Under heavy physical exertion, the normal sinus rhythm increases to 150–160 per minute (for athletes - up to 200–220).

Etiology

Sinus tachycardia: Signs, Symptoms

Clinical manifestations

Sinus tachycardia: Diagnosis

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Purpose of stage: arrhythmias preceding circulatory arrest require necessary treatment in order to prevent cardiac arrest and stabilize hemodynamics after successful resuscitation.

The choice of treatment is determined by the nature of the arrhythmia and the patient's condition.

It is necessary to call an experienced specialist for help as soon as possible.

I47.2 Ventricular tachycardia

physiological sequence of cardiac contractions as a result of disorders of the functions of automatism, excitability, conduction and contractility. These disorders are a symptom of pathological conditions and diseases of the heart and related systems, and have an independent, often urgent clinical significance.

In terms of the response of ambulance specialists, cardiac arrhythmias are clinically significant, since they represent the greatest degree of danger and must be corrected from the moment they are recognized and, if possible, until the patient is transported to the hospital.

There are three types of periarestal tachycardia: tachycardia with wide QRS complexes, tachycardia with narrow QRS complexes, and atrial fibrillation. However, the basic principles of treatment for these arrhythmias are general. For these reasons, they are all combined into one algorithm - the algorithm for the treatment of tachycardia.

UK, 2000. (Or arrhythmias with dramatically reduced blood flow)

Sick sinus syndrome,

(Stage II atrioventricular block, especially II degree atrioventricular block

degree type Mobitz II,

III degree atrioventricular block with a wide QRS complex)

Paroxysmal ventricular tachycardia,

Torsade de Pointes,

Wide QRS complex tachycardias,

Tachycardias with a narrow QRS complex,

PZhK - extrasystoles of high degree of danger according to Law (Lawm)

during diastole. With an excessively high heart rate, the duration of diastole is critically reduced, which leads to a decrease in coronary blood flow and myocardial ischemia. The frequency of the rhythm at which such disturbances are possible, with a narrow-complex tachycardia, is more than 200 per 1 minute and with a wide-complex

tachycardia more than 150 in 1 minute. This is due to the fact that wide-complex tachycardia by the heart is worse tolerated.

Rhythm disturbances are not a nosological form. They are a symptom of pathological conditions.

Rhythm disturbances act as the most significant marker of damage to the heart itself:

a) changes in the heart muscle as a result of atherosclerosis (CHD, myocardial infarction),

d) myocardial dystrophies (alcoholic, diabetic, thyrotoxic),

e) heart defects,

Causes of non-cardiac arrhythmias:

a) pathological changes in the gastrointestinal tract (cholecystitis, peptic ulcer stomach and duodenum, diaphragmatic hernia),

b) chronic diseases of the bronchopulmonary apparatus.

c) disorders of the central nervous system

G) various forms intoxication (alcohol, caffeine, medications, including antiarrhythmics),

e) electrolyte imbalance.

The fact of the onset of arrhythmia, both paroxysmal and constant, is taken into account in

syndromic diagnosis of diseases underlying cardiac arrhythmias and conduction disorders.

Treatment for most arrhythmias is determined by whether the patient has adverse signs and symptoms. On the instability of the patient's condition

due to the presence of an arrhythmia, the following indicates:

Signs of activation of the sympatho-adrenal system: pallor of the skin,

excessive sweating, cold and damp limbs; build-up of signs

impairment of consciousness due to a decrease in cerebral blood flow, Morgagny syndrome -

Adams-Stokes; arterial hypotension (systolic pressure less than 90 mm Hg)

Excessively fast heart rate (more than 150 in 1 min) decreases the coronary

blood flow and can cause myocardial ischemia.

Left ventricular failure is indicated by pulmonary edema, and increased pressure in the jugular veins (swelling of the jugular veins), and enlarged liver is

an indicator of right ventricular failure.

The presence of chest pain means that the arrhythmias, especially tachyarrhythmias, are due to myocardial ischemia. The patient may or may not complain about

increased rhythm. Can be noted during examination "dance of carotids"

The diagnostic algorithm is based on the most obvious characteristics of the ECG

(width and regularity of QRS complexes). This eliminates the need for indicators,

reflecting the contractile function of the myocardium.

Treatment of all tachycardias is combined into one algorithm.

In patients with tachycardia and unstable condition (presence of threatening signs, systolic blood pressure less than 90 mm Hg, ventricular rate more than

150 in 1 minute, heart failure or other signs of shock) recommended

immediate cardioversion.

If the patient's condition is stable, then according to the 12-lead ECG (or

one) tachycardia can be quickly divided into 2 variants: with wide QRS complexes and with narrow QRS complexes. In the future, each of these two variants of tachycardia is subdivided into tachycardia with a regular rhythm and tachycardia with an irregular rhythm.

In hemodynamically unstable patients, when assessing the rhythm and subsequently during transportation, priority is given to ECG monitoring.

The assessment and treatment of arrhythmias is carried out in two directions: the general condition of the patient (stable and unstable) and the nature of the arrhythmia. There are three options

Antiarrhythmic (or other) medicines

Pacemaker (pacing)

Compared to electrical cardioversion, antiarrhythmic drugs act more slowly and the conversion of tachycardia to sinus rhythm is less effective when used. Therefore, drug therapy is used in stable patients without adverse symptoms, and electrical cardioversion is generally preferred in patients with unstable conditions and adverse symptoms.

1. Oxygen 4-5 liters per minute

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Paroxysmal tachycardia ICD code 10

The information posted on the site is for reference only and is not official.

Wiktionary contains an article "paroxysm"

Paroxysm (from ancient Greek παροξυσμός "irritation, anger; encouragement") - an increase in any painful seizure (fever, pain, shortness of breath) to the highest degree; sometimes this word also denotes periodically recurring attacks of illness, for example, marsh fever, gout. Paroxysms reflect the presence of dysfunction of the autonomic nervous system and can be a manifestation of a number of diseases. The most common cause is neurosis. In second place are organic (usually not gross) brain lesions: hypothalamic disorders, stem (especially dysfunction of the vestibular systems). Often, crises accompany attacks of temporal lobe epilepsy, migraine. They can also occur against the background of severe allergies. Cerebral autonomic paroxysms should be differentiated from primary lesions of the endocrine glands. So, pheochromocytoma is characterized by sympathetic-adrenal paroxysms, and insulomas are characterized by vago-insular paroxysms. Studies of the excretion of catecholamines and the glycemic profile are also needed. Contrast examination of the retroperitoneal region (aortography, pneumoren) allows to differentiate these conditions.

Treatment is primarily causal. Normalization of emotional disorders (see. Neuroses), desensitization, decreased vestibular excitability. When using vegetotropic agents, one should focus on the nature of the vegetative tone in the intercrisis period: sympatholytic agents with tension of the sympathetic system (chlorpromazine, ganglion blockers, ergotamine derivatives), anticholinergic agents with increased parasympathetic manifestations (amizil, atropine drugs). In the case of amphotropic shifts - combined means: belloid, bellaspon. During an attack - sedative, tranquilizing drugs, muscle relaxation, deep slow breathing and symptomatic drugs (for sympathetic-adrenal crises - dibazol, papaverine, chlorpromazine, for vago-insular - caffeine, cordiamine).

Vegetative-vascular paroxysms begin either with a headache, or with pain in the region of the heart and palpitations, redness of the face. Blood pressure rises, pulse quickens, body temperature rises, chills begin. Sometimes there is an unreasonable fear. In other cases, general weakness occurs, dizziness, darkening of the eyes, sweating, nausea appear, blood pressure decreases, and the pulse decreases. Attacks last from a few minutes to 2–3 hours, and many go away without treatment. With an exacerbation of vegetative-vascular dystonia, the hands and feet become purple-cyanotic, wet, cold. The areas of blanching against this background give the skin a marbled appearance. Numbness, crawling, tingling, and sometimes pain appear in the fingers. Sensitivity to cold increases, hands and feet become very pale, sometimes fingers become puffy, especially with prolonged hypothermia of the hands or feet. Overwork and excitement cause more frequent attacks. After an attack, a feeling of weakness and general malaise may remain for several days.

One of the forms of vegetative-vascular paroxysms is fainting. When fainting, the eyes suddenly darken, the face turns pale, and severe weakness sets in. The person loses consciousness and falls. Seizures usually do not occur. In the supine position, fainting passes faster, this is also facilitated by inhalation of ammonia through the nose.

Paroxysmal supraventricular tachycardia - Tachycardia supraventricularis paroxismalis

Against the background of stable hemodynamics and a clear consciousness of the patient, relief of paroxysm begins with techniques aimed at irritating the vagus nerve and slowing down the conduction through the atrioventricular node. Vagal testing is contraindicated in the presence of acute coronary syndrome, suspected pulmonary embolism, in pregnant women.

■ Sharp straining after a deep breath (Valsalva test).

■ Stimulation of vomiting by pressing on the root of the tongue.

■ Swallowing a crust of bread.

■ The use of verapamil, digoxin in WPW syndrome (wide QRS complexes).

■ Simultaneous combination of several drugs that slow down AV conduction. In particular, with the ineffectiveness of verapamil, only no earlier than 15 minutes after its administration, procainamide (novocainamide *) can be prescribed, provided that stable hemodynamics are maintained.

■ Prescribing verapamil to patients taking β-blockers.

■ Prophylactic use of phenylephrine (mezatone) with initially normal blood pressure, as well as insufficient knowledge of contraindications to this drug.

Male 41 g. Complaints of palpitations, weakness, dizziness. A similar state - within half an hour. Suffers from congenital heart disease - an open oval hole. Rarely there are attacks of palpitations. She is taking verapamil.

Objectively: The condition is serious, the consciousness is clear. The skin is pale, normal moisture. BP = 80/60 mm. Heart rate 210 per minute. Breathing is vesicular. The abdomen is soft and painless. ECG shows supraventricular tachycardia.

DS. Supraventricular paroxysmal tachycardia. (I47.1)

IV through a catheter, 200 ml of saline solution, 0.2 ml of 1% mezaton solution were introduced. At the stage of the introduction of the mezaton, the rhythm recovered on its own. Repeated ECG showed sinus rhythm, heart rate 65 per minute. BP - 130/80 mm Hg. The patient was left at home.

The woman is 62 years old. Complaints about palpitations, general weakness.

This morning, about an hour ago, palpitations appeared, dizziness in an upright position. Periodically, attacks of heartbeat occur, which are removed by intravenous administration of verapamil.

Suffering from ischemic heart disease. He does not take medications all the time. The presence of other masses. diseases and drug allergies are denied. The usual blood pressure is 130/80 mm.

Objectively. Consciousness is clear. The skin and mucous membranes are pale, of normal moisture. Breathing is vesicular. Heart rate 180 per minute, the rhythm is correct. BP 100/80 mm Hg The abdomen is soft and painless. ECG shows supraventricular tachycardia.

Ds. Supraventricular paroxysmal tachycardia

IV slowly (within 1-2 minutes) began the introduction of 4 ml of 0.25% solution of verapamil without dilution. After the introduction of 3 ml, the rhythm was restored.

Notes an improvement in well-being. BP 120/70 mm, heart rate 85 per minute.

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Drug catalog

Sinus tachycardia

An increase in heart rate can be both a physiological reaction of the body and a sign of serious pathology.

• Causes of occurrence
• Diagnostics and treatment

Sinus tachycardia (heart rate more than 100 per 1 minute) is one of the most common forms of paroxysmal tachycardia, sinus tachycardia code according to ICD 10 I47.1. Cardiologists and general practitioners use the code of this disease according to the international classification of diseases of the tenth revision to record the incidence and correct medical documentation.

Causes of occurrence

The occurrence of tachycardia should not always be regarded as a manifestation of the disease. An increase in heart rate is a normal response to strong emotions (both positive and negative), exercise, and lack of oxygen. Sinus tachycardia is also a consequence of such pathological processes:

• external or internal bleeding;
• anemia of any etiology;
• hypotension;
• high fever;
• hyperfunction of the thyroid gland;
• dysfunction of the left ventricle of the heart;
• cardiopsychoneurosis.

An increase in heart rate in the presence of the above diseases occurs at rest and is often accompanied by other unpleasant symptoms. Sometimes arrhythmia (violation of the correct rhythm of heart contractions) can join the increase in heart rate. An increase in heart rate can occur with atrial and ventricular block, Wolff-Parkinson-White syndrome.

Diagnostics and treatment

Paroxysmal tachycardia in ICD 10 has code I47 and belongs to the section of heart diseases. If there is an increase in heart rate at rest, it is necessary to consult a therapist or cardiologist. An obligatory instrumental method of research for patients with an increase in heart rate or rhythm disturbances is an ECG, echocardiography and a number of other studies are also additionally performed to determine the cause of the disease. Tachycardia and bradycardia (heart rate less than 60 per minute) are serious symptoms, so you need to see a doctor promptly.

Treatment depends on the cause that caused the increase in heart rate, the presence of rhythm disturbances, concomitant diseases. You also need to limit your caffeine intake, alcoholic beverages quitting smoking. Lifestyle modification gives a good result for all patients, regardless of the stage and severity of the underlying disease.

Paroxysmal tachycardia (I47)

Excluded:

• complicating:
  • abortion, ectopic or molar pregnancy (O00-O07, O08.8)
  • obstetric surgical procedures and procedures (O75.4)
• tachycardia:
  • NOS (R00.0)
  • sinoauricular NOS (R00.0)
  • sinus NOS (R00.0)

In Russia, the International Classification of Diseases of the 10th revision (ICD-10) has been adopted as a single normative document to take into account the incidence, the reasons for the population's visits to medical institutions of all departments, and the causes of death.

ICD-10 was introduced into health care practice throughout the Russian Federation in 1999 by order of the Ministry of Health of Russia dated 05/27/97. No. 170

A new revision (ICD-11) is planned by WHO in 2017 2018.

As amended and supplemented by WHO

Processing and translation of changes © mkb-10.com

Paroxysmal tachycardia code 10

Ventricular paroxysmal tachycardia (VT) - in most cases it is a sudden and just as suddenly ending attack of increased frequency of ventricular contractions up to 150-180 beats. per minute (less often - more than 200 beats per minute or within the range of 100-120 beats per minute), usually while maintaining the correct regular heart rate.

Paroxysmal ventricular tachycardia ranks first among all life-threatening arrhythmias (both ventricular and supraventricular). since it is not only extremely unfavorable for hemodynamics in itself, but also really threatens with a transition to flutter and ventricular fibrillation, in which the coordinated contraction of the ventricles stops. This means the arrest of blood circulation and, in the absence of resuscitation measures, - the transition to asystole ("arrhythmic death").

Classification of ventricular paroxysmal tachycardia Clinical classification ventricular paroxysmal tachycardia # 9726; Paroxysmal unstable ventricular tachycardia. # 9726; They are characterized by the appearance of three or more ectopic QRS complexes in a row, which are recorded during the monitoring ECG recording within no more than 30 s.

# 9726; Such paroxysms do not affect hemodynamics, but increase the risk of VF and sudden cardiac death.

# 9726; Paroxysmal sustained ventricular tachycardia. # 9726; Lasts more than 30 s.

# 9726; This type of ventricular tachycardia is characterized by a high risk of sudden cardiac death and is accompanied by significant changes in hemodynamics (arrhythmogenic shock, acute left ventricular failure).

Special forms of ventricular tachycardia

There are special forms of ventricular tachycardia, the diagnosis of which is of clinical importance, since they reflect the increased readiness of the ventricular myocardium to develop fibrillation:

# 9726; Bidirectional ventricular tachycardia.

Correct alternation of QRS complexes due to the propagation of impulses from two different parts of the ventricles or different conduction of impulses from one source.

# 9726; "Pirouette" ("torsade de pointes").

Unstable (up to 100 complexes) bidirectional ventricular tachycardia with a wave-like increase and decrease in the amplitude of QRS complexes. The rhythm is wrong, with a frequency / min. and higher. The development of "pirouette" is usually preceded by lengthening of the QT interval and early ventricular extrasystoles. Unstable bidirectional ventricular tachycardia with a wave-like increase and decrease in the amplitude of the complexes is prone to recurrence.

# 9726; Polymorphic (multiforme) ventricular tachycardia.

It occurs when there are more than two ectopic foci.

# 9726; Recurrent ventricular tachycardia.

Resumes after periods of basic rhythm.

Epidemiology of ventricular paroxysmal tachycardia

Most often, ventricular tachycardia develops in patients with coronary artery disease (about 85%).

In men, ventricular tachycardia develops 2 times more often than in women.

Only in 2% of cases, ventricular tachycardia is recorded in patients without reliable clinical and instrumental signs of organic heart disease (“idiopathic” form of ventricular tachycardia).

ICD-10 code I47.2 - Ventricular tachycardia.

when there is a powerful PA, where to look for this very person, at the bottom of which well

This is 2-10 minutes, nothing more.

And I don't mind experiencing a couple of panic attacks right now, preferably more powerful. It's just anxiety. I do not see this as prohibitively critical. You know, even if I were sick with these PAs to death, I would also continue to work, drive cars back and forth - in general, do practically everything that I do without PAs. Of course, it is not better without PA, but nevertheless, with PA it is quite worthy to function, to benefit society, at work - not just possible, but necessary. This PA did not scare me critically and in years, and does not scare me even now. Let's not classify F41.0 as Phobos and Deimos. Although I do not argue - it is very difficult to be under PA for five minutes.

I did it, without the pills, I will note. This does not mean that my personality is any special, it rather means that the diagnosis of F41.0 is just nonsense.

This suggests, rather, that everyone has very different things. For example, I managed to somehow stabilize everything, but complete cure failed to reach. Therefore, I understand people who have failed at something, and I believe that all these passions. which are written here are very real and not always eradicated, although not all of them I went through myself. I believe that people tried their best to overcome them,

but for some it turned out to be beyond their strength.

but for some it turned out to be beyond their strength.

F41.0 is not a severe, lingering illness. The pathogenetic mechanism is unknown; according to some theories, this is not a disease at all, but a psychogenic reaction to unresolved conflicts.

Or, to put it even simpler, the depletion of the nerve centers as a result of severe stress. Ten years, and exhaustion on powerful drugs? Somehow you don’t find much? And what kind of exhaustion is this that it is impossible to work on it and more or less function in society?

How does this exhaustion on a powerful farm not only fail, but even worsen? You see how many questions there are. This is all according to the very story.

Whatever the PA - severe, not severe, protracted, not protracted - they arise against the background of other diseases that the patient can fight all his life, maneuvering on the verge of borderline states. These are neuroses, and phobic disorders, etc., from which it is not so easy to get rid of, and not everyone succeeds.

Has PA already ceased to be a neurosis?

Whatever the PA - heavy, not heavy, protracted, not protracted

I'm talking about the framework in comparison with other diseases according to ICD-10.

These are neuroses and phobic disorders.

phobic disorders have already become psychosis? F40-49 seems to belong to the neurotic spectrum.

maneuvering on the verge of borderline states

How PR / PA can go beyond the line. The mechanisms of neuroses and psychosis are completely different.

Diagnostic criteria.

I47 Paroxysmal tachycardia

I 47.0 Recurrent ventricular arrhythmia

I47.1 Supraventricular tachycardia

I47.2 Ventricular tachycardia

I47.9 Paroxysmal tachycardia, unspecified

I48 Atrial fibrillation and flutter

I49 Other cardiac arrhythmias

I49.8 Other specified cardiac arrhythmias

I49.9 Unspecified cardiac arrhythmia

Definition: Rhythm disturbances are changes in the normal physiological sequence of cardiac contractions as a result of dysfunction of automatism, excitability, conduction and contractility. These disorders are a symptom of pathological conditions and diseases of the heart and related systems. In terms of the response of ambulance specialists, cardiac arrhythmias are clinically significant, since they represent the greatest degree of danger and must be corrected from the moment they are recognized and, if possible, until the patient is transported to the hospital.

Correct identification and treatment of arrhythmias in critically ill patients can prevent cardiac arrest. If the patient's condition is not unstable or acute, several treatment options are possible, including medication. If it is ineffective, it is possible to call a specialized team.

Wide QRS complex tachycardia:

regular tachycardia with a wide QRS complex:

supraventricular tachycardia with bundle branch block

irregular wide-complex tachycardia:

atrial fibrillation with a bundle branch block,

atrial fibrillation with premature ventricular excitation (WPW syndrome)

Narrow QRS complex tachycardia:

regular tachycardia with a narrow QRS complex:

AV nodal tachycardia,

AV nodal tachycardia with Wolff-Parkinson White syndrome (WPW-syndrome),

Atrial flutter with regular AV conduction (2: 1),

Irregular tachycardia with a narrow QRS complex:

atrial flutter with variable AV conduction

The presence or absence of adverse signs dictates the treatment tactics for most arrhythmias. The following adverse signs indicate instability associated with arrhythmia.

1. Shock- pale cold skin, impaired consciousness. hypotension (systolic blood pressure 90 mm Hg).

2. Syncope attacks.

3. Heart failure... manifested ALVO (pulmonary edema) or ALVO (increased pressure in the jugular veins, swelling of the liver).

4. Myocardial ischemia... manifested in the form of attacks of angina pectoris or in the form of painless ischemia - focal changes on the ECG.

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Encyclopedia of Diseases

Catecholinergic polymorphic ventricular tachycardia

Synonyms: Bidirectional tachycardia, Bidirectional tachycardia induced by catecholamine, CPVT, Catecholaminergic polymorphic ventricular tachycardia, Double tachycardia induced by catecholamines, Malignant paroxysmal ventricular tachycardia, Syntifricular tachycardia, MKB .2 Orpha No. ORPHA3286 MIM No.,

A serious genetic arrhythmogenic disorder characterized by adrenergic-induced ventricular tachycardia (VT), which manifests itself in episodes of loss of consciousness and sudden death.

The prevalence of CPVT in Europe is 1 case per population.

Clinic. Typically, CPVT appears at the age of 7-9 years and is not related to the gender of the patient. The first symptoms are episodes of loss of consciousness due to physical exertion or strong emotions. Sudden death, as the first manifestation of the disease, occurs in 10-20% of patients. Typical arrhythmias in CPVT are bidirectional ventricular tachycardia and, less commonly, supraventricular tachycardia and atrial fibrillation.

Diagnosis. Patients with a family history of CPVT, sudden death stress or physical activity / emotion-induced fainting should undergo exercise tests and Holter monitoring. Usually, arrhythmias in this nosology are reproducible, and thus, the assessment of the stress test is of extremely important diagnostic value. Holter monitoring is indicated in those rare cases where strong emotions are the main trigger. ECHO-KG and ECG at rest, as a rule, have no diagnostic value.

The differential diagnosis is with long QT syndrome, arrhythmogenic right ventricular cardiomyopathy, and Andersen-Tawil syndrome.

Treatment. Beta blockers (propranolol and nadolol) are the drugs of choice. For the prevention of arrhythmias, they should be prescribed in the maximum tolerated doses.

Recently, the sodium channel blocker flecainide has shown its effectiveness.

In patients with recurrent syncope, cardioverter defibrillator implantation is recommended to prevent cardiac arrest and sudden death despite therapy with high doses of beta-blockers and flecainide.

In several cases, impaired denervation of the left heart has shown a good result in eliminating arrhythmias, but its effectiveness has not yet been confirmed.

To avoid provoking an attack, it is necessary to limit physical activity in patients with CPVT.

Forecast. Although CPVT is a serious and often fatal disease, early diagnosis and correct treatment can significantly increase life expectancy. In patients with recurrent symptoms, restriction of physical activity, in combination with beta-blocker therapy and installation of a cadioverter-defibrillator, leads to a favorable prognosis.

Paroxysmal tachycardia

ICD-10 code

Associated diseases

Symptoms

Causes

Paroxysmal tachycardia is characterized by severe rhythm and pulse rate per minute. Ventricular complexes can be seen on the ECG, and a slightly deformed P wave is often observed in front of them. Often the disease is accompanied by intraventricular and (or) atrioventricular conduction. In this case, most often - along the right leg of the bundle of His.

The difference between atrioventricular tachycardia is precisely in the presence of the P wave, which either overlaps with the QRST complex, or is located in front of it.

When the carotid sinus is massaged, the heart rate is temporarily normalized. This applies to all forms of supraventricular tachycardia.

Ventricular tachycardia - tachycardia with a frequency of beats per minute, with a significant deformation of the QRST complex. The atria are excited independently of the ventricles in the correct rhythm, but the P wave is difficult to distinguish. The shape and amplitude of the QRST complex and the contour of the baseline vary slightly from cycle to cycle. The rhythm is often not strictly correct.

Ventricular tachycardia - tachycardia with a frequency of one minute, with significant deformation of the QRST complex. The atria fire independently of the ventricles in the correct rhythm, but the P wave is difficult to distinguish. The shape and amplitude of the QRST complex and the contour of the baseline vary slightly from cycle to cycle. The rhythm is often not strictly correct. Massaging the carotid sinus does not change the frequency of the rhythm. Sometimes, within a few days after a paroxysm of tachycardia, negative T waves are recorded on the ECG, less often - with a displacement of the ST segment - poettachycal syndrome: such patients require careful observation and exclusion of small focal myocardial infarction.

Paroxysmal tachycardia mcb

Clc syndrome

CLC gets its name from the names of the scientists who described it - Clerk, Levy, and Critesco. Another name for this condition is LGL (Launa-Ganong-Levine) syndrome. In this article we will talk about how and why this syndrome occurs, how dangerous it is for health and life, how to be treated and live with this diagnosis.

Development mechanism

Conductive system of the heart

The heart contracts under the influence of impulses that are produced in the accumulation of nerve cells located in the right atrium - the sinus node. It is a kind of battery that regularly sends electrical signals to the cells of the heart muscle. The impulses travel along the nerve pathways in the atria, causing them to contract. During this process, blood from the atria is squeezed out into the ventricles.

So that the ventricles of the heart are well filled with blood and contract a little later than the atria, nature has provided a special filter on the border between them - the atrioventricular node. Excitation, getting into it, goes slowly. Only after passing the atrioventricular junction, electrical impulses quickly spread through the myocardium of the ventricles and cause their contraction. As a result, blood is pushed into the aorta and pulmonary trunk.

It takes up to 0.1 s for nerve impulses to travel along the intra-atrial pathways. It takes them the same time to overcome the atrioventricular node. Therefore, the total time from the onset of atrial contractions to the signal output from the atrioventricular junction and the onset of ventricular contraction does not normally exceed 0.2 s. On the electrocardiogram, this distance corresponds to the P-Q interval.

However, in some people, from birth in the heart, bypass paths for impulses are formed, bypassing the atrioventricular junction. One of these additional conduction routes is the James beam. Passing through it, excitement does not linger on the border between the atria and ventricles. Therefore, the duration of the P-Q interval is shortened to less than 0.11 seconds. The CLC phenomenon emerges. This is just an electrocardiographic term that reflects changes in the ECG recording itself.

However, sometimes the impulses, having traveled along the short path of James, return back through the atrioventricular node and again follow this path. In other cases, the impulse passes through the atrioventricular node, and returns along the James bundle. A circular course of excitation is formed. In this circle, the impulse circulates very quickly, causing the development of cardiac arrhythmias - a paroxysm of supraventricular tachycardia. When such deviations appear, accompanied by the patient's complaints and changes in the electrocardiogram, they talk about the CLC syndrome. Thus, the CLC syndrome differs from the phenomenon by the presence of clinical manifestations. The same applies to the Wolff-Parkinson-White phenomenon / syndrome.

Reasons for development

CLC phenomenon and syndrome - congenital diseases. The exact reason for them is unknown. It can only be assumed that it is associated with a harmful effect on the fetus at the time of pregnancy, when the heart and its pathways are laid. A genetic cause is not excluded - a "breakdown" of a certain gene responsible for the development of intracardiac pathways.

A shortening of the P-Q interval is observed in two out of a hundred healthy people, more often in middle-aged men. CLC can also be caused by coronary artery disease, hypertension, myocardial infarction, rheumatism, thyroid hyperfunction, hypovitaminosis B and other conditions that affect the nerve cells and blood supply to the heart.

Symptoms and Diagnosis

Patients with CLC syndrome may not be aware of their disease for a long time, since it does not always cause any symptoms. Only an ECG study allows you to correctly diagnose.

The CLC phenomenon is manifested by a shortening of the P-Q interval on the electrocardiogram and does not cause any symptoms. A person can live his whole life with such changes and not feel any health problems.

The development of the CLC syndrome is accompanied by the appearance of sudden attacks of heartbeat - paroxysms of supraventricular tachycardia. Paroxysmal heart rhythm disturbances with this type of ventricular preexcitation occur less frequently than in patients with Wolff-Parkinson-White (WPW) syndrome.

Paroxysmal supraventricular tachycardia is clinically manifested by a sudden onset of heartbeat with a heart rate of 140 to 220 beats per minute (usually 150 to 180 beats per minute). Before this, the patient sometimes feels a jolt in the area of ​​the heart or neck. An attack of palpitations may be accompanied by dizziness, noise in the head, constricting pain behind the sternum, fainting. In some cases, sweating, bloating, nausea, or even vomiting appear. At the beginning or at the end of a prolonged paroxysm of arrhythmia, there may be profuse urination.

The attack can be stopped with the help of vagal tests - straining while inhaling, lowering the face into cold water while holding the breath, massage the carotid sinus area on the neck.

In rare cases, CLC may be accompanied by paroxysmal fibrillation atria: frequent irregular heartbeat.

CLC syndrome is diagnosed using electrocardiography and 24-hour monitoring of the electrocardiogram. In addition to these studies, a transesophageal electrophysiological examination of the heart is recommended.

Treatment

In many cases, CLC syndrome special treatment does not require. When an attack of arrhythmia occurs, it is recommended to independently perform vagal tests, and if they are ineffective, call an ambulance. To stop (stop) the paroxysm of supraventricular tachycardia or atrial fibrillation, you can use drugs such as sodium adenosine triphosphate (ATP), verapamil, beta-blockers, novocainamide, amiodarone and others.

It should be noted that with different forms of tachycardia, some of the listed drugs are contraindicated, therefore, only a doctor should stop the paroxysm with medication. After the rhythm is restored, some patients may be prescribed antiarrhythmic drugs to prevent seizures.

In arrhythmology departments, the doctor can restore the normal rhythm with the help of electrical cardioversion. This method consists of applying a series of electrical impulses to stop the circular excitation.

With frequently recurring paroxysms that worsen the patient's quality of life, preventing him from performing his professional duties, it is carried out surgery... It is aimed at destroying the additional pathway. Such an intervention is carried out after an intracardiac electrophysiological study, which is carried out using a special probe inserted into the heart through a vessel. The operation is called radiofrequency catheter ablation. This intervention is less traumatic, after which the patient quickly returns to normal life.

How to decipher the cardiogram of the heart? Formation of the conclusion on the electrocardiogram (ECG) is carried out by a functional diagnostics doctor or cardiologist. This is a difficult diagnostic process, tr ...

Ventricular extrasystole: causes, signs, treatment Ventricular extrasystoles (VES) are extraordinary contractions of the heart that occur under the influence of premature impulses that originate from the intragland ...

Right atrial hypertrophy: causes, symptoms, diagnosis Right atrial hypertrophy (HRP) is a term for an enlargement of this part of the heart. Recall that venous blood enters the right atrium ...

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not intended for self-diagnosis and treatment of diseases!

Copying of materials is allowed only with an active link to the source.

Most often this is manifested by a violation of the vascular tone.

According to ICD 10 of the International Classification of Diseases, this pathology is attributed to the class of diseases of the nervous system and in a certain way affects the work of all internal organs and systems of the body. It can be observed in infants, but most often the manifestations of VSD affect children of primary school age and adolescents. After reaching puberty, in most cases, the negative manifestations of the disease go away.

Today, vegetative-vascular dystonia is not considered a specific disease, but rather is a condition that signals a malfunction in the body. Therefore, narrow specialists are engaged in the study of the manifestations of pathology and treatment: a pediatric neuropathologist, cardiologist, endocrinologist, gastroenterologist and others.

Who is at risk of VSD

According to statistics, signs of autonomic disorders are observed in more than half of all children aged five years and up to the end of puberty.

However, there are risk groups, which include children most susceptible to the influence of this pathology:

1. Girls are more prone to developing vascular disorders. This is due to fluctuations in their hormonal levels during restructuring of the body and the lag in the development of the nervous system in comparison with physical growth. The female nervous system is more susceptible to stress, psychological and emotional stress.
2. Teenagers. VSD of the pubertal period is associated with a discrepancy between the development of the nervous system and physical data, as well as changes in the hormonal background in a teenager. In addition, it is during this period that school loads increase, bad habits appear, relationships in the team are most acutely perceived, competition between adolescents intensifies, and an increased interest in the opposite sex is manifested.
3. Dystonia is very often manifested in preschool children and newborns who have suffered a birth trauma, suffering from congenital pathologies of the cardiovascular and nervous systems, who have suffered cerebral circulatory disorders in infancy, whose mothers suffered from preeclampsia and other disorders during pregnancy.
4. Heredity, especially on the maternal side, increases the risk of developing vascular disorders in a child.

In addition, there are a number of reasons and external conditions due to which any child may experience disturbances in the work of the autonomic nervous system. Parents should promptly pay attention to deviations in the behavior and well-being of the child. Seeking help from specialists is mandatory, since manifestations of pathology can affect the functioning of vital body systems and cause dangerous complications and disorders.

Causes of vegetative-vascular disorders

VSD in children and adolescents is most often observed during the period of active growth and restructuring of the body.

"Triggers" can be very diverse:

1. Circumstances that traumatize the child's psyche - conflicts in the family and in the environment of peers, psychological and mental overload associated with mastering the school curriculum.
2. Acute and chronic diseases - neurological, infectious, endocrine, allergic.
3. Improper nutrition and irrational daily routine (night wakefulness at the computer), lack of physical activity or excessive overload of the body.
4. Climatic conditions, meteorological dependence, unfavorable ecological conditions.

What symptoms should alert parents

Children, as a rule, are not always able to objectively assess their condition and clearly formulate a health problem. They are mobile and impulsive, subject to frequent mood swings, but there are a number of signs that cannot be ignored. Symptoms of vegetative vascular dystonia in children are determined by the nature of the disorders.

Parents should be alerted to changes in the child's behavior, and should also be attentive to his complaints, including:

• headaches and dizziness;
• constant fatigue;
• poor memory;
• absent-mindedness, forgetfulness;
• insomnia or drowsiness.

Alarming signs are such as tearfulness and fearfulness, anxiety and apathy, unfounded fears, hysteria, depression.

The cardiac symptoms of VSD are characterized by the following features:

• tachycardia, bradycardia;
• fluctuations in blood pressure - hypertension or hypotension;
• ringing in the ears, darkening in the eyes;
• pain in the heart, very rapid pulse.

These symptoms cannot be ignored, as they may indicate the presence of serious disorders in the body.

Sometimes parents can hear from a child complaints about respiratory manifestations with VSD:

• shortness of breath both when walking and at rest;
• feeling short of breath;
• Bursting chest, cough;
• subfebrile temperature.

The child may complain of chills or a feeling of heat, intolerance to cold or heat.

Manifestations of VSD due to disruption of the gastrointestinal tract.

Vegetative vascular dystonia in adolescents and children can also manifest itself in a disorder of the digestive tract, which is often expressed in the form of:

• abdominal pain;
• diarrhea, flatulence, constipation;
• nausea and vomiting;
• loss of appetite.

Parents should pay attention if the child is losing weight or gaining weight rapidly.

Vegetative-vascular dystonia manifests itself in children and in disorders of the urinary system, the symptoms of which are as follows:

• very frequent urination or urinary retention;
• swelling of the face and limbs;
• pain in lumbar region or in the lower abdomen.

Activity disorders endocrine system with VSD in adolescents, they can manifest themselves in the form of:

Methods for the treatment of vegetative-vascular disorders

Treatment of VSD is complex and takes into account the nature of autonomic disorders. If no serious concomitant pathologies are found in the diagnostic process, preference is given to non-drug methods. Treatment of VSD in children also requires lifestyle changes and the consultation of a psychologist.

What parents can do to help their child:

1. Review your diet. Provide the body with vitamins and microelements by including more vegetables, fruits, cereals, nuts in the menu. Eliminate foods containing "empty" calories, preservatives, trans fats. Minimize the consumption of salt and sugar, animal fats, carbonated drinks, fast food.
2. Normalize the daily routine, sleep and rest. Try to minimize the interaction of the child with a computer, smartphone and TV, especially at night.
3. Get interested in sports, outdoor activities, communication with peers and pets.
4. Provide the child with positive communication in the family, support and understanding of loved ones, protect him from stress, balance the stress with rest and help him find an interesting activity.

It is very important to provide the child with emotional balance and more positive emotions. If there is a need, it will not be superfluous to contact a psychologist.

In addition, the following will have a positive effect on the state of the child's or adolescent's body and his psycho-emotional mood:

• physiotherapy activities - electrophoresis, acupuncture, magnetic laser therapy and others;
• massage - it can be done even by the smallest;
• water procedures - cold and hot shower and baths;
• physiotherapy exercises and swimming.

Children and adolescents suffering from vegetative-vascular disorders are registered with a pediatrician, who monitors their condition every few months.

Atrial heart palpitations: features and treatment

What is atrial tachycardia, and what factors influence the development of pathology? This is a condition in which accelerated atrial automatism is observed as a result of damage to certain areas of myocardial tissue. In the supraventricular zone, the conduction of electrical impulses generated by the sinus node is disturbed. This provokes the appearance of an abnormal focus of circulation, due to which there is an overstimulation of cardiac activity and an acceleration of the frequency of contractions, fluctuating in the range of beats per minute.

The disease is most often detected in elderly people and children, according to statistical data, it is about 20% of all arrhythmic disorders, according to ICD 10, the code is assigned - 147.2 (paroxysmal ventricular tachycardia).

Classification

Atrial tachycardia can be chronic or paroxysmal. In the first case, there is a prolonged chaotic contraction of cardiomyocytes during the day, days or even months, in the second, the attack lasts from several minutes to two to three hours. Depending on the nature of the origin, the pathology is classified into the following subspecies:

1. Trigger. This form of the disease is extremely rare and is detected, as a rule, in older people taking cardiac drugs of the glycoside group, which eventually lead to intoxication of the body. Excessive exercise and increased sympathetic tone can also be a cause.
2. Reciprocal. A distinctive feature of pathology is that the paroxysm is not stopped by antiarrhythmic drugs. The onset of flutter occurs when the electrical impulse re-enters the atrium. One of the methods for removing the pathological condition is extrastimulation of the affected area. The etiology of this form of the disease is not fully understood, but there is a certain relationship between atrial tachycardia and other types of arrhythmias, for example, atrial fibrillation.
3. Polytopnaya. This form is found in both the elderly and young people. Often accompanied by pathologies of the respiratory system and heart failure. Not much different from supraventricular arrhythmia. Treatment usually addresses the underlying cause of the tachycardia, but antiarrhythmic drugs may be prescribed if necessary.
4. Automatic. This type of arrhythmia often occurs against the background of heavy physical exertion. Young people are most susceptible to this form of pathology. With a long absence of treatment, there may be a deterioration of the clinical picture with the appearance of acute pain and, as a result, a state of shock.

Causes of the disease

Sometimes it is impossible to determine the exact origin of the pathology, especially if the patient has not sought medical help for a long time.

In rare cases, in the absence organic lesions heart and other destructive processes, unexpressed atrial tachycardia can be taken as a variant of the norm.

The negative factors that provoke the development of the disease include:

• infectious cardiovascular diseases;
• arterial hypertension;
• endocrine disorders;
• respiratory diseases, especially pneumonia;
• obesity;
• poisoning of toxic genesis.

Tachycardia is most often a consequence chronic diseases... In a child, pathology can develop in the presence of congenital heart defects, in adults with an atrial septal defect, blockade, and also after surgical procedures.

It is possible to diagnose atrial tachycardia only at the time of paroxysm, which makes it difficult to identify the disease itself and determine further treatment tactics.

In this regard, the doctor may ask the patient to undergo several types of examinations at different times.

Symptoms of the disease

In young and old people, the clinical picture can be very different. So, for example, persons suffering from severe diseases of the cardiovascular system sometimes do not notice an acceleration of heart rate and other minor signs of the progression of pathology at all, which usually happens in old age. In relatively healthy patients, a change in state in the worst side rarely goes unnoticed. But in most cases, patients are worried about the same symptoms, such as:

• chest pain;
• dyspnea;
• dizziness;
• light-headedness;
• feeling of palpitations.

Untimely, as well as improperly selected treatment can lead to the development of a multifocal form of atrial tachycardia, which is an advanced degree of the disease and is much more difficult to treat.

Diagnostics

The most informative way to diagnose atrial tachycardia is an ECG (electrocardiogram), which must be performed right at the time of an attack, which is usually difficult to implement in practice. In this regard, daily monitoring by the Holter method is often used: the patient is at home or in a stationary environment with sensors connected to him that record any changes in the rhythm of the heart rate.

Also, blood and urine samples are taken for laboratory research. This procedure allows you to identify the decay products of adrenaline and the concentration of erythrocytes. This is necessary in order to exclude the likelihood of the patient having leukemia and other serious diseases.

Treatment

Since atrial tachycardia is not an independent disease, treatment should be directed at the main cause of the pathology. For example, for heart injuries, a surgical operation is used, for an infectious lesion of the membranes of the organ (pericarditis), anti-inflammatory therapy is required.

In other cases, antiarrhythmic drugs are prescribed, such as: "Amiodarone" or "Propafenone". To eliminate excessive stimulation of the heart by impulses generated inside the atria, beta-blockers are used. Drugs in this group can lower the heart rate and have a pronounced hypotensive effect, which is important if a person has arterial hypertension. If drug therapy was not enough, according to the indications of the attending physician, catheter ablation is performed, which allows destroying the pathological bundles of tissues that produce impulses.

Patients with asymptomatic and short-term attacks of atrial tachycardia are not prescribed treatment, since in this case arrhythmia is a natural reaction to internal pathological processes. Prevention of paroxysms consists in maintaining a healthy lifestyle and treating existing diseases.

Complications and prognosis

The life prognosis with minor hemodynamic disturbances and the rare occurrence of paroxysms is favorable. This pathology, even with systematic relapses, does not lead to dysfunction of the cardiovascular system, and also tends to self-cure. Possible complication is a weakening of the myocardium and, as a consequence, an increase in the symptoms of tachycardia, which, as a rule, does not affect the patient's life expectancy.

Accessory chord of the left ventricle

An additional chord in the left ventricle is a diagnosis that is established only on the basis of ultrasound; it cannot be detected either by listening or by ECG. Of course, if a young patient has a heart murmur and a serious defect is not suspected, then the doctor may assume that this is either an additional chord or a valve prolapse.

Very often doctors who are not clean on hand, especially pediatricians, after listening to the child and pretending to look thoughtful, say that the child has a murmur in the heart and this is an additional chord, and it is urgent to do an ultrasound of the heart in a "such and such" place and write out a direction, on a beautiful the letterhead of a private clinic, putting your stamp there. At the same time, they do not write a word about noise in the outpatient card, and if you go to an uninterested expert, it turns out that there is no noise either. Indeed, with an additional chord, heart murmur is extremely rare.

By itself, the additional chord is a strand that is attached with one side to the valve leaf and the other to the heart wall. Each person has several such chords, and their main function is to help the valve not to bend and retain blood while the heart is contracting. If one or more of these chords is thicker or denser, then it becomes visible on ultrasound. They certainly write about this in the conclusion, most often adding the word "hemodynamically insignificant" - i.e. not affecting the work of the heart. Such a chord does not require treatment and generally should not be overlooked.

If the additional chord is nevertheless hemodynamically significant, then it is necessary to consult a cardiac surgeon. But do not worry, this does not mean at all that it will have to be excised, you just need to understand the current situation.

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Sinus tachycardia - description, causes, symptoms (signs), diagnosis, treatment.

Short description

Sinus tachycardia (CT) is an increase in heart rate at rest, more than 90 per minute. Under heavy physical exertion, the normal sinus rhythm increases to 150–160 per minute (for athletes - up to 200–220).

Causes

Etiology - generation of excitation impulses by the sinus - atrial node with an increased frequency Physiological causes Fever (an increase in body temperature by 1 ° C causes an increase in heart rate by 10 per minute) Excitation (hypercatecholaminemia) Hypercapnia Exercise Diseases and pathological conditions Thyrotoxicosis MI Endocarditis Thyroidism vegetative-vascular dystonia Mitral stenosis Aortic valve insufficiency Pulmonary tuberculosis Shock Left ventricular failure Cardiac tamponade Hypovolemia drugs (epinephrine, ephedrine, atropine) Pain.

Symptoms (signs)

Clinical manifestations Palpitations, a feeling of heaviness, sometimes pain in the region of the heart Symptoms of the underlying disease.

Diagnostics

ECG - identification of heart rate at rest - 90–130 per minute Each P wave corresponds to a QRS complex, the P – P intervals are equal to each other, but when combined with sinus arrhythmia, they can differ by more than 0.16 s. the T waves preceding them, mimicking atrial or atrioventricular paroxysmal tachycardia. Differential sign - vagal reflexes (massage of the carotid sinus, Valsalva test) for a short time slow down the rhythm, helping to recognize the P waves.

Differential diagnosis Supraventricular paroxysmal tachycardia Atrial flutter with regular conduction to the ventricles 2: 1.

Treatment

Treatment Elimination of the identified risk factor: exclusion of smoking, alcohol consumption, strong tea, coffee, spicy food, sympathomimetic drugs (including nasal drops) Treatment of the underlying disease b - Adrenergic blockers in small doses by mouth (rarely prescribed) Sedatives With concomitant heart failure - cardiac glycosides, pathogenetic therapy.

Reduction. CT - sinus tachycardia.

Sinus tachycardia

An increase in heart rate can be both a physiological reaction of the body and a sign of serious pathology.

Sinus tachycardia coding according to ICD-10

Sinus tachycardia (heart rate more than 100 per 1 minute) is one of the most common forms of paroxysmal tachycardia, sinus tachycardia code according to ICD 10 I47.1. Cardiologists and general practitioners use the code of this disease according to the international classification of diseases of the tenth revision to record the incidence and correct medical documentation.

Causes of occurrence

The occurrence of tachycardia should not always be regarded as a manifestation of the disease. An increase in heart rate is a normal response to strong emotions (both positive and negative), exercise, and lack of oxygen. Sinus tachycardia is also a consequence of such pathological processes:

• external or internal bleeding;
• anemia of any etiology;
• hypotension;
• high fever;
• hyperfunction of the thyroid gland;
• dysfunction of the left ventricle of the heart;
• cardiopsychoneurosis.

An increase in heart rate in the presence of the above diseases occurs at rest and is often accompanied by other unpleasant symptoms. Sometimes arrhythmia (violation of the correct rhythm of heart contractions) can join the increase in heart rate. An increase in heart rate can occur with atrial and ventricular block, Wolff-Parkinson-White syndrome.

Diagnostics and treatment

Paroxysmal tachycardia in ICD 10 has code I47 and belongs to the section of heart diseases. If there is an increase in heart rate at rest, it is necessary to consult a therapist or cardiologist. An obligatory instrumental method of research for patients with an increase in heart rate or rhythm disturbances is an ECG, echocardiography and a number of other studies are also additionally performed to determine the cause of the disease. Tachycardia and bradycardia (heart rate less than 60 per minute) are serious symptoms, so you need to see a doctor promptly.

Treatment depends on the cause that caused the increase in heart rate, the presence of rhythm disturbances, concomitant diseases. You also need to limit the use of caffeine, alcoholic beverages, quit smoking. Lifestyle modification gives a good result for all patients, regardless of the stage and severity of the underlying disease.

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Self-medication can be hazardous to your health. At the first sign of disease, consult a doctor.

Ventricular tachycardia according to microbiology 10

Sinus tachycardia mkb 10

When making a diagnosis

The level of consciousness, frequency and efficiency of breathing, heart rate, pulse, blood pressure, ECG, anamnesis if possible

Additional (according to indications)

Laboratory tests: hemoglobin, blood gases, indicators of CBS,

electrolytes (K, Na, Mg, Ca, Cl), blood glucose, leukocytes, blood count, enzymes CPK, ALAT, ASAT

R-graphy of the chest organs

During treatment

Monitoring according to clause 1.5. Repeatedly according to indications # 8212; ECG, laboratory parameters, depending on the clinical situation

Cancellation of drugs that lengthen the PQ interval on the ECG. Providing adequate ventilation, oxygen inhalation, intravenous access

Atropine 0.5-1 mg IV, up to a total dose of 0.04 mg / kg

Percutaneous external pacing, if impossible or as a temporary alternative until transvenous pacing # 8212; dopamine 5-20 μg / kg / min. adrenaline 2-10 mcg / min. in the form of a continuous metered infusion

Correction of water and electrolyte balance

Extracardial pathological sinus tachycardia occurs with an increase in body temperature, acidosis, hypoglycemia, hypoxemia associated with anemia or lung damage, with pheochromocytoma and thyrotoxicosis, infectious toxicosis (neurotoxicosis when taking or overdose of drugs: adrenaline, inhalydine, atropine agonists of 2-adrenergic receptors (terbutaline, salbutamol, etc.).

Lymphostasis, syndrome chronic fatigue... Osteopathy helps at any age. Even babies will benefit from osteopathic treatment. two to three treatment sessions can help restore normal sleep, to get rid of unreasonable whims and anxiety. The course of pediatric osteopathy helps to improve the child's appetite, helps to normalize reflexes and muscle tone.

Hypercatecholaminemia, sinus node hypersensitivity to catecholamines, as well as hypovagotonia determine the pathogenesis, clinical picture and treatment tactics of this type of tachycardia 35. According to ON. Voronina 9, in children with chronic sinus tachycardia, pronounced autonomic dysfunction with a high tone of the parasympathetic division of the autonomic nervous system is the leading one.

Any symptoms of cardiac dysfunction, adolescents' complaints of poor health should alert parents and be a reason to see a doctor. Also pay attention to outdoor games of younger children. When the child's behavior changes during the game: Rapid fatigue, shortness of breath, pallor of the skin, it should be examined by a cardiologist.

In this case, it is necessary to remove an electrocardiogram for the child. Heart murmurs are not always audible. With obvious tachycardia, extrasystole, we can talk about the late manifestation of cardiopathy in children. Therefore, it is important to timely identify this pathology. To do this, you should constantly maintain the child's health, observe preventive measures, and also appear at a cardiologist's appointment at least once a year, with a mandatory examination.

In children, heart rate depends on age (Table 1). Distinguish sinus tachycardia: 1) moderate (I degree) increased heart rate by 1020 higher age norm; 2) medium (II degree) by 2040; 3) pronounced (III degree) on. Sinus tachycardia can be physiological and pathological, and pathological is subdivided into extracardiac and cardiac 2, 21.

V. I. Starodubov dated March 6, 2008 N 1619-Sun organization of selection of patients for high-tech treatment methods according to profile # 171; cardiovascular surgery # 187; guidelines

Unspecified heart rhythm disorder

For selection for high-tech methods of treating arrhythmias, it is rational to classify on the basis of their clinical significance.

When examining young people, it is advisable to distinguish two types of arrhythmias: I type # 8212; unstable, not significantly affecting well-being and prognosis; II type # 8212; persistent arrhythmias affecting the patient's condition and having prognostic value.

Type I (unstable arrhythmias): supraventricular extrasystoles, rare ventricular extrasystoles (up to 10 per hour), migration of the pacemaker, sinus bradycardia and sinus tachycardia, if they do not manifest themselves clinically. When detecting such arrhythmias, these persons usually do not need additional research; in most cases, these arrhythmias are a finding when examining young people.

Type II (persistent, significant arrhythmias): frequent (more than 10 per minute or 100 per hour) and polytopic ventricular extrasystoles, paroxysmal cardiac arrhythmias (supraventricular and ventricular tachycardias, atrial fibrillation and flutter), sick sinus syndrome. This group also includes WPW syndrome and CLC syndrome, since it can be combined with latent WPW syndrome. If arrhythmias of the II group are detected, these persons need additional examination in order to clarify the nature and severity of arrhythmias, identify the mechanisms of arrhythmia development and resolve the issue of the need for their correction. The main instrumental methods for diagnosing cardiac arrhythmias are presented in Table 6.

Basic instrumental diagnostic methods

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The main types of ventricular arrhythmias include ventricular tachycardia and ventricular premature beats.

1. Name of the protocol: Premature depolarization of the ventricles (ventricular premature beats). Ventricular tachycardia (VT).

3. Duration (days) of days.

4. Profile: cardiological

5 Indications for hospitalization: ventricular premature beats varying degrees severity (11-5 gradation according to Law), first-emerging or recurrent episodes of ventricular tachycardia.

Admission: planned or emergency (prolonged attack of tachycardia)

6. Definition: Ventricular arrhythmias are arrhythmias in which the source of ectopic impulses is located below the His bundle, that is, in the branches of the His bundle. in Purkinje fibers or in the ventricular myocardium.

Ventricular extrasystole (PVC) is called a premature (extraordinary) contraction of the heart (from the above sections), directly related to the previous contraction of the main rhythm. Three or more ventricular complexes with a frequency of 100 to 240 beats per minute are considered to be ventricular tachycardia.

7. Classification of ventricular arrhythmias B. Lown and M. Wolf (1971,1983)

1. Rare single monomorphic extrasystoles - less than 30 per hour (1A-less than 1 per minute and 1 B-more than 1 per minute).

2. Frequent single monomorphic extrasystoles - more than 30 per hour.

3. Polymorphic (multimorphic) ventricular extrasystoles.

4. Repeated forms of ventricular arrhythmias:

4A- paired verses.

4B-group (volleys), including short episodes of ventricular tachycardia.

5. Early ventricular extrasystoles - type R on T.

VT and PVC can be monomorphic and polymorphic. Polymorphic VT can be bidirectional (more often with glycosidic intoxication), as well as bidirectional spindle-shaped, such as "pirouette" (with extended OT syndrome). Ventricular tachycardia can be paroxysmal or chronic. If VT lasts more than 30 seconds, it is called stable.

The main diagnostic criteria (clinical and instrumental): interruptions in the work of the heart, episodes of palpitations, accompanied by shortness of breath, pain in the heart, dizziness, rarely episodes of loss of consciousness.

ECG with PVC and VT: wide QRS complexes (more than 0.12 seconds) of various configurations depending on the location of the arrhythmogenic focus (discordant changes in the terminal part of the ventricular complex - the ST segment, the T wave). With PVC, a complete compensatory pause is usually recorded. With VT, artioventricular (a-c) dissociation and the presence of conducted and / or confluent QRS complexes are often observed.

Basic differential diagnostic ECG signs tachyarrhythmias (with broadened QRS complexes).

Supraventricular tachycardia with functional IV block (occurring at the time of paroxysm)

Supraventricular tachycardia (in patients with a previous violation of intravenous conduction, i.e. with sinus rhythm.

Supraventricular tachyarrhythmias (patients with ventricular pre-excitation syndrome - WPW syndrome)

1. QRS complexes more often than 0.14 seconds. 2. Mono or biphasic QRS complexes in holes V1 V6 are characteristic. 3. The presence of RSR in holes V1 R | S -1.0 in holes V6 in combination with EOS deviation to the left. 4. There may be a-in dissociation with the capture of the ventricles by sinus impulses (confluent complexes).

1. QRS complexes no more than 0.14 seconds, more often up to 0.12 seconds. 2. Often QRS complexes are in the form of blockade right leg of the His bundle with three-phase complexes in holes V1 V6. (rSR type in V1 and qRS type in V6.

QRS complexes during tachycardia are the same as during sinus rhythm.

1. QRS complexes during supraventricular tachycardia are the same as during sinus rhythm (the rhythm during tachycardia is regular) There may be an increase in the degree of pre-excitation at the time of tachycardia - an increase in delta waves. 2. In patients with atrial fibrillation or atrial flutter, the QRS complexes during tachyarrhythmia are the same as in sinus rhythm (the rhythm at the time of tachycardia is often irregular, with flutter it can be regular). I can note an increase in the degree of pre-excitation at the time of tachyarrhythmia - an increase in the delta wave.

Mandatory minimum examinations before hospitalization:

2.general analysis blood.

3. general urine analysis.

4. study of feces for helminths.

Tachycardia

Tachycardia is a condition in which the heart rate exceeds 90 beats per minute. Tachycardia can occur as a result of an increase in heart rate due to physical exertion, stressful situations or excitement, and be a consequence of an increase in heart rate at rest.

In some cases, tachycardia can be uneventful, however, it can seriously disrupt the normal function of the heart, increase the risk of stroke, or can lead to sudden cardiac arrest and death. Risk factors for developing tachycardia are obesity and type 2 diabetes. Allocate sinus tachycardia, paroxysmal and ventricular fibrillation.

Sinus tachycardia

Sinus tachycardia is a condition when impulse conduction from the sinus node to the ventricles is disturbed or the generation of impulses by the sinus nodes that control the heart rhythm is disturbed. It is detected using an electrocardiogram, and its causes can be both external factors and malfunctioning of the sinus node.

Paroxysmal tachycardia

Paroxysmal tachycardia is a condition in which an attack of rapid heartbeat suddenly occurs and stops, with a frequency of beats per minute. There are three forms of paroxysmal tachycardia:

The immediate causes of this type of tachycardia are increased activity of the nervous system and dystrophic changes in the myocardium.

Ventricular fibrillation

Ventricular fibrillation is a condition in which, with a frequency of beats per minute, a chaotic contraction of myocardial fibers occurs, which leads to the absence of ventricular contractions and cardiac arrest. Often, ventricular fibrillation is a consequence of complications caused by extensive myocardial infarction.

Causes of tachycardia

The most common causes of tachycardia are disorders of the autonomic nervous system and hemodynamics, various forms of arrhythmias and disorders of the endocrine system.

Often, tachycardia is a consequence of hypertension. coronary heart disease, myocardial infarction and heart defects. Also, one of the causes of tachycardia is excessive consumption of caffeine, alcoholic beverages and tobacco smoking. Diseases of the thyroid gland and various infectious diseases contribute to the development of tachycardia.

Tachycardia symptoms

The symptoms of tachycardia are:

In some cases, tachycardia can occur without the above symptoms. In such cases, as a rule, the condition is detected by physical examination or heart monitoring.

Diagnosis of tachycardia

Diagnosis of tachycardia occurs through a medical examination, a series of examinations, analyzes and tests. Common tests for making a diagnosis are:

• Electrophysiological study, with the help of which it becomes possible to determine the source of problems of the cardiac system;
• Electrocardiography, which determines the type of tachycardia and its effect on heart rate;
• Holter monitoring, on the basis of which it becomes possible to obtain a complete symptomatic picture of the disease.

Tachycardia treatment

The main areas of treatment for tachycardia are to prevent its attacks in the future, minimize the complications caused and bring the heart rate to a normal state. Treatment of tachycardia can be medication, with the appointment of special medications, or it can consist in changing the patient's lifestyle, avoiding stressful situations and having good rest.

International Statistical Classification of Diseases and Related Health Problems - a document used as a leading framework in public health. ICD is a regulatory document that ensures the unity of methodological approaches and international comparability of materials.

Currently, the International Classification of Diseases of the Tenth Revision (ICD-10, ICD-10) is in force.

In Russia, health authorities and institutions made the transition of statistical accounting to ICD-10 in 1999.

ICD 10 - International classification of diseases 10th revision

Supraventricular (supraventricular or atrial) tachycardia characterized by a sudden rapid heartbeat, which is felt even without probing the pulse. The heart rate is 140-250 beats per minute. Impulses during supraventricular tachycardia are formed above the level of the ventricles, namely in the atria or atrioventricular node.

Classification

There are several types of supraventricular tachycardia, depending on the localization of the ectopic center of increased automatism or a constantly circulating wave of excitation (re-entry):

Paroxysmal atrial tachycardia (AT)

There are the following types of atrial paroxysmal tachycardia, which differ in the localization of the arrhythmogenic focus, as well as in the mechanisms of development:
1. Sinoatrial (sinus) reciprocal paroxysmal tachycardia (PT) caused by the re-entry mechanism in the sinoatrial zone.
2. Reciprocal atrial paroxysmal tachycardia (PT) caused by the re-entry mechanism in the atrial myocardium.
3. Focal (focal, ectopic) atrial paroxysmal tachycardia (PT), which is based on the abnormal automatism of the atrial fibers.
4. Multifocal (“chaotic”) atrial paroxysmal tachycardia (PT), which is characterized by the presence of several foci of ectopic activity in the atria.

5. Atrioventricular paroxysmal tachycardia (PT)
- atrioventricular nodal (AV-nodal) reciprocal paroxysmal tachycardia (PT) without the participation of additional conduction pathways;
- typical (slow-fast) - with antegrade conduction along the slow path as part of the atrioventricular connection (AV connection) and retrograde along the fast path;
- atypical (fast-slow) - with antegrade conduction along the fast path as part of the atrioventricular connection (AV connection) and retrograde along the slow path;
- atrioventricular reciprocal (AV-reciprocal) paroxysmal tachycardia (PT) with the participation of additional pathways;
- orthodromic - the impulse is conducted antegrade through the atrioventricular junction (AV junction) and retrograde along an additional path;
- antidromic - the impulse is carried out antegrade along an additional path and retrograde through the atrioventricular junction (AV junction);
- with the participation of hidden additional retrograde conduction pathways (fast or slow);
- focal (focal, ectopic) paroxysmal tachycardia (PT) from the atrioventricular junction (AV junction).

It should be noted that until now there are discrepancies in the classification and terminology of paroxysmal tachycardia (PT) in different authors. Given the complexity of diagnosing paroxysmal rhythm disturbances, all tachyarrhythmias are divided into two types, according to international recommendations:
- tachycardia with a narrow QRS complex (antegrade conduction through the AV node); usually supraventricular paroxysmal tachycardia;
- tachycardia with a wide QRS complex (antegrade conduction through the accessory pathway); requires urgent differential diagnosis between various supraventricular and ventricular tachycardias (VT), and if it is impossible to completely exclude ventricular tachycardias (VT), treatment is carried out in the same way as with proven paroxysm of ventricular tachycardias (VT) ("to the maximum"); with unstable hemodynamic parameters, immediate cardioversion is indicated.

Depending on the localization of the ectopic center of increased automatism or a constantly circulating wave of excitation (reentry), there are:

• Paroxysmal atrial tachycardia (AT)

  Depending on the localization of the arrhythmogenic focus and development mechanisms, they are distinguished:

  • Sinoatrial (sinus) reciprocal paroxysmal tachycardia (PT) caused by the reentry mechanism in the sinoatrial zone.
  • Reciprocal atrial paroxysmal tachycardia (PT) due to the reentry mechanism in the atrial myocardium.
  • Focal (focal, ectopic) atrial paroxysmal tachycardia (PT), which is based on abnormal automatism of atrial fibers.
  • Multifocal (“chaotic”) atrial paroxysmal tachycardia (PT), which is characterized by the presence of several foci of ectopic activity in the atria.

• Atrioventricular paroxysmal tachycardia (PT)
  • Atrioventricular nodular (AV-nodular) reciprocal paroxysmal tachycardia (PT) without the involvement of additional conduction pathways
    • Typical (slow-fast) - with antegrade conduction along the slow path as part of the atrioventricular junction (AV junction) and retrograde along the fast path.
    • Atypical (fast-slow) - with antegrade conduction along the fast path as part of the atrioventricular junction (AV junction) and retrograde along the slow path.
  • Reciprocal atrioventricular (AV-reciprocal) paroxysmal tachycardia (PT) involving accessory pathways
    • Orthodromic - the impulse is conducted antegrade through the atrioventricular junction (AV junction) and retrograde along an additional path.
    • Antidromic - the impulse is carried out antegrade along the accessory path and retrograde through the atrioventricular junction (AV junction).
    • With the participation of hidden additional retrograde conduction pathways (fast or slow).
  • Focal (focal, ectopic) paroxysmal tachycardia (PT) from the atrioventricular junction (AV junction).

It should be noted that until now there are discrepancies in the classification and terminology of the description of paroxysmal tachycardia (PT) by different authors. Given the difficulties in diagnosing paroxysmal rhythm disturbances, according to international recommendations, all tachyarrhythmias are divided into two types:

Tachycardia with a narrow QRS complex (antegrade conduction through the AV node); most often it is supraventricular paroxysmal tachycardia.
- Tachycardia with a wide QRS complex (antegrade conduction through the accessory pathway); requires urgent differential diagnosis between various supraventricular and ventricular tachycardias (VT), and if it is impossible to completely exclude ventricular tachycardias (VT), treatment is carried out in the same way as with proven paroxysm of ventricular tachycardias (VT) ("to the maximum"); with unstable hemodynamic parameters, immediate cardioversion is indicated.

Etiology and pathogenesis

Etiology

Organic (dystrophic, inflammatory, necrotic and sclerotic) damage to the heart muscle and the cardiac conduction system (in acute myocardial infarction, chronic ischemic heart disease, myocarditis, cardiopathy, heart disease).
- Additional abnormal conduction pathways (eg, WPW syndrome).
- Severe vegetative-humoral disorders (for example, in patients with NCD).
- The presence of viscerocardiac reflexes and mechanical influences (additional chords, mitral valve prolapse, adhesions).

Often, in children, adolescents and young people, it is not possible to identify a disease that could cause atrial or atrioventricular paroxysmal supraventricular tachycardia (PNT). In such cases, cardiac arrhythmias are usually regarded as essential, or idiopathic, although most likely the cause of arrhythmias in these patients is minimal, not detected by clinical and instrumental methods dystrophic lesions of the myocardium.

In all cases of paroxysmal supraventricular tachycardia (PNT), it is necessary to determine the level of thyroid hormones; although thyrotoxicosis is rarely the only cause of PNT, it creates additional difficulties in the selection of antiarrhythmic therapy.

Pathogenesis

The main mechanisms of paroxysmal tachycardia (PT) are:

Reentry and circular movement of the excitation wave (reentry) underlies the pathogenesis of paroxysmal supraventricular tachycardias (PNT) in the vast majority of cases - in the presence of sinus, atrial and atrioventricular nodal (AV-nodal) reciprocal tachycardia, including with ventricular pre-excitation syndromes.
- Increased automatism of the cells of the cardiac conduction system - ectopic centers of the II and III order and the trigger mechanism are the basis of the pathogenesis of paroxysmal supraventricular tachycardia (PNT) much less often - with ectopic atrial and atrioventricular (AV-tachycardia) tachycardia.

Epidemiology

Sign of prevalence: Widespread

Sex ratio (m / f): 0.5

The prevalence of paroxysmal supraventricular tachycardia in the population is 2.29 per 1000 people. In women, it is registered twice as often as in men. The risk of its development is more than 5 times higher in persons over 65 years of age.

In this case, atrial tachycardias account for 15-20%, atrioventricular - 80-85% of cases.

Clinical picture

Clinical diagnostic criteria

Sudden palpitations, weakness, dizziness,

Symptoms, course

Subjective tolerance of paroxysmal supraventricular tachycardias (PNT) largely depends on the severity of tachycardia: with a heart rate (HR) of more than 130-140 beats / min, paroxysm rarely remains asymptomatic. However, sometimes patients do not feel the paroxysm of tachycardia, especially if the heart rate during the attack is low, the attack is short-lived, and the myocardium is intact. Some patients perceive the heartbeat as moderate, but they feel weakness, dizziness and nausea during an attack. Generalized manifestations of autonomic dysfunction (tremors, chills, sweating, polyuria, etc.) with PNT are less pronounced than with attacks of sinus tachycardia.

Clinical picture to some extent depends on the specific type of arrhythmia, however, common to all PNT are complaints of a completely sudden onset of an attack of a sharp heartbeat. The rate of heart contractions, as it were, instantly switches from normal to very fast, which is sometimes preceded by a more or less long period of sensation of interruptions in the work of the heart (extrasystole). The end of an attack of PNT is as sudden as its onset, regardless of whether the attack stopped on its own or under the influence of drugs.

With very prolonged attacks, cardiovascular failure develops in most cases.

Auscultation during an attack reveals frequent rhythmic heart sounds; A heart rate of 150 beats / min and above excludes the diagnosis of sinus tachycardia, a heart rate of more than 200 makes ventricular tachycardia unlikely. It should be remembered about the possibility of atrial flutter with a conduction ratio of 2: 1, in which vagal tests can lead to a short-term deterioration in conduction (up to 3: 1, 4: 1) with a corresponding abrupt decrease in heart rate. If the duration of systole and diastole become approximately equal, the second tone in terms of volume and timbre becomes indistinguishable from the first (the so-called pendulum rhythm, or embryocardia). For most paroxysmal supraventricular tachycardias (PNT), rhythm rigidity is characteristic (its frequency is not influenced by intense breathing, physical activity, etc.).

However, auscultation does not allow to find out the source of tachycardia, and sometimes to distinguish sinus tachycardia from paroxysmal.

Occasionally, for example, with a combination of paroxysmal supraventricular tachycardia (PNT) and atrioventricular blockade of the II degree with periods of Samoilov-Wenckebach or with chaotic (multifocal) atrial tachycardia, the regularity of the rhythm is disturbed; while the differential diagnosis with atrial fibrillation possible only by ECG.

Blood pressure usually goes down. Sometimes the attack is accompanied by acute left ventricular failure (cardiac asthma, pulmonary edema).

Diagnostics

ECG:

Stable correct rhythm with heart rate from 140-150 to 220 beats / min. With a heart rate of less than 150 beats / min, sinus non-paroxysmal tachycardia is more likely. With a very high frequency of supraventricular tachycardia or latent disturbance of atrioventricular conduction during an attack, atrioventricular block II degree often develops with periods of Samoilov-Wenckebach or loss of every second ventricular contraction.

Ventricular complexes during an attack have the same shape and amplitude as outside the attack. Narrow QRS complexes (less than 0.12 sec) are characteristic. A wide QRS complex does not exclude PNT: sometimes in the presence of latent conduction disturbances in the branches of the intraventricular conduction system during an attack of tachycardia of a supraventricular nature, the ventricular QRS complexes are deformed and widened, usually as a complete blockade of one of the legs of the bundle of His (see below, as well as "Blocks hearts "). Deformation of the QRS complex (pseudo R-wave in lead V1 or pseudo S-wave in leads II, III, aVF) may be due to the imposition of a P wave on it in AV-nodal tachycardia.

Ventricular complexes are in one way or another associated with atrial P waves. The relationship of QRS complexes with atrial P waves can be different: the P wave can precede the ventricular complex (and the PQ interval is always greater or less than with sinus rhythm), can merge with the QRS complex, or follow him. The P wave must be actively sought (it can overlap the QRS complex or the T wave, deforming them). Sometimes it does not differentiate, completely merging with the T wave of the preceding ventricular complex or superimposed on the T wave following the QRS complex (as a result of slowing retrograde conduction during AV block). The absence of a P wave is possible with reciprocal AV tachycardia (P is "hidden" in the QRS complex) and does not exclude the diagnosis of PNT.

The P waves during an attack differ in shape, amplitude, and often in polarity from those recorded in a given patient against the background of a sinus rhythm. P wave inversion during an attack most often indicates atrioventricular genesis of tachycardia.

Holter monitoring
Holter monitoring allows you to record frequent paroxysms (including short - 3-5 ventricular complexes - "jogging" PNT, subjectively not perceived by the patient or felt as interruptions in the work of the heart), assess their beginning and end, diagnose transient ventricular preexcitation syndrome and concomitant arrhythmias ... Reciprocal arrhythmia is characterized by the beginning and end of an attack after supraventricular extrasystoles; a gradual increase in the frequency of the rhythm at the beginning of paroxysm ("warming up") and a decrease - at the end - indicate the automatic nature of tachycardia.

Exercise ECG tests
PNT is usually not used for diagnostics - it is possible to provoke paroxysm. If it is necessary to diagnose coronary artery disease in a patient with a history of syncope, it is preferable to use transesophageal cardiac stimulation (TEE).

Transesophageal heart stimulation (TPSS)
It can be used even in patients with poor tolerance of PNT, since it is well controlled by extrastimuli. Shown for:
- Clarification of the mechanism of tachycardia.
- Identification of PNT in patients with rare seizures that cannot be “caught” on the ECG.

Intracardiac electrophysiological study (EPI)
Allows you to accurately determine the mechanism of PNT and indications for surgical treatment.

Differential diagnosis

In the absence of organic heart disease in patients with PNT, the following conditions should be excluded:

Sick sinus syndrome (SSS). If it is not detected, PNT therapy can be not only unsuccessful, but also dangerous.
- Syndromes of pre-excitation of the ventricles. According to some data, the incidence of WPW syndrome in patients with PNT is up to 70%.

Should be performed with the following rhythm disturbances

PNT with aberrant conduction to the ventricles.
- PNT in combination with blockade of the pedicle of Hisa (ref I44.7, I45.0).
- Antidromic supraventricular tachycardia in WPW syndrome (ref I45.6).
- Atrial fibrillation / flutter in WPW syndrome.
- Atrial fibrillation / flutter with aberrant conduction to the ventricles.
- Ventricular tachycardia (ref I47.2)

Differential diagnosis of wide-complex PNT and ventricular tachycardia presents significant difficulties; it is advisable to navigate according to the signs given in table.

• Tab. Differential diagnosis of tachycardia with a wide QRS complex (A.V. Nedostup, O.V. Blagova, 2006)

  Sign	Paroxysmal supraventricular tachycardia (PNT)	Ventricular tachycardias (VT)
  Heart rate	150-250 bpm	140-220 bpm
  Typical start	With supraventricular extrasystoles	With ventricular premature beats
  Having a full compensatory pause after an attack	Uncharacteristic	Characteristically
  RR Interval Stability	Very high	Possible fluctuations within 0.03sec
  P wave	Determined before each QRS complex or completely absent	Occasionally, a slower atrial rhythm with sinus P, not associated with the QRS, or separate negative ones in lead II P after QRS with PR "> 0.10-0.12 s, can be determined.
  "Ventricular grips"	Not typical	Characteristic (narrow QRS preceded by sinus P and normal PQ)
  Drain QRS complexes	Not typical	Characteristic (intermediate between sinus and ectopic QRS, preceded by sinus P)
  Sharp EOS deviation to the left	For initial conduction disturbances	Characteristic as a feature of VT itself
  The characteristic QRS shape	V1 - RsR ", RS R", rS R ",	V1 RR ", qR, QR, Rsr" or monomorphic (especially negative) in V1-6; V6 - QR, QS, rS
  Transesophageal / endocardial electrogram	Identification of P waves clearly associated with ventricular complexes	Complete atrioventricular dissociation

With stable hemodynamics and a relatively low heart rate (HR), vagal tests can also be used for differential diagnosis of PNT and VT, as well as a test with IV injection of ATP (contraindicated in the presence of bronchial asthma, as well as previously established conduction disturbances), which are interpreted as follows:

Relief of an attack - paroxysmal supraventricular tachycardia (PNT).

Preservation of atrial tachycardia with an increase in conduction rate - atrial flutter or ectopic atrial tachycardia.

A gradual slowing down of the rhythm with a subsequent increase in frequency - non-paroxysmal tachycardia, ectopic atrial tachycardia.

No change - inadequate dose of ATP or VT.

Table Differential diagnosis of various variants of paroxysmal supraventricular tachycardia (PNT) (A.V. Nedostup, O.V. Blagova, 2006)

• • 
    

    ECG sign	Ectopic atrial tachycardia	Reciprocal sinus tachycardia	AV nodal reciprocal tachycardia *	AV nodal ectopic tachycardia
    RR stability	Gradual shortening of the RR at the beginning and lengthening at the end of the cycle	Rhythm frequency is subject to vegetative influences	Very high	Possible gradual changes in heart rate during paroxysm
    P wave	Positive / negative	Sinus		Missing or negative
    Ratio of PQ and QP	PQ is shorter than QP	PQ> sinus and shorter than QP	PQ is longer than QP, QP<100см без WPW, QP >100ms at WPW	PQ is longer than QP, QP> 70ms
    Multiple AV conduction blockade	Typically at atrial rate> 150-170	Typically at atrial rate> 150-170	Does not occur	Does not occur
    Reaction to IV injection of ATP	Slowing down of the ventricular rate, increasing the rate of AV block or stopping	Relief of paroxysm	Relief of paroxysm	Deceleration of the ventricular rate
    Transesophageal heart stimulation (TPSS)	Rarely - induction (triggered PT); does not stop (slowing down the rhythm)		Induction and relief by extrastimulus	Not induced or stopped

    * AV-nodal reciprocal tachyacardia refers to the following forms of reentry involving the AV-node:
    - AV nodal tachycardia without the involvement of additional pathways.
    - Orthodromic AV nodal tachycardia in WPW syndrome.

Complications

With very prolonged attacks, cardiovascular failure develops in most cases. If PNT appears in a patient with severe myocardial lesions (heart attack, congestive cardiomyopathy), a cardiogenic (arrhythmogenic) shock may develop in the first minutes after the onset of an attack. Dangerous are also such violations of hemodynamics, which sometimes occur against the background of PNT, as disorders of consciousness up to syncope, attacks of Morgagni-Adams-Stokes. Fainting occurs in about 15% of PNT cases and usually occurs either at the onset of the attack or after its end. Some patients experience anginal pain during an attack (most often with ischemic heart disease); shortness of breath often develops (acute heart failure - up to pulmonary edema).

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Treatment

Relief of an attack of paroxysmal supraventricular tachycardia (PNT)

PNT is characterized by a stopping effect vagal samples... The most effective is usually the Valsalva test (straining with holding the breath for 20-30 seconds), but deep breathing, the Danini-Aschner test (pressure on the eyeballs for 5 seconds), squatting down, lowering the face into cold water for 10 -30 sec, massage of one of the carotid sinuses, etc.
The use of vagal tests is contraindicated in patients with conduction disorders, CVS, severe heart failure, glaucoma, as well as with severe discirculatory encephalopathy and a history of stroke. Massage of the carotid sinus is also contraindicated with a sharp decrease in pulsation and the presence of noise over the carotid artery.
In the absence of the effect of vagal tests and the presence of pronounced hemodynamic disorders, emergency relief of paroxysm is indicated with the help of transesophageal heart stimulation (TPSS) or electroimpulse therapy (EIT)... NPVS is also used in case of intolerance to antiarrhythmics, anamnestic data on the development of serious conduction disturbances during recovery from an attack (with CVS and AV blocks). In multifocal atrial tachycardia, EIT and HRV are not used; they are ineffective in ectopic atrial and ectopic AV-nodular forms of PNT.

For paroxysmal supraventricular tachycardia (PNT) with narrow QRS complexes

In the absence of a positive effect of vagal tests, patients with stable hemodynamics begin intravenous administration antiarrhythmic drugs. It is permissible to use these funds without electrocardiographic control only in critical situations or in the presence of reliable information that the patient was repeatedly injected with this agent in the past and this did not cause complications. All ampouled preparations, except for triphosadenine (ATP), are diluted before administration in 10-20 ml of isotonic sodium chloride solution. The drugs of choice are adenosine (sodium adenosine triphosphate, ATP) or nonhydropyridine calcium channel antagonists.

Adenosine (adenosine phosphate) at a dose of 6-12mg (1-2 amp. 2% solution) or Sodium adenosine triphosphate (ATP) rapidly in a dose of 5-10mg (0.5-1.0ml 1% solution) only in the intensive care unit under monitor control (it is possible to exit the PNT through stopping the sinus node for 3-5 seconds or more!).
- Verapamil is injected slowly in a stream at a dose of 5-10 mg (2.0-4.0 ml 2.5% solution) under the control of blood pressure and rhythm frequency.
- Procainamide (Novocainamide) is injected in / in a jet slowly or drip at a dose of 1000 mg (10.0 ml of 10% solution, the dose can be increased to 17 mg / kg) at a rate of 50-100 mg / min under the control of blood pressure (with a tendency to arterial hypotension - together with 0.3-0.5 ml of 1% solution of phenylephrine (Mezaton) or 0.1-0.2 ml of 0.2% solution of norepinephrine (noradrenaline)):
- Propranolol is injected intravenously in a stream at a dose of 5-10 mg (5-10 ml of 0.1% solution) for 5-10 minutes with a short pause after half the dose is administered under the control of blood pressure and heart rate; in case of initial hypotension, its introduction is undesirable even in combination with mezaton.
- Propafenone is injected intravenously in a jet at a dose of 1 mg / kg for 3-6 minutes.
- Disopyramide (Ritmilen) - at a dose of 15.0 ml of a 1% solution in 10 ml of saline (if novocainamide was previously administered).

During vagal administration or administration of drugs, ECG registration is required; the reaction to them can help in diagnosis, even if the arrhythmia has not stopped. After the introduction of an antiarrhythmic, which was not complicated by the development of bradycardia or stopping the sinus node, it makes sense to repeat vagal techniques.

Approximate frequency and sequence of drug administration:

1. Sodium adenosine triphosphate (ATP) 5-10mg IV push.
2. No effect - after 2min ATP 10mg IV push.
3. No effect - after 2 min of verapamil 5 mg IV.
4. No effect - after 15 minutes verapamil 5-10 mg IV.
5. Repeat vagal techniques.
6. No effect - after 20 minutes novocainamide, or propranolol, or propafenone, or disopyramide - as indicated above; however, in many cases, hypotension is aggravated and the likelihood of bradycardia after restoration of sinus rhythm increases.

An alternative reuse the above drugs can serve as an introduction:

Amiodarone (Cordarone) at a dose of 300 mg in a stream for 5 minutes or drip, however, taking into account the delay of its action (up to several hours), as well as the effect on the conductance and duration of QT, which may prevent the administration of other antiarrhythmics. A special indication for the administration of amiodarone is a paroxysm of tachycardia in patients with ventricular pre-excitation syndromes.
- Etacizin (Etacizin) 15-20mg IV for 10 min, which, however, has a pronounced proarrhythmic effect, and also blocks conduction.
- Nibentan 10-15mg drip - with resistance to the main drugs, only under BIT conditions (!) - has a pronounced proarrhythmic effect, a high incidence of severe ventricular arrhythmias.

If there are no conditions for intravenous administration of drugs, use (chew tablets!):

Propranolol (Anaprilin, Obzidan) 20-80mg.
- Atenolol (Atenolol) 25-50mg.
- Verapamil (Isoptin) 80-120 mg (in the absence of pre-excitation!) In combination with phenazepam (Phenazepam) 1 mg or clonazepam 1 mg.
- Or one of the previously effective antiarrhythmics in a double dose of quinidine (Quinidin-durules) 0.2 g, procainamide (Novocainamide) 1.0-1.5g, disopyramide (Ritmilen) 0.3g, ethazizin (Etacizin) 0.1g, propafenone (Propanorm) 0.3g , sotalol (Sotagexal) 80mg).

With PNT with wide QRS complexes

The tactics are somewhat different, since the ventricular nature of the tachycardia cannot be completely excluded, and the possible presence of a pre-excitation syndrome imposes certain restrictions.

Electric pulse therapy (EIT) is indicated for hemodynamically significant tachycardia; if paroxysm is tolerated satisfactorily, transesophageal cardiac stimulation (TEE) is desirable. Medical relief is carried out with drugs that are effective both for paroxysmal supraventricular tachycardia (PNT) and for ventricular tachycardia: the most commonly used are procainamide (Novocainamide) and / or amiodarone; if they are ineffective, relief is carried out as with ventricular tachycardia (VT).

For unspecified wide-complex tachycardia, adenosine (ATP) and aymaline can also be used (with a very likely supraventricular genesis, tachycardia helps in differential diagnosis supraventricular tachycardia (NVT) and ventricular tachycardia (VT), lidocaine, sotalol.

Cardiac glycosides and verapamil, diltiazem, β-blockers (propranolol, atenolol, nadolol, metoprolol, etc.) should not be used because of the possibility of improving conduction along the additional path and the occurrence of flutter or ventricular fibrillation.

In patients with left ventricular dysfunction, only amiodarone, lidocaine and electrical pulse therapy (EIT) are used to relieve tachycardia with wide complexes of an unspecified nature.

After testing 1 or 2 drugs, further attempts at pharmacological relief of the attack should be stopped and switched to PPVS or (in the absence of technical feasibility or ineffectiveness) - to EIT.

Surgery

Surgical treatment is indicated for patients with severe PNT course and refractory to drug therapy; with WPW syndrome there are additional indications to surgery

Two fundamentally different surgical approaches are used:

Destruction (mechanical, electrical, chemical, cryogenic, laser) of additional pathways or foci of heterotopic automatism
- Implantation of pacemakers operating in pre-programmed modes (paired stimulation, "exciting" stimulation, etc.).

Forecast

The prognosis is determined by the type of paroxysmal supraventricular tachycardia (PNT) that caused it, the frequency and duration of attacks, the presence or absence of complications during an attack, the state of the contractile myocardium (severe myocardial damage predispose to the development of acute heart or cardiovascular failure, sudden arrhythmic death, ischemia myocardium, etc.).

The prognosis in patients with "essential" PNT is usually favorable: most patients remain fully or partially able to work for many years or decades, although complete spontaneous cure is rarely observed.

If supraventricular tachycardia is due to myocardial disease, the prognosis largely depends on the rate of development and the effectiveness of treatment of this disease.

Hospitalization

Urgent hospitalization is necessary for an attack of supraventricular tachycardia, if it cannot be stopped outside the hospital or is accompanied by acute cardiovascular or heart failure.

Routine hospitalization is indicated for patients with frequent (more than 2 times a month) attacks of tachycardia for in-depth diagnostic examination and determination of patient treatment tactics, including indications for surgical treatment.

Prophylaxis

Prevention of essential paroxysmal supraventricular tachycardia (PNT) is unknown; for PNT in heart disease, primary prevention coincides with prevention of the underlying disease. Secondary prophylaxis should be considered treatment of the underlying disease, continuous drug antiarrhythmic therapy, and surgical treatment.

Supportive antiarrhythmic therapy for PNT

Constant anti-relapse therapy is indicated for patients who have attacks twice a month or more often, and medical help is needed to stop them.

• Tab. Recommendations for the appointment of prophylactic antiarrhythmic therapy for PNT (ACC / AHA / ESC, 2003)

  Resistant to beta-blockers and verapamil, AV-nodal

  Vagus tests I V Rare, well-tolerated AV nodal

It is advisable to start therapy with beta-blockers with a clear effect of vagal tests that stops paroxysm. Non-selective beta-blockers are often more effective antiarrhythmics, therefore, in the absence of contraindications and conditions requiring the mandatory appointment of highly selective beta-blockers, atenolol (Atenolol) 50-100 mg / day should be used (or propranolol (Anaprilin, Obzidan) 40-160 mg / day in 4 reception). Also used: metoprolol (Vasokardin, Egilok) 50-100mg / day, betaxolol (Lokren) 10-20mg / day, bisoprolol (Concor) 5-10mg / day;

Verapamil (Isoptin) at a dose of 120-480 mg / day or diltiazem (Diltiazem, Cardil) 180-480 mg / day, preferably in retard form, is prescribed in the absence of WPW syndrome. High doses should not be avoided - the prophylactic efficacy of drugs is dose-dependent.

It is necessary to exclude the use of drugs that cause sinus tachycardia, if against their background PNT paroxysms become more frequent, and also limit the intake of alcohol, tea, coffee, smoking; it should be remembered that the patient may use (often hidden) various drugs (amphetamine, ecstasy, etc.).

Information

Information

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• MedElement website and mobile applications "MedElement", "Lekar Pro", "Dariger Pro", "Diseases: Therapist's Guide" are exclusively information and reference resources. The information posted on this site should not be used to unauthorized changes in the doctor's prescriptions.
• The editors of MedElement are not responsible for any damage to health or material damage resulting from the use of this site.