What arrhythmias indicate digoxin toxicity?

Arrhythmias Indicating Digoxin Toxicity

The most characteristic arrhythmias of digoxin toxicity include enhanced atrial, junctional, or ventricular automaticity (with ectopic beats or tachycardia) combined with atrioventricular block, and bidirectional or fascicular ventricular tachycardia, which is highly specific for digoxin toxicity. 1

Classic Arrhythmia Patterns

Bradyarrhythmias and Conduction Disturbances

• Atrioventricular block (first-degree, second-degree Wenckebach, or third-degree heart block including asystole) is a hallmark finding that results from digoxin's direct and vagotonic effects on the AV node 1, 2
• Sinus bradycardia with marked slowing of the sinus rate occurs in severe toxicity, particularly important in infants and children where it may be the earliest sign of impending intoxication 1, 2
• Sinus arrest with junctional bradyarrhythmias represents combined enhanced automaticity and conduction block 3

Tachyarrhythmias (Highly Specific for Digoxin Toxicity)

• Atrial tachycardia with variable AV block is one of the most characteristic rhythms of digoxin toxicity, reflecting enhanced atrial automaticity combined with AV nodal suppression 1, 4
• Accelerated junctional (nodal) rhythm, especially occurring in the setting of atrial fibrillation, is highly suggestive of toxicity 1, 2, 4
• Bidirectional ventricular tachycardia is pathognomonic for digoxin toxicity and should immediately raise suspicion 1, 5
• Fascicular ventricular tachycardia is another highly specific pattern for digoxin toxicity 1, 5

Ventricular Arrhythmias

• Unifocal or multiform ventricular premature contractions, particularly in bigeminy or trigeminy patterns 2
• Ventricular tachycardia (non-fascicular types) 2
• Ventricular fibrillation in severe cases 2, 6

Important Clinical Context

ECG Changes That Are NOT Toxicity

• PR prolongation and ST segment depression are expected pharmacologic effects of digoxin and should not by themselves be considered evidence of toxicity 2

Age-Specific Considerations

• In infants and children, cardiac arrhythmias (especially sinus bradycardia) are the earliest and most frequent manifestation of overdosage, rather than gastrointestinal or CNS symptoms that predominate in adults 2
• Any arrhythmia developing in a child taking digoxin should be assumed to be caused by digoxin until proven otherwise 2

Severe Toxicity Indicators

• Cardiac standstill occurs with severe digoxin overdose, typically accompanied by hyperkalemia 1, 5
• Competing rhythms such as AV dissociation or atrial tachycardia with competing junctional rhythm suggest significant toxicity 6

Diagnostic Approach

The diagnosis requires the combination of characteristic rhythm disturbances, ancillary symptoms (visual disturbances, nausea, changes in mentation), and elevated serum concentrations 1, 5. However, toxicity can occur even when serum digoxin concentration is within the therapeutic range (0.5-1.2 ng/mL), particularly in the presence of potentiating factors 5.

Key Potentiating Factors That Lower Arrhythmia Threshold

• Hypokalemia is the most critical factor—significantly increases risk of digoxin-induced arrhythmias even at therapeutic drug levels 1, 5, 7
• Hypomagnesemia compounds the arrhythmogenic risk 1, 5
• Hypercalcemia sensitizes the myocardium to digoxin effects 5
• Renal dysfunction and advanced age increase susceptibility 5
• Hypothyroidism potentiates toxicity 1, 5

Management Implications

For any sustained ventricular arrhythmia potentially due to digoxin toxicity, administration of digoxin-specific Fab antibodies is recommended (Class I, Level B-NR). 1, 5 Response typically occurs within 30 minutes to 4 hours, with a 54% survival rate even in patients presenting with cardiac arrest 1, 5.

Treatment Algorithm Based on Arrhythmia Severity

• Mild toxicity (ectopic beats, first-degree AV block): Discontinue digoxin, monitor rhythm continuously, maintain serum potassium >4.0 mEq/L (ideally 4.0-5.5 mEq/L) 1, 5, 7
• Moderate toxicity (ventricular arrhythmias without hemodynamic compromise): Administer intravenous magnesium sulfate even if serum magnesium is normal 1, 5
• Severe toxicity (sustained VT, VF, high-degree AV block with hemodynamic compromise, serum digoxin >4 ng/mL): Immediate digoxin-specific Fab antibody administration 1, 5
• Symptomatic bradyarrhythmias: Temporary cardiac pacing is safe and effective in accidental overdose (though contraindicated in acute intentional overdose/suicide attempts) 1, 3

Critical Pitfall

Transvenous temporary cardiac pacing, while safe in accidental digoxin overdose with symptomatic bradycardia, has been associated with fatal arrhythmias in acute intentional overdose (suicide attempts) and should be avoided in that specific context 3.