Cardiology Practice Questions

Q: What does the ECG show?

Mobitz type 1 heart block. ***Mobitz type 1 heart block*** - Shows **progressive lengthening of PR intervals** followed by a **dropped QRS complex**, creating the characteristic **Wenckebach phenomenon**. - After the dropped beat, the **PR interval resets** to its shortest duration and the cycle repeats, indicating intact but fatiguing AV conduction. *First degree heart block* - Characterized by a **fixed prolonged PR interval** (>0.20 seconds) with **no dropped beats**. - All P waves are followed by QRS complexes, unlike the intermittent dropped beats seen in this ECG. *Complete heart block* - Shows **complete AV dissociation** with P waves and QRS complexes occurring independently at different rates. - The **ventricular escape rhythm** is typically slower (30-50 bpm) with no relationship between P waves and QRS complexes. *Mobitz type II heart block* - Features **fixed PR intervals** with **sudden dropped QRS complexes** without prior PR prolongation. - Carries a **worse prognosis** than Mobitz type I and often requires pacemaker implantation due to risk of progression to complete heart block.

Q: What type of mutation is most commonly associated with Brugada syndrome?

Loss of function mutation. **Explanation:** **Brugada Syndrome** is an autosomal dominant genetic channelopathy characterized by a predisposition to ventricular arrhythmias and sudden cardiac death. **1. Why "Loss of Function" is correct:** The most common genetic defect in Brugada Syndrome involves the **SCN5A gene**, which encodes the alpha subunit of the cardiac **sodium channel (Nav1.5)**. The mutation leads to a **Loss of Function (LOF)** of these sodium channels. This reduction in inward sodium current ($I_{Na}$) during Phase 0 of the action potential causes an imbalance between inward and outward currents, particularly in the right ventricular outflow tract (RVOT) epicardium. This results in the characteristic ST-segment elevation (Coved pattern) and provides the substrate for re-entrant arrhythmias. **2. Why other options are incorrect:** * **Gain of Function (GOF):** GOF mutations in the SCN5A gene lead to **Long QT Syndrome Type 3 (LQT3)**, where the sodium channel fails to inactivate properly, prolonging the action potential. * **Antimorphic mutation:** This refers to a dominant-negative effect where the mutant gene product actively opposes the wild-type. While some SCN5A mutations may show this, the primary underlying mechanism is classified as LOF. * **Lethal mutation:** While Brugada syndrome can cause sudden death, the mutation itself is not "lethal" in a genetic sense (embryonic lethal), as individuals survive to adulthood. **High-Yield Clinical Pearls for NEET-PG:** * **ECG Hallmark:** "Coved" ST-elevation >2mm followed by a negative T-wave in V1-V2 (Type 1 pattern). * **Triggers:** Fever, large meals, and certain drugs (Sodium channel blockers like Ajmaline/Flecainide). * **Inheritance:** Autosomal Dominant. * **Management:** The only proven effective treatment for symptomatic patients or survivors of cardiac arrest is an **Implantable Cardioverter Defibrillator (ICD)**. Quinidine can be used for electrical storms.

Q: Pulse deficit may be seen in all of the following, except:

Bradyarrhythmias. **Explanation:** **Pulse deficit** is defined as the difference between the **apical heart rate** (measured by auscultation) and the **peripheral pulse rate** (measured by palpation). It occurs when ventricular contractions are too weak or happen too early to generate a pressure wave strong enough to open the aortic valve or reach the peripheral arteries. **Why Bradyarrhythmias is the Correct Answer:** In bradyarrhythmias (e.g., complete heart block), the heart rate is slow, allowing for prolonged diastolic filling time. This ensures that every ventricular contraction results in a significant stroke volume, producing a palpable peripheral pulse for every audible heartbeat. Therefore, the apical and radial rates are equal, and there is **no pulse deficit**. **Analysis of Other Options:** * **Atrial Fibrillation (AF):** This is the most common cause of pulse deficit. Variable diastolic filling times and "short cycles" result in some contractions being too weak to be felt peripherally. * **Ventricular Premature Contractions (VPC):** An early beat occurs before the ventricles have filled sufficiently. The resulting stroke volume is often inadequate to produce a palpable radial pulse, though the beat is heard on auscultation. * **Tachyarrhythmias:** Rapid heart rates shorten diastole significantly, leading to reduced stroke volume in many beats, thereby creating a deficit. **Clinical Pearls for NEET-PG:** * **Diagnostic Threshold:** A pulse deficit of **>10 beats/minute** is clinically significant and highly suggestive of Atrial Fibrillation. * **Measurement:** To be accurate, the apical and radial pulses should be counted simultaneously by two observers for one full minute. * **Pulsus Alternans:** Do not confuse pulse deficit with pulsus alternans (seen in left ventricular failure), where every beat reaches the periphery but with alternating strength.

Q: A dicrotic pulse is observed in which condition?

Dilated Cardiomyopathy (DCM). **Explanation:** A **dicrotic pulse** is characterized by two peaks in the arterial pulse waveform during a single cardiac cycle: one in systole and the second in diastole (following the dicrotic notch). It occurs due to an exaggerated dicrotic wave, typically seen in states with **low cardiac output** and **high systemic vascular resistance** (high peripheral resistance) [1]. **1. Why Dilated Cardiomyopathy (DCM) is correct:** In DCM, the stroke volume is significantly reduced (low cardiac output) [1]. This leads to a low-amplitude systolic peak. Simultaneously, the compensatory increase in peripheral resistance makes the dicrotic wave (rebound of blood against the closed aortic valve) more prominent [2]. The combination of a small systolic peak and a prominent diastolic peak results in the classic "double-peaked" dicrotic pulse. **2. Analysis of Incorrect Options:** * **HOCM:** Characterized by a **Bisferiens pulse** (two systolic peaks). The first peak is due to rapid ejection, followed by a dip due to mid-systolic obstruction, and a second peak as ejection continues. * **Restrictive Cardiomyopathy (RCM):** Usually presents with signs of right heart failure and Kussmaul’s sign, but not typically a dicrotic pulse. * **Left Ventricular Failure (LVF):** While LVF can lead to a dicrotic pulse if severe, it is more classically associated with **Pulsus Alternans** (alternating strong and weak beats) [1]. **3. High-Yield NEET-PG Pearls:** * **Dicrotic Pulse:** Seen in DCM, severe Heart Failure, and sometimes in young patients with Febrile illnesses (e.g., Typhoid). * **Bisferiens Pulse:** Seen in AR (Aortic Regurgitation), AS+AR, and HOCM. * **Anacrotic Pulse (Slow-rising):** Classic for Aortic Stenosis [3]. * **Pulsus Paradoxus:** Seen in Cardiac Tamponade [4], Severe Asthma, and COPD. * **Water-hammer Pulse:** Seen in AR, PDA, and High-output states [2].

Q: What is the drug of choice for persistent unstable ventricular arrhythmia?

Amiodarone. **Explanation:** **Amiodarone** is the drug of choice for persistent unstable ventricular arrhythmias (such as Ventricular Tachycardia or Ventricular Fibrillation) that are refractory to electrical cardioversion or defibrillation. As a Class III antiarrhythmic, its primary mechanism is blocking potassium channels, which prolongs the action potential duration and effective refractory period. However, it also possesses Class I (sodium channel), Class II (beta-blocking), and Class IV (calcium channel) properties, making it highly effective across various myocardial tissues. **Why other options are incorrect:** * **Procainamide (Option A):** While a Class IA antiarrhythmic used for stable VT (especially in Wolff-Parkinson-White syndrome), it is not the first-line choice for persistent unstable arrhythmias due to its slower onset and risk of hypotension. * **Calcium Gluconate (Option B):** This is used for cardioprotection in hyperkalemia or for calcium channel blocker toxicity; it has no direct antiarrhythmic effect on ventricular tachycardia. * **Digoxin (Option C):** Used primarily for rate control in atrial fibrillation or in heart failure. It can actually *induce* ventricular arrhythmias in toxic doses. **NEET-PG High-Yield Pearls:** * **ACLS Protocol:** In pulseless VT/VF, Amiodarone is administered after the third shock. Lidocaine is the alternative if Amiodarone is unavailable. * **Side Effects:** Long-term use is associated with "6 Ps": **P**ulmonary fibrosis, **P**hotodermatitis (Blue-grey skin), **P**rolonged QT, **P**eripheral neuropathy, and **P**eripapillary (corneal) deposits, and Thyroid **P**athology (Hypo/Hyperthyroidism due to high iodine content). * **Drug of Choice:** Amiodarone is also the drug of choice for arrhythmias in patients with structural heart disease or decreased ejection fraction.

Question 1

Which of the following differentiates ventricular tachycardia from Wolff-Parkinson-White (WPW) pattern with atrial fibrillation?

Accepted Answer

Regular RR interval

Answer

Irregular RR interval

Answer

Broad QRS

Answer

Increased heart rate

Question 2

A 41-year-old woman presents with chest pain, shortness of breath, and worsening fatigue for the past day. The chest pain initially worsened with lying down and improved with leaning forward, but now it seems equal in intensity over all positions. On examination, she has labored, fast breathing and appears to be in pain. She has jugular venous distention. She is tachycardic, and has distant heart sounds with a friction rub. Her lungs are clear to auscultation bilaterally, and she has no limb edema. Her pulse is 126/min, BP is 89/66 mm Hg, respiratory rate is 32/min, and oxygen saturation is 98% on room air. Which of the following is the most likely diagnosis?

Accepted Answer

Cardiac tamponade

Answer

Acute Pericarditis

Answer

Congestive heart failure

Answer

Panic attack

Question 3

Which of the following statements regarding the ECG findings in acute pericarditis is FALSE?

Accepted Answer

T wave inversion develops after ST elevations return to baseline.

Answer

Global ST segment elevation is seen in early pericarditis.

Answer

Sinus tachycardia is a common finding.

Answer

PR segment depression is present in the majority of patients.

Question 4

What does the ECG show?

Accepted Answer

Mobitz type 1 heart block

Answer

First degree heart block

Answer

Complete heart block

Answer

Mobitz type II heart block

Question 5

What type of mutation is most commonly associated with Brugada syndrome?

Accepted Answer

Loss of function mutation

Answer

Gain of function mutation

Answer

Antimorphic mutation

Answer

Lethal mutation

Question 6

Pulse deficit may be seen in all of the following, except:

Accepted Answer

Bradyarrhythmias

Answer

Ventricular Premature Contraction (VPC)

Answer

Atrial Fibrillation (AF)

Answer

Tachyarrhythmias

Question 7

A dicrotic pulse is observed in which condition?

Accepted Answer

Dilated Cardiomyopathy (DCM)

Answer

Hypertrophic Obstructive Cardiomyopathy (HOCM)

Answer

Restrictive Cardiomyopathy (RCM)

Answer

Left Ventricular Failure

Question 8

What is the most common cause of mitral stenosis?

Accepted Answer

Rheumatic heart disease

Answer

Infective endocarditis

Answer

Diabetes mellitus

Answer

Congenital

Question 9

What is the drug of choice for persistent unstable ventricular arrhythmia?

Accepted Answer

Amiodarone

Answer

Procainamide

Answer

Calcium gluconate

Answer

Digoxin

Question 10

Pseudo resistant hypertension is seen in which situation?

Accepted Answer

Patient at the office

Answer

Patient at home

Answer

Patient at the hospital

Answer

None of the above

Cardiology — MCQs

Cardiology — MCQs

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