Everything about digoxin in one place, in the order a patient meets it: what it is, how it works, what it does and does not do, who gets it, how toxicity shows up, what raises the risk and how it is reversed.
| Topic | What to know | Source |
|---|---|---|
| What it is | A cardiac glycoside. The lactone ring and steroid nucleus are essential for activity; the sugar molecules change absorption, half-life and metabolism. | L9 slide 61 |
| Older mechanism: inotropic | Inhibits the sodium-potassium ATPase, so intracellular sodium rises; the sodium-calcium exchanger then lets calcium accumulate and fiber shortening (contraction) increases. It increases the force of cardiac muscle contraction. | L9 slide 62 slide 63 |
| Newer mechanism: neurohormonal | Lower sympathetic and higher parasympathetic activity (lower heart rate, more atrioventricular nodal slowing), resensitized baroreflex, less renin-angiotensin-aldosterone activity, less remodeling and better tissue perfusion; cardiac output rises. | L9 slide 63 slide 64 slide 65 |
| Benefits | Better symptoms, exercise tolerance and quality of life, and fewer hospitalizations, but no survival benefit: the symptoms-only side of the survival rule. | L9 slide 66 |
| Place in therapy | No evidence of slowed disease progression. Used in symptomatic patients already on optimal ACE inhibitor, beta blocker and diuretic therapy; an option for rate control in atrial fibrillation with heart failure; considered in symptomatic heart failure with systolic dysfunction. | L9 slide 67 |
| Level and narrow margin | A level is checked (reference target 0.5 to 1 ng/mL); higher concentrations may be associated with worse outcomes in heart failure. A very narrow therapeutic index: small excess causes major toxicity. | L9 slide 65 |
| Toxicity: gastrointestinal and visual | Anorexia and nausea; visual disturbances: blurred vision, photophobia, xanthopsia (shining lights, yellow-green halos around objects). | L9 slide 68 |
| Toxicity: central | Delirium, fatigue, confusion, dizziness, abnormal dreams. | L9 slide 69 |
| Toxicity: cardiac | Nodal slowing (longer PR interval, shorter QT interval, depressed ST segment), bradycardia (most common), and digoxin-induced after-depolarizations that cause ventricular arrhythmias such as premature ventricular beats. | L9 slide 70 slide 71 |
| What raises the risk | Low potassium, low magnesium, high calcium. Loop diuretics and thiazides lower potassium and magnesium, so the combination is hazardous; keep potassium above 4.0 mEq/L with a thiazide. | L9 slide 71 slide 19 slide 29 |
| Do not use with | Advanced atrioventricular block; severe bradycardia or sick sinus syndrome; premature ventricular beats and ventricular tachycardia; Wolff-Parkinson-White syndrome; electrolyte disturbances (low potassium, low magnesium, high calcium). | L9 slide 71 |
| Antidote | Digoxin immune Fab: an antibody fragment made by immunizing healthy sheep with digoxin; it binds digoxin with higher affinity than digoxin has for the sodium-potassium ATPase and rapidly reverses toxicity. The condition digoxin was treating can return after reversal. | L9 slide 72 |