Cardiology — MCQs

Cardiology Indian Medical PG Practice Questions and MCQs

Question 1391: What is the primary concern for a patient with third-degree heart block?

A. Increased heart rate
B. Decreased heart rate (Correct Answer)
C. Fluctuating heart rate
D. Irregular heart rhythm

Explanation: ***Decreased heart rate*** - In a **third-degree heart block**, there is a complete **disassociation between atrial and ventricular activity**, meaning no impulses from the atria reach the ventricles [2]. - The ventricles fire independently at a very slow escape rhythm (typically 20-40 bpm), leading to significant **bradycardia** and reduced cardiac output [1]. *Increased heart rate* - An increased heart rate, or **tachycardia**, is not characteristic of third-degree heart block [1]. - The block prevents rapid atrial impulses from being conducted to the ventricles. *Fluctuating heart rate* - While the heart rate can be variable with certain arrhythmias, a third-degree heart block typically presents with a **persistently slow and regular ventricular escape rhythm**, rather than wide fluctuations. - The heart rate is consistently low due to the complete block [1]. *Irregular heart rhythm* - Although there is **AV dissociation**, the ventricular rhythm in a third-degree heart block is often **regular but slow**, due to the consistent firing of an escape pacemaker [2]. - Increased irregularity might suggest a co-existing arrhythmia but is not the primary issue in complete heart block itself.

Question 1392: What is the most appropriate initial management for a 65-year-old male with ST-elevation myocardial infarction (STEMI) presenting with crushing chest pain and diaphoresis?

A. Thrombolysis followed by transfer for PCI
B. Delayed PCI after medical stabilization
C. Medical management with antiplatelets and anticoagulants
D. Immediate PCI to restore coronary perfusion (Correct Answer)

Explanation: ***Immediate PCI to restore coronary perfusion*** - For **STEMI**, the primary goal is to **promptly restore blood flow** to the ischemic myocardium. **Primary percutaneous coronary intervention (PCI)** is the preferred reperfusion strategy, ideally performed within **90 minutes** of first medical contact [2]. - PCI directly opens the occluded coronary artery, significantly reducing **infarct size**, improving ventricular function, and lowering mortality [2]. *Thrombolysis followed by transfer for PCI* - **Thrombolysis** is an alternative when primary PCI is not available within recommended timelines (e.g., if transfer to a PCI-capable center would take too long) [2]. - However, if PCI is readily available, it is **superior to thrombolysis** due to higher rates of successful reperfusion and lower rates of reocclusion and bleeding complications [2]. *Delayed PCI after medical stabilization* - Delaying reperfusion therapy in STEMI is **contraindicated**, as **time is myocardium**. Rapid reperfusion is critical to preserve myocardial tissue and improve patient outcomes. - Medical stabilization alone without reperfusion therapy is insufficient to address the underlying occluded coronary artery. *Medical management with antiplatelets and anticoagulants* - **Antiplatelet (e.g., aspirin, P2Y12 inhibitors)** and **anticoagulant (e.g., heparin)** therapies are crucial adjuncts to reperfusion in STEMI, helping to prevent further clot formation and stabilize the plaque [2]. - However, these medications alone cannot effectively open a fully occluded artery characteristic of STEMI [1]; **mechanical reperfusion (PCI)** or **pharmacological reperfusion (thrombolysis)** is required.

Question 1393: A 62-year-old man with type 2 diabetes and a history of myocardial infarction is being treated for heart failure with reduced ejection fraction (HFrEF). According to the latest guidelines, which of the following medications should be added to optimize his treatment?

A. Sodium-glucose cotransporter-2 (SGLT2) inhibitor (Correct Answer)
B. Sacubitril/valsartan
C. Ivabradine
D. Digoxin

Explanation: ***Sodium-glucose cotransporter-2 (SGLT2) inhibitor*** * **SGLT2 inhibitors** are now recommended as a foundational therapy for HFrEF, regardless of diabetes status, due to their proven benefits in reducing **cardiovascular death** and **heart failure hospitalizations**. * In this patient with **type 2 diabetes** and **HFrEF**, an SGLT2 inhibitor would provide both glycemic control and significant cardiovascular protection. * *Sacubitril/valsartan* * **Sacubitril/valsartan** is a neprilysin inhibitor/angiotensin receptor blocker (ARNI) that is a cornerstone of HFrEF treatment, often replacing an **ACE inhibitor** or **ARB** [1]. * However, the question asks which medication *should be added* to *optimize* treatment, implying other foundational therapies might already be in place, and SGLT2 inhibitors offer an additional, distinct benefit. * *Ivabradine* * **Ivabradine** is indicated for HFrEF patients who are in **sinus rhythm** with a resting heart rate ≥ 70 bpm despite being on maximally tolerated doses of **beta-blockers**, to further reduce hospitalizations [1]. * The question does not provide information about his sinus rhythm or heart rate, or current beta-blocker status. * *Digoxin* * **Digoxin** may be considered in patients with HFrEF to reduce **heart failure hospitalizations**, particularly in those with **atrial fibrillation** or persistent symptoms despite optimal guideline-directed medical therapy [1]. * It does not improve survival in HFrEF and is generally reserved for patients who remain symptomatic after other foundational therapies.

Question 1394: A 50-year-old male with severe hypertension and a history of headaches presents for evaluation. Which physiological phenomenon is most likely increased in this patient?

A. Renal plasma flow
B. Systemic vascular resistance (Correct Answer)
C. Capillary hydrostatic pressure
D. Glomerular filtration rate

Explanation: - Severe **hypertension** is primarily characterized by chronically elevated **systemic vascular resistance (SVR)**, reflecting constricted arterioles. [2] - This increased resistance forces the heart to pump harder, leading to higher blood pressure, which can cause symptoms like **headaches**. *Renal plasma flow* - In chronic severe hypertension, **renal arterioles** may constrict, leading to a **decrease** in renal plasma flow rather than an increase. [2] - Reduced renal plasma flow can contribute to kidney damage over time. *Capillary hydrostatic pressure* - While overall blood pressure is elevated, the **capillary hydrostatic pressure** specifically within the systemic capillary beds may not be uniformly or significantly increased across all tissues. [1] - Capillary pressure is more strongly influenced by local regulatory mechanisms and venular tone than by systemic arterial pressure in many cases. *Glomerular filtration rate* - Initially, the **glomerular filtration rate (GFR)** might be maintained through autoregulation, but in severe and prolonged hypertension, renal damage can lead to a **decrease** in GFR. - Sustained high pressures can damage the **glomeruli**, impairing their filtering capacity.

Question 1395: What is the most appropriate initial treatment for a 58-year-old female with a history of breast cancer who presents with pulmonary embolism?

A. Low Molecular Weight Heparin (LMWH) (Correct Answer)
B. Inferior Vena Cava (IVC) filter without anticoagulation
C. Systemic thrombolysis for immediate treatment
D. Oral anticoagulants as initial therapy

Explanation: ***Low Molecular Weight Heparin (LMWH)*** - **LMWH** is the preferred initial treatment for **pulmonary embolism** in patients with **cancer** due to its superior efficacy in preventing recurrence and ease of administration. - It has a lower risk of bleeding compared to unfractionated heparin and is more effective than vitamin K antagonists in cancer-associated thrombosis [2]. [3] *Inferior Vena Cava (IVC) filter without anticoagulation* - An **IVC filter** is reserved for patients with absolute **contraindications to anticoagulation** or recurrent VTE despite adequate anticoagulation [2]. - It does not treat the existing clot or prevent new clot formation in the pulmonary circulation; it only prevents further embolization from the lower extremities. *Systemic thrombolysis for immediate treatment* - **Systemic thrombolysis** is indicated only for patients with **massive pulmonary embolism** presenting with **hemodynamic instability** due to a high risk of major bleeding [1]. - The patient's presentation does not suggest hemodynamic instability, making thrombolysis highly risky and unnecessary as an initial treatment [1]. *Oral anticoagulants as initial therapy* - While **oral anticoagulants** (e.g., DOACs or warfarin) are used for long-term management of PE, they are generally not suitable for **initial treatment** of acute PE, especially in cancer patients, as they have a slower onset of action or require bridging with parenteral anticoagulants [2]. - **LMWH** provides rapid and reliable anticoagulation, which is crucial in the acute phase of PE to prevent further clot propagation and embolization [3].

Question 1396: A 72-year-old female presents with dyspnea on exertion and an ejection systolic murmur best heard at the right upper sternal border. Echocardiography reveals a calcified aortic valve with restricted movement. What is the most likely diagnosis?

A. Aortic stenosis (Correct Answer)
B. Mitral regurgitation
C. Tricuspid regurgitation
D. Ventricular septal defect

Explanation: ***Aortic stenosis*** - The classic presentation of **dyspnea on exertion** and an **ejection systolic murmur** at the **right upper sternal border** in an elderly patient is highly suggestive of aortic stenosis [1]. - **Echocardiography demonstrating a calcified aortic valve with restricted movement** definitively confirms the diagnosis by showing the pathological changes to the valve [1]. *Mitral regurgitation* - Characterized by a **holosystolic murmur** best heard at the **apex** and radiating to the axilla, associated with conditions like papillary muscle dysfunction or leaflet prolapse [2]. - While it can cause dyspnea, the murmur's location and timing, along with the specific echo findings of a calcified aortic valve, differentiate it from the patient's presentation [2]. *Tricuspid regurgitation* - Presents with a **holosystolic murmur** that increases with inspiration (Carvallo's sign) and is best heard at the **left lower sternal border**, often associated with and secondary to pulmonary hypertension. - This condition does not typically involve a calcified aortic valve or an ejection systolic murmur at the right upper sternal border. *Ventricular septal defect* - Typically causes a **harsh holosystolic murmur** best heard at the **left sternal border**, often associated with a thrill, and is usually diagnosed earlier in life. - While it can lead to dyspnea, the specific murmur features and echocardiographic findings presented in an elderly patient are inconsistent with an isolated VSD.

Question 1397: A 70-year-old man with a long history of hypertension presents with sudden severe chest pain radiating to the back. CT angiography shows aortic dissection. What is the most common predisposing factor?

A. Hypertension (Correct Answer)
B. Marfan syndrome
C. Bicuspid aortic valve
D. Atherosclerosis

Explanation: ***Hypertension*** - A **long history of hypertension** is the most significant predisposing factor for aortic dissection, as it increases the wall stress of the aorta [1]. - It can lead to **degeneration of the aortic media**, making it more susceptible to dissections [1]. *Bicuspid aortic valve* - While it can lead to **aortic stenosis** and other complications, it is not the **most common** predisposing factor for aortic dissection. - This condition primarily affects younger individuals, whereas dissection is more associated with **older age** and chronic hypertension. *Atherosclerosis* - Atherosclerosis contributes to **cardiovascular disease** but does not directly lead to aortic dissection as primarily as hypertension does. - It affects atherosclerotic plaque formation rather than the **structural integrity** of the aorta, which is pivotal in dissections [1]. *Marfan syndrome* - Although it is associated with aortic dissection [1], it is less common compared to **hypertension** in the general population. - Marfan syndrome is a genetic disorder, affecting connective tissue, which leads to dissection but is not as prevalent as chronic high blood pressure.

Question 1398: 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 1399: What is the diagnostic utility of high-sensitivity troponin assays in the early detection of myocardial infarction?

A. Low sensitivity; high specificity for detecting myocardial infarction.
B. High sensitivity; low specificity for detecting myocardial infarction.
C. Low sensitivity and specificity for detecting myocardial infarction.
D. High sensitivity and specificity for detecting myocardial infarction. (Correct Answer)

Explanation: ***High sensitivity and specificity for detecting myocardial infarction.*** - **High-sensitivity troponin assays** are designed to detect very low concentrations of troponin, allowing for earlier detection of myocardial injury. - Their **high sensitivity** means fewer true positives are missed, while their **high specificity** ensures that elevated levels are very likely due to myocardial injury, improving diagnostic accuracy [1]. *Low sensitivity; high specificity for detecting myocardial infarction.* - This statement is incorrect because high-sensitivity troponin assays are specifically developed for their **high sensitivity**, meaning they are very good at picking up even small amounts of myocardial damage [1]. - While they are indeed specific to cardiac muscle, their primary advantage in early detection lies in their ability to detect subtle increases that traditional assays might miss. *High sensitivity; low specificity for detecting myocardial infarction.* - While high-sensitivity troponins do offer **high sensitivity**, stating they have "low specificity" is inaccurate in the context of their use for myocardial infarction. - Although troponin can be elevated in conditions other than MI (e.g., heart failure, renal failure), these assays are still highly specific for **cardiac muscle injury**, and clinical context helps differentiate MI from other causes [1]. *Low sensitivity and specificity for detecting myocardial infarction.* - This option is incorrect because the very purpose of **high-sensitivity troponin assays** is to overcome the limitations of older troponin assays, which might have had lower sensitivity, especially in the early stages of MI. - These newer assays offer superior performance in both detecting and accurately identifying cardiac injury [1].

Question 1400: 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.

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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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