Supraventricular tachyarrhythmias in children

Supraventricular (supraventricular) tachyarrhythmias include tachyarrhythmias with the localization of the electrophysiological mechanism above the bifurcation of the His bundle - in the atria, AV junction, as well as arrhythmias with the circulation of the excitation wave between the atria and ventricles. In a broad sense, supraventricular tachyarrhythmias include sinus tachycardia caused by the acceleration of the normal automaticity of the sinus node, supraventricular extrasystole and supraventricular tachycardia (SVT). SVT is the largest part of clinically significant supraventricular tachyarrhythmias in childhood.

Sinus tachycardia is diagnosed when a high-frequency sinus rhythm (heart rate at the 95th percentile and above) is recorded on all resting ECGs. If sinus tachycardia is recorded for 3 months or more, it is considered chronic. Sinus tachycardia occurs with increased psychoemotional arousal, accompanies hyperthermic reactions, hypovolemia, anemia, thyrotoxicosis, and occurs as a result of taking a number of medications. Chronic sinus tachycardia may be a manifestation of persistent neurohumoral regulation of the heart rhythm. The frequency of chronic sinus tachycardia in childhood is unknown.

The term supraventricular heterotopic tachycardia refers to a high-frequency atrial rhythm (at least three consecutive heart contractions) that occurs due to abnormal myocardial excitation. The rhythm source is localized above the bifurcation of the His bundle. Supraventricular tachyarrhythmias originating from the atria or involving atrial tissue as part of the arrhythmogenic substrate are most common in childhood. They are rarely accompanied by the development of life-threatening conditions (except for prolonged attacks of paroxysmal tachycardia), but are often clinically significant. Children complain of a feeling of palpitations and a deterioration in well-being. With prolonged existence, this condition leads to remodeling of the heart with expansion of its cavities, the development of arrhythmogenic myocardial dysfunction and arrhythmogenic cardiomyopathy. Supraventricular tachycardias in the pediatric population occur with a frequency of 0.1-0.4%. The most common electrophysiological mechanisms of supraventricular tachycardia in children are AV reciprocating tachycardia (ventricular pre-excitation syndrome), AV nodal reciprocating tachycardia (20-25% of all supraventricular tachycardias), atrial (10-15% of all supraventricular tachycardias) and AV nodal ectopic tachycardia. Atrial fibrillation is rare in childhood.

Between 30 and 50% of supraventricular tachycardias detected in the neonatal period may spontaneously resolve by the age of 18 months as a result of maturation of the cardiac conduction system structures. When arrhythmias occur at an older age, spontaneous recovery is extremely rare.

In 95% of cases, supraventricular tachycardia is detected in children with a structurally normal heart. Extracardiac factors that provoke the development of supraventricular tachycardia in children include autonomic disorders with a predominance of parasympathetic reactions, connective tissue dysplasia, hereditary predisposition (an aggravated family history of heart rhythm and conduction disorders), psychoemotional instability, diseases of the central nervous system, endocrine pathology, metabolic diseases, acute and chronic infectious diseases, as well as excessive physical activity relative to the child's physical capabilities (especially associated with increased parasympathetic effects on the heart - swimming, diving, martial arts). Age periods of risk for the development of clinically significant supraventricular tachycardia in children are the neonatal period and the first year of life, 5-6 years, puberty.

Pathogenesis

Intracardiac mechanisms of supraventricular tachyarrhythmia development include anatomical and electrophysiological conditions for the occurrence of abnormal electrophysiological mechanisms of cardiac excitation: the presence of additional impulse conduction pathways, foci of abnormal automatism, and trigger zones. The basis of sinus tachycardia is the increased automatism of the sinus node pacemakers themselves. The occurrence of abnormal electrophysiological processes in the myocardium may be due to anatomical causes (congenital cardiac anomalies, postoperative scars). For the formation of the electrophysiological substrate of heterotopic arrhythmia in childhood, the preservation of the embryonic rudiments of the conduction system is important; the role of mediators of the autonomic nervous system has been experimentally demonstrated.

Pathogenesis of supraventricular tachyarrhythmias

Classification of supraventricular tachyarrhythmias

Supraventricular tachyarrhythmias are classified taking into account the localization and characteristics of the electrophysiological mechanism and clinical and electrocardiographic manifestations.

• Supraventricular extrasystole is divided into typical extrasystole and parasystole.
• Extrasystole is divided into atrial (left and right) and nodal.
• A distinction is made between monomorphic (one morphology of the ventricular complex) and polymorphic (polytopic) extrasystole.
• According to their severity, they are divided into single, paired (two consecutive extrasystoles), interpolated or intercalated (an extrasystole occurs in the middle between two sinus contractions in the absence of a compensatory pause), allorhythmia (an extrasystole occurs after a certain number of sinus complexes) - bigeminy (every second contraction is an extrasystole) and trihymeny (every third contraction is an extrasystole), etc.

Classification of supraventricular tachyarrhythmias

Symptoms of supraventricular tachyarrhythmias

The clinical manifestation of chronic sinus tachycardia is a sensation of palpitations, which increases with exertion. This arrhythmia is typical for school-age children, and is often encountered during puberty. Despite the constantly increased heart rate (100-140 per minute), children experience palpitations during emotional and physical stress. Other symptoms include difficulty falling asleep, sleepwalking and sleep talking, neurotic reactions, tics, stuttering, and increased sweating of the palms and feet. Girls suffer from this type of rhythm disorder 3 times more often than boys. An ECG records craniocaudal (sinus) morphology of the P wave. Chronic sinus tachycardia should be differentiated from heterotopic tachycardia from the upper part of the right atrium, which, as a rule, is absent from complaints of a sensation of palpitations and reveals rhythm rigidity.

Symptoms and diagnosis of supraventricular tachyarrhythmias

Treatment of supraventricular tachyarrhythmias

Emergency therapy of paroxysmal supraventricular tachycardia is aimed at interrupting the paroxysm of tachycardia and normalizing hemodynamics.

Stopping an attack begins with vagal tests: turning upside down, handstand, Aschner's test, Valsalva's test, carotid sinus massage, pressing on the root of the tongue. In young children, turning upside down for several minutes is most effective.

The tactics of emergency drug therapy depends on the electrophysiological substrate of paroxysmal supraventricular tachycardia. Emergency therapy of paroxysmal supraventricular tachycardia with a narrow QRS complex, as well as with a wide QRS due to functional blockade of the His bundle branches, begins with intravenous administration of adenosine phosphate (1% solution intravenously by jet stream: up to 6 months - 0.5 ml, from 6 months to 1 year - 0.8 ml, from 1 year to 7 years - 1 ml, 8-10 years - 1.5 ml, over 10 years - 2 ml). If ineffective, the administration can be repeated twice more with an interval of at least 2 minutes. Adenosine phosphate slows conduction through the AV node, interrupts the re-entry mechanism and helps restore sinus rhythm. The drug can cause cardiac arrest, so it should be administered under conditions that allow resuscitation if necessary.

Treatment of supraventricular tachyarrhythmias

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