Mechanisms of Atrial Extrasystole
Normally, the primary pacemaker is the sinoatrial node (SAN). In atrial extrasystole, an ectopic focus of excitation forms in the atrial myocardium—acting as an irritant that generates an electrical impulse earlier than expected.
Because this focus is located outside the SAN, the propagation of the depolarization wave across the atria is atypical. However, once the premature impulse reaches the atrioventricular node (AVN), its subsequent pathway is no different from normal. The excitation passes through the AVN and spreads through the ventricular conduction system via the standard route.
On the ECG, this manifests with the following features:
- A premature contraction is recorded.
- The preceding P wave is modified and deformed because the atria are depolarized along an abnormal vector.
- The QRS complex retains its normal morphology and remains narrow. This is a critical diagnostic marker indicating that intraventricular conduction is completely intact.
Ventricular Extrasystole: Phase of Excitation
In ventricular extrasystole, the ectopic focus is located directly within the ventricular tissue. In this scenario, the propagation mechanism changes fundamentally: excitation sweeps through the ventricular myocardium entirely bypassing the specialized conduction system, particularly the bundle of His.
Impulse propagation through the contractile working myocardium is significantly slower than through specialized fibers. This deceleration creates a specific ECG pattern:
- The atrial P wave is completely absent before the premature complex.
- The ventricular QRS complex becomes high-voltage, significantly widened, and deformed. This complex morphology directly reflects the slow, asynchronous propagation of the impulse through the ventricular working myocardium.
Rhythm Interaction and Compensatory Pause
Of particular physiological interest is how a ventricular extrasystole interacts with the underlying normal sinus rhythm. The ectopic ventricular focus may function via spontaneous phase-4 depolarization or a re-entry mechanism.
The essence of the compensatory pause phenomenon lies in temporary myocardial refractoriness:
- After the ventricles contract in response to the premature ectopic impulse, they enter a refractory state.
- Simultaneously, the SAN continues to fire at its intrinsic rate and generates the next normal impulse.
- When this sinus impulse descends to the ventricles, they have not yet recovered from refractoriness. Consequently, they cannot be excited, and one normal contraction is predictably "dropped."
The ventricles will respond with a contraction only to the subsequent sinus impulse. This dropped contraction creates a full compensatory pause. Measuring the interval encompassing the pre-extrasystolic and post-extrasystolic periods (from the end of the extrasystole to the onset of the next normal contraction) shows its duration equals exactly two normal cardiac cycles—i.e., the 2 R-R interval.