TOXICOLOGY
■ AMS and coma
■ Seizures with lipophilic agents (eg, propranolol)
■ Hypoglycemia (potentially, in children)
■ HyperkalemiaDIFFERENTIAL
■ Calcium channel blocker, clonidine, or digoxin toxicityDIAGNOSIS
■ Should be considered in the differential of any patient with bradycardia
and hypotensionTREATMENT
■ Supportive therapy
■ GI decontamination
■ Gastric lavage: If early presentation with a large overdose, given lack of
antidote and potential lethality of these agents
■ Activated charcoal: Give in all cases (with patent airway)
■ Whole-bowel irrigation: If large overdose of sustained-release preparation
■ Bradycardia and hypotension
■ Treat initially with atropine and vasopressors.
■ Calciumsupplementation
■ After ruling out digoxin toxicity
■ Increases movement of calcium into the cell
■ Glucagon
■ Requires high doses (5–10 mg)
■ Activates adenyl cyclase and increases cyclic AMP, resulting in
increased calcium influx into the cell
■ High-dose insulin (with glucose to maintain euglycemia)
■ Increases cardiac output via unclear mechanisms
■ Cardiac pacing, intra-aortic balloon pump, and bypass should be con-
sidered if these pharmacologic measures fail.Calcium Channel BlockersPrescribed for the treatment of hypertension, arrhythmias, and migrainesMECHANISM/TOXICITY
■ Blockade of L-type voltage gated Ca++channels→decreased Ca++influx
into cells.
■ In cardiac muscle cells →decreased SA node activity, decreased con-
tractility, slowed AV conduction.
■ In smooth muscle cells (peripheral vascular system) →relaxation and
vasodilitation.
■ Agent specificity:
■ Verapamil: Major effect at sinoatrial and atrioventricular nodes
■ Diltiazem: Intermediate activity at both cardiac and peripheral
vasculature
■ Dihydroperidines (eg, nifedipine): Major effect on peripheral vasculaturePropranolol, due to its
lipophilicity, can cause
delirium in the absence of
cardiovascular effects.Specificity between peripheral
and central cardiovascular
effect may be lost in overdose.