Calcium Channel Blockers (CCBs):** Non-dihydropyridines (Verapamil/Diltiazem) are contraindicated in HFrEF due to their negative inotropic effects. While Amlodipine is safe, it does not provide the mortality benefits seen with ACEIs. * **Nitrates:** These are primarily venodilators (reducing preload). While useful in acute failure or in combination with Hydralazine (especially in African American populations), they are not the primary choice for long-term management of hypertensive heart failure compared to ACEIs [2]. **High-Yield Clinical Pearls for NEET-PG:** * **The "Big Three" for Mortality Benefit:** ACEIs/ARNs, Beta-blockers (Carvedilol, Metoprolol succinate, Bisoprolol), and Mineralocorticoid Receptor Antagonists (Spironolactone) [4]. * **Side Effect:** If a patient develops a dry cough on ACEIs (due to bradykinin accumulation), switch to **ARBs** (Candesartan/Valsartan) [1]. * **Contraindications:** Avoid ACEIs in bilateral renal artery stenosis, pregnancy (teratogenic), and hyperkalemia [3].

Question 513: An axis deviation between -30 and -60 degrees is seen in which of the following conditions?

A. Left Ventricle Hypertrophy (Correct Answer)
B. Right Ventricle Hypertrophy
C. Left Posterior Fascicular Block
D. Lateral wall Myocardial Infarction

Explanation: ### Explanation **Correct Answer: A. Left Ventricle Hypertrophy** The normal QRS axis ranges from **-30° to +90°** [1]. Left Axis Deviation (LAD) is defined as an axis more negative than -30°. In **Left Ventricular Hypertrophy (LVH)**, the increased muscle mass of the left ventricle shifts the mean electrical vector further to the left and posteriorly. While mild LVH may stay within normal limits, significant hypertrophy typically results in an axis between **-30° and -60°**. **Analysis of Options:** * **B. Right Ventricular Hypertrophy (RVH):** This causes **Right Axis Deviation (RAD)**, typically > +90°. The electrical vector shifts toward the hypertrophied right ventricle. * **C. Left Posterior Fascicular Block (LPFB):** This is a classic cause of **RAD** (usually +120° to +180°). Conversely, Left *Anterior* Fascicular Block (LAFB) is the most common cause of extreme LAD (more negative than -45°). * **D. Lateral Wall MI:** Infarction of the lateral wall leads to a loss of electrical forces on the left, causing the axis to shift away from the lesion toward the right (**RAD**). **High-Yield Clinical Pearls for NEET-PG:** * **LAD Causes:** LVH, Left Anterior Fascicular Block (LAFB), Inferior Wall MI (due to loss of inferior forces), and WPW syndrome (right-sided bypass tract). * **RAD Causes:** RVH, Left Posterior Fascicular Block (LPFB), Lateral Wall MI, Pulmonary Embolism (Acute Cor Pulmonale), and Dextrocardia. * **Quick Rule:** If Lead I is positive (upright) and Lead aVF is negative (downward), LAD is present. To confirm if it is pathological (<-30°), Lead II must also be negative.

Question 514: Which of the following is NOT a true statement regarding ECG changes?

A. Hypokalemia is associated with U waves.
B. Hyperkalemia is associated with tall, peaked T waves.
C. Hyponatremia is associated with Q waves. (Correct Answer)
D. Hypocalcemia is associated with a prolonged QT interval.

Explanation: This question tests your knowledge of electrolyte imbalances and their characteristic manifestations on an Electrocardiogram (ECG), a high-yield topic for NEET-PG. ### **Explanation of the Correct Option** **Option C (Hyponatremia is associated with Q waves)** is the correct answer because it is a **false statement**. Sodium levels (hyper- or hyponatremia) generally do not produce specific, diagnostic changes on an ECG [1]. Pathological Q waves are typically markers of a transmural myocardial infarction (old or evolving) [2] or certain types of cardiomyopathy, not electrolyte disturbances. ### **Analysis of Other Options** * **Option A (Hypokalemia):** This is a true statement. Classic findings include flattened T waves, ST-segment depression, and the appearance of prominent **U waves** (best seen in V2-V4). * **Option B (Hyperkalemia):** This is a true statement. The earliest sign of hyperkalemia is **tall, "tented" or peaked T waves** with a narrow base [1]. As levels rise, you may see P-wave flattening and QRS widening ("Sine wave" pattern) [1]. * **Option C (Hypocalcemia):** This is a true statement. Calcium affects the plateau phase (Phase 2) of the action potential. Low calcium leads to ST-segment lengthening, which results in a **prolonged QT interval**. ### **High-Yield Clinical Pearls for NEET-PG** * **Hypercalcemia:** Causes a **shortened QT interval** (the opposite of hypocalcemia). * **Hypomagnesemia:** Often co-exists with hypokalemia and can lead to **Torsades de Pointes** (prolonged QT). * **Digoxin Effect:** Characterized by "reverse tick" or **scooped-out ST-segment depression**. * **Osborn Waves (J waves):** Characteristic of **Hypothermia**, seen at the junction of the QRS and ST segment.

Question 515: A patient complains of intermittent claudication, dizziness, and headache. What is the likely cardiac lesion?

A. Tetralogy of Fallot (TOF)
B. Atrial Septal Defect (ASD)
C. Patent Ductus Arteriosus (PDA)
D. Coarctation of the aorta (Correct Answer)

Explanation: The clinical presentation of **intermittent claudication** (leg pain on exertion) combined with symptoms of **upper body hypertension** (headache and dizziness) is a classic hallmark of **Coarctation of the Aorta**. [1] **1. Why Coarctation of the Aorta is correct:** Coarctation is a focal narrowing of the aortic lumen, typically near the ductus arteriosus. This creates a pressure gradient: * **Proximal to the obstruction:** Hypertension occurs in the upper extremities and head, leading to **headaches, dizziness, and epistaxis**. * **Distal to the obstruction:** Hypotension and reduced perfusion occur in the lower extremities, leading to **intermittent claudication**, cold feet, and delayed/diminished femoral pulses. [1] **2. Why other options are incorrect:** * **Tetralogy of Fallot (TOF):** A cyanotic heart disease characterized by "tet spells," cyanosis, and clubbing [3]. It does not typically cause differential blood pressure or claudication. * **Atrial Septal Defect (ASD):** Usually asymptomatic in early life or presents with exercise intolerance and palpitations. It is characterized by a fixed split S2, not upper body hypertension. * **Patent Ductus Arteriosus (PDA):** Presents with a continuous machinery murmur [2]. While a large PDA can cause "differential cyanosis" (blue toes, pink fingers), it does not cause the hypertension-claudication complex seen here. **High-Yield Clinical Pearls for NEET-PG:** * **Physical Exam:** Look for **Radio-femoral delay** and a BP systolic difference >20 mmHg between upper and lower limbs [1]. * **Chest X-ray:** Look for the **"3" sign** (pre- and post-stenotic dilatation) and **rib notching** (due to enlarged intercostal collateral arteries). * **Association:** Frequently associated with **Bicuspid Aortic Valve** (most common) and **Turner Syndrome** [1]. * **Complication:** Increased risk of **Berry aneurysms** (leading to Subarachnoid Hemorrhage) due to chronic hypertension.

Question 516: Which of the following is NOT true regarding hypertrophic cardiomyopathy?

A. Digoxin is useful. (Correct Answer)
B. Abdominal pain can be a symptom.
C. Jaundice can be a symptom.
D. Bleeding can be a symptom.

Explanation: **Explanation:** **1. Why Option A is the correct answer (Why Digoxin is NOT useful):** Hypertrophic Cardiomyopathy (HCM) is characterized by left ventricular hypertrophy and dynamic outflow tract obstruction. **Digoxin is contraindicated** in obstructive HCM because it is a positive inotrope. By increasing myocardial contractility, Digoxin worsens the Left Ventricular Outflow Tract (LVOT) obstruction and increases the pressure gradient, thereby exacerbating symptoms. Management typically focuses on negative inotropes like Beta-blockers or Verapamil to improve diastolic filling. **2. Why the other options are wrong (How they relate to HCM):** * **Abdominal pain & Jaundice (Options B & C):** These are symptoms of **Right-sided Heart Failure**. While HCM primarily affects the left ventricle, chronic disease can lead to pulmonary hypertension and subsequent right heart failure. This causes systemic venous congestion, leading to **congestive hepatopathy** ("nutmeg liver"), which manifests as RUQ abdominal pain and jaundice. * **Bleeding (Option D):** HCM is strongly associated with **Heyde’s Syndrome**. High-shear stress caused by the narrowed LVOT leads to the destruction of **von Willebrand Factor (vWF) multimers** (Acquired Type 2A vWD). This deficiency often results in bleeding from gastrointestinal angiodysplasias. **NEET-PG High-Yield Pearls:** * **Murmur Dynamics:** The systolic murmur of HCM **increases** with Valsalva and standing (decreased preload) and **decreases** with squatting and handgrip (increased preload/afterload). * **Classic Sign:** Jerky pulse (Double-peaked/Bisferiens pulse). * **ECG Finding:** Dagger-like Q waves in lateral/inferior leads. * **Sudden Cardiac Death (SCD):** HCM is the most common cause of SCD in young athletes [1], with mutations in sarcomeric proteins like Beta-myosin heavy chain often identified [2].

Question 517: Which of the following statements regarding Dressler's Syndrome is true?

A. Usually occurs 1-4 days after myocardial infarction
B. Occurs in 10% of patients with acute myocardial infarction
C. Treatment of choice is aspirin (Correct Answer)
D. Complication of early pericarditis

Explanation: ### Explanation: Dressler’s Syndrome **Dressler’s Syndrome** (also known as Post-Cardiac Injury Syndrome) is an immune-mediated pericarditis that occurs as a late complication following myocardial infarction (MI), cardiac surgery, or trauma. **1. Why Option C is Correct:** The treatment of choice is **High-dose Aspirin** (750–1000 mg every 6–8 hours) plus **Colchicine**. Aspirin is preferred over other NSAIDs (like Ibuprofen) in the post-MI period because other NSAIDs can interfere with myocardial healing and increase the risk of ventricular free wall rupture [1]. Corticosteroids are reserved only for refractory cases. **2. Why the Other Options are Incorrect:** * **Option A:** Dressler’s syndrome typically occurs **2 to 6 weeks** (late onset) after an MI. Symptoms occurring within 1–4 days are characteristic of *Peri-infarction Pericarditis*, which is due to direct inflammatory extension from the necrotic myocardium. * **Option B:** Due to the advent of reperfusion therapy (PCI/Thrombolysis), the incidence has significantly decreased and is now estimated to be **<1%**, far less than the historical 10%. * **Option C:** Dressler’s is a **late, immune-mediated** phenomenon (Type III hypersensitivity) involving anti-myocardial antibodies. It is distinct from early pericarditis, which is a localized inflammatory response to transmural necrosis. **3. High-Yield Clinical Pearls for NEET-PG:** * **Clinical Triad:** Fever, pleuritic chest pain, and pericardial effusion. * **ECG Findings:** Diffuse ST-segment elevation with PR-segment depression (except in lead aVR) [1]. * **Key Difference:** Unlike early pericarditis, Dressler’s is often associated with an elevated ESR and leukocytosis. * **Avoidance:** Avoid anticoagulants during the acute phase to prevent hemorrhagic pericardial effusion and cardiac tamponade.

Question 518: Which of the following is prolonged QT interval associated with?

A. Hypercalcemia
B. Type Ia antiarrhythmic drugs
C. Torsade de pointes (Correct Answer)
D. Atrial fibrillation

Explanation: Explanation: The **QT interval** represents the total time for ventricular depolarization and repolarization. A prolonged QT interval (corrected QT or QTc >440ms in men, >460ms in women) indicates delayed repolarization, which creates a vulnerable period for "early after-depolarizations" (EADs) [1]. **Why Torsade de Pointes (TdP) is correct:** Prolongation of the QT interval is the primary precursor to **Torsade de Pointes**, a specific form of polymorphic ventricular tachycardia characterized by the QRS complexes "twisting" around the isoelectric line [1]. If the QT interval is long enough, an EAD can trigger a premature ventricular contraction (PVC) that falls on the T-wave (R-on-T phenomenon), initiating TdP [2]. **Analysis of Incorrect Options:** * **A. Hypercalcemia:** This actually **shortens** the QT interval (specifically the ST segment). **Hypocalcemia** is a classic cause of QT prolongation. * **B. Type Ia antiarrhythmic drugs:** While Type Ia (e.g., Quinidine, Procainamide) and Type III drugs *do* cause QT prolongation, the question asks what the prolonged QT is **associated with** (i.e., its clinical consequence). TdP is the direct pathological result of a prolonged QT. * **D. Atrial fibrillation:** This is a supraventricular arrhythmia characterized by absent P-waves and an irregularly irregular rhythm; it is not directly caused by or associated with QT prolongation. **High-Yield Clinical Pearls for NEET-PG:** * **Congenital Long QT Syndromes:** Romano-Ward (Autosomal Dominant, pure cardiac) and Jervell and Lange-Nielsen (Autosomal Recessive, associated with sensorineural deafness) [2]. * **Electrolyte triggers:** Hypokalemia, Hypomagnesemia, and Hypocalcemia (The "3 Hypos"). * **Drug triggers:** Macrolides, Fluoroquinolones, Antipsychotics (Haloperidol), and Tricyclic Antidepressants (TCAs). * **Management of TdP:** Intravenous **Magnesium Sulfate** is the drug of choice, even if magnesium levels are normal.

Question 519: Assays of which of the following biomarkers is most commonly used in the diagnosis of heart failure?

A. Brain Natriuretic Peptide (BNP) (Correct Answer)
B. Atrial Natriuretic Peptide (ANP)
C. Endothelin-1 (ET-1)
D. Adrenomedullin

Explanation: The diagnosis of heart failure (HF) relies on clinical assessment supported by biomarkers that reflect ventricular wall stress [1]. **Brain Natriuretic Peptide (BNP)** and its inactive cleavage product, **NT-proBNP**, are the gold-standard biomarkers used in clinical practice [3]. **Why BNP is the Correct Answer:** BNP is synthesized primarily by the **ventricular myocardium** in response to increased wall tension, stretch, or pressure overload [3]. It acts as a compensatory hormone by promoting natriuresis, diuresis, and vasodilation to reduce preload and afterload [2]. Its high **negative predictive value** makes it exceptionally useful in the emergency department to rule out HF in patients presenting with acute dyspnea [1]. **Analysis of Incorrect Options:** * **Atrial Natriuretic Peptide (ANP):** Produced mainly by the atria. While elevated in HF, it has a very short half-life (approx. 2 minutes) compared to BNP (approx. 20 minutes) [3], making it clinically impractical for routine assays. * **Endothelin-1 (ET-1):** A potent vasoconstrictor. While levels correlate with the severity of HF and pulmonary hypertension, it is not used for diagnosis due to lack of specificity and standardized testing. * **Adrenomedullin:** A vasodilator peptide. Though it increases in HF, it is not a standard diagnostic tool and lacks the established clinical cut-offs that BNP possesses. **NEET-PG High-Yield Pearls:** * **Cut-off values for Acute HF:** BNP <100 pg/mL or NT-proBNP <300 pg/mL effectively rules out heart failure. * **Neprilysin Inhibitors (Sacubitril):** These drugs prevent the breakdown of BNP. Therefore, in patients on ARNI therapy, **NT-proBNP** must be used for monitoring instead of BNP, as BNP levels will be pharmacologically elevated. * **False Positives:** BNP can be elevated in old age, renal failure, and atrial fibrillation. It is characteristically **lower** in obese patients.

Question 520: Which of the following can cause Right Bundle Branch Block (RBBB)?

A. It can occur in a normal person
B. Pulmonary embolism
C. Corpulmonale
D. All of the above (Correct Answer)

Explanation: **Explanation:** Right Bundle Branch Block (RBBB) occurs when there is a delay or blockage of electrical conduction through the right bundle branch. Unlike Left Bundle Branch Block (LBBB), which is almost always pathological, RBBB can be found in a variety of clinical scenarios ranging from benign to life-threatening. 1. **Normal Individuals (Option A):** RBBB can be an isolated, incidental finding in individuals with no structural heart disease. It is estimated to occur in approximately 1% of the healthy population and its prevalence increases with age. 2. **Pulmonary Embolism (Option B):** Acute right ventricular (RV) strain caused by a massive pulmonary embolism can lead to a new-onset RBBB [1]. This is a classic high-yield association, often seen alongside the S1Q3T3 pattern. 3. **Cor Pulmonale (Option C):** Chronic right heart strain or hypertrophy resulting from primary lung disease (e.g., COPD, pulmonary hypertension) frequently leads to RBBB due to the stretching or remodeling of the right ventricular conduction system. **Clinical Pearls for NEET-PG:** * **ECG Criteria:** Look for an **rsR' pattern** (M-shaped) in leads V1-V2 and wide, slurred S-waves in leads I, aVL, and V5-V6. The QRS duration is $\geq$ 120 ms. * **Heart Sounds:** RBBB causes a **wide, fixed splitting of the S2** (second heart sound) because the delayed depolarization of the right ventricle leads to delayed closure of the pulmonary valve. * **Differential:** If you see RBBB with **Left Axis Deviation**, suspect **Bifascicular Block** (RBBB + Left Anterior Hemiblock) [2]. * **New Onset:** A new-onset RBBB in a patient with chest pain or dyspnea should always raise suspicion for acute myocardial infarction or pulmonary embolism [1].

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Cardiomyopathies

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Congenital Heart Disease in Adults

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Cardiology — MCQs

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