Overview
Digoxin is a cardiac glycoside which can be associated with significant toxicity. Certain ECG findings are characteristic.
Pathogenesis
Digoxin inhibits the Na+/K+ ATPase pump, which results in sodium influx and potassium efflux. This subsequently increases the activity of the Na+/Ca2+ exchange pump, resulting in calcium influx which increases automaticity and has a positive inotropic effect (increases contractility). Digoxin also increases parasympathetic (vagal) tone, causing reduced conduction through the AV node.
Effects of Digoxin
- Increased automaticity - due to an increase in intracellular calcium
- Reduced conduction via the AV node - due to an increase in parasympathetic (vagal) tone
Diagnosis
Certain ECG changes with digoxin may purely indicate a therapeutic effect (such as the ST depression and T wave flattening), while other changes (such as T wave inversion and arrhythmias) indicate toxicity.
ECG Findings in Digoxin Toxicity
- ST depression - down-sloping or scooped
- T wave changes - flattening, inversion or biphasic T waves
Due to Increased Automaticity
- QT shortening (due to reduced ventricular repolarisation time)
- Premature beats - atrial, junctional or ventricular
- Tachyarrhythmias - atrial tachycardia, accelerated junctional tachycardia
Due to Reduced Conduction
- Prolonged PR interval
- Bradyarrhythmias - sinus bradycardia, bundle branch block, AV block
The ST depression of digoxin toxicity is characteristically scooped - this is often referred to as a reverse tick or Salvador Dali's moustache ST depression.
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