Cardiology — MCQs

Cardiology Indian Medical PG Practice Questions and MCQs

Question 1401: Sinus bradycardia with myocardial infarction is best treated with:

A. Atropine (Correct Answer)
B. Isoproterenol
C. Dopamine
D. Temporary pacing

Explanation: ***Atropine*** - **Atropine** is a **parasympatholytic agent** that blocks acetylcholine's action on muscarinic receptors, increasing heart rate. - It is the **first-line treatment** for hemodynamically significant **bradycardia** in the context of **myocardial infarction** to improve cardiac output [2]. *Dopamine* - While dopamine can increase heart rate and blood pressure, it is typically used for **hemodynamically unstable bradycardia** unresponsive to atropine. - Its **vasoconstrictive effects** can increase myocardial oxygen demand, which might be detrimental in **myocardial infarction**. *Isoproterenol* - **Isoproterenol** is a **non-selective beta-agonist** that increases heart rate and contractility. - Its use in **myocardial infarction** is generally avoided due to significant **tachycardic** and **arrhythmogenic effects**, which can worsen myocardial ischemia. *Temporary pacing* - **Temporary pacing** is reserved for **severe, symptomatic bradycardia** that is **refractory to pharmacological management** (e.g., atropine, dopamine) [2]. - It is an **invasive procedure** and not the initial treatment for sinus bradycardia with myocardial infarction unless other measures fail [1].

Question 1402: A 40-year-old male presents with severe chest pain, hypotension, and distended neck veins. His ECG shows electrical alternans. What is the most likely diagnosis?

A. Myocardial infarction
B. Pulmonary embolism
C. Pericardial tamponade (Correct Answer)
D. Aortic dissection

Explanation: ***Pericardial tamponade*** - The combination of **chest pain**, **hypotension**, and **distended neck veins** (Beck's triad), along with **electrical alternans** on ECG, is highly indicative of pericardial tamponade. - **Electrical alternans** is caused by the heart "swinging" within the fluid-filled pericardial sac, leading to beat-to-beat variations in QRS amplitude. *Myocardial infarction* - While it can cause **chest pain** and **hypotension**, **distended neck veins** and **electrical alternans** are not typical findings. - ECG usually shows **ST-segment elevation** or depression, and/or **T-wave inversion**, depending on the type and location of the infarction. *Pulmonary embolism* - It can cause **chest pain** and **hypotension**, but **distended neck veins** are less common and typically associated with right heart strain, and **electrical alternans** is not a characteristic ECG finding. - ECG often shows **S1Q3T3 pattern** or **right bundle branch block**, acute right ventricular strain, and sinus tachycardia. *Aortic dissection* - It presents with severe, tearing **chest pain** that may radiate to the back and can cause **hypotension** due to hypovolemic shock (rupture into the pericardium/pleural space) or cardiac tamponade. - However, **electrical alternans** is not a direct consequence of aortic dissection, though it may occur if dissection leads to significant pericardial effusion and tamponade.

Question 1403: A 58-year-old man presents with chest pain and sweating. His ECG shows ST elevation in leads II, III, and aVF. What is the most likely location of the myocardial infarction?

A. Anterior wall
B. Posterior wall
C. Inferior wall (Correct Answer)
D. Lateral wall

Explanation: Detailed Analysis: ***Inferior wall*** - **ST elevation** in leads **II, III, and aVF** is the classic electrocardiographic finding for an **inferior wall myocardial infarction** [1]. - These leads correspond to the **diaphragmatic surface** of the heart, supplied primarily by the **right coronary artery** (RCA) in most individuals. *Anterior wall* - An **anterior wall myocardial infarction** typically shows **ST elevation** in leads **V1-V4** [2]. - This region is usually supplied by the **left anterior descending** (LAD) coronary artery. *Posterior wall* - A **posterior wall myocardial infarction** is often characterized by **ST depression** in leads **V1-V3** and prominent R waves, which are reciprocal changes to posterior ST elevation [2]. - This area is usually supplied by the **circumflex artery** or a dominant RCA. *Lateral wall* - A **lateral wall myocardial infarction** is indicated by **ST elevation** in leads **I, aVL, V5, and V6** [1]. - The lateral wall is primarily supplied by the **circumflex artery** or marginal branches of the LAD. *Symptoms* - Presenting symptoms such as chest pain and sweating (signs of sympathetic activation) are characteristic of acute myocardial ischemia [3].

Question 1404: In a 60-year-old man with chronic heart failure, what is the most likely cause of decreased exercise tolerance?

A. Decreased cardiac output (Correct Answer)
B. Decreased total peripheral resistance
C. Increased systemic vascular resistance
D. Increased stroke volume due to compensatory mechanisms

Explanation: ***Decreased cardiac output*** - **Chronic heart failure** is characterized by the heart's inability to pump sufficient blood to meet the body's metabolic demands, directly leading to **decreased cardiac output**. [1] - Reduced cardiac output limits oxygen delivery to muscles during exertion, causing **fatigue** and decreased **exercise tolerance**. [1] *Increased systemic vascular resistance* - While **increased systemic vascular resistance (SVR)** can occur in heart failure as a compensatory mechanism (due to activation of the **renin-angiotensin-aldosterone system** and sympathetic nervous system), it primarily raises afterload and further impedes cardiac output, rather than being the direct cause of exercise intolerance. - The direct cause of reduced exercise capacity is the resultant **lowered cardiac output**, which this increased resistance contributes to. *Decreased total peripheral resistance* - **Decreased total peripheral resistance** would typically improve cardiac output by reducing afterload, and thus would not be a cause of decreased exercise tolerance in chronic heart failure. - In fact, in chronic heart failure, compensatory mechanisms often lead to **increased**, not decreased, peripheral resistance. *Increased stroke volume due to compensatory mechanisms* - In heart failure, the **stroke volume** is typically **reduced** due to impaired contractility or filling. [1] - While compensatory mechanisms like **Frank-Starling law** (increased preload) can transiently increase stroke volume, chronic heart failure is fundamentally marked by a **failing heart** and an overall inability to maintain adequate stroke volume and cardiac output, especially during exertion. [1]

Question 1405: Which of the following is the most important preoperative test for a patient with a history of cardiovascular disease?

A. Complete blood count
B. Electrocardiogram (Correct Answer)
C. Chest X-ray
D. Urinalysis

Explanation: ***Electrocardiogram*** - An **ECG** is crucial for patients with a history of **cardiovascular disease** to assess for existing or new cardiac rhythm abnormalities, ischemia, or infarction that could impact surgical risk. - It helps identify patients who may require further cardiac evaluation or optimization before surgery to prevent **perioperative cardiac events**. *Complete blood count* - A **complete blood count (CBC)** assesses overall health, detects anemia, infection, and platelet disorders, which are important for surgical planning. - While important, it doesn't directly evaluate the function or status of the **cardiovascular system** itself in the same way an ECG does. *Chest X-ray* - A **chest X-ray** provides information about lung fields, heart size, and major blood vessels. It is useful for detecting pulmonary issues or significant cardiomegaly. - However, it does not offer the same detailed functional assessment of the heart's electrical activity or potential ischemic changes as an **ECG**. *Urinalysis* - **Urinalysis** screens for kidney disease, urinary tract infections, and diabetes, which are important general health indicators. - It provides no direct information about the **cardiovascular system** or its operative risk secondary to cardiac disease.

Question 1406: A 35-year-old male experiences sudden chest pain and shortness of breath. An ECG reveals ST-segment elevation. What is the most likely underlying physiological process?

A. Aortic dissection
B. Pulmonary embolism
C. Myocardial infarction (Correct Answer)
D. Pericarditis

Explanation: ***Myocardial infarction*** - **ST-segment elevation** on an ECG is a classic sign of an **ST-elevation myocardial infarction (STEMI)**, indicating transmural ischemia [2]. - This is caused by a complete and sustained occlusion of a **coronary artery**, leading to myocardial cell death [1] [3]. *Aortic dissection* - While it causes sudden severe chest pain, an aortic dissection typically presents with a **tearing or ripping pain** and often involves pulse deficits or blood pressure differentials. - ECG findings are usually non-specific or show signs of left ventricular hypertrophy, but **ST-segment elevation** is not characteristic. *Pulmonary embolism* - Pulmonary embolism presents with sudden chest pain and shortness of breath, but its hallmark ECG finding is often **tachycardia** and signs of right heart strain (e.g., S1Q3T3 pattern). - It does not typically cause **ST-segment elevation** unless it's a massive PE leading to severe myocardial ischemia secondary to profound hypotension. *Pericarditis* - Pericarditis causes chest pain that is often **sharp, pleuritic**, and relieved by leaning forward, and it can cause diffuse **ST-segment elevation** on ECG. - However, in pericarditis, the ST elevation is typically **concave up** and widespread, rather than localized to specific coronary territories as seen in myocardial infarction [3].

Question 1407: A 60-year-old patient presents with chest pain and a crescendo-decrescendo systolic murmur that radiates to the neck. What is the most likely diagnosis?

A. Mitral valve prolapse
B. Aortic stenosis (Correct Answer)
C. Mitral regurgitation
D. Aortic regurgitation

Explanation: ***Aortic stenosis*** - A **crescendo-decrescendo systolic murmur** radiating to the **neck** is a classic finding in aortic stenosis, indicative of turbulent flow through a narrowed aortic valve during systole [1]. - Chest pain in this context is often due to increased myocardial oxygen demand from the pressure overload [2]. *Mitral valve prolapse* - Characterized by a **mid-systolic click** followed by a **late systolic murmur**, and typically does not radiate to the neck [1]. - Symptoms can include atypical chest pain and palpitations, but the murmur presentation is distinct. *Mitral regurgitation* - Produces a **holosystolic murmur** that radiates to the **axilla**, not the neck, due to blood flowing back into the left atrium [3]. - The murmur in mitral regurgitation is usually plateau-shaped, unlike the crescendo-decrescendo pattern. *Aortic regurgitation* - Causes a **diastolic decrescendo murmur** best heard at the left sternal border, resulting from blood leaking back into the left ventricle during diastole [4]. - This condition does not present with a systolic murmur radiating to the neck.

Question 1408: Which of the following best describes the initial management of a patient with Klippel-Trenaunay syndrome?

A. Conservative management with compression stockings (Correct Answer)
B. Immediate surgical intervention
C. Sclerotherapy for varicose veins
D. Lymphatic drainage

Explanation: ***Conservative management with compression stockings*** * **Klippel-Trenaunay syndrome (KTS)** is a congenital disorder characterized by a triad of capillary malformations (port-wine stains), venous malformations (varicose veins), and limb overgrowth. * Initial management focuses on alleviating symptoms and preventing complications through non-invasive methods, with **compression garments** being crucial for managing lymphedema, venous insufficiency, and pain. *Immediate surgical intervention* * **Surgical intervention** in KTS is typically reserved for severe complications or functional impairment, like limb length discrepancy or arterial-venous fistulas, which are not the primary initial approach. * Non-conservative measures are usually explored only after conservative treatment fails or if there are life-threatening complications. *Sclerotherapy for varicose veins* * While sclerotherapy can be used for **varicose veins** in KTS, it is usually considered after or in conjunction with conservative management. * It specifically targets the venous malformations but does not address the other components like **limb overgrowth** or comprehensive symptom management in the initial phase. *Lymphatic drainage* * **Manual lymphatic drainage (MLD)** is a component of complete decongestive therapy for managing lymphedema. * While lymphedema can be a feature of KTS, **lymphatic drainage** alone is usually part of a broader conservative strategy that often includes compression therapy.

Question 1409: A 72-year-old patient presents with the acute onset of chest pain and electrocardiographic changes indicative of an anterior wall myocardial infarction. What is the most effective initial treatment?

A. High-dose aspirin therapy
B. Intravenous nitroglycerin
C. Oral beta-blocker therapy
D. Primary percutaneous coronary intervention (PCI) (Correct Answer)

Explanation: ### Primary percutaneous coronary intervention (PCI) - For **ST-segment elevation myocardial infarction (STEMI)**, primary PCI is the most effective initial treatment as it directly restores blood flow to the ischemic myocardium by opening the occluded coronary artery [2]. - Guidelines recommend PCI within **90 minutes door-to-balloon time** or 120 minutes if transfer to a PCI-capable facility is required. *High-dose aspirin therapy* - While **aspirin** is crucial for its antiplatelet effects and is part of the initial management of MI, it is not the definitive treatment for reperfusion. - It helps prevent further thrombus formation but does not actively dissolve or remove the existing occlusive clot. *Intravenous nitroglycerin* - **Nitroglycerin** helps relieve angina by causing vasodilation, reducing preload and afterload, and improving coronary blood flow, but it does not directly open a completely occluded artery. - It is contraindicated in cases of **inferior wall MI with right ventricular involvement** due to the risk of severe hypotension. *Oral beta-blocker therapy* - **Beta-blockers** reduce myocardial oxygen demand, limit infarct size, and prevent arrhythmias, but they do not provide immediate reperfusion [1]. - They are typically initiated after the acute phase, once the patient is hemodynamically stable, or in specific clinical scenarios [1].

Question 1410: What is the first-line treatment for a patient diagnosed with symptomatic bradycardia?

A. Atropine (Correct Answer)
B. Beta-blockers
C. Pacemaker
D. Digoxin

Explanation: ***Atropine*** - **Atropine** is the **first-line pharmacological agent** for symptomatic bradycardia because it blocks the action of acetylcholine at muscarinic receptors, thereby enhancing **sinoatrial (SA) node automaticity** and **atrioventricular (AV) node conduction**. - It rapidly increases **heart rate** and improves symptoms such as hypotension and syncope in patients with bradycardia attributable to increased vagal tone or AV nodal block. *Beta-blockers* - **Beta-blockers** decrease heart rate and slow AV nodal conduction [2], which could **worsen bradycardia**, making them contraindicated in acute symptomatic bradycardia [4] unless used to treat an underlying tachyarrhythmia, which is not the case here. - Their primary use is for conditions like **hypertension**, **angina**, and **tachyarrhythmias**, not initially for bradycardia. *Pacemaker* - A **pacemaker** is considered for **symptomatic bradycardia** if **atropine** and other temporary measures (like transcutaneous pacing) fail, or in cases of ** Mobitz II AV block**, **complete heart block**, or **sick sinus syndrome** with persistent symptoms [1]. - It is a **definitive treatment** for persistent and severe bradycardia but not the first-line pharmacological intervention. *Digoxin* - **Digoxin** is a **cardiac glycoside** that slows the heart rate by increasing vagal tone and prolonging AV nodal refractory period, making it **contraindicated in symptomatic bradycardia** as it would further depress heart rate and conduction [3]. - Its primary uses are in conditions like **heart failure** and **atrial fibrillation with rapid ventricular response** where slowing the heart rate is desired, but not in existing bradycardia.

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Coronary Artery Disease and Angina

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Acute Coronary Syndromes

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Heart Failure

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Cardiac Arrhythmias

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Valvular Heart Diseases

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Cardiomyopathies

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Pericardial Diseases

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Congenital Heart Disease in Adults

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Hypertension and Hypertensive Emergencies

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Pulmonary Hypertension

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Non-invasive Cardiac Diagnostics

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Preventive Cardiology

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Cardiology — MCQs

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