TOXICOLOGYSYMPTOMS/EXAM
■ Varying degrees of hypotension, bradycardia
■ Patient may present in cardiogenic shock.
■ Respiratory depression, apnea, QRS and QT prolongation
■ AMS, seizures, and coma
■ Fewer CNS effects when compared to β-blockers
■ Hyperglycemia (mild)
DIFFERENTIAL
■ β-Blockers, clonidine, digoxin
DIAGNOSIS
■ Should be considered in the differential of any patient with bradycardia,
hypotension, and hyperglycemia
TREATMENT
■ GI decontamination
■ Gastric lavage: If early presentation with a large overdose, given lack of
antidote and potential lethality of these agents
■ Activated charcoal: Give to all patients (with patent airway).
■ Whole-bowel irrigation: Consider if large overdose of sustained release
preparations.
■ Bradycardia and hypotension
■ Treat initially with atropine and vasopressors.
■ IV calcium
■ After ruling out digoxin toxicity
■ Increases movement of Ca++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
■ May be less successful than with β-blocker toxicity
■ 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.
Digoxin
Digoxin is a cardiac glycoside derived from the foxglove plant. It is used to
increase the force of myocardial contraction in systolic heart failure and to decrease
AV conduction in atrial fibrillation. Digoxin has a narrow therapeutic-toxicwindow
and is eliminated primarily via renal excretion.
MECHANISM/TOXICITY
■ Inactivation of the Na+K+ATPase pump on the cardiac cell membrane →
increased intracellular Ca++and extracellular K+.
■ Increased automaticity
■ Decreases conduction through the AV node via increased vagal tone
Hyperglycemia is suggestive
of calcium channel blocker
overdose in the
undifferentiated hypotensive
and bradycardic patient.