Cardiology Practice Questions

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.

Q: Which of the following is NOT an ECG finding in Wolff-Parkinson-White syndrome?

Narrow QRS complexes. **Explanation:** Wolff-Parkinson-White (WPW) syndrome is a pre-excitation syndrome caused by an accessory pathway (the **Bundle of Kent**) that bypasses the AV node [1]. This allows electrical impulses to reach the ventricles earlier than usual [1]. **1. Why "Narrow QRS complexes" is the correct answer:** In WPW, the QRS complex is **wide (>120ms)**, not narrow [1]. This occurs because the ventricle is activated via two fronts: early activation through the accessory pathway (causing the slurred start) and subsequent activation through the normal His-Purkinje system [1]. This "fusion" of electrical signals results in a widened, distorted QRS complex. **2. Analysis of incorrect options:** * **Short PR interval (<0.12s):** This is a hallmark of WPW [1]. Because the accessory pathway lacks the physiological delay of the AV node, the time from atrial to ventricular depolarization is shortened [1]. * **Slurred and tall QRS (Delta wave):** The delta wave represents the initial slow, intramyocardial conduction through the accessory pathway [1]. It is the most characteristic finding of WPW. * **Normal QT interval:** While the QRS is widened, the repolarization (T-wave) usually adjusts such that the overall QT interval remains within normal limits [1], unless there is secondary repolarization abnormality. **Clinical Pearls for NEET-PG:** * **The WPW Triad:** Short PR interval + Delta wave + Wide QRS [1]. * **Pseudo-infarction pattern:** Delta waves can sometimes mimic Q-waves, leading to a false diagnosis of myocardial infarction. * **Treatment:** **Radiofrequency ablation** of the accessory pathway is the definitive treatment. * **Contraindication:** Avoid "ABCD" (Atrioventricular nodal blockers) in WPW with Atrial Fibrillation: **A**denosine, **B**eta-blockers, **C**alcium channel blockers, and **D**igoxin, as they can paradoxically increase conduction through the accessory pathway, leading to Ventricular Fibrillation [2].

Q: Inverted T waves are seen in which of the following conditions?

Wellen syndrome. **Explanation:** **Wellens Syndrome** is a clinical manifestation of critical stenosis of the **proximal Left Anterior Descending (LAD) artery**. It is a "pre-infarction" state where the patient is currently pain-free but at high risk for a massive anterior wall MI. The hallmark ECG finding is deeply and symmetrically **inverted T waves** (Type B) or biphasic T waves (Type A) in the precordial leads (V2–V3) [1]. **Analysis of Options:** * **Hyperkalemia (A):** Characterized by **Tall, tented (peaked) T waves** with a narrow base [2]. As potassium levels rise further, it leads to PR prolongation, loss of P waves, and QRS widening (sine wave pattern) [2]. * **Hyperthermia (B):** Typically causes sinus tachycardia. While extreme physiological stress can cause non-specific ST-T changes, it is not a classic cause of T-wave inversion. * **Coronary Syndrome (D):** While "Acute Coronary Syndrome" (ACS) can cause T-wave inversions, the option is too broad. Wellens Syndrome is the *specific* eponymous condition defined by these characteristic T-wave changes in a stable patient, making it the most precise answer in a competitive exam context. **High-Yield Clinical Pearls for NEET-PG:** * **Wellens Criteria:** History of angina, normal/minimally elevated cardiac enzymes, no precordial Q-waves, and characteristic T-wave changes in V2-V3. * **Contraindication:** Do **NOT** perform a Stress Test in suspected Wellens Syndrome, as it can precipitate a fatal MI. These patients require urgent coronary angiography. * **Differential for Deep T-wave Inversion:** Wellens Syndrome, CNS injury (Cerebral T-waves), Hypertrophic Cardiomyopathy (Apical variant), and Massive Pulmonary Embolism (S1Q3T3).

Q: Following an attack of myocardial infarction, what indicates the mortality and morbidity of the patient?

Left ventricular ejection fraction. The **Left Ventricular Ejection Fraction (LVEF)** is the single most important predictor of long-term mortality and morbidity following an acute myocardial infarction (MI). 1. **Why LVEF is the Correct Answer:** LVEF is a direct measure of the heart's systolic function and reflects the extent of myocardial damage (infarct size). A reduced LVEF (typically <40%) indicates significant ventricular dysfunction, which predisposes the patient to congestive heart failure and sudden cardiac death due to ventricular arrhythmias [1], [3]. Clinical trials have consistently shown that as LVEF decreases, the risk of post-MI complications and death increases proportionally. 2. **Why Other Options are Incorrect:** * **Ventricular Extrasystole (PVCs):** While common post-MI, isolated PVCs are not reliable independent predictors of long-term mortality unless they occur in the setting of a low LVEF [1]. * **Duration of Syncope:** Syncope may occur during an MI (due to arrhythmias or profound hypotension), but its duration does not correlate linearly with long-term prognosis or the extent of myocardial necrosis [2]. * **Percentage of Narrowness:** While coronary anatomy is important for deciding intervention (PCI/CABG), the *functional* outcome (how much muscle survived) is more critical for survival than the degree of stenosis in a vessel that has already caused an infarct. **High-Yield Clinical Pearls for NEET-PG:** * **Killip Classification:** Used to clinically risk-stratify patients with acute MI based on the severity of heart failure (Killip IV = Cardiogenic shock, highest mortality). * **Gold Standard:** Echocardiography is the most common initial tool to assess LVEF post-MI [1]. * **Sudden Cardiac Death (SCD):** Patients with LVEF ≤35% post-MI are at high risk for SCD and are often candidates for an Implantable Cardioverter Defibrillator (ICD).

Question 1

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 2

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 3

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 4

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 5

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 6

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

Question 7

Which of the following is NOT an ECG finding in Wolff-Parkinson-White syndrome?

Accepted Answer

Narrow QRS complexes

Answer

Normal QT interval

Answer

Slurred and tall QRS (delta wave)

Answer

Short PR interval

Question 8

Inverted T waves are seen in which of the following conditions?

Accepted Answer

Wellen syndrome

Answer

Hyperkalemia

Answer

Hyperthermia

Answer

Coronary syndrome

Question 9

All of the following may be seen in a patient with cardiac tamponade, except?

Accepted Answer

Kussmaul's sign

Answer

Pulsus paradoxus

Answer

Electrical alternans

Answer

Right ventricular diastolic collapse on echocardiogram

Question 10

Following an attack of myocardial infarction, what indicates the mortality and morbidity of the patient?

Accepted Answer

Left ventricular ejection fraction

Answer

Ventricular extrasystole

Answer

Duration of syncope

Answer

Percentage of narrowness of coronary artery

Cardiology — MCQs

Cardiology — MCQs

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