ECG signs of ventricular fibrillation. Causes and treatment of ventricular fibrillation

Fibrillation of ventricles - this is a life-threatening heart rate disorder ( cardiac arrhythmia ) for which the absence of a whole reduction is characteristic hearts Due to the fact that each cell of the heart muscle is excited and reduced by itself. With ventricular fibrillation, the number of all muscle muscle contiglies ( cardiac muscle) exceeds 300 in 1 minute. This is the amount of non-reduction of the whole heart, but the number of pulses that are produced in the ventricles. Such inconspicuous and chaotic activity does not provide an effective reduction in the heart, which leads to a circulatory stop and clinical death.

Circulatory stop It is characterized by a sudden cessation of effective blood pumping by arteries and veins, which is normal due to the pumping ( contractile) Heart function.

Clinical death - this is a reversible transitionality between life and biological death ( biological death - an irreversible state).

The fibrillation of the ventricles is one of the causes of sudden cardiac death ( 85% of the heart stops are due to the fibrillation of ventricles).

Sudden heart death(WSS) It has the following features:

  • her reason is always cardiac pathology (it does not matter whether it was known about this disease to the patient or not);
  • among the causes there is no injury or violent impact from outside;
  • there is necessarily a sudden loss of consciousness;
  • developed within 1 hour after the development of the first symptoms.

Anatomy and heart physiology

The heart is a hollow organ ( it has cavity), the work of which is to carry out blood flow through the vessels. The heart, working as a pump, shakes blood throughout the body, and in a minute it pumped around 5 - 6 liters of blood ( at rest), and during exercise this amount increases at times. The heart has 2 ventricles - left and right. Golders are large heart chambers that have a thick muscular wall. It is the ventricles that pushed blood from the heart in the artery. Right ventricle shakes blood into the pulmonary artery, and the left ventricle - in Aorta ( home Arteri Organism). Normally there is no message between them, they are separated by the interventricular partition. In the heart there are 2 more tops, smaller cameras are atrium. The main function of the atrial is to get blood from large veins and push it into the ventricles.

The ventricles make the following actions:

  • Systole - Reduction that pushes blood in artery.
  • Diastole - relaxation ( time between two systolates), which is necessary to fill the ventricles with a new portion of blood. In addition, blood flow in the heart muscle itself depends on the degree of relaxation of the ventricles. When the muscle relaxes, the blood on the heart vessels flows easier and nourishes all the departments of the heart muscle.

Accordingly, the ability of the heart to make a reduction is called systolic function, and the ability to relax and fill with blood - diastolic.

The main part of the mechanical work of the heart falls on the left ventricle. He is much more powerful than the right, because he directs blood in big circle blood circulation ( blood delivery to all organs), and right ventricles operate under less pressure, directing blood on a small circulation of blood circulation ( in oxygen enrichment).

Due to the fact that it is the left ventricle that performs the main part of the pump function of the heart, then this function itself is calculated by its parameters.

The main parameters of the left ventricle are:

  • Emission fraction - An indicator that reflects how much blood from the entire volume, which was in the ventricle before the reduction, is thrown into the aorta. This amount is expressed as a percentage. Normally, 55 - 70% of blood, which is available in it falls in the aort of the left ventricular systole. The emission fraction is estimated by echocardiography ( Ehoche) or catheterization of the heart ( introduction to the cavity of the heart of the catheter). The indicator reflects the systolic function of the left ventricle.
  • Type of blood flow through a mitral valve. Estimated with ECCG. The harder the blood fills the left ventricle, the higher the pressure in it. The pressure depends on its stiffness, that is, the ability to relax and expand to the desired degree. This indicator reflects the diastolic function of the left ventricle.

Conductive heart system

The heart muscle is the only muscle in the body that can produce nerve impulses itself for themselves. This is carried out through a conductive heart system, which consists of a special group of cardiac cells - atypical cardiomyocytes ( typical cardiomyocytes are the cells of the heart muscle that will reduce the heart). This system is called, because the purpose of its existence is reduced to conducting a pulse from the hearth, where it was formed to the heart muscle.

The conductive heart system consists of the following departments:

  • sinus knot - Located in the upper part of the right atrium, between the upper and lower hollow veins, in a place like a sinus ( sinus - sickness);
  • atrioventricular node ( Av-nodes) - Located between the atrium and the ventricle ( atriya - atrium, ventricul - ventricle);
  • bunch of Gis - this is the lower and thin part of the Av-node, which has two legs, while each leg passes along its side of the interventricular partition and is sent to one of the ventricles ( right leg - to the right ventricle, and left - to the left);
  • fiber Purkinje - It is branching the legs of the beam of Gis inside the vesting wall, which in contact with the heart muscle and transmit nerve impulse.

Cells of the conductive heart system can perform the following functions:

  • automatism - the ability to produce electrical pulses independently;
  • conductivity - the ability to transmit pulse along the fibers and from one cell another;
  • excitability - the ability to operate the necessary ion channels under the influence of pulses ( sodium, potassium, calcium), stimulating the current of charged particles inside the cell, which leads cells to the state of readiness to reduce.

Sinus node, Av-node, a beam of His and fibers Purkinier possess the properties of automatism, however in different degrees. Normally, the heart rhythm dictates a sinus node, as it produces impulses more often than everyone else. For this ability, it is called the center of automatism of 1 order. The sinus node is able to produce up to 160 per minute, however, at rest, the frequency of generation of pulses is 60 - 90 per minute. If the sinus node "turns off", the Av-Node takes on the function of the "substituent", but it works slower, produces pulses with a frequency of 40 - 60 per minute ( therefore, it is called the center of automatism of 2 orders).

The feature of the automation is also a beam cells of Gis ( its lower part legs) And Fiber Purkinier. Their ability to form an electric pulse is small - approximately 20 - 45 pulses per minute. These cells are referred to as the center of automatism of 3 orders.

Under normal conditions, this hierarchy is not violated, and the centers of automatic 2 and 3 orders do not have chances to "capture power" and become a rhythm driver. That is why all these sites are considered ectopic foci ( ectopia - a phenomenon that is not observed wherever usually), and the heart rhythm, dictated by impulses from these foci - ectopic rhythm.

Regulation of cardiac functions

The heart should be able to adapt to the requirements of the body, so it has several modes of operation. The main modes are "peace" and "load". Switch from one mode to another heart 2 systems are helped - intracardiac and extraordinary.

An intracardial nervous system can change the following parameters:

  • heart rate;
  • the speed of the pulse on the conductive heart system;
  • strength reduction of ventricles;
  • the speed of relaxation of the ventricles.

The intracardiac regulation system consists of the following parts:

  • Intracellular mechanisms - an increase in the muscle mass of myocardium by elevated protein formation ( observed in athletes and with heart disease requiring increased heart work).
  • Hemodynamic mechanisms ( gemo - Blood, Dynamics - Movement) - the reduction force of the heart depends on the amount of blood in the gastroincing cavity, that is, the more blood, the more the muscle is stretched, and the stronger ( the more stretch the gum, the stronger she "hit").
  • Outdoor reflexes - Work through cells inside the heart wall, which independently regulate some of the parameters of cardiac activity through a reflex arc. The reflex arc is a response system to a certain stimulus consisting of 3 nerve cells - perceiving transmitting and motor ( the same principle lies in the development of conditional reflexes). Perceiving cells persistently react to stretching the wall of the ventricle, so they are called mechanoreceptors ( for their irritation, it is necessary to change the degree of mechanical pressure on the wall of the heart).

The extraordinary regulation system consists of the following 2 departments:

  • sympathetic nervous system - activated during the physical and emotional load, stimulates the work of the heart;
  • parasympathetic nervous system - activated in a dream and in pathology of internal organs, inhibits heart function.

Both systems affect the heart through sensitive nerve endings - receptors. Impact occurs through biologically active substances transmitters ( mediators). These include adrenaline, norepinephrine ( for the sympathetic nervous system) and acetylcholine ( for parasympathetic nervous system). The prevailing effect on the heart depends not only on the activity of a system or another, but also on the number of receptors belonging to the specific nervous system.

Causes of ventricular fibrillation

Ventricular fibrillation is arrhythmia ( ), which always has a serious reason. The ventricular fibrillation is one of the forms of ventricular tachycardia, or rather the most severe option of all ventricular rhythm disorders. The ventricular tachycardia is an attack of a rapid heartbeat, which occurs if the center of arrhythmia is located inside the ventricles, or rather below the place where the Gis beam is divided into two branches. However, unlike ventricular tachycardia, during ventricular fibrillation, there is not one source of arrhythmias, but a plurality of small waves moving along a random path that constantly changing their direction. That is why when fibrillation, the heart is reduced chaotic and irregularly.

The fibrillation of ventricles is developing against the background of the electrical instability of myocardium. This condition of the heart muscle can be described as "increased preparedness for arrhythmia." Such readiness has a reason, because the cell stability is not so easy to disrupt, since in the heart there are mechanisms that impede the development of arrhythmias - this is the period when muscle fibers are immune to new impulses .

Electrical instability develops due to electrical negrogeneity ( heterogeneity) Cardiac muscle. It arises in all those cases when two hearths with different properties are located in the heart next door, for example, muscle fibers that are well suited, and those that blood supply not enough have different electrical properties ( in the second focus, all processes proceed slower).

The electrical instability of the heart muscle can cause the following violations of the rhythm and conductivity of the pulse:

  • ventricular extrasystoles ( extra - except, over, systole - reduction) - Extraordinary reductions in the heart, which arise because of the center of arrhythmia in the ventricles;
  • repeating stomach tachycardia attacks - an attack of heartbeat, which on the ECG is visible as a number of coming in front of each other in the rapid pace of ventricular extrasystole;
  • atrial fibrillation and trembling - an attack of heartbeat, for which the regular ( with treputania) or irregular ( with fibrillation) Rhythm, which comes from atrium ( unlike ventricular fibrillation in these arrhythmias of the circulatory stop does not occur);
  • full av-blockade - the fallout of the Av-site function, as a result of which the impulse from the atria cannot reach the ventricles ( stomachs are forced to produce "their" pulses);
  • intraventricular blockades - A pronounced slowdown in the speed of the pulse along the legs of the Gis beam or the fibers of Purkinier.

All of the above arrhythmias are developing independently, but due to various heart and extraimatic diseases. Otherwise, these situations doctors call markers of high risk of ventricular fibrillation. The presence of these markers indicates the possibility of the transition of these rhythm disorders into ventricular fibrillation. Thus, those pathologies that are reasons for the appearance of risk markers of ventricles are caused to fibrillation of ventricles.

Risk markers of ventricular fibrillation can develop in the following mechanisms:

  • Enhanced automatic in the ectopic node. Ectopic ( located not where you need) It is called any focus outside the sinus node. The enhancement of automatic means that this focus begins to produce more pulses per minute than a sinus node, so it can claim the role of the driver's rhythm driver.
  • Circular motion of excitation wave.If a certain "trench" is formed in the heart or vicious circle, loop, then the impulse of excitement, entering this loop, begins to spin through it, generating pulses to excite the heart. Inside the ventricles, or rather between the most distant shallow sprigs fibers Purkinne anatomically, there is the possibility of a circular motion. Such a structure in the norm gives you the opportunity to have an area and distribute the impulse if the blockade arose on one side ( "back door") However, the local "local" ( ventricular) Imparals.
  • Trigger activity. Trigger is a factor, "induced" to the desired goal. The trigger impulse is additional electrotocks that can stimulate the excitation wave. They are "induced" on the threshold of cell excitability. If the trigger comes to an excitability threshold, then it causes a new impetus and a new reduction. The cause of trigger activity is a high level of calcium.

The heterogeneity of the heart muscle can be represented as chaos that is going on in the city, where the police are unevenly distributed. Conditionally, the police are electrical impulses from the sinus node, and the criminals are an impulse from the center of arrhythmia in the ventricle. Arrhythmia can develop in two cases - the police work slowly ( the impulse does not reach) Or criminals in a kind of area have become more active ( the automatism of arrhythmia rose). The area where crime is the highest ( hearth arrhythmia), will try to "capture" the whole city and dictate your conditions. The same thing happens in the heart muscle. If the myocardium ventricles are unstable, this means that overlying centers of the conductive heart system ( police) Do not cope, and the restraining mechanisms have ceased to work.

The fibrillation of the ventricles itself develops according to the mechanism of the circular motion of the wave, but not a single wave, but a set of small. This mechanism is called micro Ratentri ( ratenter - re-entry). It happens as follows. The heart muscle loses its homogeneity, that is, while one plot of muscle "sleeps", the other is in the "wakefulness" state ( ready to reduce if he gets momentum). This means that the circular impulse constantly finds those areas that awake, and causes them to reduce them. While the wakey areas are reduced, "sleeping" muscle fibers "wake up" and become "awake". Moreover, these little waves constantly change their direction. Several child waves are formed from one wave, and it happens until the heart muscle remains inhomogeneous. Heart cannot recover from fibrillation of ventricles. Return the homogeneity of myocardium or to arrange a "reset" can only a strong impulse, which "pulls" all the small foci of arrhythmia.

Ventricular fibrillation happens:

  • primary - occurs in the absence of circulatory disorders, that is, with such states as heart failure or cardiogenic shock ( 80% of cases fibrillation of ventricles);
  • secondary - develops against the background of severe heart disease ( usually existing for a long time).

The characteristic feature of the primary fibrillation of ventricles is that it is easily treated with electric thermal therapy ( electrocker, defibrillation). Such fibrillation is considered as a "confusion" reaction of a healthy heart at a sharply occurring pathological situation. With a secondary form, the fibrillation of ventricles is a manifestation of the final stage of the disease, that is, the natural outcome of the severe heart damage, which leads to its stop.

The reasons for ventricular fibrillation can be:

  • acute myocardial infarction;
  • vazospadic angina;
  • chronic ischemic heart disease;
  • aneurysm left ventricle;
  • post-infarction cardiosclerosis;
  • myocardial reperfusion;
  • medical interventions on the heart;
  • hypertrophic cardiomyopathy;
  • "Sports Heart";
  • restrictive cardiomyopathy;
  • dilatation cardiomyopathy;
  • acquired heart defects;
  • prolapse mitral valve;
  • acute and chronic heart failure;
  • cardiogenic shock;
  • hypokalemia;
  • hypercalcemia;
  • brugada syndrome;
  • catecholaminideduced ventricular tachycardia;
  • WPW syndrome;
  • medical ventricular tachycardia;
  • idiopathic fibrillation of ventricles.

Acute myocardial infarction

A sharp myocardial infarction is the death of a portion of the heart muscle, which bloodslled by the clogged artery. Termination of blood flow for 30 minutes and longer causes myocardial infarction. Up to 30 minutes, the heart muscle can recover. The reason for the blockage of the artery is an atherosclerotic lesion, damage to atherosclerotic plaques and the layering of thrombotic masses ( from glued thrombocyte). A sharp cessation of blood flow on a certain section of the heart muscle causes a violation of electrophysiological properties in this zone. The electrical pulse first slows down its turn, and then stops spread to this zone at all, but something similar to the trench is created around this zone. For this trench around the hearth, the circular motion of the excitation wave can begin.

Vazospadic angina ( variant angina, angina printela)

Angina is a heart attack that does not lead to myocardial infarction. Ordinary angina develops against the background of atherosclerosis of coronary arteries, which narrows the clearance of the vessel, reducing the amount of blood that goes to myocardium. In contrast to conventional angina, variant angina develops at a completely different mechanism. The cause of a heart attack with this angina - vasospasm, that is, spasm of vessels ( vasa - Vessel). If, with a conventional angina, the artery is narrowed, but a certain amount of blood, still passes, then with a vazosphaise, the narrowing of the vessel can be almost completely closed of two walls ( burning). If you compare with the highway, then at ordinary angina, instead of three tracks there is one, and the area for the entire width of the road is temporarily blocked during vasospadic. In fact, the pronounced attack of the variant angina is comparable to myocardial infarction, especially if it lasts longer than 30 minutes and leads to the same electrical instability of myocardium.

Chronic ischemic heart disease

Ischemia is the poor blood supply to a certain area of \u200b\u200bthe organ, the cause of which is the defeat of the feeding artery. Feeding heart vessels are called coronary. If the bloodstream decreases sharply, but does not stop completely, it causes starvation of the heart muscle and a heart attack, that is, angina. It is anginary that is synonymous with chronic ischemic Disease Hearts. In contrast to acute myocardial infarction, angina tests, when the load on the heart increases. Chronic ischemic heart disease can lead to ventricular fibrillation if large coronary artery is affected - left coronary artery, feeding left ventricles. If it is narrowing more than 50 - 70%, then with the accession of spasm, the lumen is completely closed, and the whole left ventricle almost ceases to get blood, ischemia develops to which the ventricle reacts arrhythmia ( fibrillation of ventricles).

Aneurysm left ventricle

Aneurysm is a sacriflement of the wall of the hollow organ. The aneurysm of the left ventricle is developing with myocardial infarction and is an expanded and thinned area of \u200b\u200bthe dead hearter muscle. Normally, after the myocardial infarction, the dead plot is compacted. If the left ventricle with myocardial infarction continues to test high load, then this process is broken. Demanding fabric is not reduced and easily deformed. There is also a "trench" for the circulation of excitation wave around the aneurysm.

Post-infarction cardiosclerosis

Cardiosclerosis is a cordial muscle seal. Post-infarction cardiosclerosis is a scar seal after a myocardial infarction. The greater the scar, the more he causes heterogeneity in the heart muscle, since its electrophysiological properties differs from healthy cells. Especially in cases where there is a risk of myocardial infarction, an existing scar can cause ventricular arrhythmia. And the ventricular arrhythmia against the background of poor blood supply to the heart always has the risk of moving into the fibrillation of ventricles.

Myocardial reperfusion

Reperfusion ( re - repeat, perfusion - infusion) Myocardial is the restoration of blood circulation in the affected artery zone. Reperfusion can be self ( sPASM stops, thrombus is destroyed independently) or due to the intervention of doctors ( introduction of drugs, balloon expansion of the coronary artery, stenting). Regardless of the process of recovering blood circulation, reperfusion can also cause arrhythmia. A sharp influx of blood after a long "bloodless" period causes the so-called reperfusion damage. Cells that have already been close to death, after the influx of blood swell sharply, and they are aggravated by metabolic disorders. The main factor that enhancing the risk of fibrillation is the accumulation of calcium in heartcards after reperfusion. Calcium, as is known, increases automatism and excitability, which means that a lot of calcium accumulates in the focus, it can potentially cause arrhythmia.

Interventions on the heart

Pibrillery fibrillation can develop with coronary and coronary vessels. In the course of the study in the coronary artery, a probe is carried out, which in some cases its tip can temporarily close the clearance of the arteries, thereby having deprived of the blood supply to the section of the heart muscle. In addition, a contrast agent is introduced to "see" a vessel on an X-ray with coronary artery coronorography. Too many contrast substances in the artery, as it were, displaces the blood itself from there, which also causes a nutritional impairment. In essence, in such cases, changes in the heart muscle are similar to change in vasospadic angina.

Hypertrophic cardiomyopathy and "Sports Heart"

Cardiomyopathy is primary changes in the heart muscle, not related to any other heart pathology. Hypertrophic cardiomyopathy is characterized by a pronounced thickening wall of the left ventricle, including the interventricular partition. With this pathology in the heart muscle against the background of general hypertrophy ( thickening) Little scar sections and areas of ischemia are mosaic. This creates electrical heterogeneity and instability of myocardium, sharply increasing the risk of developing ventricular arrhythmias.

"Sports Heart" is hypertrophy of the myocardium of ventricles, which is caused by a high load on the heart during training. Despite the fact that the "sports" heart is not a disease or pathological condition, yet, in the presence of some hereditary predisposition or physical overloads against the background of myocardial hypertrophy, arrhythmias may occur that can go into ventricular fibrillation. In contrast to hypertrophic cardiomyopathy, hypertrophy with the "sports heart" may disappear or become less pronounced when stopping regular training.

Restrictive cardiomyopathy

Restrictive cardiomyopathy ( restriction - limit) is characterized by the damage to the heart muscle and endocardium ( the inner shell of the heart), which dramatically limits filling ventricles during diastole. This pathology can be primary ( independent) or secondary ( develops under a number of other diseases).

The group of restrictive cardiomyopathies also includes heart lesions in the following pathologies:

  • amyloidosis - the disease affecting the whole organism is characterized by accumulation of amyloid protein ( pathological protein), which begins to disturb the normal function of the organ and gradually leads to its destruction;
  • collagenoses (rheumatic diseases) - diseases affecting collagen ( connective) the cloth ( frame of any organ);
  • sarcoidosis - autoimmune disease for which the formation of tubercles consisting of cells involved in the inflammatory response ( leukocytes);
  • gemohromatosis - disease transmitted by inheritance for which iron accumulation in tissues is characteristic.

All these diseases increase the "hardness" of myocardium. Any substance that accumulates in tissues stimulates the growth of scar tissue. As a result, gradually healthy tissue of the heart is replaced by the scar. The dense scar tissue prevents the expansion of the ventricles and violates the homogeneity of the heart muscle. In addition, in these pathologies, intraventricular blockades arise, which are risk markers for the development of ventricular fibrillation.

Dilatium cardiomyopathy

Dilatium cardiomyopathy is characterized by a sharp expansion ( dilatation) Stomats. Impripated muscle fibers are bad bloodshed, the impulse is moving slower, intraventricular blockades are developing - all this contributes to the development of arrhythmia.

Arrhythmogenic dysplasia right ventricle

Arrhythmogenic dysplasia of the right ventricle is a hereditary disease for which the replacement of normal cells of the heart muscle with scar-fatty tissue is characteristic. This violates the homogeneity of the heart muscle and causes serious, threatening arrhythmias that are risk markers of ventricular fibrillation. Often the disease flows in a hidden form, that is, no way manifests itself until a certain point, and the first symptom is precisely fibrillation of ventricles.

Myocarditis

Myocarditis is inflammation of the heart muscle. Any inflammation is accompanied by infiltration - flooding, filling with inflammatory tissues and liquid. The liquid squeezes the heart, and inflammation disrupts the pulse.

Acquired heart defects

The acquired vices of the heart are damage to valves, which leads either to narrow the valve hole ( stenosis), or to the destruction of sash and incomplete closure ( failure). In both cases, blood movement is disturbed in the heart chambers and increases the load on any of its department. If the load falls on the left ventricle ( usually, when damaged aorta valve), then the ventricle is hypertrophy and expands. Next, the mechanism of development of arrhythmia is similar to that with hypertrophic and dilated cardiomyopathy.

Mitral valve prolapse

The mitral valve is located between the left atrium and the left ventricle, it has 2 sash, so it is also called bivalve. Prolapse refer to the empty of the sash of the mitral valve towards the left atrium during the reduction of ventricles. As a result, part of the blood ( in the form of a jet) Under pressure from the left ventricle is thrown back to the left atrium. With severe, third degree of prolapse of disorders are comparable to severe defects of the mitral valve ( failure). The consequences of heavy prolapse are an increased load on the left atrium and the left ventricle. In addition, during the prolapse of the mitral valve, there is often disruption of the nervous control of the heart - an increased tone of the sympathetic nervous system, and the valve muscles are stretched, which causes a slowdown in the pulse in this part. It is also important to know that the mitral valve prolapse is often combined with other congenital changes. It is a combination of several pathologies in the prolapse of a mitral valve can cause arrhythmia.

Hypokalemia and hypercalcemia

Hypokalemia is a low level of potassium in the blood, and hypercalcemia is a high level of calcium. These two ions are constantly competing. Potassium - slows down, calcium - speeds up. Therefore, with a deficiency of potassium and excess calcium, the healing of heartbeat occurs, the tissue excitability increases and the pulse is slowed down, that is, all conditions are created for the occurrence of arrhythmias.

Electrotramma

Electricalrama is physical damage to the body when exposed to electric current. The electric current becomes the cause of injury if it is by force exceeding the level of the body's sensitivity. Electrotok disrupts the conductivity of the heart and the excitability of the heart, which is manifested by fibrillation of ventricles.

Acute and chronic heart failure

Heart failure is the result of any other lesion of the heart. It is characterized by a violation of the pumping function of the ventricle or the inability to fill blood. Both types of disorders reduce the amount of blood, which comes through the aorta to different organs. If blood is less than it is required - this is insufficient blood circulation or heart failure.

Acute heart failure develops quickly, for several hours, and sometimes minutes. If any factor suddenly breaks the movement of blood to heart, then the heart simply does not have time to adapt to new conditions, and the blood stagnation develops in the veins, and little blood is emitted into the aorta. If the disease increases the load on the heart gradually, then it has time to adapt, and only when the heart of the heart "hold" is depleted, heart failure develops, which is called chronic.

Cardiogenic shock

Cardiogenic shock is the extreme degree of deficiency of the left ventricle ( one of the forms of acute heart failure or exacerbation of chronic heart failure). In other words, these are pronounced symptoms of heart failure ( chief, arrhythmia, dizziness, weakness and so on), caused by a sharp deterioration of the contractile function of the left ventricle or an increase in the load on it.

Cardiogenic shock leads:

  • common ( extensive) myocardial infarction;
  • "New" myocardial infarction against the background of the existing scar after the "old" ( transferred);
  • heart breaks ( interventricular partition, nipple muscles valves).

Syndrome of the extended interval Q-T

The syndrome of the elongated interval Q-T is a state that is diagnosed with ECG. This syndrome is characterized by a high risk of hazardous ventricular tachycardia, which is highly likely to go into ventricular fibrillation.

The Q-T interval is the distance between the K and T. It is important that it reflects the entire process of propagation of the impulse, excitement and reduction of the myocardial of ventricles, as well as the return process to its original state. In fact, it is all electrophysiological processes occurring in the myocardium of ventricles, which are caused by the movement of sodium ions, potassium and calcium inside the cell and back across special channels.

Q-T interval syndrome happens:

  • congenital - there is a genetic defect of sodium and potassium channels ( is 50% of all cases of this syndrome);
  • acquired - develops on the background of various pathologies ( hypokalemia, strokes, vasospadic angina, mitral valve prolapse, cardiomyopathy, alcoholism, hormonal diseases, poisoning poisons, some tumors and more).

The length of this interval depends on the cardiac frequency. The norm for each person is calculated by a special formula. The elongation of the Q-T interval is diagnosed in cases where the calculated time is significantly less than the duration of the ECG interval ( electrocardiogram) Patient.

Brugada syndrome

Brugada syndrome is characterized by a genetic anomaly, which violates the work of sodium channels in the cells of the heart muscle. As a result, the ventricles are formed in the ventricles. This focus becomes the cause of ventricular tachycardia, and it quickly goes into fibrillation of ventricles. Brugada syndrome is diagnosed according to ECG data. The origin of arrhythmia at night is characteristic of it. Sometimes the disease is provoked by the appointment of a number of antiarrhythmic drugs ( preparenon, Novocainamide), which exacerbate the available disorders of the function of the ion channels ( these drugs affect these channels.).

Catecholaminidated ventricular tachycardia

This arrhythmia occurs due to increased individual sensitivity to catecholaminams. Catecholamines are adrenaline and norepinephrine. High sensitivity to these substances increases the excitability of ventricular cells and contributes to the development of ventricular tachycardia ( pickpoint attack) And its transition to fibrillation. This arrhythmia is provoked by a physical or emotional load when the adrenal glands allocate more catecholamines.

WPW syndrome

A special type of hereditary arrhythmia is WPW or Wolf-Parkinson-White ( Wolff-Parkinson-White). The WPW syndrome feature is that additional conductive nerve paths are found in the heart, for which the pulse can get from the atrium into the ventricle, bypassing the Av-node. Characteristic feature The extension path is the absence of a pulse delay function that has an Av-site. Thanks to this delay, not every impulse from the atria is getting into the ventricles. If a person has an additional way that passes all impulses, then there is a risk of transition of atrial arrhythmias ( supported paroxysmal tachycardia, atrial fibrillation and trembling) In the fibrillation of ventricles. This syndrome is diagnosed if a "step" is visible on the ascending part of the highest oscillation of the cardiogram.

Ventricular fibrillation caused by medicines

Ventricular fibrillation caused by intoxication ( overdose) or side effects drugs, arises either due to the elongation of the Q-T interval, or the strengthening of the electrophysiological disorders of the hereditary and acquired nature in the heart muscle.

To fibrillation of ventricles can cause the wrong use of the following drugs:

  • antiarrhythmic drugs - County, Novocainamide, Dizeciramide, Curdaron, Satolol, PropaPenon;
  • cardiotonic drugs ( strengthen the reduction of heart) - Cardiac glycosides ( digoxin);
  • bronchoranting drugs ( broncholitiki) - Salbutamol, Terbutalin;
  • antihistamines ( antiallergic) Preparations - Asthemisol, Terfenadine;
  • diuretic - Furosemid, Indapamide;
  • antifungal drugs - ketoconazole, fluconazole;
  • antibiotics and antimalarial preparations - erythromycin, chlorookhin;
  • antiwheat preparations - metoclopramide;
  • tricyclic antidepressants - imipramine, doxypin.

Idiopathic fibrillation of ventricles

The term "idiopathic" is used in medicine if the disease does not have explicit and objective causes, as well as in cases where pathology is developing independently ( often in the presence of hereditary predisposition). Idiopathic fibrillation of ventricles, according to some doctors, has a completely definite reason, which was simply not revealed earlier, and the first manifestation of the disease is precisely fibrillation of ventricles. The diagnosis of idiopathic ventricular fibrillation is established only in cases where all other reasons are excluded, especially hereditary arrhythmias.

Symptoms of ventricular fibrillation

Before the actual ventricular fibrillation occurs, a patient develops one of the forms of heart rate impaired, which can go into ventricular fibrillation. These are the arrhythmias that are high-risk markers. Therefore, symptoms that correspond to the fibrillation itself of ventricles should be distinguished ( circulatory stop, clinical death) and the symptoms that precede fibrillations ( correspond to the symptoms of risk markers). The faster the transition from arrhythmia to ventricular fibrillation occurs, the faster the loss of consciousness arises - the main sign of life-focused arrhythmia.

Symptoms of ventricular fibrillation

Symptom

Development mechanism

Manifestations

Tachycardia

  • Tachycardia is the beginning of an attack of ventricular fibrillation, characterized by frequent heart rate. The causes of tachycardia can be either loop Ratenter in the ventricles, or an ectopic focus, less often ventricular arrhythmia develops by type of trigger activity ( with a high level of calcium and low level potassium).
  • If the attack of ventricular tachycardia lasts longer than 30 seconds, it is called sustainable. This means that in the ventricle there is persistent inhomogeneity.
  • Frequent rhythm sharply reduces the emission fraction, that is, the amount of blood, which goes to the brain is sharply reduced.
  • Within 1 minute after the start of the attack, tachycardia can go into ventricular fibrillation.
  • picking attack;
  • weakness;
  • dizziness;

Arrhythmic shock

  • The arrhythmic shock develops if the heart practically ceases to swing blood due to arrhythmia. Due to the too large number of pulses of fibrillation and lack of synchronism, the heart cannot push the blood in the aorta. In such conditions, the reflex spasm of blood vessels of limbs and skin is developing, so that more blood gets vital organs. All the same blood is not enough and to the brain and other bodies almost stops.
  • threaded pulse ( pulse without hesitations, weak);
  • decrease in blood pressure ( top pressure less than 90 mm Hg.);
  • reducing the amount of urine released ( oliguria) or the absence of urine ( anuria);
  • violation of consciousness ( lethargy, lack of reaction to external stimuli);
  • pallor and skin sinusiness;
  • sticky cold sweat;
  • cold limbs.

Circulatory stop

  • Circulatory stop occurs as a result of the absence of heart cuts. If the pump ceases to act, the organs cease to receive blood. First of all, he suffers from the brain, which is constantly necessary to obtain oxygen and glucose from blood ( there are almost no stocks in the cells). That is why when stopping the blood circulation related to the heart stop, it is necessary to disable those functions that lead the brain - consciousness, breathing. This state leads to clinical death.
  • loss of consciousness;
  • agonal breathing ( frequent, superficial and hoarse);
  • lack of breathing;
  • no pulse on radial artery ( at the brush) and on the carotid artery ( on the neck);
  • expansion of pupils;
  • pallor and gray skin shade.

Diagnosis of ventricular fibrillation and causes of this state

The diagnosis of ventricular fibrillation is made solely on the basis of the electrocardiogram data ( ECG). In the absence of pulse, consciousness and respiration in the patient there is a clinical death ( this is done quickly, for 10 - 15 seconds) And reanimation measures begin. What a specifically arrhythmia led to a heart stop, it turns out already during the first medical care (some basic events need to start before installing electrodes for ECG registration). After the electrocardiograph is connected ( apparatus for registration ECG), the doctor finds out the specific type of arrhythmia. However, often the cause of the circulatory stop is determined by the effectiveness of certain resuscitation activities. For example, if the normal heart rhythm has been restored after defibrillation, the patient had fibrillation or ventricular flutter. In the absence of effects from the electric shock, the doctor revises the alleged diagnosis.

In addition to fibrillation and trembling ventricles, clinical death can cause the following arrhythmias:

  • electric activity without pulse - the electrical activity of the heart is stored, but the mechanical cut is not carried out ( therefore, there is no pulse), which is due to a sharp decrease in energy reserves in the heart muscle and a decrease in its insensitive to electric stimuli;
  • asistolia- termination of the electrical activity of the heart, which on the ECG corresponds to a flat line without oscillations ( injection).

Methods for diagnosing ventricular fibrillation and high-risk markers

Study

How is it held?

What does it reveal?

Electro-cardiography

The ECG execution technique may differ somewhat in life-giving arrhythmias or in cases where the doctor fixes the circulatory stop. Often ventricular fibrillation begins in the intensive therapy separation when the patient is already connected to the monitor. In this case, the number of electrodes that is established by the patient may be different. An ordinary ECG in 12 leads can be carried out, at which 4 electrodes are installed in the ankle area and wrists, and another 6 - above the heart area. In other cases, 3 electrodes are installed - one by one under each collar and one left at the bottom of the abdomen. The doctor chooses the desired mode on the monitor and then the lead, where all important elements of the cardiogram are best visible. Especially use monitors defibrillators. Such devices are designed not only for electrical treatment ( electroshok), but also for tracking the main life indicators ( pressure, breathing, blood saturation with oxygen and other parameters). Under ambulance, ECG is recorded after the implementation of resuscitation measures to assess their effectiveness ( it all depends on the equipment of the hospital or ambulance).

  • ventricular fibrillation;
  • ventricular high-risk arrhythmias;
  • hereditary arrhythmias ( brugada syndrome);
  • arritmogenic dysplasia of the right ventricle;
  • acute myocardial infarction;
  • vazospadic angina;
  • aneurysm left ventricle;
  • post-infarction cardiosclerosis;
  • the elongated interval Q-T syndrome;
  • brugada syndrome;
  • wPW syndrome.

Halter monitoring

This method of monitoring cardiac activity includes a continuous ECG record in the mode of conventional daily life of the patient. Electrodes ( usually from 4 to 7) They are superimposed on the chest similar to the installation of electrodes when monitoring in resuscitation. The registrar himself is fixed in the waist area with a special belt or is worn around the neck, if it is miniature. Usually, the HALTER monitoring ECG is carried out within 1 day, sometimes it is necessary to wear the device longer ( up to 7 days). During the entire monitoring period, the patient must have its actions or leisure periods to celebrate in the diary.

  • ventricular arrhythmias ( high risk markers);
  • vazospadic angina;
  • brugada syndrome;
  • wPW syndrome;
  • catecholaminined tachycardia.

Long monitoring ECG

If an ECG recording is required for a long time ( months), then the so-called "event registrars" or loop registrars are used. They register the ECG within a few minutes before, during and after the attack. The remaining data is removed from the memory. There are external and implantable devices. Exterior devices are worn with themselves in a special handbag. When an attack occurs ( or feeling his approach) The patient presses the apparatus button, and it writes an ECG through an electrode attached to the patient's body ( how in halter monitoring). The implantable devices are implanted subcutaneously into the region of the left side of the chest into a specially created "pocket" of soft tissues. The device also consists of a registrar and electrodes, but in a more miniature version. It works this unit is not constantly, but only during the attack, it turns on. Some devices can forward the ECG with the episode of arrhythmias to the doctor through a mobile phone.

  • the same as in the halter monitoring.

Echo cardiography

(Ehoche)

EchoCG is a method of studying the structures of the heart and its contractile function using ultrasound. During the study, the patient takes the position lying on his back, slightly turning to the left side. Left hand need to lift and put under the head. The doctor sets an ultrasonic sensor over the heart area. Ehovolny reach the structures of the heart, reflected and captured by the sensor. The doctor observes the reduction in the heart, the valve movement and calculate the necessary parameters.

  • acute myocardial infarction;
  • post-infarction cardiosclerosis;
  • aneurysm left ventricle;
  • acquired heart defects;
  • mitral valve prolapse;
  • heart failure;
  • myocarditis;
  • sports Heart;
  • dilatation cardiomyopathy;
  • restrictive cardiomyopathy;

Sample C. exercise

Samples with physical activity are rarely used in suspected ventricular fibrillation due to the danger provoke an attack. However, in some cases, such a study is carried out to clarify the diagnosis and appoint proper treatment, as some drugs that are effective at some arrhythmias are completely contraindicated with others. The sample involves the registration of ECG while walking the patient on the treadmill or rotation of the bike pedals for 15 to 20 minutes with the increasing load. In the office during the study necessarily there is a defibrillator ( machine for electric shock).

  • acute myocardial infarction;
  • chronic ischemic heart disease;
  • catecholaminidated ventricular tachycardia.

ECG with provocation

The essence of this method is that the introduction of drugs that provoke arrhythmia allows you to establish a mechanism for its development, which means to put an accurate diagnosis. Characteristic ECG changes in some arrhythmias appear before the bout of ventricular fibrillation or when other ventricular arrhythmia appear. Such drugs like Aimalin and freakinide are administered intravenously and monitor changes to the ECG. It is important that during the sample in the office everything was ready for emergency recovery of rhythm ( defibrillator and drugs).

  • brugada syndrome.

Magnetic resonance imaging

(MRI)

MRI ( magnetic resonance imaging) Hearts are carried out in the patient's position lying on the retractable tomograph table. A coil is installed on the chest, which allows you to adjust the signal frequency. The patient is fixed so that during the study he could not do sharp movements ( movement distort the picture). The principle of operation of MRI consists in changing the position of hydrogen atoms, which in a strong magnetic field begin to radiate signals. These signals captures the detector and converts to the image. Usually, at MRI of the heart, the introduction through a vein of a contrast agent is used, which enhances the signal.

  • hypertrophic cardiomyopathy;
  • restrictive cardiomyopathy;
  • myocardial infarction;
  • vazospadic angina;
  • heart defects;
  • arrhythmogenic dysplasia right ventricle.

Electro Physio-Great Study

(EFI)

EFI is an intracardiac cardiogram, that is, the register of electrical activity of different departments of the conductive system of the heart with the help of the electrodes of the "delivered" to the cavity of the heart through the femoral, shoulder or subclavian vein. The "conveyor" of the electrodes serves the wire, which is called the probe. Promotion of the probe is carried out under control of x-ray research ( metal probe itself, so it is visible on x-ray) with the introduction of a contrast agent that paints the "path" itself for the probe ( blood vessels and heart cavity). In the right heads of the heart, three or four electrodes are installed - the first in the upper part of the right atrium, the second in the area of \u200b\u200bthe valve, the third in the cavity of the right ventricle, and the fourth in the vein itself of the heart itself. EHF allows you to reproduce arrhythmia and stop ( stop) It, affecting the specific sections of the conductive system during the desired period ( when you can start or stop arrhythmia). In addition, with the help of Ethi, the doctors recognize the exact location of the pathological focus to then affect it by surgical methods.

  • brugada syndrome;
  • arritmogenic dysplasia of the right ventricle;
  • wPW syndrome;
  • hypertrophic cardiomyopathy;
  • post-infarction cardiosclerosis;
  • chronic ischemic heart disease.

Corono-graphic and catheterization of the heart

Coronaryography is an X-ray-contrast study of the coronary arteries. The study is carried out almost as EFI. The difference is that the probe is introduced into the femoral artery and promote through the aorta to the coronary arteries, after which a contrast substance is served and make a series of X-rays. On the screen it is seen as a contrast fills the flowable artery or does not fill the sections where there is a blockage.

Heart catheterization is the introduction of a catheter in the cavity of the heart. The technique of the introduction of the catheter resembles coronary artwork, but the catheter is not introduced into the coronary artery, but in the left and / or right ventricle cavity. This allows you to measure the pressure inside the heart and evaluate its contractile function.

  • myocardial infarction;
  • chronic ischemic heart disease;
  • vazospadic angina;
  • cardiogenic shock.

Miocardium biopsy

Biopsy is a lifetime taking a piece of viable tissue for analysis. The myocardium biopsy is carried out either under X-ray control or ultrasound. In most cases, the first option is used ( Uzi control is also shown during pregnancy). Special biopsy catheter ( bioptom) Enter into a subclavian, jugular or femoral vein, if we need a material from the right heart departments, and through the femoral artery, if the material from the left ventricle is needed. After the biopt reaches the desired section of the heart muscle ( usually it is a native partition) It "opens" and take the material from several places. Then the biopt is removed. The resulting material is sent to the laboratory.

  • hypertrophic cardiomyopathy;
  • restrictive cardiomyopathy;
  • dilatation cardiomyopathy;
  • arritmogenic dysplasia of the right ventricle;
  • myocardits.

On ECG, you can observe the following stages of ventricular fibrillation:

  • tahisistolia - Frequent, but also regular ventricular tachycardia waves ( lasts a few seconds);
  • convulsive stage of ventricular fibrillation - the transition from tachiisistolia to fibrillation, which lasts up to 1 minute, while waves gradually become irregular ( new arrhythmia foci appear), and the rate of abbreviations increases;
  • stage of Flicker - actually fibrillation of ventricles, for which the frequent irregular waves of different amplitudes and form are characterized ( lasts 1 - 3 minutes);
  • aTONIC STADE - It is characterized by a gradual extinction of cardiac activity, so fibrillation waves become small ( since the start of the attack, it usually takes 5 minutes);
  • asistolia- This is the transition of ventricular fibrillation with small waves into the state of complete cessation of the electrical activity of the heart.

An important part of the diagnosis of ventricular fibrillation is to find out the reasons that led to this arrhythmia, but it is done after successful resuscitation.

During the search for the reasons for fibrillation of ventricles(after eliminating the attack) The doctor prescribes the following tests:

  • general blood test and general urine analysis;
  • blood chemistry ( hepatic enzymes, creatinine, urea, glucose);
  • ionogram ( level of potassium, calcium, magnesium and other ions);
  • lipidogram ( level of cholesterol, triglycerides and lipoproteins);
  • myocardial damage markers ( troponin, MB-fraction Creatinginase, LDH), which are indicators of myocardial infarction, myocarditis;
  • coagulogram ( analysis of blood clotting, which includes many, Protrombin, AFTT, D-dimer, fibrinogen and other indicators);
  • analysis on a brain sodium treatment peptide ( NT-PROBNP), which is an indicator of heart failure.

The list of analyzes increases if the patient shows surgical treatment.

When is needed drug treatment of ventricular fibrillation?

The treatment of ventricular fibrillation starts with resuscitation activities, as this arrhythmia is the cause of the heart stop. The use of medicines is not the first paragraph in the treatment of the attack of fibrillation. It is important to provide first medical care to a person at the time of the attack of fibrillation. For this, the doctor, as well as any person who turned out to be near the sick, should appreciate the signs of stopping blood circulation.

Resuscitation during ventricular fibrillation(stop heart) it happens:

  • basic;
  • extended.

The basic resuscitation can be used without medical education, if he was next to the patient who lost consciousness, checked the pulse, breathing, and they are absent.

Basic resuscitation includes the following items:

  • BUT ( air Way - Best Ways) - Restoration of respiratory tract. For this, the triple reception of the Safar is carried out - throw the head back, put forward the lower jaw ( the lower teeth should be ahead of the upper), open the mouth and exempt it from foreign substances ( if there).
  • B ( breathing - Breathing) - Artificial respiration. A person without medical education and equipment should take advantage of an artificial respiration "mouth in the mouth". Doctors and trained Paramedics use the AMBU apparatus - this is a bag of mask. The mask is worn on the face so that it gripped the mouth tightly and the patient's nose, and begin to squeeze and squeeze the balloon itself. Compression corresponds to inhale, and the rally is exhaled. In a minute you need to do 8 - 10 compression and rally ( every 6 - 8 seconds). Each "inhale" should last 1 second. How efficiently "breathes" the victim is assessed with the eye in the movements of the chest ( she rises in breathe and falls on exhalation), as well as the sound that occurs during the exhalation. Oxygen is also supplied through the AMBU apparatus.
  • C ( circulation - blood circulation) - Ensuring blood circulation, that is, a closed heart massage. The patient must lie on the solid surface smoothly, the lower limbs should be lifted a bit ( blood to heart will come more). Providing first help puts hands on the sternum ( on the bone and not on the heart). Hand position - right hand from above left, the fingers of the right hand worst fingers of the left hand as a castle ( for the left "top hand" left). Number of compressions ( pressure on the sternum) per minute should be 100.

ABC items are performed for 2 minutes, after which it is necessary to appreciate the presence of a pulse, breathing and consciousness. According to modern recommendations, it should be focused on not artificial respiration, but to the compression of the chest, and begin the basic resuscitation from clause C. If the basic resuscitation makes one person, then after every 30 compresses it performs 2 breaths. If there are two resuscators, then one performs compression ( constantly), and another 8 - 10 breaths per minute.

Point "D" of extended resuscitation during ventricular fibrillation includes:

  • defibrillation - cessation of ventricular fibrillation using electropulse therapy;
  • drugs ( drugs - medicine) - apply only after defibrillation;
  • differential diagnosis - Revision of the preliminary diagnosis, by connecting the patient to the cardiomonitor and cardiac rhythm analysis ( for this, temporarily compression and artificial respiration stop and write down the ECG).

Defibrillation

The main difference of ventricular fibrillation from other reasons for stopping the blood circulation is that it can be eliminated by defibrillation. It is defibrillation that eliminate the attack. If ventricular fibrillation developed in the hospital, then the medical staff should immediately perform defibrillation. If the heart stop occurred outside the hospital, defibrillation exercises either a challenge of ambulance brigade, or a person who knows how to use the automatic outer defibrillator ( defibrillation apparatus). In Western countries, defibrillators are available in almost all public places, and staff trained them.

The testimony for defibrillation of the heart includes:

  • no Pulse - Pulse needs to determine on sleepy arteries On both sides ( on the sides of the neck), for this, you need to put my fingers on the cartilage of the neck and "slip" to the right and left ( towards) in the "snaps" on the side parts of the neck;
  • lack of consciousness and reaction to external stimuli - the patient does not respond to questions, does not respond to painful irritation, there is no reaction of pupils on the light ( normally, he must be);
  • no breath - To assess, you need to tilt the head to the mouth of the patient with cheek, with the skin of the cheek you can feel a warm jet of exhaled air, and to the eye to determine the movements of the chest when inhaling and exhale.

It is important to know that the successful application of defibrillation depends on the effectiveness of basic resuscitation ( points ABC.). These activities are needed, since the fibrillation of ventricles, which lasts a few minutes, completely depletes the reserves of oxygen and the energy of the heart muscle. After the reserves are exhausted fibrillation of ventricles will also stop, but at the same time the chances of restoring heart activities will almost be equal to zero. Heart massage and artificial respiration make it possible to extend the viability of the heart muscle, that is, to preserve its sensitivity to electrical impulses ( while there is a ventricular fibrillation, the heart is sensitive to the therapy with electric shock). That is why before defibrillation for 2 minutes the doctor performs the pectoral compression and artificial respiration.

Defibrillation includes the following steps:

  • The inclusion of the defibrillator. The automatic external defibrillator is similar to a small laptop with 2 electrodes. Many "professional" defibrillators are equipped with a cardiomonitor, which requires the main parameters of vital activity that the doctor interprets. Defibrillators for people without medical education instruct the person who has the first medical assistance, at all stages. These can be voice instructions or detailed video.
  • Installing electrodes. Electrodes are installed on the chest so that the heart turns out to be between them. One electrode must be applied under the right clavicle to the right of the sternum ( it is important not to put on the bone itself), and the second is in the left lower part of the chest at 5 - 6 intercostal. While the defibrillator includes and install electrodes, it is important not to interrupt the compression of the chest ( therefore, resuscitation is carried out two).
  • Automatic cardiac rhythm analysis.The defibrillator analyzes the heart rhythm itself. During the analysis of the rhythm compression temporarily stop. Conductive defibrillation should warn others do not touch the patient during rhythm analysis. If the defibrillator recognizes ventricular fibrillation waves or dangerous ventricular tachycardia, then the signal is triggered.
  • Automatic, semi-automatic or manual decomposition.Some defibrillators after discovering ventricular fibrillation immediately apply a discharge ( automatic devices), others inform resuscitative about the fact that there is ventricular fibrillation, and the resuscator must press the digit button itself ( semi-automatic devices). With a manual defibrillator, the doctor itself determines the power of the discharge.

Immediately after the first time was applied, the reanior evaluates whether normal rhythm is restored. If fibrillation persists, the outer heart massage continues and artificial respiration. If the rhythm is not restored, the power of the charge increases to the maximum ( 360 J.) And the second category is applied. In the absence of the effect of the second category, the catheter is introduced into the vein and begin to enter medications.

Preparations for the treatment of ventricular fibrillation

Medical therapy for ventricular fibrillation is carried out only by a doctor. It is important to know that some drugs are applied only during resuscitation activities, while others - and for resuscitation, and for the prevention of repeated attacks of ventricular fibrillation. Preventive antiarrhythmic therapy is effective in half of patients with ventricular arrhythmias, moving to fibrillation. The rest of the patients are shown surgical treatment.

Preparations for the treatment of ventricular fibrillation

Medication

Mechanism of therapeutic action

Indications

Mode of application

Adrenalin

Adrenaline affects specific receptors that are available in different organs and name adrenoreceptors. Most of all these receptors are in vessels and in the heart, so the introduction of adrenaline causes a spasm of blood vessels ( enhances blood pressure). Adrenaline increases the excitability of the heart muscle. Against the background of fibrillation of ventricles, the higher the excitability of myocardium, the higher the chances that defibrillation will be successful ( excitable myocardium is sensitive to stool). After restoring the rhythm, adrenaline, affecting the heart, allows you to increase the reduction of the heart muscle and restore the pump function.

Intravenously or intraosnially every 3 - 5 minutes against the background of continuing basic cardiovascular intensive care and defibrillation.

Amiodar

(cordaron)

Amiodaron is an antiarrhythmic drug that acts on the ionic channels of cardiac cells. By blocking these channels, the amiodarone changes the excitability of cells in the ventricles and the speed of the wave for all small rhenium waves. As a result, the movement of the pulse in a closed loop slows down so much that the impulse "late" to the cell at the time of her willingness and finds it in a state of sleep. As a result, the loop is interrupted.

  • an attack of ventricular fibrillation;
  • prevention of repeated ventricular arrhythmia after successful resuscitation and recovery.

It is introduced after the third discharge of the defibrillator intravenously quickly. For prevention, intravenously drip ( in the intensive care unit) or assigned in the form of tablets ( already after discharge from the hospital).

Lidocaine

Lidocaine is also an antiarrhythmic drug. It acts solely on the beam cells of the Gis and Fiber Purkinier, as well as on contractile myocardium, changing the speed of the pulse. The slowdown of the pulse leads to the same effect as when the amiodarone is used - the excitation wave is "late" and is interrupted.

  • the fibrillation attack of ventricles.

Enter intravenously.

Bicarbonate of soda

Sodium bicarbonate is introduced to increase the efficiency of major drugs. The sodium bicarbonate effect is due to alkaline properties, it restores the acid essential equilibrium of the body ( often broken with many arrhythmias) and reduces blood acidity ( acidosis).

  • long resuscitation activities ( 30 minutes and more);
  • arrhythmia caused by overdose of other drugs ( tricyclic antidepressants) and hyperkalemia.

Intravenously drip.

Beta adrenoblocators

(bisoprolol, Carvedilol)

Beta adrenoblocators are a group of drugs that blocks beta class receptors of the sympathetic nervous system. It is through these receptors that the function of the conductive heart system and some properties of the heart muscle are regulated. The blockade of these receptors has a "soothing" impact on the heart - Rhythm penetrates ( the sinus node is oppressed), the excitability of cells decreases ( the number of calcium is reduced). All this makes it easier for the work of the heart muscle and reduces the risk of repeated attacks of ventricular fibrillation.

  • prevention of bouts of ventricular fibrillation, thanks to the prevention of the development of other ventricular arrhythmias.

Preparations are accepted inside.

The main drugs that are included in the expanded resuscitation point are amiodar and adrenaline. Lidocaine is usually used in the absence of amiodarone. It is important to know that Lidocaine is never introduced if the patient has already entered amiodaron.

When is the surgical treatment of ventricular fibrillation with the introduction of a pacemaker?

Surgical treatment of ventricular fibrillation is aimed at treating the main heart disease, which led to arrhythmia, and prevent repeated attacks, if the main reason cannot be eliminated. Surgical treatment can be in the form of an open operation on the heart or minimally invasive interventions. Invasive interventions on the heart are carried out with a catheter, which is injected through large vessels and bring to the heart.

From the point of view of the forecast and tactics of treatment, the following 2 large groups of ventricular fibrillation are distinguished:

  • ischemic origin - includes rhythm disorders in the presence of serious lesions of the coronary arteries ( ischemic heart disease, vasospadic angina, acute myocardial infarction);
  • non-ahemic origin - Includes all other heart pathology.

If ventricular fibrillation has ischemic origin, then its treatment is to restore the coronary arteries. This is carried out due to balloon dilatation and stenting, as well as thrombolesis ( the introduction of drugs that destroy the thrombus blocking the coronary artery), that is, the treatment of such ventricular fibrillation corresponds to the treatment of acute myocardial infarction.

Fibrillation of ventricles of non-ahemal origin is treated by the following methods:

  • implantation of cardioverte-defibrillator;
  • catheter ablation;
  • surgical ablation;
  • open operation.

A pacemaker, that is, a device that sends pulses to reduce the heart, with the most fibrillation of ventricles does not apply. The need for a pacemaker arises only when a person has rarely beats a heart ( this is called Brady Country), Against this background, ventricular tachycardia develops, which can potentially go to ventricular fibrillation. Thus, the main indication for the dwelling of the pacemaker is not fibrillation of ventricles, but by other arrhythmias from a group of high-risk markers.

With ventricular fibrillation, the patient implan the other device is a cardioverter-defibrillator, which resembles a pacemaker, but the principle of its action is completely different.

Cardoverter-Defibrillator implantation

Cardioverter defibrillator ( cardio - Heart, Veto - Rotate), unlike the pacemaker, need to interrupt the starting attack of ventricular tachycardia and prevent its transition to ventricular fibrillation. Thus, the implantation of the cardioverte-defibrillator is the methods for the prevention of sudden cardiac death.

The cardioverter defibrillator performs the following two functions:

  • recognizes hazardous arrhythmias ( constantly controls heart rhythm);
  • inflicts an electrical discharge to restore normal rhythm.

The cardioverter defibrillator can be configured if necessary so that it performs the functions of the single-chamber ( stimulation of one heart chamber - either atrium, or ventricle) or two-chamber ( stimulation of two heart cameras - and atrium, and ventricle) Cardimulator. However, in contrast to the implantable defibrillator, the pacemaker cannot stop the attack of ventricular tachycardia or ventricular fibrillation.

The implantable cardioverter defibrillator consists of the following components:

  • impulse generator;
  • electrodes.

The pulse generator contains a battery, a condenser ( accumulates and converts electric current) and the so-called "reasonable" electronic part or "brain". Electrodes are divided into two types - perceive heart rhythm and applying discharge. Electrodes are injected through a femoral vein. One electrode is installed in the right atrium, and the second is in the right ventricle. The box is implanted into soft fabrics under the left clavicle. After implantation, the cardioverter defibrillator is set up. One month after the impact, check the operation and settings of the cardioverter-defibrillator using a special device.

Cardoverter-defibrillator implanted according to the following readings:

  • ventricular fibrillation not related to reassembly;
  • ventricular fibrillation with severe chronic heart failure ( II - III degrees) and a reduced contractile function of the left ventricle ( emission fraction less than 35%);
  • lack of effect from medication therapy arrhythmia for three months;
  • arritmogenic dysplasia of the right ventricle;
  • cardiomyopathy ( hypertrophic, dilatational);
  • the elongated interval Q-T syndrome;
  • brugada syndrome.

The cardioverter-defibrillator "Fights" with arrhythmia in the following ways:

  • Antitachycardial electrostimulation. After the start of arrhythmia, cardioverter analyzes the rhythm frequency and begins to send signals that stimulate the heart more often than the arrhythmia itself. As a result, the impulses from the center of arrhythmia begin to "be late", reaching at the moment when muscle fibers are restored after cutting and cannot be repeated. Thus, arrhythmia is interrupted. Such an interriety of arrhythmia is often unnoticed for the patient.
  • Electric shock. If the heart beats too often or arrhythmia has already passed into ventricular fibrillation, then the first way is ineffective. In such cases, cardioverter, recognizing arrhythmia, causes an electrical discharge and performs the same defibrillation as during resuscitation. A short discharge, nevertheless, is felt sick and often happens painful.

The cardioverter-defibrillator is not implanted in the following cases:

  • constantly repeated attacks of ventricular tachycardia;
  • wPW syndrome;
  • the final stage of heart failure ( when a heart transplant is required);
  • the cause of ventricular fibrillation can be eliminated.

Against the background of an implanted cardioverte-defibrillator, some drugs can be prescribed to the patient. The fact is that the cardioverter-defibrillator works only when arrhythmia attacks, that is, the purpose of its implantation is the prevention of sudden heartfelt death in patients with life-in-lawy arrhythmias, but not adjusting the heart rate outside the attack. The medications are prescribed to reduce the rapid rhythm of the heart - a phenomenon that is observed in the majority of patients with heart pathology ( heart overload always activates the stress systems of the body, and they are rapidly rhythm).

In patients with an implanted cardioverter-defibrillator, amiodarons and beta-adrenoblays are used. These drugs have a property to increase the fibrillation threshold - the probability of the appearance of a pulse. If the threshold is low, then the impulse occurs easy, if high - with difficulty. That is, an electrical impulse should be so powerful to reach the threshold. If the excitability of cells to decrease, the threshold will increase, and the impulse will not reach the desired mark, will not be able to cause a violation of the rhythm.

The service life of a cardiovertere-defibrillator is about 5 to 8 years, depending on the model.

Catheter ablation

Ablation is called the destruction of any changed area of \u200b\u200bthe organ using the effects of physical factor. In most cases, this focus is migrated, less often frozen. The catering catheter is introduced into the heart just as with other invasive operations - through artery or vein, depending on what the heart is the arrhythmic hearth. With the help of EFI in the midstime, the arrhythmias find where the pulse moves slower everything is the so-called experiencing. This "critical point" is migrated, which makes it impossible to re-entry the excitation wave and interrupts Ratentri loop. That is why catheter ablation is used only if the source of arrhythmia is one source in which the loop and the circular motion of the excitation wave is formed. Such a focus is the cause of ventricular tachycardia, therefore it will be more correct to say that catheter ablation is not aimed at the treatment of the fibrillation itself of ventricles, but to eliminate arrhythmia with a high risk of transition to ventricular fibrillation.

Catheter ablation is shown in the following cases:

  • there is an arrhythmic substrate - an obvious pathological structure, which becomes the source of arrhythmia, for example, a scar after myocardial infarction, an additional beam;
  • "Arrhythmic Storm" - Frequent attacks of arrhythmia in patients with an implanted cardioverter-defibrillator, which arise in cases where the main cause of arrhythmias ( disease or violation) Not eliminated, and cardioverter defibrillator works often, causing discomfort in the patient.

The arrhythmic storm is observed in the following cases:

  • defeat several coronary arteries ( the risk of myocardial infarction);
  • aggravation of heart failure;
  • changing the level of potassium, calcium and magnesium in the body;
  • side effects of some antiarrhythmic drugs.

Open operation on the heart and surgical ablation

Practically in 90 - 95% of cases, ventricular fibrillation is due to the pathology of the heart. If the cause of the rhythm violation is a pathology that requires an open operation on the heart, then doctors can perform surgical ablation, that is, the same migration but not through the catheter, but a tool introduced into the chest cavity. In these cases, cryoablation is most often used - freezing.

Surgical ablation at a high risk of ventricular fibrillation is carried out in conjunction with the following operations:

  • aneurysmismectomy - removal of the aneurysm of the left ventricle;
  • prosthetics of valve - replacement of the affected mitral valve;
  • coronary shunting - sewing bypass vessels to restore heart blood flow ( one end of the vessel is stitched with aorta, and the other is below the location of the coronary artery).

In addition, surgical ablation is shown in cases where catheter ablation has not been effective. The fact is that the causing of the selected loop area must be carried out at the entire depth of the wall. In this part there should be a scar. The scar can not carry out the impulse. If migrating, leaving at least a bit of a healthy tissue, the possibility of holding a pulse on the loop will be saved.



How to identify bouts of ventricular fibrillation?

It is possible to identify the fibrillation of ventricles only to the ECG ( electrocardiogram), but, since the attack of ventricular fibrillation often occurs outside the hospital, then with a sudden loss of consciousness, the absence of pulse and respiration in humans, it is precisely the fibrillation of ventricles as the most frequent cause of the heart stop. On ECG fibrillation of ventricles are frequent irregular waves of different amplitude.

What does the ventricular fibrillation lead to?

Pibrillation of ventricles leads to a stop of the heart, since one-piece reduction of the heart is impossible to implement this rhythm disorder ( with fibrillation, each group of muscular fibers is excited and reduced by itself). This condition is called a circulatory stop. Circulatory stop is the cessation of blood flow through the vessels due to the fact that the heart stopped shrinking. Circulatory stop leads to clinical death ( reversible). Those cases that lead to death due to ventricular fibrillation are called a sudden heartfelt death. This means that the patient had any heart disease ( a person could know about him or not to know), which manifested itself with a violation of the heart rhythm in the form of ventricular fibrillation.

How does ventricular fibrillation feel?

The fibrillation of the ventricles itself is not felt by the patient, as it immediately leads to the loss of consciousness, stop the heart and stopping the breath. However, a person can feel the symptoms of those violations of the heart rhythm, which go into ventricular fibrillation. Usually, any arrhythmia begins with extrasystole - premature reduction of the heart, which is caused by one impulse from the center of arrhythmia. Extrasystoles are felt as a feeling of "fall" of something in the chest, interruption in work or fading. If the extrasystoles follow one after another, they are transferred to the ventricular tachycardia, which is manifested by the seating of rapid heartbeat, dizziness, weakness, pain in the chest in the heart, shortness of breath. This state corresponds to the pre-imaging. If the attack continues, and the heart beats very often, then the pre-arrangement state is fainted ( blood ceases to reach the brain).

If ventricular tachycardia goes into ventricular fibrillation, except for the loss of consciousness, the respiratory stop occurs or it becomes noisy and superficial ( agonal breathing), ceases to take care of the pulse at carotid arteries ( on the neck), and after 40 seconds, convulsions begin, sometimes involuntary urination or feces are observed. Gradually, pupils expand and begin to respond poorly to light ( if the light is sent to the pupil, it is normal in the normal). The maximum expansion of pupils is observed 1.5 minutes after stopping the heart.

What is the difference between shimmer arrhythmia from ventricular fibrillation?

Cleaning arrhythmia is the atrial fibrillation, that is, arrhythmia that violates the reduction of the upper and smaller heart chambers. The mechanism for the development of atrial fibrillation and ventricular fibrillation is the same - many loops are formed in the heart muscle, in which the electrical impulse is constantly moving.

These multiple loops are called Ratentri ( from english word. Re-Entry, Ri - Repeat, Entry - Entrance), And the arrhythmia mechanism is "re-entry of the excitation wave", then the situation when the impulse does not fuss in the ventricles, but continues to spin, constantly changing its direction. Given the small size of these loops, they are called micro Ratentri.

Between the flickering arrhythmia and fibrillation of ventricles there are the following differences:

  • Cleaning arrhythmia becomes the reason for the cessation of the reduction of only atrium, which, of course, worsens the work of the heart, but does not lead to its stop. The fibrillation of the ventricles violates the coordinated reduction of ventricles, which swing blood along the vessels. That is why ventricular fibrillation leads to a heart stop and requires resuscitation activities.
  • The attack of flickering arrhythmia can pass on its own, but the attack of ventricular fibrillation never independently passes. The developed ventricular fibrillation is the result of severe heart damage, and often the transition from severe heart disease to clinical death, that is, the mechanism for which a person with a severe heart pathology "refuses the heart".
  • On ECG ( cardiogram) With flicker arrhythmia there are minor irregular waves of flicker, but there are necessarily high sharp oscillations up and down - this is a reduction in ventricles. With ventricular fibrillation, there are only irregular waves of different shapes, large and small size.

Can the atrial fibrillation go to ventricle fibrillation?

Atrial fibrillation can move into ventricular fibrillation in the presence of an additional way from the atrium in the ventricles. The presence of such paths is called WPW syndrome ( Wolf-Parkinson-White). This syndrome can not be felt. The symptoms appear only when its consequences occur - the attack of arrhythmias ( heartbeat with a frequency greater than 150 per minute).

Normally, the conduct of a large number of impulses from atria in the ventricles is not warned, due to the ability of the Av-node ( preservative knot) To delay the impulse for a while or block some pulses if there are too many. Thus, the Av-assembly warns the development of ventricular fibrillation in patients with atrial fibrillation. If a person with WPW syndrome develops atrial fibrillation, then a very frequent rhythm, which is observed during atrial fibrillation, can pass the ventricles, that is, without exception, the impulses, bypassing the Av-node, will be held to the ventricles and will cause them fibrillation.

What is the difference in fibrillation of ventricles from trembles?

Trepping ventricles - this means very frequent, but regular oscillation of something, in this case it is frequent ( 200 - 300 per minute), but regular cutting of ventricles. The fibrillation of ventricles is a chaotic, irregular reduction in each muscular fiber in the ventricles separately ( the term fibrillation comes from the word "fibril" - fiber). The difference between fluttering and ventricular fibrillation is visible on the electrocardiogram ( ECG).

The trembling of ventricles on the ECG is characterized by:

  • sinusoidal regular waves;
  • lack of isolated ( flat line on an ECG, which is normal between the teeth, that is, the oscillations of the cardiogram);
  • the amount of waves is usually no more than 300 per minute.

The cause of the trembling of the ventricles is one large loop in the ventricles, according to which the impulse is moving in a circle, causing excitement and reduction of the heart.

Fibrillation of ventricles on the ECG is characterized by:

  • waves of different shapes and amplitude;
  • irregular waves;
  • the number of oscillations of the cardiogram ( wave) More than 300 per minute.

The cause of ventricular fibrillation is a plurality of small loops and waves in the ventricles.

It is believed that the flourishing of ventricles due to the preservation of the whole reduction of the heart provides at the minimum level of vital functions ( breathing, blood circulation), However, it depends on the frequency of abbreviations. With the number of pulses of 300 per minute, the trembling of ventricles leads to the same ineffective reduction in the heart as ventricular fibrillation.

The fluttering of ventricles is considered the first stage of ventricular fibrillation, that is, potentially can go ( and usually goes) To fibrillation. This is because due to electrical instability, one big wave disintegrates into a plurality of small waves.

Both arrhythmias lead to a heart stop and, therefore, blood circulation, as such a frequent reduction does not lead to efficient blood pumping. Both arrhythmias lead to clinical death, and to restore rhythm, it is required to carry out resuscitation.

What is the difference between ventricular tachycardia and ventricular fibrillation?

And ventricular tachycardia, and ventricular fibrillations are ventricular arrhythmia ( ). Ventricular tachycardia ( tahi - Often, Cardio - Heart) Is an attack of a rapid heartbeat, in which the heart is reduced 120 - 300 times per minute ( on average, 180 shots per minute), while cutting regular. The cause of ventricular tachycardia is one or two focus of arrhythmia in ventricular, which generate pulses faster than this can make the main driver of the heart rhythm - sinus knot ( his features - maximum, 160 beats per minute). The reason for the fibrillation of ventricles is the movement of the wave excitement by random path, while the wave constantly changes its direction. There are many such waves for fibrillation, and each acts independently. That is why, with ventricular fibrillation, each muscle group is excited and reduced in its rhythm, and the result is 300 or electrical pulses per minute emanating from the heart.

You can distinguish both arrhythmias from each other both by symptoms and according to electrocardiography ( ECG).

The ventricular fibrillation has the following features:

  • each muscular beam is reduced intermittently ( a signal, as it were, flashes or flickering);
  • there is no period when all the muscles "resting" ( while decreases alone fibers, other fibers are preparing to reduce);
  • it is chaotic and irregularly registered then large, then small oscillations of different shapes.

Stomatricular tachycardia is manifested by the following symptoms:

  • sudden start and sudden ending attack ( often alone);
  • extended and deformed cardiogram oscillations ( if they are compared with fluctuations in normal ECG);
  • the atrium is reduced by a rhythm of the sinus node, and the ventricle - rhythm of the ventricles themselves;
  • periodically arise normal complexes on ECG ( if the impulse from the sinus node finds the ventricles in their finished to excitement).

How to provide first help if ventricular fibrillation arose?

If a person suddenly lost consciousness fails to determine the pulse and there is no breathing, then immediately proceed to the provision of first aid. For this you do not need to be a medical worker. It is also impossible to stay indifferent and wait for an ambulance. Such a delay can cost the patient's life, and in time perfect correct actions can save it.

First aid for ventricular fibrillation should be provided in the following sequence:

  • Make sure the person is unconscious. To do this, ask loud questions, shake, pat on the cheeks, determine the reaction of pupils into the light. The reaction of pupils can be assessed either with the help of the palm ( get down with palms both eyes, then quickly remove the palms), either by flashlight ( side Light eye). Normally, pupils must be driving. If they remain expanded, this is a sign of clinical death.
  • Check for pulse. To do this, put the fingers of the right hand to the carotid artery, which passes through the side surfaces of the neck. To grope it, you should put your fingers on the center of the neck and without tearing them, move to the right or leftAt the same time, the fingers will "fall" in a sneaker - this is the location of the carotid artery. Checking the pulse must be required on both carotid arteries.
  • Check no breathing. Bend to the victim, bringing the cheek to his mouth. In the presence of breathing, the cheek will feel warm. At the same time, you should evaluate the movement of the chest when inhaling and exhale. To evaluate the breathing, you can also bring the sick mirror to the mouth. If there is breath, then the mirror is notice.
  • Start resuscitation activities. Resuscitation during fibrillation begins with a closed heart and artificial respiratory massage. A closed heart massage is compression ( pressure, push) On the sternum with two hands and the entire severity of the body in order to pump out blood from the heart into the vessels. Thus, a person providing first medical care ( not necessarily doctor) Temporarily becomes a pump instead of a heart. You need to put it on the bone ( breast), with two hands. The right hand is placed on the left, and the tops of the top hand wrap the fingers of the bottom. Artificial respiration is carried out according to the "mouth in the mouth" method, that is, you need to hold the nose of the patient, to breathe in and exhale in the mouth of the patient ( it is important to tightly squeeze the mouth of the affected mouth so that the air gets into the airways, and not outward). After every 30 chest compressions, you need to make 2 breaths. If the first medical assistance can have two, then one conducts only compression, and the second only artificial respiration. Periodically, you need to change in places ( hands of a person who produces compression quickly get tired).
  • Ask someone to call ambulance. It is undesirable to stop "swing blood" and call himself. If there is no one near anyone, then you should first call the ambulance, and then start providing first medical care.
  • Defibrillation ( electric shock) . If there is a device for defibrillation nearby ( defibrillator), then you should immediately use it. Outside the hospital, such devices are designed for people without medical education, and when turned on, you begin to instruct a person providing assistance. The success of defibrillation depends on the effectiveness of the main resuscitation activities.

After defibrillation, the heart rhythm can recover immediately. In this case, the pulse and breathing will appear. If fibrillation continues, then you need to continue compression and artificial respiration for another 2 minutes ( rhythm can recover in a few minutes). Repeated the discharge of the electric shock can after 5 cycles of compressions and the breathing "mouth in the mouth" ( 1 cycle - 30 compressions and 2 inhales).

Vottricular fluttering is ventricular tahiarhythmia, which has the right frequent rhythm (about 200-300 shots in one minute). Most often a state may be accompanied by a decrease arterial pressure. The loss of consciousness, pallor, diffuse cyanosis of skin, agonal breathing, convulsions, expansion of pupils are not excluded.

In addition, it can provoke sudden coronary death. The diagnosis of such pathology is carried out on the basis of electrocardiographic studies and clinical data. In the event of the trembling of ventricles includes immediate defibrillation and cardiovascular resuscitation.

What is the trembling of ventricles?

A similar phenomenon is a disorganized electrical activity of myocardium, which is characterized by frequent and rhythmic reduction in ventricles. The frequency of such cuts exceeds 200 shots per minute. It can also go to fibrillation (flicker), which will be frequent, up to 500 shots, but irregular and disorderly ventricular activity.

In the cardiology department, specialists include fibrillation and fluttering to rough-type arrhythmias, which can lead to ineffective hemodynamics. In addition, they are the most frequent reasons Arrhythmic death. In accordance with epidemiological data, fibrillation and fluttering most often arise in persons whose age is in the range from 47 to 75 years. A characteristic feature is that men are manifested three times more often than women. In 70-80% of cases, the cause of sudden death is precisely fibrillation of ventricles.

The reasons why pathology arises?

The trembling of ventricles may arise against the background of various heart diseases, with a variety of extracardial pathologies. Quite often, organic lesion of myocardium, which develops on the background of IBS, can be complicated by ventricular fibrillation and trembling. In addition, this pathology accompanies the following diseases:


Other reasons

It is less likely to develop this impairment due to intoxication of cardiac glycosides, violations of the balance of electrolytes, high-level in the blood of catecholamines, electricians, contusions of the heart, hypoxia, acidosis, hypothermia. Also, ventricular tachycardia can be caused by some of the drugs, such as sympathomimetics, barbiturates, narcotic analgesics, antiarrhythmic agents.

Another reason for the occurrence of trepidation is a cardiac surgical procedure. These include coronary artwork, electric cardioversion, defibrillation in the cardiology department.

Pathogenesis of ventricular trembles

The development of such a disease is directly related to the Re-Entry mechanism having a circular nature of circulation of excitation wave passing through the myocardium of ventricles. It leads to the fact that the ventricles are often reduced and rhythmically, and there is no diastolic interval. The re-entry loop can be located around the perimeter of the entire infarct zone, or a plot of ventricular aneurysm. The CSS table is normal as follows below.

Multiple random waves RE-Entry play the main role in the pathogenesis of ventricular fibrillation, which provoke the reduction of individual myocardial fibers while there are no entire ventricles. This phenomenon is due to the electrophysiological heterogeneity of myocardium: at the same time, various parts of the ventricles can be in the period of repolarization and in the period of depolarization.

What does it start?

Fibrillation and trembling of ventricles, as a rule, launches ventricular and superstricular extrasystole. Initiate ventricular and Wolf-Parkinson-White's syndrome, atrial flicker, and then support the Re-Entry mechanism.

In the process of the development of trembles and flicker, it is rapidly declining, and then becomes zero impact volume of the heart. As a result, blood circulation ceases instantly. The fluttering of paroxysmal nature and ventricular fibrillation are always accompanied by trimmed states, and the stable form of tachyarhythmia entails first clinical, and then biological death.

Classification of ventricular trembles

In the process of development, such heart diseases such as ventricular flickering and tremies pass four stages:

The first is the tachiisistolic stage of ventricular trembles. The duration of this stage is a maximum of two seconds. It is characterized by frequent, coordinated heart abbreviations. The ECG of this stage corresponds to 3-6 ventricular complexes with a sharp high amplitude oscillation.

The second stage is the convulsive ventricular tachyritium. Its duration is from 15 to 50 seconds. It is characterized by frequent, local abbreviations of the myocardial of an irregular nature. ECG reflects this stage in the form of high-voltage waves having different magnitude and amplitude.

Third stage is the stage of flickering ventricles. The duration of this stage is 2-3 minutes. It is accompanied by multiple irregular contractions of individual myocardial zones that have different frequency.

The fourth is the stage of Atonia. This stage develops approximately 2-5 minutes after the flickering of the ventricles has occurred. For the fourth stage, small, irregular abbreviation waves are characterized, the increasing number of areas that ceased to decrease. The ECG is reflected in the form of irregular waves, the amplitude of which is gradually decreasing.

Cardiologists distinguish ventricular flickering and trembles according to the variant of their clinical development. So, allocate constant and paroxysmal forms. In this case, the flutter of the second form can be recurrent, that is, can be repeated several times during the day.

Symptoms

Heart diseases - ventricular fibrillation and trembles, in fact, correspond to clinical death. If fluttering occurred, then for a short time, it is possible to preserve low heart emissions, consciousness and arterial hypotension. Occasionally, ventricular flutters can end with spontaneous recovery of sinus type rhythm. Most often there is a transition of such an unstable rhythm into ventricular fibrillation.

Trepping and fibrillation of ventricles accompany the following symptoms:


If such symptoms are observed and it is established that fibrillation and trembling of ventricles occurred, then the patient is necessary to provide urgent medical care. The CNS and other organs are irreversibly affected if within 4-5 minutes it is not to restore normal heart rhythm.

Complications

Death is the most unpleasant outcome of such deviations. As a result, the following complications are possible:


Diagnosis of ventricular trembles

You can recognize and diagnose ventricular flickering and tremies using clinical and electrocardiographic data. If such a deviation is available, then on an electrocardiographic study, it will be displayed as regular, rhythmic waves having almost the same shape and amplitude. They resemble a sinusoidal type curve with a frequency of oscillations 200-300 per minute. Also on the ECG there is no isoelectric line between the waves, the teeth of P and T.

If ventricular fibrillation is observed, waves with heart rate (heart rate) of 300-400 oscillations per minute will be recorded, which continuously change their duration, shape, direction and height. There is no isoelectric line between the waves.

Golden flickering and fluttering should be differentiated from the heart tamponade, massive tel, supertoday arrhythmia, paroxysmal tachycardia of the ventricles.

The CSS table is normal in the ages below.

Treatment of ventricular trembles

In the case of the development of ventricular flutters or fibrillations, immediate resuscitation assistance should be provided, which is aimed at restore the sinus heart rate. Primary resuscitation should include applying a precondial impact or performing artificial respiration in a tandem with an indirect heart massage. Specialized cardiovary and pulmonary resuscitation includes an IVL and electrical defibrillation of the heart.

Simultaneously with the measures of a resuscitation nature, it is necessary to introduce solutions of atropine, adrenaline, sodium hydrocarbonate, procainamide, lidocaine, amiodarone, magnesium sulfate intravenously. In parallel, it is required to re-electrodefibrillation. At the same time, with each series, an energy from 200 to 400 j. If recurrence of ventricular fibrillation and fluttering occurs, which arises as a result of a complete atrioventricular blockade of the heart, then it is necessary to resort to the time stimulation of cardiac ventricles with a rhythm, which exceeds the frequency of their own oscillations.

special instructions

If the patient has no restoration of spontaneous breathing, cardiac activity, consciousness, does not occur, there is no reaction to the light of pupils, the measures of resuscitation should be discontinued. If resuscitation has been successful, then the patient for further observation is transferred to the orort. Subsequently, the attending cardiologist decides whether to implant the cardioverter-defibrillator or a two-chamber cardiac card.

The fibrillation of the ventricles of the heart is the hardest form of the violation of its rhythm. It leads to a stop of the heart and the development of clinical death within a few minutes. This is a border state that requires immediate resuscitation activities. Therefore, the life of a person after an attack depends on the timeliness and literacy of the actions of people who were near.

According to statistics, men are subject to men over the age of 45, having various forms of heart pathologies. It is the diseases of this body that are the main cause of the development of ventricular fibrillation.

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    Basic concept

    Fibrillation of ventricles, or their flicker, is an urgent state characterized by non-coordinated cuts of the ventricles of the heart. Often their frequency exceeds 300 shots per minute. During this period, the function of this organ for pumping blood is broken, and after a while it stops at all.

    Preceded by a row of a condition called "Verbs' Vrestorchkov" - unstable arrhythmic heart cuts with a frequency of 220 to 300 per minute, which quickly go into fibrillation.

    Fibrillation of ventricles

    The disease is at the heart of the disease lies a violation of the electrical activity of myocardium and the cessation of full heart cuts, leading to a circulatory stop.

    Men are three times more often women suffer from ventricular fibrillation. It accounts for about 80% of all cases of cardiac arrest.

    The mechanism of development of pathology

    The essence of the mechanism for the development of ventricular fibrillation lies in the uneven electrical activity of the heart muscle - myocardium. This leads to a reduction in individual muscle fibers with a different speed, as a result, different portions of myocardium are located in different phases of reduction. The frequency of abbreviations of some fibers reaches 500 per minute. The whole process is accompanied by chaotic cardiac muscle, which is not able to provide normal blood circulation. After some time, the human heart stops and clinical death comes. If you do not start cardiovascular resuscitation, then after 5-6 minutes there will be irreversible changes in the body and the death of the brain.

    Trepping and fibrillation of ventricles are the most dangerous types of arrhythmia. Their difference lies in the fact that the correct rhythm of the contractions of myocardial cells - cardiomyocytes remains preserved, and their frequency does not exceed 300 per minute. Fibrigration is distinguished by indiscriminate reduction in cardiomyocytes and irregularity of the rhythm.

    Trepping and fibrillation of ventricles

    Trepping ventricles is the first stage of fibrillation.

    Causes and predisposing factors

    There are many factors affecting the conductivity of myocardium and its ability to reduce. Of these, 90% fall on cardiovascular diseases.

    The main causes of ventricular fibrillation:

    FactorPathology
    Cardiovascular diseases
    • stomatricular paroxysmal tachycardia - a sudden attack of a rapid heartbeat arising under the influence of pulses that replace the normal sinus rhythm of the heart;
    • ventricular extrasystole - a violation of the heart rhythm, in which an extraordinary reduction of ventricles occurs;
    • myocardial infarction is the mass death of the cells of the muscular tissue of the heart due to lack of supply of blood;
    • acute coronary insufficiency - circulatory disruption in the heart;
    • cardiomegaly, or "bullish heart", - anomalous increase in the size or mass of the organ;
    • brugada syndrome is a genetically determined impairment of the heart;
    • an atrioventricular blockade is a disorder of electrical conductivity between ventricles and atria, leading to arrhythmia;
    • vices for the development of the heart and its valves;
    • cardiomyopathy - the pathology of myocardium of unclear nature, characterized by an increase in the dimensions of the heart and its cameras, a violation of rhythm, heart failure;
    • cardioosclerosis is a gradual substitution of myocardium with a connecting cloth;
    • myocarditis - Inflammation of the Heart Muscle
    Balance violation of electrolyte
    • insufficient flow of potassium into the body, leading to the electrical instability of myocardium;
    • excess calcium accumulation inside cells
    Reception of medicinesInxication caused by the following groups of drugs:
    • sympathomimetics - orciprenaline, epinephrine, salbutamol;
    • heart glycosides - Digitoxin, Digoxin;
    • means against arrhythmia - amiodar, sotalol;
    • narcotic analgesics - levomepromazine, chlorpromazine;
    • catecholamines - Dopamine, Noraderenalin, adrenaline;
    • barbiturates - Sectional, Phenobarbital;
    • medical anesthesia - chloroform, cyclopropane
    Injuries
    • electric shock;
    • blunt heart injuries;
    • penetrating injuries of the chest
    Medical manipulations
    • coronaryography is the introduction of a contrast agent into the blood circulation system with subsequent radiography;
    • cardoversion - Treatment of heart rate disorders by means of electrical impulses
    Burns, overheating
    • temperature increase;
    • fever with sharp temperature drops
    Insufficient oxygen provision
    • skull injuries;
    • suffocation
    Other reasons
    • acidosis - a decrease in the pH of the body, that is, the shift of the acid-alkaline balance towards increasing the acidity;
    • dehydration associated with blood loss various character;
    • hypovolemic shock - critical condition resulting from a sharp loss of circulating blood in the body

    Myocardial infarction as a cause of ventricular fibrillation.

    Risk factors include:

    • male gender;
    • age older than 45 years old.

    Clinical picture

    Fibrillation of ventricles occurs suddenly. Their function is dramatically violated, which leads to a circulatory stop. This process entails the development of acute ischemia (oxygen starvation) of internal organs and brain. The patient stops moving and loses consciousness.

    The main symptoms of pathology:

    • cardiac rhythm;
    • sharp pain in the head;
    • dizziness;
    • sudden disconnection of consciousness;
    • stopping cardiac activity;
    • intermittent breathing or its absence;
    • skin pallor;
    • akricyanosis (skin sinusiness), especially in the area of \u200b\u200bthe nasolabial triangle, nose and ears tips;
    • the inability to try the pulse on sleepy and femoral arteries;
    • expansion of pupils and the absence of their reaction to light;
    • hypotension (relaxation) muscles or convulsions;
    • sometimes - involuntary defecation and urination.

    All signs arise almost simultaneously, while the fatal outcome occurs throughout the hour since the appearance of the first symptom in 98% of cases.

    After a complete stop of the heart, you can return the person to life for seven minutes. Throughout this time, changes in the body are considered reversible. Then the irreversible processes of the cellular decay and biological death of the brain begin.

    Stages of fibrillation of ventricles and ECG testimony

    The fibrillation attack is manifested by the symptoms of clinical death. It is possible to recognize this condition using electrocardiography (ECG) - the most informative diagnostic method.

    ECG readings

    ECG advantages:

    • rapid resulting;
    • the ability to conduct a procedure outside the clinic or hospital.

    Characteristic features of the flicker of ventricles on the ECG:

    1. 1. Lack of registration of the excitation of the ventricles of the heart on the ECG, that is, the ventricular complex or QRS complex.
    2. 2. Determination of irregular, different duration and amplitude of fibrillation waves, the intensity of which reaches 400 per minute.
    3. 3. No insion.

    Based on the size of the waves, ventricular fibrillation is two types:

    1. 1. Large - excess of the reduction force above one cell (0.5 cm) when writing electrocardiography. The definition of this type of flicker is noted in the first minutes of the attack and means the beginning of arrhythmia.
    2. 2. Melkovo-wave - manifests itself in the exhaustion of cardiomyocytes, the increase in the signs of acidosis and disorders of metabolic processes in the body, which is characterized by a large risk of death.

    The sequence of the stage of arrhythmias determined by the ECG:

    1. 1. Tahisistolic - fluttering a duration of about two seconds.
    2. 2. Supervinas - loss of regularity of heart muscle cuts and an increase in their frequency. The duration of the stage is not longer than one minute.
    3. 3. Cleaning - irregular frequent reductions in different intensity that do not have pronounced teeth and intervals. Stage duration 2-5 minutes.
    4. 4. ATONIC - change of large fibrillation waves on small as the result of the depletion of myocardium. Stage time - up to 10 minutes.
    5. 5. Finishing - complete cessation of cardiac activity.

    Ventricular fibrillation on ECG

    Depending on the duration of the attack, the fibrillation of the ventricles is divided into two forms:

    1. 1. Paroxysmal - short-term episodes of the development of pathology.
    2. 2. Permanent - a violation of the rhythm characterized by a clinic of sudden death.

    Urgent Care

    ECG is necessary in the diagnosis of ventricular fibrillation, but the reanimation measures should be started immediately, without waiting for its results. Otherwise, a person can die.

    The main principle of emergency assistance is its beginning in the shortest possible time, because the death of the patient may occur within a few minutes. In case of impossibility of emergency defibrillation, the victim is shown indirect heart massage and artificial ventilation of the lungs. The correct heart massage for 4 minutes provides blood saturation with oxygen to 90% even in the absence of artificial respiration. Thus, the maintenance of vital bodies prior to the arrival of specialized assistance increases the chances of a person to life.

    • assessment of the patient's condition;
    • definition of breathing and pulse;
    • providing a sick horizontal position lying on the back with a backward back head with a lower jaw reducing;
    • inspection of the patient's oral cavity for the presence of foreign bodies;
    • in the absence of breathing and pulse - immediate resuscitation activities. If reanimizing one, the ratio of air blowings and pages on the chest is 2:30. If two people reanimate, then it is 1: 5.

    Non-specialized resuscitation activities

    Specialized assistance includes the use of a defibrillator and medication therapy. Before that, an ECG is made (in parallel with the conduct of cardiovascular intensive care) to confirm the flicker of ventricles, since in other cases the defibrillator may not have a proper effect.

    Specialized emergency care is carried out in several stages, of which each subsequent begins with the ineffectiveness of the previous one:

    Stage Order of conduct
    First
    1. 1. Determination of the presence of consciousness in the patient.
    2. 2. Ensuring the opening of the respiratory tract.
    3. 3. After controlling the pulse and breathing - conducting cardiovascular intensive care (SLR). The frequency of pages on the chest is 100 per minute. At the same time, artificial ventilation of the lungs (IVL) "mouth in the mouth" is performed. If a bag of AMBU is used, the ratio of IVL and the indirect heart massage (NMS) is 2:30.
    4. 4. In parallel with the SLR - removal of ECG readings
    Second
    1. 1. Holding an ECG analysis to determine the need for defibrillation.
    2. 2. When clarifying the flicker of ventricles through an ECG - defibrillation of 360 J + 2 more times in the absence of a result.
    3. 3. At the same time - preparation of the toolkit for conducting trachea intubation (aspirator, laryngoscope, air duct and other) and a solution for endotracheal administration (adrenaline 3 mg and sodium chloride 0.9% 7 ml)
    The third
    1. 1. Conducting the CLP for a minute.
    2. 2. Four intubation on half a minute.
    3. 3. In parallel - NMS.
    4. 4. Introduction of the catheter in the main vein.
    5. 5. Intravenous inkjet pouring 1 ml of adrenaline or endotracheal introduction of its solution.
    6. 6. IVL + NMS
    Fourth
    1. 1. Defibrillation 360 J.
    2. 2. The introduction of cordaron (amiodarone) 150-300 mg or lidocaine 1 mg per kilogram of weight intravenously.
    3. 3. NMS + IVL.
    4. 1. Defibrillation 360 J.
    5. 5. If ineffectiveness is the re-administration of cordaron and NMS + IVL after 3-5 minutes.
    6. 6. With ineffectiveness - intravenously 10 ml of Novocainamide 10% and repeated cardiovary and pulmonary resuscitation.
    7. 1. Defibrillation 360 J.
    8. 8. With ineffectiveness - the introduction of intravenously orinids at the rate of: 5 mg per kilogram of weight every 5-10 minutes until the dose is 20 mg per one kg of weight. After each introduction of Ornida - Defibrillation 360 J

    Places of proper installation of electrodes.

    If the effects performed did not give, then the question of the subsequent implementation of resuscitation actions is solved.

    According to statistics using a defibrillator, the work of the heart is restored in 95% of cases if there is no serious organic lesion of the heart muscle. Otherwise, the positive effect does not exceed 30%.

    Complications

    After the return of a person to life, it is a prerequisite for the resuscitation department, and then in the ward of intensive therapy. This is due to the instability of blood circulation and the consequences of the oxygen starvation of the brain and other organs.

    The consequences of transferred arrhythmia:

    1. 1. POSTABANCE ENECTIONFAALOPATH - the damage to the neurons of the brain as a result of a long oxygen starvation. This condition is manifested by neurological and psycho-emotional disorders of various nature. In a third of the patients who have undergone clinical death, neurological complications incompatible with life are developing. In the second third there are impairment of motor activity and sensitivity.
    2. 2. Resistant reduction in blood pressure - hypotension against the background of myocardial infarction.
    3. 3. ASISTOLY - Full Heart Stop. It is the complication of the most attack of ventricular fibrillation.
    4. 4. Fractures of ribs and other damage to the chest as the consequences of intense indirect heart massage.
    5. 5. Hemotorax - blood cluster in the pleural cavity.
    6. 6. Pneumothorax - the appearance of gases or air in the cavity of the pleura.
    7. 7. Myocardial dysfunction is a violation of the heart muscle.
    8. 8. Aspiration pneumonia is inflammation of the lungs as a result of falling into them from the vomit masses or other substances from the oral and nose.
    9. 9. Other types of arrhythmia (heart rate disorders).
    10. 10. Thrombommbolia - entering the pulmonary artery of blood clots and its blockage.

    Light artery thromboembolism as a complication of resuscitation activities

    When restoring the heart of the heart after 10-12 minutes of clinical death, there is a high probability of the development of coma, physical and mental disability. This is due to long brain hypoxia and the emergence of irreversible processes in it. The lack of violations of the brain activity is observed only in 5% of the people who have moved the heart stop.

    Prevention and forecast

    Prevention of ventricular fibrillation can significantly extend the human life. This is relevant both with the probabilities of the development of pathology and after the attack. In the case of the last risk of recurrence increases several times.

    Preventive measures against ventricular fibrillation:

    1. 1. Timely and high-quality treatment of cardiovascular pathology.
    2. 2. Regular use of drugs with antiarrhythmic effect.
    3. 3. Installing a cardioverte-defibrillator or pacemaker.

    Installed pacemaker

    Mortality from ventricular fibrillation in people over 45 years old is more than 70% annually. The forecast is not always favorable and depends on the efficiency and professionalization of resuscitation activities, as well as on the time of finding the patient in a state of clinical death.

    The fatal outcome in the flickering of ventricles occurs in 80% of cases. The cause of 90% of attacks are diseases of the cardiovascular system (heart patterns, cardiomyopathy, cardiosclerosis, myocardial infarction). Ischemic heart disease becomes the cause of sudden death in women in 34% of cases, men in 46%.

    Cured ventricular fibrillation is impossible. Emergency resuscitation measures make it possible to extend the life only in 20% of patients. A positive result is 90% when assisting on the first minute of the heart stop. Resuscitation for the fourth minute reduces this indicator three times and does not exceed 30%.

    Fibrillation, or flickering of ventricles, is a formidable violation with a high risk of fatal outcome. A favorable forecast depends on timely and high-quality first aid. Of particular importance is prevention aimed at preventing the development of pathology.

Etiology and pathogenesis

The fibrillation (flicker) of the ventricles occurs in the acute period of myocardial infarction and is often the cause of sudden death.

I.A. Chernogorov repeatedly observed in the experiments on the heart of the dog's flickering of ventricles during the dressing of the large branches of the left corneous artery. At the same time, the reduction in the heart was first weakened, then single and group extrasystoles, passing into long-term ventricular tachycardia, and finally, in the flickering of ventricles.

According to M.E. Raisian, in the experiment, the abandonment of the anterior downward branch of the left coronary artery in the upper third causes ventricular fibrillation in 70%, ventricular tachiisistol - in 40%, ventricular extrasystole - in 90% of animals. Analysis of prefabral violations of the heart rate showed that ventricular fibrillation precedes extrasystole in 100% of cases, with extrasystole, ventricular fibrillation occurs in 77% of cases. The ventricular tachiisistolia is preceded by fibrillation in 50% of cases, and in ventricular tachiisistolia, fibrillation occurs in 88% of cases.

According to M. E. Risky, the main condition for the transition of extrasystole in group extrasystole and ventricular fibrillation is early appearance Extrasystole in a heart cycle, which contributes to a further increase in the dispersion, the time of repolarization of the heart.

With the help of cardiomonitorial systems with permanent electrocardiographic control, you can find in some cases short-term periods of flickering ventricles. In particular, E.I. Chazov and V.M. Bogolyubov noted such violations of the rhythm in patients with myocardial infarction after the introduction of stanfantine K.

The flickering of the ventricles may arise against other lesions of the heart, with intoxication by drugs and stroophantine K. The individual sensitivity of myocardium to cardiac glycosides depends on the severity of myocardial lesions, lowering the level of intracellular potassium, catecholamines, the degree of myocardial ischemia.

Ventricular fibrillation arises as a complication after anesthesia, heart catheterization, operational interventions on the heart, acute infections (in particular, diphtheria), renal and liver failure. Sometimes the flickering of ventricles is developing after the introduction of some drugs (chinidine, Novocainamide, adrenaline).

In the experiment after the dressing of several branches of the coronary arteries and prolonged adrenaline infusion (hypercathecholamine leads to histotoxic hypoxia myocardium), with the developed weakness of the heart muscle, ventricular fibrillation may occur.

It is necessary to allocate fibrillation arising from patients with a full transverse blockade, which is often the cause of attacks of Morgali-Adams-Stokes. The peculiarity of ventricular fibrillation in such patients is often spontaneous or after one heart massage the cessation of attacks without electrical defibrillation, which in patients without atrial stomach blockade is observed quite rarely.

The flickering of the ventricles is the terminal manifestation of many organic diseases of the heart, especially when hypokalemia after energetic treatment with diuretic and massive doses of cardiac glycosides.

Sometimes the flickering of ventricles occurs as a result of a strong blow to the chest, as well as the extraordinary excitation of the vegetative nervous system, for example, under the influence of strong psycho-emotional factors, sudden frightened or fear.

The flickering of the ventricles in etiology is close to the flickering of the atria, with the only difference that, with ventricular fibrillation, one ectopic focus or several focus of high-frequency excitation are located in the muscles of the ventricles (see Cleaning Arrhythmia).

Prof. A.I. Gritsyuk

"Causes of ventricular fibrillation, development mechanism" - Section Emergency States

Fibrillation of ventricles

The fibrillation of the ventricles is the random electrical activity of the heart, in which its effective reductions are missing and there is no cardiac output. QRS complexes There are no ecg.

Fibrillation of ventricles for 5-7 minutes. Almost inevitably leads to death. Ventricular fibrillation is often preceded by ventricular tachycardia.

Risk factors and causes of ventricular fibrillation are about the same as for ventricular tachycardia. The fibrillation of ventricles may occur suddenly, without any provoking factors.

In 75% of cases, the community-wide circulation stop is caused by ventricular fibrillation. Among the reanimated 75% there is a pronounced damage to coronaryarters, in 20-30% - a transmural myocardial infarction. In the absence of IBA, the risk of re-stopping blood circulation, but those who have a circulatory stop occurred against the background of myocardial infarction, the risk of sudden death during the year is only 2%. The risk of sudden death is higher in patients who have undergone forehanded myocardial infarction. The risk factors of the sudden death include ischemia myocardium, systolic dysfunction of the left ventricle, ten or more ventricular extrasystole per hour, induced or spontaneous ventricular tachycardia, arterial hypertension, left ventricular hypertrophy, smoking, male floor, obesity, hyperlipopoprotemia, elderly age, alcohol abuse.

Treatment

As mentioned above, the fibrillation of ventricles very quickly leads to death and almost never stops independently. It is necessary to quickly start cardiovascular resuscitation and defibrillation. At least 200 J, the uninfective discharge is applied, with ineffectiveness, the discharge increases to 300 and 360 j. If after three digits, blood circulation is not restored, adrenaline is quickly introduced. 1 mg V / B, and repeat defibrillation. The introduction of adrenaline, if necessary, repeat every 3-5 min. With ineffectiveness of resuscitation activities, lidocaine is introduced. In addition, procanamide is used. Britia Tosylate and Amiodaron. In the recommendations of the American Cardiology Association, it is indicated that, as the experience gained, amiodarone can become a major drug used to treat ventricular rhythm disorders in the ineffectiveness of lidocaine.

Ventricular fibrillation and sudden heart death

fibrillation of ventricles and sudden heart death

Fibrillation, or flashing, ventricles - These are arrhythmical, non-coordinated and inefficient reductions in individual muscle gastric fiber groups with a frequency of more than 300 per 1 min with the termination of the pump function of the heart. Close to fibrillation of ventricles is their flutter, which is a ventricular tachy-arrhythmia with a frequency of 220-300 in 1 min. As in the fibrillation, the reduction of ventricles at the same time ineffective and cardiac output is practically no. Verbutania - unstable rhythm, mainly pretty quickly goes into their fibrillation, occasionally - in sinus rhythm.

Ventricular fibrillation is the main cause of sudden cardiac death.

Sudden heart death - Natural death due to heart reasons for 1 hour after the appearance of sharp symptoms, which precedes the loss of consciousness; Probably the presence of heart diseases in history, but the time and method of death is unexpected. The frequency of ventricular fibrillation among the direct causes of sudden cardiac death is 75-80%.

Etiology. Among men aged 60-69 years with a preliminary history of heart disease, the level of sudden cardiac death is 8 per 1000 population.

Most often the cause of sudden heartfall is

- Myocardial infarction

- heart failure

- Hypertrophic cardiomyopathy

- Dilatation Cardiomyopathy

- Aorta Stenosis

- mitral valve prolapse

- Violation of the conductive heart system

- Wolff-Parkinson-byte Syndrome

- the elongated Qt syndrome

- Brugada syndrome

- arrhythmogenic dysplasia right ventricle

- Anomalous development of coronary arteries

- Myocardial bridge

1. Transient trigger events (toxic, metabolic, electrolyte imbalance; vegetative and neurophysiological disorders; ischemia or reperfusion; ge-modinamic changes).

2. Violations of high-risk repolarization (congenital or acquired syndromes of the elongated Qt, the arrhythmogenic effect of drugs, the interaction of drugs).

3. Clinical hidden heart disease (unrecognized disease).

4. Idiopathic ventricular fibrillation (factors not installed).

Diseases leaking with structural changes of the heart are well-known factors of sudden cardiac death. First of all, it concerns the diseases in which the left ventricle hypertrophy is developing (AG, heart remodeling after myocardial infarction and others.).

Pathophysiological mechanisms. The occurrence of ventricular fibrillation is based on multiple rhenium foci in myocardium with ever-changing paths, as well as an increase in automatic in one or more portions of myocardium. This is due to the heterogeneity of the electrophysiological state of myocardium.

The ventricular fibrillation in more than 90% of patients is caused by monomorphic or polymorphic ventricular tachycardia, much less often it can be induced by 1-2 "Early", according to R per t, ventricular extrasystoles, which cause the occurrence of an unequal degree of depolarization in various muscle fibers. The fibrillation of the ventricles in humans cannot stop spontaneously. Only electrical defibrillation is capable of restore the sinus rhythm, the effectiveness of which depends on the nature of the main disease, the severity of the associated heart failure, as well as the timeliness of the application.

Clinical picture. Since in the occurrence of ventricular fibrillation, the pump function is stopped, a picture of a sudden stopping of blood circulation and clinical death is noted. Patients lose consciousness after 15-30 seconds from the beginning of ventricular fibrillation, after 40-45, convulsions, involuntary urination and defecation develop. Pupils are expanded and not react to light. Loud and frequent breathing is usually stopped on the 2nd minute. Diffuse cyanosis develops, there is no pulsation on major arteries (sleepy and femoral) and breathing. If within 4 minutes it fails to restore effective heart rate, the irreversible changes occur in the central nervous system and other organs.

With ventricular tachycardia, ventricular fibrillation is often preceded, Mos, Consciousness and AT, usually low, can be saved for a short time. But more often this unstable rhythm quickly turns into fibrillation of ventricles.

On ECG, ventricular fibrillation is manifested by various amplitude and duration by chaotic flicker waves with teeth, not differentiated, and frequency of more than 300 per 1 min. The dependences of their amplitude can be allocated to Velikhville and Dribnochville the fibrillation of ventricles (Fig. 61). In the case of the last amplitude of the flicker waves, up to 0.2 mV and the likelihood of successful defibrillation is significantly lower.

Differential diagnosis. The possibility of a sudden stopping circulation should be remembered in all cases of loss of consciousness. Although during the sudden cessation of cardiac activity during the first 1-2 minutes, agonal respiratory can be kept, an early sign of this state is the absence of pulsation on large arteries and, that is not so secure, the tones of the heart.

Cyanosis develops rapidly and pupils are expanding. Confirm the diagnosis and establish the immediate cause of the sudden stop of the heart (fibrillation, ventricular asistol, electromechanical dissociation) allows registration of an ECG.

Velikhville the fibrillation of ventricles on the ECG is sometimes difficult to distinguish from the trembling of ventricles and polymorphic ventricular tachycardia. For both these forms, arrhythmia is characterized by a smaller frequency of ventricular complexes, and for fluttering - also the large stability of their amplitude.

In the development of ventricular fibrillation, 4 stages are distinguished:

Stage fluttering ventricles - high-amplitude waves with a frequency of 250-300 per 1 min (duration 2 s) are recorded on ECG.

The convulsive stage (1 min), in which chaotic non-coordinated reductions of certain portions of myocardium occur with the appearance of high-amplitude waves at an ECG to 600 per 1 min.

Stage of flickering of ventricles (microwave fibrillation of ventricles) up to 3 minutes. On ECG - low-amplitude waves with a frequency of up to 1000 per 1 min.

ATONIC STAGE - a violation of individual portions of myocardium, go out, the duration increases on the ECG and the amplitude of the waves is reduced at their frequency up to 400 in 1 min.

Treatment Includes urgent help - cardiovascular resuscitation and, if successful, measures to prevent re-occurrence of ventricular fibrillation and sudden death.

Cardiovary and pulmonary resuscitation is to ensure adequate ventilation of lungs and blood circulation until the cause of the cessation of respiration and blood circulation is eliminated.

The primary event algorithm when stopping a heart includes:

1) checking reactions

2) Opening of the airways

3) breathing check

4) if there is self-breathing - conducting an indirect heart massage (within 10 s)

5) If the blood circulation has not recovered, continuing the heart massage (100 in 1 min, the ratio of 15: 2).

The most important determinant survival of patients after sudden death is the time from the beginning of the blood circulation stop before conducting electrical disfigure defibrillation. Optimal is the conduct of electrical thermal therapy during the period of vessels of ventricular fibrillation in the fluttering stage and the convulsive stage of fibrillation. In this regard, to improve the effectiveness of assistance to patients with a sudden cessation of blood circulation, it is necessary as early as possible to provide qualified and specialized medical care on the Advanced Cardiac Life Support algorithm (ACLS).


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    The leadership is designed to help the doctor in the diagnosis and treatment of the most common diseases of children's age, already at first contact with the patients, to determine the range of preventive tasks, assign treatment according to the modern requirements of evidence-based medicine. Special attention is paid to issues of feeding children early age, child infections and their prevention. All drugs are given with the international non-specific names registered in the Russian Federation.

    1 890 R


    In this edition, in algorithmized form, modern approaches to the diagnosis and treatment of patients with dementia are considered. The material is presented in accordance with the logic of the diagnostic and therapeutic process: from screening cognitive testing to a deployed clinical and neuropsychological study, which allows to refine a syndromal and nosological diagnosis and optimally lined up the therapy scheme. The techniques of brief neuropsychological testing, modern criteria for the diagnosis of major diseases leading to dementia are described, the principles of their differential diagnosis are described. The problems of formulating the diagnosis and its coding are considered in accordance with the International Classification of Diseases of the 10th Revision.

    1 590 R


    The book contains the latest data on the diagnosis and treatment of hepatology. Designed for practitioners. The book was composed in the form of specific algorithms and schemes, convenient for daily work, reduces the time to choose the treatment and selection of the drug, is made in a comfortable selection format.

    1 890 R


    The book details the issues of general and oncological gynecology, reproductive endocrinology and infertility, contraception and planning of family, children's and teenage gynecology, yorkiology, etc. In some chapters, psychological aspects of gynecology are revealed, the problems of homemade cruelty and sexual violence.

    2 790 R


    The book details the basics of reproduction, normal obstetrics, diagnosis and tactics of conducting various complications during pregnancy and childbirth, urgent states in obstetrics. Attention is paid to extragenital diseases (including surgical) during pregnancy. A separate chapter is devoted to resuscitation of newborns and care for children from high-risk groups.

    2 690 R


    In the leadership of dental doctors at the present level, issues of etiology, pathogenesis, diagnosis, prevention and treatment of periodontal diseases are presented. The publication is recommended by practicing dental physicians, students of dental faculties and clinical interns, as well as listeners of additional professional education programs in the specialties "Therapeutic dentistry", "Dentistry of general practice", "Dentistry surgical", "Orthopedic" dentistry.

    2 890 R


    Management is devoted to the problems of diagnosis and treatment of pancreatic cancer and periampular zone organs. Contains an algorithm of ultrasonic and intra-speech diagnostics of pancreatic cancer, surgical technologies of pancreatopodenal resection. Addressed to the doctors-specialists of ultrasound diagnostics; Surgeons of specialized medical and outpatient polyclinic institutions.

    2 290 R


    Currently, there are cases when a student is already a month after passing state exams enter the clinic and must perform a pediatrician function. For many years he studied Pediatrics, but only 10 days of them - ophthalmology; At the same time, the doctors working with children are significantly more responsible in contrast to doctors working with adult patients, for the state of the visual system of the newborn - immature, gentle, developing, very vague, rich in congenital disposable and unreasonable pathology, anomalies.

    1 590 R


    Reflects anatomy, histology and embryogenesis of parathyroid glands. A comparative assessment of the capabilities of various visualization methods in hyperparathyroidism is presented. In detail describes the research methodology and the ultrasonic picture of the parathyroid glands in normal and under various pathological conditions. Particular attention is paid to the differential diagnosis of the pathology of the parathyroid glands. The possibilities of the ultrasound method in assessing the treatment of hyperparathyroidism are described.

    1 890 R


    More than two hundred color illustrations. Allocation of essential diagnostic elements. Isolation in a compressed form of major morphological and immunohistochemical symptoms. A description of the needle biopsy is a rapidly propagating technique that opens up new opportunities for histopathologists.

    2 230 R


    This leadership is developed on the basis of the analysis of domestic and international clinical experience in physical therapy and medical rehabilitation of patients with various diseases. It contains information about the algorithm for the appointment and use of therapeutic physical methods and funds with proven effectiveness on international criteria.

    3 890 R


    The textbook gives an idea of \u200b\u200bthe basic principles of the systemic approach in osteopathy. Describes methods of osteopathy, their integrity and sequence of study. The features of the biomechanical method of osteopathy are revealed in detail. Much attention is paid to BLT as a transitional therapeutic model between biomechanical and functional methods.

    850 R


    The authors will introduce you to a scientifically based gymnastics for the face, literally turning back the processes of aging of the skin. You will learn how to "pull up" the face in just a few minutes with the help of fast Miolifting, discover the secrets of a unique physiological system of rejuvenation and prevention of aging

    2 190 R


    It contains information about the technique and procedures of procedures that are used in physiotherapy. As well as classic apparatus And the techniques are represented by new, such as laser therapy, EDF therapy, halotherapy, describe the features of physiotherapy procedures in children. Characteristics of apparatus, physiotherapy techniques, safety appliances when working with equipment were performed.

    1 590 R


    Atlas includes the test criteria for preoperative cytological diagnostics on the Bethesda system, as well as new categories of thyroid tumors and the criteria for their diagnosis in accordance with the new international histological classification of WHO. On the Atlas pages, the changes made to the international TNM classification of malignant tumors of the thyroid gland were reflected

    1 990 R


    The study guide addresses the issues of clinical physiology, etiology, pathogenesis, clinics and therapy of a number of critical states, the foundations of modern anesthesia and anesthesia, maintaining the postoperative period.

    2 099 R


    This reference edition combined these directions of medicine. On the pages of the book, issues of diagnosis and treatment male infertion, sexual disorders, characterized by sexually transmitted infections, benign and malignant neoplasms of genital organs. The book was created specifically for practicing doctors and is built in such a way that it allows you to get quick access to the results of the latest research and decisions of discussion issues of clinical practice.

    1 790 R


    Cosmetology allowance is intended for students of professional retraining courses, advanced training, internships in the preparation of cosmetologists and doctors - plastic surgeons; preparation of nurses in cosmetology; training specialists with the qualifications "Technologist-astretis" under the Program "Applied Aesthetics" and "Specialist in Applied Aesthetics" under the program "Technology of Aesthetic Services" (for the professions of cosmetics, manicure, pedicuress), a wide range of people interested in issues of care and decoration of their Body, hands, legs, faces, hair and nails.

    1 990 R


    The textbook is a laminated color card, on the front side each contains an illustration from the course of anatomy with digital signs, on the turnover - Russian and Latin names of anatomical structures. This form of material representation is particularly convenient when studying anatomy.

    1 390 R


    The general principles of topical diagnosis in neurology are considered. The entire spectrum of neurological pathology is presented in detail, ranging from the damage to the peripheral nerves and ending with the defeat of the cortex of the Hemispheres of the brain. The features of clinical manifestations depending on the individual variations of the structure of the nervous system are discussed. The syndromes of vascular lesions of the brain and comatose states are considered separately.

    2 630 R


    The biological, methodological foundations of acupuncture and approaches to acupuncture diagnostics are presented. The patterns in the principles of selection of acupuncture points with anatomical-physiological positions are analyzed. The original tables reflecting the diversity of the functional relationships of meridians are presented. The integral approaches are formulated to the principle of the selection of acupuncture recipe of exposure points, the understanding of which makes it possible to individualize the treatment of patients.

    2 790 R


    The book examined the basic principles of patients with complaints about pain, the most common causes of pain and the most common ways to deal with it are given numerous examples from practice. A separate section is devoted to invasive methods of treating pain under fluoroscopic control.

    2 890 R


    It is an exhaustive work on acupuncture, but will be useful for beginner specialists and students interested. Moreover, the book reflects the achievements of the latest scientific research in this area.

    4 090 R


    Collection of lectures. Abuzus headache, back pain, miastic, dizziness, comatose states, mioclon, paramy, fibromyalgia, botulinitherapy, motor multifocal neuropathy. Lectures are addressed primarily to practical neurologist physicians and contain the most complete information to date on the specified problems.

    2 090 R


    The book provides a justification for the use of adhesive techniques in cosmetic restorative dentistry, the minimum invasive dentistry is discussed, the individual problems with which the doctor may face, using adhesive techniques when working with ceramic and polymer composite restorations.

    0 R


    Principles of assistance to children with impaired adaptation and meteo sensitivity, which is characteristic of children with chronic diseases. Cruel-handling syndrome with a child reflects the option of the maximum possible stress in children. The foundations of organizing the prevention and treatment of the most common diseases, taking into account disadaptation and the influence of the child of adverse weather factors on the body of the child.

    1 790 R


    The main differential symptoms and features of the flow of diseases that are manifested on the mucous membrane of the mouth, language and lips with similar clinical signs are considered. The features of changes in the mucous membrane of the mouth, language and lips are described at the most frequent pathological conditions that have differential diagnostic importance, which are shown in the tables.

    1 990 R


    Clinical guidance contains basic information about epidemiology, risk factors, etiology and pathogenesis, clinical picture, diagnostics, including using modern research, treatment and prevention of acute brain circulation disorders. A large place in it is assigned to various modes of drug therapy with a list of appropriate drugs, information about their doses, efficiency and side effects.

    1 990 R


    Modern approach To the treatment of ischemic stroke - systemic thrombolytic therapy. The data on the management of patients both in the prehospital stage and during and after therapy are presented; The methods of treatment, testimony, contraindications, complications are considered; Information about the concomitant therapy is given.

    1 590 R


    Practical guide may be useful specialists encountered with the problems of diagnosis, treatment and rehabilitation of septic patients, including patients with diseases of the reproductive system.

    790

    Microbiology with the basics of epidemiology and methods of microbiological research - Sabychakov VB


    The textbook consists of six sections. The 1st section is devoted to the history of the development of microbiology as science, as well as various aspects of biology of microorganisms. In the 2nd section, the peculiarities of the interaction of micro and macroorganism are considered, a review of the methods of etiotropic therapy is given. The 3rd section includes microbiology issues current bacterial infections, 4th - microbiology relevant viral infections. The 5th section contains a description of the morphology and physiology of microscopic fungi. The 6th section covers the issues of sanitary microbiology and emergency microbiology.

    2 390 R


    This manual is intended for listeners of the Faculty of Postgraduate and Additional Education, as well as for doctors, graduate students, orders, internals in Psychiatry, "psychotherapy" and related disciplines (narcology, psychophysiology, suicidology, medical psychology, etc.)

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

    Tasks are given clinical cases on all topics of the curriculum. Special attention is paid clinical examplesillustrating the main urgent states in patients wounded and affected neurosurgical profile.

    990 R


    The second volume contains chapters in which diseases of the blood system, the internal secretion glands, systemic lesions of the connective tissue and diseases of the joints, immunodeficiency, chronic fatigue syndrome, pharmacotherapy in geriatric practice, as well as allergic diseases.

    1 890 R


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

    1 890 R


    The manual covered the principles of organizing orthodontic assistance, methods of examination and basic methods of treatment of dental anomalies, correcting the irregular position of teeth and bite. This section of dentistry Students of the Dental Faculty are beginning to study from the 4th year.

    1 790 R


    The functional importance of the basic anatomical formations in each brain department is shown and the most characteristic clinical manifestations are presented under their lesions. Considered modern ideas about the dynamic localization of functions in the core of a large brain hemispheres are considered, the main conducting ways of the central nervous system and functional disorders are described in detail. The text is illustrated by classic and original drawings.

    1 590 R


    In these methodological guidelines, scientific data and personal professional experience of the organization of the X-ray service are summarized, radiation diagnostics methods are described. The methods of studying organs and systems of a person with normal anatomy, embryogenesis, x-rayanatomy, as well as x-ray age-selection of various pathological conditions in adults and children are illuminated.

    1 690 R


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

    1 590 R


    Practicing doctors are proposed simple, easily accessible, designed before the details of clinical and instrumental criteria for identifying the norm and various violations of the erection of the penis. This allows you to take a fresh look at the emergence, development and prevention of erectile dysfunction, taking into account early, preclinical changes in erection. Much attention is paid to the clinical characteristics of diseases, the risk factors for their development and their corresponding semiotic signs arising from the study of erection violations

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

    The directory describes in detail the issues of neurovalization, methods of recanalization and secondary prevention of ischemic stroke. Chapters on the differential diagnosis of ischemic stroke and states that imitate ischemic strokes, basic therapy, methods of recanalization of cerebral arteries (including thromboemboloxtraction) are expanded and supplemented. In detail the recommendations for the correction of risk factors, prevention and treatment of complications, as well as the rehabilitation of patients with ischemic stroke.

    790 R

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