Cardiology Pharmacology: MRCEM Primary questions with answers

Cardiology Pharmacology belongs to the pharmacology section, which carries 24 of the 180 questions in MRCEM Primary. The topic covers basic and advanced life support, tachyarrhythmias, bradycardias, hypertensive emergency, beta blockers, calcium channel blockers, antiplatelets, statins, nitrates, fibrinolytics, anticoagulants and digoxin. These are the drugs an emergency physician reaches for in cardiac arrest, acute coronary syndromes and arrhythmias.

5 free questions below, each with the answer and the full explanation · 154 in the full bank · Last updated after the 27 October 2026 MRCEM Primary sitting.

1. Question 1 · Betablocker and Calcium channel blockers

   Which one of the following receptors is mainly responsible for smooth muscle contraction and constriction of blood vessels?

   1. ABeta 2
   2. BBeta 3
   3. CBeta 1
   4. DAlpha 1
   5. EAlpha 2
   Show answer and explanation

   Answer: D. Alpha-1 receptors mediate smooth muscle contraction and vasoconstriction.

   • A: Beta-2 causes smooth muscle relaxation.
   • B: Beta-3 mediates lipolysis and bladder relaxation.
   • C: Beta-1 acts mainly on the heart.
   • E: Alpha-2 mediates inhibition of noradrenaline release.

   Full explanation

   A useful way to remember: Alpha 1 for constriction, Alpha 2 for inhibition, B 1 for heart, and B2 for relaxation

   High yield:

   Note: Nitroprusside is metabolized to nitric oxide, which causes both arterial and venous dilation This effect is immediate and results in a decrease in both preload and afterload.

    

2. Question 2 · Cardiology Pharmacology

   A woman aged 65 with hypertension is being treated with thiazide, and her blood pressure responds well and reads at 120/75. After several months on the medication, she complains of being tired and weak. Which one of the following complications has she likely developed?

   1. ADecreased potassium
   2. BDecreased Sodium
   3. CDecreased glucose
   4. DDecreased calcium
   5. EDecreased Uric acid
   Show answer and explanation

   Answer: A. Thiazides commonly cause hypokalaemia, which produces tiredness and weakness.

   • B: Hyponatraemia occurs but typically causes confusion; hypokalaemia best fits weakness.
   • C: Thiazides tend to raise glucose.
   • D: Thiazides raise calcium.
   • E: Thiazides raise uric acid.

   Full explanation

   • Hypokalemia is common adverse effect of thiazide and furosemide, and cause fatigue and lethargy in the patient.
   • Food rich in potassium, potassium chloride can correct the hypokalemia alternatively potassium sparing diuretics e.g., spironolactone may be added

   Note: Calcium uric acid and glucose are usually elevated by thiazide. Sodium loss wouldn't weaken the patient.

3. Question 3 · Digoxin

   A patient with a history of heart failure is prescribed digoxin. Which one of the following ecg changes shows the digoxin effect?

   1. AST segment elevation
   2. BShortening of PR interval
   3. CQT interval prolongation
   4. DPeaked T waves
   5. EPR Prolongation
   Show answer and explanation

   Answer: E. PR prolongation is a recognised digoxin effect on the ECG.

   • A: Digoxin causes ST depression with a reverse tick.
   • B: PR interval is prolonged, not shortened.
   • C: Digoxin shortens the QT interval.
   • D: Peaked T waves suggest hyperkalaemia; digoxin flattens or inverts T waves.

   Full explanation: Digoxin

   Digoxin

   Digoxin is a cardiac glycoside derived from the plant foxglove that primarily works by inhibiting the Na+/K+ ATPase in the myocardium.

   Mechanism: Digoxin has positive inotropic effects and negative chronotropic effects 

   • Binds to and inhibits the Na+/K+ pump on the myocyte cell membrane (competes with the K+ ion) Increases intracellular Na+ concentration.
   • Reduces the extrusion of intracellular Ca2+ via the Na+/Ca2+ exchange transporter Increased Ca2+ is stored in the sarcoplasmic reticulum Increased amounts of Ca2+ released during each action potential force of contraction increased.
   •  Digoxin also increases vagal tone by enhancing Ach release at muscarinic receptors, thus slowing the heart rate, atrioventricular (AV) conduction, and the AV nodal refractory period.

   Indications: Heart failure, persistent and permanent atrial fibrillation and flutter.

   Note: In heart failure digoxin is useful in patient with reduced ejection fraction, with an ejection fraction below 40%. However, it has no benefit in mortality reduction.

   • Digoxin can only be used as monotherapy in sedentary patients because it controls ventricular response at rest.

   Monitoring: Digoxin has narrow therapeutic index. Narrow therapeutic index means difference between the effective therapeutic dose and the potentially toxic dose is relatively small. This narrow window makes proper dosing and monitoring critically important to ensure the medication’s safety, effectiveness and to prevent toxicity. The therapeutic plasma levels of digoxin are usually between 1.0-1.5 nmol/l. The likelihood of toxicity rises dramatically at levels above 2 nmol/l.

   Dose adjustments in renal failure and liver failure:

   Renal failure: Digoxin is excreted renally, and impaired renal function can cause increased digoxin levels and leads to digoxin toxicity. In this case the patient should have their digoxin dose reduced and their digoxin level and electrolytes should be carefully monitored.

   Liver failure: Liver failure has little influence on digoxin metabolism or clearance; therefore, no dose adjustment is necessary.

   Digoxin toxicity: Precipitated by hypokalemia or drugs causing hypokalemia, hypercalcemia, acidosis and renal failure.

   The features of digoxin toxicity include:

   •  Hyperkaliemia
   •  Nausea, vomiting and diarrhea.
   • Abdominal pain
   • Confusion, dizziness and psychosis
   • Tachyarrhythmias or bradyarrhythmia’s
   •  Xanthopsia (yellow-green vision)

   Treatment: Digoxin immune fab is the reversal agent (Antidote) of digoxin toxicity.

4. Question 4 · Tachyarrhythmia

   A patient aged 65 who attended ED with chest pain suddenly collapses in the waiting room. He is not breathing and has no pulse, and you begin chest compressions after calling for the resuscitation team. Monitoring shows ventricular fibrillation. After three shocks, there is still no pulse. You ask a colleague to give intravenous adrenaline. What dose of adrenaline should be given:

   1. A10 ml of 1 in 10,000 adrenaline solution
   2. B5 ml of 1 in 1000 adrenaline solution
   3. C0.5 ml of 1 in 1000 adrenaline solution
   4. D10 ml of 1 in 1000 adrenaline solution
   5. E0.5 ml of 1 in 10,000 adrenaline solution
   Show answer and explanation

   Answer: A. The dose is 1 mg adrenaline, which is 10 mL of 1 in 10,000.

   • B: 5 mL of 1 in 1000 is 5 mg, an overdose.
   • C: 0.5 mL of 1 in 1000 is 0.5 mg, not the arrest dose.
   • D: 10 mL of 1 in 1000 is 10 mg, a dangerous overdose.
   • E: 0.5 mL of 1 in 10,000 is only 0.05 mg.

   Full explanation: Life Support Algorithms

   Basic Life Support

   • For chest compressions in adult basic life support the heel of one hand should be placed over the middle of the lower half of the patient's sternum with the other hand on top.
   • The sternum should be depressed to a depth of 5 - 6 cm.
   • Chest compressions should be performed at a rate of 100 - 120 per minute.
   • Thirty compressions should be given before two breaths and that ratio continued (30:2).
   • The person giving CPR should be changed every 2 minutes if possible to avoid exhaustion and poor quality chest compressions.
   • Interruptions should be minimised (pauses should be < 5 seconds).

   Advanced Life Support

   • In adult advanced life support, basic life support should continue whilst the defibrillator pads are attached and the airway managed.
   • The pads should be positioned one to the right of the upper sternum below the clavicle and the other in the left midaxillary line in the 5th intercostal space.
   • Chest compressions should be paused briefly (< 5 secs) to assess the rhythm and then continued as the defibrillator charges if a shockable rhythm is identified or continued for a further two whole minutes if a non-shockable rhythm is identified.
   • When delivering a shock, everybody should be clear of the patient (and any GTN patches and oxygen sources removed).
   • Once the shock has been delivered, compressions should resume immediately and continue for a further two minutes before checking the rhythm again or feeling for a pulse.

   Shockable Rhythm (ventricular fibrillation or pulseless ventricular tachycardia)

   • IV adrenaline 1 mg (10 mL of 1:10,000 solution) should be given after 3 shocks and every 3 - 5 minutes/after alternate shocks thereafter.
   • IV amiodarone 300 mg should be given after 3 shocks. A further dose of IV amiodarone 150 mg may be considered after a total of five defibrillation attempts. Lidocaine (1 mg kg^-1) may be used as an alternative if amiodarone is not available but may not be given if amiodarone has been given already.

   Non-shockable Rhythm (asystole or pulseless electrical activity)

   • IV adrenaline 1 mg should be given as soon as IV access is achieved and then given every 3 - 5 minutes thereafter.

5. Question 5 · Hypertensive emergency

   Thiazide diuretics are primarily indicated for which of these:

   1. AAcute angle-closure glaucoma
   2. BAscites secondary to liver cirrhosis
   3. CCerebral oedema
   4. DAcute pulmonary oedema
   5. EOedema in chronic heart failure
   Show answer and explanation

   Answer: E. Thiazides relieve oedema in chronic heart failure and treat hypertension.

   • A: Acetazolamide or mannitol is used for glaucoma.
   • B: Spironolactone is first-line for cirrhotic ascites.
   • C: Mannitol is used for cerebral oedema.
   • D: Loop diuretics are used for acute pulmonary oedema.

   Full explanation: Thiazide Diuretics

   Thiazide diuretics are moderately potent diuretics, and are used to relieve oedema in chronic heart failure, and in the management of hypertension. They act within 1 to 2 hours of oral administration and most have a duration of action of 12 to 24 hours.

   Mechanism of Action

   Thiazides act mainly on the early segments of distal tubule where they inhibit NaCl reabsorption by binding to the the Na+/Cl- cotransporter. Excretion of Cl-, Na+ and accompanying water is increased. The increased Na+ load in the distal tubule stimulates Na+ exchange with K+ and H+, increasing their excretion and causing hypokalaemia and a metabolic alkalosis. Excretion of Ca2+ is reduced.

   Indications

   Bendroflumethiazide is used for oedema in mild or moderate heart failure. Combination diuretic therapy (with loop and thiazide diuretics) may be effective in patients with oedema resistant to treatment with one diuretic.

   Thiazide diuretics are licensed for the treatment of hypertension but are no longer considered the first line diuretic for this indication. In the management of hypertension a low dose of a thiazide produces a maximal or near-maximal blood pressure lowering effect, with very little biochemical disturbance. Higher doses cause more marked changes in plasma potassium, sodium, uric acid, glucose, and lipids, with little advantage in blood pressure control.

   Contraindications

   Thiazide diuretics are contraindicated in:

   • Addison’s disease
   • Hypercalcaemia
   • Hyponatraemia
   • Refractory hypokalaemia
   • Symptomatic hyperuricaemia
   • Severe hepatic impairment (may precipitate encephalopathy)

   Cautions

   Thiazide diuretics should be used with caution in:

   • Diabetes mellitus (may exacerbate)
   • Gout (may exacerbate)
   • Systemic lupus erythematosus (may exacerbate)
   • Hyperaldosteronism
   • Malnourishment
   • Nephrotic syndrome

   Side Effects

   Lower initial doses of diuretics should be used in the elderly because they are particularly susceptible to the side effects. The dose should then be adjusted according to renal function.

   Common side effects of thiazide diuretics include:

   • Excessive diuresis
     • Postural hypotension, dehydration, renal impairment
   • Acid-base and electrolyte imbalance
     • Hypokalaemia, hyponatraemia, hypomagnesaemia, hypercalcaemia, hypochloraemic alkalosis
   • Metabolic imbalance
     • Hyperuricaemia and gout
     • Impaired glucose tolerance and hyperglycaemia
     • Altered plasma-lipid concentrations
   • Mild gastrointestinal disturbances

   Hypokalaemia

   Hypokalaemia can occur with both thiazide and loop diuretics. The risk of hypokalaemia depends on the duration of action as well as the potency and is thus greater with thiazides than with an equipotent dose of a loop diuretic. Hypokalaemia is dangerous in severe cardiovascular disease and in patients also being treated with cardiac glycosides. Often the use of potassium-sparing diuretics avoids the need to take potassium supplements.