• Tachycardia Symptoms and Treatment

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    Among paroxysmal tachycardia tachycardias of supraventricular localization prevail. Most VT occurs with myocardial infarction.

    Causes of

    Myocardial infarction: myocardial infarction, myocardial ischemia, cardio-myopathy, hypertensive heart, pulmonary heart, heart defects, myocarditis, trauma, surgery, swelling.
    Medications: cardiac glycosides, sympathomimetics, antiarrhythmics, theophylline.
    Metabolic disorders: hypokalemia, hypomagnesemia, renal failure, intoxication( alcoholic, nicotinic, caffeine).
    Hypoxia: bronchopulmonary diseases, heart failure, anemia.
    Endocrine diseases: diabetes mellitus, hyperthyroidism.
    Vegetative influences: vagotonia, sympathicotonia.
    Other reasons: reflex( trauma), braditahicardia syndrome, WPW syndrome.
    Idiopathic( primary electrical heart disease).

    Reentry( riaintrie, reciprocal, recurrent tachycardia).Under certain conditions, a wave of excitation appears in the myocardium, propagating along a closed loop. First, the electric pulse( extrasystolic or sinus) meets the block of the blockade in one of the directions, then this pulse bypassing the unexcelled obstacle returns through the originally blocked area with the formation of a continuous movement of the pulse along the closed loop and further excitation of the atria and ventricles.

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    Most tachyarrhythmia( about 80%) develops according to this mechanism, called in the English literature reentry( re-entry).
    Many NTVs are caused by congenital structural changes in the heart, predisposing to the development of reciprocal tachycardias. The additional AV pathway promotes the development of orthodromic tachycardia, and the longitudinal dissociation of the AV node is manifested by the AV nodal reciprocal tachycardia. Ventricular reciprocal tachycardias are usually caused by acquired ventricular lesions, for example, due to myocardial infarction.

    Reciprocal tachycardia begins and ends suddenly. Usually, this "rapid" tachycardia with a heart rate of 140-200 per minute. Spontaneous extrasystoles and increased sinus rhythm trigger the occurrence of reciprocal tachycardia.
    Such a tachycardia is caused and stopped with a programmable pacing. Vagal tests often help with supraventricular reciprocal tachycardias. Effective antiarrhythmic drugs, electrocardiostimulation and especially EIT.With EFI in cases of ULT, less often with VT, it is possible to accurately map the reentry loop and conduct ablation of the loop sites.

    Ectopic automaticity( ectopic, automatic, focal tachycardia).Tachycardia is caused by increased electrical activity of the cells of the conduction system and the myocardium. Automatic tachycardia account for up to 10% of all tachycardias.

    Most often, automatic tachycardia are caused by metabolic disorders: hypokalemia, hypomagnesemia, sympathicotonia or sympathomimetics, changes in acid-base balance, ischemia. Such arrhythmias are common in intensive care wards in patients with acute diseases.

    Automatic tachycardia is characterized by a gradual onset and termination. Usually, these are "slow" tachycardia with a heart rate of 110-150 per min, without hemodynamic disorders.
    Automatic tachycardia is not induced and does not stop with a programmable or accelerated pacemaker. Extrasystoles do not cause tachycardia, and vagal tests are not able to stop HPV.

    In treatment, elimination of the metabolic cause of arrhythmia is important. Ectopic automatism is usually difficult to treat with antiarrhythmic drugs and EIT.

    Determination of the location of the arrhythmogenic focus in the myocardium by means of electric cardiac mapping allows one to identify effectively and by ablation eliminate arrhythmia with the help of catheter ablation.

    Trigger activity( trigger, focal tachycardia).After passing the excitation wave, the trace electrical processes of sufficient intensity can lead to the development of tachycardia. Trigger tachycardia are characterized by features of automatic and reciprocal tachyarrhythmias: gradual onset and termination, call and stopping during pacing( significantly worse than reciprocal).

    Note that a conventional ECG is not sufficiently informative to diagnose the mechanism of tachycardia and requires an EFI.
    Knowledge of the mechanism of tachycardia largely determines the choice of the method of treatment of arrhythmia and antiarrhythmic drug. In 1990, the classification of antiarrhythmic drugs( "Sicilian Gambit") was developed, based on the effect of drugs on electrophysiological mechanisms and vulnerable parameters of arrhythmias. However, the complexity of classification and the inability in many cases to accurately determine the electrophysiological properties of arrhythmia impede the widespread use of this classification.

    Recently, it has been proposed to classify atrial tachycardias into focal( focal) ones, including arrhythmias with increased ectopic automatism, trigger activity and micrrientri( very small rounds of recurrent excitation), and with the participation of macririentri.

    Patients suffering from tachyarrhythmias most often report complaints of heart beat. This symptom is found in epidemiological studies in 16% of the population.

    However, the subjective feeling of palpitation is not always due to arrhythmias. For example, with daily monitoring of the ECG, only 17-61% of the heartbeats were accompanied by cardiac rhythm disturbances.

    The most common cause of heart rhythm not associated with arrhythmia is considered to be mental disorders. For example, in the study B. E. Weber et al.(1996) among 190 patients with palpitations in 31% of cases the symptom was due to a psychopathological cause. Most often among mental dysfunctions in the presence of palpitation, there is a panic disorder.

    Arrhythmias, in particular ventricular extrasystoles, can be the cause of chronic cough, which is eliminated by antiarrhythmic therapy.

    In the absence of a life-threatening situation, glycoside intoxication, hypokalemia and uncompensated heart failure are considered a temporary contraindication for cardioversion. If there are no clinical or electrocardiographic signs of an overdose of cardiac glycosides, it is not necessary to cancel the digoxin before EIT.Otherwise, it is better to postpone cardioversion, usually more than 24 hours, due to the risk of refractory ventricular tachyarrhythmias.

    In the case of a low heart rate for non-drug-related HTP, there is a damage to the conductive system. Therefore, in connection with the risk of severe bradycardia, replacement cardiac pacemaking may be required.

    When the patient is conscious and there is no possibility of general anesthesia, diazepam( > 10 mg) and morphine are injected intravenously to reduce discomfort from the electrical discharge.

    For anesthesia, short-acting drugs are recommended so that after a cardioversion the patient quickly recovered and it was not necessary to leave the patient in the hospital for the night.

    One of the most common errors is the insufficient level of anesthesia. In this case, patients not only experience severe discomfort, but also can remember this sensation.

    Complications of

    A strong electrical discharge can cause damage to the myocardium, causing changes in the ECG and an increase in the level of cardiac biomarkers in the blood.

    There is often a rise or depression of the ST segment( 35%), a negative T wave( 10%).Usually these changes take place within 5 minutes, but in rare cases can persist up to 30-60 minutes. Negative T wave can persist for several days.
    In 7-10% of cases after cardioversion, the level of cardiac biomarkers in blood increases. Note that the activity of troponins, unlike CK and myoglobin, does not increase, which is important in the diagnosis of myocardial infarction.

    Asystole with a slipping rhythm is caused by a massive release of acetylcholine and usually occurs within 5 seconds. With persistent bradycardia prescribe atropine.

    Cardiovascular non-synchronized cardioversion may be complicated by VF( 0.4%), which is easily eliminated by repeated discharge.

    In 2-3% of cases, the development of pulmonary edema is possible 1-3 hours after the restoration of sinus rhythm, the origin of which is unclear. The collapse of unspecified nature develops at 3% and can last several hours.

    Increasing cardioversion efficiency

    The following are the most popular methods for increasing cardioversion efficiency:

    high-energy discharge with external( 720 J with two defibrillators) and internal( 200-300 J) cardioversion,
    electrode position change,
    chest compression,
    biphasic discharge,
    administration of an antiarrhythmic drug and repetition of the procedure,
    electrical cardioversion in the background of antiarrhythmic treatment.

    Causes and predisposing factors

    If possible, identify and eliminate the cause of tachyarrhythmia( hyperthyroidism, coronary atherosclerosis, hypokalemia) and eliminate predisposing factors( hypoxia, sympathicotonia).Often there are situations where a combination of several factors leads to the appearance of tachyarrhythmias and requires a comprehensive treatment.

    In the case of severe symptomatic tachyarrhythmias, tachycardia is usually first stopped, and then the problem of eliminating the cause of arrhythmia arises. It is also necessary to take into account the peculiarities of arrhythmia treatment depending on the existing cause and the presence of concomitant pathology.

    To prevent recurrence of tachycardia the following measures are used:

    Elimination of the cause of arrhythmia: myocardial revascularization, correction of valve defect, treatment of hyperthyroidism.
    Medication antiarrhythmic treatment.
    Non-pharmacological treatment methods( catheter radiofrequency ablation, surgical treatment, ICD, antitachikardicheskii EKS).
    Elimination of provoking factors.
    Provoking factors tachyarrhythmias
    Physical activity.
    Mental factors: stress, anxiety, depression.
    VNS dysfunction. Alcohol, smoking, coffee.
    Reflex effects: cholelithiasis, swallowing, hiatal hernia, constipation, eating, sharp turn, osteochondrosis, etc.
    Change in blood pressure.
    Changing heart rate.
    Eticrolytic disorders: hypokalemia, hypomagnesemia.
    Drugs: theophylline, diuretics, thyroid hormones, etc.

    Note the importance of identifying provoking factors that facilitate the onset of tachycardia. Elimination or correction of these factors often helps reduce the frequency of relapses and the dose of antiarrhythmic drugs. At the same time, the relationship between factors that can cause arrhythmia, and heart rhythm disturbances is not always proven. For example, in patients with recurrent VT, the need for ICD therapy did not depend on a violation of the potassium balance.
    Often in the first months-years after the advent of paroxysmal tachycardia, there are one or two provoking factors, and in later stages, usually, numerous situations contribute to arrhythmia.

    Medication or surgical prophylaxis of tachycardia attacks has an alternative - relief of recurrent seizures. Therefore, in the beginning it is necessary to solve the problem of the need for preventive treatment.

    The constant reception of antiarrhythmic drugs has its drawbacks, for example, the side effects of drugs( including arrhythmogenic drugs).

    The decision on preventive treatment is taken if positive changes in the result of treatment significantly outweigh possible negative aspects. Prophylactic treatment is indicated in the following cases:

    Tachycardia attacks are accompanied by severe hemodynamic disorders( syncope, angina, shock, acute cerebrovascular accident).
    Tachycardia can cause VF( resistant VT in IHD).
    Tachycardia with mild hemodynamic disturbances( dyspnea, fatigue), occurs frequently( eg,> 1 time per week) and requires intravenous administration of drugs.
    Tachycardia often recurs and causes subjective discomfort without significant hemodynamic disturbances.

    Criteria for the effectiveness of treatment

    To assess the effectiveness of preventive treatment in symptomatic paroxysmal tachycardias, one can focus on the patient's feelings. In this case, an observation period exceeding the maximum interval between tachycardia attacks is not less than 3 times.

    The results of treatment of frequent daily paroxysms of tachycardia can be assessed using daily ECG monitoring by comparing the frequency of arrhythmia episodes before and after treatment. In this case, the frequency of arrhythmia must be taken into account on different days.

    The effectiveness of prevention of reciprocal tachycardia is also determined with EFI, when the possibility of provoking tachycardia after the appointment of an antiarrhythmic drug is evaluated.

    Note that the evaluation of drugs for oral administration is carried out in the same doses that the patient will use.

    To prevent paroxysms, tachycardia uses antiarrhythmic drugs. Preference is given to long-acting, cheap and safe drugs.

    You also need to consider the concomitant pathology. For example, in patients who underwent myocardial infarction, undesirable use of 1C class drugs( propafenone, flecainide), due to increased lethality. This recommendation is extended to other structural diseases of the heart. Note that the use of these drugs in patients without heart lesions is safe. With systolic heart failure, 1A class drugs( especially disopyramide), 1C class and calcium antagonists can cause progression of heart failure.

    Selection of antiarrhythmic treatment

    Stage 1: antiarrhythmic monotherapy - select one antiarrhythmic drug. At the outset, a drug that has a good effect with this arrhythmia is selected according to large randomized controlled trials. In practice, it is not uncommon to select an antiarrhythmic drug using the "trial and error" method.

    Stage 2:

    a) combination therapy - select a combination of 2 antiarrhythmic drugs. In this case, it is necessary to remember the potential risks of combined treatment, including proarrhythmic effects. B) heart rate control - with ULT, AV reduction and, respectively, heart rate with beta-blockers, calcium antagonists, digoxin, or a combination of these drugs. More rarely, amiodarone is used for this purpose.

    c) invasive treatment - radiofrequency catheter ablation of arrhythmogenic focus or reentry loop area, implantation of cardioverter-defibrillator.

    It is important to note that in severe tachyarrhythmias, more aggressive invasive treatment( radiofrequency ablation, cardioverter-defibrillators) is now often selected.

    Practical recommendations of

    The complaint of heart palpitations is not always due to tachyarrhythmia. Palpitation can be associated with anxiety, medications, anemia, hyperthyroidism, hypoglycemia and other conditions.
    It is necessary to strive to identify the cause of arrhythmia and try to eliminate it.
    With a small effect of the average therapeutic dose of an antiarrhythmic drug, it is preferable not to increase the dose, but to change the drug.
    If there is no effect of the drug of one group, then often other drugs of the same group are ineffective.
    With a combination of drugs, a qualitatively different effect may appear than with a single drug.
    It is desirable in the hospital to pick up 2-3 drugs for prevention and relief of tachycardia.
    With prolonged antiarrhythmic treatment, resistance to treatment often develops, which can be overcome by a break in treatment, increasing the dose or changing the drug.

    Tachycardia is the excitation of the atria and / or ventricles with a frequency greater than 100 per min. Only three consecutive excitations of one heart chamber( waves, teeth or complexes on the ECG) are enough to determine a tachycardia. The clinical significance of tachycardia is determined primarily by an increase in the heart rate, which is not always recorded with supraventricular arrhythmias. How to use folk remedies for this disease look here.

    The terminology of the flow of tachyarrhythmias has not yet been sufficiently standardized.
    In the latest international recommendations on atrial fibrillation, the first episode of arrhythmia was first described, and recurring episodes were recurrent. In case of spontaneous end of the episode, tachycardia is defined as paroxysmal, and if cardioversion is required - as persistent.

    Some specialists distinguish acute course - with the appearance of tachycardia in the period of acute disease, for example, viral myocarditis. For individual tachyarrhythmias, a continuously-recurrent course characterized by alternating arrhythmias with short episodes of sinus rhythm is characteristic.

    Localization: sinus, atrial, atrioventricular, associated with DP, ventricular.
    Course: acute, paroxysmal, recurrent.
    Mechanism: returnable, automatic, trigger.
    Symptoms: asymptomatic, symptomatic( heart failure, arterial hypotension, angina pectoris, syncope).

    ECG of rest
    Holter monitoring of ECG
    Event and transtelephone monitoring of ECG
    Electrophysiological study of
    Load tests

    Treatment of

    The tactic of arresting a tachycardia depends on the presence of hemodynamic disorders and prognosis. In case of severe complications, tachycardia( shock, acute heart failure, acute disorders of cerebral circulation, myocardial ischemia) is indicated by EIT, since antiarrhythmic drugs are less effective, they do not always act quickly and can even worsen the situation, for example, by lowering blood pressure.

    With dysfunction of the sinus node or AB blockade of 2-3 degrees, the risk of developing severe bradycardia, up to asystole, interferes with the treatment of tachyarrhythmia.

    Preservation of the cause of tachyarrhythmia( hyperthyroidism, severe heart disease), unsuccessfulness of arresting previous seizures or the inability to maintain a sinus rhythm for a long time make it unpromising to restore sinus rhythm.

    Asymptomatic tachycardias often do not require treatment. At the same time, with coronary atherosclerosis and increased risk of VF, restoration of sinus rhythm is shown.

    For non-severe symptoms( fatigue, palpitations, dyspnoea with exercise), antiarrhythmic drugs are usually used.

    Antiarrhythmic drugs used to stop tachyarrhythmias

    Class 1A: giluritmal, disopyramide, procainamide, quinidine sulfate.
    Class 1B: lidocaine, mexiletine, phenytoin.
    Class 1C: allapinin, moracizin, propafenone, flecainide, etatsizin.
    Class 2: beta-blockers: propranolol, esmolol.
    Class 3: amiodarone, brethil tosylate, dofetilide, ibutilide, nibentane, sotalol.
    Class 4: calcium antagonists: verapamil, diltiazem.
    Other drugs: ATP, potassium, magnesia.

    Note that the effect of amiodarone, unlike other drugs, develops slowly enough: for example, with AF, an average of 5.5 hours( from 2 hours to 48 hours).This inhibits the use of the drug in threatening conditions that require immediate effect.

    Nibentane, which has been shown to be quite effective in treating atrial fibrillation and flutter, can be complicated by the syndrome of prolonged QT interval with dangerous VT.

    In medical practice, there are often situations where the form of tachycardia is unknown, for example, if it is not possible to register an ECG or it is difficult to interpret it. In these cases, treatment is required, using the most rational approach.

    Treatment should take place in a relaxed business atmosphere, as stress and hyperkatecholamineemia increase heart rate. The presence of unauthorized persons hinders the work and increases the likelihood of errors. It is necessary to provide monitoring of ECG and blood pressure, to install an infusion system. In the ward where arrhythmia is treated, there should be everything necessary for resuscitation. Since sometimes after a cupping of a tachycardia there is a pronounced bradycardia( brady-tachycardia syndrome), temporary pacing may be required.

    In acute heart failure, oxygen therapy is connected. Antitumor therapy requires drug interactions, for example, diazepam can enhance the effect of ATP on sinus and AV nodes. If there are electrolyte disorders( hypokalemia, hypomagnesemia) or they are highly probable, appropriate correction should be made.

    Outside acute myocardial infarction, NTDs are much more common. The choice of tactics of relief depends on the rhythm of tachycardia, which can be determined auscultatory or by pulse.

    Rhythmic tachycardia can be caused by various HT and VT, among which the most common AV reciprocal tachycardia( nodular or orthodromic).

    In the case of rhythmic tachycardia, it is recommended first to carry out a vagal test, and if it does not help, then inject 6-12 mg of ATP.The effect of ATP is characteristic for AV reciprocal tachycardia, and sinus reciprocal and ventricular tachycardia are much less common in this situation.

    Decrease in heart rate or the appearance of pauses after vagal samples or ATP indicates atrial location of tachycardia, most often atrial flutter or atrial tachycardia.

    In case of preservation of a tachycardia at achievement of blockade AV of a site with a high degree of confidence it is possible to speak about ZHT.

    Note that with this approach, the assumption of localization of tachycardia in rare cases may be erroneous. For example, a stable VT with a BNPG configuration is sometimes stopped by vagal samples and ATP.

    In case of irregular tachycardia, atrial fibrillation is more common, atrial flutter is more common with a varying degree of AV blockade and even less often - atrial tachycardia. All these forms of supraventricular tachyarrhythmias can be both narrow-complex and wide-complex with concomitant BNPG.In addition, there are irregular forms of VT: bi-directional-fusiform and polytopic.

    In the case of unstable tachycardia of unknown type, it seems reasonable to use methods of arresting atrial fibrillation.

    Treatment of arrhythmic, unspecified tachycardia

    When recording narrow narrow QRS complexes( <120 ms) on ECG, supraventricular tachyarrhythmia can be suggested, since VT with narrow complexes is very rare. Note that the term "supraventricular( supraventricular) tachycardia" can be used only if it is impossible to determine the localization and mechanism of tachyarrhythmia.

    Differential diagnosis of narrow-complex tachyarrhythmias on the surface ECG is based on the evaluation of the morphology of the P wave and its location in the cardiocycle. For 12 leads ECG can be diagnosed the type of narrow-complex tachycardia in 81-84% of cases.

    Differential diagnostics of the

    In cases where the P wave can be seen indistinctly, long-term ECG recording in one lead( II, V,), signal amplification( 2: 1), a different recording speed( 25-50-100 mm / s).

    AB dissociation - independent excitation of the atria and ventricles - can be recorded with a narrow complex tachycardia. In this case, the tachycardia is localized in the AV node - the trunk of the bundle of the Hisnia or the intraventricular conduction system, and the impulses to the atria are blocked( retrograde AV blockade).

    EFI allows to cause reciprocal tachycardia, to determine the localization of tachyarrhythmias and to choose the optimal treatment.

    Indications for electrophoresis in narrow complex tachycardia

    I class( proven effectiveness)

    1. Patients with frequent or poorly tolerated episodes of tachycardia, inadequately responding to medication, for which knowledge of the localization of the source, mechanism and electrophysiological properties of the tachycardia pathways is important for selecting the appropriatetreatment( medication, catheter ablation, electrocardiostimulation, surgery).

    2. Patients who prefer ablatsiya medicamental treatment.

    Class II( conflicting performance data)

    Patients with frequent episodes of tachycardia requiring medication, for which information about the proarrhythmic effect of antiarrhythmic drugs, their effect on the sinus node or AV conduction is important.

    The tactics of treating narrow-set tachycardia are practically the same as those described in the section of unspecified tachycardia.

    With tachycardia with wide QRS complexes( & gt; 120 ms), three situations can be assumed:

    • VT;

    • NTT with persistent or frequency-dependent violation of intraventricular conduction( BNPG);

    • UWT in WPW syndrome.

    Because knowledge of the type of tachycardia allows for more effective treatment, differential diagnosis becomes important. The greatest problems are the differentiation of VT and NWT with aberration.

    Numerous criteria have been proposed to distinguish between NRT and aberration( BNPG) and VT.Each of these criteria individually has low information content, but with a combination of several criteria, the accuracy of diagnosis is 80-90% or more. Note that symptomatology and hemodynamic signs do not help in differential diagnosis.

    Diagnostic signs of HPLC and VT

    When analyzing ECG, it is important to know well the typical picture of BNPG, since the differences can be assumed by the ventricular source of excitation.

    Of great importance for diagnosis is the similarity of morphology and wide complexes during tachycardia and sinus rhythm. Often with prolonged ECG recording, transient changes in QRS morphology can be recorded, which help to clarify the type of tachycardia( Fig. 1.13,1.15).

    The determination of independent atrial excitation( AV dissociation) on the ECG may be important in the differential diagnosis of broad-based tachycardias. The frequency of the atrial rhythm, which exceeds the frequency of the ventricular rhythm, is characteristic for ULT, and in the opposite case, VT occurs.

    It is more difficult to interpret associated excitations of the atria and ventricles, since with VT in 25-30% of cases it is possible to retrograde the impulses to the atria. True, the frequency of VT in this case is usually 120-140 per minute, which is not typical for reciprocal UHT.It is difficult to diagnose and have a pseudo-P tooth that is part of the QRS complex with VT.

    The frequency of the atrial and ventricular rhythm can be estimated by ECG, vascular pulse wave and echocardiography.

    To assess the localization of tachycardia, an evaluation of the venous and arterial pulse( heart tones), reflecting the contraction of the right atrium and left ventricle, is used. To identify the pulse on the jugular veins use hepato-yugular reflux. Determine atrial contractions possible with echocardiography.

    You can use the day of diagnosis of tachycardia methods of slowing down AV-carrying: vagal and ATP.

    Decrease in the frequency of ventricular rhythm or relief of tachycardia is characteristic of supraventricular localization of tachyarrhythmias. Note that verapamil with VT sometimes causes significant arterial hypotension and acceleration of the ventricular rhythm, so its use in this situation is less desirable.

    The variability of heart rate and sonority of heart sounds caused by VAS asynchronous atrial and ventricular contractions may have a diagnostic value.

    Informativeness of heart rate and heart rate variability in the diagnosis of AS AS6969D In addition, with ULT with LNPG, a distinct cleavage of II tone is usually recorded, which persists on exhalation.

    Note also that a large-scale tachycardia developed in patients after myocardial infarction or with heart failure, usually( up to 80-90% of cases) is ventricular.

    Diagnosis of atrial fibrillation or flutter, antidromic tachycardia within the WPW syndrome has its own characteristics.

    The high frequency of ventricular excitations( & gt; 220-250 / min), the QRS morphology from the classical picture of BNPG( smoothed delta wave, unidirectional QRS), narrowing of QRS in the administration of drugs blocking DP( 1A, 1C,3 classes), the presence of classical pre-excitation features on previous ECG with sinus rhythm.

    It is important to note that blockade of AV-conducting with verapamil or digoxin not only does not reduce heart rate, but it can increase it.

    On the surface ECG it is often impossible to distinguish the forms of a wide-complex tachycardia. For example, VT with a reentry in the leg of the bundle of the Hisnia or atrio-fascicular tract has the morphology of QRS, which is characteristic of ULT with aberration. Arrhythmias with pre-excitation can be indistinguishable from VT on the basis of one analysis of QRS morphology.

    Conducting EFIs may be advisable in cases of severe tachycardia, when knowledge of the localization and mechanism of tachycardia is important in the choice of therapy.

    In heart disease, especially myocardial infarction and heart failure, VT occurs much more often than the ULC and can go to VF.Therefore, if it is impossible to clarify the localization of broad-based tachycardia, the tactics of treatment of VT are used.

    The drug treatment of VT involves the administration of lidocaine, and in the absence of the effect of procainamide or amiodarone. If medications do not help, then EIT is carried out.

    Recall that severe complications( shock, acute heart failure, myocardial ischemia, syncope) require immediate EIT.In other cases, with rhythmic tachycardia, procainamide, sotalol and amiodarone are recommended, and for arrhythmic tachycardia( eg, atrial fibrillation within the WPW syndrome) - procainamide, ibutilide or flecainide.

    Coping of a wide-range tachycardia

    The clinical significance of tachycardia is determined by its risk to the patient's life, suffering, disability and other limitations. An important factor determining the clinic of tachycardia is a violation of systemic hemodynamics, which is most often caused by a decrease in cardiac output at high heart rate. In addition, adequate blood supply to vital organs depends on the state of peripheral vascular tone, the system of local blood flow luteregulation and other factors. For example, in young people with ULT with a heart rate of> 200 per min, a significant reduction in cerebral blood flow and fainting is rare, and in elderly patients, a tachycardia with a heart rate of 150-170 beats / min can lead to impaired consciousness.

    In some cases, an increase in heart rate with a relatively preserved stroke volume leads to an increase in cardiac output and an increase in blood pressure.

    The presence of symptoms during tachycardia significantly influences the choice of treatment tactics. Asymptomatic tachycardia, unlike symptomatic, usually does not require treatment.

    Patient complaints of palpitations and interruptions, as shown above, are highly unreliable signs of arrhythmia, therefore the following techniques and methods are used to confirm the association of arrhythmia and symptoms:

    • Recording of heart rate or ECG during a symptomatic episode.

    • Holter monitoring of ECG, daily monitoring of blood pressure.

    • Event-based monitoring of ECG.

    • Provocation of tachycardia with EFI( intracardiac or transesophageal pacing).

    • Trial treatment( "exjuvantibus"): antiarrhythmic drugs, implantation of antiarrhythmic devices.

    With tachycardia, a decrease in the time of filling the ventricles and the volume of ejected blood can lead to impaired pumping function of the heart. Usually severe acute heart failure( class 3-4 Killip) develops with initially available left ventricular dysfunction caused most often by myocardial infarction, cardiomyopathy or heart valve defects. This is evidenced by symptoms of heart failure in history, signs of myocardial infarction on the ECG, an increase in the left ventricle during echocardiography.

    In this case, the traditional treatment of acute heart failure with vasodilators( nitroglycerin, sodium nitroprusside), diuretics and sympathomimetics( dopamine) will not only be ineffective, but even dangerous. The introduction of vasodilators against the background of tachycardia can cause severe arterial hypotension. Furosemide displays potassium, which contributes to the refractivity of arrhythmia to treatment. Sympathomimetics increase heart rate due to increased automatism of arrhythmogenic focus and acceleration of AB-conduction.

    It should be understood that often tachycardia reduces cardiac output and makes a decisive contribution to the heart failure clinic. The method of choice in the treatment of "tachycardic" acute heart failure is EIT, which most effectively reduces arrhythmia and does not reduce ventricular contractility.

    If there is no possibility to conduct EIT, then it is necessary to prescribe antiarrhythmic drugs, even despite the negative inotropic effect. For example, beta-blockers and calcium antagonists( verapamil, diltiazem) can stop pulmonary edema caused by the HPLC.At the same time, if left ventricular dysfunction was present before the development of tachycardia, the administration of antiarrhythmic drugs may, after elimination of tachycardia, increase the short duration of manifestation of heart failure. In this situation, drugs with minimal effect on myocardial contractility, for example lidocaine or amiodarone, are shown. The disadvantage of amiodarone in this situation is the slow development of the effect.

    With tachycardia with heart rate & gt;170 180 per min usually begins a decrease in cardiac output and blood pressure. With arterial hypotension the traditional treatment of sympathy and meticam and fluid infusion can be ineffective and even dangerous. The effect of sympathomimetics with tachycardia hypotension is associated with vasopressor action, and not with an increase in cardiac output. Therefore, dopamine should be given in sufficient doses or preparations with a predominantly vasopressor effect( norepinephrine).Note that sympathomimetics can increase the frequency of tachycardia and reduce the effect of antiarrhythmic drugs.

    The method of choice is EIT because it is more effective and safer than antiarrhythmic drugs. If there is no possibility of cardioversion, then tachycardia, the main cause of hypertension, should be suppressed. For example, with ULT, beta-blockers and calcium antagonists decrease heart rate and increase blood pressure.

    If lowered blood pressure was present before the development of tachycardia, then preference is given to antiarrhythmic drugs with minimal hypotensive effect. Note that intravenous amiodaron, especially with rapid administration, reduces BP in 20-26% of cases due to vasodilation.

    Attention is drawn to the information on the decrease in the hypotensive effect of calcium antagonists after the preliminary administration of calcium preparations, for example, I ml 10% calcium chloride. In this case, the antiarrhythmic effect of calcium antagonists does not decrease. Doctors also use co-administration of procainamide and sympathomimetics.

    With tachycardia, myocardial oxygen demand is significantly increased, and in the case of significant atherosclerotic stenosis of the coronary arteries, ischemia or even necrosis of the myocardium is possible. However, the diagnosis of the latter is often very difficult, which is due to a number of factors.

    With narrow-complex tachycardia in 70% of cases there is depression of ST segment, which is associated with sympathoadrenal activity. The literature describes depression of the ST segment 1-8 mm deep and slightly distinguishable from ischemic changes. Note also that after the end of tachycardia often( up to 40% of cases) there is a negative tooth T, which can persist for 6 hours to 2-6 weeks. This repolarization disorder in> 90% of patients is not associated with ischemic heart disease.

    Due to the existing difficulties in the interpretation of the ECG in diagnosis, it is necessary to take into account the presence of IHD in history, anginal pains, increase in plasma markers of myocardial necrosis( troponins, MB CK), ST segment displacement after

    tachycardia, risk factors for IHD( male, elderly, arterial hypertension, diabetes mellitus, hypercholesterolemia, smoking).It is possible to conduct a test with physical activity after tachycardia is stopped.

    Myocardial ischemia requires an emergency recovery of sinus rhythm, preferably with EIT.Note that during tachycardia, the effectiveness of nitrates is reduced, and sometimes severe arterial hypotension may develop.

    Atrial fibrillation occurs in 0.4% of the population, mainly in the elderly and senile, and up to 25 years, atrial fibrillation is very rare.

    In the presence of atrial fibrillation, the risk of death doubles, the main cause of which is the embolic stroke, which develops more often after 60 years.

    According to the latest ACC recommendations, /AHA/ ESC secrete paroxysmal, persistent and permanent forms of atrial fibrillation. With paroxysmal form, spontaneous recovery of the sinus rhythm takes place, usually in the period up to 7 days. If cardiac arrest or electrical cardioversion is required to arrest arrhythmia, then it is called persistent. Usually, persistent atrial fibrillation persists for more than 7 days. This category also includes cases of prolonged arrhythmia( for example, more than 1 year), when cardioversion was not performed.

    In the case of the first recording of an arrhythmia, it is designated as the first occurrence. With two or more episodes of atrial fibrillation - paroxysmal or persistent - the arrhythmia is additionally qualified as recurrent.

    Heart diseases affecting the atria

    • Hypertonic heart

    • IHD

    • Cardiomyopathies( primary, secondary, myocarditis)

    • Defects of the mitral valve, atrial septal defect

    • Pulmonary heart( acute, chronic)

    • Cardiosurgery: coronary bypass, mitralvalvulotomy, mitral valve prosthetics

    • Additional route for Kent( WPW syndrome)

    Other arrhythmias

    • SSSU

    • Tachyarrhythmias: atrial flutter, othere atrial tachycardia, AV nodal reciprocating tachycardia, orthodromic tachycardia, ventricular tachycardia

    System disorders

    • Hyperthyroidism

    • Metabolic disorders: hypokalemia, hypoxia, alcohol intoxication

    • Medications: cardiac glycosides, sympathomimetics, theophylline

    absence of heart disease and systemic violation

    • Idiopathic

    • If atrial fibrillation occurs, heart rate can be controlled up to 24 h, waiting for spontaneous recovery of sinus rhythm.

    • If atrial fibrillation continues> 2 days, anticoagulant therapy is required for 3 weeks before cardioversion and 4 weeks after it, regardless of the method of cardioversion.

    • If atrial fibrillation continues & gt; 2 days, it is preferable to restore the sinus rhythm with electrical cardioversion.

    • In the absence of an obvious cause of atrial fibrillation, it is necessary to evaluate the level of thyroid-stimulating hormone in the plasma.

    • Before starting treatment, try to avoid an overdose of digoxin, in which many drugs are not shown.

    • When restoring sinus rhythm, one should remember about the possibility of brady-tachycardia syndrome, especially in the elderly, with a history of dizziness or fainting, and a low heart rate.

    • At an HR of> 250 per min, there is usually an additional route, accelerated through the AV node or hyperthyroidism.

    • In case of paroxysmal, especially frequent and prolonged, atrial fibrillation, prophylactic anticoagulant treatment is performed in a similarly constant form.

    • In case of increased risk of injury at work or during sports, taking non-steroidal anti-inflammatory drugs, prolonged use of indirect anticoagulants is undesirable.

    With atrial flutter, the excitation wave spreads by the mechanism of macro-reentry around large anatomical formations, for example, tricuspid ring or fibrosis foci.

    It seems that the term "atrial flutter" denotes several varieties of atrial tachycardia, which is reflected in various classifications of tachyarrhythmias( types I and II, typical and atypical forms).

    The causes of atrial flutter differ little from those at atrial fibrillation. In paroxysmal form, structural damage to the heart may be absent, while a permanent form is usually associated with rheumatic or ischemic heart disease, cardiomyopathy. However, it should be noted drug-induced atrial flutter, which occurs in the treatment of atrial fibrillation with 1C preparations, as well as 1A and 3 classes. In this case, antiarrhythmic drugs contribute to the formation of slower and rhythmic atrial excitation.

    The frequency of atrial flutter is 2.5 times higher in men and increases with age: from 5 cases per 100 000 population to 50 years to 587 cases per 100 000 population over 80 years.

    Atrial flutter on the ECG instead of the P wave, rhythmic waves F with a frequency of more than 240 per min( in the absence of antiarrhythmic treatment) are determined. The difference in FF intervals is usually less than 20 ms.

    Isolate a typical form of atrial flutter, which is about 85%.The waves F in the II and III leads have a "sawtooth" shape, and in the lead V, they usually resemble the positive tooth R. In the atypical form in the II and III leads, F waves are recorded in the form of positive or negative teeth resembling a tooth R.-

    In a widespread classification, H. Wells( 1979) distinguishes between types I and II of atrial flutter.

    With type I, the frequency F of waves is 240-340 per min. This type of atrial flutter is caused by the mechanism of reentry, so tachyarrhythmia is well-controlled with increasing electrocardiostimulation. Atrial flutter I type is close to the typical form.

    With type II, the frequency F of waves is 340-430 per min. This type of tachyarrhythmia is associated with the emergence of a hotbed of increased automatism, so electrocardiostimulation is ineffective.

    In some cases, the atrial waves on the ECG are practically invisible and are only detected in the transesophageal VE lead or when creating an AV blockade with carotid sinus massage or medications( ATP, verapamil, propranolol).

    The frequency of the excitation of the ventricles with atrial flutter is limited to the physiological AV blockade of 2: 1-3: 1.If a blockade of 4: 1 and above is registered, then there is usually an organic lesion or the influence of medicines.

    The intervals RR can be the same, for example, with a robust AB blockade of the 2nd degree I type 2: 1 or 3: 1.With AB blockade of 2 degrees of type 1 or type II with varying degrees of blockade, the RR intervals differ.

    In young patients, the AV node is capable of transmitting up to 300 pulses per minute, so atrial flutter, usually associated with operations for congenital heart disease, is very dangerous. For example, in 6 years in patients without HR control, a sudden arrhythmic death was recorded in 20%, and in the presence of heart rate control, 5% of cases.

    With a heart rate of more than 3000 per minute, there is usually an additional route, accelerated through the AV node or hyperthyroidism.

    In the treatment of antiarrhythmic drugs 1A and 1C class, the frequency of atrial excitation( FF) can be reduced to 120-200 per minute and, accordingly, atrial impulses through the AV node with an increase in heart rate improve.

    Often flutter and atrial fibrillation occur together: one tachyarrhythmia may be preceded by another, or there is an intermittent pattern on the ECG.

    1. Viral myocarditis, the first arising atrial flutter of type I with AV blockade of 2 degrees( 4-6: 1) and heart rate of 40-60 per min.

    2. Idiopathic recurrent paroxysmal atrial flutter of type II with syncope.

    The treatment of atrial flutter is similar to the treatment of atrial fibrillation, but there are some features described below.

    Non-pharmacological cardioversion

    Atrial flutter is easily suppressed by EIT.It is preferable to begin cardioversion with a discharge of 100 J effective in 85% of cases, since at a discharge of 50 J the efficiency is lower - 75%.After a discharge of> 100 J( 100-200-360 J), the sinus rhythm is restored in 95% of cases.

    With Type I flutter, in 80%, electrocardiostimulation is effective, which is usually performed through the esophageal electrode. Conducting stimulation with a frequency of 15-25% higher than the spontaneous frequency of atrial flutter or salvos of super-rapid stimulation( up to 40 stimuli with a frequency of 10 per second).After the administration of antiarrhythmic drugs or digoxin, the effectiveness of CHPP increases.

    Medication cardioversion

    Drug treatment is generally less effective than with atrial fibrillation. Preference is given to intravenous administration of ibutilide, which restores the sinus rhythm in 38-76% of cases. Apparently, sotalol, amiodarone and preparations of 1C and 1A classes are less effective.

    When atrial fluttering is necessary, one should be afraid of an increase in heart rate after administration of antiarrhythmic drugs 1A or 1C class, which is associated with a cholinolytic effect and a decrease in the frequency of atrial excitation caused by slowing down.

    Drugs 1A and 1C class reduce intraventricular conduction and can lead to a significant expansion of QRS complexes. In this case, a wide-complex tachycardia similar to VT can develop.

    In the absence of the effect of cardioversion of atrial flutter, heart rate control is performed with the help of calcium antagonists, beta-blockers, digoxin.

    In addition, you can try to translate the flutter into atrial fibrillation. The latter is better tolerated, it is easier to control heart rate and more often the sinus rhythm is restored spontaneously. For this purpose saturation with digoxin, verapamil or CPP is used.

    Prophylaxis of thromboembolism in cardioversion

    Several studies reported an increase in the incidence of thromboembolism in cardioversion in patients with constant atrial flutter. Based on these data, some experts consider it necessary to prevent thromboembolism before cardioversion( conventional or based on transesophageal echocardiography).

    There was also a later restoration of atrial function after cardioversion in atrial flutter. According to recent studies, the risk of thromboembolism during the following month was 0.6-2.2%, which makes it reasonable to prescribe anticoagulants within 4 weeks after cardioversion.

    Drug treatment

    Prophylactic medication is performed similarly to that described in the section on atrial fibrillation. It should be emphasized once again the danger of severe tachycardia in the recurrence of atrial flutter when taking drugs of 1C class.

    Radiofrequency catheter ablation

    With a typical form of atrial flutter( type I), the excitation propagates around the circle of the reentry around the tricuspid valve ring in the right atrium. Radiofrequency catheter ablation in the region of the isthmus( the area between the inferior vena cava and the tricuspid valve ring) is effective in 81 to 95% of cases, but the frequency of recurrence of the tachycardia within 10-33 months is 10-46%.After the procedure, at 11-36% of cases, atrial fibrillation develops or persists, which is not surprising, since usually there is atrial disease. We note that in patients with atrial flutter during drug treatment, the risk of atrial fibrillation reaches 60%.The effectiveness of the method is reduced by the combination of flutter and atrial fibrillation.

    Indications for radiofrequency catheter ablation for atrial fibrillation and atrial flushing

    1 class( proven effectiveness)

    Patients with atrial flutter if medication is ineffective, or is poorly tolerated, or the patient does not want to take medicine for a long time.

    Class II( conflicting performance data)

    Patients with flutter and atrial fibrillation if medication is ineffective, or is poorly tolerated, or the patient does not want to take long-term medications.

    Heart rate control

    Temporarily before cardioversion and with the constant form of atrial flutter, the goal of treatment is to reduce the impulse conduction on the AV connection.

    With atrial flutter, it is more difficult to control heart rate as compared to atrial fibrillation. Often, 2 or even 3 drugs( beta-blocker, calcium antagonist and digoxin) are required to achieve the optimal ventricular rhythm.

    In the appointment of calcium antagonists and / or beta-blockers, the change in ventricular response does not occur gradually, as in atrial fibrillation, but in a leap, for example from 2: 1 to 3: 1 -4: 1.

    Prevention of thromboembolism

    The risk of stroke with constant atrial flutter was increased by 41% in retrospective data of 17413 cases of atrial flutter in the work of L. A. Biblo et al. In the study, K. Seidl et al. In 191 patients with atrial flutter for 26 ± 18 months, thromboembolism was detected in 7% of cases.

    At the same time, in patients with atrial flutter, thrombi in the appendix of the left atrium were found only in 1-1.6% of cases, and in the right atrium in 1% of cases. Given the relative rarity of thrombi in the atria with atrial flutter, it can be assumed that thromboembolic complications were caused by unregistered atrial fibrillation. In addition, cases have been described where flutter develops in one atrium, in the other - atrial fibrillation, and the picture of atrial flutter was recorded on the ECG.

    The validity of the ongoing antithrombotic treatment with constant atrial flutter is currently not clear. According to a number of American and European experts, the recommendations of antithrombotic treatment for atrial fibrillation and atrial flutter should be extended.

    • With heart rate & lt;100 per minute there is an AV block of grade 2, which requires caution in the treatment.

    • At a heart rate of more than 3000 rpm, there is usually an additional route, an AV node with accelerated conduction or hyperthyroidism.

    • Before starting treatment, try to avoid an overdose of digoxin, in which many drugs are not shown.

    • Class 1C and 1A preparations can increase the delivery of impulses to the ventricles, therefore, calcium antagonists or beta-blockers must be preselected.

    In some people, there is usually a congenital longitudinal dissociation of the AV node, predisposing to AV reciprocal tachycardia. The latter develops more often in young people( under 40 years) without structural damage to the heart.

    In this case, the AV node includes "fast" and "slow" fibers, respectively, with the front and back localization of the atrial connections.

    In the 1980s, it was shown that the impulse for tachycardia can occur in a number of cases along the near-node pathways of the right atrium and the intersection of these paths leads to the cessation of tachycardia. In this case, the term "reciprocal tachycardia from the AV compound" is often used.

    In most cases, with AV nodal reciprocal tachycardia, the impulse is anterograde along the "slow" pathway and retrograde along the "fast" pathway. There is a tachycardia with pulse circulation anterograde in a fast and retrograde slow pathway or atrial tissues. In very rare cases, the movement of the pulse occurs along the slow anterograde and retrograde pathways.

    With AV nodal reciprocal tachycardia, a rhythmic tachycardia with a heart rate in the range of 140-200 rpm is usually recorded.

    The electrocardiographic picture for this tachycardia depends on the electrophysiological properties of the AV node and adjacent tissues. The form of tachycardia( the path of the circulation of impulses) is determined by the position of the P wave in the cardiocycle.

    Electrocardiographic signs of AV nodular reciprocal tachycardia in different ways of pulse circulation

    On the ECG with a typical AV node reciprocal tachycardia( "slow-fast") a rhythmic narrow-complex( if not BNPG) tachycardia without P 'teeth is recorded. Such an ECG is detected in 66-74% of cases of this tachyarrhythmia. The teeth of P 'are hidden in the QRS complex, as simultaneous excitation of the atria and ventricles occurs. In transoesophageal lead VE, the P 'teeth are usually well visible.

    Less frequently the retrograde tooth P 'can be seen behind the QRS as a pseudo-S-wave in the II lead or pseudo-z'-tooth in lead V1.Such ECG is recorded in 22-30% of cases of AV nodal reciprocal tachycardia. In contrast to orthodromic tachycardia in WPW syndrome, the interval RP '& lt;100 ms.

    In the atypical form of a fast-slow tachycardia, the retrograde tooth P 'is located in front of the QRS complex, i. E.RP '& gt;P'R( 4-10%).In some patients, the retrograde tooth P is located in the middle of the cardiocycle while the pulse is being circulated along slow paths( "slow-slow").

    It should be noted the possibility of changing the position of the P 'tooth in the cardiocycle under the influence of antiarrhythmic drugs, which significantly complicates the diagnosis.

    AV node nasal reciprocating tachycardia is usually initiated after the atrial extrasystole with an extended PR interval. With this form of tachycardia, the RR intervals are usually the same, sometimes with slight changes due to variations in the AV conductivity. Possible shortening of RR intervals in the first few and lengthening in the last few cardiac cycles of tachycardia. A vagal test often stops the tachycardia, and sometimes only slows it down a little.

    Occurrence of AV blockade without interruption of tachycardia practically excludes AV reciprocal tachycardia, since blockade at the level of the trunk of the bundle of the His with this tachycardia occurs extremely rarely.

    AV reciprocal tachycardia is sufficiently easily induced and stopped with the help of rapid or programmed pacemaker.

    Tachycardia is provoked during a rapid pacemaker, usually in the range of the stimulation frequency close to the Wenkebach point.

    With programmed pacing as the extrastimulus adhesion interval( eSt) decreases, the eSt-R interval is significantly extended and then tachycardia is induced.

    Most often it is necessary to differentiate AV nodal reciprocal tachycardia with AV tachycardia( ortodromic) associated with carrying out a pulse through a retrograde DP functioning only. This form of tachycardia accounts for up to 30% of all NTV.

    On the ECG without an attack, signs of DP characteristic for WPW syndrome - shortening of PR interval, delta wave and wide QRS complex> are not visible.120 ms. Typically, this tachycardia appears on the ECG by placing the retrograde tooth P 'on the ST segment or the T wave( RP'> 100 ms).

    The final diagnosis of AV tachycardia involving latent DP is possible only with EFI, when ventricular stimulation previously excites atria than the trunk of the bundle of His.

    Treatment of this tachycardia is practically the same as treatment of AV nodular reciprocal tachycardia. In this situation, there is no danger of using calcium antagonists and beta-blockers, since DP functions only retrograde.

    The diagnosis of

    1. Idiopathic paroxysmal atrioventricular nodal reciprocal tachycardia with presyncop.

    2. Idiopathic paroxysmal atrioventricular nodal reciprocating tachycardia( "fast-slow") with a heart rate of 200 per min, angina.

    Causing an attack of

    With AV nodal reciprocal tachycardia, vagal tests and many antiarrhythmic drugs are effective. The most optimal treatment scheme is shown in Table.

    Efficacy of drugs for the treatment of AV nodal reciprocal tachycardia

    Closing tactic for AV node nasal reciprocating tachycardia

    We note the rather high efficiency of vagal samples( 60-80%).Preference is given to the massage of the carotid sinus. However, if there are acute disorders of cerebral circulation in the anamnesis, noise on carotid arteries or old age, the sample is not shown. The test with straining of Valsalva is also quite popular.

    If vagal tests do not help, then tachycardia in more than 90% of cases is stopped by calcium or ATP antagonists. Note that the effectiveness of vagal samples after administration of antiarrhythmic drugs is increased. Very rarely, other antiarrhythmics are required( 1A, 1C or 3 grade).

    It is easy to restore sinus rhythm during pacing.

    Some patients, in case of rare attacks of tachycardia and the impossibility of parenteral treatment, successfully use seizure with an oral medication:

    • verapamil 160-320 mg

    • propranolol 80 mg + diltiazem 120 mg

    • pindolol 20 mg + verapamil 120 mg

    • Propafenone 450 mg

    Oral medications have an average effect of 30-40 minutes( 4 minutes - 3.5 hours).Faster effect occurs if drugs take sublingual and chew.

    In the case of the choice of oral treatment, it is advisable in the hospital to make sure that such treatment does not cause serious complications,

    for example symptomatic arterial hypotension, decrease ADS & lt;80 mm Hg.sine sinus bradycardia <50 min, AB blockages of 2-3 degrees, etc.

    Most often, treatment is started with beta-blockers or calcium antagonists that have a better risk-benefit ratio. If these drugs are ineffective, radiofrequency catheter ablation is preferred, and preparations of 1C or 3 classes are less often prescribed.

    Efficacy of drugs for preventing AV nodal reciprocating tachycardia

    Since the 1990s, radiofrequency catheter ablation has become widely used to treat AV nodular reciprocal tachycardia. Preference is given to ablation of slow( posterior) ways, since in this case the incidence of AV blockade is about lower( about 1%) and the effect is higher in atypical forms of tachycardia. The ablation of slow pathways is effective in 90-96% of cases. In rare cases, the ablation of slow pathways leads to ablation of the fast( anterior) pathways. In this case, the effectiveness is 70-90% and the full AV blockade, which requires the implantation of EKS( about 8% of cases) develops more often.

    Indications for radiofrequency catheter ablation

    I class( proven effectiveness)

    Patients with symptomatic stable AV nodal reciprocal tachycardia if medication is ineffective, or is poorly tolerated, or patients do not want to take long-term medications.

    Class II( conflicting performance data)

    1. Patients with persistent AV nodal reciprocal tachycardia detected during EFI, or if necessary, catheter ablation of another arrhythmia.

    2. Detection of double pathways in the AV node and atrial echocomplexes without provocation of tachycardia during EFI in patients with suspected AV node-reciprocal tachycardia.

    • If the patient complains of palpitations occurring after vagal tests, this is usually AV reciprocal tachycardia.

    • In the case of AV reciprocal tachycardia, it is necessary to find out whether there are any additional routes.

    • Before carotid sinus stimulation should be evaluated the risk of possible complications( auscultation of carotid arteries, acute cerebrovascular accident in the anamnesis, elderly age).

    • Verapamil and ATP are the most effective drugs for arresting AV reciprocal tachycardia.

    Ectopic foci of excitation in focal tachycardia from AV joints most often occurs in the bundle of His. As a rule, this tachycardia occurs in children and newborns, and in adults it develops rarely. The recurrent course of tachyarrhythmia is characteristic, and chronic forms are rare.

    • Medications: glycoside intoxication, sympathomimetics

    • Myocardial ischemia, myocardial infarction( inferior)

    • Myocarditis

    • Cardiomyopathies

    • Heart operations( defect of the interventricular septum)

    • SSU

    The excitation frequency for AV focal tachycardia is usually 110-250 pulsesper minute The excitation of the atria is most often due to the sinus rhythm with the picture of AV dissociation( relatively rare, positive in the II lead of the P-wave, not associated with the rhythm of the ventricles).Less often the atria are raised retrograde from the AV focus. In this case on the ECG negative negative P 'in the 2nd lead behind the QRS complex or the P' teeth are hidden in the QRS complex.

    In adults, a "slow" tachycardia with a heart rate of 70-120 per minute, sometimes referred to as non-paroxysmal tachycardia from the AV compound, may be recorded in adults and treated separately from focal AB tachycardia. The term "tachycardia" at first glance is not fully correct for frequencies in the range of 70-100 per minute, but this is a very high frequency for the pacemaker from the AV connection.

    The characteristic for the work of the ectopic focus is the gradual onset and termination of tachycardia. The frequency of tachycardia changes with autonomic influences.

    Tachycardia with a low heart rate usually does not violate hemodynamics and does not require treatment. If therapy is necessary, difficulties are encountered in selecting an effective drug.

    First you need to try to eliminate the cause( cardiac glycosides, sympathomimetics, the underlying disease).In a number of cases, tachycardia can be suppressed with the help of drugs 1A, 1C and 3 grade. Cardioversion is usually ineffective, and with glycosidic intoxication is even dangerous. To prevent episodes of tachycardia, propafenone, sotalol and amiodarone can be used.

    With persistent tachycardia with a high heart rate, medications that slow the AV conduction can be prescribed, which, however, will not be effective when the focus is located in the bundle of His.

    In case of ineffectiveness or intolerance of drug treatment, radiofrequency catheter ablation of the ectopic focus is indicated.

    With sinus reciprocal tachycardia, excitation wave circulation occurs in the sinus node. Assume the dissociation of the conduction in the sinus node is similar to the AV node. Often, excitation occurs in the adjacent areas of the right atrium, so some researchers use the term "sinoatrial reciprocal tachycardia."Tachycardia is relatively rare and accounts for 1-10% of all UHT.

    • CHD

    • Atrial septal defect

    • Myocarditis

    • Cardiomyopathies

    Morphology P waves during sinus tachycardia reciprocal similar to that in normal sinus rhythm, or may be slightly different when the pulse circulating in okolouzlovoy atrial tissue.

    In contrast to sinus tachycardia due to the increase in sympathetic activity, the PR interval increases and the AV blockade with Wenckebach periodicals is often recorded.

    Sinus reciprocal tachycardia is relatively "slow" - the heart rate is usually 100-150 per minute, and the episode of tachyarrhythmias includes more often <10-20 complexes and rarely exceeds several minutes.

    Tachycardia occurs and ends after the atrial extrasystole. However, sometimes tachycardia begins without a previous extrasystole, which distinguishes it from other reciprocal tachycardias.

    It should be noted that half of the patients have sinus node dysfunction.

    Tachycardia attacks usually have a low heart rate and are short, so arrhythmia is rarely needed. Vagal samples eliminate sinus reciprocal tachycardia much less often than AV reciprocal tachycardia. Verapamil, beta-blockers and ATP are effective enough, but

    should be remembered about the possible concomitant sinus node dysfunction. Class 1 drugs poorly restore sinus rhythm with this tachycardia. In addition, seizures can be stopped with the help of pacing.

    Verapamil, beta-blockers and amiodarone are used to prevent paroxysms of tachycardia. For the selection of treatment is applied CHPES, which allows provoking tachycardia.

    With symptomatic recurrent tachycardia and inefficiency or intolerance of drug treatment, radiofrequency catheter ablation is possible, sometimes followed by implantation of ECS.

    Paroxysmal reciprocal atrial tachycardia is rare and accounts for about 5% of all UHT.

    • IAD

    atrial septal defect •

    myocarditis •

    cardiomyopathy •

    cardiomyopathy •

    hypokalemia •

    heart glycoside intoxia • Idiopathic

    Predictive P wave signals are registered before the QRS complex. In the case of arrhythmia localization in the upper parts of the atrium, the P-wave is positive in the II lead, and when the arrhythmia is localized in the lower parts of the atrium, they are negative. The frequency of tachycardia is 120-220 per min. The PR interval is usually prolonged, but the AV block of the 2nd degree develops rarely.

    Spontaneous termination of a tachycardia can be sudden, with a gradual slowdown or an alternating change in the duration of a cardiocycle( long-short).

    Vagal tests usually do not stop tachycardia, even if they cause AV blockade. In some patients, tachycardia is stopped by adenosine, beta-blockers or verapamil.

    For the treatment of atrial reciprocal tachycardia, 1C class drugs and amiodarone are used. Sotalol and Class 1A preparations are somewhat less effective. Beta-blockers and calcium antagonists have little effect on conduction in the atria and are used primarily to control heart rate.

    Paroxysmal focal atrial tachycardia occurs in 0.3% of the population and accounts for about 5% of all UHT.In children, this tachycardia occurs much more often - about 10-23% of all NTV.

    myocardial ischemia •

    dilated cardiomyopathy •

    myocarditis •

    myocarditis •

    mitral valve prolapse •

    atrial septal defect correction • Chronic lung diseases, especially with acute

    infection • Digitalis into

    • Hypokalemia

    • Alcohol intoxication

    • Idiopathic

    With tachycardiathe teeth P of the altered morphology before the QRS complex are recorded. The P tooth is often hidden in the preceding T wave. The PQ interval is at the isoline. Tachycardia is usually unstable with a frequency of 100-200 per min.

    Recently, atrial tachycardia has been described, the source of which is most often localized in pulmonary veins, having heart rate & gt;250 per minute and often turning into atrial fibrillation.

    Tachycardia can be caused by late atrial extrasystoles without the same adhesion interval. The first tooth P of tachycardia is similar to subsequent teeth of P with tachycardia, in contrast to most forms of reciprocal atrial tachycardia.

    The first PP intervals progressively decrease( "warming up" of the ectopic focus).The variation of the PP intervals is usually negligible( <50 ms).It is possible to block the output of the 2nd degree of the first type with a progressive decrease in the interval PP and the appearance of a pause less than 2 * PP or block 2 of the second type with the appearance of pauses that are multiples of the PP interval.

    Vagal tests do not stop tachycardia, even if they cause AV blockade.

    Tachycardia often does not respond to treatment. Antiarrhythmic drugs( 1A and 1C class, sotalol, amiodarone) are selected empirically. Beta-blockers, calcium antagonists and cardiac glycosides are used to control heart rate.

    At present, radiofrequency catheter ablation is usually performed, the efficiency of which reaches 90%.

    Chronic focal atrial tachycardia is common in children and rarely in adults. Among the URT in adults, this rhythm disturbance is recorded in 2.5-10% of cases, and among children - in 13-20% of cases. There is a continuous recurrence or a constant course of arrhythmia.

    • Correction of

    atrial septal defect •

    myocarditis •

    dilated cardiomyopathy •

    dilated cardiomyopathy • Idiopathic

    In chronic atrial tachycardia, the P tooth of altered morphology is recorded before the QRS complex. Often there are fluctuations in the PP intervals due to instability of the ectopic focus. The frequency of atrial excitation is in adults 120-150 per min, and in children 180-250 per min. The focus of excitation may be sensitive to vegetative influences. It is possible to block the exit from the focal point of the 2nd degree of the first type with a progressive decrease in the RR interval and the appearance of a pause 2 2 * PP or a block 2 of the second type with the appearance of pauses that are multiples of the PP interval.

    In most cases of continuous recurrence the first 2-4 intervals of the PP progressively decrease( "warming up" the ectopic focus).Tachycardia ends with a gradual increase in PP intervals or suddenly.

    Tachycardia often does not respond to treatment. You can try 1C class drugs, amiodarone, magnesium. Cardioversion and electrocardiostimulation are ineffective. Beta-blockers, calcium antagonists and cardiac glycosides are used to control heart rate.

    Destruction of the arrhythmogenic focus is a method of choice for severe tachycardia and inefficiency of antiarrhythmic drugs. Applied catheter radiofrequency ablation of arrhythmogenic focus, surgical resection or isolation of the focus.

    Recently, a continuous-recurring monomorphic atrial tachycardia of an unknown mechanism has been described that is easily suppressed by lidocaine and insensitive to other anti-arrhythmic drugs.

    In polytopic( "chaotic", multifocus) atrial tachycardia due to hypoxia, toxic effects, organic changes in the atria, several foci of pathological impulses arise. Usually arrhythmia develops in elderly people who have numerous medical problems. This is the most common form of automatic atrial tachycardia.

    The course of tachycardia is usually paroxysmal, less often chronic. Mortality with this tachycardia reaches 30-60% and is caused in a significant majority of cases by the main disease.

    • Chronic obstructive pulmonary diseases( 65-80% of all causes)

    • Heart failure

    • Medications: theophylline, sympathomimetics, cardiac glycosides

    • Sepsis

    • Myocardial infarction

    • Pneumonia

    • Pulmonary embolism

    • Diabetes mellitus

    • Hypokalemia

    Pins of P are recorded in at least 3 varieties, the rhythm is irregular, the intervals PP, PR and RR vary considerably. Usually, heart rate is 100-130 per minute and rarely, mostly in children, is higher. Most pulses are carried in the ventricles.

    Sometimes polytopic atrial tachycardia is regarded by doctors as atrial fibrillation. At the same time in 50-70% of cases, this polytopic atrial tachycardia is combined or passes over time into atrial fibrillation.

    Apparently, tachycardia from one ectopic focus with multiple pathways of pulse propagation is possible. A case of transition of polytopic tachycardia to a tachycardia with the same morphology P and a constant heart rate after intravenous administration of a beta-blocker during an EFI is described. With the help of radiofrequency catheter ablation, tachycardia was cured.

    It is necessary to try to reduce the negative impact of the underlying disease, for example, to prescribe effective bronchodilators and oxygen therapy in exacerbation of chronic obstructive pulmonary disease. Oxygenation should maintain oxygen saturation & gt; 90%.

    In many situations, including resistant forms, magnesia is effective with simultaneous correction of hypokalemia. In case of an overdose, theophylline is administered dipyridamole.

    Beta-blockers( metoprolol) restore sinus rhythm in 70% of cases, but caution is required for bronchial obstruction, especially caused by asthma. Verapamil arrests arrhythmia in 20-50% of cases. The effectiveness of amiodarone has been studied little.

    Blockade of AV-conduction( verapamil, metoprolol) is usually achieved with great difficulty, therefore in resistant cases a catheter modification of the AV-connection is used.

    Cardioversion is rarely effective. Catheter ablation is not used because there are multiple ectopic foci in the atria.

    Arrhythmia and thromboembolism are indications for antithrombotic treatment( disaggregants, anticoagulants).

    The source of the VT is distal to the branch of the bundle and can be located both in the conducting system( the bundle bundle legs, Purkinje fiber) and in the ventricular myocardium.

    Classification of ventricular tachycardias

    • coronary heart disease( myocardial infarction, myocardial infarction, aneurysm, angina pectoris)

    • Dilated cardiomyopathy and myocarditis

    • Heart defects( congenital, acquired)

    • Prolapse of the mitral

    valves • Hypertrophic cardiomyopathy

    • Arrhythmogenic right ventricular dysplasia

    •Syndrome of the extended interval QT

    • Idiopathic

    In the vast majority of cases( 67-79%), VT develops in patients with IHD, less often with other heart diseasesAnd in 2-10% of cases, the cause can not be identified. In this connection, the data of J. Strain et al., Who examined 18 patients with VT for an average duration of 3 years without IHD, valvular defects, heart failure and a normal QT interval, are of interest. With myocardial biopsy of the right ventricle, anomalies were revealed in 89% of cases: a picture of dilated cardiomyopathy( in normal size and contractility) in 50%, myocarditis in 17%, arrhythmogenic dysplasia in 11% and lesion of small coronary arteries in 11% of cases.

    1. Wide complexes with QRS = 120-200 ms. Rarely there is a narrow complex VT with a picture of an anterior-superior blockade or a posterior-inferior branching of LNG.

    2. The heart rate is usually 150-180 rpm, tachycardia <130 and> 200 rpm is rarely seen.

    3. Rhythmic tachycardia with a small variability of RR( <20 ms).Irregularity of the rhythm may be due to the capture of the ventricles by sinus pulses, changes in the length of the loop reentry, instability of the focus or blockade of the exit from the ectopic center.

    4. Atrial pts P most often not visible. If nevertheless it is possible to register them, then these are usually independent of the ventricles, a rarer rhythm of the sinus node. In 25% of cases of VT, retrograde VA-holding( 1: 1 or VA of type 2 and 2 block of degree 2) occurs with the registration of the P 'teeth on the ST segment or the T wave. The BA of the blockade can be caused by a vagal test.

    Recall that the presence of three consecutive ventricular complexes on the ECG should be considered as VT, and not a group extrasystole.

    Isolate monomorphic VT with identical complexes of QRS-T and polymorphic VT.The latter is caused both by sources of different localization and by the generation in one place with varying paths of propagation of the excitation wave in the ventricle.

    It is important to consider the possibility of artifacts in the Holter ECG monitoring, which are very similar to the ventricular( wide-complex) tachycardia.

    The causes of artifacts are the movements of patients, poor contact of electrodes with skin and electromagnetic interference.

    It is interesting to note that among therapists, artifacts of 6% were accurately determined, among cardiologists 42%, and among electrophysiologists - 62%.The rest of the doctors diagnosed most often with ventricular or broad-complex tachycardia.

    The correct definition of artifacts is based on the identification of elements of QRS complexes at intervals multiple of sinus RR intervals, unstable baseline before or after an episode of artefacts, registration of the QRS complex immediately after the end of the episode, which is physiologically impossible, as well as well-being for tachycardia with high heart rate.

    With the help of special methods for processing the electrocardiogram signal( averaging with the imposition of several complexes, filtration), it is possible to identify the so-called late ventricular potentials. The latter are low-amplitude( 1-25 μV) deviations in the terminal area of ​​the ventricular complex.

    The following characteristics of the filtered ventricular complex are considered as criteria for late potentials:

    1) duration> 114-120 ms;

    2) the terminal portion of the signal with an amplitude <40 μV for> 39 ms;

    3) Signal amplitude <20 μV in the last 40 ms.

    Such late potentials are recorded in patients after myocardial infarction with sustained ventricular tachycardia in 70-90%, without ventricular tachycardia in 7-15% and in healthy people in 0-6% of cases. Late potentials can be determined already through

    3 hours after the onset of anginal pain and are usually recorded during the first week, disappearing in some patients after 1 year.

    IHD: postinfarction cardiosclerosis( 12,02,94), angina of stress 2 FC, paroxysmal resistant polymorphic VT with presincopy.

    Idiopathic dilated cardiomyopathy, cardiac failure 3 FC, paroxysmal resistant monomorphic VT with a picture of BLNPH and episodes of pulmonary edema.

    Idiopathic continuously recurring monomorphic VT with a pattern of BPNAP.

    In case of serious hemodynamic disorders( pulmonary edema, angina pectoris, syncope, hypotension), EIT is indicated. The initial discharge of EIT is selected depending on the form of the stable VT: with monomorphic VT without hemodynamic disorders begin with a discharge of 50 J, with a monomorphic VT with hemodynamic disturbances - from a discharge of 100 J. Rapid polymorphic VT is assessed similarly to VF, and cardioversion begins with a discharge of 200 J.

    If the situation does not require emergency EIT, then prescribe medication. It is important to consider the possible cause of VT( myocardial ischemia, hypokalemia) and try to eliminate it.

    Monomorphic VT is usually associated with the mechanism of reentry and is more common in patients with myocardial infarction and postinfarction cicatrix.

    At first it is useful to ask the patient to cough, which can lead to the restoration of sinus rhythm due to improved coronary circulation. Stroke on the sternum can be dangerous because of the risk of VF development.

    Tactics of ventricular tachycardia,

    Usually, treatment with lidocaine, although less effective, but with little effect on contractility of the myocardium and blood pressure, is usually started. If there is no effect, then appoint procainamide, which is superior to lidocaine for antiarrhythmic activity, but has more side effects. With moderate arterial hypotension, heart failure or conduction disorder, amiodarone is recommended. The FDA recommends the following scheme for the administration of the drug: dilute 150 mg in 100 ml of 5% glucose and inject for 10 minutes( rate 10 ml / min or 15 mg / min), then 900 mg diluted in 500 ml 5% glucose andInitially, 360 mg for 6 hours( rate of 1 mg / min or 33 ml / min), and then 540 mg at a rate of 16 ml / min or 0.5 mg / min).If persistent tachycardia persists, bolus administration of 150 mg of amiodarone can be repeated every 15-30 minutes.

    Given the high risk of switching to ventricular fibrillation, the cupping of polymorphic VT is usually performed by the EIT method. If it is not possible to conduct electrical cardioversion, lidocaine is used, and in the absence of effect, amiodarone is prescribed.

    There is usually a bi-directional-fusiform VT.In this case, it is necessary to cancel preparations that increase the QT interval, and to correct the metabolic disorders( hypokalemia, hypomagnesemia).

    In this situation, antiarrhythmic drugs are ineffective, and preparations of 1A and 3 classes are even dangerous.

    For the treatment of arrhythmia, intravenous magnesia is indicated: a bolus of 2 g of magnesium sulfate( 8 ml of 25% magnesium sulfate per 1 minute) tachycardia almost instantaneously. In the absence of effect, repeat the introduction after 5-15 minutes. After arresting tachycardia, supportive administration of magnesia is carried out at a rate of 3-20 mg / min for 24-48 hours. An increase in the sinus rhythm frequency to 100-120 per minute with the help of sympathomimetics reduces the risk of relapse of VT.

    The goal of preventive treatment is to prevent recurrence of symptomatic VT and reduce the risk of sudden arrhythmic death, usually associated with the transition of rapid VT to ventricular fibrillation.

    The risk of recurrence of resistant VT within 2 years is 30-50%, therefore, after the first attack of VT, preventive measures should be taken.

    Of course, you need to identify heart disease, usually( in 90-95% of cases) available with a stable VT.For this purpose, echocardiography and coronary angiography are performed. In the case of coronary atherosclerosis, myocardial revascularization( coronary bypass or angioplasty) and antianginal therapy, including beta-blockers, are required. With reduced left ventricular function, ACE inhibitors and beta-blockers are prescribed with a careful correction of the electrolyte balance in the case of diuretics.

    The choice of preventive treatment of VT( medication, ICD) depends on the risk of arrhythmic sudden death.

    Patients with stable VT in the presence of heart diseases with hemodynamic complications( syncope, heart failure, arterial hypotension) with left ventricular dysfunction( PV <35-40%) showed implantation of a cardioverter-defibrillator( AVID, C IDS).

    In cases of impossibility of implantation of a cardioverter-defibrillator, antiarrhythmic drugs are used: amiodarone, sotalol or a combination of amiodarone and beta-blockers.

    It is possible to select an antiarrhythmic drug empirically, based on the results of studies of drugs with VT in a large group of patients. In addition, individual evaluation of the effectiveness of drugs according to the results of Holter monitoring or EFI is possible. It is believed that empirical treatment is less effective, but reliable controlled studies comparing different approaches are virtually non-existent.

    In connection with the revealed advantage of amiodarone and sotalol, as well as the possibility of implantation of a cardioverter-defibrillator, the selection of antiarrhythmic drugs with the help of special tests is currently less relevant. Moreover, the evaluation of the efficacy of amiodarone is hampered by the slow development of the effect and prolonged withdrawal of the drug, which interferes with the testing of other drugs.

    Holter monitoring and EFI can be used to select preventive antiarrhythmic therapy.

    Evaluation of the effect of the drug using holter monitoring is based on a reduction in the number of initially available

    arrhythmias. Therefore, this method can not always be applied. For example, with stable VT in patients with IHD, spontaneous ventricular arrhythmias are absent in 17-34% of cases. Due to the pronounced variability of arrhythmias from day to day, treatment is considered effective if, with daily ECG monitoring, the number of ventricular extrasystoles decreases by 70%, paired - by 80%, episodes of unstable VT by> 90%, and episodes of resistant VT disappear.

    By the method of EFI, it is possible to induce reciprocal VT at a stable monomorphic VT in 90%, and in VF - in 30-60%.After the introduction of the drug, a second attempt is made to induce tachyarrhythmia and, if this is considered unsuccessful, consider this drug effective. Unfortunately, according to EFI, an effective drug can be selected only in 15-40% of cases, and in these cases the annual frequency of relapses of tachycardia is about 5%.

    Which of the two methods of selecting antiarrhythmic therapy should be preferred? According to the faulty data of the ESVEM study, both approaches have approximately the same information, although most experts prefer the EFI.

    The prophylactic efficacy of antiarrhythmic drugs for relapses of VT is rather low. No less important characteristic of antiarrhythmic drugs is the ability to reduce the risk of sudden death, which is elevated in patients with VT.Not all antiarrhythmic drugs are capable of effectively solving these two problems.

    Given to randomized controlled trials, class I drugs and especially 1C subclasses( CAST, CASH), preventing recurrence of VT, may increase the risk of sudden death, which limits the use of these drugs. Note that the studies were conducted mainly in patients after myocardial infarction and they did not always include patients with resistant VT.Nevertheless, these results are also transferred to patients with stable VT and other structural lesions of the heart.

    Beta-blockers, although they prevent recurrence of VT and reduce the risk of sudden death, but are considered less effective than amiodarone.

    A number of studies have noted the preventive effect of sotalol, apparently somewhat inferior to the effect of amiodarone( AVID).

    Prophylactic efficacy of antiarrhythmics with stable VT and VF

    The most common and apparently effective means of preventing VT is amiodarone( CASCADE, CASH, CIDS).Amiodarone is first prescribed in a high dose for a quicker effect( 800-1600 mg / day 1-3 weeks), and then switch to a maintenance dose( 200-400 mg / day).

    What to do with VT with severe symptoms, ineffectiveness of amiodarone or sotalol and the patient's lack of ICD?There remains an attempt to strengthen the effect of antiarrhythmic drugs with the help of other means. Unfortunately, there are currently no randomized studies of the effectiveness of combined treatment.

    Based on the data from the CAMIAT and EMIAT studies, it is possible to suggest an increase in the effect when beta-blockers and amiodarone are combined. Of the other drugs, preference should be given to those who have not been shown to have a significant increase in mortality in controlled studies. Even if there is an individually small increase in the risk of sudden death, in the case of a good effect, patients can get rid of severe attacks.

    Although there is an increased risk of using Class 1 drugs( especially 1C class), the combination of these drugs with amiodarone, sotalol or beta blockers can not be ruled out. Moreover, in this case, lower doses of antiarrhythmics can be used.

    Let's give an approximate scheme of combined treatment:

    1. Amiodarone 200 mg / day + atenolol 50 mg / day.

    2. Amiodarone 200 mg / day + mexiletine 400 mg / day or prolonged disopyramide 200 mg / day or morazizin or neogylu-rhythmal 20 mg / day 400 mg / day in 2 divided doses.

    3. Sotalol 320 mg / day + preparations listed in point 2.

    4. Metoprolol 200 mg / day + preparations listed in point 2.

    Currently, surgical resection of the arrhythmogenic focus is rarely used, because the arrhythmogenic focus is difficult to locate( mappingis performed on the beating heart, and during the operation cardioplegia is needed) and the risk of death( 5-20%) is high. This method is chosen for aneurysm after myocardial infarction and left ventricular function.

    In the vast majority of cases, ICDs and radiofrequency catheter ablation are now used.

    If there is evidence of a high risk of sudden death( who underwent VF, syncopal VT, symptomatic VT in the presence of a heart attack, especially with PV <35%), then a cardioverter-defibrillator implantation is indicated, since this method is more effective than amiodarone( AVID, CIDS, CASH).

    In patients undergoing cardiac arrest, the ICD reduces the risk of sudden death to 2% within 1 year and to 6% within 5 years. While the operational mortality in the installation of ICDs currently does not exceed 1%.

    The goal of radiofrequency catheter ablation is to create an obstacle in the narrowest part of the circular movement of the reentry wave.

    The method is used only for monomorphic VT caused by the mechanism of reentry, and is effective on average in 70-72% of patients. With a structurally normal heart, the ablation efficiency is 85-90%, with idiopathic dilated cardiomyopathy( reentry in the Gys system) - 61%, with IHD - 54-73%.Complications occur in 3% of procedures without reported deaths.

    The technique of ablation depends on the type of VT.Patients without structural heart disease usually have a monotopic VT and ablation is usually effective. With extensive damage to the heart, especially after myocardial infarction, there is often a polytope VT.In these cases, the catheter ablation of one VT in such patients does not exclude other methods of antiarrhythmic treatment.

    Indications for radiofrequency catheter ablation [ASA / ASA, 1995]

    I class( proven effectiveness)

    1. Patients with symptomatic resistant monomorphic VT, if the tachycardia is resistant to treatment, or the patient does not tolerate medication, or does not wish to take medications for a long time.

    2. Patients with VT and reentry in the His system.

    3. Patients with stable monomorphic VT and ICD who underwent multiple cardioversion without the effect of reprogramming or concomitant medication.

    Class II( conflicting performance data)

    Unsustainable symptomatic VT with resistance to drug treatment, or drug intolerance to the patient, or unwillingness to take drugs for a long time.

    Treatment of unstable ventricular tachycardia

    The tactics of treating unstable VT are determined by the risk of sudden death, which is almost completely dependent on the presence and severity of the underlying disease-usually a heart attack or left ventricular dysfunction( PV <40%).In patients without heart disease, the risk of sudden death is not increased and treatment is usually not required. The questions of prevention of sudden death are considered in the corresponding section below.

    The unstable VT usually does not lead to a significant disturbance of hemodynamics and a worsening of the patient's condition. Comparative effectiveness of antiarrhythmic drugs for suppression of ventricular arrhythmia is presented in Table.

    Efficacy of drugs with unstable VT and ventricular extrasystole

    When monitoring ECG in patients with acute myocardial infarction, VT occurs in 45-60% of cases, mainly in the first 48 hours. Development or preservation of a stable VT after 48 hours from the onset of myocardial infarction leads to an increased riskdeath from VF.In this case, for example, given the GISSI-3 study, within 6 weeks the lethality increased more than 6-fold.

    In patients with myocardial infarction with unstable VT( monomorphic or polymorphic), beta-blockers are used( atenolol 100 mg 1 time, metoprolol 100 mg 2 times).According to a meta-analysis of randomized trials, amiodarone reduces overall mortality. In the case of left ventricular dysfunction( PV <40%), the ACE inhibitor is shown.

    In controlled trials of the use of Class I drugs in patients after myocardial infarction, a significant increase in the lethality was revealed, therefore these preparations are not shown.

    With stable VT, it is recommended, first of all, to conduct angiography and revascularization of the myocardium( coronary bypass, angioplasty), aneurismectomy.

    With a low-symptom-resistant VT, it is possible to use medications, among which amiodarone is preferred. The combination of amiodarone and beta-blockers deserves attention. Apparently, sotalol is also quite effective. Beta-blockers are not able to effectively prevent stable VT.With frequent attacks of VT without hemodynamic disorders, radiofrequency catheter ablation reduces the frequency of recurrence of tachycardia.

    In patients with syncopal VT or resistant symptomatic VT( with pre-obstruction or angina or arterial hypotension) with left ventricular dysfunction( PV <35-40%), the cardioverter-defibrillator implantation( AVID, CIDS) is indicated.

    It should be noted the high frequency of ventricular arrhythmias with thrombolysis, reaching a maximum 30 minutes after the restoration of coronary blood flow. The frequency of reperfusion VT can reach 40%, and VF - 10%.However, the effect of prophylactic administration of lidocaine or other antiarrhythmic drugs has not been established.

    An extended QT interval syndrome is a condition with an increase in the QT interval and the presence of a bidirectional-spindle VT.

    • Drugs: antiarrhythmic drugs( 1A, 3 classes and to a lesser extent 1C class), phenothiazine derivatives( aminazine, alimamazine, frenolone, thioridazine, chlorpromazine, neuleptil, haloperidol, droperidol, diprazine, etatsizin), heterocyclic antidepressants( amitriptyline, imipramine, doxepin, maprotiline), indapamide, antihistamine( astemizole, terfenadine), macrolides( erythromycin), cotrimoxazole, cisapride.

    • Organic heart damage: myocardial infarction, cardiomyopathy, myocarditis, mitral valve prolapse.

    • Bradyarrhythmias: SSSU, AB blockade of the 3rd degree.

    • Electrolyte disorders: hypokalemia, hypomagnesemia, hypocalcemia.

    • Endocrine disorders: diabetes, pheochromocytoma, hypothyroidism.

    • Central nervous system damage: thrombosis, embolism, tumors, infection, hemorrhagic stroke.

    • Congenital forms: Jerwell-Lange-Nielsen syndrome( deaf-mute, syncope, & gt; QT), Romano-Word syndrome( syncope, & gt; QT), sodium channel gene mutation( SCN5A).

    The QT interval reflects the repolarization rate in the His-Purkinje system. The interval QT is determined from the origin of the tooth Q( R) to the point of intersection of the downward bend of the tooth T with the isoline.

    Despite the doubts about the accuracy of the technique, the estimate of the corrected QT interval using the Basett formula is widely used: QTc = QT /( RR) 1/2.

    According to the European Society for the Evaluation of Medicines, the upper limit of the QTc rate for men is 450 ms, and for women, 470 ms.

    Interval specifications QTc

    An estimate of the absolute value of the QT interval is considered less informative. Usually, the risk increases if the QT interval exceeds 500 ms, and in the case of 600 ms or more, VT is almost always developed.

    The QT interval extension can be variable. Often, in Holter monitoring, before the development of VT, there is a significant increase in the QTc interval.

    If there is no VT, then the term "extended QT interval phenomenon" is recommended.

    For torsade de pointes, a gradual change in the polarity of QRS complexes from positive to negative and vice versa is characteristic. The RR intervals are irregular with a change of magnitude up to 200-300 ms. Tachycardia is characterized by high frequency( 200-300 per minute), instability( episodes from 6 to 100 complexes) and a tendency to relapse. The main danger of bi-directional-spindle VT lies in the risk of transition to VF.

    Episodes of tachycardia in the acquired syndrome are usually due to trigger activity and appear usually against a background of a rare sinus rhythm. Therefore, this tachycardia is called "tachycardia, depending on pauses."

    In the case of congenital( idiopathic) syndrome of the prolonged QT interval, tachycardia occurs in more than half of cases with emotional stress or physical exertion.

    Unstable VT can be asymptomatic, and in the case of a resistant VT, dizziness, fainting, and circulatory arrest occur. VNS and catecholamines can affect the manifestation and severity of both the congenital and acquired syndrome of the extended QT interval.

    Isolate acute( medications, craniocerebral trauma, myocarditis) and chronic( postinfarction cardiosclerosis, cardiomyopathy, congenital form) course of the syndrome.

    The drug of choice is magnesium, the introduction of which in a dose of 2 g( 8 ml of 25% magnesium sulphate) bolus within 1 minute tachycardia almost instantly. If there is no effect, repeat the introduction after 5-15 minutes, and if necessary, carry out EIT.

    Note the low efficacy of lidocaine and brethil tosylate. Sometimes they describe the effect of verapamil. It is dangerous to administer drugs 1A and 3 class, which can increase the interval of QT and the severity of the syndrome.

    After cupping of tachycardia, supportive administration of magnesia is carried out at a rate of 3-20 mg / min for 24-48 hours. Increase in heart rate with the help of sympathomimetic infusion also prevents recurrence of brady-dependent VT.

    To suppress and prevent tachycardia, in addition to sympathomimetics, frequent atrial or ventricular pacing is used.

    Since bidirectional-fusiform VT usually occurs in the background of a bradycardia or during long sinus pauses, in order to reduce the frequency of relapses, tachycardias tend to increase the heart rate to 100-120 rpm with the help of ECS or temporarily prior to the installation of EKS by sympathomimetics.

    If it is not possible to eliminate the cause, it is recommended to implant a cardioverter-defibrillator or a permanent ECS in a brady-dependent form. It is possible to use mexiletine or tokaineide, which do not change the QT interval.

    When the phenomenon of an extended QT interval occurs, the cause should be eliminated and care should be taken when using potentially dangerous drugs.

    Mortality in the congenital syndrome of the extended QT interval is 50-70%.Highlights the risk factors for sudden death, presented in Table.

    Risk factors for sudden death in patients with prolonged QT interval syndrome

    I class

    1. Syncope.

    2. Bi-directional-spindle VT( FV) cardiac arrest.

    3. Jerwell-Lange-Nielsen is a recessive option.

    4. 3 genetic variant.

    Pa class

    1. QTc & gt;600 ms.

    2. Cardiac events in newborns.

    3. Postpartum period.

    4. Female gender.

    5. Syndactyly and AB blockade.

    6. Macroscopic alternative to T.

    116 class

    1. Family history.

    2. Dispersion of the QT interval.

    For cupping bi-directional-spindle VT, propranolol is injected with 5-10 mg at an rate of 1 mg / min. Primary prevention of sudden death in patients with prolonged QT interval syndrome

    I class( proven effectiveness)

    1. Avoidance of severe physical stress in symptomatic patients.

    2. Beta-blockers in symptomatic patients.

    Pa class( more data in favor of efficacy)

    1. Avoiding drugs that extend the QT interval in patients with or without symptoms, carriers of the latent gene.

    2. Avoiding severe physical strain in patients without symptoms or carriers of the latent gene.

    3. Beta-blockers in patients without symptoms.

    4. And CD + beta-blockers with relapse of symptoms on the background of beta-blockers.

    Given the association of VT with an increase in sympathetic activity, prevention is performed with high( maximally tolerated) doses of beta-blockers, without missing a single dose. In case of inefficiency, a permanent ECS is used to prevent bradycardia in combination with large doses of beta-blockers.

    With a high risk of sudden death, along with beta-blockers, IK is used, which works in the electrocardiostimulation mode and is able to replace VT or ventricular fibrillation.

    In recent years, mutations of the sodium cardiac channel gene( SCN5A) have been described, the electrophysiological properties of which can be corrected by 1C class drugs. Recently, the results of a study showing the possibility of a significant decrease in the QTc interval after prolonged treatment with potassium preparations( potassium chloride, spironlactone) in patients with a gene mutation( HERG or KNCH2) of potassium channels have recently been published.

    Do not forget about the exclusion of heavy physical stress and drugs that extend the QT interval.

    • For long-term treatment with antiarrhythmic drugs 1A class, amiodarone and sotalol, it is necessary to monitor the QT interval.

    • If patients experience dizziness or fainting with treatment with the above described drugs, arrhythmogenic complications should be avoided.

    • QT interval prolongation may be transient, therefore it is better to conduct ECG monitoring of

    for diagnostic purposes. • Pay attention to the form of a wide-complex tachycardia: in the presence of spindle-shaped complexes it is necessary to exclude the syndrome of the extended QT interval.

    • Bidirectional-spindle VT with extended QT interval syndrome is treated with magnesium.

    The arrhythmogenic cardiomyopathy of the right ventricle is considered as a myocardial disease, mainly affecting the right ventricle and characterized by the replacement of myocytes with fat and fibrous tissue.

    The incidence of this disease is approximately estimated at 1 case per 5000 population, although there are difficulties in identifying this pathology. A hereditary predisposition, transmitted by an autosomal dominant type, has been identified. In family forms, genetic abnormalities are found in 1( 14q23-q24) and 10 chromosomes.

    Arrhythmogenic cardiomyopathy of the right ventricle in more than 80% of cases is detected before the age of 40 years. The disease can be suspected in young people in case of fainting, VT or cardiac arrest, as well as in adults with heart failure.

    After 40-50 years, right ventricular heart failure may develop. The clinic for heart failure usually appears 4-8 years after the ECG has been registered with a complete BPNG.

    It is also possible to involve the left ventricle( biventricular dysplasia) in the pathological process, which reaches up to 60% of cases in the developed forms of the disease.

    In echocardiographic studies, the most characteristic signs are dilatation of the right ventricle with a local aneurysm during diastole and dyskinesia of the lower basal region. An important feature is the ratio of the end-diastolic diameter of the right ventricle to the left & gt; 0.5.

    In 54% of patients with arrhythmogenic cardiomyopathy of the right ventricle, an inversion of the T wave in the precordial leads V2 is recorded on the ECG. 3. Note that this sign is quite common in children.

    A characteristic manifestation of arrhythmogenic cardiomyopathy of the right ventricle is the widening of the QRS complex in the leads V, 3 compared to the V6 derivation. In the case of complete LTPG, the width of the QRS complexes in the V2 3 leads is 50 ms longer than the V6 lead.

    In 30% of patients with arrhythmogenic cardiomyopathy of the right ventricle at the end of the QRS complex and the beginning of the ST segment on the ECG, a low-amplitude epsilon wave is determined.

    In 18% of cases, incomplete BNPG is recorded, and in 15% - complete BNPG.These signs are also nonspecific, since they can occur in healthy people.

    VT manifests itself as a monomorphic BLNGH, since the source of tachyarrhythmia is the right ventricle. The development of VT is caused by the formation of circular excitation near the centers of fibrotic-lipid degeneration of myocytes.

    Right ventricular arrhythmogenic cardiomyopathy accounts for about 5% of sudden deaths in people under 65 and 3-4% of deaths associated with physical activity in young athletes. The annual mortality rate is 3% without treatment and 1% in treatment, including ICD.

    VT and ventricular fibrillation most often develop with physical activity, in addition, arrhythmias are usually reproduced by the introduction of sympathomimetics( isoprenaline).

    Ventricular arrhythmias are preceded by an increase in the frequency of the sinus rhythm, and directly episodes of VT are initiated by extrasystoles of the same morphology, in contrast to IHD.


    1. Pronounced dilatation or reduction of right ventricular ejection without( or with a small) left ventricular dysfunction.

    2. Local aneurysm of the right ventricle.

    3. Expressed segmental dilatation of the right ventricle.

    4. Fibrous-lipid replacement of the right ventricular myocardium with endomyocardial biopsy.

    5. Epsilon wave or local magnification( & gt; 110 ms) of the QRS width in the right precordial leads( Vl3).


    1. Easy dilatation or reduction of right ventricular ejection with unchanged left ventricle.

    2. Easy segmental dilatation of the right ventricle.

    3. Regional hypokinesia of the right ventricle.

    4. Late potentials.

    5. Inversion of T-wave in precordial leads( V23) in patients after 12 years of age and in the absence of

    BPNPG 6. VT with a picture of BLNPH.

    7. Frequent ventricular extrasystole and I( & gt; 1000/24 ​​h).

    8. Family history of premature sudden death( <35 years) due to presumed right ventricular dysplasia.

    9. Family history of arrhythmogenic cardiomyopathy of the right ventricle.

    For diagnosis, two large or one large and two small criteria are sufficient.


    Beta-blockers, sotalol, amiodarone and calcium antagonists are considered to be the most effective antiarrhythmic drugs nor prevent ventricular arrhythmias. Preparations of the first class are practically ineffective.

    Non-pharmacological treatment of

    Radiofrequency catheter ablation was effective in 32.45 and 66% of cases after the first, second and third procedures, respectively, when observed for 4.5 years. The main obstacle to the effect of treatment is the progressive nature of the disease, leading to the formation of more and more arrhythmogenic foci.

    Patients with an episode of cardiac arrest, a history of fainting, or a life-threatening VT have been shown to implant a cardioverter-defibrillator in combination with medication to reduce the frequency of discharges.

    Early excitation( pre-excitation) of the ventricular myocardium by sinus or atrial pulses occurs through congenital microscopic fibers - the so-called additional pathways( DP).Most often, the atrioventricular or Kent bundles are of greatest clinical significance.

    The clinical significance of James' pathway between the atria and the bundle of His is insufficiently established. Currently, there is no conclusive evidence of a specific LGL syndrome characterized by a short PR interval, normal QRS complex and tachycardia associated with the atrial-giassic tract.

    Under the syndrome WPW( Wolf-Parkinson-White) is meant the attacks of the UHT associated with the presence of the atrioventricular connection or the bundle of Kent. A mutation of the gene( 7q34-q36), responsible for the familial form of the WPW syndrome, has been identified.

    Congenital Kent beam is found in 0.1-0.3% of the population, with men predominating( 60-70%).The frequency of paroxysmal tachyarrhythmias in the presence of electrocardiographic signs of DP is estimated at 10-36%.

    If there is a DP, in most cases the ventricle base is first excited, and this leads to the following ECG changes:

    1. PR interval shortening: PR & lt;120 ms, but the PJ interval is normal, unlike BNPG.

    2. Broad Ventricular Complex: QRS & gt;100 ms.

    3. Delta-wave: a shallow ascending knee of the R wave with a duration of 20-70 ms and a height of 2-5 mm. Often there are atypical variants of a delta wave: two-phase or negative in the form of a tooth q( Q), appearing in only one or two leads.

    Note that it is very difficult to determine the localization of DP by the presence and polarity of the delta wave in different leads of the ECG.For example, the assumed localization of types A to C coincides with the EFI data only in 30-40%, and according to the table J. Gallagher - in 60%.To carry out the destruction, the informativeness of these methods is insufficient, and for medical treatment the knowledge of the localization of the Kent beam does not matter.

    Sympathetic activation speeds up DP, while changes in the tone of the parasympathetic nervous system change the procedure slightly.

    Sometimes there are ECG with signs of pre-excitation and a picture of BLNPG.In this case, most often there is an atrial fascicular or nodophascicular additional pathway, the fibers of which are usually implanted in the right leg of the bundle.

    There are forms with a normal PR interval and no delta wave. With latent form, such a picture is due to a slow DP, left-sided localization of the DP or a transient blockade of the DP.In these cases, techniques that enhance the manifestation of the WPW phenomenon can help:

    • Vagal test.

    • Blockade of AV-conduction( verapamil, ATP).

    • Electrophysiological study.

    In the case of latent DP, holding the pulse is only possible retrograde( from the ventricles to the atria), so the signs of pre-excitation on the ECG are not visible. Retrograde DP may be detected by intracardiac electrophoresis or during a reciprocal rhythmic narrow-complex tachycardia with RP '& gt;100 ms.

    If intraventricular conduction is disturbed, changes in the QRS complex, similar to delta wave, are possible. Such cases are most often met with myocardial infarction, myocarditis, cardiomyopathy, left ventricular myocardial hypertrophy.

    The need to clarify the nature of conduction disorders occurs when there is paroxysmal tachycardia. In these situations, in addition to ECG analysis at the time of tachycardia, the following diagnostic techniques are useful:

    • Vagal test - the delta wave is amplified.

    • Test with verapamil or ATP - the delta wave is amplified.

    • Atropine test - the delta wave decreases.

    • Test with procainamide or giluritmal - delta wave decreases, manifestations of intraventricular blockade increase.

    • Electrophysiological study.

    Note that a change in the conduct of the AV node does not change the ECG in the case of nocinodicular fibers of Maheima.

    Congenital DP predisposes to the occurrence of paroxysmal tachycardias. For example, in half of patients with a bundle of Kent, tachycardia is recorded, among which are the following:

    • Orthodromic AV reciprocal tachycardia( 70-80%).

    • Atrial fibrillation( 10-38%).

    • Atrial flutter( 5%).

    • Antidromic AV reciprocal and pre-excitatory tachycardia( 4-5%).

    The prognosis for most tachycardias is favorable, and the rate of sudden death is about 0.1%.

    In 20% of cases, orthodromic AV reciprocal tachycardia is combined with paroxysmal atrial fibrillation.

    Note that the presence of signs of DP does not exclude the possibility of development in these patients and other types of tachycardia. For example, AV node nasal reciprocating tachycardia is often detected.

    Orthodromic( AV reciprocal) tachycardia develops by the mechanism of reentry, when impulses pass from the atrium to the ventricles through a normal conducting system( AV node, the Gisa- Purkinje system), and return to the atrium via DP.On ECG, this tachycardia is characterized by the following symptoms:

    • Retrograde teeth P '(negative in II lead).

    • The P wave is located behind the QRS complex with RP '& gt;100 ms and typically P'R & gt;RP '.

    • Tachycardia rhythmic, without AV blockade.

    The atrial teeth are best seen in the transesophageal lead.

    In rare cases of slow retrograde conduction along the DP, the P-teeth are located far behind the QRS complex and P'R & lt;RP '.

    Tachycardia suddenly begins and ends, is characterized by rhythm and a higher heart rate( 150-250 per min) than with AV nodal reciprocal tachycardia. Broad QRS complexes during tachycardia are due to the presence of BNPG and occur in 38-66%, i.e.much more often than with AB node tachycardia.

    If the blockage develops in the ventricle in which the DP is located, the interval of RP 'increases and the rhythm of tachycardia becomes less frequent( Kumel-Slam effect).Antidromic tachycardia

    Antidromic tachycardia is rare and develops by the mechanism of reentry, when impulses pass from the atrium to the ventricles through the DP, and return to the atrium along a normal conducting system( the Gisa- Purkinje system, the AV node).On ECG, such a tachycardia is characterized by wide QRS complexes. The tooth P is not visible behind the wide QRS complexes.

    With WPW syndrome in 5-16% of cases, several DPs occur. In this case, it is possible to develop a pre-excitatory tachycardia, in which the impulse passes anterograde and retrograde along the DP.Many specialists consider a pre-excited tachycardia within the framework of antidromic tachycardia, since there are no differences between them on the ECG and in the tactics of treatment.

    Usually patients with atrial fibrillation and flutter also have AV reciprocal tachycardia. Rare cases of orthodromic tachycardia transition( with a heart rate of 180-200 per min) to ventricular fibrillation are described.

    Atrial fibrillation and flutter are very dangerous in "fast" DP because the ventricles are very often excited and severe hemodynamic disorders develop. Atrial fibrillation recorded a frequency of ventricular response of 360 per min.

    The trigger factor of atrial fibrillation may be atrial myocarditis, which can be detected in 50% of patients with signs of an additional route of execution who died suddenly.

    If the incidence of ventricular excitations reaches 250 per minute, then there is a real threat of VF.At high heart rate( & gt; 250 rpm), the first attack of tachyarrhythmia can end fatal. On the ECG, wide complexes are constantly or periodically recorded.

    The frequency of sudden death in WPW syndrome is estimated at 0.15% per year, and in asymptomatic patients it is lower. The factors of low and high risk of VF.Note that syncope is not a predictor of an increased risk of sudden death.

    • Atrial fibrillation, the minimum RR & lt;250 ms

    • ERP DP & lt;270 ms

    • Multiple DP

    Predictors of low risk of FF

    • Signs of the phenomenon of WPW on the ECG are unstable

    • Delta wave suddenly( not gradually) disappears with physical exertion

    • The disappearance of the delta wave with medication( procainamide 10 mg / kg, giluritmal1 mg / kg, disopyramide 2 mg / kg)

    • Atrial fibrillation, the minimum RR & gt;250 ms

    • ERP DP & gt;270 ms, Wenkebach point DP & lt;250 per min

    EFI can be performed in patients with WPW syndrome to assess the mechanism of tachyarrhythmia, the electrophysiological properties of the DC( Wenkebach and ERP DP points) and the normal conductive system, the number and localization of DP, the effectiveness of antiarrhythmic therapy, or the possibility of ablation of DP.

    Transesophageal EFI allows:

    1. Identify latent or intermittent forms. For example, with left-sided localization of the Kent beam on the ECG, pre-excitation is often not detected.

    2. Evaluate the functional properties of the DP.For example, with "fast" DP( ERP <220-270 ms, Wenkebach point> 250 rpm), the risk of VF is increased.

    3. Diagnose reciprocal tachycardia.

    4. To select preventive treatment for tachycardia.

    At the same time, you should be aware that the normal refractory period of DP does not exclude the risk of atrial fibrillation with a rapid ventricular response.

    Intra-cardinal ECP, in contrast to the transesophageal study, allows to estimate the exact localization and quantity of

    DP, to reveal latent DP.This information is necessary for carrying out the destruction of DP and monitoring the effectiveness of treatment.

    Indications for EFI

    1 class( proven effectiveness)

    1. Diagnostic examination before catheter or surgical ablation of DP.

    2. Patients who survive a circulatory arrest or have unexplained syncope.

    3. Patients with symptoms in whom the definition of the arrhythmia mechanism or knowledge of the properties of the DP and the normal conductive system should help in choosing the appropriate treatment.

    4. Patients with AV reciprocal tachycardia, fibrillation, or atrial flutter who are scheduled for permanent medication.

    II class( conflicting performance data)

    1. Patients without symptoms who have a family history of sudden death in whom knowledge of the properties of DP or induced tachycardia can help in the choice of treatment or recommendations for future work.

    2. Patients without arrhythmias performing high-risk work, in which knowledge of the properties of DP or induced tachycardia can help in the choice of treatment or recommendations for future work.

    3. Patients who undergo heart surgery for other reasons.

    The course of WPW

    syndrome The usual course of WPW syndrome can be represented as follows:

    Stage 1: short-term( <20-30 min) attacks of orthodromic tachycardia, stop reflexively.

    Stage 2: increased frequency and duration( 30 minutes - 3 hours) of seizures, arrest with one antiarrhythmic drug, sometimes in combination with vagal samples. To prevent tachycardia apply medication.

    Stage 3: frequent and prolonged( > 3 h) attacks of orthodromic tachycardia, occurrence of attacks of atrial fibrillation, VT, FF, disturbances of the conduction system( SSSU, BNPG, AV blockade), tolerance to antiarrhythmic drugs. Catheter ablation of DP is indicated.

    There is no such a bad situation that could not get any worse.

    Single cases of DP involution have been described in adults due to focal fibrosis, calcification of the fibrous ring, mechanical isovolytic damage of the muscle bridges between the fibrous ring and ventricular myocardium.

    Mortality from arrhythmia in WPW syndrome is 1.5%.

    Diagnosis of myocardial infarction

    Kent bunches are often manifested by pseudo-infarction ECG.Pathological tooth Q( negative delta wave) with a discordant rise of the ST segment occurs in 53.5-85% of cases of the WPW phenomenon. We note that the magnitude of the shift of the ST segment can vary, which depends on the vegetative effects on the conductivity along the DP.

    In a number of cases, electrocardiographic manifestations of myocardial infarction resemble the phenomenon of WPW with negative delta wave. The wide and altered QRS complex, the discordant shift of the ST segment and the T wave, create great difficulties in the diagnosis of myocardial infarction in patients with the WPW phenomenon. In this case, it is necessary to focus on long-term anginal pain, increased activity of markers of myocardial necrosis( CFC MB, troponins), disruption of isotope accumulation in left ventricular myocardium, akinesia according to echocardiography.

    Various pharmacological tests help diagnose myocardial infarction. For example, a blockade of DP can lead to the disappearance of electrocardiographic signs caused by a change in the course of excitation. A similar result can be obtained in 30-50% of cases when accelerating the AV node with atropine. After the introduction of ATP, the development of the Kent beam on the ECG is enhanced. Note that after the disappearance of the signs of pre-excitation, the negative tooth of T.

    may persist. In the presence of electrocardiographic signs of the DP, the term "WPW phenomenon" is used on the proposal of the WHO Working Group of Experts, and in the case of tachycardia, WPW syndrome ".

    The following clinical forms of the WPW phenomenon are distinguished:

    Manifesting - constant ECG changes( truncated PQ, delta wave, wide QRS).

    Intermittent - transient ECG changes, including brady- and tachycardic blockade of the DP.With daily ECG monitoring, typical changes periodically disappear in 30-40% of cases, which is usually associated with a transient DP blockade.

    Latent - ECG changes appear only with EFI.

    Hidden - there is only a retrograde pulse in the DP, so the rest ECG is always normal and ortho-phomic( AV reciprocal) tachycardia is possible.

    1. The phenomenon of WPW, intermittent form.

    2. WPW syndrome, latent form, paroxysmal atrioventricular reciprocal tachycardia.

    3. WPW syndrome, paroxysmal atrial fibrillation with heart rate to 240 rpm, syncope and transient ischemic attacks.

    No treatment is required if there is an asymptomatic WPW phenomenon. Individuals of certain professions( pilots, divers, public transport drivers) are recommended by the EFI in order to determine the properties of DP and the provocation of tachycardia, which will allow choosing the correct tactics of reference. In the presence of fainting, electrophoresis and catheter destruction of the DP are performed. Preventive antiarrhythmic treatment is currently rarely prescribed.

    Coupling ortodromic AV reciprocal tachycardia is similar to treatment of AV nodal reciprocal tachycardia. A vagal test, verapamil( diltiazem) and CHPES have a good effect.

    In rare cases, spontaneous transition of orthodromic tachycardia to atrial fibrillation is possible, and then blocking AV by verapamil will be undesirable. For such situations, an emergency EIT may be required.

    It is important to consider the increased risk of atrial fibrillation with intravenous administration of ATP.

    For the prevention of tachycardia, drugs 1A, 1C or 3 grade are recommended. Apparently, long-term use of beta-blockers is possible, especially in the absence of signs of a "fast" DP( ACC /AHA/ ESC, 2003).If the antiarrhythmic drugs are ineffective or intolerant, catheter destruction of the DP is indicated.

    With high heart rate and severe hemodynamic disorders, it is necessary to conduct an immediate cardioversion. In other cases, for the management of tachycardia, usually drugs with a strong and rapid antiarrhythmic effect are chosen that block DP well, for example, propafenone, procainamide, and also Ibutilide or flecainide. Amiodarone is effective, but the relatively slow development of the effect in severe cases limits its use.

    Recently introduced into clinical practice, dofetilide has shown a good arresting effect in WPW syndrome with atrial fibrillation. Single or repeated administration of the drug eliminated arrhythmia in 82% of cases.

    Influence of antiarrhythmic drugs on

    AS We note that the assessment of the effect of drugs on the rate of VOCD has a value primarily for the treatment of broad-spectrum tachycardias, especially atrial fibrillation and flutter, rather than orthodromic tachycardia. In connection with the possibility of accelerating the procedure for DP and the development of VF, intravenous administration of calcium antagonists, beta-blockers and digoxin is contraindicated.

    If there are factors of an increased risk of sudden death, then destruction of the DP is necessary. In other cases, you can try to prevent seizures with drugs 1C or 3 class.

    Note that with oral administration of verapamil, the risk of VF does not increase. In our observation, after taking 80 mg of verapamil, a paradoxical disappearance of the WPW phenomenon was recorded on the ECG.Moreover, during the previous and subsequent diurnal ECG monitoring without verapamil there were no signs of blockade of the DP.Apparently, DPs with different electrophysiological properties and different reactions to pharmacological agents are also used.

    To stop and prevent antidromic tachycardia apply drugs 1A, 1C and 3 classes. Unlike orthodromic tachycardia, in this case, verapamil and digoxin are not shown, since it is possible to increase the heart rate. If the antiarrhythmic drugs are ineffective or intolerant, catheter destruction of the DP is indicated.

    The safety, efficacy and relatively low cost of radiofrequency catheter ablation of DPs make this treatment the method of choice in most patients with WPW syndrome. The method of treatment consists in conducting the electrodes to the location of the DP, previously identified with EFI, and the destruction of the connection by electric discharge.

    The effectiveness of treatment for DP located in the left free wall is 91-98%, in the septal region 87%, on the right free wall 82%.

    The overall incidence of complications and death is 2.1% and 0.2% of complications include valve damage, pericardial tamponade, AV blockade, pulmonary and systemic embolisms. It is important to note that after successful ablation, AF often recurs atrial fibrillation: in 12% in patients under 50 years, 35% in patients over 50 years and in 55% of patients over 60 years.

    I class( proven effectiveness)

    1. Patients with symptomatic AV reciprocal tachycardia, if drug treatment is ineffective, is poorly tolerated or the patient does not want to take drugs for a long time.

    2. Patients with atrial fibrillation( or other atrial tachyarrhythmia) and rapid ventricular response via DP, if medication is ineffective, is poorly tolerated, or the patient is not willing to take long-term medications.

    Class II( conflicting performance data)

    1. Patients with AV reciprocal tachycardia or atrial fibrillation with a high incidence of ventricular arthritis detected during the EFI of another arrhythmia.

    2. Patients without symptoms with pre-excitation of the ventricles, if their vital activity, or profession, or mental state, or public safety can be worsened by spontaneous tachyarrhythmias or abnormalities on the ECG.

    3. Patients with atrial fibrillation and a controlled ventricular response via DP.

    4. Patients with a family history of sudden death.

    Operative treatment

    Currently, surgical treatment is rarely used. Operative destruction is carried out under conditions of artificial circulation or without it, through endo- or epicardial access. Destruction of DP is carried out by means of acute intersection, cryodestruction, electrodestruction, chemical denaturation.

    The effectiveness of treatment is about 100%.The lethality of the method is about 1.5%, and if the correction of heart disease is carried out simultaneously, 2-5%.AV block of the 3rd degree appears in 0.8% of cases, which is due to the division of the atria and ventricles in the zone of DP during the operation. Repeated destruction is required in 0-3% of cases.

    • Normal ECG does not exclude the presence of DP.

    • Determination of localization of DP by the presence and polarity of the delta wave in various leads of the ECG is not of significant clinical significance.

    • Kent's congenital bundle can manifest itself on the ECG with pseudo-infarct changes.

    • The tactics of ventricular pre-excitation syndrome are determined by the presence of tachycardia and the conductive properties of DP.

    • Patients in certain professions with signs of pre-excitation on the ECG need to determine the electrophysiological properties of DP in connection with the high risk of adverse situations already at the first attack of tachycardia.

    • Verapamil and digoxin accelerate the process along an additional pathway of Kent and can be dangerous in the development of atrial fibrillation or flutter.

    • AV nodal reciprocal tachycardia can be caused by a retrograde-functioning DP.

    • For tachycardia with a very high heart rate( & gt; 200-250 per min), the ventricular pre-excitation syndrome should be excluded.