Written questions
Model answers available
Catalogued
Questions without a written answer yet
- (a)Compare and contrast the pharmacological mechanisms by which intravenous adenosine and amiodarone terminate tachyarrhythmias with respect to the following:
- (i)Primary site of action in the heart.1 mark
- (ii)Mechanism of action and ion channel effects.3 marks
- (iii)Cardiac electrophysiological consequences and ECG changes.4 marks
- (b)Outline the differences in the onset and duration of antiarrhythmic action of both drugs.2 marks
Single best answer
9 SBAs on cardiovascular drugs
Viva
4 viva questions
Aspirin’s half-life is 20 minutes. Why stop it a week before surgery?
Show the answerSay it out loud first
Because the effect is not related to the drug being present. Aspirin irreversibly acetylates cyclo-oxygenase-1, and the platelet is anucleate so it cannot make more enzyme. The inhibition therefore lasts that platelet’s entire lifespan. Recovery depends on new platelets entering the circulation at about 10 to 12% per day, which is a matter of days regardless of how fast the drug itself disappears.
A patient had a drug-eluting stent two months ago and needs an elective hernia repair. What do you advise?
Show the answerSay it out loud first
Defer the surgery. Elective surgery is conventionally postponed for at least six months after a drug-eluting stent, with three months acceptable where it genuinely cannot wait. Stopping dual therapy at two months risks stent thrombosis, which carries a high mortality, and a hernia repair does not justify that. If it had to proceed, continue aspirin throughout and involve cardiology.
Why might vasopressin work when escalating noradrenaline has stopped helping?
Show the answerSay it out loud first
Because it uses a different receptor. In prolonged sepsis, adrenoceptors are downregulated and desensitised and their response is further blunted by acidosis, so more noradrenaline achieves progressively less. The V₁ receptor pathway is independent of that and relatively preserved, and there is a relative vasopressin deficiency from depletion of endogenous stores — so giving it replaces a missing mechanism rather than flogging an exhausted one.
Why would vasopressin lower cardiac output?
Show the answerSay it out loud first
Because it raises afterload with no inotropic support. It has no β₁ activity at all, unlike noradrenaline, so the ventricle must eject against a higher systemic vascular resistance without any increase in contractility. In a heart with poor reserve, stroke volume falls. That is why it is added at a fixed low dose rather than escalated.