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 completely healthy individuals during marked physical exertion or acute emotional stress. Naturally, various diseases also serve as a frequent cause of premature impulses. In laboratory settings, for example, during classic experiments on an isolated frog heart, such rhythm disturbances can easily be modeled by direct electrical stimulation of the muscle tissue.
Depending on the exact location of the ectopic focus (the source of abnormal excitation), there are two main types of arrhythmias:
- Atrial premature contractions.
- Ventricular premature contractions.
Atrial Extrasystole
In this type of arrhythmia, the source of premature excitation is localized directly within the atrial tissue, and most often the ectopic focus is the sinus node itself.
The primary condition for the successful formation of such a contraction is the precise entry of the impulse into a specific temporal window. The myocardial tissue must have already fully recovered from refractoriness (the unexcitable period), but the next regular automatic action potential must not yet have had time to form.
An important electrophysiological distinguishing feature of the atrial type is the nature of the subsequent muscle recovery. The pause that occurs immediately after an atrial extrasystole is absolutely equal in duration to a normal diastolic pause between regular contractions. In normal physiology, this phenomenon is referred to as 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 physiological rule in this case is that premature ventricular excitation does not affect the normal automaticity of the main pacemaker—the sinoatrial (SA) node. The SA node continues to function in its normal rhythm and generates the next normal signal strictly according to the physiological schedule.
Mechanism of Prolonged Compensatory Pause Formation:
- The sinoatrial node timely generates and sends its scheduled impulse.
- This normal signal reaches cardiomyocytes at the exact moment they are in a refractory state caused by the just-occurred ventricular extrasystole.
- As a result, the muscle cells of the atria and ventricles are unable to contract in response to this correct sinus impulse.
- Full myocardial excitability is restored only after the premature contraction has completely finished.
- The heart is forced to skip the current beat and wait for the next impulse from the SA node to respond with a full contraction.
The result of this superimposition of electrophysiological processes is the appearance of a compensatory pause, which lasts significantly longer than the usual intercycle interval. An obvious rhythm irregularity is registered in the heart's activity, but the total heart rate remains unchanged, as the time of the prolonged pause compensates for the shift.
Mechanical Features of Premature Contractions
Premature contractions have distinct features 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 muscle contraction compared to a normal sinus cycle.
The fundamental cause of this hemodynamic phenomenon is the sharp shortening of the diastole duration (the relaxation and filling period). By the time of the sudden onset of the premature contraction, the heart chambers simply do not have time to receive an adequate volume of venous blood. Due to this partial filling, the ventricles physically cannot provide a full ejection of blood, which manifests as a weak contraction force.