Cardiology Practice Questions

Q: What is the best initial pharmacotherapy management option for a 30-year-old male who presents to the emergency department with palpitations, has a regular broad complex tachycardia on ECG, and is haemodynamically stable if DC cardioversion is not available?

IV procainamide. ***IV procainamide*** - **Procainamide** is a Class Ia antiarrhythmic drug and is an effective initial pharmacotherapy for **stable broad complex tachycardia (BCT)** if direct current cardioversion (DCC) is not immediately available - It works by blocking sodium and some potassium channels, prolonging the **action potential duration** and **effective refractory period**, which helps terminate re-entrant rhythms and slow conduction - Particularly useful when the origin of BCT (ventricular vs. supraventricular with aberrancy) is uncertain *IV amiodarone* - **Amiodarone** is a Class III antiarrhythmic drug that is effective for both supraventricular and ventricular arrhythmias - It is also an acceptable option for stable BCT and is preferred by some guidelines, though it has a **slower onset of action** compared to procainamide - May be preferred in patients with structural heart disease or heart failure *IV verapamil* - **Verapamil** is a non-dihydropyridine **calcium channel blocker** that primarily slows AV nodal conduction - It is **contraindicated** in broad complex tachycardia (BCT) of uncertain or ventricular origin because it can worsen hypotension and precipitate ventricular fibrillation - Can cause hemodynamic collapse in ventricular tachycardia or pre-excitation syndromes (e.g., Wolff-Parkinson-White syndrome) *IV adenosine* - **Adenosine** is primarily used for the acute termination of **supraventricular tachycardias (SVTs)**, especially those involving the AV node - It is **contraindicated** in broad complex tachycardia as it can lead to hemodynamic collapse or ventricular fibrillation, particularly if the BCT is due to **ventricular tachycardia** - May cause paradoxical acceleration in **Wolff-Parkinson-White syndrome** with antegrade conduction down an accessory pathway

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: 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: 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: 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: Straight back syndrome is associated with?

Mitral valve prolapse. ***Mitral valve prolapse*** - **Straight back syndrome** refers to a reduction in the normal thoracic kyphosis, which can decrease the **anteroposterior diameter** of the chest. - This flattened chest can compress the heart, particularly the **mitral valve**, leading to auscultatory findings suggestive of prolapse, even in the absence of true valvular dysfunction. *Ankylosing spondylitis* - This is a chronic inflammatory disease primarily affecting the **axial skeleton**, leading to spinal fusion and stiffness, which is distinct from a flattened thoracic spine. - While it affects the spine, it causes an abnormal **kyphosis or lordosis** rather than a simply straightened back that predisposes to cardiac compression. *Osteopetrosis* - This is a rare genetic disorder characterized by abnormally dense bones due to a defect in **osteoclast function**. - Its musculoskeletal manifestations involve increased bone fragility and hematological issues, not a specific spinal curvature anomaly like straight back syndrome. *Cor-triatriatum* - This is a rare congenital heart defect where the **left atrium (cor triatriatum sinistrum)** or, less commonly, the **right atrium (cor triatriatum dextrum)** is divided by a fibromuscular membrane. - It is a primary cardiac structural anomaly and has no association with musculoskeletal conditions such as straight back syndrome.

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: 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: 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.

Question 1

What is the best initial pharmacotherapy management option for a 30-year-old male who presents to the emergency department with palpitations, has a regular broad complex tachycardia on ECG, and is haemodynamically stable if DC cardioversion is not available?

Accepted Answer

IV procainamide

Answer

IV verapamil

Answer

IV amiodarone

Answer

IV adenosine

Question 2

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 3

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

Accepted Answer

Amiodarone

Answer

Esmolol

Answer

Vernakalant

Answer

Lignocaine

Question 4

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

Accepted Answer

CK-MB

Answer

Troponins

Answer

Myoglobin

Answer

LDH

Question 5

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 6

Straight back syndrome is associated with?

Accepted Answer

Mitral valve prolapse

Answer

Osteopetrosis

Answer

Cor-triatriatum

Answer

Ankylosing spondylitis

Question 7

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 8

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 9

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 10

Absolute contraindication to thrombolytic therapy is:

Accepted Answer

History of hemorrhagic stroke in past one year

Answer

Patients on nitrates

Answer

Hypertension

Answer

Pregnancy

Cardiology — MCQs

Cardiology — MCQs

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