MEDizzy - Patient, who has excessively slow AV nodal conduction rates

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Pharmacology of the cardiovascular system 2

Patient, who has excessively slow AV nodal conduction rates that unfortunately haven’t been recognized, is started on a drug. As soon as blood levels climb towards the usual therapeutic range, the patient goes into a complete heart block. Which of the following drugs most likely provoked this further prolongation of the P-R interval, ultimately leading to the complete heart block?

ExplanationIn essence, we are asking “Which drug can suppress AV nodal conduction velocity?” Verapamil (and the very similar non dihydropyridine calcium channel blocker, diltiazem) do that. Recall the profile of verapamil and diltiazem: a vasodilator effect plus a direct cardiac “depressant” effect that includes slowing of AV conduction (and potential depression of other cardiac contractile and electrophysiologic phenomena). (Be sure you can contrast this dual vasodilator/cardiac depressant pro-file for verapamil and diltiazem with that of the dihydropyridines [e.g., nifedipine; answer c]. Dihydropyridines cause vasodilation but lack any cardiac depressant actions. Indeed, with dihydropyridine dosages sufficient to lower blood pressure enough and quickly enough, there will be reflex (baroreceptor) activation of the sympathetic nervous system. One consequence of increased norepinephrine release at the heart would be increased (faster) AV nodal conduction velocity, which could be construed as an “unblocking” of the AV node—precisely the opposite of what may happen with verapamil or diltiazem.) Captopril (ACE inhibitor) and losartan (angiotensin receptor blocker) have no significant effects on AV nodal conduction. Nitroglycerin (nitrovasodilator) and prazosin (vasodilator that acts by competitive α1 blockade) also have no direct effect on the AV node but are likely to lead to an indirect quickening of AV conduction via baroreceptor activation. On a final and important note, be sure you understand that all β- adrenergic blockers (including those with some α-blocking activity, e.g., labetalol and carvedilol) can slow AV nodal conduction and can cause or worsen heart block.