Cardiology Practice Questions

Q: Which of the following ECG changes is NOT typically seen in hyperkalemia?

Inverted T waves. ***Inverted T waves*** - **Hyperkalemia** typically causes **tall, peaked T waves** (narrow-based and symmetric), not inverted T waves. - **Inverted T waves** are more commonly associated with **hypokalemia**, **ischemia**, or **digitalis toxicity**. *Prolonged PR interval* - This is a **typical finding** in hyperkalemia as potassium affects **cardiac conduction**. - Occurs as the second stage of hyperkalemic ECG changes after **peaked T waves** develop. *Wider QRS complex* - **QRS widening** is a **characteristic finding** in severe hyperkalemia (>7.0 mEq/L). - Results from **impaired sodium channel function** and indicates potential for **cardiac arrest**. *ST segment depression/elevation* - **ST segment changes** are commonly seen in moderate to severe hyperkalemia. - Can progress to a **sine wave pattern** in extreme hyperkalemia, which is life-threatening.

Q: A 58-year-old man had a myocardial infarction 1 year ago. He now wants to prevent another acute coronary event and is advised to begin a program of exercise and to change his diet. A reduction in the level of which of the following serum laboratory findings 1 year later would best indicate the success of his diet and exercise regimen?

Cholesterol. **Explanation:** The primary goal of secondary prevention after a myocardial infarction (MI) is to reduce the progression of atherosclerosis. **Cholesterol**, specifically Low-Density Lipoprotein (LDL), is the most significant modifiable risk factor for coronary artery disease (CAD). 1. **Why Cholesterol is Correct:** Atherosclerosis is driven by the accumulation of cholesterol in the arterial walls, leading to plaque formation. Diet (reducing saturated fats) and aerobic exercise effectively lower serum LDL and total cholesterol while increasing HDL ("good" cholesterol). A reduction in serum cholesterol directly correlates with a decreased risk of recurrent coronary events and improved cardiovascular outcomes. 2. **Why Other Options are Incorrect:** * **Calcium:** While coronary artery calcification is a marker of atherosclerosis, serum calcium levels are tightly regulated by the parathyroid hormone and do not reflect the success of a cardiovascular diet or exercise regimen. * **Glucose:** While managing blood sugar is vital for diabetic patients, a reduction in glucose is not the *best* specific indicator for preventing a second MI in a general post-MI patient compared to lipid profile improvement. * **Potassium:** Serum potassium levels are critical for cardiac rhythm but are influenced by renal function and medications (like ACE inhibitors or diuretics), not by long-term lifestyle changes aimed at atherosclerosis. **High-Yield Clinical Pearls for NEET-PG:** * **Target LDL:** For post-MI patients (Very High Risk), the current goal is often LDL <55 mg/dL. * **Exercise Effect:** Exercise primarily increases **HDL** and lowers **Triglycerides** by increasing the activity of **Lipoprotein Lipase (LPL)**. * **Dietary Impact:** Saturated fats downregulate LDL receptors; reducing them increases receptor expression, lowering serum LDL.

Q: Stokes-Adams syndrome is associated with which of the following conditions?

High-degree AV block. **Explanation:** **Stokes-Adams Syndrome** (or Adams-Stokes attacks) refers to sudden, transient episodes of syncope caused by a drastic decrease in cardiac output due to a paroxysmal change in heart rate or rhythm. **Why High-degree AV block is correct:** The most common underlying cause of Stokes-Adams syndrome is a sudden transition into **Complete (3rd-degree) Heart Block** or high-grade AV block [1]. When the conduction between the atria and ventricles fails, there is a period of ventricular standstill (asystole) before a ventricular escape rhythm takes over [2]. During these few seconds of asystole, cerebral perfusion drops sharply, leading to sudden loss of consciousness [3]. **Analysis of Incorrect Options:** * **Sinoatrial arrest:** While SA arrest can cause syncope (often part of Sick Sinus Syndrome), the classic description of Stokes-Adams is historically and clinically tied to the failure of the distal conduction system (AV block) [3]. * **Tachyrhythmias:** Although rapid rhythms can cause syncope, Stokes-Adams specifically refers to the "brady-asystolic" mechanism. * **Polymorphic Ventricular Tachycardia (Torsades de Pointes):** This is a specific type of tachyarrhythmia associated with Long QT Syndrome, not the classic Stokes-Adams mechanism [4]. **NEET-PG High-Yield Pearls:** * **Clinical Presentation:** Sudden collapse without warning, pallor followed by flushing (hyperemia) upon recovery, and rapid return to consciousness [3]. * **ECG Findings:** Between attacks, the ECG often shows evidence of conduction system disease, such as **Bifascicular block** or **Trifascicular block** [1]. * **Management:** The definitive treatment for recurrent Stokes-Adams attacks due to AV block is the implantation of a **Permanent Pacemaker** [1]. * **Distinction:** Unlike vasovagal syncope, there is usually no prodrome (nausea/sweating) in Stokes-Adams syndrome.

Q: A 65-year old man presents with crushing chest pain for 2 hours. On examination, BP = 80/60 mm Hg and JVP are elevated 4 cm above the sternal angle. All are true about the condition shown except?

ST segment depression in leads II, III, aVF. ***ST segment depression in leads II, III, aVF*** - In **right ventricular infarction** with inferior STEMI, leads II, III, and aVF show **ST elevation**, not depression. - **ST depression** in these leads would be seen in **posterior wall MI** or **reciprocal changes** from anterior MI, not RV infarction. *ST elevation in V4R* - **V4R (right-sided V4)** shows characteristic **ST elevation** in right ventricular infarction. - This is a **diagnostic hallmark** of RV involvement and helps differentiate from isolated inferior MI. *Right ventricular infarction* - The clinical presentation of **hypotension (80/60 mmHg)** and **elevated JVP** is classic for RV infarction. - **Right heart failure** occurs due to impaired RV filling and reduced cardiac output. *Kussmaul sign +* - **Kussmaul sign** (JVP rise with inspiration) is positive in RV infarction due to **impaired ventricular compliance**. - This paradoxical JVP response occurs because the rigid RV cannot accommodate increased venous return during inspiration.

Q: What is the treatment of choice for ST-elevation myocardial infarction?

Percutaneous coronary intervention. The primary goal in the management of ST-elevation myocardial infarction (STEMI) is the rapid restoration of coronary blood flow to salvage myocardium. **Why Percutaneous Coronary Intervention (PCI) is the Correct Answer:** Primary PCI is the **gold standard** and treatment of choice for STEMI. Clinical trials have consistently demonstrated that PCI is superior to fibrinolysis in achieving higher rates of vessel patency (TIMI 3 flow), lower rates of re-infarction, and reduced mortality [1]. It is preferred if it can be performed within **120 minutes** of first medical contact. **Analysis of Incorrect Options:** * **A. Thrombolysis with Streptokinase:** While thrombolysis is an alternative, it is only indicated if primary PCI cannot be performed within the recommended 120-minute window [1]. It carries a higher risk of intracranial hemorrhage and is less effective at opening the artery compared to PCI. * **C. Anticoagulate with heparin:** Heparin is an *adjunctive* therapy used during PCI or thrombolysis to prevent further clot propagation; it is not a definitive treatment for mechanical obstruction [2]. * **D. Aspirin and clopidogrel:** Dual Antiplatelet Therapy (DAPT) is a mandatory *supportive* treatment for all STEMI patients to prevent stent thrombosis, but it cannot mechanically open a totally occluded coronary artery. **High-Yield Clinical Pearls for NEET-PG:** * **Door-to-Balloon Time:** Should be <90 minutes (at PCI-capable centers) or <120 minutes (if transfer is required). * **Door-to-Needle Time:** If PCI is unavailable, thrombolysis should be initiated within **30 minutes**. * **Pharmacoinvasive Strategy:** If thrombolysis is performed first, the patient should still be transferred for PCI within 3-24 hours. * **Contraindication:** Remember that Streptokinase is antigenic; it should not be repeated in a patient who has received it previously.

Q: Which of the following drugs should not be used empirically in a patient with severe hypertension, especially in the elderly?

Prazosin. **Explanation:** The correct answer is **Prazosin (Option D)**. **Why Prazosin is avoided empirically:** Prazosin is a selective alpha-1 blocker. Its empirical use in severe hypertension, particularly in the elderly, is discouraged due to the **"First-dose phenomenon."** This refers to sudden, severe orthostatic hypotension and syncope occurring shortly after the initial dose [1]. In elderly patients, baroreceptor sensitivity is already diminished, making them highly susceptible to falls and related injuries (e.g., hip fractures). Furthermore, the **ALLHAT trial** demonstrated that alpha-blockers are less effective than other classes in preventing heart failure and cardiovascular events when used as monotherapy. **Analysis of Incorrect Options:** * **A. Enalapril (ACE Inhibitor):** A first-line agent for hypertension [1]. While it requires monitoring for renal function and potassium, it is a standard empirical choice, especially in patients with diabetes or heart failure. * **B. Amlodipine (Calcium Channel Blocker):** A preferred first-line agent for elderly patients and those of African descent [2]. It is highly effective in reducing systolic blood pressure and has a low risk of metabolic side effects [1]. * **C. Chlorthalidone (Thiazide-like Diuretic):** Often considered the "gold standard" diuretic for hypertension due to its long half-life and proven efficacy in reducing cardiovascular mortality in the elderly (SHEP trial) [2]. **NEET-PG High-Yield Pearls:** * **Drug of Choice (DOC) for Hypertension in Elderly:** Thiazide-like diuretics (Chlorthalidone) or Long-acting CCBs (Amlodipine) [2]. * **Prazosin Indications:** Now primarily used for Benign Prostatic Hyperplasia (BPH) or as add-on therapy in resistant hypertension. * **First-dose phenomenon prevention:** Start with a low dose (0.5–1 mg) and administer at bedtime ("Bedtime dosing").

Q: A 50-year-old man had an attack of myocardial infarction and developed ventricular ectopics and a low ejection fraction. Which of the following antiarrhythmic drugs should be given?

Beta-blocker. ### Explanation **Correct Answer: C. Beta-blocker** The management of post-myocardial infarction (MI) arrhythmias focuses on reducing mortality and preventing sudden cardiac death (SCD). **Why Beta-blockers are the drug of choice:** In patients with a history of MI and a low ejection fraction (EF), **Beta-blockers** (e.g., Metoprolol, Carvedilol) are the first-line therapy [1]. They reduce myocardial oxygen demand, decrease sympathetic overactivity, and prevent ventricular remodeling [2]. Most importantly, they are the only class of drugs in this list proven to **reduce mortality** and the risk of arrhythmic death in patients with coronary artery disease and heart failure [1, 2]. **Why other options are incorrect:** * **Flecainide (Class IC):** The landmark **CAST (Cardiac Arrhythmia Suppression Trial)** study proved that Class IC agents increase mortality in post-MI patients due to their pro-arrhythmic effects in scarred myocardium [3]. They are strictly contraindicated in structural heart disease. * **Mexiletine (Class IB):** While it can suppress ventricular ectopics, it has not shown a mortality benefit and is generally reserved as an adjunct therapy for refractory cases. * **Radio-frequency ablation:** This is typically indicated for symptomatic, drug-refractory ventricular tachycardia or specific focal ectopics, but it is not the initial medical management for post-MI ventricular ectopics. **High-Yield Clinical Pearls for NEET-PG:** * **CAST Trial Key Takeaway:** Never use Class IC antiarrhythmics (Flecainide, Propafenone) in patients with prior MI or CAD [3]. * **Low EF + Post-MI:** The most effective intervention to prevent SCD is an **ICD (Implantable Cardioverter Defibrillator)** if the EF remains ≤35% despite optimal medical therapy. * **Amiodarone:** It is "neutral" regarding mortality in post-MI patients; it suppresses arrhythmias but does not improve survival like Beta-blockers do.

Question 1

Which of the following ECG changes is NOT typically seen in hyperkalemia?

Accepted Answer

Inverted T waves

Answer

Prolonged PR interval

Answer

Wider QRS complex

Answer

ST segment depression/elevation

Question 2

A 58-year-old man had a myocardial infarction 1 year ago. He now wants to prevent another acute coronary event and is advised to begin a program of exercise and to change his diet. A reduction in the level of which of the following serum laboratory findings 1 year later would best indicate the success of his diet and exercise regimen?

Accepted Answer

Cholesterol

Answer

Calcium

Answer

Glucose

Answer

Potassium

Question 3

Stokes-Adams syndrome is associated with which of the following conditions?

Accepted Answer

High-degree AV block

Answer

Sinoatrial arrest

Answer

Tachyrhythmias

Answer

Polymorphic ventricular tachycardia

Question 4

A 65-year old man presents with crushing chest pain for 2 hours. On examination, BP = 80/60 mm Hg and JVP are elevated 4 cm above the sternal angle. All are true about the condition shown except?

Accepted Answer

ST segment depression in leads II, III, aVF

Answer

ST elevation in V4R

Answer

Right ventricular infarction

Answer

Kussmaul sign +

Question 5

What is the treatment of choice for ST-elevation myocardial infarction?

Accepted Answer

Percutaneous coronary intervention

Answer

Thrombolysis with Streptokinase

Answer

Anticoagulate with heparin

Answer

Aspirin and clopidogrel

Question 6

A 38-year-old male presents with a two-week history of progressive shortness of breath. He has a past medical history of type II diabetes mellitus. An echocardiogram revealed an ejection fraction (EF) of 25% with anterior, septal, and lateral wall motion defects. He was admitted and stabilized on furosemide, spironolactone, bisoprolol, and ramipril. What would be the next investigation in the course of management?

Accepted Answer

Angiogram

Answer

Endomyocardial biopsy

Answer

Viral titres

Answer

Exercise tolerance test

Question 7

Which of the following drugs should not be used empirically in a patient with severe hypertension, especially in the elderly?

Accepted Answer

Prazosin

Answer

Enalapril

Answer

Amlodipine

Answer

Chlorthalidone

Question 8

Which of the following EKG findings are characteristic of ventricular premature beats?

Accepted Answer

Fusion beat, AV dissociation, Wide QRS complex, Capture beat

Answer

Narrow QRS complex, Wide QRS complex, Capture beat

Answer

Fusion beat, Narrow QRS complex, AV dissociation, Wide QRS complex

Answer

Fusion beat, Narrow QRS complex, Wide QRS complex, Capture beat

Question 9

Which of the following is the first-line vasopressor in the management of cardiogenic shock?

Accepted Answer

Norepinephrine

Answer

Epinephrine

Answer

Dopamine

Answer

Dobutamine

Question 10

A 50-year-old man had an attack of myocardial infarction and developed ventricular ectopics and a low ejection fraction. Which of the following antiarrhythmic drugs should be given?

Accepted Answer

Beta-blocker

Answer

Flecainide

Answer

Mexiletine

Answer

Radio-frequency ablation technique

Cardiology — MCQs

Cardiology — MCQs

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