Digoxin

Digoxin does not bind directly to cardiac receptors but stimulates the vagus nerve,

it does not fit into the classical Vaughan–Williams classification and is therefore categorized as an “other anti-arrhythmic drug”.
“Other anti-arrhythmic drugs” are sometimes referred to as Class V.

Classification:

Mechanism:

Effect on AF:

Slows ventricular response during an episode of atrial fibrillation (AF) because it inhibits the AV node

Digoxin has a limited effect during increased sympathetic tone: physical or psychological exertion, stress-related occupations,
in such situations, beta-blockers are recommended for AF rate control.

Digoxin and atrial fibrillation (AF)
Brand names
Digoxin, Lanoxin, Lanicor, Lanacordin
Indications
Acute control of ventricular response during AF mainly in patients with ejection fraction < 40 % Chronic control of ventricular response during AF mainly in patients with ejection fraction < 40 %
Dosing
Acute rate control in AF (intravenous) 0.25–0.5 mg (intravenous) over 5–10 minutes A second dose of 0.25 mg (intravenous) every 6 hours if adequate rate slowing is not achieved Maximum dose within 24 hours is 1.5 mg Chronic rate control in AF (oral) 0.0625–0.25 mg once daily; the dose is highly individualized
Onset of action
5–60 min. (intravenous) 1–2 h (oral)
Effect
Reduces AF rate by 10–30 %
Duration of action
3–4 days (intravenous) 3–4 days (oral)
Therapeutic serum level
0.8–2 ng/ml – outside this range, treatment is ineffective
Contraindications
Pre-excited AF (delta wave on ECG) Ventricular fibrillation Ventricular tachycardia AV block II or III degree Bradycardia (< 50/min.) Sick sinus syndrome Hypertrophic obstructive cardiomyopathy Acute myocardial infarction Severe hypo-/hyperkalaemia, hypomagnesaemia Acute myocarditis Restrictive cardiomyopathy Hypothyroidism Allergy to digoxin

Patient monitoring after initiation of digoxin:

Patient monitoring after initiation of digoxin
Time since initiation	What to monitor	Reason for treatment interruption
Week 1	ECG Heart rate Potassium level (K⁺) Serum digoxin level	Bradycardia < 50/min. AV block II or III degree Serum digoxin level > 2.0 ng/ml Hypokalaemia
Month 1	ECG Heart rate Potassium level (K⁺) Serum digoxin level	Bradycardia < 50/min. AV block II or III degree Serum digoxin level > 2.0 ng/ml Hypokalaemia Inadequate clinical response
6–12 months	ECG Heart rate Potassium level (K⁺) Serum digoxin level	Bradycardia < 50/min. AV block II or III degree Serum digoxin level > 2.0 ng/ml Hypokalaemia Inadequate clinical response

Adverse effects:

Ventricular arrhythmias (ventricular extrasystoles, bigeminy, trigeminy, ventricular tachycardia [VT], bidirectional VT, R-on-T phenomenon)
Visual disturbances (blurred vision, yellow or green vision – xanthopsia)
Skin rash (maculopapular, bullous, etc.)
Headache
Anxiety, confusion, depression, hallucinations
AV block (II and III degree)
Diarrhoea
Thrombocytopenia
Atrial tachycardia

Digoxin and beta-blockers are used for ventricular rate control in AF (not for maintenance of sinus rhythm).

Digoxin vs. beta-blockers in atrial fibrillation (AF)
Characteristic	Digoxin	Beta-blockers
Preferred patients	Sedentary patients with ejection fraction < 40 %	Most patients – especially with coronary artery disease and chronic stress
Effect	Slows rate mainly at rest	Slow rate at rest and during exertion
Use	Often as add-on therapy to beta-blockers or non-DHP calcium channel blockers	First-line drug for rate control
Limitations	Limited effect during exertion, risk of toxicity	Caution in bradycardia, asthma/COPD, hypotension
Adverse effects	Nausea, vomiting, arrhythmias (AV block, ventricular tachyarrhythmias), visual disturbances (xanthopsia)	Bradycardia, hypotension, fatigue, bronchospasm, worsening HF in decompensated patients

CAD – coronary artery disease, BB – beta-blockers, non-DHP CCB – non-dihydropyridine calcium channel blockers