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Pharmacology · Cardiovascular drugs: lignocaine selectivity
Sample itemA 55-year-old man with an anterior myocardial infarction has sustained ventricular tachycardia and is given intravenous lignocaine. Why is it more effective in ischaemic myocardium than in healthy tissue?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
B. It binds preferentially to open and inactivated sodium channels, which are more frequent in depolarised tissue
Lignocaine is a class IB agent with fast on-off kinetics. It binds open and inactivated sodium channels, and ischaemic cells are partially depolarised so that many channels sit in the inactivated state. Hence it suppresses arrhythmias from diseased tissue with little effect on normal conduction, and it shortens the action potential.
Option by option
A. It blocks L-type calcium channels that are overactive in ischaemia
Calcium channel blockade is the action of verapamil and diltiazem, not lignocaine.
B. It binds preferentially to open and inactivated sodium channels, which are more frequent in depolarised tissue (correct)
Correct. State-dependent binding gives selectivity for abnormal, depolarised myocardium.
C. It blocks potassium channels and prolongs the action potential in ischaemic cells
Class III agents such as amiodarone block potassium channels; lignocaine shortens rather than prolongs the action potential.
D. It blocks beta-1 receptors that are upregulated in ischaemic cells
Beta-blockade is the action of drugs such as esmolol, not lignocaine.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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