Medicine chapters
Atrial fibrillation and atrial flutter
The two common atrial tachyarrhythmias: causes, irregularly irregular pulse, ECG features (no P waves vs sawtooth flutter waves), complications such as stroke, and management by rate control, rhythm control and anticoagulation.
- AF = chaotic atrial activity at 300–600/min; irregularly irregular pulse, no P waves, irregular narrow QRS; the main danger is stroke from left atrial appendage clot.
- Flutter = a regular re-entry circuit in the right atrium at about 300/min; sawtooth F waves, often 2:1 block giving a rate of 150; best long-term cure is ablation.
- Management rests on three pillars: rate control (beta-blocker, rate-limiting calcium channel blocker, digoxin), rhythm control (cardioversion, antiarrhythmics, ablation) and anticoagulation guided by CHA2DS2-VASc.
On this page
Overview
Atrial fibrillation (AF) is the commonest sustained arrhythmia. It affects about 1–2% of the population and 5–15% of people over 75. Atrial flutter is less common, often coexists with AF, and is managed in a similar way.
Both matter because they cause palpitations, heart failure and, above all, stroke. MCQs test the pulse, the ECG, causes (thyroid!), CHA2DS2-VASc, cardioversion rules and drug choices.
Causes of atrial arrhythmias
Anything that stretches, scars or inflames the atria:
- Cardiac: hypertension (commonest in developed countries), heart failure, ischaemic heart disease, rheumatic mitral valve disease (especially mitral stenosis, common in Pakistan), cardiomyopathy, pericarditis, myocarditis, ASD, after cardiac surgery (about one third of patients).
- Systemic: thyrotoxicosis, alcohol (binge drinking, "holiday heart"), pneumonia and other acute infections, pulmonary embolism, COPD, electrolyte disturbance, obesity, diabetes, sleep apnoea, older age.
- Lone AF: no cause found, usually in younger patients; some have a family history.
Check thyroid function in every patient with new AF. In the elderly, AF may be the only sign of hyperthyroidism.
Atrial fibrillation
Mechanism
Many small wandering re-entry wavelets, often triggered by ectopic foci in the pulmonary veins, activate the atria chaotically at 300–600/min. There is no effective atrial contraction. The AV node lets through only some impulses, so the ventricular rate is irregular, usually 120–180/min untreated.
Classification
| Type | Definition |
|---|---|
| First detected | First time found, whatever the duration |
| Paroxysmal | Stops by itself (or with treatment) within 7 days |
| Persistent | Lasts more than 7 days |
| Long-standing persistent | Continuous more than 1 year, rhythm control still being tried |
| Permanent | Accepted by doctor and patient; no further attempts to restore sinus rhythm |
Clinical features
- About a third have no symptoms.
- Palpitations, breathlessness, fatigue, reduced exercise tolerance, chest pain, dizziness.
- Presentation with stroke or TIA or other embolism (acute limb ischaemia, mesenteric ischaemia).
- Irregularly irregular pulse, varying in volume.
- Pulse deficit: the apical rate (counted at the heart) is higher than the radial rate, because some beats come so early that the ventricle has not filled and no pulse wave reaches the wrist.
- Absent a waves in the JVP; no fourth heart sound (no atrial contraction); varying intensity of S1.
- In mitral stenosis, the onset of AF causes sudden worsening (loss of atrial kick) and the presystolic accentuation of the murmur disappears.
An irregularly irregular pulse is AF (or multiple ectopics). A regularly irregular (grouped) pulse suggests Wenckebach or regular ectopics. The irregularity of AF persists on exercise, whereas ectopic beats often disappear.
ECG findings
- No P waves.
- Fine or coarse fibrillatory (f) waves on an undulating baseline.
- Irregularly irregular RR intervals.
- Narrow QRS (unless bundle branch block or WPW).
Investigations
- 12-lead ECG (Holter or event recorder for paroxysmal AF).
- Thyroid function, electrolytes, renal and liver function, full blood count, clotting (before anticoagulation).
- Echocardiography: valve disease (mitral stenosis), LV function, left atrial size. Transoesophageal echo to exclude left atrial appendage thrombus before early cardioversion.
- Chest X-ray if heart failure or lung disease suspected.
Complications
- Stroke and systemic embolism: blood stagnates in the left atrial appendage and forms clot.
- Heart failure and tachycardia-induced cardiomyopathy (from a persistently fast rate).
- Haemodynamic collapse in stiff hearts (aortic stenosis, hypertrophic cardiomyopathy, mitral stenosis).
- Reduced quality of life, dementia risk, bleeding from anticoagulants.
Management of AF
1. Acute AF
Haemodynamically unstable (shock, syncope, myocardial ischaemia, acute heart failure): urgent synchronised DC cardioversion, with heparin.
Stable:
- Treat the trigger (sepsis, thyrotoxicosis, alcohol, electrolytes).
- Onset clearly under 48 hours: rhythm control is reasonable now: DC cardioversion or drug cardioversion (flecainide if no structural heart disease; amiodarone if structural disease), after starting heparin.
- Onset over 48 hours or unknown: rate control first and anticoagulate for at least 3 weeks before elective cardioversion, or do a TOE to exclude clot and then cardiovert.
- Continue anticoagulation for at least 4 weeks after cardioversion (atrial "stunning" means clot can still form), then decide long-term by CHA2DS2-VASc.
The 48-hour rule: after 48 hours of AF, clot may already be present, so cardioversion needs 3 weeks of anticoagulation first (or a clear TOE), and 4 weeks after.
2. Rate control vs rhythm control
Large studies showed no survival difference between the two strategies; choose by patient.
| Rate control (usual for most) | Rhythm control |
|---|---|
| Older, fewer symptoms, permanent AF | Younger, symptomatic, active patients |
| Failed cardioversion or antiarrhythmics | First episode, reversible cause |
| Beta-blocker or verapamil/diltiazem; digoxin for sedentary patients or with heart failure; combinations if needed | DC cardioversion; flecainide or propafenone (normal heart); sotalol (coronary disease); amiodarone (heart failure, LVH, structural disease) |
| Target resting rate under 110/min (stricter if still symptomatic) | Catheter ablation (pulmonary vein isolation) for paroxysmal or early persistent AF |
| "Ablate and pace" (AV node ablation plus pacemaker) when drugs fail | Pill-in-the-pocket flecainide for infrequent paroxysms |
Digoxin alone controls the rate at rest only (it works through vagal tone). It fails during exercise in active patients; a beta-blocker or rate-limiting calcium channel blocker is preferred.
Flecainide (class Ic) is avoided in coronary artery disease or LV dysfunction because it increases mortality (proarrhythmia). Dronedarone is avoided in heart failure.
3. Anticoagulation (stroke prevention)
Use CHA2DS2-VASc for non-valvular AF:
| Letter | Risk factor | Points |
|---|---|---|
| C | Congestive heart failure / LV dysfunction | 1 |
| H | Hypertension | 1 |
| A2 | Age 75 or over | 2 |
| D | Diabetes mellitus | 1 |
| S2 | Prior stroke, TIA or thromboembolism | 2 |
| V | Vascular disease (MI, peripheral arterial disease, aortic plaque) | 1 |
| A | Age 65–74 | 1 |
| Sc | Female sex | 1 |
- Score 0 (men) or 1 (women, from sex alone): no anticoagulation.
- Score 1 in a man: consider anticoagulation.
- Score 2 or more: offer oral anticoagulation.
A 77-year-old woman with hypertension and diabetes, no previous stroke
Age 75 or over = 2; female = 1; hypertension = 1; diabetes = 1
Score = 2 + 1 + 1 + 1 = 5 → oral anticoagulation advised
- Drugs: DOACs (apixaban, rivaroxaban, edoxaban: factor Xa inhibitors; dabigatran: direct thrombin inhibitor) or warfarin with INR 2.0–3.0. DOACs need no INR checks and have fewer interactions.
- Valvular AF (moderate to severe mitral stenosis or a mechanical valve): warfarin, not a DOAC.
- Antiplatelets (aspirin) should not be used for stroke prevention in AF.
- HAS-BLED estimates bleeding risk (Hypertension, Abnormal renal or liver function, Stroke, Bleeding, Labile INR, Elderly over 65, Drugs or alcohol). A high score means correct the modifiable risks and monitor closely; it is not by itself a reason to withhold anticoagulation.
- Left atrial appendage occlusion if anticoagulation is impossible.
- Reversal: idarucizumab for dabigatran; vitamin K and prothrombin complex for warfarin.
CHA2DS2-VASc: the two "2s" are the two big ones: Age 75 or over and Stroke.
Atrial flutter
Mechanism
A single macro re-entry circuit, typically in the right atrium around the tricuspid annulus, passing through the cavotricuspid isthmus (between the IVC and tricuspid valve). Usually anticlockwise. Atrial rate about 250–350/min, typically 300/min.
ECG findings
- Sawtooth flutter (F) waves, best seen in II, III, aVF (negative in typical flutter) and V1.
- No isoelectric baseline between F waves.
- AV block gives a regular ventricular rate: 2:1 → 150/min (commonest), 3:1 → 100/min, 4:1 → 75/min. Variable block gives an irregular pulse.
- Vagal manoeuvres or adenosine briefly increase the block and unmask the F waves (they do not usually terminate flutter).
A regular narrow-complex tachycardia at exactly 150/min should make you think of atrial flutter with 2:1 block.
Class Ic drugs (flecainide) slow the flutter rate, which can allow 1:1 conduction with a dangerously fast ventricular rate. Give an AV nodal blocker with them.
Management
- Unstable: synchronised DC cardioversion (flutter responds to low energy).
- Stable: rate control (beta-blocker, verapamil, diltiazem), but flutter is harder to rate-control than AF.
- Cardioversion: electrical is most effective; same anticoagulation rules as AF (48 hours; 3 weeks before, 4 weeks after).
- Prevention: sotalol or amiodarone.
- Definitive: catheter ablation of the cavotricuspid isthmus, which cures typical flutter in about 90–95%; AF may still develop later.
- Anticoagulate by the same CHA2DS2-VASc rules as AF.
AF and flutter compared
| Feature | Atrial fibrillation | Atrial flutter |
|---|---|---|
| Atrial rate | 300–600/min, chaotic | About 300/min, organised |
| Atrial waves | Fibrillatory f waves, no P | Sawtooth F waves |
| Ventricular rhythm | Irregularly irregular | Usually regular (fixed block) |
| Typical rate | 120–180 untreated | 150 with 2:1 block |
| Best long-term cure | Pulmonary vein isolation (selected) | Cavotricuspid isthmus ablation |
| Stroke prevention | CHA2DS2-VASc | Same |
AF in Wolff-Parkinson-White syndrome
Impulses can race down the accessory pathway, giving a fast, irregular, broad-complex tachycardia that can degenerate into VF.
- Avoid AV nodal blockers: digoxin, verapamil, diltiazem (and adenosine, beta-blockers). Blocking the node pushes more impulses down the accessory pathway.
- Treat with DC cardioversion if unstable, or flecainide or procainamide if stable. Definitive: ablation of the pathway.
Expect: irregularly irregular pulse and pulse deficit; ECG with no P waves vs sawtooth flutter waves; flutter with 2:1 block at 150/min; thyroid function in new AF; CHA2DS2-VASc scoring and that aspirin is not used; warfarin INR 2–3 and warfarin (not DOAC) for mitral stenosis or mechanical valves; 3 weeks before and 4 weeks after cardioversion; rate control drugs and why digoxin alone fails in active patients; flecainide contraindicated with structural heart disease; avoiding digoxin and verapamil in WPW with AF; and isthmus ablation for flutter.
Quick revision
- AF: no P waves, irregularly irregular RR, atrial rate 300–600.
- Causes: hypertension, heart failure, IHD, mitral stenosis, thyrotoxicosis, alcohol, infection, PE.
- Unstable: synchronised DC cardioversion.
- Over 48 h: 3 weeks anticoagulation (or TOE) before, 4 weeks after cardioversion.
- Rate control: beta-blocker or verapamil/diltiazem; digoxin for sedentary or heart failure.
- Rhythm: flecainide (normal heart), amiodarone (structural disease), ablation.
- CHA2DS2-VASc 2 or more: anticoagulate (DOAC or warfarin INR 2–3); no aspirin.
- Flutter: sawtooth waves, 2:1 block at 150/min, isthmus ablation curative.
- WPW with AF: avoid digoxin and verapamil.
Written by The House Job from standard references (Kumar and Clark's Clinical Medicine).
FAQ
Why is there a pulse deficit in atrial fibrillation?
Some beats come so soon after the previous one that the ventricle has hardly filled. The heart can be heard to beat at the apex, but too little blood is ejected to produce a pulse at the wrist.
Why is aspirin not used to prevent stroke in AF?
Studies show it gives little protection against AF-related stroke while still increasing bleeding. Oral anticoagulants are effective.
When can AF be cardioverted without 3 weeks of anticoagulation first?
When the AF has clearly lasted under 48 hours, or when transoesophageal echo shows no clot in the left atrium; heparin is still given and anticoagulation continued afterwards.
Why are digoxin and verapamil dangerous in AF with WPW?
They block the AV node, so more impulses pass down the accessory pathway, which can speed the ventricular rate and trigger ventricular fibrillation.