An older man with a known history of chronic atrial fibrillation presents to the clinic in Abu Dhabi complaining of frequent episodes of lightheadedness and palpitations over the past month. He has not been on any cardiac medications for over one year. On examination, he is alert with no signs of acute distress. His blood pressure is 115/75 mmHg, and his heart rate is 125 beats per minute and irregularly irregular. An electrocardiogram confirms atrial fibrillation with a rapid ventricular response. There are no clinical signs of acute heart failure. What is the most appropriate initial medication to manage his symptoms?

• Digoxin

• Warfarin

• Metoprolol

• Amiodarone

• Lisinopril

Answer explanation

The patient is symptomatic (lightheadedness, palpitations) due to a rapid ventricular rate in atrial fibrillation. The primary therapeutic goal is rate control. Beta-blockers, such as metoprolol, are first-line agents for rate control in stable patients with atrial fibrillation, particularly in the absence of decompensated heart failure. They effectively reduce the heart rate by decreasing atrioventricular nodal conduction.

A 4 year old girl is brought to the ED by her parents for being “unrousable.” O/E, she is pale with cool extremities. BP 65/40 mmHg, HR 230/min, RR 35/min, Temp 37.1°C. Capillary refill is 4 seconds. GCS is 9. A bedside cardiac monitor displays a narrow-complex tachycardia. IV access has just been established. What is the most appropriate immediate management?

• Administer vagal maneuvers

• Administer IV adenosine

• Perform synchronized cardioversion

• Administer IV amiodarone

• Secure airway with endotracheal intubation

Answer explanation

The patient presents with supraventricular tachycardia (SVT) and clear signs of hemodynamic instability (hypotension, poor perfusion, altered mental status). According to Pediatric Advanced Life Support (PALS) guidelines, unstable tachycardia requires immediate synchronized cardioversion (0.5-1 J/kg) to prevent progression to cardiac arrest.

A female patient presents to the Emergency department of Emirates hospital Jumeirah c/o sudden-onset palpitations & dizziness x1hr. She denies chest pain or syncope. O/E, she is anxious but alert. BP 115/75 mmHg, HR 160/min, RR 18/min, SpO2 99% on RA. Cardiac monitor shows a regular, narrow-complex tachycardia. A 12-lead ECG confirms SVT with no visible P waves. Carotid sinus massage was performed without effect. What is the most appropriate next pharmacologic intervention?

• IV Adenosine

• IV Metoprolol

• IV Amiodarone

• IV Verapamil

• IV Procainamide

Answer explanation

The patient has hemodynamically stable SVT that is unresponsive to vagal maneuvers. According to ACLS guidelines, the first-line drug of choice is IV adenosine (6 mg rapid push) due to its high efficacy and ultra-short half-life, which makes it both diagnostic and therapeutic.

A 68 Y/O M with a Hx of HTN and CAD presents for a routine check-up. He reports feeling occasional dizziness over the past month but denies syncope or chest pain. O/E, his HR is 65/min and irregular. An in-office ECG is performed, and a representative rhythm strip is shown. What is the most accurate interpretation of this rhythm strip?

• First-degree AV block

• Mobitz Type I AV block (Wenckebach)

• Mobitz Type II AV block

• Third-degree (complete) AV block

• Sinus pause

Answer explanation

The ECG shows a consistent PR interval for all conducted beats, followed by a P wave that is not conducted (a "dropped beat"). This pattern of a fixed PR interval with intermittent non-conducted P waves is the classic definition of Mobitz Type II AV block.

A patient with known HTN is evaluated for recurrent dizziness and one episode of syncope. A 12-lead ECG demonstrates a left bundle branch block and first-degree AV block (PR interval 340 ms). The patient is currently asymptomatic with a heart rate of 60/min. What is the most appropriate definitive management for this patient?

• Implantation of a permanent pacemaker

• IV Atropine and observation

• Holter monitoring for 48 hours

• Electrophysiology (EP) study

• Discontinue all AV-nodal blocking agents

Answer explanation

International guidelines give a Class I indication for permanent pacemaker implantation in patients with bifascicular block (like LBBB) and syncope that is likely due to AV block, even if the block is not captured on the ECG at the time of presentation. The combination of ECG findings and syncope indicates a high risk of progression to complete heart block.

A patient presents with acute cardiogenic pulmonary edema, characterized by severe respiratory distress, bibasilar crackles, and a BP of 170/100 mmHg. An ECG shows sinus tachycardia but no acute ischemic changes. The patient is placed in an upright position and given supplemental oxygen. What is the most appropriate initial medication to administer to this patient?

• Intravenous labetalol

• Intravenous normal saline

• Intravenous furosemide

• Intravenous digoxin

• Intravenous morphine

Answer explanation

The primary goal in acute cardiogenic pulmonary edema is to rapidly reduce preload (pulmonary congestion). Intravenous loop diuretics, such as furosemide, are the first-line treatment. They promote rapid diuresis and also have an immediate venodilating effect, both of which decrease pulmonary capillary pressure and improve symptoms.

A patient with a known history of severe COPD presents with new-onset bilateral pedal edema and exertional dyspnea. O/E, the JVP is elevated. Auscultation of the lungs reveals diminished breath sounds but no crackles. What is the most likely diagnosis?

• Cor pulmonale

• Acute myocardial infarction

• Decompensated left-sided heart failure

• Constrictive pericarditis

• Cirrhosis of the liver

Answer explanation

 The presentation is a classic triad: 1) underlying chronic lung disease (COPD), 2) signs of right ventricular failure (elevated JVP, edema), and 3) absence of left ventricular failure (clear lungs). This clinical picture defines cor pulmonale, which is right-sided heart failure caused by pulmonary hypertension secondary to lung pathology.

A patient with heart failure is on a stable dose of digoxin. Furosemide is initiated to manage volume overload. Several weeks later, the patient develops bradycardia and nausea, and lab tests confirm digoxin toxicity despite no change in the digoxin dose or renal function. What is the primary mechanism responsible for the increased risk of digoxin toxicity in this patient?

• Furosemide-induced hypokalemia

• Decreased renal clearance of digoxin

• Displacement of digoxin from plasma protein binding sites

• Inhibition of hepatic CYP450 metabolism

• Increased gastrointestinal absorption of digoxin

Answer explanation

The core mechanism of this interaction is electrolyte disturbance. Digoxin exerts its effect by inhibiting the Na+/K+-ATPase pump. Potassium (K+) and digoxin compete for the same binding site on this pump. When furosemide causes hypokalemia (low potassium), there is less competition for digoxin, leading to increased binding and an exaggerated pharmacologic effect, resulting in toxicity.

A patient with long-standing, untreated dyslipidemia is being counseled on the pathogenesis of coronary artery disease. The physician explains how certain lipids cross the arterial endothelium and accumulate in the vessel wall, initiating an inflammatory cascade. The subendothelial accumulation and subsequent oxidation of which of the following lipoproteins is the key initiating event in the formation of an atherosclerotic plaque?

• Chylomicrons

• High-density lipoprotein (HDL)

• Very-low-density lipoprotein (VLDL)

• Low-density lipoprotein (LDL)

•  Lipoprotein(a) [Lp(a)]

  
  

Answer explanation

The pathophysiology of atherosclerosis begins when Low-density lipoprotein (LDL) particles, particularly small, dense ones, migrate from the bloodstream across the endothelium into the subendothelial space (tunica intima). There, they become oxidized, triggering an inflammatory response that attracts macrophages. These macrophages engulf the oxidized LDL, becoming "foam cells," which are the hallmark of the early atherosclerotic lesion, the fatty streak.

A patient is hospitalized following a recent myocardial infarction. Several days after the event, the patient suddenly develops severe dyspnea. O/E, tachycardia and bibasilar crackles are noted. Auscultation reveals a new, loud holosystolic murmur at the cardiac apex. Which investigation is most critical for identifying the cause of this patient's acute deterioration?

• Echocardiography

• 12-lead ECG

• Coronary Angiography

• Serial Troponin measurement

• Chest X-ray

Answer explanation

The presentation of acute heart failure with a new murmur post-MI strongly suggests a mechanical complication, such as papillary muscle rupture causing acute mitral regurgitation. An echocardiogram provides a rapid, non-invasive way to directly visualize cardiac structures, confirm the valvular lesion, assess its severity, and evaluate overall ventricular function, which is crucial for urgent surgical planning.