Ventricular tachycardia symptoms. Unsustained tachycardia

In addition, when carrying out emergency therapy it is necessary to take into account the interaction of antiarrhythmic drugs with other drugs.

Great importance has an assessment of the effectiveness of drugs previously used to relieve rhythm disturbances. Thus, if a patient has traditionally been helped by the same drug, there is good reason to assume that the same drug will be effective this time.

In addition, in difficult diagnostic cases, the nature of rhythm disturbances can be clarified ex juvantibus. Thus, in case of tachycardia with wide QRS, the effectiveness of lidocaine indicates, rather, in favor of ventricular tachycardia, and ATP, on the contrary, in favor of nodal tachycardia.

Was there any fainting, suffocation, pain in the heart area, involuntary urination or defecation, cramps.

Need to identify possible complications arrhythmias.

• General principles of stopping paroxysm of ventricular tachycardia

  Even in the absence of certainty about the ventricular origin of wide complex tachycardia, its relief is carried out according to the principles of stopping paroxysm of ventricular tachycardia.

  • In case of severe hemodynamic disturbances, emergency electrical cardioversion is performed.
    • For synchronized cardioversion, a charge of 100 J is most often effective.
    • If during ventricular tachycardia the pulse and blood pressure are not determined, a 200 J discharge is used, and in the absence of effect - 360 J.
    • If immediate use of a defibrillator is not possible, cardioversion is preceded by a precordial shock, chest compressions, and artificial ventilation lungs.
    • If the patient loses consciousness (persistence or immediate relapse of ventricular tachycardia / ventricular fibrillation), defibrillation is repeated against the background of intravenous jet (in the absence of pulse - into the subclavian vein or intracardiac) injection of adrenaline, magnesium sulfate 10.0-20.0 ml of 20% solution (at 20.0 ml of 5% glucose solution for 1-2 minutes under the control of blood pressure and respiratory rate) followed by intravenous drip administration (in case of relapses) 100 ml of 20% magnesium sulfate solution per 400 ml of saline at a speed of 10 -40 drops/min.
    • If there is no effect, electrical pulse therapy is performed.
    • In the future (at the second stage), treatment tactics are determined by the preservation of left ventricular function, 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) in a slow stream under blood pressure control, or IV infusion at a rate of 30-50 mg/min to a total dose of 17 mg/kg.
      • Novocainamide is effective in 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!
      • In the future, after the first day of infusion, you can continue the maintenance infusion at a rate of 0.5 mg/min.
      • If a repeated episode of ventricular tachycardia or ventricular fibrillation develops, you can additionally administer 150 mg of amiodarone in 100 ml of 5% glucose solution over 10 minutes.
    • After stabilization of the condition, amiodarone is prescribed orally for maintenance therapy.
    • If there is no effect from the therapy carried out at the second stage, electropulse therapy is performed, or they move on to the third stage of treatment.
• STAGE 3
  • In patients with frequent relapses of ventricular tachycardia, especially with myocardial infarction, to increase the effectiveness of repeated attempts at electrical pulse therapy, bretylium tosylate (ornid) 5 mg/kg is administered intravenously for 5 minutes in 20-50 ml of saline.
  • If there is no effect after 10 minutes, you can repeat the administration at a double dose.
  • Maintenance therapy – 1-3 mg/min bretylium tosylate intravenously.

After stopping paroxysms of ventricular tachycardia, intravenous administration of antiarrhythmics and/or potassium supplements is indicated for at least 24 hours.

Paroxysmal tachycardia (PT) is an accelerated rhythm, the source of which is not the sinus node (normal pacemaker), but a focus of excitation that arises in the underlying part of the conduction system of the heart. Depending on the location of such a focus, atrial ATs, from the atrioventricular junction and ventricular ATs are distinguished. The first two types are combined with the concept “supraventricular or supraventricular tachycardia.”

How does paroxysmal tachycardia manifest?

An attack of PT usually begins suddenly and ends just as suddenly. The heart rate ranges from 140 to 220 - 250 per minute. An attack (paroxysm) of tachycardia lasts from a few seconds to many hours, in in rare cases The duration of the attack reaches several days or more. Attacks of PT tend to recur (relapse).

The heart rhythm during PT is correct. The patient usually feels the beginning and end of the paroxysm, especially if the attack is prolonged. Paroxysm of PT is a series of extrasystoles following each other with a high frequency (5 or more in a row).

High heart rate causes hemodynamic disorders:

• decreased filling of the ventricles with blood,
• decrease in stroke and cardiac output.

As a result, there is oxygen starvation brain and other organs. With prolonged paroxysm, spasm of peripheral vessels occurs, increases arterial pressure. An arrhythmic form of cardiogenic shock may develop. Coronary blood flow worsens, which can cause an attack of angina or even the development of myocardial infarction. Decreased blood flow to the kidneys leads to decreased urine production. Oxygen starvation of the intestines can manifest itself as abdominal pain and flatulence.

If PT exists for a long time, it can cause the development of circulatory failure. This is most typical for nodal and ventricular ATs.

The patient feels the onset of paroxysm as a push behind the sternum. During an attack, the patient complains of rapid heartbeat, shortness of breath, weakness, dizziness, and darkening of the eyes. The patient is often frightened and has motor restlessness. Ventricular AT can be accompanied by episodes of loss of consciousness (Morgagni-Adams-Stokes attacks), and can also transform into ventricular fibrillation and flutter, which can be fatal if left untreated.

There are two mechanisms for the development of PT. According to one theory, the development of an attack is associated with increased automatism of the cells of the ectopic focus. They suddenly begin to generate electrical impulses at a high frequency, which suppresses activity sinus node.

The second mechanism for the development of AT is the so-called re-entry, or repeated entry of the excitation wave. In this case, a similarity is formed in the conduction system of the heart vicious circle, through which the impulse circulates, causing rapid rhythmic contractions of the myocardium.

Paroxysmal supraventricular tachycardia

This arrhythmia can first appear at any age, most often in people between 20 and 40 years old. Approximately half of these patients do not have organic heart disease. The disease can cause an increase in sympathetic tone nervous system, which occurs during stress, abuse of caffeine and other stimulants, such as nicotine and alcohol. Idiopathic atrial PT can be triggered by diseases of the digestive system (peptic ulcer, cholelithiasis, etc.), as well as traumatic brain injury.

In another part of patients, PT is caused by myocarditis, heart defects, and coronary heart disease. It accompanies the course of pheochromocytoma (a hormonally active tumor of the adrenal glands), hypertension, myocardial infarction, lung diseases. Wolff-Parkinson-White syndrome is complicated by the development of supraventricular AT in approximately two thirds of patients.

Atrial tachycardia

The impulses for this type of AT originate from the atria. The heart rate ranges from 140 to 240 per minute, most often 160 to 190 per minute.

Diagnosis of atrial AT is based on specific electrocardiographic signs. This is an attack of rhythmic heartbeat that suddenly begins and ends at a high frequency. Before each ventricular complex, a modified P wave is recorded, reflecting the activity of the ectopic atrial focus. Ventricular complexes may not change or be deformed due to aberrant conduction through the ventricles. Sometimes atrial AT is accompanied by the development of functional atrioventricular block of the first or second degree. With the development of permanent atrioventricular block of the second degree with 2:1 conduction, the rhythm of ventricular contractions becomes normal, since only every second impulse from the atria is conducted to the ventricles.

An attack of atrial AT is often preceded by frequent atrial extrasystole. The heart rate does not change during an attack and does not depend on physical or emotional stress, breathing, or atropine intake. With a sinocarotid test (pressure on the area of ​​the carotid artery) or a Valsalva maneuver (straining and holding your breath), sometimes the heart attack stops.

The recurrent form of AT is a constantly repeating short paroxysms of heartbeat that last for a long time, sometimes for many years. They usually do not cause any serious complications and can occur in young, otherwise healthy people.

To diagnose PT, a resting electrocardiogram and 24-hour Holter electrocardiogram monitoring are used. More full information obtained during an electrophysiological study of the heart (transesophageal or intracardiac).

Paroxysmal tachycardia from the atrioventricular junction (“A-V nodal”)

The source of tachycardia is a focus located in the atrioventricular node, which is located between the atria and ventricles. The main mechanism for the development of arrhythmia is the circular movement of the excitation wave as a result of longitudinal dissociation of the atrioventricular node (its “division” into two paths) or the presence of additional impulse paths bypassing this node.

The reasons and methods for diagnosing A-B nodal tachycardia are the same as atrial tachycardia.

On the electrocardiogram, it is characterized by a sudden onset and ending attack of rhythmic heartbeat with a frequency of 140 to 220 per minute. P waves are absent or recorded behind the ventricular complex, while they are negative in leads II, III, aVF; the ventricular complexes are most often unchanged.

The sinocarotid test and the Valsalva maneuver can stop an attack of palpitations.

Paroxysmal ventricular tachycardia

Paroxysmal ventricular tachycardia (VT) – sudden attack frequent regular contractions of the ventricles with a frequency of 140 to 220 per minute. The atria contract independently of the ventricles under the influence of impulses from the sinus node. VT significantly increases the risk of severe arrhythmias and cardiac arrest.

VT is more common in people over 50 years of age, predominantly in men. In most cases, it develops against the background serious illnesses heart: with acute myocardial infarction, cardiac aneurysm. Sprawl connective tissue(cardiosclerosis) after a heart attack or as a consequence of atherosclerosis in coronary heart disease is another common cause of VT. This arrhythmia occurs in hypertension, heart defects, and severe myocarditis. It can be triggered by thyrotoxicosis, a violation of the potassium level in the blood, or bruises of the chest.

Some medications can provoke an attack of VT. These include:

• cardiac glycosides;
• adrenalin;
• procainamide;
• quinidine and some others.

Largely due to the arrhythmogenic effect, they are trying to gradually abandon these drugs, replacing them with safer ones.

VT can lead to serious complications:

• pulmonary edema;
• collapse;
• coronary and renal failure;
• cerebrovascular accident.

Often patients do not feel these attacks, although they are very dangerous and can be fatal.

Diagnosis of VT is based on specific electrocardiographic signs. There is a sudden onset and ending attack of frequent rhythmic heartbeat with a frequency of 140 to 220 per minute. The ventricular complexes are dilated and deformed. Against this background, there is a normal, much rarer sinus rhythm for the atria. Sometimes “captures” are formed, in which the impulse from the sinus node is nevertheless carried out to the ventricles and causes their normal contraction. Ventricular “traps” are a hallmark of VT.

To diagnose this rhythm disorder, resting electrocardiography and 24-hour electrocardiogram monitoring are used, which provide the most valuable information.

Treatment of paroxysmal tachycardia

If an attack of rapid heartbeat occurs for the first time in a patient, he needs to calm down and not panic, take 45 drops of Valocordin or Corvalol, and perform reflex tests (holding your breath with straining, inflating a balloon, washing with cold water). If palpitations persist after 10 minutes, seek medical attention.

Treatment of supraventricular paroxysmal tachycardia

To relieve (terminate) an attack of supraventricular AT, you should first use reflex methods:

• hold your breath while inhaling while straining (Valsalva maneuver);
• immerse your face in cold water and hold your breath for 15 seconds;
• reproduce the gag reflex;
• inflate the balloon.

These and some other reflex methods help stop an attack in 70% of patients.
The most commonly used medications to relieve paroxysm are sodium adenosine triphosphate (ATP) and verapamil (isoptin, finoptin).

If they are ineffective, it is possible to use procainamide, disopyramide, gilurhythmal (especially in PT due to Wolff-Parkinson-White syndrome) and other class IA or IC antiarrhythmics.

Quite often, amiodarone, anaprilin, and cardiac glycosides are used to stop the paroxysm of supraventricular PT.

If there is no effect of medication to restore normal rhythm, electrical defibrillation is used. It is carried out in the event of the development of acute left ventricular failure, collapse, acute coronary insufficiency and consists of applying electrical discharges that help restore the function of the sinus node. In this case, adequate pain relief and medicated sleep are necessary.

Transesophageal pacing can also be used to relieve paroxysm. In this procedure, impulses are delivered through an electrode inserted into the esophagus as close to the heart as possible. It's safe and effective method treatment of supraventricular arrhythmias.

In cases of frequently recurring attacks and ineffective treatment, surgical intervention is performed - radiofrequency ablation. It involves the destruction of the focus in which pathological impulses are produced. In other cases, the conduction pathways of the heart are partially removed and a pacemaker is implanted.

To prevent paroxysms of supraventricular PT, verapamil, beta-blockers, quinidine or amiodarone are prescribed.

Treatment of ventricular paroxysmal tachycardia

Reflex methods for paroxysmal VT are ineffective. Such paroxysm must be stopped with medication. To the means for medication interruption attacks of ventricular PT include lidocaine, procainamide, cordarone, mexiletine and some other drugs.

If medications are ineffective, electrical defibrillation is performed. This method can be used immediately after the onset of an attack, without using medications, if the paroxysm is accompanied by acute left ventricular failure, collapse, or acute coronary failure. Electric current discharges are used to suppress the activity of the tachycardia focus and restore normal rhythm.

If electrical defibrillation is ineffective, cardiac pacing is performed, that is, imposing a slower rhythm on the heart.

With frequent paroxysms of ventricular AT, installation of a cardioverter-defibrillator is indicated. This is a miniature device that is implanted into the patient's chest. When an attack of tachycardia develops, it performs electrical defibrillation and restores sinus rhythm.
To prevent repeated paroxysms of VT, antiarrhythmic drugs are prescribed: procainamide, cordarone, rhythmilene and others.

If there is no effect from drug treatment may be carried out surgery, aimed at mechanical removal areas of increased electrical activity.

Paroxysmal tachycardia in children

Supraventricular PT occurs more often in boys, while congenital heart defects and organic heart damage are absent. main reason such arrhythmia in children is the presence of additional conduction pathways (Wolf-Parkinson-White syndrome). The prevalence of such arrhythmia ranges from 1 to 4 cases per 1000 children.

In children younger age supraventricular PT is manifested by sudden weakness, anxiety, and refusal to feed. Signs of heart failure may gradually appear: shortness of breath, blue discoloration of the nasolabial triangle. Older children complain of palpitations, which are often accompanied by dizziness and even fainting. In chronic supraventricular PT, external signs may be absent for a long time until arrhythmogenic myocardial dysfunction (heart failure) develops.

The examination includes a 12-lead electrocardiogram, 24-hour electrocardiogram monitoring, and a transesophageal electrophysiological study. Additionally prescribed ultrasonography heart, clinical blood and urine tests, electrolytes, if necessary, examine the thyroid gland.

Treatment is based on the same principles as in adults. To stop an attack, simple reflex tests are used, primarily cold tests (immersion of the face in cold water). It should be noted that the Aschner test (pressure on the eyeballs) is not performed in children. If necessary, sodium adenosine triphosphate (ATP), verapamil, procainamide, and cordarone are administered. To prevent repeated paroxysms, propafenone, verapamil, amiodarone, and sotalol are prescribed.

In case of severe symptoms, decreased ejection fraction, or ineffectiveness of drugs in children under 10 years of age, radiofrequency ablation according to vital indications. If it is possible to control the arrhythmia with the help of medications, then the question of carrying out this operation is considered after the child reaches the age of 10 years. Efficiency surgical treatment is 85 – 98%.

Ventricular PT in childhood is 70 times less common than supraventricular PT. In 70% of cases, the cause cannot be found. In 30% of cases, ventricular AT is associated with severe heart diseases: defects, myocarditis, cardiomyopathies and others.

In infants, VT paroxysms are manifested by sudden shortness of breath, rapid heartbeat, lethargy, swelling and enlarged liver. At an older age, children complain of rapid heartbeat, accompanied by dizziness and fainting. In many cases, there are no complaints with ventricular AT.

Relief of an attack of VT in children is carried out using lidocaine or amiodarone. If they are ineffective, electrical defibrillation (cardioversion) is indicated. In the future, the issue of surgical treatment is being considered, in particular, implantation of a cardioverter-defibrillator is possible.
If paroxysmal VT develops in the absence of organic heart disease, its prognosis is relatively favorable. The prognosis for heart disease depends on the treatment of the underlying disease. With the introduction of surgical treatment methods into practice, the survival rate of such patients has increased significantly.

Extrasystole: causes, symptoms, treatment Extrasystole is a premature contraction of the entire heart or its parts under the influence of an extraordinary impulse. Such an extraordinary impulse appears...

Bundle branch block on ECG You can often find the term “bundle branch block” in the electrocardiographic report. The blockade can be complete or incomplete, cover the right...

Cardiac arrhythmia: what is dangerous, the main types of arrhythmias Arrhythmia is a disturbance of the heart rhythm, which is accompanied by the improper functioning of electrical impulses that cause the heart to beat…

Classification and causes of supraventricular extrasystole

Supraventricular extrasystole is special condition, directly related to heart rhythm disturbances. The disease is expressed in an extraordinary contraction of either the entire heart or its individual sections.

• Classification of the disease
• Causes
• Symptoms
• Diagnosis of the disease
• Treatment
• Possible complications
• Preventive measures and forecasts

Supraventricular extrasystole is also called supraventricular extrasystole, and it is characterized by premature impulses that occur in ectopic foci located in the atria.

Classification of the disease

In medicine, it is customary to classify supraventricular extrasystole according to several characteristic features:

According to the location of the outbreak:

• atrioventricular (occur in the septum between the atria and ventricles);
• atrial (occurs in upper sections hearts).

By frequency (per minute):

• group (several extrasystoles in a row are observed at once);
• single (up to five contractions are observed);
• multiple (from five extraordinary reductions);
• doubles (two in a row).

According to the number of emerging outbreaks:

• monotopic (there is one focus);
• polytopic (there are several foci).

By order:

• ordered extrasystoles (meaning the alternation of normal contractions with extrasystoles);
• disordered extrasystoles (implies the absence of any pattern in the alternation).

By time of appearance:

• early (appear during atrial contraction);
• medium (appears in the interval between contractions of the atria and ventricles);
• late (appear during contraction of the ventricles with complete relaxation of the heart).

Causes

There are several reasons that can lead to the development of supraventricular extrasystole:

1. Cardiac, that is, cardiac causes. These include the presence of diseases such as:
   • Ischemic disease. In this case, this is due to insufficient blood supply and oxygen starvation;
   • Myocardial infarction. The death of an entire section of the heart muscle occurs, which is subsequently replaced by scar tissue;
   • Cardiomyopathy. In such cases, damage to the heart muscle occurs;
   • Myocarditis. This is inflammation of the heart muscle;
   • Congenital/acquired heart defects (implies a violation of the structure of the heart);
   • Heart failure. Here we are talking about conditions when the heart is not able to fully perform its function of pumping blood.

1. Drug treatment. In this case, it is meant that the causes of the disease can be various drugs, which were taken by the patient, either uncontrollably or over a long period of time. Among these medications are the following:
   • drugs against arrhythmia (they can cause heart rhythm disturbances);
   • cardiac glycosides, which are aimed at improving heart function while reducing the load on it;
   • diuretics, which increase the production and excretion of urine.

1. Violations of the level of electrolytes, that is, a change in the existing proportions of the ratio of salt elements: potassium, magnesium, sodium.
2. Toxic effects on the body, namely, the effects of cigarettes and alcohol.
3. Disorders of the autonomic nervous system.
4. The presence of the following hormonal diseases:
   • diabetes mellitus (the pancreas is affected, which leads to disturbances in glucose metabolism);
   • adrenal gland diseases;
   • thyrotoxicosis ( thyroid releases an increased amount of hormones that have a destructive effect on the body).

1. Chronic oxygen starvation (hypoxia). This is possible if the patient has diseases such as sleep apnea (short-term stops in breathing during sleep), bronchitis, and anemia (anemia).
2. Idiopathic cause, that is, the case when the disease occurs without any reason.

Symptoms

Supraventricular extrasystoles are insidious in that they often do not have any pronounced symptoms.

Patients often do not have any complaints, and the disease proceeds unnoticed, but only for some time.

Supraventricular extrasystole may have the following symptoms:

1. Shortness of breath, feeling of suffocation.
2. Dizziness (this occurs due to decreased blood flow and oxygen starvation).
3. Weakness, increased sweating, discomfort.
4. Interruptions in the work of the heart (feeling of beats out of rhythm or even “reversals”).
5. "Hot flashes" without reason.

The most important and a common symptom the presence of the disease is a feeling as if the heart stops for a while. Most often this causes panic, anxiety, paleness, etc. in people.

Generally speaking, then ventricular extrasystole accompanies a large number of heart diseases. Sometimes it is associated with the presence of vegetative or psycho-emotional disorders.

Diagnosis of the disease

Diagnosis of the disease is based on the following points:

• Analysis of patient complaints, which refers to a feeling of “interruptions” in the work of the heart, general weakness and shortness of breath. The doctor will definitely ask how long ago all these symptoms appeared, what treatment was carried out previously, if any, and how the signs of the disease changed during this time;
• Analysis of anamnesis. The cardiologist must find out what operations and diseases the patient has had previously, what kind of lifestyle he leads, what bad habits he has, if any. Heredity is also important, namely, the presence of heart disease in close relatives;
• General inspection. The doctor feels the pulse, listens and taps the heart in order to identify any changes in the boundaries of the organ;
• Taking a biochemical analysis of blood, urine, analysis of hormone levels;
• ECG data. It is this moment that makes it possible to identify changes characteristic of the disease;
• Holter monitoring indicators. This diagnostic procedure involves the patient wearing a machine that performs an ECG throughout the day. In this case, a special diary is kept where absolutely all the patient’s actions are recorded. The ECG and diary data are subsequently compared, which makes it possible to identify unknown heart rhythm disturbances;
• Echocardiography data. The procedure allows us to identify the fundamental causes of the disease, if any.

Consultation with a therapist and cardiac surgeon is also important, so if you have the above symptoms, it is better to contact them along with a visit to a cardiologist.

Treatment

Treatment of supraventricular extrasystole has two types:

• conservative;
• surgical.

The choice of medication depends on the type of extrasystole and the presence/absence of contraindications to the drug.

Commonly prescribed medications include the following:

• etacizin;
• anaprilin;
• obzidan;
• allapinin;
• arrhythmil;
• verapamil;
• amiodarone.

Also, the doctor, at his discretion, can prescribe cardiac glycosides to the patient, which are designed to improve heart function while reducing the load on it. It is also possible to prescribe medications that lower blood pressure.

Surgical intervention is used only if there is a complete lack of improvement after taking it medicines from different groups. The operation is most often recommended for young patients.

Possible the following types interventions:

• Radiofrequency catheter ablation. Via major blood vessel a catheter is inserted into the atrium cavity, through which, in turn, an electrode is passed, cauterizing the altered area of ​​the patient’s heart;
• Open heart surgery, which involves excision of ectopic foci (those areas of the heart where an additional impulse occurs).

Possible complications

How dangerous is the disease? It can cause the following complications:

• Ischemic disease. In this case, the heart ceases to perform its function correctly;
• Change the structure of the atria;
• Create atrial fibrillation (that is, defective heart contractions).

Preventive measures and forecasts

• Maintain a rest regime, control the duration of sleep;
• Eat right, exclude spicy foods, fried, salty, canned foods from your diet. Doctors recommend eating more greens, fruits, and vegetables;
• Any medication intake should be carried out under the supervision of a specialist;
• Quitting smoking, alcohol;
• Contact a cardiologist at the first manifestation of symptoms of the disease.

In conclusion, I would like to note that if you consult a doctor in a timely manner and follow all norms and recommendations, patients are given a good prognosis.

Ventricular extrasystole (VC) is detected in almost all patients with MI. PVCs themselves do not have any significant effect on hemodynamics and myocardial perfusion. However, some of them indicate the presence of severe inhomogeneity of the LV myocardium, which can be the cause of other life-threatening arrhythmias: ventricular tachycardia (VT) and ventricular fibrillation (VF). Prognostically unfavorable PVCs, which are associated with a high risk of VT and VF, traditionally include:

Frequent PVCs (more than 30 per hour);

Polytopic and polymorphic ZhE;

Early PVCs (type “R to T”);

Paired PVCs;

Group and “volley” ZhE.

These types of PVCs are regarded as peculiar precursors of VT and VF. At the same time, in recent years it has been convincingly shown that other types of PVCs (for example, late PVCs) often precede VF. On the other hand, the listed types of “threatening” PVCs (including early, polytopic, paired and even group PVCs) are sometimes detected in young healthy individuals. This indicates that the question of the prognostic significance of ventricular extrasystole in patients with MI is still far from being resolved. In all likelihood, the appearance of any ventricular ectopic activity in a patient with myocardial infarction, especially in the first hours of the disease, should serve as a reason for the physician to be especially wary regarding the possibility of VF. At the same time, PVCs are not a reason for the immediate prophylactic administration of antiarrhythmic drugs (for example, lidocaine), as was believed quite recently, since the unjustified use of these drugs in patients with MI increases the risk of developing ventricular asystole and sudden cardiac death (R.

Campbell, 1975, V.A. Lyusov, 2000).

WITH for preventive purposesβ-blockers can be used (in the absence of contraindications for their use).

Ventricular tachycardia. Short episodes (“jogging”) of ventricular tachycardia (VT), consisting of several successive VVCs, do not affect hemodynamics, blood pressure levels and coronary blood flow and often go unnoticed by patients. As a rule, they are detected during ECG monitoring. Just like infrequent PVCs, they do not require special antiarrhythmic treatment, with the exception of the possible prescription of β-blockers.

Persistent VT with a rhythm frequency of 160–220 per minute can lead to an expansion of the zone of necrosis and myocardial ischemia, a decrease in the pumping function of the heart and peripheral hypoperfusion. Adverse outcomes of this form of VT are:

Pulmonary edema;

Arrhythmic shock;

VF development;

Syncope (fainting) up to the occurrence of typical Morgagni–Adams–Stokes attacks with loss of consciousness and convulsions.

In case of persistent VT, emergency relief of paroxysm is necessary. If the clinical situation allows, the following sequence of treatment measures can be used:

1. Punch to the chest. This technique often allows you to interrupt the pathological circulation of the excitation wave.

2. Drug relief of paroxysm. Lidocaine is administered intravenously as a bolus at a dose of 50 mg. If there is no effect after 2 minutes, the drug can be re-administered at the same dose. After stopping the paroxysm of VT, a slow intravenous infusion of lidocaine is prescribed at a dose of 100–150 mg.

3. If there is no effect from the administration of lidocaine, electrical cardioversion is performed (see.

chapter 3). Remember

If persistent paroxysm of VT is accompanied by pulmonary edema, cardiogenic shock, or loss of consciousness, electrical cardioversion is immediately performed after delivering a precordial blow with the fist. After stopping the paroxysm of VT, lidocaine is administered intravenously for 24 hours. Sometimes attacks of VT can be stopped with the help of rapid programmed electrical stimulation of the heart (see Chapter 3).

Ventricular fibrillation (VF) is clinically characterized sudden loss consciousness, absence of heart sounds and arterial pulse. Blood pressure is not determined. Agonal breathing occurs, which soon stops completely (clinical death). There are:

Primary fibrillation, which develops in the first minutes and hours of MI. Primary VF accounts for about 80% of all cases of this complication;

Secondary VF, which occurs a few days after the onset of MI and is usually combined with acute left ventricular failure and/or cardiogenic shock;

Late VF, which develops at 2–6 weeks of the disease.

The most unfavorable prognosis is secondary VF.

Remember

The only treatment for VF is emergency electrical cardioversion. In patients with MI, a shock of 200–300 J is usually used. In case of successful defibrillation, the patient is administered intravenous bolus lidocaine (50 mg), and then intravenous drip at a rate of 2 mg/min for 24 hours. The risk of recurrence of VF and sudden death in patients who have undergone successful cardioversion, it is extremely high.

Myocardial infarction

Ventricular paroxysmal tachycardia. Short bursts of ventricular tachycardia may be well tolerated and do not require treatment, but longer episodes may cause hypotension and heart failure. Lidocaine is the first choice of medication, but there are several other medications that may also be effective. An initial dose of lidocaine of 1 mg is usually given. kg-1 intravenously, half of this dose is repeated every 8-10 minutes, reaching a maximum of 4 mg. kg-1. This may be followed by intravenous infusion to prevent relapse. Electropulse therapy is indicated if hemodynamically significant ventricular tachycardia remains stable. Sale of used used Opel Insignia cars.

It is important to distinguish true ventricular tachycardia from accelerated idioventricular rhythm, a usually harmless consequence of reperfusion, in which the ventricular rate is below 120 beats. min.

Ventricular fibrillation. If you have a defibrillator, you should defibrillate. If it is not there, then it is worth striking a sharp blow to the lower third of the sternum. Follow the recommendations of the European Society for Resuscitation (Fig. 1).

SUPRAVENTRICULAR ARRHYTHMIAS

Atrial fibrillation is a complication in 15-20% of myocardial infarctions and is often associated with severe left ventricular damage and heart failure. Usually it stops on its own. IN different cases it can last from several hours to several minutes, very often with relapses. In many cases, the ventricular rate is not very fast, the arrhythmia is well tolerated, and no treatment is required. In other cases, a fast rhythm contributes to heart failure and requires immediate treatment. Digoxin is effective in reducing the rhythm in many cases, but amiodarone may be more effective in stopping the arrhythmia. Electropulse therapy can also be used, but should be used selectively only if relapses become more frequent.

Other forms of supraventricular arrhythmias are rare and usually self-limiting. They may react when pressure is applied to the carotid sinus. Beta blockers may be effective if no contraindications However, verapamil is not recommended. If the arrhythmia is not well tolerated, electrical impulse therapy should be tried.

SINUS BRADYCARDIA AND HEART BLOCK

Sinus bradycardia often occurs in the first hour, especially with inferior myocardial infarction. In some cases, as a result of the action of narcotic drugs. It may be accompanied by severe hypotension, in which case atropine should be used intravenously, starting with 0.3-0.5 mg, repeating until a total dose of 1.5-2.0 mg is administered. Later, during the treatment of myocardial infarction, it is a favorable sign and does not require treatment. Sometimes, however, it can be combined with hypotension. If there is no response to atropine, then short-term pacing may be advised.

VENTRICULAR OR VENTRICULAR FIBRILLATION

PAROXYSMAL TACHYCARDIA WITH NO PULSE

Ventricular fibrillation and ventricular tachycardia - basic principles and diagnostic criteria

Ventricular fibrillation and ventricular tachycardia –

Basic provisions and diagnostic criteria

G.G.Ivanov, V.A.Vostrikov

Department of Cardiology, National Research Center MMA named after. I.M.Sechenova,

The presented work discusses the validity of the formulation of electrocardiographic conclusions in tachysystolic forms of ventricular arrhythmias and differential diagnosis with ventricular fibrillation. The results of studies of ventricular fibrillation and its stages are illustrated, and the most typical ECG examples are given.

Fibrillation, i.e. frequent (more than 300 pulses/min.) non-rhythmic disorganized electrical activity of the atria or ventricles (VF), is the movement of multiple waves of excitation along a random path. Constantly encountering areas that are partially or completely impervious to excitation, they are forced to constantly change the direction of movement in search of excitable tissue. Despite more than a century of research, the mechanisms of the onset and maintenance of VF remain largely unexplored. Experimental and clinical researches, as well as work using mathematical modeling that complements previously existing electrophysiological data on the genesis and mechanisms of development of heterogeneity in the electrical properties of the myocardium, which underlie the disturbance of the excitation wave front during the development of VF.

Everyday clinical practice indicates that VF, as a rule, is an irreversible process and requires cardiopulmonary resuscitation and defibrillation. In patients with primary cardiac pathology, VF, when detected early during the provision of first aid at the prehospital stage, accounts for up to 60-80% of cases of sudden cardiac arrest (SCA), with prolonged SCA - about 40%. Such a significant decrease in VF registration during prolonged SVO is associated with its transformation into asystole. Only at

7-10% of patients record sustained ventricular tachycardia (VT) with a high heart rate, the so-called, as the initial rhythm leading to cardiac arrest. VT without pulse. Brady-asystole, depending on the start of monitoring of a patient with sudden cardiac arrest, is observed in ≥ 20-40% of patients. It should be noted that about 80% of cases of SCA caused by VF/VT occur in the prehospital stage and less than 20% occur in hospitals and other medical institutions.

In recent years, a number of researchers have become interested in the problem of spontaneously reversible VF. The cases of spontaneous cessation of VF presented in published articles, unfortunately, often do not give an accurate idea of ​​the type of tachyarrhythmia being illustrated: whether it is true VF or one of the varieties of polymorphic VT with a high frequency of ventricular contractions, for example, “pirouette” VT. The authors do not provide data on the frequency and amplitude of the main fibrillary oscillations and their dynamics during a long-term (≥ 60 s) course of possible VF; do not indicate the relationship between VF amplitude and EGC characteristics before and after fibrillation. Electrocardiographic data are often presented in one lead (mainly the results of Holter ECG monitoring), from which it is quite difficult to assess the true type of tachyarrhythmia (amplitude and duration of oscillations). In this regard, both theoretical and practical points of view deserve discussion. next questions: 1) is spontaneous recovery of ventricular fibrillation possible in an adult? If this is possible, then at what stage of VF and what electrophysiological mechanisms underlie spontaneous cessation; 2) whether the VF pattern in a person can be attributed to the VT pattern (especially when recorded in one lead), or should they be separated, classifying VT as an early stage of VF. 3) for all controversial cases, it is advisable to use such definitions as VT/VF or VF/VT.

As N.L. Gurvich pointed out in his monograph, FZh is distinguished by continuity of uncoordinated excitation. which is supported by random and intermittent excitations individual elements and irregular activation of the myocardium with the appearance of multiple small waves, while VT is characterized, in general, by the remaining synchrony of the process of activation and contraction. It has been established that when true VF develops rapidly complete desynchronization of myofibril contractions, while in all types of VT their minimal synchrony and coronary blood flow, as a rule, are preserved.

Paroxysmal monomorphic ventricular tachycardia (MVT) ) . Definition: VT is a series of 3 or more consecutive wide QRS complexes. Paroxysmal MVT usually occurs after ventricular extrasystole (PV) or against the background of an increase in the general rhythm. In addition, VTs are often preceded by frequent or paired VTs. VT is considered stable if the paroxysm lasts more than 30 s. The heart rate (HR) during paroxysmal VT is usually in the range of 140-220 per 1 min (Fig. 1).

The QRS complex is widened (> 0.12 s), the ST segment and T wave are directed opposite to the QRS complex. There are no fixed P waves before the QRS. VT, which develops according to the reentry mechanism (circulation of excitation around the anatomical block) has the form of monomorphic tachycardia. This is due to the fact that the excitation wave front circulates along a fixed path from cycle to cycle

Figure 1. Examples of monomorphic VT (top row) -150 per minute and bottom - 200 per minute (arrow indicates 1 sec)

Paroxysmal polymorphic VT (PVT) . Bidirectional fusiform VT (BDVT) or ‘torsade de pointes’ (“pirouette”) . DVVT is characterized by periodic changes in direction electrical axis ventricular QRS complex. This is accompanied by a change in the same ECG lead in the shape and direction of the main teeth of the QRST complex to the opposite. Heart rate usually ranges from 150 to 250 bpm; the rhythm is irregular with fluctuations in R-R intervals of ≥ 0.20-0.30 s (Fig. 2a).

Rice. 2b. Jog VT starting with early VT (D)

Not all polymorphic ventricular tachycardia - “torsade de pointes”. Polymorphic (multiform) VT must be differentiated from ventricular fibrillation. The incidence of multiforme VT varies from 150 to 250 per minute Often progresses to ventricular fibrillation; unlike VF, it often stops spontaneously.

Rice. 3 Multiform VT

A number of researchers have noticed that single ventricular ectopic complexes with very short clutch interval initiate a quick polymorphic ventricular tachycardia, which then transforms into VF. Pause-dependent polymorphic arrhythmias have also been described. Most authors are inclined to believe that the re-entry mechanism underlies the pathogenesis of idiopathic VF. There are opinions that the focus of arrhythmogenesis is located in the anterior wall and outflow tract of the right ventricle.

Ventricular flutter . During the development of flutter, the ECG records large ventricular waves of large amplitude and width, resembling a sinusoid, in which the individual teeth of the QRST complex are not differentiated.

Drawing. 4 Ventricular flutter with heart rate 200/min

Most often, the need for emergency care occurs with hemodynamically ineffective cardiac arrhythmias, when heart contractions are not able to provide adequate cardiac output. Emergency conditions also include those types of arrhythmias that, being hemodynamically effective at the time of occurrence, can quickly lead to circulatory arrest. Hemodynamically ineffective arrhythmias are primarily ventricular fibrillation, regarded as circulatory arrest with the appropriate diagnosis and measures described above. Then - ventricular paroxysmal tachycardia, accompanied by severe hemodynamic disturbances: without treatment, most often it turns into ventricular fibrillation. Hemodynamic disorders requiring emergency care are also observed with tachyforms atrial fibrillation, paroxysmal supraventricular tachycardia, frequent extrasystoles (especially ventricular), as well as severe bradycardia (sick sinus syndrome, complete AV block).

Life-threatening tachyarrhythmias

General considerations emergency diagnostics and treatment of tachyarrhythmias are as follows.

1. It is necessary to clearly distinguish between the concepts: stopping an attack and slowing down the heart rate. Stopping an attack is a set of recovery measures sinus rhythm. The goal of reducing the attack is to slow down the frequency of ventricular contractions.

2. The differentiation of concepts helps to make the right decision about the need to stop an attack. An attack definitely needs to be stopped immediately if it is accompanied by severe hemodynamic disturbances, namely: cerebral phenomena (fainting, Morgagni-Edams-Stokes attack) or cardiac phenomena (pulmonary edema, acute coronary insufficiency, arrhythmogenic shock). If there are significant but non-life-threatening signs of hemodynamic disturbance (moderate arterial hypotension, moderate shortness of breath, etc.), the advisability of emergency relief of the attack is questionable. In this situation, it is preferable to consider the issue of reducing the heart rate with a subsequent attempt to stop it in a specialized hospital.

If the attack is not accompanied by obvious hemodynamic disturbances, it is recommended to transport the patient to a specialized hospital.

3. Most patients tolerate attacks of tachyarrhythmia poorly, especially if they occur rarely or this is the first attack in the patient’s life. Therefore, when assessing the need for its relief, it is important not to confuse the patient’s subjective feelings with objective examination data.

Conditions that require urgent relief or reduction of an attack will be discussed below. Some measures can lead to a slowdown in the rhythm and to stopping the attack.

Criteria for the diagnosis of life-threatening tachyarrhythmias:

patient complaints

palpitations, feeling like “your heart is beating in your throat” and “ready to fly out of your chest”;

weakness;

chest pain;

dizziness;

darkening of the eyes;

sweating;

urge to urinate and defecate;

inspection data

rapid heart rate (usually 150 per minute) can be either rhythmic or irregular;

decrease in blood pressure (from moderate hypotension to significant, accompanying arrhythmogenic shock);

shortness of breath, tachypnea, orthopnea;

discharge of foamy sputum (white or pink) with pulmonary edema;

bulging and pulsating neck veins.

Types of life-threatening tachyarrhythmias:

paroxysmal ventricular tachycardia;

frequent ventricular extrasystole and ventricular tachycardia;

paroxysmal supraventricular tachycardia;

frequent supraventricular extrasystole and jogging supraventricular tachycardia;

atrial tachyarrhythmia (atrial fibrillation and flutter with a rapid ventricular rhythm) can be of regular and irregular shape.

Differential diagnosis

There is no doubt that diagnosing a variant of tachyarrhythmia is difficult in the absence of the ability to register an ECG. Nevertheless, such situations may occur. The data in the table below will help determine the approximate type of tachyarrhythmia without ECG diagnostics. To use the table, you must first perform the following diagnostic procedures:

give the patient a horizontal position (or as close as possible if the patient does not tolerate it well);

palpation and counting the pulse simultaneously with auscultation of heart sounds for 3–4 minutes;

determination of venous pulse in the jugular veins;

auscultation of bowel sounds;

reflex stimulation of the vagus - performing vagal techniques.

Notes

1. The coincidence of venous pulsation with heart contractions during supraventricular tachycardia is caused by the presence of a focus of excitation in these types of tachycardias above the AV node or in it itself, therefore both the ventricles and atria are stimulated with the same frequency. With ventricular tachycardia, the source of excitation is located below the AV node and its impulses are blocked in the AV node, so the atria contract at a slower rhythm - the coincidence of venous pulsation with heart contractions is not observed.

2. With ventricular tachycardia, the appearance of a loud, “cannonball” tone is associated with periodic random coincidences of the rhythm of the atria and ventricles.

3. With frequent extrasystole and jogging tachycardia, ventricular and supraventricular, clinical diagnosis is approximately similar to that for paroxysms. Longer auscultation makes it possible to identify moments of arrhythmias and evaluate them according to the relevant criteria indicated in the table.

4. It must be borne in mind that even the most accurate clinical diagnosis of tachyarrhythmias is not a reason to refuse an ECG study. If an attack of tachyarrhythmia occurs, it is necessary to do an electrocardiogram!

ECG signs of life-threatening tachyarrhythmias are shown in the table.

Notes

1. Widening and distortion of the QRS complex, called aberration, can also be observed with supraventricular tachycardias the following reasons: initial disturbance of intraventricular conduction, Wolff-Parkinson-White syndrome, as well as due to the development of functional ventricular block during an attack. This type of tachycardia is called supraventricular tachycardia with aberrant conduction.

2. Supraventricular tachycardia with aberrant conduction can be distinguished by clinical signs indicated in this table, as well as when compared with previous electrocardiograms. Further, ventricular tachycardias, in contrast to supraventricular tachycardias with aberrant conduction, are characterized by a more significant widening of the complex (over 0.14 s) and a sharp deviation of the electrical axis to the left.

3. ECG signs of frequent extrasystoles and tachycardia runs are identical to those of paroxysms, with the exception of their inconsistent registration on the ECG.

List and sequence of actions:

registration and subsequent monitoring of ECG;

determine the type of arrhythmia;

prepare the defibrillator for use;

blood pressure monitoring;

provide venous access (peripheral or central);

call a specialized team or an ambulance;

stop an attack or slow down the heart rate;

in parallel, carry out symptomatic therapy depending on the patient’s condition (described above for the corresponding clinical conditions).

An algorithm for stopping attacks accompanied by severe hemodynamic disturbances is presented on p. 526.

ALGORITHM FOR TERMINATION OF SEIZURES WITH SPECIFIC HEMODYNAMIC DISORDERS

Notes

1. Simultaneously with urgent measures to stop the attack, it is necessary to call a specialized team or an ambulance team.

2. Be sure to find an opportunity for cardioversion!

3. If, as a result of the measures, an acceptable decrease in heart rate is achieved (subject to stabilization of hemodynamic parameters), it is not recommended to restore the rhythm at any cost outside a specialized hospital.

Cardioversion

Cardioversion is an electrical pulse therapy for arrhythmias, which differs from defibrillation in the following ways: it is carried out, as a rule, when the patient is conscious; requires premedication and anesthesia; may be accompanied by certain types of complications.

Indications for cardioversion outside a specialized department:

treatment of life-threatening arrhythmias accompanied by severe hemodynamic disturbances;

treatment of life-threatening arrhythmias accompanied by moderate hemodynamic disturbances, when drug treatment is impossible (lack of medications, individual allergic reactions of the patient) and there is a clear threat of deterioration of the patient’s condition.

Cardioversion is performed in the same way as defibrillation, but cardioversion requires short-term superficial anesthesia, which can cause complications characteristic of it (for example, respiratory arrest). In addition, it is preferable to perform cardioversion in synchronized mode. This mode implies synchronization of the discharge with the R wave on the ECG, thereby eliminating the discharge from entering dangerous period(T wave). Modern defibrillators have an automatic synchronization system. In some clinical situations, when, for example, a paroxysm of ventricular tachyarrhythmia is accompanied by fulminant pulmonary edema or arrhythmogenic shock, cardioversion, as an exception, can be performed without prior anesthesia.

Note

Complications of cardioversion are associated with anesthesia (nausea, vomiting, bronchospasm, respiratory arrest, hypotension) and defibrillation (skin burns, fever, secondary rhythm and conduction disorders, thromboembolism).

Drug relief of tachyarrhythmia attacks

Basic therapy for all tachyarrhythmias is aimed at creating an electrolyte bed for the action of antiarrhythmic drugs, since with a deficiency of potassium and magnesium their action is less effective. It is advisable to carry out all antiarrhythmic measures against the background of infusion of a polarizing mixture of the following composition:

1 g of potassium chloride + 200 ml of 5% glucose solution + 10 units of insulin, IV drip at a rate of 25–30 drops per minute.

You can add 3-5 ml of 25% magnesium sulfate solution to the mixture.

Note

Schemes for drug relief of ventricular and supraventricular tachyarrhythmias, tachyforms of atrial fibrillation are presented on p. 529, 530 and 531.

Note on the scheme for drug relief of ventricular tachyarrhythmias

Isoptin is not recommended to be further diluted: dilution leads to its inactivation by whey proteins (already quite quickly) and sharply reduces its stopping activity. If necessary, isoptin can be administered several times at intervals of 5–10 minutes until a total dose of 60 mg is reached.

Note on the scheme for drug management of supraventricular tachyarrhythmias

If visualization of the arrhythmia is impossible (there is no technical possibility for ECG diagnostics or it is difficult to determine the type of arrhythmia from the ECG), and also if there is no possibility for it specific treatment(no antiarrhythmic drugs, venous access, etc.), then the following actions are recommended:

calling a specialized team or an ambulance team;

precordial blow (with a fist on the middle third of the sternum);

reflex stimulation of the vagus – vagal methods;

oral potassium saturation - give the patient 80-100 ml of a 10% solution of potassium chloride to drink at once, or Panangin - 4 tablets at a time, or - 10 ml IV in a stream (can be in a solution of 10 ml of 5% glucose). If necessary oral administration potassium can be repeated after 15–20 minutes, remembering that it is almost impossible to overdose on potassium when taken orally;

Corvalol or Valocordin - 50-60 drops in sugar or dissolved in water.

Notes

1. Before ECG diagnosis of the type of arrhythmia, it is not recommended to administer specific antiarrhythmic drugs, since there is no universal antiarrhythmic drug, and almost blind administration of an antiarrhythmic drug can significantly worsen the patient’s condition.

2. One of the frequently used antiarrhythmic drugs is procainamide, which is not included in these regimens for stopping arrhythmias. The reason is the pronounced side effects of the drug, one of which is acute hypotension. Although novocainamide is used with great success to relieve various kinds arrhythmias, it is preferable to use it in specialized hospitals, where there is everything necessary for leveling side effects. In urgent situations, about which we're talking about in this chapter, when there are already pronounced hemodynamic disturbances, and the possibilities for their relief are limited, the use of this drug, as many authors believe, is dangerous and inappropriate.

Methods of reflex stimulation of the vagus (vagal techniques)

Valsalva maneuver:

straining, trying to exhale with a closed glottis.

Cermak–Goering maneuver:

alternate massage of the carotid sinuses located below the angle of the lower jaw at the level of the upper edge of the thyroid cartilage, where pulsation of the carotid arteries is usually palpated. It is preferable to start on the left side, which is richer in nerve endings.

Muller's maneuver:

Danini-Aschner maneuver:

pressing on the eyeballs. This technique is a subject of debate, since it is impossible to accurately calculate the safe force and duration of pressure, which can lead to retinal detachment. Most authors do not recommend using this technique.

Inducing the gag reflex:

mechanical irritation of the pharynx.

Life-threatening bradyarrhythmias

Decrease in heart rate, requiring urgent measures, in clinical practice observed much less frequently than tachycardia. Not every severe bradycardia is an indication for emergency care. The main criterion for the need to provide emergency treatment for bradycardia is hemodynamic disorders.

Most often, bradycardia develops gradually. However, there are also acute clinical situations, for example acutely developed complete AV block(for myocardial infarction, acute myocarditis, etc.), sinus bradycardia with SSSU with a heart rate of less than 40, leading to fainting-convulsive syndrome (Morgagni-Edams-Stokes). Such conditions require emergency assistance due to increased heart rate.

In any case, bradycardia recorded in the patient (heart rate less than 60 per minute) is a direct indication for examination and identification of its causes.

Absolute indications for emergency treatment of bradycardia

Fainting-convulsive attacks (Morgagni - Edens - Stokes). A single attack that ends on its own, as a rule, does not worsen the patient’s condition. The need for emergency care most often occurs when there are several attacks following one after another with short time intervals (see below), or if severe bradycardia is recorded immediately after the attack.

Low heart rate of any nature, accompanied by severe hemodynamic disturbances.

Moderate bradycardia (40–60 per minute) with a tendency to progression (decrease in heart rate), accompanied by a deterioration in the patient’s hemodynamic status.

General considerations for the diagnosis and treatment of life-threatening bradyarrhythmias

To treat bradyarrhythmias, medications and cardiac pacing are used. It is better to start emergency care with drug therapy, and here's why.

Firstly, unlike cardioversion, cardiac pacing (both invasive and external) requires special equipment, which non-specialized institutions are unlikely to have; skills are also required to carry out this manipulation - most doctors do not have them. Therefore, when life threatening bradycardia, it is necessary to call a specialized team and immediately begin medication to increase the heart rate.

Secondly, the most commonly used temporary endocardial pacing is an invasive procedure, therefore it is possible serious complications. External cardiac pacing does not have these disadvantages, but the equipment for its implementation is not yet available in many clinics, and in addition, it is less effective than endocardial pacing.

Thirdly, many bradycardias can be stopped quite successfully and quickly with medication. Achieving an acceptable heart rate (usually about 50) allows you to gain time and arrange for the patient to be transferred to a specialized hospital, where they will conduct a detailed examination and determine the advisability of cardiac pacing (temporary or permanent). Sometimes an increase in heart rate even by 5–6 per minute is enough to stabilize his hemodynamic status.

General activities:

ECG registration and monitoring;

blood pressure monitoring;

ensuring venous access, peripheral or central (in parallel with the previous steps, call a specialized team with the necessary skills and equipment for temporary cardiac pacing);

drug treatment of bradycardia according to the scheme (in parallel - symptomatic therapy according to the patient's condition, described above for the relevant clinical conditions).

Hemodynamic disorders requiring emergency care most often occur when the ventricular rate is 40 or lower. Such bradycardia can be observed with the following conduction and automaticity disorders:

idioventricular rhythm with complete AV block (AV dissociation);

failure of the SA node, when replacement rhythms are caused by impulse formation from low-lying pacemakers (with SSSS);

severe sinus bradycardia (rarely, most often with an overdose of drugs or SSSS).

Diagnosis criteria:

patient complaints

severe weakness;

dizziness;

heaviness in the head;

darkening of the eyes, fog before the eyes, various vision disorders (grids, floaters, etc.);

presyncope and fainting, up to attacks of MES (see below);

chest pain;

inspection data

decreased heart rate (most often 40 or less);

decrease in blood pressure ( NB! in some cases it may be increased);

swelling of the neck veins;

shortness of breath, dry cough, orthopnea;

pale skin, cyanosis of mucous membranes, acrocyanosis.

A Morgagni–Edems–Stokes attack is a clinical expression of acute cerebral hypoxia and is characterized by the following symptoms: unexpected loss of consciousness (without warning signs and gradual deterioration in well-being); epileptiform seizures. An attack is most often (but not always!) provoked by exercise stress, it usually lasts several minutes and disappears on its own or (depending on the cause of its occurrence) may result in circulatory arrest.

NB! MES attacks can occur not only with bradycardia.

The main causes of an attack of MES

Ventricular asystole for more than 5–10 seconds, caused by a failure (stop) of the SA node before the generation of impulses from lower order pacemakers begins, as well as when rhythms change (for example, at the end of a paroxysm of tachyarrhythmia, when the SA node fails to keep up for several seconds start work or if it turns on on time, but the pulse frequency is low).

Chronotropic heart failure: when there is no increase in heart rate adequate to physical activity.

Note

MES attacks are not easily distinguished from other forms of disorders of consciousness accompanied by motor disorders. It is rare that it is possible to record electrical activity heart at the time of the attack, and after its end there may not be any pathological ECG changes. Therefore, any episode of MES should serve as a basis for hospitalization and a detailed examination of the patient.

The drug treatment regimen for life-threatening bradycardia, regardless of its type, is presented on p. 537.

Notes

1. In the absence of the above drugs, you can use Zelenin drops (the so-called Kremlin drops) containing belladonna: 30-40 drops per dose, and if there is no effect, repeat the dose 3-4 times every 10-15 minutes.

2. You should remember about the possibility of drug-induced bradycardia. Drugs that can cause it should be discontinued immediately. These include cardiac glycosides, almost all antiarrhythmic drugs, beta blockers, etc. Cardiac glycosides are especially dangerous, since bradycardia that develops as a result of glycoside intoxication is difficult to correct with medication.

If there is no possibility of treating bradyarrhythmia and the patient’s condition is progressively deteriorating, a supportive method can be used. closed massage hearts. If it is possible for ECG monitoring, then massage shocks are performed during the ECG pause between individual ventricular contractions, thereby replenishing (replacing) the missing contractions. The indirect massage technique is described above. If there is no possibility for ECG monitoring, then massage shocks are performed rhythmically with a frequency of about 40–50 per minute.

| |

Heart disease is the leading cause of death worldwide. Ventricular paroxysmal tachycardia (ICD-10 code – I47.2) is considered especially dangerous. Without medical care pathology disrupts circulatory function and reduces human life expectancy.

What is paroxysmal tachycardia

A type of arrhythmia caused by the activation of frequent electrical impulses in the ventricles or interventricular septa, called Bouveret's disease or ventricular paroxysmal tachycardia (VPT).

The disease leads to a sudden increase in heart rate to 140-200 beats per minute.

In various forms, pathology is diagnosed in 20-30% of patients of all ages. In older people, it is caused by organic changes in the myocardium; in young people, tachycardia is functional in nature. GPT occurs more often in men.

Features of the ventricular form

The coordinated work of the atria and ventricles and the production of electrical impulses are regulated by the His bundle. With ventricular ventricle, the excitation wave covers the left ventricle, then, with great delay, moves to the right and spreads along it in the usual way.

Due to the change in wave duration, the repeated impulse appears too early, a process of repolarization occurs - the work of the ventricles and atrium becomes uncoordinated (dissociated). The paroxysm begins and ends suddenly.

Depending on the location of generation of electrical discharges, three forms of the disease are distinguished:

• atrial;
• atrioventricular;
• ventricular

The first two are combined into one group under common name supraventricular or supraventricular paroxysmal tachycardia. The ventricular form of the pathology accelerates the pulse to a maximum of 200 beats per minute, but diagnostic tests with excitation are negative.

Supraventricular paroxysmal tachycardia occurs in 6-10% of patients. Leads to increased heart rate up to 250 beats per minute. In this case, vagal maneuvers help to stop the attack: pressure on the eyeballs, deep inhalation and exhalation with effort.

Types of pathology

Based on the duration of the attack, the following types of paroxysmal tachycardia are distinguished:

• Sustainable. Increased heart rate persists for longer than 30 seconds.
• Unstable. Lasts up to 30 seconds.

Forms of tachycardia that increase the readiness of the myocardium for the occurrence of ventricular fibrillation are as follows:

• Bidirectional. Characterized by the correct alternation of the QRS complex, electrical impulses emanate from two sources or from one section of the His bundle and travel in different ways.
• Recurrent (chronic). Appear after the normal heart rhythm has resumed.
• Pirouette. The QRS complex is characterized by a wave-like increase and decrease in amplitude. Heart rhythm is disturbed.
• Polymorphic. Occur when there are more than two sources of electrical impulses.

Possible complications

A stable form of tachycardia is accompanied by changes in hemodynamics. Without treatment, it leads to a lack of oxygen, the development of arrhythmogenic shock, heart failure, and myocardial muscle necrosis. Unsustained paroxysm of ventricular tachycardia does not affect the speed of blood flow, but increases the chance of ventricular fibrillation and arrhythmic death.

Signs of ventricular AT

The patient clearly feels the time of the onset of paroxysm. This is indicated by a painful shock in the heart area, followed by a gradual or sharp increase in the pulse. Additionally, the following symptoms are observed:

• decreased blood pressure;
• dizziness;
• pallor of the skin and mucous membranes;
• weakness;
• burning, squeezing in the chest;
• increased sweating;
• lightheadedness or fainting;
• attacks of nausea;
• trembling in the limbs;
• increased feeling of fear, anxiety;
• frequent urination.

Causes of ventricular paroxysmal tachycardia

Heart palpitations are often caused by organic lesions myocardium, only in 2-4% of patients the pathology is of unknown origin. The following causes of paroxysmal tachycardia are distinguished:

• myocardial infarction – a lack of blood supply to the myocardium resulting from blockage (thrombosis) of the arteries;
• acquired defects or congenital heart defects;
• infection of the heart muscle with adenovirus, cytomegalovirus, enterovirus and other groups of viruses;
• protrusion of the walls mitral valve(prolapse);
• acute myocarditis – inflammatory disease heart muscle;
• thinning of the walls (aneurysm) of the left ventricle;
• coronary heart disease - impaired blood supply to the heart muscle due to damage to the coronary arteries;
• toxic effects of cardiac glycosides;
• arrhythmogenic dysplasia – isolated damage to the right or left ventricle;
• thyrotoxicosis – hyperfunction of the thyroid gland;
• diabetes;
• cardiosclerosis – proliferation of connective tissue in the myocardium;
• heart failure;
• Wolff-Parkinson-White syndrome – ventricular preexcitation.

Provoking factors of PT paroxysm

The pathology is sometimes observed in pregnant women. Tachycardia is caused by accelerated metabolic processes and compression of the heart muscle by the uterus. The disturbances disappear after childbirth and do not cause negative consequences. Other risk factors include:

• caffeine and alcohol abuse;
• smoking;
• frequent stress;
• hard physical labor;
• hereditary predisposition;
• large blood loss;
• premenopausal period.

Diagnostics

If any unpleasant symptoms consult a physician or cardiologist. The doctor will conduct an external examination, take a medical history, and measure blood pressure and pulse. Differential analysis is carried out to exclude organic heart pathologies and identify the cause of tachycardia.

Patients are prescribed the following studies:

• Coronary angiography. To assess the state of the circulatory system, diagnose coronary heart disease.
• Stress tests on an exercise bike or treadmill. The study determines how heart rate changes with increasing exercise.
• 24-hour electrocardiogram monitoring. Helps to identify the number of attacks per day, their duration, and the location of the source of excitation.
• General blood and urine analysis. Prescribed to determine the level of cholesterol, sugar, blood electrolytes and exclude concomitant diseases.
• Echocardiography. Determines the condition of the myocardium and its individual structures, identifies valvular disorders.
• Multislice computed tomography (MSCT), ultrasound, magnetic resonance imaging. The methods help to exclude concomitant diseases and identify myocardial defects.
• Radionuclide research. Finds the area of ​​damage to the heart muscle.

Ventricular tachycardia on ECG

Electrocardiography determines the contractility of the heart and the conduction of electrical impulses. Characteristic signs of ventricular tachycardia are:

1. Sudden onset and end of an attack with increased heart rate up to 220 beats per minute.
2. The presence of AB dissociation is a widening of the QRS complex with multidirectionality of the ST segment and T wave. For comparison: paroxysmal supraventricular tachycardia more often leads to the appearance of a narrow QRS complex.

What to do during an attack of tachycardia

If your heart rate increases rapidly, call an ambulance. Before doctors arrive, provide first aid to the victim:

1. Place the patient on his back. Place a pillow or elastic cushion under your head.
2. Unbutton your clothes and loosen your tie.
3. Provide fresh air access to the room - open windows and doors.
4. Wipe the victim cool water.
5. Try to induce artificial vomiting.
6. For increased anxiety, give Phenazepam (0.0005 g).
7. Ask the victim to take a deep breath, then lightly cover his mouth and nose with your palm. The patient must strain to expel the air.

How to treat the ventricular form of paroxysmal tachycardia

The choice of treatment tactics depends on the type of arrhythmia, the frequency of its occurrence and the duration of attacks.

An acute attack of paroxysm is treated in a hospital setting.

The exception is unstable forms of tachycardia with a favorable course, which are easily eliminated by taking medications.

To relieve an attack, electrical pulse therapy is performed (treatment of heart rhythm disturbances). electric shock). If it is impossible to use such tactics, antiarrhythmic drugs are prescribed - Amiodarone, Sotahexal, Cordarone.

The survival prognosis is favorable. If there are no complications, the life expectancy of patients with gastrointestinal tract is 8-10 years. Death is possible in people with heart defects, concomitant diseases and those who refused treatment or experienced clinical death.

In severe cases of paroxysmal tachycardia, anti-relapse therapy and heart surgery are performed. During rehabilitation, patients are advised to adhere to a diet, eliminate psycho-emotional stress, do gymnastics and visit physical therapy more often. fresh air.

Drug therapy

On initial stages treatment, the patient is intravenously injected with a glucose solution mixed with lidocaine. Droppers are alternated with magnesium sulfate to restore rhythm. To prevent an attack in the future, the patient is prescribed the following medications:

• Beta blockers – Anaprilin, Vedicardol. Normalizes pulse and reduces blood pressure.
• Calcium channel blockers – Verapamil, Cinnarizine. Restore heartbeat, dilate blood vessels.
• Electrolytes – Panangin, Asparkam. Replenishes the deficiency of potassium and magnesium ions.
• Sedatives – Corvalol, Validol. To normalize the psycho-emotional state.

Surgical methods

If conservative therapy does not bring results, the doctor prescribes surgery. Surgical treatment is performed for the following indications:

• uncoordinated ventricular contraction in the past;
• persistent extrasystolic arrhythmia;
• recurrent attacks of tachycardia;
• hemodynamic changes in patients after a heart attack;
• dilated cardiomyopathy (stretching of the myocardial cavities) with impaired functioning of the left ventricle.

To exclude attacks of paroxysm, the following surgical treatment methods are used:

• Radiofrequency ablation is destruction (destruction) of the source of arrhythmia by electric current. The operation is performed through the femoral or subclavian vein under local anesthesia.
• Implantation (installation) of a cardioverter-defibrillator. The device prevents heart palpitations and normalizes myocardial function.

Alternative treatment of paroxysmal tachycardia

Herbal decoctions and tinctures are used as auxiliary methods. Before your appointment folk remedies, consult your doctor. The following recipes help normalize the pulse and prevent an attack:

• Grind 100 g of hawthorn berries. Pour in 500 ml of alcohol. Insist for a week. Take 50 drops 3 times a day. The course of treatment is 2 weeks.
• Mix hawthorn, calendula, chamomile, and chicory in equal quantities. Pour 1 liter of boiling water over 3 tbsp. l. raw materials. Leave for 3 hours. Take 30 ml 5-7 times a day. Duration of treatment is 3-4 weeks.
• Grind 160 g dried apricots, 20 pcs. almonds and 4 lemons. Mix with 200 g of honey. Eat 20 g of the mixture before breakfast. The treatment regimen is 30 days on, a month off.

Video