Cardiology — MCQs
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Which of the following ECG features are characteristic of ventricular tachycardia?
Prolonged QT interval is seen in all of the following except
Levine sign is seen in
Which of the following is NOT a clinical sign of widened pulse pressure seen in patients with aortic regurgitation?
Episode of stable angina pectoris typically lasts for
Ejection click of pulmonary stenosis is better heard in
What is the PRIMARY complication that requires lifelong management in patients with mechanical prosthetic heart valves?
38 yr old patient with high risk of coronary artery disease and hypertension, which of the following antihypertensive drugs will be suitable as a first line treatment for this patient?
Most frequent time period between myocardial infarction and subsequent myocardial rupture is -
What is commonly referred to as the widow's artery in myocardial infarction?
Cardiology Indian Medical PG Practice Questions and MCQs
Question 1471: Which of the following ECG features are characteristic of ventricular tachycardia?
- A. Bizarre QRS complexes (Correct Answer)
- B. Presence of AV dissociation [fusion beats]
- C. Prolonged duration of QRS complexes
- D. P pulmonale
Explanation: ### Original Explanation ***Bizarre QRS complexes*** - In **ventricular tachycardia (VT)**, the electrical impulse originates from the ventricles, bypassing the normal conduction system [1]. - This leads to **aberrant ventricular activation**, resulting in **wide** and **unusual-looking QRS complexes** [1]. *Presence of AV dissociation [fusion beats]* - While **AV dissociation** can be present in VT, it is **not a universal characteristic** and is often seen in other wide complex tachycardias as well [1]. - **Fusion beats** are a specific type of AV dissociation where a ventricular and supraventricular impulse simultaneously activate the ventricles, which reinforces the diagnosis of VT; however, bizarre QRS complexes are a more direct visual indicator of ventricular origin [1]. *Prolonged duration of QRS complexes* - A prolonged QRS duration (typically **>0.12 seconds**) is characteristic of **wide complex tachycardias**, including VT [1]. - However, the term "bizarre" goes beyond simple prolongation to describe the **unusual morphology and irregular shapes** that are highly suggestive of a ventricular origin [1]. *P pulmonale* - **P pulmonale** refers to a **tall, peaked P wave** in leads II, III, and aVF, indicative of **right atrial enlargement**. - This finding is associated with conditions like **pulmonary hypertension** or **pulmonary embolism** and has no direct relevance to the diagnosis of ventricular tachycardia.
Question 1472: Prolonged QT interval is seen in all of the following except
- A. Hypokalemia
- B. Hypocalcemia
- C. Hypernatremia (Correct Answer)
- D. Use of macrolide antibiotics
Explanation: ***Hypernatremia*** - **Hypernatremia** does not typically cause a prolonged QT interval; instead, it tends to cause **shortening of the QT interval** due to its effect on cardiomyocyte repolarization. - The primary cardiac effects of hypernatremia involve alterations in **myocardial contractility** and **arrhythmia risk**, but not QT prolongation. *Hypokalemia* - **Hypokalemia** leads to changes in myocardial repolarization, causing **QT prolongation** which increases the risk of **Torsades de Pointes** [1], [2]. - This occurs because low potassium levels affect the outward potassium currents, extending the action potential duration. *Hypocalcemia* - **Hypocalcemia** prolongs the **QT interval** by extending the ST segment duration without significantly affecting the T wave morphology directly. - Reduced extracellular calcium levels interfere with the voltage-gated calcium channels, impacting the plateau phase of the cardiac action potential. *Use of macrolide antibiotics* - Many **macrolide antibiotics**, such as **azithromycin** and **erythromycin**, are known to inhibit cardiac potassium channels (specifically **IKr current**), thereby prolonging the QT interval [2]. - This effect can lead to a significant risk of **ventricular arrhythmias**, including **Torsades de Pointes** [2], [3].
Question 1473: Levine sign is seen in
- A. Acute Myocardial Infarction (Correct Answer)
- B. Esophageal spasm
- C. Aortic dissection
- D. Pulmonary embolism
Explanation: ***Acute Myocardial Infarction*** - The **Levine sign** is a classic nonverbal gesture where a patient clenches their fist over the sternum, indicating **retrosternal chest pain** [1]. - This sign is highly suggestive of **ischemic chest pain**, often associated with an **acute myocardial infarction** [1]. *Pulmonary embolism* - Chest pain in pulmonary embolism is typically **pleuritic**, sharp, and localized, often worsened by breathing. - It does not usually present with the diffuse, constrictive quality expressed by the **Levine sign**. *Esophageal spasm* - Chest pain from esophageal spasm can mimic cardiac pain, but it is often described as a **squeezing or crushing sensation** behind the sternum and may be relieved by nitrates. - While it can be severe, it is less consistently associated with the **Levine sign** compared to myocardial infarction. *Aortic dissection* - The pain of aortic dissection is typically described as **sudden, severe, tearing, or ripping** and often radiates to the back. - It usually has a unique quality that is distinct from the constrictive pain signaled by the **Levine sign**.
Question 1474: Which of the following is NOT a clinical sign of widened pulse pressure seen in patients with aortic regurgitation?
- A. Corrigan's pulse
- B. Quincke's sign
- C. Pulsus paradoxus (Correct Answer)
- D. De Musset's sign
Explanation: ***Pulsus paradoxus*** - **Pulsus paradoxus** is an abnormally large decrease in **systolic blood pressure and pulse wave amplitude** during inspiration, which is typically associated with **cardiac tamponade** or severe respiratory conditions like **asthma** or **COPD**, not specifically widened pulse pressure in aortic regurgitation. - While it reflects pulse examination, it reflects impaired ventricular filling due to extrinsic compression or lung overinflation, not primarily the consequence of increased stroke volume and rapid diastolic runoff as seen in aortic regurgitation. *Corrigan's pulse* - **Corrigan's pulse** is a **bounding and forceful pulse** that rapidly collapses, often described as a **water-hammer pulse**, which is a classic sign of **aortic regurgitation** due to a high stroke volume and rapid fall in diastolic pressure [1]. - This sign directly reflects the **widened pulse pressure**, where a large systolic ejection causes a strong pulse, followed by a sudden decrease in peripheral pressure [1]. *Quincke's sign* - **Quincke's sign** refers to visible **capillary pulsations** in the nail beds, which are blanching and flushing of the capillaries when gentle pressure is applied to the fingernail, typically indicative of **aortic regurgitation**. - This phenomenon occurs because of the **capillary vasodilation** and the significant **systolic-diastolic pressure difference** transmitted to the peripheral circulation. *De Musset's sign* - **De Musset's sign** is a rhythmic **head nodding with each heartbeat**, which is an uncommon but specific sign of **severe aortic regurgitation** [1]. - This physical manifestation results from the **large stroke volume** and **widened pulse pressure** leading to significant movement of the head and neck vessels with each cardiac contraction [1].
Question 1475: Episode of stable angina pectoris typically lasts for
- A. Less than 1 min
- B. 2 - 5 mins (Correct Answer)
- C. 5 - 10 mins
- D. > 10 mins
Explanation: ***2 - 5 mins*** - Episodes of **stable angina pectoris** are typically brief, lasting between 2 and 5 minutes [1]. - The chest discomfort is usually relieved by **rest** or sublingual **nitroglycerin** [1]. *Less than 1 min* - Anginal episodes usually last longer than 1 minute; very brief chest pain is often not typical for angina. - This duration might suggest a different etiology, potentially **musculoskeletal pain** or **esophageal spasm**. *5 - 10 mins* - While a single episode can sometimes last up to 10 minutes, this duration is at the upper limit for typical stable angina. - If pain persists for this long or longer, it raises suspicion for **unstable angina** or **myocardial infarction** [1]. *> 10 mins* - Chest pain lasting longer than 10 minutes is usually concerning for **unstable angina** or an **acute myocardial infarction** [1]. - It requires urgent medical evaluation to rule out more serious cardiac events.
Question 1476: Ejection click of pulmonary stenosis is better heard in
- A. Patient bending forward
- B. Patient lying in left lateral position
- C. Expiration
- D. Inspiration (Correct Answer)
Explanation: Inspiration - The **pulmonic ejection click** is associated with the opening of a **domed pulmonary valve** during systole [1]. - During **inspiration**, increased right ventricular filling causes more blood to be ejected, leading to earlier and louder opening of the stenotic pulmonary valve, making the click more prominent. Expiration - During **expiration**, venous return to the right side of the heart is reduced, decreasing right ventricular volume and making the pulmonic ejection click less noticeable or even absent. - This respiratory variation helps distinguish a pulmonic ejection click from an aortic ejection click, which does not vary with respiration [1]. Patient bending forward - **Bending forward** is a maneuver primarily used to accentuate **aortic regurgitation** murmurs, not to optimize the hearing of a pulmonic ejection click. - This position brings the heart closer to the chest wall, enhancing sounds originating from the left side of the heart. Patient lying in left lateral position - The **left lateral position** is commonly used to accentuate **mitral valve** sounds, such as the opening snap of mitral stenosis or the murmur of mitral regurgitation [1]. - This position does not specifically improve the audibility of a pulmonic ejection click.
Question 1477: What is the PRIMARY complication that requires lifelong management in patients with mechanical prosthetic heart valves?
- A. Thromboembolism (Correct Answer)
- B. Immediate valve failure
- C. Pulmonary edema
- D. Acute myocardial infarction
Explanation: ***Thromboembolism*** - Mechanical prosthetic heart valves are inherently **thrombogenic** due to non-endothelialized surfaces that interact with blood components, necessitating lifelong **anticoagulation** to prevent clot formation [2]. - Clots can form on the valve and embolize, leading to serious complications such as **stroke** or **peripheral arterial occlusion** [1]. *Immediate valve failure* - While possible, **immediate valve failure** is a rare event typically related to surgical error or a manufacturing defect and is not a primary, ongoing management concern. - The durability of modern mechanical valves is excellent, so failure generally occurs over a long period, if at all, due to structural degradation or infection, rather than immediately post-op. *Acute myocardial infarction* - **Acute myocardial infarction** is primarily caused by **coronary artery disease** and is not a direct complication of the prosthetic heart valve itself. - While valve surgery can be associated with cardiac complications, MI is not a unique, lifelong management issue specifically attributable to the presence of a mechanical valve. *Pulmonary edema* - **Pulmonary edema** can occur in the setting of heart failure due to severe valve dysfunction or other cardiac issues, but it is not a direct or primary complication of the mechanical valve itself requiring lifelong management unique to the valve. - Effective valve function, whether native or prosthetic, is aimed at *preventing* pulmonary edema, not causing it.
Question 1478: 38 yr old patient with high risk of coronary artery disease and hypertension, which of the following antihypertensive drugs will be suitable as a first line treatment for this patient?
- A. Calcium channel blockers
- B. Beta-adrenergic blockers
- C. Diuretics
- D. ACE inhibitors (Correct Answer)
Explanation: ### ACE inhibitors - **ACE inhibitors** are particularly suitable as first-line treatment for patients with hypertension and a high risk of **coronary artery disease (CAD)** because they have proven benefits in **cardiovascular protection** and **mortality reduction** [1]. - They improve **endothelial function** and can prevent **cardiac remodeling**, which is crucial in managing high-risk cardiovascular patients [4]. ### Calcium channel blockers - While effective for hypertension, **calcium channel blockers** do not offer the same level of **cardioprotection** in high-risk CAD patients as ACE inhibitors [1]. - They primarily act as **vasodilators** but lack the direct benefits on cardiac remodeling and atherosclerosis progression seen with ACE inhibitors. ### Beta-adrenergic blockers - **Beta-blockers** are generally not recommended as first-line monotherapy for essential hypertension unless there are specific compelling indications like **post-myocardial infarction** or **heart failure** [5]. - Their routine use as initial therapy for uncomplicated hypertension, especially in high-risk CAD patients without a recent event, is less favored compared to ACE inhibitors. ### Diuretics - **Diuretics**, particularly **thiazide diuretics**, are effective in lowering blood pressure and are often used, especially in elderly patients or those with salt sensitivity [3]. - However, for patients with high CAD risk, ACE inhibitors generally provide superior **cardiovascular benefit** beyond just blood pressure reduction, including preventing adverse cardiac events [2].
Question 1479: Most frequent time period between myocardial infarction and subsequent myocardial rupture is -
- A. 3-4 days (Correct Answer)
- B. 4-8 days
- C. 1-3 weeks
- D. 3-6 weeks
Explanation: ***3-4 days*** - This period corresponds to the peak of **macrophage infiltration** and **collagen degradation** in the infarcted myocardial tissue, making it most vulnerable. - The necrotic tissue is mechanically weak and susceptible to the **intracardiac pressure**, leading to rupture. *4-8 days* - By this stage, **scar formation** has usually begun, with fibroblasts appearing and laying down new collagen. - While still a vulnerable period, the initial peak of degradation and risk of rupture typically occurs earlier. *1-3 weeks* - During this time, significant **fibrosis and scar maturation** are occurring, leading to increased structural integrity of the infarct zone. - The risk of rupture significantly decreases as the **scar tissue** strengthens. *3-6 weeks* - At this point, the infarct is generally well-healed, with a dense **fibrous scar** largely replacing the necrotic tissue [1]. - The myocardial wall has regained considerable strength, making rupture highly unlikely at this late stage.
Question 1480: What is commonly referred to as the widow's artery in myocardial infarction?
- A. Left anterior descending artery (Correct Answer)
- B. Right coronary artery
- C. Posterior interventricular artery
- D. Left circumflex artery
Explanation: ***Left anterior descending artery*** - The **left anterior descending (LAD) artery** is often called the "widow maker" due to its critical role in supplying blood to a large area of the left ventricle, which is the heart's main pumping chamber [1]. - An **occlusion** in the LAD artery can lead to extensive damage, significantly increasing the risk of sudden cardiac death and making it a particularly dangerous site for a **myocardial infarction**. *Right coronary artery* - The **right coronary artery (RCA)** primarily supplies the **right ventricle**, the inferior wall of the left ventricle, and the SA/AV nodes. - While an RCA occlusion can cause a myocardial infarction, it is generally associated with a **better prognosis** and less extensive damage compared to an LAD occlusion. *Posterior interventricular artery* - The **posterior interventricular artery (PDA)**, also known as the posterior descending artery, typically branches off the RCA (in 85% of individuals) or the circumflex artery (in 15%) [2]. - It supplies the **diaphragmatic surface** of both ventricles and the posterior interventricular septum, but its occlusion is generally less critical than the LAD. *Left circumflex artery* - The **left circumflex artery (LCX)** supplies the lateral and posterior walls of the left ventricle [2]. - Although an LCX occlusion can lead to a significant myocardial infarction, it usually involves a **smaller territory** and is not as acutely life-threatening as an LAD occlusion.
Practice by Chapter
Coronary Artery Disease and Angina
Practice Questions
Acute Coronary Syndromes
Practice Questions
Heart Failure
Practice Questions
Cardiac Arrhythmias
Practice Questions
Valvular Heart Diseases
Practice Questions
Cardiomyopathies
Practice Questions
Pericardial Diseases
Practice Questions
Congenital Heart Disease in Adults
Practice Questions
Hypertension and Hypertensive Emergencies
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Pulmonary Hypertension
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Non-invasive Cardiac Diagnostics
Practice Questions
Preventive Cardiology
Practice Questions
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