Arrhythmias in children and their treatment

A relatively common cause of circulatory failure in pediatric practice is the development of various types of heart rhythm disturbances - arrhythmia in children. It is known that the highest activity in generating impulses is possessed by the pacemaker cells of the sinoatrial (SA) node, which is the source of impulse formation or first-order automatism.

Pacemaker cells located in the atria, atrioventricular (AV) junction, and His system are referred to as 2nd and 3rd order automaticity centers. Normally, they are suppressed by impulses emanating from the SA node, but under certain circumstances they can take on a leading role, causing disturbances in the heart rhythm and reducing the efficiency of its pumping function, which is why arrhythmias can cause AHF.

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Symptoms of arrhythmia in children

When arrhythmia occurs in children, they complain of increased heartbeat, anxiety, weakness. Not only the heart rhythm is disturbed, but also blood circulation (decreased blood pressure, microcirculation disorders). Arrhythmia in children is often detected accidentally during a medical examination, since patients do not experience painful sensations. Particular attention is drawn to arrhythmias accompanied by circulatory failure, hypoxic encephalopathy (for example, in the form of Morgagni-Adams-Stokes attacks with complete AV block). Stable, serial ventricular extrasystoles (bigeminy, trigeminy), AV and ventricular tachycardia, ventricular fibrillation and flutter, tachyform atrial fibrillation also have a significant effect on blood circulation.

What types of arrhythmias are there in children?

There is no generally accepted classification of arrhythmia in children yet, but one can use the classification of A.P. Meshkov (1996), which forms 2 groups based on the source of impulse generation:

1st group - nomotopic arrhythmias in children (from the SA node):

• sinus tachycardia,
• sinus bradycardia.

Group 2 - ectopic arrhythmias in children (other sources of impulses):

• passive (replacing the absence of impulses from the SA node):
  • slow AV rhythm,
  • slow idiopathic (ventricular) rhythm;
• active (manifesting, in addition to impulses from the SA node, competitively):
• accelerated ectopic rhythms originating from different parts of the heart,
  • extrasystole and parasystole,
  • atrial fibrillation and flutter,
  • ventricular fibrillation and flutter.

Arrhythmias in children of the 1st group usually occur as a result of changes in the autonomic regulation of the heart (neuroses, stress, etc.), which is why they are also called functional arrhythmias. The second group is related to the organic nature of arrhythmias associated with toxic, inflammatory or morphological damage to the heart. Organic arrhythmias include rhythm disturbances in Wolff-Parkinson-White syndrome (WPW), SA node weakness syndrome and other types of premature ventricular excitation. In their genesis, additional (shunting) pathways for impulse conduction from the atria to the ventricles bypassing the SA node (Kent, James, etc. - there are 6 of them in total) play a significant role. ECG signs of these anomalies are shortening of the PQ segment < 0.09 s, the presence of a sigma wave on the ascending limb with widening of the ARS complex and a decrease or inversion of the T wave.

Treatment of arrhythmia in children

Determining the pulse helps in diagnosing arrhythmias, although an accurate diagnosis is only possible with recording and analysis of the ECG.

A distinction is made between paroxysmal and chronic arrhythmias in children. Paroxysmal rhythm disturbance is understood as sudden onset and disappearance. A distinctive feature of paroxysmal supraventricular tachycardia (PVT) is the presence of a correctly positioned P wave and a narrow (< 0.12 s) QRS wave on the ECG. The diagnosis is established if there are more than 3 complexes with a heart rate of 120 to 300 per minute on the ECG. Sinus PVT is more often observed in children. In AV nodal PNT, the P waves may be ahead of the complex (2Я8 (the rhythm source is in the upper part of the AV node), merge with it, or follow it (in the middle and lower parts of the node, respectively). Only in PNT are reflex therapy methods effective (ice to the cheek, unilateral irritation of the carotid sinus, Aschner's reflex, Valsalva's reflex - straining, vomiting). Beta-blockers are effective intravenously by slow jet. Novocainamide (at a dose of 5 mg/kg) with mesaton (0.1 ml for each year of life; no more than 1 ml in total) can be used to prevent possible arterial hypotension.

Cordarone can be used in a dose of 8-10 mg/kg-day) in 2-3 doses orally for 5-6 days with subsequent reduction of the dose by 2 times. During the administration and 15-20 days after the cancellation of cordarone, attacks of paroxysmal tachycardia do not recur. Unfortunately, this drug has a number of side effects that limit its long-term use (for example, the development of fibrosing alveolitis, hypothyroidism or thyrotoxicosis).

Cardiac glycosides (digoxin in a saturation dose of 0.05 mg/kg administered fractionally over 24-36 hours) are used to treat supraventricular tachycardia in children. Digoxin is usually prescribed after stopping an attack of supraventricular tachycardia with antiarrhythmic drugs for several days or weeks. Their use is most often indicated in infants with low initial blood pressure and decreased myocardial contractility. In newborns, the saturation dose of digoxin is lower - 0.01-0.03 mg/kg.

The effect of antiarrhythmic treatment is enhanced by the administration of potassium preparations to children in the form of a polarizing mixture, asparkam, and then non-steroidal anabolics (potassium orotate, riboxin), as well as the use of sedative therapy, neurometabolic agents (piracetam, aminalon, pyriditol, phenibut, etc.) in the presence of vegetative-vascular dystonia in patients.

In case of repeated and frequent attacks of PNT, it is necessary to resort to electropulse therapy, as well as surgical destruction of additional conduction pathways in the myocardium.

Cardiac glycosides and verapamil (finoptin, etc.) are contraindicated in WPW syndrome and other types of premature ventricular contraction.

Supraventricular extrasystoles also differ from ventricular ones by the presence of the P wave. Extrasystoles that occur more often than 6-15 times per minute require targeted treatment. Obzidan (0.1 mg/kg intravenously by jet stream) or finoptin (0.1 mg/kg intravenously by jet stream), potassium preparations, sedatives are used.

Ventricular extrasystoles are characterized by the absence of the P wave and extended (> 0.12 s) QRS complexes. They can be monotopic; allorhythmias (bigeminy, trigeminy), polyfocal and salvo extrasystoles also belong here. Patients require emergency therapy with lidocaine (1-2 mg/kg is administered as a bolus, then 2 mg/kg per hour by drip). If there is tolerance to lidocaine, electropulse therapy is prescribed followed by the administration of cordarone (2-3 mg/kg by drip, then orally).

Ventricular paroxysmal tachycardia (VPT) is characterized by the appearance on the ECG of 3 or more widened (>0.12 s) deformed QRS complexes without a preceding or superimposed P wave on the QRS complex. Bidirectional and fusiform (pirouette) forms of VPT may be observed. Lidocaine is the most effective; mexitil, rhythmilene, cordarone, or novocainamide may be used. If ineffective, electropulse therapy is prescribed, since in the absence of rhythm conversion, arrhythmogenic collapse and pulmonary edema inevitably develop. Cardiac glycosides are not indicated in the treatment of VPT.

Paroxysmal atrial fibrillation (PAF) is caused by atrial flutter (220-350 beats per minute) or flickering (> 350 beats per minute) and an independent, slower rhythm of the ventricles. According to the frequency of ventricular contractions, brady-, normo- and tachyforms of PA are distinguished. In atrial flutter, the ECG shows a separate regular rhythm of P waves instead of P waves, reflecting the occurrence of an impulse in the atrium, and periodic occurrence of QRS complexes associated with the T wave (or not). The ventricular rhythm can be regular or irregular. In atrial fibrillation, "heart delirium" with a pulse deficit in the periphery is clinically observed. There are no P waves on the ECG, the duration of RR varies.

According to M.A. Shkolnikova et al. (1999), digoxin is used in the treatment of MPA (especially in tachyform MPA) in combination with antiarrhythmic agents of subgroup 1a (quinidine, novocainamide, kinilentin, ajmaline) or 1c (ritmonorm, flecainide). Anaprilin, finoptin, amiodarone, and sotalol are used to control the ventricular rhythm in chronic forms of atrial fibrillation in children. In bradyforms of MPA, the use of antiarrhythmic drugs and cardiac glycosides is strictly not indicated.

Of great importance is the use of membrane-stabilizing (cytochrome C, polarizing mixture - potassium, glucose), antioxidant (dimephosphone, aevit, etc.) and neurometabolic (trental, coenzymes, cavinton, cinnarizine, nootropics, etc.) drugs that affect the neurovegetative and metabolic mechanisms of arrhythmia. The particular effectiveness of dimephosphone (100 mg/kg per day) intravenously by drip (course duration 10-14 days) in the complex therapy of arrhythmia in children was noted by L. A. Balykova et al. (1999).

General principles of arrhythmia treatment:

• etiotropic treatment of arrhythmia in children, including psychotherapy, sedatives for neuroses, drugs that stabilize neurovegetative regulation, as well as treatment of diseases that cause organic damage (myocarditis, myocardial ischemia, rheumatism, intoxication, infections, etc.);
• basic treatment of arrhythmia in children, which means restoration of electrolyte (primarily potassium-sodium) and energy balance (panangin, polarizing mixture, potassium orotate, etc.) in cardiomyocytes;
• drugs belonging to different groups of antiarrhythmic agents.

1. sodium channel blockers or membrane depressants (subgroup 1a - quinidine, novocainamide. 1b - lidocaine. 1c - etacizine, etc.);
2. beta-blockers that limit the sympathetic effect on the heart (propranolol, cordanum, trazicor, etc.);
3. drugs that increase the repolarization phase and the duration of the action potential (cordapon, etc.);
4. calcium channel blockers (veragtamil, diltiazem, etc.);
5. mixed-action drugs (ritmonorm, bonnecor, etc.).

Bradycardia is registered at heart rate> 60 per minute. It can be in healthy adults and adolescents. In pathology, bradycardia is distinguished by the source of automatism:

1. Sinus: myogenic, neurogenic.
2. Replacement idiopathic or AV rhythm.
3. Ventricular rhythm: sinoatrial block 2:1 (II degree), complete AV block (III degree).

In sinus bradycardia, there is always a positive P wave before the QRS complex on the ECG. Neurogenic sinus bradycardia is observed in autonomic dysfunction, gastrointestinal diseases, meningitis and is accompanied by a distinct respiratory arrhythmia (an increase in heart rate is detected during inhalation, and a decrease in heart rate during exhalation). In myogenic bradycardia with myocardial damage, there is no connection with the respiratory cycle or breath holding. In addition to myocardial inflammation (past or present), myogenic bradycardia can be caused by the toxic effects of drugs. With a pulse of less than 40 per minute, the probability of sinus bradycardia is low.

In the treatment of sinus bradycardia, atropine is usually used in a dose of 0.05-0.1 ml of 0.1% solution per 1 year of life (no more than 0.7 ml per injection) subcutaneously, intravenously; it can also be prescribed orally (1 drop per 1 year of life). Belladonna extract, becarbon, besalol can also be used. Bellaspon and belloid should not be prescribed.

Replacement bradycardia, such as AV rhythm, may occur with sick sinus syndrome. SA block 2:1 on the ECG is represented by the rhythmic loss of every 2nd complex of the pulmonary artery block with the preservation of a single P wave at a strictly defined interval.

Complete AV block is accompanied by two independent rhythms: a more frequent rhythm of the atria (P wave) and a rare rhythm of the ventricles. There are no patterns in the relationship between the P and QRS waves.

Stable heart block accompanied by Morgagni-Adams-Stokes attacks (loss of consciousness, convulsions) and bradycardia of ventricular origin is an indication for the use of an endocardial pacemaker. In the preoperative period, the required cardiac output can be maintained with dobutamine, isadrine, sometimes adrenaline, and also by using a transesophageal pacemaker. The same treatment regimen is used for sick sinus syndrome accompanied by bradycardia.

The probability of an antiarrhythmic effect for most antiarrhythmic drugs is 50% and only in a few clinical forms of arrhythmia does it reach 90-100%.

All antiarrhythmic agents for the treatment of arrhythmia in children are contraindicated in stage III AHF, SA block, grade II and III AV block, and sick sinus syndrome. In these cases, cardiotonics, M-anticholinergics (atropine), and pacemakers are used. In addition, antiarrhythmic agents that contain glycosides can themselves cause an arrhythmogenic effect, which often develops against the background of hypokalemia and severe myocardial damage (inflammatory or toxic-metabolic genesis).