Calcium Channel Blockers (CCB) decrease calcium entry thru L-type calcium channels in the heart, vascular smooth muscle and the pancreas. Some CCB (amlodipine, nifedipine) act primarily on blood vessels causing vasodilatation and others (verapamil, diltiazem) also act on the heart, decreasing heart rate and contractility. Most texts would list the following actions of CCB:
Simplistically, the blocked L-type Ca channels in the following locations cause the clinical picture seen with CCB OD:
1)Heart -a)SA/AV node which decreases rate
b) myocardial smooth muscle which decreases force of contraction
2) Vascular Smooth Muscle-decreases vascular tone i.e., vasodilatation
3) Beta Islet pancreas-dose-related inhibition of glucose-induced insulin release (so called insulin resistance)
Clinically, the blocked calcium channels cause
One of the important pathophysiological changes that occur during CCB OD is that hypotension shifts myocardial energy substrate preference from fatty acid (FFA) to carbohydrates (CHO).
Not surprisingly, one of the treatments of the hypotension is insulin-which allows maximal myocardial CHO utilization.
Treatment of CCB OD next week.
The question of the week was prepared by Donna Seger, MD
Last week’s Question explained the reason for administering glucagon for beta-blocker induced hypotension. Dr. Cosby Stone (Assistant Professor Allergy/Immunology, VUMC) noted that glucagon also reverses the effects of a beta-blocker if someone is having anaphylaxis and needs epinephrine. Great comment, Dr. Stone.
I am interested in any questions you would like answered in the Question of the Week. Please email me with any suggestion at firstname.lastname@example.org.
Donna Seger, MD
Tennessee Poison Center www.tnpoisoncenter.org
Poison Help Hotline: 1-800-222-1222