Mechanisms of atrial extrasystole
Normally, the main pacemaker is the sinuatrial node (SAN). In atrial extrasystole, an ectopic focus of excitation forms in the atrial myocardium—a kind of irritant that generates an electrical impulse prematurely.
Since this focus is located outside the SAN, the propagation of the depolarization wave through the atria itself is atypical. However, once the premature impulse reaches the atrioventricular node (AVN), its further path does not differ from normal. The excitation passes through the AVN and spreads through the ventricular conduction system via a completely standard route.
On the ECG tracing, this manifests with the following signs:
- A premature contraction is registered.
- The preceding P wave is necessarily altered and deformed, as the atria are excited along a non-standard vector.
- The QRS complex retains its normal shape and remains narrow. This is a critical diagnostic marker indicating that intraventricular conduction is completely unimpaired.
Ventricular extrasystole: excitation phase
In ventricular extrasystole, the ectopic focus is located directly within the ventricular tissue itself. In this case, the propagation mechanism changes dramatically: the excitation covers the ventricular myocardium, completely bypassing the specialized conduction system, particularly the bundle of His.
The movement of the impulse through the working contractile myocardium occurs much slower than through specialized fibers. This deceleration creates a specific pattern on the ECG tracing:
- 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 conduction of the impulse through the contractile tissue of the ventricles.
Rhythm interaction and compensatory pause
Of particular physiological interest is how ventricular extrasystole interacts with the main, normal sinus rhythm. The ectopic focus in the ventricle can function via the mechanism of spontaneous depolarization or re-entry of the excitation wave.
The essence of the compensatory pause phenomenon lies in the temporary refractoriness of the myocardium:
- After the ventricles have contracted under the influence of the premature ectopic impulse, they enter a refractory state.
- At the same time, the SAN continues to operate at its own rhythm and generates the next normal impulse.
- When this sinus impulse descends to the ventricles, they have not yet exited the refractory state. Consequently, they cannot be excited, and one normal contraction naturally "drops out".
The ventricles will respond with a contraction only to the next sinus impulse. Due to this dropped contraction, a full compensatory pause is formed. If the interval combining the pre-extrasystolic and post-extrasystolic periods (the distance from the end of the extrasystole to the start of the next normal contraction) is measured, its duration will be strictly equal to two normal cardiac cycles—that is, the 2 R-R interval.
Briefly: answers to topical questions
What is the mechanism of formation of an incomplete compensatory pause in atrial extrasystole?
The mechanism of formation of an incomplete compensatory pause is due to the retrograde propagation of the ectopic impulse to the atria and the premature "resetting" of the sinuatrial node. The ectopic impulse propagates antegradely to the ventricles and retrogradely reaches the SA node. A "reset" of the node occurs due to the premature impulse, after which the pause includes the time required to prepare a new impulse. As a result, the interval including the extrasystole is only slightly longer than a normal cycle, and the total sum of intervals is less than two normal cardiac cycles.
What is an interpolated extrasystole?
An interpolated extrasystole is a premature heart contraction that occurs during bradycardia very early, immediately following the previous contraction. The main feature of this form is that it does not cause a compensatory pause. In this case, the regular sinus impulse arrives exactly on time because it falls into the period after the myocardial refractoriness has ended.
What are the types of extrasystoles according to the type of allorhythmia?
Allorhythmia represents a regular alternation of premature extrasystoles and normal complexes. According to the type of such alternation, the following forms are distinguished:
- Bigeminy — an extrasystole follows every single regular (normal) impulse.
- Trigeminy — a premature contraction follows every two regular impulses.
- Quadrigeminy — an extrasystole follows every three normal contractions.
To avoid confusing ECG signs: "Atrial — distorted P and narrow QRS, Ventricular — no P and wide QRS, plus a compensatory pause (2 R-R)"
Class and exam questions
Why does the QRS complex remain narrow in atrial extrasystole?
The QRS complex remains narrow because the premature impulse, having originated in the atria, passes through the atrioventricular node and descends to the ventricles via normal pathways of the conduction system. Intraventricular conduction remains undisturbed.
What happens to the P wave in ventricular extrasystole?
In ventricular extrasystole, the atrial P wave preceding the premature complex is absent because the ectopic focus is located in the ventricular myocardium, and excitation encompasses only the ventricles without preceding ventricular contraction.
Why does the phenomenon of a "dropped" normal contraction occur?
The drop-out occurs because the regular normal impulse from the sinuatrial node reaches the ventricles at a time when they are in a refractory (non-excitable) state following the premature contraction from the ectopic focus.
What is the duration of the full compensatory pause?
The duration of the full compensatory pause (including the pre-extrasystolic and post-extrasystolic periods) is equal to the time of two normal cardiac cycles, which corresponds to the 2 R-R interval on the ECG tracing.
What else to study on this topic
- Mechanism of spontaneous depolarization of ectopic foci
- Mechanism of re-entry of the excitation wave
- Changes in the P wave with various localizations of the atrial focus
- Features of excitation propagation through the contractile myocardium
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