Ventricular tachycardia of the "pirouette" type. What is pirouette type tachycardia Pirouette type cardiac arrhythmia

General principles therapy coincide with the principles of therapy for monomorphic VT. Most patients develop hemodynamic instability and are therefore indicated for external defibrillation. Polymorphic VT (pirouette type) occurs in the following cases requiring specific therapy:

• ischemic polymorphic VT in AMI;
• non-ischemic VT with prolongation of the QT interval.
• polymorphic VT accompanying Brugada syndrome.

Symptoms and signs of polymorphic ventricular tachycardia of the pirouette type

Usually collapse/arrest of the heart with a long course.

With short-term symptoms, stable hemodynamics is possible.

Ischemic polymorphic ventricular tachycardia

• Occurs in acute myocardial infarction or chronic myocardial ischemia.
• Monomorphic VT in myocardial infarction can turn into polymorphic VT.
• Initial treatment consists of complete revascularization. Then Holter monitoring, stress tests with ECG registration and electrophysiological examination should be performed to determine the arrhythmia threshold.
• Some patients, especially those with impaired left ventricular function, as well as the transformation of monomorphic VT into polymorphic, may require implantation of a defibrillator.

Non-ischemic polymorphic ventricular tachycardia with a prolonged OT interval

Irregular polymorphic VT (usually stopping on its own), "wrapping" on the ECG isoline. It occurs when the QT interval is prolonged (QT >500 ms), but QT length does not predict the risk of serious arrhythmias. May present with recurrent fainting or dizziness. Often given state patients are erroneously described as convulsions.

Brugada syndrome

• Usually found in Japan, Southeast Asia. Men are more often affected.
• Mutations in sodium channels of cardiomyocytes are noted.
• It is required to consult an electrophysiologist and conduct an electrophysiological study in order to determine the indications for the implantation of a defibrillator.
• Diagnosis is based on a series of ECGs after administration of flecainide.< 2 мг/кг внутривенно или прокаинамида 10 мг/кг внутривенно. Проба положительна если после назначения препарата сегмент ST поднимается на 1 мм. При положительной пробе необходимо произвести электрофизиологическое исследование и в дальнейшее специальное обследование.
• electrolyte disorders.
• Severe bradycardia.
• Heart disease (IHD, myocarditis).
• Intracranial hemorrhage (especially subarachnoid).

Reasons for lengthening the OT interval

• Congenital (long QT syndrome).
• Medicines.
• Electrolyte imbalance (low K +, Mg 2+).
• Bradycardia/episodic asystole.
• myocardial ischemia.
• Others (significant metabolic disorder, subarachnoid hemorrhage).

Medicines:

• Antiarrhythmics: Quinidine, procainamide, disopyramide, amiodarone, sotalol.
• Antipsychotics: Pimozide, thioridazine.
• Antihistamines: Terfenadine, astemizole, especially when interacting with other drugs taken, such as ketoconazop, erythromycin.
• Antimalarials: Especially hapofantrine.
• Organophosphate poisoning.

ECG diagnostics

Regular change in QRS morphology and axis (variations around the isoelectric baseline).

Congenital long QT syndrome

• Syndrome Jervel, Lange-Nielsen (aortic insufficiency and deafness).
• Romano-Ward syndrome (aortic insufficiency, normal hearing).

Note! Although amiodarone and sotalol prolong the OT interval, polymorphic VT is rarely observed with these drugs.

Treatment of polymorphic ventricular tachycardia

Congenital long WC syndrome

• In this case, polymorphic VT has an adrenergic origin, therefore, it requires the appointment of long-acting β-blockers (for example, propranolol).
• Additionally, implantation of a pacemaker and ganglionectomy of the stellate ganglion on the left may be required.
• The possibility of implanting a defibrillator should be discussed. Decision making can be difficult due to the young age of the patient.

Acquired Long WC Syndrome

• The priority is the correction of the extended OT interval.
• It is necessary to identify and stop the impact of causative factors.
• Polymorphic VT in acquired QT interval prolongation usually occurs secondarily during the lengthening of the pauses between beats, which should be avoided.
• All patients should be given magnesium sulfate (8 mmol as a 2–5 minute bolus followed by 60 mmol as a daily infusion).
• Temporary pacing (both ventricular and atrial) interrupts the arrhythmia. Long-term pacing prevents recurrence of polymorphic VT.
• Isoprenaline may be given to prepare for pacing. It enhances the atrial rhythm and suppresses the ventricular. Target frequency is 110-120 per minute.

Urgent measures for polymorphic ventricular tachycardia of the pirouette type

With a stable arrhythmia, hemodynamic collapse usually develops or there is a threat of its inevitable development. An urgent cardioversion is required. In the absence of a pulse - an algorithm for CPR.

If the patient is conscious and stable, or polymorphic VT recurs and is unstable, urgent treatment is required, as the patient's condition may deteriorate rapidly.

• Correction of electrolyte balance (especially K + , Mg 2+), goal> 4.5 mmol / l.
• Simultaneous treatment possible causes arrhythmias such as MI.
• If the corrected QT interval is prolonged (> 0.45 s) in sinus rhythm, aim treatment to increase heart rate and shorten QT:
• cancel any provoking drug;
• useful intravenous magnesium sulfate, if there is no hypomagnesemia - give 1-2 g (4-8 mmol) for 5-10 minutes in 100 ml of 5% glucose, then infusion of 0.5-1 g / h;
• consider administering atropine/isoprenaline as a temporary measure;
• temporary stimulation with a frequency of 90 bpm.
• Amiodarone may worsen the condition by prolonging the QT.
• If the QT interval is normal in sinus rhythm, there is no bradycardia (in this case, usually due to myocardial ischemia or an obvious systemic cause):
• consider using atropine/isoprenaline as a temporary measure;
• if necessary, prescribe lidocaine.

Further measures for polymorphic VT

• Maintain potassium > 4.5 mmol/L.
• Avoid drugs that prolong QT.
• Urgent examination by a cardiologist.

Often found in clinical practice and require careful evaluation of patients to determine the individual prognosis of these arrhythmias and the possible risk of ventricular fibrillation (VF) and sudden cardiac death. Frequent ventricular arrhythmias include: ventricular extrasystole (PV); ventricular tachycardia (VT); ventricular fibrillation (VF); accelerated idioventricular rhythm.

Ventricular extrasystole

Ventricular extrasystole (PV) is a premature excitation of the heart that occurs under the influence of impulses emanating from various parts of the ventricular conduction system. Single monomorphic PVCs can occur as a result of both the formation of a re-entry of the excitation wave (re-entry) and the functioning of the post-depolarization mechanism. Repetitive ectopic activity in the form of several successive PVCs is usually due to the re-entry mechanism. The source of PVCs in most cases are branches of the bundle of His and Purkinje fibers. During PVC, the sequence of repolarization changes, there is a shift of the RS-T segment above or below the isoline, the formation of an asymmetric negative or positive T wave. The shift of RS-T and the polarity of the T wave are discordant to the main wave of the ventricular complex, directed in the direction opposite to this wave.

An important sign of PVC is the absence of a P wave in front of the extrasystolic QRS complex, as well as the presence of a complete compensatory pause. During PVC, the SA node usually does not "discharge" because the ectopic impulse originating in the ventricles cannot pass retrograde through the AV node and reach the atria and SA node. In this case, the next sinus impulse freely excites the atria, passes through the AV node, but in most cases cannot cause another depolarization of the ventricles, since after PVC they are still in a state of refractoriness. With left ventricular ES, there is an increase in the interval of internal deviation in the right chest leads V1, V2 (more than 0.03 s), and with right ventricular ES - in the left chest leads V5, V6 (more than 0.05 s).

To assess the prognostic significance of PVCs, V. Lown and M. Wolf (1971) proposed a system of gradations. Based on the results of 24-hour Holter ECG monitoring, 6 classes of PVCs are distinguished: class 0 — no PVCs within 24 hours of monitoring; class 1 - less than 30 PVCs are recorded for any hour of monitoring; Grade 2 - more than 30 PVCs are registered for any hour of monitoring; Grade 3 - polymorphic PVCs are registered; class 4a — monomorphic paired PVCs; Grade 46 — polymorphic paired PVCs; Grade 5 - 3 or more PVCs in a row are registered within no more than 30 s. Class 2-5 PVCs are associated with a greater risk of ventricular fibrillation (VF) and sudden cardiac death.

65-70% healthy people separate, monomorphic isolated PVCs are registered, belonging to the 1st class according to the classification of V. Lown and M. Wolf, are not accompanied by clinical and echocardiographic signs of organic heart disease. Therefore, they are called "functional PVCs". Functional PVCs are recorded in patients with hormonal profile disorders, cervical osteochondrosis, NCD, with the use of aminophylline, glucocorticoids, antidepressants, diuretics, in vagotonics.

In individuals with increased activity of the parasympathetic system, the PVC system disappears during physical activity.

Organic PVCs are characterized serious forecast, occur in patients with ischemic heart disease, myocardial infarction, postinfarction cardiosclerosis, hypertension, heart defects, MVP, myocarditis, pericarditis, DCM, HCM, CHF. More often, polytopic, polymorphic, paired PVCs and even short episodes (“jogging”) of unstable VT are recorded. The presence of "organic" extrasystole does not exclude a certain role of neurohormonal disorders in the occurrence of arrhythmias. Patients in whom organic PVCs are detected undergo: biochemical analysis blood (K+, Mg2+ and other parameters); 24-hour Holter ECG monitoring; EchoCG with the definition of EF, diastolic dysfunction; variability study heart rate. These studies make it possible to estimate the possible risk of VF and sudden cardiac death, to determine the tactics of treating patients.

Ventricular tachycardia

Ventricular tachycardia (VT) is a sudden onset and just as suddenly ending attack of increased ventricular contractions up to 150-180 bpm. (less often - more than 200 beats or within 100-120 beats per minute), usually while maintaining the correct regular heart rate). Mechanisms of VT paroxysms: re-entry of the excitation wave (re-entry), localized in the conduction system or the working myocardium of the ventricles; ectopic focus of increased automatism; ectopic focus of trigger activity.

In most cases, VT in adults develop by the reentry mechanism and are reciprocal. Reciprocal VT is characterized by a sudden acute onset immediately after the PVC that induces the onset of an attack. Focal automatic VT is not induced by extrasystoles and often develops against the background of increased heart rate caused by physical activity and an increase in the content of catecholamines. Trigger VT also occurs after a PVC or an increase in heart rate. Automatic and triggered VT are characterized by tachycardia with a gradual achievement of a rhythm rate at which sustained VT is maintained.

There are streets with cardiac pathology (acute myocardial infarction, postinfarction aneurysm, DCMP, HCM, arrhythmogenic pancreatic dysplasia, heart defects, MVP, digitalis intoxication). In 85% of cases, VT develops in patients with coronary artery disease, and in men 2 times more often than in women. ECG signs: 1. A sudden onset and just as suddenly ending attack of increased heart rate up to 140-150 beats per minute (less often - more than 200 or within 100-120 beats per minute) while maintaining the correct rhythm. 2. Deformation and expansion of the QRS complex more than 0.12 by its discordant location of the RS-T segment and the T wave. 3. The presence of AV dissociation - complete dissociation of the frequent ventricular rhythm (PU complexes) and normal atrial sinus rhythm (P waves).

Differential Diagnosis VT and supraventricular PT with wide QRS is of paramount importance because the treatment of these two arrhythmias is based on different principles, and the prognosis of VT is much more serious than supraventricular PT. A reliable sign of this or that form of PT is the presence of VT or the absence of AV dissociation with periodic "captures" of the ventricles. This in most cases requires intracardiac or transesophageal registration of P waves of the ECG. However, already during a routine clinical examination of a patient with paroxysmal tachycardia, when examining the veins of the neck and auscultation of the heart, it is possible to identify signs characteristic of each type of PT. With supraventricular tachycardia with AV conduction of 1:1, there is a coincidence in the frequency of arterial and venous pulses. Moreover, the pulsation of the cervical veins is of the same type and has the character of a negative venous pulse, and the volume of the first tone remains the same in different cardiac cycles. Only in the atrial form of supraventricular PT, episodic prolapse is observed. arterial pulse associated with transient second degree AV block.

Figure 30.

Ventricular tachycardia

(M.L. Kachkovsky)

There are three clinical variants of VT: 1. Paroxysmal non-sustained VT is characterized by the appearance of three or more ectopic QRS complexes in a row, which are recorded during an ECG monitor recording within no more than 30 s. Such paroxysms increase the risk of VF and sudden cardiac death. 2. Paroxysmal sustained VT lasting more than 30 s. It is characterized by a high risk of sudden cardiac death and significant changes in hemodynamics. 3. Chronic or continuously recurrent VT - long-term recurring relatively short tachycardic "jogs" that are separated from each other by one or more sinus complexes. This variant of VT increases the risk of sudden cardiac death and leads to a gradual increase in hemodynamic disturbances.

Polymorphic ventricular tachycardia tina "pirouette"

A special form of paroxysmal VT is polymorphic VT (pirouette - torsade de pointes), which is characterized by an unstable, constantly changing form of the QRS complex and develops against the background of a prolonged QT interval. It is believed that bidirectional fusiform VT is based on a significant prolongation of the QT interval, which is accompanied by a slowdown and asynchronism of the repolarization process in the ventricular myocardium, which creates conditions for the reentry of the excitation wave (reentry) or the appearance of foci of triggered activity. In some cases, bidirectional VT can develop against the background of a normal QT interval.

The most characteristic for VT of the "pirouette" type is a constant change in the amplitude and polarity of ventricular tachycardia complexes: positive QRS complexes can quickly transform into negative ones and vice versa. This type of VT is caused by the existence of at least two independent but interacting reentry circuits or multiple foci of trigger activity. There are congenital and acquired forms of VT of the "pirouette" type.

The morphological substrate of this VT is inherited - long QT interval syndrome, which in some cases (with an autosomal recessive type of inheritance) is combined with congenital deafness. The acquired form is much more common than the hereditary form. It develops against the background of a prolonged Q-T interval and pronounced asynchronism of ventricular repolarization.

ECG signs of VT: 1. The frequency of the ventricular rhythm is 150-250 per minute, the rhythm is irregular with fluctuations R-R intervals within 0.2-0.3 s. 2. QRS complexes of large amplitude, their duration exceeds 0.12 s. 3. The amplitude and polarity of the ventricular complexes changes within a short time. 4. In cases where P waves are recorded on the ECG, a dissociation of the atrial and ventricular rhythm (AV dissociation) can be observed. 5. VT paroxysm usually lasts a few seconds, stopping spontaneously, but there is a pronounced tendency to multiple recurrence of seizures. 6. Attacks of VT are provoked by PVC. 7. Outside the attack of VT on the ECG, a significant lengthening of the QT interval is recorded. Since the duration of each attack of VT of the "pirouette" type is short, the diagnosis is more often established on the basis of the results of Holter monitoring and assessment of the duration of the QT interval in the period between attacks.

Figure 31.

Ventricular tachycardia type "pirouette"

(M.A. Kachkovsky)

Flutter and ventricular fibrillation

Ventricular flutter (VT) is a frequent (200-300 per minute) and rhythmic excitation and contraction. Ventricular fibrillation (flicker) is equally frequent (200-500 per minute), but erratic, irregular excitation and contraction of individual muscle fibers, leading to the cessation of ventricular systole (ventricular asystole). The main ECG signs: 1. With ventricular flutter - frequent (200-300 per minute), regular and identical in shape and amplitude flutter waves, resembling a sinusoidal curve. 2. With fibrillation (flicker) of the ventricles - frequent (200-500 per minute), but irregular random waves that differ from each other in different shapes and amplitudes.

The main mechanism of TA is rapid and rhythmic Roundabout Circulation waves of excitation along the ventricular myocardium (re-entry) along the perimeter of the infarcted zone or the area of ​​the LV aneurysm. VF is based on the occurrence of multiple random micro-re-entry waves, which are formed as a result of pronounced electrical inhomogeneity of the ventricular myocardium.

The causes of TG and VF are severe organic lesions of the ventricular myocardium (acute MI, chronic ischemic heart disease, postinfarction cardiosclerosis, hypertensive heart, myocarditis, cardiomyopathy, aortic heart disease).

Figure 32.

ventricular flutter

(M.A. Kachkovsky)

Distinguish between primary and secondary VF. Primary fibrillation is associated with acutely developing electrical myocardial instability in patients who do not have fatal circulatory disorders, severe heart failure, or cardiogenic shock. The causes of primary VF can be acute coronary insufficiency (MI, unstable angina pectoris), myocardial reperfusion after effective revascularization of the heart muscle, surgical manipulations on the heart.

Primary VF is successfully treated with electrical cardioversion in most cases, although patients remain at high risk of recurrent VF later in life. Secondary VF is a mechanism of death in patients with severe organic pathology: cardiogenic shock, CHF, postinfarction cardiosclerosis, DCMP, heart defects. Secondary VF is usually very difficult to treat and in most cases ends in the death of the patient.

Polymorphic ventricular tachycardia with prolongation of the Q-T interval (pirouette type)

polymorphic ventricular tachycardia with prolongation of the Q-T interval (pirouette type)

Ventricular tachycardia of the "pirouette" type is associated with an increase in the duration of cardiomyocyte repolarization, is determined on the ECG by a prolongation of the Q-T interval (congenital or acquired), and its immediate triggering factor is a slowing of the heart rate, which leads to a sharp prolongation of the interval.

Diagnostic criteria there are such ECG signs (Fig. 58):

1) cyclic changes in the direction of the QT complex vector in the range of 180 ° with a frequency of 10-15 complexes on average

2) connection of the occurrence of ventricular tachycardia with a decrease in heart rate. Ventricular tachycardia is often preceded by severe sinus bradycardia, complete atrioventricular block

3) prolongation of the Q-T interval in sinus rhythm complexes immediately preceding ventricular tachycardia.

The frequency of the ventricular rhythm in paroxysmal ventricular tachycardia of the "pirouette" type ranges from 150-250 per 1 min.

Clinical picture and course. Most attacks end spontaneously and are asymptomatic or accompanied by dizziness and temporary loss of consciousness. However, in such patients, the risk of transformation of ventricular tachycardia into ventricular fibrillation and sudden death is significantly increased.

Treatment and secondary prevention. The method of choice is temporary electron rocardiostimulation, preferably atrial, with a heart rate of 90-100 per 1 min, which allows to reduce the duration of the QT interval. The class IV antiarrhythmic drugs lidocaine and mexiletine have the same ability. Even in the absence of hypomagnesemia, iatrogenic ventricular tachycardia of the "pirouette" type can be suppressed by the administration of magnesium sulfate at a dose of 2-3 g, which is associated with the elimination of trigger activity due to blockade of calcium channels. good effect also gives intravenous administration of potassium salts. In the event of a prolonged attack, they resort to electrical defibrillation, which, however, gives an unstable effect.

To prevent recurrence of polymorphic ventricular tachycardia, the “culprit drug” should be discontinued. Subsequently, the appointment of other drugs that cause prolongation of the QT interval should be excluded. It is also important to prevent the development of hypokalemia and hypomagnesemia.

Pirouette type tachycardia

The concept of "pirouette-type tachycardia" was introduced by Dessertenne in 1966. It denotes a rapid ventricular tachycardia with a repetitive change of QRS complexes around the isoline every 5-10 complexes. Most often, pirouette-type tachycardia is observed in the syndrome of prolongation of the QT interval (Schwartz, 1985). In this case, it is pathognomonic along with prolongation of the QTC interval. It can also be observed on the basis of other arrhythmogenic substrates.

(!) Pirouette-type tachycardia can stop spontaneously or turn into ventricular fibrillation. It should always be regarded as a life-threatening condition.

Therapy. Based on the following principles. Emergency treatment depending on the clinical condition of the patient. With unstable hemodynamic parameters - resuscitation measures. Ventricular arrhythmias should be treated as quickly as possible by cardioversion or defibrillation. Up to this point, it is necessary to maintain blood circulation through chest compressions. With slow and satisfactorily tolerated by the patient, arrhythmias can begin with pharmacological therapy. If relief does not occur, the next step is intracardiac overstimulation or cardioversion. Long-term therapy: pharmacological therapy is indicated if the child is too young for radiofrequency ablation, or if the arrhythmia is rapid, to reduce the frequency

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Heart rhythm failure is one of the most frequently reported pathologies in cardiology. Arrhythmias are diverse and can arise from different sources of impulses. The pirouette form of tachycardia belongs to a special type of ventricular paroxysmal tachycardia and is characterized by an increased risk of developing disorders incompatible with life.

Arrhythmia is a common heart rhythm disorder that is either higher or lower normal indicators, and covers a large group of diseases. One of the most severe forms failure of the heart rhythm is an arrhythmia, which was given the name "pirouette" in connection with the peculiarities of changes in the work of the organ. This pathology refers to paroxysmal disorders.

Paroxysmal (paroxysmal) tachycardia is a spontaneously started and also suddenly ended attack of increased heart contractions in the range of 145-245 beats / min. In this case, the regularity of the rhythm can be either preserved or changed.

With ventricular paroxysmal tachycardia, the source of ectopic impulses is located in the conducting system of the ventricles - the bundle of His, its branches and Purkinje fibers. The impulse current through the ventricles is sharply and pathologically changed, it first excites one ventricle, and then, with a significant delay, passes to another and spreads through it in a non-standard way.

As a result, the repolarization process is also disrupted. A typical picture of this disorder is formed on the cardiogram. An important factor is atrioventricular dissociation - the atrial and ventricular parts contract in different rhythms.

Pirouette type tachycardia is described by the above signs and is characterized by polymorphism of the ventricular complex on the electrocardiogram. What is pirouette and polymorphism?

Polymorphic - that is, diverse in its form, and pirouette - turning around one, two or more times. Is the heart capable of changing its shape and making such revolutions? In fact, these are conventional names for what happens with this type of pathology.

Violations can be clearly seen on the cardiogram:

1. Pathology is characterized by a significant increase in the Q-T interval.
2. An atypical change in the QRS complex is fixed - they have different amplitudes and shapes.

Why does a violation occur?

All causes and factors that stimulate the formation of pirouette tachycardia can be differentiated into acquired and congenital.

Causes of innate character:

• Romano-Ward syndrome;
• Jervell-Lange-Nielsen syndrome;
• anomalies of sodium and calcium channels.

Acquired Causes:

• heart lesions with morphological damage to the organ: chronic coronary artery disease, myocardial infarction, prolapse mitral valve, cardiomyopathy, myocarditis;
• CNS damage, anorexia nervosa;
• decompensated diseases of the endocrine system;
• mercury poisoning, insecticides;
• electrolyte imbalance: lack of calcium, magnesium.

Pathology can occur as a result of an overdose of drugs of such groups:

Main risk factors:

• chronic psycho-emotional overexcitation;
• addiction to alcohol and drugs;
• low-protein diets and insufficient fluid intake;
• hypothermia.

Characteristic symptoms

Outside of an attack of paroxysm, the main clinical picture presents with symptoms of the underlying disease. The main symptoms of polymorphic pirouette tachycardia are as follows:

• syncopal conditions, which are based on an increase in heart rate up to 250 beats / min and a violation of brain oxygenation against this background;
• feeling of palpitations and interruptions in the chest;
• rapid rhythmic pulse of weak filling and low blood pressure;
• feeling short of breath;
• general weakness;
• anxiety;
• frequent dizziness;
• periodic pain in the region of the heart.

Pirouette arrhythmia is an extremely dangerous malfunction of the organ, which can provoke the development of ventricular fibrillation and increases the risk of death.

Diagnostic Measures

If you experience the above symptoms, you should immediately seek help from a cardiologist. Important in making a diagnosis are: careful collection of anamnesis, complaints and their detail, objective examination and instrumental diagnostics hearts. The most informative method is the electrocardiogram.

The main ECG signs of the disease:

Additional diagnostic procedures:

• Holter ECG;
• echocardiography.

Main therapeutic measures

Treatment of pirouette arrhythmia is complex and can be conservative (medication) and surgical treatment. In the event of an attack, it is urgent to start resuscitation measures, otherwise the development of a lethal outcome is possible. If the attack is provoked by taking antiarrhythmic, psychotropic or drugs of another group (listed above), they must be canceled.

Stages of emergency care:

It is strictly forbidden to administer antiarrhythmic drugs of class Іа, ІІс, ІІІ as it contributes to the prolongation of the QT interval.

With inefficiency drug therapy, and if the attacks are repeated often, the patient needs surgical intervention: implantation of an automatic defibrillator-cardioverter. If symptoms of bradycardia are still noted, the installation of an electrical stimulator is recommended.

Another method is the removal of areas of pathological impulses by radiofrequency ablation under X-ray control. It is also called catheter destruction.

Prevention and prognosis

Main preventive measures are the following:

Forecast this disease adverse. At the first occurrence of complaints and a timely appeal to a cardiologist, the prognosis can be improved, since effective therapy will be prescribed in a timely manner.

If you neglect the "cry for help" of your body, polymorphic pirouette-tachycardia can turn into ventricular fibrillation and be fatal.

It is extremely important to tell the doctor all the details of the course of the disease: the time and frequency of the onset of symptoms, the medication taken, the presence of similar manifestations in the next of kin.

No matter how serious the disease is, you can always improve the quality of life if you seek help in a timely manner. Pirouette arrhythmia often requires only ECG monitoring and an integrated approach to treatment for its confirmation. The outcome and prognosis, subject to elementary rules, can have a favorable course.

This term is used to describe one of the forms of ventricular tachycardia, which is called pirouette tachycardia or ventricular tachycardia of the pirouette type.

1 When does the heart dance?

Recall that ventricular tachycardia is a variant of heart rhythm disturbance, in which the frequency of ventricular contractions reaches high numbers up to 150-250 per minute, and even higher. This arrhythmia can be paroxysmal (if the tachycardia starts abruptly and ends abruptly) and chronic (lasting for months, years).

Pathological impulses that cause the ventricles to contract so rapidly can be produced by one source, then this kind of ventricular tachycardia is called monomorphic. And there may be several sources of impulsation, in this case there is a polymorphic arrhythmia. In the classification of arrhythmias, there is a form of polymorphic paroxysmal tachycardia - pirouette tachycardia or ventricular tachycardia of the Torsades de pointes type.

These are paroxysmal episodes of frequent ventricular beating from 200 to 300 per minute, which last from 30 seconds to 1 minute. There are always several sources that set such impulses, so the ventricular complexes on the cardiogram have different shape and amplitude. A feature of ventricular tachycardia of the pirouette type is that it develops against the background of extended interval QT on ECG. Normally, this interval reflects the process of excitation and recovery of the ventricles.

2 Causes of tachycardia type Torsades de pointes

All causes can be divided into congenital and acquired. Congenital ventricular tachycardia pirouette develops with long QT syndrome, which is caused by a mutation of certain genes. There are several forms of congenital long QT syndrome: Roman-Ward syndrome, Jervell-Lange-Nielsen syndrome. These syndromes, and pirouette-type tachycardia, as a consequence, are inherited.

But much more common are the acquired causes of the development of this arrhythmia. All these reasons cause the development of secondary (acquired) prolongation of the QT interval. Acquired causes include:

3 Clinical picture

Symptoms of paroxysmal pirouette tachycardia: palpitations, severe dizziness, fainting, a prolonged attack may be complicated by the transition to ventricular fibrillation, which can be fatal. Outside of the paroxysm, the symptoms will be determined by the underlying disease of the patient. Against the background of an attack, the patient has a frequent rhythmic pulse, weak filling, low blood pressure, increased tone I during auscultation of the heart.

The attack may stop on its own, or it may turn into ventricular fibrillation. If the patient has fainted, it is necessary, if possible, to take a cardiogram from the patient in a fainting state, and be sure to analyze it in terms of the presence of the syndrome long Q-T. Collection of complaints, symptoms, thorough diagnosis will allow the doctor to establish a diagnosis and begin treatment.

Ventricular tachycardia "pirouette" is a dangerous arrhythmia that can lead to fibrillation and death. The prognosis for this form of arrhythmia is often poor.

4 Diagnostics

ECG, ECG Holter monitoring, EchoCG are successfully used in diagnostics. But the most common, simple and affordable method remains the removal of an electrocardiogram against the background of an attack.

Signs of pirouette tachycardia of the ventricles on the ECG will be:

1. The frequency of the ventricular rhythm is from 200 to 300 per minute and higher, the amplitude of the complexes is different, their direction alternates: they are either higher or lower than the isoline, as if rotating, “dancing pirouette” around it. QRS complexes expanded 0.12 s;
2. R-R intervals are not the same, fluctuations are within 0.2-0.3 sec;
3. outside the attack, the length of the QT interval is greater than normal.

Since the duration of the attack is not so long, it is rarely possible to fix the ECG directly at the time of the attack. The attack may stop on its own, or it may turn into ventricular fibrillation. Therefore, more often the diagnosis is made by deciphering the data of the daily monitoring of the ECG according to the Holter and by analyzing the Q-T interval on the cardiogram outside the attack.

5 Treatment

With a paroxysm of ventricular tachycardia of the pirouette type, accompanied by hemodynamic disturbances, loss of consciousness, cardioversion is used. Start electrical defibrillation with a discharge of 75-100 kJ. If necessary, continue defibrillation with a 200 kJ discharge, and if ventricular tachycardia persists, apply 360 kJ. If the paroxysm is caused by taking any of the drugs that can affect the length of the QT interval, it is necessary to cancel this drug.

If the patient has hypokalemia, intravenous injections of potassium chloride are performed. Also in the treatment, a 20% solution of magnesium sulfate 10-20 ml in 20 ml of a 5% glucose solution is used, the drug is administered intravenously for 1-2 minutes. At the same time, it is necessary to carefully control the rhythm of breathing and the level blood pressure because it is possible to fall blood pressure and respiratory depression.

If tachycardia is repetitive, prone to recurrence, 100 ml of a 20% solution of magnesium sulfate is injected intravenously with 400 ml of isotonic sodium chloride at a rate of 10-35 drops per minute. It is effective to prescribe lidocaine or B-blockers for pirouette ventricular tachycardia. If a conservative treatment did not have the desired effect, there is a congenital form of the disease.

With frequent paroxysms, implantation of a cardioverter-defibrillator is used - a special device that can recognize emerging heart rhythm disturbances and eliminate them with a special electrical signal. Pirouette-type ventricular tachycardia is a severe form of arrhythmia, the prognosis for life with this form of arrhythmia is always serious. There is a high probability of this tachycardia turning into ventricular fibrillation, which can be fatal.

The risk of sudden cardiac death is also high. To combat these complications, patients suffering from ventricular arrhythmias are given prophylactic maintenance antiarrhythmic therapy, an implanted cardioverter-defibrillator, or surgically ablated sources of pathological impulses.

Ventricular paroxysmal tachycardia (VT) - most often suddenly starting and just as suddenly ending attack of increased ventricular contractions up to 150-180 beats per minute (less often - more than 200 beats per minute or within 100-120 beats per minute), as a rule, while maintaining the correct regular heart rhythm.

Ventricular paroxysmal tachycardia is in first place among all arrhythmias, life threatening the patient (both ventricular and supraventricular), as it is not only dangerous for hemodynamics in itself, but also seriously threatens the transition to flutter and ventricular fibrillation. In this case, the coordinated contraction of the ventricles stops, which means circulatory arrest and transition to asystole ("arrhythmic death"), if timely resuscitation is not carried out.

Classification

Clinical classification of ventricular paroxysmal tachycardias

Paroxysmal nonsustained ventricular tachycardia

They are characterized by the appearance of three or more ectopic QRS complexes in a row, which are recorded during an ECG monitor recording within up to 30 seconds. Such paroxysms do not affect hemodynamics, but increase the risk of ventricular fibrillation (VF) and sudden cardiac death.

Paroxysmal sustained ventricular tachycardia

These ventricular tachycardias are at high risk of sudden cardiac death and are accompanied by significant hemodynamic changes. Hemodynamics - 1. A section of the physiology of blood circulation that studies the causes, conditions and mechanisms of blood movement in cardiovascular system based on the use of the physical laws of hydrodynamics. 2. The totality of the processes of blood movement in the cardiovascular system
(acute left ventricular failure, arrhythmogenic shock). Duration - more than 30 seconds.

special shapes ventricular tachycardia

The diagnosis of such tachycardias is of clinical importance, since they indicate an increased readiness of the ventricular myocardium to develop fibrillation:

1. Bidirectional ventricular tachycardia - the correct alternation of QRS complexes, caused by the propagation of impulses from two different parts of the ventricles or different conduction of impulses from one source.

2. "Pirouette" ("torsade de pointes") - unstable (up to 100 complexes) bidirectional ventricular tachycardia with a wave-like increase and decrease in the amplitude of QRS complexes, with an irregular rhythm, with a frequency of 200 - 300 per 1 minute and above. The development of "pirouette" is most often preceded by prolongation of the QT interval and early ventricular premature beats. Extrasystole - a form of heart rhythm disturbance, characterized by the appearance of extrasystoles (a contraction of the heart or its departments that occurs earlier than the next contraction should normally occur)
. For unstable bidirectional ventricular tachycardia with a wave-like increase and decrease in the amplitude of the complexes, relapses are characteristic.

3. Polymorphic (multiform) ventricular tachycardia, which occurs when there are two or more ectopic foci.

4. Recurrent ventricular tachycardia, resuming after periods of the main rhythm.

Etiology and pathogenesis

Etiology of ventricular paroxysmal tachycardias

1. Coronary ventricular paroxysmal tachycardia:
- acute myocardial infarction;

Postinfarction aneurysm;

reperfusion arrhythmias.

2. The main non-coronary ventricular paroxysmal tachycardias:

Acute myocarditis;

Postmyocarditis cardiosclerosis;

Hypertrophic cardiomyopathy;

dilated cardiomyopathy;

Restrictive cardiomyopathy;

Heart defects (congenital and rheumatic);

Arterial hypertension;

Amyloidosis;

Sarcoidosis;

Heart surgeries (correction of tetralogy of Fallot, ventricular septal defect, etc.);

Arrhythmogenic action medicines and ventricular arrhythmias against the background of electrolyte disturbances - with electrolyte disturbances (hypokalemia, hypomagnesemia, hypocalcemia), it is possible to develop paroxysmal ventricular tachycardia of the "pirouette" type, implemented through a prolongation of the QT interval;

thyrotoxicosis;

Digitalis intoxication;

Genetically determined diseases in which ventricular extrasystoles / ventricular paroxysmal tachycardias are the main clinical manifestation.

- Athlete's heart.

The idiopathic form of ventricular tachycardia is especially distinguished, which is detected, according to available data, in about 4% of people (about 10% of all detected ventricular tachycardias). The prognosis for this form of tachycardia is favorable, it is usually asymptomatic. The causes of occurrence have not yet been sufficiently studied.

Pathogenesis of ventricular paroxysmal tachycardias

In the event of paroxysms, all 3 arrhythmia mechanisms can be participants:

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

2. Ectopic focus of trigger activity.

3. Ectopic focus of increased automatism.

Fascicular ventricular tachycardia is a special form of left ventricular tachycardia, when the conduction system is involved in the formation of the re-entry loop (a branching of the left leg of the His bundle, passing into Purkinje fibers). Fascicular tachycardia has a characteristic ECG morphology, refers to idiopathic tachycardia. It is observed mainly in boys and young men, is symptomatic (palpitations, without fainting), is stable. Its treatment requires a special approach (radiofrequency ablation).

Etiology and pathogenesis of ventricular paroxysmal tachycardias of the "pirouette" type ("torsade de pointes")

A special form of paroxysmal ventricular tachycardia is polymorphic (bidirectional) spindle-shaped ventricular tachycardia ("pirouette", "torsade de pointes"). This form of tachycardia is characterized by an unstable, constantly changing form of the QRS complex, and it develops against the background of a prolonged QT interval.

It is believed that the basis of bidirectional fusiform ventricular tachycardia is a significant lengthening of the QT interval, accompanied by a slowdown and asynchronism of the repolarization process in the ventricular myocardium. This creates conditions for the re-entry of the excitation wave (re-entry) or the appearance of foci of trigger activity.

There are congenital (hereditary) and acquired forms of ventricular tachycardia such as "pirouette".

It is assumed that the morphological substrate of this ventricular tachycardia is inherited - the syndrome of a long Q-T interval, which in some cases (with an autosomal recessive type of inheritance) is combined with congenital deafness.

The acquired form of ventricular tachycardia of the “pirouette” type is much more common than hereditary. In most cases, it also develops against the background of a prolonged QT interval and severe asynchronism in ventricular repolarization. True, it must be borne in mind that in some cases bidirectional ventricular tachycardia may develop against the background of a normal duration of the QT interval.

Reasons for prolongation of the QT interval:

electrolyte disorders (hypokalemia, hypomagnesemia, hypocalcemia);

Myocardial ischemia (patients with coronary artery disease, acute myocardial infarction, unstable angina pectoris);

Severe bradycardia of any origin;

Mitral valve prolapse;

Syndrome of congenital long QT interval;

The use of antiarrhythmic drugs of classes I and III (quinidine, novocainamide, disopyramide, amiodarone, sotalol);

Intoxication with cardiac glycosides;

Sympathectomy;

Implantation of a pacemaker.

Epidemiology

Prevalence sign: Common

Sex ratio (m/f): 2

Ventricular tachycardia most often develops in patients with coronary artery disease (about 85%).

Among patients with ventricular tachycardia disease, there are 2 times more men than women.

Only in 2-4% of cases, ventricular tachycardia is recorded in patients who do not have reliable clinical and instrumental signs of organic heart damage, it is called the "idiopathic" form of ventricular tachycardia.

Clinical picture

Clinical Criteria for Diagnosis

Sudden palpitations, pain in the region of the heart, severe autonomic symptoms in the form of agitation, hand tremor, sweating

Symptoms, course

As a rule, an attack of paroxysmal tachycardia (PT) has a sudden onset and ends just as abruptly. The patient experiences a push in the region of the heart (initial extrasystole), after which a strong heartbeat begins. Very rarely, patients complain only of a feeling of discomfort in the region of the heart, a light heartbeat, or do not experience it at all. discomfort. Sometimes, before an attack, it is possible to fix extrasystole. Very rarely, some patients feel an aura before an attack approaches - slight dizziness, noise in the head, a feeling of constriction in the region of the heart.

Patients often experience severe pain during an attack of PT. The electrocardiogram during this period registers the presence of coronary insufficiency.
Pain can also be accompanied by disorders of the central nervous system: agitation, muscle cramps, dizziness, darkening of the eyes. Very rarely transient focal neurological symptoms- hemiparesis, aphasia.
During an attack of PT, there may be increased sweating, increased peristalsis, flatulence, nausea and vomiting.
Important diagnostic sign PT attack - urina spastica Urina spastica (med. lat. spastic urine) - profuse urination observed after emotional arousal, a vegetative crisis, an attack of paroxysmal tachycardia or angina pectoris
- frequent and profuse urination for several hours. At the same time, urine is light, with a low relative density (1.001-1.003). emergence given symptom associated with relaxation of the sphincter Bladder spasmodic during an attack. After the attack ends, breathing and cardiac activity return to normal, the patient experiences a feeling of relief.

When an attack of PT occurs, the skin and visible mucous membranes become pale; the jugular veins sometimes swell, pulsate synchronously with the arterial pulse; breathing quickens; there is a rhythmic, sharply accelerated pulse of weak filling, the counting of the pulse is difficult.
At the beginning of the attack, the dimensions of the heart are not changed or correspond to those in the underlying disease.

Auscultatory revealed pendulum rhythm with a heart rate of 150-160 to 200-220 in 1 minute. With the ventricular form of paroxysmal tachycardia, the frequency of the heterotopic rhythm can be up to 130 per 1 minute.

With an increase in cardiac activity, previously heard noises disappear, heart sounds become clear. Due to insufficient filling of the ventricles, the first tone acquires a clapping character, the second tone is weakened.
Systolic pressure decreases, diastolic pressure remains normal or slightly reduced. Blood pressure after the cessation of the attack gradually returns to its original level.

The decrease in blood pressure in PT is due to a decrease in minute volume due to a shortening of diastole and a decrease in stroke volume. In patients with a sharply altered cardiac muscle, a distinct decrease in blood pressure is noted even with a picture of collapse.

It is important to distinguish between atrial PT and ventricular PT.

Ventricular PT usually develops against the background of organic damage to the heart, and atrial is more often accompanied by functional changes. In the origin of ventricular PT importance have extracardiac factors and disorders of the autonomic nervous system.

Atrial PT characterized by the fact that at the beginning or at the end of an attack, as a rule, there is frequent and profuse urination (up to 3-4 liters). In addition, there is usually an aura in the form of slight dizziness, a feeling of constriction in the region of the heart, noise in the head. With ventricular PT, such phenomena are rarely observed.
In atrial PT, massage in the carotid sinus usually relieves the attack, while in the ventricular form, it most often does not affect the heart rhythm.

Diagnostics

ECG signs of ventricular paroxysmal tachycardia:

1. A sudden onset and just as suddenly ending attack of increased heart rate up to 140-180 beats per minute (less often - up to 250 or within 100-120 beats per minute), while maintaining the correct rhythm in most cases.

2. Deformation and expansion of the QRS complex for more than 0.12 seconds, reminiscent of the graphics of the bundle branch block, mainly with a discordant arrangement of the RS-T segment and the T wave.

3. The presence of AV dissociation - complete dissociation of the frequent ventricular rhythm (QRS complexes) and normal atrial sinus rhythm (P waves) with occasionally recorded single unchanged QRST complexes of sinus origin (“captured” ventricular contractions).

ECG signs of ventricular tachycardia of the "pirouette" type:

1. The ventricular rate is 150-250 per minute, the rhythm is irregular.

2. QRS complexes of large amplitude, duration - more than 0.12 seconds.

3. The amplitude and polarity of the ventricular complexes changes within a short time (resembles a continuous chain of spindles).

4. In cases where P waves are recorded on the ECG, there is a disconnection of the atrial and ventricular rhythm (AV dissociation).

5. Paroxysm of ventricular tachycardia most often lasts a few seconds (up to 100 complexes), stopping spontaneously (unsustained ventricular tachycardia). However, there is a pronounced tendency to multiple recurrence of seizures.

6. Attacks of ventricular tachycardia are provoked by ventricular extrasystoles (usually "early" ventricular extrasystoles).

7. Outside of an attack of ventricular tachycardia, the ECG shows a prolongation of the QT interval.

Since attacks of ventricular tachycardia of the "pirouette" type are short, the diagnosis is often established on the basis of the results of Holter monitoring and assessment of the duration of the QT interval in the interictal period.

The source of ventricular tachycardia is determined by the shape of the QRS complexes in various leads, similar to the source of ventricular extrasystole.

Coincidence of the QRS shape with the shape of the previous ventricular extrasystoles allows you to more confidently regard the paroxysm as ventricular tachycardia.

Most ventricular tachycardias during myocardial infarction and postinfarction aneurysm are left ventricular.

The division of ventricular extrasystoles / ventricular tachycardias into left and right ventricular has a certain clinical significance. This is due to the fact that most left ventricular arrhythmias are coronarogenic, while a number of specific hereditary diseases should be excluded when right ventricular ectopia is detected.

Fascicular ventricular tachycardia - tachycardia with a narrow QRS complex and a sharp deviation of the electrical axis of the heart to the right, has a characteristic morphology on the ECG.

Accurate topical diagnosis of ventricular tachycardias in therapeutic practice of great importance does not, it is used by cardiac surgeons mainly as an aid in conducting an intracardiac electrophysiological study, and is carried out with the help of ECG mapping.

Holter ECG monitoring

This type of study to detect ventricular tachycardia is indicated in all (including asymptomatic) patients with diseases that are the etiological causes of tachycardia, as well as in all patients with suspected these diseases. ECG monitoring can serve as Holter monitoring in the acute period of myocardial infarction. In patients with idiopathic ventricular tachycardia, Holter ECG monitoring reveals the relationship between ventricular arrhythmias and nocturnal bradycardia. Holter ECG monitoring is indispensable for monitoring the effectiveness of therapy.

Tests with physical activity

Physical activity can provoke automatic ventricular tachycardia (which, as a rule, is not preceded by ventricular extrasystole), ventricular tachycardia with arrhythmogenic right ventricular dysplasia, WPW syndrome, long QT interval syndrome, idiopathic ventricular tachycardia from the outflow tract of the right ventricle.

Only if the above variants of ventricular tachycardia are suspected (excluding WPW syndrome), exercise tests can be used to provoke a paroxysm. In these cases, exercise tests (treadmill or bicycle ergometry) can be performed to monitor the effectiveness of therapy.

When conducting tests with physical activity in patients with ventricular tachycardia, it is necessary to create conditions for emergency defibrillation and resuscitation. Exercise tests can be used in patients with ventricular tachycardia only if other diagnostic methods are ineffective.

Intracardiac electrophysiological study and transesophageal electrophysiological study

Indications for carrying out:

The need for differential diagnosis in wide-complex tachycardia;

Assessment of the mechanism of ventricular tachycardia;

Topical diagnosis of tachycardia and selection of therapy.

A contraindication to these invasive studies is hemodynamically unstable, continuously recurrent, polymorphic ventricular tachycardia, when ECG mapping is dangerous and technically impossible.

Intracardiac electrophysiological study is the main method for accurate diagnosis of various pathogenetic types of ventricular tachycardias. A separate indication for its implementation is the resistance of ventricular tachycardia to drug therapy.

Programmed stimulation is carried out in various parts of the myocardium in order to provoke a "clinical" variant of ventricular tachycardia.

Drugs during an intracardiac electrophysiological study are administered intravenously. Attempts to re-induce ventricular tachycardia after the administration of a particular drug and relief of ventricular tachycardia are carried out in one study.

echocardiography

Evaluation of the functioning of the left ventricle by echocardiography is no less important part of the examination of patients with ventricular tachycardia than the identification of the mechanism of development of arrhythmias or its topical diagnosis. Echocardiography makes it possible to assess the functional parameters of the ventricles (ejection fraction), which is of great prognostic value.

Differential Diagnosis

Differential Diagnosisventricular paroxysmal tachycardia and supraventricular atrial tachycardia with wide QRS complexes (aberrant conduction) is of paramount importance. This is because the treatment of these two arrhythmias is based on different principles, and the prognosis of ventricular paroxysmal tachycardia is much more serious than that of supraventricular atrial tachycardia.

Ventricular paroxysmal tachycardias and supraventricular atrial tachycardias with aberrant QRS complexes are distinguished on the basis of the following features:

1. Signs of ventricular tachycardia in chest leads, including lead V1:

QRS complexes are monophasic (R or S type) or biphasic (qR, QR or rS type) appearance;

Three-phase complexes like RSr are not typical for ventricular paroxysmal tachycardias;

When registering a transesophageal ECG or with an intracardiac electrophysiological study, it is possible to detect AV dissociation, which proves the presence of ventricular tachycardia;

The duration of the QRS complexes exceeds 0.12 seconds.

2. Signs of supraventricular atrial tachycardias with aberrant QRS complexes:

In lead V1, the ventricular complex looks like rSR (triphasic);

The T wave may not be discordant to the main wave of the QRS complex;

When registering a transesophageal ECG or during an intracardiac electrophysiological study, P waves are recorded corresponding to each QRS complex (absence of AV dissociation), which proves the presence of supraventricular paroxysmal tachycardia;

The duration of the QRS complex does not exceed 0.11-0.12 seconds.

As you can see, the most reliable sign of one form or another of atrial tachycardia is the presence (with ventricular paroxysmal tachycardia) or the absence (with supraventricular atrial tachycardia) of AV dissociation with periodic "captures" of the ventricles. In most cases, this requires a transesophageal or intracardiac electrophysiological study in order to register P waves on the ECG.

Even with the usual clinical (physical) examination of a patient with paroxysmal tachycardia, for example, when examining the veins of the neck and auscultation of the heart, signs characteristic of each type of paroxysmal tachycardia can often be observed. However, these signs are not sufficiently accurate and specific, and the task of the medical staff is to provide ECG diagnostics (preferably monitor), access to a vein and the availability of therapeutic agents.

For example, in supraventricular tachycardia with 1:1 AV conduction, arterial and venous pulse rates coincide. At the same time, the pulsation of the cervical veins is of the same type and has the character of a negative venous pulse, and the volume of the first tone remains the same in different cardiac cycles.

Only in the atrial form of supraventricular paroxysmal tachycardia is an episodic loss of the arterial pulse associated with transient second-degree AV blockade observed.

With ventricular tachycardia, AV dissociation is observed: a rare venous pulse and a much more frequent arterial one. At the same time, enhanced “giant” waves of a positive venous pulse are periodically recorded, caused by a random coincidence of atrial and ventricular contractions with closed AV valves. At the same time, the I heart sound also changes its intensity: from weakened to very loud (“cannon”) when the systole of the atria and ventricles coincides.

Differential diagnosis of ventricular tachycardias with various pathogenic mechanisms

Reciprocal ventricular tachycardias caused by the re-entry mechanism have the following features:

1. The possibility of eliminating ventricular tachycardia by electrical cardioversion, as well as by premature extrastimuli.

2. The possibility of reproducing a typical tachycardia attack for a given patient during programmed electrical stimulation of the ventricle with single or paired extrastimuli with a varying length of the coupling interval.

3. Intravenous administration of verapamil or propranolol does not stop the already developed reciprocal ventricular tachycardia and does not prevent its reproduction, while the introduction of novocainamide is accompanied by a positive effect (MS Kushakovsky).

For ventricular tachycardia due to abnormal automatism of the ectopic focus, the following is characteristic:

1. Ventricular tachycardia is not induced by programmed electrical pacing.

2. Ventricular tachycardia can be induced intravenous administration catecholamines or exercise, as well as norepinephrine.

3. Ventricular tachycardia is not corrected by electrical cardioversion, programmed or frequent pacing.

4. Ventricular tachycardia is often eliminated with verapamil.

5. Ventricular tachycardia is eliminated by intravenous administration of propranolol or novocainamide.

For ventricular tachycardia due to trigger activity, it is characteristic:

1. The occurrence of ventricular tachycardia against the background of increased sinus rhythm or under the influence of imposed frequent electrical stimulation of the atria or ventricles, as well as under the influence of single or paired extrastimuli.

2. Provoking ventricular tachycardia by the introduction of catecholamines.

3. Prevention of induction of trigger ventricular tachycardia with verapamil.

4. Slowing the rhythm of trigger ventricular tachycardia with propranolol, procainamide.

Complications

It was found that in paroxysmal tachycardia (PT), when 180 or more contractions per 1 minute are recorded, coronary blood flow is significantly reduced. It can cause myocardial infarction in patients with coronary heart disease.

Sometimes an attack of PT ends with thromboembolic complications. During Wenckebach's atrial blockage, intracardiac hemodynamics are disturbed, as a result of stagnation of blood in the atria, blood clots form in their ears. When sinus rhythm is restored, loose thrombi in the atrial appendages can break off and cause an embolism.

Against the background of prolonged attacks of PT (more than a day), an increase in temperature can be observed, sometimes up to 38-39 ° C, leukocytosis and eosinophilia appear in the blood. ESR normal. Such manifestations may be associated with a pronounced autonomic reaction of the body, but one should not forget about the possible development of myocardial infarction. In such cases, as a rule, an attack of angina pectoris occurs, after the disappearance of leukocytosis, the ESR increases, the content of enzymes in the blood increases, and the ECG dynamics characteristic of myocardial infarction is observed.

Ventricular PT is a serious arrhythmia, especially in myocardial infarction, as it can be complicated by ventricular fibrillation. An increase in the ventricular rate to 180-250 per minute is especially dangerous - such an arrhythmia is an emergency.

It is important to remember that after an attack of PT, the development of post-tachycardia syndrome is possible (more often observed in patients with coronary atherosclerosis, sometimes in young patients without signs of organic heart damage). Negative T waves appear on the ECG, occasionally with some shift in the ST intervals, and the QT interval lengthens. Such ECG changes can be observed within hours, days, and sometimes weeks after the cessation of the attack. In this situation, dynamic monitoring and additional laboratory research(determination of enzymes), in order to exclude myocardial infarction, which can also be the cause of PT.

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Treatment

Sustained monomorphic (classic) ventricular tachycardiarefers to severe and life-threatening arrhythmias. With this form of ventricular tachycardia, immediate relief and effective prevention paroxysms.

Unsustained ventricular tachycardia(4B gradation according to B. Lown) usually does not require immediate intervention, but the prognosis for patients with organic lesion hearts in this case are worse.

General principles for the relief of paroxysmal ventricular tachycardia

Even when there is no certainty in the ventricular origin of wide complex tachycardia, its relief is carried out according to the principles of relief of paroxysmal ventricular tachycardia:

1. In severe hemodynamic disorders, emergency electrical cardioversion is performed.

2. With synchronized cardioversion, a charge of 100 J is most often effective.

3. If pulse and blood pressure are not detected during ventricular tachycardia, use a discharge of 200 J, and in the absence of effect - 360 J.

4. If it is impossible to immediately use a defibrillator before cardioversion, a precordial beat should be performed, indirect massage heart and mechanical ventilation.

5. If the patient has lost consciousness (preservation or immediate recurrence of ventricular tachycardia / ventricular fibrillation), defibrillation is repeated against the background of an IV jet (in the absence of a pulse - in subclavian vein or intracardiac) administration of adrenaline - 1.0 ml of 10% solution per 10.0 ml of saline.

6. In the absence of a pulse, adrenaline is injected into the subclavian vein or intracardiac.

7. Together with adrenaline, antiarrhythmic drugs are administered (necessarily under ECG control!):

Lidocaine IV 1-1.5 mg/kg or

Bretylium tosylate (Ornid) IV 5-10 mg/kg or

Amiodarone IV 300-450 mg

You should immediately stop the drug, which could cause ventricular tachycardia. Stop taking the following medicines: quinidine (quinidine durules), disopyramide, ethacizine (etacizine), sotalol (sotahexal, sotalex), amiodarone, nibentan, dofetilide, ibutilide, as well as tricyclic antidepressants, lithium salts and other drugs that can provoke changes in QT.

Drug relief of paroxysm of ventricular tachycardia is carried out in the following order - in stages:

STAGE 1:

Lidocaine in / in 1-1.5 mg / kg once in a stream for 1.5-2 minutes (usually 4-6 ml of a 2% solution per 10 ml of saline);

If the introduction of lidocaine is ineffective, and stable hemodynamics is maintained, continue administration at 0.5-0.75 mg / kg every 5-10 minutes (up to a total dose of 3 mg / kg for an hour);

After stopping the paroxysm of ventricular tachycardia, 4.0-6.0 ml of 10% lidocaine solution (400-600 mg) is prophylactically administered intramuscularly every 3-4 hours;

Lidocaine is effective in 30% of cases;

Lidocaine is contraindicated in severe transverse conduction disorders;

With ventricular tachycardia of the "pirouette" type, which has developed against the background of an elongated QT, relief can be started with an intravenous administration of magnesium sulfate 10.0-20.0 ml of 20% solution (20.0 ml of 5% glucose solution for 1-2 minutes under control of blood pressure and respiratory rate) followed by intravenous drip (in case of relapses) 100 ml of 20% magnesium sulfate solution per 400 ml of saline at a rate of 10-40 drops / min .;

Electropulse therapy is carried out in the absence of effect.

In the future (at the second stage), the treatment tactics is determined by the preservation of the function of the left ventricle, that is, the presence of heart failure.

STAGE 2:

In patients with preserved left ventricular function (more than 40%):

Novocainamide IV 1000 mg (10 ml 10% solution) bolus slowly under the control of blood pressure, or IV infusion at a rate of 30-50 mg/min. up to a total dose of 17 mg/kg; novocainamide is effective up to 70% of cases;

The use of novocainamide is limited, since most patients with ventricular tachycardia have circulatory failure, in which novocainamide is contraindicated!

Or sotalol 1.0-1.5 mg / kg (Sotahexal, Sotalex) - IV infusion at a rate of 10 mg / min.; restrictions on the use of sotalol are the same as those of novocainamide.

In patients with reduced left ventricular function (less than 40%):

Amiodarone IV 300 mg (6 ml 5% solution), over 5-10 minutes in 5% glucose solution;

In the absence of the effect of the introduction of amiodarone, one should proceed to electrical cardioversion;

If there is an effect, it is necessary to continue therapy according to the following scheme:

The total daily dose of amiodarone on the first day should be about 1000 (up to a maximum of 1200) mg;

To continue the slow infusion, 18 ml of amiodarone (900 mg) is diluted in 500 ml of 5% glucose solution and administered first at a rate of 1 mg / min. within 6 hours, then - 0.5 mg / min. - the next 18 hours;

In the future, after the first day of infusion, you can continue the maintenance infusion at a rate of 0.5 mg / min .;

With the development of a repeated episode of ventricular tachycardia or with ventricular fibrillation, you can additionally introduce 150 mg of amiodarone in 100 ml of 5% glucose solution for 10 minutes;

After stabilization of the condition, amiodarone is administered orally for maintenance therapy.

If the therapy carried out at the second stage turned out to be ineffective, electrical impulse therapy is carried out or they proceed to the third stage of treatment.

STAGE 3:

In patients with frequent relapses ventricular tachycardia, especially in myocardial infarction, in order to increase the effectiveness of repeated attempts at electrical impulse therapy:
- Bretylium tosylate (ornid) 5 mg/kg is administered intravenously, over 5 minutes, for 20-50 ml of saline;

If there is no effect after 10 minutes, you can repeat the introduction in a double dose;

Supportive therapy - 1-3 mg/min bretylium tosylate IV drip.

After relief of paroxysms of ventricular tachycardia, intravenous administration of antiarrhythmics and / or potassium preparations is indicated for at least the next 24 hours.

Relief of paroxysms of special forms of idiopathic ventricular tachycardia:

1. Special forms of idiopathic ventricular tachycardia, which usually have a blockade morphology right leg bundle of His and well tolerated by the patient, may be sensitive to the introduction of Isoptin 5-10 mg intravenously by bolus.

With the normal functioning of the left ventricle, the risk of high-grade ventricular arrhythmias, including ventricular fibrillation, as well as sudden cardiac death, is very low in the near future.

There is a very high risk of recurrence of ventricular arrhythmias or sudden cardiac death with a low ejection fraction.

Intracardiac electrophysiological testing (EPS) and attempts to provoke tachycardia with electrical stimulation can provide important information about the prognostic value of ventricular tachycardias. Patients in whom it is possible to induce ventricular tachycardia in this way, accompanied by clinical symptoms or sustained ventricular tachycardia (lasting more than 30 seconds) have the highest risk of sudden cardiac death. However, it must be remembered that ventricular tachycardias of different mechanism have varying degrees reproducibility during EFI.

The risk of complex cardiac arrhythmias (sustained ventricular tachycardia and ventricular fibrillation) and sudden cardiac death is 3-5 times higher in patients who have slow fragmented electrical activity of the ventricular myocardium, which is recorded using a signal-averaged ECG in the terminal part of the QRS complex with a duration of more than 40 ms.

The prognosis for bidirectional (fusiform) ventricular tachycardia of the "pirouette" type is always serious. In this type, as a rule, there is a transformation of polymorphic ventricular tachycardia into ventricular fibrillation or stable monomorphic ventricular tachycardia. The risk of sudden cardiac death is also quite high.

Hospitalization

After renderingfirst medical care in the event of paroxysmal ventricular tachycardia, hospitalization is always necessary in order to select long-term antiarrhythmic therapy.

Prevention

Supportive antiarrhythmic therapy is used to prevent sudden death in patients with malignant ventricular arrhythmias. Prevention of sudden death should be carried out not only with antiarrhythmic drugs, but also with other drugs with a proven effect. For patients after myocardial infarction, these drugs include aspirin, ACE inhibitors, statins and aldosterone receptor blockers, and beta-blockers.

The reason for the use of more effective methods for life-threatening arrhythmias may be the lack of effectiveness of drug therapy:

Implantable cardioverter defibrillator

When conducting multicenter studies comparing drug therapy and implantation of cardioverter-defibrillators, the effectiveness of implantation was higher.

There are absolute indications for implantation of cardioverter-defibrillators in ventricular tachycardias:

1. clinical death caused by ventricular tachycardia/ventricular fibrillation not associated with a transient cause.

2. Spontaneous paroxysms of sustained ventricular tachycardia.

3. Unsustainable ventricular tachycardia, which is reproduced during EPS, is not stopped by novocainamide and is combined with postinfarction cardiosclerosis and left ventricular dysfunction.

4. Unexplained syncope in combination with EPS induction of significant ventricular tachycardia or ventricular fibrillation and ineffectiveness/inability to prescribe antiarrhythmics.

5. Primary prevention for patients who have had a myocardial infarction and have a left ventricular ejection function of less than 30%.

6. Primary prevention for post-MI patients with less than 40% left ventricular ejection function with asymptomatic nonsustained ventricular tachycardia.

7. Primary prophylaxis for patients with idiopathic congestive cardiomyopathy, left ventricular ejection function less than 30%, and syncope/presyncope or supraventricular tachycardia.

8. Secondary prevention for patients with dilated cardiomyopathy (DCM), with left ventricular ejection function less than 30% and a history of persistent ventricular tachycardia/ventricular fibrillation.

9. Secondary prevention for patients with documented ventricular arrhythmias. Such patients are candidates for a heart transplant.

Patients with continuously recurrent ventricular tachycardia, with WPW syndrome, terminal congestive insufficiency, etc., are contraindicated in the installation of cardioverter-defibrillators.

The need to prescribe antiarrhythmics after implantation of cardioverter-defibrillators remains in 70% of cases, mainly to reduce the frequency of ventricular tachycardia and reduce heart rate during paroxysms of ventricular tachycardia. Of the drugs, only amiodarone (possibly in combination with beta-blockers) and sotalol do not affect the defibrillation threshold, which is necessary for the effective operation of an implantable cardioverter-defibrillator.

RF ablation

Indications:

1. Hemodynamically significant prolonged monomorphic ventricular tachycardia, resistant to antiarrhythmics (or there are contraindications to taking them).

2. Ventricular tachycardia with a relatively narrow QRS due to re-entry in the bundle branch system (fascicular ventricular tachycardia). The effectiveness of radiofrequency ablation in this case is about 100%.

3. Frequent discharges of the implantable cardioverter-defibrillator in patients with prolonged monomorphic ventricular tachycardia, which are not eliminated after reprogramming the implantable cardioverter-defibrillator and connecting antiarrhythmics.

Aneurysmectomy

Aneurysmectomy is the preferred intervention in patients with ventricular arrhythmias / ventricular paroxysmal tachycardias with postinfarction aneurysm.

Indications:

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