Cardiology — MCQs

A 16-year-old male is referred for a physical examination before joining the football team. His elder brother died suddenly during football practice; no autopsy was performed. The patient has a loud systolic murmur on chest auscultation. Which of the following findings is inconsistent with hypertrophic cardiomyopathy?

Q654Medium

All of the following are true about pulsus parvus EXCEPT?

Q655Medium

Prolonged QT interval is not seen in which of the following conditions?

Q656Medium

An asymptomatic 19-year-old female student presents for routine follow-up. Echocardiogram shows congenital mitral regurgitation. What are the most typical clinical and auscultation findings?

Q657Medium

Which of the following heart diseases is the most common cause of sudden death in young athletes?

Q658Medium

What is characteristic of unstable angina?

Q659Medium

In ECG leads II, III, and aVF, abnormalities are noted. Which of the following vessels is most likely blocked?

Q660Easy

Loud P2 is found in which of the following conditions?

Cardiology Indian Medical PG Practice Questions and MCQs

Question 651: Antibiotic prophylaxis is mandatory before dental extraction in patients with which of the following cardiac conditions?

A. Ischemic heart disease
B. Hypertension
C. Congestive cardiac failure
D. Congenital heart disease (Correct Answer)

Explanation: ### Explanation The primary goal of antibiotic prophylaxis before dental procedures is to prevent **Infective Endocarditis (IE)**. Dental extractions cause transient bacteremia (commonly *Viridans group streptococci*), which can seed onto damaged endocardium or prosthetic material, leading to life-threatening infections. **Why Congenital Heart Disease (CHD) is correct:** According to the latest AHA/ACC and ESC guidelines, antibiotic prophylaxis is only indicated for "High-Risk" conditions [1]. **Congenital Heart Disease** falls into this category under specific circumstances [3]: 1. **Cyanotic CHD** that has not been repaired. 2. CHD repaired with **prosthetic material** (for the first 6 months post-procedure) [1]. 3. Repaired CHD with **residual defects** at or adjacent to the site of a prosthetic patch/device. 4. Patients with a prior history of IE or those with prosthetic heart valves [1]. **Why other options are incorrect:** * **A, B, and C (IHD, Hypertension, CCF):** While these are significant cardiovascular morbidities, they do not involve the structural valvular abnormalities or high-velocity turbulent flow required to create a substrate (vegetation) for bacterial attachment. Therefore, the risk of IE in these patients is not significantly higher than in the general population. [2] **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Oral **Amoxicillin (2g)** given 30–60 minutes before the procedure. * **If Penicillin allergic:** Use Clindamycin (600mg), Cephalexin (2g), or Azithromycin/Clarithromycin (500mg). * **Procedures requiring prophylaxis:** Only those involving manipulation of gingival tissue, the periapical region of teeth, or perforation of the oral mucosa. * **Not recommended anymore:** Prophylaxis is no longer required for routine mitral valve prolapse (MVP) or simple bicuspid aortic valves unless other high-risk criteria are met [1].

Question 652: Sukhia Rani, a 16-year old girl, presents with non-pitting edema of recent onset affecting her right leg and no other symptoms. Which of the following statements is true regarding this patient?

A. Prophylactic antibiotics are indicated.
B. A lymphangiogram will show hypoplasia of the lymphatics. (Correct Answer)
C. Elastic stockings and diuretics will lead to a normal appearance of the limb.
D. A variety of operations will ultimately lead to a normal appearance of the limb.

Explanation: ### Explanation The clinical presentation of a 16-year-old girl with unilateral, non-pitting edema of the leg is classic for **Lymphedema Praecox** (a form of Primary Lymphedema). **1. Why Option B is Correct:** Primary lymphedema is caused by developmental abnormalities of the lymphatic system. Lymphedema praecox (Meige disease) typically manifests around puberty and is more common in females. In approximately 70-80% of these cases, a lymphangiogram reveals **lymphatic hypoplasia** (fewer and smaller lymphatics). Other patterns include lymphatic aplasia or hyperplasia (varicosity), but hypoplasia is the most frequent finding. **2. Analysis of Incorrect Options:** * **Option A:** Prophylactic antibiotics are not indicated for the edema itself. They are only prescribed if the patient suffers from recurrent episodes of cellulitis or lymphangitis, which is not mentioned here. * **Option C:** While elastic stockings and physical therapy (Complex Decongestive Therapy) are the mainstays of management, they control the swelling but **do not restore a "normal appearance"** to the limb. Diuretics are generally ineffective for lymphedema as they remove water but leave behind the protein-rich interstitial fluid. * **Option D:** Surgical interventions (e.g., Charles procedure or lymphovenous anastomosis) are reserved for severe, refractory cases. These operations are palliative or functional; they rarely, if ever, result in a perfectly "normal" looking limb and often leave significant scarring. **3. NEET-PG High-Yield Pearls:** * **Classification by Age:** * *Lymphedema Congenita:* Present at birth (e.g., Milroy's disease). * *Lymphedema Praecox:* Onset between ages 1–35 (most common primary type). * *Lymphedema Tarda:* Onset after age 35. * **Stemmer’s Sign:** Inability to pinch the skin on the dorsal surface of the second toe; a pathognomonic clinical sign of lymphedema. * **Gold Standard Investigation:** **Lymphoscintigraphy** (using Technetium-99m labeled colloid) has largely replaced the older, invasive lymphangiogram in modern practice.

Question 653: A 16-year-old male is referred for a physical examination before joining the football team. His elder brother died suddenly during football practice; no autopsy was performed. The patient has a loud systolic murmur on chest auscultation. Which of the following findings is inconsistent with hypertrophic cardiomyopathy?

A. A crescendo-decrescendo systolic murmur
B. Murmur radiating to the neck
C. Brisk carotid upstroke
D. Increase in murmur intensity during Valsalva maneuver or standing (Correct Answer)

Explanation: The correct answer is **B. Murmur radiating to the neck.** In **Hypertrophic Obstructive Cardiomyopathy (HOCM)**, the murmur is caused by dynamic left ventricular outflow tract (LVOT) obstruction [1]. This occurs due to asymmetrical septal hypertrophy and systolic anterior motion (SAM) of the mitral valve. 1. **Why Option B is the correct choice (Inconsistent finding):** Radiation to the neck (carotids) is a hallmark of **Aortic Stenosis (AS)**, not HOCM [1]. In HOCM, the murmur typically radiates to the axilla or remains localized at the lower left sternal border, as the turbulence is directed away from the aortic valve. 2. **Why other options are consistent with HOCM:** * **Option A:** The murmur is characteristically **crescendo-decrescendo** (ejection systolic) because the obstruction develops mid-systole as the heart contracts. * **Option C:** Unlike the *pulsus parvus et tardus* (weak and late) seen in AS, HOCM features a **brisk carotid upstroke** (often "spike and dome") because initial ejection is rapid before the obstruction occurs [1]. * **Option D:** This is a classic HOCM feature. **Valsalva and standing** decrease preload, reducing LV volume. A smaller LV cavity increases the proximity of the septum to the mitral valve, worsening the obstruction and **increasing murmur intensity.** **High-Yield Clinical Pearls for NEET-PG:** * **Dynamic Maneuvers:** HOCM and Mitral Valve Prolapse (MVP) are the only two murmurs that **increase** in intensity with Valsalva/Standing (decreased preload). * **Handgrip/Squatting:** These increase afterload/preload, increasing LV volume and **decreasing** the HOCM murmur. * **Sudden Cardiac Death (SCD):** HOCM is the most common cause of SCD in young athletes due to ventricular arrhythmias [1]. * **Drug of Choice:** Beta-blockers (first-line) to improve diastolic filling. Avoid Nitrates and Diuretics.

Question 654: All of the following are true about pulsus parvus EXCEPT?

A. Seen in aortic stenosis
B. Decreased left ventricular output
C. Decreased peripheral resistance (Correct Answer)
D. Decreased pulse pressure

Explanation: **Explanation:** **Pulsus parvus** refers to a pulse with low amplitude (small volume). It is frequently associated with **pulsus tardus** (delayed peak), collectively known as *pulsus parvus et tardus*, which is the hallmark of severe aortic stenosis [2]. **Why Option C is the correct answer:** Pulsus parvus is caused by conditions that lead to a narrow pulse pressure [1]. **Decreased peripheral resistance** (seen in distributive shock or high-output states) typically leads to a rapid stroke volume ejection and lower diastolic pressure, which often results in a **bounding pulse** (large volume) rather than a small volume pulse [1]. In contrast, *increased* peripheral resistance is a compensatory mechanism in low-output states to maintain blood pressure, which contributes to the "small" feel of the pulse. **Analysis of Incorrect Options:** * **A. Seen in aortic stenosis:** This is true. The mechanical obstruction to left ventricular outflow limits the stroke volume and slows the rate of pressure rise in the peripheral arteries [2]. * **B. Decreased left ventricular output:** This is true. Any condition that reduces stroke volume (e.g., heart failure, hypovolemia, or mitral stenosis) will manifest as a low-amplitude pulse [1], [3]. * **C. Decreased pulse pressure:** This is true. Pulse pressure is the difference between systolic and diastolic pressure. A low stroke volume directly reduces systolic pressure, narrowing the pulse pressure and resulting in pulsus parvus [1]. **Clinical Pearls for NEET-PG:** * **Pulsus Parvus et Tardus:** Classic sign of **Aortic Stenosis** [2]. * **Pulsus Alternans:** Alternating strong and weak beats; pathognomonic for **Left Ventricular Failure**. * **Pulsus Paradoxus:** An exaggerated drop in systolic BP (>10 mmHg) during inspiration; classic for **Cardiac Tamponade**. * **Water-hammer pulse (Corrigan’s):** Large volume, bounding pulse seen in **Aortic Regurgitation** [1].

Question 655: Prolonged QT interval is not seen in which of the following conditions?

A. Hypokalemia
B. Hypocalcemia
C. Hypomagnesemia
D. Hypercalcemia (Correct Answer)

Explanation: **Explanation:** The QT interval on an ECG represents the total time for ventricular depolarization and repolarization. It is primarily influenced by the duration of the action potential. **Why Hypercalcemia is the correct answer:** In **Hypercalcemia**, the increased extracellular calcium levels shorten the phase 2 (plateau phase) of the cardiac action potential. This leads to faster repolarization, which manifests on the ECG as a **shortened QT interval**. In severe cases, the ST segment may be completely absent, with the T wave starting immediately after the QRS complex. **Analysis of incorrect options (Conditions that prolong QT):** * **Hypocalcemia (B):** Low calcium levels prolong phase 2 of the action potential, leading to a lengthened ST segment and a **prolonged QT interval**. * **Hypokalemia (A):** Low potassium levels delay repolarization and often lead to the appearance of prominent **U waves** [1]. While the "true" QT may be normal, the fusion of the T and U waves creates a "QU interval," which is clinically interpreted as a prolonged QT. * **Hypomagnesemia (C):** Magnesium is a cofactor for the Na+/K+-ATPase pump. Its deficiency impairs repolarization and is frequently associated with both hypokalemia and hypocalcemia, collectively leading to QT prolongation. **High-Yield Clinical Pearls for NEET-PG:** * **Formula:** The corrected QT (QTc) is calculated using **Bazett’s Formula**: $QTc = QT / \sqrt{RR}$. * **Torsades de Pointes:** Prolonged QT interval is the primary precursor for this life-threatening polymorphic ventricular tachycardia [2]. * **Drug-induced QT prolongation:** Common culprits include Class IA and III antiarrhythmics, Macrolides, Fluoroquinolones, and Antipsychotics (e.g., Haloperidol). * **Congenital Syndromes:** Romano-Ward (autosomal dominant, pure cardiac) and Jervell and Lange-Nielsen (autosomal recessive, associated with sensorineural deafness) [3].

Question 656: An asymptomatic 19-year-old female student presents for routine follow-up. Echocardiogram shows congenital mitral regurgitation. What are the most typical clinical and auscultation findings?

A. Soft S1 and holosystolic murmur radiating from the apex to the axilla (Correct Answer)
B. Early and midsystolic murmur, pulmonary edema, and elevated JVP
C. Diminished S1
D. Clear lungs and elevated JVP

Explanation: **Explanation:** **1. Why Option A is Correct:** In chronic Mitral Regurgitation (MR), the mitral leaflets fail to coapt properly. The **Soft S1** occurs because the leaflets are already partially closed or poorly apposed at the onset of ventricular systole, reducing the intensity of the closure sound. The **holosystolic (pansystolic) murmur** is the hallmark of MR; it begins immediately with S1 and continues through S2 as blood leaks from the high-pressure left ventricle into the low-pressure left atrium [1]. Because the regurgitant jet is usually directed posterolaterally, the murmur characteristically **radiates to the axilla** [1]. **2. Why Other Options are Incorrect:** * **Option B:** Early and midsystolic murmurs are more typical of acute MR or aortic stenosis [2]. Pulmonary edema and elevated JVP suggest acute heart failure or right heart failure, which are unlikely in an **asymptomatic** 19-year-old with chronic compensated MR. * **Option C:** While a diminished S1 is a feature of MR, this option is incomplete compared to Option A, which provides the classic murmur description essential for diagnosis. * **Option D:** While lungs are clear in compensated MR, an elevated JVP indicates right-sided heart failure (late-stage disease). In an asymptomatic young patient, the JVP is typically normal. **3. NEET-PG High-Yield Pearls:** * **S3 Gallop:** In severe chronic MR, an S3 may be heard due to rapid filling of the dilated left ventricle; it does *not* necessarily indicate heart failure in this context [1]. * **Dynamic Auscultation:** The MR murmur **increases** with handgrip (increased afterload) and **decreases** with Valsalva or standing (decreased preload). * **Apex:** The apex is usually displaced inferolaterally due to left ventricular volume overload. * **Commonest Cause:** Globally, Rheumatic Heart Disease remains a major cause, but in developed settings, Mitral Valve Prolapse (MVP) is more common.

Question 657: Which of the following heart diseases is the most common cause of sudden death in young athletes?

A. Aortic stenosis
B. Mitral regurgitation
C. Aortic regurgitation
D. Hypertrophic cardiomyopathy (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Hypertrophic cardiomyopathy (HCM)** **Why it is correct:** Hypertrophic cardiomyopathy is the most common cause of sudden cardiac death (SCD) in young athletes (typically defined as <35 years) [1]. It is an autosomal dominant genetic disorder characterized by asymmetric septal hypertrophy and myofibrillar disarray [1]. The mechanism of sudden death is usually a **lethal ventricular arrhythmia** (Ventricular Tachycardia or Ventricular Fibrillation) triggered during intense physical exertion [1]. The thickened myocardium, combined with fibrosis and ischemia, creates a substrate for these re-entrant arrhythmias [2]. **Why the other options are incorrect:** * **A. Aortic Stenosis:** While congenital bicuspid aortic valve can lead to stenosis and SCD in young individuals, it is significantly less common than HCM in the athletic population [1]. * **B & C. Mitral and Aortic Regurgitation:** Chronic valvular regurgitant lesions generally lead to progressive heart failure over years rather than sudden, unexpected death in an otherwise asymptomatic young athlete. **High-Yield Clinical Pearls for NEET-PG:** * **Murmur Dynamics:** The systolic murmur of HCM **increases** with Valsalva and standing (decreased preload) and **decreases** with squatting or handgrip (increased preload/afterload). This is a classic "opposite" behavior compared to most other murmurs. * **EKG Findings:** Look for "dagger-like" Q waves in lateral (I, aVL, V5-V6) and inferior leads. * **Management:** Beta-blockers are the first-line medical therapy. For those at high risk of SCD (e.g., history of syncope, massive hypertrophy >30mm), an **Implantable Cardioverter Defibrillator (ICD)** is the treatment of choice. * **Note:** In athletes >35 years, the most common cause of SCD shifts from HCM to **Coronary Artery Disease**.

Question 658: What is characteristic of unstable angina?

A. CK-MB is elevated
B. Troponin I is elevated
C. Myoglobin is elevated
D. The levels of cardiac markers remain unchanged. (Correct Answer)

Explanation: ### Explanation The core distinction between **Unstable Angina (UA)** and **Non-ST Elevation Myocardial Infarction (NSTEMI)** lies in the presence or absence of myocardial necrosis. Both conditions fall under the spectrum of Acute Coronary Syndrome (ACS) and may present with similar clinical symptoms (chest pain at rest) and ECG changes (ST-depression or T-wave inversion) [1]. **1. Why the Correct Answer is Right:** In Unstable Angina, there is transient or sub-total occlusion of a coronary artery leading to myocardial ischemia, but the ischemia is not severe or prolonged enough to cause irreversible cell death (necrosis) [2]. Since cardiac biomarkers like Troponin and CK-MB are only released into the bloodstream when the myocardial cell membrane is damaged, **the levels of cardiac markers remain within the normal range in UA.** [1] **2. Why the Incorrect Options are Wrong:** * **Options A, B, and C:** Elevation of **CK-MB**, **Troponin I**, or **Myoglobin** signifies myocardial injury/necrosis. If any of these markers are elevated in the clinical setting of ACS, the diagnosis automatically shifts from Unstable Angina to **Myocardial Infarction (NSTEMI or STEMI)** [1]. **3. NEET-PG Clinical Pearls:** * **Troponins (T and I):** These are the most sensitive and specific markers for cardiac injury. They begin to rise 3–6 hours after injury and can remain elevated for 7–14 days. * **CK-MB:** Useful for detecting **re-infarction** because it returns to baseline quickly (within 48–72 hours). * **Myoglobin:** The earliest marker to rise (1–2 hours), but it lacks specificity for cardiac muscle. * **Braunwald Classification:** Used to grade the severity of Unstable Angina based on the clinical presentation and intensity of treatment. * **Rule of Thumb:** UA = Ischemia (Normal Markers); NSTEMI = Necrosis (Elevated Markers, no ST-elevation); STEMI = Necrosis (Elevated Markers + ST-elevation).

Question 659: In ECG leads II, III, and aVF, abnormalities are noted. Which of the following vessels is most likely blocked?

A. Left coronary artery
B. Left anterior descending artery
C. Right coronary artery (Correct Answer)
D. Right circumflex artery

Explanation: **Explanation:** The ECG leads **II, III, and aVF** are known as the **inferior leads**. They look at the diaphragmatic (inferior) surface of the heart. In approximately 80-85% of individuals (right-dominant circulation), the **Right Coronary Artery (RCA)** gives rise to the Posterior Descending Artery (PDA), which supplies the inferior wall of the left ventricle. Therefore, ST-elevation or Q-waves in these leads typically signify an **Inferior Wall Myocardial Infarction (IWMI)** caused by an RCA occlusion [1]. **Analysis of Options:** * **Right Coronary Artery (Correct):** As the primary vessel supplying the inferior wall in the majority of the population, its blockage leads to changes in leads II, III, and aVF [1]. * **Left Coronary Artery (LCA):** This is the main trunk. A proximal occlusion here would typically cause massive anterolateral infarction (leads V1–V6, I, aVL) and is often fatal. * **Left Anterior Descending (LAD):** Known as the "widow maker," it supplies the anterior wall and septum. Blockage results in changes in leads **V1 to V4** [1]. * **Right Circumflex Artery:** This is a distractor. The **Left Circumflex (LCx)** artery supplies the lateral wall (leads I, aVL, V5, V6). In "left-dominant" individuals (10%), the LCx may supply the inferior wall, but the RCA remains the most common answer for exams. **High-Yield Clinical Pearls for NEET-PG:** * **Right Ventricular Infarction:** About 40% of IWMIs involve the right ventricle. Always check **Lead V4R**; if ST-elevation is present, avoid nitrates (due to preload dependence). * **Bradycardia:** The RCA supplies the SA node (60%) and AV node (90%). Thus, IWMI is frequently associated with sinus bradycardia or AV blocks. * **Lead III > Lead II:** If ST-elevation in lead III is greater than in lead II, it highly suggests RCA over LCx involvement [1].

Question 660: Loud P2 is found in which of the following conditions?

A. Pulmonary Hypertension (Correct Answer)
B. Mitral Stenosis
C. Mitral Regurgitation
D. Aortic Incompetence

Explanation: The second heart sound (S2) consists of two components: **A2** (Aortic valve closure) and **P2** (Pulmonary valve closure). The intensity of P2 depends on the pressure gradient across the pulmonary valve and the velocity of its closure. **1. Why Pulmonary Hypertension is Correct:** In **Pulmonary Hypertension (PH)**, the pressure in the pulmonary artery is significantly elevated [1]. This high back-pressure causes the pulmonary valve leaflets to slam shut with greater force and velocity at the end of ventricular systole, resulting in a **loud (accentuated) P2** [1]. This is a hallmark physical finding of PH and is best heard at the left second intercostal space. **2. Analysis of Incorrect Options:** * **Mitral Stenosis:** While long-standing Mitral Stenosis eventually leads to reactive pulmonary hypertension (which would cause a loud P2), the primary finding of Mitral Stenosis itself is a **loud S1** and an **Opening Snap**. PH is a secondary complication, not the defining feature of the valve lesion. * **Mitral Regurgitation:** This typically leads to a soft S1 and a pansystolic murmur. While it can eventually cause pulmonary venous congestion, it is not the classic cause of an isolated loud P2. * **Aortic Incompetence (Regurgitation):** This affects the A2 component or creates an early diastolic murmur. It does not directly increase pulmonary arterial pressure in its early or mid-stages. **High-Yield Clinical Pearls for NEET-PG:** * **Loud P2** is the most sensitive physical sign of Pulmonary Hypertension [1]. * **Soft/Absent P2:** Seen in Pulmonary Stenosis and Tetralogy of Fallot (due to reduced flow/pressure). * **Wide Fixed Split S2:** Characteristic of Atrial Septal Defect (ASD). * **Reverse (Paradoxical) Splitting:** Seen in Left Bundle Branch Block (LBBB) and Aortic Stenosis.

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Cardiomyopathies

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Pericardial Diseases

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Congenital Heart Disease in Adults

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Hypertension and Hypertensive Emergencies

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Cardiology — MCQs

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