MYOCARDIAL INFARCTION (Latin infarctus from infarcire to fill, fill; a myocardium) — the acute disease caused by development of one or several centers of an ischemic necrosis in a cardiac muscle, which is shown various disturbances of cordial activity and clinical syndromes determined by the nature of the reflex reactions connected with development of acute ischemia and a necrosis of a myocardium.
And. the m can be considered as a complication of diseases at which the coronary blood stream, first of all atherosclerosis is broken. However independent wedge, value I. m it is so essential that it is allocated with the accepted classifications, and in theories and a wedge, to practice the form — option of an acute form is studied as separate nozol, coronary heart disease (see). And. the m should distinguish from inflammatory necroses of a myocardium (focal myocardites), from damages of a myocardium at an injury of heart and coronary vessels, from the so-called nekoronarogenny necroses of a myocardium resulting from disturbances of metabolism at effect of toxic and biologically active agents or disturbances of electrolytic balance.
On a wedge. - morfol, the characteristic distinguish macrofocal and small - focal And. m with the indication of a zone of defeat (front, side, lower walls of a left ventricle, an interventricular partition, a top of heart etc.).
Depending on prevalence of a necrosis on wall thickness allocate the following forms I. m: transmural (defeat extends to all thickness of a myocardium and an adjacent endocardium and a pericardium), intramural (the necrosis develops vnutristenochno, without extending to an epicardium and an endocardium), subepicardial (a necrosis in a layer of a myocardium, adjacent to a visceral layer of a pericardium) and subendocardial (a necrosis in a layer of a myocardium, adjacent to an endocardium).
- 1 HISTORY
- 2 STATISTICS
- 3 AETIOLOGY AND PATHOGENY
- 4 An experimental myocardial infarction
- 5 PATHOLOGICAL ANATOMY
- 6 CURRENT AND SYMPTOMS
- 7 COMPLICATIONS
- 8 NERVOUS AND MENTAL DISORDERS
- 9 DIAGNOSIS
- 10 TREATMENT
- 11 the FORECAST
- 12 PREVENTION
- 13 Tables
until the end of 19 century. And. the m was described as the casuistry which was found during the opening of the dead from not clear disease. In Russia the doctor K. Knopf in 1878 for the first time described a wedge, a picture I. the m complicated by cardiogenic shock and a cardiorrhesis. In 1892 the English clinical physician U. Osler pointed to a possibility of a feedforward of a necrosis of a myocardium with defeat of a coronary artery of heart. The same year the Russian therapist V. M. Nernig (1892) in detail described a wedge, a picture of an epistenokardialny pericardis which as now it is known, is a complication And. m.
In 1909 P. Obraztsov and N. D. Strazhesko for the first time in the world gave the developed description various a wedge. forms I. m, having connected its development with thrombosis of coronary arteries of heart. In three years Herrick (J. Century of Herrick, 1912) published article devoted to clinic and a patomorfologiya And. m.
History of studying And. by m it is closely connected with development of a method electrocardiography (see). The first data on changes of an ECG at experimental injury of heart were obtained by A. F. Samoylov (1910). About the beginnings of the 20th of work devoted to an etiology, a pathogeny, patol, to anatomy, clinic, diagnosis and treatment And. m, are intensively conducted in the majority of the countries of the world. In 1969 for development of new methods of treatment of Pi of the organization of the help to patients I. m to group of scientists of our country (V. N. Vinogradov, P.E. Lukomsky, E. I. Chazov, 3. I. Yanushkevichus, B. P. Kushelevsky) the State award USSR is awarded.
Most often And. the m is observed at men 50 years are more senior though cases of its development in persons to 30 years are noted. Up to 60 years it occurs at women almost by 3 times less than at men, after 60 years this distinction decreases. In the large cities And. the m is registered considerably more often than in rural areas.
According to researches Ying-that cardiology of the USSR Academy of Medical Sciences (1974), carried out according to the program of WHO, the frequency of emergence And. the m at men is more senior than 40 years averages annually in Moscow 3 on 1000, in Kaunas — 2,3, in Warsaw — 2,7, in London — 4,9 and in Helsinki — 5,9 on 1000 men.
In 20 century in all economically developed countries sharp increase in incidence of coronary heart disease and mortality from it is noted, and the leading cause of death is And. m and its effects. In the USSR coronary heart disease mortality increased from 1965 for 1971 by 16% in the cities and for 52% — in rural areas. The largest frequency of deaths at women (83,7%) belongs to 60 — 79 years of life, at men is after 50 years.
From 60th increase in frequency is noted And. m at men at young age (30 — 40 years). According to WHO data, mortality at this disease at the age of 35 — 44 years increased by 60%.
AETIOLOGY AND PATHOGENY
Development And. by m it is always connected with ischemia of the site of a cardiac muscle or owing to full occlusion of a coronary artery — embolism (see), hemorrhage in the basis of an atherosclerotic plaque, thrombosis (see), or in connection with serious discrepancy of volume of a blood-groove on coronary vessels (usually patholologically changed) to the needs of a myocardium for oxygen and nutrients.
The most frequent reason And. the m is the termination of inflow of blood to the site of a myocardium in the coronary arteries which are sharply changed by atherosclerosis (see. Atherosclerosis ). The embolism of coronary arteries meets extremely seldom — hl. obr. at patients with a subacute septic endocarditis, at patol, the processes leading to formation of blood clots in cardial cavities during surgeries on heart. Are the rare reasons of obstruction of a coronary artery also massive hemorrhage in the basis of an atherosclerotic plaque and formation of blood clot in the artery changed not owing to atherosclerosis, and as a result of inflammatory defeats (A thromboangitis, a rheumatic coronaritisis, etc.) or injuries (e.g., after the selection coronary angiography).
Most often And. the m develops at coronary heart disease. Emergence And. the m at persons without defeat of coronary arteries of heart is observed, apparently, seldom. A number of researchers considers that in the absence of changes of coronary arteries And. the m, except for embolic and hemorrhagic (connected with an ekstravazation of large amounts of blood from a large arterial trunk), does not meet at all. Rather not numerous data of intravital selection coronary angiography at patients in an acute stage And. m demonstrate that occlusion of the main coronal arteries is observed at all patients macrofocal And. m. Special analysis of cases And. the m, developed without occlusion of coronary arteries, practically always reveals coronary atherosclerosis. H. N. Anichkov found atherosclerosis of coronary arteries in 89% of the dead from And. m, A. I. Strukov and soavt. — at 97%, A. M. Vikhert (t. 10, additional materials) — at 100% of the dead.
At the same time it is known that at many patients with the crushing stenosing defeat of coronary arteries And. the m does not develop, and they die of other reasons; on the other hand, at rather small atherosclerotic defeat of coronary arteries are observed extensive transmural And. m. Apparently, functional frustration of coronary circulation are important in development And. m. However they are not exhausted only by a spasm of arteries, and include as well dysfunctions of collaterals, both strengthening of thrombogenic properties of blood, and increase in need of a myocardium for oxygen at activation of sympathoadrenal system, etc. According to a role of these disturbances it is possible to speak about etiol, value of certain risk factors of development And. the m Since atherosclerosis of coronary arteries is a basis of the changes bringing to And. m, risk factors of development And. m in many respects match risk factors of emergence and progressing atherosclerosis (see). To the factors increasing danger of development I.m., carry advanced age, belonging to a male, the increased maintenance of lipids in blood serum, arterial hypertension, genetic predisposition, disturbance of tolerance to glucose (diabetes mellitus), obesity, existence of gout, insufficient physical. activity, some features of the personality (the increased emotionality), smoking (especially smoking of cigarettes), the use of soft drinking water. Danger of emergence And. m it is especially high at simultaneous influence of two or several risk factors. The mechanism of action of a number of the known risk factors is insufficiently clear (e.g., gouts, the uses for drink of soft water).
Hypercholesterolemia and the increased maintenance of lipids, in particular triglycerides, in blood serum at patients And. m are observed considerably more often than at healthy faces of the same age. Depending on the structural maintenance of lipids in blood serum allocate five types of a lipidemia (see. Hypercholesterolemia ); And. the m most often develops at a lipidemia II and III types. A role of arterial hypertension (in 80 — 90% of cases it is about an idiopathic hypertensia) in increase in probability of development And. to m it is also established (see. Idiopathic hypertensia ). Men have 30 — 59 years with the diastolic pressure of 105 mm of mercury. and more And. the m arises by 3 times more often than at men of the same age with diastolic pressure within 75 — 84 mm of mercury.
Value of smoking of tobacco (especially cigarettes) as risk factor of development And. to m it is shown at mass inspections of the population. According to 10 years' observation, among men there are 30 — 59 years which were daily smoking throughout this term on a pack and more cigarettes in day, PI. the m developed in 3,3 times more often than among non-smoking. The mechanism of action of smoking on development And. the m is completely not found out, but its adverse influence on cardiovascular system is known. Under the influence of nicotine heart rate increases, there can occur tranzitorny increase in the ABP, stroke and minute output, speed of reduction of a myocardium, to increase requirement it in oxygen and to arise various disturbances of a heart rhythm. Besides, the substances which are contained in tobacco smoke promote a thrombogenesis and emergence of a spasm of coronary arteries of heart. Content of carboxyhaemoglobin makes non-smoking 0,4% in blood and reaches 10% in blood of smokers that reduces transport function of hemoglobin, promoting development of ischemia of heart and a myocardial infarction.
Communication between frequency And. m and obesity (see) it is opened not completely, but its existence is established. Most of researchers considers that one of the essential factors increasing danger of development And. the m, is a shortcoming physical. activities. It is interconnected with development of obesity therefore quite often these factors are combined. On the other hand, in an etiology And. the m quite often plays a role physical. the overstrain which is sharply increasing the need of a myocardium for oxygen of edge cannot be satisfied with adequate increase in a coronary blood-groove at patients with atherosclerosis of coronary arteries. The same discrepancy between requirements of a myocardium and opportunities of a coronary bed plays a role in development And. m after psychoemotional tension. Sometimes the last is combined with acute abuse of nicotine that significantly increases risk of development And. m.
Frequency of the thrombosis of coronary arteries revealed at And. the m, varies, according to different authors, from 30 to 92%, but its role as proximate cause And. the m is estimated differently since it is not excluded that in some cases thrombosis in relation to And. the m develops for the second time.
In development of thrombosis at atherosclerosis of coronary arteries allocate the general and local pathogenetic factors. From local factors major importance has disturbance of an integrity of an endothelium of a vascular wall over an atherosclerotic plaque and the related delay and turbulence of a blood flow, and also reduction of fibrinolitic activity in a vascular wall and the local increase in coagulating properties of blood which is especially expressed at hemorrhage in a plaque or at its disintegration. From the general disturbances promoting thrombosis at atherosclerosis, the crucial role belongs not to increase in maintenance of coagulants as thought earlier, and to decrease funkts, opportunities of anticoagulative system, in particular due to increase in content in blood of inhibitors of heparin and fibrinolysin. It is shown that at And. the m decreases quantity of the so-called mast cells producing heparin.
Development And. the m is followed by the short period of increase in anti-coagulating and fibrinolitic properties of blood in response to the conditions creating threat of formation of blood clot. At atherosclerosis this reaction is short-term and insignificant; after it there occurs sharp increase in the thrombogenic properties promoting loss of fibrin and formation of blood clot in coronary vessels.
Great value in development And. m give to disturbances microcirculation (see) in which origin change of adhesive properties of thrombocytes at atherosclerosis along with reduction of life expectancy of thrombocytes and increase in a possibility of their disintegration plays a role.
Searches of immunocompetent systems, to some extent responsible for development And. m, did not result in certain results. The producing antibodies in the course of formation of the center of a necrosis in a myocardium is secondary that, apparently, matters only in genesis of some complications of this disease.
The question of an origin is most difficult And. m with serious discrepancy between the need of a myocardium for oxygen and nutrients and a possibility of their receipt in the absence of thrombosis of coronary arteries of heart. Sharp narrowing of a gleam of coronary arteries (most often an atherosclerotic plaque) can create conditions for emergence of acute coronary insufficiency (see). In the conditions of the heavy stenosing atherosclerosis function of an interkoronarny anastomosis is reduced and their development not always compensates reduction of a blood-groove on the main coronary trunks. Thereof even small increase in need of a myocardium for oxygen or insignificant additional narrowing of a gleam of an artery (a spasm, increase in an atherosclerotic plaque) can lead to development of a necrosis in a muscle of heart.
In similar cases on opening the located atherosclerotic plaques with massive deposits of salts of calcium and a stenozirovaniye of a gleam of a vessel are found most often tsirkulyatorno.
Important pathogenetic value can have also decrease in elasticity of a vascular wall. Some researchers assume, as. the m can develop as a result only funkts, frustration, in particular a long spasm of coronary arteries, an opportunity to-rogo at the person is proved by data of intravital coronary arteriography.
In formation wedge, manifestations acute And. the m participates a number of the pathogenetic factors connected with acute ischemia and a necrosis of a myocardium. In most cases the following effects of ischemia and a necrosis matter: 1. Reirritation of interoceptors of a myocardium, an endocardium and visceral layer of a pericardium with irradiation of irritation in the corresponding segments of a spinal cord, and also in subcrustal structures and in a cerebral cortex that creates stressful reaction. As well as at anything stress (see), at And. the m is activated system a hypothalamus — a hypophysis — adrenal glands with strengthening in blood of catecholamines (the first phase of a stress). Are connected with it observed during the most acute period And. m arterial hypertension (see. arterial hypertension ), tachycardia (see). One of manifestations of stressful reaction is also the aneosinophilia. However extremely the megalgia can cause development of arterial hypotension and be the cause collapse (see). 2. Acute reduction of cordial emission owing to the termination of sokratitelny activity nekrotiziruyushchegosya the site of a myocardium is one of the reasons of development both passing arterial hypotension, and irreversible cardiogenic shock (see). Same explain also development at And. m. cardiac asthma (see), fluid lungs (see), and also damages of internals: a brain (disturbance of cerebral circulation), went. - kish. path (erosive gastritis, pancreatitis), liver, kidneys, etc. At the same time in defeat of the specified bodies play a role the increased allocation of the catecholamines causing a vasospasm, and also viscerovisceral reflexes (e.g., paresis of a stomach and intestines) and, perhaps, toxic influence of decomposition products of the necrotic center. 3. Development of a rezorbtsionno-necrotic syndrome and aseptic inflammation. From nekrotizirovanny cells of a myocardium enzymes and toxic products which cause temperature increase, a neutrophylic leukocytosis with band shift, and further acceleration of ROE are released. 4. Redistribution of electrolytes in the area, adjacent to the center of a necrosis (a periinfarktny zone). Balance upset inside - and extracellular potassium and sodium leads to emergence of electric instability of a myocardium in a periinfarktny zone that creates premises to development of disturbances of a heart rhythm: ventricular premature ventricular contraction (see), ventricular tachycardia (see. Bouveret's disease ), fibrillations of ventricles and to other types arrhythmias of heart (see). 5. Distribution of a necrosis or periinfarktny zone on conduction system of heart creates passing or stable disturbances of conductivity which at And. m can be localized at the different levels of conduction system (see. Heart block ). Ischemia or a necrosis of a sinus node serve as premises to emergence of a number of arrhythmias (e.g., blinkings or atrial flutters, etc.) or cardiac standstills.
Except the listed pathogenetic factors defining the main, the most general a wedge, manifestations macrofocal And. m, in some cases work also others, the defining private wedges, symptoms. The increased end diastolic pressure at the extensive and deep center of a necrosis creates premises to development acute or subacute aneurisms of heart (see), and also to a rupture of a myocardium. Existence of the small centers of dystrophy or a necrosis of a myocardium on a distance from the main, large center is a possible origin at And. m. ciliary arrhythmia (see), edges can be also a consequence of an acute overload and overstrain of the left auricle because of insufficiency of a left ventricle. Distribution of a necrosis on a papillary muscle conducts to a heavy congestive left ventricular failure since damage of a papillary muscle serves as the reason of insufficiency of the mitral valve at the expense of a prolapse of its shutter in a cavity of the left auricle during a ventricular systole.
Right ventricular insufficiency, edges in the acute period And. the m is observed seldom, can be connected with several reasons: 1) a heart attack of a right ventricle or spread of a heart attack of a left ventricle on right; 2) rupture of an interventricular partition; 3) aneurism of an interventricular partition with its protrusion in a cavity of a right ventricle (Berngeym's syndrome); 4) the accompanying embolism of a pulmonary trunk and its branches.
An experimental myocardial infarction
the First attempts of experimental creation of ischemic necroses of a myocardium at animals consisted in obstruction of coronal vessels in the mechanical way. It was carried out at animals by either bandaging of coronary arteries, or closing of their gleam with various suspensions (metal balls, mercury, seeds). Though bandaging of coronary arteries at animals was made in 17 century, detailed studying patofiziol, and patomorfol, changes at experimental obstruction of vessels of heart began at the end of 19 century. In 1883 G. M. Lukyanov and in 1896 A. I. Talyantsev, using this method, proved, contrary to the existing representation, existence of collateral bonds in vessels of heart. Further various schemes of bandagings of coronary arteries allowing to receive, as a rule, necroses of a myocardium not only a certain size, but also a certain localization were in details developed.
For receiving experimental And. m most often use high bandaging of a front interventricular artery. At the same time there are extensive necroses of a myocardium, is frequent with damage of papillary muscles and development of aneurism of heart. For studying of features of a row patofiziol, and biochemical, processes at And. m (studying of a condition of fermental systems in blood, reflex reactions of coronary vessels) are developed the methods allowing to exclude influence of an operational injury. For this purpose the ligature is brought under a coronary vessel and, without tightening a node, bring her in various ways out of a chest cavity through an operational wound. After scarring of a wound the ligature is tightened, causing impassability of a coronary artery. Use creation of embolic necroses of a myocardium by introduction of mechanical suspensions (mercury, plastic balls etc.) much less often the syringe or through a catheter in chest department of an aorta and directly in the mouth of the left coronal artery. At this method necroses of a myocardium are formed much less often and much more often there are complications connected with a drift of suspensions in various departments of vascular system.
Methods of mechanical obstruction of coronary arteries allowed to study and find out a number of questions of morphology, a pathophysiology and a pathogeny And. m, including processes of a rassasyvaniye of necrotic masses and development of a hem, feature morfol, and biochemical, changes in a periinfarktny zone, formation of sites of dystrophy and small necroses of a myocardium out of a zone of a heart attack. By means of bandaging of coronary arteries sources of collateral circulation in heart are in detail studied, to-rymi three groups of an anastomosis — an anastomosis between large coronary arteries (the main source of a collateral blood-groove), an anastomosis between coronary vessels and cardial cavities, the noncardiac anastomosis connecting vessels of heart to vessels of other bodies are. These researches played an important role in development of methods of surgical treatment of coronary insufficiency, in particular methods of bypass shunting of the struck coronary arteries. At experimental And. the m noted emergence of a reflex spasm of coronary arteries out of a zone I. m, emergence in connection with a spasm or paralysis of vessels funkts, insufficiency of collateral bonds.
Experimental studying of changes of a hemodynamics at And. showed m that in development of cardiogenic shock an essential role is played by the falling of sokratitelny ability of a myocardium which is followed by falling of minute emission of heart. It turned out also that arterial hypertension considerably burdens a current experimental And. the m, promotes increase in the sizes of a heart attack.
Use of a pilot model And. diagnostic value of increase in blood of level of aminotransferases, isoenzymes of a lactate dehydrogenase, kreatinfosfokinaza and others biochemical allowed to study m, changes, to investigate features of exchange of carbohydrates, amino acids, lipids in a zone of a necrosis and in the remote sites of heart. At last, this model was successfully used for dynamic studying of features of an ECG at And. m of various localization.
Both clinical physicians, and pathologists point to basic distinction And. m as patol, process at the person and an experimental necrosis of the myocardium caused in a healthy animal in the mechanical way. Some researchers tried to bring closer a pilot model And. m to estimated conditions of its emergence in clinic. H. N. Kipshidze found out that excessive physical. loading (long run in the tredbena) leads to development of necroses of a myocardium in rabbits with the heavy lipoidosis of arteries caused long (4 — 5 months) keeping of animals on a diet rich with cholesterol. For disclosure of mechanisms of formation of blood clots in coronary arteries in an experiment on rabbits action of three factors was studied, the Crimea the important pathogenetic part in development is assigned And. m at the person: a lipoidosis of vessels of the heart (caused by feeding of animals cholesterol), a spasm of coronary arteries (introduction of Pituitrinum) and increase in thrombogenic properties of blood (intravenous administration of thrombin). At a combination of these mechanisms it is possible to reproduce blood clots in coronary vessels with development of necroses of a myocardium. The large role in reproduction of thrombosis is played by oppression of anticoagulative mechanisms (reduction of production of heparin, decrease in fibrinolitic activity of blood) which is observed at an experimental lipoidosis of vessels (E. I. Chazov).
In a series of researches with reproduction of failure of century of N of by an overstrain of nervous processes in a brain at monkeys (collision of defensive and food excitement), and also way of irritation of various departments of a brain (administration of air in cerebral cavities, his irritations electric current etc.) showed value of a neurogenic factor in emergence And. m. At the same time the expressed reaction of sympathoadrenal system to neurogenic influence was noted. This reaction, according to a number of authors, plays an important role in a pathogeny And. m.
Focal necrotic changes in a myocardium were reproduced also in other ways. So. A Selye (1959) noted emergence of necroses in a myocardium at simultaneous introduction by an animal 2 - alpha methyl - 9 - an alpha chlorcortisone and sodium orthophosphate (a so-called electrolytic and steroid cardiopathy). However such necroses do not model And. m, they are nekoronarogenny necroses.
Experimental studying to lay down. influences at And. by m it was carried out in various directions. One of the important directions is connected with studying of an opportunity to lyse fresh blood clot in coronary arteries by introduction to a venous bed or directly in a coronary artery of anticoagulants of direct action, fibrinolysin or activators of a fibrinolysis. It was noted that in some cases, at small prescription of blood clot, its lizirovaniye, recovery of a coronary blood-groove and disappearance of specific changes of an ECG is possible. The second direction is connected with impact on cells of a periinfarktny zone which under certain conditions can survive and recover the functional full value whereas under other circumstances they perish, increasing a zone of a necrosis. Recovery of full-fledged viability of cells of a periinfarktny zone, according to experimental data, is promoted by a number of substances, including lowering the need of a myocardium for oxygen (blockers of beta and adrenergic receptors, gliosiz, etc.), the coronary arteries causing dilatation (e.g., verapamil, or Isoptinum) having anticoagulating properties (heparin, fibrinolysin and activators of a fibrinolysis) and interfering aggregation of thrombocytes (Persantinum, or curantyl, etc.), and also some enzymes (hyaluronidase).
In experimental conditions influence of different types was studied artificial circulatory support (see) on the current of cardiogenic shock and a fluid lungs at And. m. One of such methods is counterpulsation, edges can be intra aortal (forcing, synchronous with a diastole, in an aorta of blood or inflating of the rubber barrel entered into an aorta) and outside (forcing of air, synchronous with a diastole, in the special rubber suit which is put on an experimental animal). Also the method of venoarterialny forcing of blood with its artificial oxygenation bypassing the heart affected with a heart attack was studied.
In an experiment also operation of so-called defoaming agents (alcohol, antifomsilan) and the numerous pharmaceuticals used in a wedge, practice for fight against a fluid lungs at patients was studied And. m, and also electric defibrillation (see) and countershock.
Morfol, picture I. m and the related complications depends on a stage of its development, and also on localization and depth of defeat of walls of heart.
Macroscopically the zone of a necrosis in a myocardium clearly comes to light only in 18 — 24 hours after the beginning of a disease. Before the myocardium in the pool of the affected artery differs in flabbiness, an uneven krovenapolneniye. At the end of the first days the site of a necrosis gains clay and reddish color; it is surrounded with a red strip of hemorrhage and eminates as a result of hypostasis a little. In the next days the zone of a necrosis sinks down in connection with disappearance of hypostasis, becomes dense, its color gradually changes on yellowish-gray. Around granulyatsionny fabric in the form of a reddish border forms. In 3 — 5 weeks on site of a heart attack the connective tissue hem is formed: in the beginning reddish-gray, and then grayish color (tsvetn. fig. A.1).
On depth of damage of a cardiac muscle distinguish transmural And. m when defeat takes all thickness of a myocardium from an epicardium to an endocardium, intramural — with localization of the center of a necrosis in the thickness of a myocardium, and also subepicardial and subendocardial And. m.
In most cases the area of a necrosis matches the pool of the artery affected with atherosclerosis or thrombosed; sometimes note a so-called heart attack at distance when the pool of the affected artery does not match the center of a necrosis that is explained with features of development of collaterals. The largest frequency of stenoses (more than for 50% of a gleam of a vessel) comes to light in a front interventricular artery. Apparently, almost exclusive localization is explained by it And. m in walls of a left ventricle of heart. The isolated heart attacks of a right ventricle meet very seldom — not more often than in 1,25% of cases; also isolated heart attacks of auricles are extremely seldom observed.
Frequency of detection of thrombosis at a pathoanatomical research depends on time between emergence And. in m and death from it. If at deaths door in the first days of fibrinferments it is found in 24,1% of cases, then at the dead by third day its frequency increases to 52,4% of cases.
Most often the myocardial infarction develops in a front wall of a left ventricle (fig. 1), i.e. in the pool of blood supply of a front interventricular artery. The second place on frequency is taken And. m of a back wall of a left ventricle. Necrotic changes, by data A. V. Smolyannikova, in an interventricular partition are noted in 10 — 20% of various options of localization And. m, on a sidewall it extends in 5 — 6% of cases, to papillary muscles — in 25% of cases.
Subendocardial And. the m is most often connected with the stenosing atherosclerosis which is not followed by occlusion or thrombosis of a vessel. In most cases subendocardial And. the m is located in a front or back papillary muscle of a left ventricle, a back or front wall of a left ventricle and in a left ventricular part of an interventricular partition.
Development of macrofocal heart attacks is connected, as a rule, with occlusion of large branches of coronary arteries. At disturbance of a blood-groove in an upper third of a front interventricular artery the heart attack is usually localized in the field of a front wall, lobbies 2/3 interventricular partitions and to a top of heart, sometimes extending to a sidewall of a left ventricle.
A heart attack of a back wall more polimorfen concerning localization and the sizes that is caused by type of blood supply of heart. Depending on features of vascularization of a back wall and interventricular partition distinguish the right, left, and also average types of blood supply of heart with their options (srednepravy and srednelevy). At the left type these departments are supplied with blood from the left coronal artery, at the right type — from right, at average type the back wall of a left ventricle receives blood from the left coronal artery, and a back wall of a right ventricle and back department of an interventricular partition — from the right coronal artery. At srednelevy type the back wall of a left ventricle and partially back department of a partition receive blood from the left coronal artery, and the right coronal artery, supplying a back wall of a right ventricle, takes part also in blood supply of back department of a partition, therefore, two sources of blood supply have edges. At the srednepravy type which is found most often (apprx. 50% of cases), a medial part of a back wall of a left ventricle and an interventricular partition receive blood from the right coronal artery, and the left coronal artery supplies with blood only a lateral part of a back wall of a left ventricle. At the right and left types of blood supply of a possibility of development of collaterals it is less, than at average types.
Emergence And. by m in a back wall of a left ventricle it is connected at average and left types of blood supply with damage of the left coronal artery, at the right and srednepravy types — with damage of the right coronal artery. At the right type of blood supply of heart the heart attack takes all back wall, at srednepravy only its medial part. Thrombosis of the main trunk of the left coronal artery at the left or srednelevy types of blood supply of heart leads to emergence circular And. the m taking all walls of a left ventricle, an interventricular partition, and partially and a back wall of a right ventricle.
At patients And. m against the background of hron. coronary heart disease quite often macroscopically find large hems, melkoochagovy cardiosclerosis (see), it is preferential in subendocardial departments of a left ventricle of heart. Hems are naturally formed at repeated And. m, but are found also at absence in the anamnesis a wedge, manifestations And. m. In a zone of hems the pristenochny endocardium is thickened at the expense of neogenic collagenic and elastic fibers (a secondary fibroelastosis of an endocardium). Fresh necroses are often localized in the zone adjacent to hems.
In most cases the weight of heart is increased to 400 g and above even in the absence of an idiopathic hypertensia. The weight of heart in the presence of hems is especially increased. The hypertrophy of heart can be total or concern preferential left, and sometimes a right ventricle of heart. The last is observed at the aneurisms of a left ventricle of heart which are complicated by hypertensia of a small circle of blood circulation in connection with hron, a left ventricular failure.
Microscopically changes in heart at And. m come to light during the first hours its development. At a svetooptichesky research if death came in the first 2 hours from the beginning a wedge, manifestations And. m, are found only focal changes in walls of the main trunks of coronal arteries — swelling of an intima, proteinaceous treatment of subendothelial departments, fibrous fabric of plaques, contents of atheromas; fresh hemorrhages in superficial departments of plaques, around neogenic vessels, in an adventitia, and also in the neogenic vessels feeding plaques are noted. These changes reflect acute disorders of permeability of vascular membranes in connection with the progressing hypoxia. In a myocardium a plethora of vessels, staza in capillaries, the expressed hypostasis of a stroma, swelling of walls of small intramural and subendocardial arteries come to light. In 2 — 3 hours from an onset of the illness initial changes in muscle fibers in the form of their uneven coloring decide on formation of rough cross strips, glybok, flows («muscular contractures» — fig. 2). In 4 — 5 hours in subendocardial departments of heart there are focuses of a fuchsinophil degeneration which are characterized by swelling of muscle cells, their intensive coloring by acid paints and a metachromasia during the coloring according to Xie in league. These changes are connected with plasmatic treatment of the perishing muscle cells.
The electronic microscopic examination applied by hl. obr. in pilot studies (an alloying of a coronary artery), reveals changes in a cardiac muscle in 15 — 20 min. Initial changes are found in mitochondrions which bulk up, their matrix is clarified, cristas bulk up and break up and mitochondrions take a form of bubbles. These changes appear in the mitochondrions located under a sarcolemma and then and in localized between myofibrils in the beginning. The gleam of tanks of an endoplasmic reticulum increases. Disks and cross strips of muscle cells do not konturirutsya, granules of a glycogen disappear. In a kernel of special changes it is not observed. During the contrasting of cuts in solution of a lead acetate uneven activity of ATP-ase is noted: the greatest number of the besieged lead is located on outside covers of mitochondrions, in its bulked-up cristas it is much less, in myofibrils activity of enzyme almost completely is absent.
At ischemia during 6 — 8 hours hypostasis of muscle fiber reaches the highest degree. A part of mitochondrions loses a cover and partially or completely is dissolved, merges with each other. Some mitochondrions sharply bulk up, are deformed. In an endoplasmic reticulum large vacuoles come to light. Myofibrils are in a condition of a relaxation, the myofibrils on site destroyed numerous fatty drops are. Activity of oxidation-reduction enzymes falls.
In 7 — 8 hours from the beginning of ischemia it is possible to see final fracture of mitochondrions. An endoplasmic reticulum vakuolizirovan, its membranes are destroyed. Activity of oxidation-reduction enzymes is absent. There are destructive changes in a kernel: it badly konturirutsya, becomes homogeneous, the cover of a kernel collapses, chromatin gets a krupnoglybchaty form and accumulates at a nuclear envelope.
At luminescent microscopy in 1 — 2 hour after an alloying of a coronary artery, and also in cases of sudden death decolourization of muscle fibers which begin to shine green light comes to light. It is caused by accumulation in fabric of acid products of exchange. In 4 — 6 hours during the processing of cuts 3,4 benzpyrene the numerous small fatty droplets which are not revealed during the coloring by Sudan by the III—IV, Sudan black and other methods are visible.
At gistokhy, a research the most precursory symptom of local ischemia is sharp reduction of maintenance of a glycogen in muscle fibers that is noted in 30 min. after an alloying of a coronary artery, and also at sudden death at early opening. The glycogen in a zone of ischemia is not defined by 4 — 6 hours, except for the separate bunches located under an endocardium and around vessels. It, and also big activity of a dehydrogenase milk to - you point to strengthening of glycoclastic processes. In 2 — 4 hours from the beginning of ischemia activity of oxidation-reduction enzymes changes. In the beginning activity of a succinatedehydrogenase quickly amplifies (distribution is broken, the quantity of granules of a formazan increases and their coloring amplifies), but in 4 — 6 hours there comes its oppression (the quantity decreases and coloring of grains of a formazan is weakened). Completely activity of enzymes disappears in 12 hours from the beginning of experience. In the created heart attack it is possible to see three zones of activity of enzymes: in the center of a necrosis — its total absence (grains of a formazan do not come to light), in a border area — hypoactivity of enzymes (reduction of amount of grains of a formazan and weakening of their coloring), in the remote sites — normal or a superactivity of enzymes.
In 6 — 10 hours from the beginning of development And. m svetooptichesky microscopy come to light accumulations of leukocytes in capillaries of the affected myocardium, migration of leukocytes for walls of vessels; diapedetic hemorrhages on the periphery of the forming center of a necrosis are found. In the next hours outlines of the bulked-up muscle fibers become wrong, disappears their cross striations. During the day there is a full necrosis of muscle fibers.
By the end of the first days the quantity of the centers of a fuchsinophil degeneration increases, they merge among themselves, forming large fields, and in a stroma leukocytic infiltrates appear. On the periphery the line of demarcation consisting of leukocytes (fig. 3) forms, to the Crimea histiocytic elements are added. The quantity of leukocytes increases, and by 48 o'clock from an onset of the illness they form plentiful accumulations on the periphery of a heart attack between the dead and the remained muscle fibers.
Typical And. the m is characterized by zonality of a structure. On the periphery of necrotic focus the zone of damage of cardiomyocytes comes to light, around the cut forms the zone of ischemia revealed morphologically only by means of a posthumous kapillyarografiya. The zone of damage is expressed unevenly. From an endocardium in usually remaining Purkinye's fibers, as well as in subepicardial departments, damage is expressed slightly. In regional departments, and also in the thickness of the center around the remained perivascular islands of a myocardium damage reaches the maximum degree, sometimes passing into a necrosis.
On 3 — the 5th days the gradual rassasyvaniye of nekrotizirovanny weight is observed. The resorption and phagocytosis are carried out by large macrophagic cells (fig. 4) appearing usually for the 4th day on the periphery of a heart attack, a knaruzha from a leukocytic shaft. During the same period the leucolysis in a zone of demarcation, proliferation of stromal cells is noted. On site the broken-up leukocytes there is a nuclear dust in the form of DNA grains. To 5 —-mu to day the sizes I. m are stabilized (though in some cases progressing of a necrosis can continue to 10 — 15 days and more — fig. 5).
Fibroblastichesky reaction arises on 4 — the 5th days. First thin argyrophil (fig. 6) and collagenic fibers in a zone of a heart attack appear on 7 — the 8th days. During the 1st and the beginning of the 2nd week the zone of a necrosis is presented by the lysing muscle fibers, deprived of vessels, impregnated with edematous liquid with the leukocytes which are breaking up on the periphery. These changes can cause developing of acute aneurism of heart, a cardiorrhesis, a separation of a papillary muscle, a rupture of an interventricular partition. After 7 — 10 days processes of a reparation proceed in the form of substitution of nekrotizirovanny fabric young granulyatsionny fabric. At small heart attacks in 3 — 6 weeks in most cases the zone of a necrosis is completely replaced with granulyatsionny fabric. Full organization large And. the m comes to the end in 2 — 2,5 months. Further the hem is condensed, vessels in it are reduced and transformed to arteries, veins and sinusoids.
Duration of the organization I. the m fluctuates over a wide range depending on its sizes and conditions in which it occurs. Terms are extended during the progressing of a necrosis, at a heavy sclerosis of coronary arteries, at a decompensation of heart. In these cases proliferative reaction is slowed down, Macrophagic reaction happens scanty, and devitalized muscle fibers are exposed to an acellular lysis. The stromal skeleton of heart is as a result bared and there is its kollabirovaniye to thinning of a wall of heart. The hem in such cases takes a form of the student invisible grayish center with yellowish dot necroses in the center. Reactive and proliferative processes around such center a long time are absent and only later 2 — 3 weeks it is possible to notice reproduction of stromal cells (areactive and atsellyulyarny And. m). At the edges of a heart attack and beyond its limits the small centers of damage and a necrosis of various prescription in most cases are found; a part them arises during the preceding infarction period, others along with And. m, and regarding cases they are morfol, an equivalent recurrent And. m.
During the organization I. m in its fringe regions and in surrounding tissue of a myocardium, and sometimes and in a distance it is possible to observe accumulations of eosinophils, and later limfogistiotsitarny infiltrates with participation of plasmocytes. These changes consider manifestation of local autoimmune reactions to the breaking-up myoproteose.
At And. m are found changes in intrakardialny nerve knots: in the acute period — swelling of separate ganglionic cells, a peripheral arrangement and pycnosis of their kernels; at deaths door during later period the sclerosis of nerve knots comes to light.
An endocardium in a zone I. m with the phenomena of hypostasis, a razvolokneniye, focal kruglokletochny infiltration. Between trabecular muscles the blood clots extending to tebeziyeva vessels are quite often formed. In an epicardium at transmural And. the m quite often arises hypostasis, leukocytic infiltration, the centers of a necrosis of fat and fibrinous imposings on a surface. During the organization I. the m happens adhesion, and then an union of leaves of a pericardium to existence in commissures of the centers of ksantomny cells, limfoplazmotsitarny infiltrates. Sometimes in the period of the organization I. the m arises a pericardis as manifestation postinfarction syndrome (see).
Unlike described typical And. the m, a morphogenesis of its clinically atypical forms (asthmatic, cerebral, arhythmic, asymptomatic, etc., except abdominal) is more difficult. Atypical And. m are more often observed at patients with the combined pathology against the background of a heavy current hron, coronary heart disease in the presence of an idiopathic hypertensia and the aggravating background diseases. In their development, except acute disorders of coronary circulation, metabolic disturbances in a muscle of heart and slowly progressing hypoxia of a myocardium play a role. Thus, the centers of a necrosis and damages at atypical And. m often have mixed — the koronarogenny and nekoronarogenny nature. Natural developing of blood clots in coronal arteries at atypical And. by m it is connected not so much with coronary atherosclerosis how many with release and receipt in blood of thromboplastic substances of a myocardium, and also with hypoxemic damage of vascular walls, disturbance of microcirculation, difficult hemodynamic conditions because the main blood stream in a myocardium in similar cases is sharply broken and blood circulation happens preferential on difficult collateral ways.
Macroscopically found in heart at atypical And. the m is large subendokardialno-intramural, and sometimes and the transmural necrotic center by outward differs from typical And. m diversity of structure and lack of zonality of a structure. Its outward often does not correspond to duration a wedge. manifestations. In pathoanatomical practice such centers are usually regarded as organized And. m. Microscopically such center represents randomly alternating sites of a fuchsinophil degeneration and coagulative necrosis being at different stages of formation and the organization and also sites of a myolysis, vacuolar, fatty dystrophy, an atrophy of muscle fibers (fig. 7); quite often also old cicatricial changes meet. In a stroma of the center note disorders of microcirculation in the form of hypostasis, a plethora of vessels, perivascular hemorrhages. Though such And. m are usually localized in a zone of blood supply of the obliterated or sharply stenosed artery, angiographically in them, unlike typical And. the m, is noted abundance of the small vessels forming dense textures (fig. 8). Sometimes in the main coronal artery find also fresh blood clots, often repeated. In these cases all originally arisen motley center nekrotizirutsya and loses morfol, an originality.
Depending on a stage of development And. m can come to light its various complications: the cardiorrhesis, aneurism, thromboembolisms, a separation of a papillary muscle, perforation of an interventricular partition, trombendokardit, etc.
The rupture of a myocardium is a complication of the early period And. m, hl. obr. in the first 3 — 10 days (tsvetn. fig. B). It occurs among the dead from a myocardial infarction in 10 — 15% of cases. The crucial role in emergence of a gap is played by the sizes of the necrotic center — the gap arises at extensive transmural heart attacks. The gap is promoted by arterial hypertension and poor development of collateral circulation. At repeated And. m gaps are observed less than at the first. More than a half of gaps arises at heart attacks of a front wall of a left ventricle (fig. 9). More often the gap is on a joint of the dead and the remained myocardium in a zone of leukocytic reaction and has a step appearance. I. V. Davydovsky connected gradualness of a gap with gradual, but not single-step character of a gap.
Rare complications of the early period And. the m (1 — 1,5% of lethal outcomes) is a separation of a nekrotizirovanny papillary muscle and perforation of an interventricular partition. One muscle comes off usually, and the separation of a back papillary muscle is 6 times more often observed. The rupture of an interventricular partition, as well as a cardiorrhesis, is more often observed at the first And. m and at the heart attack which developed against the background of arterial hypertension. The rupture of an interventricular partition leads to development of acute right ventricular heart failure.
In 20 — 30% of cases And. m, preferential transmural, are complicated by aneurism of heart. Aneurisms are more often localized in the field of a front wall of a left ventricle near a top of heart, in a back wall at the basis of heart, more rare in the field of a top of heart and in an interventricular partition. Distinguish acute (to 3 weeks), subacute (3 weeks — 3 months) and hron, aneurisms (St. 3 months). Most often they form in terms of 4 — 14 days. Their development is promoted disturbance of durability of fibrous structures and muscular tissue of heart in connection with their hypostasis, destruction, swelling in the conditions of the accruing acidosis, by multiple internal anguishes of heart in a zone of a heart attack, progressing of a necrosis, delay and inferiority of reparative processes. The sizes and a form of aneurism of heart depend on depth and extent And. m. At transmural And. the m of an aneurysm can arise even at defeat, small on the area; at intramural And. the m of an aneurysm forms only at the extensive center of a necrosis; the more deeply and more aneurysm of heart there is more than the area of defeat, the. By the size distinguish small aneurisms (to dia, to 4 cm), averages (to dia. 4 — 7 cm) and large (to dia. St. 7 cm); they can be diffusion and sacculate.
The wall of acute aneurism of heart is area of a heart attack and morphologically all evolution typical for a heart attack is reflected in it. In process of formation and consolidation of a hem acute protrusion of a wall of a ventricle can disappear, however most often acute aneurism of heart passes in subacute, and then and into chronic. At subacute aneurism, in addition to devitalized fabrics with the phenomena of the organization, the wall of aneurism is usually made by the stuck together leaves of a pericardium and a reinforced endocardium. Hron, aneurism can be fibrous (at transmural And. m) or fibromuscular (at intramural And. m). In a wall hron, aneurisms sharply expressed hypertrophy of the remained muscle bundles and a new growth of elastic fibers in hems, and also reorganization of vessels as arteries of the closing type is noted. The cavity of aneurism is almost always filled with layered blood clot; over time trombotichesky masses is condensed, and sometimes and obyzvestvlyatsya (see. Thrombosis ).
Acute aneurism of heart is quite often broken off; at subacute and hron, aneurisms gaps are rare, at them there is a progressing heart failure or tromboembolic episodes more often (see. Thromboembolism ), leading patients to death.
Tromboembolic episodes And. m can be observed as in a big, and small circle of blood circulation. Their frequency in connection with broad use of fibrinolitic and anticoagulating drugs considerably decreased. A source of vascular embolisms of a big circle are trombotichesky imposings in a cavity of a left ventricle or in a cavity of an aneurysmal bag. At And. m find blood clots in vessels of a small circle of blood circulation or in connection with an embolism from pelvic veins and veins of the lower extremities, or in connection with local thrombosis of branches of a pulmonary artery.
After 5 — the 10th day from development And. m quite often are found morfol. signs of a syndrome of Dressler (see. Postinfarction syndrome ).
CURRENT AND SYMPTOMS
Klin, manifestations And. the m and its current in many respects are defined by localization of a necrosis and its volume, and also degree of a metastasis ad nervos of various vegetative functions. A metastasis ad nervos can sometimes be leaders in a picture of a disease, creating certain syndromes, and also atypical forms of a current And. m
Macrofocal myocardial infarction
Typical current And. the m includes five periods. 1. The prodromal stage, or the period of harbingers (a so-called preinfarction angina), is characterized by emergence or change of signs of coronary insufficiency with increase of their weight; it proceeds from several hours to one month. 2. The most acute period — time between the beginning of heavy ischemia of the site of a myocardium and emergence of signs of its necrosis — takes 30 min. to the 2nd hour. There are data that if during this period there is a resorption of blood clot, involution of symptoms is possible And. m 3. The acute period, during to-rogo is formed the site of a necrosis and myoma of a lyation, lasts from 2 to 10 days (sometimes — at a long or recurrent current And. m — longer). 4. The subacute period, in time to-rogo initial processes of the organization of a hem come to the end: necrotic masses is completely replaced with granulyatsionny fabric by the end 4 — 5th week from the beginning of a disease (apart from a prodromal stage). 5. The postinfarctive period which is characterized by increase in density of a hem and the greatest possible adaptation of a myocardium to new operating conditions of cardiovascular system proceeds within 3 — 6 months from the moment of formation of a necrosis.
For every period And. m are in most cases characteristic certain changes of an ECG.
The prodromal stage is lit in literature insufficiently fully. Most of authors considers that the period of harbingers is observed approximately at a half of patients And. m. Carry the attacks arising for the first time in life to harbingers stenocardias (see); at the patients having stenocardia — increase, lengthening and increase in weight of attacks, accession of stenocardia of rest to an angina of exertion («unstable» stenocardia). The important symptom — absence to lay down. effect of use of nitroglycerine for patients at whom he stopped pains earlier. Sometimes in this period the changes of an ECG reflecting ischemia of a myocardium in area where further develops are noted And. m.
The most acute period is most often characterized by an attack of a megalgia, edges is localized behind a breast (status anginosus), is more rare in other areas of a thorax or in epigastriums (status gastralgicus). Pain can irradiate in a hand, a shoulder, a shoulder girdle, a clavicle (especially in left), in a neck and a mandible, in a back (is more often in interscapular space). Pain has the squeezing, pressing, arching or burning character; many patients are not capable to describe the pain precisely. Pain reaches the maximum intensity very quickly: within several seconds or minutes. Certain patients note wavy strengthening and reduction of pain. Its duration fluctuates of 20 — 30 min. till several o'clock; longer pain is usually connected with accession of an epistenokardialny pericardis or with the prolonged current And. m when the necrosis gradually takes the increasing mass of a myocardium. In some cases pain is absent or is so insignificant that the patient does not pay attention to it.
Pain is followed by sharply arising sharp general weakness, frequent nausea, vomiting (especially at localization And. m in back departments of a left ventricle), fear of death, feeling of shortage of air * perspiration. The first minutes or hours of a disease at many patients the ABP raises; further relative or absolute arterial hypotension develops (see. Hypotension arterial ).
Arterial hypotension serves as manifestation in many cases not only reflex vascular insufficiency (see), but also the acute heart failure arising owing to falloff of sokratitelny function of a left ventricle of heart where the center of a necrosis is usually localized. The extensive center of a necrosis leads to falloff of cordial emission and development true (most often irreversible) cardiogenic shock. In many cases the left ventricular failure is shown by cardiac asthma and a fluid lungs in combination with cardiogenic shock; occasionally acute And. the m begins with an asthma, but not with pain (status asthmaticus). Both acute vascular, and an acute heart failure almost naturally are followed by tachycardia.
In the most acute period And. m often develop heavy disturbances of a cordial rhythm, cardiogenic shock which along with a fluid lungs are the reason of early death more than a half of patients.
The diseases given a physical research in the most acute period are defined by hl. obr. such complications as various forms of heart failure and disturbance of a heart rhythm. The cantering rhythm can be an important auskultativny symptom (see. Gallop rhythm ). Other physical signs, such as tachycardia, dullness of cardiac sounds, expansion of its borders to the left, are less specific. If the acute left ventricular failure is connected with a heart attack or a rupture of a papillary muscle, over a top of heart and in the V point rough systolic noise of mitral insufficiency appears.
The acute period is connected with the end of formation of the center of a necrosis. Considerably pain decreases or disappears. Residual pain can be connected with ischemia of a periinfarktny zone or with the joined epistenokardialny pericardis. Displays of heart failure and arterial hypotension in this period remain or arise at many patients and can progress. The tendency to development of disturbances of a rhythm and conductivity which, according to the round-the-clock monitor observation, are noted practically at all patients remains.
According to V. A. Lyusov and BB. B. Belousova, during the first hours And. the m increases viscosity of blood and aggregation ability of erythrocytes and thrombocytes.
In several hours since the beginning of a disease there is a feverish reaction (usually body temperature reaches 38 — 38,5 ° and only occasionally surpasses this size). There is a neutrophylic leukocytosis (10 — 12 thousand in 1 mkl blood), the few patients have a hyperleukocytosis (more than 20 000 cells in 1 mkl blood). A bit later ROE accelerates. In blood activity of a number of enzymes increases: kreatinfosfokinaza, lactate dehydrogenases, generally at the expense of its first isoenzyme (in 3 — 4 hours from the beginning of a disease), aminotransferases, or transaminases, in particular asparaginic and to a lesser extent — alanine (usually by the end of the first days of a disease). The hyperglycemia, and also disturbance of ratios of protein fractions of blood is quite often observed (content of albumine decreases, and globulins and fibrinogen — increases, appears patol. S-reactive protein).
The subacute period begins after a full otgranicheniye of the center of a necrosis from not changed myocardium. In this period the wedge, symptoms connected with a degrowth of functionally full-fledged myocardium and its electric instability remain.
Anginous pains at many patients are absent. Sometimes they disappear also at those patients at whom before development And. the m noted stenocardia. In some cases attacks of stenocardia remain or appear if they were not to And. m. Displays of heart failure in most cases begin to decrease, but can be stable or even to accrue. The ABP, especially systolic, gradually raises though usually does not reach initial size. If. the m developed against the background of arterial hypertension, the so-called beheaded hypertensia can be defined: diastolic pressure remains raised, and systolic can be a little reduced or normal. Further at many patients also systolic pressure increases, but pulse usually remains reduced. Disturbances of a rhythm are observed less than in the most acute and acute periods And. the m, and frequency of arrhythmias decreases every day of a disease. In 2 — 3 weeks at many patients PI broken in the acute period is recovered. m conductivity. Quite often the arrhythmias connected with an acute overload of the left auricle, napr, a ciliary arrhythmia disappear.
Manifestations of a rezorbtsionno-necrotic syndrome in the subacute period decrease. Since 3 — the 4th day from the beginning of a disease fever gradually decreases and by the end of the first week body temperature is usually normalized. If it does not occur, it is necessary to think of accession of complications — pneumonia, a thrombendocarditis, Dressler's syndrome (see. Postinfarction syndrome ).
The leukocytosis, expressiveness to-rogo considerably is defined by the sizes I. the m, gradually decreases and by the end of the first week the quantity of leukocytes in blood is normalized, and the band shift disappears. Longer existence of a leukocytosis indicates emergence of inflammatory complications or the prolonged course of a myocardial infarction. ROE reaches the maximum size to 5 — to the 7th day of a disease. Further acceleration of ROE can remain within several weeks or months before full substitution of the center of a necrosis granulyatsionny fabric. The sugar content in blood is, as a rule, normalized within several days from the moment of development And. m. Increase in activity of serumal enzymes — kreatinfosfokinaza and lactate dehydrogenases — remains within 10 — 12 days. Activity of aminotransferases is normalized to 3 — to the 4th day from the beginning of a disease. Disturbances in the ratio of protein fractions of blood can come to light during 4 weeks and more.
The postinfarctive period is characterized by manifestations of processes of adaptation of cardiovascular system to new operating conditions. Signs of a compensatory hypertrophy of the departments of a myocardium which are not affected with a heart attack come to light. Heart failure at many patients disappears or decreases, but at very extensive and especially repeated And. the m compensation happens impossible and stabilization or even weighting of symptoms of heart failure is observed. Arrhythmias (hl. obr. ventricular premature ventricular contraction) remain at most of patients, but usually do not pose hazard to life. If in the postinfarctive period disturbances of conductivity do not disappear, the probability of its recovery is insignificant further. Manifestations of a rezorbtsionno-necrotic syndrome remain only in the form of acceleration of ROE and shifts of protein fractions of blood.
The Melkoochagovy myocardial infarction
Frequency during small - focal And. to m it is less expressed, than at macrofocal. Nevertheless sometimes allocate the period of harbingers, the acute period and the period of reconvalescence in its current. Anginous pain at this form I. the m usually has rather small intensity and duration though between expressiveness of pain and extensiveness of damage of a myocardium there is no strict parallelism. Long pain at melkoochagovy And, m can speak formation of new ochazhok of a necrosis or long ischemia of a periinfarktny zone. If pain is rather intensive, the collapse can develop though more often the ABP tends to increase, and the subsequent arterial hypotension is noted not at all patients. Sonority of cardiac sounds at most of patients practically does not change. Tachycardia is observed not always and has reflex character. Heart failure develops only when the centers of a necrosis are multiple and arise against the background of a cardiosclerosis after postponed earlier And. m. Disturbances of a heart rhythm and conductivity meet considerably less than at macrofocal And. m though occasionally have extremely difficult character (fibrillation of ventricles, total cross block). Premises for formation of aneurism of heart are absent. At the same time at subendocardial localization of a necrosis if it takes also an endocardium, the mural thrombosis and tromboembolic episodes is possible. Changes of blood are expressed much more weakly, than at macrofocal And. m, also remain during rather short time. The leukocytosis usually does not exceed 10 — 12 thousand in 1 mkl blood, the band shift and an aneosinophilia are registered not always. Not at all patients also increase in ROE comes to light. Increase in activity of enzymes is short-term and insignificant, at the same time changes of an ECG can remain a long time. Sometimes melkoochagovy And. the m serves as a harbinger of macrofocal, including transmural damage of a myocardium.
Atypical forms of a myocardial infarction. In certain cases completely is absent characteristic for And. m pain syndrome. The disease can begin with acute vascular or heart failure (cardiac asthma, a fluid lungs, cardiogenic shock). Occasionally as the first symptom of a disease serves disturbance of a heart rhythm, most often ventricular tachycardia, quite often fibrillation of ventricles. And. the m proceeding without pain almost never begins with developing of supraventricular arrhythmias (atrial tachycardia, blinking and an atrial flutter). At the same time these arrhythmias with coronary insufficiency and the high frequency of ventricular reductions can lead to development of melkoochagovy necroses of a myocardium. To atypical forms I. m carry also the beginning of a disease from an attack of Morganyi — Adams — Stokes (see. Morganyi — Adams — Stokes a syndrome ). Sometimes the disease is shown only by the general weakness, an indisposition, an adynamia. At some patients And. the m or a postinfarction cardiosclerosis comes to light only at accidental research ECG (an asymptomatic current).
A repeated myocardial infarction
Unlike the prolonged current And. the m connected with additional necroses of a myocardium in the pool of the same arteries which damage caused development of primary necrotic center (most often owing to the continued thrombosis) allocate repeated And. m, development to-rogo it is not connected with proximate causes of primary necrosis, has independent! character also usually arises in pools of other branches of a coronary artery.
An interval between the first and repeated And. the m fluctuates from several days to many years. Almost in 70% of cases repeated And. the m arises within the first 3 years after previous. According to V. G. Popov (1971), approximately at 1/3 died from repeated And. m it arose in terms up to 2 months after the first.
On a wedge, to a picture and a current repeated And. the m most often does not differ from the first. A number of authors specifies that bezbolevy forms at repeated And. m meet more often than at the first. However according to V. G. Popov, repeated macrofocal And. the m in 82,2% is followed by development of a heavy painful attack. Bezboleva option repeated macrofocal And. the m is, as a rule, characterized by acute cardiovascular insufficiency: cardiogenic shock, collapse or cardiac asthma, fluid lungs; more rare the main its wedge, manifestation are disturbances of a cordial rhythm (ventricular tachycardia, sometimes supraventricular tachycardia, blinking or an atrial flutter), but the most frequent reason of sudden death in the most acute stage And. m happen arrhythmias of heart (fibrillation of ventricles).
Localization of pains, as well as at the first And. the m, can be not only retrosternal that sometimes serves as the reason of diagnostic mistakes at repeated macrofocal And. m (up to establishment of the diagnosis of a ruptured ulcer of a stomach, on the basis to-rogo make a laparotomy). Body temperature during the first hours and days repeated macrofocal And. the m is usually increased. At most of patients the leukocytosis, further acceleration of ROE, increase in activity of a number of enzymes of blood serum is observed (aspartate aminotransferases, the 1st fraction of a lactate dehydrogenase, a kreatinfosfokinaza). At the same time changes of an ECG often happen less typical, than at the first And. m since are quite often combined with the changes which remained after previous And. m that complicates their interpretation.
Repeated melkoochagovy And. m more often than the first And. the m (irrespective of its extensiveness), proceeds in a bezbolevy form. Nevertheless at most of patients typical anginous pains are noted. In some cases retrosternal pains arise repeatedly during many days, months or even years, and their intensity is sometimes so big that they do not concede to effect of drugs. The similar course of a disease, a cut quite often treat as an aggravation hron, coronary heart disease or as the preinfarction angina, usually is followed by formation of the small centers of dystrophy or a necrosis (repeated small - focal And. m).
Quite often repeated melkoochagovy And. the m is shown by asthmatic option or in the form of disturbances of a cordial rhythm. In the latter case it is sometimes difficult to solve whether melkoochagovy necroses in a myocardium are the reason of a tachyarrhythmia or its investigation since it is known that the long paroxysm of tachycardia or a ciliary arrhythmia at patients with the stenosing damage of coronal arteries can lead to development of necrotic changes in a myocardium.
Temperature reaction is noted approximately at 3/4 patients repeated melkoochagovy And. m, as well as changes from blood. Increase in activity of enzymes though all these signs do not reach such expressiveness, as is more often observed at macrofocal And. m.
Electrocardiographic diagnosis of repeated melkoochagovy PI. m it is often difficult, especially if the necrosis develops in areas of the cicatricial field after postponed earlier macrofocal And. m. In certain cases changes of an ECG after postponed earlier melkoochagovy And. m are completely leveled owing to emergence of melkoochagovy defeats on an opposite wall of a myocardium.
Repeated repeated And. m, unlike the first, quite often become the reason of development acute or hron. the heart failure connected with defeat of the increasing mass of a sokratitelny myocardium, emergence of the new centers of ectopic activity leading to disturbances of a cordial rhythm which can be a cause of death, including and sudden. With increase in number transferred the patient macrofocal And. the m weight of their current accrues, congestive heart failure develops more often, the labor forecast worsens, both the hospital lethality, and a lethality after an extract from a hospital raises.
Cardiac asthma and a fluid lungs — frequent manifestations of acute weakness of a left ventricle, its tonogenny dilatation with relative insufficiency of the mitral valve. The left ventricular failure proceeds especially hard at a heart attack or a rupture of a papillary muscle.
Attack cardiac asthma (see) begins with feeling of shortage of air, a cut quickly passes into suffocation. Breath is speeded up, at a breath wings of a nose are inflated. The patient aims to accept a sitting position (orthopnea). The percussion and auskultativny picture over lungs is mosaic: in different departments of a thorax areas of dullness of a percussion sound appear, in other sites it can have a bandbox shade. In places, especially over zadnenizhny departments of lungs, it is more on the right, non-constant wet rattles are listened. With increase of a left ventricular failure the fluid lungs develops.
Cardiogenic shock — one of the most terrible complications in the most acute and acute period And. m; often is a cause of death of patients at early stages of a disease.
Cardiogenic shock (see) most often develops the first minutes or hours of a disease. Emergence of shock is usually preceded by the expressed pain though it can develop also at bezbolevy And. m. Outward of the patient is characteristic: the pointed features, pallor with a grayish and cyanochroic shade. Skin is cold, it is covered with a clammy sweat. The patient is adynamic, almost or at all does not react to surrounding. Pulse is frequent, threadlike. Falling of the ABP, especially systolic, and also reduction of pulse pressure is most characteristic. At patients with initial arterial hypertension symptoms of shock can develop already at decrease in systolic pressure to 120 — 100 mm of mercury. If initial pressure is normal, shock usually comes with a systolic pressure below 80 mm of mercury. Important and predictively a heavy sign of true cardiogenic shock — anury (see).
Right ventricular insufficiency of heart seldom complicates And. m in the acute period. At its emergence it is necessary to think about accompanying And. m of a thromboembolism of pulmonary arteries, about aneurism of an interventricular partition, its gap; the heart attack of a right ventricle can be very rare cause. The main symptom of acute right ventricular insufficiency — the acute congestive swelling of a liver which is often followed by severe pain in right hypochondrium. Also swelling of cervical veins is noted. Further there are hypostases of feet and shins. With progressing of right ventricular insufficiency hypostases extend to hips, a crotch, a waist; arises hydrothorax (see) and ascites (see). Sometimes right ventricular insufficiency develops in the subacute or postinfarctive period; in these cases it is connected with is long the existing left ventricular failure and exhaustion of compensatory mechanisms.
The Epistenokardialny pericardis — very frequent complication transmural And. m though clinically it is distinguished seldom. The only objective symptom of a pericardis — — it is possible to listen to a pericardial rub not at all localizations And. m (only at defeat of a front wall of a left ventricle and top of heart). This noise is listened short time, usually within several hours. With the advent of exudate in a cavity of a cordial shirt noise disappears. Noise is defined in the field of a top, is more often in Botkin's point — Erba. The pericardis quite often is followed by the pain having other character, than anginous pain at the beginning And. m. Frequent communication of intensity of pain with phases of breath is especially important for the diagnosis of a pericardis that it is explained by a reactive inflammation of an adjacent pleura.
Disturbances of a cordial rhythm and conductivity — almost constant complication macrofocal And. m; they are frequent and at melkoochagovy defeats. According to long monitor observation (see), they occur practically at all patients macrofocal And. m in the first days of a disease and more than at a half of patients — on second day. Ventricular is most often observed premature ventricular contraction (see). Polytopic, group and early ventricular extrasystoles quite often serve as a harbinger of ventricular tachycardia and fibrillation of ventricles. Early call the extrasystoles matching a so-called vulnerable phase of a cardial cycle, the corresponding top of a tooth of T on an ECG. There are instructions that at And. the m «a vulnerable phase» can be extended. Approximately at a quarter of patients atrial premature ventricular contraction is registered, edges can be a harbinger of Bouveret's atrial disease, blinking or an atrial flutter. Bouveret's atrial disease and an atrial flutter are observed at And. m it is rather rare (in 1 — 7% of cases), a ciliary arrhythmia — at 10 — 25% of patients, and according to data of some authors — and is more often. With a little smaller frequency there is nodal atrioventricular tachycardia (actually nodal tachycardia and the accelerated atrio-ventricular rhythm). Data on the frequency of ventricular tachycardia at And. m are extremely contradictory and depend on methods of their registration and on what authors understand as ventricular tachycardia (some designate this term and group premature ventricular contraction, if number of extrasystoles more than two). It is long the existing Bouveret's disease or a tachyarrhythmia (see. Ciliary arrhythmia ) leads to development of congestive heart failure and aritmogenny shock. The heaviest disturbances of a rhythm are trembling and ventricular fibrillation (see. Arrhythmias of heart ). Distinguish primary fibrillation (blinking) of ventricles resulting from difficult disturbances of neurohumoral regulation of a cordial rhythm and the secondary fibrillation occurring in connection with heavy necrotic changes of considerable mass of a myocardium and which is essentially an agonal rhythm. Primary fibrillation can be stopped by the category of a defibrillator, at secondary fibrillation of ventricles treatment is most often inefficient.
At And. m are observed all types of disturbances of conductivity (see. Heart block ). They develop, as a rule, in the acute period of a disease. Considerable danger to the patient is constituted by a total atrioventricular block, edges occurs at 2 — 10% of patients acute And. m. Clinically full atrioventricular block is shown by aritmogenny shock, and regarding cases and attacks of Morganyi — Adams — Stokes. Usually total block remains within 3 — 7 days. If blockade does not disappear in 10 days since the beginning of a disease, it is the most probable that it is irreversible.
Tromboembolic episodes in connection with broad use of anticoagulants and earlier activation of patients began to meet rather seldom. If in 1948 — 1956 they were noted at 14 — 30% of patients, then in the next years their frequency decreased to 2 — 5%. A source of thromboembolisms at And. the m most often serves intracavitary thrombosis. Formation of blood clots in cardial cavities is promoted by release of thromboplastic substances from the destroyed endothelium. Destruction of an endothelium leads to adhesion of thrombocytes and formation of blood clot. Formation of blood clot in cavities of auricles at a complication is possible And. m ciliary arrhythmia. Often trombotichesky masses is formed in an aneurysmal bag where the thrombogenesis is promoted by delay and turbulence of a blood flow. Friable trombotichesky masses can partially collapse and with a blood flow to get into arteries of a big circle of blood circulation, causing their obstruction with the advent of corresponding a wedge, symptoms (see. Thromboembolism ). In the field of an arrangement of pristenochny endocardiac blood clot the aseptic inflammation (thrombendocarditis) can develop, a cut in rare instances is complicated by development of an infection. Clinically the thrombendocarditis is shown by long subfebrile condition, more rare high fever, the general weakness, perspiration, fatigue, in some cases a thromboembolism of arteries of a big circle of blood circulation. Changes of blood of a malospetsifichna. The moderate neutrophylic leukocytosis with small band shift, an eosinophilia, acceleration of ROE can be observed. At And. m, especially at elderly people, in connection with hemodynamic disturbances, changes of coagulability of blood and long restriction of mobility sometimes develop fibrinferments of peripheral veins which can become the reason of an embolism of a pulmonary trunk and its branches.
The rupture of a wall of a ventricle of heart can arise at extensive transmural And. m. Usually it occurs during the period between the second and tenth days of a disease. As a rule, it is preceded by considerable strengthening of a retrosternal pain. The gap is followed by the most severe pain, and in several seconds of the patient faints. If the patient does not perish at the time of a cardiorrhesis, the heavy cardiogenic shock connected with develops cardiac tamponade (see). On an ECG at the time of a cardiorrhesis the sinoatrial or idioventricular rhythm, sometimes an asystolia is registered, it is extremely rare — fibrillation of ventricles. Longevity from the moment of a cardiorrhesis is estimated for minutes, in the few cases — hours. (Hemorrhage to the sacculated site of a cavity of a pericardium) patients live in exclusively exceptional cases of the covered perforation several days and even months.
The rupture of an interventricular partition, as well as a rupture of a wall of a ventricle, usually is followed by sharp pain in heart, a faint or reflex cardiogenic shock. Quickly the phenomena of congestive right ventricular insufficiency accrue. There is a rough systolic noise on both sides of a breast at the level of III — the IV intercostal spaces, noise extends from left to right. In the field of listening of noise systolic trembling is defined. Quite often there are disturbances of a heart rhythm and especially conductivity (total cross block).
The rupture of a papillary muscle is shown by symptoms of an acute congestive left ventricular failure (fluid lungs). Quite often there is cardiogenic shock. Emergence of rough systolic noise with epicenter over a top of heart where often it is possible to reveal also systolic trembling is characteristic.
Aneurism of heart develops at extensive, usually transmural And. m. In the acute period protrusion of a wall of heart in the field of the center of a necrosis is noted practically at all patients macrofocal And. m. Further this protrusion in most cases disappears in connection with the pulling together action of a connective tissue hem. True aneurism forms at persons with initially raised ABP more often, and also probably at gross violation of a bed rest in the first days of a disease. Quite often at development of aneurism systolic noise appears. The pulsation in precardiac area is characteristic of aneurism of a front wall of a left ventricle patol. Aneurism of heart at many patients is shown by symptoms of a congestive left ventricular failure. Aneurism of an interventricular partition with protrusion in a cavity of a right ventricle leads it to development of congestive right ventricular insufficiency (Berngeym's syndrome). In an aneurysmal bag blood clots are quite often formed and the thrombendocarditis develops. The diagnosis is specified by data of an ECG, echocardiography, electro-and rentgenokimografiya, and further — a contrast ventrikulografiya of heart (see. Aneurism of heart ).
Paresis of a stomach and intestines, and also erosive gastritis, pancreatitis — complications And. the m connected with a hypoxia, disturbances of microcirculation and a nervous trophicity of internals. Sometimes they significantly influence the current And. m also demand urgent to lay down. actions. A wedge, manifestations of damages of a liver and kidneys are found seldom.
Rather late there are complications connected with a sensitization of an organism decomposition products of a myocardium — Dressler's syndrome, a syndrome of a front wall of a thorax, a syndrome of a shoulder combined by the general concept a postinfarction syndrome.
NERVOUS AND MENTAL DISORDERS
Nervous and mental disorders at a myocardial infarction are substantially connected with disturbance cerebral circulation (see), is more often than functional character, and sometimes owing to thrombosis or a thromboembolism of small vessels of a brain. Nevrol, frustration in such cases can become conducting a wedge, manifestations of the acute period, especially in the presence of a focal nevrol, symptomatology and oppression of consciousness up to a coma (an apoplektiformny syndrome). An essential pathogenetic role can be played a hypoxia of a brain (I eat. Hypoxia) owing to developing at And. m of heart failure and toxic influence of decomposition products of the center of a necrosis in a muscle of heart on a brain.
Mental disturbances meet at persons of the senior age groups, especially after 60 years more often. Psikhopatol, a syndrome arises in connection with a complex of factors of both psychogenic, and somatic character. Already in the most acute period And. the m can appear the fear of death which is followed by concern, alarm, melancholy. Some patients are silent, are not mobile, others, on the contrary, are extremely irritable.
In a further current And. the m of disturbance of mentality can be divided into two groups: not psychotic and psychotic. The first group includes asthenic and neurosis-like states, affective syndromes — depressive, alarming and depressive, euphoric; the second group represents various disorders of consciousness — conditions of an oglushennost and a sopor, delirious and twilight states.
In clinic psikhopatol, disturbances at And. m figure prominently emotional frustration. The alarming depression which is followed by steady and long melancholy can be the reason of suicide actions. At deterioration in a somatic state, increase of the hypoxia expressed to intoxication a depression can be replaced by euphoria. At improvement of a somatic state the depression can develop again.
In the first days And. m most often are found emotional frustration, an alarming and depressive syndrome which can be replaced by the periods of euphoria. The fear of death, melancholy, alarm, an alarming depression can be replaced by psychomotor excitement. Patients in such state try to get up, go, speak much. Despite objectively serious condition, mood at such patients raised. During this period can appear, though it is rare, psychotic states with change of consciousness. Short duration is characteristic of them, usually they proceed of a minute to 5 — 6 days.
At a heavy current And. the m at patients is more senior than 60 years sometimes the condition of an oglushennost is observed, a cut can pass into a sopor. The wedge, death, a hypoxia, heavy disturbances of a rhythm lead a heavy pain syndrome, a state in certain cases to emergence of twilight conditions of consciousness, various on depth, sometimes to development of a delirium.
True reactive states are most often observed during the period between 2 — the 3rd and 15th days of a disease. In later period in a condition of patients the adynamy of different shades dominates, morbid depression, hysteriform reactions, conditions of persistence can develop.
Neurosis-like syndromes at And. m differ in a variety of symptomatology. Persistence and hypochiondrial states have character or exaggerations, or patol. prikovannost of attention to the available feelings.
In the postinfarctive period psychotic states are observed seldom. Sleep disorders and an adynamy are often noted, and at patients with cerebral atherosclerosis the oglushennost and confusion of consciousness are possible. During this period «leaving» of patients in a disease with heavy neurotic reactions, hysteria and phobias is possible.
Recognition of a prodromal stage And. the m is based on establishment of the first attacks of stenocardia or its equivalents, changes of character of their current, developing of stenocardia of rest, disappearance to lay down. effect of nitroglycerine, symptoms of ischemia of a myocardium on an ECG.
The diagnosis developed And. the m at the typical course of a disease comes easy. The long intensive retrosternal pain is most characteristic, arterial hypotension, a cut in some cases precedes more or less long increase in the ABP, tachycardia, a priglushennost of cardiac sounds, further temperature increase, changes of blood (a leukocytosis with shift to the left, an aneosinophilia, change of ratios of protein fractions, acceleration of ROE, increase in activity of a number of enzymes). At such a wedge, data of an ECG most often confirm to a picture the diagnosis.
It is much more difficult to distinguish And. m at the atypical and erased current. Sometimes the pain syndrome is absent or is expressed so poorly that patients do not see a doctor. The diagnosis at such current And. the m can be delivered only retrospectively, on the basis of data of an ECG and careful collecting the anamnesis. As it was specified, And. the m can begin with manifestations of an acute congestive left ventricular failure (cardiac asthma, a fluid lungs), with cardiogenic shock, disturbances of a heart rhythm and conductivity. At development of these symptoms even if there is no retrosternal pain, the urgent electrocardiographic research, and also a research of activity of enzymes in blood — kreatinfosfokinaza, a lactate dehydrogenase and aminotransferases is necessary. Difficult and recognition And. m at atypical localization of pains (in the right half of a thorax, hands, a neck and a mandible, .mezhlopatochny space and epigastric area). In similar cases to assume an opportunity And. the m allows a serious general condition of the patient (weakness, an adynamia, arterial hypotension, heart and vascular failure, disturbances of a rhythm and conductivity of heart). As a rule, research ECG helps to finalize the diagnosis, a cut it is necessary to carry out at the slightest suspicion on existence And. m.
If diagnosis And. the m is established not during the first hours its development, about time of emergence And. m to a certain extent allow to judge carefully collected anamnesis, given an electrocardiography and a research of activity of enzymes of blood: activity of aminotransferases is normalized to 4 — 5th days of a disease, activity of a lactate dehydrogenase and kreatinfosfokinaza — to 10 — to the 14th day. Disturbances in the ratio of protein fractions of blood and acceleration of ROE can remain several weeks.
by the Main method of specification of the diagnosis And. the m, its localization, extensiveness, and also identification of a number of complications (an aneurysm of heart, disturbance of a cordial rhythm and conductivity) is an electrocardiographic research. ECGs register in 12 assignments: three standard, three strengthened from extremities and six single-pole chest according to F. N. Wilson; in certain cases resort to use of additional assignments on W. Nehb, across Gurevich, etc. (see. Elektrokardiografiya ), allowing to obtain additional information at so-called elektrokardiografichesk negative And. m the Vektorkardiografichesky research (see. Vektorkardiografiya ) in diagnosis And. the m has no essential advantages before the usual scalar ECG.
Leading electrocardiographic sign of emergence macrofocal And. the m is registration of so-called monophase curve (tab. 1). If on the usual ECG two positive deviations (a tooth In and a tooth of) divided by the isoelectric line are accurately fixed, then in a monophase curve it is not possible to differentiate these elements strictly: the S T segment rises over the isoelectric line and merges a monophase curve it is possible with T. Zaregistrirovat's tooth not in all cases And. m. So, at a zadnebazalny heart attack in usually applied assignments it can be absent. To rum of that, at signs of monostaging quickly (during the days and even hours) decrease; they are more weakly expressed in the assignments reflecting capacities of the sites of a myocardium remote from a zone of a necrosis.
For transmural And. m disappearance of a tooth of R is characteristic. Instead of the normal QRS complex the QS complex expressed by one deep and wide negative tooth forms patol. If in the field of scarring there is no functioning muscle fiber left, patol, the QS complex remains also after the full organization of the center of a necrosis.
Characteristic sign intramural And. m — emergence patol, a tooth of Q at. preservation of a tooth of R though amplitude of the last can be reduced. Patol, consider a tooth of Q if it arises in those assignments where is absent normal if its amplitude is more, than registered usually in this assignment, and duration is equal to 40 ms or more. Most often at acute And. m at the same time are available other electrocardiographic signs of damage of a myocardium, napr, disturbances of a rhythm.
Injury of a myocardium is expressed on an ECG by raising of a segment of ST in assignments in which registration is made in the point turned to the depolarized or not completely polarized area, and decrease in a segment of ST in positionally opposite assignments. It is considered that an ECG at And. the m allows to reveal three zones. Changes of the QRS complex are connected with a zone of a necrosis; shift of a segment of ST — with a zone of damage, or a periinfarktny zone, and, at last, inversion of a tooth of T — with a peripheral zone of ischemia. Such division is to a certain extent conditional. So, development of granulyatsionny fabric usually is followed by formation of a negative «coronary» tooth of T.
At melkoochagovy defeat, as a rule, there is no main electrocardiographic sign of destruction of fabric — a negative initial deviation in a ventricular complex (patol, a tooth of Q or the QS complex). Only occasionally are registered a superficial tooth of Q. Changes of an ECG are limited to the small shift of a segment of ST up (at subepicardial) or down (at subendocardial And. m) and inversion of a tooth of T (fig. 10 — 12 and tsvetn. fig. C.).
Electrocardiographic diagnosis repeated is extremely difficult And. m. Again arisen changes can level completely signs postponed earlier And. m and, on the contrary, quite often mask old changes. Difficulties of electrocardiographic diagnosis are especially considerable at emergence of fresh focal changes in area, opposite to a hem. Interpretation of an ECG at simultaneous development of necrotic defeats on opposite walls of a left ventricle is not less difficult. In such cases can promote the diagnosis the ECG loudspeaker in the course of treatment.
Quite often And. the m should be differentiated, according to an ECG, with blockade of the left leg of a ventriculonector. At the same time it must be kept in mind, as. the m can develop against the background of blockade of a leg or lead to its emergence. In similar cases take into account existence of dynamic changes of an ECG at And. m, emergence of teeth of Q in assignments in which they are not registered at uncomplicated blockade of a leg, increase in a tooth of IS at blockade of a leg without heart attack and decrease it at a combination of blockade and a heart attack. In all similar cases careful comparison of electrocardiographic data with data of clinic and laboratory methods of a research is necessary. The changes of an ECG characteristic for And. m, undergo characteristic dynamics in time (tab. 1).
Because of a forced immovability of the patient at early stages And. m rentgenol, diagnostic methods get practical value only by then when the patient is rather activated and can face the screen, i.e. by the end 3 — 4th week at macrofocal And. m. The separate observations made at early stages of a disease show that rentgenol, the picture almost does not differ at this time from observed in later terms. The only sign characteristic for And. the m in the acute period, is the change of a shape of heart connected with decrease in its tone: heart widely prilezhit to a diaphragm, its contours come nearer to rectilinear (the «settled» heart); in further heart gets a usual form.
The greatest diagnostic value in a subacute stage And. m have rentgenokimografiya (see) and elektrokimografiya (see). The usual roentgenoscopy allows to reveal in certain cases on a contour of a shadow of a left ventricle of heart in a straight line or in the left slanting projection sites hypo - or akineziya, the respective areas of damage of a myocardium. More patognomonichn paradoxical pulsation: protrusion of the site of the contour of a shadow corresponding to a zone of defeat of a left ventricle in the period of a systole. Emergence of this protrusion is connected with loss of sokratitelny properties of a myocardium in a zone of a necrosis owing to what increase in intracavitary pressure during a systole leads to stretching of the struck area. Paradoxical pulsation, or systolic expansion, maybe partial: in this case the specified symptom is observed only at the beginning of a systole. At the expressed paradoxical pulsation the roentgenoscopy finds simultaneous shift in the lateral directions of contours of an aorta and an affected area of a ventricle (contours of an aorta and ventricles are normal move in opposite directions); at partial systolic expansion the contour of an affected area makes the double movement during each systole.
The paradoxical pulsation especially clearly comes to light at rentgeno-and an elektrokimografichesky research. If in usual conditions synchronously registered teeth rentgeno-and elektrokimogrammma of an aorta and a left ventricle have absolutely various, close to mirror the form, then at a paradoxical pulsation the teeth reflecting the movement of a contour of an aorta and a contour of an affected area of a left ventricle become almost identical. Rentgeno-and an elektrokimografiya promote also identification of sites hypo - and akineziya of a myocardium which, unlike a paradoxical pulsation, meet not only at And. m, but also at many other heart diseases. Rentgenol, data promote recognition And. m, localized in a front wall, a top and a sidewall of a left ventricle; at localization And. m in a back wall rentgenol. research maloinformativno. Rentgenol, signs And. the m manages to be revealed approximately at 75% of patients in a subacute stage of a disease. Further they can decrease and even to disappear.
Rentgenol, methods can give essential help in diagnosis of a so-called elektrokardiograficheska negative And. m. These methods are important in diagnosis of the pericardis complicating a current And. m.
For the solution of a question of a possibility of surgical treatment in the acute period And. the m (aortocoronary shunting), and also for specification of localization of blood clot for the purpose of attempt of its dissolution by local introduction of fibrinolitic means carry sometimes out the selection coronary angiography (see). Blood clot in a coronal artery is distinguished on a koronarogramma on break of a shadow of the contrasted artery.
Attempts of visualization of the center of damage of a myocardium and by means of radio-gramophones, methods are made: scannings of heart, a stsintigrafiya with a number of labeled substances.
The differential diagnosis
two types of mistakes in diagnosis Meet And. m: or And. m mistakenly regard as other disease, or, on the contrary, accept this or that disease for And. m. Mistakes arise at more often atypically proceeding And. m, including at its bezbolevy current. E.g., an acute left ventricular failure at And. m if it proceeds against the background of the raised ABP, quite often regard as display of hypertensive crisis; cardiogenic shock at bezbolevy And. the m when it is followed by a soporous state, can be the cause of the wrong diagnosis nevrol, a coma.
Differential diagnosis is very difficult And. m with a pain syndrome of atypical localization. The most often gastralgichesky form I. m, especially if it is followed by vomiting, take for food poisoning, a ruptured ulcer of a stomach, acute cholecystitis. In similar cases the wrong tactics of the doctor can be the cause of death of a disease. More rare (e.g., at right-hand localization of pains) to the patient I. m make the diagnosis of pneumonia or pleurisy. Localization of pain in those areas where it usually irradiates, can lead to the wrong diagnosis of a plexitis or osteochondrosis with a radicular syndrome. Unlike these diseases, And. the m practically is always followed by symptoms of the general character (weakness, an adynamia, tachycardia, changes of the ABP). The diagnosis of neuralgia is helped by the analysis of nature of pains (pains long and are often localized on the course of intercostal nerves), identification of painful points at a palpation of intercostal nerves and a backbone, efficiency of usual analgetics (analginum, pyramidon), lack of changes on an ECG and with peripheral blood.
Sometimes wrong diagnosis of PI. the m or stenocardias can be delivered to the patient with shingles (see. Herpes ), especially if at survey of the patient the rash of bubbles on the hyperemic basis on the course of an intercostal nerve is not found yet. Specifies the diagnosis in a preexanthematous stage lack of changes on an ECG, registration a cut in such cases is necessary.
Differentiation of acute coronary insufficiency is very difficult and embolisms of a pulmonary artery (see). Thorax pain at an embolism of branches of a pulmonary trunk usually has no retrosternal localization, however the reflex collapse is quite often observed. Changes of an ECG differ from arising at And. m though in some cases the electrocardiographic picture reminds a picture of a heart attack of a back wall of a left ventricle, differing from it in signs of an overload of the right departments of heart. Though non-constant, a symptom of an embolism the pneumorrhagia serves important. The embolism arises in the postoperative period, after the delivery, at patients with heart diseases, thrombophlebitis and especially a phlebothrombosis more often. At a massive embolism acute right ventricular insufficiency often develops, edges belongs to rare complications And. m. In some cases specification of the diagnosis is promoted rentgenol, by a research. Also features of change of a fermental range of a lactate dehydrogenase (increase in the second peak) have diagnostic value. It is necessary to remember a possibility of a combination of an embolism of branches of a pulmonary trunk with And. m.
In differential diagnosis with the stratifying aortic aneurysm (see. stratifying ) also datas of laboratory (at the stratifying aneurism there are no changes of an ECG and activity of enzymes of blood serum) have the leading value electrocardiographic.
Sometimes And. the m should be differentiated with acute pericardis (see). The acute pericardis more often happens a complication hron, diseases (rheumatism, tuberculosis, uraemia) though so-called primary (virus) pericardis occasionally meets. The pericardial rub usually appears from the first hours of this disease and remains longer, than at And. m. This noise amplifies during the pressing by a stethoscope on a chest wall. Activity of a kreatinfosfokinaza, lactate dehydrogenase and aminotransferases is not increased. Changes of an ECG if they come to light, have both similarity and distinctions with observed at And. the m therefore assessment the ECG loudspeakers is important, edges at these diseases significantly differs, and comparison of changes of an ECG to clinical displays of a disease.
Picture acute And. the m can remind spontaneous pheumothorax (see), especially left-side. Pain at pheumothorax can be so intensive that there is shock. The diagnosis of spontaneous pheumothorax is so simple that if the patient is investigated rather carefully, it is difficult not to distinguish this state (a tympanites over the corresponding half of a thorax). Are absent characteristic for And. m of change of blood, activity of enzymes, ECG.
The question of the differential diagnosis is represented especially difficult between And. in m and so-called nekoronarogenny necroses of a myocardium. The last can be caused by a significant amount of factors since dystrophy of a myocardium and its inflammatory defeats of any origin can be transformed to a necrosis. The necrosis such, as a rule, is melkoochagovy and develops gradually.
Emergence of harbingers And. the m demands urgent hospitalization of the patient since adequate treatment in a prodromal stage allows to prevent sometimes development And. m. Hospitalization of patients And. for m from the first hours of a disease it is obligatory; it is made whenever possible in specialized kardi-ol. or the therapeutic departments equipped with the necessary equipment and provided with highly qualified personnel.
Organization of treatment of patients And. by m it is based on four philosophy. 1. The organization of the specialized ambulance crews equipped with special transport, the equipment and completed with well prepared shots. A task of these crews — rendering on site the highly skilled help to the patient I. the m and its transportation in to lay down. establishment. 2. Perhaps early hospitalization of patients. 3. Creation of specialized chambers for overseeing by a condition of patients And. m and their treatments (so-called chamber of intensive observation). These chambers shall be provided with a highly qualified medical personnel and are equipped with monitor systems for constant control of an ECG of sick and vital parameters (see. Monitor observation ), the equipment for artificial ventilation of the lungs, defibrillators, electrocardiostimulators. The term of stay of the patient in such chamber depends on weight of his state and usually fluctuates from 3 to 5 days 4. Creation of system of recovery treatment (rehabilitation). The solution of the listed organizational issues allows to lower a lethality in extra hospital conditions, in particular during the transportation, and in a hospital. So, in scientific research institute of cardiology of A. L. Myasnikov of the USSR Academy of Medical Sciences improvement of the organization of the help to patients I. allowed m from 1963 for 1975 to lower a lethality from 26,4 to 16,2%.
Treatment of a pain syndrome — the first task of the doctor at a bed patient I. m since pain can cause complications, up to development of reflex cardiogenic shock. It does not concern only to patients with bezbolevy forms I. m, and also to those cases when the doctor comes to the patient after the termination of an anginous attack. Quite often for stopping of pain at acute And. m it is necessary to resort to repeated, including intravenous, to injections of drugs. For the prevention of a number of side effects of the drugs of group of opium connected with excitement of a vagus nerve them usually enter 0,1% of solution of atropine in combination with 0,5 ml, and at threat of oppression of a respiratory center combine 2 — 3 ml of Cordiaminum with introduction.
A merit of the Soviet cardiology is implementation in practice of therapy of a pain syndrome at And. m of an anesthesia nitrous oxide with oxygen. However such anesthesia allows to achieve bystry and full anesthesia only in half of cases. Apply to increase in its efficiency as exponential means small doses of morphine, Omnoponum (1 ml of 1% of solution) or Promedolum (1 ml of 2% of solution). Use for potentiation of an anesthesia of aminazine (1 ml of 2,5% of solution intramusculary; not to enter intravenously!) it is undesirable since it causes tachycardia and decrease in the ABP. These shortcomings the haloperidol is deprived (1 ml of 0,5% of solution intramusculary). Effect of the narcotic, anesthetizing substances pi of nitrous oxide is exponentiated by also antihistaminic drugs — Dimedrol (1 ml of 1% of solution intramusculary or intravenously) and especially Pipolphenum or isopromethazine (1 — 2 ml of 2,5% of solution intramusculary or 1 ml intravenously).
One of the most effective methods of anesthesia — neyroleptanalgeziya (see), i.e. combination antipsychotic and anesthetics. The combination of a degidrobenzperidol, or Droperidolum (2,5 — 5,0 mg intramusculary) with an analgetic fentanyl is most often used (0,05 — 0,1 mg intramusculary or kapelno intravenously). The dosage of each of components depends on a number of factors: Droperidolum removes psychomotor excitement, feeling of tension, alarm; fentanyl on the action is close to morphine, however side effects at its use are observed less often and are less expressed.
Treatment by fibrinolitic and anticoagulating drugs is directed first of all to the prevention of education and growth of intra coronary blood clots, but it matters also for the prevention of tromboembolic episodes. Also spasmolytic and analgetic properties are inherent in heparin.
In the absence of contraindications to use anticoagulants (see) purpose of heparin and fibrinolitic means shall be earlier. Complex anticoagulative therapy in the most acute and acute periods And. the m includes intravenous drop administration of 15 000 PIECES of heparin in 250 ml of isotonic solution of sodium chloride with addition 60 000 — 90 000 PIECES of fibrinolysin or 700 000 — 1 000 000 PIECES of Streptoliasum (Streptasums). This mix is entered within 6 — 10 hour. Further the dose of heparin is determined by a blood clotting time, a cut in the first two days of treatment there should not be less than 15 — 20 min. In the next 5 — 7 days intravenously or intramusculary enter heparin in the doses sufficient for maintenance of a blood clotting time at the level of 10 — 20 min. A day before alleged cancellation of heparin appoint anticoagulants of indirect action (neodicoumarin, or Pelentanum, Phenilinum, Syncumarum, etc.). At selection of doses of these drugs are guided by achievement of an optimum prothrombin ratio (40 — 50%). In the USSR the method of direct introduction of fibrinolitic means to coronary arteries of heart during the first hours is developed And. m.
At complex therapy heparin and fibrinolitic drugs note more favorable current And. m. The lethality in group of the patients receiving such complex therapy is almost twice less, than in control group, and the frequency of tromboembolic episodes decreases from 15 — 20 to 3 — 6%.
The treatment directed to reduction a feather of an infarctive zone. For recovery of function of cells of a periinfarktny zone and restriction of the sizes of a necrosis numerous medicamentous means and methods of treatment are offered. Efficiency of the most part of these means and methods still demands confirmation though the role in this respect of fibrinolitic and anticoagulating therapy is estimated as positive.
Expediency of use of the drugs expanding coronary vessels of heart in an acute stage And. the m is called in question because of the assumption that these drugs, dilatiruya equally all arteries of heart, lead to deterioration in blood supply in a zone of the corked artery (a syndrome of «burglarizing»). Nevertheless at treatment And. m try to apply the same pharmaceuticals, as at treatment stenocardias (see). Searches and other substances promoting preservation of viability of the cells of a periinfarktny zone in particular improving transport of oxygen and nutritious substances from vessels in cells of a myocardium are conducted (e.g., hyaluronidase). Use of the drugs reducing the need of a myocardium for oxygen (blockers of beta and adrenergic receptors of a myocardium) is limited because of their possible negative inotropic effect. There are messages on beneficial effect on survival of cells of a periinfarktny zone of counterpulsation (see. Artificial circulatory support ) and hyperbaric oxygenation (see). In specialized institutions according to strictly limited indications during the first hours diseases apply an operative measure — aortocoronary shunting (see. Arterialization of a myocardium , Myocardial infarction, surgical treatment ). The method did not gain the general recognition.
For improvement of a trophicity of a myocardium use a significant amount of pharmaceuticals (vitamins, cocarboxylase, ATP, anabolic steroids, etc.). However accurate indications to use of these drugs at And. m are not developed yet. Believe that some of them accelerate formation of a hem (orotat potassium, inozy-f, etc.). Expediency of use of these means is doubtful and demands a further research.
Treatment of cardiogenic shock. Reflex shock, as a rule, is quickly stopped at effective treatment of a pain syndrome. At preservation of arterial hypotension intravenously enter a phenylephine hydrochloride (0,1 — 0,5 ml of 1% of solution in isotonic solution of sodium chloride), noradrenaline (1 ml of 0,2% of solution into 200 — 250 ml of 5% of solution of glucose — intravenously kapelno).
At true cardiogenic shock apply the same pressor amines, and also cardiac glycosides (strophanthin, Korglykonum), plasma substitutes (reopoliglyukin, a high-molecular dextran, etc.), corticosteroid hormones (sometimes in very high doses), however at true, especially areactive shock, all these measures are usually ineffective. Surgical methods of treatment are developed: an artificial circulatory support in the form of venoarterialny forcing of oxygenic blood or counterpulsation — artificial increase in blood pressure, synchronous with a diastole, in an aorta by means of a special barrel (see. Artificial circulatory support ).
Treatment of aritmogenny shock comes down to recovery of the broken heart rhythm or conductivity.
Treatment of disturbances of a rhythm and conductivity. At ventricular premature ventricular contraction and ventricular tachycardia most often apply lidocaine — 100 — 150 mg of drug intravenously struyno then immediately pass to drop injection with a speed of 1 — 2 mg of 1 min. Drug is terminated almost immediately after the end of its introduction. It eliminirutsya more slowly novokainamid which it is necessary to apply intramusculary (5 — 10 ml of 10% of solution) or orally not less than 4 times a day (on 0,75 — 1,0 g on reception) since at intravenous administration of this drug the collapse quite often develops. At purpose of a novokainamid rather frequent control of an ECG in connection with the oppressing influence of drug on atrioventricular and intra ventricular conductivity is necessary. Blockers of beta and adrenergic receptors of a myocardium, napr, anaprilin (Obsidanum), appoint in small doses (0,01 — 0,02 g 4 times a day) and carefully in connection with their cardiodepressive, hypotensive action and negative influence on conductivity. In some cases there is effective dipheninum (diphenylhydantoin) in a daily dose of 0,1 — 0,3 g. In certain cases ventricular disturbances of a rhythm are stopped by use of Pananginum and the so-called polarizing mixes containing insulin (8 — 20 PIECES), potassium chloride (2 — 4 g) and glucose (200 — 300 ml of 10% of solution) in different proportions.
At a supraventricular Bouveret's disease the good antiarrhythmic effect can give bystry intravenous administration of 10 mg of Isoptinum. Is less effective novokainamid, and lidocaine at this disturbance of a rhythm does not render to lay down. actions. A ciliary arrhythmia and an atrial flutter at patients And. m usually demand use of cardiac glycosides.
In case of inefficiency of medicamentous cure for supraventricular and especially ventricular tachycardia, and also at an atrial flutter it is carried out countershock (see), and sometimes urezhayushchy cardiac activation in various forms — stimulation by the pair or combined impulses, etc. (see. Cardiostimulation ). The only method of controlling with trembling and ventricular fibrillation — emergency electric defibrillation (see).
Treatment of disturbances of atrioventricular conductivity begin with introduction 0,5 — 1,0 ml of 0,1% of solution of atropine subcutaneously, intramusculary or intravenously. In some cases under the influence of atropine atrioventricular conductivity improves. Use of other means — glikokortikoidny hormones in high doses (100 — 200 mg in recalculation on Prednisolonum), the drugs removing potassium (hypothiazid), an izopropilnoradrenalin (Isadrinum, Isuprelum) usually ineffectively is also often limited in connection with a possibility of undesirable action of these drugs.
At a total atrioventricular block at patients And. m electric cardiac activation by means of the bipolar catheter electrode entered under rentgenol or electrocardiographic control through a subclavial, kubitalny or femoral vein in a right ventricle is most efficient. Sometimes the electrode is entered into heart preventively at threat of development of a total block (the progressing atrioventricular block, development of the bifastsikulyarny block).
If total cross block remains more than 3 weeks, resort to implantation of a constant stimulator.
Treatment of an acute heart failure, the shown cardiac asthma, a fluid lungs, begin with introduction 1 — 2 ml of 1% of solution of morphine or Promedolum (1 ml of 2% of solution), or fentanyl in combination with Droperidolum — intramusculary or slowly intravenously on isotonic solution of sodium chloride. Most of authors indicates uses of cardiac glycosides of bystry action (strophanthin, Korglykonum) the need though there is an opinion that introduction of cardiotonic means by the patient I. to m with a fluid lungs it is not shown. This point of view is based on the assumption that glycosides strengthen activity of the unimpaired right ventricle to a large extent, than the struck left; as a result pressure in system of a pulmonary trunk increases. Klien, experience proves groundlessness of such assumption. Apply drop introduction to a vein of strophanthin (0,3 — 0,5 ml of 0,05% of solution) or Korglykonum (0,5 — 1,0 ml of 0,06% of solution) in 200 — 300 ml of isotonic solution of sodium chloride or the polarizing mix. At a fluid lungs of 0,5 ml of Korglykonum previously enter into a vein slowly struyno. Apply also diuretics — furosemide of 40 — 80 mg intravenously, osmotic diuretics — a mannitol (30 g in 120 — 140 ml of 5% of solution of glucose, enter into a vein with a speed of 15 ml/min.), urea (30% the solution prepared in 10% solution of glucose; enter into a vein kapelno with a speed of 60 — 120 thaws of 1 min.). A single dose of a mannitol and urea select proceeding from a ratio 1 — 1,5 g of nonvolatile solid on 1 kg of weight of the patient. In edematous liquid apply inhalation of vapors of 70 — 80% of solution of alcohol which is filled in instead of water in a humidifier of the oxygen device, and also an aerosol of an antifomsilan (see to defoaming. Fluid lungs, treatment ).
Treatment of mental disturbances. For fight against psychomotor excitement in the acute period And. m use diazepam in injections or neuroleptics — Droperidolum, a haloperidol intramusculary. The patient with the expressed concern, depression appoint small tranquilizers in widely varying doses (Seduxenum on 5 — 50 mg a day, Elenium of 10 — 100 mg a day, etc.), sometimes in combination with neuroleptics. Because effect of antidepressants (amitriptyline, Azaphenum) is shown slowly, in the acute period And. m do not appoint these drugs. In the subacute and postinfarction periods if necessary therapy is carried out: psychotropic drugs of all groups (neuroleptics, small tranquilizers, antidepressants) in combination with rational psychotherapy (direct and indirect suggestion, explanatory conversations, auto-training etc.).
Restoration of vital activity can be reached if resuscitation is begun not later than through 2 — 3 think. after approach a wedge, death. A proximate cause of death at And. the m usually is fibrillation of ventricles or an asystolia. If a wedge, death came out of a hospital and the person giving help has no make-shifts, resuscitation begin with indirect cardiac massage (see) and an artificial respiration of companies in a mouth or a mouth in Nov (see. Artificial respiration, artificial ventilation of the lungs ). These actions allow to bring in some cases the patient out of a state a wedge, death or not to allow development biol, death before arrival of specialized emergency medical service.
In the presence of the special equipment if there is no electrocardiographic information at the moment a wedge, death, resuscitation are begun with electric cardiac defibrillation (see. Defibrillation ). At inefficiency of the first defibrillating category immediately begin an indirect cardiac massage and an artificial respiration of companies in a mouth (a mouth in Nov). At this time adjust registration of an ECG and hardware artificial ventilation of the lungs. If on an ECG fibrillation of ventricles is registered, carry out a repeated defibrillation by categories of more and more high tension (to 7 kV).
At an asystolia sometimes it is possible to recover cordial activity by sharp blow of a fist from distance of 20 — 25 cm on the bottom of a breast of reanimated. For increase in efficiency of resuscitation at an asystolia enter adrenaline (1 ml of 0,1% of solution) and calcium chloride (2 — 5 ml of 10% of solution) into a cardial cavity. Sometimes there is successful electric cardiac activation, to-ruyu carry out by means of the electrode entered through a vein into a cavity of a right ventricle or by means of the special electrode needle entered through a chest wall into a myocardium.
Holding resuscitation events, korrigirut disturbances of acid-base equilibrium intravenous administration of 150 — 200 ml of freshly cooked 5% of solution of hydrosodium carbonate.
Resuscitation actions continue before recovery of blood circulation and breath or before emergence of reliable signs biol, death.
From the first days of a disease the events directed to the prevention possible and treatment of the arisen complications and also on mobilization of compensatory opportunities of an organism are held. It is recommended to adhere to the following terms of stay of patients of II. m in a hospital: at melkoochagovy And. m without essential complications — 20 — 25 days, with complications — 25 — 35 days; at uncomplicated intramural And. m — 25 — 35 days, with complications — 40 — 45 days; at transmural And. m without essential complications — 40 — 50 days, with complications — more than 50 days. Recovery therapy includes use not only medicamentous drugs, but also LFK, psycho - and physiotherapeutic, a dignity. - hens. and other influences. Is important adequate to a state physical. activity of patients And. the m, edges is defined individually for each patient. Terms of activation of patients are presented in table 2.
Diet during the first hours and days acute And. the m when appetite of the patient is sharply reduced, is limited to the fruit juice, mineral water which are easily acquired and high-calorific products. Since 3 — the 4th day the diet is gradually expanded at the expense of products from the wiped meat, cottage cheese and other lactic products by 7th day of a disease of the patient it was transferred to a diet No. 10 (see. Clinical nutrition ).
Medical physical culture — one of methods in system of recovery therapy of patients And. m. It promotes stimulation of auxiliary, noncardiac factors of blood circulation that promotes simplification of cardiac performance, a training of sokratitelny function of the weakened cardiac muscle, development of more perfect adaptation of coronary circulation to exchange requirements of a myocardium. LFK promotes also moderate activation of breath, to increase in a tone of a nervous system, improvement of functions went. - kish. a path that plays a role and in prevention of hypostatic pneumonia and other possible undesirable effects of a high bed rest. During the carrying out LFK the principles of a shchazheniye of a myocardium shall not be broken and electrocardiographic control is obligatory.
Indications by the beginning of use of LFK are satisfactory condition of the patient, lack of an asthma at rest, the termination of severe and frequent pains in heart, decrease in elevated temperature of a body, moderate ROE, lack of a tendency to a lowering of arterial pressure, absence on an ECG of the data indicating negative dynamics of process.
LFK at And. m — a component of the general motive regime of the patient; she is carried out to lay down in shape. gymnastics. Expansion of the motive mode and increase in intensity applied physical. exercises are carried out strictly individually, taking into account age, sex of the patient, extensiveness of a heart attack, dynamics of a disease, a physical activity of the patient in the past. The movements of the patient were more for a long time and more sharply limited, the expansion of the motive mode shall be carried out more slowly.
Occupations of LFK can be begun at And. moderately severe m on 2 — the 3rd day, at heavier — on 3 — the 7th and later days of a disease; in the beginning they are carried out individually to time before lunchtime when the patient is not tired. Exercises to lay down. gymnastics shall be simple, be made rhythmically, smoothly, without breakthroughs. Each exercise should be alternated to respiratory. As exercises of LFK apply the patient in the conditions of a bed rest in the beginning, it is recommended to lie periodically with the legs bent in knees that provides the best inflow of blood to heart and gives the feeling of a support necessary at the subsequent rise in vertical position. For improvement of peripheric circulation the movements in distal departments of extremities are used. For strengthening of a venous blood-groove the free and rhythmical strictly dosed movements in large joints of extremities, are applied by hl. obr. lower, alternating with breathing exercises and pauses of rest. Exercises in relaxation of muscles are widely used that promotes improvement of peripheric circulation. For the prevention of weakness of skeletal muscles and the copular device developing at a long bed rest apply exercises to strengthening of the arch of foot, muscles of the lower extremities and spins.
For patients And. it is important to m to master the most facilitated options of raising of a basin, turns sideways, transition to a sitting position and standing. At first carries out these movements of the patient by means of the methodologist and the servicing medical staff, and then independently, but without natuzhivaniya and breath holdings. During training of the patient for transition to a standing position with problems of LFK are recovery of adaptation of cardiovascular system to physical. to loading upon transition to a sitting position, and then costing. For a training of a vestibular mechanism gradually enter the movements into occupations of LFK the head at first in a prone position, and then sitting and standing.
Indicators of proper response of cardiovascular system to loading are increase of pulse at height of loading and the first 3 min. after it to 20 ud. in 1 min., breath — to 6 — 8 in 1 min., increase in systolic pressure on 20 — 30 mm of mercury. and diastolic — on 10 mm of mercury. or an urezheniye of pulse to 10 ud. in 1 min., decrease in the ABP no more than on 10 mm of mercury. At emergence of adverse reactions in response to the loadings offered for the first time, depending on expressiveness of negative indicators, exercises carry out at slower rate or temporarily stop.
In the recovery period And. the m expansion of the motive mode is produced due to increase in duration of walking and bigger volume of exercises, the gradual training in walking on a ladder is especially important. If the patient after a hospital is directed to an out-patient and polyclinic aftercare, then in the first 2 — 3 days of stay in house conditions, considering raised physical. and mental loading, it shall limit a physical activity in comparison with reached in a hospital. If the condition of the patient remains steadily satisfactory, it resumes a training in walking on a ladder again, increases distance in walking on the level ground. Stay on air where walking shall alternate with rest is allowed to it. After the patient begins to visit policlinic, the attending physician sends it to an office of LFK of policlinic or a medical and sports clinic where studies are continued to lay down. the gymnastics also gives further consultations on the organization of the motive mode.
If patient from to lay down. institutions transfer to an aftercare in a dignity. - hens. establishment (specialized kardiol. sanatoria of the same climatic zone, in a cut of the patient lives constantly), 3 — 4 days it adhere to the mode of activity ordered at the end of stay in-tse. In subsequent 2 once a day within 20 — 40 min. the patient is engaged in a complex to lay down. gymnastics; besides, to it 2 times a day the dosed walking are appointed (see. Terrainkur ): in the first 3 — 4 days 10 — 15 min., further 30 — 60 min., from the 3rd week the speed of walking increases. At an uncomplicated current And. the m at the end of stay in sanatorium of the patient in two steps makes a way of 5 — 8 km with speed of 2 — 4 km/h. Expansion of the mode of a physical activity is carried out under control of pulse, the ABP and an ECG according to the program, the approximate statement a cut is presented in table 3.
Treatment at repeated And. the m essentially does not differ from treatment at the first And. the m is also defined by the general condition of the patient, the anamnesis (a possibility of use of anticoagulants), existence and character of complications. The same treats also the mode, actions for rehabilitation and LFK. If repeated And. the m occurred in several days or weeks after the first, terms of activation of the patient are respectively extended and counted from the moment of development repeated And. m
Despite considerable progress in treatment And. m it remains to one of the most serious cardiovascular illness. A lethality in the first 28 days of a disease, according to N. A. Masur, among the diseased And. the m of residents of Moscow makes 35,1%. Almost at a half of the dead death comes in the first hour of a disease and at 78% — in the first days from the beginning of a disease. More than 60% of all deaths fall on the first 6 hours from the moment of emergence And. m. Further the lethality sharply decreases, and after 5 days from the beginning And. m perish from late complications only certain patients. In most cases (apprx. 70%) patients perish out of a hospital; the intrahospital lethality makes about 20%. It is connected with the fact that the most part of heavy complications And. m (cardiogenic shock, disturbances of a heart rhythm and conductivity etc.) arises during the first hours and days And. m. During this period death from fibrillation of ventricles or a cardiorrhesis is most probable. Therefore the forecast of a disease depends on that, the patient how fast gets to a hospital, under constant medical observation. According to N. V. Kalinina, etc., a lethality of the patients who transferred the first And. the m and written out from a hospital, makes 11,0% within the first year. Repeated And. m, it is frequent from the death, it is observed within the first year after the first And. m at 13 — 17% of patients.
According to scientific research institute of cardiology of A. L. Myasnikov of the USSR Academy of Medical Sciences, thanks to implementation of new methods of treatment and rehabilitation of patients And. m in 1970 — 1975 of 80% of the patients who are written out from hospitals after the first And. m, returned to former work. The reason of disability of the patients who transferred And. the m, most often serves heart failure, heavy stenocardia and disturbances of a heart rhythm are slightly more rare.
Forecast And. the m in many respects depends on extensiveness of the site of damage of heart, though not completely is defined by this factor. Krupnoochagvy, especially transmural And. m, are the reason of the most part of deaths and invalidism of patients. At perforation of an interventricular partition and at a rupture of a papillary muscle the forecast is adverse: life expectancy of patients usually does not exceed 10/Russian cabbage soup. If defect of a partition is small, patients sometimes live months and even years. At melkoochagovy And. m the lethality is insignificant. Use of modern methods of emergency treatment and rehabilitation considerably improves the forecast.
Prevention And. the m consists of system of the actions directed to the prevention of atherosclerosis and an exception, whenever possible, of risk factors of a disease And. m.
Primary prevention is based on broad promotion of medical recommendations about the prevention of coronary heart disease, and also on mass inspections of the population for identification of the contingent subject to influence of risk factors for the purpose of their possible elimination. Object of secondary prevention are the persons who transferred And. m and the medical examinations which are subject for this reason.
The first-priority attention is paid to elimination of such risk factors as arterial hypertension, a lipidemia (hypercholesterolemia), smoking of tobacco, obesity, small physical. activity. To persons with coronary heart disease the active treatment directed to the prevention of attacks of stenocardia and to development of collaterals in vessels of a myocardium is carried out, besides. Persons with arterial hypertension are subject to the dispensary account and observation. Depending on the nature of hypertensia the pathogenetic therapy providing normal or close to normal (achievable for this patient) the ABP level and the excluding possibility of hypertensive crises is carried out. The patient with an idiopathic hypertensia for this purpose appoints hypotensive pharmaceuticals in the combinations dictated by a stage of a disease and identity of the patient (see. Idiopathic hypertensia, treatment ). In the presence of a hypercholesterolemia fats of animal origin in a diet shall be, according to most of authors, are considerably replaced with seed fats. Most effectively reduce the content of cholesterol in blood serum polyunsaturated fats of a plant origin. Content in blood serum of triglycerides is in direct dependence on quantity in food of carbohydrates. Therefore at identification of a triglitseridemiya recommend to adhere to the diet poor in carbohydrates. For a korrigirovaniye of lipidic composition of blood, except various diets, the large number vitamin and medicines, including ascorbic to - that, the estrogen, thyroxine, means influencing absorption and metabolism of cholesterol is offered (Clofibratum, Atheromidum, holesteramin). Attempts of operational treatment of patients with a steady lipidemia (in particular with a gipertriglitseridemiya) by creation of a bypass way in distal department of a jejunum are made. A role of the listed dietary, medicinal and surgical actions directed to a korrigirovaniye of the broken lipidic exchange in prevention And. by m it is still finally not found out in connection with difficulty of carrying out enough long, the standardized and representative researches. It is established that use of a number of the transferred funds (estrogen, thyroxine and their analogs) is in most cases inexpedient in connection with small effect or the expressed side effects. On the other hand, it is established that use of Clofibratum promotes decline in mortality of patients with stenocardia though this decrease does not depend on influence of drug on the level of a hypercholesterolemia. These data are provided in Oliver's works (M. by F. Oliver, 1971), the Dewar (N. A. Dewar, 1971, 1972), Is red also Kidera (L. R. Krasno, G. F. Kidera, 1972). Long purpose of anticoagulants for the purpose of secondary prevention And. the m, according to preliminary data, does not influence significantly probability of development repeated And. m.
An important role in primary prevention And. m play the actions directed to fight against smoking of tobacco. Effective fight against smoking among healthy faces — a complex problem, edges can be successfully solved only by joint efforts of workers of health care and not medical public (see. Tobacco ). Role physical. trainings in a complex of secondary prevention And. by m it is studied it is incomplete though its value for primary prevention is considered established.
The training increases overall performance of heart. Sufficient physical. activity reduces tendency to a thrombogenesis, to development of endogenous obesity. Promotion and active organization physical. the greatest value for persons, physical has cultures. which activity by the nature of the carried-out professional activity is insufficient. One of the most important components of prevention And. m — the qualified treatment of patients with stenocardia. Epid. inspection (I. K. Shkhvatsabaya, V. I. Metelitsa, 1977) among men of 50 — 59 years receiving Intensainum for the purpose of secondary prevention of coronary heart disease showed the vital forecast, more favorable at them, for 2 years of observation, than in control group. At unstable stenocardia, increase of its attacks hospitalization of the patient with purpose of a bed rest, the koronaroaktivny means and means reducing the need of a myocardium for oxygen is necessary. If necessary appoint the anesthetizing drugs and drugs. The effect of the drugs promoting reduction of bent of thrombocytes to aggregation is studied (acetilsalicylic to - that, Dipiridamolum).
Correctly organized physical. and mental rehabilitation allows to reduce considerably the frequency of development repeated And. m
Table 1. ELECTROCARDIOGRAPHIC CHANGES AT VARIOUS FORMS of CORONARY INSUFFICIENCY (The table is illustrated by color drawings [tsvetn. fig. C.])
Table 2. AVERAGE TERMS of VARIOUS STAGES of ACTIVATION of PATIENTS AT DIFFERENT FORMS AND the COURSE of the MYOCARDIAL INFARCTION
Table 3. The NATURE of USE of PHYSIOTHERAPY EXERCISES in the course of EXPANSION of the MOTIVE MODE AT PATIENTS with the MYOCARDIAL INFARCTION (According to V. S. Lebedeva, 197 4)
Bibliography: Vinogradov A. V., etc. Myocardial infarction, M., 1971, bibliogr.; Ganelina I. E., B r and to-kerv. N to an ivolperta. I. Acute period of a myocardial infarction, L., 1970, bibliogr.; A myocardial infarction, under the editorship of T. Sempl, the lane with English, M., 1976, bibliogr.; A myocardial infarction, under the editorship of 4 K. Fridberg, the lane with English, M., 1975; Lebedeva V. S. Medical physical culture at a myocardial infarction, L., 1974, bibliogr.; Blizzard V. I. and Masur of N. A. Epidemiologiya and prevention of coronary heart disease, M., 1976, bibliogr.; The multivolume guide to internal diseases, under the editorship of E. M. Tareeva, t. 2, page 327, M., 1964, bibliogr.; A. L. butchers, etc. Experimental necroses of a myocardium, M. 1963, bibliogr.; P at d and M. Ya. and 3 y with to about A. P. Myocardial infarction, M., 1977; Smolyannikov A. V. and Naddach and on T.A. Questions of pathological anatomy and pathogeny of coronary insufficiency, M., 1963, bibliogr.; they, To a morphogenesis of an atypical heart attack, Arkh. patol., t. 39, No. 7, page 14, 1977, bibliogr.; Strukov A. II., L at sh N and to about in E. T. and about the district and to K. A. Gistokhimiya of a myocardial infarction, M., 1967, bibliogr.; H and-z about in E. I. Sketches of urgent cardiology, M., 1973; Epidemiology of cardiovascular diseases, under the editorship of. I. K. Shkhvatsaby, etc., M., 1977; Acute myocardial infarction, ed. by D. G. Julian a. M. F. Oliver, Edinburgh — L., 1968; Aliumada G., Roberts R. a. 5 o b e 1 B. E. Evaluation of myocardial infarction with enzymatic indices, Progr, cardiovasc. Dis., v. 18, p. 405, 1976; Biochemistry and pharmacology of myocardial hypertrophy, hypoxia and infarction, ed. by P. Harris a. o., Baltimore, 1976; The early phase of acute myocardial infarction, Ann. intern. Med., v. 78, p. 918, 1973; H an u ss W. H. u. K o with h R. Koronar-sklerose und Herzinfarkt, Stuttgart, 1976; Innovations in the diagnosis and management of acute myocardial infarction, ed. by A. N. Brest, Philadelphia, 1976; Matz-d o r f f F. Herzinfarkt, Prevention und Rehabilitation, Miinchen, 1975, Bibliogr.; Myocardial infarction, ed. by E. Corday a. H. J. C. Swan, Baltimore, 1973; The myocardium, failure and infarction, ed. by E. Braunwald, N.Y. 1974, bibliogr.; Obrastzow Vv'. P. u. S t r a s-c h e s k o N. D. Zur Kenntnis der Thrombose der Koronararterien des Herzens, Z. klin. Med., Bd 71, S. 116, 1910; P a n t r i d g e I. F. a. o. The acute coronary attack, L., 1975; Protection of the ischemic myocardium, Circulation, Suppl. 1, v. 53, N 3, 1976; Russell R. O. a. RackleyC. E. Hemodynamic monitoring in a coronary intensive care unit, N. Y., 1974; Shock in myocardial infarction, ed. by R. M. Gunnar a. o., N. Y. — L., 1974; Symposium on the management of jeopardized ischemic myocardium, Amer. J. Cardiol., v. 37, p. 461, 1976; W i t A. L. a. Friedman P. L. Basis for ventricular arrhythmias accompanying myocardial infarction, Arch, intern. Med., v. 135, p. 459, 1975.
E. I. Chazov, V. A. Bogoslovsky; T. A. Naddachina, A. V. Smolyannikov (stalemate. An.).