Myocardial infarction etiology clinic diagnostics. myocardial infarction

Cardiac ischemia

(modern aspects of clinic, diagnostics, treatment,

prevention, medical rehabilitation, expertise)

The main cause of MI is atherosclerosis of the coronary arteries (95%). In 35% of patients, MI can develop as a result of CA embolism (infective endocarditis, intraventricular thrombi), congenital defects in the development of coronary vessels and other CA lesions (coronaritis in systemic lupus erythematosus, rheumatism, rheumatoid arthritis). However, in these cases, MI is not regarded as a clinical form of coronary artery disease, but as a complication of one of the listed diseases. In most cases, the cessation or sharp restriction of coronary blood flow occurs as a result of coronary thrombosis, which usually develops in the area of a “complicated” atherosclerotic plaque, the thinned capsule of which is damaged (tear, ulceration, exposure of the lipid core of the plaque). This contributes to the activation of platelet and plasma coagulation factors by tissue thromboplastin and collagen. MI can occur as a result of spasm of the coronary artery against the background of atherosclerosis or with severe stress, the use of cocaine, amphetamines. The causes of MI may be congenital anomalies of the coronary arteries, thrombosis in arteritis and heart injury, dissection of the coronary artery and aorta. In young women, MI is more likely to develop with a combination of tobacco smoking and the use of hormonal contraceptives.

Initially, a platelet “white” parietal thrombus is formed. At the same time, a number of biologically active substances with a powerful vasoconstrictor effect (endothelin, serotonin, thrombin, antithrombin A2) are released in this area. As a result, a pronounced spasm of the stenotic coronary artery occurs, further limiting the blood flow through the coronary artery.

Small platelet aggregates can embolize coronary vessels at the microcirculatory level, further limiting coronary blood flow. Gradually, the size of the parietal thrombus increases and, if it does not spontaneously lysis as a result of natural activation of its own fibrinolytic system or thrombolytic therapy is not carried out, the thrombus completely occludes the lumen of the vessel and transmural MI (infarction with a Q wave) develops.

When, for various reasons, complete occlusion of the coronary artery does not occur or spontaneous thrombus lysis occurs, subendocardial or intramural MI (non-Q wave infarction) may develop. The latter can also develop with complete occlusion of the coronary artery, if collaterals are well expressed. In 75% of cases, the process of formation of a total thrombus, completely blocking the lumen of a large CA, can take from 2 days to 2-3 weeks. During this period, the clinical picture of a progressive deterioration in coronary blood flow generally corresponds to the symptoms of unstable angina pectoris (preinfarction syndrome). In 1/4 patients with MI, the process of formation of a total, completely occluding thrombus proceeds at lightning speed. In these cases, there are no symptoms of the prodromal period in the clinical picture of the disease.

The rapid formation of a focus of necrosis in the heart muscle can be facilitated by 3 additional factors: pronounced spasm of the CA; poor development of collateral vessels; a pronounced increase in myocardial oxygen demand as a result of physical or psycho-emotional stress, an increase in blood pressure and other reasons. All three factors lead to an increase in the rate of formation of the focus of necrosis and its volume. Under conditions of well-developed collateral circulation, even complete, but gradual, occlusion of the coronary artery in some cases may not be accompanied by the development of MI.

Morphological data

The earliest morphological changes in the myocardium in MI can be detected using electron microscopy. As early as 15-20 minutes after coronary occlusion, mitochondrial swelling and glycogen depletion are detected. 60 minutes after the cessation of coronary circulation, irreversible ischemic damage to the cell is revealed in the form of nuclear chromatin decay and pronounced contracture of sarcomeres. When using light microscopy, the first changes in the focus of MI are detected only after 12-18 hours from the onset of a heart attack. There is an expansion of capillaries, swelling of muscle fibers. After 24 hours, fragmentation of muscle fibers and infiltration with polymorphonuclear leukocytes are detected. Macroscopically, the picture of MI begins to be detected only after 18-24 hours from the onset of the disease. The focus of necrosis looks pale and edematous, and after 48 hours the area of necrosis acquires a gray tint and becomes flabby. In an uncomplicated course, the process of scar formation is completed approximately 6 weeks after the onset of MI.

During the formation of MI, the diastolic and systolic functions of the left ventricle are disturbed, and the process of its remodeling begins. At the same time, there are significant changes in the functional state of other organs and systems. LV diastolic dysfunction is one of the first manifestations of ischemia and developing MI. Diastolic dysfunction is caused by increased stiffness (reduced compliance) of the heart muscle during diastole. The initial stages of diastolic dysfunction are characterized by a decrease in the rate of diastolic relaxation and the volume of early diastolic filling (in the phase of rapid filling of the ventricle). The volume of blood flow in the LA systole increases. A significant part of LV diastolic filling occurs only at the end of diastole, during LA systole. Further worsening of the LV diastolic function leads to an increase in LV blood pressure, filling pressure and mean pressure in the LA and veins of the pulmonary circulation, which significantly increases the risk of blood stasis in the lungs.

LV systolic dysfunction manifests itself in impaired regional LV contractility and in the appearance of signs of global LV systolic dysfunction. Violations of local LV contractility in MI develop very early. At first, they resemble those found in patients with stable angina during exercise tests or in patients with NS after an anginal attack. However, already a day after the onset of MI, hypokinesia of the necrotic area of the heart muscle, reflecting the function of the hibernating (“sleeping” under conditions of severe ischemia) myocardium, is replaced by its akinesia - the absence of contraction of the necrotic area of the heart muscle during systole. The most serious violation of local contractility is dyskinesia - a paradoxical bulging of the area of necrosis at the time of systole. In the area of intact cardiac muscle, there is often an increase in the contractility of intact LV sections, of a compensatory nature.

The decrease in the global systolic function of the left ventricle in MI consists in a decrease in EF, SV, SI, MO, BP; in increasing KDD and KDO LV; in the appearance of clinical signs of left ventricular failure and stagnation of blood in the pulmonary circulation; in the appearance of signs of systemic disorders of the peripheral circulation, including at the microcirculatory level. The pumping function of the left ventricle in MI is determined by the extent of the necrosis focus. In each case, this dependence can be significantly violated, since an even greater deterioration in hemodynamics may be associated with the development of acute LV aneurysm, the appearance of mitral regurgitation in papillary muscle infarction or perforation of the IVS, severe myocardial hypertrophy, the presence of diastolic dysfunction of the heart muscle, the state of myocardial areas adjacent to the infarction. not involved in the process of infarction.

LV remodeling in MI is a set of changes in the structure and function of the LV, due to the formation of MI in the heart muscle. The most significant changes occur in transmural MI. An extensive focus of necrosis formed in the LV wall experiences high intraventricular pressure created by the intact ventricular myocardium during systole. LV remodeling is more pronounced in patients with extensive anterior transmural MI. In these cases, remodeling begins as early as 24 hours after the onset of infarction and continues for a long time (weeks and months).

The severity of the remodeling process is influenced by several factors:

The size of the MI (the larger the area of the infarction, the more pronounced are the structural changes in the left ventricle).
The size of the peri-infarction zone (the area of ischemic or hibernating myocardium, directly bordering the zone of necrosis).
Mechanical properties of the necrosis zone.
The magnitude of the afterload, including the level of blood pressure, peripheral vascular resistance, the size of the LV cavity
Preload value (volume of venous return of blood to the heart).
SAS hyperactivation.
Hyperactivation of the RAAS, including tissue RAS.
Hyperproduction of endothelin and other vasoconstrictor substances.

The last three factors are of particular importance for the formation of compensatory hypertrophy of the intact myocardium, the development of cardiofibrosis and LV dilatation. Therefore, limiting the activity of the CAS, RAAS, and tissue RAS with the help of β-blockers, ACE inhibitors, and some other drugs can reduce the severity of the remodeling process. LV remodeling in patients with transmural MI leads to increased mortality, rapid progression of heart failure, frequent formation of LV aneurysms, and increased risk of myocardial rupture.

Functional and morphological changes in other organs and systems are determined by several main factors: hypoxia of organs associated with their hypoperfusion due to impaired pumping function of the heart (decrease in cardiac output, bcc, systemic blood pressure); increased pressure in the small and venous bed of the systemic circulation due to left ventricular or right ventricular failure; activation of the sympathetic-adrenal system, RAAS and tissue RAS; activation of the blood coagulation system and platelet aggregation; systemic microcirculation disorders.

An increase in pressure in the pulmonary veins and pulmonary capillaries, due to systolic and diastolic LV dysfunction, leads to an increase in the volume of extravascular fluid, impaired pulmonary ventilation and gas exchange, and the development of interstitial pulmonary edema. A decrease in cerebral perfusion is accompanied by a number of neurological manifestations, up to the development of ischemic stroke. Renal perfusion disorders in MI are often accompanied by proteinuria, microhematuria, and cylindruria. With cardiogenic shock, acute renal failure develops.

Increased activity of the blood coagulation system, characteristic of patients with MI, is accompanied by pronounced hematological changes, which are important not only for the formation of CA thrombosis, but also for the formation of platelet aggregates in the microcirculatory vascular bed. Excessive activation of the SAS that occurs during MI contributes to increased peripheral vasoconstriction and the development of severe cardiac arrhythmias.

ATHEROSCLEROSIS

Pavlova T.V., Pichko G.A.

1.2 Pathogenesis

1.4 Laboratory and instrumental diagnostics 1.5 Treatment and prevention

ATHEROSCLEROSIS IN DIABETES MELLITUS

Shustov S.B.

2.1. Definition, features of pathogenesis in diabetes mellitus 2.2. Clinical manifestations 2.3. Diagnosis of diabetic foot syndrome 2.4. Differential diagnosis of diabetic foot forms 2.5. Prevention of diabetic macroangiopathies 2.6. Conservative treatment 2.7. Surgery

CARDIAC ISCHEMIA

Kryukov N.N., Nikolaevsky E.N.

3.2 Etiology and pathogenesis

SUDDEN CARDIAC DEATH

Nikolaevsky E.N., Polyakov V.P.

4.6 Treatment and prevention

STABLE ANGINA

Kryukov N.N., Nikolaevsky E.N., Polyakov V.P., Pavlova T.V., Pichko G.A.

5.3 Laboratory and instrumental diagnostics 5.4 Conservative treatment 5.5 Prevention of angina attacks 5.6 Surgical treatment

SPECIAL FORMS OF CORONARY HEART DISEASE

Nikolaevsky E.N., Kryukov N.N.

6.1 Spontaneous (variant) angina pectoris 6.2 Silent myocardial ischemia 6.3 Cardiac syndrome X

UNSTABLE ANGINA

7.5 Laboratory and instrumental diagnostics 7.6 Conservative treatment 7.7 Surgical treatment

MYOCARDIAL INFARCTION

Kryukov N.N., Nikolaevsky E.N., Polyakov V.P., Kachkovsky M.A., Pichko G.A.

8.3 Etiology and pathogenesis

8.5 Laboratory and instrumental diagnostics 8.7 Quality of life in patients with myocardial infarction 8.8 Myocardial infarction of the right ventricle 8.9 Complications of myocardial infarction 8.10 Depression in patients with myocardial infarction

ACUTE CORONARY SYNDROME

Svistov A.S., Ryzhman N.N., Polyakov V.P.

9.3. Diagnosis of acute coronary syndrome 9.4. Imaging techniques in the diagnosis of ACS 9.6. Principles of treatment of acute coronary syndrome

HEART FAILURE

Kryukov N.N., Nikolaevsky E.N.

10.5 Chronic systolic heart failure 10.6 Classification of chronic heart failure 10.7 Laboratory and instrumental diagnostics 10.9 Chronic diastolic heart failure

DIAGNOSIS AND TREATMENT OF REVERSIBLE ISCHEMIC DYSFUNCTION

Svistov A.S., Nikiforov V.S., Sukhov V.Yu.

11.3 Methods for diagnosing reversible ischemic myocardial dysfunction 11.4 Positron emission tomography 11.5 Methods for assessing myocardial perfusion 11.6 Echocardiographic techniques 11.7 Magnetic resonance imaging 11.8 Basic approaches to the treatment of reversible ischemic myocardial dysfunction

RHYTHM AND CONDUCTIVITY DISORDERS

Kryukov N.N., Nikolaevsky E.N., Polyakov V.P., Pichko G.A.

12.4 Classification of arrhythmias 12.6 Instrumental diagnostics 12.7 Supraventricular arrhythmias 12.8 Ventricular arrhythmias 12.9 Medical treatment 12.10 Pacing 12.11 Electrical cardioversion 12.12 Surgical treatment

CURRENT STATE AND PROSPECTS OF CARDIAC SURGERY FOR CORONARY HEART DISEASE

Khubulava G.G., Payvin A.A., Yurchenko D.L.

13.1. Evolution of surgical treatment of coronary heart disease 13.3. Surgical myocardial revascularization 13.4. Catheterization methods of myocardial revascularization 13.7. Surgical treatment of heart failure 13.8. The role of the cardiologist in the postoperative management of patients 13.9. Prospects for cardiac surgical treatment of coronary heart disease

EXAMINATION OF TEMPORARY INABILITY OF PATIENTS WITH CORONARY HEART DISEASE

Dodonov A.G., Nikolaevsky E.N.

14.1 Examination of temporary disability 14.2 Medical and social examination 14.3 Rehabilitation of the disabled 14.4 Examination of disability in patients with myocardial infarction 14.5 Examination of disability in patients with angina pectoris 14.6 Examination of disability in patients with unstable angina pectoris

REHABILITATION TREATMENT OF PATIENTS WITH CORONARY HEART DISEASE

Udaltsov B.B., Nikolaevsky E.N., Dodonov A.G.

15.2 Rehabilitation treatment of patients with ischemic heart disease 15.3 Rehabilitation treatment of patients with myocardial infarction 15.4 Rehabilitation treatment of patients with stable angina pectoris 15.6 Rehabilitation treatment of patients with rhythm disturbances 15.7 Rehabilitation treatment of patients after coronary artery bypass grafting

MEDICAL AND PSYCHOLOGICAL REHABILITATION OF PATIENTS WITH MYOCARDIAL INFARCTION

Sukhova E.V.

16.1 Psychological aspects of myocardial infarction 16.3 Active muscle relaxation technique 16.4 Passive muscle relaxation technique 16.5 Autogenic training technique

www.medpro.ru

Infarct_myocarda

Myocardial infarction. Brief description of the disease

Etiopathogenetic aspects of myocardial infarction

Myocardial infarction is ischemic myocardial necrosis due to acute discrepancy between coronary blood flow and myocardial needs associated with coronary artery occlusion, most often due to thrombosis.

Etiology. In 97-98% of patients, atherosclerosis of the coronary arteries is of primary importance in the development of myocardial infarction. In rare cases, myocardial infarction occurs due to embolism of the coronary vessels, inflammation in them, pronounced and prolonged coronary spasm. The cause of an acute violation of the coronary circulation with the development of ischemia and necrosis of a portion of the myocardium, as a rule, is thrombosis of the coronary artery.

Pathogenesis. The occurrence of thrombosis of the coronary arteries is facilitated by local changes in the intima of the vessels (rupture of an atherosclerotic plaque or a crack in the capsule covering it, less often hemorrhage into the plaque), as well as an increase in the activity of the coagulation and a decrease in the activity of the anticoagulant system. When the plaque is damaged, collagen fibers are exposed, adhesion and aggregation of platelets occur at the site of damage, the release of platelet coagulation factors and the activation of plasma coagulation factors. A thrombus forms, closing the lumen of the artery. Thrombosis of the coronary artery, as a rule, is combined with its spasm. The resulting acute occlusion of the coronary artery causes myocardial ischemia and necrosis. The accumulation of underoxidized metabolic products during myocardial ischemia leads to irritation of myocardial interoreceptors or blood vessels, which is realized in the form of a sharp anginal attack.

Classification of myocardial infarction

According to the depth of the focus of necrosis, myocardial infarction happens:

Large focal and transmural myocardial infarction with Q wave,

Small focal myocardial infarction without Q wave.

According to the localization of the focus of necrosis, myocardial infarction happens:

right ventricle,

Anterior wall of the left ventricle

Inferior wall of the left ventricle

Lateral wall of the left ventricle

circular infarction,

high lateral divisions,

Apex of the heart

Interventricular septum.

By localization in the layers of the myocardium, there are:

subendocardial,

subepicardial,

Intramural.

2.3 Clinical forms of myocardial infarction

Clinically, there are 5 periods during myocardial infarction:

1). The prodromal period lasts from several hours to 30 days. The main feature of this period is considered to be recurrent pain syndrome and electrical instability of the myocardium, which is most often manifested by ventricular extrasystoles or paroxysmal ventricular tachycardia. It may often be absent.

2) The most acute period from the onset of acute myocardial ischemia to the appearance of signs of necrosis (from 30 minutes to 2 hours). The classical beginning in 70-80% of cases is characterized by the appearance of an anginal attack. The pain syndrome is often accompanied by a feeling of fear, agitation, anxiety, as well as autonomic disorders, such as increased sweating. In 20-30% of cases there may be atypical forms:

Arrhythmic. It is manifested by the occurrence of acute rhythm and conduction disturbances. These include polytopic, group, early ventricular extrasystole, paroxysmal ventricular tachycardia, ventricular fibrillation. Clinically, it can manifest as syncope.

Cerebrovascular. It is observed in patients with a burdened neurological history, manifested by the appearance of focal neurological symptoms.

Asthmatic. It occurs in patients with initial heart failure, with postinfarction or severe atherosclerotic cardiosclerosis, prolonged hypertension, and diabetes mellitus. The asthmatic form of myocardial infarction is suggested in cases where the leading symptom of the disease is a sudden, often unmotivated attack of shortness of breath or pulmonary edema.

Abdominal. It is more often observed with the localization of necrosis on the lower wall of the left ventricle. It is manifested by the appearance of pain in the epigastric region, nausea, vomiting, flatulence, stool disorder, and intestinal paresis. Often there is cyanosis, shortness of breath, while the abdomen remains soft and there are no symptoms of peritoneal irritation.

Asymptomatic. It is manifested by such non-specific symptoms as weakness, deterioration in sleep or mood, discomfort in the chest. It is usually observed in elderly and senile patients, especially those suffering from diabetes mellitus.

3) Acute period. Corresponds to the time of formation of the focus of necrosis and the emergence of the so-called resorption-necrotic syndrome associated with the general reaction of the body to the absorption (resorption) of necrotic masses into the blood, accompanied by a violation of the functional state of the cardiovascular system. With an uncomplicated course of myocardial infarction, the acute period usually lasts about 7-10 days.

4) Subacute period. In the subacute period of myocardial infarction, a connective tissue scar gradually forms, replacing necrotic masses. The duration of the subacute period varies widely and depends primarily on the volume of the focus of necrosis, the state of the surrounding myocardium not involved in the necrotic process, the degree of development of collaterals, the presence of concomitant diseases and complications of myocardial infarction. The duration of the subacute period is 4-6 weeks.

Postinfarction period. In the immediate post-infarction period, the amount of collagen increases in the scar area and its compaction (scar consolidation) is completed. At the same time, the formation of a number of compensatory mechanisms aimed at maintaining hemodynamics at the proper level continues.

diagnosis of myocardial infarction at the prehospital stage

The basis for the diagnosis of myocardial infarction at the prehospital stage is a thorough analysis of the pain syndrome, taking into account the anamnesis indicating the presence of coronary artery disease or relevant risk factors, the appearance of specific myocardial troponin T protein (tropanin test) and dynamic changes in the ECG.

Change on the ECG: the appearance of a pathological Q wave (wider than 0.03 s and deeper than ¼ 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, the formation of a negative T wave, the presence of reciprocal changes in opposite leads.

Complications of myocardial infarction

1. Cardiac rhythm and conduction disorders (early, reperfusion,

2. Asystole.

3. Cardiogenic shock.

4. Acute heart failure.

5. Ruptures of the heart (early and late, external and internal, complete and incomplete, slow and simultaneous) with the development of tampo-

6. Acute aneurysm of the heart.

7. Thrombosis of the left ventricle.

8. Early postinfarction angina pectoris.

Basic principles of medical care

at the prehospital stage

When starting to provide assistance for myocardial infarction, it should be well understood that the first minutes and hours from the moment it starts is the time when pharmacotherapy is most effective and the sooner treatment is started, the more likely it is to improve the prognosis of this extremely serious disease.

The provision of medical care at the prehospital stage is aimed at:

Adequate pain relief

Restoration of coronary blood flow,

Limiting the size of necrosis,

Treatment and prevention of early complications of myocardial infarction.

A patient with a myocardial infarction or suspected of having it should be immediately transferred to a horizontal position (lying, semi-lying, half-sitting, depending on the intensity of congestion in the lungs), oxygen therapy with 100% humidified oxygen should be started, and peripheral vein catheterization should be performed.

Anesthesia

Relief of an anginal attack is a prerequisite for all further therapeutic measures. Persistent anginal pain supports hyperactivation of the sympathadrenal system, which is accompanied by tachycardia, a positive inotropic effect, an increase in myocardial oxygen demand, and ultimately leads to an increase in the area of necrosis. Also, against the background of activation of the sympathadrenal system, the threshold for ventricular fibrillation decreases, which in itself can have fatal consequences.

In all cases, if there is no severe arterial hypotension (systolic pressure not lower than 90 mm Hg) and severe tachycardia or bradycardia, treatment is started with an aerosol form of nitroglycerin (nitrocor, nitrospray) or sodium isosorbide (isoket) 0.4 mg or sublingual forms of nitroglycerin 0.5 mg. Further, with severe anginal syndrome, nitroglycerin is prescribed intravenously, and with a relatively mild one, repeatedly sublingually.

Narcotic analgesics

The classic means of pain relief in patients with myocardial infarction is the use of narcotic analgesics.

Morphine, which is an opioid receptor agonist, in addition to the rapid relief of pain, reduces venous tone and, consequently, reduces venous blood return to the heart, preload and myocardial oxygen demand. In addition, morphine has a pronounced sedative effect. It is administered intravenously fractionally in 2-3 stages at a dose of 10 mg (1 ml of a 1% solution). First, within 2 minutes, 3-5 mg of the drug, then, if necessary and in the absence of side effects, repeat up to a total dose of 10 mg until the pain syndrome is completely relieved. Morphine should not be used in elderly debilitated patients with signs of respiratory depression. It is relatively contraindicated

with severe damage to the right ventricle and lower myocardial infarction with

bradycardia-hypotension syndrome.

Fentanyl has a powerful, fast-growing, but short-lived

noah analgesic activity. Administered intravenously at a slow dose

0.1 mg (2 ml of 0.005% solution) in 2 steps. Elderly patients 0.05 mg (1 ml of 0.005% solution). The action of the drug occurs after 1 minute, reaches a maximum after 3-7 minutes, but lasts no more than 25-30 minutes.

Neuroleptanalgesia

To enhance and prolong the effect of fentanyl, it can be combined with the antipsychotic droperidol. Its mechanism of action is due to the blockade of alpha-adrenergic receptors, which interrupts the flow of afferent impulses to the central nervous system and causes peripheral vasodilation. In addition, droperidol slightly slows down AV conduction and has a powerful antiemetic effect. Due to its effect on blood pressure, the dose of droperidol is selected depending on its initial level: with a systolic pressure of 100-110 mm Hg. administer 2.5 mg, 120-140 mm Hg - 5 mg, 140-160 mm Hg - 7.5 mg.

Ataranalgesia

The use of narcotic analgesics together with tranquilizers (usually diazepam) is possible, but significantly increases the risk of respiratory failure.

Nitrous oxide

Currently, the use of nitrous oxide in myocardial infarction is considered insufficiently effective, and the mask method of anesthesia is poorly tolerated by patients. Therefore, nitrous oxide in patients with myocardial infarction is inappropriate to use.

Limiting the size of the focus of myocardial necrosis

Intravenous administration of nitroglycerin in the first hours of the disease is more effective in limiting the size of necrosis than oral administration of drugs.

Indications for intravenous administration of nitroglycerin:

1. Persistent or recurrent anginal pain.

2. Persistent or recurrent acute congestive heart failure

failure.

3. The need for controlled antihypertensive therapy.

Contraindications to the appointment of nitropreparations:

1. Systolic pressure below 90 mm Hg. Art.

2. Heart rate 100 in 1 min.

3. Suspicion of damage to the right ventricle.

Aqueous solutions of nitroglycerin (perlinganite) or isosorbide dinitrate (isoket) are administered intravenously by drip or through a dispenser, selecting an individual injection rate until a clinical effect is achieved, but not allowing an excessive decrease in systolic pressure (not lower than 100-110 mm Hg) starting at a rate of 5 mcg /min The optimal infusion rate most often ranges from 40-60mcg/min.

Beta blockers

Patients who do not have contraindications need an early appointment of beta-adrenergic receptor blockers (propranolol, metoprolol). Early appointment of beta - blockers helps to reduce the size of ischemic damage to the myocardium, significantly reduces the incidence of complications and mortality.

Beta-blockers are especially effective in patients with additional risk factors:

1. Age over 60 years.

2. Myocardial infarction in history.

3. Arterial hypertension.

4. Heart failure.

5. Angina.

6. Treatment with cardiac glycosides and diuretics.

7. Diabetes.

The safest at the prehospital stage is the appointment of beta-blockers inside.

Propranolol is prescribed at a dose of 20 mg orally or sublingually. Metoprolol - 50 mg orally or sublingually.

Restoration of coronary blood flow

One of the most important stages in the provision of emergency care for myocardial infarction, taking into account the etiology and pathogenesis, is the restoration of blood flow in the ischemic zone and the correction of the rheological properties of blood, i.e. thrombolytic, anticoagulant and antiplatelet therapy.

Thrombolytic therapy

The basis of thrombolytic therapy is that all thrombolytic drugs activate plasminogen, a key proenzyme of the fibrinolytic system. As a result, plasminogen is converted into an active fibrinolytic enzyme - plasmin, which converts fibrin into a soluble state.

Indications for thrombolysis:

Anginal pain persisting without supporting factors for more than 30 minutes. and not inferior to repeated administration of nitroglycerin, accompanied by ST elevation in at least two leads or the appearance of bundle branch block. Thrombolytic therapy is indicated in the first 6 hours of the disease (with persistent or recurrent pain - 12-24 hours).

Contraindications for thrombolysis:

Absolute contraindications:

Severe injury, surgery or head trauma before -

marching 3 weeks;

Gastrointestinal bleeding in the previous 30 days;

Blood diseases (hemophilia, hemorrhagic diathesis);

Dissecting aortic aneurysm;

Oncological diseases;

Varicose veins of the esophagus;

Severe damage to the liver and kidneys;

bronchiectasis;

Pregnancy.

Relative contraindications:

Age over 70;

Transient cerebrovascular accident in previous 6

Type 2 diabetes

Treatment with indirect anticoagulants;

Puncture of non-compressible vessels;

Uncontrolled arterial hypertension (systolic blood pressure above 180

mmHg.);

allergic reactions;

Drugs used for systemic thrombolysis:

streptokinase,

Actelise (alteplase),

urokinase,

Tissue plasminogen activator.

Currently, streptokinase, Actelise are most often used for thrombolytic therapy.

Streptokinase is administered intravenously (drip or through a dispenser) at a dose of 1500,000 IU per 100 ml of isotonic sodium chloride solution for 30 minutes. At a high risk of allergic reactions, it is recommended to inject 30-60 mg of prednisolone intravenously into the streptokinase before the introduction of streptokinase. When prescribing streptokinase, it should be remembered that it has antigenic properties and after its administration, the titer of antibodies to streptokinase increases hundreds of times and remains high for several months. Therefore, streptokinase is not recommended to be re-administered for at least 2 years after the first application.

Unlike streptokinase, thrombolytic actilyse (alteplase) does not have antigenic properties, does not cause pyrogenic and allergic reactions, and at the same time is the most effective thrombolytic. Approximate regimen of administration: intravenously 15 mg as a bolus and 50 mg as an infusion over 30 minutes. and 35 mg IV drip over the next 60 minutes.

Signs of the effectiveness of thrombolytic therapy:

1. Termination of anginal pain.

2. Normalization or significant shift of the ST segment to the isoline.

Complications of thrombolytic therapy:

1. Reperfusion arrhythmias are the most common complication of thrombolytic therapy and, at the same time, indirect evidence of restoration of coronary blood flow. Most often it is an accelerated ideoventricular rhythm, ventricular extrasystoles, paroxysms of unstable ventricular tachycardia, transient AV blockade, ventricular fibrillation). Occurs in 20-60% of cases.

2. The phenomenon of "stunned myocardium" - a violation of the contractile function of the heart after the restoration of coronary blood flow - is manifested by signs of congestive heart failure.

3. Reocclusion of the coronary artery is observed in 15-20% of cases and is often asymptomatic. May be manifested by the resumption of anginal pain and deterioration of hemodynamics. At the same time, nitroglycerin, heparin and acetylsalicylic acid are prescribed intravenously.

4. Bleeding. Most often they develop from vein puncture sites. In this case, it is enough to apply a pressure bandage. In 1% of cases, bleeding can be significant.

5. Arterial hypotension. Usually corrected by reducing the rate of thrombolytic administration. If this is not enough, then the administration of the thrombolytic drug should be stopped and the patient's lower limbs raised by 20 degrees.

6. Allergic reactions. An immediate cessation of the administration of a thrombolytic is required and the appointment, depending on the severity and clinical manifestations, of antihistamines, glucocorticoid hormones, bronchodilators, and with the development of anaphylactic shock - adrenaline.

7. Hemorrhagic stroke. May develop in elderly patients with uncontrolled arterial hypertension and burdened neurological history. Therefore, thrombolytic therapy is not indicated for patients in this category. With the development of hemorrhagic stroke, it is necessary to stop the administration of thrombolytic and continue to treat in the same way as without thrombolytic therapy.

Since thrombin lysis releases thrombin, which stimulates platelet aggregation, antiplatelet agents are recommended.

Antiplatelet therapy

Acetylsalicylic acid, as a direct antiplatelet agent, is indicated from the first hours of myocardial infarction, regardless of whether thrombolytic therapy is performed or not. Treatment should be started as early as possible with a dose of 250 mg (chewed).

Plavix is indicated at a dose of 75 mg/day in combination with acetylsalicylic acid, both with and without thrombolytic therapy.

Anticoagulant therapy

Heparin is a direct acting anticoagulant. Heparin "slows down" all three phases of blood coagulation: the phases of formation of thromboplastin, thrombin and fibrin, and also to a certain extent prevents platelet aggregation. Heparin is indicated during thrombolytic therapy with actelise intravenously in a stream at a dose of 60 units / kg, but not more than 4000 units. When conducting thrombolytic therapy with streptokinase, heparin may not be prescribed if there are no other indications for the use of the drug. If thrombolytic therapy is not carried out, heparin is administered intravenously in a stream at a dose of 5000 - 10000 units.

Prevention of early complications of myocardial infarction

All of the above listed activities, including gentle transportation on a stretcher, are the prevention of early complications of myocardial infarction.

Currently, lidocaine, previously used to prevent ventricular fibrillation, is not used, due to a significant increase in the number of cases of asystole.

The use of previously used magnesium sulfate, in the course of long-term clinical trials, did not confirm the positive effect of this drug on the course and outcome of myocardial infarction. Therefore, at present, the prophylactic use of magnesium sulfate in the acute period of myocardial infarction is considered unindicated.

studfiles.net

myocardial infarction

Myocardial infarction is a necrosis (death) of the heart muscle, caused by an acute violation of the coronary circulation as a result of a mismatch between the need of the heart muscle for oxygen and its delivery to the heart.

myocardial infarction

Over the past 20 years, mortality from myocardial infarction in men has increased by 60%. The infarction is much younger. Now it is not uncommon to see this diagnosis in thirty-year-olds. While he spares women up to 50 years, however, then the incidence of heart attack in women and men levels off. Heart attack is also one of the main causes of disability, and mortality among all patients is 10-12%.

In 95% of cases of acute myocardial infarction, its cause is coronary artery thrombosis in the area of atherosclerotic plaque.

When an atherosclerotic plaque ruptures, erodes (formation of an ulcer on the surface of the plaque), cracks in the inner lining of the vessel under it, platelets and other blood cells adhere to the site of damage. A so-called "platelet plug" is formed. It thickens and grows rapidly in volume and eventually blocks the lumen of the artery. This is called occlusion.

The supply of oxygen to the cells of the heart muscle, which was fed by the blocked artery, is enough for 10 seconds. For about 30 minutes, the heart muscle remains viable, then the process of irreversible changes in the heart muscle begins, and by the third to sixth hour from the start of occlusion, the heart muscle in this area dies.

There are five periods of development of myocardial infarction:

Pre-infarction period

Lasts from a few minutes to 1.5 months. Usually during this period, angina attacks become more frequent, their intensity increases. If treatment is started on time, a heart attack can be avoided.

The most acute period

Duration up to 3 hours. The main in the clinic is the pain syndrome (presented in 80-95% of patients).

The intensity of pain varies widely, there are severe pains in the precordial region with wide irradiation, less often in the epigastrium (abdominal variant of a heart attack, more often with damage to the posterior wall). Pain, as a rule, is not stopped by nitroglycerin and lasts more than 30 minutes. in 15% of patients, myocardial infarction proceeds without pain (painless form of ischemia). In the elderly, the main manifestation may be acute left ventricular failure. Myocardial infarction can be manifested by severe weakness, syncope. Almost all patients may manifest various rhythm disturbances, up to ventricular fibrillation, less often - conduction disturbances. With an extensive heart attack, cardiogenic shock or pulmonary edema may develop.

Physical examination reveals a change in the number of contractions, deafness of tones, the presence of pathological tones, arrhythmias, stagnation in the pulmonary circulation.

According to the presence of certain symptoms, several variants of the course of a heart attack are distinguished: anginal (painful), when the pain is localized in the region of the heart, abdominal (pain in the epigastrium), asthmatic (dyspnea and pulmonary edema are characteristic), arrhythmic (manifested only by rhythm disturbance) and cerebral ( dizziness, visual disturbances, focal lesions).

Acute period

It lasts approximately 10 days. During this period, the zone of the dead heart muscle is finally formed and a scar begins to form at the site of necrosis. Pain syndrome is usually absent. The clinical picture is dominated by fever. The most frequent complications of this period are arrhythmias, blockades, heart failure, aneurysm. Perhaps the formation of aseptic pericarditis (inflammation of the heart bag), parietal endocarditis. In some patients, there is a detachment of the papillary muscle, a rupture of the interventricular septum. One of the most common causes of death during this period is heart failure.

myocardial infarction

Subacute period

Lasts up to 8 weeks. During this period, the state of health of patients remains satisfactory. Significantly reduces the risk of complications. Formed chronic heart failure and aneurysm of the heart. One of the rare complications of this period is Dresler's syndrome, the development of which is associated with immune disorders. Manifested by pericarditis, rarely pleurisy.

Postinfarction period

Duration 6 months. In the same period, repeated myocardial infarction, the occurrence of angina pectoris or heart failure are possible.

The diagnosis is established by the presence of three criteria:

typical pain syndrome
changes on the electrocardiogram (an early ECG sign is an increase in the ST segment, the presence of giant T waves, a decrease in R wave voltage, the appearance of pathological Q, sometimes a fusion of R and T; by the end of the first day, ST decreases, T becomes negative). With a heart attack without Q, only changes in the T wave are detected. In many patients, changes in the ECG remain for life.
changes in clinical and biochemical blood tests indicating damage to heart muscle cells (neutrophilic leukocytosis in the first hours and up to 7-10 days, increased ESR up to 2-3 weeks, increased AST, CPK, LDH and troponin T in the blood, myoglobin in the urine up to 7 days). Among the various markers of myocardial necrosis, troponin T has the maximum specificity and sensitivity. An increase in the content of C-reactive protein, fibrinogen, and globulins is also characteristic.

EchoECG reveals a zone of impaired contractility, a decrease in the ejection fraction.

The use of scintigraphy with technetium isotopes makes it possible to visualize the affected area.

Differential diagnosis is carried out with pulmonary embolism, acute periacrditis, dissecting aortic aneurysm.

As a rule, at least 25% of patients die suddenly before the arrival of an ambulance, hospital mortality is 7-15%, another 5% of patients die during the first year.

Treatment

First aid - physical and emotional rest, take 1 tablet of nitroglycerin under the tongue and half an aspirin tablet, an oxygen cushion (if any), correction of blood pressure (with increased pressure, take an antihypertensive drug).

After the arrival of the ambulance, the main task is to relieve the pain syndrome, for which narcotic analgesics and neuroleptanalgesia are used (promedol 1-2 ml of a 1% solution or fentanyl 1-2 ml of a 0.005% solution and droperidol 1-2 ml of a 0.25% solution intravenously).

With hospitalization in the early stages (up to 8 hours), anticoagulant and thrombolytic therapy is mandatory. For thrombolysis, streptokinase is used (the first dose is 200-250 thousand IU intravenously, then slowly drip for 1-2 hours until the total dose is not more than 1,000,000-1,500,000 IU), urokinase, tissue plasminogen activator. Streptokinase ensures the restoration of coronary blood flow in 50-60% of patients, urokinase - in 60-70% of cases. An absolute contraindication for thrombolytic therapy is: extensive trauma or surgery within the previous 2 months, strokes within 6 months, the presence of high hypertension, gastrointestinal ulcers, hemorrhagic diathesis during hospitalization, anaphylaxis. At the same time, heparin is administered intravenously (once 10 thousand units, then 1 thousand drops per hour. In the next 7-10 days, heparin is administered subcutaneously (no more than 10 thousand units 2 times a day).

Nitrates are an essential component of therapy. They reduce the work of the heart, relieve spasm of the coronary arteries, increase blood flow in them. Assigned both inside and intravenously.

Beta blockers are widely used. With their use, mortality is reduced by 20-25%, mainly due to antiarrhythmic and anti-ischemic effects.

From the first day of hospitalization, antiplatelet agents are prescribed (aspirin at a dose of 100-125 mg per day).

ACE inhibitors are prescribed in the formation of heart failure (ejection fraction less than 45%).

The use of cardiac glycosides in myocardial infarction is undesirable.

Physiotherapy exercises begin in the absence of pain already on the 2nd day after hospitalization.

Angioplasty, stenting, coronary artery bypass grafting are rarely used in our country.

Share the article!

Myocardial infarction: pathogenesis

A myocardial infarction usually occurs due to the fact that a thrombotic occlusion occurs in an atherosclerotic coronary artery and blood flow stops. Occlusion or subtotal stenosis. developing gradually, are less dangerous, because during the growth of an atherosclerotic plaque, a network of collaterals has time to develop. Thrombotic occlusion, as a rule, occurs due to rupture, splitting, ulceration of an atherosclerotic plaque. what smoking does. arterial hypertension and dyslipoproteinemia. and systemic and local factors predisposing to thrombosis. Particularly dangerous are plaques with a thin fibrous cap and a high content of atheromatous masses.

Platelets adhere to the injury site; isolation of ADP. adrenaline and serotonin causes activation and adhesion of new platelets. Platelets secrete thromboxane A2. which causes arterial spasm. In addition, when platelets are activated, the conformation of glycoprotein IIb/IlIa changes in their membrane. and it acquires affinity for the Arg-Gly-Asp sequence of the Aalpha chain and the 12 amino acid sequence of the fibrinogen gamma chain. As a result, the fibrinogen molecule forms a bridge between two platelets, causing them to aggregate.

Blood coagulation is triggered by the formation of a complex of tissue factor (from the site of plaque rupture) with factor VII. This complex activates factor X. which converts prothrombin into thrombin. Thrombin (free and thrombus-bound) converts fibrinogen to fibrin and accelerates many of the steps in blood clotting. As a result, the lumen of the artery is closed by a thrombus consisting of platelets and fibrin filaments.

Less commonly, myocardial infarction is caused by an embolism. spasm, vasculitis, or congenital anomalies of the coronary arteries. The size of the infarction depends on the caliber of the affected artery, myocardial oxygen demand, and the development of collaterals. on whether its lumen is completely blocked, whether spontaneous thrombolysis has occurred. The risk of myocardial infarction is high in unstable and vasospastic angina. several risk factors for atherosclerosis. increased blood clotting. vasculitis. cocainism. thrombosis of the left heart (these conditions are less common).

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.

MI is more common in men than in women, especially in younger age groups. In the group of patients aged 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) has increased significantly.

Classification. MI is subdivided taking into account the size and localization of necrosis, the nature of the course of the disease.

Depending on the size of necrosis, large-focal and small-focal myocardial infarction is distinguished.

Given 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,

previously called "large-focal");

♦ MI without Q wave (changes affect only the segment ST and G wave;

previously called "small-focal") non-transmural; How

usually subendocardial.

According to localization, anterior, apical, lateral, sep-

tal, inferior (diaphragmatic), posterior and inferior basal.

Combined lesions are possible.

These localizations refer to the left ventricle as the most frequently affected by MI. Right ventricular infarction is extremely rare.

Depending on the nature of the course, myocardial infarction with prolonged

recurrent MI, recurrent MI.

A protracted course is characterized by a long (from several days to a week or more) period of pain attacks following one after another, slow repair processes (protracted reverse development of ECG changes 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 processes of scarring (the appearance of new foci of necrosis during the first 72 hours - the expansion of the MI zone, and not its recurrence).

The development of recurrent MI is not associated with primary myocardial necrosis. Usually, recurrent MI occurs in the pools of other coronary arteries in terms, as a rule, exceeding 28 days from the onset of the previous infarction. These terms are established by the International Classification of Diseases of the X revision (previously this period was indicated as 8 weeks).

Etiology. The main cause of MI is atherosclerosis of the coronary arteries, complicated by thrombosis or hemorrhage in the atherosclerotic plaque (atherosclerosis of the coronary arteries is found in 90-95% of cases in those who died from MI).

Recently, significant importance in the occurrence of MI has been attached 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 myocardial oxygen and nutrient needs.

Rarely, the causes of MI are embolism of the coronary arteries, their thrombosis in inflammatory lesions (thrombangiitis, rheumatic corona-ritis, etc.), compression of the mouth of the coronary arteries by a dissecting aortic aneurysm, etc. They lead to the development of MI in 1% of cases and do not apply to manifestations of IBS.

Factors contributing to the occurrence of MI are:

1) insufficiency of collateral connections between coronary vessels

ladies and violation of their function;

2) strengthening of thrombogenic properties of blood;

3) increased myocardial oxygen demand;

4) violation of microcirculation in the myocardium.

Most often, MI is localized in the anterior wall of the left ventricle, i.e. in the pool of blood supply to the most frequently affected atherosclerosis

14.12.2018

Myocardial infarction is a lesion of the heart muscle that occurs as a result of an acute violation of its blood supply due to blockage of one of the arteries of the heart with atherosclerotic plaque. As a result, the part of the muscle that was left without blood supply dies off, that is, it becomes necrotic.

Have you been through a full round of doctors in the last 3 years?

YesNo

Classification

Depending on the stage of development, the following periods of myocardial infarction are distinguished:

sharpest usually lasts less than 5-6 hours from the onset of the attack. The stage reflects the initial changes caused by the cessation of blood supply to the affected area of the heart muscle.
Spicy takes up to 2 weeks from the moment of the onset of a heart attack, is characterized by the formation of a necrotic tissue area in the area of the dead part of the heart muscle. In this period, the area of the affected myocardium is already determined, which is of decisive importance in the development of complications.
Subacute- from the 14th day to the end of the 2nd month after a heart attack. In this period, the process of replacing the area of necrosis with connective tissue (scarring) begins. Cells that were slightly damaged as a result of an attack restore their functions.
Scarring- also called the post-infarction period, which begins 2 months after the first signs of a heart attack and ends with the final formation of a scar, which thickens over time.

The total duration of all stages from the onset of acute circulatory disorders to the formation of a scar takes from 3 to 6 months.

The contractile apparatus of the heart in the region of the scar tissue of the heart is no longer active, which means that healthy muscle fibers must now work in an increased load mode, resulting in myocardial hypertrophy.

In addition, replacement of a portion of the myocardium with connective tissue leads to a change in the pattern of conduction of cardiac impulses.

According to the size of the pathological focus

Depending on the size of the necrotic focus, a heart attack is distinguished:

Large-focal (transmural or Q-infarction).
Small-focal (not Q-infarction).

According to the department of heart disease

Myocardial infarction captures various parts of the heart muscle, depending on what is divided into:

Subepicardial- the outer shell of the heart is involved in the pathological process.
Subendocardial- violation in the inner layer of the shell of the central organ of blood circulation.
intramural- infarction in the middle section of the myocardium.
transmural- damage to the entire thickness of the heart muscle.

According to the presence of complications

There are groups of complications:

The most acute period.
acute period.
Subacute period.

Classification according to the localization of the focus

Myocardial infarction affects the following areas of the heart muscle:

Left ventricle (anterior, lateral, inferior or posterior wall).
Apex of the heart (isolated infarction of the apex of the heart).
Interventricular septum (septal infarction).
Right ventricle.

Variants of combined lesions of various parts of the heart muscle, different walls of the left ventricle are possible. Such a heart attack will be called posterior-inferior, anterior-lateral, etc.

Causes of myocardial infarction

The group of main factors that most often cause the development of myocardial infarction include:

inflammatory lesions of the coronary arteries;
trauma;
thickening of the arterial wall;
embolism of the coronary arteries;
discrepancy between the needs of the myocardium and oxygen delivery;
blood clotting disorder;
postoperative complications;
anomalies in the development of the coronary arteries.

In addition, in rare cases, the occurrence of a heart attack can provoke:

surgical obturation - as a result of ligation of an artery or in case of tissue dissection during angioplasty;
spasm of the coronary arteries.

All of the above conditions are united by the ability to cause a complete stoppage of the blood supply to a certain area of the heart muscle.

Risk factors

People at increased risk of myocardial infarction include:

Abusing cigarettes (passive smoking is also included), alcoholic beverages.
Suffering from obesity, high levels of low and very low density lipoproteins, triglycerides in the blood, low levels of high density lipoproteins.
Patients with rheumatic heart disease.
Patients who have a history of a previous myocardial infarction or had previously asymptomatic forms of coronary vascular disease, which are currently represented by a pronounced clinical picture.
living in polluted areas.
Previously transferred diseases caused by streptococcus and.
The elderly, especially the sick.

According to statistics, belonging to the male sex can also be included in the list of risk factors for myocardial infarction, because the frequency of an attack in a strong half of humanity is 3-5 times higher than that of women.

The mechanism of development of myocardial infarction

There are 4 stages in the development of myocardial infarction:

Ischemic. It is characterized by the development of acute ischemia, fatty and protein degeneration. In some cases, ischemic tissue damage develops for a long time, being a harbinger of an attack.
The pathological process is based on a violation of the blood supply to areas of the heart muscle, gradually gaining a "critical mass" when the lumen of the artery is narrowed by 70% or more of the total cross-sectional area. Initially, a decrease in blood supply can be compensated by collaterals and other vessels, but with such a significant narrowing, there can no longer be sufficient compensation.
Necrobiotic (damage stage). As soon as compensatory mechanisms are exhausted and metabolic, functional disorders in the tissues of the heart muscle are revealed, they indicate damage. The duration of the necrobiotic stage is about 5-6 hours.
Necrotic. The infarction area in this period, which develops over several days - 1-2 weeks, is represented by necrotic (dead) tissue, clearly delimited from healthy myocardial areas. In the necrotic stage, not only necrosis of ischemic, damaged areas of the heart muscle occurs, but also the onset of deep dyscirculatory and metabolic disorders of tissues outside the lesion.
Scarring. It starts a few weeks after the attack, ends in 1-2 months. The duration of the stage is directly affected by the area of the affected area of the myocardium and the state of the patient's body to adequately respond to various stimuli (reactivity).

As a result of myocardial infarction, a dense, shapeless scar forms in its place, and post-infarction large-focal cardiosclerosis develops. Areas of healthy heart muscle located on the edge with newly formed scar tissue are hypertrophied - a response compensatory mechanism of the body, due to which these areas take on the function of dead tissue.

Only in the stage of ischemia is the reverse process possible, when the tissues are not yet damaged, and the cells can return to normal functions.

Symptoms

The clinical picture in myocardial infarction is presented:

Chest pain. It must be distinguished from angina pain. Infarction pain is usually extremely intense, in severity many times greater than the pain syndrome in angina pectoris. Pain is described as tearing, spilled over the entire chest or only in the region of the heart, radiating (radiating) to the left arm, shoulder blade, half of the neck and lower jaw, interscapular space. It differs in duration of more than 15 minutes, sometimes reaching up to an hour or more, without loss of intensity. It is not possible to stop pain in myocardial infarction with nitroglycerin.
Skin blanching. Patients often show cold extremities and loss of healthy skin color. If a heart attack affects a large area of the heart muscle, a pale cyanotic, "marble" skin tone is observed.
Loss of consciousness. Usually develops due to intense pain syndrome.
Cardiac arrest. It may be the only clinical symptom of an attack. The development is based on arrhythmias (usually extrasystole or atrial fibrillation).
Increased sweating. The sweat accompanying the attack is described as profuse, clammy.
Fear of death. The emergence of this feeling is associated with the basics of the work of the first human signaling system. Even before the onset of a heart attack, a person may feel the fear of imminent death, but this is not always the case. A distinctive feature of such a subjective sensation in a heart attack from that in neurosis and psychosis is immobility.
Shortness of breath. It can both accompany the main pain syndrome, and be the only manifestation of a heart attack. Patients are concerned about the feeling of lack of air, difficulty breathing, suffocation.

In addition to the main symptoms, an attack may be accompanied by:

feeling of weakness;
nausea, vomiting;
headache, dizziness.

Atypical forms of myocardial infarction

Myocardial infarction can be difficult to diagnose due to the atypical clinical presentation seen in:

Peripheral form with atypical localization of pain. The pain syndrome differs in different intensity, localized in the throat, left hand, distal phalanx of the left little finger, lower jaw, cervicothoracic spine. The pericardial region remains painless.
Abdominal (gastralgic) form. The patient has nausea, vomiting, hiccups, bloating, pain in the upper abdomen. The clinical picture resembles that of food poisoning or acute pancreatitis.
Asthmatic form. Patients are worried about shortness of breath, which tends to increase. Symptoms of myocardial infarction in this case resemble an attack of bronchial asthma, can lead to pulmonary edema.
Brain (cerebral) form. The clinical picture resembles a stroke, includes dizziness, clouding or loss of consciousness, neurological symptoms. A variant of the course of the pathology is often found in the elderly, who have a history of cerebral circulation disorders.
Silent (painless) form. It is rare, mainly in patients with severe complications of decompensated diabetes mellitus (diabetic neuropathy - in patients, the sensitivity of the limbs decreases, later on the heart and other internal organs). Subjectively, patients complain of severe weakness, the appearance of sticky cold sweat, deterioration of the general condition. After a short period of time, a person may feel only weakness.
arrhythmic form. This type of flow is the main sign of the paroxysmal form, in which pain may be absent. Patients are concerned about the increase or decrease in heart rate, in some cases there is a loss of consciousness, reflecting a complete atrioventricular block.
Collaptoid form. There is no pain syndrome in the region of the heart, the patient has a sharp and significant decrease in blood pressure, dizziness, darkening in the eyes, consciousness is usually preserved. More often occurs in the case of repeated, transmural or.
edematous form. In the clinical picture, shortness of breath, weakness, palpitations, edema that appeared relatively quickly, and in some cases ascites are distinguished. In patients with an edematous type of myocardial infarction, it may appear, which indicates acute right ventricular failure.
Combined atypical form. Such a variant of the course implies a combination of manifestations of several atypical forms.

Consequences of myocardial infarction

Complications of a heart attack are divided into 2 groups:

Early.
Late.

The first group includes complications that arose from the onset of a heart attack and up to the first 3-4 days from an attack. They belong to:

Rupture of the heart muscle- most often the free wall of the left ventricle suffers. An urgent operation is required to keep the patient alive.
Acute heart failure- the cause of the development of cardiogenic shock, pulmonary edema, cardiac asthma, acute renal failure.
- the heart muscle temporarily loses the ability to actively contract. This happens due to acute left ventricular failure. Cardiogenic shock leads to a decrease in blood supply to organs and tissues, manifested by a significant decrease in systolic blood pressure, pulmonary edema, a decrease in the amount of urine excreted (oliguria), blanching of the skin, an increase in its moisture, and stupor. It can be treated with medication (the main task is to restore the normal level of blood pressure) or surgically.
- often causes death due to insufficient attention. When viewing the above complications, it seems that heart rhythm disturbance is not the worst thing that can happen to a person after a heart attack. In fact, the victim may develop ventricular fibrillation, which, without emergency assistance in the form of a defibrillator, is fatal.
Thromboembolism- a blood vessel is clogged by a thrombus detached from the place of its formation, as a result of which the blood supply to organs and tissues stops. Clinical manifestations are varied and depend on the location of the affected area.
Pericarditis- the serous membrane of the heart becomes inflamed, without treatment leads to the development of heart failure. Among all the complications of myocardial infarction, the least dangerous.

Late complications include:

Dressler syndrome- also called post-infarction syndrome, the essence of which is an inadequate response of the body to the connective tissue, which came to replace dead cardiomyocytes in the heart. Protective mechanisms of immunity are activated, which gives rise to an autoimmune reaction leading to inflammation of various organs and tissues (pericarditis, pleurisy, pneumonitis).
chronic heart failure- areas of the heart that hypertrophy and take on the function of dead cells become depleted over time and can no longer perform not only compensatory, but also their own functions. A person with chronic heart failure can hardly endure stress, which affects his lifestyle.
- the wall of the myocardium in a certain area becomes thinner, protrudes, completely loses its contractility. As a result of prolonged existence, it can provoke heart failure. Most often amenable to surgical removal.

Mortality in myocardial infarction is about 30%, while mortality is high due to complications or a second attack during the first year after the onset of acute circulatory disorders of the heart muscle.

First aid

Considering that in our time the frequency of cardiovascular diseases has increased and continues to increase, you should know the rules for providing first aid for myocardial infarction:

If you suspect a seizure in a person, seat him or lay him down, bending his knees. If there are tight clothing, belts, ties, remove them or unfasten them, try to free the upper respiratory tract, if something prevents the victim from breathing normally. A person must be in complete physical and psycho-emotional peace.
If there is a nearby Nitroglycerin, fast-acting drugs for retrosternal pain, put the victim one tablet under the tongue. If there are no such drugs at hand, or the effect of them did not come 3 minutes after ingestion, you should immediately call an ambulance.
If there is Aspirin nearby, when you know that the victim is not allergic to it, give him 300 mg of the drug, help him chew (if necessary) so that the remedy works as quickly as possible. If the patient is taking a medical therapy that includes Aspirin and has already taken it today, give the patient an amount of the drug that is not enough to reach 300 mg.

What to do if a person's heart stops? The victim needs urgent cardiopulmonary resuscitation. If the attack happened in a public place, like a restaurant, airport, ask the staff of the institutions about the availability of a portable defibrillator.

If a person has lost consciousness, his breathing is not rhythmic, immediately proceed to active actions, it is not necessary to check for a pulse.

For more information on performing cardiopulmonary resuscitation, see the video below:

Further assistance will be provided by medical personnel. This is usually accompanied by:

Taking patients Propranolol tablets (10-40 mg) under the tongue.
Intramuscular injection of 1 ml of a 2% solution of Promedol with 2 ml of a 50% solution of Analgin, 1 ml of a 2% solution of Diphenhydramine and 0.5 ml of a half-percent solution of Atropine sulfate.
Intravenous injection of 20,000 IU of Heparin, then another 5,000 IU of the drug is injected subcutaneously into the paraumbilical region.
With systolic pressure below 100 mm Hg. Art. the victim is injected intravenously with 60 mg of Prednisolone, diluted in advance with 10 ml of saline.

Patients are transported on a stretcher in a supine position.

Which doctor is treating?

If a person survives an attack, he is sent to the hospital, where he undergoes all the necessary examinations that could confirm the diagnosis of myocardial infarction.

The treatment is usually carried out by a cardiologist. If the patient needs an operation due to the presence of early complications, a cardiac surgeon takes over.

Depending on the presence of concomitant diseases that could provoke the occurrence of damage to the heart muscle, pulmonologists, endocrinologists, nutritionists, physiotherapists and other specialists can supplement the treatment.

Diagnostic methods

Despite the fact that in most cases it is difficult to confuse a heart attack with other diseases due to a bright specific picture (if you do not take into account), however, due to the existence, only diagnostic measures taken by specialists can make an accurate diagnosis.

Physical examination allows you to determine the patient's complaints on the spot, assess his general condition, degree of consciousness, blood pressure, heart rate and breathing. For people who have had a myocardial infarction, an intense pain syndrome is characteristic, which is not stopped by taking Nitroglycerin, a decrease in blood pressure, while the pulse rate can be both increased (compensatory reaction to a decrease in blood pressure) and reduced (in the first stages of an attack).

Laboratory research methods:

General blood analysis. In patients with myocardial infarction, a decrease in the erythrocyte sedimentation rate and an increase in the content of leukocytes are detected.
Blood chemistry. The amount of cholesterol, fibrinogen, albumin is increased, as well as aspartate and alanine aminotransferase.

Particular attention is paid to the performance of the last two enzymes. When the heart is damaged, their number increases unevenly: AST activity increases up to 10 times, while ALT activity increases only 1.5-2 times.

Biochemical markers of myocardial necrosis

These markers are divided into:

early;
later.

The first group includes an increase in the content:

Myoglobin is a muscle protein that performs the function of providing working muscle fibers with oxygen. Its concentration in the blood gradually increases during the first 2 hours from the onset of the attack.
The cardiac form of creatine phosphokinase is an enzyme found in human muscle tissue. When diagnosing, it is the mass of a given chemical compound that is of decisive importance, and not its activity. An increase in serum levels is determined 3-4 hours after the onset of myocardial infarction.
The cardiac form of a protein that binds fatty acids. It is characterized by high sensitivity in detecting necrosis of the heart muscle.

The first two markers have a lower sensitivity, which is why during the diagnosis attention is paid to the concentration of all of the above indicators.

Most late markers of myocardial necrosis are characterized by high sensitivity. They are determined after 6-9 hours from the beginning of the pathological process. They belong to:

Lactate dehydrogenase is an enzyme that has 5 isoforms. In the diagnosis of myocardial infarction, LDH 1 and LDH 2 isoenzymes are of decisive importance.
Aspartate aminotransferase.
Cardiac troponins I and T are the most specific and sensitive in cardiac muscle necrosis. They are defined as the “gold standard” in the diagnosis of myocardial lesions accompanied by tissue necrosis.

Instrumental research methods

Electrocardiography refers to the methods of early diagnosis of myocardial infarction.

It is characterized by low cost and good information content in relation to the work of the heart as a whole.

The pathology is characterized by the following ECG signs:

The appearance of a pathological Q wave, the duration of which is more than 30 ms, as well as a decrease in the amplitude of the R wave or the ventricular QRS complex. These changes are detected in the area of necrosis.
Displacement of the RS-T segment above the isoline or below the isoline for transmural and subendocardial myocardial infarction, respectively. It is typical for the zone of ischemic damage.
The appearance of an equilateral and peaked T wave is also called coronary. It can be negative (with transmural infarction) or high positive (subendocardial infarction). Deviations from the normogram in the area of ischemic damage are determined.

echocardiography- a method of ultrasound diagnostics, which allows to identify morphological and functional changes in the heart, its valvular apparatus. For myocardial infarction:

The contractile activity in the area of the affected area of the heart muscle decreases, which makes it possible to determine the department of the organ lesion.
Decreased ejection fraction of the heart.
An echocardiogram may reveal an aneurysm of the heart, an intracardiac thrombus.
An assessment is made of morphological changes in the pericardium, the presence of fluid in it.
The echocardiography method allows you to assess the level of pressure in the pulmonary artery and identify signs of pulmonary hypertension.

The ejection fraction of the heart is an indicator that determines the volume of blood ejected by the left ventricle into the lumen of the aorta during its contraction.

Myocardial scintigraphy- one of the radioisotope methods for diagnosing a heart attack, used if the patient's ECG picture is doubtful and does not allow a final diagnosis. This procedure involves the introduction into the body of a radioactive isotope (technetium pyrophosphate), which accumulates in the foci of necrosis of the heart muscle. After scanning, the lesion is seen as intensely colored.

Coronary angiography- a radiopaque method of research, in which a special catheter is inserted into the lumen of the coronary arteries through the femoral artery and the upper part of the aorta (or through the artery of the forearm) after local anesthesia. A radiopaque substance is injected through the catheter. The method allows assessing the degree of damage to the coronary vessels and determining further treatment tactics.

If coronary angiography is performed in case of suspected myocardial infarction, keep the cardiac surgeon in full readiness, as an urgent operation may be required.

Magnetic resonance imaging allows you to determine the localization, size of the focus of myocardial infarction. It can be used for early diagnosis of pathology, assessment of the severity of ischemic damage to the tissues of the heart muscle.

Contrast magnetic resonance imaging- Myocardial infarction can be freely defined. Used to detect small lesions.

Less common among instrumental diagnostic methods CT scan. The method provides comprehensive cross-sectional information about the central circulatory organ, which makes it possible to identify aneurysms and intracardiac thrombi. Although the method is not widely accepted in myocardial infarction, it has a higher sensitivity than echocardiography in diagnosing complications.

How to treat myocardial infarction?

If a patient has a suspected myocardial infarction, then as soon as possible appoint:

Means that inhibit platelet aggregation (antiplatelet agents). Acetylsalicylic acid (Aspirin) is the most common among these agents. The drug significantly reduces the risk of complications.
thrombolytic drugs. The clinical efficacy of Streptokinase has been time-tested. However, the drug also has disadvantages, among which immunogenicity is noted, as a result of which antibodies are formed in the patient's body, which reduce the effectiveness of the drug when it is re-administered within 5 days from the date of the first appointment. Streptokinase also leads to the active production of bradykinin, which has a pronounced hypotensive effect.

The recombinant tissue plasminogen activator Alteplase causes a more pronounced reduction in mortality and a favorable course of the disease in general, in contrast to Streptokinase.

Currently, certain schemes of thrombolytic therapy are used, according to which the optimal regimen for a course of treatment in 1 week includes:

Fibrinolytic (Fibrinolysin).
Acetylsalicylic acid.
Clopidogrel (antithrombotic agent, inhibitor of platelet aggregation).
Enoxaparin / Fondaparinux (an antithrombotic drug from the heparin group and a synthetic selective inhibitor of active factor X, respectively). These drugs are classified as anticoagulants.

In the treatment of myocardial infarction, the following groups of drugs are also used:

Analgesics. Removing pain or reducing its intensity plays a significant role in the further recovery of the heart muscle and reducing the risk of complications. In a heart attack, Morphine hydrochloride and Promedol (among opioid or narcotic analgesics), as well as Tramadol and Nalbuphine (painkillers - partial agonists of opioid receptors) are widely used.
Antipsychotics. They are used to relieve pain during a heart attack in combination with analgesics, which helps to slow down the central nervous system, restore hormone balance and normal functioning of the autonomic nervous system. Most often, the antipsychotic Droperidol is used, and Fentanyl, Tramadol, Analgin are added to it.
Nitrous oxide (an inhalation anesthetic) can also be used to relieve pain from a heart attack. Analgesic effect occurs at a concentration of 35-45%, and loss of consciousness - at 60-80%. The agent has practically no adverse effect on the body at a concentration below 80%.
Angiotensin-converting enzyme inhibitors. In myocardial infarction, the affected area (necrosis) is reduced when administered at the first stages of the pathological process by increasing the level of bradykinin, reducing the load on the heart by reducing pressure (limiting the stimulation of hypertrophy of healthy areas of the heart muscle after an attack). The drugs of this group are prescribed in the acute period of a heart attack. Typical representatives: Lisinopril, Captopril, Ramipril.
Beta blockers. If the funds are administered intravenously in the first hours of an attack, the myocardial oxygen demand decreases, the delivery of the latter improves, the intensity of the pain syndrome and the risk of arrhythmias decrease. With prolonged therapy, the likelihood of a recurrent heart attack decreases. The most famous representatives: Propranolol, Atenolol, Metoprolol.
Tranquilizers. They are used as part of complex treatment in the rehabilitation period to eliminate heart pain. Typical representatives of the group: Meprotan, Phenibut, Phenazepam.

Surgical intervention

Indications for surgical treatment of myocardial infarction:

The lack of effect of thrombolytic therapy or the impossibility of its use due to the presence of contraindications.
Recurrent vascular thrombosis.
Progressive heart failure or recurrent attacks of retrosternal pain during active drug therapy.

The main types of operations for a heart attack:

Transluminal balloon coronary angioplasty- a catheter equipped with a balloon is inserted into the vessel on the thigh or arm and advanced to the clogged (narrowed) coronary vessel under X-ray control. Upon reaching the desired location, the balloon is inflated, which leads to an increase in pressure, destruction of the plaque under its action and restoration of the lumen of the vessel.
Stenting of the coronary artery is the preferred operation. A metal stent (framework) is installed in the vessel, which improves coronary circulation.
In recent years, drug-eluting stents have been used - after the frame is installed in the coronary artery, a pharmacological agent is released into its lumen for several weeks, preventing excessive growth of the inner lining of the vessel and the formation of plaques on it.
Aspiration thrombectomy- an operation in which the mechanical removal of blood clots from the affected blood vessels is performed using special catheters installed by percutaneous puncture.
Excimer laser coronary angioplasty- a modern method of treating severe lesions of the coronary arteries, less traumatic and more effective in comparison with the above. Together with a fiber-optic catheter, a laser is delivered to the affected vessel, the excimer energy of which causes the appearance of mechanical waves that destroy formations located on the inner lining of the arteries.

Folk remedies

Among folk remedies used after a heart attack, garlic is considered the most effective. This product inhibits the formation of sclerotic plaques, preventing them from sticking together and attaching to the walls of blood vessels. From garlic you can do:

Infusion. Cut into thin slices 2 cloves of garlic, pour a glass of water and let it brew for 12 hours (best done in the evening). In the morning we drink all the infused liquid. We can again pour the remaining garlic with water and leave to infuse until the evening. The course of treatment is a month.
Oil. Finely grind the head of garlic and pour it with 200 ml of unrefined sunflower oil, let it stand for a day. Then add the squeezed juice of one lemon, carefully stir the resulting product and leave for a week, stirring occasionally. Take garlic oil 1 teaspoon 3 times a day 30 minutes before meals. The course of treatment is 3 months.

Therapy with the use of garlic can be started only in the rehabilitation period. It is strictly forbidden to use the product immediately after a heart attack.

Diet

In the first days after a heart attack, portions are reduced for victims, the diet consists of soups, pureed foods without salt and spices.

In the future, the amount of food consumed becomes normal.

Nutrition rules:

Limited consumption of sweets, salt, fatty meats, spices.
Inclusion in the diet of an abundance of fresh vegetables, fish and seafood.
Limited fluid intake in the early stages of rehabilitation (usually no more than 1.5-2 liters / day).
General reduction in calorie intake for obese people.

Recovery period

Rehabilitation begins after the acute phase of myocardial infarction and is divided into 3 periods:

Stationary. It usually lasts 1-3 weeks, depending on the severity of the patient, and includes drug treatment. At this stage, the patient is assigned strict bed rest with minimal physical activity.
Post-stationary. The essence of the period is to stabilize the general condition of the patient, the introduction of a new diet, lifestyle, and the psychological state is normalized. Patients can go through this period at home, rehabilitation centers, specialized sanatoriums, boarding houses for the elderly. Lasts for 6-12 months.
supportive. Includes diet, healthy lifestyle, exercise, medication, regular visits to doctors. Lasts the entire subsequent life of the victims.

For the most part, successful completion of the first two periods of rehabilitation provides a minimal risk of complications.

Forecast

Due to the occurrence of irreversible changes, which is the cause of frequent and serious complications, the prognosis of the disease is conditionally unfavorable.

Disease recurrence

Recurrent myocardial infarction- a second attack that occurs between 72 hours and 8 weeks after the first. Mortality among all patients with this type of infarction is about 40%. The reason is the defeat of the same coronary artery as in the first attack.

Recurrent myocardial infarction- an attack that occurs 28 days after the first due to damage to another coronary artery. Mortality is about 32.7%. Most often observed in women - 18.9%.

Prevention

Prevention of a heart attack is based on:

Proper nutrition, containing an abundance of vitamins, trace elements and vegetable fiber, foods with omega-3 fats.
Weight loss (if necessary).
Control of cholesterol, blood sugar, blood pressure.
Minor physical exertion, allowing you to deal with hypodynamia.
Maintain preventive drug therapy.

To avoid a myocardial infarction, you should lead a healthy lifestyle, but if an attack occurs, be careful and follow rehabilitation and preventive measures to improve the quality of life and reduce the risk of death.

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.

Classification. MI is subdivided taking into account the size and localization of necrosis, the nature of the course of the disease.

Depending on the size of necrosis, large-focal and small-focal myocardial infarction is distinguished.

Given 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,
previously called "large-focal");

♦ MI without Q wave (changes affect only the segment ST and G wave;
previously called "small-focal") non-transmural; How
usually subendocardial.

According to localization, anterior, apical, lateral, sep-
tal, inferior (diaphragmatic), posterior and inferior basal.
Combined lesions are possible.

These localizations refer to the left ventricle as the most frequently affected by MI. Right ventricular infarction is extremely rare.

Depending on the nature of the course, myocardial infarction with prolonged
recurrent MI, recurrent MI.

Factors contributing to the occurrence of MI are:

1) insufficiency of collateral connections between coronary vessels
ladies and violation of their function;

2) strengthening of thrombogenic properties of blood;

3) increased myocardial oxygen demand;

4) violation of microcirculation in the myocardium.

Most often, MI is localized in the anterior wall of the left ventricle, i.e. in the pool of blood supply to the most frequently affected atherosclerosis

The basis for the development of MI is a pathophysiological triad, including rupture (tear) of an atherosclerotic plaque, thrombosis, and vasoconstriction.

In most cases, MI develops with a sudden onset of a sharp decrease in coronary blood flow due to thrombotic occlusion of the coronary artery, the lumen of which is significantly narrowed by the previous atherosclerotic process. With a sudden complete closure of the lumen of the coronary artery by a thrombus in the absence or insufficient development of collaterals, a tracemural MI develops. With intermittent thrombotic occlusion of a coronary artery (due to spontaneous or therapeutic thrombolysis) in pre-existing collaterals, a non-transmural MI is formed. In this case, necrosis is most often located in
subendocardial regions or in the thickness of the myocardium, not reaching the epicardium.

Instability (“vulnerability”) of an atherosclerotic plaque is due to the development of aseptic inflammation in it. Modified LDL entering the plaque is a powerful stimulator of this inflammation. Inflammation occurs with the participation of macrophages and T-lymphocytes. activated
T-lymphocytes, macrophages secrete a large number of proteolytic enzymes (collagenase, gelatinase, etc.), which destroy collagen
structures of the fibrous cap and drastically reduce its strength. Under the influence of gamma-interferon secreted by T-lymphocytes, collagen synthesis decreases, which also reduces the strength of the plaque cover.

Plaque destabilization factors can be factors such as a significant increase in blood pressure, intense physical
load. Rupture (tear) or erosion of the atherosclerotic plaque activates
mechanisms of hemostasis with the formation of a thrombus.

There are two types of coronary artery thrombosis in MI. The first type of thrombosis develops in 25% of cases - a thrombus is formed on the surface of an atherosclerotic plaque protruding into the lumen of the vessel, when it is superficially damaged. As a result of damage to the endothelium, adhesion occurs
platelets during the interaction of GP-Ib on the membrane of activated platelets with the von Willebrayd factor, an adhesion molecule produced by endotheliocytes when they are damaged. Then comes the process of platelet aggregation (the connection of neighboring platelets with fibrinogen molecules, interacting
GP IIb/IIIa expressed on the platelet membrane), release of aggregation stimulators from platelets and other cells (ADP, thromboxane A 2, thrombin, etc.), release of mediators that cause coronary spasm, and thrombus formation. The second type of thrombosis is observed in 75% of patients and is caused by plaque rupture, as a result of which blood penetrates into the plaque, where it interacts with tissue thromboplastin and collagen. The thrombus first forms inside the plaque, filling its volume, and then spreads into the lumen of the vessel.

The cessation of blood flow to the myocardium

Activation of the renin-angiotensin-II-aldosterone system

Atherosclerosis of the coronary arteries

endothelial dysfunction

Pathophysical triad:

Rupture of atherosclerotic plaque

Thrombosis

coronary spasm

Hypercoagulability

Main manifestations:

Intense pain in the heart

ECG changes

Resorption-necrotic syndrome

Inadequate angiogenesis and collaterals

Immunological disorders

Myocardial infarction (necrosis, aseptic inflammation, metabolic electrolyte disturbances, myocardial remodeling)

Activation of the kinin system

Decreased cardiac output

Violation of microcirculation, tissue hypoxia

Complications:

myocardial rupture

arrhythmias, blockade

Cardiogenic shock

Asystole

ventricular fibrillation

Activation of the sympathoadrenal system

Rice. 2. Pathogenesis of acute myocardial infarction

Coronary spasm plays a huge role in the obstruction of the coronary artery. Its development is due to endothelial dysfunction, which leads to a decrease in the production of vasodilators (nitric oxide, prostacyclin, adrenomedullin, hyperpolarizing factor) and a significant increase in the synthesis of vasoconstrictors (endothelin, angiotensin II, serotonin, thromboxane A2). Spasm increases the degree of coronary artery obstruction caused by plaque and thrombus and leads to occlusive obstruction causing myocardial necrosis. MI is a stress response that activates the sympathoadrenal system. The release of excess catecholamines into the blood increases myocardial oxygen demand, contributes to the progression of necrosis. In addition, catecholamines increase platelet aggregation and release of the vasoconstrictor thromboxane A 2 . Of great importance in the pathogenesis of MI is the degree of compensation of impaired coronary blood flow by collateral circulation. Thus, slowly developing stenosis of the epicardial arteries may not lead to the development of MI with a well-developed collateral vascular network in the myocardium. Functional inferiority of collateral blood flow, as one of the pathogenetic mechanisms, is of great importance in the majority of young patients with insufficient development of their coronary anastomoses. An essential role in the development of MI belongs to insufficient angiogenesis.

DISTURBANCE OF HEART FUNCTION IN MYOCARDIAL INFARCTION

The development of MI is accompanied by a violation With istolic and diastolic functions of the heart and p e simulation of the left ventricle. The severity of these changes is directly proportional to the size of the zone of necrosis of the heart muscle. There is a violation of the contractile function, tk. the necrotic area of the myocardium is not involved in the contraction of the heart. Soon after
development of MI in the unaffected nearby zone, hyperkinesia may be observed. It is caused by compensatory mechanisms, including activation of the sympathetic nervous system and the Frapka-Starlpng mechanism. Compensatory myocardial hyperkinesia gradually decreases within 9-14 days from
start IM. In some patients, already in the first days, there is a decrease in the contractile function of the myocardium in the peri-infarction zone. This may be due to prior infarction obstruction of the coronary artery supplying blood to non-infarct areas of the left ventricular myocardium, and insufficiently developed collateral blood flow. During the formation of an acute aneurysm of the heart, a paradoxical pulsation may develop - the movement of part of the blood during systole from the left ventricle into a protruding aneurysmal sac, which worsens hemodynamics. There may also be a slowdown
contraction processes compared to the intact myocardium (dyssynchrony).

A decrease in the ejection fraction (the main indicator of impaired systolic function) occurs when contractility is impaired by more than 10% of the mass
myocardium. If contractility is impaired by more than 15% of the mass of the myocardium, an increase in the end-diastolic volume (EDV) and pressure (EDV) of the left ventricle is observed. With necrosis of more than 25% of the mass of the myocardium, left ventricular failure develops, and with necrosis of more than 40% of the mass of the myocardium of the left
ventricle - cardiogenic shock.

Violation of the diastolic function of the heart is due to a decrease in the elasticity and extensibility of the myocardium, which is explained by a slow transition
calcium ions from myofibrils to the sarcoplasmic reticulum due to a lack of energy substrates. As a result of this, the diastole of the left ventricle becomes defective, because. the myocardium does not relax enough, as a result of which the end-diastolic pressure (EDP) increases and coronary blood flow worsens. Violation of diastolic function is observed when less than 10% of the mass of the myocardium of the left ventricle is affected.

Remodeling of the left ventricle consists in myocardial stretching both in the area of the necrosis zone and in unaffected, viable areas (i.e., dilatation of the left ventricular myocardium develops). This pathological process is most pronounced in transmural MI and is due to the following factors: thinning of the myocardium in the area of necrosis; decrease in myocardial tone in the area of necrosis and in the peri-infarction zone; the development of a state of hibernation in the peri-infarction zone, activation of the circulating and local (cardiac) RAAS; activation of the sympathoadrenal system; overproduction of endothelin by the endothelium. Under the influence of these neurohumoral stimulants, growth factors are activated, intracellular synthesis of proto-oncogenes and nuclear transcription factors increases, which is accompanied by hypertrophy of cardiomyocytes. With extensive transmural necrosis, myocardial remodeling develops within 24 hours from the onset of infarction and may persist for several weeks or even months.

CLINICAL PICTURE OF MYOCARDIAL INFARCTION

In the clinical course of MI, 5 periods are distinguished:

1. Prodromal (pre-infarction)

2. The most acute period

3. Acute period

4. Subacute period

5. Post-infarction period

Prodromal (pre-infarction) period characterized by an increase in the severity of coronary insufficiency preceding the development of MI. This period can last from several hours to one month. It is observed in 70-80% of patients and occurs as one of the variants of unstable
angina. The most common variant of this period should be considered progressive angina pectoris, i.e. we are talking about the increase in the severity of the already existing stable angina pectoris. The main manifestations of this period are: an increase in the intensity and duration of retrosternal pain;
expansion of the zone of distribution of pain and the area of irradiation of pain; progressive decrease in exercise tolerance; a sharp decrease in the effectiveness of nitroglycerin taken sublingually; attachment to angina pectoris tension angina pectoris; the appearance of new symptoms (shortness of breath, heart rhythm disturbance, general weakness, sweating).

The most acute period- this is the period from the moment of myocardial ischemia to the beginning of the formation of a focus of necrosis. The duration of the most acute period ranges from 30 minutes to 2 hours. The following provoking factors contribute to the development of this period: intense physical activity; stressful
situation; binge eating; pronounced hypothermia or overheating. These factors increase myocardial oxygen demand, increase blood pressure,
cause coronary spasm. The most characteristic clinical sign of the most acute MI is pain syndrome, which has the following characteristics: in most patients, pain is extremely intense, localized in the retrosternal region, often captures the precordial or the entire anterior surface of the chest; radiate to the left arm, shoulder and shoulder blade, to the interscapular region,
neck, lower jaw, ear, throat; the duration of pain is always more than 20-30 minutes, sometimes several hours; they are stopped by narcotic analgesics (administration of morphine in / vein), the use of neuroleptanalgesia, anesthesia with nitrous oxide. During a painful attack, patients experience a feeling of fear of death, doom, melancholy, they can be restless, excited (Status anginosus develops).

The development of pain syndrome is associated with the action of the following factors:

a) lowering the threshold of pain sensitivity;

b) acute dilatation of the heart;
c) an increase in the concentration of extracellular potassium

due to its loss by cardiomyocytes;

d) an increase in the concentration of such mediators as

bradykinin, substance P, serotonin, adenosine,

histamine, etc.;

e) the development of metabolic acidosis. However, until the end, the mechanisms of development of the pain syndrome have not yet been
studied. The range of severity of pain is very large - from insignificant in a small number of patients to extremely intense in most patients. In this case, the localization of myocardial damage, its prevalence and other characteristics can be very similar. In addition, sometimes (with an atypical course) a painless form of MI develops.

On examination, attention is drawn to the pallor, moisture of the skin, cyanosis of the lips, nose, ears, subungual spaces. The bradycardia developing in the first minutes is replaced by tachycardia. Blood pressure in the first minutes (sometimes hours) rises, and then hypotension develops with a decrease in systolic and pulse pressure. The weakening of the I tone above the apex of the heart is characteristic. During acute period the focus of necrosis with myomalacia is finally formed. It lasts from 2 to 10-14 days. In the acute period, as a rule, the pain disappears. The persistence of pain may be due to the expansion of the necrosis zone in progressive MI, an increase in the peri-infarction ischemic zone, or the addition of fibrinous pericarditis. In the study of the cardiovascular system, an accelerated pulse is determined, the tendency to decrease in blood pressure remains, the heart sounds are muffled, a systolic murmur is heard at the apex. With extensive anterior transmural MI, a pericardial friction rub is heard in the zone of absolute dullness of the heart, which is due to the development of fibrinous pericarditis.

Characteristic of this period is the development of resorption-necrotic syndrome with the following symptoms: 1) fever; 2) leukocytosis; 3) increase in ESR; 4) detection of "biochemical signs of inflammation"; 5) the appearance in the blood of biochemical markers of the death of cardiomyocytes. Subfebrile temperature is noted for 2-3 days. The duration of the temperature increase is about 3-7 days. The development of neutrophilic leukocytosis with a shift of the formula to the left is due to the development of an acute phase response. Leukocytosis develops after 3-4 hours, reaches a maximum on the 2-4th day and persists for about 3-7 days. An increase in ESR is noted from 2-3 days, reaches a maximum between 8-12 days, then gradually decreases and normalizes after 3-4 weeks. The phenomenon of "scissors" between leukocytosis and ESR is considered characteristic of MI: at the end of the 1st - the beginning of the 2nd week, the number of leukocytes
begins to decrease, and ESR increases. OOF develops in the body, which is confirmed by an increase in the content of OOF mediators and proteins in the blood. IN
blood, biochemical markers of death of cardiomyocytes appear (see section: Laboratory diagnostics).

Subacute period characterized by complete replacement of necrotic masses with granulation tissue and corresponds to the time of formation of a connective tissue scar at the site of the focus of necrosis. In uncomplicated MI, the subacute period lasts from 6 to 8 weeks. The general condition of the patient is satisfactory, there is no pain syndrome. In the study of the cardiovascular system, the normalization of heart rate, blood pressure, the disappearance of systolic murmur in the region of the apex of the heart is revealed. In the subacute period, manifestations of the resorption-necrotic syndrome disappear.

Postinfarction period (period of postinfarction cardiosclerosis) corresponds to the period of complete consolidation of the scar in the focus of necrosis and adaptation
of the cardiovascular system to new conditions of functioning - turning off the contractile function of the myocardium. This period continues
throughout the rest of the patient's life. Allocate the nearest (2-6 months) and remote (after 6 months) postinfarction period. Most patients have no pain in the region of the heart. However, often in the future, angina pectoris resumes again, which bothered the patient before the development of MI.

Myocardial infarction etiology clinic diagnostics. myocardial infarction

Infarct_myocarda

myocardial infarction

Pre-infarction period

The most acute period

Acute period

Subacute period

Postinfarction period

Treatment

Share the article!

More articles on this topic

Myocardial infarction: pathogenesis

MYOCARDIAL INFARCTION

Classification

According to the size of the pathological focus

According to the department of heart disease

According to the presence of complications

Classification according to the localization of the focus

Causes of myocardial infarction

Risk factors

The mechanism of development of myocardial infarction

Symptoms

Atypical forms of myocardial infarction

Consequences of myocardial infarction

First aid

Which doctor is treating?

Diagnostic methods

Biochemical markers of myocardial necrosis

Instrumental research methods

How to treat myocardial infarction?

Surgical intervention

Folk remedies

Diet

Recovery period

Forecast

Disease recurrence

Prevention