Cardiology Practice Questions

Q: Which of the following ECG findings would indicate a posterior wall myocardial infarction?

ST elevation in V1-V3 leads. ### Explanation **Correct Answer: A. ST elevation in V1-V3 leads** In clinical practice, a **Posterior Wall Myocardial Infarction (PWMI)** is often diagnosed using a standard 12-lead ECG by looking for **reciprocal changes** in the anterior leads (V1-V3) [1]. Because the posterior wall is opposite to the anterior leads, the typical "STEMI" findings are "flipped": * ST-segment depression (instead of elevation) * Tall, broad R waves (instead of Q waves) * Upright, tall T waves (instead of T-wave inversion) [1] **Note on the Question:** While the standard ECG finding for PWMI is ST-depression in V1-V3, the diagnosis is **confirmed** by placing posterior leads (**V7-V9**). In these specific leads, the finding that indicates infarction is **ST-elevation** [3]. Therefore, in the context of posterior-specific leads, ST-elevation is the definitive finding. #### Analysis of Incorrect Options: * **B & D (Tall/Significant R waves):** These are indeed features of PWMI on a standard ECG (representing the "inverted" Q wave of the posterior wall). However, they are secondary diagnostic criteria compared to ST-segment changes. * **C (Tall T waves):** While tall, symmetric T waves in V1-V3 are seen in PWMI, they are non-specific and can also be seen in hyperkalemia or early de Winter’s T-waves. #### NEET-PG High-Yield Pearls: * **Artery Involved:** Most commonly the **Right Coronary Artery (RCA)** or the Left Circumflex (LCx). * **The "Mirror Test":** If you flip a standard ECG upside down and look at it through the back of the paper, the V1-V3 leads in a PWMI will look like a classic STEMI. * **Associated Infarcts:** PWMI rarely occurs in isolation; it is frequently associated with **Inferior Wall MI** (leads II, III, aVF) [2]. Always check posterior leads if you see ST-depression in V1-V3 that is not explained by ischemia.

Q: Which valve is most commonly affected in subacute bacterial endocarditis?

Mitral. In subacute bacterial endocarditis (SABE), the **Mitral valve** is the most commonly affected valve. This is because SABE typically occurs on valves that have pre-existing structural abnormalities, such as mitral valve prolapse (the most common underlying condition in developed countries) or chronic rheumatic heart disease (common in developing countries) [1]. The high-pressure gradient across the mitral valve creates turbulent blood flow, leading to endothelial damage and the formation of sterile fibrin-platelet vegetations (Non-Bacterial Thrombotic Endocarditis), which then become seeded by low-virulence organisms like *Streptococcus viridans* [1]. **Analysis of Options:** * **Mitral Valve (Correct):** It is the most frequent site of involvement overall. If the question specifies both Mitral and Aortic involvement, the combination is also very common, but individually, the Mitral valve leads. * **Tricuspid Valve (Incorrect):** This is the most common valve affected in **Intravenous Drug Users (IVDUs)**, typically associated with *Staphylococcus aureus* [1]. In the general population, right-sided involvement is much less common than left-sided. * **Pulmonary Valve (Incorrect):** This is the least commonly affected valve in infective endocarditis. **High-Yield Clinical Pearls for NEET-PG:** * **Most common organism (SABE):** *Streptococcus viridans* (low virulence, follows dental procedures) [1]. * **Most common organism (Acute IE):** *Staphylococcus aureus* (high virulence, affects normal valves) [1]. * **IVDU classic triad:** *S. aureus*, Tricuspid valve involvement, and multiple septic pulmonary emboli [1]. * **Prosthetic Valve Endocarditis:** *Staphylococcus epidermidis* is the most common cause within the first year of surgery. * **Culture-negative IE:** Most commonly due to prior antibiotic use or HACEK group organisms.

Q: A 62-year-old male with underlying COPD develops a viral upper respiratory infection and begins taking an over-the-counter decongestant. Shortly thereafter, he experiences palpitations and presents to the emergency room, where the given rhythm strip is obtained, demonstrating:

Atrial flutter. ***Atrial flutter*** - **Sympathomimetic decongestants** can precipitate atrial flutter in patients with underlying **COPD** due to increased sympathetic stimulation and hypoxemia. - Classic ECG features include **sawtooth flutter waves** at ~300 bpm atrial rate with regular ventricular response due to **2:1 or 3:1 AV block**. *Junctional tachycardia* - Originates from the **AV junction** and typically shows a **narrow QRS complex** with absent or inverted P waves. - Usually occurs at rates of **100-180 bpm** and is less commonly triggered by **sympathomimetics** compared to atrial arrhythmias. *Paroxysmal atrial tachycardia* - Characterized by **sudden onset and termination** with discrete P waves that differ from sinus P waves. - Atrial rate is typically **150-250 bpm** with **1:1 AV conduction**, unlike the organized flutter waves seen in atrial flutter. *Complete heart block* - Shows **complete AV dissociation** with independent atrial and ventricular rhythms at different rates. - Ventricular rate is typically **slow (30-50 bpm)** due to escape rhythm, inconsistent with palpitations from sympathomimetic use.

Q: Which of the following conditions presents with an ECG pattern that mimics myocardial infarction, often referred to as 'myocardial stunning'?

Takotsubo cardiomyopathy. **Explanation:** **Takotsubo Cardiomyopathy** (also known as "Broken Heart Syndrome" or "Stress-induced Cardiomyopathy") is the correct answer. It is characterized by transient left ventricular apical ballooning, typically triggered by intense emotional or physical stress. 1. **Why it is correct:** The pathophysiology involves a massive surge of catecholamines leading to microvascular dysfunction or direct catecholamine toxicity, resulting in **"myocardial stunning."** On ECG, it frequently presents with ST-segment elevation and T-wave inversions, closely mimicking an Acute Coronary Syndrome (ACS). However, coronary angiography reveals **no obstructive coronary artery disease.** 2. **Why the other options are incorrect:** * **Restrictive Cardiomyopathy:** Typically presents with low-voltage QRS complexes and signs of diastolic heart failure, not an MI-mimicking pattern. * **Brugada Syndrome:** Shows a characteristic "coved" ST-elevation in V1-V3 followed by a negative T-wave (Type 1 pattern). It is a sodium channelopathy associated with sudden cardiac death, not myocardial stunning. * **Pericardial Effusion:** Classically presents with low-voltage complexes and **electrical alternans** [1] (beat-to-beat variation in QRS amplitude). **High-Yield Pearls for NEET-PG:** * **Demographics:** Most common in post-menopausal women. * **Echocardiography:** Shows apical ballooning with hypercontractile basal segments (resembling a Japanese octopus trap, or *Takotsubo*). * **Cardiac Biomarkers:** Troponins are often mildly elevated, but the rise is disproportionately low compared to the extent of wall motion abnormalities. * **Prognosis:** Generally excellent, with ventricular function returning to normal within weeks.

Q: The ECG in hyperkalemia classically shows:

Increased QRS duration. **Explanation:** Hyperkalemia is a life-threatening electrolyte abnormality that significantly alters cardiac conduction. As serum potassium levels rise, the resting membrane potential of myocytes becomes less negative (partially depolarized), which decreases the velocity of the upstroke of the action potential (Phase 0) [1]. This results in **slowed intraventricular conduction**, which manifests on the ECG as an **increased QRS duration** (widening) [1]. If untreated, this can progress to a "sine wave" pattern and eventually ventricular fibrillation or asystole. **Analysis of Options:** * **B. Shortened PR interval:** Incorrect. Hyperkalemia actually causes **prolongation of the PR interval** due to slowed AV conduction [1]. Eventually, P waves may disappear entirely (atrial standstill) [1]. * **C. Prominent U waves:** Incorrect. Prominent U waves are a classic hallmark of **hypokalemia**, not hyperkalemia. * **D. Increased R wave amplitude:** Incorrect. In hyperkalemia, the R wave amplitude typically **decreases**, and the S wave depth increases as the QRS widens. **NEET-PG High-Yield Pearls:** * **Sequential ECG Changes:** 1. Tall, "tented" or peaked T waves (earliest sign, usually K+ >5.5 mEq/L) [1]. 2. PR prolongation and P wave flattening [1]. 3. QRS widening (K+ >6.5 mEq/L) [1]. 4. Sine wave pattern (K+ >8.0 mEq/L). * **Treatment Priority:** The first step in managing hyperkalemia with ECG changes is **Intravenous Calcium Gluconate** to stabilize the cardiac membrane, followed by insulin/dextrose to shift potassium intracellularly [2].

Q: Which gene alteration is most commonly associated with dilated cardiomyopathy?

Titin. **Explanation:** **1. Why Titin is the Correct Answer:** Dilated Cardiomyopathy (DCM) is characterized by ventricular dilation and systolic dysfunction. While DCM can be idiopathic, toxic, or infectious, approximately 30-40% of cases are familial. Mutations in the **TTN gene**, which encodes the protein **Titin**, are the most common genetic cause, accounting for roughly **25% of familial DCM** cases and 10-15% of sporadic cases. Titin is the largest protein in the human body and acts as a molecular spring, maintaining the structural integrity and passive stiffness of the sarcomere. Truncating mutations (TTNtv) lead to haploinsufficiency and impaired sarcomere function, resulting in ventricular remodeling. **2. Analysis of Incorrect Options:** * **Dystrophin:** Mutations in the dystrophin gene cause Duchenne and Becker muscular dystrophies. While these patients frequently develop DCM, it is not the *most common* genetic cause in the general population. * **Sarcomere (e.g., MYH7, TNNT2):** Mutations in sarcomeric proteins (Beta-myosin heavy chain, Troponin T) are the hallmark of **Hypertrophic Cardiomyopathy (HCM)**. While they can cause DCM, they are less frequent than Titin mutations. * **Mitochondrial genes:** These are associated with syndromic cardiomyopathies (e.g., MELAS) and typically present in pediatric populations with multi-organ involvement; they are a rare cause of isolated DCM. **3. High-Yield Clinical Pearls for NEET-PG:** * **Most common genetic cause of DCM:** Titin (TTN). * **Most common genetic cause of HCM:** Beta-myosin heavy chain (MYH7) or Myosin-binding protein C (MYBPC3). * **Arrhythmogenic Right Ventricular Dysplasia (ARVD):** Associated with desmosomal protein mutations (e.g., Plakoglobin, Desmoplakin). * **Lamin A/C (LMNA) mutations:** A high-yield cause of DCM associated with significant conduction system disease (AV blocks).

Q: Comment on the diagnosis of the patient based on ECG?

Multifocal atrial tachycardia. ***Multifocal atrial tachycardia*** - Characterized by **≥3 distinct P-wave morphologies**, **heart rate >100 bpm**, and **irregularly irregular rhythm** with varying **PR intervals**. - Commonly associated with **COPD exacerbations**, **hypomagnesemia**, and **theophylline toxicity**. *Atrial fibrillation* - Shows **absence of discrete P waves** with **fibrillatory waves** creating a wavy baseline between QRS complexes. - Results in **irregularly irregular rhythm** but lacks the multiple distinct P-wave morphologies seen in MAT. *Mobitz II heart block* - Presents with **intermittently dropped QRS complexes** following normal P waves with **fixed PR intervals**. - The **atrial rate remains regular** (typically 60-100 bpm) with periodic **non-conducted P waves**. *Wolff-Parkinson-White syndrome* - Characterized by **delta waves** (slurred upstroke of QRS), **short PR interval** (<0.12 seconds), and **wide QRS complex**. - May present with **supraventricular tachycardia** but shows consistent **pre-excitation pattern**, not multiple P-wave morphologies.

Q: A fixed PR interval with occasional dropped beats in a 2:1, 3:1, or 4:1 pattern, accompanied by a wide QRS complex, is characteristic of which condition?

Mobitz Type II block. The correct answer is **Mobitz Type II block**. This condition is characterized by an intermittent failure of conduction through the His-Purkinje system. Unlike Type I, the **PR interval remains constant (fixed)** before and after the dropped beat. It often presents in fixed ratios (2:1, 3:1, etc.) [1]. Because the block occurs below the AV node (infra-nodal), the escape rhythm or conducted beats usually exhibit a **wide QRS complex**, indicating bundle branch involvement. **Why other options are incorrect:** * **Wenckebach (Mobitz Type I):** This involves a progressive lengthening of the PR interval until a beat is dropped [1]. The QRS is typically narrow because the block is at the level of the AV node. * **WPW Syndrome:** This is a pre-excitation syndrome characterized by a short PR interval and a delta wave [2]. It does not cause dropped beats in a fixed PR ratio. * **Complete Heart Block (CHB):** In CHB, there is total AV dissociation. The P waves and QRS complexes have no relationship with each other, meaning the PR interval is not "fixed" but completely variable. **High-Yield Clinical Pearls for NEET-PG:** * **Site of Block:** Mobitz I is usually **intranodal** (reversible, better prognosis); Mobitz II is **infranodal** (permanent, high risk of progression to CHB) [1]. * **Vagal Maneuvers:** Carotid sinus massage worsens Mobitz II (by increasing AV conduction but exposing the distal block) but improves Mobitz I. * **Management:** Mobitz Type II always requires a **permanent pacemaker**, even if the patient is asymptomatic, due to the high risk of sudden cardiac arrest [1].

Q: What is the most common cause of embolism leading to cerebrovascular disease?

Non-rheumatic atrial fibrillation. ### Explanation **Correct Answer: B. Non-rheumatic atrial fibrillation** **Concept:** Embolic strokes account for approximately 20% of all ischemic strokes. The most common source of these emboli is the heart (cardioembolism). Among all cardiac conditions, **Non-rheumatic Atrial Fibrillation (AF)** is the leading cause [1]. In AF, the ineffective contraction of the atria (particularly the left atrial appendage) leads to blood stasis, thrombus formation, and subsequent embolization to the cerebral circulation [2]. The risk increases significantly with age and the presence of other comorbidities (calculated via the CHA₂DS₂-VASc score) [2]. **Analysis of Incorrect Options:** * **A. Prosthetic valves:** While mechanical prosthetic valves carry a high risk of thromboembolism, they are statistically less common in the general population compared to the high prevalence of AF. * **C. Paradoxical embolus:** This occurs when a venous thrombus enters the systemic circulation through a Right-to-Left shunt (e.g., Patent Foramen Ovale). While a significant cause of "cryptogenic" stroke in young adults, it is not the most common cause overall. * **D. Paroxysmal supraventricular tachycardia (PSVT):** Unlike AF, PSVT (like AVNRT) does not typically cause atrial stasis or thrombus formation and is not a recognized major risk factor for systemic embolism. **NEET-PG High-Yield Pearls:** * **Most common source of cardioembolism:** Non-rheumatic Atrial Fibrillation. * **Most common site of thrombus in AF:** Left Atrial Appendage (LAA). * **Most common site of embolization in the brain:** Middle Cerebral Artery (MCA) territory [4]. * **Anticoagulation:** In non-valvular AF, DOACs (Apixaban, Rivaroxaban) are now preferred over Warfarin unless there is moderate-to-severe mitral stenosis or a mechanical heart valve [3].

Q: A 45-year-old man presents to the emergency department with dizziness. He has a history of supraventricular beats and is currently taking aspirin, atenolol, and quinine. His EKG reveals Torsades De Pointes. How should he be managed?

Magnesium. The patient is presenting with **Torsades de Pointes (TdP)**, a specific form of polymorphic ventricular tachycardia characterized by a "twisting of the points" around the isoelectric line [1]. This condition is typically associated with a **prolonged QT interval** [1]. In this clinical scenario, the patient’s use of **Quinine** (a Class IA antiarrhythmic property drug) is the likely precipitant of QT prolongation. **1. Why Magnesium is Correct:** Intravenous **Magnesium Sulfate** is the first-line treatment for Torsades de Pointes, regardless of the patient's serum magnesium levels. It works by stabilizing the cardiac membrane and suppressing the early afterdepolarizations (EADs) that trigger the arrhythmia, even if the baseline magnesium is normal [2]. **2. Why Other Options are Incorrect:** * **Digoxin:** This drug shortens the refractory period and can increase myocardial excitability. It is contraindicated here as it can worsen ventricular arrhythmias. * **Calcium:** While used in hyperkalemia-induced arrhythmias, it has no role in treating TdP and may theoretically worsen triggered activity. * **Atropine:** Used for bradycardia. While increasing the heart rate can sometimes shorten the QT interval (overdrive pacing), Magnesium remains the definitive immediate pharmacological intervention. **Clinical Pearls for NEET-PG:** * **Drug-Induced QT Prolongation:** Remember the mnemonic **"ABCDE"**: **A**ntiarrhythmics (Class IA, III), **B**iotics (Macrolides, Quinolones), **C**isapride (Antipsychotics/Antiemetics), **D**epressants (TCAs), and **E**lectrolytes (Hypokalemia, Hypomagnesemia, Hypocalcemia) [2]. * **Management Algorithm:** If the patient is unstable, immediate **Defibrillation** is required. If stable, IV Magnesium is the drug of choice. * **Secondary Prevention:** Discontinue the offending agent (Quinine in this case) and correct electrolyte imbalances [2].

Question 1

Which of the following ECG findings would indicate a posterior wall myocardial infarction?

Accepted Answer

ST elevation in V1-V3 leads

Answer

Tall and broad R waves

Answer

Tall T waves

Answer

Significant R waves

Question 2

Which valve is most commonly affected in subacute bacterial endocarditis?

Accepted Answer

Mitral

Answer

Tricuspid

Answer

Pulmonary

Answer

None of the above

Question 3

A 62-year-old male with underlying COPD develops a viral upper respiratory infection and begins taking an over-the-counter decongestant. Shortly thereafter, he experiences palpitations and presents to the emergency room, where the given rhythm strip is obtained, demonstrating:

Accepted Answer

Atrial flutter

Answer

Junctional tachycardia

Answer

Paroxysmal atrial tachycardia

Answer

Complete heart block

Question 4

Which of the following conditions presents with an ECG pattern that mimics myocardial infarction, often referred to as 'myocardial stunning'?

Accepted Answer

Takotsubo cardiomyopathy

Answer

Restrictive cardiomyopathy

Answer

Brugada Syndrome

Answer

Pericardial effusion

Question 5

The ECG in hyperkalemia classically shows:

Accepted Answer

Increased QRS duration

Answer

Shortened PR interval

Answer

Prominent U waves

Answer

Increased R wave amplitude

Question 6

Which gene alteration is most commonly associated with dilated cardiomyopathy?

Accepted Answer

Titin

Answer

Dystrophin

Answer

Sarcomere

Answer

Mitochondrial genes

Question 7

Comment on the diagnosis of the patient based on ECG?

Accepted Answer

Multifocal atrial tachycardia

Answer

Atrial fibrillation

Answer

Mobitz II heart block

Answer

Wolff-Parkinson-White syndrome

Question 8

A fixed PR interval with occasional dropped beats in a 2:1, 3:1, or 4:1 pattern, accompanied by a wide QRS complex, is characteristic of which condition?

Accepted Answer

Mobitz Type II block

Answer

Wenckebach (Mobitz Type I) block

Answer

Wolff-Parkinson-White (WPW) syndrome with reentrant tachycardia

Answer

Complete heart block with atrial fibrillation

Question 9

What is the most common cause of embolism leading to cerebrovascular disease?

Accepted Answer

Non-rheumatic atrial fibrillation

Answer

Prosthetic valves

Answer

Paradoxical embolus

Answer

Paroxysmal supraventricular tachycardia (PSVT)

Question 10

A 45-year-old man presents to the emergency department with dizziness. He has a history of supraventricular beats and is currently taking aspirin, atenolol, and quinine. His EKG reveals Torsades De Pointes. How should he be managed?

Accepted Answer

Magnesium

Answer

Digoxin

Answer

Calcium

Answer

Atropine

Cardiology — MCQs

Cardiology — MCQs

On this page

Practice by Chapter

Want unlimited practice?