Relationship of digoxin and potassium levels

>Digoxin’s primary action is inhibiting sodium-potassium-activated adenosine triphosphatase on the

myocyte, promoting movement of calcium from extracellular to intracellular cytoplasm and strengthening
myocardial contraction. Since the sodium-potassium ATPase pump normally causes sodium to leave cells
and potassium to enter cells, blocking this mechanism results in increased intracellular sodium levels
higher serum potassium levels. Digoxin toxicity, therefore, can cause hyperkalemia.

In addition, since digoxin normally binds to the ATPase pump on the same site as potassium, when
potassium levels are low, digoxin can more easily bind to ATPase pump, exerting the inhibitory effect.
Thus, when a patient has electrolyte imbalance (hypomagnesemia, hypercalcemia, and hypokalemia),
they have increased sensitivity to digoxin making toxicity more likely even with a lower concentration of
serum digoxin. Conversely, when a patient has hyperkalemia, digoxin’s effectivness diminishes.

Digoxin also has direct effects on conduction through increased vagal tone. Digoxin stimulates the vagus
nerve leading to prolonged conduction through the sinuatrial (SA) and atrioventricular (AV) nodes.