Cardiology — MCQs
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Subclavian steal syndrome is
What is the most likely cause of fluid overload in a patient presenting with shortness of breath?
Which of the following is associated with WPW syndrome?
In the management of a patient with acute myocardial infarction, which of the following is the most critical step in the initial treatment?
Treatment of choice for prinzmetal's angina
Which of the following is a non- modifiable risk factor for CHD -
Creatine kinase is elevated in MI after
Which condition is associated with a left axis deviation of -30° to -60°?
Kussmaul's sign is classically described in:
Which biomarker is typically elevated in the plasma of patients with chronic heart disease?
Cardiology Indian Medical PG Practice Questions and MCQs
Question 1541: Subclavian steal syndrome is
- A. Reversal of blood flow in the ipsilateral vertebral artery (Correct Answer)
- B. Reversal of blood flow in the contralateral carotid artery
- C. Reversal of blood flow in the contralateral vertebral artery
- D. B/L reversal of blood flow in vertebral arteries
Explanation: ***Reversal of blood flow in the ipsilateral vertebral artery*** - Subclavian steal syndrome occurs due to a **proximal stenosis** or **occlusion of the subclavian artery**. - This causes blood to be "stolen" from the **ipsilateral vertebral artery**, flowing retrograde to supply the arm and thereby reducing blood flow to the brainstem. *Reversal of blood flow in the contralateral carotid artery* - The carotid arteries supply blood to the brain directly and are typically not directly involved in thesteal phenomenon in this specific syndrome. - Reversal of flow in the carotid artery would indicate a much more severe and different pathology, not characteristic of subclavian steal. *Reversal of blood flow in the contralateral vertebral artery* - The steal phenomenon specifically involves the vertebral artery on the **same side (ipsilateral)** as the subclavian artery obstruction. - The contralateral vertebral artery would typically continue to supply blood to the brain without a reversed flow in this syndrome. *B/L reversal of blood flow in vertebral arteries* - Subclavian steal syndrome is generally a **unilateral phenomenon**, affecting the vertebral artery ipsilateral to the subclavian artery stenosis. - Bilateral reversal would imply bilateral subclavian artery obstruction or other severe cerebrovascular disease, which is not the definition of subclavian steal syndrome itself.
Question 1542: What is the most likely cause of fluid overload in a patient presenting with shortness of breath?
- A. Nephritic syndrome
- B. Cardiac failure (Correct Answer)
- C. TB
- D. Portal hypertension
Explanation: ***Cardiac failure*** - **Cardiac failure** leads to reduced cardiac output, causing blood to back up in the **pulmonary and systemic circulation**, resulting in fluid accumulation in the lungs (pulmonary edema), which manifests as **shortness of breath** [1]. - The heart's inability to pump efficiently results in increased hydrostatic pressure in capillaries, pushing fluid into interstitial spaces and pleural effusions, exacerbating respiratory distress [1]. *Nephritic syndrome* - **Nephritic syndrome** is characterized by inflammation of the glomeruli, leading to **hematuria, proteinuria, and hypertension**. While it can cause fluid retention due to impaired kidney function, it primarily presents with acute renal injury and less direct, rapid onset pulmonary edema compared to cardiac failure. - The fluid accumulation in **nephritic syndrome** is more generalized (edema) rather than acutely focused on pulmonary congestion leading to shortness of breath, as seen in heart failure. *TB* - **Tuberculosis (TB)** primarily affects the lungs, causing **inflammation, granuloma formation, and tissue destruction**, but usually does not directly cause acute fluid overload and pulmonary edema leading to shortness of breath in the manner that heart failure does. - While **TB** can cause pleural effusions, it is not typically associated with widespread fluid overload and acute pulmonary congestion as a primary mechanism of shortness of breath. *Portal hypertension* - **Portal hypertension** is an increase in blood pressure within the **portal venous system**, usually due to liver cirrhosis. This primarily leads to fluid accumulation in the **abdominal cavity (ascites)** and sometimes peripheral edema. - While significant ascites can indirectly limit diaphragmatic movement and cause some breathlessness, it does not directly cause the acute **pulmonary edema** and fluid overload that are hallmarks of cardiac failure presenting with severe shortness of breath.
Question 1543: Which of the following is associated with WPW syndrome?
- A. Ebstein anomaly (Correct Answer)
- B. TOF
- C. VSD
- D. TAPVC
Explanation: ***Ebstein anomaly*** - **Ebstein anomaly** is a congenital heart defect characterized by apical displacement of the septal and posterior leaflets of the tricuspid valve, which is strongly associated with **Wolff-Parkinson-White (WPW) syndrome.** - WPW syndrome, involving an **accessory pathway** that bypasses the AV node [1], is found in 5-25% of patients with Ebstein anomaly, predisposing them to re-entrant tachycardias [3]. *TOF* - **Tetralogy of Fallot (TOF)** is a complex cyanotic congenital heart defect that includes four main features: VSD, pulmonary stenosis, overriding aorta, and right ventricular hypertrophy [2]. - There is no direct or strong association between TOF and WPW syndrome. *VSD* - A **Ventricular Septal Defect (VSD)** is a common congenital heart defect where there is an opening in the interventricular septum, allowing blood to flow between the ventricles [4]. - While VSDs can occur with other cardiac anomalies, there is no specific or frequent association with WPW syndrome. *TAPVC* - **Total Anomalous Pulmonary Venous Connection (TAPVC)** is a rare congenital heart defect where all four pulmonary veins connect to the systemic venous circulation instead of the left atrium. - This condition does not have a recognized association with WPW syndrome.
Question 1544: In the management of a patient with acute myocardial infarction, which of the following is the most critical step in the initial treatment?
- A. Administering beta-blockers
- B. Administering aspirin (Correct Answer)
- C. Performing coronary angiography
- D. Initiating thrombolytic therapy
Explanation: - **Aspirin** is crucial in the immediate management of **acute myocardial infarction (AMI)** due to its **antiplatelet effects**, which prevent further thrombus formation in the coronary arteries [1]. - It rapidly inhibits **cyclooxygenase-1 (COX-1)**, reducing **thromboxane A2** production and thus platelet aggregation, limiting infarct size and improving outcomes. *Performing coronary angiography* - While essential for definitive diagnosis and revascularization (e.g., PCI), **coronary angiography** is typically performed after initial medical stabilization and is not the *first* critical step [2]. - Delay in initial medical therapy to prioritize angiography can worsen myocardial damage. *Initiating thrombolytic therapy* - **Thrombolytic therapy** is a revascularization strategy, similar to PCI, used when immediate catheterization is not available, but it comes with a risk of bleeding [3]. - It is often initiated after **aspirin** and other immediate stabilizing medications, and its use depends on specific criteria and contraindications [3]. *Administering beta-blockers* - **Beta-blockers** are important in AMI management to reduce myocardial oxygen demand, control arrhythmias, and improve long-term outcomes. - However, their administration typically follows **aspirin** and other initial stabilizing measures, and they may be contraindicated in certain conditions like **acute heart failure** or **bradycardia** [2].
Question 1545: Treatment of choice for prinzmetal's angina
- A. Nitroglycerin
- B. Prazosin
- C. Beta-blockers
- D. Calcium Channel Blockers (CCBs) (Correct Answer)
Explanation: ***Calcium Channel Blockers (CCBs)*** - **Dihydropyridine** CCBs like nifedipine or amlodipine, and **non-dihydropyridine** CCBs like diltiazem or verapamil, are the **first-line agents** for Prinzmetal's angina [1]. - They work by **relaxing coronary smooth muscle**, preventing the vasospasm that causes the angina [1]. *Nitroglycerin* - **Nitroglycerin is effective** for acute relief of Prinzmetal's angina symptoms due to its **vasodilatory properties**. - However, it's typically used as **rescue therapy** and not as a long-term preventative treatment. *Beta-blockers* - Beta-blockers are **contraindicated** in Prinzmetal's angina as they can **worsen coronary vasospasm** by blocking beta-2 mediated vasodilation, leaving unopposed alpha-1 vasoconstriction [2]. - They can increase the **frequency and severity of attacks**. *Prazosin* - Prazosin is an **alpha-1 adrenergic blocker** used primarily for **hypertension** and benign prostatic hyperplasia. - While it can cause vasodilation, it is **not the treatment of choice** for Prinzmetal's angina and is less effective than CCBs in preventing coronary spasm.
Question 1546: Which of the following is a non- modifiable risk factor for CHD -
- A. Diabetes
- B. Smoking
- C. Hypertension
- D. Old age (Correct Answer)
Explanation: Old age - Age is a **non-modifiable risk factor** for Coronary Heart Disease (CHD) because it is an inherent biological process that cannot be changed [3]. - The risk of developing CHD **increases with age** due to cumulative exposure to other risk factors and natural wear and tear on the cardiovascular system [3]. *Diabetes* - Diabetes is a **modifiable risk factor** for CHD because it can be managed and controlled through lifestyle changes, medication, and regular monitoring [2]. - **Poorly controlled diabetes** significantly increases the risk of heart disease by damaging blood vessels and promoting atherosclerosis. *Smoking* - Smoking is a highly **modifiable risk factor** for CHD as it can be completely stopped [1], [2]. - **Cessation of smoking** significantly reduces the risk of heart attack and stroke over time [1]. *Hypertension* - Hypertension is a **modifiable risk factor** for CHD because blood pressure can be lowered through lifestyle interventions, such as diet and exercise, and pharmacotherapy [2]. - **Uncontrolled high blood pressure** places increased stress on the heart and blood vessels, accelerating the development of atherosclerosis [1].
Question 1547: Creatine kinase is elevated in MI after
- A. 4-8 hours
- B. >24 hours
- C. 12-24 hours
- D. 2-4 hours (Correct Answer)
Explanation: ***2-4 hours*** - **Creatine kinase (CK)** levels typically begin to rise within **2-4 hours** after the onset of myocardial infarction. - This early elevation makes CK an effective, though non-specific, marker for **acute MI** in the initial stages [1]. *4-8 hours* - While CK levels may continue to rise during this period, the initial measurable elevation usually occurs earlier, within **2-4 hours**. - A significant elevation at 4-8 hours would indicate that the myocardial event occurred at least several hours prior. *12-24 hours* - Creatine kinase levels typically peak much earlier, between **12-24 hours**, rather than just beginning to elevate at this time. - By this time, other more specific markers like **troponins** would also be significantly elevated and are often preferred for diagnosis [1], [2]. *>24 hours* - Beyond 24 hours, CK levels usually start to decline, making it less useful for the initial detection of an acute MI that began many hours earlier. - For events occurring over 24 hours ago, a positive CK would indicate that the event had happened, but it's not the first time it would be elevated.
Question 1548: Which condition is associated with a left axis deviation of -30° to -60°?
- A. Left ventricular hypertrophy (LVH) (Correct Answer)
- B. Right ventricular hypertrophy (RVH)
- C. Aortic stenosis (AS)
- D. Left atrial enlargement (LAE)
Explanation: ***Left ventricular hypertrophy (LVH)*** - **Left ventricular hypertrophy** often leads to an increased mass of the left ventricle, causing the electrical axis to shift leftward, potentially resulting in **left axis deviation** between -30° and -90° [1]. - The electrical activity generated by the hypertrophied left ventricle dominates, pulling the mean QRS vector towards the **left and inferior direction** [1]. *Right ventricular hypertrophy (RVH)* - **Right ventricular hypertrophy** typically causes a **right axis deviation**, pushing the electrical axis beyond +90° [1]. - The increased muscle mass of the right ventricle pulls the electrical vector towards the **right and inferior direction**. *Aortic stenosis (AS)* - While **aortic stenosis** can *cause* **left ventricular hypertrophy** due to increased afterload, it is not the direct ECG finding. LVH is the direct ECG manifestation. - The primary ECG change in AS is often **LVH**, which consequently leads to **left axis deviation**, but AS itself is a valvular disease. *Left atrial enlargement (LAE)* - **Left atrial enlargement** primarily affects the P wave, causing changes such as a **notched P wave (P mitrale)** or a prolonged P wave duration. - While LAE can occur with conditions that cause LVH, it does not directly lead to **left axis deviation** of the QRS complex.
Question 1549: Kussmaul's sign is classically described in:
- A. Acute myocardial damage
- B. Acute cardiac compression
- C. Chronic ventricular stiffening
- D. Chronic inflammatory heart condition (Correct Answer)
Explanation: ***Chronic inflammatory heart condition*** - **Kussmaul's sign**, characterized by a paradoxical rise in **jugular venous pressure (JVP)** during inspiration, is classically seen in conditions like **constrictive pericarditis** [1], which is often a chronic inflammatory heart condition. - This sign reflects the heart's inability to accommodate increased venous return during inspiration due to a rigid, fibrotic pericardium [1]. *Acute cardiac compression* - **Cardiac tamponade** [3], a form of acute cardiac compression, typically presents with **pulsus paradoxus** and muffled heart sounds, not Kussmaul's sign. - While it involves elevated JVP, the paradoxical inspiratory rise is less common compared to constrictive pericarditis. *Acute myocardial damage* - **Acute myocardial infarction** [2] or myocarditis, leading to acute myocardial damage, primarily causes symptoms related to reduced cardiac output and arrhythmias, such as chest pain or dyspnea. - Kussmaul's sign is not a typical feature of acute myocardial damage because the pericardium is usually not rigid or constricting. *Chronic ventricular stiffening* - Conditions involving **chronic ventricular stiffening**, such as **restrictive cardiomyopathy**, can mimic some features of constrictive pericarditis, including elevated JVP and sometimes Kussmaul's sign. - However, the classic description and most prominent cases of Kussmaul's sign are associated with external compression from a diseased pericardium rather than intrinsic myocardial stiffness, although differentiation can be challenging.
Question 1550: Which biomarker is typically elevated in the plasma of patients with chronic heart disease?
- A. Endothelin-1
- B. Troponin T
- C. B-type natriuretic peptide (BNP) (Correct Answer)
- D. Cortisol
Explanation: ***B-type natriuretic peptide (BNP)*** - **BNP** is a hormone secreted by **ventricular cardiomyocytes** in response to increased wall stretch and pressure overload, making it a strong indicator of **myocardial stress** and **chronic heart failure** [1]. - Elevated levels correlate with the **severity of heart failure**, aiding in diagnosis and prognosis [1]. *Endothelin-1* - **Endothelin-1** is a potent **vasoconstrictor** involved in vascular tone regulation and endothelial dysfunction. - While it can be elevated in conditions like **pulmonary hypertension** and **atherosclerosis**, it is not a primary diagnostic biomarker for chronic heart disease in general. *Troponin T* - **Troponin T** is a cardiac-specific protein that is released into the bloodstream following **myocardial injury or necrosis**. - While it is a crucial biomarker for **acute coronary syndromes** (e.g., heart attack), persistently elevated levels are not typical for stable chronic heart disease unless there is ongoing subclinical myocardial damage. *Cortisol* - **Cortisol** is a **stress hormone** produced by the adrenal glands, involved in metabolism, immune response, and blood pressure regulation. - While chronic stress can impact cardiovascular health, cortisol itself is not a specific diagnostic biomarker for chronic heart disease.
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
Practice Questions
Pulmonary Hypertension
Practice Questions
Non-invasive Cardiac Diagnostics
Practice Questions
Preventive Cardiology
Practice Questions
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