Atrial fibrillation
Unstable means shock it. Stable means control the rate, treat the trigger and decide about anticoagulation. Rheumatic mitral stenosis means warfarin, not a DOAC.
A 62-year-old woman admitted with pneumonia has a pulse of 152, irregularly irregular. BP 118/76, SpO₂ 94%, no chest pain. She is breathless but talking. Temperature 38.6 °C.
Is she stable, and what do you treat first?
- 12-lead ECGConfirm AF: irregularly irregular, no P waves. Check for ischaemia and pre-excitation.
- Is she unstable?Shock, fainting, chest pain from ischaemia, or acute heart failure.
- Unstable: synchronised DC cardioversionWith sedation, by a senior. Up to 3 shocks, then amiodarone.
- Look for the triggerSepsis, dehydration, low potassium or magnesium, thyroid, heart attack, PE, alcohol, after surgery.
- Stable: control the rateTreat the trigger. Beta-blocker or diltiazem, or digoxin if heart failure or inactive.
- When did it start?Under 48 hours, or not known. This decides about cardioversion.
- BloodsElectrolytes including magnesium, CBC, TSH, troponin if pain, sugar, creatinine.
- AnticoagulationCHA₂DS₂-VA score and bleeding risk. Rheumatic mitral stenosis: warfarin.
- Shock, collapse, ischaemic chest pain, acute heart failure
- Heart rate above 150 not settling
- Irregular, broad and very fast (pre-excited AF)
- Fever, sepsis or dehydration driving it
- Sudden cold, painful limb or stroke symptoms
- Unstable AF
- Pre-excited AF (WPW)
- Thyrotoxicosis
- Sepsis-driven AF
- Embolic stroke, limb or mesenteric ischaemia
- Rheumatic mitral stenosis
| Unstable | Synchronised DC shock, up to 3 attempts, then amiodarone 300 mg IV |
| Rate target | Resting heart rate below 110 at first |
| Potassium | Keep 4–5 mmol/L (mEq/L). Magnesium above 0.8 mmol/L |
| Cardioversion | Only if onset clearly under 48 hours, or after 3 weeks of anticoagulation (or TOE) |
| Anticoagulation | CHA₂DS₂-VA of 2 or more: anticoagulate. 1: consider |
Check every dose against a current drug reference and your hospital protocol.
On this page
What it is
In atrial fibrillation (AF), the atria quiver chaotically instead of contracting. The AV node lets through some of the impulses at random, so the pulse is irregularly irregular. Two problems follow:
- A fast rate reduces the time the heart has to fill, so BP falls and the lungs congest.
- Clots form in the still left atrium and can travel to the brain (stroke), gut or limbs.
In Pakistan, remember rheumatic heart disease, especially mitral stenosis, in younger patients with AF.
Stable or unstable?
- Shock (low BP, cold, confused)
- Fainting
- Ischaemic chest pain
- Acute heart failure
- Synchronised DC cardioversion with sedation, by a senior
- Treat the trigger
- Control the rate
- Decide about rhythm control and anticoagulation
Fast AF in a septic, dry or bleeding patient is often the body's response to illness. Treat the sepsis, give fluids and correct potassium first. Slowing the heart of a patient who needs that rate can drop the BP further.
Unstable AF
Stable AF: rate control
Bisoprolol by mouth (or IV metoprolol for faster control)
- Digoxin
- Bisoprolol at a low dose once heart failure is treated
Amiodarone IV, senior decision
Irregular, very fast (often above 200), broad complexes that vary in shape. Do not give AV-node blockers (digoxin, verapamil, diltiazem, beta-blockers, adenosine): they can push the rhythm into VF. Call your senior: DC cardioversion if unstable, or procainamide or flecainide if available and stable.
Rhythm control
- Onset clearly under 48 hours: cardioversion (electrical, or flecainide or amiodarone) can be considered by a senior, with heparin cover. Some newer guidelines use a 24-hour limit.
- Over 48 hours or unknown: rate control first. Cardioversion only after 3 weeks of effective anticoagulation, or after a transoesophageal echo shows no clot.
- After any cardioversion, anticoagulate for at least 4 weeks.
Anticoagulation
- Congestive heart failure: 1
- Hypertension: 1
- Age 75 or over: 2
- Diabetes: 1
- Stroke, TIA or clot elsewhere before: 2
- Vascular disease (MI, peripheral arterial disease, aortic plaque): 1
- Age 65–74: 1
Score 2 or more: anticoagulate. Score 1: consider. Older guidelines added a point for female sex (CHA₂DS₂-VASc). Use the calculator.
AF with moderate or severe mitral stenosis or a mechanical heart valve needs warfarin (INR target per valve and cardiology), whatever the score. DOACs are not used in these patients.
- Assess bleeding risk too (for example HAS-BLED), and fix what can be fixed: BP, alcohol, NSAIDs. A high bleeding score is a reason to monitor closely, not usually a reason to withhold anticoagulation.
- Aspirin is not a substitute for anticoagulation in AF.
Investigations
| Test | Why |
|---|---|
| 12-lead ECG | Confirm AF, ischaemia, pre-excitation |
| Potassium, magnesium, calcium | Correct to help control the rate |
| CBC, creatinine, LFTs | Before anticoagulation, drug dosing |
| TSH | Thyrotoxicosis |
| Troponin | Only if chest pain or ischaemic ECG. Fast AF alone can raise it slightly |
| Chest X-ray | Pneumonia, heart failure |
| Echo | Valve disease (rheumatic), heart function, left atrial size |
Common mistakes
- Giving bisoprolol to fast AF caused by septic shock or dehydration.
- Giving digoxin or verapamil to pre-excited AF.
- Cardioverting AF of unknown duration without anticoagulation.
- Starting a DOAC in rheumatic mitral stenosis.
- Using aspirin instead of anticoagulation.
- Forgetting potassium and magnesium.
Frequently asked questions
What is the first-line drug for rate control in AF?
A beta-blocker such as bisoprolol, or diltiazem if a beta-blocker cannot be used and there is no heart failure with a weak heart. Digoxin for heart failure or inactive patients.
When should AF be cardioverted?
Immediately if the patient is unstable. Electively if the onset is clearly under 48 hours, or after 3 weeks of anticoagulation or a transoesophageal echo showing no clot.
Which patients with AF need warfarin rather than a DOAC?
Those with moderate or severe mitral stenosis (usually rheumatic) and those with mechanical heart valves.
What is the digoxin loading dose?
0.5 mg IV or by mouth, then 0.25 mg every 6 hours for 2 doses (total 1 mg), with lower doses in kidney failure and the elderly.
Test yourself
Exam-style questions on this guide, from our two question banks. Choose an answer to see why each option is right or wrong.
1. A patient in AF at 150/min has BP 76/40 and is confused. What is the next step?
Answer: Synchronised DC cardioversion. Adverse features (shock, syncope, ischaemia, heart failure) in a tachyarrhythmia mean electrical cardioversion.
- IV digoxin: Too slow for an unstable patient.
- IV verapamil: Dangerous with hypotension.
- Start apixaban and wait: Instability needs immediate treatment.
- Oral bisoprolol: Too slow, and may worsen hypotension.
2. A 34-year-old woman in AF has a loud first heart sound, an opening snap and a mid-diastolic murmur. Which anticoagulant should be used?
Answer: Warfarin. AF with rheumatic mitral stenosis (or a mechanical valve) needs warfarin. DOACs are for non-valvular AF.
- No anticoagulation as she is young: Mitral stenosis with AF carries a very high stroke risk.
- Aspirin: Inadequate stroke prevention.
- Rivaroxaban: Same problem.
- Apixaban: DOACs are not used with moderate-severe rheumatic mitral stenosis.
3. A patient has an irregular, broad-complex tachycardia at 230/min. Which drugs should be avoided?
Answer: AV-node blocking drugs. Irregular broad complexes at a very fast rate suggest AF with a pre-excitation pathway (WPW). Blocking the AV node can speed conduction down the accessory pathway and cause VF.
- Amiodarone: Not the main concern.
- Oxygen: Not harmful.
- Magnesium: Not harmful.
- Electrical cardioversion: Appropriate if unstable.
4. A 55-year-old has palpitations from AF that started 3 days ago. He is stable and not anticoagulated. Rhythm control is desired. What is needed before cardioversion?
Answer: 3 weeks anticoagulation or TOE. AF > 48 hours (or unknown duration) has risk of left atrial thrombus; before elective cardioversion either anticoagulate for ≥ 3 weeks or exclude LA appendage thrombus by transoesophageal echo. Continue anticoagulation ≥ 4 weeks after (and long-term according to CHA₂DS₂-VASc). AF < 48 h: can cardiovert with heparin cover. Unstable patients → immediate synchronised DC cardioversion.
- Immediate DC cardioversion: Immediate cardioversion after 48 hours risks stroke.
- Aspirin for 1 week: Aspirin is inadequate.
- No anticoagulation needed: Without anticoagulation there is a stroke risk.
5. A 68-year-old with permanent AF has a ventricular rate of 130/min at rest. He has normal LV function and no asthma. What is first-line rate control?
Answer: Bisoprolol. Rate control (target resting < 110/min, lenient) uses beta-blockers or rate-limiting calcium-channel blockers (diltiazem, verapamil — avoid in HFrEF). Digoxin is added or used in sedentary patients or heart failure. Rhythm control (cardioversion, flecainide if no structural heart disease, amiodarone, ablation) for symptomatic patients. Anticoagulate by CHA₂DS₂-VASc regardless of strategy.
- Digoxin first-line: Digoxin is less effective during activity.
- Amiodarone: Amiodarone is a rhythm drug with significant toxicity.
- Flecainide: Flecainide is a rhythm drug, contraindicated after MI.
6. A boy with acute rheumatic fever develops a new murmur. Which murmur is most typical of acute rheumatic carditis?
Answer: Apical pansystolic murmur. Acute rheumatic carditis is a pancarditis; the mitral valve is most affected, causing mitral regurgitation (pansystolic murmur). A soft mid-diastolic Carey Coombs murmur can occur from valvulitis. Mitral stenosis develops years later as fibrosis and fusion progress. Aschoff bodies are typical on histology.
- Mid-diastolic rumble at the apex: Develops after years of chronic rheumatic heart disease.
- Ejection systolic murmur: Not typical in acute disease.
- Continuous machinery murmur: Patent ductus arteriosus.
- Early diastolic murmur at the left edge: Not typical.
7. Three days after starting warfarin without heparin cover, a woman develops painful dark skin patches on her thigh and breast. What is the underlying problem?
Answer: Skin necrosis from falling protein C. Protein C has a short half-life, so it falls before factors II, IX and X when warfarin starts. This causes a brief prothrombotic state, with thrombosis in small skin vessels (fatty areas), especially in people with protein C deficiency. Starting with heparin cover prevents it.
- Heparin-induced thrombocytopenia: Heparin was not given.
- Vitamin K overdose: Would reverse warfarin, not cause necrosis.
- Allergic vasculitis to warfarin dye: Not the mechanism.
- DIC from infection: Not the cause here.
References and dose sources
- ESC 2024 guidelines for atrial fibrillation
- NICE NG196: Atrial fibrillation
- Resuscitation Council UK: tachycardia algorithm
- NICE NG128 — stroke
- Resus Council UK — adult ALS
- Amiodarone dosing: Drugs.com: Amiodarone dosage (see also our amiodarone dose page)
- Bisoprolol dosing: Drugs.com: Bisoprolol dosage (see also our bisoprolol dose page)
- Diltiazem dosing: Drugs.com: Diltiazem dosage (see also our diltiazem dose page)
- Digoxin dosing: Drugs.com: Digoxin dosage (see also our digoxin dose page)
- Apixaban dosing: Drugs.com: Apixaban dosage (see also our apixaban dose page)
- Rivaroxaban dosing: Drugs.com: Rivaroxaban dosage (see also our rivaroxaban dose page)
- Warfarin dosing: Drugs.com: Warfarin dosage (see also our warfarin dose page)
International guidance is linked where it reflects good practice. Where your hospital’s protocol differs, follow your hospital.