At higher plasma levels atrial tachyarrhythmias and ventricular tachyarrhythmias may occur. This initially manifests with premature beats (premature atrial beats or premature ventricular beats), which are considered an early sign of overdosing. Increased automaticity occurs both in the atria and the ventricles.One should always suspect digoxin as the trigger of an arrhythmia (in patients using digoxin) if there is evidence of increased automaticity and diminished impulse conduction. However, none of the ECG changes or arrhythmias are unique to digoxin. Arrhythmias caused by digoxinĭigoxin may cause virtually all known arrhythmias. Arrhythmias may occur already at therapeutic plasma levels of digoxin in the setting of hypokalemia. Potassium levels must always be assessed in patients using digoxin whenever they seek medical attention. Hypokalemia always potentiates the pro-arrhythmic effects of digoxin. Hypokalemia potentiates the digoxin effect Thus, digoxin is rather unpredictable in terms of arrhythmia risk. However, arrhythmia may occur at plasma levels below 2 ng/mL and arrhythmias may not occur even at higher plasma levels. Plasma levels >2 ng/mL are considered an overdose. Hence, arrhythmias may occur in the absence of ECG changes and vice versa (i.e ECG changes may be pronounced without any arrhythmias occurring). It is important to note that the association between ECG changes and the risk of arrhythmia is weak. The effect on automaticity should be distinguished from the effect on impulse conduction because digoxin slows impulse conduction. This increases the automaticity in cells with natural automaticity but it may also provoke abnormal automaticity in cells that normally do not exhibit automaticity. Digoxin shortens the action potential in all cardiac cells, both in the atria and the ventricles. This is explained by the increase in intracellular calcium levels, which causes a shortening of the action potential. Digoxin is very pro-arrhythmic, meaning that it increases the probability of arrhythmias occurring. The incidence of adverse drug reactions is high, owing to the narrow therapeutic index of the drug. ST segment depression due to digoxin treatment. The most classical ECG finding is generalized ST segment depressions with curved ST segment (generalized implies that the depressions may occur in most ECG leads). Increased Vagus activity diminishes the automaticity in the sinoatrial node (which lowers heart rate) and also slows conduction over the atrioventricular (AV) node. Lowering of the heart rate is due to increased Vagus nerve activity caused by digoxin. Inhibition of Na-K-ATPase leads to increased intracellular concentration of sodium, which affects the sodium-calcium exchanger such that ultimately intracellular calcium concentration increases. This makes more calcium available to the contractile proteins which therefore produce stronger contractions. The positive inotropic effect is due to inhibition of the sodium-potassium adenosine triphosphatase (NaK-ATPase) in ventricular myocardium. Digoxin effects on cardiac function and ECGĭigoxin has a positive inotropic effect and negative chronotropic effect, meaning that it enhances ventricular contractility but lowers heart rate. Because digoxin may cause life-threatening arrhythmias, every health care provider must be able to recognize common digoxin ECG changes and arrhythmias. Moreover, digoxin is used frequently in the emergency setting to slow ventricular rate during supraventricular tachycardia (e.g atrial fibrillation). However, it has kept coming back and it is still used in patients who do not achieve satisfactory effect by first line therapies. Due to its profound pro-arrhythmic effects and lack of compelling data regarding morbidity and mortality benefit, digoxin has been expelled repeatedly from the treatment arsenal. Digoxin ECG changes: arrhythmias, conduction defects and waveform changesĭigoxin may be used in patients with heart failure, atrial fibrillation, atrial flutter and in selected cases of paroxysmal supraventricular tachycardia.
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