Related Experiment Videos
Which cardiac disturbances should be treated with digoxin immune Fab (ovine) antibody?
F E Marchlinski1, B G Hook, D J Callans
1Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia 19104.
Insights
Digoxin excess causes dangerous heart rhythm problems and high potassium. Digoxin-specific antibody fragments are the preferred treatment for severe toxicity, especially with hemodynamic compromise.
Area of Science:
- Cardiology
- Clinical Toxicology
- Pharmacology
Background:
- Digoxin toxicity presents with bradyarrhythmias, tachyarrhythmias, and hyperkalemia.
- Bradyarrhythmias stem from direct and vagotonic effects on cardiac nodes.
- Digoxin enhances automatic and triggered electrical activity, leading to arrhythmias.
Purpose of the Study:
- To outline the electrophysiologic effects of digoxin excess.
- To identify characteristic arrhythmias associated with digoxin toxicity.
- To discuss the role of digoxin-specific antibody fragments in managing toxicity.
Main Methods:
- Review of electrophysiologic mechanisms of digoxin toxicity.
- Analysis of characteristic arrhythmias: atrial tachycardias, accelerated junctional rhythms, fascicular tachycardias.
- Evaluation of indications for digoxin-specific Fab fragment therapy.
Main Results:
- Digoxin excess causes conduction disturbances and blocks at AV and sinus nodes.
- Characteristic arrhythmias include atrial tachycardias with variable AV block and accelerated junctional rhythms.
- Hyperkalemia in acute severe digoxin toxicity is an indication for Fab therapy.
Conclusions:
- Digoxin-specific antibody fragments are the treatment of choice for hemodynamically compromising digoxin toxicity.
- Risk-benefit assessment for Fab therapy involves toxicity severity, renal function, and patient factors.
- Careful consideration of alternatives and patient predispositions is crucial.
Abstract:
Digoxin excess can produce characteristic bradyarrhythmias, tachyarrhythmias, and hyperkalemia. The bradyarrhythmias, which consist of disturbances in conduction and block at the level of the atrioventricular and sinus nodes, are mediated by a direct and vagotonic effect. The vagotonic effect of excess digoxin may also result in a marked slowing of the sinus rate in the setting of severe toxicity. Digoxin increases automatic and triggered electrical activity in atrial muscle, His-Purkinje system, and ventricular muscle, which predisposes to tachycardias. Many of the tachyarrhythmias are relatively specific for the toxic effects of digoxin. Atrial tachycardias with variable atrioventricular block, accelerated junctional rhythms (especially in the setting of atrial fibrillation), and fascicular tachycardias are characteristic digoxin toxic rhythms. Digoxin-specific antibody fragments should be considered the treatment of choice for any digoxin toxic arrhythmia associated with hemodynamic compromise or the threat of hemodynamic compromise. Hyperkalemia, when due to acute severe digoxin toxicity, is also an appropriate indication for digoxin-specific Fab fragment therapy. When assessing the risk:benefit ratio for using digoxin-specific Fab fragment therapy, one needs to determine, in addition to the electrocardiographic manifestations and patient's hemodynamic status (1) the severity of toxicity, as indexed by the amount ingested and/or the serum digoxin concentration; (2) the expected time course for reversal of toxicity, which is usually determined by the status of renal function; (3) the need for digoxin to provide ventricular rate control or improved ventricular contractility and therapeutic alternatives to digoxin; (4) the presence of a strong allergy history; (5) the presence of such factors as increased age and severity of heart disease that may predispose to digoxin toxicity.(ABSTRACT TRUNCATED AT 250 WORDS)