Myocardial infarction etiology and pathogenesis. Myocardial infarction
Myocardial infarction (MI)- an acute disease caused by the occurrence of one or more foci of ischemic necrosis in the heart muscle due to absolute or relative insufficiency of coronary blood flow.
In men, MI is more common than in women, especially in young age groups. In the group of patients aged from 21 to 50 years, this ratio is 5:1, from 51 to 60 years - 2:1. In later age periods, this difference disappears due to an increase in the number of heart attacks in women. Recently, the incidence of myocardial infarction in young people (men under 40 years of age) has increased significantly.
Classification. MI is subdivided taking into account the size and location of necrosis and the nature of the disease.
Depending on the magnitude of necrosis, large-focal and small-focal myocardial infarction are distinguished.
Taking into account the prevalence of necrosis deep into the heart muscle, the following forms of MI are currently distinguished:
♦ transmural (includes both QS-, and Q-myocardial infarction,
formerly called "large focal");
♦ MI without a Q wave (changes affect only the segment ST and G wave;
formerly called "fine-focal") non-transmural; How
usually occurs subendocardial.
According to localization, they distinguish anterior, apical, lateral, septal
tal, inferior (diaphragmatic), posterior and inferiorbasal.
Combined lesions are possible.
These locations refer to the left ventricle as the one most often affected by MI. Right ventricular infarction is extremely rare.
Depending on the nature of the course, MI is distinguished with protracted
reading, recurrent myocardial infarction, repeated myocardial infarction.
A protracted course is characterized by a long (from several days to a week or more) period of painful attacks following one another, slow repair processes (protracted reverse development of changes in the ECG and resorption-necrotic syndrome).
Recurrent MI is a variant of the disease in which new areas of necrosis appear within 72 hours to 4 weeks after the development of MI, i.e. until the end of the main scarring processes (the appearance of new foci of necrosis during the first 72 hours is an expansion of the MI zone, and not its relapse).
The development of recurrent myocardial infarction is not associated with primary myocardial necrosis. Typically, recurrent MI occurs in the territories of other coronary arteries within a period usually exceeding 28 days from the onset of the previous infarction. These periods are established by the International Classification of Diseases, X Revision (previously this period was specified as 8 weeks).
Etiology. The main cause of MI is atherosclerosis of the coronary arteries, complicated by thrombosis or hemorrhage into an atherosclerotic plaque (in those who die from MI, atherosclerosis of the coronary arteries is detected in 90-95% of cases).
Recently, significant importance in the occurrence of MI has been attributed to functional disorders leading to spasm of the coronary arteries (not always pathologically altered) and an acute discrepancy between the volume of coronary blood flow and the myocardial needs for oxygen and nutrients.
Rarely, the causes of MI are embolism of the coronary arteries, their thrombosis during inflammatory lesions (thromboangiitis, rheumatic coronaryitis, etc.), compression of the mouth of the coronary arteries by dissecting aortic aneurysm, etc. They lead to the development of MI in 1% of cases and are not related to manifestations of ischemic heart disease.
Factors contributing to the occurrence of MI are:
1) insufficiency of collateral connections between coronary vessels
dami and disruption of their function;
2) strengthening of blood clot-forming properties;
3) increased myocardial oxygen demand;
4) disturbance of microcirculation in the myocardium.
Most often, MI is localized in the anterior wall of the left ventricle, i.e. in the blood supply basin most often affected by atherosclerosis
Etiology of myocardial infarction- multifactorial (in most cases, not one factor acts, but a combination of them). Risk factors for ischemic heart disease (there are more than 20): hypertension, hyperlipidemia, smoking, physical detraining, overweight, diabetes (in elderly diabetics against the background of myocardial infarction, arrhythmias appear 4 times more often and AHF and CABG 2 times more often), severe stress. Currently, we can list the circumstances with the maximum risk coefficients for IHD (in descending order): the presence of close relatives in whom IHD occurred before the age of 55, hypercholesterolemia more than 7 mmol/l, smoking more than 0.5 packs per day, physical inactivity, diabetes.
Major factor in myocardial infarction(in 95%) - unexpected thrombosis of the coronary artery in the area of atherosclerotic plaque with blockage of the artery or its subtotal stenosis. Already at the age of 50, atherosclerosis of the coronary arteries is observed in half of people. Typically, a thrombus occurs on damaged endothelium at the site of rupture of the fibrous “cap” of the plaque (the pathophysiological substrate of ACS). This zone also accumulates mediators (thromboxane Ag, serotonin, ADP, platelet activating factor, thrombin, tissue factor, etc.), which stimulate further aggregation of platelets, erythrocytes and mechanical narrowing of the coronary artery. This process is dynamic in nature and can cyclically take on different forms (partial or complete occlusion of the coronary artery or its reperfusion). If there is not sufficient collateral circulation, the thrombus closes the lumen of the artery and causes the development of MI with an increase in the ST segment. The thrombus measures 1 cm in length and is composed of platelets, fibrin, red blood cells and white blood cells.
At autopsy thrombus often not found due to its postmortem lysis. After occlusion of a coronary artery, the death of myocardial cells does not begin immediately, but after 20 minutes (this is the prelethal phase). The oxygen supply in the myocardium is only enough for 5 contractions, then the heart “starves” with the development of the “ischemic cascade” - the sequence of events after coronary occlusion. Diastolic relaxation of myocardial fibers is disrupted, which subsequently leads to a decrease in systolic contractility of the heart, the appearance of signs of ischemia on the ECG and clinical manifestations. With transmural damage to the myocardium (the entire wall), this process is completed after 3 hours. But histologically, the cardiomyocyte becomes necrotic only 12-24 hours after the coronary blood flow stops. More rare causes of MI:
prolonged coronary artery spasm(in 5%), especially in young people, against the background of Prinzmetal’s angina. Angiographically, pathology in the coronary arteries may not be detected. Coronary artery spasm caused by endothelial dysfunction can damage the integrity of the endothelium of an atherosclerotic plaque, and usually occurs against the background of prolonged negative emotions, mental or physical stress, excessive alcohol or nicotine intoxication. In the presence of such factors, “adrenal necrosis” of the myocardium often occurs due to a large release of catecholamines. This type of MI occurs more often in young “introverts” (who “digest everything within themselves”). Typically, these patients do not have severe TS or indications of it in the anamnesis, but are exposed to coronary risk factors;
coronary artery lesions(coronaritis) with panarteritis nodosa (ANGLA), SLE, Takayasu's disease, rheumatoid arthritis, acute rheumatic fever (2-7% of all MI), i.e. MI can be a syndrome, a complication of other diseases;
coronary embolism with infective endocarditis, thromboembolism from the left chambers of the heart against the background of existing mural thrombosis of the LV or LPR, congenital anomalies of the coronary arteries;
mural thickening of the coronary arteries against the background of metabolic or proliferative diseases of the intima (homocysteinuria, Fabry disease, amyloidosis, juvenile intimal sclerosis, coronary fibrosis caused by chest X-ray irradiation);
myocardial oxygen imbalance- discrepancy between blood flow through the coronary arteries and oxygen consumption by the myocardium (for example, with aortic defects, thyrotoxicosis, prolonged hypotension). Thus, in a number of patients with fairly severe atherosclerotic lesions of the coronary arteries, but without plaque rupture, MI occurs in conditions where oxygen delivery to the myocardium is significantly reduced. The ECG in these patients usually shows a deep negative T wave and ST segment depression;
hematological disorders- polycythemia, thrombocytosis, severe hypercoagulation and DIC syndrome.
Myocardial infarction
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Introduction
Coronary heart disease is the main problem in the clinic of internal diseases; in WHO materials it is characterized as an epidemic of the twentieth century. The basis for this was the increasing incidence of coronary heart disease in people in various age groups, the high percentage of disability, and the fact that it is one of the leading causes of mortality.
Coronary heart disease has become notorious, becoming almost epidemic in modern society.
Coronary heart disease is the most important problem of modern healthcare. For a variety of reasons, it is one of the leading causes of death among the population of industrialized countries. It strikes able-bodied men (more than women) unexpectedly, in the midst of vigorous activity. Those who do not die often become disabled.
Coronary heart disease is understood as a pathological condition that develops when there is a violation of the correspondence between the need for blood supply to the heart and its actual implementation. This discrepancy can occur when the myocardial blood supply remains at a certain level, but the need for it has sharply increased, or when the need remains, but the blood supply has decreased. The discrepancy is especially pronounced in cases of decreased blood supply and an increasing need for blood flow from the myocardium.
Currently, coronary heart disease in all countries of the world is regarded as an independent disease and is included in<Международную статистическую классификацию болезней, травм и причин смерти>. The study of coronary heart disease has a history of almost two centuries. To date, a huge amount of factual material has been accumulated indicating its polymorphism. This made it possible to distinguish several forms of coronary heart disease and several variants of its course. The main attention is drawn to myocardial infarction - the most severe and common acute form of coronary heart disease.
Myocardial infarction. Definition
Myocardial infarction is one of the clinical forms of coronary heart disease, accompanied by the development of ischemic myocardial necrosis resulting from impaired coronary circulation. Myocardial infarction is a disease that attracts a lot of attention from doctors. This is determined not only by the frequency of myocardial infarction, but also by the severity of the disease, the severity of the prognosis and high mortality. The patient and those around him are always deeply impressed by the catastrophic nature with which the disease often develops, leading to long-term disability. The concept of “myocardial infarction” has an anatomical meaning, indicating myocardial necrosis - the most severe form of ischemia resulting from pathology of the coronary vessels.
Contrary to existing opinion, the meaning of the terms “occlusion of coronary vessels”, “thrombosis of coronary vessels” and “myocardial infarction” does not completely coincide, from which it follows that there are:
· heart attacks with coronary occlusion due to vascular thrombosis arising on an atheroma plaque (most);
· infarctions with coronary occlusion of another nature: embolism, coronaryitis (aortic syphilis), diffuse, stenosing atherosclerosis, intramural hematoma with protrusion of a thickened vascular wall into the lumen of the vessel or with intimal rupture and thrombosis at the site of its damage (but not on the atheroma plaque);
· heart attacks without occlusion: significant decreases in coronary blood flow during collapse, massive pulmonary embolism (reflex narrowing of the coronary vessels, decreased cardiac blood flow and blood flow in the coronary vessels, congestion in the coronary venous system due to hypertension in the right atrium);
· significant and prolonged tachycardias that reduce diastole in a hypertrophied heart;
· metabolic disorders (excess of catecholamines, which lead to myocardial anoxia by increasing metabolism in it;
· intracellular decrease in potassium level and increase in sodium content.
Practice shows that, even if there is no obvious coronary occlusion, which in itself would be sufficient to cause a heart attack (only if it exceeds 70% of the lumen of the vessel), occlusion is still, in most cases, involved in the pathogenesis of a heart attack. Cases of myocardial infarction without coronary artery occlusion usually occur against the background of atheromatous coronary pathology.
Myocardial infarction. Classification
By stages of development:
1. Prodromal period (2-18 days)
2. The most acute period (up to 2 hours from the onset of MI)
3. Acute period (up to 10 days from the onset of MI)
With the flow:
1. -monocyclic
2. - protracted
3. - recurrent myocardial infarction (in the first coronary artery, a new focus of necrosis occurs from 72 hours to 8 days)
4. - repeated MI (in another cor. art., a new focus of necrosis 28 days after the previous MI)
Info myocardial ct. Etiology and pathogenesis
The development of myocardial infarction is based on atherosclerotic damage to large and medium-sized heart vessels.
Of great importance in the development of myocardial infarction are the disturbances in blood properties that accompany atherosclerosis, a predisposition to increased coagulability, and pathological changes in platelets. On the atherosclerotic vascular wall, accumulations of platelets form and a thrombus is formed, which completely closes the lumen of the artery.
Myocardial infarction usually develops at the end of the fifth, but more often in the sixth decade of life. There are more men than women among the patients. There is currently evidence of a family predisposition to myocardial infarction. The development of myocardial infarction is predisposed by profession and work associated with intense mental work and overexertion with insufficient physical activity. Hypertension is a factor contributing to the development of myocardial infarction. Smoking and alcoholism also contribute to the development of the disease. In half of the patients, among the factors contributing to the development of myocardial infarction, mental trauma, anxiety, and nervous strain are found. If circulatory failure in the area of the heart vessels occurs quickly, which is observed with reflex spasm or vascular thrombosis, the myocardium quickly undergoes necrosis, resulting in a heart attack.
In the mechanism of development of myocardial infarction, the following are essential:
· spasm of the arteries, in which there are atherosclerotic changes that have an irritating effect on the receptors of the vessels, causing spasmodic contractions of the arteries;
· thrombosis of an artery altered by an atherosclerotic process, often developing after a spasm;
· functional discrepancy between the myocardium’s need for blood and the amount of inflowing blood, which also arises as a result of atherosclerotic changes in the arteries.
With a rapidly developing discrepancy between the blood flow and the functional need for it in the myocardium (for example, during severe physical activity), small-focal necrosis of muscle tissue (microinfarctions) can occur in different parts of the myocardium.
Myocardial infarction. Pathanatomy
Disorders in the heart muscle are associated with the development of ischemic necrosis, which undergoes several stages in its development:
· Ischemic (acute period) is the first few hours after blockage of a coronary vessel before the formation of myocardial necrosis. Microscopic examination reveals foci of destruction of muscle fibers, expansion of capillaries with impaired blood flow in them.
· Acute period - the first 3-5 days of the disease, when necrosis processes with a borderline inflammatory reaction predominate in the myocardium. The walls of the arteries in the infarction zone swell, their lumen is filled with a homogeneous mass of red blood cells, and at the periphery of the necrosis zone, leukocytes emerge from the vessels.
· The subacute period lasts 5-6 weeks, during which time loose connective tissue forms in the area of necrosis.
· The scarring period ends 5-6 months from the onset of the disease with the formation of a full-fledged connective tissue scar.
Sometimes not one, but several heart attacks occur, as a result of which a series of scars are formed in the heart muscle, which give the picture of cardiosclerosis. If the scar is large and covers a significant part of the wall thickness, then due to blood pressure it gradually bulges, resulting in the formation of a chronic cardiac aneurysm.
Macroscopically, myocardial infarctions are ischemic or hemorrhagic in nature.
Their size varies within very significant limits - from 1-2 cm in diameter to the size of a palm.
The division of infarctions into large and small focal ones is of great clinical importance. Necrosis may cover the entire thickness of the myocardium in the affected area (transmural infarction) or be located closer to the endocardium and epicardium; isolated infarctions of the interventricular septum and papillary muscles are possible. If necrosis extends to the pericardium, there are signs of pericarditis.
Blood clots are sometimes detected in damaged areas of the endocardium, which can cause embolism of the arteries of the systemic circulation. With an extensive transmural infarction, the heart wall in the affected area is often stretched, which indicates the formation of a cardiac aneurysm.
Due to the fragility of the dead heart muscle in the infarction zone, it may rupture; in such cases, massive hemorrhage into the pericardial cavity or perforation (perforation) of the interventricular septum is detected.
Myocardial infarction. Clinical picture
Most often, the main manifestation of myocardial infarction is intense pain behind the sternum and in the heart area. The pain occurs suddenly and quickly becomes severe.
May spread to the left arm, left scapula, lower jaw, interscapular space. Unlike the pain of angina, with myocardial infarction the pain is much more intense and does not go away after taking nitroglycerin. In such patients, the presence of coronary heart disease during the course of the disease, displacement of pain in the neck, lower jaw and left arm should be taken into account. However, it should be taken into account that in elderly people the disease may manifest itself as shortness of breath and loss of consciousness. If these symptoms are present, it is necessary to take an electrocardiogram as quickly as possible. If the ECG shows no changes characteristic of myocardial infarction, frequent re-registration of the ECG is recommended.
Myocardial infarction in some cases develops suddenly. There are no signs that foreshadow it, sometimes in people who have not previously suffered from coronary heart disease. This explains cases of sudden death at home, at work, in transport, etc.
In some patients, prior events are observed before the onset of a heart attack; they occur in 50% of patients. Precursors of myocardial infarction are changes in the frequency and intensity of angina attacks. They begin to occur more often, with less physical stress, become more persistent, last longer, in some patients they occur at rest, and in the intervals between painful attacks, sometimes a dull ache or a feeling of pressure remains in the area of the heart. In some cases, myocardial infarction is preceded not by pain, but by symptoms of general weakness and dizziness.
Typical for myocardial infarction are high intensity and long duration of pain. The pain is pressing and squeezing in nature. Sometimes they become unbearable and can lead to blackout or complete loss of consciousness. The pain is not eliminated by the use of conventional vasodilators, and sometimes does not stop with morphine injections. In almost 15% of patients, a painful attack lasts no more than an hour, in a third of patients - no more than 24 hours, in 40% of cases - from 2 to 12 hours, in 27% of patients - over 12 hours.
In some patients, the occurrence of myocardial infarction is accompanied by shock and collapse. Shock and collapse develop suddenly in patients. The patient feels severe weakness, dizziness, turns pale, sweats, and sometimes there is a blackout or even a short-term loss of consciousness. In some cases, nausea and vomiting, and sometimes diarrhea, appear. The patient feels very thirsty. The limbs and tip of the nose become cold, the skin is moist and gradually takes on an ash-gray tint.
Blood pressure drops sharply, sometimes not being detected. The pulse on the radial artery is weak or not palpable at all; the lower the blood pressure, the more severe the collapse.
The prognosis is especially difficult in cases where blood pressure in the brachial artery is not determined.
The number of heartbeats during collapse can be normal, increased, sometimes decreased, and tachycardia is more often observed. Body temperature becomes slightly elevated.
The state of shock and collapse can last for hours or even days, which has a poor prognostic value.
The described clinical picture corresponds to the first phase of shock. Some patients experience symptoms of the second phase of shock at the very beginning of myocardial infarction. During this period, patients are excited, restless, rushing about and cannot find a place for themselves. Blood pressure may be increased.
The occurrence of symptoms of congestion in the small circle changes the clinical picture and worsens the prognosis.
Some patients develop acute progressive left ventricular failure with severe shortness of breath and suffocation, and sometimes an asthmatic condition. Right ventricular failure usually develops in the presence of left ventricular failure.
Objective symptoms include an increase in the borders of the heart to the left. Heart sounds are unchanged or muffled. In some patients, a gallop rhythm is heard, indicating weakness of the heart muscle. A murmur is heard on the mitral valve.
The appearance of a diffuse cardiac impulse or pulsation in the area of the heart may indicate a cardiac aneurysm. Listening to a pericardial friction rub in rare cases is of some importance, which indicates the spread of necrosis up to the pericardium. Patients with myocardial infarction may experience significant disorders of the gastrointestinal tract - nausea, vomiting, pain in the epigastric region, intestinal paresis with symptoms of obstruction.
Very significant disorders can occur in the central nervous system. In some cases, a sharp pain attack is accompanied by fainting and short-term loss of consciousness. Sometimes the patient complains of severe general weakness; some patients develop persistent, difficult to eliminate hiccups. Sometimes intestinal paresis develops with severe bloating and abdominal pain. Of particular importance are the more serious disorders of cerebral circulation that develop during myocardial infarction and sometimes come to the fore. Poor cerebral circulation is manifested by a coma, convulsions, paresis, and speech impairment. In other cases, brain symptoms develop later, most often between the 6th and 10th day.
In addition to the specific symptoms described above from various systems and organs, patients with myocardial infarction also experience general symptoms, such as fever, an increase in the number of red blood cells in the blood, as well as a number of other biochemical changes. A temperature reaction is typical, often developing in the first day and even hours. Most often the temperature does not exceed 38°C. In half of the patients it falls by the end of the first week, in the rest - by the end of the second.
Thus, the following clinical forms of myocardial infarction can be distinguished:
· anginal form (begins with an attack of pain behind the sternum or in the heart area);
· asthmatic form (begins with an attack of cardiac asthma);
collaptoid form (begins with the development of collapse);
· cerebral form (begins with the appearance of pain and focal neurological symptoms);
· abdominal form (appearance of pain in the upper abdomen and dyspeptic symptoms);
· painless form (hidden onset of myocardial infarction);
· mixed form.
Myocardial infarction. Diagnostics
Clinical diagnosis. Myocardial infarction can develop asymptomatically if there are enough collaterals that begin to function at the right time (the phenomenon is more often observed in the area of the right coronary artery).
The most common and pronounced subjective sign of myocardial infarction is pain, which clinically characterizes the onset of a heart attack. It usually occurs suddenly without obvious dependence on physical stress. If the patient previously had painful attacks, then the pain during the development of myocardial infarction may be more severe than before; its duration is measured in hours - from 1 to 36 hours and is not relieved by the use of nitro derivatives.
Unlike coronary pain attacks, which are not accompanied by the development of myocardial infarction, pain during a heart attack may be accompanied by a state of agitation, which may continue after its disappearance. In 40% of cases, a heart attack is preceded by an intermediate syndrome on average 15 days (which in 10% of cases is the first manifestation of pain of coronary origin). The resumption of disappeared pain that arose in connection with a heart attack is a threatening sign, as it indicates the appearance of a new heart attack, the spread of an old one, or the occurrence of embolism of the branches of the pulmonary artery.
Severe pain accompanies 75% of cases of myocardial infarction. Along with it, accompanying subjective symptoms of the second plan are usually noted: disorders of the digestive system (nausea, vomiting, hiccups), neurovegetative disorders (sweating, cold extremities, etc.).
In 25% of cases, myocardial infarction begins without pain (hence, often remains unrecognized) or the pain is less pronounced, sometimes atypical in nature and therefore is regarded as a secondary sign, giving way to other symptoms that are usually a sign of complications of myocardial infarction. These include dyspnea (heart failure) - in 5% of cases, asthenia; lipotomy with impairment of: peripheral circulation (collapse) - in 10% of cases; various other manifestations (pleuropulmonary) - in 2% of cases. On objective examination, the patient is pale, with cold, sometimes cyanotic, extremities. Tachycardia usually occurs; bradycardia (block) is less common.
Systolic and diastolic blood pressure levels are usually reduced. This decrease appears early, is progressive, and if pronounced, indicates the development of collapse.
The apical impulse is weakened. On auscultation, heart sounds may be muffled. In diastole, a fourth sound (atrial gallop) and less often a third sound (ventricular gallop) are often heard, and in systole, a systolic murmur is heard, which is relatively often (50% of cases) associated with hypotension and dysfunction of the papillary muscles.
In 10% of cases, the appearance of a pericardial friction rub of an intermittent nature is also described.
Hyperthermia is observed constantly. It appears 24 - 48 hours after the onset of pain and lasts 10 - 15 days. There is a relationship between the height and duration of temperature, on the one hand, and the severity of the heart attack, on the other.
Electrocardiographic diagnostics
Electrocardiographic changes that accompany a heart attack develop parallel to the process in the myocardium. However, there is not always a close relationship between electrocardiographic data, on the one hand, and clinical symptoms, on the other.
Clinically “silent” infarctions with a typical electrocardiographic manifestation are known.
After a long time after an unrecognized heart attack, the ECG reveals data characteristic of the cicatricial period of a heart attack.
Clinically and biochemically obvious infarctions, but “silent” electrocardiographically, are also known. In these infarctions, the absence of electrocardiographic manifestations appears to be the result of the localization of the process being “inconvenient” for routine recording.
After the occurrence of myocardial infarction, electrocardiographic studies indicate a number of characteristic changes, consisting in the appearance of some specific pathological vectors.
Electrocardiographic diagnosis of myocardial infarction is based on the following three elements:
1. Coexistence of three characteristic ECG changes:
· QRS deformations (pathological Q, decreased R wave voltage) - “necrosis”;
· increased ST segment—“damage”;
· deformation of the T wave—“ischemia.”
2. Characteristic orientation of pathological vectors that “give birth” to these three modifications:
· damage vectors that appear at the moment of formation of the ST segment are oriented towards the infarction zone;
· “running away” from the infarction zone to the healthy zone, the “necrosis” vectors are oriented, which arise at the moment of formation of the Q wave, causing deep negative Q waves and the “ischemia” vectors, which appear at the end of the ECG, during the formation of the T wave, causing negative T waves
3. Evolution over time of these three types of changes, among which Q(-) and ST(+) appear within the first hour after the onset of necrosis, and a change in the T wave occurs approximately after 24 hours.
Typically, the appearance of Pardieu waves is Q(-), ST(+) and T(-) during the first day. Subsequently, gradually (4-5 weeks) the ST segment returns to the isoelectric line, a pathological Q wave is formed, and a negative T wave remains.
An ECG with an elevated ST segment, an abnormal wave, but a normal T wave corresponds to a very recent myocardial infarction (less than 24 hours). If there is also a negative T, then the infarction lasts more than 24 hours, but less than 5-6 weeks. If ST is isoelectric and there are only pathological Q and negative T, the infarction has already healed and is more than 6 weeks old.
We should also not forget that in a relatively large number of cases of heart attacks (up to 30%), the ECG does not leave any pathological signs.
The electrocardiographic localization of the infarction does not differ from the localization of the pathological focus in the myocardium.
Infarcts localized only in the left ventricle will be recorded on the ECG in the case of an anterolateral (“anterior”) infarction with typical changes (Q abnormal, ST elevated and T negative) in leads I, aVL and V6, and in cases of diaphragmatic infarction ( "posterior"), typical changes will be noted in leads III, II and aVF. There are many possible locations that are variations of the main two types. The main thing for topographic analysis is to identify the relationship between pathological vectors and leads with optimal orientation. All types are widely described in specific manuals.
Nevertheless, it is necessary to discuss the point that will reduce the difficulties encountered in the electrocardiographic diagnosis of myocardial infarction, namely the combination of a heart attack and blockade of the pedicle (nerve bundle).
The interventricular septum has an approximately sagittal orientation, while the two branches of the bundle of His are located: the right one in front (cranial), the left with two branches in the back (caudal).
Thus, an “anterior” infarction can be combined with a blockade of the right leg, and a “posterior” one with a blockade of the left leg, which is more rare, since it is difficult to imagine a simultaneous conduction disorder due to a necrotic process in the myocardium due to the fact that each of the branches forming the left leg receives blood supply from different sources.
Since with bundle branch blocks the deformations of the QRS complex and the ST-T segment are usually very significant, they can mask the signs of a heart attack. There are four possible combinations:
· blockade of the right leg with “anterior” or “posterior” infarction;
· blockade of the left leg with “anterior” or “posterior” infarction.
Right leg block is characterized by the appearance in leads with right-left orientation (I, aVL, Ve) of an extended QRS complex in the terminal negative part (S), a positive T wave.
An “anterior” infarction is detected in the same leads and is expressed by the appearance of a pathological Q, a change in RS-T and a negative T. With a combination of blockade of the right bundle branch and an “anterior” infarction against the background of a branch block, signs of a heart attack appear in leads I, aVL and V6: Q wave, decrease in R amplitude or disappearance of wave 5, negative T waves.
“Posterior” infarction is more pronounced in leads with a cranial-caudal orientation (III, aVF, II), where the block of the right leg changes the image of the QRS complex and the T wave less.
Consequently, it is easier to establish the presence of signs of infarction in the case of a combination of right leg block and “posterior” infarction.
Left leg block is less often combined with a heart attack. In leads with a right-left orientation (I, aVL, V6), it is characterized by an expansion of the QRS complex in the central positive part (R flattened); negative T wave.
With an anterior (combined) infarction, Q waves or a decrease in R amplitude, and an upward shift of the ST segment may appear in these leads.
When blockade of the left bundle branch is combined with a “posterior” infarction in leads with a cranial-caudal orientation (III, aVF, II), the increased ST is smoothed out, negative T waves appear (very pronounced, because in these leads there are T waves with blockade of the left bundle positive).
Laboratory diagnostics
Laboratory diagnostics. The clinical diagnosis is confirmed by a number of biohumoral tests. Leukocytosis with polynucleosis appears early (in the first 6 hours) and persists for 3-6 days, less often 2-3 weeks.
There is a certain relationship between the amount of leukocytosis and the extent of infarction. Prolonged leukocytosis should raise suspicion of the development of complications (repeated infarction, embolism of the branches of the pulmonary artery, bronchopneumonia).
ROE increases in parallel with the necrotic process and scarring in the myocardium. It increases slowly in the first 2 days and reaches its highest levels in the first week, and then decreases over 5-6 weeks.
Hyperfibrinogenemia: fibrinogen increases from 2-4 g% to 6-8 g% in the first 3 days, then returns to normal after 2-3 weeks. Like leukocytosis, the level of hyperfibrinogenemia increases parallel to the size of the infarction. Hypercoagulability and hyperglycemia are less predictive of infarction because these tests are variable. An increase in the level of some enzymes is a relatively specific factor.
There are two groups of enzymes whose levels increase during a heart attack:
1. enzymes with a rapid increase in level - TGO (transaminase glutamoxalacet and CPK (creatine phosphokinase). Their level begins to increase in the first hours and is restored within 3-5 days.
2. enzymes whose levels increase more slowly - LDH (lactate dehydrogenase). It increases from the first hours and returns to normal by 10-14 days.
The most reliable enzyme test is TGO, which is observed in 95% of heart attack cases.
This test has the advantage that it is not observed in pathologies that require differential diagnostic decisions regarding myocardial infarction (intermediate syndrome, pericarditis). If the increase in the level of this enzyme in another pathology is still significant, then it is lower than in myocardial infarction.
It should not be forgotten, however, that TGO numbers can also increase with infarctions of the spleen, intestines, kidneys, acute pancreatitis, hemolytic crises, severe injuries and burns, muscle damage, after the use of salicylates and anticoagulant drugs of the coumarin series, with venous stasis due to liver pathology . Therefore, practically from biohumoral tests the following should be taken into account:
· leukocytosis, which appears early and allows us to draw some conclusions about the extent of the infarction;
· TGO, which appears very early but disappears quickly and is a more or less specific test;
· ROE, the acceleration of which occurs concomitantly with the development of a heart attack and appears later than the previous two tests.
With the simultaneous analysis of the listed clinical, electrocardiographic and biohumoral elements, the problem of differential diagnosis of myocardial infarction is significantly simplified. However, in some cases, diagnostic doubts may arise, so one should keep in mind a number of diseases with which myocardial infarction is sometimes confused.
A common symptom of diseases that should be distinguished from myocardial infarction is chest pain. Pain during myocardial infarction has a number of distinctive features regarding localization, intensity and duration, which generally give it a unique character.
Myocardial infarction. Differential diagnosis
Differential diagnosis. There are still difficulties in distinguishing myocardial infarction from a number of other diseases.
1. Milder forms of ischemic cardiopathy, when the pain symptom is of a dubious nature. In such cases, the absence of other clinical symptoms present during a heart attack (tachycardia, decreased blood pressure, increased temperature, dyspnea), the absence of changes in biohumoral parameters and electrocardiographic data (pathological Q, elevated ST and negative T), and all this is noted against the background of significantly better condition than a heart attack. In this case, biohumoral signs of a heart attack may occur, with the exception of an increase in TGO.
2. Embolism of the branches of the pulmonary artery (with pulmonary infarction). With this pathology, symptoms such as pain and collapse may be common to myocardial infarction. Other clinical symptoms of infarction may also be present, but more intense dyspnea (asphyxia, cyanosis) should be noted with embolism of the branches of the pulmonary artery. Biohumoral signs are the same as during a heart attack, with the exception of TGO, the activity of which is absent in embolism of the branches of the pulmonary artery. An electrocardiographic study may also raise doubts. In the case of pulmonary embolism, there is the possibility of the same three typical symptoms of a heart attack appearing on the ECG: pathological Q, elevated ST, negative T.
The orientation of pathological vectors and the speed (hours - days) of electrocardiographic manifestations in pulmonary embolism sometimes allow differential diagnosis, which is generally difficult. Valuable signs indicating pulmonary embolism are bloody sputum, hydrobilirubinemia, an increase in the level of LDH along with the preservation of normal TGO numbers and, most importantly, radiological changes - the identification of pulmonary infiltrate with a pleural reaction.
Anamnesis can also help clarify this or that pathology. Thus, embolism of the branches of the pulmonary artery is indicated by embolic pathology in the venous system (lower limbs, etc.).
Widespread emboli of the branches of the pulmonary artery can themselves contribute to the development of myocardial infarction. In this case, the nature of ECG changes is practically the only sign for diagnosing a new pathology.
3. Acute pericarditis may also begin with pain in the cardiac region and other clinical, electrocardiographic and biochemical signs of myocardial infarction, with the exception of increased blood enzyme levels, arterial hypotension and electrocardiographic signs of necrosis (Q). Anamnesis is important in differential diagnosis.
The development of the process over time eliminates doubts if the problem of differential diagnosis was initially difficult to resolve.
4. Acute pancreatitis with its acute onset, intense pain, sometimes of atypical localization, can in some cases simulate myocardial infarction. Suspicion of it may increase due to the presence of electrocardiographic changes that are more or less characteristic of a heart attack (ST elevated, T negative and even pathological Q), as well as the presence of a number of laboratory signs common to both pathologies (increased ROE, increased leukocytosis).
Distinctive differential diagnostic features, in addition to indications of diseases of the gastrointestinal tract characteristic of pancreatitis, are some laboratory tests characteristic of this pathology: increased amylasemia (between the 8th and 48th hour), sometimes transient hypoglycemia and subicterus, hypocalcemia in severe cases.
Differential diagnostic difficulties usually occur at the onset of the disease.
5. Infarction of the mesenteric vessels is another acute disease of the abdominal cavity, which can lead to differential diagnostic doubts the more easily the more similar the anamnestic data are (generalized atherosclerosis with pathological manifestations in both the coronary and mesenteric vessels). Atypical pain accompanied by collapse and electrocardiographic signs of injury-ischemia (ST-T) (possibly pre-existing, and sometimes having no connection with acute mesenteric pathology) can lead to an erroneous diagnosis of myocardial infarction, instead of mesenteric vascular infarction. The presence of blood in the stool, the detection of bloody fluid in the abdominal cavity and the evolution of existing signs can make it possible to establish this diagnosis, which is very difficult to recognize at the first moment.
6. Dissecting aortic aneurysm has a pronounced picture, in which substernal pain predominates. Great diagnostic difficulties are possible. With this pathology, there are usually no laboratory signs characteristic of a heart attack: increased temperature and electrocardiographic signs of a necrotic focus in the myocardium.
Characteristic signs, in addition to pain, are the diastolic murmur of aortic insufficiency, the difference in pulse and blood pressure between the corresponding limbs (different effects on the mouths of the arteries), and progressive dilation of the aorta (x-ray).
The often observed tendency to maintain or increase blood pressure may be a pathognomonic sign. The difficulty of differential diagnosis is aggravated by the possibility of coexistence of myocardial infarction, electrocardiographic signs of ischemic cardiopathy, which is quite possible in a patient with long-standing vascular pathology, as well as the possibility of a slight increase in temperature, ROE and leukocytes in the blood in cases where destruction of the aortic wall is more widespread.
7. Abdominal, renal, biliary and gastrointestinal colic are easily distinguishable from myocardial infarction even when the nature of the pain is atypical. The absence of characteristic biochemical, electrocardiographic and anamnestic data in the presence of specific signs and anamnesis characteristic of various types of colic allows differential diagnosis in most cases without difficulty.
8. Painless heart attack. Heart failure (acute pulmonary edema), which appeared or worsened for no reason, especially in the presence of a history of angina pectoris, should increase suspicion of a heart attack. The clinical picture, which includes hypotension and fever, increases this suspicion. The appearance of electrocardiographic signs confirms the diagnosis. If the disease begins with collapse, then the same problems arise.
However, here too the data of laboratory and electrocardiographic studies resolve the issue.
Finally, we should not forget that cerebrovascular pathology can also cause the appearance of signs of myocardial infarction on the ECG. Completely different clinical and biochemical data make it easy to reject the diagnosis of myocardial infarction.
Myocardial infarction. Treatment. Anesthesia
The first problem that arises in the treatment of myocardial infarction is pain relief. To eliminate pain, the classic drug is morphine in an amount of 10-20 mg under the skin. If the pain remains very intense, this dose of medication can be re-administered after 10-12 hours. Treatment with morphine, however, is associated with some risk.
Dilatation of peripheral vessels (capillaries) and bradycardia can have fatal consequences in patients with collapse. This also applies to hypoxemia caused by depression of the respiratory center, which is especially dangerous during a heart attack. We should also not forget that in combination with the hypotensive effects of MAO inhibitors, which persist for up to 3 weeks after cessation of treatment, morphine during a heart attack can cause collapse. In addition to morphine, and usually before starting its use, you should try using antipsychotic drugs (chlorpromazine), minor tranquilizers (meprobamate, diazepam) and (or) hypnotics (phenobarbital).
It must be borne in mind that phenobarbital enhances the destruction of anticoagulant substances of the coumarin series, therefore, if it is used simultaneously with these drugs, the latter should be administered in increased doses.
The pain usually disappears within the first 24 hours.
Drug treatment
Anticoagulant drugs. The effectiveness of anticoagulant therapy in reducing mortality and complications of myocardial infarction is still a matter of debate. In the treatment of thromboembolic complications of myocardial infarction, the need to use anticoagulant drugs is beyond doubt; as for the prevention of other complications of myocardial infarction and the development of the infarction itself, statistics have not established any great benefit of this therapy.
In addition, there are formal contraindications and risks, such as bleeding from hepatopathy, bleeding from the digestive tract (ulcer), cerebral hemorrhage (bleeding, arterial hypertension with diastolic pressure above 120 mm Hg)
Contrary to the above and especially due to the lack of statistical justification, anticoagulant therapy for myocardial infarction in most cases is carried out taking into account known theoretical premises. This therapy is indicated for all long-term infarctions (long-term immobilization, subendocardial necrosis with thrombosis), for infarctions with heart failure (congestion, pulmonary embolism) and, of course, for thromboembolic complications. We noted the peculiarities of the use of anticoagulant drugs when presenting the issue of “precursor syndrome” of myocardial infarction. Based on the above, we believe that anticoagulant therapy is indicated:
· with the syndrome of precursors and pain crises, often and suddenly recurring, with an increasing intensity of pain, and in cases of sharp deterioration, despite specific therapy. In all these cases, we are talking about situations that “threaten the risk of developing a heart attack,” so hypocoagulolability can delay, reduce, or possibly prevent the formation of a blood clot that clogs the lumen of the vessel;
· for long-term heart attacks or those accompanied by complications (thromboembolic, heart failure);
· for uncomplicated heart attacks, when anticoagulant drugs are used to limit the prevalence of vessel thrombosis. However, this aspect of the use of anticoagulants is controversial.
The duration of anticoagulant therapy varies. It is recommended to carry out emergency therapy for 3-4 weeks, followed by a course of maintenance doses of the drug for 6-12 months. The implementation of the second part of this therapy, which has a preventive purpose, is usually difficult, since the patient is already at home.
Treatment with thrombolytic (fibrinolytic) drugs. Thrombolytic drugs are among the promising drugs in the treatment of fresh vascular occlusions. The method of administration into the body, the timeliness of application and the effectiveness of treatment have not yet been fully established, but at present there are enough indicative points that allow for rational treatment of the disease. As is known, fibrinolysis is a process that limits the coagulation process.
In principle, plasminogen, circulating inertly in the plasma, is activated by a number of endo- or exogenous substances (thrombin, some bacterial enzymes, etc.) and is converted into a proteolytic enzyme - plasmin. The latter exists in two forms: circulating in the plasma (quickly destroyed by antiplasmins) and in a fibrin-bound form (less destroyed). In its bound form, plasmin exhibits proteolytic activity, i.e. fibrinolysis. In its free form, plasmin, if it circulates in the blood in large quantities, destroys other proteins circulating in the blood (coagulation factors II, V, VIII), giving rise to pathological proteolysis with subsequent inhibition of the coagulation process. Streptokinase and urokinase are used as artificial plasminogen activators.
If thrombosis of the coronary vessels causes occlusion of the vascular lumen, then irreversible myocardial necrosis occurs within 25-30 minutes; incomplete occlusion causes a slower development of the necrotic process. A coronary thrombus measuring 5-10 mm is quite sensitive to the fibrinolytic activity of plasmin and streptokinase in the first 12 hours from the time of thrombus formation, which in itself determines the first requirement of this treatment - an early period.
Timely initiation of treatment with thrombolytic drugs is not always possible.
An older thrombus, of which a sclerotic plaque is a component, is not amenable to thrombolytic treatment. As a result of thrombolytic therapy, not only the main thrombus dissolves, but sometimes also the fibrin reserves deposited in the capillaries of the areas adjacent to the infarction, which improves the oxygen supply to these areas. To obtain an optimal therapeutic effect, it is necessary to determine the fibrinolytic activity of plasma, since fibrinogen breakdown products have an anticoagulant (antithrombin) effect and a quantitative decrease in factors I, II, V, VIII enhances this effect.
It is advisable to carry out early treatment in a short period of time (24 hours) with large and repeated doses at short intervals (4 hours): a) in the first 20 minutes: 500,000 units of streptokinase in 20 ml of sodium chloride 0.9%; b) after 4 hours: 750,000 units of streptokinase in 250 ml of sodium chloride 0.9%; c) after 8 hours: 750,000 units of streptokinase in 250 ml of sodium chloride 0.9%; d) after 16 hours: 750,000 units of streptokinase in 250 ml of sodium chloride 0.9%.
Small doses (up to 50,000 units of streptokinase) are inactivated by antistreptokinase, medium doses (less than 100,000 units) predispose (paradoxically) to bleeding. This fact is explained by the fact that the given doses cause increased and prolonged plasminemia with the persistent presence of fibrinogen breakdown products in the blood, which results in, along with fibrinolysis, the destruction of factors II, V and VIII, blood coagulation with subsequent significant hypocoagulolability. At large doses (more than 150,000 units), the activity of streptokinase in relation to the plasma fibrinolytic system and blood coagulation factors is significantly reduced, but the effect on fibrin of the blood clot (thrombolysis) is more intense. In the first hours of treatment, there is a rapid and significant decrease in fibrinogenemia with significant hypocoagulolability. After 24 hours, fibrinogen levels begin to increase.
Anticoagulant therapy begins in the second phase of thrombolytic treatment.
In practice there are two possibilities:
1. the use of coumarin drugs from the first moment of thrombolytic therapy is based on the fact that their effect begins to manifest itself 24-48 hours after administration into the body, therefore, after the end of the action of thrombolytic drugs;
2. administration of heparin after 24 hours, i.e. at the end of thrombolytic therapy (the effect of heparin is almost instantaneous).
We should not forget that the antithrombin and antifibrin activity of heparin is superimposed on the process of the anticoagulant action of fibrinolytic substances, therefore, heparin therapy in these conditions should be carried out with special attention. The risk of thrombolytic therapy is low if treatment is carried out carefully.
Cases of bleeding, the mechanism of which was discussed above, can become dangerous if there is a need for bloody intervention (heart massage) with the combined use of thrombolytic and anticoagulant drugs. In such cases, it is necessary to use inhibitors of anticoagulant drugs, protamine sulfate, vitamin K and e-aminocaproic acid, a fibrillolysis inhibitor (3-5 g intravenously or orally, then 0.5-1 g every hour until bleeding stops).
Hemorrhagic diathesis and bleeding from internal organs are contraindications to thrombolytic treatment, which, in addition, is associated with the risk of rupture of the muscular elements of the heart (papillary muscles, septum, parietal myocardium).
Cases of anaphylactic shock associated with the introduction of streptokinase into the body require, along with the use of this drug, simultaneous administration with the first dose of 100-150 mg of hydrocortisone.
If you adhere to the treatment regimen, if therapy is carried out in a timely manner and if you do not forget about contraindications, then the advantages of thrombolytic therapy are undeniable. Due to the short-term implementation of this therapy for myocardial infarction, there is no need for special laboratory tests. Most statistics indicate a clear reduction in mortality from myocardial infarction in the case of targeted use of thrombolytic drugs. A decrease in the number of cases of arrhythmias, a rapid improvement in the ECG picture, as well as an almost complete absence of cases of bleeding are also described if the duration of treatment does not exceed 24 hours.
Treatment with ionic solutions. Theoretically and experimentally substantiated treatment with ionic solutions did not produce the desired results in the clinic. Intravenous administration of solutions of potassium and magnesium with glucose and insulin is justified by the fact that myocardial fibers in the infarction zone lose potassium and magnesium ions, accumulating sodium ions. The result of a violation of the relationship between intra- and extracellular ionic concentrations is an increase in bathmotropism, as a result of which arrhythmias arise: extrasystoles, ectopic tachycardias, tachyarrhythmias. In addition, potassium and magnesium have been shown to have a protective effect against the development of myocardial necrosis.
Insulin facilitates the penetration of glucose into cells, the role of which in muscle metabolism and in potassium-sodium polarization is known.
Treatment with vasodilators. Conventional therapy, which is carried out for painful anginal crises, is inappropriate in the acute stage of myocardial infarction. Nitro derivatives can intensify the state of collapse due to the expansion of all blood vessels in the body.
The effect of b-blockers during a heart attack can be twofold: due to their bathmotropic and negative chronotropic effect, they reduce cardiac load and the risk of arrhythmias, but as a result of their negative and inotropic and dromotropic effect, the tendency to decompensation and the occurrence of blockades increases. In addition, b-blockers cause a decrease in blood pressure by reducing peripheral resistance; The so-called vasoconstrictive coronary effect (reduction of vasoconstrictors due to decreased oxygen demand) was also mentioned. In this combination of positive and negative effects in the acute phase of myocardial infarction, negative factors seem to predominate, and therefore one should not resort to the use of the above drugs. The possibility of using vasodilating drugs such as carbochromene (intensain), dipyridamole (persantine), hexabendine (ustimon) is also debatable.
Myocardial infarction. Oxygen therapy
Due to its mechanism of action, oxygen therapy is an effective treatment for long-term ischemia of coronary origin and myocardial infarction. Its action is justified by the causal relationship between anoxia and anginal pain, especially considering the often observed decrease in the partial pressure of arterial oxygen (pO2 of arterial blood) during a heart attack. With the introduction of oxygen, it is possible to increase the concentration (and therefore the partial pressure) of this gas in the alveolar air from 16%, which is the normal value, to values approaching 100%. An improvement in alveolar-arterial pressure leads to a corresponding increase in the penetration of oxygen into the blood. Arterial blood hemoglobin, which is completely saturated with oxygen under normal conditions (97.5%), is affected by an improvement in this indicator only slightly (98-99%), however, the amount of oxygen dissolved in plasma and pO2 increases significantly. An increase in arterial blood pO2 leads, in turn, to improved diffusion of oxygen from the blood to the tissues around the infarction zone, from where the gas further penetrates to the ischemic zones.
Oxygen causes a slight increase in heart rate, peripheral resistance, cardiac output and stroke volume, which is sometimes an undesirable effect of treatment.
Oxygen can be introduced into the body in several ways:
· Insufflation methods: by injection; through a nasal tube or in an oxygen chamber (supply 8-12 liters per minute) - methods by which you can achieve oxygen concentration in the alveolar air up to 30-50%;
· mask inhalation (with a valve mechanism that regulates the gas flow and ensures the concentration of oxygen in the alveolar air within the range of 50-100%).
Myocardial infarction. Therapeutic measures
One of the first therapeutic measures is the cessation of pain. For this purpose, injections of painkillers (morphine, pantopon), preferably intravenously, droperidol 0.25% solution, 1-4 ml, intravenously or as a bolus, depending on blood pressure, are used. Before administration, if well tolerated, 0.5 mg nitroglycerin is prescribed sublingually, then again after 3-5 minutes (up to 3-4 tablets in total).
Hypotension and bradycardia that occur in some patients are usually eliminated with atropine, and respiratory depression with naloxone. Intravenous beta-blockers or the use of nitrates are considered as additional measures in case of insufficient effectiveness with repeated administration of opiates.
A number of prescriptions are aimed at preventing complications and reducing the likelihood of adverse outcomes. They should be carried out in all patients who do not have contraindications.
Myocardial infarction
Myocardial infarction is ischemic necrosis of the myocardium due to an acute discrepancy between the coronary blood flow and the needs of the myocardium, associated with occlusion of the coronary artery, most often caused by thrombosis.
Etiology
In 97-98% of patients, atherosclerosis of the coronary arteries plays a major role in the development of myocardial infarction (MI). In rare cases, myocardial infarction occurs as a result of embolism of the coronary vessels, the inflammatory process in them, and severe and prolonged coronary spasm. The cause of acute coronary circulatory disorders with the development of ischemia and necrosis of a portion of the myocardium, as a rule, is thrombosis of the coronary artery (CA).
Pathogenesis
The occurrence of coronary artery thrombosis is facilitated by local changes in the vascular intima (rupture of an atherosclerotic plaque or a crack in the capsule covering it, less commonly, hemorrhage into the plaque), as well as an increase in the activity of the coagulation system and a decrease in the activity of the anticoagulation system. When a plaque is damaged, collagen fibers are exposed, and at the site of damage, platelet adhesion and aggregation occurs, platelet-derived coagulation factors are released, and plasma coagulation factors are activated. A blood clot forms, closing the lumen of the artery. Thrombosis of the coronary artery is usually combined with its spasm. The resulting acute occlusion of the coronary artery causes myocardial ischemia and, if reperfusion does not occur, its necrosis. The accumulation of under-oxidized metabolic products during myocardial ischemia leads to irritation of myocardial interoreceptors or blood vessels, which is realized in the form of a sharp pain attack. The factors that determine the size of the infarction include: 1. Anatomical features of the coronary artery and the type of blood supply to the myocardium. 2. Protective effect of coronary collaterals. They begin to function when the lumen of the coronary artery decreases by 75%. A pronounced network of collaterals can slow down the rate and limit the extent of necrosis. Collaterals are better developed in patients with inferior MI. Therefore, anterior MI affects a larger area of the myocardium and more often ends in death. 3. Reperfusion of occluded coronary artery. Restoring blood flow in the first 6 hours improves intracardiac hemodynamics and limits the size of the MI. However, an unfavorable effect of reperfusion is also possible: reperfusion arrhythmias, hemorrhagic MI, myocardial edema. 4. Development of “stunning” of the myocardium (stunned myocardium), in which the restoration of myocardial contractile function is delayed for a certain time. 5. Other factors, incl. the influence of medications that regulate the oxygen needs of the myocardium. The localization of myocardial infarction and some of its clinical manifestations are determined by the localization of the coronary circulation disorder and the individual anatomical features of the blood supply to the heart. Total or subtotal occlusion of the anterior descending branch of the left coronary artery usually leads to infarction of the anterior wall and apex of the left ventricle, the anterior part of the interventricular septum, and sometimes the papillary muscles. Due to the high prevalence of necrosis, bundle branch ischemia and distal atrioventricular block often occur. Hemodynamic disturbances are more pronounced than with posterior myocardial infarction. Damage to the circumflex branch of the left coronary artery causes in most cases necrosis of the lateral wall of the LV and (or) its posterolateral sections. In the presence of a more extensive basin of this artery, its proximal occlusion also leads to infarction of the posterior diaphragmatic region of the left, partially right ventricle and the posterior part of the interventricular septum, which also leads to the occurrence of atrioventricular block. Impaired blood supply to the sinus node contributes to the occurrence of arrhythmias. Occlusion of the right coronary artery is accompanied by an infarction of the posterior phrenic region of the left ventricle and quite often an infarction of the posterior wall of the right ventricle. Damage to the interventricular septum is less commonly observed. Ischemia of the atrioventricular node and trunk of the His bundle often develops, and somewhat less frequently, the sinus node with corresponding conduction disturbances.
There are also variants of myocardial infarction: according to the depth of the lesion: transmural, intramural, subepicardial, subendocardial; by location: anterior, lateral, posterior walls of the left ventricle, interventricular septum, right ventricle; by periods: pre-infarction state (prodromal period), acute period, acute period, subacute period, scarring period. Acute myocardial infarction with the presence of a pathological Q wave (transmural, macrofocal) Clinic and diagnosis. Clinically, there are 5 periods during MI: 1.
Prodromal (pre-infarction), lasting from several hours, days to one month, may often be absent. 2.
The most acute period is from the onset of severe myocardial ischemia to the appearance of signs of necrosis (from 30 minutes to 2 hours). 3.
Acute period (formation of necrosis and myomalacia, perifocal inflammatory reaction) - from 2 to 10 days. 4.
Subacute period (completion of the initial processes of scar organization, replacement of necrotic tissue with granulation tissue) - up to 4-8 weeks from the onset of the disease. 5.
The stage of scarring is an increase in scar density and maximum adaptation of the myocardium to new operating conditions (post-infarction period) - more than 2 months from the onset of MI. A reliable diagnosis of myocardial infarction requires a combination of both | at least two of the following three criteria: 1) prolonged attack of chest pain; 2) ECG changes characteristic of ischemia and necrosis; 3) increased activity of blood enzymes.
The typical clinical manifestation is severe and prolonged cardiac pain. The pain is not relieved by taking nitrates and requires the use of drugs or neuroleptanalgesia (status anginosus).
It is intense, can be pressing, squeezing, burning, sometimes sharp, “dagger-like”, most often localized behind the sternum with varying irradiation. The pain is wave-like (it intensifies and then weakens), lasts more than 30 minutes, sometimes for several hours, accompanied by a feeling of fear, excitement, nausea, severe weakness, and sweating.
There may be shortness of breath, disturbances in heart rhythm and conduction, and cyanosis. A significant proportion of these patients have a history of angina attacks and risk factors for ischemic heart disease. Patients experiencing intense pain are often agitated, restless, and tossing around, unlike patients with angina who “freeze” during a painful attack.
When examining the patient, pale skin, cyanosis of the lips, increased sweating, weakening of the first tone, the appearance of a gallop rhythm, and sometimes a pericardial friction noise are noted. Blood pressure decreases more often.
On the first day, tachycardia and various heart rhythm disturbances are often observed; by the end of the first day, an increase in body temperature to subfebrile levels, which persists for 3-5 days. In 30% of cases there may be atypical forms of MI: gastralgic, arrhythmic, asthmatic, cerebrovascular, asymptomatic, collaptoid, similar to recurrent attacks of angina, in the right ventricular localization.
The gastralgic variant (1-5% of cases) is characterized by pain in the epigastric region, there may be belching, vomiting that does not bring relief, bloating, and intestinal paresis. Pain can radiate to the area of the shoulder blades, the interscapular space.
Acute stomach ulcers often develop with the occurrence of gastrointestinal bleeding. The gastralgic variant is more often observed with posterior phrenic localization of myocardial infarction.
In the asthmatic variant, which is observed in 10-20%, the development of acute left ventricular failure eliminates the pain syndrome. Characterized by an attack of cardiac asthma or pulmonary edema.
It is more often observed with repeated MI or in patients with existing chronic heart failure. The arrhythmic variant is manifested by the occurrence of acute rhythm and conduction disturbances, often life-threatening for patients.
These include polytopic, group, early ventricular extrasystole, paroxysmal ventricular tachycardia. Recurrent myocardial infarction is characterized by a long, protracted course of 3-4 weeks or longer, with the development of a repeated painful attack of varying intensity, which may be accompanied by the occurrence of acute rhythm disturbances and cardiogenic shock.
According to ECG data, stages are distinguished: ischemic, acute (damage), acute (necrosis stage), subacute, scarring. The ischemic stage is associated with the formation of an ischemic focus and lasts 15-30 minutes.
Above the lesion, the amplitude of the T wave increases, it becomes high, pointed (subendocardial ischemia). This stage is not always possible to register.
The damage stage (acute stage) lasts from several hours to 3 days. In areas of ischemia, subendocardial damage develops, which is manifested by an initial shift of the ST interval downward from the isoline.
Damage and ischemia quickly spread transmurally to the subepicardial zone. The ST interval shifts dome-shaped upward, the T wave merges with the ST interval (monophasic curve).
The acute stage (necrosis stage) is associated with the formation of necrosis in the center of the lesion and a significant ischemic zone around the damage zone, lasting 2-3 weeks. ECG signs: the appearance of a pathological Q wave (wider than 0.03 s and deeper than 1/4 of the R wave); reduction or complete disappearance of the R wave (transmural infarction);) dome-shaped displacement of the ST segment upward from the isoline - Purdy wave, formation of a negative T wave.
The subacute stage reflects ECG changes associated with the presence of a zone of necrosis, in which the processes of resorption, repair, and ischemia occur. There is no longer a damage zone.
The ST segment descends to the isoline. The T wave is negative, in the form of an isosceles triangle, then gradually decreases and can become isoelectric.
The scarring stage is characterized by the disappearance of ECG signs of ischemia with persistent preservation of scar changes, which is manifested by the presence of a pathological Q wave. The ST segment is located on the isoelectric line.
The T wave is positive, isoelectric or negative, there is no dynamics of its changes. If the T wave is negative, it should not exceed 5 mm and be less than 1/2 the amplitude of the Q or R waves in the corresponding leads.
If the amplitude of the negative T wave is greater, then this indicates concomitant myocardial ischemia in the same area. Thus, the acute and subacute period of large-focal MI is characterized by: the formation of a pathological, persistently persistent Q wave or QS complex, a decrease in the R wave voltage with ST segment elevation and T wave inversion, and there may be conduction disturbances.
DIFFERENT LOCALIZATIONS OF MI ON ECG Septal V1,V2, V1-V2 Median V3,V4 Anteroseptal V1-V4 Lateral I, aVL, V5-V6 Anterolateral I, aVL, V3 -V 6 Postodiaphragmatic II, III, aVF Posterobasal V7 - V9. an increase in the R wave, a decrease in the ST segment and an increase in the T wave in leads V1 V2 Complications of the acute period of myocardial infarction (in the first 7-10 days) include rhythm and conduction disturbances, cardiogenic shock; acute left ventricular failure (pulmonary edema); acute cardiac aneurysm and its rupture; internal ruptures: a) rupture of the interventricular septum, b) rupture of the papillary muscle; thromboembolism. In addition, acute stress erosions and ulcers of the gastrointestinal tract may occur, which are often complicated by bleeding, acute renal failure, and acute psychosis.
Rhythm and conduction disturbances are observed in 90% of patients in the acute period of myocardial infarction. The form of rhythm and conduction disturbances sometimes depends on the location of the MI.
Thus, with lower (diaphragmatic) MI, bradyarrhythmias associated with transient dysfunction of the sinus node and atrioventricular conduction, sinus arrhythmia, sinus bradycardia, and atrioventricular block of varying degrees are more common. In anterior MI, sinus tachycardia, intraventricular conduction disturbances, and grade III AV block are more often observed.
type Mobitz-2 and complete distal AV block. In almost 100% of cases, supraventricular and ventricular extrasystoles occur, including polytopic, group, and early ones.
Paroxysmal ventricular tachycardia is a prognostically unfavorable rhythm disorder. The most common immediate cause of death in patients with acute MI is ventricular fibrillation.
Cardiogenic shock is a syndrome that develops as a result of a sharp decrease in the pumping function of the left ventricle, characterized by inadequate blood supply to vital organs with subsequent disruption of their function. Shock during MI occurs as a consequence of damage to more than 30% of the cardiomyocytes of the left ventricle and its inadequate filling.
A sharp deterioration in the blood supply to organs and tissues is caused by: a decrease in cardiac output, narrowing of peripheral arteries, a decrease in circulating blood volume, the opening of arteriovenous shunts, intravascular coagulation and a disorder of capillary blood flow (“sludge syndrome”). The main criteria for cardiogenic shock include: - peripheral signs (pallor, cold sweat, collapsed veins) and dysfunction of the central nervous system (excitement or lethargy, confusion or temporary loss of consciousness); - a sharp drop in blood pressure (below: 90 mm Hg.
Art.) and a decrease in pulse pressure below 25 mm Hg.
Art.; - oligoanuria with the development of acute renal failure; - wedge pressure in the pulmonary artery is more than 15 mm Hg.
Art.; — cardiac index less than 2.2 l/(min-m2).
In myocardial infarction, the following types of cardiogenic shock are distinguished: reflex, true cardiogenic, arrhythmic and associated with myocardial rupture. In severe cardiogenic shock, refractory to therapy, they speak of areactive shock.
Reflex shock develops against the background of anginal status. The leading mechanism of its development is reflex hemodynamic reactions to pain.
This type of shock is more often observed with posterior myocardial infarction. Usually this is shock with vasodilation, with a decrease in both systolic and diastolic blood pressure and with relative preservation (within 20-25 mm Hg).
Art.) pulse blood pressure.
After timely and adequate pain relief and a single administration of adrenergic agonists, hemodynamics are usually restored. In true cardiogenic shock, the main pathogenetic mechanism is a sharp decrease in the contractile function of the myocardium with extensive ischemic damage (more than 40% of the myocardium), a decrease in cardiac output.
As shock progresses, the syndrome of disseminated intravascular coagulation develops, microcirculation disorders with the formation of microthrombosis in the microvasculature. In arrhythmic shock, the leading role is played by hemodynamic disturbances caused by disturbances of heart rhythm and conduction: paroxysmal tachycardia or a high degree of atrioventricular block.
Areactive cardiogenic shock is shock: in an irreversible stage as a possible outcome of its previous forms, most often true. It manifests itself as a rapid decline in hemodynamics, severe multiple organ failure, severe disseminated intravascular coagulation and ends in death.
The main mechanisms of development of acute left ventricular failure include segmental disorders of myocardial contractility, its systolic and/or diastolic dysfunction. In accordance with the Killip classification, there are 4 classes of acute left ventricular failure.
Classification of acute left ventricular failure in patients with acute myocardial infarction according to Killip Characteristics of class I No signs of heart failure II Moist rales, mainly in the lower parts of the lungs, three-part rhythm (gallop rhythm), increased central venous pressure III Pulmonary edema IV Cardiogenic shock, often in combination with pulmonary edema As a rule, the development of pulmonary edema is associated with extensive myocardial damage involving more than 40% of the LV myocardial mass, the occurrence of acute LV aneurysm or acute mitral regurgitation due to avulsion or dysfunction of the papillary muscles. Acute interstitial pulmonary edema, manifested by a typical attack of cardiac asthma, is associated with massive accumulation of fluid in the interstitial space of the lungs, significant infiltration of serous fluid into the interalveolar septa, perivascular and peribronchial spaces, and a significant increase in vascular resistance.
An important pathogenetic link in alveolar pulmonary edema is the penetration of transudate into the cavity of the alveoli and its formation. Breathing becomes bubbling, foamy, sometimes pink sputum is released in large quantities - “drowning in one’s own phlegm.”
The wedge pressure in the capillaries of the lungs increases sharply (up to 20 or more mm Hg.
), cardiac output decreases (less than 2.2 l/min/m2). Heart rupture usually occurs on days 2-14 of the disease.
The provoking factor is the patient’s insufficient compliance with bed rest. Characterized by severe pain followed by loss of consciousness, pallor, cyanosis of the face, neck with swelling of the jugular veins; pulse and blood pressure disappear.
A characteristic symptom of electromechanical dissociation is the cessation of the mechanical activity of the heart while maintaining the electrical potentials of the heart for a short period, which is manifested on the ECG by the presence of sinus or idioventricular rhythm. Death occurs within a few seconds to 3-5 minutes.
A rupture of the interventricular septum is characterized by sharp pain in the heart, a drop in blood pressure, the rapid development of right ventricular failure (swelling of the neck veins, enlargement and tenderness of the liver, increased venous pressure); a rough systolic murmur over the entire region of the heart, best heard over the middle third of the sternum and in the 4-5 intercostal space to the left of it. When the papillary muscle ruptures, severe pain occurs in the region of the heart, collapse, acute left ventricular failure quickly develops, a rough systolic murmur appears, conducted to the left axillary region, due to regurgitation of blood into the left atrium, and sometimes a squeaking noise.
A cardiac aneurysm can form in the acute and, less commonly, subacute periods. Criteria for aneurysm: progressive circulatory failure, precordial pulsation in the third-lV intercostal space on the left, systolic or (less often) systolic-diastolic murmur in the area of pulsation, on the ECG - a “frozen” monophasic curve, typical of transmural myocardial infarction.
An x-ray examination reveals paradoxical pulsation of the aneurysm; an x-ray kymogram or an ultrasound scan of the heart reveals zones of akinesia. Often, cardiac aneurysm is complicated by parietal thromendocarditis, which is manifested by a prolonged febrile state, leukocytosis, increased ESR, stable angina, and the occurrence of trogloembolic syndrome - in the vessels of the brain, great vessels of the extremities, mesenteric vessels, and in case of septal localization - in the pulmonary artery system.
In the subacute period, post-infarction Dressler syndrome develops, which is based on autoimmune processes. Manifested by pericarditis, pleurisy, pulmonitis, fever.
There may be polyarthralgia, leukocytosis, increased ESR, eosinophilia, hypergammaglobulinemia, increased titer of anticardiac autoantibodies. Late complications of MI also include the development of chronic heart failure.
Post-infarction circulatory failure occurs mainly of the left ventricular type, but later right ventricular failure can also join. POST-INFARCTION CARDIOSCLEROSIS Diagnosis.
The diagnosis is made no earlier than 2 months after the onset of myocardial infarction. Postinfarction cardiosclerosis is diagnosed on the basis of pathological ECG changes in the absence of clinical and biochemical (increased enzyme activity) signs of acute myocardial infarction.
If the ECG does not show signs of a previous myocardial infarction, the diagnosis of post-infarction cardiosclerosis can be made on the basis of medical documentation (ECG changes and a history of increased enzyme activity). The severity of the condition of a patient with coronary artery disease with post-infarction cardiosclerosis is determined by the presence and nature of the arrhythmia, the presence and severity of heart failure.
Heart failure is characterized by a staged course: initially it occurs in the left ventricular type and only in the later stages becomes biventricular. It is often accompanied by atrial fibrillation, initially paroxysmal, then permanent, as well as cerebrovascular insufficiency.
Physical examination findings are not specific. In severe cases, orthopnea may be observed, attacks of cardiac asthma and pulmonary edema are possible, especially with concomitant arterial hypertension, alternating pulse.
Signs of right ventricular failure appear relatively late. The apical impulse gradually shifts to the left and down.
On auscultation, a weakening of 1 tone at the apex is noted; a gallop rhythm and a short systolic murmur in the projection of the mitral valve can be heard. The ECG reveals focal changes after myocardial infarction, as well as diffuse changes of varying degrees of severity.
Signs of a chronic cardiac aneurysm are possible, but the diagnostic value of the ECG in this case is less than the information content of echocardiography. Left ventricular hypertrophy and bundle branch block are often observed.
In some cases, signs of silent subendocardial ischemia can be detected in the form of ST segment depression of more than 1 mm, sometimes in combination with a negative T wave. The interpretation of these changes may be ambiguous due to their nonspecificity.
More informative is the registration of transient ischemia (painless or painful) during stress tests or Holter monitoring. On X-ray examination, the heart is moderately enlarged, mainly due to the left sections.
An echocardiogram reveals dilatation of the left ventricle, often its moderate hypertrophy. Local disturbances of segmental contractility are characteristic, including signs of an aneurysm.
In advanced cases, hypokinesia is diffuse in nature and is usually accompanied by dilatation of all chambers of the heart. As a manifestation of papillary muscle dysfunction, a slight disturbance in the movement of the mitral valve leaflets is possible.
Similar changes are observed with ventriculography. Myocardial scintigraphy helps to identify persistent foci of hypoperfusion of various sizes, often multiple, and transient focal hypoperfusion during stress tests due to increased myocardial ischemia.
It is impossible to accurately assess the patient's condition based on the size of the scar. The functional state of the coronary circulation in areas of the myocardium outside the scar is of decisive importance.
This condition is determined by the presence or absence of angina attacks in the patient, and by tolerance to physical activity. Coronary angiography shows that the condition of the coronary arteries in patients with post-infarction cardiosclerosis can vary significantly (from three-vessel lesions to unchanged coronary arteries).
There may be no stenosing changes in the coronary arteries in patients with post-infarction cardiosclerosis if complete recanalization of the vessel has occurred in the area whose damage led to myocardial infarction. Typically these patients do not have angina.
In addition to occlusive lesions in the vessel of the scar zone, damage to one or two main coronary arteries is possible. These patients experience angina pectoris and decreased exercise tolerance.
The presence of angina pectoris, which is one of the most important clinical criteria for the condition of a patient with post-infarction cardiosclerosis, significantly affects the course and prognosis of the disease. It is known that transient myocardial ischemia leads to dysfunction in the affected area. During an anginal attack caused by physical activity, disturbances in the contractile function of the myocardium can be so pronounced that an attack of cardiac asthma or pulmonary edema develops.
A similar asthma attack in patients with post-infarction cardiosclerosis can develop in response to a severe attack of spontaneous angina. The progression of coronary atherosclerosis is accompanied by increasing damage to the myocardium - its dilatation, decreased contractility, leading to heart failure.
With further progression, a period comes when the patient always reacts to physical activity with shortness of breath, and not with an anginal attack. The clinical manifestations of attacks of myocardial ischemia are transformed.
Usually during this period, patients show clinical signs of severe congestive heart failure. Stable exertional angina pectoris that persists after an MI also aggravates the prognosis of life.
If effortful angina pectoris persists after an MI, it is necessary to determine the indications for coronary angiography to determine the possibility of radical intervention - CABG or transluminal angioplasty, possibly with the use of vessel agency. Women with post-infarction angina have a worse prognosis after MI than men.
Diagnostics
Laboratory studies in the acute period of MI reflect the development of resorption-necrotic syndrome. By the end of the first day, leukocytosis is observed in the blood, which reaches a maximum by the 3rd day, aneosinophilia, a shift to the left, from 4-5 days - an increase in ESR with the beginning of a decrease in leukocytosis - a symptom of crossover. From the first day, there is an increase in the activity of creatine phosphokinase (CPK), the MB fraction of CPK, LDH-1, aspartate aminotransferase (AST), and an increase in the content of myoglobin in the urine and blood. The titer of monoclonal antibodies to myosin and troponin increases. An increase in the content of troponins T and I is detected in the first 2-3 hours from the onset of MI and persists for up to 7-8 days. A characteristic feature is hypercoagulation syndrome - an increase in the blood level of fibrinogen and its degradation products, and a decrease in the level of plasminogen and its activators. Ischemia and myocardial damage cause changes in the protein structures of cardiomyocytes, and therefore they acquire the properties of an autoantigen. In response to the appearance of autoantigens, anticardiac autoantibodies begin to accumulate in the body and the content of circulating immune complexes increases. Radionuclide testing reveals the accumulation of technetium pyrophosphate in the focus of necrosis, which is important especially in the late stages (up to 14-20 days) of the disease. At the same time, the thallium isotope - 2C1 TI accumulates only in areas of the myocardium with preserved blood supply in direct proportion to the intensity of perfusion. Therefore, the necrosis zone is characterized by a decrease in isotope accumulation (“cold focus”). An echocardiographic study reveals signs of focal myocardial damage - passive paradoxical movement of the interventricular septum and a decrease in its systolic excursion of less than 0.3 cm, a decrease in the amplitude of movement of the posterior wall and akinesia or hypokinesia of one of the walls of the left ventricle. Radionuclide angiography indicates the total contractility of the left ventricle, the presence of its aneurysm and segmental disorders. In recent years, positron emission tomography and nuclear magnetic resonance have been used to diagnose myocardial ischemia and MI.
Myocardial infarction is a clinical emergency requiring urgent hospitalization in an intensive care unit. Mortality is highest in the first 2 hours of MI; emergency hospitalization and treatment of ventricular arrhythmias contribute to its significant reduction. The leading cause of death from MI in the prehospital stage is a pronounced decrease in left ventricular contractility, shock and ventricular fibrillation.
The main task of the doctor at the prehospital stage is to carry out emergency measures, including resuscitation, pain relief, elimination of severe rhythm disturbances, acute circulatory failure, and correct and gentle transportation of patients to the hospital. At the hospital stage, it is necessary to eliminate life-threatening dysfunctions of various body systems, activate the patient, constantly expanding the motor mode, and prepare the patient for post-hospital rehabilitation.
In the acute phase, strict bed rest is required. Relief of a painful attack is achieved by intravenous administration of narcotic analgesics, mainly morphine, less often - omnopon, promedol; neuroleptoanalgesia, carried out using intravenous injection of 1-2 ml of a 0.005% solution of the analgesic fentanyl and 2-4 ml of a 0.25% solution of the neuroleptic droperidol.
You can use a ready-made mixture of fentanyl and droperidol - talamonal, 1 ml of which contains 0.05 mg of fentanyl and 2.5 mg of droperidol. The use of non-narcotic analgesics is not very effective.
Inhalation anesthesia with nitrous oxide and oxygen is relatively rarely used. Oxygen inhalation using a nasal catheter is recommended for all patients with myocardial infarction, especially with severe pain, left ventricular failure, and cardiogenic shock.
In order to prevent ventricular fibrillation, β-blockers and potassium preparations (potassium chloride as part of a polarizing mixture, panangin) are administered at the prehospital stage. In the presence of arrhythmias, appropriate antiarrhythmic drugs are used (lidocaine, cordarone, etc.
) (see “Arrhythmias”).
In recent years, active treatment tactics have been used including reperfusion therapy (thrombolytics, balloon angioplasty or CABG), which is regarded as the most effective method of limiting the size of myocardial infarction and improving the immediate and long-term prognosis. Early (up to 4-6 hours from the onset of the disease) use of intravenous thrombolysis by administering streptokinase (cabikinase), recombinant tissue plasminogen activator (Actilyse) and other similar drugs reduces hospital mortality by 50%.
Streptokinase (cabikinase) is administered intravenously in a dose of 1-2 million (average 1.5 million).
) ME for 30-60 min. Streptokinase is the drug of choice in the elderly (over 75 years of age) and in severe arterial hypertension.
With its use, the smallest number of intracranial hemorrhages is observed. According to a number of multicenter studies, the most effective thrombolytic agent is tissue plasminogen activator (actilyse).
Actilyse, unlike streptokinase, does not have antigenic properties and does not cause pyrogenic or allergic reactions. An approximate regimen for using tPA: 60 mg during the first hour (of which 10 mg as a bolus and 50 mg intravenously), then 20 mg/hour during the second and third hours, i.e.
i.e. only 100 mg in 3 hours.
In recent years, accelerated tPA administration regimens have also been used: 15 mg as a bolus, 50 mg as an infusion over 30 minutes, and 35 mg over the next 60 minutes. Before treatment, 5000 units are administered intravenously.
heparin, and then an infusion of heparin 1000 units/hour is carried out for 24-48 hours under the control of aPTT (activated partial thromboplastin time), which should be extended no more than 1.5-2.5 times compared to the initial level (up to 60-85 seconds with the norm being 27-35 seconds). In recent years, third-generation thrombolytics have been created based on genetic modification of the human tissue plasminogen activator molecule: reteplase, lanoteplase, tenecteplase.
The main indications for thrombolytic therapy: 1. AMI with a Q wave in the period from 30 minutes to 12 hours and with ST segment elevation > 1 mm in two or more adjacent leads 2.
AMI with a Q wave lasting more than 12 hours and less than 24 hours, provided that the patient continues to have ischemic pain. 3.
Chest pain and ST segment depression in the anterior precordial leads, combined with impaired segmental contractility of the posterior wall of the LV (signs of MI of the inferior wall of the LV, provided that less than 24 hours have passed since the onset of pain). 4.
No major contraindications. Contraindications for thrombolysis include hemorrhagic diathesis, gastrointestinal or urogenital bleeding in the last month, blood pressure > 200/120 mmHg.
history of cerebrovascular accident, recent skull injury, surgery at least 2 weeks before MI, prolonged resuscitation, pregnancy, dissecting aortic aneurysm, diabetic hemorrhagic retinopathy. If thrombolysis is clearly ineffective (persistent pain, ST segment elevation), coronary balloon angioplasty is indicated, which allows not only to restore coronary blood flow, but also to establish stenosis of the artery supplying the infarction area.
In the acute period of MI, emergency coronary bypass surgery is successfully performed. The development of thromboembolic complications, an increase in the coagulating properties of blood and a decrease in fibrinolytic activity are the basis for the early prescription of anticoagulants and antiplatelet agents.
For myocardial infarction, direct (heparin) and indirect anticoagulants are used. Heparin is recommended to be prescribed as an intravenous drip continuous infusion at a rate of approximately 1000 - 1500 IU/hour after preliminary bolus administration of 5000 -10000 IU (100 IU/kg).
The dose is initially adjusted every 4 hours after determining the APTT or blood clotting time, then, after stabilization, heparin is administered less frequently. Intravenous jet administration at a dose of 10-15 thousand units, then subcutaneously at 5 thousand units after 4-6 hours under the control of blood clotting time is associated with a high frequency of hemorrhagic complications.
Heparin therapy is continued for an average of 5-7 days, rarely more, followed by gradual withdrawal or, in isolated cases, in the presence of special indications, with a transition to oral indirect anticoagulants. Doses of indirect anticoagulants (syncumar, phenyline) are selected in such a way as to constantly maintain the prothrombin index at the level of 40-50%.
Acetylsalicylic acid has a positive effect in AMI, which is associated with its antiplatelet and antiplatelet effect (inhibition of the synthesis of trsmboxane A2). The most commonly used daily dose of acetylsalicylic acid is 325-160 mg, with the first dose prescribed immediately after the occurrence of myocardial infarction.
Limitation of the peri-infarction zone is achieved by taking nitroglycerin sublingually every 15 minutes for 1-2 hours or by drip administration of nitro drugs followed by switching to long-acting nitrates (see Treatment of Angina).
In recent years, b-adrenergic receptor blockers have been widely used to treat patients with MI. Their positive effect.
MI is caused by the following effects: antianginal effect due to slowing heart rate and reducing myocardial oxygen demand, preventing arrhythmogenic and other toxic effects of catecholamines; possibly by increasing the threshold for fibrillation. Therapy with b-blockers helps reduce hospital mortality and improve long-term prognosis, especially with Q-wave MI. Treatment with b-blockers is advisable for at least 1 year after MI, and possibly for life.
The administration of beta-blockers intravenously in the acute period of myocardial infarction with a further transition to tablet forms is recommended for patients with myocardial infarction without severe symptoms of heart failure, shock or bradycardia (less than 50 min-1). A relative contraindication for β-blockers is a sharp decrease in ejection fraction - less than 30%.
For LV dysfunction, a short-acting b-blocker, esmolol, is prescribed, the effect of which quickly ceases after administration. The most effective b-blockers without internal symlatomimetic activity are: metoprolol (vasocordin, egilok, corvitol) 50-100 mg 2 times a day.
atenolol 50-100 mg 1 time per day. bisoprolol 5 mg/day.
propranolol (obzidan, anaprilin) -180-240 mg per day. in 3-4 doses.
LV remodeling and dilatation that occurs during MI can be reduced or even eliminated by prescribing angiotensin-converting enzyme inhibitors (ACE inhibitors). An approximate scheme for using captopril: immediately after hospitalization of the patient - 6.25 mg, after 2 hours - 12.5 mg, after another 12 hours - 25 mg, and zggem - 50 mg 2 times a day for a month or more.
The first dose was pril or lisino-pril - 5 mg. Next, the drug is prescribed at a dose of 10 mg 1 time per day.
Absolute contraindications to the use of ACE inhibitors are arterial hypotension and cardiogenic shock. The results of clinical studies indicate that there is no positive effect of calcium antagonists on the size of necrosis, the incidence of relapses and mortality in patients with AMI with Q wave, and therefore their use in the acute period of MI is inappropriate.
To improve the functional state of the myocardium, it is possible to use metabolic therapy. In the first three days, it is advisable to use cytochrome C - 40-60 mg of the drug in 400 ml of 5% glucose solution intravenously at a rate of 20-30 cal per minute, neoton (creatine phosphate) - in the first day up to 10 g (2 g intravenously in a stream and 8 g drip), and then, from the second to the sixth day, 2 g 2 times a day intravenously, for a course of treatment - 30 g.
Subsequently, trimetazidine (Preductal) 80 mg per day in three doses is used. If necessary, sedatives are prescribed.
The diet in the first days after an MI should be low-calorie (1200-1800 kcal per day), without added salt, low in cholesterol, and easily digestible. Drinks should not contain caffeine or be too hot or cold.
Most patients with large-focal myocardial infarction remain in the intensive care unit during the first 24-48 hours. In uncomplicated cases, the patient can get out of bed by the beginning of the second day and he is allowed independent nutrition and self-care; on days 3-4 he can get out of bed and walk on a flat surface for 100-200 m.
Patients whose MI is complicated by heart failure or serious arrhythmias should remain in bed for a significantly longer period of time, and their subsequent physical activity should be increased gradually. At the time of discharge from the hospital, the patient must achieve such a level of physical activity that he can take care of himself, climb the stairs to the first floor, and walk up to 2 km in two steps during the day without negative hemodynamic reactions.
After the hospital stage of treatment, rehabilitation in specialized local sanatoriums is recommended. Treatment of the main complications of myocardial infarction In case of reflex cardiogenic shock, the main treatment measure is rapid and complete pain relief in combination with drugs that increase blood pressure: mesaton, norepinephrine.
In case of arrhythmic shock, electrical pulse therapy is performed for health reasons. When treating true cardiogenic shock, treatment tactics include complete pain relief, oxygen therapy, early thrombolytic therapy, increasing myocardial contractility and reducing peripheral vascular resistance.
Hypovolemia should be excluded - with low CVP values (less than 100 mm of water column), an infusion of low molecular weight dextrans - rheopolyglucin, dextran-40 - is necessary. When blood pressure is low, inotropic agents are administered to increase blood pressure.
The drug of choice is dopamine. If blood pressure does not normalize with dopamine infusion, norepinephrine should be administered.
In other cases, the administration of dobutamine (Dobutrex) is preferable. Large doses of corticosteroids may be used.
To prevent microthrombosis in the capillaries, the administration of heparin is indicated. To improve microcirculation, rheopolyglucin is used.
To correct the acid-base state, a 4% sodium bicarbonate solution is prescribed. In case of an areactive version of true cardiogenic shock, balloon counterpulsation is used.
Transluminal balloon angioplasty or orthocoronary bypass surgery performed in the early stages of the disease can improve the survival of patients. In case of myocardial rupture, the only measure to save the patient’s life is surgical intervention.
Heart rhythm and conduction disturbances are treated according to the general principles of treatment of arrhythmias (see Chap.
Arrhythmias). Treatment of acute left ventricular failure is carried out taking into account the Killip classification.
At. degree, no specific treatment is required. In grade II, it is necessary to reduce preload with the help of nitroglycerin and diuretics, which helps to reduce pulmonary artery wedge pressure (PAWP). In grade III, pronounced hemodynamic disturbances are observed - an increase in PAWP and a significant decrease in cardiac index (CI).
To reduce PAWP, diuretics and nitroglycerin are used, and to increase CI, sodium nitroprusside is used, which increases CI, reducing afterload. The use of inotropic agents that increase myocardial oxygen demand should be avoided.
Treatment of stage IV acute heart failure is the treatment of true cardiogenic shock. At the same time, measures are being taken to reduce foaming in the respiratory tract - oxygen inhalation through alcohol, antifomsilane; oxygen therapy.
To reduce transudation into the interstitial tissue of the lungs and into the alveoli, glucocorticoids (prednisolone - 60-90 mg) are prescribed intravenously; for high blood pressure, antihistamines are used: diphenhydramine, piprfen, suprastin, tavegil, etc.
For the treatment of Dressler's syndrome, corticosteroids (prednisolone) are prescribed in medium doses - 30-40 mg / day, NSAIDs - diclofenac sodium up to 100 mg / day, it is possible to use epsilon-aminocaproic acid. Treatment for cardiac aneurysm involves surgery.
Aneurysmectomy is performed no earlier than after 3 months. after myocardial infarction.
In the first days of MI, acute “stress” ulcers of the gastrointestinal tract may occur, which are often complicated by gastrointestinal bleeding. Treatment of gastroduodenal bleeding consists of intravenous administration of 400 ml of fresh frozen plasma (under central venous pressure control), 150 ml of a 5% solution of aminocaproic acid.
It is also recommended to take antacids; in the absence of contraindications, H2-histamine receptor blockers and/or selective anticholinergics (gastrocepin). For paresis of the gastrointestinal tract, fasting, removal of the stomach contents and its rinsing with a sodium bicarbonate solution, and infusion therapy are recommended. With a chain of stimulation of gastric and intestinal motility, 20 ml of 10% sodium chloride solution, 0.5-0.75 ml of 0.05% proserin solution or 1 ml of 0.01% carbocholine solution are prescribed intravenously, metoclopramide orally 0.01 4 times per day or intramuscularly, cisapride 0.01 3 times a day.
For painful hiccups, aminazine is administered intramuscularly (under blood pressure control) or a phrenic nerve block is performed. To relieve acute psychosis, intravenous administration of 1-2 ml of seduxen and 1-2 ml of 0.25% droperidol solution is recommended.
Acute myocardial infarction without a pathological Q wave (small-focal myocardial infarction) Characterized by the development of small foci of necrosis in the myocardium. Clinic and diagnostics.
The clinical picture of small-focal myocardial infarction resembles the picture of extensive MI. The difference is the shorter duration of the pain attack, the rare development of cardiogenic shock and a lower degree of hemodynamic disturbances.
The course is relatively favorable compared to large-focal MI. Small focal MI, as a rule, is not complicated by circulatory failure, but various rhythm and conduction disturbances, including fatal ones, often occur.
Although the area of necrosis in patients with MI without a Q wave is usually smaller than in those with a Q wave, they are more likely to develop recurrent infarctions, and the long-term prognosis is the same in both groups. On the ECG: the QIRS complex usually does not change, in some cases the amplitude of the R wave decreases, the ST segment may shift downward from the isoline (subendocardial infarction), the T wave becomes negative, “coronary”, sometimes biphasic and remains negative for 1-2 months.
An increase in body temperature to subfebrile levels persists for 1-2 days, laboratory data are characterized by the same manifestations of resorption-necrotic syndrome as with large-focal myocardial infarction, but they are less pronounced and less durable. Treatment is carried out according to the same principles as for large-focal myocardial infarction.
The effectiveness of thrombolysis in small focal MI has not been proven.
Attention! The described treatment does not guarantee a positive result. For more reliable information, ALWAYS consult a specialist.
Myocardial infarction is a clinical form of coronary artery disease characterized by the development of ischemic myocardial necrosis caused by complete cessation of coronary circulation. It is based on thrombosis of the coronary arteries.
Etiology: In most cases, the basis for the development of MI is atherosclerotic damage to the coronary arteries, causing a narrowing of their lumen. Often, atherosclerosis of the arteries is accompanied by acute thrombosis of the affected area of the vessel, causing a complete or partial cessation of blood supply to the corresponding area of the heart muscle. Thrombosis is promoted by increased blood viscosity. In some cases, MI occurs against the background of spasm of the branches of the coronary arteries. Other causes may be embolization of the coronary artery (thrombosis due to coagulopathy, fat embolism), congenital defects of the coronary arteries. The development of MI is facilitated by risk factors such as diabetes mellitus, hypertension, obesity, physical inactivity, dyslipidemia, heredity (for ischemic heart disease), age, mental stress, alcoholism, smoking, etc.
Pathogenesis: violation of the integrity of the endothelium, erosion or rupture of an atherosclerotic plaque -> platelet adhesion, formation of a “platelet plug” -> layers of erythrocytes, fibrin, platelets with rapid growth of a parietal thrombus and complete occlusion of the arterial lumen -> ischemic damage to the myocardial region supplied by the given coronary artery ( 15-20 minutes, reversible condition) -> myocardial necrosis (more than 20 minutes, irreversible condition).
Classification:
1. By volume of lesion:
- Large-focal (transmural), Q-infarction
- Small focal, non-Q infarction
2. According to the depth of the lesion:
- Transmural
- Intramural
- Subendocardial
- Subepicardial
3. By stages of development (with Q-infarction):
- Extremely acute, or developing (up to 6 hours)
- Acute or developed (6 hours – 7 days)
- Subacute, or scarring, or healing (7 – 28 days)
- Healed, or scar (starting from 29 days)
4. By localization:
- Left ventricular MI (anterior, posterior, lateral, inferior)
- Isolated apex myocardial infarction
- MI of the interventricular septum (septal)
- Right ventricular MI
- Combined localizations: posterior-inferior, anterior-lateral, etc.
5. Downstream:
- Monocyclic
- Lingering
- Recurrent MI
- Repeated MI
Clinical variants of “uncomplicated” MI. The most common is the anginal variant of MI. It manifests itself as intense chest pain, usually of a pressing, squeezing, burning nature, radiating to the left arm and shoulder blade, neck, lower jaw, and may be accompanied by a feeling of fear of death, anxiety, agitation, and cold sweat. Lasts 20 minutes or more. In most cases, it is not completely relieved by taking nitroglycerin, and sometimes by repeated injections of narcotic analgesics. The pain syndrome may have a “wavy” character, decreasing slightly and then intensifying again.
In the asthmatic variant, the leading manifestations are acute left ventricular failure - cardiac asthma or pulmonary edema, and chest pain
may be either absent or mild. It occurs more often in elderly patients suffering from CHF. More often develops with repeated MI.
The gastralgic (abdominal) variant of MI is manifested by epigastric pain and may be accompanied by nausea, vomiting, and bloating. An objective examination may even register tension in the muscles of the anterior abdominal wall, which sometimes leads to laparotomy. Therefore, it must be remembered that all patients with suspected “acute abdomen” must have an ECG recorded. More often observed with diaphragmatic MI.
The arrhythmic variant is characterized by various rhythm disturbances, for example, atrial fibrillation, supraventricular, ventricular tachycardia. Atrioventricular and sinoauricular blocks can also be recorded. Pain syndrome may be absent or mild. Therefore, especially if tachy- or bradyarrhythmia occurs for the first time, especially in individuals with risk factors for coronary artery disease, analysis of biomarkers of myocardial necrosis is necessary to exclude MI.
The cerebrovascular variant is manifested by cerebral symptoms of a different nature: fainting, dizziness, focal neurological symptoms, nausea, vomiting, sometimes signs of a transient cerebrovascular accident, and sometimes have the character of a severe stroke. Cerebral ischemia develops due to a decrease in myocardial contractility. Symptoms can be either reversible or persistent. It most often occurs in elderly patients with initially stenotic extracranial and intracranial arteries, often with cerebrovascular accidents in the past.
The low-symptomatic (painless) form of MI is not so rare. In this case, signs of a previous myocardial infarction are a random finding on an ECG or during an autopsy, and a careful history taking does not reveal an episode of anginal pain.
Diagnosis: 1. medical history (risk factors, whether there have been previous myocardial infarctions, the presence of angina pectoris, heredity). 2. examination (pallor and moisture of the skin, there may be cyanosis, decreased skin temperature; precordial pulsation, charged jugular veins, their pulsation). 3. physical examination (increased blood pressure, increased heart rate (in complicated cases, vice versa), moist rales in the lungs; muffled tones, pericardial friction noise, systolic murmur, proto-diastolic gallop rhythm).
4. laboratory diagnostics: CBC (leukocytosis may be observed several hours after the onset of MI, then an increase in ESR and a decrease in leukocytes), markers (troponins T and I begin to increase after 3-4 hours and remain at a high level for up to 14 days; CK-MB – rise after 4-5 hours, up to 3-4 days; myoglobin 2 hours after the onset of the attack).
5.instrumental diagnostics: ECG (in the acute period - ST elevation, high T wave; in the acute period - ST elevation, pathological Q wave, T wave inversion; in the subacute period - ST descends to the isoline, negative T, pathological Q; in the scar stage – pathological Q wave, ST on the isoline, T positive),
Additional: Ultrasound (hypo- and akinesia zones), radioisotope diagnostics (cold and hot foci), CT, MRI, angiography and coronary angiography.
Treatment: Emergency care:
1. Bed rest;
2. If the patient has not taken nitroglycerin: 0.5 mg of short-acting nitroglycerin under the tongue once and then up to 3 times every 5 minutes under the control of heart rate (heart rate ≤100 beats/min) and systolic blood pressure (BP ≥ 100 mmHg).
3. Ensuring reliable intravenous access: peripheral intravenous catheter;
4. Acetylsalicylic acid in a dose of 150–300 mg, chew the tablet, take orally.
5. β-blockers in minimal doses for oral administration (bisoprolol 1.25 mg or metoprolol succinate 12.5 mg, or carvedilol 3.125 mg, or nebivolol 1.25 mg) should be prescribed if the patient does not have: 1) signs of heart failure ; 2) proven reduction in left ventricular ejection fraction ≤35%; 3) high risk of cardiogenic shock (age >70 years, systolic blood pressure 110 or 0.24 seconds or atrioventricular block II–III degree; 5) bronchial asthma.
6. The drug of first choice for pain relief is morphine, which also reduces feelings of fear and anxiety. Morphine is administered exclusively intravenously and in fractions: 10 mg (1 ml of 1% solution) is diluted in 10 ml of physiological solution and administered slowly, first 4–8 mg, then an additional 2 mg at intervals of 5–15 minutes until the pain syndrome is completely eliminated or until side effects (nausea and vomiting, hypotension, bradycardia and respiratory depression). Hypotension and bradycardia are stopped by slow intravenous administration of atropine: 1 mg (1 ml of 0.1% solution) is diluted in 10 ml of saline and 0.1–0.2 mg is administered at intervals of 15 minutes (maximum dose 2 mg). If breathing slows down to less than 10 per minute or Cheyne-Stokes type breathing occurs, it is recommended to use slow intravenous administration of naloxone: 0.4 mg (1 ml of solution) diluted in 10 ml of saline and administered 0.1–0.2 mg at intervals of 15 minutes (maximum dose 10 mg). If there is severe anxiety, sedatives are administered, but in many cases morphine is sufficient. An effective method of pain relief for ACS is neuroleptanalgesia: simultaneous administration of the narcotic analgesic fentanyl (1–2 ml of a 0.005% solution) and the neuroleptic droperidol (2–4 ml of a 0.25% solution). The mixture in one syringe diluted in 10 ml of saline is administered intravenously, slowly, under the control of blood pressure and respiratory rate. The dose of fentanyl is 0.1 mg (2 ml), and for persons over 60 years of age with a body weight of less than 50 kg or chronic lung diseases - 0.05 mg (1 ml). The effect of the drug lasts up to 30 minutes, which must be taken into account when pain returns and before transporting the patient. Droperidol causes pronounced vasodilation, so its dose depends on the initial level: with systolic blood pressure up to 100 mm Hg. - 2.5 mg (1 ml of 0.25% solution), up to 120 mm Hg. - 5 mg (2 ml), up to 160 mm Hg. - 7.5 mg (3 ml), above 160 mm Hg. - 10 mg (4 ml).
7. To relieve breathing problems: shortness of breath, acute heart failure, hypoxia (blood oxygen saturation measured by pulse oximeter (SaO2) less than 95%), oxygen is administered at a rate of 2–4 l/min through a mask or nasal cannula.
Groups of drugs used for MI:
- Thrombolytics (streptokinase, alteplase) for STEMI
- Anticoagulants (unfractionated heparin, low molecular weight heparin - enoxaparin), fondaparinux. Heparin IV bolus
- Antiplatelet agents (acetylsalicylic acid, clopidogrel, ticlopidine)
- Nitrates
- Beta blockers
- Statins (atorvastatin, rosuvastatin)
- iAPF (sartans)
Primary and secondary prevention: Primary prevention: addressing risk factors to inhibit atherosclerotic events. Secondary prevention: prevents complications and inhibits the worsening of clinical manifestations.
Primary prevention consists of non-drug measures that are aimed at improving lifestyle and influencing risk factors. Modifiable risk factors include dyslipidemia, low physical activity, smoking, arterial hypertension, overweight and obesity, and diabetes. Prevention measures: quit smoking, increase physical activity (aerobic, dynamic, which involve most muscle groups, train the cardiorespiratory system and increase endurance - running, brisk walking, swimming, aerobics, etc.; frequency control is used to determine the duration and severity of physical activity heart contractions: submaximal heart rate = (220-age) * 0.75. Correction of dyslipidemia (cholesterol less than 4 mmol/l, LDL less than 1.5 mmol/l). Healthy nutrition (with calculation of calorie content of the daily diet, diets: sea fish, 1-2 tablespoons of vegetable oils, legumes, vegetables, herbs, fruits, soybeans, plant products high in fiber, with pectin) Educational work among the population.
Secondary prevention: non-drug (smoking cessation, diet, physical activity, blood pressure control, diabetes mellitus), drug therapy: antiplatelet agents (aspirin 75-100 mg,
clopidogrel 75 mg/day) - duration of dual antiplatelet therapy 12 months, beta-blockers, ACE inhibitors, sartans (valsartan), aldosterone receptor blockers (eplerenone), statins (atorvastatin 80 mg/day, rosuvastatin, simvastatin), dihydropyridine calcium antagonists, nitrates. Immunization against influenza.
Stages of rehabilitation:
- inpatient (starting and performed in a regular ward of the infarction department of a hospital or vascular center)
- inpatient rehabilitation (carried out in an inpatient cardiac rehabilitation department)
- outpatient (performed in the dispensary and outpatient department of a specialized Rehabilitation Center, including cardiology, or in a territorial outpatient clinic). At this stage, in the first months after discharge from the hospital, these measures should be carried out under medical supervision, and then independently.
The positive effect of physical training is explained by the following effects: anti-ischemic, anti-atherosclerotic, antithrombotic, antiarrhythmic, mental.
Principles of rehabilitation:
- individual approach
- early start
- strict dosage and phasing
- continuity and regularity
Myocardial infarction (MI) is ischemic necrosis of a region of the heart that occurs as a result of an acute discrepancy between the myocardial oxygen demand and its delivery through the coronary arteries.
Epidemiology: MI is one of the most common causes of death in developed countries; in the USA, 1 million patients annually, 1/3 of them die, ½ of them die within the first hour; incidence of 500 men and 100 women per 100 thousand population; Until the age of 70, men get sick more often, then - equally with women.
Etiology of MI: coronary artery thrombosis in the area of atherosclerotic plaque (90%), less often - coronary artery spasm (9%), thromboembolism and other causes (coronary embolism, congenital defects of the coronary arteries, coagulopathy - 1%).
Pathogenesis of myocardial infarction: violation of the integrity of the endothelium, erosion or rupture of an atherosclerotic plaque; adhesion of platelets, formation of a “platelet plug”; layering of red blood cells, fibrin, platelets with rapid growth of a parietal thrombus and complete occlusion of the lumen of the artery; ischemic damage to the myocardial region supplied by blood (15-20 min, reversible condition) myocardial necrosis (irreversible condition).
Clinical picture and variants of the course of MI.
In the clinical course of a typical MI, there are 5 periods:
1. Prodromal, or pre-infarction, period (from several minutes to 1-1.5 months) – clinically manifested by the clinic of unstable angina with transient ischemic changes on the ECG.
2. The most acute period (from 2-3 hours to 2-3 days) – often occurs suddenly, is determined by the appearance of signs of necrosis on the ECG, various variants of the course are characteristic:
a) anginal variant (status anginosus, typical variant) - extremely intense, wavy, pressing (“a hoop, iron pincers squeezing the chest”), burning (“a fire in the chest, a feeling of boiling water”), squeezing, bursting, sharp (“ dagger") pain behind the sternum, grows very quickly, widely radiates to the shoulders, forearms, collarbones, neck, lower jaw on the left, left scapula, interscapular space, lasts from several hours to 2-3 days, accompanied by excitement, a feeling of fear, motor restlessness , vegetative reactions, are not relieved by nitroglycerin.
b) asthmatic variant (AFV) – manifested by the clinical manifestations of cardiac asthma or alveolar pulmonary edema; more common in patients with repeated MI, severe hypertension, in old age, with dysfunction of the papillary muscles with the development of relative mitral valve insufficiency
c) arrhythmic variant - manifested by paroxysmal tachycardia, ventricular fibrillation, complete AV block with loss of consciousness, etc.
d) abdominal (gastralgic) variant - pain suddenly occurs in the epigastric region, accompanied by nausea, vomiting, gastrointestinal paresis with severe bloating, tension in the muscles of the abdominal wall; more common with lower localization of necrosis
e) cerebral variant - can begin with clinical manifestations of dynamic disorders of cerebral circulation (headache, dizziness, motor and sensory disorders).
f) peripheral with atypical localization of pain (left-handed, left-scapular, laryngeal-pharyngeal, upper vertebral, mandibular)
g) erased (low-symptom)
Other rare atypical variants of MI: collaptoid; hydropic
3. Acute period (up to 10-12 days) – the boundaries of necrosis are finally determined, myomalacia occurs in it; pain disappears, resorption-necrotic syndrome is characteristic (increase in body temperature to subfebrile, neutrophilic leukocytosis, increase in ESR from 2-3 days for 4-5 days, increase in the activity of a number of cardiac-specific enzymes in the LHC: AST, LDH and LDH1, CPK, CPK- MV, myoglobin, TnT, TnI).
4. Subacute period (up to 1 month) – a scar is formed; Manifestations of resorption-necrotic syndrome and heart failure soften and disappear.
5. Post-infarction cardiosclerosis: early (before 6 months) and late (after 6 months) – consolidation of the formed scar.
1. characteristic pain syndrome (status anginosus), not relieved by nitroglycerin
2. ECG changes typical of myocardial necrosis or ischemia
According toBayley, ECG during MI is formed according to the influence of three zones: zones of necrosis– located in the center of the lesion (Q wave), damage zones– located on the periphery of the necrosis zone (ST segment), ischemic zones– located on the periphery of the damage zone (T wave)
Typical changes characteristic ofQ-myocardial infarction:
1) the most acute period– first, a high, pointed T wave (there is only an ischemic zone), then a dome-shaped elevation of the ST segment appears and its fusion with the T wave (a zone of damage appears); in leads characterizing the myocardial zones opposite to the infarction, reciprocal depression of the ST segment can be recorded.
2) acute period– a zone of necrosis appears (pathological Q wave: duration more than 0.03 s, amplitude more than ¼ R wave in leads I, aVL, V1-V6 or more than ½ R wave in leads II, III, aVF), the R wave may decrease or disappear ; The formation of a negative T wave begins.
3) subacute period– the ST segment returns to the isoline, a negative T wave is formed (characterized by the presence of only zones of necrosis and ischemia).
4) post-infarction cardiosclerosis– the pathological Q wave remains, the amplitude of the negative T wave may decrease, and over time it may become smoothed or even positive.
For nonQ myocardial infarction, changes in the ECG will occur, depending on the stage, only with the ST segment and T wave. In addition to the typical changes in the ECG, MI may be indicated the first complete blockade of the left bundle branch.
TopClinical diagnosis of MI based on ECG data: anterior septal – V 1 -V 3; anterior apical – V 3, V 4; anterolateral – I, aVL, V 3 -V 6; anterior extensive (widespread) – I, II, aVL, V 1 -V 6; anteroposterior – I, II, III, aVL, aVF, V 1 -V 6; lateral deep – I, II, aVL, V 5 -V 6; lateral high – I, II, aVL; posterior phrenic (lower) – II, III, aVF.
If the standard ECG is not very informative, you can take an ECG in additional leads (along the Sky, etc.) or do a cardiotopographic study (60 leads).
Myocardial infarction is necrosis of a section of the heart muscle that occurs as a result of the combined effect of impaired coronary blood flow and myocardial hypoxia, leading to dysfunction of the heart, blood vessels and other organs.Depending on the prevalence of necrosis, large-focal and small-focal infarctions are distinguished. Taking into account the location of necrosis according to the thickness of the ventricular wall, transmural, intramural, subendocardial and subepicardial infarctions are distinguished. Based on the location of necrosis, the anterior, lateral, and posterior walls of the left ventricle and septal infarctions are most often distinguished. Often, patients have simultaneous damage to different parts of the myocardium.
Etiology:
The cause of myocardial infarction is a violation of the neuroendocrine regulation of coronary circulation, respiration and thrombus formation. Disturbances of coronary blood flow: this is anatomical narrowing, spasm, thrombosis, embolism of coronary vessels, hypoxia and deep disturbances of metabolic processes in the myocardium, a combination of the effects of coronary sclerosis and myocardial hypoxia.Factors contributing to the development of myocardial infarction: smoking, irregular and unbalanced diet, obesity, mental and physical stress, genetic deficiency of regulation.
Pathogenesis:
Factors leading to myocardial necrosis are disruption of coronary blood flow, hypoxia and changes in metabolism.Factors arising from the appearance of myocardial necrosis: acute heart failure, acute vascular failure, cardiac arrhythmia, rupture of the heart muscle, the formation of thromboendocarditis.
Necrosis of an area of the myocardium occurs after two to three hours of cessation of coronary blood flow with little compensation due to collaterals, and this determines the severity of clinical manifestations. Necrosis formation can be longer with intensive compensation of impaired blood flow and with the action of hypoxia as the main pathogenic factor. The action of pathogenic factors can be simultaneous, which creates favorable opportunities for scarring of the resulting myocardial necrosis and restoration of its functions.
Clinical picture:
The main clinical symptom of myocardial infarction is a painful attack. The localization and irradiation of pain during myocardial infarction do not differ significantly from those during an attack of angina. Often there is the development of an intense pain attack in the retrosternal region, precordial region, in some cases the pain spreads to the entire anterolateral surface of the chest, less often an atypical localization may appear.Pain in a typical myocardial infarction radiates to the left arm, shoulder, scapula; in some cases, pain radiates to the right arm, scapula, and jaw.
The nature of the pain is very diverse: pressing, squeezing, cutting. The pain is not relieved by taking nitroglycerin and requires the use of drugs, neuroleptoanalgesia and even anesthesia. The duration of a painful attack can vary - from 1–2 hours to several days.
On auscultation, muted tones are noted; in a number of patients, a presystolic gallop rhythm is heard at Botkin's point. During the first day of the disease, a pericardial friction noise may appear, associated with reactive pericarditis, which can persist for a short time - from one to three days.
Thirty percent of myocardial infarction cases may present atypically. The following forms are distinguished: asthmatic, gastrological, arrhythmic, cerebral and asymptomatic.
The gastralgic variant of myocardial infarction is characterized by the appearance of a painful attack in the epigastric region with spread to the retrosternal space. At the same time, dyspeptic complaints arise: belching with air, hiccups, nausea, repeated vomiting, bloating with a feeling of expansion of the abdominal cavity. The gastrolgic variant of myocardial infarction should be differentiated from foodborne toxic infection, perforated gastric ulcer, and pancreatitis.
The asthmatic variant of myocardial infarction is characterized by the development of acute left ventricular failure, which seems to obscure the pain syndrome and manifests itself in the form of an attack of suffocation.
The arrhythmic variant of myocardial infarction is characterized by the occurrence of an acute rhythm disturbance with the development of a life-threatening arrhythmia. These include polytopic ventricular extrasystole, ventricular tachycardia, ventricular fibrillation, paroxysmal tachycardia, atrial fibrillation, and cardiac conduction disturbances.
Cerebral variant of myocardial infarction. Caused by the development of cerebral circulatory disorders in the acute period of myocardial infarction, which is associated with a decrease in blood supply to the brain, especially with the development of cardiogenic shock. It will manifest itself by the appearance of general cerebral symptoms with symptoms of cerebral ischemia: nausea, dizziness, impaired consciousness, with the development of fainting and also in the form of focal symptoms in the brain, simulating a violation of cerebral circulation in one or another area of the brain.
The asymptomatic variant of myocardial infarction is characterized by the absence of clinical manifestations of myocardial infarction and the unexpected manifestation of acute myocardial infarction on the ECG. The frequency of this variant ranges from one to ten percent among all atypical forms of the disease.
Recurrent myocardial infarction is characterized by a long, protracted course of 3–4 weeks or longer. This form of the disease is based on slow processes of connective tissue replacement of areas of necrosis in the heart muscle.
The clinical picture of recurrent myocardial infarction is characterized by the manifestation of particularly frequent paroxysmal chest pain, the development of a painful attack of varying intensity, which may be accompanied by the development of acute rhythm disturbances and cardiogenic shock. Often, recurrent myocardial infarction develops according to the asthmatic variant of the course.
Diagnostics:
Diagnosis of myocardial infarction is based on data from an electrocardiographic study, biochemical parameters, increased levels of creatine phosphokinase (CPK), lactate dehydrogenase (LDH), AST and ALT. Signs of myocardial infarction are noted on the ECG by the appearance of a pathological Q wave, a decrease in the voltage of the R wave or an increase in the S-T interval, and T wave inversion.The diagnosis of myocardial infarction is made on the basis of the clinical picture of an anginal attack, characteristic changes on the ECG: the appearance of a pathological Q wave, elevation of the S-T segment, monophasic curve, negative T wave.
The typical clinical picture of an attack with the appearance of characteristic sequences (hyperleukocytosis, hyperthermia, increased erythrocyte sedimentation rate, signs of pericarditis) suggests a heart attack and treats the patient even if there are no changes on the ECG that are evidence of a heart attack.
The diagnosis is confirmed by analysis of the further course of the disease, identification of hyperfermentemia, complications, especially left ventricular failure of the heart. In the same way, a retrospective diagnostic assumption about myocardial infarction complicating the course of other diseases or the postoperative period is justified.
To diagnose a small-focal infarction, the patient must have the three above-mentioned components (intensity and duration of a painful attack, reactive changes in the blood, body temperature, serum enzymes, and changes on the ECG are usually less pronounced).
The reliability of the diagnosis is based only on the appearance of a negative T wave (in the absence of convincing clinical and laboratory data, this is doubtful). As a rule, small-focal infarction is observed in people who have long suffered from coronary heart disease and cardiosclerosis.
