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Sinus node arrest is a type of impulse formation disorder when the sinus node, the main pacemaker, stops functioning for some period.

Sinoatrial blockade is a type of conduction disorder in which an impulse, having originated in the sinus node, cannot “pass” to the atria. What happens when you stop sinus node. what about sinoatrial blockade , the clinical picture is identical. Moreover, even on an ECG it is not always possible to distinguish one from the other. Therefore, we will combine them into one article.

With these arrhythmias, pauses of varying durations occur both on the ECG and in the work of the heart. This does not mean that if the sinus node stops, the person will instantly die. Nature took care of the safety net.

If the sinus node fails, the atria or atrioventricular node takes over the pacemaker function. If for some reason these two sources also fail, then the last backup sources are the ventricles. However, they cannot maintain adequate heart function for a long time, since the frequency they can generate does not exceed 30-40 beats per minute, and this is at best.

It must be said that a stop of the sinus node can occur for a short time; for such a description of the electrocardiogram to appear, it is enough to record one stop and after a few seconds the native rhythm returns, so it is not always possible to reach backup sources.

There are many reasons for sinus node arrest, and in any case it is necessary to undergo a full cardiac examination, since sinus node arrest does not occur out of the blue, and it is the cause that will determine the treatment tactics and prognosis of the disease.

In conclusion, it must be said that the hearts of some patients throughout their lives work in the atrial rhythm or the rhythm of the atrioventricular junction. These backup sources are quite capable of ensuring adequate functioning of the heart, and if they fail, then there is only one way out - implantation of a pacemaker.

Sinoauricular block heart - a disturbance in the conduction of impulses from the sinus (sinoatrial) node to the atrial myocardium. This type of B. s. usually observed with organic changes in the atrial myocardium, but sometimes occurs in practically healthy people when the tone of the vagus nerve increases. There are three degrees of sino-auricular block (SAB): I degree - slowing down the transition of the excitation impulse from the sinus node and atrium; II degree - blocking the conduction of individual impulses; III degree - complete cessation of impulses from the node to the atria.

The causes of sinoauricular (SA) blockade may be coronary atherosclerosis of the right coronary artery, inflammatory changes in the right atrium with the development of sclerotic changes due to myocarditis, metabolic disorders in the atria, various intoxications and primarily cardiac glycosides, β-blockers, antiarrhythmic drugs quinidine series, poisoning with organophosphorus substances. Immediate causes of SA blockade:

1) the impulse is not generated in the sinus node;

2) the strength of the sinus node impulse is insufficient to depolarize the anterior heart;

3) the impulse is blocked between the sinus node and the right

Sinoauricular block can be I. II. III degree.

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Sinoauricular block

Sinoauricular block. When conduction disturbances of this type occur, the impulse is blocked at the level between the sinus node and the atria.

Etiology and pathogenesis. Sinoauricular block can be observed after heart surgery, in the acute period heart attack myocardium, in case of intoxication with cardiac glycosides, while taking quinidine, potassium supplements, beta-blockers. More often it is recorded with damage to the atrial myocardium, especially near the sinus node, by a sclerotic, inflammatory or dystrophic process, sometimes after defibrillation, very rarely in practically healthy individuals with increased tone of the vagus nerve. Sinoauricular block occurs in individuals of all ages; more often in men (65%) than in women (35%).

The mechanism of sinoauricular blockade has not yet been clarified. The question has not been resolved whether the blockade is caused by a decrease in atrial excitability, or whether the impulse is suppressed in the node itself. In recent years, sinoauricular block is increasingly considered a sick sinus syndrome.

Clinic. Patients with sinoauricular block usually do not show any complaints or experience short-term dizziness during cardiac arrest. Occasionally during long stops hearts Morgagni-Edams-Stokes syndrome may occur.

By palpation of pulse and auscultation hearts loss of heart contractions and a large diastolic pause are detected. Loss of a significant number of heartbeats leads to bradycardia. Rhythm hearts regular or more often irregular due to changes in the degree of blockade, jumping contractions, extrasystole.

There are three degrees of sinoauricular block. With first degree blockade, the time of impulse transition from the sinus node to the atria is prolonged. Such a conduction disorder cannot be registered on an electrocardiogram and is detected only with the help of an electrogram. Second degree sinoauricular block in clinic observed in two versions: without Samoilov-Wenckebach periods and with Samoilov-Wenckebach periods.

First option recognized electrocardiographically by long pauses in which the P wave and the associated QRST complex are absent. If one cardiac cycle falls out, then the increased R-R interval is equal to twice the main R-R interval or slightly less. The value of the R-R interval depends on the number of heartbeats that occur. Usually there is a loss of one sinus impulse, but sometimes there are dropouts after each normal contraction (allorhythmia). Such sinoauricular block (2:1) is perceived as sinus bradycardia. Clinically, it can be determined only after a test with atropine or physical activity by the doubling of the rhythm, or by an electrocardiogram.

Second degree sinoauricular block with Samoilov-Wenckebach periods (second option) has the following features:

1) the frequency of discharges in the sinus node remains constant;

2) a long R-R interval (pause), including a blocked sinus impulse, shorter in duration than the double R-R interval preceding the pause;

3) after a long pause, a gradual shortening of the R-R intervals occurs;

4) the first R-R interval following a long pause is longer than the last R-R interval preceding the pause. In some cases, with this type of blockade, before long pauses (losses of impulses), there is not a shortening, but an extension of the R-R interval.

III degree sinoauricular block characterized by complete blockade of impulses from the sinus node with a persistent rhythm from the underlying parts of the conduction system (more often popping up replacement rhythms from the atrioventricular junction).

Diagnostics. Sinoauricular block should be distinguished from sinus bradycardia, sinus arrhythmia, blocked atrial extrasystoles, and second degree atrioventricular block.

Sinoauricular block and sinus bradycardia can be differentiated using an atropine or exercise test. U sick with sinoauricular block during these tests, the heart rate doubles, and then suddenly decreases by 2 times (elimination and restoration of the blockade). With sinus bradycardia, a gradual increase in rhythm is observed. With sinoauricular block, the extended pause is not associated with the act of breathing, but with sinus arrhythmia it is associated.

With a blocked atrial extrasystole, the electrocardiogram shows an isolated P wave, while with sinoauricular block there is no P wave and the associated QRST complex (i.e., the entire cardiac cycle is missing). Difficulties arise if the P wave merges with the T wave preceding the extended pause.

With atrioventricular block of the second degree, in contrast to sinoauricular block, the P wave is constantly recorded, an increasing increase in time or a fixed time of the P-Q interval is noted, followed by a blocked (without the QRST complex) P wave.

Treatment of sinoauricular block should be aimed at eliminating the cause that caused it (intoxication with cardiac glycosides, rheumatism, ischemic disease hearts and etc.).

With a significant decrease in heart rate, which causes dizziness or short-term loss of consciousness, it is necessary to reduce the tone of the vagus nerve and increase the tone of the sympathetic nervous system. For this purpose, 0.5-1 ml of a 0.1% atropine solution is prescribed subcutaneously or intravenously or in drops (5-10 drops in the same solution 2-3 times a day). Sometimes they give Effect adrenomimetic facilities- zphedrine and drugs isopropylnorepinephrine (orciprenaline or alupent and isadrin). Ephedrine is used orally at 0.025-0.05 g 2-3 times a day or subcutaneously in the form of a 5% solution of 1 ml. Orciprenaline (alupent) is injected slowly into a vein, 0.5-1 ml of a 0.05% solution, intramuscularly or subcutaneously, 1-2 ml, or given orally in tablets of 0.02 g 2-3 times a day. Izadrin (novodrin) is prescribed under the tongue (until complete resorption) 1/g-1 tablet (1 tablet contains 0.005 g) 3-4 or more times a day. It must be remembered that an overdose of these drugs may cause headache, palpitations, tremors of the limbs, sweating, insomnia, nausea, vomiting (see also “Antiarrhythmics”).

In severe cases, especially when Morgagni-Edams-Stokes syndrome occurs, electrical stimulation of the atria is indicated (in acute cases - temporary, in chronic cases - permanent).

Prognosis for sinoauricular block depends on the nature of the underlying disease, as well as on its degree and duration, and the presence of other rhythm disturbances. In most cases, it is asymptomatic and does not lead to severe hemodynamic disturbances. However, if the blockade is accompanied by Morgagni-Edams-Stokes syndrome, the prognosis is unfavorable.

Prevention of sinoauricular blockade is a difficult task, since its pathogenesis is not clear enough. As with other rhythm disturbances, attention should be paid to treatment the underlying disease causing the blockade.

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