Does ventricular fibrillation always end in clinical death? Ventricular fibrillation: clinical presentation, ECG readings and emergency care

a common part

Ventricular fibrillation (fibrillation) (VF) is a disorganized electrical activity of the ventricular myocardium, which is based on the re-entry mechanism.

During ventricular fibrillation, their full contractions stop, which is clinically manifested by a cessation of blood circulation, accompanied by loss of consciousness, absence of pulsation and blood pressure in large arteries, absence of heart sounds and respiration. At the same time, frequent (300 to 400 per minute), irregular, not having a clear configuration, electrical oscillations with varying amplitude are recorded on the ECG.

Close to ventricular fibrillation is ventricular flutter (VF) , which is a ventricular tachyarrhythmia with a frequency of 200-300 per minute.

As with fibrillation, ventricular contractions are ineffective and cardiac output is virtually absent. With flutter on the ECG, regular flutter waves of the same shape and amplitude are noted, resembling a sinusoidal curve. Flutter of the ventricles is an unstable rhythm, which in most cases quickly turns into their fibrillation, occasionally into sinus rhythm.

Fibrillation (fibrillation) of the ventricles is the leading cause of sudden cardiac death.

Treatment of ventricular fibrillation (fibrillation) is the use of emergency cardiopulmonary resuscitation, including immediate defibrillation.

• Epidemiology of ventricular fibrillation (fibrillation)

  Ventricular fibrillation occurs in 70% of cardiac arrests. Of the 300,000 deaths from sudden cardiac death in the United States, 75% -80% of cases are due to the development of ventricular fibrillation (atrial fibrillation).

  Ventricular fibrillation is more common in men than in women (3: 1).

  Most often, ventricular fibrillation is noted among people aged 45-75 years.

• ICD-10 code

  I49.0 Ventricular fibrillation (flicker).

Etiology and pathogenesis

• Etiology of ventricular fibrillation (fibrillation)

  In most patients, ventricular fibrillation develops against the background of various heart diseases, as well as other extracardiac disorders.

  The reasons for the development of ventricular fibrillation can be the following diseases and pathological conditions:

  • Ischemic heart disease.

    First of all, the cause of the development of ventricular fibrillation is an acute violation of the coronary circulation, acute and postponed myocardial infarction.

    According to the Framingham study, in CHD, sudden cardiac death accounts for 46% of deaths among men and 34% among women. Similar data were obtained in other studies. The highest incidence of ventricular fibrillation and sudden cardiac death is observed at the height of myocardial ischemia in the first 12 hours of acute infarction.

    An increased risk of ventricular fibrillation and sudden cardiac death is also noted in patients with Q-wave myocardial infarction due to the presence of a morphological substrate for the occurrence of potentially fatal ventricular arrhythmias (paroxysmal ventricular tachycardias).

  • Hypertrophic cardiomyopathy.

    In hypertrophic cardiomyopathy, sudden cardiac death most often occurs in young people during intense physical activity. The risk of sudden cardiac death decreases with age.

    During the cessation of blood circulation in such patients, polymorphic ventricular tachycardia is usually recorded, turning into ventricular fibrillation. It must be remembered that loss of consciousness and severe hemodynamic disturbances in them can also be caused by any supraventricular tachycardia with a rapid ventricular rhythm.

  • Dilated cardiomyopathy.

    The proportion of patients with dilated cardiomyopathy accounts for about 10% of successfully resuscitated after sudden cardiac arrest.

    Sudden death usually occurs against the background of severe hemodynamic disorders in about half of patients with dilated cardiomyopathy. It must be remembered that in such patients, as in patients with hypertrophic cardiomyopathy, sudden death is equally often caused by ventricular fibrillation and bradyarrhythmias.

  • Canalopathy.

    Canalopathies are the following pathological syndromes: Brugada syndrome, arrhythmogenic dysplasia (cardiomyopathy) of the right ventricle, long QT interval syndrome, Wolff-Parkinson-White syndrome (WPW).

    By the degree of malignancy of ventricular arrhythmias, this group is close to ischemic heart disease.

    The "harbinger" of ventricular fibrillation (atrial fibrillation) in Brugada syndrome and long QT syndrome is most often ventricular tachycardia of the "pirouette" type, in arrhythmogenic dysplasia (cardiomyopathy) of the right ventricle - monomorphic ventricular tachycardia, in WPW syndrome - polymorphic ventricular tachycardia.

  • Valvular heart disease.

    Among valvular heart diseases, ventricular fibrillation and sudden cardiac death are most often caused by stenosis of the aortic orifice (congenital and acquired), which, as in the case of hypertrophic cardiomyopathy, is caused by hypertrophy of the left ventricular myocardium and the possibility of a sharp deterioration in its filling and expulsion.

    In patients with mitral valve prolapse, despite the significant frequency of ventricular arrhythmias, ventricular fibrillation occurs extremely rarely and is usually associated with disturbances in the electrophysiological properties of the myocardium.

  • Specific cardiomyopathies.

    Specific cardiomyopathies leading to ventricular fibrillation and sudden cardiac death primarily include inflammatory cardiomyopathies, especially cardiomyopathy in sarcoidosis.

  • More rare causes of ventricular fibrillation:
    • Intoxication with cardiac glycosides, as well as side effects when taking medium doses of cardiac glycosides (strophanthin K).
    • Electrolyte disturbances.
    • Electric shock.
    • Hypothermia.
    • Hypoxia and acidosis.
    • Coronary angiography, cardioversion.
    • Side effects when taking certain drugs: sympathomimetics (epinephrine, orciprenaline, salbutamol), barbiturates, anesthetics (cyclopropane, chloroform), narcotic analgesics, TAD, phenothiazine derivatives (chlorpromazine, levomepromazine), amiodarone, sotalol drugs, class I antiarrhythmias ( most often - against the background of "pirouette" tachycardia due to prolongation of the QT interval).

• Pathogenesis of ventricular fibrillation (fibrillation)

  With ventricular fibrillation, multiple re-entry loops are formed in the ventricular myocardium. In this case, there are contractions of individual myocardial fibers, but there is no effective contraction of the entire ventricles. This is due to the heterogeneity of the electrophysiological state of the myocardium, when its individual sections are simultaneously in different time periods of depolarization and repolarization.

  The development of fibrillation is facilitated by a number of factors that reduce the electrical stability of the myocardium; among them, the most important is an increase in the size of the heart, the presence of foci of sclerosis and degeneration in the contractile imocardium and the conducting system, an increase in sympathetic activity. Electrical instability of the myocardium is usually indicated by the presence of malignant and potentially malignant ventricular arrhythmias.

  Ventricular fibrillation in more than 90% of patients is caused by ventricular tachycardia, monomorphic or polymorphic, much less often it can be induced by 1-2 early, type R to T, ventricular extrasystoles, causing the occurrence of an unequal degree of depolarization in various muscle fibers.

Clinic and complications

• The clinical picture with flutter and ventricular fibrillation

  With flutter and ventricular fibrillation, there is a cessation of blood circulation with loss of consciousness, absence of pulse (including on the carotid and femoral arteries) and breathing. Diffuse cyanosis develops.

  There is an expansion of the pupils and the lack of their response to light.

  Often, flutter and ventricular fibrillation are accompanied by convulsions, involuntary urination and defecation.

  With ventricular flutter, cardiac output, consciousness, and blood pressure (usually low) may persist for a short time. In most cases, however, this erratic rhythm quickly turns into ventricular fibrillation.

  Ventricular fibrillation always comes on suddenly. After 15-20 seconds from its onset, the patient loses consciousness, after 40-50 seconds, characteristic convulsions develop - tonic muscle contraction. At the same time, the pupils begin to dilate. Breathing gradually decreases and stops at the 2nd minute of clinical death. If within 4 minutes it is not possible to restore an effective heart rate, irreversible changes occur in the central nervous system and other organs.

• Complications of flutter and ventricular fibrillation

  Human ventricular fibrillation cannot spontaneously stop; accordingly, the main complication is death.

  Only cardiopulmonary resuscitation is capable of restoring sinus rhythm, the main point of which is electrical defibrillation, the effectiveness of which depends on the nature of the underlying disease, the severity of the associated heart failure, as well as on the timeliness of use. These factors are associated with the presence and severity of non-fatal complications during flutter and ventricular fibrillation, which are observed after the restoration of an effective heart rate almost always, with the exception of relatively rare cases of early electrical defibrillation.

  Complications are associated with both circulatory arrest and the resuscitation measures themselves.

  Potential lung complications include aspiration pneumonia and lung damage from broken ribs.

  During cardiac arrest, total myocardial ischemia develops, and after restoration of coronary circulation, its more or less pronounced transient dysfunction due to reperfusion syndrome and the so-called stunning (Stunning).

  In the postresuscitation period, very often there are also a wide variety of arrhythmias, caused either by the same cause as the preceding ventricular fibrillation, or by violations of the bioelectrical and mechanical functions of the myocardium associated with the postponed circulatory arrest.

  Neurological complications (anoxic encephalopathy) are manifested by convulsive syndrome and coma, up to decortication. It should be noted that severe brain damage after successful cardiac resuscitation is extremely rare, primarily because if resuscitation measures are carried out untimely or poorly, then cardiac activity cannot be restored.

  The degree of impairment of consciousness after prolonged cardiopulmonary resuscitation can be assessed on the scale of the depth of the coma.

  The scale is intended for an objective assessment of the severity of a coma of any etiology in patients who are not under the influence of drugs that depress the central nervous system, respiration, and muscle tone. At 30-34 points, the state of consciousness can be assessed as stunning; at 20-29 points - as stupor; with 8-19 points - as to whom. At 7 points, brain death is assumed.

  Table

  In some cases, even after a relatively long, up to 72 hours, period of unconsciousness, consciousness can recover without residual neurological disorders. If the duration of the coma exceeds 3 days, the prognosis for survival and recovery of brain function is poor.

Diagnostics

• Differential diagnosis of atrial flutter and ventricular fibrillation

  The possibility of a sudden arrest of blood circulation should be borne in mind in all cases of loss of consciousness.

  With ventricular fibrillation, clinical death always occurs suddenly, at once; its onset is accompanied by a characteristic single tonic contraction of skeletal muscles. Although with a sudden cessation of cardiac activity, agonal breathing may persist for the first 1–2 minutes, an early sign of this condition is the absence of pulsation in the large arteries and, less reliably, of heart sounds.

  Cyanosis develops rapidly and the pupils dilate.

  ECG recording allows to confirm the diagnosis and establish the immediate cause of sudden cardiac arrest (fibrillation, ventricular asystole, electromechanical dissociation).

  With the progression of heart blockages, circulatory disturbance occurs gradually, and the symptoms are extended in time: first there is a clouding of consciousness, then motor excitement with moaning, wheezing, then tonic-clonic seizures (Morgagni-Adams-Stokes syndrome - MAS).

  In the acute form of massive pulmonary embolism, circulatory arrest occurs suddenly, more often at the time of physical exertion, often debuts with respiratory arrest and sharp cyanosis of the upper body.

  Cardiac tamponade usually develops after severe pain syndrome, blood circulation stops suddenly, breathing persists for 1-3 minutes. and fades away gradually, there is no convulsive syndrome.

  It should be emphasized that cardiopulmonary resuscitation should be started without waiting for the ECG data, immediately after the clinical diagnosis of sudden cardiac arrest.

Treatment

With flutter and ventricular fibrillation, emergency care is reduced to immediate defibrillation.

In the absence of a defibrillator, a single fist blow to the sternum should be used, which sometimes interrupts ventricular fibrillation.

If it was not possible to restore the sinus rhythm, then it is necessary to immediately begin chest compressions and artificial ventilation (ALV).

Cardiopulmonary resuscitation at a specialized stage begins with electrical defibrillation, which is carried out with an electric discharge with an energy of 200 J.

It is best to deliver the shock after prior ECG confirmation of ventricular fibrillation. If the clinical picture does not cause serious doubts, the pulse on the large arteries is not determined and it is possible to perform defibrillation within 30 seconds without wasting time on diagnostic measures, then it is carried out blindly, without a preliminary assessment of the heart rate according to ECG data.

The concept of the importance of the earliest possible electrical impulse therapy is based on the following facts:

• Ventricular fibrillation and ventricular tachycardia, accompanied by the disappearance of the pulse, account for the vast majority (at least 80%) of cases of sudden cardiac arrest in adults.
• Ventricular fibrillation in a person cannot stop spontaneously, but is stopped only with the help of electrical defibrillation. Electrical defibrillation is also the most effective method of restoring sinus or other hemodynamically effective supraventricular rhythm and ventricular tachycardia.
• The effectiveness of defibrillation decreases rapidly over time. According to the available data, the probability of success of resuscitation decreases by 7-10% with every minute that has passed since the onset of clinical death. This is due to the transition of large-wave ventricular fibrillation to small-wave fibrillation and asystole, which are associated with a significantly worse prognosis.

All ambulance teams and all departments of medical institutions must be equipped with a defibrillator, and all health workers must own this method of resuscitation.

With flutter and ventricular fibrillation, the heart rhythm may be restored after the discharge immediately or after a short period of rapidly changing post-conversion arrhythmias.

If ventricular fibrillation persists, then immediately repeat the discharge with an energy of 300 J. In the absence of effect, the next defibrillation is carried out with a discharge of maximum energy (360 J). If, after that, a contour line with a duration of more than 1 standard interval is recorded on the ECG, which may be due to electrical or mechanical stunning, it is necessary to continue cardiopulmonary resuscitation for 1 minute, after which the rhythm is reassessed.

In cases of persistence of ventricular fibrillation or ventricular tachycardia, to ensure optimal ventilation of the lungs, tracheal intubation is performed and access is established to the central - jugular or subclavian - or peripheral vein, through which 1 mg of epinephrine hydrochloride is administered as a bolus.

The effectiveness of epinephrine hydrochloride in cardiopulmonary resuscitation is due to its ability to prevent the collapse of the carotid arteries and increase blood pressure in general, both during pressure on the sternum and during diastole, as well as to cause centralization of blood flow by spasm of the arteries of the abdominal cavity and kidneys.

The possibility of further improving resuscitation outcomes in humans with higher than 1 mg doses of epinephrine hydrochloride has not yet been confirmed in placebo-controlled studies; however, in difficult cases, repeated injections of Adrenaline hydrochloride 1 mg every 3-5 minutes of cardiopulmonary resuscitation are used.

All drugs for cardiopulmonary resuscitation are administered intravenously quickly.

When using a peripheral vein, the preparations are mixed with 20 ml of isotonic sodium chloride solution.

In the absence of venous access, adrenaline (as well as atropine, lidocaine) can be injected into the trachea in a double dose in 10 ml of isotonic solution.

Intracardiac injections (with a thin needle with strict adherence to the technique of administration and control) are permissible only in exceptional cases, when it is absolutely impossible to use other routes of administration.

While maintaining ventricular fibrillation after two series of discharges, the next discharge with energy of 360 J is carried out 1 minute after the administration of Lidocaine at a dose of 1.5 mg / kg. If ventricular fibrillation persists, then the introduction of Lidocaine in the same dose and the discharge of energy 360 J is repeated.

If the result is negative, you can try to conduct defibrillation after the introduction of Ornid at a dose of 5 mg / kg, then 10 mg / kg, or after the introduction of Novocainamide 1000 mg. If these drugs are ineffective or lacking, Amiodarone 300-450 mg and Magnesium sulfate 2 g are used before applying the next discharge.

The required amount of the drug (mmol) is calculated by multiplying 0.3 by the base deficit (mol / l) and by the body weight (kg). Half of the calculated dose is injected intravenously in a stream, the other half - by drip, trying to reduce the base deficit to 5 mmol / L at a blood pH value of 7.3-7.5.

In case of out-of-hospital sudden cardiac arrest, sodium bicarbonate is used only with prolonged cardiopulmonary resuscitation, with unsuccessful defibrillation, adequate mechanical ventilation, the administration of Adrenaline hydrochloride and antiarrhythmic drugs. Sodium bicarbonate is administered first at a dose of 1 mmol / kg, and then at 0.5 mmol / kg every 10 minutes of cardiopulmonary resuscitation. The use of sodium bicarbonate is permissible only in patients with effective mechanical ventilation.

Calcium preparations are contraindicated in cardiopulmonary resuscitation; they are used only in patients with initial hyperkalemia, for example, with chronic renal failure or an overdose of calcium antagonists.

At one stage or another of resuscitation, ventricular fibrillation can turn into idioventricular rhythm and / or asystole.

The termination of resuscitation measures is possible if within 30 minutes there are no signs of their effectiveness: there is no consciousness, spontaneous breathing, electrical activity of the heart, pupils are maximally dilated without reacting to light.

After successful resuscitation of patients, it is necessary to be hospitalized in a block or department of intensive observation and treatment.

• Treatment measures after cardiopulmonary resuscitation

  After successful resuscitation, patients usually have hemodynamic instability, inadequate gas exchange and anoxic encephalopathy phenomena for a more or less long time, so they must be hospitalized in a block or department of intensive observation and treatment.

  In the intensive care unit, oxygen therapy and peripheral vein catheterization are indicated.

  The most sensitive to developing during the arrest of blood circulation ischemia and hypoxia of the central nervous system. Approximately 1/3 of successfully resuscitated patients die from neurological complications, and in 1/3 of survivors there remain persistent motor or sensory impairments.

  There are no specific treatments for encephalopathy. In such cases, symptomatic therapy is aimed at correcting and preventing arterial hypotension, hypoxia, hypo- or hypercapnia, electrolyte and carbohydrate metabolism disorders.

  In cases of short resuscitation after a short period of ventricular fibrillation, spontaneous breathing of oxygen at high concentrations under the control of pulse oximetry data is usually sufficient to correct hypoxemia. In this case, the saturation of hemoglobin with oxygen should be at least 95%.

  Inadequate spontaneous ventilation and acidosis increase the risk of recurrent cardiac arrest and contribute to secondary brain damage. Therefore, such patients are shown tracheal intubation and artificial ventilation.

  In a number of patients, after successful resuscitation, arterial hypotension is noted, which may be associated with the development of acute myocardial infarction or myocardial stunning as a manifestation of reperfusion. Such patients require inotropic therapy.

  A variety of cardiac arrhythmias are common postresuscitation complications. For its prevention, it is important to control the level of K + in the blood plasma, which should be maintained within the range of 4-4.5 mmol / l.

  Correction of acidosis begins with ensuring adequate ventilation of the lungs and hemodynamics, resorting to the introduction of sodium bicarbonate only with insufficient effectiveness of these measures.

  Taking into account the negative effect of postresuscitation hyperglycemia on the neurological status, according to indications, it is corrected with simple insulin.

• Treatment of ventricular fibrillation in the acute stage of myocardial infarction and after reperfusion

  There are several types of ventricular fibrillation, depending on the time of its occurrence from the onset of myocardial infarction, the severity of the existing structural changes in the myocardium and the severity of hemodynamics, as well as depending on the prognosis for life.

  Distinguish between early ventricular fibrillation, which occurs in the first 24–48 hours from the onset of myocardial infarction, and late, which develops after 48 hours from the onset of the disease.

  In addition, a distinction is made between primary and secondary fibrillation.

  Primary fibrillation occurs in patients without signs of cardiogenic shock or severe heart failure; its appearance is explained by electrical instability in the area of \u200b\u200bischemic or necrotic myocardium. It is believed that primary ventricular fibrillation that occurs in the first 24 hours of myocardial infarction is not prognostically unfavorable and does not significantly affect long-term survival.

  Unlike primary ventricular fibrillation, secondary fibrillation, which develops in the presence of severe organic myocardial damage or against the background of cardiogenic shock or acute left ventricular failure, has a poor prognosis.

  In patients with myocardial infarction, ventricular fibrillation most often occurs in the first hours of the disease: about 60% of all cases of ventricular fibrillation develop in the first 4 hours and 80% of all cases - in the first 12 hours of myocardial infarction.

  In the last 10 years, there has been a decrease in the incidence of ventricular fibrillation in patients with myocardial infarction, which is probably associated with the wider use of thrombolytic drugs, Aspirin, β-blockers, as well as percutaneous coronary interventions.

  Regardless of whether ventricular fibrillation has developed as a result of myocardial reperfusion or as a result of persistent ischemia, the only effective way to eliminate it is electrical cardioversion according to the algorithm described above.

  From pharmacological preparations, intravenous administration of 1 mg of Adrenaline can be used.

  In cases of ventricular fibrillation that are resistant to electrical discharges, the likelihood of success in resuscitation and the effectiveness of cardioversion can be increased using intravenous amiodarone.

  Currently, there are no clear recommendations on the duration of antiarrhythmic drug therapy after successful elimination of primary ventricular fibrillation in patients in the first hours of myocardial infarction. Typically, intravenous infusion of antiarrhythmic drugs continues from 48 hours to several days - until there is confidence in the absence of recurrent ventricular fibrillation.

  When episodes of ventricular fibrillation recur, in addition to continuing antiarrhythmic therapy (usually amiodarone), correction of acid-base and electrolyte balances, the maximum possible doses of β-blockers are used, implantation of two-chamber pacemakers, cardioverter-defibrillators, procedures for myocardial revascularization (percutaneous coronary artery bypass grafting).

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2 090 R




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2 290 R




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2 390 R




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2 690 R




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2 790 R




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2 790 R




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4 190 R




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5 590 R




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2 890 R




The introduction describes the main types of damage to the anatomical elements of the skin (stratum corneum, epidermis, dermo-epidermal junction, dermis, subcutaneous fat), which underlie the syndromes and diseases considered in the atlas. A strict step-by-step description of these diseases is given: the main clinical manifestations are listed, then histomorphology at low and high microscope magnifications. Various

2 790 R




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2 590 R




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2 390 R




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1 890 R




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2 290 R




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2 990 R




The manual is devoted to blood, urine and cerebrospinal fluid tests, most often performed in the practice of intensive care for patients in a critical condition, for example, with bleeding, sepsis, myocardial infarction, inflammatory processes and other diseases and conditions leading to damage to the functions of vital organs and systems ... The normal (reference) values \u200b\u200bof various parameters, their deviations from the norm, and the diagnostic value of these deviations are given. Brief recommendations are given for intensive care for various disorders of homeostasis.

2 090 R




A practical guide to outpatient care includes materials on the most important sections of obstetrics and gynecology, gynecological endocrinology and gynecological oncology. Issues of etiology, pathogenesis and diagnostics of pathological conditions are considered in detail in the light of the latest achievements of domestic and foreign authors. The modern methods of prevention and therapy in obstetrics and gynecology are presented.

2 190 R




The guide is intended to help the doctor diagnose and treat the most common childhood diseases, determine the range of preventive tasks already at the first contact with the patient, and prescribe treatment in accordance with the modern requirements of evidence-based medicine. Particular attention is paid to the issues of feeding young children, childhood infections and their prevention. All medicinal products are listed taking into account international non-proprietary names registered in the Russian Federation.

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This publication in an algorithmized form discusses modern approaches to the diagnosis and treatment of patients with dementia. The material is presented in accordance with the logic of the diagnostic and treatment process: from screening cognitive testing to a detailed clinical and neuropsychological study, which makes it possible to clarify the syndromic and nosological diagnosis and optimally build a therapy regimen. The methods of brief neuropsychological testing, modern diagnostic criteria for the main diseases leading to dementia, and the principles of their differential diagnosis are described in detail. The problems of formulating the diagnosis and its coding in accordance with the International Classification of Diseases of the 10th revision are considered.

1 590 R




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1 890 R




The book covers in detail the issues of general and oncological gynecology, reproductive endocrinology and infertility, contraception and family planning, pediatric and adolescent gynecology, urogynecology, etc. The psychological aspects of gynecology, problems of domestic cruelty and sexual violence are revealed in separate chapters.

2 790 R




The book covers in detail the basics of reproduction, normal obstetrics, diagnostics and management tactics of various complications during pregnancy and childbirth, emergency conditions in obstetrics. Attention is paid to extragenital diseases (including surgical ones) during pregnancy. A separate chapter is devoted to the resuscitation of newborns and the care of children from high-risk groups.

2 690 R




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2 890 R




The manual is devoted to the problems of diagnosis and treatment of cancer of the pancreas and organs of the periampullary zone. Contains an algorithm for ultrasound and intrascopic diagnostics of pancreatic cancer, surgical technologies for pancreatoduodenal resection. Addressed to medical specialists in ultrasound diagnostics; surgeons of specialized medical and outpatient clinics.

2 290 R




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More than two hundred color illustrations. Isolation of essential diagnostic elements. Isolation in a condensed form of the main morphological and immunohistochemical signs. Description of needle biopsy - a rapidly expanding technique that opens up new possibilities for histopathologists.

2 230 R




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3 890 R




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850 R




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2 190 R




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2 099 R




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1 790 R




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1 990 R




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1 390 R




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2 630 R




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2 790 R




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2 890 R




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4 090 R




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2 090 R




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0 R




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1 790 R




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1 590 R




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790

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The tutorial is divided into six sections. The first section is devoted to the history of the development of microbiology as a science, as well as to various aspects of the biology of microorganisms. In the second section, the features of the interaction of micro- and macroorganisms are considered, an overview of the methods of etiotropic therapy is given. The third section includes questions of microbiology of actual bacterial infections, the fourth - the microbiology of actual viral infections. The 5th section contains a description of the morphology and physiology of microscopic fungi. Section 6 covers issues of sanitary microbiology and microbiology of emergencies.

2 390 R




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Situational tasks in neurosurgery for the faculties of training doctors - A. I. Gaivoronsky, D. V. Svistov




The tasks provide clinical cases for all topics of the curriculum. Particular attention is paid to clinical examples illustrating the main emergency conditions in patients, wounded and injured neurosurgical profile.

990 R




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1 890 R




The presentation is structured according to the traditional plan with a description of the etiology and pathogenesis, modern classification, clinical manifestations, methods of diagnosis and treatment of diseases of internal organs. Each section contains examples of the formulation of diagnoses, describes the most common complications of diseases and methods of their prevention.

1 890 R




The manual covers the principles of organizing orthodontic care, examination methods and the main methods of treating dentoalveolar anomalies, correcting the incorrect position of teeth and occlusion. Students of the Faculty of Dentistry begin to study this section of dentistry from the 4th year.

1 790 R




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1 590 R




These guidelines summarize scientific data and personal professional experience in organizing an X-ray service, describe methods of radiation diagnostics. Methods for studying organs and systems of a person with normal anatomy, embryogenesis, X-ray anatomy, as well as X-ray semiotics of various pathological conditions in adults and children are covered.

1 690 R




The textbook reflects modern views on the etiology, pathogenesis and classification of the main diseases of the cardiovascular system. Information on epidemiology, clinical picture of diseases of the cardiovascular system, criteria for their diagnosis, differential diagnosis, treatment and prevention are presented.

1 590 R




Practitioners are offered simple, easily accessible, clinical and instrumental criteria for identifying the norm and various disorders of penile erectile dysfunction. This allows you to take a fresh look at the occurrence, development and prevention of erectile dysfunction, taking into account the early, preclinical changes in erection. Much attention is paid to the clinical characteristics of diseases, risk factors for their development and the corresponding semiotic signs that arise in the study of erectile dysfunction.

Diagnostics, treatment, rehabilitation and prevention of ischemic stroke (pocket guide) - Vinogradov O.I.




The handbook discusses in detail the issues of neuroimaging, methods of recanalization and secondary prevention of ischemic stroke. Chapters on differential diagnosis of ischemic stroke and conditions mimicking ischemic stroke, basic therapy, methods of recanalization of cerebral arteries (including thromboembolic extraction) have been expanded and supplemented. Recommendations for correction of risk factors, prevention and treatment of complications, as well as rehabilitation of patients with ischemic stroke are presented in detail.

790 R

From this article you will learn: what kind of arrhythmia is called ventricular fibrillation, how dangerous it is. The mechanism of development of arrhythmia, causes and main symptoms of fibrillation, diagnostic methods. Treatment, first aid and professional cardiac resuscitation techniques.

Date of publication of the article: 05.07.2017

Date of article update: 02.06.2019

Ventricular fibrillation is a life-threatening form of heart rhythm disturbance () caused by an uncoordinated, asynchronous contraction of certain groups of cardiomyocytes (myocardial cells) of the ventricles.

Conduction of electrical impulses in normal conditions and during ventricular fibrillation

Normally, the rhythmic contraction of the heart muscle is provided by bioelectric impulses that generate special nodes (sinus in the atria, atrioventricular at the border of the atria and ventricles). Impulses sequentially propagate through the myocardium, excite the cardiomyocytes of the atria, and then the ventricles, forcing the heart to rhythmically push blood into the vessels.

The conducting system of the heart is responsible for the rhythmic contraction of the entire myocardium (heart muscle)

In pathology for various reasons (cardiomyopathy, myocardial infarction, drug intoxication), the sequence of the bioelectric impulse is disrupted (it is blocked at the level of the atrioventricular node). The ventricular myocardium generates its own impulses, which cause a chaotic contraction of individual groups of cardiomyocytes. The result is ineffective work of the heart, the volume of cardiac output drops to a minimum.

Ventricular fibrillation is a dangerous, life-threatening condition; it is fatal in 80% of cases. It is possible to save the patient only by emergency cardiac resuscitation measures (defibrillation).

It is impossible to cure fibrillation - arrhythmia occurs suddenly, most often (90%) against the background of serious organic changes in the heart muscle (irreversible transformations of functional tissue into non-functional). It is possible to improve the prognosis and prolong the life of a patient who has survived an attack by implanting a cardioverter-defibrillator. In some cases, the device is installed for prophylaxis, with predicted development of arrhythmia.

Cardiac resuscitation measures are carried out by the ambulance team or the doctors of the intensive care unit. In the future, the patient is led and monitored by a cardiologist.

The mechanism of development of pathology

In the walls of the ventricles, there are groups of cells that can independently generate bioelectric impulses. With a complete blockade of the atrioventricular node, this ability leads to the appearance of many isolated impulses circulating through the cardiomyocytes of the ventricles.

Atrioventricular block is the cause of ventricular fibrillation

Their strength is sufficient to cause weak, scattered contractions of individual groups of cells, but not enough to contract the ventricles as a whole and for a full cardiac output of blood.

The frequency of ineffective ventricular fibrillation varies from 300 to 500 per minute, while the impulse does not weaken or interrupt, so the arrhythmia cannot stop on its own (only after or artificial defibrillation).

As a result, the force of the heart contractions, the volume of the ejection, and the blood pressure drop rapidly, resulting in a complete cardiac arrest.

Causes of the disease

The immediate causes of fibrillation are disturbances in the conduction and contractility of the ventricular myocardium, which develop against the background of cardiovascular diseases (90%), metabolic disorders (hypokalemia) and certain conditions (electric shock).

Group of reasons	Specific pathologies
Cardiovascular pathology	Arrhythmias (ventricular,) Heart and valve defects (, mitral stenosis, cardiac aneurysm) Hypertrophic (with thickening of the heart walls) and dilated (with enlargement of the heart chambers) cardiomyopathy (pathology of the heart muscle) Cardiosclerosis (scarring of the heart muscle) Myocarditis (myocardial inflammation)
Electrolyte imbalance	Potassium deficiency causes repolarization (electrical instability of the myocardium) Accumulation of intracellular calcium (myocardial repolarization)
Drug intoxication	Cardiac glycosides (digoxin, digitoxin) Catecholamines (adrenaline, norepinephrine, dopamine) Sympathomimetics (salbutamol, epinephrine) Antiarrhythmics (amiodarone) Narcotic analgesics (chlorpromazine) Barbiturates (phenobarbital) Medicinal anesthesia (cyclopropane)
Trauma	Mechanical trauma to the heart Blunt and Penetrating Injuries to the Chest Electrical injury
Medical procedures	Coronary angiography (diagnostic method with the introduction of a catheter into the vessel) Electrical cardioversion (treatment with electrical impulses) Coronary angiography (diagnostics of the heart with the introduction of contrast agents) Defibrillation (electrical pulse restoration of the heart rhythm)
Hyperthermia and hypothermia	Hypothermia and overheating, feverish states (with sudden changes in temperature), burns
Hypoxia	Oxygen deficiency (asphyxiation, head injury)
Acidosis	Increased acidity of the internal environment of the body
Dehydration	Bleeding (as a result of large fluid loss)

Fallot's tetralogy (combination of four heart anomalies) - one of the possible causes of ventricular fibrillation

Risk factors for developing ventricular fibrillation:

• age (after 45 years);
• gender (in women it develops 3 times less often than in men).

Typical symptoms

Ventricular fibrillation is a symptomatic life-threatening condition equivalent to clinical death.

During arrhythmia, the function of the ventricles is impaired, blood does not enter the vascular system, its movement stops, acute ischemia (oxygen starvation) of the brain and other organs rapidly increases. The patient is unable to move, quickly loses consciousness.

Death in 98% occurs within an hour after the first signs of ventricular fibrillation appear (the time interval can be much shorter).

All symptoms of atrial fibrillation appear almost simultaneously:

• violation of the rhythm of the heart;
• sharp headache;
• dizziness;
• heart failure;
• sudden loss of consciousness;
• interrupted breathing or its complete absence;
• sharp pallor of the skin;
• uneven cyanosis (cyanosis of the nasolabial triangle, tips of the ears, nose);
• lack of pulse in the large arteries (carotid and femoral);
• dilated pupils of the eyes that do not respond to bright light;
• convulsions or complete relaxation;
• involuntary urination, defecation (optional).

The period of clinical death (until the changes in the body have become irreversible) lasts for 4-7 minutes from the moment of complete cardiac arrest, then biological death occurs (when the process of cellular decay begins).

Diagnostics

Ventricular fibrillation is diagnosed, focusing on external symptoms (lack of pulse, breathing, pupil reaction to light). Several stages of arrhythmia development are sequentially recorded on the electrocardiogram:

1. Short tachysystole or ventricular flutter (15–20 seconds).
2. Convulsive stage (the frequency of contractions increases rapidly, the rhythm is disturbed, cardiac output weakens, takes up to 1 minute).
3. Fibrillation of the ventricles of the heart itself (quite large, but chaotic and frequent (300-400) flicker waves without pronounced intervals and teeth, changing the height, shape, length, the stage lasts from 2 to 5 minutes).
4. Atony (small, small length and height, low-amplitude waves appear, lasts up to 10 minutes).
5. Complete absence of heartbeats.

Since any condition with similar symptoms is a direct threat to life, resuscitation begins immediately, without waiting for the ECG data.

The manifestation of pathology on the ECG

Treatment

It is impossible to cure fibrillation, this form of arrhythmia is a deadly complication that usually occurs unexpectedly. In some cardiovascular diseases, it can be predicted and prevented by installing a pacemaker or cardioverter-defibrillator.

Treatment of fibrillation consists in first aid and cardiac resuscitation measures, in 20% of the victim's life can be saved.

First aid

If cardiac arrest due to ventricular fibrillation does not occur in a hospital, first aid should be provided prior to the arrival of a professional medical team. Very little time is allowed for it - the heart must be started within 7 minutes, then the chances of the victim are rapidly falling.

First stage of emergency care

Hail the person, shake it up, hit it hard on the cheek, perhaps the person will come to his senses.

Place your hand on your chest, its movement indicates the presence of breathing.

Place your ear against your chest in the sternum (palm below the subclavian fossa), so you can catch the sound of a heartbeat or feel the chest rise in time with breathing.

With your fingers (middle and forefinger) folded together, try to feel for a pulse on any accessible large blood vessel (carotid, femoral artery).

Lack of pulse, breathing, chest movements is a signal for first aid.

Second stage of emergency care

Lay the victim face up on a flat surface.

Tilt his head back, try to determine with your fingers what is interfering with breathing, clear the respiratory tract of foreign objects, vomit, take the falling tongue aside.

Ventilate the lungs: hold the victim's nose with one hand, and forcefully blow air “mouth to mouth”. At the same time, evaluate how much the chest rises (artificial respiration does not allow the lungs to collapse, stimulates the movement of the chest).

Get on your knees to the side of the victim, fold your hands on top of each other (crosswise), begin rhythmically pressing on the lower third of the sternum with crossed palms on outstretched arms.

For every 30 rhythmic chest pressures, take 2 deep mouth-to-mouth breaths.

After several cycles of direct massage and ventilation of the lungs, assess the condition of the victim (perhaps he has a reaction, pulse, breathing).

Direct heart massage is done intensively, but without sudden movements, so as not to break the victim's ribs. Do not try to kick the heart with an elbow strike in the sternum - only very qualified specialists can do this.

First aid is provided before the arrival of the medical team, who must be called before the start of resuscitation. The time during which it makes sense to provide first aid is 30 minutes, then biological death occurs.

Professional cardiac resuscitation techniques

After the arrival of doctors, measures to restore the work of the heart and hemodynamics continue in the ambulance car and in the intensive care unit of the hospital.

Apply:

• Electrical defibrillation of the heart (with the help of electrical impulses of different frequency and strength, they eliminate conduction and excitability disorders of the ventricular myocardium, restore the rhythm). If there are no serious organic changes in the myocardium, in the first minutes, the defibrillator restores the work of the heart in 95%, against the background of serious pathologies (cardiosclerosis, aneurysms), stimulation is effective only in 30%.
• Artificial lung ventilation device (ventilate the lungs manually, using an Ambu bag or connect to an automatic device, supplying the breathing mixture through a tube or mask).

The administration of drugs corrects electrolyte metabolism disorders, eliminates the consequences of the accumulation of metabolic products (acidosis), maintains the heart rhythm, and has a positive effect on the conductivity and excitability of the myocardium.

After an attack of ventricular fibrillation, patients spend some time in intensive care units, during this period the attending cardiologist decides how to improve the prognosis (the options under consideration are implantation of a cardioverter-defibrillator or pacemaker).

Complications of the postresuscitation period

Resuscitation measures (direct massage, defibrillation) save the lives of 20% of patients.

Typical complications of the postresuscitation period:

• chest injuries and rib fractures (due to intense direct massage);
• hemothorax and pneumothorax (accumulation of blood or air in the pleural cavity of the lungs);
• aspiration pneumonia (due to ingestion of the contents of the stomach, nasopharynx and oral cavity into the respiratory tract and lungs);
• disturbances in the work of the heart (myocardial dysfunction);
• arrhythmia;
• thromboembolism (blockage of a pulmonary artery by a blood clot);
• disturbances in the work of the brain (against the background of hemodynamic disturbances and oxygen starvation).

The result of the restoration of the work of the heart and hemodynamics after a long time (10-12 minutes after the onset of clinical death) can be irreversible changes in brain tissue caused by oxygen deficiency, coma, complete loss of mental and physical capacity for work. Only 5% of cardiac arrest survivors have no significant brain impairment.

Forecast

The appearance of ventricular fibrillation is a poor prognostic sign, a cause of cardiac arrest and death (80%).

In most cases (90%), arrhythmia becomes a complication of serious cardiovascular diseases (congenital defects, cardiosclerosis, cardiomyopathy) with organic changes in the myocardium (small or large foci of scarring). With ischemic heart disease, the death rate is 34% in women and 46% in men.

It is impossible to cure fibrillation; it is possible to prolong the patient's life (20%) only by emergency resuscitation measures. The effectiveness of first aid directly depends on the time of cardiac arrest - in the first minute it is 90%, by 4 it decreases 3 times (30%).

In some cases, it is possible to predict its occurrence in advance and prevent it by implanting a pacemaker or defibrillator (Brugada syndrome). The same methods improve the prognosis after an attack of fibrillation.

Ventricular fibrillation is the most common cause of sudden death between the ages of 45 (about 70–74% annually).

Content

Violation of the rhythm of the heart is a life-threatening condition. Due to fibrillation, blood flow stops, an increase in metabolic disorders in the body begins. This is the cause of 80% of deaths diagnosed with sudden death. Pathology is more common in men 45–70 years old with cardiac disorders. Arrhythmia can be found anywhere, so it is important to know the first aid measures to save the victim's life. Timely resuscitation methods will help the patient hold out until the ambulance arrives and increase the chances of survival.

What is ventricular fibrillation

The normal contraction of the heart muscle is provided by bioelectric impulses. They are generated by the atrioventricular and sinus nodes. The impulses affect the myocardium, cardiomyocytes of the atria and ventricles, provoking the heart to push blood into the vessels. When impulse conduction is disrupted, arrhythmia occurs. Ventricular fibrillation is a condition in which there is a chaotic movement of myocardial muscle fibers. They start to work ineffectively, with a frequency of 300-500 beats per minute. For this reason, urgent resuscitation of the patient is required.

Fibrillation results in a rapid decrease in the number of heartbeats. The volume of ejected blood decreases along with blood pressure, leading to complete cardiac arrest. If it is not started with the help of special resuscitation measures, the patient will live no more than 3-5 minutes. The arrhythmia cannot stop on its own, therefore, artificial defibrillation is required.

The reasons

Fibrillation often occurs due to cardiovascular causes. The main ones are:

• Complete blockade of the atrioventricular node.
• Complication of myocardial infarction.
• Cardiomyopathies - hypertrophic (thickening of the heart wall), dilatational (enlargement of the heart chambers), idiopathic (violation of the structure of the heart).
• Arrhythmias - ventricular premature beats, paroxysmal tachycardia.
• Heart defects, valves (aneurysm, mitral stenosis).
• Acute coronary insufficiency (narrowing of large vessels).

There are less common causes of ventricular fibrillation. These include:

• Cardiomegaly (enlargement of the heart).
• Cardiosclerosis (scarring of the heart muscle).
• Brugada syndrome (hereditary ventricular arrhythmia).
• Myocarditis (inflammation of the myocardium).
• A sharp decrease in the volume of blood pushed out by the heart, due to problems of unclear etiology.

The causes of ventricular fibrillation can be caused by processes not associated with a violation of the heartbeat. They are shown in the table:

	Possible states
Electrolyte imbalance	Lack of potassium leads to myocardial instability
Overdose of diuretics or cardiac glycosides	Severe poisoning with thiazide diuretics, narcotic analgesics, barbiturates
Medical manipulations	Coronary angiography, cardioversion, coronary angiography, defibrillation
Hypoxia	Lack of oxygen
	Increased acidity in the body

There are factors that rarely provoke the development of fibrillation. These include:

• Hypo- and hyperthermia - hypothermia and overheating of the body with sudden changes in temperature.
• Dehydration - can cause bleeding and hypovolemic shock (rapid loss of large amounts of fluid).
• Injuries - mechanical to the sternum, electric shock, blunt and penetrating.
• Hormonal imbalance due to thyroid abnormalities.
• Chronic stress, excessive nervous tension.

Classification

Fibrillation of the ventricles is usually divided into 3 stages - primary, secondary and late. Primary fibrillation occurs 1-2 days after myocardial infarction. Electrical instability of cardiomyocytes is due to acute ischemia. More than half of cases of primary fibrillation are observed in the first 4 hours, 40% - within 12 hours after a heart attack, which is the main cause of death in patients with this pathology.

Secondary fibrillation develops due to a lack of blood circulation in the left ventricle and is accompanied by cardiogenic shock. This stage is difficult to eliminate by defibrillation, while the primary one passes after a single electrical impulse. Late atrial fibrillation is noted 48 hours after myocardial infarction or at 5-6 weeks of heart disease related to ventricular dysfunction. At this stage, the mortality rate is 40-60%.

Symptoms

Arrhythmia is characterized by symptoms identical to complete cardiac arrest (asystole). Signs of ventricular fibrillation:

• violation of the heart rhythm;
• weakness, dizziness;
• sudden loss of consciousness;
• rapid breathing or lack of it, wheezing;
• pallor of the skin and mucous membranes;
• cyanosis (cyanosis of the tips of the ears, nasolabial triangle);
• pain in the heart, its stoppage;
• lack of pulse in large arteries (carotid, femoral);
• dilated pupils;
• complete relaxation or cramps;
• involuntary emptying of the bladder, intestines.

Arrhythmia begins suddenly, its appearance cannot be predicted. The signs of fibrillation determine the state of clinical death, when the changes in the body are still reversible and the patient can survive. After 7 minutes of arrhythmia, oxygen starvation leads to irreversible disturbances in the cerebral cortex and the process of cell decay begins, i.e. biological death.

Diagnostics

The likelihood of fibrillation is indirectly determined by signs of cardiac arrest or sudden death. This condition can only be confirmed using one diagnostic method - ECG (electrocardiography). The advantages of the study are the speed and the possibility of carrying out the procedure anywhere. For this reason, resuscitation teams are equipped with cardiographs.

ECG ventricular fibrillation

An electrocardiogram records the main stages of development of fibrillation. These include:

1. Ventricular flutter or short (20 seconds) tachysystole.
2. Convulsive stage - takes 30-60 seconds, accompanied by an increase in the frequency of contractions, weakening of cardiac output, rhythm disturbance.
3. Fibrillation - 2-5 minutes. Large, chaotic frequent scintillation waves are observed without pronounced intervals. The P wave is also missing.
4. Atony - up to 10 minutes. Large waves are replaced by small (low-amplitude) ones.
5. Complete absence of heart contractions.

Urgent care

A person with atrial fibrillation should receive emergency treatment before the arrival of the resuscitation team. It consists in carrying out resuscitation measures. First step:

1. It is necessary to hit the person in the face if he lost consciousness. This will help bring him to his senses.
2. Determine the presence of pulsation in the carotid or femoral arteries, observe if there is movement of the chest.
3. If there is no pulse and breathing, you should proceed to providing first aid.

The second stage consists in performing a closed heart massage and mechanical ventilation. The algorithm is as follows:

1. Lay the victim on a flat, hard surface.
2. Tilt your head back, clear your mouth of vomit, take your tongue out if it is fused.
3. With one hand, pinch the victim's nose and blow air through the mouth.
4. After blowing in, fold the hands crosswise and apply rhythmic pressure to the lower third of the sternum. 2 deep breaths, then 15 presses.
5. After 5-6 cycles of resuscitation, assess the condition of the victim - check for the presence of pulse, breathing.

A closed heart massage is performed rhythmically, but without sudden movements, so as not to break the ribs of a person with fibrillation. You should not try to inflict a precordial blow to the heart area if you do not have special skills. The provision of emergency care should be carried out in the first 30 minutes of the onset of arrhythmia and before the arrival of medical specialists, who should be called even before the start of resuscitation measures.

Treatment of ventricular fibrillation

Sudden cardiac arrhythmia cannot be treated. You can prevent fibrillation in some heart conditions by installing a pacemaker or cardioverter defibrillator. Therapy involves first aid to the victim and the use of special resuscitation equipment:

• Defibrillation is the restoration of the heart rhythm using electrical impulses of varying strength and frequency.
• Artificial ventilation of the lungs - manually using an Ambu bag or through a breathing mask with a ventilator.
• The use of the drug for cardiac resuscitation - Epinifrin, Amiodorona.

Professional cardiac resuscitation techniques

Specialized resuscitation of the heart and lungs begins with taking data from a portable cardiograph to determine the type of arrhythmia. If this is not an attack of fibrillation, then the use of the electrical stimulation machine will be ineffective. Next, you need to hit the heart area, if the pulse and breathing did not appear, you should use a defibrillator. If doctors are inclined to diagnose ventricular fibrillation, resuscitation using an electric current is performed immediately.

Using an AC or DC machine to normalize heart rate is dangerous without certainty about the diagnosis. The indications for defibrillation are as follows:

• Arrhythmia, when a chaotic contraction of cardiomyocytes occurs.
• EKG with ventricular flutter while maintaining rhythm. This condition is dangerous because it turns into fibrillation.

Emergency cardiac defibrillation is performed in a specific order. The algorithm is as follows:

1. Release the patient's chest while lying down.
2. Lubricate the defibrillator electrodes with a special gel or soak gauze in 7% sodium chloride solution.
3. Select the required power and charge the electrodes.
4. Place the right electrode on the subclavian area, and the left electrode just above the heart.
5. Apply a discharge by pressing the electrodes firmly to the body.
6. The result is evaluated - waves will appear on the monitor.
7. If the fibrillation fails, a higher power charge is delivered.

The first discharge is delivered with a power of 200 J. After it, the normalization of the heart rate often occurs. If this does not happen, a second pulse of 300 J is carried out.Then antiarrhythmics are administered intravenously or intracardiacally - Lidocaine 1.5 mg / kg body weight and a third discharge of 360 J is performed. artificial oxygenation of the respiratory organs. Epinephrine is given to prevent the carotid artery from collapsing and blood pressure to rise.

Medication combined with defibrillation and mechanical ventilation increases the chances of survival. The main drugs are shown in the table:

If emergency resuscitation measures have led to the restoration of the heart rate and the appearance of vital signs, the patient is taken to the intensive care unit for further treatment and observation. When 30 minutes have passed after the start of cardiac resuscitation measures, and breathing, pulse and pupil response are absent, the victim's biological death is stated.

Complications of the postresuscitation period

Emergency resuscitation at fibrillation helps 20% of patients survive. There are complications after emergency resuscitation:

• Injuries to the chest and fractures of the ribs - too intense heart massage.
• Pneumothorax, hemothorax - accumulation of air, blood in the pleural cavity of the lungs.
• Arrhythmia.
• Myocardial dysfunction - disturbances in the work of the heart.
• Aspiration pneumonia is the entry of the contents of the mouth, nose, stomach into the respiratory tract.
• Disorders in the brain caused by impaired blood flow and oxygen deprivation.
• Thromboembolism is a blockage of a pulmonary artery by a blood clot.

Fatal neurological disorders (postanoxic encephalopathy) occur in 1/3 of patients after resuscitation with fibrillation. Among the survivors, 1/3 have persistent disorders of sensitivity and motor activity. A complication can be burns from a defibrillator, hypotension after myocardial infarction. It is treated with medications (Isoprenaline, sodium bicarbonate). The first time after emergency resuscitation there is a high risk of recurrence of fibrillation, which is often fatal.

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Fibrillation and flutter of the ventricles are life-threatening cardiac arrhythmias, which are inherently chaotic contractions of parts of the ventricular myocardium. With fibrillation, the rhythm is irregular, and with ventricular flutter, the appearance of regular electrical activity of the heart remains. However, with both types of arrhythmia, there is hemodynamic inefficiency, that is, the heart does not perform its main function: pumping. The outcome of such rhythm disturbances is usually cardiac arrest and clinical death.

Ventricular fibrillation is usually accompanied by contractions of individual groups of muscle fibers of the heart with a frequency of 400 to 600 per minute, less often from 150 to 300 contractions. With ventricular flutter, individual parts of the heart muscle contract at a frequency of about 250 - 280 per minute.

The development of these rhythm disturbances is associated with the re-entry mechanism, or re-entry. The electrical impulse circulates in a circle, causing frequent contractions of the heart muscle without normal diastolic relaxation. With ventricular fibrillation, many such re-entry loops appear, which leads to complete disorganization of myocardial contractility.

Fibrillation and flutter of the ventricles can occur as a consequence of other cardiac arrhythmias, as well as for "nonarrhythmic" reasons.

The development of such a severe complication may be the result of recurrent persistent or unstable ventricular tachycardia, frequent polymorphic and polytopic. Bidirectional ventricular tachycardia in long Q-T syndrome, paroxysmal fibrillation or atrial flutter in the background can transform into such a violation. Fibrillation and flutter of the ventricles can occur with side effects of cardiac glycosides and some. In this case, arrhythmia develops against the background of electrical instability of the myocardium.

In 25% of cases, the development of fibrillation and ventricular flutter is not preceded by ventricular arrhythmias. These conditions can develop with acute coronary insufficiency, including with. It is believed that undiagnosed atherosclerosis of the main coronary arteries is one of the most common causes of ventricular flutter and fibrillation.

These pathologies are often found in patients with left ventricular enlargement due to various reasons (,). Complete atrioventricular and nonspecific intraventricular block also predispose to the development of these arrhythmias. Other causes can be electrical trauma, hypokalemia, severe emotional stress, accompanied by an intense release of adrenaline and other catecholamines. Anesthetic overdose and hypothermia during cardiac surgery can also provoke such severe complications.

Often the development of such rhythm disturbances is preceded by sinus in combination with an adrenaline rush. Therefore, ventricular flutter and fibrillation is one of the main causes of sudden death in young people, in particular during sports.

Symptoms

The precursors of the development of such rhythm disturbances can be short-term episodes of loss of consciousness of unknown origin, associated with ventricular extrasystole or paroxysmal ventricular tachycardia. Also, painless myocardial ischemia can precede ventricular fibrillation, manifested by an unreasonable decrease in exercise tolerance.

At the beginning of the paroxysm of ventricular flutter, several contractions with a high amplitude are recorded on the electrocardiogram, then frequent irregular contractions of the myocardium occur. Gradually, the waves of contractions become more rare, their amplitude decreases, and eventually the electrical activity of the heart fades away. Usually the duration of such an attack is up to 5 minutes. In rare cases, sinus rhythm can then recover on its own.

After 3 - 4 seconds after the development of ventricular flutter, the patient feels dizzy, after 20 seconds he loses consciousness due to a sharp oxygen starvation of the brain. After 40 seconds, tonic convulsions are recorded once.

Flutter and ventricular fibrillation are accompanied by cessation of pulse in large arteries, severe pallor or cyanosis (cyanosis) of the skin. Agonal breathing occurs, which gradually stops in the second minute of clinical death. After 60 seconds from the onset of the attack, the pupils expand, they stop responding to light. Involuntary urination and defecation are likely. In the absence of help, after 5 minutes, irreversible changes in the nervous system develop, death occurs.

Treatment principles

If paroxysm of flutter or ventricular fibrillation is documented (for example, on an electrocardiogram monitor screen), in the first 30 seconds, a precordial beat in the area of \u200b\u200bthe lower third of the sternum may be used. In some cases, it helps restore normal electrical activity in the heart.

Should begin immediately, including airway restoration, artificial respiration and chest compressions.

The main treatment for ventricular fibrillation and flutter is electrical defibrillation. It is carried out by trained personnel using a series of electrical impulses of increasing energy. At the same time, artificial lung ventilation is performed. Intravenous drugs are injected that stimulate the basic functions of the cardiovascular system: adrenaline, lidocaine and others.

With correct and timely cardiopulmonary resuscitation, the survival rate is up to 70%. In the postresuscitation period, lidocaine is prescribed to prevent ventricular arrhythmias, atropine, dopamine, and the syndrome of disseminated intravascular coagulation and brain dysfunctions are corrected.

The question of further tactics is being decided. One of the modern methods of treatment of paroxysms of fibrillation and ventricular flutter is the installation of a cardioverter-defibrillator. This device is implanted into the chest and helps to recognize ventricular arrhythmias in time, while delivering a series of impulses that restore sinus rhythm. In other cases, implantation of a two-chamber pacemaker is indicated.

Medical animation on the theme "Atrial fibrillation":