Cardiology Practice Questions

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

Congenital heart disease. ### 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].

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

Decreased peripheral resistance. **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].

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

Hypercalcemia. **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].

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

Hypertrophic cardiomyopathy. ### 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**.

Q: What is characteristic of unstable angina?

The levels of cardiac markers remain unchanged.. ### 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).

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

Right coronary artery. **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].

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

Pulmonary Hypertension. 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.

Question 1

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

Accepted Answer

Congenital heart disease

Answer

Ischemic heart disease

Answer

Hypertension

Answer

Congestive cardiac failure

Question 2

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?

Accepted Answer

A lymphangiogram will show hypoplasia of the lymphatics.

Answer

Prophylactic antibiotics are indicated.

Answer

Elastic stockings and diuretics will lead to a normal appearance of the limb.

Answer

A variety of operations will ultimately lead to a normal appearance of the limb.

Question 3

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?

Accepted Answer

Increase in murmur intensity during Valsalva maneuver or standing

Answer

A crescendo-decrescendo systolic murmur

Answer

Murmur radiating to the neck

Answer

Brisk carotid upstroke

Question 4

All of the following are true about pulsus parvus EXCEPT?

Accepted Answer

Decreased peripheral resistance

Answer

Seen in aortic stenosis

Answer

Decreased left ventricular output

Answer

Decreased pulse pressure

Question 5

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

Accepted Answer

Hypercalcemia

Answer

Hypokalemia

Answer

Hypocalcemia

Answer

Hypomagnesemia

Question 6

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?

Accepted Answer

Soft S1 and holosystolic murmur radiating from the apex to the axilla

Answer

Early and midsystolic murmur, pulmonary edema, and elevated JVP

Answer

Diminished S1

Answer

Clear lungs and elevated JVP

Question 7

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

Accepted Answer

Hypertrophic cardiomyopathy

Answer

Aortic stenosis

Answer

Mitral regurgitation

Answer

Aortic regurgitation

Question 8

What is characteristic of unstable angina?

Accepted Answer

The levels of cardiac markers remain unchanged.

Answer

CK-MB is elevated

Answer

Troponin I is elevated

Answer

Myoglobin is elevated

Question 9

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

Accepted Answer

Right coronary artery

Answer

Left coronary artery

Answer

Left anterior descending artery

Answer

Right circumflex artery

Question 10

Loud P2 is found in which of the following conditions?

Accepted Answer

Pulmonary Hypertension

Answer

Mitral Stenosis

Answer

Mitral Regurgitation

Answer

Aortic Incompetence

Cardiology — MCQs

Cardiology — MCQs

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