Introduce digitalis and digoxin, the type of drug they are, their drug action. And their changes in ECG.
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Digitalis and digoxin
Digitalis is the general term for cardiac-active substances derived from foxglove plants (Digitalis species). It includes cardiac glycosides such as digoxin and digitoxin. Digoxin is the commonly used clinical preparation, historically obtained from Digitalis lanata.
Type of drug
Digoxin is a:
- Cardiac glycoside
- Positive inotropic drug: increases myocardial contractile force
- Negative chronotropic and dromotropic drug: slows heart rate and atrioventricular (AV) nodal conduction
- Used mainly in selected patients with:
- Heart failure with reduced ejection fraction, to improve symptoms and reduce hospital admissions
- Atrial fibrillation or atrial flutter, for ventricular-rate control, especially when heart failure coexists
It has a narrow therapeutic index, so modest increases in exposure can cause toxicity. [Fuster and Hurst's The Heart, p. 1539]
Drug action
1. Direct myocardial action: positive inotropy
Digoxin inhibits the Na+/K+-ATPase pump in cardiac myocytes.
Sequence:
- Na+/K+-ATPase inhibition raises intracellular Na+.
- The Na+/Ca2+ exchanger then removes less Ca2+ from the cell.
- Intracellular and sarcoplasmic-reticulum Ca2+ increase.
- More Ca2+ is released with each heartbeat.
- Cardiac contraction becomes stronger.
Therefore, digoxin produces a positive inotropic effect. [Fuster and Hurst's The Heart, p. 1539]
2. Autonomic and AV-nodal actions
Digoxin also:
- Increases vagal (parasympathetic) tone
- Reduces sympathetic activity
- Slows sinoatrial-node firing
- Slows conduction through the AV node
- Increases AV nodal refractoriness
This explains its role in reducing the ventricular rate in atrial fibrillation.
ECG changes
A. Therapeutic digoxin effect: not necessarily toxicity
Typical ECG effects at therapeutic doses are:
| ECG finding | Explanation |
|---|---|
| PR interval prolongation | Slower AV-nodal conduction |
| Shortened QT interval | Shorter ventricular action-potential duration |
| ST-segment depression | Classically downsloping, curved, or "scooped" ST depression, called the digitalis effect |
| T-wave flattening or inversion | Altered ventricular repolarization |
| Sometimes sinus bradycardia | Increased vagal effect |
The classic appearance is scooped ST depression, often described as a "reverse tick" or “Salvador Dalí moustache” pattern. These changes alone are expected pharmacologic effects and do not prove digoxin toxicity. The FDA prescribing information specifically notes PR prolongation and ST depression with therapeutic digoxin.
B. ECG features of digoxin toxicity
Toxicity can cause both increased automaticity and impaired conduction. Hence, many arrhythmias are possible.
Important patterns include:
- Sinus bradycardia
- First-degree AV block
- Second-degree AV block, including Wenckebach block
- Complete heart block
- Junctional rhythm or junctional tachycardia
- Frequent premature ventricular complexes, often bigeminy
- Atrial tachycardia with AV block: a classic digoxin-toxicity rhythm
- Bidirectional ventricular tachycardia: highly characteristic, though uncommon
- Ventricular tachycardia or ventricular fibrillation in severe toxicity
Memory point:
Digoxin toxicity = tachyarrhythmia plus AV block, particularly atrial tachycardia with block.
Digoxin toxicity = tachyarrhythmia plus AV block, particularly atrial tachycardia with block.
Hypokalemia, hypomagnesemia, hypercalcemia, renal impairment, advanced age, and interacting drugs can increase susceptibility to toxicity. Acute severe toxicity may cause hyperkalemia because of Na+/K+-ATPase inhibition. [Tintinalli's Emergency Medicine, Clinical Presentation of Digitalis Glycoside Toxicity]
Recent literature includes a 2025 expert consensus on diagnosis and management of digoxin toxicity, PMID 39265879.
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