Paroxysmal ventricular tachycardia

Paroxysmal ventricular tachycardia

Ventricular paroxysmal tachycardia (VPT) – sudden onset and sudden cessation of tachycardia attacks caused by pathological foci of automatism in the ventricular myocardium. Heart rate —> 100 per minute. The localization of the arrhythmogenic zone is determined according to the rules for the topical diagnosis of ventricular extrasystoles (see Ventricular extrasystole). The predominant gender is male (69%). Etiology

    • Acquired VT
    • ischemic heart disease
    • THEM
    • Postinfarction cardiosclerosis
    • Aneurysm of the left ventricle
    • Alcoholic cardiomyopathy
    • Myocarditis
    • Heart defects
    • Cardiomyopathy
    • Poisoning with cardiac glycosides
    • hypokalemia
    • Hypercalcemia
    • The presence of a catheter in the cavity of the ventricles
    • Stress
    • Congenital VT
    • Heart defects
    • Mitral valve prolapse
    • Arrhythmogenic ventricular dysplasia
    • Syndrome of premature excitation of the ventricles
    • Long QT syndrome (Romano-Ward syndrome)
    • In 2% of cases, VT is observed in people who do not have visible organic changes in the myocardium (idiopathic VT or primary electrical heart disease).

Pathogenesis. Sources of gastrointestinal tract: Purkinje fibers, AUC bundle pedicles, ventricular contractile myocardium. The electrophysiological mechanisms of ZHPT are similar to those of ventricular extrasystoles – early post-depolarization and trigger activity, the phenomenon of re-entry (see Ventricular extrasystole).

Clinical picture

    • Caused by low cardiac output (pale skin, low blood pressure)
    • The heart rate, traditionally regular, is 100-200 per minute. Most often – 150-180 per minute.

ECG identification

    • Heart rate – 100-200 per minute.
    • Deformation and widening of the QRS complex more than 0.14 s in 75% of cases, from 0.12 to 0.14 s in 25% of cases of VT.
    • R wave missing.
    • Signs that allow you to reliably diagnose VT
    • The appearance of normal-width QRS complexes among deformed ventricular complexes (complete ventricular captures) and / or confluent complexes (partial or combined ventricular captures), indicating the passage of a sinus impulse to the ventricles during the extra-refractory period. Difficulties in identifying: in the majority of cases, it can be registered only with long-term, multi-minute registration of chest leads V,, V2, V3
    • Identification of an independent (slower) atrial rhythm – atrioventricular dissociation (P waves do not have a fixed connection with ventricular complexes). Difficulties in identifying: in the bulk

cases, the P waves are completely hidden in the altered ventricular complexes.

    • According to the results of the ECG, several types of GI are distinguished.
    • Sustained VT with a frequency of 140-250 per minute and the same type of ventricular complexes
    • Repeated episodes of VT in the form of groups of 3-5-10 QRS complexes, having the form of ventricular extrasystoles, interspersed with periods of sinus rhythm
    • Slow VT with a frequency of 100-140 per minute for a duration of 20-30 seconds (within 30 QRS complexes).


Lead tactics. GI is an emergency. The main method of treatment is electropulse therapy (see Cardioversion). Drug therapy is in the presence of a pulse (BP is not reduced to critical values) and the improbability of using electropulse therapy.

    • Lidocaine IV bolus 80–120 mg (1.5 mg/kg) over 3–5 minutes. Then, without delay, its constant drip administration of 2-4 mg / min is started. After 10-15 minutes, against this background, an IV bolus is repeated at a half dose (40-80 mg). In total, no more than 300 mg is administered within 1 hour. In the following hours (sometimes up to 1-2 days), a maintenance infusion of lidocaine is continued at a rate of 1 mg / min.
    • In the absence of a drip system, it is possible, after an intravenous administration of the first bolus (approximately 80 mg) or an intramuscular injection of 400 mg of lidocaine, to continue intramuscular injections of 400-600 mg after 3 hours for the entire necessary treatment period.
    • Amiodarone at a dose of 300 mg IV over 10 minutes (in a critical situation as soon as possible), then at a dose of 360 mg IV drip over the next 6 hours.
    • Phenytoin in / in a dose of 10-15 mg / kg for 1 hour, then 400-600 mg / day in tablets or capsules.
    • Etatsizin IV 50-100 mg in 20 ml of 0.9% NaCl solution at a rate of 10 mg / min for 5-10 minutes.
    • Novocaine mid 1,000 mg (10 mg/kg) IV no faster than 100 mg/min or IM.
    • Magnesium sulfate 2–2.5 g IV slowly is indicated for bidirectional ventricular tachycardia that occurs against the background of a prolongation of the QT interval (for example, in the treatment of quinidine). Then treatment with lidocaine or phenytoin is due.
    • B-blockers, bretylium tosylate, disopyramide are also used.


    • Indications for surgical treatment
    • An episode of ventricular fibrillation in a patient with a postinfarction aneurysm
    • Relapses of gastrointestinal tract in patients with postinfarction cardiosclerosis
    • Congestive circulatory insufficiency in patients with postinfarction biliary tract
    • Persistent extrasystolic allorhythmia
    • Ineffectiveness of antiarrhythmic drugs
    • Patients with postinfarction aneurysm of the left ventricle and paroxysms of gastrointestinal tract resistant to drug therapy are indicated for aneurysmectomy with excision of the ectopic focus.

Course and forecast

    • Sustained VT that occurs during the first 2 months after the development of MI: mortality 85%. Maximum life expectancy – 9 months
    • VT not associated with macrofocal

myocardial changes: death within 4 years in 75% of cases. Drug therapy increases life expectancy to an average of 8 years. See also Cardioversion Reduction. VT – ventricular paroxysmal tachycardia of the ICD. 147 Paroxysmal tachycardia

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