Fibrillation of ventricles

Description:

Fibrillation of ventricles  are arrhythmic, in-coordinate and inefficient reductions of separate groups of muscle fibers of ventricles with a frequency more than 300 of 1 min. At the same time ventricles do not develop pressure, and pumping function of heart stops. Their trembling which represents a ventricular tachyarrhythmia with a frequency of 220-300 of 1 min. is close to fibrillation of ventricles. As well as at fibrillation, reductions of ventricles at the same time are inefficient and cordial emission is practically absent. Trembling of ventricles - an unstable rhythm which in most cases quickly enough turns into their fibrillation, occasionally - in a sinoatrial rate. Also frequent ventricular tachycardia with a loss of consciousness is clinically equivalent to fibrillation of ventricles (so-called ventricular tachycardia without pulse).

Fibrillation of ventricles is the main reason for the sudden cardiac death arising against the background of a stable hemodynamics during 1-b h from emergence of symptoms of disturbance of a state. Recently most of specialists limits it "a temporary window" 1 h. Specific weight of fibrillation of ventricles among proximate causes of a sudden cardiac death makes 75-80%.

Symptoms of Fibrillation of ventricles:

As at emergence of fibrillation of ventricles pumping function of heart stops, the picture of a sudden stop of blood circulation and clinical death is noted. Patients faint that often is followed by spasms, an involuntary urination and defecation. Pupils are expanded and do not react to light. Diffusion cyanosis develops, are absent a pulsation on large arteries - sleepy and femoral - and breath. If within 4 min. it is not possible to recover an effective cordial rhythm, there occur irreversible changes in the central nervous system and other bodies.

On an ECG fibrillation of ventricles is shown by chaotic waves of blinking, various on amplitude and duration, with not differentiated teeth and with a frequency more than 300 in 1 min. Depending on their amplitude it is possible to allocate krupnovolnovy and melkovolnovy fibrillation of ventricles. At the last amplitude of waves of blinking makes less than 0,2 mV and the probability of an urgent defibrillation is much lower.

Complications and the result of fibrillation of ventricles depend on timeliness of delivery of health care - cardiopulmonary resuscitation. Efficiency of the last, in turn, is defined by the nature of an organic heart disease, first of all expressiveness of its dysfunction, and timeliness of the beginning of resuscitation actions.

Aspiration pneumonia and injury of lungs at a fracture of edges belong to possible complications from lungs. During a cardiac standstill total ischemia of a myocardium, and after recovery of coronary circulation - its more or less expressed passing dysfunction owing to a reperfusion syndrome and so-called devocalization (Stunning) develops. During the postresuscitatic period very often there are also most various arrhythmias caused or the same reason, as the previous fibrillation of ventricles, or the disturbances of bioelectric and mechanical functions of a myocardium connected with the postponed blood circulation stop. Neurologic complications (anoxic encephalopathy) are shown by a convulsive syndrome and a coma, up to a decortication. Even after rather long, to 72 h, the unconsciousness period, consciousness can be recovered without residual neurologic disturbances. If duration of a coma exceeds 3 days, the forecast concerning survival and recovery of function of a brain bad.

Reasons of Fibrillation of ventricles:

Etiological factors of fibrillation of ventricles and the related sudden cardiac death as the decreasing frequency are:

    * An ischemic heart disease, first of all an acute disorder of coronary circulation, the acute and postponed myocardial infarction. At an ischemic heart disease 46% of lethal outcomes among men and 34% - among women fall to the share of a sudden cardiac death. The largest frequency of fibrillation of ventricles and a sudden cardiac death is noted at myocardium ischemia height in the first 12 h an acute heart attack;
    * Hypertrophic cardiomyopathy. At a hypertrophic cardiomyopathy the sudden cardiac death most often comes at persons of young age during an intensive exercise stress. With age its risk decreases. In recent years its communication with certain options of genovariations from among responsible for developing of this disease is found;
    * Idiopathic dilatatsionny cardiomyopathy. About 10% which are successfully reanimated after a sudden cardiac standstill fall to the share of such patients. Sudden death comes usually against the background of the expressed frustration of a hemodynamics approximately at a half of patients with a dilatatsionny cardiomyopathy. It is necessary to remember that at such patients, as well as at patients with a hypertrophic cardiomyopathy, sudden death is equally often caused by fibrillation of ventricles and bradyarrhythmias;
    * Aritmogenny cardiomyopathy of a right ventricle. Though such patients are very subject to monomorphic ventricular tachycardia with frequent transformation in fibrillation of ventricles, owing to rare occurrence of this disease its specific weight among the reasons of sudden death from arrhythmia is very small;
    * Valve heart diseases. Among them most often leads a stenosis of the mouth of an aorta to emergence of fibrillation of ventricles and a sudden cardiac death (inborn and acquired) that, as well as in case of a hypertrophic cardiomyopathy, is caused by a hypertrophy of a myocardium of a left ventricle and a possibility of sharp deterioration in its filling and exile.
    * At patients with a prolapse of the mitral valve, despite the considerable frequency of ventricular arrhythmias, fibrillation of ventricles arises extremely seldom and is usually connected with disturbances of electrophysiologic properties of a myocardium;
    * Specific a cardiomyopathy, first of all inflammatory character, especially a cardiomyopathy at a sarcoidosis;
    * Primary disturbances of electrophysiologic properties of a myocardium in the absence of visible structural heart diseases. Belong to this category a syndrome of lengthening of an interval of Q-T (inborn and acquired, an iatrogenic origin) and supraventricular tachycardia at a syndrome of premature excitement of ventricles.

Also cases of idiopathic fibrillation of ventricles which presumably connect with dysfunction of the autonomic nervous system meet.

Risk of emergence of sudden death the greatest at transferred a sudden stop of blood circulation at which it makes 10-30% a year. At patients with an idiopathic dilatatsionny cardiomyopathy it is approximately equal to 10% a year, within the first year after a myocardial infarction - 5%, at a hypertrophic cardiomyopathy and a syndrome of the extended interval of Q-T-of 1-3%. For comparison it is possible to provide such data: at adult population of the USA the frequency of sudden death makes 0,22% a year and at patients with a prolapse of the mitral valve without regurgitation - 0,019% (G. Naccareffl, 1966).

Except the listed cases of development of fibrillation of ventricles as the reasons of a sudden cardiac death as a result of primary disturbances of the electrophysiologic properties of a myocardium connected or not connected with organic heart diseases it can be the terminal arrhythmia arising against the background of the progressing frustration of the central and peripheral hemodynamics.

Treatment of Fibrillation of ventricles:

Treatment includes acute management - cardiopulmonary resuscitation and, in case of success, an action for the prevention of repeated emergence of fibrillation of ventricles and sudden death.

Cardiopulmonary resuscitation. Cardiopulmonary resuscitation consists in ensuring adequate ventilation of the lungs and blood circulation before elimination of the reason of the termination of breath and blood circulation. Cardiopulmonary resuscitation at a specialized stage is begun with an electric defibrillation which is carried out "blindly", without preliminary estimate of a cordial rhythm according to an ECG.

If fibrillation of ventricles remains, the defibrillation is repeated 1-3 360 J categories. In cases of inefficiency or bystry resuming of fibrillation introduction of Adrenalinum hydrochloricum is repeated by each 3-5 min. according to an algorithm fibrillation - a defibrillation - cardiopulmonary resuscitation - Adrenalinum hydrochloricum - rhythm assessment according to an ECG.

At preservation of fibrillation of ventricles after two series of categories and the first introduction of Adrenalinum hydrochloricum to the program of resuscitation include antiarrhytmic therapy. However its efficiency is not proved in the controlled researches yet. Treatment is usually begun with intravenous administration of lidocaine in the form of a bolus in a dose 1-1,5¼ú/kg which it is possible to repeat each 3-5 min. before receiving a total dose of 3 mg/kg. It is established that at the person, unlike animals, administration of this drug before an electric defibrillation does not exert negative impact on its threshold.

As alternative to lidocaine antiarrhytmic drug III of a class the bretylium capable to raise a threshold of fibrillation of ventricles can serve and to reduce heterogeneity of duration of the refractory period in an ischemic and not ischemic myocardium. The bretylium is entered intravenously in the form of a bolus in a dose of 5 mg/kg then in 1-2 min. repeat transthoracic depolarization. In the absence of effect the dose is raised to 10 mg/kg which it is possible to enter each 15-30 min., but all - no more than 30-35 mg/kg.

Row drug III at recurrent fibrillation of ventricles or ventricular tachycardia without pulse is новокаинамид which enter in an initial dose 1 g at a speed of infusion of 20-30 mg of 1 min. At inefficiency of the listed drugs it is possible to try to enter intravenously ß adrenoblockers - propranolol 1 mg each 5 min. to the general dose of 0,1 mg/kg or эсмолол. These drugs are especially shown to patients with an acute myocardial infarction. There are single messages on efficiency of high doses (1000-1500 mg a day) Amiodaronum when which using less expressed arterial hypotension in comparison with a bretylium and novokainamidy is noted.