What is sinoatrial blockade of the 2nd degree. Sinoauricular (sinoarterial) blockade: features of the diagnosis and treatment of the disease

Sinus arrest- this is a type of violation of the formation of an impulse, when sinus node- the main pacemaker, for some period ceases to function.

Sinoatrial blockade- this is a type of conduction disorder in which an impulse, originating in the sinus node, cannot "pass" to the atria. What's when you stop sinus node. what at 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 various durations occur both on the ECG and in the work of the heart. This does not mean that when the sinus node stops, a person will instantly die. Nature took care of the safety net.

In case of failure of the sinus node, the function of the pacemaker is taken over by the atria or the atrioventricular node. If, for some reason, these two sources fail, then the ventricles are turned on as the last backup sources. However, they cannot maintain adequate heart function for a long time, since the frequency that they can generate does not exceed 30-40 beats per minute, and this is at best.

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

There are many reasons for stopping the sinus node, and in any case, it is necessary to undergo a complete cardiological examination, since the stop of the sinus node does not occur out of the blue, and it is the reason that will determine the tactics of treatment and the prognosis of the disease.

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

Sinoauricular blockade heart - a violation of the impulse 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 with an increase in tone vagus nerve. There are three degrees of sino-auricular blockade (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 conduction of impulses from the node to the atria.

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

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

2) the strength of the impulse of the sinus node is insufficient for the depolarization of the ppedserdia;

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

Sinoauricular blockade can be I. II. III degree.

+ Means of treatment

Sinoauricular blockade

Sinoauricular block. In violation of the conduction of this type, the impulse is blocked at the level between the sinus node and the atria.

Etiology and pathogenesis. Sinoauricular blockade can be observed after heart surgery, in the acute period heart attack myocardium, with intoxication with cardiac glycosides, against the background of taking quinidine, potassium preparations, 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 vagal tone. Sinoauricular blockade is observed in persons of all ages; in men more often (65%) than in women (35%).

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

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

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

There are three degrees of sinoauricular blockade. With blockade of the first degree, the time of transition of the impulse 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. Sinoauricular blockade of the II degree in clinic observed in two versions: without Samoilov-Wenckebach periods and with Samoilov-Wenckebach periods.

First option It is recognized electrocardiographically by long pauses in which the P wave and the QRST complex associated with it are absent. If one cardiac cycle falls out, then the increased R-R interval is equal to twice the main R-R interval or somewhat less. The value of the interval R-R depends on the number of dropped heart beats. Usually there is a loss of one sinus impulse, but sometimes there is a loss after each normal contraction (allorhythmia). This 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 onset of a doubling of the rhythm, or by an electrocardiogram.

Sinoauricular block II degree with Samoilov-Wenckebach periods (second variant) 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, is shorter in duration than the doubled R-R interval preceding the pause;

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

4) the first R-R interval following the long pause is longer than the last R-R interval preceding the pause. In a number of cases, with this variant of the blockade, before long pauses (dropouts of impulses), there is not a shortening, but a lengthening of the R-R interval.

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

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

Sinoauricular block and sinus bradycardia can be differentiated using atropine or exercise testing. At sick with sinoauricular blockade in these tests, doubling occurs heart rate, and then its sudden decrease by 2 times (elimination and restoration of the blockade). With sinus bradycardia, there is a gradual increase in the rhythm. With sinoauricular blockade, an extended pause is not associated with the act of breathing, but with sinus arrhythmia it is.

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

In second-degree atrioventricular block, in contrast to sinoauricular block, a 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 QRST complex) P wave.

Treatment of sinoauricular blockade 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, against which dizziness or a short-term loss of consciousness occur, 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% solution of atropine is prescribed subcutaneously or intravenously or in drops (in the same solution, 5-10 drops 2-3 times a day). Sometimes they give the effect adrenomimetic facilities- zfedrine and drugs isopropylnorepinephrine (orciprenaline or alupent and isadrin). Ephedrine is applied orally at 0.025-0.05 g 2-3 times a day or subcutaneously as 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. Isadrin (Novodrin) is prescribed under the tongue (until complete resorption) at 1/g-1 tablet (0.005 g per tablet) 3-4 or more times a day. It must be remembered that in case of an overdose of these drugs, headache, palpitations, trembling of the limbs, sweating, insomnia, nausea, vomiting (see also "Antiarrhythmics").

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

Prognosis for sinoauricular block depends on the nature of the underlying disease, as well as on its degree and duration, 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-Edems-Stokes syndrome, the prognosis is poor.

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

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