atrial tachycardia. Atrial heart palpitations: features and treatment Atrial tachycardia on the ECG is characterized by

Atrial PT is a relatively rare form of PT; its frequency does not exceed 10–15% of the total number of supraventricular PTs. Depending on what is the localization of the arrhythmogenic focus and which of the listed mechanisms underlies atrial PT, there are:

sinoatrial reciprocal PT due to the re-entry mechanism in the sinoatrial zone, where the tissue of the SA node passes into the atrial myocardium;

reciprocal atrial PT, also due to the re-entry mechanism localized in the atrial myocardium;

focal (focal) or ectopic atrial PT, which are based on abnormal automatism of atrial fibers.

The causes of atrial PT are:

1. Organic heart diseases (CHD, MI, cor pulmonale, hypertension, rheumatic heart disease, mitral valve prolapse, atrial septal defect, etc.).

2. Digitalis intoxication, hypokalemia, acid-base balance shifts.

3. Reflex irritation with pathological changes in other internal organs (peptic ulcer of the stomach and duodenum, cholelithiasis, etc.), as well as alcohol abuse, nicotine and other intoxications. Atrial PTs that develop due to these causes are often referred to as idiopathic a form of supraventricular PT, since, in this case, no organic pathology is usually found in the heart.

Clinical manifestations depend on the heart rate during an attack, as well as on the nature and severity of heart disease. With the sinoatrial form of atrial PT, in which the heart rate usually does not exceed 120–130 per minute (rarely more than 160 per minute), patients tolerate an attack of tachycardia relatively easily. In more severe cases, for example, with atrial reciprocal or focal (focal) PT with a heart rate of up to 170-180 per minute, shortness of breath, pain in the region of the heart and a feeling of palpitations appear during an attack.

ECG signs of atrial PT(Fig. 3.45):

1. A sudden onset and just as suddenly ending attack of increased heart rate up to 140-250 beats per minute while maintaining the correct rhythm.

2. The presence in front of each ventricular QRS complex of a "reduced, deformed, biphasic or negative P wave".

3. Normal unchanged ventricular QRS complexes, similar to QRS, recorded before the onset of an PT attack.

4. In some cases (Fig. 3.46), there is a deterioration in AV conduction with the development of AV blockade of the 1st degree (prolongation of the P-Q (R) interval for more than 0.02 s) or the 2nd degree with periodic dropouts of individual QRS complexes "(non-permanent signs).

It should be added that each of the listed forms of atrial PT has some features. So, with the sinoatrial form of atrial tachycardia, the heart rate usually does not exceed 120–130 per minute, and the P waves are practically unchanged (positive P in leads II, III and aVF). Reciprocal tachycardia is characterized by an acute sudden onset and the same sudden cessation of paroxysm, as well as some lengthening of the P–Q (R) interval, and therefore the P wave often overlaps with the T wave of the previous complex. Focal (focal) atrial PT, caused by an increase in automatism or trigger activity of the atria, is characterized by a gradual increase in heart rate (the “warm-up” phenomenon) at the beginning of an attack and a gradual decrease in heart rate at the end. This form of PT is also characterized by functional instability of the ectopic center, which affects the regularity of the QRS and the duration of the P–P interval. Sometimes in clinical practice there is another form of atrial tachycardia - multifocal (“chaotic”) atrial PT. It is characterized by the presence of several foci of ectopic activity in the atria, which determines some features of this form of PT. With an increase in heart rate to 100–250 per minute, an irregular rhythm with different P–P intervals is detected on the ECG. The morphology of the P waves and the duration of the P–Q (R) interval are continuously changing (Fig. 3.47). The most common cause of multifocal atrial PT is cor pulmonale (see Chapter 13). It should be noted that in some cases, with any form of atrial PT, the ventricular rhythm becomes irregular due to the functional blockade of the II degree AV junction, which leads to periodic prolapse of the ventricular QRS complex.

Fibrillation (flicker) and atrial flutter

Fibrillation (flicker) and atrial flutter are two cardiac arrhythmias similar in their mechanism of occurrence, which often transform into each other in the same patient. More common is atrial fibrillation (AF) or atrial fibrillation, which may be paroxysmal or chronic. In terms of prevalence and frequency of occurrence, AF is second only to extrasystole, ranking first among arrhythmias requiring hospitalization and treatment in a hospital setting. Atrial fibrillation is a condition in which there is frequent (up to 400–700 per minute), erratic, chaotic excitation and contraction of individual groups of atrial muscle fibers. With atrial flutter (AF), the latter are excited and reduced also with a high frequency (about 300 per minute), but the correct atrial rhythm is usually maintained. In both cases, the AV node cannot "pass" to the ventricles such a large number of atrial impulses, since some of them reach the AV node when it is in a state of refractory. Therefore, in AF, there is an irregular chaotic ventricular rhythm (“absolute ventricular arrhythmia”), and the number of ventricular contractions depends on the duration of the effective refractory period of the AV junction. At bradysystolic form of AF, the number of ventricular contractions is less than 60 per minute; at normosystolic- from 60 to 100 per minute; at tachysystolic form - from 100 to 200 per min. With AFL, every second (2:1) or every third (3:1) atrial impulse is usually conducted to the ventricles. This functional AV block that develops in atrial fibrillation prevents the ventricles from overworking and inefficiently. For example, if the frequency of regular atrial excitations is 300 per minute, then with a ratio of 2: 1, the ventricular rhythm is only 150 per minute. If the degree of slowing of AV conduction remains constant, the correct ventricular rhythm is recorded on the ECG, characterized by the same R-R intervals ( correct form of TP). If the same patient has an abrupt change in the degree of AV blockade and then every second, then only the third or fourth atrial impulse is carried out to the ventricles, an irregular ventricular rhythm is recorded on the ECG ( wrong form of TP). Both arrhythmias are based on electrical inhomogeneity of the atrial myocardium, some limited areas of which differ in different electrophysiological properties, in particular, in different durations of effective refractory periods. Under these conditions, the wave of excitation propagating through the atria encounters areas of non-excitable tissue, changing its direction. Under certain “favorable” conditions, a circular motion of the excitation wave (re-entry) may occur in the atrium, which is the direct mechanism for the occurrence of these types of arrhythmias (Fig. 3.55). It is believed that TP is based on the rhythmic circulation of a circular wave of excitation (macro-re-entry) in the atria, for example, around the annulus of the tricuspid valve or at the base of the RA, between the tricuspid valve and the mouth of the vena cava (F. Cosio, G. Taylor). The formation of AF is based on the formation of many micro-re-entry loops in the atria, and most of them are formed in the LA (A.F. Samoilov, L.V. Rozenshtraukh, M.S. Kushakovsky, M. Allesie et al. .).

Atrial fibrillation occurs predominantly in patients with organic changes in the atrial myocardium, primarily in the left atrium (acute myocardial infarction, postinfarction cardiosclerosis, chronic forms of coronary artery disease, mitral stenosis, thyrotoxicosis, hypertension, intoxication with cardiac glycosides, etc.). In the past, the most common causes of AF were considered to be three diseases (three …oz”), which are characterized by damage to the LA in the form of its dilatation, hypertrophy and / or focal fibrosis:

cardiosclera oz(atherosclerotic and postinfarction);

mitral walls oz;

thyrotoxic oz.

However, the range of diseases and pathological syndromes in which AF occurs, especially its paroxysmal form, turned out to be much wider. In addition to the cardiosclerosis, mitral stenosis and thyrotoxicosis listed above, these include:

obesity;

diabetes;

arterial hypertension;

alcohol intoxication;

mitral valve prolapse;

electrolyte disturbances (eg, hypokalemia);

congestive heart failure;

dyshormonal secondary heart diseases;

the so-called “vagal” variants of paroxysmal AF (M.S. Kushakovsky, R. Сoumel), which occur at night, at rest as a result of a reflex effect on the heart of the vagus nerve, which shortens the effective refractory period of the atria and slows down conduction in them (including persons with pathology of the gastrointestinal tract, hiatal hernia, gastric ulcer, chronic constipation, etc.);

hyperadrenergic variants of AF that occur during the day, with physical and psycho-emotional stress in individuals with increased SAS activity.

The presence of WPW syndrome or SSSU in patients with paroxysmal atrial fibrillation significantly complicates the course and prognosis of this rhythm disturbance and has a decisive influence on the choice of a method for treating fibrillation.

atrial flutter occurs in the same pathological conditions as AF. However, the cause of this heart rhythm disturbance is more often caused by diseases characterized by PP overload (dilation, hypertrophy, dystrophic changes), including pulmonary embolism, chronic obstructive pulmonary disease, etc. Table 3.6 presents the differential diagnostic signs of “vagal” and hyperadrenergic AF paroxysms. There are several important factors to be aware of that increase the risk of paroxysms of atrial fibrillation or flutter. These include:

atrial expansion (the most important, but still not a mandatory feature);

the presence of interatrial and intraatrial blocks (see below);

frequent atrial stimulation;

ischemia and dystrophy of atrial myocardium;

increased tone of the vagus nerve;

increase in the tone of the SAS, etc.

Table 3.6 Some differential diagnostic signs of “vagal” and “hyperadrenergic” variants of idiopathic paroxysmal AF (according to A.P. Meshkov)

Since there is no simultaneous atrial contraction in AF and AFL, the efficiency of diastolic filling of the ventricles decreases by 15–25%, which in one way or another leads to a decrease in cardiac output, an increase in KDD in the ventricles and an increased risk of congestion in the pulmonary and systemic circulation. In other words, long-term atrial fibrillation or atrial fibrillation inevitably leads to the development of heart failure.

ECG signs of atrial fibrillation are (Fig. 3.56):

1. The presence on the ECG of frequent (up to 200-400 per minute), regular, similar atrial F waves, which have a characteristic sawtooth shape (leads II, III, aVF, V 1, V 2).

2. In most cases, the correct, regular ventricular rhythm is maintained with the same F-F intervals (with the exception of cases of a change in the degree of atrioventricular block at the time of ECG registration).

3. The presence of normal, unchanged (narrow) ventricular complexes, each of which is preceded by a certain (usually constant) number of atrial waves F (2: 1; 3: 1; 4: 1, etc.).

ECG signs of AF(fig. 3. 57):

1. Absence of P wave in all ECG leads.

2. The presence throughout the entire cardiac cycle of random small waves f, having a different shape and amplitude. Waves f are better recorded in leads V 1 , V 2 , II, III and aVF.

3. Irregularity of ventricular QRS complexes - irregular ventricular rhythm (R-R intervals of different duration).

4. The presence of QRS complexes, which in most cases have a normal, unchanged appearance without deformation and widening.

Depending on the magnitude of the wave f, coarse and finely wavy forms of the FP are distinguished (Fig. 3.58). With a coarse-wave form, the amplitude of the f waves exceeds 0.5 mm, and their frequency usually does not exceed 350–400 per minute. Such waves are usually well recognized on the ECG. Coarse-wavy form of AF is often found in patients with thyrotoxicosis, mitral stenosis, and some other pathological conditions. With a finely wavy form of AF, the wave frequency f reaches 600–700 per minute, and their amplitude is less than 0.5 mm. Sometimes the f waves are not visible at all on the ECG in any of the electrocardiographic leads. This form of atrial fibrillation is often observed in elderly people suffering from coronary artery disease, acute myocardial infarction, atherosclerotic cardiosclerosis.

Ventricular arrhythmias

Ventricular arrhythmias are quite common in clinical practice and in most cases require a thorough examination of patients not only to clarify the nature and source of the arrhythmia, but also to determine the individual prognosis of these arrhythmias and the possible risk of developing ventricular fibrillation (VF) and sudden cardiac death. The most common ventricular arrhythmias include:

ventricular extrasystole (PV);

ventricular tachycardia (VT), including torsades de pointes;

ventricular fibrillation (VF);

accelerated idioventricular rhythm.

Ventricular extrasystole

Ventricular extrasystole (PV) is a premature excitation of the heart that occurs under the influence of impulses emanating from various parts of the ventricular conduction system. Single monomorphic PVCs can occur as a result of both the formation of a re-entry of the excitation wave (re-entry) and the functioning of the post-depolarization mechanism. Repetitive ectopic activity in the form of several successive PVCs is usually due to the re-entry mechanism. The source of PVCs in most cases are branches of the bundle of His and Purkinje fibers. This leads to a significant disruption in the process of propagation of the excitation wave along the RV and LV: first, the ventricle in which the extrasystolic impulse arose is excited, and only after that the depolarization of the other ventricle occurs with a great delay. This leads to a significant increase in the total duration of the extrasystolic ventricular QRS complex. The extrasystolic complexes at the same time are very similar in shape to the QRS complexes in the blockade of the legs of the bundle of His. With PVC, the sequence of repolarization also changes, in connection with which there is a shift of the RS–T segment above or below the isoline, as well as the formation of an asymmetric negative or positive T wave. At the same time, the shift of the RS–T segment and the polarity of the T wave are discordant to the main wave of the ventricular complex, those. directed in the direction opposite to this tooth (Fig. 3.59).

An important sign of PVC is the absence of a P wave in front of the extrasystolic QRS complex, as well as the presence of a complete compensatory pause. The SA node is not usually “discharged” during PVC, because the ectopic impulse that originates in the ventricles, as a rule, cannot pass retrograde through the AV node and reach the atria and the SA node. In this case, the next sinus impulse freely excites the atria, passes through the AV node, but in most cases cannot cause another depolarization of the ventricles, since after PVC they are still in a state of refractoriness. The usual normal excitation of the ventricles will occur only after the next (second after PVC) sinus impulse. Therefore, the duration of the compensatory pause in PVC is noticeably longer than the duration of the incomplete compensatory pause. The distance between the normal (sinus origin) ventricular QRS complex preceding the PVC and the first normal sinus QRS complex recorded after the extrasystole is equal to twice the R–R interval and indicates a complete compensatory pause. Only sometimes, usually against the background of a relatively rare main sinus rhythm, there may be no compensatory pause after PVC. This is explained by the fact that the next (first after the extrasystole) sinus impulse reaches the ventricles at the moment when they have already left the state of refractoriness. As seen in fig. 3.60, in these cases, the PVC is, as it were, inserted between two sinus ventricular complexes without any compensatory pause. These are the so-called interpolated or interpolated PVCs. A compensatory pause may also be absent during PVC against the background of atrial fibrillation.

At left ventricular ES(Fig. 3.61) there is an increase in the interval of internal deviation in the right chest leads V 1 and V 2 (more than 0.03 s), and with right ventricular ES(Fig. 3.62) - in the left chest leads V 5 and V 6 (more than 0.05 s). To assess the prognostic significance of PVCs, V. Lown and M. Wolf (1971) proposed a gradation system, further modified by M. Ryan et al. Based on the results of 24-hour Holter ECG monitoring, 6 PVC classes are distinguished:

Grade 0 - no PVC within 24 hours of monitoring;

1 class - less than 30 PVCs are registered for any hour of monitoring;

Grade 2 - more than 30 PVCs are registered for any hour of monitoring;

Grade 3 - polymorphic PVCs are registered;

4a class - monomorphic paired PVCs;

4b class - polymorphic paired PVCs;

Grade 5 - 3 or more consecutive PVCs are recorded within no more than 30 s (considered as “unsustainable” paroxysmal ventricular tachycardia).

In general, higher grade PVCs (grades 2–5) are associated with a greater risk of ventricular fibrillation (VF) and sudden cardiac death, although there are exceptions to this general rule. prognostic value. Assessing the prognostic value of PVCs, it should be emphasized that in approximately 65–70% of people with a healthy heart, Holter monitoring registers individual PVCs, the source of which in most cases is localized in the pancreas. Such monomorphic isolated PVCs, as a rule, belonging to the 1st class according to the classification of V. Lown and M. Wolf, are not accompanied by clinical and echocardiographic signs of organic heart disease and hemodynamic changes. That's why they got the name “functional PVCs”. It should, however, be noted that often the patients themselves regard such “harmless” extrasystoles as signs of a serious heart disease, very colorfully describing their feelings when an arrhythmia occurs. Functional PVCs are recorded in patients with hormonal disorders, cervical osteochondrosis, NCD, as well as in the use of certain drugs (eufillin, glucocorticoids, antidepressants, diuretics, etc.), in vagotonics. In individuals with increased activity of the parasympathetic nervous system, PVCs usually disappear during exercise, reappearing at rest. “Organic ZhE”, which have a more serious prognosis, usually occur in patients with organic heart disease (chronic coronary artery disease, acute myocardial infarction, postinfarction cardiosclerosis, hypertension, heart defects, MVP, myocarditis, pericarditis, DCM, HCM, CHF, etc.). In these cases, polytopic, polymorphic, paired PVCs and even short episodes (“jogging”) of unstable VT are more often recorded. It should be remembered that even the presence of “organic” extrasystole, which is based on the inhomogeneity of the electrophysiological properties of the heart muscle, does not exclude a certain role of neurohormonal disorders in the occurrence of arrhythmia. Of even greater importance in patients with cardiac pathology are electrolyte disturbances, primarily hypokalemia and hypomagnesemia, which often occur with prolonged unsystematic use of diuretics. Therefore, patients who are suspected to have organic PVCs should be subjected to a thorough clinical and instrumental examination, which, at a minimum, should include:

biochemical blood test (including the content of K, Mg 2 and other parameters);

24-hour Holter ECG monitoring;

EchoCG study with the definition of EF, diastolic dysfunction and other hemodynamic parameters;

study of heart rate variability;

registration of signal-averaged ECG, etc.

These studies, along with an analysis of the clinical picture of the disease, make it possible to reliably assess the possible risk of VF and sudden cardiac death and determine the general tactics of treating patients with PVC.

Ventricular tachycardia

Ventricular tachycardia (VT) - in most cases, this is a sudden onset and just as suddenly ending attack of increased ventricular contractions up to 150–180 bpm. per minute (less often - more than 200 beats per minute or within 100–120 beats per minute), usually while maintaining the correct regular heart rate (Fig. 3.63).

All 3 arrhythmia mechanisms described in Section 3.2 may be involved in the occurrence of VT paroxysms:

re-entry of the excitation wave (re-entry), localized in the conduction system or the working myocardium of the ventricles;

ectopic focus of increased automatism;

ectopic focus of trigger activity.

In most cases, VT in adults develop according to the re-entry mechanism, i.e. are reciprocal. Reciprocal VT is characterized by a sudden acute onset immediately after PVC (less often after atrial ES), which induces the onset of an attack. The paroxysm of reciprocal tachycardia breaks off as suddenly as it began. Focal automatic VT is not induced by extrasystoles and often develops against the background of an increase in heart rate caused by exercise and an increase in the content of catecholamines. Finally, triggered VTs also occur after a PVC or an increase in heart rate. Automatic and triggered VT are characterized by the so-called “warm-up” period of tachycardia with a gradual achievement of the rhythm rate, at which stable VT is maintained. In almost all cases, VT occurs in patients with cardiac pathology (acute myocardial infarction, postinfarction aneurysm, DCMP, HCM, arrhythmogenic pancreatic dysplasia, heart defects, MVP, digitalis intoxication). Most often (about 85%), VT develops in patients with coronary artery disease, and in men 2 times more often than in women. Only in 2% of cases, VT is registered in patients who do not have reliable clinical and instrumental signs of organic heart damage (“idiopathic” form of VT).

ECG signs of VT are (Fig. 3.64):

1. Suddenly starting and just as suddenly ending attack of increased heart rate up to 140-150 beats. per minute (less often - more than 200 or within 100-120 beats per minute) while maintaining the correct rhythm in most cases.

2. Deformation and expansion of the QRS complex for more than 0.12 s with a discordant location of the RS–T segment and the T wave.

3. The presence of AV dissociation is a complete dissociation of the frequent ventricular rhythm (QRS complexes ") and the normal sinus rhythm of the atria (P waves") with occasionally recorded single unchanged QRST complexes of sinus origin ( “trapped” ventricular contractions).

Evaluation of patients with VT (or suspected VT) has several goals:

1. Verify that there is indeed ventricular, and not supraventricular, tachycardia with aberrant electrical impulse conduction and widened QRS complexes.

2. Specify the clinical variant of VT (according to ECG Holter monitoring data).

3. Determine the leading mechanism of VT (reciprocal, automatic, or triggered VT) (intracardiac EPS and programmed cardiac pacing).

4. If possible, clarify the localization of the ectopic focus (intracardiac EPS).

5. Assess the prognostic value of VT, the risk of VF and sudden cardiac death (intracardiac EPS, signal-averaged ECG with determination of late ventricular potentials, echocardiography with assessment of global and regional LV function, etc.).

6. To select effective drugs for the relief and prevention of recurrent VT, as well as to evaluate the feasibility of surgical methods for the treatment of tachycardia (intracardiac EPS).

In the practice of cardio intensive care units of hospitals, where the majority of patients with VT are hospitalized on an emergency basis, the most important is the solution of the first, second and fifth tasks. The rest are usually solved in specialized, including cardiac surgery, institutions. Differential diagnosis of VT and supraventricular PT with wide QRS complexes (aberrant conduction) is of paramount importance, since the treatment of these two rhythm disorders is based on different principles, and the prognosis of VT is much more serious than supraventricular PT.

Thus, the most reliable sign of one form or another of PT is the presence (VT) or absence (supraventricular PT) of AV dissociation with periodic “captures” of the ventricles, which in most cases requires intracardiac or transesophageal registration of ECG P waves (Fig. 3.65). However, already during the usual clinical examination of a patient with paroxysmal tachycardia, in particular, when examining the neck veins and auscultation of the heart, it is possible to identify signs characteristic of each type of PT. So, with supraventricular tachycardia with AV conduction 1: 1, there is a coincidence in the frequency of arterial and venous pulses (Fig. 3.66, a). Moreover, the pulsation of the cervical veins is of the same type and has the character of a negative venous pulse, and the volume of the I tone remains the same in different cardiac cycles (Fig. 3.67, a). Only in the atrial form of supraventricular PT is there an episodic loss of the arterial pulse associated with transient second-degree AV block. In VT, AV dissociation is observed: a rare venous pulse and a much more frequent arterial one. At the same time, enhanced “giant” waves of a positive venous pulse appear periodically, due to a random coincidence of contraction of the atria and ventricles with closed AV valves (Fig. 3.66, b). At the same time, the I heart sound also changes its intensity: from weakened to very loud (“cannon”) when the systole of the atria and ventricles coincides (Fig. 3.67, b).

Clarification of the clinical variant of VT is carried out using daily Holter ECG monitoring. There are three clinical variants of VT.

1. Paroxysmal unstable VT is characterized by the appearance of three or more ectopic QRS complexes in a row, which are recorded during an ECG monitor recording within no more than 30 s (Fig. 3.68). Such paroxysms do not affect hemodynamics, but increase the risk of VF and sudden cardiac death.

2. Paroxysmal sustained VT lasting more than 30 seconds (see Figures 3.64 and 3.65). This type of VT is characterized by a high risk of sudden cardiac death and is accompanied by significant hemodynamic changes (arrhythmogenic shock, acute left ventricular failure).

3. Chronic or constantly recurrent (continuously relapsing) VT - long-term (weeks and months) recurring relatively short tachycardic "runs" that are separated from each other by one or more sinus complexes (Fig. 3.69). This variant of VT also increases the risk of sudden cardiac death and leads to a gradual, relatively slow increase in hemodynamic disturbances. LV function assessment Echocardiography is no less important part of the examination of patients with VT than the identification of the mechanism of development of arrhythmias or its topical diagnosis. Normal LV function indicates a low risk of high-grade ventricular arrhythmias, including VF, and sudden cardiac death in the near future. Low EF is usually associated with a high risk of recurrent ventricular arrhythmias or sudden cardiac death. These data are usually confirmed by the study of heart rate variability (HRV) and the assessment of late ventricular potentials, although the results of these tests are not strictly specific.

Rice. 3.68. Two short paroxysms of ventricular tachycardia recorded during Holter ECG monitoring

Important information about predictive value of VT can be obtained by intracardiac EPS and attempts to provoke tachycardia with electrical stimulation. Patients who successfully induce sustained VT (lasting more than 30 s) or symptomatic VT in this manner are at greatest risk of sudden cardiac death. True, it should be borne in mind that VTs with different mechanisms have different degrees of reproducibility during EPS. Finally, the risk of sudden cardiac death and the occurrence of complex cardiac arrhythmias (sustained VT and VF) increases by 3-5 times in patients who have slow fragmented ventricular myocardial electrical activity (PVA), which is recorded using a signal-averaged ECG in the terminal parts of the QRS complex lasting more than 40 ms. To be sure specific mechanisms of VT, on the knowledge of which the tactics of further management of patients depends, intracardiac EPS is usually used.

Propranolol was one of the first B-blockers that began to be used for the treatment of cardiovascular pathology. This drug is better known as anaprilin. Since the drug is a non-selective blocker of B-adrenergic receptors, its use is currently limited. But there are situations when this medicine has advantages.

Features of the action of non-selective B-blockers

Like any drug in this group, anaprilin blocks B1-adrenergic receptors located in the heart and kidneys. Due to this, the formation of renin decreases and the activity of the RAAS is suppressed. Propranolol reduces the frequency of heart contractions, their intensity, which is accompanied by a decrease in cardiac output. Through these mechanisms, the drug helps lower blood pressure.

Anaprilin reduces the activity of the sinoatrial node, as well as foci of pathological activity located in the atria, AV junction, and ventricles. The drug has a membrane-stabilizing effect. That is why the drug can be used for rhythm disturbances.

Since the strength of heart contractions and their frequency decreases, the need for oxygen in the heart muscle decreases, due to which angina attacks occur less often.

Unlike selective B-blockers, anaprilin additionally acts on B2-adrenergic receptors, which are located in the wall of the bronchi, uterus, intestines, in the smooth muscles of arteries, in skeletal muscles, salivary glands, eyes and other organs. That is why blocking the stimulating effect of catecholamines leads to the corresponding effects. Propranolol increases the tone of the uterus, lowers intraocular pressure, due to which the indications for the use of the drug are expanding compared to selective B-blockers. But the number of adverse reactions also increases significantly.

After oral administration, propranolol is absorbed fairly quickly. Already after 1-1.5 hours, the concentration of the active substance in the blood reaches a maximum. The hypotensive effect lasts up to a day. Bioavailability is about 30%, but after a meal it increases. The half-life is two to three hours. It binds to plasma proteins by 90-95%. The drug is excreted mainly by the kidneys. Penetrates into breast milk and through the placental barrier.

Indications for use

You can take anaprilin in tablets for many diseases:

1. Elevated blood pressure in essential and symptomatic hypertension.
2. IHD: stable and unstable angina, myocardial infarction (from the fifth day).
3. Tachyarrhythmias, including against the background of various diseases. Propranolol helps to effectively deal with sinus tachycardia. Treatable: supraventricular tachycardia, extrasystole, atrial fibrillation.
4. Heart disease: subaortic stenosis, mitral valve prolapse, hypertrophic cardiomyopathy.
5. Autonomic disorders: sympathetic-adrenal crises in patients with diencephalic syndrome, neurocirculatory dystonia, panic attacks, autonomic disorders during menopause.
6. Portal hypertension syndrome in liver cirrhosis.
7. Thyrotoxicosis - to eliminate tachycardia, relieve thyrotoxic crisis, in preparation for surgical treatment.
8. Essential tremor.
9. Complex treatment of pheochromocytoma (mandatory with alpha-blockers).
10. withdrawal syndrome.
11. Prevention of migraine attacks.
12. Primary weakness of labor activity and prevention of postpartum complications.
13. Hemangiomas in newborns.

Contraindications for treatment

Anaprilin can be used only in the absence of contraindications:

• low pressure;
• sinoatrial and AV blockade of 2-3 degrees;
• Heart rate less than 55 per minute;
• SSS (sick sinus syndrome);
• severe heart failure (acute and chronic);
• variant angina (Prinzmetal);
• bronchial asthma and a tendency to bronchospasm;
• cardiogenic shock;
• the first days after acute myocardial infarction;
• circulatory disorders in the peripheral arteries (Raynaud's disease, etc.);
• hypersensitivity.

Take pills with caution in the following conditions:

• diabetes mellitus and a tendency to hypoglycemia;
• chronic diseases of the bronchopulmonary system, emphysema;
• disruption of the liver and kidneys;
• psoriasis;
• spastic colitis;
• muscle weakness;
• advanced age;
• pregnancy;
• lactation period.

Methods of treatment

In the presence of high pressure, tablets begin to take 40 mg in the morning and evening. Gradually increase the dosage to the required. The daily dose can be divided into 2 or 3 doses. Such treatment is most effective at the initial stage of hypertension or an episodic increase in blood pressure, accompanied by a rapid heartbeat. Preferably used in young people.

If you have to treat angina pectoris, then start with 20 mg 3 times a day. The dosage can be increased over time to a maximum, but not more than 240 mg.

You can take anaprilin and with essential tremor, and for the prevention of migraine attacks. Small doses are used: 40 mg 2-3 times a day, maximum 160 mg. Do not forget that propranolol lowers blood pressure, as a result of which the use of large doses can cause hypotension.

The drug is sometimes used to stimulate labor, as well as to prevent postpartum complications, as it stimulates uterine contractions. Doses are small: 20 mg three to six times a day.

There is an injectable form of the drug. It is used to stop arrhythmias and angina attacks. The medicine is administered intravenously. There are also eye drops that help with glaucoma.

Side effect

The negative consequences after taking anaprilin are much greater than those of selective B-blockers.

1. First of all, the drug acts on the cardiovascular system, often causing a pronounced decrease in the frequency of heart contractions, intracardiac blockade, hypotension, heart failure. Violated peripheral circulation due to spasm of the arteries.
2. The reaction of the nervous system is manifested in the form of dizziness, headaches, sleep disturbances. There are nightmares. Emotional lability is often observed, the speed of mental and motor reactions decreases. Hallucinations, depression, disorientation in space and time, short-term amnesia, sensory disturbances and paresthesias are possible.
3. The gastrointestinal tract reacts to the medication with dyspeptic disorders, which is manifested by nausea, vomiting, and stool disorders. Since the drug increases the tone of the smooth muscles of the intestines, as well as the arteries, abdominal pains appear. Mesenteric artery thrombosis and ischemic colitis may develop.
4. The respiratory organs also respond with a characteristic reaction to the drug. Increased muscle tone of the bronchi manifests itself in the form of bronchospasm and laryngospasm, shortness of breath, cough, chest pain.
5. Eye changes: keratoconjunctivitis, visual disturbances and dry eyes.
6. Disturbances in the blood system: a decrease in the content of leukocytes, agranulocytosis, thrombocytopenic purpura, an increase in liver parameters, cholesterol and its atherogenic fractions.
7. Other reactions: skin manifestations in the form of rashes, alopecia, itching, exacerbation of psoriasis; sexual dysfunction up to impotence; Peyronie's disease; pain in the joints; hypoglycemia and fever.

What to know

If propranolol has to be used for a long time and it becomes necessary to cancel it, then this should be done very carefully. The dosage is reduced gradually. If you stop taking the pills immediately, then a withdrawal syndrome occurs. This is manifested in an increase in the symptoms of the underlying disease.

It is necessary to constantly monitor blood glucose in patients with diabetes mellitus, so as not to miss hypoglycemia. This condition is much more dangerous than high sugar, because the brain suffers from a lack of energy.

Given that propranolol lowers the reactivity of the body (motor and mental), people who drive a vehicle or work in hazardous conditions should be especially careful.

You can not use the drug simultaneously with certain drugs:

• antipsychotic and anxiolytics;
• calcium channel blockers (diltiazem and verapamil);
• alcoholic products.

Various antihypertensive drugs, sympatholytics, MAO inhibitors, anesthetics enhance the ability to lower blood pressure. Reduce the effectiveness of treatment with NSAIDs, glucocorticoids and estrogens.

Propranolol itself increases the activity of thyreostatic drugs and drugs that tone the uterus. But reduces the effectiveness of allergy medications. Slows down the excretion of lidocaine and aminophylline, prolongs the action of coumarins and non-depolarizing muscle relaxants.

If surgical treatment is planned using anesthesia (chloroform, ether), treatment should be discontinued.

If the treatment of coronary heart disease with the help of this B-blocker is planned to be carried out for a long time, then it is advisable to take cardiac glycosides at the same time.

Tablets may contain 10 and 40 mg of the active substance. One package contains 30 or 50 pieces. The shelf life is 4 years.

Conclusion

Anaprilin has its own niche for use. But if its additional effects are not needed, then the drug should be replaced with a selective B-blocker. How long the treatment will last, what dose to take, only a doctor can determine. He is able to take into account all the risks from such therapy, which the patient himself cannot do. Self-medication is dangerous and often leads to a deterioration in the course of the underlying disease, as well as the general condition.

Atrioventricular heart block

Atrioventricular blockade (atrioventricular) is a disorder of the conduction of excitation from the atria to the ventricles. Clinical symptoms and electrocardiographic manifestations can be observed with conduction disorders at the level of:

• atrial tract,
• in the atrioventricular node
• in the stem
• in the bundle of His.

According to the classification of V. Doshchitsin, in functional diagnostics, 4 types of atrioventricular blockades are distinguished, respectively, 3 proximal (located at the beginning of the conduction system of the heart, listed first) and one - distal (final):

• atrial
• nodal,
• stem,
• trifascicular (trifascicular).

What is an atrioventricular node?

The atrioventricular node (Ashof-Tavara) is an accumulation of special myocardial cells in the lower part of the right atrium near the interatrial septum. The size of the knot is 3x5 mm. According to the importance of the rank, it represents an automatic center of the second order (following the sinus node) and is designed to take on the role of a pacemaker in case of failure of a higher pacemaker.

The Czech scientist Jan Purkinje was the first to describe the special cells of the heart: they consist, like myocytes, of actin and myosin, but do not form a clear structure for contraction, they are oversaturated with calcium ions. It turned out that these features make it possible to create electrical impulses or spontaneously excited. This makes them related to neurons. Subsequently, 2 types of cells were identified in the conduction system of the heart:

• some create electrical impulses;
• others organize their conduction from the atria to the ventricles.

Nutrition is delivered to the cells in 90% of cases by a branch of the right coronary artery, in 10% of cases - from the left circumflex artery of the heart.

Depending on the density, the knot is formed by three layers of different compactness. And in the longitudinal size, it is functionally divided into two channels:

• α - slow;
• β - fast.

Proper functioning of the cells and channels ensures the uninterrupted flow of impulses from the sinus node to the ventricles and synchronizes the work of all parts of the heart.

Reasons for the blockade

The reasons for the blockade can be:

• functional influence of the central nervous system through the vagus nerve (observed in healthy people, athletes);
• the effect of drugs from the foxglove group;
• inflammatory process in rheumatic attack, myocarditis of various etiologies caused by childhood infections, tonsillitis, influenza;
• area of ​​necrosis or ischemia in the development of myocardial infarction;
• focal and diffuse cardiosclerosis;
• hyperkalemia and acidosis;
• myocardial dystrophy in the area of ​​the conduction system;
• consequences of hypertrophic changes in hypertension, myocardiopathies;
• post-traumatic scars on the heart.

Types of atrioventricular blockade

Atrioventricular blockade is divided into:

• incomplete - despite impaired conduction, most impulses, albeit late, reach the ventricles;
• complete - there is a rupture of the atrioventricular message.

By time:

• short-term and permanent;
• random and periodic.

In addition to these types, blockade is distinguished according to three degrees of severity. They have ECG differences and characterize the depth of the lesion of the pathways.

Characteristics of violations in the blockade of the first degree

Atrioventricular blockade of the 1st degree means a slowdown in the time of passage of the impulse from the atria to the ventricles to 0.2 seconds or more (this corresponds to a widening of the PQ interval on the ECG) at a normal rhythm rate.

In cases of proximal blockade, the shape of the ventricular complex does not change. In the distal variant, the QRS complex is deformed and expanded. Its width is over 0.3 sec. indicates a sign of a combined conduction disorder.

The diagnostic value of the blockade of the 1st degree is most significant in myocarditis. After treatment, she disappears. But it is impossible to make a diagnosis only on the basis of one ECG sign. Clinical symptoms must be taken into account in the first place.

Characteristics of violations in the blockade of the II degree

2 degree of blockade means that part of the impulses from the atria is not conducted to the ventricles. The ECG shows "loss" of ventricular complexes. In this case, the atrial and ventricular contractions are counted separately and the ratio is calculated (for example, blockade 3:1 or 5:1).

There are 3 types of atrioventricular blockade of the second degree:

• Type I is also called the type of Wenckebach or Mobitz I - on the ECG, PQ intervals are detected with gradual lengthening, then there is a loss of ventricular contraction. The sign is called the Wenckebach-Samoilov period. More typical for blockade in the proximal sections, so the ventricular complexes are not changed. Rarely, atrioventricular blockade of the first type is combined with impaired conduction in the His bundles, due to which the QRS widens.
• Type II or Mobitz II - ventricular prolapse also occurs, but there is no prior PQ elongation. Associated with impaired incomplete conduction at the level of the trifascicular bundle, so the ventricular complexes are more often dilated and deformed.
• Type III - prolapse occurs in the correct fixed order (every second, third or quadruple complex from the ventricles), while bradycardia is observed. It is considered an indicator of the progression of the cause of the blockade. It is possible both at the proximal and distal levels. The QRS complex either changes or retains the correct shape.

Characteristics of violations in the blockade of the III degree

The third degree equates to a complete atrioventricular block. Impulses from the atria do not enter the ventricles at all, so the atria and ventricles of the heart contract independently of each other at their own pace. As a rule, the ventricles are more difficult to excite, so they “work” more slowly.

As well as the two milder degrees, complete atrioventricular block may be due to proximal or distal lesions.

Proximal complete blockade causes a ventricular rhythm that has arisen in the atrioventricular node, bradycardia is about 50 per minute, ventricular complexes are not changed, contractions occur synchronously.

The distal block is distinguished by altered QRS complexes. The number of contractions slows down to 25-30.

Clinical picture

With a first-degree blockade, as a rule, the patient does not present any specific complaints. Altered well-being is associated with the underlying disease. In the second or third degree, circulatory disorders of a compensatory and adaptive nature occur: each contraction of the ventricles becomes larger in volume, which leads to myocardial hypertrophy. Cardiac pathology is usually accompanied by a number of symptoms:

• Bradycardia of 30 beats per minute causes insufficient blood flow in the brain, dizziness appears, and a short-term loss of consciousness is possible.
• Patients feel rare strong shocks (beats) of the heart in the chest. This is caused by the imposition of the rhythm of atrial and ventricular contractions and the formation of single complete regular systoles.
• When listening to the patient's heart, they have the characteristic of a "cannon shot". During examination of the neck, a pronounced pulsation of the veins is detected due to the back wave of blood into the jugular vein.
• For diagnosis, an important point is the absence of an acceleration of the pulse after exercise, any fluctuations when holding the breath on a deep breath.

If the blockade is caused by an inflammatory process or incomplete scarring, then all the signs are unstable.

In patients with pathological menopause, vegetovascular dystonia, the influence of the vagus nerve is pronounced. This is found out by conducting a test with Atropine. After subcutaneous administration of a small dose, the blockade is removed.

Treatment

Treatment of atrioventricular blockade is determined by the causes that caused the pathology.

If the rhythm disorder is associated with an acute overdose of digitalis preparations:

• immediately cancel the medication;
• gastric lavage is usually ineffective, 30 minutes after ingestion, activated charcoal has a greater effect, which should be given several times;
• Antidigoxin and Atropine are injected;
• Phenytoin and Lidocaine are indicated for the combination of blockade with ventricular arrhythmias;
• in the absence of the possibility of immediate administration of Antidigoxin, the concentration of potassium should be lowered by intravenous administration of a glucose solution with insulin, ingestion of the ion-exchange resin Polystyrenesulfonate, Hypothiazide;
• in order to eliminate acidosis, a solution of sodium bicarbonate (soda) is dripped.

It is necessary to remember about the inefficiency of forced diuresis, hemosorption and hemodialysis methods in this case.

In the absence of effect and stable bradycardia, external pacing is used. The endocardial type of stimulation is not indicated, since the risk of ventricular fibrillation and death remains.

When the blockade is associated with an increased tone of the vagus nerve, the following have a good effect:

• preparations with Atropine (candles with belladonna, Zelenin drops);
• Adrenaline, Izadrin have the opposite effect.

For the treatment of an inflammatory focus that interrupts the conduction of impulses, the following are used:

• antibiotics;
• large doses of corticosteroid hormones;
• Hypothiazide as a drug that removes potassium is recommended for concomitant hyperkalemia;
• small doses of an alkaline solution are used to remove local acidification.

With the ischemic nature of blockades, a full set of drugs is used to dilate blood vessels, eliminate disturbed metabolism in cells, and reduce the ischemic zone:

• nitrates of fast and prolonged action;
• coronary drugs;
• β-blockers even with bradycardia 50 per minute.

Atropine solution is used when there is a threat of transition to a more severe degree.

With frequent attacks of Morgagni-Adams-Stokes, defibrillation is performed, the issue of installing an artificial pacemaker is being decided.

Treatment for atrioventricular blockade requires caution and frequent monitoring of electrocardiographic changes. Therefore, patients need to regularly come to the scheduled examination. It is not recommended to use any folk remedies.

Features of paroxysmal supraventricular (supraventricular) tachycardia

Characteristics of the disease

The supraventricular form of the disease occurs when the impulse occurs at the level of the atrial tissues. The heart rate increases to 140-250 per minute.

Such tachycardia develops according to 2 scenarios:

• The normal source of impulses ceases to control heart contractions. They arise under the influence of abnormal foci that are above the level of the ventricles of the heart.
• The impulse circulates in a circle. Because of this, the elevated heart rate persists. This state is called "rebreathing" of excitation. It develops if the excitation impulse has detours.

Paroxysmal supraventricular tachycardias are potential life-threatening conditions. But the prognosis when they occur is more favorable than with the development of intense ventricular contractions. They rarely indicate left ventricular dysfunction and organic heart disease.

Prevalence and development process

In women, the supraventricular form is diagnosed 2 times more often than in men. People who have crossed the 65-year mark are 5 times more likely to develop it. But it does not occur too often: its prevalence does not exceed 0.23%.

The atrial form of tachycardia occurs in 15-20%, and atrioventricular - in 80-85%. Seizures develop at any time.

Many people are diagnosed with this disease in childhood. But it can also develop as a complication after cardiac diseases. Paroxysmal supraventricular arrhythmia is considered an intermediate link between fatal and benign heart rhythm problems.

Attacks of paroxysm come and end suddenly. The rest of the time, patients do not complain about the rhythm, it is normal, fluctuations in the frequency of contractions are not significant.

Classification and signs on the ECG

Depending on the type of arrhythmia, the mechanism of the course of the attack differs.

• Sinoatrial tachycardia appears due to the recirculation of the impulse through the sinus node and the myocardium of the right atrium. On the ECG in this condition, the R wave is preserved. It is he who is responsible for the contraction of the atria. The frequency of contractions reaches 220 bpm.
• Atrial arrhythmia appears with an increase in the activity of the pathological focus, which has its own automation apparatus.

  The shape of the P wave on the ECG is modified: it becomes negative or biphasic. With this form, the attack can develop gradually. The heart contracts at a rate of 150-250 beats/min.

• Paroxysmal AV nodal tachycardia appears when 2 parallel pathways for impulses appear in the area of ​​\u200b\u200bthe junction of the atria and ventricles. Their functionality is different.

  The fast and slow paths form a ring, because of this, the exciting impulse begins to circulate in a circle. Excitation of the atria and ventricles occurs simultaneously, so there is no P wave on the ECG.

Causes, risk factors

Doctors distinguish physiological and pathological tachycardia. In the first case, the increase in rhythm is a response to physical activity or stress. The pathological condition develops due to a failure of the impulse formation mechanism in the physiological source.

Doctors distinguish between cardiac and non-cardiac causes of the disease. These include:

In some cases, the cause cannot be determined. Risk factors for developing the disease include:

• hereditary predisposition;
• the use of diuretics.

In childhood and adolescence, tachycardia appears against the background of:

• electrolyte disturbances;
• psycho-emotional or physical overstrain;
• exposure to adverse conditions: with an increase in body temperature, lack of fresh air in the room.

Symptoms

Patients who have experienced PNT describe their condition in different ways. For some, seizures are almost asymptomatic. For others, the condition worsens markedly.

Paroxysmal supraventricular tachycardia is manifested as follows:

• acceleration of the heartbeat in the chest;
• the appearance of shallow breathing;
• palpable pulsation of blood vessels;
• dizziness;
• hand tremor;
• darkening in the eyes;
• hemiparesis: damage to the limbs on one side;
• speech disorders;
• increased sweating;
• increase in the number of urination;
• fainting.

Symptoms appear suddenly and disappear unexpectedly.

Carrying out diagnostics

When attacks of a sharp heartbeat appear, you should contact a cardiologist. An accurate diagnosis is established after a special examination. To detect supraventricular paroxysms use:

• physical examination;
• ultrasound, MRI, MSCT of the heart: they are done to exclude organic pathology if paroxysmal tachycardia is suspected;
• instrumental examination: ECG, ECG during exercise, Holter and electrophysiological intracardiac study.

A characteristic feature of the disease is the rigidity of the rhythm. It does not depend on the load and respiratory rate. Therefore, an important part of the diagnosis is an auscultatory examination.

It is important to determine the type of tachycardia: supraventricular or ventricular. The second state is more dangerous.

If it is not possible to accurately establish the diagnosis of PNT, then the disease is regarded as ventricular tachycardia and treated accordingly.

Also, patients with PNT should be examined to exclude the following syndromes:

• weakness of the sinus node;
• ventricular excitation.

Urgent care

There are several methods to reduce the symptoms of an attack by a patient. The patient is recommended:

• throw back your head;
• immerse your face in cold water for 10-35 seconds, its temperature should be about 2 0C;
• put an ice collar on the neck;
• press on the eyeballs;
• tighten your abdominals and hold your breath for 20 seconds.

To stop an attack of supraventricular paroxysmal tachycardia, vagal techniques are used:

• sharp exhalation through the closed nose and mouth (Valsalva test);
• massage of the carotid arteries (with caution done to people who have atherosclerosis or impaired cerebral blood flow);
• inducing a cough that ruptures the diaphragm.

Treatment and rehabilitation

After examining and determining the nature of the disease, the doctor determines whether the patient needs special antiarrhythmic treatment.

To prevent seizures, drugs are prescribed that restore the heart rhythm. But long-term use of certain antiarrhythmic drugs negatively affects life expectancy. Therefore, a cardiologist should select drugs.

Means that are intended for stopping seizures are also chosen by the doctor, taking into account the patient's history. Some advise doing breathing exercises that slow down the rhythm.

If there are indications against paroxysmal supraventricular tachycardia, surgery is used. It is necessary:

• with frequent attacks that the patient does not tolerate well;
• while maintaining the manifestations of the disease against the background of taking antiarrhythmic drugs;
• people with professions in which loss of consciousness is life-threatening;
• in situations where long-term drug therapy is undesirable (at a young age).

Surgeons perform radiofrequency ablation of the source of the pathological impulse. Learn more about these operations in this video:

Therapy is aimed not only at eliminating the arrhythmia, but also at changing the quality of life of the patient. Rehabilitation will be impossible if you do not follow the recommendations of the doctor. Diet and lifestyle are important in the treatment of arrhythmias.

Possible consequences, complications and prognosis

Short-term unexpressed attacks do not cause serious discomfort, so many underestimate their seriousness. PNT can cause disability of the patient or lead to sudden arrhythmic death.

The prognosis depends on:

• type of paroxysmal supraventricular tachycardia;
• concomitant diseases that provoked its appearance;
• the duration of attacks and the presence of complications;
• myocardial conditions.

With prolonged PNT, some develop heart failure, which impairs the ability of the myocardium to contract.

Ventricular fibrillation is a serious complication of tachycardia. This is a chaotic contraction of individual myocardial fibers, which, without emergency resuscitation, leads to death.

Seizures also affect the intensity of cardiac output. With their decrease, coronary circulation worsens. This leads to a decrease in the blood supply to the heart and can cause angina pectoris and myocardial infarction.

Preventive measures

It is impossible to prevent the development of seizures. Even regular use of antiarrhythmic drugs does not guarantee that PNT will not appear. And to get rid of arrhythmia allows surgical intervention.

Doctors say that it is necessary to treat the underlying disease that provokes arrhythmia. Also need:

• exclude alcohol and drugs;
• revise the diet: the menu should not contain excessively salty foods, fried and fatty foods, smoked meats;
• control the concentration of glucose in the blood.

If signs of tachycardia appear, a complete examination should be performed. If the doctor diagnoses paroxysmal supraventricular tachycardia, then you will have to constantly monitor your condition. It is necessary to identify the underlying disease and direct all efforts to combat it. This will prevent the occurrence of complications.

A complex course and a not entirely favorable prognosis are characteristic of recurrent tachycardia. What it is and how dangerous the disease is in its development can be reliably said after a thorough examination of the patient. For this, not only a standard ECG is used, but also other diagnostic methods.

Recurrent tachycardia (RT) is also referred to as non-paroxysmal or continuously recurrent. In its development, it can affect various parts of the heart (atria, ventricles). It is diagnosed at various ages, including in infants.

Cases of recurrent tachycardia are recorded much less frequently than with paroxysmal tachycardia. For example, among infants, the incidence of pathology is 1 RT per 333,300 live children according to studies in the UK.

Very often the disease is asymptomatic, but it can quickly lead to the development of heart failure. Therefore, at the slightest suspicion of cardiac pathology, it is important to perform diagnostics followed by, in most cases, catheter ablation.

Video Tachycardia. What's this? What to do? Tips for parents

Description of recurrent tachycardia

To date, the pathological physiology of RT has not been studied to the end. According to some assumptions, recurrent tachycardia is formed as a result of the action of microscopic tumors, which may be similar to myocardial hamartomas. In the clinic, such a pathology is known as histiocytic cardiomyopathy.

Other researchers point out that the pathology is based on a disorder in the formation of electrical impulses, which can be presented in two versions. The first is associated with trigger activity, which is created against the background of the action of late depolarizations. In the second case, pathological automatism is observed, which triggers the formation of a rapid heartbeat.

Symptoms of recurrent tachycardia

The disease is characterized by prolonged attacks of palpitations. Patients may complain of a feeling of "jumping heart", "jumping out of the heart from the chest", it becomes difficult to take a full breath.

With recurrent tachycardia, 10% of the time during the day is spent on attacks.

In some cases, the pathology is asymptomatic or the signs of the disease are mild. Then the symptoms of rhythm disturbance are determined using instrumental research methods or during auscultatory listening to the heart by a doctor.

Causes of recurrent tachycardia

To date, it has not been fully explored. The development of the disease in infancy, often after 3 to 30 months, indicates that a hereditary factor is involved. Sometimes there is a dependence of paroxysms with physical activity. Some cases of development of RT in professional athletes are described. Nevertheless, it is not yet possible to reliably name the causes of the appearance of recurrent tachycardia.

Types / photos of recurrent tachycardia

The pathological process can affect such parts of the heart as the atria and ventricles. Accordingly, a distinction is made between recurrent ventricular tachycardia and recurrent atrial (supraventricular) tachycardia.

Recurrent ventricular tachycardia

The second common designation of pathology is non-paroxysmal continuously recurrent ventricular tachycardia (NPVT). With this form of the disease, pathological rhythms most often follow from the right ventricle, namely from the outflow tract. Therefore, ventricular RT is also known as ventricular tachycardia from the outflow tract (right ventricle).

The course of the disease is characterized by short, but frequent "volleys" of the heartbeat, when the heart rate rises to 150 beats / min. In children, the heart rate can range from 170 to 440 beats / min. Sometimes, instead of attacks, single extrasystoles are noted, combined with a prolonged sinus rhythm. Nevertheless, according to research, such manifestations of the disease still resemble RT.

Recurrent atrial tachycardia

During an attack of RT, the heart rate can rise to 140-180 beats / min. With daily monitoring of the patient, a larger run-up of the indicator is often noted - from 105 to 170 beats / min. Patients often do not show special complaints, the whole disease has a clear clinical significance. This is primarily due to the fact that the long course of the pathology can lead to a decrease in the ejection fraction, the development of arrhythmogenic ventricular dysfunction. In some cases, dilatation of the right and left atria develops.

Diagnosis of recurrent tachycardia

First of all, a standard electrocardiogram is performed. With its help, the following signs of RT are determined:

• With ventricular recurrent tachycardia, widened ventricular complexes and high-amplitude R waves are often determined, which, depending on the lead, may have positive or negative deviations.
• With atrial recurrent tachycardia, a change in sinus rhythm, deformation of the P wave, and an increase in heart rate can be observed.

Additionally, Holter monitoring is used, which helps to determine the duration and frequency of attacks for a day or three. An electrophysiological study is also carried out, which is especially important in the case of focusing on performing radiofrequency catheter ablation.

Dosed load tests help in the diagnosis of ventricular RT. With their help, the dependence of tachycardia on sinus rhythm is clarified. In some patients, there is an increase in sinus activity during exercise, and against this background, the manifestation of ventricular ectopic activity decreases. If physical activity is reduced, then RT begins to occur.

ECHO KG is another study that is shown to all patients on RT. It is carried out to assess the activity of the heart valves, the thickness of the heart muscle, confirmation or exclusion of myocardial hypertrophy.

Treatment and prevention of recurrent tachycardia

Emergency assistance is provided to eliminate seizures. In particular, lidocaine is used, which is administered at a dose of 1-2 mg/kg. This drug slows down the heart rate. If it is impossible to use lidocaine, or after its administration there is no effect, then amiodarone is administered.

During recurrent tachycardia, the use of cardioversion is inappropriate, since it does not give the desired result.

Prevention of recurrent tachycardia is to prevent the development of arrhythmia after stopping the attack. To do this, use the same amiodarone or flecainide. If necessary, therapy is supplemented with beta-blockers. RFA is a last resort treatment and can be performed after an assessment of the patient's condition.

If the patient is a professional athlete and he has a question about participation in competitions, then radical treatment using RFA and further observation should be carried out. The absence of seizures for 4 weeks after therapy allows you to return to training under medical supervision.

The prognostic value for recurrent tachycardia is relatively favorable. Pathology does not provoke the development of ventricular fibrillation, but with a protracted course, it can complicate the patient's condition, contributing to the occurrence of heart failure.

Foci located both in the right atrium (RA) and in the left atrium (LA) can serve, as a result of which discrete P waves of a modified shape are formed, following in an accelerated regular rhythm. An exception is multifocal atrial tachycardia, which is characterized by an irregular atrial rhythm with P waves of different morphology.

Causes are damage myocardium, respiratory diseases and damage to the valvular apparatus of the heart. Often atrial tachycardia is idiopathic.

As with atrial flutter(TP), in some cases, the AV node can conduct all atrial impulses to the ventricles, but AV blockade of varying degrees is often observed. Antiarrhythmic agents may be effective. In difficult cases, catheter RFA is required.

source of atrial tachycardia can serve as foci located both in the PP and in the LP. It may be persistent or paroxysmal. In a practical sense, the difference between atrial tachycardia and TP is that in the first case, the atrial rate is lower (120-240 bpm). As with AFL, in some cases the AV node can conduct all atrial impulses to the ventricles, but AV block of varying degrees is often observed.

Frequency atrial contractions lower than with TP, and there is no sawtooth change in the isoline. In the absence of preexisting bundle branch block or aberrant intraventricular conduction, the ventricular complexes will be narrow. As with AFL, atrial activity is usually best seen in lead V1.

May occur atrial tachycardia with AV conduction 1:1. Massage of the carotid sinus can be helpful in making a diagnosis. Adenosine can also be used for diagnosis, however, in some cases, the drug stops atrial tachycardia without causing transient AV block.

At AV conduction 1:1 it is difficult to distinguish atrial tachycardia from sinus. In sinus tachycardia, the PR interval is usually short because catecholamines, which increase sinus node activity, also increase AV conduction velocity. Thus, a prolonged PR interval is more likely to indicate the presence of atrial rather than sinus tachycardia.

Positive P wave in lead V1 or a negative P wave in leads I or aVL indicate that the source of the tachycardia is in the LA, while a positive P wave in lead aVL indicates the origin of the tachycardia from the RA.

In the presence of AV blocks high degree due to the fact that the ventricular rate is relatively low, an erroneous conclusion can be made about the presence of complete heart block. As a consequence, an unreasonable question about the appropriateness of the pacemaker is likely, if the high frequency of atrial contractions is not properly assessed!

Atrial tachycardia usually paroxysmal. However, with prolonged continuous flow, it can lead to the development of heart failure.

Multifocal atrial tachycardia

Multifocal atrial tachycardia, also called chaotic atrial rhythm, is characterized by the presence of a high-frequency irregular atrial rhythm with P waves of different morphology. It is usually due to pulmonary pathology or severe systemic pathology such as sepsis.

Causes of atrial tachycardia

Causes of atrial tachycardia include cardiomyopathy, ischemic left ventricular (LV) dysfunction, rheumatic heart disease, cardiac surgery for valvular or congenital heart disease, chronic obstructive pulmonary disease, and SSS. It is often idiopathic. With left atrial tachycardia, the place of its occurrence is often the transition zone between the atrium and the pulmonary vein: these tachycardias have the same mechanism as paroxysmal AF, and may be its precursor.

Occasionally, an arrhythmia occurs after successful AVNRT ablation of the slow conduction pathway, and its source is localized in the immediate vicinity of the RF application site.

Atrial tachycardia with AV block may be due to digitalis intoxication. This arrhythmia is called "paroxysmal atrial tachycardia with blockade." The term "paroxysmal" is inappropriate because the tachycardia is usually sustained.

Treatment of atrial tachycardia

If sinus rhythm is needed to be restored, cardioversion or frequent atrial pacing is performed. Antiarrhythmic drugs (such as sotalol, flecainide, and amiodarone) may be effective in maintaining sinus rhythm. In persistent atrial tachycardia, the ventricular rate can be controlled with drugs that block AV node conduction. If the patient is receiving digoxin, digitalis intoxication should be suspected and the drug discontinued.

In cases refractory to medical treatment, consideration should be given to catheter RFA of the source of tachycardia, which is often located in the lateral or infero-septal region of the RA or near the orifices of the pulmonary veins in the LA, or ablation of the AV node.

ECG training video for supraventricular tachycardia (sinus tachycardia, atrial fibrillation, atrial flutter)

Atrial tachycardias account for approximately 20% of all supraventricular tachycardias. According to the electrophysiological mechanisms of development, three types of atrial tachycardias are distinguished: automatic, trigger (post-depolarization) and reciprocal (re-entry). Reciprocal atrial tachycardias are more often paroxysmal, and automatic ones are chronic (permanent or continuously recurrent). In addition, almost all researchers agree that in children, a violation of automatism can be considered the predominant cause of the development of atrial tachycardia, and the arrhythmia itself is often persistent or chronic, lasting for months, and sometimes years, and can lead to the development of cardiomegaly.

Electrocardiographic diagnosis and clinical manifestations

Electrocardiographically, atrial tachycardias are characterized by the presence of a P wave, the shape of which usually differs from its morphology in sinus rhythm, located in front of the QRS complex of the supraventricular type (PR interval less than the RP interval). The frequency of tachycardia in adults, as a rule, ranges from 140 to 180 beats per minute. With an increase in the atrial rate, the PR interval may increase, and the P wave merges with the previous T wave. Deterioration of atrioventricular conduction is sometimes accompanied by the development of second-degree AV block (Samoilov-Wenckebach period) without cessation of tachycardia, which distinguishes atrial tachycardia from most atrioventricular reciprocal tachycardia. Although it is difficult to distinguish automatic atrial tachycardia from re-entry arrhythmia on the basis of clinical and ECG data, there are also a number of differential diagnostic signs. Automatic atrial tachycardia cannot be induced and stopped by pacing, which is just typical for reciprocal arrhythmias. Stimulation of the atria at a rate exceeding the rate of automatic atrial tachycardia only temporarily suppresses the arrhythmia, after cessation of stimulation it resumes.

The first P wave of automatic atrial tachycardia is similar to subsequent P waves. In reciprocal tachycardia, the shape of the atrial extrasystole complex, with which an attack usually begins, differs from subsequent P waves, the morphology of which depends on the place of impulse circulation. In contrast to arrhythmias caused by the re-entry mechanism, the frequency of automatic atrial tachycardias often increases gradually. This phenomenon in electrophysiology is figuratively called "warming up" ("warms up"). In clinical practice, the determination of the electrophysiological mechanism for the development of atrial tachycardia is necessary, mainly, only when deciding on the use of pacing.

Vector analysis of the atrial ECG complex during tachycardia helps to establish its localization. A positive or biphasic P wave in lead aVL indicates the presence of an ectopic focus in the right atrium, while a positive P wave (“dome and dart”) in lead V1 and negative in leads V4-V6 indicate the origin of the arrhythmia from the left atrium.

Atrial tachycardia in some cases has to be differentiated from sinus tachycardia. Differential diagnosis can be difficult, but it is important for the choice of treatment tactics. Physical activity and vagal techniques significantly affect the frequency characteristics of sinus tachycardia and have little or no effect on them with atrial tachycardia. Long-term ECG recording in patients with chronic atrial tachycardia can reveal short periods of sinus rhythm (especially at night), which also helps in the differential diagnosis.

Atrial tachycardia often develop in patients with organic heart disease. They are diagnosed with diseases such as coronary artery disease, myocardial infarction, arterial hypertension, heart valve damage, dilated cardiomyopathy, cor pulmonale, etc. The role of digitalis intoxication, alcohol intake and hypokalemia in the appearance of atrial tachyarrhythmias is known. At the same time, a number of patients (primarily with automatic atrial tachycardia) are not diagnosed with cardiovascular diseases that could be the cause of arrhythmia.

In patients with atrial tachycardia, the prognosis is usually determined by the underlying disease. Mortality among them in the absence of other pathology, except for cardiac arrhythmias, is very low. However, if the arrhythmia occurs with a high frequency, for a long time, then even in patients without organic heart damage, cardiomegaly develops, the ejection fraction decreases and congestive heart failure appears.

Treatment. Patients with asymptomatic, rare, short paroxysms of atrial tachycardia do not need treatment. They should be examined in order to identify the cause of the rhythm disturbance and eliminate it. Pharmacotherapy or non-drug treatment is necessary only for patients with severe attacks of arrhythmia, as well as for its chronic course, even in the absence of hemodynamic disturbances and good tolerance of arrhythmia due to the high risk of developing cardiomegaly and heart failure. Many cardiologists in the treatment of such patients currently prefer not antiarrhythmic drugs, but interventionist interventions, given their high efficiency with a small number of complications.

Paroxysms of atrial tachycardia with unstable hemodynamics should be stopped with an EIT discharge of medium energy (50-100 J). Pharmacotherapy of atrial tachycardias has not been developed enough, although, in principle, it is carried out, as in other atrial tachyarrhythmias. With stable hemodynamics, drugs that worsen atrioventricular conduction are used to slow down high heart rate: calcium antagonists (verapamil, diltiazem), beta-blockers, cardiac glycosides, or a combination thereof. The effectiveness of these drugs in terms of restoring and maintaining sinus rhythm is small. If the paroxysm remains, then the restoration of sinus rhythm is carried out in / in the introduction of antiarrhythmics 1A, 1C and III classes (novocainamide, propafenone, amiodarone, sotalol, etc.), and with reciprocal atrial tachycardia, pacing can be used for this purpose.

In order to prevent repeated attacks of arrhythmia, according to our experience and literature data, first of all, class 1C and III drugs (propafenone, flecainide, encainide, amiodarone, sotalol) should be used, less effective are class 1A antiarrhythmics such as quinidine, disopyramide, novocainamide, aymalin. K. Koike et al. (13), evaluating for several years the effectiveness of 5 antiarrhythmic drugs of various classes, as well as digoxin and its combinations with propranolol, metoprolol, quinidine in automatic atrial tachycardia in children, came to the conclusion that it is advisable to start therapy for this heart rhythm disorder with sotalol, since in 75% of cases he restored sinus rhythm or significantly reduced the frequency of ventricular contractions. If it is ineffective or there are contraindications, according to the authors, class 3 antiarrhythmics (with the exception of etmozine, which is ineffective in ALRT) or amiodarone should be used. Chronic atrial tachycardia in most cases is difficult to respond to mono- and combined antiarrhythmic therapy. EIT in this case is also ineffective. If antiarrhythmics do not work, in patients with chronic atrial tachycardia, it is necessary to achieve a decrease in the frequency of ventricular contractions to prevent the development of congestive heart failure. For this purpose, verapamil, diltiazem, cardiac glycosides or even amiodarones are used (their combinations are possible); in addition, the issue of non-drug treatment should be addressed.

Radiofrequency catheter destruction has been successfully used to treat atrial tachycardia, regardless of the electrophysiological mechanism of its development (automatic, trigger or reciprocal) and localization (right or left atrium). The main indication for radiofrequency catheter destruction is the ineffectiveness of pharmacotherapy or the patient's unwillingness to take antiarrhythmic drugs for a long time. In the USA, according to some reports, the effectiveness of such an intervention is 75%, and the number of complications is 0.8%. Destruction of the atrioventricular connection with the implantation of a pacemaker or its "modification" (partial destruction) is carried out if the radiofrequency catheter destruction of the arrhythmia focus is ineffective or it is impossible to carry it out. In patients with symptomatic recurrent supraventricular tachycardias that stop with pacing, in whom drug treatment and radiofrequency catheter destruction have been ineffective, implantation of an antitachycardiac pacemaker is possible. Surgical interventions (isolation, resection or destruction of the arrhythmogenic zone) are now rarely performed in case of failure of radiofrequency catheter destruction or if another cardiac surgery is planned.

Sinoatrial reciprocal tachycardia

One of the forms of atrial tachycardia, which differs somewhat in its clinical course, electrophysiological and ECG diagnostics, as well as pharmacotherapy, is sinus nodal reentrant tachycardia. The development of sinoatrial reciprocal tachycardia is associated with the circulation of an excitation wave in the sinus node, with the inclusion, in some cases, in the circulation circuit of a nearby portion of the right atrial myocardium.

This arrhythmia is usually paroxysmal in nature, and the heart rate with it varies from 100 to 220 beats per minute, but in general it is less than with other supraventricular tachycardias, and in most cases does not exceed 150 beats per minute. Attacks of tachycardia in this case are most often short (from 5-20 complexes to several minutes), prolonged attacks are observed very rarely. It is difficult to talk about the true prevalence of sinoatrial reciprocal tachycardia. The incidence of sinoatrial re-entry, according to most researchers, ranges from 2 to 10% among all supraventricular tachycardias. There is much less evidence of its wider distribution. Thus, SART was diagnosed in 11 of 65 patients (16.9%) with supraventricular tachycardia who underwent intracardiac electrophysiological studies.

Since the mechanism of development of sinoatrial reciprocal tachycardia is associated with the re-entry of the excitation wave, it is successfully caused and stopped by extrastimulation of the atria (sometimes even the ventricles) and increased atrial stimulation. Unlike most atrial tachycardias, the P wave located before the QRS complex is identical or very similar to that recorded in sinus rhythm. The PR interval is shorter than the RP interval. Sudden onset and, in most cases, sudden cessation of an attack, as well as the possibility of its relief by vagal techniques (sinus tachycardia and PRT do not stop with them) can serve as important differential diagnostic signs of sinoatrial reciprocal tachycardia.

Since the frequency of attacks in sinoatrial reciprocal tachycardia is usually low, and the attacks themselves are of short duration, they may be asymptomatic and do not require treatment. The relief and prophylactic antiarrhythmic therapy of symptomatic sinoatrial reciprocal tachycardia resembles that which is carried out with atrioventricular nodal reciprocal tachycardia. Cupping begins with vagal maneuvers (Valsalva maneuver, carotid sinus massage), and in case of resistance to them, intravenous antiarrhythmics are administered: ATP 10-20 mg (adenosine 6-12 mg, very quickly) or calcium antagonists (verapamil 5-10 mg or diltiazem 0.25-0.35 mg/kg for 2 minutes). Perhaps in / in the use of digoxin, beta-blockers and amiodarone. When the patient's condition is unstable (severe anginal pain, a significant decrease in blood pressure, cardiac asthma or pulmonary edema), an emergency electrical cardioversion is performed (the first shock with a power of 50-100 J). Paroxysms of tachycardia can be successfully stopped by pacing. For the prevention of attacks of sinoatrial reciprocal tachycardia, verapamil, diltiazem, beta-blockers, digoxin, as well as class III antiarrhythmic drugs - amiodarone and sotalol are primarily used. There are reports of the effective use of radiofrequency catheter destruction of the focus of arrhythmia.

Multifocal (chaotic) atrial tachycardia

Multifocal atrial tachycardia is diagnosed in 0.13-0.4% of hospitalized adult patients. It most often affects older people (average age is over 70 years). This rhythm disturbance is recorded in approximately the same proportion in men and women. More than 60% of patients with multifocal atrial tachycardia are diagnosed with lung disease. Chronic obstructive pulmonary disease is the most common. Less commonly, arrhythmia acts as a complication of acute pneumonia, pulmonary embolism, lung tumors. Drugs such as eufillin, isoproterenol, used in the treatment of chronic obstructive pulmonary disease, may play a role in the occurrence of arrhythmia, and also cause its more severe course. In addition to pulmonary pathology, such patients often have cardiovascular diseases (IHD, hypertension, less often valvular heart disease, etc.), accompanied by congestive heart failure. It is important to note that in many cases (according to some reports, up to 70%) carbohydrate metabolism disorders accompany multifocal atrial tachycardia. Mortality among adult patients with multifocal atrial tachycardia is high and amounts to 29-62%. The cause of death is usually serious illness, which affects most patients with multifocal atrial tachycardia, and not the rhythm disorder itself.

Electrocardiographic criteria for the diagnosis of multifocal atrial tachycardia are:

• the presence of three or more P waves of different morphology in one ECG lead;
• the presence of an isoline between the P waves;
• irregular PR, PP and RR intervals.

The shape of the P waves depends on the location of the ectopic arrhythmia and changes in intraatrial conduction.

Most often, multifocal atrial tachycardia has to be differentiated from atrial fibrillation. Unlike the latter, with multifocal atrial tachycardia, P waves of a changing shape and an isoline between them are clearly visible.

In the management of patients with multifocal atrial tachycardia, an important place is occupied by the treatment of the underlying disease and the correction of factors predisposing to its development: the fight against infection during exacerbation of chronic lung disease, the treatment of heart failure, the normalization of acid-base balance and electrolyte disorders, streamlining the use of beta-adrenergic receptor agonists and methylxanthine derivatives. These activities sometimes allow normalization of the rhythm even without the use of antiarrhythmic drugs.

Antiarrhythmic therapy of multifocal atrial tachycardia is associated with great difficulties. Some studies have shown the ineffectiveness of quinidine, novocainamide, lidocaine and phenytoin. Cardiac glycosides are also ineffective and often cause intoxication due to the presence of hypoxia and a number of severe metabolic disorders in patients. Electrical impulse therapy does not restore sinus rhythm and is therefore ineffective.

Analysis of works on antiarrhythmic treatment of multifocal atrial tachycardia shows that verapamil, beta-blockers (however, they are contraindicated in patients with bronchospastic syndrome) and amiodarone are most effective in slowing down, converting the rhythm and preventing recurrence of arrhythmia. There is a small number of studies devoted to the study of the effect of class 1C arthyarrhythmics on multifocal atrial tachycardia. Thus, in particular, a case of relief of tachycardia due to intravenous administration of flecainide to a 57-year-old patient is described, in whom verapamil, metaprolol, sotalol, disopyramide and some other antiarrhythmic drugs were ineffective; the possibility of successful parenteral and oral use of propafenone in this type of arrhythmia in pediatric practice has been shown. Interesting data were obtained regarding the high stopping efficacy of magnesium sulfate (in some cases in combination with potassium preparations): in 7 out of 8 patients with multifocal atrial tachycardia (87.7%), sinus rhythm was restored with intravenous administration for 5 hours from 7 to 12 g MgSO4. It should be noted that a decrease in the level of magnesium and potassium in the blood plasma was observed only in 3 patients.

Thus, it is advisable to start pharmacotherapy of multifocal atrial tachycardia with beta-blockers (if there are no contraindications to them) or verapamil, if they are ineffective, use amiodarone and class 1C antiarrhythmics, and intravenous administration of magnesium sulfate is also possible to stop arrhythmia.

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