Cardiology — MCQs

Cardiology Indian Medical PG Practice Questions and MCQs

Question 1061: Resistant hypertension is defined as?

A. Hypertension resistant to 3 or more antihypertensive drugs
B. Hypertension resistant to 3 or more antihypertensive drugs, including a thiazide diuretic (Correct Answer)
C. Hypertension resistant to aldosterone
D. Hypertension with resistance of Angiotensin II receptors

Explanation: ### Explanation **Definition and Concept** Resistant Hypertension (RH) is a clinical diagnosis made when a patient’s blood pressure remains above the goal (typically >140/90 mmHg) despite the concurrent use of **three antihypertensive drug classes** of different mechanisms. The definition specifically requires that: 1. The drugs are prescribed at **optimal/maximal tolerated doses**. 2. One of the three drugs must be a **diuretic** (classically a long-acting thiazide or thiazide-like diuretic such as Chlorthalidone). 3. Patients whose BP is controlled but require **four or more** drugs are also classified as having resistant hypertension [1]. **Analysis of Options** * **Option A:** This is partially correct but incomplete. The inclusion of a diuretic is a mandatory criterion for the formal definition to rule out volume overload as the cause of resistance. * **Option B (Correct):** This aligns with the AHA/ACC and ESC guidelines, emphasizing the triad of triple therapy including a diuretic. * **Option C & D:** These are pathophysiological distractions. While aldosterone excess (Primary Aldosteronism) is the most common secondary cause of resistant hypertension, and Angiotensin receptors are targets for therapy (ARBs), they do not define the clinical syndrome of "Resistant Hypertension." **High-Yield Clinical Pearls for NEET-PG** * **Pseudoresistance:** Before diagnosing RH, rule out "White Coat Hypertension" (using ABPM) and medication non-adherence [1]. * **Most Common Secondary Cause:** Primary Aldosteronism (Conn’s Syndrome). * **Drug of Choice for Add-on Therapy:** If BP remains uncontrolled on three drugs, the 4th drug added should be a **Mineralocorticoid Receptor Antagonist (MRA)** like **Spironolactone** (as per the PATHWAY-2 trial). * **Screening:** Always screen for Obstructive Sleep Apnea (OSA) and Chronic Kidney Disease (CKD) in these patients.

Question 1062: Which of the following statements is NOT true regarding right-sided infective endocarditis?

A. Unlikely in the absence of a murmur (Correct Answer)
B. It is commonly seen in intravenous drug users
C. Emboli to organs other than the lung are rare
D. Can occur following septic abortion

Explanation: In Right-Sided Infective Endocarditis (RSIE), the correct answer is **Option A** because the statement "Unlikely in the absence of a murmur" is **false**. Unlike left-sided endocarditis, where murmurs are present in over 85% of cases, a murmur is frequently **absent** in RSIE (occurring in only about 35-50% of patients). This is because the pressure gradient across the tricuspid valve is lower than the mitral or aortic valves, making the resulting turbulence less audible. **Analysis of other options:** * **Option B:** IV drug use (IVDU) is the most common risk factor for RSIE, typically involving the tricuspid valve [1]. *Staphylococcus aureus* is the most frequent pathogen in this cohort [1]. * **Option C:** Since the vegetation is on the right side (tricuspid/pulmonary valves), fragments embolize via the pulmonary artery [1]. This leads to **septic pulmonary emboli**, causing cough, chest pain, and hemoptysis. Systemic emboli (to brain or spleen) are rare unless a right-to-left shunt (e.g., Patent Foramen Ovale) exists. * **Option D:** Septic abortion or pelvic infections can lead to RSIE via the pelvic venous plexus, which drains into the inferior vena cava and reaches the right heart. **High-Yield Clinical Pearls for NEET-PG:** * **Most common valve involved in IVDU:** Tricuspid Valve. * **Triad of RSIE:** Fever, anemia, and multiple patchy pulmonary infiltrates (septic emboli). * **Chest X-ray:** Often shows "flea-bitten" appearance or multiple peripheral cavitary lesions. * **Treatment:** Often requires longer courses of antibiotics; surgery is less common than in left-sided IE but indicated for large vegetations (>20mm) or persistent infection.

Question 1063: What is/are the positive ECG sign(s) of ischemia in a treadmill test?

A. Upsloping depression of the ST segment 1 mm below baseline
B. Downsloping depression of the ST segment >0.1 mm below baseline (Correct Answer)
C. Junctional ST-segment changes
D. Tachycardia

Explanation: **Explanation:** In a Treadmill Test (TMT), the primary objective is to identify exercise-induced myocardial ischemia. The most reliable ECG indicator of ischemia is the morphology and depth of ST-segment depression measured at the J-point [1]. **Why Option B is Correct:** A positive (abnormal) TMT is defined by a **horizontal or downsloping ST-segment depression of ≥1 mm (0.1 mV)** occurring 60–80 ms after the J-point [1]. Downsloping depression is the most specific indicator of coronary artery disease (CAD) and carries a higher predictive value for multivessel disease compared to other patterns. **Analysis of Incorrect Options:** * **Option A (Upsloping depression):** Rapidly upsloping ST depression is often a physiological response to tachycardia and is generally considered a **negative** or "borderline" result unless it is "slow-upsloping" (where the ST segment is still ≥1.5 mm depressed at 80 ms after the J-point). * **Option C (Junctional changes):** J-point depression with rapid upward return to baseline is a common finding in healthy individuals during peak exercise due to atrial repolarization (Ta wave) and does not signify ischemia. * **Option D (Tachycardia):** Tachycardia is a normal physiological response to exercise. While a failure to increase heart rate (chronotropic incompetence) is abnormal, tachycardia itself is not a sign of ischemia. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Criteria:** ≥1 mm horizontal or downsloping ST depression [1]. * **ST Elevation:** If ST elevation occurs in leads without prior Q-waves (infarct), it is highly specific for severe transmural ischemia (e.g., vasospasm or high-grade stenosis). * **Duke Treadmill Score:** Used for prognosis; it combines exercise time, ST deviation, and the presence of angina [1]. * **Contraindication:** Do not perform TMT in patients with unstable angina, acute MI (within 2 days), or severe symptomatic aortic stenosis.

Question 1064: In left ventricular hypertrophy (LVH), what is the typical criteria for the sum of SV1 and RV6 in millimeters?

A. 25 mm
B. 30 mm
C. 35 mm (Correct Answer)
D. 45 mm

Explanation: ### Explanation **1. The Correct Answer: C (35 mm)** The question refers to the **Sokolow-Lyon Criteria**, one of the most widely used ECG tools for diagnosing Left Ventricular Hypertrophy (LVH). In LVH, the increased muscle mass of the left ventricle generates higher electrical voltages during depolarization. Because the left ventricle is posterior and to the left, these increased forces are directed away from the right-sided precordial leads (causing a deep **S wave in V1**) and toward the left-sided leads (causing a tall **R wave in V5 or V6**). * **Criteria:** SV1 + (RV5 or RV6) ≥ 35 mm (in adults >35 years). **2. Analysis of Incorrect Options:** * **Option A (25 mm) & B (30 mm):** These values are below the established threshold for the Sokolow-Lyon index. While a sum of 30 mm might be suggestive in older patients with thin chest walls, it lacks the specificity required for a formal diagnosis of LVH. * **Option D (45 mm):** This value is significantly higher than the standard diagnostic cutoff. While a sum of 45 mm is highly specific for LVH, using it as the "typical criteria" would result in many false negatives (low sensitivity). **3. Clinical Pearls for NEET-PG:** * **Cornell Criteria:** Another high-yield index. It is defined as **R in aVL + S in V3 > 28 mm (men)** or **> 20 mm (women)**. It is often considered more accurate than Sokolow-Lyon. * **Strain Pattern:** Look for asymmetrical ST-segment depression and T-wave inversion in lateral leads (V5, V6, I, aVL); this indicates chronic pressure overload. * **Romhilt-Estes Point System:** A scoring system where a score of ≥5 is definitive for LVH. * **Limitation:** ECG has high specificity but **low sensitivity** for LVH; Echocardiography remains the gold standard for assessing ventricular mass.

Question 1065: For the diagnosis of Acute Rheumatic Fever, which of the following is essential?

A. Prior history of rheumatic fever
B. Recent sore throat infection
C. One major and two minor Jones criteria (Correct Answer)
D. Erythema marginatum

Explanation: The diagnosis of **Acute Rheumatic Fever (ARF)** is clinical and relies on the **Revised Jones Criteria**. Because no single laboratory test or clinical sign is pathognomonic, a combination of findings is required to ensure diagnostic accuracy. [1] ### Why Option C is Correct According to the Revised Jones Criteria (AHA), the diagnosis of a **first episode** of ARF requires: * **Evidence of a preceding Group A Streptococcal (GAS) infection** (e.g., elevated ASLO titer, positive throat culture, or rapid antigen test) **PLUS** [1] * Two Major criteria **OR** * **One Major and two Minor criteria.** ### Why Other Options are Incorrect * **A. Prior history of rheumatic fever:** While a history of ARF increases the risk of recurrence, it is not a requirement for diagnosing a new or initial episode. [1] * **B. Recent sore throat infection:** While a GAS infection is the trigger, a "sore throat" is a subjective symptom. Diagnosis requires objective evidence (ASLO/Culture). Furthermore, the infection itself is a prerequisite, not the diagnostic threshold. [1] * **D. Erythema marginatum:** This is one of the five **Major criteria**. While its presence is highly suggestive, it is not "essential" on its own; the diagnosis can be made using other combinations (e.g., Carditis and Polyarthritis). ### NEET-PG High-Yield Pearls * **Major Criteria (J♥NES):** **J**oints (Migratory Polyarthritis), **♥** (Carditis), **N**odules (Subcutaneous), **E**rythema marginatum, **S**ydenham’s chorea. * **Minor Criteria:** Arthralgia, Fever, Elevated ESR/CRP, Prolonged PR interval on ECG. * **Exceptions:** Sydenham’s chorea or indolent carditis can be used to diagnose ARF without strict adherence to the Jones Criteria or evidence of preceding GAS infection. [1] * **Joint Involvement:** In high-risk populations, **monoarthritis** or **polyarthralgia** may be considered a Major criterion. * **Secondary prevention:** Patients are susceptible to further attacks of rheumatic fever if another streptococcal infection occurs, and long-term prophylaxis with penicillin should be given. [2]

Question 1066: A 61-year-old male presented to the OPD with complaints of dyspnea, chest pain, and syncope. What is he most likely suffering from?

A. Mitral Stenosis (MS)
B. Aortic Stenosis (AS) (Correct Answer)
C. Mitral Regurgitation (MR)
D. Tricuspid Regurgitation (TR)

Explanation: The classic triad of **Dyspnea, Angina (chest pain), and Syncope** is the hallmark clinical presentation of **Symptomatic Aortic Stenosis (AS)**. ### 1. Why Aortic Stenosis is Correct In AS, the narrowing of the aortic valve causes a fixed left ventricular outflow tract obstruction [1]. * **Angina:** Occurs due to increased myocardial oxygen demand (from LV hypertrophy) and decreased supply (due to high wall tension and compression of coronary arteries). * **Syncope:** Typically exertional, caused by the inability of the heart to increase cardiac output during exercise, leading to reduced cerebral perfusion, or due to the baroreceptor reflex causing vasodilation. * **Dyspnea:** Indicates the onset of heart failure as the left ventricle fails to pump against the high pressure, leading to pulmonary congestion [2]. ### 2. Why Other Options are Incorrect * **Mitral Stenosis (MS):** Primarily presents with dyspnea, hemoptysis, and palpitations (due to Atrial Fibrillation). Syncope and chest pain are rare. * **Mitral Regurgitation (MR):** Presents with chronic fatigue and exertional dyspnea [3]. It does not typically cause syncope unless associated with severe arrhythmias. * **Tricuspid Regurgitation (TR):** Presents with signs of right-sided heart failure, such as peripheral edema, hepatomegaly, and elevated JVP, rather than the classic AS triad. ### 3. High-Yield Clinical Pearls for NEET-PG * **The "SAD" Mnemonic:** **S**yncope, **A**ngina, **D**yspnea (in order of worsening prognosis). * **Average Survival:** Once symptoms appear, survival is roughly: Angina (5 years), Syncope (3 years), Dyspnea/HF (2 years). * **Physical Exam:** Look for **Pulsus Parvus et Tardus** (slow-rising, low-volume pulse) and a **harsh crescendo-decrescendo systolic murmur** radiating to the carotids [1]. * **Management:** Symptomatic severe AS is an absolute indication for **Aortic Valve Replacement (AVR/TAVI)** [2].

Question 1067: Which of the following is NOT true about hypertrophic obstructive cardiomyopathy?

A. Asymmetric hypertrophy of the septum
B. Systolic anterior motion of the mitral valve leaflet
C. Left ventricle outflow obstruction
D. Beta-blockers are not effective (Correct Answer)

Explanation: ### Explanation **Hypertrophic Obstructive Cardiomyopathy (HOCM)** is an autosomal dominant genetic disorder characterized by myocardial hypertrophy, primarily affecting the interventricular septum [1]. **Why Option D is the correct answer (The "False" statement):** Beta-blockers (e.g., Metoprolol, Propranolol) are actually the **first-line medical treatment** for symptomatic HOCM. They work by decreasing the heart rate (increasing diastolic filling time) and reducing contractility (negative inotropy). This reduces the pressure gradient across the Left Ventricular Outflow Tract (LVOT), decreases oxygen demand, and improves symptoms like angina and dyspnea [1]. Therefore, saying they are "not effective" is incorrect. **Analysis of Incorrect Options (True statements about HOCM):** * **Option A:** **Asymmetric Septal Hypertrophy (ASH)** is the hallmark of HOCM. The septum is typically $\geq1.5$ times the thickness of the posterior wall. * **Option B:** **Systolic Anterior Motion (SAM)** occurs when the mitral valve's anterior leaflet is sucked toward the septum during systole due to the Venturi effect, contributing to obstruction. * **Option C:** The combination of ASH and SAM leads to **LVOT obstruction**, which is dynamic and worsens with factors that decrease preload or increase contractility. **NEET-PG High-Yield Pearls:** 1. **Murmur Dynamics:** The harsh systolic murmur of HOCM **increases** with Valsalva and standing (decreased preload) and **decreases** with squatting or handgrip (increased preload/afterload). 2. **Drugs to Avoid:** Nitrates, Diuretics, and ACE inhibitors (they decrease preload/afterload, worsening the obstruction) and Digitalis (increases contractility). 3. **ECG Findings:** Giant T-wave inversions (precordial leads) and "dagger-like" Q waves in lateral leads. 4. **Sudden Cardiac Death (SCD):** HOCM is the most common cause of SCD in young athletes [1].

Question 1068: Reverse splitting of S2 is seen in which of the following conditions?

A. Aortic stenosis (Correct Answer)
B. Aortic stenosis
C. Pulmonary artery hypertension
D. Pulmonary stenosis

Explanation: The second heart sound (S2) is composed of two components: **A2** (Aortic valve closure) and **P2** (Pulmonary valve closure). Normally, A2 precedes P2, and the gap increases during inspiration (physiological splitting). **Reverse (paradoxical) splitting** occurs when P2 precedes A2. This happens when there is a significant delay in the closure of the aortic valve. **1. Why Aortic Stenosis (AS) is correct:** In severe Aortic Stenosis, the left ventricular ejection time is prolonged because the blood must be forced through a narrowed orifice [1]. This delays the closure of the aortic valve (A2) so much that it occurs after P2. During inspiration, P2 moves later (normal physiology), narrowing the gap between P2 and A2; during expiration, P2 moves earlier, widening the gap. This "paradoxical" behavior is a hallmark of severe AS [1], Left Bundle Branch Block (LBBB), and HOCM. **2. Why the other options are incorrect:** * **Pulmonary Stenosis:** This causes a delay in P2, leading to a **wide and fixed/variable split** (A2 occurs first, but P2 is significantly delayed) [3]. * **Pulmonary Artery Hypertension:** This typically results in a **loud P2** and a narrow split, but the sequence (A2 before P2) remains normal. * **Atrial Septal Defect (ASD):** (Commonly confused) This causes a **wide, fixed split** S2, not reverse splitting [2]. **Clinical Pearls for NEET-PG:** * **Normal Split:** Increases with inspiration (P2 moves later). * **Wide Split:** Seen in RBBB and Pulmonary Stenosis [3]. * **Fixed Split:** Pathognomonic for **ASD** [2]. * **Reverse Split:** Think **"L-A-H"** — **L**BBB, **A**ortic Stenosis, **H**OCM. * If a question mentions "splitting disappears on inspiration," it is referring to reverse splitting.

Question 1069: Which of the following is NOT a typical ECG feature of primary pulmonary hypertension?

A. Sinus tachycardia
B. ST elevation (Correct Answer)
C. Increased P wave amplitude
D. Right axis deviation

Explanation: Primary Pulmonary Hypertension (PPH) leads to chronic pressure overload of the right side of the heart, resulting in **Right Ventricular Hypertrophy (RVH)** and **Right Atrial Enlargement (RAE)** [1, 3]. **Why ST Elevation is the correct answer:** ST elevation is typically a marker of acute myocardial infarction or pericarditis [3]. In the context of pulmonary hypertension, the ECG usually shows signs of right heart strain, which manifests as **ST-segment depression** and **T-wave inversion** in the right precordial leads (V1–V3), rather than ST elevation [1, 3]. **Analysis of incorrect options:** * **Sinus Tachycardia:** This is a common, non-specific finding in pulmonary hypertension as the heart attempts to maintain cardiac output despite increased pulmonary vascular resistance [1]. * **Increased P wave amplitude:** Known as **P-pulmonale**, this refers to a peaked P wave >2.5 mm in lead II. it is a classic sign of right atrial enlargement due to high pulmonary pressures [2]. * **Right Axis Deviation (RAD):** As the right ventricle hypertrophies, the mean electrical axis shifts toward the right (usually >+90°), making this a hallmark feature of the condition [1, 3]. **High-Yield Clinical Pearls for NEET-PG:** * **ECG Triad of RVH:** Right Axis Deviation, dominant R wave in V1 (>7mm), and right ventricular strain pattern (ST depression/T wave inversion in V1-V3) [1, 3]. * **S1Q3T3:** While classic for Pulmonary Embolism (acute cor pulmonale), it is less common in chronic primary pulmonary hypertension [1]. * **Gold Standard Diagnosis:** Right heart catheterization (Mean Pulmonary Artery Pressure >20 mmHg at rest).

Question 1070: A patient with rheumatic heart disease, mitral stenosis, and atrial fibrillation is on oral warfarin. On an OPD visit, his INR is found to be 6. What is the recommended action?

A. Stop warfarin, and review (Correct Answer)
B. Stop warfarin, and administer fresh frozen plasma
C. Stop warfarin, and administer oral vitamin K
D. Stop warfarin, and administer intramuscular vitamin K

Explanation: **Explanation:** The management of supratherapeutic INR in patients on Warfarin is a high-yield topic governed by the **ACCP (American College of Chest Physicians) guidelines**. The primary factors determining management are the **INR value** and the **presence or absence of bleeding.** **1. Why Option A is Correct:** In this scenario, the patient has an INR of 6.0 but is **asymptomatic** (no mention of bleeding). According to guidelines, for patients with an **INR between 4.5 and 10.0 and NO clinically significant bleeding**, the recommended action is to **omit the next few doses of Warfarin** and monitor (review) the INR frequently [1]. Warfarin can be resumed at a lower dose once the INR returns to the therapeutic range. **2. Why Other Options are Incorrect:** * **Option B (FFP):** Fresh Frozen Plasma (or Prothrombin Complex Concentrate) is reserved for patients with **major or life-threatening bleeding**, regardless of the INR level. It is not indicated for asymptomatic elevation. * **Option C (Oral Vitamin K):** Oral Vitamin K (1–2.5 mg) is generally reserved for asymptomatic patients with an **INR > 10.0**. At an INR of 6.0 without bleeding, it is not routinely required. * **Option D (IM Vitamin K):** Intramuscular administration of Vitamin K should be **avoided** in patients on anticoagulants due to the high risk of hematoma formation at the injection site. **Clinical Pearls for NEET-PG:** * **INR < 4.5 (No bleeding):** Reduce dose or skip one dose; monitor. * **INR 4.5 – 10.0 (No bleeding):** Hold 1–2 doses; monitor. * **INR > 10.0 (No bleeding):** Hold Warfarin and give **Oral Vitamin K** (2.5–5 mg). * **Any INR with Serious/Life-threatening Bleeding:** Hold Warfarin + **IV Vitamin K** (10 mg) + **4-factor PCC** (preferred) or **FFP**. * **Target INR for Mitral Stenosis with AF:** 2.0 – 3.0 [2].

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