Digoxin inhibits Na+/K+/ATPase pump. By inhibiting this pump, digoxin increases the force of ventricular contraction, which is known as inotropy. This drug also increases cardiac output, by increasing stroke volume per beat.
Because digoxin can increase the inotropy/contractility of the heart, it is sometimes used in patients who have heart failure who remain symptomatic despite adequate diuretic and ACE inhibitor treatment. However, it is no longer the first-line drug used in heart failure due to its toxic effects and the availability of other treatment options.
Digoxin is used in people with atrial fibrillation by slowing down the conduction in the AV node, thereby reducing ventricular rate.
Digoxin increases vagal activity, thereby decreasing heart rate by slowing depolarization of pacemaker cells in the AV node.
Fatigue is a common side effect of digoxin and may also include dizziness, headache, and malaise.
Digoxin is contraindicated in patients with heart block, as well as, in pregnancy, acute myocardial infarction, and hypokalemia.
Before administering medication, take an apical pulse for 1 full minute noting rate and rhythm and quality. Withhold the medication and notify the health care provider if rate falls below 60.
Never give digoxin to a patient who is already hypokalemic, as this potentiates digoxin toxicity. Because digoxin normally competes with K+ ions for the same binding site on the Na+/K+/ATPase pump, hypokalemia can make toxicity present more quickly.
Signs and symptoms of digoxin toxicity become more frequent with levels above 2 ng/ml, and may include anorexia, nausea, vomiting, diarrhea, confusion, and visual disturbances, such as blurry vision that often has a yellow hue. Levels are usually checked every 6 months along with other lab values.
Digibind is an antidote for digoxin toxicity. It works by binding to digoxin and preventing it from working in the body.
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