Write a short note on atrial fibrillation, including digoxin therapy and toxicity.

Definition

Atrial fibrillation (AF) is a supraventricular tachyarrhythmia characterised by uncoordinated atrial activation with consequent deterioration of atrial mechanical function. It is the commonest sustained arrhythmia, and its prevalence rises steeply with age.

ECG features: absent P waves, replaced by fibrillatory (f) waves; an irregularly irregular ventricular response; and a narrow QRS complex unless there is aberrancy or pre-existing bundle branch block.

Classification: paroxysmal (self-terminating within 7 days), persistent (> 7 days or requiring cardioversion), long-standing persistent (> 1 year), and permanent (accepted, with no further attempts at rhythm control).

Aetiology

Also: heart failure, cardiomyopathy, pericarditis, congenital heart disease, obesity, and "lone AF" with no identifiable cause.

Clinical Features

• Palpitations, breathlessness, fatigue, reduced exercise tolerance, chest discomfort, dizziness and syncope.
• May be entirely asymptomatic and detected incidentally — or present for the first time with a stroke.
• Irregularly irregular pulse with a pulse deficit (apical rate exceeding radial rate, because weak beats do not transmit to the periphery).
• Loss of the atrial contribution to ventricular filling (about 20–30% of cardiac output) causes marked deterioration in patients with stiff ventricles — which is why AF so often precipitates decompensation in mitral stenosis, HFpEF and hypertrophic cardiomyopathy.
• Complications: STROKE and systemic embolism (a fivefold increased risk), heart failure, and tachycardia-mediated cardiomyopathy.

Investigations

• ECG (and Holter or event monitoring for paroxysmal AF)
• thyroid function
• CBC, electrolytes, magnesium, renal and liver function
• echocardiography (valve disease — especially mitral stenosis, chamber size, LV function, left atrial thrombus on transoesophageal imaging)
• chest X-ray
• investigation for precipitants (sepsis, pulmonary embolism, alcohol, sleep apnoea).

Management — Three Decisions

1. ANTICOAGULATION — the decision that saves lives

Assess stroke risk with CHA₂DS₂-VASc:

Anticoagulate men scoring ≥ 2 and women scoring ≥ 3 (consider at 1 and 2 respectively). Assess bleeding risk with HAS-BLED — to identify and correct modifiable risk factors, NOT to withhold anticoagulation.

Choice of agent:

• DOACs (apixaban, rivaroxaban, dabigatran, edoxaban) are preferred in NON-VALVULAR AF — comparable or better efficacy, less intracranial haemorrhage, no monitoring, fewer interactions.
• WARFARIN (target INR 2–3) IS MANDATORY in "VALVULAR" AF — that is, MODERATE-TO-SEVERE RHEUMATIC MITRAL STENOSIS and MECHANICAL PROSTHETIC VALVES. DOACs are contraindicated in these settings. This distinction is of major importance in India, where rheumatic AF is common.
• Left atrial appendage occlusion for patients with a genuine contraindication to long-term anticoagulation.
• Aspirin is NOT an acceptable alternative for stroke prevention in AF — an outdated practice that persists and leaves patients unprotected.

2. RATE versus RHYTHM CONTROL

• Rate control is appropriate for most older, minimally symptomatic patients: beta-blockers or non-dihydropyridine calcium channel blockers (diltiazem, verapamil — avoid in heart failure) first-line; digoxin as an adjunct or in sedentary patients and those with heart failure. Target a resting rate under about 110 (lenient) or under 80 (strict) depending on symptoms.
• Rhythm control — preferred in younger patients, those with symptoms despite rate control, new-onset AF, heart failure, or where AF is precipitated by a reversible cause. Recent evidence (EAST-AFNET 4) supports early rhythm control within a year of diagnosis to improve outcomes.
• Cardioversion: electrical (synchronised DC) or pharmacological (flecainide or propafenone in structurally normal hearts; amiodarone where there is structural disease). If AF has lasted more than 48 hours or is of unknown duration, anticoagulate for at least 3 weeks beforehand and 4 weeks afterwards, OR exclude left atrial thrombus with transoesophageal echocardiography — otherwise cardioversion can dislodge thrombus and cause a stroke.
• Catheter ablation (pulmonary vein isolation) — highly effective for symptomatic paroxysmal AF, and superior to drugs in selected patients including those with heart failure.

Treat the Underlying Cause and Risk Factors

Thyrotoxicosis, hypertension, heart failure, valve disease, sleep apnoea, obesity, alcohol excess — aggressive risk factor management substantially reduces AF burden and recurrence after ablation.

Digoxin — Uses, Toxicity and Management

Mechanism: inhibits the Na⁺/K⁺-ATPase pump, raising intracellular sodium and thereby intracellular calcium (via the sodium-calcium exchanger) — producing a positive inotropic effect. It also increases vagal tone, slowing conduction through the AV node — which is the basis of its rate-controlling action.

Uses: rate control in atrial fibrillation (particularly with heart failure or in sedentary patients — note it controls resting but not exertional rate) and symptom control in HFrEF (it reduces hospitalisation but does not improve survival).

Digoxin has a NARROW THERAPEUTIC INDEX, and toxicity is common and frequently missed.

Factors precipitating toxicity:

• HYPOKALAEMIA — the most important (potassium competes with digoxin for the pump; hypokalaemia increases binding). Also hypomagnesaemia and hypercalcaemia.
• Renal impairment — digoxin is renally excreted; doses must be reduced. Elderly patients with unrecognised renal impairment are the classic victims.
• Drug interactions — amiodarone, verapamil, quinidine, spironolactone, macrolides and itraconazole all raise digoxin levels.
• Hypothyroidism; low body weight; hypoxia.

Clinical features of toxicity:

Note the "reverse tick" or "Salvador Dali" sagging ST depression is a sign of digoxin EFFECT, not toxicity — it occurs at therapeutic levels and does not require action.

Management of digoxin toxicity:

1. STOP digoxin.

2. Correct electrolytes — particularly potassium and magnesium. (Note: in acute massive overdose, hyperkalaemia occurs and is a marker of severity; calcium must be avoided in that setting because of the risk of precipitating fatal arrhythmia.)

3. Continuous cardiac monitoring; treat bradyarrhythmias with atropine and temporary pacing if needed.

4. DIGOXIN-SPECIFIC ANTIBODY FRAGMENTS (Fab, "Digibind") — the specific antidote, indicated for life-threatening arrhythmia, haemodynamic instability, severe hyperkalaemia, or massive ingestion. Response is rapid and dramatic.

5. Avoid class Ia antiarrhythmics and cardioversion where possible (which may precipitate ventricular fibrillation in the digoxin-toxic heart); use lidocaine or phenytoin for ventricular arrhythmias if required.

6. Dialysis is ineffective — digoxin has a large volume of distribution.