Diagnosis is carried out using a surface ECG. Treatment of prolonged episodes is with cardioversion or antiarrhythmics, depending on symptoms. If necessary, long-term treatment is carried out using an implantable cardioverter defibrillator.

Some experts use a rate >100 beats/min to verify VT.

Most patients with VT have significant illness hearts. Electrolyte disturbances (especially hypokalemia and hypomagnesemia), acidemia, hypoxemia, and side effects of medications can contribute to the occurrence of VT.

Typically, patients with a history of VT have ischemic disease heart disease or non-ischemic cardiomyopathy, but VT can also occur with acute ischemia myocardium or even in a “normal heart” as a result of abnormal automaticity or triggered activity.

The frequency of ventricular contractions can be in the range of 100-300 beats/min. Tachycardia may be sustained (> 30 sec) or unstable. In most cases, VT is monomorphic, i.e., the conduction path is not changed and the QRS morphology is the same. There is a group of idiopathic monomorphic VTs that have a better prognosis. Polymorphic VT associated with changes in QRS morphology from beat to beat and with prolongation of the corrected QT interval on an ECG with sinus rhythm is called torsade de pointes. Polymorphic VT usually causes collapse and is often unstable, although it can be stable and develop into VF.

Ventricular tachycardia (VT) is common in patients with coronary artery disease and cardiomyopathies. In this case, the development of VT is considered a serious situation, since VT can lead to hemodynamic disturbances or progress to ventricular fibrillation (see earlier), which is caused by abnormal activity, or triggered activity of ischemic tissue, or the presence of re-entry around the affected ventricular tissue.

Causes of ventricular tachycardia

VT can be monomorphic and polymorphic, as well as unstable and stable. Monomorphic VT occurs from a single pathological focus or has a reentry mechanism and regular QRS complexes identical in morphology. Polymorphic VT originates from several different foci or accessory pathways with a reentry mechanism and is therefore irregular, with different QRS complexes. Unsustained VT has a duration<30 сек; устойчивая ЖТ длится >30 seconds, or it is stopped earlier due to hemodynamic collapse.

Typical causes of VT are acute myocardial infarction, cardiomyopathy, chronic ischemic heart disease, especially when combined with ventricular aneurysm or LV dysfunction.

Patients recovering from a heart attack may have periods of idioventricular rhythm (“slow” VT) at a rate slightly higher than the preceding sinus rhythm and below 120 bpm. These episodes often reflect reperfusion of the infarcted area and may good sign. They are usually self-limiting and asymptomatic, requiring no treatment.

Other forms of VT, if they last more than a few beats, require treatment and often urgently.

VT sometimes occurs in people with a healthy (other than VT) heart (“normal heart VT”) due to abnormal automaticity in the RV outflow tract. The prognosis is good, the treatment method is catheter ablation.

Symptoms and signs of ventricular tachycardia

VT of short duration or slow VT may be asymptomatic. Sustained VT is almost always symptomatic, causing palpitations, symptoms of hemodynamic compromise, or sudden cardiac death.

Patients may have low cardiac output(dizziness, shortness of breath, syncope). The ECG shows tachycardia with wide deformed QRS complexes with a frequency of 120 per minute. VT can sometimes be difficult to distinguish from SV - from tachycardia to complain of symptoms with bundle branch block or pre-excitation (WPW syndrome). A 12-lead ECG, intracardiac ECG, or transesophageal ECG will help make the diagnosis. If the diagnosis is unclear, it is safer to treat the condition as VT.

Signs indicating VT in the differential diagnosis of wide-complex tachycardia

• History of myocardial infarction.
• AV dissociation (pathognomonic).
• Trapped/confluent ventricular complexes (pathognomonic sign).
• Strong deviation of the EOS to the left.
• Very wide QRS (>140 ms).

Diagnosis of ventricular tachycardia

Diagnosed by ECG. Any tachycardia with wide QRS complexes (QRS >0.12 sec) should be considered VT until another tachycardia is proven. The diagnosis is confirmed by the presence of dissociation of P waves, confluent complexes or supraventricular “captures” on the ECG, uniformity of QRS vectors in the precordial leads with a discordant T-wave vector (opposite QRS vectors), and the location of the QRS axis in the frontal plane in the northwestern quadrant. The use of drugs suitable for the treatment of supraventricular tachycardia in patients with VT may cause hemodynamic collapse and death.

Wide complex tachycardia should be considered VT. If the diagnosis is uncertain, remember that it is safer for the patient to treat SVT as VT rather than the other way around.

80% of wide complex tachycardias are VT, this figure increases to 95% if there is a history of MI or CAD.

Always make a diagnosis using a 12-lead ECG, not a three-lead ECG.

IN clinical practice the speed of development and degree of hemodynamic disturbances are a poor criterion for differential diagnosis.

The following clinical signs support the diagnosis of VT;

• old age;
• history of coronary artery disease or structural heart pathology;
• decreased LV function.

The following ECG signs suggest SVT with RBBB:

• Typical RBBB/LBBB:
• especially if the QRS morphology and axis are identical to those of sinus rhythm;
• otherwise, wide complex VT tachycardia should be suspected.

In some cases, adenosine is useful in making a diagnosis.

Treatment of ventricular tachycardia

• Acute: sometimes synchronized electrical cardioversion, sometimes class I and III antiarrhythmic drugs,
• Long-term: usually an implantable cardioverter defibrillator.

Typically, sinus rhythm should be restored immediately, followed by prophylactic therapy. Cardioversion is the method of choice for systolic blood pressure<90 мм рт.ст. Если аритмия переносится хорошо, можно начать с болюсной внутривенной инфузии амиодарона, после чего продолжить его капельное введение. Внутривенное введение лидокаина используют, но оно может снизить функцию ЛЖ, вызвать гипотензию или острую СН. Гипокалиемия и гипомагниемия, ацидоз и гипоксемия ухудшают ситуацию и требуют коррекции.

β-blockers effectively prevent VT. Amiodarone can be added if additional monitoring is needed. Class I antiarrhythmics should be used in an acute situation, but their long-term use is dangerous in patients with coronary artery disease. In patients at high risk of arrhythmogenic death (eg, patients with severe LV dysfunction, or in patients in whom VT causes hemodynamic compromise), an implantable defibrillator should be used. IN in rare cases Surgery or catheter ablation may interrupt the focus or vicious cycle of the arrhythmia.

Acute treatment

Treatment depends on symptoms and duration of VT. Hypotension during VT requires synchronized electrical cardioversion with energy >100 J. Stable sustained VT can be treated with class I and III antiarrhythmic drugs. Lidocaine acts quickly but is often ineffective. If lidocaine is ineffective, the class IV drug procainamide can be used, but the wait for its effect may take up to 1 hour. The ineffectiveness of the class IV drug procainamide is an indication for cardioversion.

Non-sustained VT does not require immediate treatment until runs become frequent or long enough to cause symptoms. In such cases, antiarrhythmics are used in the treatment of sustained VT.

Long-term treatment

The primary goal is to prevent sudden death rather than simply suppress the arrhythmia. The decision of who to treat with an implantable cardioverter-defibrillator-like procedure is complex and depends on the expected likelihood of life-threatening ventricular tachycardia and the severity of the underlying cardiac disease.

Long-term treatment is not required when the VT episode is due to a transient cause or a reversible cause (acid-base disturbances, electrolyte disturbances, proarrhythmic drug effects).

In the absence of a transient or reversible cause, patients who experience an episode of sustained VT usually require implantation of an implantable cardioverter defibrillator. Most patients with sustained VT and significant structural heart disease also receive beta blockers. If it is not possible to use an ICD, amiodarone may be the preferred antiarrhythmic drug for the prevention of sudden death.

If VT prevention is important, it is required antiarrhythmic therapy or ablation of an arrhythmogenic substrate. Any - la, lb, lc, II or III class of antiarrhythmic drugs can be used. Due to their safety, β-blockers are the drugs of choice in the absence of contraindications. If it is necessary to use additional drugs, sotalol is usually used, then amiodarone.

Transcatheter radiofrequency ablation is used most often in patients with well-known syndromes and otherwise healthy hearts.

Long QT syndrome and ventricular tachycardia

Ventricular tachycardia is specific form polymorphic VT in patients with long QT syndrome. It is characterized by fast, irregular QRS complexes that appear to “roll” around the ECG baseline. It causes significant hemodynamic failure and often death. Diagnosed by surface ECG. Treatment is IV MD under control of the duration of the QT interval and electrical defibrillation when it transforms into ventricular fibrillation.

Long QT syndrome, which can cause ventricular tachycardia, can be congenital or drug-induced.

Congenital long QT syndrome

At least 10 described separate forms congenital long QT syndrome. Most cases fall into the first 3 subgroups:

• Long QT syndrome type 1, caused by loss of function due to mutation of the KCNQ1 gene, which encodes the catecholamine-sensitive cardiac potassium channel l Ks.
• Long QT syndrome type 2, caused by loss of function due to a mutation in the HERG gene, which encodes another cardiac potassium channel I Kr).
• Long QT syndrome type 3 is caused by a mutation in the SCN5A gene, which impairs the rapid inactivation of the cardiac sodium channel (lNa).

These forms are inherited as autosomal dominant disorders with incomplete penetration and were formerly referred to as Romano-Ward syndrome. In rare cases, in patients with 2 pathological copies of a genetic abnormality (especially LQT1), the disorder is associated with deafness and was in the past called Jervell-Lange-Nielsen syndrome. Patients with long QT syndrome are prone to recurrent syncope and sudden death secondary to ventricular tachycardia, transforming into ventricular fibrillation.

Symptoms

Patients often experience syncope due to cessation of cerebral perfusion at a ventricular rate of 200-250 beats/min. Conscious patients usually experience palpitations. Sometimes a prolonged QT interval is discovered after successful resuscitation.

Diagnostics

The ECG shows a wavy QRS axis, with multidirectional polarity of the complexes relative to the isoelectric line. The ECG between episodes of VT shows a prolonged QT interval (after correction for rhythm frequency (corrected QT)). The normal mean is 0.44 sec, although it varies between individuals and gender. Family history suggests a congenital syndrome.

Treatment

• Usually unsynchronized electrical cardioversion.
• Sometimes magnesium sulfate (MgSO 4 w/v).

An acute episode long enough to cause hemodynamic failure is treated with unsynchronized electrical cardioversion starting at 100 J. Despite this, early relapses are common. Patients often respond to Mg, usually MgSO 4 2 g, IV over 1-2 minutes. If there is no effect, a 2nd bolus is given and magnesium infusion is started in patients without renal failure. Lidocaine (class lb) shortens the QT interval and may be effective especially in the treatment of drug-induced ventricular tachycardia. Class Ia, Ic and III antiarrhythmic drugs should be avoided.

If the reason is medicinal product, it is discontinued, but until this drug is completely eliminated, a patient with frequent or long runs of ventricular tachycardia requires treatment with drugs that reduce the QT interval. Because an increase in heart rate is associated with a decrease in the QT interval, temporary electrical pacing and IV isoproterenol, used alone or together, are often effective. Long-term treatment is necessary for patients with congenital long OT syndrome. First-line treatment options include the use of β-blockers, permanent pacing, implantable cardioverter defibrillators (ICDs), or a combination of these. Family members should perform an ECG recording.

Patients with congenital long QT syndrome should completely avoid drugs that prolong the QT interval, and patients with exercise-related symptoms should avoid strength exercises. Treatment options include the use of beta blockers, electrical pacing to maintain a faster heart rate (which shortens the QT interval), and an ICD. These guidelines outline the indications for ICDs in patients resuscitated from cardiac arrest and in patients with syncope, regardless of β-blocker therapy.

Torsades de pointes (torsades de pointes)

This type of polymorphic ventricular tachycardia is a complication of prolonged ventricular repolarization. The ECG shows fast, irregular complexes that appear as a constantly changing electrical QRS axis. The arrhythmia is usually intermittent and recurrent, but it can progress to VF. During sinus rhythm, the ECG shows extended interval Q-T.

Reasons

Causes of QT prolongation and TDP

Bradycardia

Bradycardia increases the influence of other factors causing Torsades de pointes (TDP)

Electrolyte disturbances

• Hypokalemia.
• Hypomagnesemia.
• Hypocalcemia

Drugs

• Disopyramide (and other class Ia antiarrhythmics).
• Sotalol, amiodarone (and other class III antiarrhythmics).
• Amitriptyline (and other tricyclic antidepressants).
• Chlorpromazine.
• Erythromycin and many others

Congenital syndromes

• Romano-Ward syndrome (autosomal dominant).
• Jervel and Lange-Nielsen syndrome (autosomal recessive, associated with congenital deafness)

Arrhythmia is more common in women and is often triggered by a combination of various etiological factors (eg, multiple drug therapy and hypokalemia). Congenital long QT syndrome is a familial genetic disorder characterized by mutations in genes that code for potassium or sodium pumps in the heart.

Treatment

Intravenous administration of magnesium (8 mmol over 15 minutes, then 72 mmol over 24 hours) should be carried out in all cases. Atrial pacing usually suppresses arrhythmia due to rhythm-dependent Q-T shortening. Intravenous isoprenaline is a reasonable alternative to stimulation, but is contraindicated in patients with congenital syndrome extended Q-T.

Long-term therapy is usually not required if the cause of TDP can be eliminated. β-blockers or left stellate ganglion blockade are effective in patients with congenital long QT syndrome. In addition, installation of a defibrillator is often recommended.

Brugada syndrome - genetic disease, which manifests itself as polymorphic VT or sudden death; characterized by a defect in sodium channels, changes in the ECG (right bundle branch block and ST elevation in V 1 and V 2, usually without prolongation 0-7).

Information relevant to “Treatment of unsustained ventricular tachycardia”

The effectiveness of radiofrequency ablation for ventricular tachycardia varies in patients with coronary artery disease, cardiomyopathies, as well as in various forms of idiopathic ventricular tachycardia. Mapping and ablation technologies vary depending on the type of ventricular tachycardia. In patients without structural heart disease, only isolated foci of ventricular tachycardia and catheter ablation are usually detected

1. The presence of atrioventricular dissociation, which is recorded on the His bundle electrogram. This criterion is very important, but not absolute, since it is detected, although very rarely, with supraventricular tachycardias with aberrant ventricular conduction. 2. Absence of H potential before ventricular complexes or significant shortening I-U interval on the histogram. 3. Frequent

The diagnosis must indicate cardiac surgery and devices used for the treatment of arrhythmias and cardiac conduction disorders (indicating the method and date of intervention) - catheter (radiofrequency and other) destruction, implantation of pacemakers and cardioverter-defibrillators, cardioversion or defibrillation (the date of the last one is noted). ) and so on. Examples of clinical

People without clinical signs heart disease, as well as in patients without anomalies coronary arteries(according to angiography) and without impaired left ventricular function, late potentials are not detected (Table 11.2). Similarly, low-amplitude potentials are not observed in the last 40 ms of the filtered QRS complex in patients without ventricular tachycardia and anamnestic data on

In adult patients, the most common arrhythmias leading to circulatory arrest are ventricular fibrillation and pulseless ventricular tachycardia. Pulseless ventricular tachycardia is understood as a prolonged paroxysm of ventricular tachycardia with severe hemodynamic disturbances, up to arrhythmic shock, in contrast to ventricular tachycardia with a pulse, which includes all others

With wide QRS complexes (>120 ms), it is important to differentiate supraventricular tachycardia from ventricular tachycardia. To distinguish supraventricular tachycardias from ventricular ones persistent symptoms tachycardias are not indicative. If the diagnosis of supraventricular tachycardia cannot be confirmed or established, then the tachyarrhythmia should be regarded as ventricular tachycardia and treated accordingly. Tachycardia with

Incremental stimulation and extrastimulation methods are also used in the assessment of supraventricular tachycardia. If the closed conduction pathway passes through the ventricle, these methods can directly induce and terminate the arrhythmia. Ventricular stimulation can initiate supraventricular tachycardia even in the case of non-participation of the ventricles in the development of arrhythmia. If retrograde conduction is intact,

This type of cardiac arrhythmia is characterized by two signs: 1. Tachycardia, i.e. excitation (and subsequent contraction) of the heart with a frequency of 130-250 per minute. 2. Paroxysm, i.e. the sudden onset and sudden end of an attack of tachycardia, which, as a rule, can be detected clinically and recorded electrocardiographically extremely rarely. The essence of paroxysmal tachycardia is

Sinus tachycardia. 2. Supraventricular tachycardia a. Paroxysmal reciprocal (re-entry) nodal tachycardia. b. Paroxysmal reciprocal (re-entry) nodal tachycardia in the presence of additional pathways (WPW and CLC syndrome). c. Paroxysmal focal atrial tachycardia. d.Paroxysmal (re-entry) sinus tachycardia. 3.

Arrhythmias Ventricular ectopic contractions are recorded during Holter monitoring in almost all patients with LV systolic dysfunction, including approximately half with unsustained ventricular tachycardia. In patients with an average number of ectopic contractions of more than 10 per 1 hour, 24-hour ECG monitoring shows increased risk occurrence of sudden cardiac death,

Atrioventricular block: basic concepts; Clinical concepts of spontaneous and induced atrioventricular block; Atrioventricular block: a non-invasive approach; Branch block and other forms of aberrant intraventricular conduction: clinical aspects; Electrophysiological mechanisms of ischemic ventricular rhythm disturbances: correlation of experimental and clinical data;

Based on wide QRS complexes (>120 ms), it is important to differentiate supraventricular tachycardias from ventricular tachycardias (Figure 5.4). When treating patients with supraventricular tachycardias, parenterally prescribed drugs, especially verapamil or diltiazem, are potentially dangerous because they can cause the development of collapse in patients with ventricular tachycardias. Persistent symptoms of tachycardia

Fig.1. A-B blockade of the second degree: Mobitz-2. Fig. 2 – Atrioventricular rhythm. Rice. 3 – Atrioventricular rhythm 4a – Sinus rhythm 4b – Atrioventricular rhythm Fig. 5 – Areas of accelerated ventricular rhythm Fig. 6 – Double supraventricular extrasystole and single supraventricular extrasystole with emerging bundle branch block (aberantine complex)

Algorithm of actions for paroxysmal reciprocal AV nodal tachycardia and orthodromic paroxysmal reciprocal AV tachycardia with the participation of additional atrioventricular connections (WPW syndrome) on prehospital stage. Medical tactics for paroxysmal supraventricular paroxysmal tachycardia with a narrow QRS complex are determined by the patient’s hemodynamic stability. Sustainable

Ventricular tachycardia and fibrillation

Ventricular tachycardia and

Electrophysiological testing with programmed ventricular pacing, originally used to study the mechanisms of ventricular tachycardia, is now an integral part of the clinical examination and treatment of patients with ventricular tachyarrhythmia. The sensitivity and specificity of various stimulation methods used in EPI have now been well studied. Adequate

Ventricular flutter and fibrillation in pathogenesis are closely related to ventricular tachycardia, and are observed in the same pathology in which ventricular extrasystole or ventricular tachycardia occurs. Rice. 25. On the upper ECG there is an episode of the onset of flutter with transition to ventricular fibrillation. The second ECG shows ventricular flutter. The third ECG shows ventricular fibrillation.

Ventricular tachycardia

Information relevant to "Ventricular tachycardia"

ventricular tachycardia, ventricular fibrillation); 5. ECG changes that do not reveal ST abnormalities; 6. Diabetes mellitus. TREATMENT STRATEGY: 1. Continue intravenous administration of UFH for 2-5 days. or subcutaneous - LMWH. 2. Add clopidogrel - initial dose 300 mg, then 75 mg per day. 3. If available, it is advisable to use intravenous infusion glycoprotein antagonists

ventricles. Heart rate - > 100 per minute. Etiology Acquired gastrointestinal tract ischemic heart disease MI Post-infarction cardiosclerosis Left ventricular aneurysm Alcoholic cardiomyopathy Myocarditis Heart defects Cardiomyopathies Poisoning with cardiac glycosides Hypokalemia Hypercalcemia Presence of a catheter in the ventricular cavity Stress Congenital ventricular ventricle Heart defects Prolapse mitral valve Pathogenesis.

ventricles. Preclinical form of ischemic heart disease characterized by painless silent myocardial ischemia. C Sudden death in most cases is caused by electrical instability of the myocardium, which has not lost high contractility at the time of ventricular fibrillation. Clinical picture and treatment - see Angina, Myocardial infarction, Special ECG studies - depression S-T segment, increase

ventricular. Supraventricular (atrial and atrioventricular) and ventricular extrasystoles can occur both with organic myocardial lesions and without heart disease. Clinical picture. At stage I diagnostic search in a patient with undoubted extrasystole, no complaints may be detected, and extrasystole will be diagnosed at subsequent stages of the study.

ventricles (mainly the left) and severe impairment of diastolic function. Hypertrophy of the left ventricular wall more than 15 mm unknown origin is considered a diagnostic criterion for HCM. There are obstructive (narrowing of the left ventricular outflow tract) and non-obstructive HCM. Hypertrophy can be symmetrical (increased thickness of the walls of the entire left ventricle) and asymmetrical (increased

ventricular complex (decrease in the amplitude of the T wave, its smoothness and even negative wave 7). Changed teeth are found more often in the right chest leads, sometimes in all chest leads (“total negativity syndrome 7>>”). Rarely (5-8% of cases) supraventricular extrasystole and automaticity disorders are observed. Rhythm disorders are caused mainly by various

ventricular septum (25% of all lesions). Pathogenesis. In the pathogenesis of MI main role belongs to the cessation of blood flow to the area of ​​the heart muscle, which leads to damage to the myocardium, its necrosis, and deterioration in the functioning of the peri-infarction zone (diagram 12). Myocardial necrosis is manifested by resorption-necrotic syndrome (laboratory data, increased body temperature) and

ventricular tachycardia, ventricular extrasystole). ^ Feverish state of a pregnant woman. The metabolism of the fetal myocardium is activated and sympathetic influences are enhanced. ^ Hyperthyroidism in a pregnant woman. Hormones thyroid gland penetrate the placental barrier and stimulate the fetal heart. ^ Amnionitis. Tachycardia may be the first manifestation of the development of an intrauterine infection. ^

ventricles caused by ischemia, but occasionally OHA can occur as a result of cardiac arrest in patients with impaired AV conduction. Pain caused by inflammation of the serous membranes or joints. Pericarditis. The visceral surface of the pericardium is usually insensitive to pain, as is the parietal surface with the exception of its lower part, which contains a relatively small number

ventricular asystole c) sinus bradycardia, sinoatrial block, cessation of activity sinus node, sick sinus syndrome d) sinocarotid syncope (see also above - inadequate mechanisms of vasoconstriction) e) neuralgia of the glossopharyngeal nerve 2. Tachyarrhythmias: a) periodic ventricular fibrillation in combination with or without bradyarrhythmias b) ventricular tachycardia c)

Unsustained ventricular tachycardia

unsustained ventricular tachycardia

Unsustained ventricular tachycardia primarily indicates an increased risk of sudden tachyarrhythmic death.

Since unsustained ventricular tachycardia resolves quickly and is often asymptomatic, it is usually detected during long-term ECG monitoring.

Etiology and prevalence. With rare exceptions, ventricular tachycardia is associated with organic pathology hearts.

Unsustained ventricular tachycardia- a fairly common complication of the early period of myocardial infarction. Its frequency in the first 24 hours of this disease reaches 45%.

To possible etiological factors also include systemic hypertension with left ventricular hypertrophy, rheumatic heart disease and various secondary cardiomyopathies, even in the absence of congestive heart failure.

Pathophysiological mechanisms. Like ventricular extrasystole, unstable monomorphic ventricular tachycardia can be based on each of the three known electrophysiological mechanisms. In any case, these mechanisms generally have little dependence on the nature of the heart disease.

Clinical picture. Unsustained ventricular tachycardia is usually asymptomatic and appears only with more or less long-term ECG monitoring. In some patients, there is a reason to perform this study is palpitations, dizziness, fainting and chest pain.

Diagnostics is based on characteristic ECG data (Fig. 56). A feature of the changes in these data of unstable ventricular tachycardia, which is formed in the outflow channel of the right ventricle in persons without structural heart diseases, is the graph of the blockade of the left leg of the atrioventricular bundle in combination with a deviation electrical axis hearts to the right.

Course and prognosis. Like complex forms of ventricular extrasystole, unstable ventricular tachycardia in almost healthy individuals, including its recurrent and symptomatic episodes occurring in the outflow canal of the right ventricle, does not significantly aggravate the prognosis. In the presence of organic heart disease, this arrhythmia causes an increased incidence of sudden death and death from all causes.

Treatment unsustained ventricular tachycardia is clearly indicated in symptomatic cases, regardless of whether or not there is organic heart disease, to improve the quality of life of patients. At the same time, antiarrhythmic therapy does not have any special features compared to patients with symptomatic ventricular extrasystole.

In the case of symptomatic ventricular tachycardia, treatment begins with the prescription of β-blockers, which are effective in approximately 50% of patients.

If P-blockers are ineffective or intolerant, propafenone and amiodarone are indicated. In resistant cases, radiofrequency catheter ablation of the ectopic focus is used.

Primary prevention is similar to that for potentially fatal ventricular arrhythmias.

Supraventricular tachycardia (VT) is one of the types of heart rhythm abnormalities characterized by sudden growth the number of contractions of the heart muscle, but maintaining their correct rhythm.

It progresses if there is an additional focus in the atrium that emits electrical impulses, or if additional conduction pathways for nerve excitation appear in the heart, in addition to one atrioventricular pathway.

In some cases, structural damage to the heart or deviations in the functional abilities of the left ventricle can provoke supraventricular tachycardia. NT damage can cause death, so it is considered a life-threatening condition.

Death occurs when the heart rhythm fails, as a result of which the heart muscle quickly wears out.

According to statistics, supraventricular tachycardia is recorded in 0.3 percent of the population, mainly in women. While ventricular tachycardia is more often diagnosed in men.

Localization of the lesion, exclusively in the atria, is recorded in fifteen percent of cases, and atrioventricular lesions in eighty-five percent of cases.

People are mainly affected old age(after 60 years), but the incidence rate in young people is also present.

How does NT damage occur?

Progression of supraventricular tachycardia occurs if one of two mechanisms for the occurrence of additional impulses occurs.

One of them is the emergence of additional foci emitting nerve impulses. This leads to the fact that in addition to electrical excitations transmitted by the sinus node, the same impulses are emitted by pathological foci in the atria.

As a result, the number of heart contractions increases, which disrupts the healthy rhythm of the heartbeat, causing supraventricular tachycardia, which is also called paroxysmal or supraventricular.

In the second case, impulses are emitted only by the sinus node. An increase in heart rate occurs because obstacles arise in the path of the impulse, which leads to repeated excitation. Such obstacles can be inflamed or scar tissue of the heart, tumor formations, and others. structural damage healthy heart.

In most cases, after the mechanisms described above, supraventricular or ventricular tachycardia progresses.

The main difference between them is that with supraventricular deviations are localized in the atrium or impulse-conducting tissues, and in the case of ventricular deviations, they are located directly inside the ventricles.

What triggers the occurrence of NT?

Certain factors can provoke increased heart rate (up to 250 beats in 60 seconds), with an accompanying feeling of fear.

Moreover, in young people, it is more associated with functional abnormalities, which are provoked by a disorder of the nervous system ( nervous tension, experiences, etc.), and in older people it progresses, in many cases, when exposed to structural changes cardiac tissues.

In the majority of cases, supraventricular tachycardia is provoked by the following influencing factors:

• Disturbances in the functional performance of the heart. He may be attracted by such pathological conditions, How vegetative-vascular dystonia, as well as dystonia of a neurocircular nature, increased emissions adrenaline in the blood, shock situations;
• Structural deformations of cardiac tissues. This group includes diseases in which the structural component of the heart muscle is disrupted or the normal one is deformed. This is the death of myocardial tissue (infarction), ischemic heart attacks, myocarditis, as well as cardiomyopathies;
• Exposure to cardiac glycoside toxins. When taking medications in excess of the norm (Digoxin, Strophanthin, etc.), often prescribed to patients with chronic forms pathologies, cause attacks of severe tachycardia, with a high mortality rate. The same effect of certain arrhythmic drugs (Propafenone, etc.);
• Metabolic failure. Severe deficiency of vitamins and nutrients, or prolonged liver and kidney disease followed by their failure. Also, constant diets with impaired protein intake lead to myocardial dystrophy (thinning of heart tissue);
• Constant stress. TO functional disorders hearts can lead and nervous breakdowns, mental disorders, strong emotional stress.
• Formation of extra signal paths. This pathology is congenital, but can manifest itself at any age.
• Excessive concentration of cardiotropic hormones in the human body. In case of excessive activity of the thyroid gland (hyperfunction), it increases quantitative indicator triiodothyronine in the blood, and if there are tumor formations on the adrenal glands, adrenaline and norepinephrine increase;
• Alcoholic drinks or drugs;
• SVC syndrome. With this syndrome, at the stage of fetal formation in the womb, an additional conduction bundle is formed;
• Pathologies of other organs, such as cholecystitis, kidney failure, stomach ulcers, gastritis;
• Idiopathic supraventricular tachycardia. It is diagnosed if the patient does not have any of the listed pathological conditions.

Various supraventricular rhythms

In many cases, the occurrence of supraventricular tachycardia is provoked by stress, increased consumption of strong tea, coffee, and drinks containing large number caffeine, excessive alcoholic drinks and cigarettes.

How do the symptoms appear?

The manifestation of supraventricular tachycardia is in the nature of attacks. They appear suddenly, increasing the heart rate up to 250 beats per minute, and last from a couple of minutes to a couple of days. In the period between attacks, the patient may feel completely healthy.

It begins with a feeling of a strong push in the chest, in the area of ​​the heart.

In a normal state, a person does not feel a contraction, but during an attack he feels a rapid beating of the heart. The beat frequency increases and is maintained in one, accelerated rhythm.

Attacks of supraventricular tachycardia are often accompanied by:

At the end of the attack, great relief is felt, ease of breathing is restored, the rapid beating of the heart ends with the same push, or a feeling of freezing in the chest.

How is the diagnosis made?

At the first visit, the doctor listens to the patient’s complaints, studies the medical history, and conducts initial examination for presence clearly severe symptoms. Diagnosis of supraventricular tachycardia usually does not find difficulties, and is checked with an ECG during the next attack.

When listening to heart sounds and recording pulse indicators, an increased but rhythmic increase in contractions is noted during an attack. Low blood pressure appears.

If the patient has supraventricular tachycardia, the following changes are displayed on the ECG:

• Atrial supraventricular tachycardia. The rhythm remains correct, sinus, with a partial fluctuation from 140 to 200 (maximum 250) beats per minute. The P-wave indicates the passage of the impulse through the atrial zone from the sinoarterial node, in front of each ventricle, with low amplitude, and this wave can be changed into biphasic or negative;
• Ventricular QRST complexes remain unchanged and do not widen;
• During an attack of tachycardia, the P wave from the atrioventricular junction is negative.

Also, in addition to the electrocardiogram, if other types of arrhythmia are suspected, a qualified doctor can refer you for the following hardware tests:

• Coronography– an examination that assesses the condition of the arteries of the heart. This type of diagnosis is the most accurate for cardiac ischemia;
• Ultrasound examination of the heart (ultrasound). Allows you to visualize the condition of the heart;
• MRI (magnetic resonance imaging) of the heart– is very complex look safe research. Very effective. During the examination, the patient is placed in a special device - a tomograph;
• Load tests (Treadmill, Bicycle ergometry). A treadmill is a study performed while exercising on a special treadmill. A bicycle ergometer is a similar test method, but using a special bicycle.

The main method for diagnosing supraventricular tachycardia is an electrocardiogram.

How to provide emergency assistance and stop an attack?

In the event of an attack of supraventricular tachycardia, you need to know how to provide first aid. It is especially important to know this for relatives who have a family member suffering from supraventricular tachycardia.

Most effective methods eliminating an attack are:

• Aschner-Dagnini test. It is necessary to lay the patient horizontally. Then simultaneously and with moderate force press on the closed eyeballs stricken. Such exposure to the eyeballs is allowed only for up to 30 seconds. If the effect occurs earlier, the effect is stopped. This test is contraindicated for patients suffering from eye diseases;
• Chermak-Goering test. The affected person is placed in a horizontal position, after which the carotid node, which is located between the carotid arrhythmia and the ear, is affected. Apply pressure for no more than 30 seconds. A contraindication to the test is atherosclerosis in the elderly, as well as in extreme stages of hypertension;
• Artificially induced vomiting;
• Rubbing the affected person with cold water;
• Strong pressure on the upper abdomen.

If the above methods do not produce results, drug treatment is used.

Treatment

Drug treatment of attacks of supraventricular tachycardia is prescribed by the attending physician. To prevent complications, do not self-medicate.

In most cases, the following drugs are prescribed:

• Verapamil (intravenously). The drug quite effectively suppresses attacks of supraventricular tachycardia. After stopping the attack, use Verapamil in tablets, one three times a day;
• Beta blockers (Anaprilin, Visken, Esmolol, Oxprenolol). Drugs in this group are used if Verapamil does not work. All drugs are administered intravenously during an attack, and subsequently prescribed in tablet form. The dosage is determined individually by the attending physician;
• Drugs against arrhythmia (Novocainamide with glucose solution). It is administered intravenously, or directly into the muscle, in a dosage of 10% from 5 to 10 ml. You can also take it orally in a dosage of 1 gram, every two hours, until the end of the attack. Taking this drug orally is allowed only after a doctor’s prescription, as it may lead to complications;
• ATP inhibitors. They are used in the form of droppers and help interrupt the pathological circulation of the electrical impulse in the heart;
• Aymalin. Is very effective means in the treatment of supraventricular tachycardia. It consists of components that are not as toxic as the above drugs, and is an invaluable tool for the treatment of severe stages of arrhythmia. Injected very slowly over 5 to 10 minutes. After the attack has stopped, its tablet form is used, up to 4 times a day;
• Pulse is normal. The drug helps eliminate mild attacks of supraventricular tachycardia. During an attack, the patient needs to take two tablets, and then take two of them every 8-12 hours;
• Procainamide. Quite an effective drug used intravenously. It is injected very slowly with a 10 percent solution;
• Trifosadenine. This drug has quick effect stopping an attack. It is also introduced quickly (1-2 seconds). If the effect does not occur within three minutes, a double dose must be administered. In the first minutes, headaches and coughing attacks may appear, but they are normal and disappear on their own.

If a patient is struck by an attack of supraventricular tachycardia, means are used to stop it as quickly as possible, and in the future, to maintain normal heart contractions and prevent relapses, regular pills are prescribed.

Each individual attack of supraventricular tachycardia requires individual treatment. That is why you should not self-medicate, but use medications only after they have been prescribed by your doctor.

In severe cases of supraventricular tachycardia, and the body does not accept drug treatment, surgical intervention is used. Deformed during surgery additional sources, emitting impulses, which restores the normal rhythm of heart contractions.

Before surgery, an electrocardiogram is measured from electrodes that are inserted into the heart muscle. This is done in order to identify the lesions.

Doctors perform an operation called radiofrequency ablation, during which additional pathways and areas of impulse formation are eliminated.

Also, foci can be destroyed by physical energy(laser, electric current therapy, low-temperature effects on the body).

In rare cases, it is necessary to install a pacemaker, which automatically restores the rhythm of the heartbeat during an attack of tachycardia. You can read about the installation and types of pacemakers at the link - h

Complications

In most cases, prolonged supraventricular tachycardia, if untreated, leads to thrombosis pulmonary artery, ischemic stroke, acute heart failure, pulmonary edema, as well as unexpected death.

Severe attacks of supraventricular tachycardia require immediate hospitalization and further effective treatment.

Expert forecast

According to statistical data, the prognosis for supraventricular tachycardia is more favorable than for ventricular tachycardia. The risk of complications should not be excluded.

Unexpected death occurs in 2-5 percent of patients with supraventricular tachycardia. The less severe the attacks, the more favorable the prognosis.

This disease is individual and requires consultation with a qualified doctor who will select treatment.

Self-use medicines may lead to complications.

Supraventricular tachycardia always manifests itself in the form of a rapid pulse, which is felt even without palpating the heartbeat. With this disease, impulses are formed above the level of both ventricles, namely in the atrium or atrioventricular node. A timely ECG helps to detect abnormalities. Therefore, ventricular tachycardia is under complete careful control.

The human heart consists of standard four chambers: the upper two are called atria, and the lower two are called ventricles. The first blood comes from everyone blood vessels- as a result of constant contractions of the walls of the atria, all the blood is pushed directly into the ventricles. Further contraction of the ventricles pushes blood from the heart itself to the lungs and other organs.

Special cells coordinate all contractions of the heart muscle using special electrical impulses. In this process, the formation of the sinoatrial or sinus node occurs, which is located in the right atrium. This small knot is natural stimulant heart, which generates all electrical signals and directly transmits them to the small atrioventricular node. Already directly, it correctly stimulates the work of the His bundle and branches, which further leads to stable contractions of the ventricles. The walls of all chambers of the heart contract sequentially. It is each of these sequences of contractions that is a heartbeat.

Hormone levels and nerve impulses directly affect heart rate. Disturbances in the process of cardiac conduction or unstable hormonal background lead to abnormal heart rhythms - arrhythmias. The progress of ventricular tachycardia is recorded on the ECG, so the doctor can reliably make a diagnosis and prescribe adequate treatment.

So, how does ventricular tachycardia manifest? Based on what indicators is the correct treatment prescribed?

Supraventricular (ventricular) tachycardia: what happens in the body?

The heart begins to beat so fast that the heart muscle simply cannot relax between its contractions. When relaxation does not occur, full work does not occur, and the heart does not pump enough blood to fully satisfy the body's needs. This is why ventricular tachycardia is dangerous.

Due to impaired and ineffective contractions of the heart, the brain simply does not receive enough blood and oxygen. Therefore, with such tachycardia, fainting and dizziness are possible.

Supraventricular tachycardia on the ECG is observed in absolutely healthy young children, adolescents, as well as in people with various diseases hearts. Most patients diagnosed with the disease lead a lifestyle without restrictions.

Ventricular tachycardia is very often episodic. Between episodes of cardiac arrhythmia, the heart beats normally. But remember that the disease can be chronic.

Supraventricular tachycardia: causes

Supraventricular or ventricular tachycardia usually occurs without symptoms that are characteristic of other diseases. But it is directly related to a number of ailments, for example:

• heart failure;
• dysfunction of the thyroid gland;
• atherosclerosis;
• chronic lung diseases;
• pneumonia;
• pericarditis;
• pulmonary embolism;
• cocaine use;
• taking certain medications;
• smoking and alcohol abuse;
• stress.

Structural abnormalities are also detected on the ECG, for example, Parkinson's syndrome - congenital disorder the structure of the heart, in which strong and premature excitation of the ventricles occurs - ventricular tachycardia.

Supraventricular tachycardia may be obvious side effect taking certain medications for asthma, colds. In some reasons the real reason the disease is simply unknown. Remember that the key to health is a timely visit to the doctor, even in connection with routine preventive care.

Supraventricular tachycardia: symptoms

Supraventricular tachycardia can cause a variety of symptoms, which depend on the patient's overall recorded health status and heart rate. Patients with various pathologies hearts and others medical problems the symptoms cause quite a lot of discomfort and are accompanied by greater complications than those that do not show serious disorders. In certain cases, ventricular tachycardia occurs without any symptoms.

Symptoms may come on suddenly and disappear on their own, even with an ECG. They last from a few minutes to a couple of days. Of course, the doctor can have time to record all the changes on the ECG. Please note that the signs are typical for a rapid heartbeat at 140-250 beats per minute:

• feeling that the patient's heart is beating too hard in the chest;
• dyspnea;
• severe dizziness or fainting;
• anxiety;
• feeling of tightness or pain in the chest.

Ventricular tachycardia is a rather insidious disease, and therefore requires prompt attention at the first manifestations.

Ventricular tachycardia: when to seek medical help?

Ventricular tachycardia poses a particular danger to life only in the presence of other heart diseases. Consult a qualified healthcare provider if the following occurs:

• Ventricular tachycardia occurs for the first time, the symptoms last quite a long time.
• You have already had certain episodes of arrhythmia, and the current period does not go away even after a reflex reaction to the vagus nerve.

• You have a very rapid heartbeat and dizziness, fainting - obvious ventricular tachycardia.
• Quite frequent contraction of the heart muscle is accompanied by severe pain in the chest.
• A rapid pulse is accompanied by shortness of breath.

Treatment of ventricular tachycardia must be timely and correct. It is necessary to monitor changes on the ECG. It is also worth remembering that the ECG must be performed dynamically so that the doctor can correctly monitor the development of the disease. Ventricular tachycardia requires attention, as it can lead to heart pathologies.

Ventricular tachycardia: proper treatment

Surgical treatment is required when ventricular tachycardia worsens and its symptoms worsen significantly. Therapy will also be required if the ECG long time disappointing.

If blood pressure drops much below normal levels, rapid cardioversion is necessary. If the pressure is stable, lidocaine or other medications are prescribed intravenously to suppress the disease. Ventricular tachycardia fades into the background. Treatment is prescribed again if attacks recur consistently.

By ECG results The following treatment may be prescribed: electrophysiological study and other drugs. The one that gives the most best results according to ECG, can be chosen as a preventive treatment.

Sustained ventricular tachycardia very often causes pathological changes in the ventricular area, so they have to be removed by professional surgically. Based on the ECG results, some patients are given a device called a modern automatic defibrillator. Treatment of this nature is effective.

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Questions and answers on: paroxysm of ventricular tachycardia

2015-06-24 02:43:09

SVETLANA asks:

My son is 16 years old, he has sinus rhythm with min. heart rate 48 beats/min during night sleep, heart rate 123 beats/min during the day, during physical activity (exercises on the horizontal bar), the average heart rate during the day is 73 beats/min, at night 54 beats/min. 1 short paroxysm of ventricular tachycardia was registered with an hour of 158 per minute (QRS?). 4983 atrial extrasystoles were recorded per day,
What treatment is prescribed for this? Is this life-threatening?

Answers Bugaev Mikhail Valentinovich:

Hello. If it really was a paroxysm of ventricular tachycardia, it could be dangerous. Or scan and send the ECG film, or to an appointment with an arrhythmologist. Films are needed at rest and at the moment of paroxysm.

2012-04-15 19:03:40

Nadezhda asks:

Previous letters: Hello! half a year ago the pressure began to jump to 180/120. drank hartil, then the pressure began to jump - sometimes 160/100, then 90/60 (associated with processing and constant voltage at work - I worked in a kindergarten as a teacher) I’m 27 years old. pain appeared in the heart (under the left breast, at rest, with physical activity the pain goes away), sometimes pain under the left shoulder blade! pressure began to jump. ECG - sinus tachycardia, ultrasound-PMC 0-1 ST, REGURGITATION ON HEART VALVES 1 ST , ARCHL-DIAGONAL APICAL! SINUS TACHYCARDIA-116 BP. IN MIN. (STRONGLY WORRIED) I began to feel a disruption in the heart rhythm. Holter results: Ventricular extrasystoles 106, pre-ectopic interval 208-720 ms. 83 during the day, 23 at night, average number per hour: 4.5, maximum quantity per hour: 24, single! supraventricular extrasystoles 2. average heart rate figures are within normal limits. No pathological changes in repolarization were detected. Analyzes: sugar 5.4, hemoglobin 146, cholesterol 5.6. X-ray of the cervical spine - signs of stage 1 osteochondrosis, THORACIC SECTION - NORMAL Kimmerli anomaly (incomplete arch). Sometimes the left leg goes numb (from the knee to the heel), AND THE LOWER LIP!. I take afobazole, BUT NO RESULTS, IT’S VERY SCARY WHEN HEART INTERRUPTIONS START! Constant anxiety, worries about health. Do you need to treat extrasystoles? Do you need to take antiarrhythmic drugs? could this be VSD? I've been living in this condition for half a year constant anxiety! WHAT TESTS ELSE NEED TO BE DONE TO IDENTIFY WHAT IS THE DISORDER, OR JUST CALM DOWN AND ACCEPT EVERYTHING AS IT IS, OR SHOULD I PLAN A PREGNANCY WITH EXTRASYSTOLS?

March 02, 2012


information about the consultant
Hello. You need to take sedatives (mild, herbal), not antiarrhythmics. Try to forget about arrhythmia, it does not threaten you in any way. Hello, dear doctor. I recently wrote to you about extrasystoles (letter dated February 29, 2012). Exactly a month passed after Holter, and I decided to check my heart again on Holter, because... I drank afobazole for a month and the herbs of hawthorn and motherwort. Ecstasystoles began to be felt less frequently and I was happy, but probably in vain, because Holter's results from 03/19/2012 are as follows: Average heart rate figures are WITHIN NORMAL LIMITS, THE CIRCADIC INDEX IS SUFFICIENT. Basic sinus rhythm. 166 monotopic, class 4-b Lown blood cells were identified. Blood cells are not evenly distributed throughout the day without a clear connection with the time of day , there is a connection with physical activity in the daytime. Paired VES 1. 2 short paroxysms of ventricular tachycardia lasting from 3 to 6 complexes were recorded. No pauses were detected. the displacement of the ST segment is insignificant (does not exceed 0.1 mV. I WAS UPset AGAIN, BECAUSE I THOUGHT THEY HAD DECREASED, BUT THERE IS THE VICE OVERSEAS. At the time when I had ventricular tachycardia, I climbed to the fourth floor almost at a run, and just felt a systole, then a second , and immediately a strong heartbeat (211 times according to Holter), is this tachycardia possible due to exercise (running), how dangerous is it, and why do I hardly feel them, but the cardiologist again diagnosed somatophoric dysfunction of the central nervous system and prescribed anaprilin. 10 mg 1t 2 times a day, but I don’t know whether to take them or not? Help me figure out where this came from. I’m tired of endless visits to doctors and hearing that you have VSD, YOU FEEL HEALTHY I’LL GO TO A PSYCHIATTER SOON! YOUR JOB! WHAT DOES IT MEAN IF ES ARE ASSOCIATED WITH PHYSICAL LOAD.

March 23, 2012
Mikhail Valentinovich Bugaev answers:
Cardiac surgeon of the highest category
information about the consultant
Hello. Unfortunately, if extrasystoles increase with exercise, then their cause is heart disease. Especially if there are episodes of ventricular tachycardia. Go to a good cardiologist, arrhythmologist, perhaps you need ECG stress tests (treadmill test), maybe a series of other studies. With “somatoform central nervous system dysfunction” there are no ventricular runs. With VSD too. Start of treatment - beta blockers (anaprilin - not best choice), cordarone is also possible, but only after examination by a good doctor (cardiologist, arrhythmologist). NADEZhDA asks:
Mikhail Valentinovich, thank you for your answer. I don’t want to seem smarter than the doctors, but I read the Holter ECG report and calculated how many systoles there were during the load - 32, the rest 65 at night with a pulse of 65 beats, and the rest during the day with a pulse of 70-80 when I was sitting at work. I didn’t keep any diaries during the study, is it the program itself that shows the connection between the ZH and the loads, or is it calculated by the diagnostician? because there is a larger number without load. I also took a test for cholesterol - 6.5, a month ago it was 5.5. Is systole possible from this. Thyroid hormone levels were normal. my spine often hurts in the sternum area, it crunches a lot, the cardiologist said that the left shoulder blade is sticking out, and left shoulder Below. Is it possible to have ZhES from the spine? 2 runs of tachycardia were the first time in all the months when I felt zhes. Bisoprolol is better to drink than anaprilin. Excuse me, but I just really don’t want to believe that there is heart disease at the age of 27 with a normal ultrasound. I myself am a very emotional person, what are the prognosis for my illness, if it comes from the heart! I really want to live and raise my daughter. THANK YOU!

March 27, 2012
Mikhail Valentinovich Bugaev answers:
Cardiac surgeon of the highest category
information about the consultant
Hello. Your forecasts are quite good. Take bisoprolol and don't worry. If the extrasystole decreases with exercise, this is a favorable sign. Usually the program counts the number of extrasystoles; it overestimates their number. Cholesterol has nothing to do with it at all. But the spine can give extraordinary contractions of the heart. thank you for your work. I wanted to ask you another question. I’ve been taking bisoprolol for almost a month now, with my blood pressure at 130/85, it drops to 90/60, sometimes I feel dizzy and nauseous. I take bisoprolol 5 mg in the morning after breakfast! Maybe you should drink it at lunch? I am undergoing acupuncture sessions, after the 7th session, the systoles became less frequent, sometimes I felt 5-10 a day. But now on weekends without needles, the systoles have become more frequent again, especially when I lie on my back. I began to notice that as soon as I think about them -they begin to manifest themselves with all their might, and when I’m busy with something, I don’t feel them at all, and recently I was running to catch the bus, and then there was just tachycardia, there were no systoles. While I'm waiting to see an arrhythmologist, I underwent an examination - electropuncture diagnostics. there they told me that my heart was normal, they diagnosed me with VNS tension (mixed type) 4 degrees, a lack of vitamins B1 and B6, as well as magnesium. Biliary dyskinesia. deviations in the cervical and thoracic spine (osteochondrosis). my back hurts terribly, especially in the thoracic region, constant crunching when turning. Is it possible to cure systoles if they are from the spine forever, and how dangerous are they if they are from the spine. How many maximum needle sessions can you do, and is it possible to do a massage? General health is good, there are no other complaints except systole. I feel each one very clearly, and when they come at 30 pieces per hour, panic begins. Thanks for your work!

Answers Bugaev Mikhail Valentinovich:

Hello. You pay too much attention to extrasystoles, which are not at all dangerous and do not need treatment, but you avoid real problems - biliary dyskinesia, problems with the spine, and, meanwhile, they may be the cause of your extrasystoles. It’s better to take care of them, and go to see a psychotherapist, maybe you won’t be able to focus so much on the extrasystoles. You can do a massage. I see no reason to panic.

2012-03-21 19:13:33

Nadezhda asks:

Hello, dear doctor. I recently wrote to you about extrasystoles (letter dated February 29, 2012). Exactly a month passed after Holter, and I decided to check my heart again on Holter, because... I drank afobazole for a month and the herbs of hawthorn and motherwort. Ecstasystoles began to be felt less frequently and I was happy, but probably in vain, because Holter's results from 03/19/2012 are as follows: Average heart rate figures are WITHIN NORMAL LIMITS, THE CIRCADIC INDEX IS SUFFICIENT. Basic sinus rhythm. 166 monotopic, class 4-b Lown blood cells were identified. Blood cells are not evenly distributed throughout the day without a clear connection with the time of day , there is a connection with physical activity in the daytime. Paired VES 1. 2 short paroxysms of ventricular tachycardia lasting from 3 to 6 complexes were recorded. No pauses were detected. the displacement of the ST segment is insignificant (does not exceed 0.1 mV. I WAS UPset AGAIN, BECAUSE I THOUGHT THEY HAD DECREASED, BUT THERE IS THE VICE OVERSEAS. At the time when I had ventricular tachycardia, I climbed to the fourth floor almost at a run, and just felt a systole, then a second , and immediately a strong heartbeat (211 times according to Holter), is this tachycardia possible due to exercise (running), how dangerous is it, and why do I hardly feel them, but the cardiologist again diagnosed somatophoric dysfunction of the central nervous system and prescribed anaprilin. 10 mg 1t 2 times a day, but I don’t know whether to take them or not? Help me figure out where this came from. I’m tired of endless visits to doctors and hearing that you have VSD, YOU FEEL HEALTHY I’LL GO TO A PSYCHIATTER SOON! YOUR JOB! WHAT DOES IT MEAN IF ES ARE ASSOCIATED WITH PHYSICAL LOAD.

Answers Bugaev Mikhail Valentinovich:

Hello. Unfortunately, if extrasystoles increase with exercise, then their cause is heart disease. Especially if there are episodes of ventricular tachycardia. Go to a good cardiologist, arrhythmologist, perhaps you need ECG stress tests (treadmill test), maybe a series of other studies. With “somatoform central nervous system dysfunction” there are no ventricular runs. With VSD too. Start of treatment - beta blockers (anaprilin is not the best choice), cordarone is also possible, but only after examination by a good doctor (cardiologist, arrhythmologist).

2016-11-11 09:35:54

Olesya asks:

Good afternoon. I am 33 years old, 2 months ago I had an attack of rapid heartbeat at night while sleeping, I woke up from this situation. The attack lasted about 40 minutes, and it was very hot and sweating. In the morning I was very weak, I did an ECG and ECHO of the heart in the evening, no changes were detected. I took potassium and magnesium tests and they were low. I also did a 24-hour Holter, it revealed heart rhythm disturbances, diagnosis: 1st degree AV block, transient. 2nd degree AV block, type 1. They prescribed magnesium and potassium droppers, after one dropper, in the evening the pressure rose to 150/100, for me this is very high blood pressure, since my norm is 90/60. I stopped the drips and took these vitamins in tablets. I took tests again:
Potassium-3.7
Sodium-138
Chlorine-107
Magnesium-0.82
T3free-4.2
T4 free-13.6
TSH-1.12
While taking potassium and magnesium, once every three nights I still wake up with a rapid heartbeat of 85/90 beats, while my blood pressure is 120/80, such night awakenings are very uncomfortable, and basically they happen if there is minimal physical activity (cleaning the apartment, brisk walking). I went in for sports for 2.5 years (strength), but I only started doing cardio in the last 3 months; the attack happened during one of my cardio classes. After the attacks, I completely excluded sports.
After taking magnesium and potassium, a 2-day Holter study was done. Results:
Basic rhythm sinus
Maximum heart rate 124 beats per minute-load
Minimum heart rate 44 beats per minute at 08:55-sleep
Average daily heart rate 61 beats per minute
A total of 438 episodes of sinus bradycardia were recorded in the evening night and early hours with a minimum heart rate of 38 beats per minute at 09:33-sleep
Ectopic rhythm disturbances were detected:
-single ventricular extrasystole only 1, at 15:00
-single supraventricular extrasystoles 549 in total, including couplets - 128 in total, maximum 55 extrasystoles per hour at 20:00
-short paroxysms of supraventricular tachycardia (atrial) lasting from 3 to 9 complexes, heart rate up to 116-120 beats per minute
An asystole pause of 2.17 seconds at 09:33 seconds is an episode of 2nd degree AV block of the Mobitz type 2. The maximum PR interval is 1.61 seconds. No prolongation of the PQ and QT intervals was detected.
No diagnostically significant changes in the ST segment were detected. Raising the ST segment along the 2-3 artifact channel.
Now, in addition to mini-attacks of palpitations at night, chest pains have appeared, which worries me very much. For pain in the chest, I take Corvalol. Tell me, based on Holter decoding, how dangerous AV block is and all the rhythm disturbances identified in me.
On the ECG, the sinus rhythm is heart rate 60 per minute, vertical position of the EOS

Answers Bugaev Mikhail Valentinovich:

Hello. A heart rate of 80-90/min usually does not pose a danger, single extrasystoles in a small number too. If the transient 2nd degree AV block is type 1, then it requires only dynamic observation, but the appearance of 2nd degree AV block, type 2, may also require surgical intervention - implantation of a pacemaker. It is better for you to consult in person (with all available cardiograms) with a specialist who deals with these problems. You can send me all your cardiograms (scans or photos), [email protected].

2014-06-09 16:02:44

Olga asks:

Hello. My husband is 49 years old, height 182, weight 85 kg. He does not drink alcohol at all and has never smoked. He has an athletic build, he used to play tennis. He works in an office, there are frequent psycho-emotional stress at work, he is an introvert by nature. In April he complained of irregularities in his heart . According to the ECG, sinus rhythm, heart rate 59 per minute. Violation of intraventricular conduction, single ventricular extrasystoles 5 per 1 minute. Metabolic changes in the myocardium. Holter - heart rate from 53 to 144 average daily - 85, sleep - 59. Single polytopic gastric extrasystoles all measurements - 11949. Day - 9770, sleep - 2179. Paired gastric extrasystoles - 1 during the day. Single supra-gastric extrasystoles - 26, during the day - 15, sleep - 11. Pauses due to sinus arrhythmia - 92. Circadian index - 144% within normal limits. During the day, heart rate - 83% of possible. Heart rate tubulence is normal. Ischemic changes in ST were not detected. Amount of work performed on staircase tests 83%. results. Rhythm variability was preserved. Late atrial potentials were detected in 10% of cases. Analysis results were obtained in 46 cases out of 142. Late ventricular intervals were obtained in 80 cases out of 142. There were no signs of AV block. ECHO KG - slight mitral and tricuspid regurgitation. Grade 1 calcification of the aortic valve, its opening of 18 mm is normal. The walls of the aorta are hyperechoic, the right atrium is not enlarged, the right ventricle is 26 mm. There are no signs of impaired diastolic dysfunction of the left ventricle using the Doppler method. EF- 67%. Myocardial mass-LV-177, left stomach myocardial mass index. -86g/m2. Thickness of the IVS - in diastole - in mm - 10, thickness of the LVSD - in diastole - mm - 10. Right ventricle in mm - 26. The cardiologist prescribed: Etatsizin, one tablet. 3 times a day for one month, Panangin, Kudesan, Magnesium B6, Panangin and Mildronate intravenously. During treatment discomfort in the heart region passed on day 3. Holter during treatment - heart rate from 47 to 133. Single polytopic gastric extrasystoles - all measurements - 223. Day - 213, sleep - 10.. Single supragastric extrasystoles - 11. Pauses due to sinus arrhythmias - 26. Circadian index - 135% within normal limits. Heart rate tubulence is normal. Ischemic changes in ST were not detected. Tolerance to physical stress is high. During the day, an extension of the corrected QT interval is observed over 450 ms for 8 minutes (1% of the time). A positive result of alteration of T within 4 min. 10 sec. -2% of 2 hours 49 minutes 20 seconds. The maximum duration of sections with positive alteration is 1 minute. 10 sec..average -1 min..Rhythm variability was preserved.Late atrial potentials were detected in 32% of cases.Analysis results were obtained in 37 cases out of 140.Late ventricular intervals were obtained in 77 cases out of 140.Transient AV block 1st stage .total duration 9 hours, 28 minutes. 3 weeks after discontinuation of etatsizin, Holter results - heart rate from 48 to 145. Single polytopic gastric extrasystoles, all measurements - 11949. Day - 9941, sleep - 2981. Paired gastric extrasystoles - 2 during the day. Single supragastric extrasystoles - 24. Paired supra-2 stomachs. Paroxysm of supra-gastric tachycardia-1 appeared. Pauses due to sinus arrhythmia - 52. Circadian index - 138% within normal limits. Heart rate turbulence is normal. Ischemic changes in ST were not detected. The volume of work performed on staircase tests was 86% of the maximum for a given age. Submaximal heart rate was achieved in two cases. Exercise tolerance is high. During the day, a lengthening of the corrected QT is observed. interval over 450 ms for now 10 minutes (1% of time) Positive result of T alteration for 1 min. 10 sec. The maximum duration of sections with positive alteration is 1 min. 10 seconds. Rate variability was preserved. Late ventricular intervals were obtained in 75 out of 158 cases. There were no signs of AV block. After the last Holter, the cardiologist re-prescribed us with Etatsizin 1.3 times a day, saying that we would have to take it for several months or maybe constantly. Or maybe we will have to perform RFA. Currently, nothing bothers my husband. We read about AAP, we are afraid to continue taking etatsizin again, and especially for a long time. Now we are taking Novopassid, motherwort, Magnerot, Kudesan. We have undergone examinations: ultrasound of the thyroid glands - nodes of the lobes and isthmus. The result of the puncture is a cytogram of a cystic goiter. TSH-0.56 T4f-16.3 The endocrinologist said that treatment is not indicated, only observation, monitoring of hormones and ultrasound. Blood and urine tests are normal, FGDS - HR. gastritis remission. Ultrasound of internal organs without pathology. Cholecystectomy in 2011. K-4.7 Ca-2.62 Magnesium-1.05 zinc-11.5 copper- 15.3 Na 142 mmol/ l Prostatspecific. Antigen - 0.3. Lipidogram - triglycerides - 1.4 cholesterol - 5.7 CLDLP1.45 CLDLP - 3.68 CLDLP - 0.64 atherogenic index - 3.0. CT scan of the chest organs local fibrosis upper lobe right lung S 2 linear fibrosis single adhesions suffered from pneumonia in 2011. Heart of normal configuration, normal size. Signs of osteochondrosis from the musculoskeletal system. We went to another cardiologist, he said that we don’t need AAP, recommended to continue taking sedatives, ECG monitoring, Holter after 3 months , and further examination - VEM, and exclude opisthorchiasis, giardiasis. Diagnosis: Idiopathic rhythm disturbance, frequent ventricular extrasystole. Please advise whom to listen to? Isn’t it dangerous to perform VEM with such frequent extrasystoles? Should we take etacizin or limit ourselves? sedative therapy with dynamic monitoring? Now I feel good, nothing bothers me. Blood pressure is always stable 120/80 mmHg. In the evening we count the pulse from 9 to 5 extrasystoles per minute! How difficult is our situation and life-threatening, because there are so many extrasystoles, almost 13,000 per day? I don’t sleep, listen to him at night, and during the day I come up with reasons to call him, although I hide my secrets from him excitement. Thank you in advance for your answer. Olga.

Answers Bugaev Mikhail Valentinovich:

Hello. I would not prescribe etatsizin; if possible, I would do bicycle ergometry; if extrasystole becomes more frequent, do coronary angiography. At the same time treat the thyroid gland; its diseases often lead to rhythm disturbances. Ablation, I think, is not very promising, because the extrasystole is polymorphic, probably not from one focus. The first thing I would try is beta blockers.

2013-09-21 00:30:16

Natalya asks:

Hello! Please tell me, for the last three days I have begun to feel strong tremors from my chest that reach my throat, sometimes somewhere in my stomach, aggravated by sitting or lying down, and during physical activity they practically don’t happen or I don’t notice them. I didn’t have them before. I passed. many doctors, did a bunch of ECGs, ultrasounds of the heart besides sinus tachycardia I was not diagnosed with anything. I am seeing a neurologist with a diagnosis of somatoform dysfunction of the autonomic nervous system with paroxysms, panic attacks, and asthenic depressive syndrome. Ultrasound from 09/20/2013 THE ANATOMY OF THE HEART IS NOT CHANGED, TYPE 1 DIASTOLIC FUNCTION OF THE LEFT VENTRICLE IS DISTURBED. Holter dated September 20, 2013, ON THE BACKGROUND OF SINUS RHYTHM WITH WAKEHING HR 67-159 BPM (AVERAGE HR 92 BPM) AND NIGHT SLEEP HR 61-78 (AVERAGE HR 68 BPM) SINUS ARRHYTHMI DETECTED I AM WEAKLY EXPRESSIVE (MAX.PAUSE 1335 MSEC, NORMAL LESS THAN 2000 MSEC); AVERAGE DAY HEART RATE-UPPER LIMIT OF NORM; REDUCTION IN HEART RATE DURING NIGHT SLEEP IS ADEQUATE (AVERAGE DAILY HEART RATE NORMAL); SINGLE SUPRAVENTICULAR EXTRASYSTOLES, SINGLE (TOTAL 5/DAY); SINGLE VENTRICULAR EXTRASYSTOLES, MONOMOFORMAL, IN PATHOLOGICAL QUANTITY (TOTAL 10640 / DAY, ECTOPIC DENSITY 530 / HOUR), FREQUENT EVENTS OF ALLORHYTHMIA BY TYPE OF BI-, TRIGEMYNY; 1 EPISODE OF PAIRED POLYFORM VENTRICLE EXTRASYSTOLIA; DAY CIRCADIAN TYPE OF ECTOPIC ACTIVITY; ISCHEMIC CHANGES SAT-T E DETECTED. Tell me, is this very dangerous and can ventricular tachycardia develop? The prescribed beta blockers (Corvitol, Egilok, Atenolol) make it difficult to breathe. The ambulance gave anaprilin under the tongue a couple of times, and there seemed to be no difficulty in breathing. But the doctors don’t prescribe it to me. The cardiologist, not seeing the Holter results, prescribed Grandaxin, Panangin, to walk more, I move very little. I took tests: thyroid hormones are normal, FSH, LH, PROLACTIN are normal, biochemistry is normal, urine normal, general analysis blood hemoglobin 145, ESR 4, PLATELETS 350. THANK YOU SO MUCH in advance!

Answers Bugaev Mikhail Valentinovich:

Hello. The risk of developing ventricular tachycardia is not very high, but choose effective drugs costs. Try sotalol (under medical supervision!). And check your digestive system.

2013-04-16 12:03:04

Lilya asks:

Hello! Please help me, I don’t know where to turn anymore, I’m tormented by extrasystoles! It started in December, I noticed interruptions in my heart, I started getting examined, and before the ambulance took me, I had a stone in the ureter, they had surgery, when I was discharged from the hospital I went to the cardiology department for an examination, they examined me and discharged me without prescribing anything! I am writing the results of the examination - Ultrasound of the heart - Completion of the mitral valve leaflets, stage 1, without the presence of hemodynamically significant mitral regurgitation, a minor anomaly in the structure of the heart, an aneurysm of the sac, without the presence of a shunt, Ultrasound of the thyroid gland - structural abnormalities not detected! Biochemical blood test - vol. protein - 73.1; bilirubin: vol. - 14.81; pr - 3.57; nepr - 11.24; AST - 24.8; ALT - 19.4; creat. - 73.0; urine - 3 .16;K-3.36;Na-146.2;magnesium-0.96 (I was injected with cardioarginine, then I drank syrup for another month) Blood test for lipid spectrum: Chol.4.28;trigl-0.34;HDL -1.03;LDL-3.09;VLDL-0.1;k.a.-3.2) Blood glucose-4.86; blood test for sugar and acetone-negative! I did Holter 2 times, I’m writing the results are done in January: Conclusion: The main rhythm is sinus. Average daytime heart rate is 82 beats per minute, average nighttime heart rate is 68 per minute. During the monitoring period, a pause was recorded against the background of sinus rhythm (1 in total), lasting 2028 ms, at 03:11; 48 , also recorded were single supraventricular ES (total 48 per day), ventricular ES, monomorphic in the number of 272 (with RBBB graphics), IPV more than 0.85 Lown-1. Type of circulatory distribution of ectopic activity - daytime! Diagnostically significant depression of the ST segment " the ischemic type was not recorded! 2 Holter for April 10, 2013. Conclusion: The main rhythm is sinus. Average heart rate is 94 beats per minute, average nighttime heart rate is 73 beats per minute (pulse control is insufficient) Pauses 135 (max 2012 ms) at night, caused by AV blockade of the 2nd degree, type 1. During the monitoring, 42 supraventricular ES, 863 paired 3. Zhel.ES, monomorphic were recorded. Deviations of the ST segment of the “ischemic” type were not recorded.
Single supraventricular ES Total 42
Bigemeny/trigemeny/paired NVE Total Not detected
Happy NJE 7
Paired NHE 3
Group PVC; Total Not detected
Paroxysm of ventricular tachycardia Total Not detected
Single PVCs Total 863 (443 during the day, 420 at night)
Bigemeny/trigemeny/paired Total 1.
There are only 4 paired PVCs.
Please tell me how dangerous this is, I’m very worried, I can’t sleep normally, I also eat very poorly, I’m afraid of everything, I constantly listen to the work of my heart, I’m tired of all this, doctors prescribe a sedative and that’s it! I’m 27 years old, height 167, weight 47 kg!

Answers Bugaev Mikhail Valentinovich:

Hello. Nothing dangerous has been found in you at the moment, there is no need to prescribe antiarrhythmic drugs (especially considering the episodes of AV block), you just don’t need to focus on extrasystoles, everyone has them.

2013-03-27 06:38:06

Marina asks:

Good afternoon My mother is 64 years old. Here are the results of her examinations. ECHOCARDIOSCOPY: aorta: aortic root 27 mm (20-37), walls thickened, amplitude 6 (5-8).
pulmonary artery: trunk 19 mm (15-22;
atria: left - 35 mm (19-31), right - 42 mm (up to 48);
ventricles: - left - KSR-34mm (25-38), KSR -47ml (25-65), FV-62 (55-70), KDR -51mm (40-55), EDV - 124ml (70-150), FS-33 (28-45), UO -74 ml (70-90). Walls: ZSLZh - thickness 11 mm (7-11), amplitude -10 (8-13), homogeneous structure. IVS - thickness 10 mm (7-11), amplitude -4 (3-8), type of movement - normal, structure heterogeneous;
-right -25mm (up to 28)
Valves: - aortic - the leaflet structures are slightly compacted, the divergence in systole is 18 mm (16-22),
- mitral: the structure of the leaflets is slightly compacted, the movement of the leaflets is multidirectional, M-shaped, the value of the diastolic opening of the leaflets is 22 mm (21-31),
- tricuspid: the valves are not changed,
- pulmonary valve: the leaflets are not changed.
Dopplerography - MR 0-1CT, E/A=0.8.
The pericardium is not changed.
No local contractility disorders were detected, global contractility was normal.
HOLTER MONITORING: daily sinus rhythm with heart rate 37-132 per minute. Average daily bradycardia. Rate variability is increased. At night, frequent episodes of bradycardia and bradyarrhythmia. Rhythm pause up to 2072 ms. Frequent unstable paroxysms of tachycardia with a wide QRS complex with a heart rate of up to 170 per minute, possibly ventricular, lasting up to 1.5 seconds (3-4 cardiac cycles) are recorded. TOTAL 212, mixed circadian. An unstable paroxysm of atrial tachycardia with a heart rate of up to 150 per minute, lasting 7 seconds during the day, was recorded. Only 1.
Frequent one-night polytopic polymorphic ventricular extrasystoles are recorded. A total of 4065 mixed circadians, including interpolated ones, including those with retrograde impulse conduction to the atria. Episodes of bigemeny, trigemeny. Frequent paired ventricular extrasystoles. There are 1003 mixed circadians in total. Rare polytopic polymorphic supraventricular extrasystoles. Total 112.
NO significant ischemic ST changes were detected.
Diagnosis: hypertension Stage II, degree II, risk III, NRS. Paroxysmal tachycardia. Ventricular estrasystole IIIgr. according to LONW.XCH Stage I, NYHA FC II.
Consultation with an endocrinologist: changes in thyroid gland not identified.
For a long time, my mother took amiadorone, then cordarone. all, of course, as prescribed by the cardiologist. For the last 6-8 months, cordarone has been discontinued and sotalol, perindopril + indapamide have been prescribed. It is not always possible to take Sotalol, because the pulse is below 60-50 beats per minute. I would like to know your opinion about the prescribed treatment? None surgical interventions, at the last consultation with the cardiologist, was not suggested. Do you need a pacemaker? or RFA? What is your opinion on this matter?