Pathophysiological mechanism and classification
Unlike automaticity and conduction disorders, extrasystole relates to disturbances of excitability. This condition is due to the pathological generation of an impulse outside the sinus node — in a heterotopic automaticity focus. Premature depolarization occurs, leading to a premature contraction of the atria or the entire heart.
Topically, all extrasystoles are divided into two large groups:
- Supraventricular: these include atrial and atrioventricular (AV) junctional extrasystoles.
- Ventricular.
If three or more consecutive extrasystoles are recorded on the ECG, this is regarded as a repeating phenomenon rather than a single disturbance. Such a "run" of three or more supraventricular complexes is a formal diagnostic criterion for supraventricular paroxysmal tachycardia.
ECG criteria for atrial extrasystole
To understand the pathology, it is important to remember the normal parameters of the atrial P wave: normally, it has an amplitude of less than 3 mm, a duration of up to 0.12 s, is always negative in lead aVR and positive in most other leads.
In atrial extrasystole, the normal picture changes. The main differential diagnostic signs on the ECG:
- A premature cardiac cycle occurs.
- The P wave is present, but it is deformed — its morphology differs from the patient's normal sinus P wave because the excitation vector originates from a heterotopic focus.
- The QRS complex is unchanged and follows immediately after the P wave.
- An incomplete compensatory pause forms after the premature contraction.
Atrioventricular junctional extrasystole
A special form of supraventricular disorders is atrioventricular junctional extrasystole. The excitation focus is located in the AV junction. The impulse travels to the ventricles via the normal (antegrade) pathway and returns to the atria retrogradely. Because of this, the P wave becomes negative.
There are three ECG variants depending on the timing of chamber excitation:
| Variant | Excitation chronology | ECG signs |
|---|---|---|
| With preceding atrial excitation | Atria are activated before the ventricles | Negative P in II, III, aVF before QRS; shortened P-Q interval (<0.12 s) |
| With simultaneous excitation | Depolarization of the chambers coincides in time | P wave merges with QRS and is not visualized on the ECG |
| With subsequent atrial excitation | The ventricles contract earlier | The negative P wave is located after QRS (superimposed on the ST segment or T wave) |
Functional extrasystole
Extrasystoles can be of both organic and functional origin. Epidemiologically, this is the dominant form of arrhythmias in childhood (40–45% of all cases), with a pronounced peak of manifestation in the prepubertal and pubertal periods against the background of autonomic and hormonal bodily adjustments.
Criteria for the functional nature of the arrhythmia:
- Inconstancy of manifestations.
- Topically, impulses originate from the supraventricular regions or the right ventricle.
- Specific response to exertion: during physical activity or changes in body position, extrasystoles disappear without a trace or their number decreases drastically.
To distinguish an atrial extrasystole from other atrial arrhythmias (e.g., fibrillation), look for the 'early bird' — a premature yet distorted (deformed) P wave followed by the usual narrow QRS complex.
Class and exam questions
How does atrial extrasystole differ from atrial fibrillation?
In atrial fibrillation, the P wave completely disappears, replaced by small f waves, and the rhythm is absolutely irregular (R-R intervals vary). In atrial extrasystole, the P wave is preserved, albeit deformed, and the rhythm disturbance manifests only as a single premature cycle.
How to distinguish atrial tachycardia from atrioventricular tachycardia on an ECG?
In marked tachycardia with a high heart rate, the P wave is often impossible to visualize. Because of this, both forms are combined in clinical practice under the term 'supraventricular paroxysmal tachycardia'.
What pathophysiological mechanism causes paroxysms of supraventricular tachycardia?
The main mechanisms are re-entry of the excitation wave in the AV junction, Wolff-Parkinson-White (WPW) syndrome involving an accessory pathway, as well as the presence of other accessory conduction pathways.
What else to study on this topic
- Ventricular extrasystoles and their topical diagnostics (mimicking bundle branch blocks)
- ECG criteria for atrial fibrillation and flutter
- Differential diagnosis of first-, second-, and third-degree AV blocks
- Re-entry mechanisms and Wolff-Parkinson-White (WPW) syndrome
- Instrumental methods for inducing myocardial ischemia on ECG and EchoCG
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