S15C189 - CCB OD

Question 1

CCB - Pharmacology

Answer 1

• decrease calcium entry during plateau phase of AP
• high doses: profound smooth muscle relaxation, weak cardiac contraction, blunted automaticity, conduction delay resultin gin HoTN and brady

Question 2

CCB - classes (3)

Answer 2

• phenylalkylamines (verapamil)
• benzothiazepines (diltiazem)
• dihydropyridines (nifedipine, amlodipine, felodipine)
• verapamil has most profound cardiac depression of the CCB
• dihydropyridines bind more selectively to vascular smooth muslce than other CCB, very little negative inotropy (used for HTN, prinzmetal angina, vasospasm)

Question 3

CCB OD - clinical picture

Answer 3

-HoTN, vasodilation, sinus brady or AV block (if mild OD may have reflex tachy)
-Sz, delirium, coma secondary to cerebral hypoperfusion
-often will have hyperglycemia
-

-in kids: one pill can kill!

Question 4

DDx Bradycardia

Answer 4

• hypothermia
• ACS
• hyperkalemia
• cardiac glycoside toxicity
• BB
• CCB
• antiarrhythmic class IA and IC
• central alpha-adrenergic agonist toxicity
• digoxin
• organophosphates

Question 5

CCB OD : Tx

Answer 5

• atropine (unlikely to work)
• Calcium (CaCl- 1-3g IV central line)
• Pacing
• Adrenergic agonists (NE)
• Glucagon
• Insulin (inotropic effects)
• Intralipid tx
• ECMO