Causes and general classification
The generation of any premature excitation impulse inevitably leads to premature myocardial contraction. This condition is not exclusively a sign of pathology. It can occur even in absolutely healthy individuals against the background of pronounced physical exertion or acute emotional stress. Of course, various diseases also serve as a frequent cause of premature impulses. In laboratory settings, for example, during classical experiments on an isolated frog heart, such a disturbance of the normal rhythm is easily modeled by direct electrical stimulation of the muscle tissue.
Depending on the exact location of the ectopic focus (the source of abnormal excitation), two main types of disorders are distinguished:
- Atrial premature contractions.
- Ventricular premature contractions.
Atrial extrasystole
In this type of disorder, the source of premature excitation is localized directly in the atrial tissue, with the sinus node itself most often acting as the ectopic focus.
The main condition for the successful formation of such a contraction is the exact fall of the impulse into a specific time window. The myocardial tissue must already have fully emerged from the refractory state (the period of non-excitability), but at the same time, the next normal automatic action potential must not yet have had time to form.
An important electrophysiological hallmark of the atrial type is the nature of the subsequent muscle tissue rest. The pause that occurs immediately after the atrial extrasystole is absolutely equal in duration to the usual normal diastolic pause between regular contractions. In normal physiology, this phenomenon is called an incomplete compensatory pause.
Ventricular extrasystole and pause formation
The ventricular type is characterized by the location of the ectopic focus in the lower parts of the conduction system — most often in the atrioventricular (AV) node. The basic rule of physiology in this case is that premature ventricular excitation does not affect the normal automatism of the main rhythm pacemaker — the sinoatrial node (SA node). The SA node continues to function in its usual rhythm and generates the next normal signal strictly according to the physiological schedule.
Mechanism of formation of a prolonged compensatory pause:
- The sinoatrial node timely generates and sends its scheduled impulse.
- This normal signal reaches cardiomyocytes at the exact moment when they are in a refractory state caused by the recently occurred ventricular extrasystole.
- As a result, the muscle cells of the atria and ventricles are unable to respond with a contraction to this correct sinus impulse.
- Full myocardial excitability is restored only after the premature contraction is completely finished.
- The heart is forced to skip the current beat and wait only for the next impulse from the SA node to respond to it with a full contraction.
The result of this overlapping of electrophysiological processes is the appearance of a compensatory pause, which lasts significantly longer than the usual intercycle interval. Clear rhythm irregularity is recorded in heart activity, but the total heart rate remains unchanged, as the time of the prolonged pause compensates for the occurred shift.
Mechanical features of premature contractions
Premature contractions have pronounced specifics not only in electrical activity but also in the mechanical work of the myocardium. Regardless of the type, any extrasystole is always characterized by marked weakness of muscular contraction compared to the normal sinus cycle.
The fundamental cause of this hemodynamic phenomenon is a sharp shortening of diastole time (the period of relaxation and filling). By the moment the premature contraction suddenly begins, the heart chambers simply do not have time to receive a sufficient volume of venous blood. Due to such partial filling, the ventricles physically cannot provide a full ejection of blood, which is visualized as the weak force of the contraction itself.
Briefly: answers to topical questions
What is the difference between a complete compensatory pause and an incomplete one?
A complete compensatory pause differs from an incomplete one in duration and the mechanism described in sources for ventricular extrasystole.
| Characteristic | Complete compensatory pause | Incomplete compensatory pause |
|---|---|---|
| Duration | Following a ventricular extrasystole, the pause lasts longer than usual; the interval combining the pre-extrasystolic and post-extrasystolic periods equals two normal cardiac cycles (2 R-R) | In atrial extrasystole, the pause after the extrasystole lasts as long as a normal pause |
| Type of extrasystole | Ventricular | Atrial; for atrioventricular extrasystole, a general feature is also indicated — an incomplete compensatory pause |
| Mechanism | Premature ventricular excitation does not affect SA node automatism; the next SA node impulse reaches cardiomyocytes in a refractory state, the normal contraction drops out, and the heart responds only to the next SA node impulse | For atrial extrasystole, the condition of occurrence is indicated: premature excitation appears after the end of the refractory period, but before the next automatic action potential |
What ECG changes are characteristic of atrial and ventricular extrasystoles?
The cited sources describe in detail the ECG signs of ventricular extrasystole; for atrial extrasystole, only the nature of the pause is indicated.
| ECG sign | Atrial extrasystole | Ventricular extrasystole |
|---|---|---|
| Pause | The pause after the extrasystole lasts as long as the normal pause: incomplete compensatory pause | As a rule, a complete compensatory pause is recorded |
| QRS complex | Not described in the literature | Significantly widened (≥ 0.12 s), deformed, notched |
| P wave before extrasystole | Not described in the literature | Absent |
| ST segment and T wave | Not described in the literature | Discordant relative to QRS: directed opposite to the main wave of the complex |
In which specific phases of myocardial refractoriness can an extrasystole occur?
The occurrence of an extrasystole is possible in the relative refractoriness phase and during the supernormal excitability period.
- Relative refractoriness phase — occurs during diastole; applying a supra-threshold stimulus causes a premature contraction.
- Supernormal excitability — a short period at the end of repolarization or the beginning of diastole when even a subthreshold stimulus can provoke premature excitation.
Class and exam questions
Why is the force of cardiac contraction noticeably weaker than usual during an extrasystole?
This happens due to a significant shortening of diastole. By the time of the premature contraction, the heart chambers have time to fill with blood only partially, so the output is weak.
Does the total minute heart rate change during ventricular extrasystole?
No, the total heart rate (HR) remains the same. The rhythm irregularity occurring at the moment of the extrasystole is completely smoothed out due to the subsequent prolonged compensatory pause.
Does a ventricular extrasystole exert an inhibitory effect on the activity of the sinoatrial node?
It has absolutely no effect. Premature ventricular excitation does not disrupt the automatism of the sinoatrial node, which continues to timely generate successive impulses in the usual rhythm.
What are the main causes of premature contractions in healthy individuals?
In healthy individuals, such premature contractions can occur against the background of intense physical exertion or during severe emotional stress.
What else to study on this topic
- Phases of absolute and relative refractoriness of cardiomyocytes
- Automatism mechanisms in sinoatrial node cells
- Dependence of heart contraction force on the degree of blood filling (diastole shortening)
- Comparative characteristics of the excitability of the atrioventricular and sinoatrial nodes
- Electrophysiological methods for modeling rhythm disorders in animal experiments
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