ECG and Atrial Fibrillation

Atrial fibrillation (AF) begins as paroxysmal AF episodes (spontaneously terminating within 7 days) that are triggered by an atrial arrhythmia:

Atrial premature beats, or
Rapid atrial activity, which is further divided into:

Atrial premature beats in runs (3–5 beats)
Non-sustained atrial tachycardia (<30 s)

The atrial arrhythmia that triggers paroxysmal AF originates from the region of the pulmonary vein ostia. These atrial arrhythmias can sometimes be captured on a 12-lead ECG.

Illustration of atrial fibrillation on ECG highlighting electrical foci at the pulmonary vein ostia as triggers of the arrhythmia.

Atrial premature beats originating from the pulmonary vein ostia can sometimes be identified by the P wave on a 12-lead ECG. These premature beats do not necessarily have to be followed by an AF paroxysm.

Rapid atrial activity originating from the pulmonary vein ostia has a rate of 200–220/min and is often followed by an AF paroxysm. During rapid atrial activity, P waves are almost always concealed within the preceding T wave and are therefore difficult to evaluate on a 12-lead ECG. Rapid atrial activity refers to the above-mentioned

atrial premature beats in runs (3–5 beats) or
non-sustained atrial tachycardia (<30 s).

Diagram of P-wave morphology and atrial premature beats originating from pulmonary vein ostia, highlighting ECG differences between right and left pulmonary veins.

ECG and atrial premature beats from the pulmonary veins
ECG features	Left-sided pulmonary veins	Right-sided pulmonary veins
P-wave width	>120 ms	<120 ms
Amplitude	II/III >1.25	II/III <1.25
Amplitude	I <0.05 mV (mm)	I >0.05 mV (mm)

ECG during an AF episode

On the ECG, P waves are absent, and fibrillatory waves are present. During an AF episode, the atria fibrillate at an irregular rate of 300–600/min. The SA node is suppressed because it is driven by a higher impulse frequency than it can generate—overdrive suppression occurs:
- an electrophysiological phenomenon in which the automaticity of pacemaker cells is suppressed because the pacemaker cells are stimulated at a faster rate than their intrinsic spontaneous rate.
QRS complexes are irregular because the AV node acts as a filter. Irregular atrial impulses at 300–600/min are conducted through the AV node to the ventricles at a lower, irregular rate, most commonly <100/min. The AV node has:

A long effective refractory period (ERP) that prolongs at higher stimulation rates (so-called use-dependent or rate-dependent conduction slowing).
Decremental conduction—the higher the frequency of incoming impulses, the slower their conduction through the AV node.

Rarely (<1 %), the RR interval during an AF episode may be regular.

This phenomenon may occur if the patient has third-degree AV block with AF and a concomitant junctional or ventricular escape rhythm.

Preexcited atrial fibrillation with a short SPERRI below 250 ms and rapid ventricular response on ECG.

ECG and pre-excited AF

Pre-excited AF is AF with a delta wave on ECG. The delta wave indicates that the patient has an anterograde accessory pathway.
An accessory pathway is present in <1 % of the population.
If atrial impulses at 300–600/min were conducted to the ventricles, the patient would develop ventricular fibrillation, which is a life-threatening condition.

This may occur if the patient has AF and a malignant anterograde accessory pathway. The risk of ventricular fibrillation increases if the patient receives drugs that slow conduction through the AV node.

A malignant accessory pathway is defined by the SPERRI parameter (<250 ms).

Diagram of typical atrial flutter with a counterclockwise reentry circuit and characteristic sawtooth flutter waves in ECG leads II, III, and aVF.

ECG and atrial flutter

20 % of patients with AF also have atrial flutter (typical or atypical).
Therefore, one ECG may show AF and another ECG may show atrial flutter in the same patient.
Typical atrial flutter produces characteristic flutter waves in the inferior leads (II, III, aVF), V1, and V6, because the impulse circulates in a re-entry circuit around the right atrium through the cavotricuspid isthmus.
Atypical atrial flutter produces flutter waves that differ from typical flutter because the impulse circulates in a different re-entry circuit. In AF patients, atypical flutter most commonly arises in the left atrium.

ECG and atrial fibrillation
The AF trigger—an atrial arrhythmia (atrial premature beats or rapid atrial activity) originating from the pulmonary vein ostia—can sometimes be captured and localized using a 12-lead ECG.
An AF episode produces irregular fibrillatory waves at 300–600/min and irregular RR intervals on ECG. P waves are absent.
An AF episode may have regular RR intervals if third-degree AV block and a junctional or ventricular escape rhythm are present; this is rare (<1 %).
Pre-excited AF produces a delta wave on ECG during an AF episode. If the accessory pathway is malignant, the patient may develop ventricular fibrillation. A malignant accessory pathway has SPERRI <250 ms.
Atrial flutter produces flutter waves on ECG. 20 % of patients with AF also have atrial flutter; therefore, these arrhythmias may alternate in the same patient.