home Polyps What is atrial tachycardia. The concept of atrial tachycardia: types, diagnosis and treatment. Atrial tachycardia of the reentry type

What is atrial tachycardia. The concept of atrial tachycardia: types, diagnosis and treatment. Atrial tachycardia of the reentry type

Atrial tachycardias account for approximately 20% of all supraventricular tachycardias. According to the electrophysiological mechanisms of development, three types of atrial tachycardia 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 quite often persistent or chronic, lasting months, and sometimes years, and can lead to the development of cardiomegaly.

Electrocardiographic diagnostics and clinical manifestations

Electrocardiographically, atrial tachycardias are characterized by the presence of a P wave, the shape of which usually differs from its morphology on a sinus rhythm located in front of the supraventricular QRS complex (the PR interval is less than the RP interval). The incidence of tachycardia in adults typically ranges from 140 to 180 beats per minute. With an increase in the frequency of 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 tachycardias from most atrial-ventricular tachycardia. Although it is difficult to distinguish between automatic atrial tachycardia and re-entry arrhythmias on the basis of clinical and ECG data, there are also a number of differential diagnostic features. Automatic atrial tachycardia cannot be induced and stopped by pacing, which is just characteristic of reciprocal arrhythmias. Atrial pacing with a frequency exceeding the frequency of automatic atrial tachycardia only temporarily suppresses the arrhythmia, after the termination of pacing it resumes.

The first P wave of automatic atrial tachycardia is similar to the subsequent P waves. In reciprocal tachycardia, the form of the atrial complex of the extrasystole, with which the attack usually begins, differs from the subsequent P waves, the morphology of which depends on the location of the pulse circulation. In contrast to arrhythmias caused by the re-entry mechanism, the frequency of automatic atrial tachycardia often gradually increases. This phenomenon is figuratively called "warms up" in electrophysiology. In clinical practice, the determination of the electrophysiological mechanism of the development of atrial tachycardia is necessary, basically, only when deciding on the use of electrocardiostimulation.

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 lesion in the right atrium, while a positive P wave ("dome and dart") in lead V1 and negative in leads V4-V6 indicates the origin of arrhythmia from the left atrium.

In some cases, atrial tachycardia has to be differentiated from sinus tachycardia. Differential diagnosis can be difficult, but it is important for the choice of treatment. Physical activity and vagal techniques significantly affect the frequency characteristics of sinus tachycardia and have little or no effect on them in 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 differential diagnosis.

Atrial tachycardia often develops in patients with organic heart disease. They are diagnosed with diseases such as coronary artery disease, myocardial infarction, arterial hypertension, heart valve lesions, 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 cause arrhythmias.

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 heart rhythm disturbances, is very low. However, if the arrhythmia proceeds 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-term paroxysms of atrial tachycardia do not need treatment. They need to 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 in its chronic course, even in the absence of hemodynamic disturbances and good tolerance of rhythm disturbances - due to the high risk of developing cardiomegaly and heart failure. Many cardiologists in the treatment of such patients now prefer interventional interventions rather than antiarrhythmic drugs, given their high efficiency with a small number of complications.

Paroxysms of atrial tachycardia with unstable hemodynamics should be stopped by an EIT discharge of medium energies (50-100 J). Pharmacotherapy of atrial tachycardia has not been sufficiently developed, although, in principle, it is carried out, as with other atrial tachyarrhythmias. With stable hemodynamics, to reduce high heart rate, drugs that worsen atrioventricular conduction are used: 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 low. If the paroxysm remains, then the restoration of the sinus rhythm is carried out by intravenous administration 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 recurrent attacks of arrhythmia, according to our experience and literature data, first of all, drugs of 1C and III classes (propafenone, flecainide, encainide, amiodarone, sotalol) should be used, class 1A antiarrhythmics such as quinidine, disopyramide, novocainamide are less effective, aymaline. 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 case of automatic atrial tachycardia in children, came to the conclusion that it is advisable to start therapy for this heart rhythm disturbance with sotalol, since in 75% of cases he restored sinus rhythm or significantly reduced the frequency of ventricular contractions. In case of its ineffectiveness or the presence of contraindications, according to the authors, it is necessary to use class 3 antiarrhythmics (with the exception of etmozin, which is ineffective in ALRT) or amiodarone. 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 ventricular rate to prevent the development of congestive heart failure. For this purpose, verapamil, diltiazem, cardiac glycosides, or even amiodarones are used (combinations are possible); in addition, the issue of conducting non-drug treatment should be resolved.

Radiofrequency catheter destruction is 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 United States, according to some data, the effectiveness of such an intervention is 75%, and the number of complications is 0.8%. Destruction of the atrioventricular connection with implantation of a pacemaker or its "modification" (partial destruction) is carried out when the radiofrequency catheter destruction of the arrhythmia focus is ineffective or impossible. In patients with symptomatic recurrent supraventricular tachycardia, arrested by pacing, in whom drug treatment and radiofrequency catheter destruction were ineffective, implantation of an antitachycardial pacemaker is possible. Surgical interventions (isolation, resection or destruction of the arrhythmogenic zone) are rarely performed at present, 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 sinoatrial reciprocal tachycardia (sinus nodal reentrant tachycardia). The development of sinoatrial reciprocal tachycardia is associated with the circulation of the excitation wave in the sinus node, with the inclusion, in some cases, in the circulation chain of the nearby portion of the right atrial myocardium.

This arrhythmia, as a rule, is paroxysmal in nature, and the heart rate 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. In this case, tachycardia attacks are most often short (from 5-20 complexes to several minutes), prolonged attacks are very rare. It is difficult to talk about the true prevalence of sinoatrial reciprocal tachycardia. The frequency of detection 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 out of 65 patients (16.9%) with supraventricular tachycardia who underwent intracardiac electrophysiological examination.

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 ventricles) and increased atrial stimulation. Unlike most atrial tachycardias, the P wave located in front of the QRS complex is identical or very similar to that recorded during sinus rhythm. The PR interval is shorter than the RP interval. A sudden onset and, in most cases, a sudden cessation of an attack, as well as the possibility of stopping it with vagal techniques (sinus tachycardia and PRT are not stopped by them) can serve as important differential diagnostic signs of reciprocal sinoatrial tachycardia.

Since the frequency of seizures in sinoatrial reciprocal tachycardia is usually low and the seizures themselves are short-lived, it may be asymptomatic and not require treatment. The curative and prophylactic antiarrhythmic therapy of symptomatic sinoatrial reciprocal tachycardia resembles that which is carried out with atrioventricular nodal reciprocal tachycardia. Cupping begins with vagal techniques (Valsalva test, massage of the carotid sinus), and in case of resistance to them, antiarrhythmics are administered intravenously: 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). Possible IV use of digoxin, beta-blockers and amiodarone. If the patient is unstable (severe anginal pain, a significant decrease in blood pressure, cardiac asthma or pulmonary edema), emergency electrical cardioversion is performed (first shock with a power of 50-100 J). Paroxysms of tachycardia can be successfully stopped with 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 arrhythmia focus.

Multifocal (chaotic) atrial tachycardia

Multifocal atrial tachycardia is diagnosed in 0.13-0.4% of hospitalized adult patients. Elderly people are more likely to suffer from it (the average age is more than 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. The most common chronic obstructive pulmonary disease. Less commonly, arrhythmia acts as a complication of acute pneumonia, pulmonary embolism, and lung tumors. Drugs such as aminophylline, isoproterenol, used in the treatment of chronic obstructive pulmonary disease, can play a role in the occurrence of arrhythmia, as well as cause its more severe course. In addition to pulmonary pathology, such patients often have cardiovascular diseases (coronary artery disease, hypertension, less often valvular heart disease, etc.), accompanied by congestive heart failure. It is important to note that in many cases (according to some data, up to 70%), disorders of carbohydrate metabolism 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 the serious illness that affects most patients with multifocal atrial tachycardia, and not the rhythm disturbance itself.

The 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 intervals of PR, PP and RR.

The shape of the P waves depends on the localization of the ectopic focus of arrhythmia and changes in intra-atrial 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, treatment of heart failure, normalization of acid-base balance and electrolyte disturbances, streamlining the use of beta-adrenergic receptor agonists and methylxanthine derivatives. These activities sometimes allow the rhythm to be normalized 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. Electro-pulse 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 reducing, 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 arrhythmias on multifocal atrial tachycardia. So, in particular, a case of tachycardia relief 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; shows the possibility of successful parenteral and oral use of propafenone in this type of arrhythmia in pediatric practice. Interesting data were obtained regarding the high stopping efficiency of magnesia 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 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 to stop arrhythmia, it is also possible to administer magnesia sulphate intravenously.

Literature

1. Pongiglione G., Strasburger J. F., Deal B. J. et al. Use of amiodarone for short-term and adjuvant therapy in young patients // Am. J. Cardiol. 1991; 68: 603-608.
2. Zeigler V., Gillette P. C., Ross A. B. et al. Flecainide for supraventricular and ventricular arrhythmias in children and young adults // Am. J. Cardiol. 1988; 62: 818-820.
3. Colloridi V., Perri C., Ventriglia F., Critelli G. Oral sotalol in pediatric atrial ectopic tachycardia // Am. Heart J. 1992; 123: 254-256.
4. Scheinman M. M. Patterns of catheter ablation practice in the United States // Pacing Clin. Electrophysiol. 1994; 17: 873-877.
5. Gomes J. A., Hariman R. J., Kang P. S. et al. Sustained symptomatic sinus node reentrant tachycardia: incidence, clinical significance, electrophysiologic observations and the effects of antiarhythmic agents // J. Am. Coll. Cardiol. 1985; 5: 45-57.
6. Scher D. L., Arsura E. L. Multifocal atrial tachycardia: mechanisms, clinical correlates and treatment // Am. Heart J. 1989; 118: 574-580.
7. Arsura E., Lefkin A. S., Scher D. L. et al. A randomized, double-blind, placebo-controlled study of verapamil and metoprolol in treatment of multifocal atrial tachycardia // Am. J. Medicine. 1988; 85: 519-524.
8. Creamer J. E., Nathan A. W., Camm A. J. Successful treatment of atrial tachycardias with flecainide acetate // Br. Heart J. 1985; 53: 164-166.
9. Reimer A., \u200b\u200bPaul T., Kallfelz H.-C. Efficacy and safety of intravenous and oral propafenone in pediatric cardiac dysrhythmia // Am. J. Cardiol. 1991; 68: 741-744.
10. Iseri L.T., Fairshter R. D., Hardemann J. L., Brodsky M. A. Magnesium and potassium theraphy in multifocal atrial tachycardia // Am. Heart J. 1985; 110: 789-794.
11. Olgin J. E., Zipes D. P. Specific arrhythmias: diagnosis and treatment. In Braunwald E. (eds). Heart disease. A textbook of cardiovascular medicine. Philadelphia: W. B. Saunders company. 2001. P. 837.

1. What is paroxysmal atrial tachycardia?

An attack associated with a very rapid and regular heartbeat that begins and ends suddenly. The heart rate usually reaches 160 to 200 beats per minute. The condition is also called paroxysmal supraventricular tachycardia.

The term paroxysmal means that the attack begins suddenly and ends also unexpectedly. Atrial tachycardia means that the upper chambers of the heart contract abnormally quickly. Paroxysmal atrial tachycardia can begin without heart disease.

2. What are the causes of paroxysmal atrial tachycardia?

Paroxysmal atrial tachycardia can be caused by premature atrial contraction, which sends a pulse of abnormal electrical activity to the ventricles. Other causes are related to stress, an overactive thyroid gland and, in some women, the onset of menstruation.

3. What are the symptoms of paroxysmal atrial tachycardia?

Although tachycardia is not life threatening, it can cause dizziness, chest pain, palpitations, anxiety, sweating, and shortness of breath.

4. How is paroxysmal atrial tachycardia diagnosed?

It is not always easy to diagnose paroxysmal tachycardia, since the attack has passed by the time the patient comes to the doctor. A thorough description of the seizure is the basis of diagnosis. If the palpitations persist, then an electrocardiogram shows it. Sometimes the doctor will order Holter monitoring to confirm the diagnosis.

5. How is paroxysmal atrial tachycardia treated?

Usually, the doctor gives advice on how to help yourself during an attack of paroxysmal atrial tachycardia. It is necessary to hold your breath after inhaling and exhale sharply, straining the lower abdomen, as during a bowel movement. You can also calm your heart by gently massaging your neck in the carotid sinus area.

If conservative measures do not help, the administration of the drug verapamil or adenosine is required. In rare cases, electrical stimulation is needed to restore normal heart rhythm.

Paroxysmal atrial tachycardia is not a disease and is rarely life-threatening. In rare cases, your doctor may recommend a catheter ablation procedure, which removes (cauterizes) the heart cells that trigger a fast heart rate.

Treatment of atrial tachycardia with grade II AV block

The severity of anterograde AV nodal block varies from Wenckebach's period. Often, the first ectopic P wave is already blocked. With significant AV block, the number of ventricular complexes becomes small.

Massage of the carotid sinus area enhances AV blockade without affecting the atrial P waves. In patients with digitalis intoxication, one should not resort to carotid massage. Atrial tachycardia with second-degree AV block tends to become fixed, i.e., acquire a chronic or intermittent course.

An important clinical and electrocardiographic problem is the differentiation of this form of tachycardia from TP.In the case of atrial tachycardia with AV block II degree caused by an overdose of cardiac glycoside, a diagnostic error (i.e., the diagnosis of TP) and, as a consequence, the continuation of digitalization is threatened with death.

At the same time, digitalis can be indispensable in the treatment of a true attack of TP. Differential diagnosis is based on the following criteria. First of all, the shape of the intervals P — P and T — P is taken into account. In atrial tachycardia, these intervals are isoelectric. In most cases of TP, a sawtooth or wavy line is recorded instead of an isoelectric line. Next, the frequency of the atrial impulses is taken into account.

For atrial tachycardia, the frequency of impulses less than 200 per minute is more characteristic, TP differs in the number of F waves of the order of 250-350 per minute. Finally, it is very important that in TP, the F waves arrive strictly regularly, whereas in atrial tachycardia with AV block, this regularity is often violated.

The occurrence of such a tachycardia during the period when patients are taking cardiac glycosides - a signal for their immediate cancellation. Intravenous drip infusion of a solution of potassium chloride (0.8-1 g per infusion) or phenotoin 50-100 mg every 5 minutes up to 1 g helps to end the attack. Sometimes potassium chloride only slows down the frequency of the tachycardic rhythm to a level of 150 per 1 min, followed by recovery AV conducting 1: 1 [Kushakovsky M. S. 1976].

Potassium chloride infusion is also used in cases where tachycardia is caused by an acute loss of potassium (massive diuresis, removal of ascitic fluid, etc.). B. Singh and K. Nademanee (1987) indicated that with a relatively early start of treatment, verapamil at a dose of 40-80 mg every 3 hours can also restore sinus rhythm in digitalis atrial PT with AV block II degree.

For tachycardia of a different genesis, subclass IA antiarrhythmic drugs are used in usual doses, but the effect is not always achieved. Electrical cardioversion is contraindicated in patients with digitalis intoxication.

"Arrhythmias of the heart", M.S. Kushakovsky

Atrial tachycardia with grade II anterograde AB block

Paroxysmal atrial tachycardia

Paroxysmal atrial tachycardia (PPT) is a sudden onset and abruptly terminating attacks of tachycardia arising from the pathological activity of heterotopic foci of automatism located in the atrial myocardium. The pulse rate reaches 150-250 (usually 160-190) per minute.

Classification

Reciprocal ( re-entry) atrial paroxysmal tachycardia

Chronic reciprocal (permanent-recurrent) PPT

Focal (focal) PPT

Multi-focal (multifocal) PPT.

Etiology. PPT is the most common form among all paroxysmal tachycardia (80-90%), especially at the age of 20-40

In 50-75% of cases, PPT occurs in people with a healthy heart after emotional stress, excessive consumption of coffee or tea, alcoholic beverages, marijuana, smoking, sleepless nights

Syndrome Wolff-Parkinson-White (up to 30% of all PPT)

Poisoning with cardiac glycosides and sympathomimetics

Changes in the heart with arterial hypertension

Hypokalemia

Hypoxia

Myocarditis

Thyrotoxicosis

Anomalies of the heart

Reflex irritation in diseases of internal organs (gallstone disease, colitis, kidney stone disease, peptic ulcer).

Pathogenesis

Circulation of excitation in the atrioventricular node (60% of PPT cases), in the atria (5% of PPT cases), foci (foci) of increased automaticity in the atria (5% of PPT cases)

In most cases, PPT is due to a mechanism re-entry (see. Cardiac arrhythmias) - the so-called. reciprocal tachycardia. For their development, the existence of two independent ways of conducting the impulse is necessary, which is possible in the following situations:

Electrical heterogeneity of areas of the heart muscle and its conducting system (coronary artery disease, myocarditis, etc.)

Developmental anomalies (additional fast-conducting beams Kent, James, longitudinal functional dissociation of the atrioventricular node)

An attack of PPT is not always indicative of heart disease. In 60-75% of cases, PPT occurs with a healthy heart muscle.

ECG identification

Heart rate - 150-250 rpm

The P wave is located in front of the QRS and can be changed

Foci of increased automatism in the atria - the shape of the P waves depends on the localization of the ectopic source

The initial part of the ventricular complex is not changed.

Management tactics

It is necessary to relieve tension and anxiety in the patient, create conditions to reduce sympathetic influences, provide access to fresh air

Stimulation of the vagus nerve (reduces the conduction of the atrioventricular junction) - massage of the carotid sinus, test Valsalva, pressure on the eyeballs (reflex Ashner)

If these measures are ineffective, drug therapy

Indications for electric pulse therapy are unstable hemodynamics, heart failure, progression of coronary artery disease.

Drug therapy - cm. Paroxysmal supraventricular tachycardia . Atrial fibrillation ; verapamil, b-blockers, novocainamide or cardiac glycosides IV.

One of the first B-blockers that began to be used for the treatment of cardiovascular disease was propranolol. This drug is more commonly known as anaprilin. Since the drug is a non-selective B-adrenergic receptor blocker, its use is currently limited. But there are situations where this medication has benefits.

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 cardiac contractions, their intensity, which is accompanied by a decrease in cardiac output. Through these mechanisms, the drug helps lower blood pressure.

Anaprilin lowers the activity of the sinus-atrial node, as well as foci of pathological activity located in the atria, AV-junction, ventricles. The medicine 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 decrease, the need of the heart muscle for oxygen 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 the arteries, in skeletal muscles, salivary glands, eyes and other organs. That is why blocking the stimulating effect of catecholamines leads to the occurrence of 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 expanded in comparison with selective B-blockers. But the number of side reactions is also significantly increased.

After taking the tablet inside, propranolol is absorbed rather quickly. After 1–1.5 hours, the concentration of the active substance in the blood reaches its maximum. The hypotensive effect lasts up to a day. Bioavailability is about 30%, but it increases after a meal. The half-life is two to three hours. 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 tablets for many diseases:

Increased blood pressure in essential and symptomatic hypertension.
IHD: stable and unstable angina pectoris, myocardial infarction (from the fifth day).
Tachyarrhythmias, including those associated with various diseases. Propranolol helps to effectively fight sinus tachycardia, Can be treated: supraventricular tachycardia, extrasystole, atrial fibrillation.
Heart disease: subaortic stenosis, mitral valve prolapse, hypertrophic cardiomyopathy.
Autonomic disorders: sympathoadrenal crises in patients with diencephalic syndrome, neurocirculatory dystonia, panic attacks, vegetative disorders during menopause.
Syndrome of portal hypertension in liver cirrhosis.
Thyrotoxicosis - to eliminate tachycardia, relieve thyrotoxic crisis, in preparation for surgical treatment.
Essential tremor.
Complex treatment of pheochromocytoma (necessarily with alpha-blockers).
Withdrawal syndrome.
Prevention of migraine attacks.
Primary weakness of labor and prevention of postpartum complications.
Hemangiomas in newborns.

Contraindications for treatment

Anaprilin can be used only in the absence of contraindications:

low pressure;
sinoatrial and AV block 2-3 degrees;
Heart rate less than 55 per minute;
SSSU (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;
violation of blood circulation 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.

Treatment methods

In the presence of high pressure, tablets begin to take 40 mg in the morning and evening. Gradually increase the dosage to the required level. 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 angina pectoris is to be treated, then start with 20 mg 3 times a day. The dosage can be increased over time to the 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 relieve rhythm disturbances and angina attacks. The medicine is administered intravenously. Eye drops are also available to help with glaucoma.

Side effect

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

First of all, the drug acts on the cardiovascular system, often causing a pronounced decrease in the heart rate, intracardiac blockade, hypotension, heart failure. Peripheral circulation is impaired due to arterial spasm.
The reaction of the nervous system manifests itself in the form of dizziness, headaches, and 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 disorders and paresthesias are possible.
The gastrointestinal tract reacts to 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 arteries, abdominal pain appears. Thrombosis of the mesenteric arteries and ischemic colitis may develop.
The respiratory organs also respond with a characteristic reaction to taking medicine. The increased tone of the muscles of the bronchi manifests itself in the form of bronchospasm and laryngospasm, shortness of breath, cough, chest pain appears.
Changes in the eyes: keratoconjunctivitis, visual disturbances and dry eyes.
Disturbances in the blood system: a decrease in the content of leukocytes, agranulocytosis, thrombocytopenic purpura, an increase in hepatic parameters, the content of cholesterol and its atherogenic fractions.
Other reactions: skin manifestations in the form of rashes, alopecia, itching, exacerbation of psoriasis; sexual dysfunction up to impotence; Peyronie's disease; joint pain; hypoglycemia and fever.

What you should know

If propranolol has to be used for a long time and there is a need to cancel it, then this should be done very carefully. The dosage is reduced gradually. If you stop taking the pills right away, you have withdrawal symptoms. This is manifested in the intensification of the symptoms of the underlying disease.

You should 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 body's reactivity (motor and mental), people who drive a vehicle or work in dangerous conditions should be especially careful.

You can not use the drug at the same time as some medicines:

antipsychotic and anxiolytics;
calcium channel blockers (diltiazem and verapamil);
alcohol-containing 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 agents and drugs that tone the uterus. But it 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 this B-blocker is planned to be carried out for a long time, then it is advisable to simultaneously take cardiac glycosides.

The tablets may contain 10 and 40 mg of active ingredient. 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, can only be determined by a doctor. 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 (atrioventricular) block 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 trunk,
in a bundle of His.

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

atrial,
nodal,
stem,
trifascicular (three-beam).

What is an atrioventricular node?

The atrioventricular node (Ashofa-Tavara) is an accumulation of special myocardial cells in the lower right atrium near the interatrial septum. The size of the knot is 3x5 mm. According to the importance of 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 the event of a refusal of a higher pacemaker.

Czech scientist Jan Purkinje was the first to describe special heart cells: 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 be spontaneously excited. This makes them related to neurons. In the future, 2 types of cells were distinguished in the conducting system of the heart:

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

Nutrition for cells is delivered in 90% of the 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 is fast.

Correct functioning of cells and channels ensures 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 action of drugs from the digitalis group;
inflammatory process during rheumatic attack, myocarditis of various etiologies caused by childhood infections, sore throat, flu;
site of necrosis or ischemia with the development of myocardial infarction;
focal and diffuse cardiosclerosis;
hyperkalemia and acidosis;
myocardial dystrophy in the area of \u200b\u200bthe conducting system;
consequences of hypertrophic changes in hypertension, myocardiopathies;
post-traumatic scars on the heart.

Types of atrioventricular block

Atrioventricular block is subdivided into:

incomplete - despite the impaired conduction, most of the impulses, albeit with a delay, reach the ventricles;
full - there is a rupture of the atrioventricular message.

By time:

short-term and permanent;
random and periodic.

In addition to the listed types, blockade is distinguished by three degrees of severity. They have ECG differences and characterize the depth of damage to the pathways.

Characteristics of violations in blockade I degree

Atrioventricular block of 1 degree means a slowdown in the transit time of the impulse from the atria to the ventricles to 0.2 sec or more (this corresponds to the broadening of the PQ interval on the ECG) at a normal rhythm frequency.

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 1st degree blockade is most significant in myocarditis. After treatment, it disappears. But it is impossible to diagnose only on the basis of one ECG sign. Clinical symptoms must be considered first.

Characteristics of violations in blockade II degree

2 degree of blockade means that some of the impulses from the atria are not conducted into the ventricles. The ECG shows a "prolapse" of the 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 second-degree atrioventricular block:

Type I is also called Wenckebach or Mobitz type I - the ECG reveals PQ intervals with a gradual lengthening, then there is a loss of ventricular contraction. The sign is called the Venkebach-Samoilov period. It is more typical for blockade in the proximal sections, therefore, the ventricular complexes are not changed. Rarely, atrioventricular block of the first type is combined with impaired conduction in the His bundles, due to which the QRS expands.
Type II or Mobitz II also occurs ventricular prolapse, but there is no previous PQ lengthening. It is associated with impaired incomplete conduction at the level of the trifascicular bundle, therefore, the ventricular complexes are more often expanded 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. Possible at both proximal and distal levels. The QRS complex either changes or retains the correct shape.

Characteristics of violations in blockade III degree

The third degree equates to 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 grades, complete AV block can occur from proximal or distal foci.

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

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

Clinical picture

With first-degree blockade, as a rule, the patient does not present any specific complaints. The altered state of health is associated with the underlying disease. In the second-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. Heart disease is usually accompanied by a number of symptoms:

Bradycardia at 30 beats per minute causes insufficient blood flow in the brain, dizziness appears, and short-term loss of consciousness is possible.
Patients experience rare strong shocks (beats) of the heart into the chest. This is caused by the overlapping of the rhythm of contractions of the atria and ventricles and the formation of single complete correct systoles.
When listening to a patient's heart, they have the characteristic of a "cannon shot". Examination of the neck reveals a pronounced pulsation of the veins due to the return wave of blood into the jugular vein.
For diagnostics, an important point is the absence of pulse acceleration after physical exertion, any fluctuations when holding the breath while taking a deep breath.

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

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

Treatment

Treatment of atrioventricular block is determined by the causes of the pathology.

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

urgently stop taking the medicine;
gastric lavage is usually ineffective, 30 minutes after ingestion, activated charcoal has a greater effect, which should be given several times;
antidigoxin and Atropine injections are injected;
Phenytoin and lidocaine are indicated when blockade is combined 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 an ion-exchange resin Polystyrene sulfonate, Hypothiazide;
in order to eliminate acidosis, a solution of sodium bicarbonate (soda) is injected drip.

It must be remembered that the methods of forced diuresis, hemosorption and hemodialysis are ineffective in this case.

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

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 and 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 blockages, a full set of drugs is used to expand blood vessels, eliminate impaired metabolism in cells, and reduce the ischemic zone:

fast and long acting nitrates;
coronary artery disease;
β-blockers even with bradycardia 50 per minute.

A solution of Atropine 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 resolved.

Treatment for atrioventricular blocks 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 an impulse occurs at the level of atrial tissue. The heart rate increases to 140-250 per minute.

Such a tachycardia develops in 2 scenarios:

A normal impulse source stops monitoring heartbeats. They arise under the influence of abnormal foci that are located above the level of the ventricles of the heart.
The impulse circulates in a circle. Because of this, the increased heart rate persists. This state is called "rebreathing" of excitement. 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 developmental 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 very often: its prevalence does not exceed 0.23%.

Atrial tachycardia occurs in 15-20%, and atrioventricular tachycardia - in 80-85%. Seizures develop at any time.

Many are diagnosed with this disease as early as childhood. But it can also develop as a complication after cardiac diseases. Paroxysmal supraventricular arrhythmias are thought to be intermediate between fatal and benign heart rhythm problems.

Paroxysmal attacks 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.

ECG classification and signs

The mechanism of the attack differs depending on the type of arrhythmia.

Sinoatrial tachycardia appears due to recirculation of the impulse along the sinus node and the myocardium of the right atrium. On the ECG, in this state, the P wave is preserved. It is he who is responsible for the contraction of the atria. The frequency of contractions reaches 220 beats / min.
Atrial arrhythmia appears when the activity of the pathological focus increases, which has its own automation apparatus.
The shape of the P wave on the ECG changes: it becomes negative or biphasic. With this form, the attack can develop gradually. The heart beats at a rate of 150-250 beats / min.
Paroxysmal AV-nodal tachycardia occurs when 2 parallel pathways of impulses arise in the area of \u200b\u200bthe junction of the atria and ventricles. Their functional characteristics differ.
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 of occurrence, risk factors

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

Doctors identify cardiac and non-cardiac causes of the development of the disease. These include:

In some cases, the reasons cannot be established. Risk factors for the development of the disease include:

hereditary predisposition;
the use of diuretics.

In childhood and adolescence, tachycardia appears against the background:

electrolyte disturbances;
psychoemotional or physical stress;
exposure to adverse conditions: with an increase in body temperature, lack of fresh air in the room.

Symptoms

Patients who have encountered PNT describe their condition differently. For some, seizures are almost asymptomatic. In others, the condition worsens markedly.

Paroxysmal supraventricular tachycardia manifests itself 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: lesion of the limbs on one side;
speech disorders;
increased sweating;
an increase in the amount of urination;
fainting.

Symptoms come on suddenly and disappear unexpectedly.

Diagnostics

If you have attacks of a sharp heartbeat, you should consult a cardiologist. An accurate diagnosis is established after a special examination. To identify supraventricular paroxysms, use:

physical examination;
conducting ultrasound, MRI, MSCT of the heart: they are done to exclude organic pathology in case of suspected paroxysmal tachycardia;
instrumental examination: ECG, ECG during exercise, Holter and electrophysiological intracardiac research.

A characteristic feature of the disease is rhythm rigidity. It does not depend on the load and breathing 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 condition is more dangerous.

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

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

weakness of the sinus node;
overexcitation of the ventricles.

Urgent care

There are several methods for reducing a patient's symptoms of an attack. The patient is recommended:

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

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

a sharp exhalation through a closed nose and mouth (Valsalva test);
carrying out massage of the carotid arteries (with caution do people who have atherosclerosis or impaired cerebral blood flow);
provoking a cough, in which the diaphragm bursts.

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 rate. But long-term use of certain antiarrhythmic drugs negatively affects the life prognosis. Therefore, the cardiologist should select the drugs.

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

In the presence of indications against paroxysmal supraventricular tachycardia, surgery is used. It is necessary:

with frequent attacks that the patient does not tolerate;
while maintaining the manifestations of the disease while 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. Read more about such operations in this video:

Therapy is aimed not only at eliminating arrhythmias, but also at changing the patient's quality of life. Rehabilitation will not be possible if the doctor's recommendations are not followed. Diet and lifestyle are important in treating arrhythmias.

Possible consequences, complications and prognosis

Short-term, unexpressed attacks do not cause serious discomfort, so their severity is underestimated by many. PNT can cause disability for the patient or lead to sudden arrhythmic death.

The forecast depends on:

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

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

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

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

Preventive measures

It is impossible to prevent the development of seizures. Even taking antiarrhythmic drugs on a regular basis 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. You also need:

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

When 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.

If the arrhythmogenic focus is located in the atrium of the myocardium, then atrial tachycardia develops. Pathology occurs regardless of the presence of other heart diseases in the patient. If the attacks are short-lived, then treatment is not carried out. If the heart rate rises for a long time, you need to seek medical help. Otherwise, the heart muscle is depleted.

What is the cause of the pathology?

Short bouts of tachycardia can occur against a background of stomach diseases.

For people of the older age group, a periodic increase in the heart rate is considered normal. The violation may be associated with the misuse of a number of drugs. Often the pathology is detected in obese people. In addition, the following factors affect the occurrence of atrial tachycardia:

How to recognize an ailment: the main signs

Against the background of this condition, the patient may complain of darkening in the eyes.

With the development of pathology, electrical impulses that stimulate the heart are generated in the atria. In the elderly, several foci are detected at once. According to statistics, in 70% of patients, tachycardia occurs due to increased activity of the right atrium, in other cases, left atrial disorder is diagnosed. Often, attacks occur intermittently, but prolonged tachycardia is possible, in which an increased heart rate is observed for several days or weeks. Heart rate can reach 140-240 beats / min. The average rate is 160―190 beats / min.

Atrial tachycardia symptoms:

What kind of examination is carried out?

There are several types of pathology. So, paroxysmal atrial tachycardia occurs suddenly and has a regular rhythm. In a non-paroxysmal disorder, prolonged attacks or frequent periods of malaise occur. In any case, if symptoms occur that indicate a malfunction of the heart, you need to be examined. The following diagnostic methods allow detecting atrial tachycardia:

Echocardiography will help identify cardiac abnormalities in a person.

Clinical analysis of urine and blood. It detects the presence of adrenaline breakdown products in the body, sets the level of hemoglobin and the presence of inflammation, excludes a number of blood diseases.
ECG. Detects the features of the heart. The main sign of atrial tachycardia is the P waves, separated by an isoline.
EchoCG. Reveals the condition of the heart muscle and the level of valve functionality.
Ultrasound of the myocardium. Indicates the presence of chronic diseases that can cause tachycardia.
Blood test for hormones. The level of work of the thyroid gland and adrenal glands is determined.

Differential diagnosis

Atrial tachycardia is often discovered incidentally during a routine ECG. For the timely detection of violations, you need to undergo regular medical examinations.

It is important to distinguish pathology from atrial flutter.

Before prescribing treatment for a patient, the doctor differentiates the examination results obtained with similar indicators inherent in other diseases. If the heart rate exceeds 220 bpm, this indicates atrial flutter. When an isoelectric line appears on the ECG between the P waves on II, III and aVF, they speak of atrial tachycardia. A comparison is made with sinus and sinus-atrial paroxysmal tachycardia. In the first case, the heart rate is 160 bpm. with gradual development and attenuation. In the second, the P waves have a normal configuration, there is a mild course and relief of pathology with the help of antiarrhythmic drugs.

What treatment is prescribed?

In most cases, the pathology does not require special therapy. If the heart rate increases, and the patient's quality of life deteriorates due to malfunctioning of the heart, a course of drug treatment is selected. The following groups of drugs are prescribed:

Beta blockers and calcium channel blockers. Control the ventricular rhythm, delay electrical conduction. Improve the condition during attacks, prevent their occurrence.
Antiarrhythmic drugs. Maintain sinus rhythm, slow down electrical conductivity. They are used with caution, as they can provoke the development of other heart diseases.