Which effect characterizes Vaughan Williams Class 1b on the cardiac action potential?

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Multiple Choice

Which effect characterizes Vaughan Williams Class 1b on the cardiac action potential?

Explanation:
Class 1b antiarrhythmics block fast sodium channels but do so with rapid dissociation, so they mainly affect tissue that is depolarized, such as ischemic myocardium. This results in a slower phase 0 upstroke (conduction slows), and importantly, a shortening of the action potential duration in ventricular tissue and Purkinje fibers. Because the action potential duration shortens, the refractory period—the time during which the cell cannot be re-excited—also shortens, i.e., the effective refractory period decreases. The net effect is a decreased ERP. The other ideas don’t fit this mechanism: these drugs do not lengthen phase 0 (they slow it), they do not lengthen the ERP (they shorten it), and they do not block calcium channels (that would be a property of calcium channel blockers).

Class 1b antiarrhythmics block fast sodium channels but do so with rapid dissociation, so they mainly affect tissue that is depolarized, such as ischemic myocardium. This results in a slower phase 0 upstroke (conduction slows), and importantly, a shortening of the action potential duration in ventricular tissue and Purkinje fibers. Because the action potential duration shortens, the refractory period—the time during which the cell cannot be re-excited—also shortens, i.e., the effective refractory period decreases. The net effect is a decreased ERP.

The other ideas don’t fit this mechanism: these drugs do not lengthen phase 0 (they slow it), they do not lengthen the ERP (they shorten it), and they do not block calcium channels (that would be a property of calcium channel blockers).

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