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Physiology · Nerve and muscle: use-dependent sodium channel block
Sample itemLidocaine given intravenously suppresses ventricular tachycardia in ischaemic myocardium, but has little effect on the normal atrial rhythm at a rate of 70 per minute. Which property of its action explains this selectivity?
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, so block accumulates in rapidly firing or depolarised tissue
Local anaesthetics and class I antiarrhythmics bind sodium channels mainly in the open and inactivated states and dissociate slowly in the resting state. Fast firing and depolarised, ischaemic tissue spend more time in these states, so use-dependent block builds up there while normal slow rhythms recover between beats.
Option by option
A. It blocks voltage-gated potassium channels and prolongs repolarisation in all cells equally
Potassium channel block is the mechanism of class III drugs such as amiodarone.
B. It binds preferentially to open and inactivated sodium channels, so block accumulates in rapidly firing or depolarised tissue (correct)
Correct. State-dependent binding gives use-dependent block.
C. It blocks L-type calcium channels in the atrioventricular node
Calcium channel block with slowed AV nodal conduction is the action of verapamil, not lidocaine.
D. It blocks only resting-state sodium channels, so it works best at slow rates
Preference for resting channels would make block strongest at slow rates, the opposite of what is seen.
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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