Cardiology Practice Questions

Q: A study of risk factors for atherogenesis in adults is performed. Which of the following substances is most likely to reduce serum cholesterol?

Omega-3 fatty acids. **Explanation:** The correct answer is **Omega-3 fatty acids (D)**. **Mechanism:** Omega-3 fatty acids (specifically EPA and DHA found in fish oil) are potent agents in lipid management [2]. They primarily reduce serum triglycerides by inhibiting hepatic synthesis of VLDL and increasing fatty acid oxidation. While their effect on LDL-cholesterol is variable, they are well-documented to increase HDL ("good") cholesterol and improve the overall lipid profile, thereby exerting a cardioprotective effect against atherogenesis [2]. **Analysis of Incorrect Options:** * **A. C-reactive protein (CRP):** This is an acute-phase reactant and a marker of systemic inflammation. High-sensitivity CRP (hs-CRP) is a strong predictor of cardiovascular risk, but it does not lower cholesterol; rather, it indicates an increased risk of plaque rupture. * **B. Homocysteine:** Elevated levels (hyperhomocysteinemia) cause endothelial damage and promote thrombosis. It is a known independent risk factor for atherosclerosis, not a lipid-lowering agent. * **C. Lipoprotein(a):** This is a low-density lipoprotein-like particle. High levels of Lp(a) are genetically determined and are strongly associated with an increased risk of coronary artery disease and aortic stenosis. **High-Yield Clinical Pearls for NEET-PG:** * **Friedewald Formula:** LDL = Total Cholesterol – HDL – (Triglycerides/5). Note: This is invalid if TG >400 mg/dL. * **Hypertriglyceridemia:** Omega-3 fatty acids and Fibrates (PPAR-α agonists) are the first-line treatments for severe hypertriglyceridemia to prevent pancreatitis [1], [3]. * **Atherogenic Triad:** High TG, Low HDL, and small dense LDL particles (common in Diabetes Mellitus). * **Lp(a):** It is structurally similar to plasminogen and can inhibit fibrinolysis, making it both pro-atherogenic and pro-thrombotic. [4]

Q: A 32-year-old man involved in a high-speed road traffic accident is found unconscious at the scene and breathing spontaneously. In the emergency department, the ECG monitor shows an irregular rhythm with no discernible P waves, QRS complexes, ST segments, or T waves, and a rapid rate. What is the best management for this patient?

CPR until a defibrillator is present. **Explanation:** The ECG description (irregular rhythm with no discernible P waves, QRS complexes, or T waves) is pathognomonic for **Ventricular Fibrillation (VF)**. In a trauma patient who is unconscious and in a shockable rhythm (VF/Pulseless VT), the immediate priority is to maintain coronary and cerebral perfusion via **Cardiopulmonary Resuscitation (CPR)** until a defibrillator is available to deliver a shock. **Why Option A is correct:** According to ACLS guidelines, the management of cardiac arrest begins with high-quality chest compressions. Defibrillation is the definitive treatment for VF, but CPR must be performed continuously until the device is ready to minimize the "no-flow" time. **Why other options are incorrect:** * **Option B (IV Adrenaline):** While used in cardiac arrest, it is administered *after* the second shock in a shockable rhythm. It does not take precedence over CPR or defibrillation. * **Option C (Pericardiocentesis):** This is the treatment for cardiac tamponade (obstructive shock). While tamponade is a "reversible cause" (H's and T's) of PEA/Asystole in trauma, the ECG here specifically indicates VF, which requires immediate electrical therapy. * **Option D (IV Amiodarone):** This is an anti-arrhythmic used in refractory VF (after the third shock). It is not the initial management. **High-Yield Clinical Pearls for NEET-PG:** * **Shockable Rhythms:** VF and Pulseless VT. * **Non-Shockable Rhythms:** PEA and Asystole. * **Commotio Cordis:** A clinical scenario where a blunt, non-penetrating blow to the chest (often in trauma/sports) triggers VF. * **The "Golden Hour":** In trauma, the first hour is critical; however, ACLS protocols for cardiac arrest remain the priority if the patient loses a pulse.

Q: Pericardial knock is heard in which condition?

Constrictive pericarditis. **Explanation:** **Constrictive Pericarditis (Correct Answer):** The **pericardial knock** is a high-pitched, early diastolic sound heard shortly after $S_2$. It occurs due to the rigid, non-compliant pericardium characteristic of constrictive pericarditis [1]. During early diastole, there is rapid ventricular filling; however, this filling is abruptly halted when the expanding ventricular volume hits the limit set by the stiff, calcified pericardium. This sudden cessation of ventricular expansion produces the "knock." It occurs earlier than an $S_3$ gallop. **Analysis of Incorrect Options:** * **Cardiac Tamponade:** This is characterized by muffled heart sounds (Beck’s Triad) due to fluid accumulation [3]. There is no "knock" because the fluid prevents the sudden tension of the ventricular wall against a rigid shell. * **Restrictive Cardiomyopathy (RCM):** While clinically similar to constriction, RCM is a disease of the myocardium, not the pericardium [2]. It is more commonly associated with an **$S_3$ gallop** rather than a pericardial knock. * **Acute Pericarditis:** The hallmark auscultatory finding here is a **pericardial friction rub** (scratchy, three-component sound), caused by the inflammation of the pericardial layers. Investigations often show specific ECG changes like ST elevation with upward concavity [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Kussmaul’s Sign:** Paradoxical rise in JVP during inspiration (Seen in Constrictive Pericarditis, NOT in Tamponade). * **Square Root Sign:** Seen on pressure tracings (dip-and-plateau pattern) in Constrictive Pericarditis. * **Chest X-ray:** Pericardial calcification is a classic diagnostic clue for constriction [1]. * **Pulsus Paradoxus:** Characteristically seen in Cardiac Tamponade (drop in SBP >10 mmHg during inspiration).

Q: A 75-year-old woman with hypertension develops fatigue and dyspnea on exertion. Her blood pressure is 160/60 mm Hg and pulse 80/min. The second heart sound is diminished and there is an early diastolic murmur that radiates from the right sternal border to the apex. Your clinical diagnosis is aortic regurgitation. What is the characteristic arterial pulse finding for this patient?

Hyperkinetic pulse. The clinical presentation of a wide pulse pressure (160/60 mmHg), a diminished S2, and an early diastolic murmur is classic for **Aortic Regurgitation (AR)**. In AR, the left ventricle (LV) receives blood from both the left atrium and the regurgitant flow from the aorta, leading to increased stroke volume [2]. 1. **Why Hyperkinetic Pulse is Correct:** The large stroke volume is ejected rapidly into the arterial system, causing a rapid rise in the pulse (water-hammer or Corrigan’s pulse) [3]. This is followed by a rapid fall due to the regurgitation of blood back into the LV and peripheral runoff. This "bounding" quality is termed a **hyperkinetic pulse**. 2. **Why Incorrect Options are Wrong:** * **Pulsus Tardus (A):** Characterized by a slow-rising, low-amplitude pulse. It is the hallmark of **Aortic Stenosis** [1]. * **Pulsus Paradoxus (B):** An exaggerated drop in systolic BP (>10 mmHg) during inspiration. It is classically seen in **Cardiac Tamponade**, severe asthma, or COPD. * **Bisferiens Pulse (D):** A pulse with two systolic peaks. While it can be seen in severe AR, it is most characteristic of **HOCM** or combined **AS + AR**. **NEET-PG High-Yield Pearls:** * **Right Sternal Border Murmur:** While AR is usually heard at the left sternal border (Erb's point), radiation to the **right sternal border** suggests **Aortic Root Dilatation** (e.g., Marfan syndrome, Aortic Dissection) [2]. * **Peripheral Signs of AR:** Look for Quincke’s pulse (capillary pulsations), De Musset’s sign (head nodding), and Traube’s sign (pistol-shot sounds over femoral arteries) [3]. * **Austin Flint Murmur:** A mid-diastolic rumble at the apex in severe AR, caused by the regurgitant jet displacing the mitral valve leaflet [2].

Q: A 36-year-old white female nurse comes to the ER due to a sensation of fast heart rate, slight dizziness, and vague chest fullness. Blood pressure is 110/70. The following rhythm strip is obtained, which shows?

Supraventricular tachycardia. ***Supraventricular tachycardia*** - **Narrow QRS complex** (<120 ms) with **regular rhythm** at rate of 150-220 bpm, with **absent or retrograde P waves** - classic features of SVT - Most commonly **AVNRT** in young females, presenting with sudden onset palpitations, dizziness, and chest discomfort *Atrial fibrillation* - Characterized by **irregularly irregular rhythm** with **absent P waves** and **fibrillatory waves** - Would show **variable R-R intervals** on rhythm strip, not the regular pattern seen here *Atrial flutter* - Shows characteristic **sawtooth flutter waves** (F waves) typically with **2:1 or 4:1 AV block** - **Atrial rate** around 300 bpm with **ventricular rate** of 150 bpm, but flutter waves would be visible *Ventricular tachycardia* - Features **wide QRS complexes** (>120 ms) with **AV dissociation** and potential **capture beats** - Usually causes more severe **hemodynamic compromise** than the stable presentation described here

Q: QT prolongation is seen in all, EXCEPT?

Digitalis toxicity. **Explanation:** The QT interval represents the total time for ventricular depolarization and repolarization. Prolongation of this interval is clinically significant as it predisposes patients to *Torsades de Pointes*. **Why Digitalis Toxicity is the Correct Answer:** Digitalis (Digoxin) acts by inhibiting the Na+/K+ ATPase pump, which leads to an increase in intracellular calcium. Electrophysiologically, Digoxin **shortens** the action potential duration and the refractory period. Consequently, it causes **QT interval shortening**, not prolongation. Other classic ECG findings in digitalis effect include the "reverse tick" or "scooped-out" ST-segment depression. **Analysis of Incorrect Options:** * **Hypothermia (A):** Characteristically causes prolongation of all ECG intervals (PR, QRS, and QT). It is also associated with the pathognomonic **Osborn waves** (J-waves) at the J-point. * **Hypocalcemia (C):** Low serum calcium levels prolong phase 2 of the ventricular action potential. This leads to a lengthened ST segment and, subsequently, a **prolonged QT interval**. (Note: Hypercalcemia shortens the QT interval). * **Romano-Ward Syndrome (D):** This is the most common form of **Congenital Long QT Syndrome (LQTS)**. It is inherited in an autosomal dominant fashion and is *not* associated with deafness (unlike Jervell and Lange-Nielsen syndrome). **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for QT Prolongation:** "ABCDE" – **A**ntiarrhythmics (Class IA, III), **B**iotics (Macrolides, Quinolones), **C**isapride/Antipsychotics, **D**epressants (TCAs), **E**lectrolytes (Hypokalemia, Hypomagnesemia, Hypocalcemia). * **Formula:** The corrected QT (QTc) is most commonly calculated using **Bazett’s Formula**: $QTc = QT / \sqrt{RR}$. * **Management:** For acquired Long QT with Torsades, the treatment of choice is **IV Magnesium Sulfate**.

Q: All of the following are true about Right Ventricular Infarcts, except?

Normal JVP. In Right Ventricular Infarction (RVI), the hallmark pathophysiology is **acute right-sided heart failure**. This leads to a sudden backup of pressure into the systemic venous circulation [3]. **1. Why "Normal JVP" is the correct (false) statement:** The most sensitive and characteristic clinical sign of RVI is an **elevated Jugular Venous Pressure (JVP)** [2]. Because the right ventricle fails to pump blood effectively into the pulmonary circulation, blood backs up into the superior vena cava. A normal JVP in a patient with suspected RVI is highly unlikely and should prompt a search for an alternative diagnosis. **2. Explanation of other options:** * **Nocturia:** In right-sided failure, dependent edema accumulates in the lower limbs during the day. At night, when the patient lies supine, this fluid is redistributed, increasing renal perfusion and venous return, leading to increased urine production (nocturia). * **Ascites:** Chronic or severe acute right heart failure leads to systemic venous congestion, causing hepatic congestion and fluid leakage into the peritoneal cavity (ascites) [2]. **3. High-Yield Clinical Pearls for NEET-PG:** * **The Triad of RVI:** Hypotension, Clear Lungs (absence of pulmonary edema), and Elevated JVP. * **Kussmaul’s Sign:** A paradoxical rise in JVP during inspiration is frequently seen in RVI. * **Diagnosis:** The most specific finding is **ST-elevation in lead V4R** (Right-sided ECG). * **Management Contraindication:** Avoid **Nitrates, Diuretics, and Morphine**, as they decrease preload. RVI is "preload dependent." * **Treatment of choice:** Aggressive **IV fluid resuscitation** (Normal Saline) to maintain right ventricular filling pressure [1].

Question 1

In a patient with wide-complex tachycardia, the presence of all of the following in the ECG indicates ventricular tachycardia except?

Accepted Answer

Typical right bundle branch block morphology

Answer

Atrioventricular dissociation

Answer

Fusion beats

Answer

Capture beats

Question 2

A study of risk factors for atherogenesis in adults is performed. Which of the following substances is most likely to reduce serum cholesterol?

Accepted Answer

Omega-3 fatty acids

Answer

C-reactive protein

Answer

Homocysteine

Answer

Lipoprotein(a)

Question 3

A 32-year-old man involved in a high-speed road traffic accident is found unconscious at the scene and breathing spontaneously. In the emergency department, the ECG monitor shows an irregular rhythm with no discernible P waves, QRS complexes, ST segments, or T waves, and a rapid rate. What is the best management for this patient?

Accepted Answer

CPR until a defibrillator is present

Answer

IV adrenaline

Answer

Urgent echo-guided pericardiocentesis

Answer

IV amiodarone

Question 4

Pericardial knock is heard in which condition?

Accepted Answer

Constrictive pericarditis

Answer

Cardiac tamponade

Answer

Restrictive cardiomyopathy

Answer

Acute pericarditis

Question 5

A 70-year-old man with a history of coronary artery disease presents with substernal chest pressure, diaphoresis, and nausea, along with difficulty catching his breath. An electrocardiogram shows septal T-wave inversion. His troponin I is elevated. He has been given aspirin and sublingual nitroglycerin. Blood pressure is 154/78 and heart rate is 72. What is the best next step in management?

Accepted Answer

Begin intravenous beta-blocker therapy

Answer

Arrange for emergent cardiac catheterization

Answer

Begin intravenous thrombolytic therapy

Answer

Admit the patient to a monitored cardiac bed and repeat cardiac enzymes and ECG in 6 hours

Question 6

A 75-year-old woman with hypertension develops fatigue and dyspnea on exertion. Her blood pressure is 160/60 mm Hg and pulse 80/min. The second heart sound is diminished and there is an early diastolic murmur that radiates from the right sternal border to the apex. Your clinical diagnosis is aortic regurgitation. What is the characteristic arterial pulse finding for this patient?

Accepted Answer

Hyperkinetic pulse

Answer

Pulsus tardus

Answer

Pulsus paradoxus

Answer

Bisferiens pulse

Question 7

A 36-year-old white female nurse comes to the ER due to a sensation of fast heart rate, slight dizziness, and vague chest fullness. Blood pressure is 110/70. The following rhythm strip is obtained, which shows?

Accepted Answer

Supraventricular tachycardia

Answer

Atrial fibrillation

Answer

Atrial flutter

Answer

Ventricular tachycardia

Question 8

QT prolongation is seen in all, EXCEPT?

Accepted Answer

Digitalis toxicity

Answer

Hypothermia

Answer

Hypocalcemia

Answer

Romano-Ward syndrome

Question 9

All of the following are true about Right Ventricular Infarcts, except?

Accepted Answer

Normal JVP

Answer

Nocturia

Answer

Nocturia

Answer

Ascites

Question 10

Which of the following results in broad complex tachycardia?

Accepted Answer

Antidromic conduction in Accessory pathway mediated tachycardia

Answer

Orthodromic conduction in accessory pathway mediated tachycardia

Answer

AV nodal re-entrant tachycardia

Answer

Atrial fibrillation

Cardiology — MCQs

Cardiology — MCQs

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