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Chapter 108: Cardiac Medications

Michael Levine

DIGITALIS GLYCOSIDES

Digoxin is used to treat atrial fibrillation, especially with concurrent congestive heart failure. Other cardiac glycosides are found in plants such as foxglove, oleander, and lily of the valley.

Clinical Features

Toxicity can occur following acute ingestion or develop during chronic therapy (Table 108-1). Acute toxicity typically presents with abrupt onset of nausea and vomiting. Characteristic cardiac effects include bradydysrhythmias and/or supraventricular tachycardia with atrioventricular block. Severe toxicity can result in ventricular dysrhythmias. Chronic toxicity is more common in the elderly and often occurs as a result of renal failure or diuretic therapy. Neuropsychiatric symptoms are more common with chronic toxicity, though cardiac effects are similar to those seen with acute toxicity.

Table 108-1

Clinical Presentation of Digitalis Glycoside Toxicity

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Table 108-1

Clinical Presentation of Digitalis Glycoside Toxicity
Acute toxicity
Clinical history Intentional or accidental ingestion
GI effects Nausea and vomiting
Central nervous system effects Headache, dizziness, confusion, coma
Cardiac effects Bradydysrhythmias or supraventricular tachydysrhythmias with atrioventricular block
Electrolyte abnormalities Hyperkalemia
Digoxin level Marked elevation (if obtained within 6 h)
Chronic toxicity
Clinical history Typically in elderly cardiac patients taking diuretics; may have renal insufficiency
GI effects Nausea, vomiting, diarrhea, abdominal pain
Central nervous system effects Fatigue, weakness, confusion, delirium, coma
Cardiac effects Almost any dysrhythmia, other than a rapidly conducted atrial fibrillation, can occur; ventricular dysrhythmias are common
Electrolyte abnormalities Normal, low, or high serum potassium, hypomagnesemia
Digoxin level Minimally elevated or within “therapeutic” range

Diagnosis and Differential

Hyperkalemia is often seen in acute poisoning, but may be absent in chronic toxicity. Serum digoxin levels are neither sensitive nor specific for toxicity. However, those patients with higher levels (>2 ng/mL) are more likely to experience toxicity. Almost any dysrhythmia, except for rapidly conducted atrial dysrhythmias, may be seen with toxicity; however, the most common finding is premature ventricular beats. The differential diagnosis includes sinus node disease or toxicity from calcium channel blockers, β-blockers, class IA antidysrhythmics, clonidine, other cardiotoxic plants, or intrinsic conduction disease.

Emergency Department Care and Disposition

All patients require continuous cardiac monitoring, intravenous (IV) access, and frequent reevaluation (Table 108-2).

  1. Administer activated charcoal 1 g/kg in cases of acute toxicity in which the patient is awake and cooperative.

  2. Use atropine 0.5 to 1 mg (0.02 mg/kg, minimum dose 0.1 mg) IV to treat bradydysrhythmias.

  3. Administer digoxin-specific Fab for ventricular dysrhythmias, hemodynamically significant bradydysrhythmias, and hyperkalemia greater than 5.5 mEq/L. Dosing of digoxin-specific Fab is calculated according to Table 108-3.

  4. Hyperkalemia that is thought to be due to cardiac glycoside toxicity is best treated with Fab fragments. Hyperkalemia that is felt to be due to intrinsic renal disease may be treated with dextrose followed by insulin; other options are sodium bicarbonate, potassium-binding resin, ...

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