Calcium channel blocker drug interactions

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Been busy in the real world, so I'm late to the new ITE keyword subforum ... I don't really do keywords, just test questions that I turn into keyword-like exercises.


I'm looking for a better reference than http://www.drugs.com/mmx/verapamil.html for explaining the answer to this question. I didn't find anything really compelling in Miller, Barash, or M&M.

Old question from the 1995 ITE:

In a patient taking a beta-adrenergic blocker, the drug most likely to produce atrioventricular junctional block
(A) diltiazem
(B) fentanyl
(C) halothane
(D) nifedipine
(E) verapamil


Fentanyl and halothane are clearly wrong answers here, so the question comes down to which calcium channel blocker is worst when it comes to beta-blocker interactions and AV block.

Not D. Dihydropyridines such as nifedipine, felodipine, nicardipine, and nimodipine cause the most vasodilation of all calcium channel blockers, with a reflex increase in HR, but SA and AV node depression don't occur.

According to a chart on that web page, diltiazem, a benzothiazepine, maybe has less negative inotropic effect than verapamil, an L-type calcium channel blocker ... but it was a small difference between a + and a +/- on the chart. My take was that verapamil probably carries the most risk for AV block and the answer key does say verapamil is the correct answer.

Originally Posted by pgg

Been busy in the real world, so I'm late to the new ITE keyword subforum ... I don't really do keywords, just test questions that I turn into keyword-like exercises.


I'm looking for a better reference than http://www.drugs.com/mmx/verapamil.html for explaining the answer to this question. I didn't find anything really compelling in Miller, Barash, or M&M.

Old question from the 1995 ITE:

In a patient taking a beta-adrenergic blocker, the drug most likely to produce atrioventricular junctional block
(A) diltiazem
(B) fentanyl
(C) halothane
(D) nifedipine
(E) verapamil


Fentanyl and halothane are clearly wrong answers here, so the question comes down to which calcium channel blocker is worst when it comes to beta-blocker interactions and AV block.

Not D. Dihydropyridines such as nifedipine, felodipine, nicardipine, and nimodipine cause the most vasodilation of all calcium channel blockers, with a reflex increase in HR, but SA and AV node depression don't occur.

According to a chart on that web page, diltiazem, a benzothiazepine, maybe has less negative inotropic effect than verapamil, an L-type calcium channel blocker ... but it was a small difference between a + and a +/- on the chart. My take was that verapamil probably carries the most risk for AV block and the answer key does say verapamil is the correct answer.

This might be of some help:
Non-dihydropyridines, of which there are only two currently used clinically, comprise the other two classes of CCBs. Verapamil (phenylalkylamine class), is relatively selective for the myocardium, and is less effective as a systemic vasodilator drug. This drug has a very important role in treating angina (by reducing myocardial oxygen demand and reversing coronary vasospasm) and arrhythmias. Diltiazem (benzothiazepine class) is intermediate between verapamil and dihydropyridines in its selectivity for vascular calcium channels. By having both cardiac depressant and vasodilator actions, diltiazem is able to reduce arterial pressure without producing the same degree of reflex cardiac stimulation caused by dihydropyridines.

In reality both can do it but verapamil more-so.

Agree with Noyac on this one: Verapamil depresses the AV conduction more than Diltiazem and this is exactly why I like it for Afib with RVR.

Originally Posted by Planktonmd

Agree with Noyac on this one: Verapamil depresses the AV conduction more than Diltiazem and this is exactly why I like it for Afib with RVR.

Is verapamil your goto drug then?

I thought one of the things that changed with the new ACLS guidelines was removal of verapamil as a first line agent for afib rate control. Am I wrong here?

I think the only place the 2005 ACLS guidelines include verapamil in the algorithm are (IIRC) as an alternative to diltiazem in stable patients with SVT and preserved LV function (stable bad hearts get digoxin or amiodarone; unstable patients get shocked, then either dilt or amio).

For rate control in afib or flutter ... after digging out my 2005 cards I don't see verapamil on the afib chart. Unstable patients get shocked but stable patients with rate >150 get digoxin if their heart sucks, amiodarone for WPW, otherwise a beta blocker or diltiazem.


I sort of vaguely remember someone telling me that the reason verapamil was de-emphasized for afib RVR was the risk it carries when given to someone who really has WPW, and that it's easy to mistake WPW for garden variety afib RVR when the rate's high and all you've got is a rhythm strip. This made little sense to me because if the patient's dying you're going to shock him, and if he's not dying there's no reason not to get a 12-lead before giving any drugs.

Originally Posted by pgg

Is verapamil your goto drug then?

I thought one of the things that changed with the new ACLS guidelines was removal of verapamil as a first line agent for afib rate control. Am I wrong here?

I think the only place the 2005 ACLS guidelines include verapamil in the algorithm are (IIRC) as an alternative to diltiazem in stable patients with SVT and preserved LV function (stable bad hearts get digoxin or amiodarone; unstable patients get shocked, then either dilt or amio).

For rate control in afib or flutter ... after digging out my 2005 cards I don't see verapamil on the afib chart. Unstable patients get shocked but stable patients with rate >150 get digoxin if their heart sucks, amiodarone for WPW, otherwise a beta blocker or diltiazem.


I sort of vaguely remember someone telling me that the reason verapamil was de-emphasized for afib RVR was the risk it carries when given to someone who really has WPW, and that it's easy to mistake WPW for garden variety afib RVR when the rate's high and all you've got is a rhythm strip. This made little sense to me because if the patient's dying you're going to shock him, and if he's not dying there's no reason not to get a 12-lead before giving any drugs.

We have discussed this before but the reason Verapamil is a favorite of mine is because it does not require an infusion because it is long acting compared to Diltiazem, this is very convenient in our type of business where you don't want to start drips that you are not going to be monitoring later.
As you mentioned Verapamil and WPW are a bad combination but the same goes for Diltiazem to a lesser degree.
The other problem (theoretically) is combining Verapamil with Digoxin which should be bad.
If you know what you are doing Verapamil in my opinion is still a great drug but I wouldn't advise everyone to use it.