Cardiology — MCQs
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In which of the following conditions is differential cyanosis observed?
A 40-year-old male patient presents to the Emergency department with central chest pain for 2 hours. The ECG shows ST segment depression and cardiac troponins are elevated. The patient has a positive history of previous PCI 3 months back. He is administered Aspirin, Clopidogrel, Nitrates, and LMWH in the Emergency Department and shifted to the coronary care unit. What is the best recommended course of further action?
Subclavian steal syndrome is
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
Creatine kinase is elevated in MI after
Which of the following is a non- modifiable risk factor for CHD -
What is the most common complication of a large Patent Ductus Arteriosus (PDA)?
Tall T waves on ECG are seen in:
Kussmaul's sign is classically described in:
Cardiology Indian Medical PG Practice Questions and MCQs
Question 1541: In which of the following conditions is differential cyanosis observed?
- A. VSD with reversal of shunt
- B. PDA with reversal of shunt (Correct Answer)
- C. ASD with reversal of shunt
- D. Tetralogy of Fallot
Explanation: ***PDA with reversal of shunt*** - **Differential cyanosis** is characteristic of a **patent ductus arteriosus (PDA)** with **Eisenmenger syndrome**, where the shunt reverses due to pulmonary hypertension [1]. - Deoxygenated blood from the pulmonary artery shunts into the **descending aorta** distal to the origin of the subclavian arteries, resulting in cyanosis of the lower extremities while the upper extremities remain pink [1]. *VSD with reversal of shunt* - A **ventricular septal defect (VSD)** with reversed shunt typically causes **generalized cyanosis** because deoxygenated blood is shunted from the right ventricle to the left ventricle, affecting both systemic circulations [2]. - It does not produce differential cyanosis unless accompanied by coexisting cardiac anomalies that selectively affect blood flow to different parts of the body. *ASD with reversal of shunt* - An **atrial septal defect (ASD)** with reversed shunt leads to **generalized cyanosis**, as deoxygenated blood from the right atrium enters the left atrium and mixes with oxygenated blood, distributing cyanosis throughout the body [2]. - The mixing of blood occurs at the atrial level, affecting systemic circulation uniformly rather than differentially. *Tetralogy of Fallot* - **Tetralogy of Fallot** causes **generalized cyanosis** due to the right-to-left shunt through a large VSD, forcing deoxygenated blood into the systemic circulation [3]. - The degree of cyanosis depends on the severity of the right ventricular outflow tract obstruction, but it is not typically differential [3].
Question 1542: A 40-year-old male patient presents to the Emergency department with central chest pain for 2 hours. The ECG shows ST segment depression and cardiac troponins are elevated. The patient has a positive history of previous PCI 3 months back. He is administered Aspirin, Clopidogrel, Nitrates, and LMWH in the Emergency Department and shifted to the coronary care unit. What is the best recommended course of further action?
- A. Early Revascularization with PCI (Correct Answer)
- B. Continue conservative management and monitoring of cardiac enzymes and ECG
- C. Continue conservative management and plan for outpatient follow-up
- D. Immediate Revascularization with Coronary Angiography
Explanation: ***Early Revascularization with PCI*** - The patient presents with **NSTEMI** (ST depression, elevated troponins) and is already on antiplatelet and anticoagulant therapy. **Early revascularization** (ideally within 24 hours for high-risk NSTEMI) is indicated to restore blood flow and prevent further myocardial damage [1]. - Given the patient's history of prior **PCI** and the current NSTEMI presentation, this suggests possible **in-stent restenosis** or progression of coronary artery disease, making revascularization crucial. *Continue conservative management and monitoring of cardiac enzymes and ECG* - While initial conservative management with medications is appropriate, simply continuing monitoring without definitive intervention is insufficient for a **high-risk NSTEMI** patient. - The elevated troponins and ST depression indicate ongoing myocardial injury that requires active management beyond just observation [1]. *Continue conservative management and plan for outpatient follow-up* - This approach is entirely inappropriate for a patient presenting with an **acute coronary syndrome (NSTEMI)**. - Outpatient follow-up is for stable conditions, not for an ongoing cardiac event that requires urgent hospital-based intervention. *Immediate Revascularization with Coronary Angiography* - **Immediate revascularization** (within 90 minutes) is primarily indicated for **STEMI** (ST elevation myocardial infarction). - While coronary angiography will precede PCI, the term "immediate" in this context usually refers to the urgency seen in STEMI; NSTEMI typically warrants "early" rather than "immediate" intervention (within 12-24 hours for high-risk patients like this one) [1].
Question 1543: 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 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: 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 1547: 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 1548: What is the most common complication of a large Patent Ductus Arteriosus (PDA)?
- A. Eisenmenger syndrome
- B. Congestive Heart Failure (CHF) (Correct Answer)
- C. Infective endocarditis
- D. None of the options
Explanation: ***Congestive Heart Failure (CHF)*** - A large PDA results in a significant **left-to-right shunt**, increasing pulmonary blood flow and leading to **pulmonary overcirculation**. [1] - This increased workload on the heart, particularly the left atrium and ventricle, can lead to **ventricular dysfunction** and ultimately CHF. [1] *Eisenmenger syndrome* - While a severe complication of an untreated large PDA, it represents a **late stage** where the left-to-right shunt has reversed due to **pulmonary hypertension**. [1] - It is not the *most common* initial complication, as CHF often develops earlier in the disease progression. *Infective endocarditis* - This is a potential long-term complication of a PDA, especially if untreated, due to the **turbulent blood flow** across the ductus. - However, it is less common than CHF, which results directly from the hemodynamic burden imposed by a large shunt. *None of the options* - This option is incorrect because **Congestive Heart Failure** is indeed a very common and significant complication of a large Patent Ductus Arteriosus.
Question 1549: Tall T waves on ECG are seen in:
- A. Hyperkalemia (Correct Answer)
- B. Hypokalemia
- C. Hypercalcemia
- D. Hypocalcemia
Explanation: ***Hyperkalemia*** - **Tall, peaked T waves** are a hallmark ECG finding in early to moderate **hyperkalemia**, reflecting altered repolarization due to elevated extracellular potassium [1]. - As potassium levels rise further, other ECG changes may include a **prolonged PR interval**, **widened QRS complex**, and ultimately a **sine wave pattern**, leading to ventricular arrhythmias [1]. *Hypokalemia* - This condition is typically associated with **flattened or inverted T waves**, prominent **U waves**, and a **prolonged QT interval** on the ECG [1]. - The ECG changes in hypokalemia reflect delayed repolarization and increased myocardial instability [1]. *Hypercalcemia* - **Hypercalcemia** is characterized by a **shortened QT interval** on the ECG due to accelerated ventricular repolarization. - T waves, if affected, are usually not tall or peaked but may be wider or slightly less prominent. *Hypocalcemia* - **Hypocalcemia** typically leads to a **prolonged QT interval** on the ECG, primarily due to a lengthened ST segment. - While it can manifest with various T wave morphologies, it does not typically cause the characteristic tall, peaked T waves seen in hyperkalemia.
Question 1550: 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.
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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