Obtaining digoxin levels in specific circumstances can be lifesaving.

Digoxin is the most widely used cardiac glycoside. These agents inhibit the sodium-potassium-adenosine triphosphate (Na⁺-K⁺ATPase) pump and, therefore, block active transport of Na⁺ and K⁺ across cell membranes. Increased intracellular Na⁺ reduces the transmembrane Na⁺ gradient and subsequently increases activity of the Na⁺-Ca⁺ exchanger, which causes intracellular calcium to rise. It is this increased intracellular Ca⁺ that augments myofibril activity in cardiac myocytes, causing a positive inotropic action and therefore is used for treatment of congestive heart failure. Digoxin is also used to slow the ventricular rate in certain tachyarrhythmias.

Digoxin can cause toxicity by increasing vagal tone that may lead to direct atrioventricular depression and arrhythmias. Clinically, a patient may present with acute or chronic digoxin toxicity. There are several dysrhythmias that can result, most commonly frequent premature ventricular beats. Bidirectional ventricular tachycardia is specific for digoxin toxicity but is rarely seen. Noncardiac symptoms of toxicity may include anorexia, nausea, vomiting headache, fatigue, depression, dizziness, confusion, memory loss, delirium, and hallucinations. Visual disturbances, specifically xanthopsia, seeing yellow halos around objects, have been reported. Vague symptoms can lead to a misdiagnosis of viral syndrome, so a high degree of suspicion must be maintained. Chronic toxicity may lead to renal failure.