The pathogenesis of supraventricular tachyarrhythmias

Intracardial mechanisms for the development of supraventricular tachyarrhythmias include the anatomical and electrophysiological conditions for the onset of abnormal electrophysiological mechanisms of cardiac excitation: the presence of additional pathways for the impulse, foci of abnormal automatism, and trigger zones. The basis of sinus tachycardia is the increased automatism of the pacemaker's pacemakers themselves.

The occurrence of abnormal electrophysiological processes in the myocardium can be caused by anatomical causes (congenital heart anomalies, postoperative scars). For the formation of the electrophysiological substrate of heterotopic arrhythmia in childhood, the preservation of embryonic rudiments of the conducting system is of importance; the role of mediators of the autonomic nervous system has been shown experimentally. The immediate electrophysiological mechanisms of the occurrence of supraventricular tachyarrhythmias are most often re-entry and anomalous automatism. The mechanism of re-entry is due to the circulation of the myocardial excitation pulse. On one branch of the loop, the re-entry excitation propagates antegrade, on the other branch - in the opposite direction, is retrograde. Depending on the size of the loop of the pulse circulation, macro- and micro-re-entry is distinguished. In macro-re-entry, circulation is carried out through anatomical pathways, for example, the Keta bundle in the Wolff-Parkinson-White syndrome. With macro-re-entry, pulse circulation occurs along functional paths. Abnormal automatism occurs in the tissues of the atria or AV-node, sometimes in vessels directly in contact with the atria (hollow, pulmonary veins). Suppression of the sinus node occurs, and ectopic focus becomes the dominant pacemaker.

The emergence and maintenance of the vegetative basis of arrhythmia (extracardiac mechanisms) is caused in childhood by the violation and peculiarities of maturation and functioning of the vegetative centers of rhythm regulation. With chronic sinus tachycardia, there is an increase in sympathetic effects on the heart. In non-paroxysmal supraventricular tachycardia in children without organic heart disease, in contrast, the lack of activating sympathetic effects on the heart (parasympathetic hyperactivity and hypo function of the sympathetic department of the autonomic nervous system) is noted. Paroxysmal supraventricular tachycardia develops against the background of a decrease in the functional reserves of adaptation of the sympathic-adrenal link in the regulation of the heart rhythm. It is considered as a variant of hyperadaptation to stress and other types of extra- and intracardial stimulation in children with special electrophysiological properties of the myocardium and the conduction system of the heart.

Extracardial and intracardial mechanisms are in interaction. In each clinical case, their contribution to the occurrence and maintenance of arrhythmia is individual. In infants and especially the first year of life, the intracardial mechanisms of supraventricular tachyarrhythmias prevail. Which is associated with the anatomical and physiological features of the maturation of the conduction system of the heart. With age until the end of the puberty period, the role of neurohumoral mechanisms increases. The impact of risk factors is mediated by their influence on the humoral regulation of cardiac activity, water-electrolyte and acid-base balance, myocardial metabolism. Inflammatory and degenerative processes in the myocardium can become the basis for the occurrence of supraventricular tachycardia.