Cardiology Practice Questions

Q: What is the best drug for managing atrial flutter with a 4:1 block?

Amiodarone. ***Amiodarone*** - **Amiodarone** is an effective antiarrhythmic drug for managing **atrial flutter** by controlling ventricular rate and potentially restoring sinus rhythm. - Its broad spectrum of action, including effects on potassium, sodium, and calcium channels, makes it suitable for various supraventricular and ventricular arrhythmias. *Esmolol* - **Esmolol** is a **beta-blocker** primarily used for rapid heart rate control in acute settings due to its short half-life. - While it can control ventricular rate in **atrial flutter**, it does not typically convert the rhythm to sinus [1]. *Vernakalant* - **Vernakalant** is an **antiarrhythmic drug** specifically approved for the rapid conversion of recent-onset atrial fibrillation to sinus rhythm. - It is not indicated for **atrial flutter** or for managing chronic arrhythmias. *Lignocaine* - **Lignocaine** (Lidocaine) is a **Class Ib antiarrhythmic drug** primarily used for **ventricular arrhythmias**. - It is generally ineffective for **supraventricular arrhythmias** like atrial flutter.

Q: A 38-year-old man presents with pain and shortness of breath. His pulse rate is 85 per minute, blood pressure is 180/80 mmHg, and the cardiac examination reveals an ejection systolic murmur. The ECG shows a LVH pattern and ST depression in the anterior leads. His Troponin T test is positive. Based on these findings, the echocardiogram is likely to reveal which of the following conditions?

Aortic stenosis. Aortic stenosis - The presence of an **ejection systolic murmur** [2], **left ventricular hypertrophy** on ECG [1], and a history of **pain and shortness of breath** are classic signs of aortic stenosis. The **wide pulse pressure** (180/80 mmHg) despite a normal pulse rate suggests increased peripheral resistance, common in advanced aortic stenosis. - **Elevated troponin T** suggests myocardial injury, which can occur due to increased myocardial oxygen demand in the context of severe aortic stenosis and LVH. *Aortic regurgitation* - This condition typically presents with a **diastolic murmur**, not an ejection systolic one [3]. - While it can cause LVH, the hallmark symptom of an **ejection systolic murmur** points away from regurgitation. *Mitral regurgitation* - This condition is characterized by a **holosystolic murmur** best heard at the apex and radiating to the axilla, different from the ejection systolic murmur described [1]. - While it can lead to LVH over time, the clinical presentation and specific murmur type are not consistent with mitral regurgitation. *Mitral valve prolapse* - This condition is often associated with a **mid-systolic click** followed by a late systolic murmur, rather than a clear ejection systolic murmur [4]. - Although it can sometimes cause chest pain, it rarely leads to the degrees of LVH and **troponin elevation** described in this scenario without other contributing factors.

Q: Cardiac biomarker used for diagnosing reinfarction 8 days after initial ischemia is?

CK-MB. ***CK-MB*** - **CK-MB** (creatine kinase-MB) levels typically return to normal within **2-3 days** after an initial myocardial infarction, making it a suitable marker for detecting reinfarction several days later because its re-elevation would indicate new damage [2]. - Its relatively rapid normalization kinetics compared to troponins allows for better discrimination of new cardiac injury following the resolution of a prior event [2]. *Troponins* - **Cardiac troponins (I and T)** remain elevated for an extended period, typically **7-10 days** or even longer, after an acute myocardial infarction [3]. - Due to their prolonged elevation, troponins would likely still be elevated from the initial infarct 8 days prior, making it difficult to detect a reinfarction based solely on their levels [3]. *Myoglobin* - **Myoglobin** is one of the earliest markers to rise after myocardial injury but also has a very rapid clearance, returning to baseline within **24 hours**. - While sensitive for early detection, its short half-life makes it unsuitable for diagnosing reinfarction 8 days after initial ischemia, as any elevation would have resolved much earlier. *LDH* - **Lactate dehydrogenase (LDH)** is a late marker of myocardial infarction, rising within 24-48 hours and remaining elevated for up to **10-14 days** [1]. - Similar to troponins, the prolonged elevation of LDH from the initial infarct would obscure the detection of a reinfarction 8 days later [1].

Q: Which of the following is a characteristic feature of Takayasu arteritis?

Intimal fibrosis is a common finding.. ***Intimal fibrosis is a common finding.*** - **Intimal fibrosis** and thickening, along with **medial degeneration**, are characteristic pathological features seen in the affected arteries in Takayasu arteritis. - This fibrosis leads to **stenosis** and **occlusion** of large and medium-sized arteries, particularly the aorta and its main branches [1]. *Renal hypertension is a complication.* - While **renal hypertension** can occur in Takayasu arteritis due to **renal artery stenosis**, it is a *complication* of the disease process rather than a defining *characteristic pathological feature* of the vessel itself. - The fundamental characteristic is the inflammatory and fibrotic change in the arterial wall that *leads* to such complications [1]. *Coronary aneurysm can occur.* - **Coronary artery involvement**, including both **stenosis** and **aneurysm formation**, can occur in Takayasu arteritis. - However, similar to renal hypertension, a coronary aneurysm is a *potential manifestation* or complication, rather than the primary microscopic or macroscopic characteristic feature of the affected arterial pathology. *All of the options are features.* - While all listed options can be associated with Takayasu arteritis, only **intimal fibrosis** describes the characteristic *pathological change* within the arterial wall. - The other options describe complications or clinical manifestations that arise *from* this underlying pathological process.

Q: Which of the following murmurs will increase with Valsalva?

HOCM. ***HOCM*** - The Valsalva maneuver decreases **preload** and **left ventricular volume**, which exacerbates the **left ventricular outflow tract obstruction** in hypertrophic obstructive cardiomyopathy (HOCM) [1], thereby **increasing the intensity of the murmur**. - Reduced ventricular volume causes the **interventricular septum** and **mitral valve leaflet** to come closer, increasing the obstruction. *Ventricular Septal Defect (VSD)* - The murmur of a VSD is typically **louder with increased systemic vascular resistance**, which Valsalva would tend to *reduce* initially. - A decrease in venous return and ventricular filling during Valsalva would generally **decrease the intensity** of a VSD murmur, as less blood flows through the defect. *Aortic Stenosis (AS)* - Valsalva decreases **preload** and **stroke volume**, leading to a **reduction in blood flow** across the stenotic aortic valve [3]. - This reduction in blood flow results in a **decreased intensity** of the aortic stenosis murmur. *Mitral Regurgitation (MR)* - The murmur of mitral regurgitation is primarily dependent on the pressure gradient between the left ventricle and left atrium, and the size of the regurgitant orifice [2]. - While Valsalva can transiently decrease preload and cardiac output, its effect on MR is typically **attenuation or no significant change**, not an increase, as it would generally *reduce* forward flow.

Q: Which drug is considered the first-line treatment for pain relief in myocardial infarction?

Morphine sulfate. **Morphine sulfate** - **Morphine sulfate** is considered the first-line opioid analgesic for pain relief in acute myocardial infarction (MI) due to its potent analgesic and anxiolytic effects [1]. - It helps reduce **myocardial oxygen demand** by causing vasodilation, thereby decreasing preload and afterload. *Pentazocine* - **Pentazocine** is an opioid agonist-antagonist that can increase **heart rate** and **blood pressure**, which is undesirable in an MI setting. - It should be avoided in acute MI due to its potential to worsen myocardial ischemia and increase oxygen demand. *Midazolam* - **Midazolam** is a benzodiazepine used for sedation and anxiolysis, but it is not a primary analgesic for acute pain. - While it can help with anxiety associated with MI, it does not directly relieve the **ischemic chest pain**. *Aspirin* - **Aspirin** is crucial in MI management for its **antiplatelet effects**, preventing thrombus formation and reducing mortality. - However, it provides minimal to no direct pain relief for the severe chest pain experienced during an MI, making it an adjunctive treatment, not a primary analgesic.

Q: A patient after myocardial infarction becomes pulseless and blood pressure crashes. Diagnosis is?

Ventricular fibrillation. ***Ventricular fibrillation*** - **Ventricular fibrillation (VF)** is a chaotic, disorganized electrical activity in the ventricles resulting in no effective cardiac output, leading to pulselessness and a rapid drop in blood pressure [1, 3]. - It is a common cause of sudden cardiac arrest in post-myocardial infarction patients due to myocardial ischemia and electrical instability [3]. *Monomorphic ventricular tachycardia* - **Monomorphic ventricular tachycardia (VT)** involves rapid, regular ventricular contractions, which may or may not cause hemodynamic instability, but it typically presents with discernable QRS complexes [4]. - While it can lead to hemodynamic collapse, the description of "pulseless" and "blood pressure crashing" suggests a more chaotic rhythm, often preceding or degenerating into VF [1]. *Bidirectional tachycardia* - **Bidirectional tachycardia** is a rare form of ventricular tachycardia characterized by a 180-degree alternating QRS axis from beat to beat, often seen in **digitalis toxicity**. - While it can be unstable, the presentation of pulselessness and blood pressure crash points more strongly towards the chaotic nature of ventricular fibrillation after an MI. *Polymorphic ventricular tachycardia* - **Polymorphic ventricular tachycardia (PVT)** is characterized by continuously changing QRS morphology, indicating multiple ventricular foci or variations in conduction pathways. - While PVT can cause severe hemodynamic compromise and lead to pulselessness (e.g., Torsades de Pointes), the immediate post-MI setting with pulselessness often rapidly deteriorates to ventricular fibrillation [2].

Q: Absolute contraindication to thrombolytic therapy is:

History of hemorrhagic stroke in past one year. **History of hemorrhagic stroke in past one year** - A **history of hemorrhagic stroke** is an **absolute contraindication** to thrombolytic therapy due to the significantly increased risk of recurrent and fatal intracranial hemorrhage. [1] - Thrombolytic agents dissolve clots, and in a vessel weakened by prior hemorrhage, this can lead to catastrophic re-bleeding. [1] *Pregnancy* - Pregnancy is generally considered a **relative contraindication** but not an absolute one, as the risk-benefit decision depends on the specific clinical scenario and urgent need for thrombolysis. - The primary concern is fetal exposure to radiation and the potential for maternal and fetal bleeding complications. *Patients on nitrates* - Being on nitrates has **no direct contraindication** to thrombolytic therapy. [2] - Nitrates are commonly used in cardiac patients for vasodilation and symptom relief, and their use does not increase the risk of hemorrhage from thrombolysis. [2] *Hypertension* - **Uncontrolled severe hypertension** (e.g., systolic BP >185 mmHg or diastolic BP >110 mmHg) is a relative contraindication to thrombolysis, as it increases the risk of intracranial hemorrhage. - However, isolated hypertension without other risk factors, or hypertension that can be controlled, is not an absolute contraindication.

Q: In which of the following conditions is left atrial enlargement least prominent?

Atrial septal defect. ***Atrial septal defect*** - In an **atrial septal defect (ASD)**, blood shunts from the left atrium (LA) to the right atrium (RA). [1] This flow **reduces the volume load on the LA**, meaning the left atrium does not directly experience a significant increase in pressure or volume. - While increased flow goes to the **right ventricle and pulmonary arteries**, the left atrium itself is spared from the overload that typically causes enlargement. [1] *Ventricular septal defect* - A **ventricular septal defect (VSD)** causes a left-to-right shunt at the ventricular level, increasing blood flow to the **pulmonary circulation** and subsequently back to the left atrium. - This **volume overload returning to the left atrium** leads to prominent left atrial enlargement. *Aortopulmonary window* - An **aortopulmonary window (APW)** results in a large left-to-right shunt from the aorta to the pulmonary artery, significantly increasing **pulmonary blood flow**. - This increased pulmonary flow returns to the left atrium, causing substantial **volume overload and prominent left atrial enlargement**. *Patent ductus arteriosus* - A **patent ductus arteriosus (PDA)** allows blood to shunt from the aorta to the pulmonary artery, leading to increased **pulmonary blood flow**. - This increased flow returns to the left atrium, leading to significant **volume overload and prominent left atrial enlargement**.

Q: Eisenmenger syndrome is characterized by all except:

Return of left ventricle & right ventricle to normal size. Return of left ventricle & right ventricle to normal size - In Eisenmenger syndrome, the structural heart changes are generally irreversible; the left and right ventricles do not return to normal size due to persistent pulmonary hypertension and shunting [1]. - The syndrome represents an advanced stage of congenital heart disease where the shunt reverses from left-to-right to right-to-left, causing progressive ventricular remodeling. *Pulmonary veins not distended* - This is a characteristic feature of Eisenmenger syndrome. The pulmonary veins are not distended because the reduced pulmonary blood flow, caused by increased pulmonary vascular resistance, leads to decreased venous return to the left atrium. - The altered hemodynamics, specifically the right-to-left shunt, bypasses significant portions of the pulmonary circulation, thus preventing engorgement of the pulmonary veins. *Pruning of peripheral pulmonary arteries* - This is a hallmark of pulmonary hypertension and Eisenmenger syndrome, representing the obliteration and narrowing of smaller pulmonary arterial branches [1]. - The progressive loss of these vessels contributes to the elevated pulmonary vascular resistance and contributes to the irreversible nature of the condition. *Dilatation of central pulmonary arteries* - This is typically seen in Eisenmenger syndrome due to the high pressure and flow through the main pulmonary artery and its larger branches. - While peripheral vessels constrict and "prune," the central arteries often undergo compensatory dilatation in response to the chronic high pressure [2].

Question 1

What is the best drug for managing atrial flutter with a 4:1 block?

Accepted Answer

Amiodarone

Answer

Esmolol

Answer

Vernakalant

Answer

Lignocaine

Question 2

A 38-year-old man presents with pain and shortness of breath. His pulse rate is 85 per minute, blood pressure is 180/80 mmHg, and the cardiac examination reveals an ejection systolic murmur. The ECG shows a LVH pattern and ST depression in the anterior leads. His Troponin T test is positive. Based on these findings, the echocardiogram is likely to reveal which of the following conditions?

Accepted Answer

Aortic stenosis

Answer

Aortic regurgitation

Answer

Mitral regurgitation

Answer

Mitral valve prolapse

Question 3

Cardiac biomarker used for diagnosing reinfarction 8 days after initial ischemia is?

Accepted Answer

CK-MB

Answer

Troponins

Answer

Myoglobin

Answer

LDH

Question 4

Which of the following is a characteristic feature of Takayasu arteritis?

Accepted Answer

Intimal fibrosis is a common finding.

Answer

Renal hypertension is a complication.

Answer

Coronary aneurysm can occur.

Answer

All of the options are features.

Question 5

Which of the following murmurs will increase with Valsalva?

Accepted Answer

HOCM

Answer

Ventricular Septal Defect (VSD)

Answer

Aortic Stenosis (AS)

Answer

Mitral Regurgitation (MR)

Question 6

Which drug is considered the first-line treatment for pain relief in myocardial infarction?

Accepted Answer

Morphine sulfate

Answer

Pentazocine

Answer

Midazolam

Answer

Aspirin

Question 7

A patient after myocardial infarction becomes pulseless and blood pressure crashes. Diagnosis is?

Accepted Answer

Ventricular fibrillation

Answer

Bidirectional tachycardia

Answer

Polymorphic ventricular tachycardia

Answer

Monomorphic ventricular tachycardia

Question 8

Absolute contraindication to thrombolytic therapy is:

Accepted Answer

History of hemorrhagic stroke in past one year

Answer

Patients on nitrates

Answer

Hypertension

Answer

Pregnancy

Question 9

In which of the following conditions is left atrial enlargement least prominent?

Accepted Answer

Atrial septal defect

Answer

Ventricular septal defect

Answer

Patent ductus arteriosus

Answer

Aortopulmonary window

Question 10

Eisenmenger syndrome is characterized by all except:

Accepted Answer

Return of left ventricle & right ventricle to normal size

Answer

Pulmonary veins not distended

Answer

Pruning of peripheral pulmonary arteries

Answer

Dilatation of central pulmonary arteries

Cardiology — MCQs

Cardiology — MCQs

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