No P waves, a restless baseline of fibrillation waves, and an irregularly irregular ventricular rhythm at the rate the AV node lets through.
On the trace
The tracing above is untreated atrial fibrillation with a rapid ventricular response. Each recording is new, so your numbers will differ a little from the ones here. Turn on the Normal switch under the tracing to draw a normal ECG in grey behind it. Every grey beat has a P wave. No trace beat has one.
- Look for a P wave in V1 and II. There is none. In its place the baseline never rests: fibrillation waves (f waves). They are uneven, about 1 mm in II, aVF and V2, and smaller in V1 and the lateral leads. No two are the same.
- Measure several R-R intervals. Here they run from about 310 ms to about 870 ms. Consecutive intervals differ by about 180 ms on average.
- Check the intervals for a pattern. There is none, over any number of beats. That is what "irregularly irregular" means.
- Count the QRS complexes in the 10-second strip. About 18: multiply by 6 for a mean rate of about 108 per minute. The readout's heart rate changes with every beat, because each R-R is different.
- Measure the QRS. 96 ms, narrow, with a normal axis of 59°. The activity is above the AV node, so the ventricles conduct normally.
- Find any wide beat. A beat that ends a short R-R after a long one can have an RBBB shape. Not every recording has one.
How to recognise it
| Feature | Value | On this tracing |
|---|---|---|
| P waves | Absent, replaced by f waves | f waves about 1 mm in II, aVF and V2 |
| Baseline | Restless, never repeating | Best seen in II, aVF and V1 |
| Rhythm | Irregularly irregular | R-R about 310 to 870 ms |
| Ventricular rate | The rate the AV node passes | About 108 per minute: a rapid ventricular response |
| QRS | Narrow, unless there is a bundle branch block, aberrancy or an accessory pathway | 96 ms |
The 2023 ACC/AHA and 2024 ESC guidelines diagnose AF from these features. A 12-lead ECG is enough, or a single-lead strip of 30 seconds or more.
A ventricular rate over 100 is a rapid ventricular response. Under 60 is a slow ventricular response. The forms beside the title show both, and a controlled rate between them.
Mechanism
In normal atria one wave of activation starts at the SA node and crosses both atria. That one wave draws the P wave.
In atrial fibrillation, many small wavelets run through the atria at the same time. Each wavelet turns into tissue that has just recovered, so the activity never stops. No single wave crosses the atria, so there is no P wave. The f waves are the sum of the wavelets.
The AV node receives about 350 to 600 impulses per minute. It cannot conduct all of them. An impulse that arrives while the node is still refractory fails, but it goes part of the way in. That leaves the node refractory for longer (concealed conduction). Which impulse conducts next therefore depends on the last ones, and the ventricular rhythm has no pattern.
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Why the atria can hold it
A wavelet needs a length of tissue: its conduction velocity × its refractory period (the wavelength). Atria that are large, or that have a short wavelength, hold enough wavelets for AF to continue. A normal atrial wavelength is about 14 cm. AF can be started when it falls below about 8 cm (Rensma, 1988).
These make the wavelength shorter, or the atria larger:
- Dilation, from mitral valve disease, heart failure or hypertension.
- Fibrosis, which slows conduction.
- Vagal tone, which shortens the atrial refractory period.
- AF itself. After hours to days of AF, the atrial refractory period shortens (electrical remodelling). AF begets AF (Wijffels, 1995).
What starts it
Most AF starts with premature atrial beats. Many come from muscle in the pulmonary veins. A premature beat that arrives in atria with a short wavelength can break up into wavelets, and AF starts.
Coarse and fine
Fewer, larger wavelets draw coarse f waves. More, smaller wavelets draw fine ones. Long-standing AF is often fine. The size of the f waves does not change management.
Wide beats in AF
After a long R-R interval the right bundle's refractory period is longer. A beat that arrives soon after can find the right bundle not yet recovered, and it is conducted with an RBBB shape (Ashman's phenomenon). A run of these beats can look like VT.
Pre-excited AF
An accessory pathway is not slowed like the AV node. In AF it can conduct impulses to the ventricles at 250 per minute or more. The result is fast, irregular and wide, with a QRS that changes from beat to beat. Do not give AV nodal blockers. They can make it faster.
Regular AF
AF with a regular, slow ventricular rhythm means the AV node has stopped conducting. A junctional or ventricular escape rhythm drives the ventricles. Digoxin toxicity is a common cause.
Fast AF can look regular
At a fast rate the R-R intervals are short, so the differences between them are small. Rapid AF can then look regular and be called SVT. Measure several R-R intervals before you decide. In SVT they are the same. In AF they never are, and the baseline has f waves.
Paroxysmal, persistent, permanent
AF is classed by how long it lasts. Paroxysmal AF stops on its own within 7 days. Persistent AF lasts longer than 7 days, or needs cardioversion to stop. Permanent AF is AF that the patient and the clinician decide not to try to stop.
Why a score decides anticoagulation
The stroke risk in AF is very different from one patient to the next: about 1.5% a year at age 50 to 59, and more than 20% a year after 80. A score such as CHA₂DS₂-VA finds the patients whose risk is low, so that anticoagulation is not given to them. Everyone else gets it. The score does not use the rate, the symptoms or the type of AF. Atria that are back in sinus rhythm still carry the risk.
The drugs
Rate control:
- Beta-blockers, and diltiazem or verapamil, slow the AV node directly.
- Digoxin is weaker and slower to act. Add it to one of the others, or use it when they are not tolerated.
- Amiodarone slows the rate and also helps keep sinus rhythm. It is useful in heart failure.
- Too much of any of them causes bradycardia and AV block. Some patients need a pacemaker before the rate can be controlled.
Rhythm control:
- Flecainide and propafenone (class Ic) work in paroxysmal AF. Do not give them with structural heart disease. They can change AF into atrial flutter.
- Sotalol, dofetilide, ibutilide and amiodarone (class III) can be given with structural heart disease. They prolong the QT and can cause torsades.
- Amiodarone is the most effective and the most toxic. It increases the effect of warfarin.
Do not give AV nodal blockers in pre-excited AF.
Clinical impact
Many patients tolerate the rhythm itself. The main harms are stroke and, over months, a rate that is not controlled. AF causes about one stroke in five, and the risk increases with age.
Management
Unstable: synchronised cardioversion
Do it for hypotension, ischaemic chest pain, acute heart failure or a decreased level of consciousness. A rapid rate is usually the cause of the instability.
Assess the stroke risk, separately from the rhythm
Use a score such as CHA₂DS₂-VA, and anticoagulate the patients it identifies. The decision does not depend on the rate, the symptoms or whether sinus rhythm returns.
Control the rate
Give a beta-blocker or diltiazem. Add digoxin when these are not enough or not tolerated. Watch for bradycardia and AV block.
Consider rhythm control
Use cardioversion, an antiarrhythmic drug or catheter ablation. Consider it for recent onset, symptoms despite a controlled rate, heart failure, or a younger patient.
Differential
Also irregular and narrow. Look at the baseline: flutter waves repeat exactly, as a sawtooth. The R-R intervals are whole multiples of the flutter cycle.
A fixed ratio makes flutter regular. For a regular, narrow rhythm near 150, look for flutter waves before you call it SVT.
Frequent premature atrial beats make sinus rhythm irregular. Each premature beat has a P wave, and the sinus beats keep their own regular spacing.
Regular, with a P wave before each QRS and a flat baseline between them. AF has neither.
References
- 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation — Circulation, 2024
- 2024 ESC Guidelines for the management of atrial fibrillation developed in collaboration with the EACTS — European Heart Journal, 2024
- Length of excitation wave and susceptibility to reentrant atrial arrhythmias in normal conscious dogs — Circulation Research, 1988
- Atrial fibrillation begets atrial fibrillation — Circulation, 1995