If digoxin toxicity causes hyperkalemia then why does it cause T wave inversion and ST segment depression in ecg changes? And how does it cause QT interval shortening?
While digoxin toxicity can indeed lead to hyperkalemia, the ECG changes associated with digoxin toxicity, such as T wave inversion and ST segment depression, are primarily due to its effects on cardiac conduction rather than hyperkalemia.
Here’s how digoxin toxicity can lead to these ECG changes:
- T wave inversion and ST segment depression: Digoxin has effects on cardiac electrophysiology, primarily by inhibiting the sodium-potassium ATPase pump in cardiac myocytes. This results in increased intracellular calcium levels, which can lead to delayed afterdepolarizations and triggered activity. These abnormal electrical impulses can manifest as T wave inversion and ST segment depression on the ECG.
- QT interval shortening: Digoxin toxicity can paradoxically shorten the QT interval. This is thought to be due to the increased intracellular calcium levels, which can enhance the activity of the rapidly activating delayed rectifier potassium current (Ikr). Activation of Ikr leads to earlier repolarization of the cardiac myocytes, resulting in QT interval shortening.
Hyperkalemia, on the other hand, typically manifests on the ECG as tall, peaked T waves, widened QRS complexes, and eventually bradyarrhythmias or even asystole. It’s important to differentiate between the ECG changes associated with digoxin toxicity and those associated with hyperkalemia, as the management approaches for each condition may differ.