Atrial tachycardia is a type of arrhythmia in which the lesion is localized in the atrial region of the myocardium. Another name for this disease is supraventricular tachycardia. This type of pathology often leads to sudden death, momentary fainting(syncope) or presyncope.
The heart rate in this pathology can range from 140 to 240. Most often, this indicator in patients is from 160 to 190 beats per minute.
The development of atrial tachycardia occurs due to the inability to control the heart rate, as pathologies or additional nodes have formed.
The main causes of atrial pathology:
Atrial tachycardia is also common due to the use of certain medications. It is especially often caused by Novocainamide, etc. And also if an overdose of cardiac glycosides occurs, a severe form of the disease may occur.
Based on the location of the arrhythmia focus, atrial pathology is divided into:
Depending on the pathogenesis, they distinguish:
The symptoms of atrial tachycardia completely coincide with arrhythmia. Namely this:
Often such tachycardia does not manifest itself at all.
To diagnose atrial tachycardia, it is used as laboratory methods, and instrumental. Do laboratory analysis blood, it is important to know the concentration of red blood cells and hemoglobin. This is necessary in order to exclude diseases such as leukemia, anemia, etc. It is also important to do a thyroid hormone test and a urine test. A urine test determines the breakdown products of adrenaline.
TO instrumental methods include electrocardiogram.
With its help, the work of the heart and the type of tachycardia are determined. They can also use a Holter ECG - this is a study in which the work of the heart is recorded over a long period of time (24, 48 days, more if necessary).
ECHO-CG is important and more informative. This study evaluates the work of the myocardium as a whole and the functionality of the heart valves.
Also, using ECHO-CG and ultrasound of the heart, it is possible to diagnose heart defects and other chronic diseases that can provoke atrial tachycardia.
There are often cases when atrial pathology does not require treatment, for example, when it is asymptomatic and does not entail any consequences. Sometimes this pathology is discovered by chance during a routine electrocardiogram.
Treatment is different if a person feels discomfort, pain and increased heart rate, that is, the symptoms of the disease clearly manifest themselves.
In this case, drug therapy or surgical intervention in the form of catheter ablation is prescribed. Surgery may also be necessary to eliminate the cause of the tachycardia.
Drug therapy includes taking antiarrhythmic drugs. They can cause side effects, therefore, the doctor carefully selects the drug according to the studies conducted and must be adhered to established dosage. The doctor increases the dosage of antiarrhythmic drugs only if it does not bring results.
Antiarrhythmic drugs can be prescribed from different chemical groups, as they complement each other's action. There are drugs that potentiate each other's effectiveness. This combination can develop blockade and provoke a reduced contractile action of the myocardium.
Also, treatment for this pathology involves taking beta-blockers.
To summarize, we can say that atrial tachycardia is a pathology that can appear from time to time or last for a long time.
If the form is advanced, for example, it can occur in old age, then several foci may form.
As a rule, atrial pathology is not life-threatening, but sometimes dangerous situations arise, for example, when the heart begins to enlarge.
As for the prevention of tachycardia, you should lead a healthy lifestyle and give up bad habits.
April 09, 2018 No comments
Atrial tachycardia is a supraventricular tachycardia that occurs without affecting the atrioventricular (AV) node, accessory pathways, or ventricular tissue. The disorder can occur both in people with a structurally normal heart and in people with heart pathologies, including people with congenital heart defects (especially after surgery to repair or correct congenital heart disease or heart valve disease).
This 12-lead electrocardiogram demonstrates atrial tachycardia at a rate of approximately 150 beats per minute. Note that the negative P waves at terminals III and aVF (vertical arrows) are different from the sine waves (down arrows). The RP interval exceeds the RR interval during tachycardia. Note also that tachycardia persists despite atrioventricular block.
In patients with a normal heart structure, atrial tachycardia is not a serious disorder and has a low mortality rate. Patients with underlying structural and functional heart disease, congenital heart defects, or pulmonary disease are less likely to tolerate this heart rhythm disorder.
Focal atrial tachycardia is usually episodic (paroxysmal). Typically, atrial tachycardia manifests itself as a sudden onset of palpitations. Atrial tachycardia, as a result of increased automatism, can be unstable, but recurring, or it can be continuous or stable, as in repeated forms of atrial tachycardia.
Atrial tachycardia may gradually accelerate soon after its onset. However, the patient may not know about this. In a patient with supraventricular tachycardia (SVT), an acceleration phenomenon on the electrocardiogram (eg, on a Holter monitor) indicates that the SVT is an atrial tachycardia.
If tachycardic episodes are accompanied by flutter, patients may also experience dyspnea, dizziness, fatigue, or chest pressure. In patients with frequent or recurrent tachycardias, decreased exercise tolerance and symptoms of heart failure may present early manifestations cardiomyopathy caused by tachycardia.
Dizziness can be a consequence of hypotension, depending on heart rate and other factors, such as hydration status and especially the presence of cardiac pathologies. The faster the heart rate, the more likely the patient will become dizzy. A fast heart rate and severe hypotension may lead to fainting.
Manifestations of atrial tachycardia include:
Patients who have multifocal tachycardia may have an underlying disease that is causing the tachycardia. Such diseases may include pulmonary, cardiac, metabolic and endocrinopathic disorders. Chronic obstructive pulmonary disease (COPD) is the most common underlying disease (60% of cases) in multifocal tachycardia.
Supraventricular atrial tachycardia is not uncommon in patients with a history of surgical intervention defect interatrial septum. Connective tissue in the atrium can lead to the formation of a reentrant circuit.
When examining a patient, the most important abnormal symptom is a fast pulse. The heart rate is usually regular, but it may be irregular in rapid atrial tachycardia with variable AV conduction. Blood pressure may be low in patients who are tired, dizzy, or lightheaded.
A number of methods are used to systematize atrial tachycardia. Classification in terms of origin may be based on endocardial activation mapping data, pathophysiological mechanisms and anatomy.
Based on endocardial activation, atrial tachycardia can be divided into the following two groups:
Focal atrial tachycardia: Arises from a localized area in the atria, such as the crista border, pulmonary veins, coronary sinus ostium, or intra-atrial septum.
Atrial reciprocal (re-entry) tachycardia: Recurrent atrial tachycardia most often occurs in patients with structural or complex heart disease, especially after atrial surgery.
Other classification methods include:
Pathophysiological Mechanisms: Atrial tachycardia can be classified as a result of increased automaticity, triggered activity, or a re-entry mechanism.
Anatomical methods: Classification of atrial tachycardia can be based on the location of the arrhythmogenic focus.
Atrial tachycardia can be of right or left atrial origin. Individual atrial tachycardias actually occur outside the normal anatomical confines of the atria in areas such as the superior vena cava, pulmonary veins, and the vein of Marshall (the oblique vein of the left atrium), into which bundles of atrial myocardium extend. Rarer locations, such as non-coronary, have also been described aortic valve and hepatic veins.
Anisotropic conduction in the atria as a result of complex fiber orientation can create an area of slow conduction. Certain atrial tissues, such as the ridge border and pulmonary veins, are standard sites of automatic or triggered activity. In addition, disease processes or age-related degeneration atria can lead to an arrhythmogenic process.
Abnormalities that have been noted at sites of atrial tachycardia may include the following:
Atrial tachycardia can occur in people with typical cardiovascular disease or in patients with organic heart disease. When it occurs in patients with congenital heart disease who have undergone corrective or palliative cardiac surgery, atrial tachycardia can have potentially life-threatening consequences.
Atrial tachycardia resulting from physical exercise, catecholamine crisis, alcohol consumption, hypoxia, metabolic disorders, or use of stimulants or narcotics (eg, caffeine, albuterol, theophylline, cocaine), is due to increased automation or trigger activity.
Atrial re-entry tachycardia tends to occur in patients with structural heart diseases, in particular ischemic, congenital, postoperative and valvular disorders. Iatrogenic atrial tachycardia has become more common and is usually caused by ablative procedures in the left atrium. Several typical sites of origin of these tachycardias have been identified, including the mitral isthmus (between the left lower pulmonary vein And mitral valve), the top of the left atrium and, in the re-entry scheme, around the pulmonary veins.
MPT is often associated with underlying medical conditions, often occurring in patients suffering from exacerbation of chronic obstructive pulmonary disease, pulmonary thromboembolism, exacerbation of heart failure, or severe illness, especially when critically treated with inotropic infusion. MPT is often associated with hypoxia and sympathetic stimulation.
Other major conditions that are commonly associated with MMT are the following:
Unnatural forms of atrial tachycardia can be observed in patients with an infiltrative process, including the pericardium and, as a continuation, the atrial wall.
The rhythm strip ECG is the primary diagnostic tool for identifying, locating, and differentiating atrial tachycardia. Laboratory tests may be ordered to rule out systemic diseases which can lead to tachycardia. An electrophysiological study may also be required. P-wave morphology allows you to obtain important information about the origin of tachycardia, and precisely for this reason for ECG with 12 leads is essential.
When diagnosing atrial tachycardia, the following diagnostic methods can be used:
At the beginning of work on atrial tachycardia, it is necessary to conduct appropriate laboratory tests to exclude systemic causes sinus tachycardia(eg, fever, hyperthyroidism, anemia, dehydration, infection, hypoxemia, metabolic disorder).
The following laboratory tests can help exclude systemic causes of sinus tachycardia:
The following tests may be helpful in diagnosing atrial tachycardia:
Radiography chest : in patients with cardiomyopathy caused by tachycardia, or complex congenital disease hearts;
Scanning computed tomography(CT): exception pulmonary embolism, assessment of pulmonary vein anatomy and imaging prior to the ablation procedure;
Echocardiography: exclusion of heart pathology and analysis of the size of the left atrium, determination blood pressure V pulmonary artery, left ventricular function and pericardial pathology.
Primary treatment during an episode of atrial tachycardia is rate control using AV node blocking agents (eg, beta blockers, blockers calcium channels). Antiarrhythmic drugs can prevent relapse; A calcium channel blocker or beta blocker may also be needed in combination therapy.
Specific antiarrhythmic therapies include the following:
Atrial tachycardia with increased activity: Verapamil, beta blockers and adenosine;
Atrial tachycardia with increased automaticity: beta blockers, but general indicators improvements with treatment are low;
Recurrent atrial tachycardia: class Ic antiarrhythmic drugs
Maintenance sinus rhythm: Class III antiarrhythmic drugs
Cardioversion: used for patients who do not have good hemodynamics of the heart rhythm or for whom medicines, controlling heart rate control were ineffective or contraindicated.
Radiofrequency catheter ablation: for patients refractory to treatment. Radiofrequency catheter ablation for atrial tachycardia has become a fairly successful and effective treatment option for symptomatic patients whose condition is intractable. drug therapy or who do not want to undergo long-term antiarrhythmic treatment. She can treat forms of re-entry and focal forms atrial tachycardia.
Surgical ablation: used for patients with complex congenital disease hearts.
Treatment for multifocal atrial tachycardia (MAT) involves treating the cause that causes the fast heart rate.
Treatment may also include the following medications:
In very rare cases where MPT is persistent and refractory, the use of AV-compatible radiofrequency ablation and permanent pacemaker implantation should be considered. This treatment may provide improvement in symptoms and hemodynamics and prevent the development of tachycardia-mediated cardiomyopathy. In general, brief and asymptomatic episodes of atrial tachycardia detected as incidental findings on ambulatory ECG do not require treatment.
In adults, tachycardia is generally defined as a heart rate greater than 100 beats per minute (bpm). In children, the definition of tachycardia varies because the normal heart rate depends on age:
As with most cases of supraventricular tachycardia, the electrocardiogram typically demonstrates a narrow QRS complex tachycardia (unless trochlear aberration occurs). Heart rate can vary greatly, ranging from 100-250 beats/min. The atrial rhythm is usually regular.
The accompanying ventricular rhythm is also usually regular. However, it may become irregular, especially with more high rates atria, due to variable conduction through the AV node, thus creating conduction patterns such as 2:1, 4:1, a combination of these, or Wenckebach AV block.
The morphology of P-waves on the ECG allows us to determine the site of origin, as well as the mechanism of atrial tachycardia. In the presence of focal tachycardia, P-wave morphology and axis depend on the location in the atrium from which the tachycardia originates. In the presence of a macro-re-entry tachycardia pattern, P-wave morphology and axis depend on activation patterns.
Multifocal atrial tachycardia is an arrhythmia with an irregular atrial rate greater than 100 beats/min. Atrial activity is well organized, with at least three morphologically distinct P waves, irregular PP intervals, and an isoelectric base between waves. Multifocal atrial tachycardia was previously called chaotic atrial rhythm or tachycardia, chaotic atrial mechanism, and repetitive paroxysmal MPT.
Atrial tachycardia can occur at any age, although it is more common in people with congenital heart defects. MPT is a relatively rare form of arrhythmia, with a prevalence of 0.05-0.32% in hospitalized patients. It is predominantly observed in men and in elderly people, in particular in elderly patients with multiple medical problems. Middle age disease is 72 years old.
In patients with normal heart structure, atrial tachycardia has a low mortality rate. However, tachycardia-induced cardiomyopathies develop in patients with sustained or frequent atrial tachycardia. Patients with underlying structural heart disease, congenital heart disease, or pulmonary disease are less likely to experience atrial tachycardia.
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 morphologies.
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 block is often observed varying degrees. Antiarrhythmic drugs may be effective. In difficult cases, catheter RFA is required.
After 3 sinus complexes, a short episode of atrial tachycardia follows: the atrial rate suddenly increases and the shape of the P wave changes.Source of atrial tachycardia can serve as foci located both in the PP and in the LA. It can be persistent or paroxysmal. In a practical sense, the difference between atrial tachycardia and AFL is that in the first case the atrial contraction rate is lower (120-240 beats/min). 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, 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. Carotid sinus massage can be helpful in making a diagnosis. Adenosine can also be used for diagnosis, but in some cases the drug stops atrial tachycardia without causing transient AV block.
Atrial tachycardia s. The atrial contraction rate is 150 beats/min.
At AV conduction 1:1 it is difficult to distinguish atrial tachycardia from sinus tachycardia. 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 negative wave A P wave in leads I or aVL indicates that the source of the tachycardia is in the left atrium, while a positive P wave in lead aVL indicates the origin of the tachycardia in the atrium.
Subject to availability AV block high degree due to the fact that the ventricular rate is relatively low, an erroneous conclusion may be made about the presence of complete blockade hearts. As a result, there is likely to be an unreasonable question about the advisability of ECS if it is not properly assessed. high frequency atrial contractions!
Atrial tachycardia usually paroxysmal. However, if it continues for a long time, it can lead to the development of heart failure.
Multifocal atrial tachycardia, also called chaotic atrial rhythm, is characterized by the presence of high-frequency irregular atrial rhythm with P waves of different morphology. It is usually caused by pulmonary pathology or severe systemic pathology, such as sepsis.
a - Lead V1. Atrial tachycardia with AV conduction 1:1. The PR interval is longer than usual with sinus tachycardia. The etiological factors of atrial tachycardia can be cardiomyopathy, left ventricular (LV) dysfunction ischemic genesis, rheumatic disease heart disease, cardiac surgery for valvular or congenital heart defects, chronic obstructive pulmonary disease and cardiovascular disease. Often it is idiopathic. In left atrial tachycardia, the site 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 can be its precursor.
Sometimes arrhythmia occurs after successful ablation of the slow pathway performed for AVNRT, and its source is localized in the immediate vicinity of the point of application of radiofrequency treatment.
Atrial tachycardia with AV block may be due to digitalis intoxication. This arrhythmia is usually called “paroxysmal atrial tachycardia with block.” The term “paroxysmal” is inappropriate because the tachycardia is usually sustained.
If it is necessary to restore sinus rhythm, 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 conduction through the AV node. If a patient is receiving digoxin, digitalis toxicity should be suspected and the drug discontinued.
In cases refractory to drug treatment, consideration should be given to catheter RFA of the source of the tachycardia, which is often located in the lateral or inferoseptal region of the RA or near the pulmonary vein ostia in the left atrium, or to ablation of the AV node.
Atrial tachycardia from the right atrium (RA) with 1:1 AV conduction. 
Paroxysmal atrial tachycardia stops after 9 complexes. 
Atrial tachycardia (leads II and V1) in a patient with digitalis intoxication. 
What is atrial tachycardia, and what factors influence the development of pathology? This is a condition in which there is accelerated automatism of the atria as a result of damage individual areas myocardial tissue. In the supraventricular zone, the conductivity of electrical impulses generated by sinus node. This provokes the appearance of an abnormal focus of circulation, which causes excessive stimulation of cardiac activity and an acceleration of the contraction frequency, fluctuating in the range of 160-240 beats per minute.
The disease is most often detected in the elderly and children; according to statistics, it accounts for about 20% of all arrhythmic disorders; according to ICD 10, the code is assigned to 147.2 (paroxysmal ventricular tachycardia).
Atrial tachycardia can be chronic or paroxysmal. In the first case, a prolonged chaotic contraction of cardiomyocytes is observed over the course of 24 hours, days or even months; in the second, the attack lasts from several minutes to two to three hours. Depending on the nature of origin, pathology is classified into the following subtypes:
Sometimes it is impossible to determine the exact origin of the pathology, especially if the patient has not sought medical help for a long time.
In rare cases, in the absence organic lesions hearts and others destructive processes unexpressed atrial tachycardia can be taken as a normal variant.
TO negative factors that provoke the development of the disease include:
Tachycardia is most often a consequence chronic diseases. In a child, pathology can develop in the presence of congenital heart defects, in adults with an atrial septal defect, blockades, and also after surgical procedures.
Atrial tachycardia can only be diagnosed at the moment of paroxysm, which makes it difficult to identify the disease itself and determine further treatment tactics.
Because of this, the doctor may ask the patient to undergo several types of tests at different times.
In young and old people clinical picture may vary greatly. For example, people suffering from serious illnesses cardiovascular system, sometimes they do not even notice the acceleration of heart rate and other minor signs of progression of the pathology, which usually happens in old age. In relatively healthy patients, a change in condition in the worst side rarely goes unnoticed. But in most cases, patients are worried same symptoms, such as:
Untimely or incorrectly selected treatment can lead to the development of a multifocal form of atrial tachycardia, which is an advanced stage of the disease and is much more difficult to treat.
The most informative way to diagnose atrial tachycardia is an ECG (electrocardiogram), which must be performed right at the time of the attack, which is usually difficult to implement in practice. In this regard, it is often used daily monitoring according to the Holter method: the patient is at home or in a hospital setting with sensors connected to him that record any changes in the heart rate.
Blood and urine samples are also collected for laboratory testing. This procedure allows you to identify the breakdown products of adrenaline and the concentration of red blood cells. This is necessary in order to exclude the possibility that the patient has leukemia and other serious diseases.
Since atrial tachycardia is not an independent disease, treatment should be aimed at the main cause of the pathology. For example, for heart injuries it is used surgery, in case of infectious damage to the membranes of the organ (pericarditis), anti-inflammatory therapy is required.
In other cases, antiarrhythmic drugs are prescribed, such as Amiodarone or Propafenone. To eliminate excessive stimulation of the heart by impulses produced within the atria, beta blockers are used. Drugs in this group allow you to lower your heart rate and have a pronounced hypotensive effect, which is important if a person has arterial hypertension. If drug therapy is not enough, according to the indications of the attending physician, catheter ablation is performed to destroy the pathological tissue bundles that produce impulses.
Patients with asymptomatic and short-term attacks of atrial tachycardia are not prescribed treatment, since in this case the arrhythmia is a natural reaction to internal pathological processes. Prevention of paroxysms involves management healthy image life and treatment of existing diseases.
The life prognosis for minor hemodynamic disturbances and the rare occurrence of paroxysms is favorable. This pathology even with systematic relapses, it does not lead to dysfunction of the cardiovascular system, and also tends to self-heal. Possible complication is a weakening of the myocardium and, as a consequence, increased symptoms of tachycardia, which, as a rule, does not affect the patient’s life expectancy.
Rapid heartbeat during pregnancy: what to do? 
First described by T. Lewis (1909), it began to be intensively studied after V. Lown and N. Levine (1958) discovered its connection with digi-thalis intoxication. Digitalis was the cause of 82 of 112 (73%) episodes of tachycardia observed by these authors. Among other pathological conditions complicated by such heart rhythm disturbances, mention should be made cor pulmonale, pulmonary embolism, acute loss of K + ions, hypoxia during congenital defects heart, IBO, including previous myocardial infarction [Bondarenko F.N. et al., 1966; Sumarokov A.V. et al., 1970; Kushakovsky M. S., 1974, 1976; Ma-kolkin V.I. et al., 1976]. We recorded such tachycardia in several young people who did not have visible signs heart damage.
Tachycardia begins both in the early and late diastole phases of the sinus cycle. Sometimes you can see a “warm-up” period, i.e. a gradual “increase in the rhythm frequency, which at the height of tachycardia fluctuates in different patients from a value of >100 to 150-200 per minute. In most cases, it less than 200 per minute. The polarity of monomorphic ectopic P waves is usually positive in leads II, III, aVF; lower atrial tachycardias with inversion of P waves are less common in these leads. atrial rhythm irregular, sometimes it depends on the blockade of the exit from the ectopic center [Ku-shakovsky M. S., 1974, 1981]. It is also possible to alternate long and short R-R intervals, and the P-P interval that encloses the QRS complex can be shorter than the free P-P interval, as in ventriculophasic sinus arrhythmia. This variability in the symptoms of this tachycardia is probably due to the fact that there are two types of it: reciprocal(re-entry) and focal(trigger) tachycardia with AV block of the second degree.
It is necessary to emphasize one more fundamental point: second degree AV block occurs, as a rule, from the very beginning of the attack; it is stable and in most cases, like tachycardia, is associated with certain diseases, in particular with digitalis intoxication. All this distinguishes this form of tachycardia from other atrial tachycardias, in which second-degree AV block sometimes also develops, but in the latter case this sign is neither obligatory nor characteristic. The uniqueness of the considered variant of atrial tachycardia, therefore, lies in the fact that the same factors that cause ectopic activity simultaneously disrupt the conduction of the impulse in the AV node. We included only such patients (10) in our statistical table under this heading.
The severity of anterograde AV nodal block varies from Wenckebach's periodicity 3 2, 4: 3 to blockade 2:1 - 4: 1, etc. (Fig. 85, 86). Often the first ectopic P wave is already blocked (Fig. 87). With significant AV block, the number of ventricular complexes becomes small. Massage of the sinocarotid region enhances AV block without affecting the atrial P waves. Patients with digitalis intoxication should not resort to sinocarotid massage. Atrial tachycardia with second degree AV block has a tendency to become fixed, that is, to acquire a chronic or intermittent course.
An important clinical and electrocardiographic problem is once-the boundary of this form of tachycardiafrom TP In the case of atrial tachycardia with second degree AV block caused by an overdose of a cardiac glycoside, a diagnostic error (i.e., the diagnosis of AFL) and, as a consequence, continued digitalization threaten fatal. 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 P-P and T-P intervals is taken into account. In atrial tachycardia, these intervals are isoelectric. In most cases, instead of an isoelectric line, a sawtooth or wavy line. Next, the frequency of atrial impulses is taken into account. For atrial tachycardia, a pulse frequency of less than 200 per minute is more typical; TP differs in the number of F waves of the order of 250-350 per minute. Finally, it is very important that in AFL the F waves arrive strictly regularly, whereas in atrial tachycardia with AV block this regularity is often disrupted.
Rice. 85. Atrial tachycardia with AV block of the second degree (2 1).
The frequency of excitation of the atria is about 200 per 1 min, of the ventricles - about 100 per min, the patient is 55 years old, suffered a myocardial infarction
Rice. 86. Atrial tachycardia with AV block of the second degree (3: 2).
A 31-year-old patient with tetralogy of Fallot (not operated on). The frequency of atrial excitation is 230 per 1 min, the ventricular rhythm is incorrect (143-187 per 1 min).
Rice. 87. Three variants (a, b, c) of focal atrial tachycardia with AV block
II degree.
Differences in the P"-P" intervals and blocking of the first P" waves are visible.
Treatment of atrial tachycardia with Second degree AV block. The occurrence of such tachycardia while patients are taking cardiac glycosides is a signal for their immediate withdrawal. An 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 the level<150 в 1 мин с последую-щим восстановлением АВ проведения 1:1 [Кушаковский М. С., 1976]. К вливанию калия хлорида прибегают и в тех случаях, когда тахикардия вызывается острой потерей калия (массивный диурез, удаление асци-тической жидкости и т. д.). В. 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 AT with second-degree AV block. For tachycardias of other origins, antiarrhythmic drugs of subclass IA are used in normal doses, but the effect is not always achieved. Electrical cardioversion is contraindicated in patients with digitalis intoxication.
The first description of this type of atrial tachycardia was made by M. Lipson and S. Naimi (1970). The ECG records a rhythm with a frequency of 100 to 130 per minute; However, isolated cases of tachycardia with a more frequent rhythm (150 per minute or more) have been described. The P waves differ from each other in shape, amplitude, and polarity; at least on the ECG there are 3 different P waves. In patients with chronic lung diseases, the P waves are pointed, “hent-shaped” (Fig. 88). In cases where the P waves are low-voltage, the electrocardiographic picture may resemble AF. This impression is further strengthened by the fact that the duration of the P-P and P-R intervals is constantly changing. For the most part, AV conduction is maintained at 1:1, sometimes the P waves are blocked or coincide with the PVCs. QRS complexes remain narrow.
Basically, tachycardia is paroxysmal (probably triggered) in nature (Fig. 89). It can occur suddenly against the background of normal sinus rhythm or after a period of atrial extrasystole. Tachycardia is short-lived, persists no longer than a few days, but often recurs. True, E Abinader and M. Cooper (1983) observed multifocal atrial tachycardia for 6 years in a young woman who had prolapse of the posterior mitral valve leaflet.
Among patients with multifocal tachycardia, persons suffering from chronic bronchopulmonaryother diseases: up to 60-85% of cases of this tachycardia. Tachycardia of this type also occurs in acute febrile illnesses, especially in elderly and weakened people; with diabetes mellitus; congestive circulatory failure. In the materials of M. Lipson and S. Naimi, AF preceded or followed multifocal atrial tachycardia in 55% of patients. Tachycardia is a transitional rhythm between AF (AF) and sinus rhythm after electrical defibrillation. It is possible that it is for this reason that there is an increase in cases of multifocal atrial tachycardia [Ostapyuk F.E., Sotskova T.V., 1979]. Rarely, multifocal atrial tachycardia occurs in newborns. Treatment of this tachyarrhythmia mainly consists of influencing the underlying disease (bronchodilators, improving blood gas composition - magnesium, potassium, etc.). Anti-arrhythmic drugs are ineffective; “vagal techniques” do not interrupt attacks, nor does digitalization.
The formation of the modern doctrine of AV reciprocal (re-entry) tachycardias is rightly attributed to the late 60s - early 70s. True, these arrhythmias have been known to clinicians since the end of the last century, but the “classical” or “essential” Buveret-Hoffmann PT was mistakenly perceived by them as “atrial tachycardia” for almost 90 years. It has now been definitively proven that behind this name was hidden a group of AV reciprocal tachycardias, constituting about 85% of all supraventricular tachycardias.
They are united by a number of common properties, among which the following should be considered mandatory: 1) the location of the re-entry circle in the AV junction, which also includes a variety of accessory atrioventricular tracts (“border” ATs); 2) stability of AV nodal conduction type 1: 1 in cases where the AV node is included in the re-entry circle; it cannot be disrupted without stopping the tachycardia itself; 3) the circular movement of the impulse is also interrupted during a simultaneous blockade in some other part of the re-entry circle.
Both theoretical and, especially, practical considerations make it advisable to divide a large number of AV reciprocal tachycardias into two subgroups: with narrow QRS complexes and with wide QRS complexes.
The clinical picture of the three main forms of AV reciprocal tachycardia (re-entry in the AV node, re-entry in WPW syndrome, re-entry in latent retrograde DP) has many similarities, so it can be presented in a single description (with the necessary reservations).
Observations of our clinic staff, made mainly by T. D. Butaev, cover 298 cases of AV reciprocal AT, of which 109 (36.5%) were AV nodal reciprocal tachycardia, 117 (39.4 %) belonged to AV reciprocal PT in patients with electrocardiographic signs of WPW syndrome and 72 (24.1%) belonged to AV reciprocal PT in patients with hidden retrograde DP. As can be seen, the total number of patients with DP was 63.5%.
A. A. Grosu (1984) among 48 patients who suffered from attacks of ventricular tachycardia, identified AV nodal re-entry in 15 (31%), re-entry in WPW syndrome - in 33 patients (69%). A. A. Grosu, N. M. Shevchenko (1987) also described the combination of AV nodal and sinoatrial reciprocal ATs. The same observation was recently made by our collaborator Yu. N. Grishkin (1988). N. Wellens et al. (1980) diagnosed WPW syndrome in 68 of 120 patients (57%) who suffered attacks of supraventricular tachycardia.
Slightly different relationships between different forms of AV reciprocating tachycardia were noted by D. Wu et al. (1978), who examined 72 patients who had attacks of supraventricular tachycardia in the cardiac catheterization laboratory. They found that re-entry in the AV node occurs more than 5 times more often than in latent retrograde AP (patients with signs of WPW syndrome on the ECG were excluded from the study). In a group of 60 patients (without WPW syndrome), M. Josephson (1978) observed AV nodal re-entry in 66% of cases, re-entry in hidden bypass tracts in 20% of patients. In the work of K. Rostock et al. (1981) reciprocal PTs in WPW syndrome and division of the AV node into two conducting channels were in a 1:1 ratio. Finally, we point out that A. M. Zhdanov (1985), during intracardiac EPI of 56 patients, discovered AV nodal reciprocal tachycardias in 27 (48.2%), AV reciprocal tachycardias associated with WPW syndrome - in 12 (21.5%), AV reciprocal tachycardia with hidden retrograde pathways - only in 2 patients (3.7%).
Such significant discrepancies in the distribution of various forms of AV reciprocal PT are likely due to the peculiarities of patient selection.
In table 8 provides some information about our patients with three main forms of AV reciprocal tachycardia. It is easy to notice that patients who suffered attacks of AV nodal reciprocal tachycardia were older than others. Only 4 of them were under 30 years of age. Attacks of tachycardia first began in these patients when they reached adulthood. Most of them suffered from organic heart diseases: almost every third had coronary artery disease, every fourth had grade I-II MVP (M- and 2D echocardiographic scanning). True, the causal relationship of tachycardia with these anatomical changes in the heart could not be established. There were more women than men, which differs from the observations of D. Wu et al. (1978).
In those individuals whose re-entry loop included DP, attacks of supraventricular tachycardia more often began in childhood or adolescence. In this regard, the data of N. Wellens et al. are even more indicative. (1980). Of the 45 patients whose first attack of supraventricular tachycardia occurred before the age of 21, 73% had ECG signs of WPW syndrome. Of the 75 patients with the first attack of tachycardia, which occurred when they were over 21 years old, 48% of them had signs of WPW syndrome. According to our observations, circular PT associated with WPW syndrome occurred significantly more often in men than in women. We found organic heart diseases in this subgroup noticeably less often than in patients who suffered attacks of AV nodal tachycardia. Every 6-8th patient had MVP.
Table 8
Clinical data on patients with three main forms of AV reciprocal PT
with narrow complexesQRS
Signs | AV reciprocal nodal tachycardia | AV reciprocal tachycardia in WPW syndrome | AV reciprocal tachycardia with hidden retrograde DP |
Ratio between women and men | |||
Average age of patients, years (±sigma) | |||
Age limits, years | |||
Onset of attacks before the age of 18 years (°/o patients) | |||
IHD (% of patients) | |||
Mitral valve leaflet prolapse (% of patients) | |||
Absence of organic heart diseases (% of patients) |
Almost 1 /z The patients examined in our clinic associated the appearance of the first heart attack in their life with emotional stress. In 11% of patients, the first attack of tachycardia was preceded by diseases such as influenza, sore throat, colds, and pneumonia; 37% of patients could not indicate the cause of heart rhythm disturbances. Worth mentioning is the fact that in 23% of patients (women) the onset of “tachycardia history” coincided with the first menstruation. Physical activity, according to our data, rarely served as an impetus for PT, especially in patients with WPW syndrome. There was also a clear predominance of the number of daytime attacks over nighttime ones, which coincides with the observations of J. Cinca et al. (1987) and J. Irwin et al. (1988). The latter found that the probability of occurrence of attacks of AV reciprocal tachycardia in the afternoon is 5 times higher than in the morning (circadian oscillations).
Relapses of tachycardia occurred under a variety of circumstances: changes in body position, sudden movements, psycho-emotional reactions (fear, anger, etc.), food intake, weather changes. In a number of women, attacks became 2-10 times more frequent with the onset of menopause. All this indicates a greater dependence of attacks of AV reciprocal tachycardia on the state of neurovegetative and endocrine regulation of the body. The role of myocardial ischemia and cardiac weakness is apparently minimal here (!). The duration of the “tachycardia history” varied in different patients from 1 month to 42 years. The attacks were repeated with varying frequency: from 2-5 times a day to 1 time a year. In several patients, the pause between the first and second attack lasted for 10-20 years. The duration of each attack was also different: from a few seconds to 2-2.5 days. In the observations of E. Pritchett et al. (1988) the average duration of attacks was 20 minutes (from 5 to 90 minutes).
Patients emphasized that frequent heartbeats always began suddenly, with a feeling of a push or puncture in the heart, its “turning over” or “stopping,” and strong pulsation in the area of the cervical vessels. This was noted by L. Bouveret (1889), who wrote that the onset of an attack of tachycardia can be heralded by 2-3 beats, which can be “slow”, but more energetic. About 20% of patients noted that with each relapse of arrhythmia, they experienced more frequent interruptions (extrasystoles) in the heart area. Others, shortly before the attack, experienced a feeling of anxiety, tension, and “fullness” of the heart. Sometimes such “pro-dromes” dragged on for several hours. These people seemed to have foreseen the approach of the next attack of tachycardia.
Patients with WPW syndrome experience tachycardia attacks differently. In a series of observations made by N. Wellens et al. (1980), palpitations were felt by 97%, shortness of breath by 57%, chest pain by 57% (mainly at a pulse rate of more than 200 per minute), weakness and dizziness by about 30% of patients. According to our data, a decrease in systolic blood pressure, a feeling of lack of air, dizziness (usually at the beginning of an attack) were noted mainly in older patients who had organic changes in the heart, in particular pronounced MVP. In 2 of our patients with AV nodal reciprocal tachycardia against the background of a very fast rhythm, an attack of cardiac asthma developed, accompanied by a protodiastolic gallop rhythm. Polyuria (spastica) occurred during an attack or immediately after its end in almost every third patient. This reaction, lasting from 10 to 30 minutes, was observed at a tachycardic rhythm frequency above 120 per minute. A similar sign, described by K. Wenckebach, H. Winterberg (1927), P. Wood (1963), gradually decreased over the years in our patients. Recent studies by J. Nicklas et al. (1986) showed that the cause of increased natriuresis and diuresis during supraventricular AT may be excessive secretion of atrial natriuretic factor (peptide), depending on an increase in pressure in the right atrium. Inhibition of vasopressin secretion is also of certain importance.
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