Cardiology Practice Questions

Q: All of the following are electrocardiographic features of hyperkalemia, except?

Prolonged QT interval. **Explanation:** Hyperkalemia is a critical electrolyte abnormality that alters the resting membrane potential of myocytes, leading to predictable sequential changes on an ECG [1]. **Why Prolonged QT Interval is the Correct Answer:** Hyperkalemia typically causes **shortening of the QT interval**, not prolongation. This occurs because high extracellular potassium levels increase the speed of repolarization (Phase 3 of the action potential), leading to narrow, peaked T waves and a shortened QT duration. In contrast, **Hypokalemia** is associated with QT prolongation (often due to prominent U waves). **Analysis of Incorrect Options:** * **Prolonged PR interval:** As potassium levels rise (typically >6.5 mEq/L), conduction through the atria and AV node slows down, leading to PR interval prolongation. * **Loss of P waves:** As toxicity progresses, the P wave flattens and eventually disappears (Atrial standstill) because the atrial myocardium becomes inexcitable [1]. * **Sine wave patterns:** This is a late, pre-terminal sign of severe hyperkalemia (>8.0 mEq/L). The QRS complex widens significantly and merges with the T wave, creating a characteristic sinusoidal appearance, which can rapidly degenerate into ventricular fibrillation or asystole [1]. **High-Yield NEET-PG Pearls:** * **Earliest sign:** Tall, "tented" or peaked T waves (best seen in V2-V4) [1]. * **Sequence of changes:** Peaked T waves → PR prolongation/P wave flattening → QRS widening → Sine wave → Asystole [1]. * **Treatment:** Calcium gluconate (stabilizes the cardiac membrane) is the first step if ECG changes are present [2], followed by insulin/dextrose and salbutamol to shift K+ intracellularly.

Q: A 50-year-old man with aortic stenosis is exercising for 11 minutes according to the Bruce protocol. Exercise is stopped due to fatigue. The regional pressure gradient between the two sides of the aortic valve is 60 mm Hg. What is the best management?

Observation. **Explanation:** The management of Aortic Stenosis (AS) is primarily guided by the presence of symptoms and the severity of the stenosis. In this scenario, the patient is **asymptomatic** (fatigue at 11 minutes of the Bruce protocol is a normal physiological response, not an exercise-induced symptom) and has a pressure gradient of 60 mmHg, which classifies as **Severe AS** (Mean gradient >40 mmHg) [1]. **Why Observation is correct:** Current guidelines (ACC/AHA) state that for asymptomatic patients with severe AS and preserved Left Ventricular Ejection Fraction (LVEF), the management is **watchful waiting** (Observation). Exercise testing is used to unmask "latent" symptoms [1]. Since this patient completed 11 minutes (Stage IV of Bruce protocol) and only stopped due to general fatigue—not chest pain, dyspnea, or hypotension—the test is considered negative for symptoms. Therefore, surgery is not yet indicated. **Why other options are incorrect:** * **Aortic Valve Replacement (B):** This is the definitive treatment but is reserved for *symptomatic* severe AS, asymptomatic severe AS with LVEF <50%, or those undergoing other cardiac surgeries. * **Angiogram (A):** Usually performed as a preoperative workup before valve surgery to check coronary anatomy; it is not indicated in an asymptomatic patient being managed conservatively. * **Aortic Ballooning (C):** Balloon Valvotomy is generally a palliative measure or a "bridge to surgery" in unstable patients or children; it is not a standard preventive treatment for stable adults [1]. **Clinical Pearls for NEET-PG:** * **Classic Triad of AS:** Dyspnea (most common), Angina, and Syncope (**SAD**). * **Severe AS Criteria:** Valve Area 40 mmHg, or Jet Velocity >4 m/s. * **Indication for Surgery in Asymptomatic AS:** LVEF 5 m/s).

Q: What is the primary treatment for torsades de pointes?

Magnesium sulfate (MgSO4). **Explanation:** **Torsades de Pointes (TdP)** is a specific form of polymorphic ventricular tachycardia characterized by a "twisting of points" around the isoelectric line. It is typically associated with a prolonged QT interval. **Why Magnesium Sulfate (MgSO4) is the Correct Answer:** Intravenous Magnesium sulfate is the **drug of choice** for both the treatment and prevention of recurrences of TdP, regardless of the patient's baseline magnesium levels. It works by stabilizing the cardiac cell membrane and suppressing the **Early Afterdepolarizations (EADs)** that trigger the arrhythmia. It achieves this by blocking L-type calcium channels and reducing the influx of calcium, thereby shortening the action potential duration in the Purkinje fibers. **Analysis of Incorrect Options:** * **A. Propranolol:** While beta-blockers are used in Congenital Long QT Syndrome (LQTS) to prevent episodes, they are not the primary acute treatment for an active episode of TdP. * **B. Calcium channel blockers:** These are generally contraindicated as they can worsen bradycardia or hypotension, potentially exacerbating the arrhythmia. * **D. Lignocaine:** This is a Class IB antiarrhythmic used for stable ventricular tachycardia but is ineffective in TdP and does not address the underlying QT prolongation. **High-Yield Clinical Pearls for NEET-PG:** * **Immediate Management:** If MgSO4 fails and the patient is hemodynamically unstable, **unsynchronized cardioversion** (defibrillation) is required. * **Heart Rate Management:** Increasing the heart rate via **isoprenaline** or **cardiac pacing** can help shorten the QT interval and "overdrive" suppress TdP. * **Avoidance:** Class IA (Quinidine, Procainamide) and Class III (Sotalol, Amiodarone) antiarrhythmics must be avoided as they further prolong the QT interval and can worsen TdP.

Q: Bacterial endocarditis is rarely seen in which of the following conditions?

Secundum Atrial Septal Defect (ASD). **Explanation:** The risk of **Infective Endocarditis (IE)** is primarily determined by the presence of high-velocity turbulent blood flow, which causes endothelial damage and creates a nidus for platelet-fibrin deposition (non-bacterial thrombotic endocarditis). **Why Secundum ASD is the Correct Answer:** In a Secundum Atrial Septal Defect, the pressure gradient between the left and right atria is relatively low [1]. This results in **low-velocity, laminar flow** across the defect rather than high-velocity turbulence. Consequently, there is minimal endocardial trauma, making the development of vegetations extremely rare. Therefore, Secundum ASD is the only common congenital heart disease that does not typically require IE prophylaxis (unless repaired with prosthetic material) [2]. **Analysis of Incorrect Options:** * **VSD (Option A):** Characterized by a high-pressure gradient between the ventricles, leading to high-velocity jets [1]. * **PDA (Option B):** Involves a high-pressure shunt from the aorta to the pulmonary artery, causing significant turbulence [3]. * **MVP (Option C):** Especially when accompanied by mitral regurgitation, the turbulent backflow of blood significantly increases the risk of IE [4]. **NEET-PG High-Yield Pearls:** * **Highest Risk Conditions:** Prosthetic heart valves [2], previous history of IE, and cyanotic congenital heart disease (e.g., Tetralogy of Fallot). * **Lowest Risk Conditions:** Secundum ASD, Ischemic Heart Disease, and Cardiac Pacemakers. * **Commonest Site of Vegetation in VSD:** On the right ventricular side of the defect (due to the jet effect). * **Commonest Organism:** *Staphylococcus aureus* (Acute IE/IV drug users) and *Viridans streptococci* (Subacute IE).

Q: A 70-year-old man with a prior anterior myocardial infarction presents for routine evaluation. He feels well and has no symptoms. He is taking metoprolol 100 mg bid, aspirin 81 mg od, enalapril 10 mg bid, and simvastatin 40 mg od for secondary prevention. Select the characteristic ECG finding for this patient.

Prolonged PR interval. ### Explanation **Correct Answer: A. Prolonged PR interval** The correct answer is derived from the patient's current medication profile. The patient is taking **Metoprolol 100 mg BID**, which is a high-dose beta-blocker. Beta-blockers act as negative dromotropes by slowing conduction through the **Atrioventricular (AV) node** [1]. On an ECG, AV nodal conduction delay is manifested as a **prolonged PR interval** (>0.20 seconds), which represents a first-degree heart block. Given the patient is asymptomatic and on high-dose beta-blockade for secondary prevention post-MI, this is a common and expected pharmacological finding. **Analysis of Incorrect Options:** * **B. Broad-notched P wave in lead II:** This is known as *P-mitrale*, characteristic of Left Atrial Enlargement (LAE). While chronic heart failure post-MI can lead to LAE, it is not a direct pharmacological effect of his current medications. * **C. Short QT interval:** This is typically seen in hypercalcemia or digoxin toxicity. Beta-blockers and ischemia do not cause a short QT; in fact, some antiarrhythmics and electrolyte imbalances (hypokalemia) prolong the QT interval. * **D. Short PR interval:** This is characteristic of pre-excitation syndromes like Wolff-Parkinson-White (WPW) syndrome, where an accessory pathway bypasses the AV node. Beta-blockers increase the PR interval, they do not shorten it [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Beta-blocker overdose:** Treatment of choice is **Glucagon** (increases cAMP bypassing the beta-receptor). * **Post-MI Secondary Prevention:** The "Big Four" medications are Aspirin (Antiplatelet), Statins, ACE inhibitors (prevent remodeling), and Beta-blockers (reduce mortality) [2]. * **ECG Changes:** Always correlate ECG findings with the drug history. Digoxin can cause "reverse tick" ST-segment depression, while Class Ia/III antiarrhythmics prolong the QTc.

Question 1

A 64-year-old male presents with dyspnea and edema. He had previous coronary bypass surgery 5 years ago, which was uncomplicated. Since then he has had no further chest pain. On examination, his JVP is at 8 cm, with prominent Kussmaul's sign. The heart sounds are easily heard but there is an early diastolic filling sound (pericardial knock). For this patient, select the most likely diagnosis.

Accepted Answer

Constrictive pericarditis

Answer

Cardiac tamponade

Answer

Restrictive cardiomyopathy

Answer

Right ventricle myocardial infarction

Question 2

All of the following are electrocardiographic features of hyperkalemia, except?

Accepted Answer

Prolonged QT interval

Answer

Prolonged PR interval

Answer

Sine wave patterns

Answer

Loss of P waves

Question 3

A 50-year-old man with aortic stenosis is exercising for 11 minutes according to the Bruce protocol. Exercise is stopped due to fatigue. The regional pressure gradient between the two sides of the aortic valve is 60 mm Hg. What is the best management?

Accepted Answer

Observation

Answer

Angiogram

Answer

Aortic valve replacement

Answer

Aortic ballooning to prevent further derangement

Question 4

What is the primary treatment for torsades de pointes?

Accepted Answer

Magnesium sulfate (MgSO4)

Answer

Propranolol

Answer

Calcium channel blocker

Answer

Lignocaine

Question 5

A 40-year-old male is admitted with acute inferior wall myocardial infarction. Half an hour later, his BP is 80/50 mmHg and heart rate is 40/min with sinus rhythm. What is the most appropriate next step in the management of this patient?

Accepted Answer

Intravenous administration of atropine sulfate

Answer

Administer normal saline 300 ml over 15 minutes

Answer

Immediate insertion of a temporary pacemaker

Answer

Intravenous administration of isoprenaline 50 mcg/minute

Question 6

A 73-year-old man with a history of hypertension and osteoarthritis, treated with metoprolol and naproxen respectively, presents with a 6-week history of gradually increasing dyspnea. He experiences occasional nocturnal dyspnea relieved by sitting up but denies peripheral edema. His vital signs are BP 148/94 mmHg, HR 96 bpm, and RR 16 bpm, with an O2 saturation of 92%. Physical examination reveals jugular venous distension of 7 cm, mild basilar crackles without wheezing, a sustained apex impulse, an S4 gallop, and no murmurs. Peripheral edema is absent. ECG shows stable left ventricular hypertrophy without Q waves. Chest x-ray reveals increased interstitial markings and cephalization of pulmonary vessels, with a boot-shaped cardiac silhouette but no definite cardiomegaly. Echocardiogram demonstrates left ventricular hypertrophy and an LV ejection fraction of 55%. What is the likely pathogenesis of this patient's dyspnea?

Accepted Answer

Impaired diastolic relaxation and filling

Answer

Increased metabolic demands leading to high-output heart failure

Answer

Occult coronary artery disease with dyspnea as an angina equivalent

Answer

Interstitial lung disease mimicking pulmonary vascular congestion

Question 7

Bacterial endocarditis is rarely seen in which of the following conditions?

Accepted Answer

Secundum Atrial Septal Defect (ASD)

Answer

Ventricular Septal Defect (VSD)

Answer

Patent Ductus Arteriosus (PDA)

Answer

Mitral Valve Prolapse (MVP)

Question 8

A 70-year-old man with a prior anterior myocardial infarction presents for routine evaluation. He feels well and has no symptoms. He is taking metoprolol 100 mg bid, aspirin 81 mg od, enalapril 10 mg bid, and simvastatin 40 mg od for secondary prevention. Select the characteristic ECG finding for this patient.

Accepted Answer

Prolonged PR interval

Answer

Broad-notched P wave in lead II

Answer

Short QT interval

Answer

Short PR interval

Question 9

Which of the following statements regarding bicuspid aortic valves (BAV) is FALSE?

Accepted Answer

BAVs are associated with aortic dilatation and aneurysm formation, but there is no increased risk of rupture or dissection.

Answer

BAVs are one of the most common congenital cardiac abnormalities with a prevalence in the general population of up to 2%.

Answer

Patients with BAV often need aortic valve intervention at an earlier age than those with tricuspid aortic valves.

Answer

They are commonly associated with coarctation of the aorta (up to 50%).

Question 10

Dicrotic pulse differs from pulse bisferiens in which characteristic?

Accepted Answer

Characterized by two palpable weak waves, one in systole and another in diastole

Answer

Seen in hypertrophic obstructive cardiomyopathy (HOCM)

Answer

Indicates high stroke output

Answer

Characterized by two palpable weak waves, both in systole

Cardiology — MCQs

Cardiology — MCQs

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