MINISTRY OF HEALTH OF UZBEKISTAN CENTRE FOR MEDICAL EDUCATION

Tashkent Medical Academy

"Approved"

Head of main department

science and education

Ministry of Health

Republic of Uzbekistan

S. E. Atakhanov

___________________________

“____”________________ 2011 y.

Protocol number

MYOCARDIAL INFARCTION

(Educational tools for students of IV courses and professors of medical schools)

Tashkent - 2011

Compiled by:

                          

Juraeva E.R. - Associate Professor and Faculty Hospital Therapy Faculty of Medicine, and Internal disease and preventive health care department.    

Ziyaeva F.K. - Assistant Professor of Faculty and Hospital medical care Department of Internal Medicine and Health prevention department.

G.T. Bekenova - Assistant Professor of Faculty and Hospital medical care Department of Internal Medicine and Health prevention department.

Reviewers:

. Yakubov A.V - Department of Clinical Pharmacology, TMA, prof.

Zohidova M.Z. - Department for the preparation of a general practitioner of the Tashkent Institute of Postgraduate Education, prof.

Educational tools considered and approved at a meeting of ICC TMA (Minutes № _____ "_____"_____ 2011).

DNC Chairman, Professor M. Sh.Karimov

Training manuals approved by the Academic Council of TMA and recommended for publication (Minutes № _____ "_____"_____ 2011.).

Scientific Secretary

Prof. G.S. Rahimbaeva

Theme : myocardial infarction

1 Venue lessons, equipment

o Cardiology, coronary care and general cardiorheumatology therapy department of laboratory and instrumental diagnostics, training rooms.

o Blood samples, clinical and biochemical tests, immunological studies, x-ray, ECG, PCG, EhoKS, training-control tests, case patients, handout.

o TV-video, overhet, multimedia, tables, slides, information and computer software.

2. Duration of training

Time to light the subject, 270 minutes

3. Session Purpose: Education students etiology, pathogenesis, clinical symptomatology, laboratory and instrumental diagnosis and rational therapy, prevention of complications, rehabilitation.

The purpose of education - the development and consolidation of theoretical knowledge. The educational goal - the formation of a physician in training relevant international standards of interest to the profession, a sense of responsibility, raising interest in expanding their knowledge, the formation of a deontological level of education, the formation of caution in the implementation of practical work, clarity and responsibility.

Developmental goal - the formation of students' independent thinking and debate, critical thinking in students (clinical, hygienic).

Tasks

1. Definition of myocardial infarction

1. The etiology of myocardial infarction 2. The pathogenesis of myocardial infarction. 3. The clinical picture of acute myocardial infarction: subjective data, a general inspection of the data

palpation, percussion and auscultation, the conclusion of laboratory and instrumental methods of research.

4. Differential diagnosis of acute myocardial infarction. 5. Basic principles of treatment and rehabilitation of myocardial infarction. 6. Course and prognosis of myocardial infarction.

The student should know:

etiology of myocardial infarction pathogenesis of myocardial infarction hospital myocardial infarction methods of diagnosing myocardial infarction basic principles of treatment The student should be able to:

o Gather medical history, patient complaints, conduct an overall inspection, palpation, percussion and auscultation

o Make a plan examination of the patient o Interpret laboratory data rates o Interpret ECG o To substantiate the clinical diagnosis by steps o Write a prescription for drugs and to explain their mechanism of action, side effects

4. Motivation

Currently, the study of myocardial infarction is of great importance because it is one of the most common causes of death and disability in the population and can lead to life-threatening complications of the patient.

5. Interdisciplinary communication and internal disciplinary

Interdisciplinary communication:

Myocardial infarction

Integrate with the following items:

I. Vertically 1. Normal anatomy 2. Normal physiology 3. Histology 4. Morbid anatomy 5. Physiopathology 6. Propaedeutics of Internal Medicine

II. Horizontal

1. Teaching surgery

2. Radiology

Normal anatomy

The human heart - is a muscular pump divided into four chambers. The two upper chambers called atria and two lower - the ventricles.

These two types of heart chambers perform different functions: the atria collect blood coming into the heart and push it into the ventricles and the ventricles eject blood from the heart into the arteries through which it enters into all parts of the body. The two atria are separated by septal and two ventricle - interventricular septum. Atrium and ventricle on each side of the heart are connected atrioventricular orifice. This hole opens and closes the atrioventricular valve. The left atrioventricular valve is also known as mitral valve, and the right atrioventricular valve as tricuspid valve.

The valves act as gates, giving the ability of blood to pass from one chamber of the heart to another and from the heart chambers in the associated blood vessels. The heart valves are as follows: tricuspid, pulmonary (pulmonary trunk), bicuspid (also known as mitral) and aortaly.

Tricuspid valve.

Tricuspid valve is located between the right atrium and right ventricle. When you open this valve moves blood from the right atrium into the right ventricle. Tricuspid valve prevents blood from flowing back into the atrium, closing during ventricular contraction The very name of this valve indicates that it consists of three wings.

The pulmonary valve

With a closed tricuspid valve blood in the right ventricle is the only way out in the pulmonary trunk. Pulmonary trunk divides into right and left pulmonary arteries, which are respectively the left and right lung. Log in pulmonary trunk is closed pulmonary valve. Pulmonary valve has three leaflets that open at the time of reduction of the right ventricle and closed at the time of relaxation. Pulmonary valve allows blood to get out of the right ventricle into the pulmonary artery, but prevents blood from flowing back from pulmonary artery into the right ventricle.

Bicuspid valve (mitral valve)

Bicuspid or mitral valve regulates blood flow from the left atrium into the left ventricle. As with tricuspid valve, butterfly valve is closed at the time of contraction of the left ventricle. Mitral valve has two flaps.

Normal physiology

Function automatic. Automatism function - is the heart's ability to generate electrical impulses in the absence of external stimuli.

Conductivity function. The function of conductivity - the ability for the excitation of fibers of the conducting system of the heart and the contractile myocardium.

The function of excitability. Excitability function - the ability of cells of the heart conduction system and myocardial contractile excited by external electric pulses.

Contractility. Contractility is the ability of the heart muscle to contract in response to stimulation. This function has basically the contractile myocardium.

As a result of successive contraction and relaxation of different parts of the heart by most - the heart pumping function. Histology

The structure of the myocardium. In light microscopy shows branching filaments consisting of cardiomyocytes. In the center of each kernel is cardiomyocytes.

The structure of the cardiomyocytes (data of electron microscopy). We see a number of parallel myofibrils, consisting of segments - the sarcomeres.

The structure of the sarcomere. The location of fibers on the cross-section of the sarcomere. In the center of the disc A (Zone M) is the only thick filament (myosin), in its peripheral regions - and the thick and thin filaments (actin), each thick filament surrounded by six thin. In the drive I have only thin filaments.

Histology

The structure of the myocardium. In light microscopy shows branching filaments consisting of cardiomyocytes. In the center of each kernel is cardiomyocytes.

The structure of the cardiomyocytes (data of electron microscopy). We see a number of parallel myofibrils, consisting of segments - the sarcomeres.

The structure of the sarcomere. The location of fibers on the cross-section of the sarcomere. In the center of the disc A (Zone M) is the only thick filament (myosin), in its peripheral regions - and the thick and thin filaments (actin), each thick filament surrounded by six thin. In the drive I have only thin filaments.

INFARCTION

Stained with iron hematoxylin

The arrows indicate the intercalated discs

Purkinje fibers in the myocardium Hematoxylin and eosin 1-purkinje fibers 2-endocardium 3 - myocardium

Purkinje fibers in the myocardium Hematoxylin and eosin 1-purkinje fibers 2-endocardium 3 - myocardium

Purkinje fibers in the myocardium Hematoxylin and eosin 1-purkinje fibers 2-endocardium 3 - myocardium

Morbid anatomy

Myocardial infarction (MI) - is ischemic necrosis of cardiac muscle, which develops as a result of acute failure of coronary circulation.

The earliest morphological changes in the cardiac muscle in the developing myocardial infarction can be detected only by using electron microscopy. Within 15-20 minutes after coronary occlusion exhibit swelling of mitochondria and depletion of glycogen. 60 min after cessation of coronary blood flow revealed irreversible ischemic cell damage in the form of the collapse of the chromatin of nuclei and marked contracture of sarcomeres. When using light microscopy, the first change in the focus of MI detected only after 12-18 hours of onset of infarction.There has been expansion of capillaries, swelling of muscle fibers. After 24 h revealed the fragmentation of muscle fibers and

infiltration of polymorphonuclear leukocytes.Macroscopically, the picture begins to identify myocardial infarction only after 18-24 hours of onset. Foci of necrosis and appears pale hydropic, and 48 h zone of necrosis becomes gray tint and becomes flabby. In the uncomplicated process of forming scar ends in about 6 weeks from the start of MI.

Physiopathology

The emergence of ischemia of the heart muscle leads to profound disturbances in the metabolism of myocardial cells and the vascular system of the heart. As a result of the termination or significant limitation of coronary blood flow develop hypoxia, which disturbs the synthesis of ATP in mitochondria. At the same cardiomyocytes contractile function rapidly decreases. A significant limitation of coronary blood flow with fatty acids and glucose, which are the main energy substrate cells, activates anaerobic glycolysis (breakdown of glycogen). Moreover, glycogen is metabolized to lactate, only that the shortage of oxygen does not oxidize further. The concentration of lactate and other unoxidized products in cardiac muscle and coronary sinus blood increases, and in the myocardium is a shift of pH in the acidic side (acidosis), which contributes to further reduction in electrical activity and myocardial contractility. ATP deficiency leads to the discovery of potassium channel cell K + ions out into the extracellular medium, thus reducing the transmembrane resting potential and excitability of cardiomyocytes. At the same time decreases the rate of growth TMPD, total duration, as well as the speed of the electric pulse. Characteristically, the extent of these violations in some parts of the ischemic myocardium is different. Therefore, during ischemia, the conditions for the occurrence of severe inhomogeneity of electrophysiological properties of heart muscle that underlies many cardiac arrhythmias. As a result of ischemia, also violated the reverse transport of Ca2 + in the sarcoplasmic reticulum and extracellular environment. Concentration Ca2 + in the cell grows and develops so-called "ischemic contracture" cardiomyocytes, leading to disruption of diastolic relaxation. Significant inhibition of K +-Na + pump, resulting from deficiency of ATP, is also accompanied by an increased concentration of Na + ions in the cell and, accordingly, its swelling. As a result of a myocardial infarction is a violation of diastolic and systolic left ventricular function, and begin the complex process of remodeling it.

Change the transmembrane action potential (TMPD) in the zone of ischemic damage.

Left ventricular remodeling in transmural myocardial infarction. a - the impact of intragastric pressure on cyto lytic necrotizing area of heart muscle (the 2nd day of MI), b - increase the area of heart disease, thinning of the walls in the area of necrosis and dilatation of the left ventricle.

Propaedeutics of Internal Medicine

During transmural myocardial infarction (heart attack with a tooth Q) are usually distinguished five periods:

1) prodrome, 2) acute and 3) sharp, and 4) subacute and 5) postinfarction period.

On examination, is not rare skin pallor, cold extremities and severe sweating. In most cases, cyanosis is defined lips pronounced cyanosis, orthopnea position, combined with the wet. finely rattling in the bottom of the lungs and increased frequency of respiratory movements indicate the presence of acute left ventricular failure.Palpation of the heart: palpation of the heart, there may be local tenderness in the left beforecardiac area.Auscultation of the heart during myocardial infarction: the weakening of the first tone and muted at the apex, the weakening of the second tone, the accent on the second tone of pulmonary artery, sinus tachycardia. Blood pressure in the first minutes and hours of MI may increase. With the development of acute vascular insufficiency of blood pressure is reduced, mainly due to systolic BP.

Dynamics of electrocardiogram changes in acute (a-e), subacute (g) and scar (s) stages of myocardial infarction.

RadiologyChest X-ray. In patients with myocardial infarction with a tooth Q, hospitalized in the department cardiac intensive care, chest X-ray is usually performed on special indications, namely, to timely diagnosis of interstitial pulmonary edema and other complications of the disease (pneumonia, pulmonary infarction, hydrothorax or effusion pericardial), radiological findings are described in the relevant chapters of the manual. The study is conducted using special portable x-ray machines directly in cardiac intensive care office with the patient lying on his back.Myocardial scintigraphy 99mTs-pyrophosphate (technetium) is used to visualize the foci of myocardial infarction, since this is a radioactive substance is selectively accumulated in necrotic tissue of the heart muscle in the event that persists in the affected area for at least 10-40% of blood flow (including collateral) necessary for the delivery of technetium to the foci of necrosis. Scintigram record in three Standard projections at 90 min after intravenous injection of an indicator. This time is necessary to cleanse the blood of the indicator due to its absorption of bone and necrotic tissue. Analysis of the scintigram performed after the procedure, the accumulation of pulses and procedures for background subtraction. Hotbed of acute myocardial infarction detected by this technique after 24 h of onset. In the ordinary course of myocardial necrosis hearth rendered up to 8-10 days of illness. If technetium continues to accumulate in heart muscle in 2 to 3 weeks from the onset, it indicates a slowing down of reparative processes, protracted course of myocardial postinfarction aneurysm or development.

Two-dimensional echocardiograms recorded in patients with postinfarction cardiosclerosis a - akinesia of interventricular septum, b - posteriodiaphragmal (lower) segment of the left ventricle

Scintigram myocardial 99m Tc-pyrophosphate, recorded in a patient with posterolateral diaphragmatic (lower) with myocardial infarction with a tooth Q. Notably the accumulation of technetium in posterolateral diaphragmatic (lower) segment of LV (light areas scintigram))

Surgery

Coronary revascularization

In the absence of the effect of drug therapy and maintaining signs of recurrent myocardial ischemia is shown holding a coronary revascularization: percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass grafting (CABG). The main indications for the emergency coronary revascularization, are features that characterize a high risk of myocardial infarction and death:

1Repeated episodes of myocardial ischemia (recurrent pain and / or negative dynamic segment of the RS-T).

2. Elevated serum troponins or CK-MB.

3. Hemodynamic instability (hypotension or progressive heart failure).

4.Threatening arrhythmias (ventricular tachycardia or recurrent episodes of ventricular fibrillation).

5. Early post-infarction angina.

Internal disciplinary communication:

Acquired in the course of training know-how can be applied in the study subjects: cardiology, pulmonology, gastroenterology.

                                 

6. Content of classes

1. Theoretical part

Myocardial infarction (MI) - is ischemic necrosis of cardiac muscle, which develops as a result of acute failure of coronary circulation .In the Russian Federation annually infarction occurs in 0.2-0.6% of men aged 40 to 59 years (NA Mazur). In men, the older age group (60-64 g) of MI incidence is even higher, reaching 1.7% per year. Women get sick infarction in 2.5-5 times less likely to men, especially in young and middle age, that is usually associated with the later (about 10 years) the development of their atherosclerosis. After menopause (age 55-60 years) the difference in incidence between men and women is significantly reduced. Modern classification of MI provides for his division:

magnitude and depth of lesions of the heart muscle; the nature of the disease; Localization of MI; on the stage of disease; by the presence of complications of MI.

1. The magnitude and depth of lesions of the heart muscle and differentiate transmural infarction notransmural .When transmural MI (myocardial infarction with a tooth Q) captures the focus of necrosis, or the entire thickness of cardiac muscle from subendocardial to subepicardial layers of

the myocardium, or a large part of that is reflected on the surface ECG as the formation of a pathological Q wave or QS complex in several ECG leads . Hence the synonym of transmural myocardial infarction - "myocardial infarction with a tooth Q". Typically, such damage to the heart muscle is extensive enough and focus of necrosis extended to two or more segments of the left ventricle (macrofocal MI).

When notransmural MI (myocardial infarction without tooth Q) captures only the focus of necrosis subendocardial or intramural divisions left ventricle and is not accompanied by pathological changes of the complex QRS ("wave myocardial infarction without Q"). For a long time in the Soviet literature to describe without Q-wave myocardial infarction using the term " small focal them." Indeed, in most cases without Q-wave myocardial infarction is much smaller in extent than transmural infarction, but often there are cases of extensive subendocardial infarction that span multiple segments of LV, but only affecting the subendocardial layers of myocardium.

2. By the nature of the disease are distinguished primary, recurrent and recurrent MI. Primary MI diagnosed in the absence of anamnestic and instrumental signs of myocardial infarction in the past IM. Repeated diagnosed in cases where the patient, in whom there is documented information of past myocardial infarction, there are credible signs of new foci of necrosis, often forming a pool of other satellites in extend beyond 28 days from the date of the previous infarction. For recurrent myocardial infarction clinical laboratory and instrumental signs of the formation of new foci of necrosis appear in a period of 72 hours (3 days) until 28 days after myocardial infarction, before the end of its basic processes of scarring.

Transmural (with a tooth Q) and notransmural (without tooth Q) myocardial infarction (Figure).

3. To localize them

anterioseptal (anteriopartition); anterior apical; anterolateral;

anteriobazalis (high-front); common anterior (septal, apical and lateral); posteriodiaphragmal (lower); posterolateral; posteriobazal; common background; Right ventricular infarction.

MI is more often localized in the left ventricle, hitting him front, back, side walls and / or the interventricular septum (MZHP), which depends on the location of the critical stenosis or occlusion of a spacecraft. Poor circulation to the LAD LCA can lead to myocardial infarction anteriopartition area, tops and much rarer - posteriodiaphragmal (lower) wall of the left ventricle. Cessation of blood flow in LCA impact assessment is accompanied by the anteriobazal, lateral or posteriobazal infarction (occlusion distal RH LCA). When blood circulation in the basin of PKA may develop posterolateral diaphragmatic (with the defeat of the proximal PCA) or posteriobazal infarction (occlusion distal PKA). Isolated right ventricular infarction is relatively rare. There is often a combination of its various localizations.

4.By stage of the disease are distinguished:

acute period - up to 2 hours from the start of it; acute period - up to 10 days from the start of MI; subacute period - from 10 days before the end of 4-8 weeks; postinfarction period - usually after 4-8 weeks.

The division of a heart attack on stage. The explanation in the text Sometimes singled out the so-called prodromal period ("preinfarction angina"), which corresponds to a certain extent, the notion of unstable angina, myocardial infarction complicated by development.

The most common complications of MI include:

acute left ventricular failure (pulmonary edema); cardiogenic shock; ventricular and supraventricular arrhythmias;

conduction abnormalities (CA-blockade, AV block, bundle-branch block, block); acute left ventricular aneurysm; external and internal discontinuities infarction, cardiac tamponade; aseptic pericarditis (epistenocarditic); thromboembolism.

Aetiology and Pathogenesis

The main cause of myocardial infarction is atherosclerosis SC (95%). It should also be borne in mind that infrequently (no more than 5% of patients), myocardial infarction may result from embolism of the SC (infective endocarditis , intraventricular blood clots), birth defects and other coronary lesions KA (koronariity in systemic lupus erythematosus, rheumatoid arthritis , rheumatoid arthritis), etc. However, in these cases they are not regarded as a clinical form of coronary artery disease, and as a complication of one of these diseases.

In most cases, termination or a sharp restriction of coronary blood flow occurs as a result of thrombosis of the spacecraft, which usually develops in the "complicated" plaque, which is thinned capsule damaged (tear, ulceration, exposure of the lipid core plaque). This contributes to platelet activation and plasma coagulation factors and tissue thromboplastins collagen. Initially formed platelet "white" parietal thrombus. At the same time in this area is allocated a number of biologically active substances with potent vasoconstrictor effect (endothelin, serotonin, thrombin, antithrombin A2.The result is a pronounced spasm of the stenotic spacecraft, further limiting blood flow to the coronary artery. In addition, small platelet aggregates may embolize to the coronary vessels microcirculatory level, which further limits coronary blood flow. Gradually increase the size of the thrombus and the wall, if it does not happen spontaneously lysis due to natural activation of the fibrinolytic system of its own, or not performed thrombolytic therapy, clot completely occluding the vessel lumen and evolving transmural myocardial infarction (heart attack with a tooth Q). In cases where for various reasons, complete occlusion of the spacecraft does not occur or a spontaneous clot lysis may develop subendocardial or mural myocardial infarction (heart attack without tooth Q). The latter may develop and complete occlusion of the SC, if well developed collaterals. The consequences of myocardial infarction. As a result of a myocardial infarction is a violation of diastolic and systolic left ventricular function, and begin the complex process of remodeling it. At the same time there are significant changes in the functional state of other organs and systems.

The clinical picture of "uncomplicated" myocardial infarction with Q waves

During transmural myocardial infarction (heart attack with a tooth Q) decided to allocate five periods: 1) prodrome, 2) acute and 3) sharp, and 4) subacute and 5) postinfarction period. The clinical picture of each of them consists of:

typical clinical manifestations of uncomplicated myocardial infarction; clinical symptoms of multiple complications.

Prodrome (preinfarction angina)

Most patients with MI with a tooth Q (70-80%) the formation of thrombotic occlusions total can range from 2 to 18 days. At this time the coronary circulation is characterized by extreme volatility, which is reflected in the clinical picture of disease, resembling, as a rule, one of the options for unstable angina:

first emerged angina (unstable and rapidly progressive course);

progressive angina; spontaneous anginal attacks pain at rest (including Prinzmetal's variant angina).

Acute period

Acute transmural myocardial infarction period - this time from the onset of clinical and / or instrumental (ECG) signs of acute myocardial ischemia prior to the formation of foci of necrosis (2-3 h). During this period, morphological changes in the cardiac muscle more reversible, and timely application of thrombolytic agents may be possible to restore coronary blood flow and prevent the formation of myocardial necrosis.

The first clinical manifestation of myocardial infarction associated with the completion of thrombotic occlusion of the full SC or a sudden its development (in the absence of patient symptoms prodromal period). There are several clinical variants of early myocardial infarction:

pain (anginal) version of the start (status anginosus); asthmatic option (status asthmaticus); abdominal option (status abdominalis); arrhythmic variant; cerebrovascular option; oligosymptomatic (asymptomatic) myocardial infarction beginning.

Complaints

Bout of intense pain in the heart is the most characteristic clinical sign of early myocardial infarction. The pain is localized in the chest, often spreading to the entire region before cardiac left and right of the sternum, and even epigastric region. In most cases, pain radiating to left arm, left shoulder blade, neck, at least - in interscapulum, the lower jaw in both hands, etc.

The intensity and nature of pain is usually distinguished from an attack of angina pectoris: myocardial infarction patients describe it as unusually severe, painful, "cruel" pain squeezing, crushing, or burning Expander nature, often accompanied by fear of death. The pain occurs suddenly, quickly reaching the maximum intensity. It is not docked with nitroglycerin sublingually or isosorbide dinitrate. Often the pain just stopped by after the application of narcotic analgesics ("marginal" or "morphine" pain). The duration of pain, in typical cases is 40-60 minutes, sometimes persisting hours and days, justifying its name - status anginosus.

Sometimes, perhaps as a "wave-like change in pain intensity: 20-30 minutes after the limit of strength," morphines "pain comes short (10-15 minutes), pain relief, after which she resumed with renewed vigor.

It should be remembered that the pain they sometimes can pass on their own, even if the patient had not received appropriate medical care.

Much less pain when they may be less intense and prolonged. In these cases, pain can be quite "tolerant" of their duration does not exceed 15-20-30 minutes, sometimes pain can cut short after taking several tablets of nitroglycerin.

Most patients with transmural infarction occurrence of intense pain attack is accompanied by signs of a painful shock. Patients complain of a sudden appeared a sharp weakness, dizziness, sweating expressed, heart rate (tachycardia), cold extremities. There is apathy and weakness, and in some cases, even a short blackout. There is a decrease in blood pressure.

Described clinical signs indicate the occurrence of acute vascular insufficiency, which develops, usually at an altitude of pain. As a result of reflex dilatation of the abdominal cavity and the skeletal muscle of blood is deposited in these vascular areas, reducing blood flow to the heart, developing hypovolemia, reduced blood pressure and cerebral hypoperfusion.

This clinical picture of acute circulatory failure is very similar to the initial clinical manifestation of true cardiogenic shock due to a sharp fall in cardiac output. However, in contrast, signs of reflex painful shock short-lived, quickly, within a few minutes, go alone or with the use of drugs that increase the vascular tone.

Shortness of breath. Subjective manifestations of acute left ventricular failure are observed more than half of patients transmural myocardial infarction, including patients with pain (anginal) option infarction. Against the background of continued pain after the attack, or relieve the feeling of lack of air, breathing discomfort, shortness of breath, which intensified in the horizontal position of a patient with a low headboard. These symptoms are associated with rapidly evolving against a background of severe myocardial ischemia, diastolic and systolic LV dysfunction, improvement of CRT in the ventricle, the average pressure in the LP and the veins of the pulmonary circulation and venous congestion in the lungs.

It should be emphasized that the development of more severe manifestations of acute left ventricular failure (cardiac asthma or alveolar pulmonary edema) in acute myocardial infarction period pain is not typical. An exception is the option early asthmatic MI, which is regarded as a complicated course of myocardial infarction and is considered by us in the section "Complications of myocardial infarction."

Arrhythmias. Most patients with transmural infarction (90%) as a monitor observation can reveal a variety of arrhythmias and conduction, including emerging in the earliest period of the disease. Most of them are accompanied by complaints of patients on heart rate and disruptions of the heart. A detailed description of certain types of arrhythmias is shown below (see: "Complications of myocardial infarction").

History. In the history of the vast majority of patients with acute myocardial infarction there are indications of clinical manifestations of coronary heart disease (angina or rest), as well as the presence of certain risk factors for aggravating heart attack (AH, LLA, smoking, diabetes, obesity, family history etc.). Details should ask the patient or relatives about the period immediately preceding the development of myocardial infarction (prodromal stage), and the factors trigger the development of myocardial infarction (excessive exercise, psycho-emotional stress, infections, etc.).

Physical examination. The purpose of physical examination of patients with MI is not so much a diagnosis of MI, which is confirmed in the main data laboratory and ECG studies, assessment of how the functional state of the cardiovascular system and timely diagnosis of severe complications infarction. Inspection. With the general examination in the first minute or 1-1.5 h, the last of the onset of the disease, attention is drawn to marked agitation and restlessness of patients experiencing at this time of pain. They are trying to change position, sometimes even walking around the room, sit in a chair, lie on the bed in search of provisions to relieve the suffering. This feature is characteristic of patients with MI, distinguishes them from patients with angina who, during the pain attack as if frozen in place. After the relief of pain stimulation in patients with developing myocardial infarction, usually takes place. The exceptions are cases of progressive left ventricular failure, accompanied by suddenly appearing and rapidly increasing dyspnea and suffocation. On examination, often marked pallor of the skin, cold extremities and severe sweating, indicating the

possible development of acute circulatory failure (short-term reflex painful shock) or the initial clinical manifestation of true cardiogenic shock. In most cases, cyanosis is determined by the lips.Severe cyanosis, orthopnea position, combined with moist finely rattling in the bottom of the lungs and increased frequency of respiratory movements indicate the presence of acute left ventricular failure. Palpation and percussion of the heart. On palpation of the heart, there may be local tenderness in the left before cardiac area. When percussion is no noticeable increase in LV cavity acute illness can not be identified. The exceptions are patients with previous myocardial diseases that are accompanied by dilatation of LV (hypertension, atherosclerotic and postinfarction cardio, etc.). Auscultation of the heart. In acutest period of MI in patients can identify several auscultatory phenomena: 1. Weakening and muted tones on top of I associated with a decrease in contractility of the ischemic left ventricular. 2. 2. Weakening II tone due to deceleration of early left ventricular diastolic relaxation and reduction of pressure in the aorta. When the pressure in the pulmonary artery, caused venous congestion in the pulmonary circulation, determined tone accent II on the pulmonary artery. Finally, some patients with myocardial infarction and severe atherosclerotic aortic seal can listen to the tone accent II aorte.3. Sinus tachycardia, which in the first 2-3 hours after the start of IM suggests, rather, not the presence of heart failure, and marked activation of the CAC, taking place against the backdrop of painful stress. 4. 4. Sinus bradycardia, sometimes detected in patients with myocardial infarction is associated, on the contrary, with a predominance of parasympathetic nervous system activity and the inhibition of CA-node automaticity, which is especially often observed in the field of left ventricular infarction posterolateral diaphragmatic. In addition, in more rare cases, bradycardia may be due to blockade of the SA-or AV-block II and even III degree.Arterial pulse and blood pressure. Blood pressure in the first minutes and hours of MI may increase, which is often associated with elevated CAC increased concentration of catecholamines in the blood, appearing as a result of the pain and emotional stress. With the development of acute vascular insufficiency of blood pressure is reduced, mainly due to systolic BP. Simultaneously, a decrease of filling, tension and magnitude of arterial pulse, as well as its acceleration.

Acute period.

Acute myocardial infarction period corresponds to the time of formation of foci of necrosis and the emergence of the so-called reabsorbision necrotic syndrome associated with a common reaction to the absorption (resorption) of necrotic masses in the blood. During this period also begins the complex process of LV remodeling is accompanied by a violation of the functional state of the cardiovascular system. In uncomplicated acute myocardial infarction during the period usually lasts about 7-10 days.Complaint. Pain in the heart. In the absence of complications, pain in the heart of this period usually does not occur. Preservation of pain for a few days of illness onset may indicate a further distribution of thrombotic process in the coronary system and expanding the zone of ischemic damage of the heart muscle or of involvement in the pathological process of the pericardium. Fever. At the 2-3rd day of illness the body temperature up to 37,2-38 ° C and above, which is one of the first clinical signs of necrotic resorption syndrome. Fever usually persists for 3-4 days, rarely about 1 week. More prolonged increase in body temperature may indicate the development of complications of myocardial infarction: pneumonia, thrombotic endocarditis, pulmonary infarction, etc.Shortness of breath and other signs of left ventricular failure frequently observed in acute transmural myocardial infarction, suggesting left ventricular dysfunction. Feeling short of breath, tachycardia, small for a short time can be detected even in cases that are considered in general as for

uncomplicated heart attack. In more severe cases may develop interstitial or alveolar pulmonary edema, which is regard as a very serious complication of MI (details - see: "Complications of myocardial infarction").Arrhythmias. In the acute stage of the disease remains a high risk of a variety of arrhythmias and conduction, including paroxysmal ventricular tachycardia and ventricular fibrillation. When uncomplicated myocardial infarction patients can be kept moderately severe sinus tachycardia or bradycardia, isolated extrasystoles.Physical examination.  Examination. Uncomplicated acute period of MI, usually not accompanied by any specific changes, detectable by the general inspection. In the study of the cardiovascular system during this period may reveal a slight decrease in systolic blood pressure.Often reveals a moderate sinus tachycardia due to heart failure or related to the presence of fever. For percussion of the heart may reveal a slight shift to the left the left border of the relative dullness, which may indicate the beginning of LV remodeling, its dilation and reduced contractility. Auscultation of the heart I relaxed tone, sometimes significantly, due to a sharp decrease in left ventricular contractility, dilatation of its occurrence or relative insufficiency of mitral valve damage as a result of papillary muscle. In the latter case, the weakening of the tone I often combined with systolic noise at the top, under way at the left armpit. Approximately one third of patients with MI in the acute stage can hear protodiastolic or presystolic gallop rhythm. Protodiastolic gallop rhythm due to the appearance of abnormal heart tones III shows the progressive fall of left ventricular contractility and volume overload. Diagnostic value of auscultatory phenomenon increases with the presence of other signs of left ventricular failure (dyspnoea, cyanosis, wheezes in the lungs, etc.). Sometimes the apex of the heart can hear presystolic gallop rhythm associated with the appearance of abnormal heart tones IV, due to increasing end- diastolic pressure in the left ventricular diastolic stiffness, and severe ischemic myocardium. 2-4 days of the disease on auscultation can hear the noise of friction pericardium due to involvement in the disease process leaves the pericardium (aseptic pericarditis), which is seen as a complication of myocardial infarction). Finally, in more rare cases, may appear at the top of the beat, coupled with the weakening of tone I caused the defeat of the papillary muscles and the relative development of mitral valve insufficiency. Maximum noise is determined at the top. The noise carried in the left armpit.

Subacute periodIn the subacute stage of MI gradually formed connective tissue scar, which replaces the necrotic masses. Work is also continuing the process of LV remodeling. The duration of subacute period varies widely and depends primarily on the volume of foci of necrosis, infarction of the surrounding state, not involved in the necrotic process, the degree of development of collaterals, the presence of concomitant diseases and complications of MI. Typically, the duration of subacute period is 4-6 weeks. In general, the subacute period are relatively more relaxed and favorable, than the two previous periods. The condition of patients gradually stabilized. In uncomplicated disease course pain in my heart and life-threatening severe arrhythmias (ventricular tachycardia and ventricular fibrillation Paroxysmal) are absent. Decreases the incidence of arrhythmias, sinus tachycardia and other arrhythmias. In patients with evidence of AV block I or II that have developed in the acute stage, often restored atrioventricular conduction. Reduced manifestations of heart failure (shortness of breath, tachycardia), if they occurred in the acute period.In other cases, with extensive damage to the heart muscle symptoms of congestive heart failure may progress, especially against the background mode is activated patient. At the same time grows short of breath, tachycardia, edema appear on the legs, increases the liver, stored moist wheezes in the lower lungs, etc. In most cases in the subacute stage of a tendency to normalization of blood pressure, although sometimes the level of systolic blood pressure is lower than before the onset of MI. Auscultation is usually kept muted tone I at the top, but protodiastolic and presystolic gallop rhythm are heard less often. In patients with relative insufficiency of the mitral valve due to valvular dysfunction (papillary muscle) continues to listen systolic murmur at the apex. Pericardial friction noise is absent.

Postinfarction period

In the immediate postinfarction period in the rumen increased amount of collagen and ends with his seal (consolidation of the scar). At the same time continuing the formation of a number of compensatory mechanisms aimed at maintaining the hemodynamics at the proper level (hyperfunction and hypertrophy of the intact myocardium, moderate dilatation of the LV, contributing, according to Starling mechanism, a slight increase in cardiac output, etc.). The clinical picture of postinfarction period is affected by many factors:

postinfarction scar size; functional state of the surrounding myocardium; of compensatory mechanisms of cardiac activity; rate of progression of coronary atherosclerosis, etc. In the near term post-infarction angina may resumeIf during this period there are

frequent anginal attacks occurring in a patient with the slightest exertion, psycho-emotional stress or at rest, it is regarded as one of the options for unstable angina (an early post-infarction angina) requiring emergency treatment. The second group of subjective symptoms observed in some patients in the postinfarction period is associated with progression of chronic heart failure (shortness of breath, tachycardia, leg swelling, increasing weakness, fatigue, etc.). Finally, in the postinfarction period remains an increased risk of occurrence of various arrhythmias and conduction. These objective study conducted in the postinfarction period, often support some degree of hemodynamic instability (wheezes in the lungs, edema, liver enlargement, cyanosis, ventricular dilation, etc.).

Features of the clinical picture of myocardial infarction without Q wave The clinical picture of myocardial infarction without wave Q (no transmural) is broadly

consistent with the above clinical manifestations of acute coronary syndromes. Since the basis of no transmural MI in most cases is the development of "complicated" plaque wall thrombus and appearance of the heart muscle area and expressed relatively a long-term ischemia, the main clinical manifestation of MI without Q-wave is pain. In most cases, are characterized by pain, prolonged rest angina (lasting more than 20-30 minutes), poorly stoped nitroglycerin. As a rule, anginal attacks do not reach the intensity characteristic of an emerging transmural infarction with a tooth Q, and more like the rest angina, characteristic of patients with NA. Sometimes retrosternal pain may be accompanied by sharp attacking weakness, sweating, shortness of breath, transient arrhythmias and conduction and / or a sudden drop in blood pressure. Less commonly, infarction without Q wave manifests less intense but more frequent bouts of angina, a rapid decrease in exercise tolerance, etc more reminiscent of progressive symptoms of the National Assembly. In all these cases the lack of persistent elevation RS-T on the background causes pain attacks carried out a differential diagnosis between HC and myocardial infarction without tooth Q. Physical examination usually provides little new information to confirm the diagnosis no transmural MI, except for transient significant weakening of the fundamental tone heart and the appearance of additional tones (III or IV) during the occurrence of anginal attack. Sometimes you can detect transient arrhythmias, and various changes in blood pressure. Thus, the analysis of clinical data in most cases, suggesting the development of coronary heart disease in a patient with acute coronary syndrome, but in order to confirm or refute the presence of myocardial infarction without tooth Q, should be targeted lab tests.

Laboratory diagnosis of myocardial infarction

Laboratory confirmation of acute myocardial infarction based on the identification of: 1) nonspecific indicator of tissue necrosis and inflammatory reaction of the myocardium, 2) hyperenzymemy and 3) increase in blood myoglobin and troponin.

Nonspecific reaction to the occurrence of acute myocardial infarction is associated primarily with the disintegration of muscle fibers, breakdown products of protein absorption into the bloodstream and local aseptic inflammation of the heart muscle, mainly in developing peryinfarct zone. The main clinical and laboratory signs of reflecting these processes are: increased body temperature (from subfebrile figures to 38,5-39 ° C), leukocytosis, usually not exceeding 12-15 x 109 / l., Aneozinofiliya, a small stab shift of the blood to the left, increasing the ESR. Markers of myocardial necrosis: Troponin. The most sensitive and specific marker of myocardial necrosis is an increased concentration of troponin I and T included, as is known in the troposphere myosin complex contractile myocardium. Normally cardio-specific troponins in blood are not detected or the concentration is less than the most minimal values established separately for each clinical laboratory. Cardiomyocyte necrosis is accompanied by a relatively rapid and significant increase in the concentration of troponin I and T levels are starting to exceed the upper limit of normal within 2-6 hours after anginal attack and remains high for 1-2 weeks from onset of infarction. Myoglobin. Very sensitive, but few specific marker of necrosis is the concentration of myoglobin in the blood. His rise is observed 2-4 hours after anginal attack and persists for 24-48 hours afterwards. The yield of myoglobin from heart muscle and increase its concentration in the blood occurs before the formation of foci of necrosis, etc expressed at the stage of ischemic heart muscle. You should also remember that increasing the concentration of myoglobin in the blood may be due to other causes (other than a heart attack): Disease and injury of skeletal muscles, a lot of physical stress, alcoholism, renal insufficiency. Unfortunately, not all clinics are now able to determine the concentration of troponin laboratory and myoglobin in the blood. Therefore, in practice retains its value determination of other, less sensitive and specific, markers of myocardial necrosis The most valuable of them for the diagnosis of acute myocardial infarction is to determine the activity of several enzymes in serum:

CK (K FA), especially its MB-fraction (CF to PC); lactate dehydrogenase (LDH) and its isoenzyme 1 (LDG1); aspartate aminotransferase (AST).

Creatine kinase (K FA) and its MB fraction to the FC. More specific laboratory test is to identify acute myocardial infarction MW fraction to FC (CF to PC). Its activity begins to increase after 4-6 h, reaching a peak after 12-18 hours and returned to their original numbers after 48-72 hours from the start of anginal attack. Of particular importance is the dynamics of enzyme activity: reliable signs of acute myocardial infarction considered to increase the activity of CF FC by 25% in two samples taken from the 4-hour intervals, or a gradual increase in enzyme activity over 24 hours is informative to the increased activity of CF FC 10 - 13 IU / liter. Activity common to FC in MI undergoing a similar trend: the end of the first day of the enzyme level in the 3-20 times higher than normal, but after 3-4 days of onset of the disease returned to baseline values. In contrast, the increased activity of MB fraction to FC, contained mainly in the myocardium, specific for heart muscle damage, primarily for acute myocardial infarction. MB-fraction to FC does not respond to damage of skeletal muscle, brain and thyroid gland. However, be aware that any cardiac intervention including coronary angiography, catheterization of heart cavities and electro-therapy, usually accompanied by a brief rise of activity-MB fraction to the FC. In the literature there are also indications of the possibility of increasing the level of CF to FC with severe paroxysmal tachycardia, myocarditis, and long strokes of rest, assessed as a manifestation of unstable angina.

Lactate dehydrogenase (LDH). The activity of this enzyme in acute myocardial infarction is growing more slowly than the CK and CF to CF, and remains elevated for longer. Peak activity occurs usually 2-3 days from onset of infarction, and return to its original level - only 8-14 days. Should be remembered that the total LDH activity also increased in liver disease, shock, congestive heart failure, hemolysis and megaloblastic anemia , pulmonary embolism, myocarditis, an inflammation of any localization, coronary angiography, cardioversion, heavy physical exertion and and so on. In this regard LDG1 isoenzyme more specific for heart disease, in particular for acute myocardial infarction, although it is also present not only in heart muscle but also in other organs and tissues, including red blood cells. Aspartate aminotransferase (AST) is also an enzyme with a relatively fast peak of the upcoming increase in activity (24-36 h of the onset of infarction). After 4-7 days the concentration of AST returned to baseline levels. Changes in the activity and AST is not specific for acute myocardial infarction: the level of AST with ALT levels increased in many pathological conditions, including liver diseases. Yet it must be remembered that in patients with lesions of the liver parenchyma to a greater extent increases the activity of ALT, and heart diseases - AST. In the MI ratio Rytis (the ratio of AST / ALT) greater than 1.33, and for diseases of the liver - less than 1.33. Given the specific characteristics of leaching of various enzymes of foci of necrosis and duration of their presence in the serum, should keep a few principles of enzymatic diagnosis of acute myocardial infarction.

Electrocardiography

Myocardial infarction with Q waves

According to the ideas Bayley, violation of the coronary circulation during myocardial infarction leads to the formation of three zones of the lesions: necrosis around the site are areas of ischemic damage and ischemia. In the leads, the active electrode which is located directly above the area of MI, each of these areas is involved in the formation of these ECG changes.

1. The zone of necrosis - pathological tooth Q (lasting more than 30 ms) and a sharp decrease in the amplitude of R wave or complex QS.

2. The zone of ischemic damage - offset RS-T segment above (transmural infarction) or lower contour (with subendocardial lesions of the heart muscle).

3. The zone of ischemia - "coronary" (equilateral and spiky), T wave (high positive in subendocardial MI and negative - with transmural infarction).

Acute stage (up to 2 hours from the start of IM) is recorded on the ECG-segment RS-T above isoline (transmural ischemic injury). RS-T segment with merges with a positive T wave, forming the so-called monophasic curve that resembles the shape of TM PD.

The acute stage is characterized by rapid, within 1 - 2 days, formation of a pathological Q wave or QS complex and reduced wave amplitude R, which indicates the formation and expansion of the zone of necrosis. At the same time for several days stored offset RS-T segment above the contour and merges with it at first positive and then negative spike T. A few days later RS-T segment is close to contour lines and by the end of 1st week or the beginning of the 2nd week of illness is isoelectric that indicates a decrease in the zone of ischemic damage. Negative coronary T wave abruptly deepens and becomes symmetrical and sharp (re-inversion of T wave).

Three zones of pathological changes in heart muscle in acute myocardial infarction (from Bayley) and their reflection on the ECG (Figure)

In the subacute stage of MI registers or pathological Q prong set QS (necrosis) and a negative coronary T wave (ischemia), whose amplitude, ranging from 20 to 25-days of myocardial infarction, is gradually reduced. RS-T segment is located on the contour. Scar stage of MI is characterized by persistence over many years of pathological Q wave or QS complex and the presence of negative, positive or smoothed the T wave. Depending on the localization of myocardial infarction and prevalence of these changes are found in different ECG leads.

ECG anteriorseptal myocardial infarction with the transition to the top of A and anterolateral myocardial infarction-B

ECG in advanced anterior myocardial infarction-A and anterior basal (high anterior) myocardial infarction: a - the usual arrangement of thoracic electrodes (myocardial infarction not detected), b - by placing electrodes on the two edges of the above (recorded typical symptoms of myocardial infarction)-B

ECG during acute posterolateral diaphragmatic (lower) myocardial infarction. In leads I, aVL, V1-V4 recorded reciprocal ECG changes.

Direct and reciprocal ECG signs of myocardial infarction with Q waves of different localization

Localization of infarction

Leads that show signs of myocardial infarction

Direct evidence:

pathological Q (QS);

elevation RS-T;

negative coronary T

Reciprocal features:

depression RS-T;

high positive T;

higher R (at the rear MI)

Myocardial infarction left ventricular anterior wall anterior septal V1 - V3 anterior apical V3, V4 The front side I, aVL, V5, V6 Anterior basal (high-front) V24 - V26 and / or V34 - V36 Common front I, aVL, V1 - V6 III, aVF, II Myocardial infarction left ventricular posterior wall Posterolateral diaphragmatic (lower)

III, aVF, II

posterior basal V7 - V9 V1 - V3 Rear side V5, V6, III, aVF Common background III, aVF, II, V5, V6, V7 — V9 III, aVF, II,

V5, V6, V7 - V9 V1 — V3 V1 - V3

Myocardial infarction without Q wave

Myocardial infarction without Q wave characterized by the development of cardiac muscle necrosis notransmural, localized subendocardial or intramural. In contrast, transmural infarction, these foci of necrosis does not violate the propagation of waves of depolarization of the heart, so the abnormal tooth Q or QS complex are absent. Significant violations are detected only during the formation of RS-T segment and during the final phase of ventricular repolarization (T wave). The most common ECG signs of myocardial infarction without Q wave are: 1) a shift RS-T segment below the contour (in rare cases, possible RS-segment elevation of T), 2) a variety of pathological changes of the T wave (usually symmetrical and sharp negative coronary T wave); 3) the emergence of these changes on the ECG after a long and intense pain attack and keep them within 2-5 weeks. Diagnostic localization of myocardial infarction without Q wave based on the same principles as the transmural MI. ECG of the two patients with non-Q-wave and anterior location posterolateral diaphragmatic

Echocardiography is one of the required research methods that are used for the diagnosis of acute myocardial infarction and assessment of hemodynamic and structural damage in this disease. The use of two-dimensional, one-dimensional and Doppler echocardiography in MI you can:

identify local disturbances of LV contractility; quantify systolic and diastolic function ЛЖ ; LV; reveal signs of LV remodeling (dilatation of the cavity ventricle, left ventricular geometry

changes, etc.); identify echocardiographic signs of left ventricular aneurysm; assess the condition of the valve apparatus and the presence of relative insufficiency of

mitral valve defect or MZHP; assess the level of pressure in the aircraft and identify the signs of pulmonary hypertension; identify morphological changes in the pericardium and the presence of fluid in the

pericardial cavity; intracardiac thrombi detect the presence of; assess the morphological and functional changes of main and peripheral arteries and veins.

One-dimensional echocardiograms recorded from various sites of patients with MI, which are clearly visible signs of hypokinesia or akinesia segments of diseased left ventricle.

One-dimensional echocardiograms recorded from the left parasternal access in a healthy person (a - scheme) and the patient postinfarction cardiosclerosis (b). visible hypokinesia septal

Two-dimensional echocardiograms recorded in patients with postinfarction cardiosclerosis a - akinesia of interventricular septum, b - posterolateral diaphragmatic akinesia (lower) segment of the left ventricle

Selective coronary angiography (CAG) in patients with acute myocardial infarction is carried out in cases where surgery is supposed to coronary vessels - percutaneous transluminal angioplasty or coronary artery bypass grafting. Obtained in the CAG are very important when choosing a method of surgical correction of obstructive lesions of the SC. Because when the CAG, as a rule, make the left ventriculography, it allows us to estimate a number of important hemodynamic parameters and verify some of the serious complications of MI (left ventricular aneurysm, rupture MZHP, etc.). The most common indications for emergency CAG and subsequent surgical repair in patients with acute myocardial infarction are:

cardiogenic shock; severe left ventricular failure, particularly if it is combined with severe mitral insufficiency or

rupture of the interventricular septum ; recurrent episodes of life-threatening ventricular arrhythmias (ventricular tachycardia,

ventricular fibrillation); Early post-infarction angina.

It should be noted that in recent years in the major cardiology centers greatly expanded indications for emergency CAG. The study is now carried out for many patients with acute myocardial infarction hospitalized in the early stages of disease onset (4-6 h) to restore coronary blood flow or limit the zone of necrosis by selective intracoronary administration of thrombolytic therapy or surgical correction of blood flow in the spacecraft.

Treatment of uncomplicated myocardial infarction with Q waves

The existing system currently in the treatment of patients with MI include:

specialized cardiac ambulance (prehospital) providing first medical care of patients with MI; specialized branch infarction with intensive care unit or coronary care department (hospital

phase); specialized rehabilitation centers (departments of hospitals and cardiology sanatorium); Cardiac consultative and diagnostic centers and clinics cardiology offices (clinical examination

of patients after myocardial infarction).

The main strategic objectives of the treatment of patients in the prehospital and hospital stages are:

1. Early reperfusion of the myocardium or coronary revascularization, as well as preventing further blood clots.

2. Limiting the focus of necrosis and coronary band periinfarction with hemodynamic and metabolic unloading of the heart.

3. Prevention or elimination of the early complications of myocardial infarction.

4. 4. Physical and psychological rehabilitation of patients with MI.

All patients with suspected myocardial infarction with a tooth forming Q, patients with acute coronary syndrome and persistent elevation RS-T, must be immediately hospitalized in intensive care specialist cardiac units. Basic therapy, which is carried out in all patients with myocardial infarction with a tooth Q, regardless of the presence or absence of certain complications, includes:

pain relief (analgesia); thrombolytic therapy (of course, tailored to individual indications and contraindications); antithrombotic and antiplatelet therapy; oxygen therapy; the use of anti-ischemic drugs; ACE inhibitors and angiotensin receptor antagonists II.

Pain

Relief of anginal attack is a prerequisite for all further therapeutic measures. Anginal pain retaining supports hyperactivation of SAS, which is accompanied by tachycardia, positive inotropic effects, increases myocardial oxygen demand and leads ultimately to an increase in infarct. In addition, SAS background activation lowers the threshold of ventricular fibrillation, which in itself can have fatal consequences. If there are no signs of a sharp fall in cardiac output and blood pressure (arterial pulse filling satisfactory and acceptable numbers of blood pressure), patients are encouraged to re-reception of nitroglycerin sublingual or inhalation irrigation of the oral mucosa by aerosol nitroglycerin or isosorbide dinitrate. These simple measures should be carried out at the first contact a patient with a doctor before ECG recording.

Morphine. The classic means of pain relief in patients with myocardial infarction is the use of narcotic analgesics. Morphine, an agonist of opioid receptors, in addition to rapid pain relief, reduces venous tone and, consequently, reduces the venous return of blood to the heart, the magnitude of preload and myocardial oxygen demand. Morphine has also pronounced sedative effect. In addition, he has a marked effect vagotonic causes sinus bradycardia and hypotension.

In patients with acute coronary syndrome, including suspected myocardial infarction, morphine is administered intravenously at an initial dose of 2-4 mg, followed by 2-6 mg every 10-15 minutes (a total of no more than 20-30 mg) up to pain relief or the appearance of side effects:

nausea, vomiting, sinus bradycardia (vagotonic effects); hypotension;

signs of depression of the respiratory center.

Keep in mind that vagotonic side effects relatively easily eliminated by intravenous (0.5-1.0 ml) of 0.1% solution of atropine sulfate, and the signs of depression of the respiratory center - 0.1-0.2 mg intravenous naloxone.

In the absence of effects from the use of morphine and maintaining pain showed intravenous drip solution of nitroglycerin and / or b-blockers, which contribute, as we know, the hemodynamic unloading of the heart and reduce myocardial oxygen demand.

Nitroglycerin (0.1% solution) is administered intravenously. Just as in the National Assembly, the initial rate of intravenous infusion of nitroglycerin is 10 mg / min. Then it increases to 10 mcg / min every 3-5 min until the reaction of blood pressure changes or symptoms. At the same systolic blood pressure should be below 110 mm Hg. Art. or in a patient with hypertension - 25% below baseline.

β-blockers. Intravenous b-blockers in the acutest period they can contribute to reduction of pain syndrome and control of areas of necrosis. b-blockers reduce contractility and myocardial oxygen demand and weaken the influence of catecholamines on the heart, reduce heart rate, blood pressure, increase the threshold for ventricular fibrillation and prevent supraventricular arrhythmias. It is recommended to use cardioselective b1-blocker (metoprolol, atenolol, and others).

Should be considered contraindications to the use of b-blockers in patients with myocardial infarction:

signs of congestive heart failure (including wet wheezes in the lower regions of the lungs); Heart rate below 60 bpm in minutes; AV block II, III and I grade at P-Q (R) with more than 0.24; systolic blood pressure below 90 mm Hg. ; concomitant presence of asthma; chronic obstructive bronchitis in the presence of dry wheeze in the lungs (one of the symptoms

of bronchial obstruction).

Oxygen therapy

Oxygen therapy is indicated for all patients with myocardial infarction with a tooth Q. The use of oxygen by mask or nasal catheter increases the saturation of arterial blood oxygen (SaO2) above 90%, resulting in an increase of its diffusion in the area of ischemic myocardium surrounding intact areas of the heart muscle, helping to reduce the size of the zone of ischemic damage (periinfarct zone). Oxygen therapy is indicated for patients of MI at least during the first 1-2 days after admission to the intensive care unit.

Antiplatelet drugs

Mandatory condition of patients with MI is the appointment of antiplatelet drugs. Most often prescribe aspirin at a dose no higher than 325 mg per day. At the first contact with the patient is recommended to chew an aspirin without membranes (250-325 mg) if this was not done before. In the presence of contraindications to its use may use ticlopidine or clopidogrel, which are inhibitors of ADP receptors of platelets. Effective is the combination of aspirin and clopidogrel

Heparins

Heparin is an effective indirect thrombin inhibitor, exerts its antithrombotic effect through activation of

physiological anticoagulant - antithrombin III. Appointment of heparin in acute coronary syndrome with elevation RS-T, including myocardial infarction with a tooth at Q, is justified primarily as a means of preventing further thrombus formation in the SC and reduces the incidence of venous thrombosis and intraventricular wall with the subsequent development of thromboembolic complications.

Anti-ischemic drugs

Anti-ischemic drugs are widely used in the treatment of patients with MI with a tooth Q. Thanks to an efficient hemodynamic unloading of the heart, they help to limit the size of infarction in the first place, the size of periinfarct zone. The latter is preserved areas of viable myocardium that directly border zone of necrosis.

The most appropriate designation of patients with MI of two groups of drugs that have the property to limit periinfarct zone: b-blockers and nitrates.

β-blockers. In the absence of β-blockers are contra-indications are encouraged to nominate all patients with MI. The positive effect of these agents in myocardial infarction due to their negative inotropic and chronotropic action, accompanied by a decrease in myocardial oxygen demand and ischemia heart rate. This is to some extent makes it possible to maintain the viability of the myocardium periinfarct zone and, thereby, limit the area of infarction. In addition, β-blockers have the ability to raise the threshold of fibrillation, which reduces the risk of fatal cardiac arrhythmias. Finally, the impact of β-blockers on the activity of the NAC and the RAAS is accompanied by a slowing and LV remodeling has a significant impact on survival in the short and long periods of MI.

Nitrates are used in patients with myocardial infarction to left ventricular hemodynamic unloading and reduced myocardial oxygen demand. The positive effect of nitrates on the value of periinfarct zone and the reduction or relief of some symptoms of the disease (pain in the heart, shortness of breath and other signs of left ventricular failure).

Metabolic drugs

Currently, patients are used, basically, two ways of actively influencing the metabolism of cardiac muscle: the use of trimetazidine (preduktala) and intravenous drip of glucose-insulin-potassium mixture.

Trimetazidine has a direct cytoprotective effect, implemented at the level of cardiomyocytes and subcellular structures. Trimetazidine administered in the usual therapeutic dose - 1 table. 3 times a day.

Glucose-insulin-potassium mixture (HEC) is widely used for the treatment of patients with MI. The use of glucose-insulin-potassium mixture based on the idea that the increase in glucose delivery to ischemic myocardium may have a protective effect by stimulating the accumulation of glycogen in cardiomyocytes. The latter is a source of glucose during anaerobic glycolysis and thus enhances the formation of ATP (GD Lopaschuk, 2000). It is not excluded that the introduction of glucose-insulin-potassium mixture helps to reduce the level of circulating fatty acids, since insulin inhibits the mobilization of free fatty acids from adipocytes.

ACE inhibitors

Recently, ACE inhibitors are increasingly used to treat patients with acute myocardial infarction and

patients with postinfarction cardiosclerosis, primarily to prevent progression of left ventricular dysfunction.

In addition to optimizing the level of blood pressure, afterload and preload values, reducing the production of aldosterone and, accordingly, sodium and water retention in the body, ACE inhibitors are able to limit the adverse effects of rapid cardiac remodeling in patients with myocardial infarction. Thus, ACE inhibitors reduce the effect of tissue angiotensin II in the processes of hypertrophy of cardiomyocytes, interstitial fibrosis, improving endothelial function, increasing the production of vasodilating substances and contributing to an increase in coronary flow reserve. In addition, ACE inhibitors promote atherosclerotic plaque stabilization and reducing the frequency of repeated acute coronary syndrome.

Thrombolytic therapy

Thrombolytic therapy is currently regarded as the primary method of restoring coronary blood flow (reperfusion) in patients with acute coronary syndrome with persistent elevation RS-T. All drugs currently used for thrombolysis in patients with myocardial infarction, are endogenous activators of plasminogen. The most common ones include:

Streptokinase - indirect plasminogen activator derived from a culture of b-hemolytic streptococcus group C. Streptokinase forms a covalent bond with the blood of plasminogen activating its conversion to plasmin. In this regard, streptokinase, in addition to effects on fibrin clot formation, has also expressed a systemic fibrinolytic action.

Urokinase - an enzyme that directly activates the conversion of plasminogen to plasmin. The drug is prepared from a culture of human embryonic kidney.

Alteplaza - is a tissue plasminogen activator (tPA), which is produced mainly by endothelial cells of blood vessels. Activation of tPA in the vascular bed occurs under the action of plasmin, trypsin, kallikrein and activated factor X clotting. Tissue plasminogen activator, in contrast to streptokinase, has an affinity to fibrin, so that it selectively acts on the fibrin clot, showing properties or fibrin selectivity of fibrin specificity. This is a positive characteristic alteplaza explains the high efficacy of the drug. It should nevertheless be borne in mind that the use of doses required for lysis of thrombus, alteplaza affects both circulating in the blood of plasminogen, also exerting systemic effects on fibrinolysis, although less pronounced than streptokinase. This leads to a decrease in fibrinogen levels in the blood serum and an increased risk of bleeding (major complications of thrombolytic therapy).

New educational technologies used in class:

Interactive game "cat in a bag"

In applying the method of "The Cat in the Bag" bag is put in a few sheets with questions on the subject. Students take turns taking out of the bag sheets with questions and answers.

Examples asked questions on the topic:1. The etiology of myocardial infarction2. The pathogenesis of myocardial infarction

3. Classification of myocardial infarction4. Clinical variants of myocardial infarction5. The clinical course of myocardial infarction6. Laboratory Methods of myocardial infarction7. ECG signs of myocardial infarction8. Differential diagnosis of acute myocardial infarction.9. Basic principles of treatment and rehabilitation of myocardial infarction.10. Complications of myocardial infarction.

6.2. The analytical part.

Situational problems

1. Patient M. age 62 turned to the clinic complaining of severe chest pain, feeling short of breath, general weakness. A patient suffering from coronary heart disease for a long time. Pain started 2 hours ago, the pain does not even nausea Paulsen receive 4 tablets of nitroglycerin. OBJECTIVE: pale skin, cold sweat, lips cyanosis, pulse 92 beats per 1min., Blood pressure 90/50 mmHgI. Your tentative diagnosis:A. CHD: myocardial infarction *B. ischemic heart disease: angina FC IV. ischemic heart disease: progressive anginaG. ischemic heart disease: angina angiospasticD. CHD: angina FC IVII. Necessary for the diagnosis methods:A. UltrasoundB. ECG *V. X-rayG. EhoKSD. radioisotope scan2. In the clinic enrolled patient complaining of pain dagger in the heart, not stoped taking nitroglycerin, accompanied by cold sweat and feeling the fear of death. Auscultation of the heart tones of the deaf.I. Your tentative diagnosis:A. CHD: myocardial infarction *B. ischemic heart disease: anginaV. hypertension, hypertensive crisisG. ischemic heart disease: angina angiospasticII. What changes in the ECG:A dome-shaped segment elevation ST *B. negative T wavesV. ST segment on the isoelectric line, the expansion of the QRS complexG. metabolic changes in the myocardium, the signs of left ventricular hypertrophy

D. ECG unchanged3. Patient A., 44. Complains of chest pain compressive nature, cold sweats, general weakness. Anamnesis: in 5 years suffer from coronary heart disease. Deterioration began this morning. Deterioration began this morning. Repeated reception of nitroglycerin pain is not docked. OBJECTIVE: The state of medium gravity, there is pallor of the skin. In the lungs, vesicular breathing. Cardiac deaf. Pulse regular, intense, 80 beats per minute. BP 180/90. The ECG - sinus rhythm in leads III, AVF ST segment above the contour lines and contour otvedeniiV3 below.I. Your diagnosis:A. CHD. Acute myocardial infarction anterior left ventricular wallB. CHD. Acute myocardial infarction anterior septal areaV. CHD. Acute myocardial infarction posterior wall *G. CHD. Acute myocardial infarction of the apical regionII. What complications can occur early in the patient?A syndrome DreslleraB. Cardiogenic shock *V. Chronic aneurysmG. postinfarction cardio4. Patient K., aged 46. Complains of chest pain compressive nature. Of history: During the 3 years of age suffer from hypertension. In the last 2-3 months periodically bothered squeezing chest pain character, who with nitroglycerin pills quickly passed. Today, because of the lack of nitroglycerin patient did not accept it. The patient was given a pill under the tongue Validol, but chest pain persisted, and he brought the ambulance to the emergency department of a hospital. OBJECTIVE: The state of medium gravity, skin pale and covered with cold sweat. In the lungs, vesicular breathing. Cardiac deaf. Pulse 74 beats rhythmic min. AD140/90. The ECG - isoelectric ST-segment elevation in I-II, AVL, V5, V6 leads.I. Your diagnosis:A. CHD. Progressive anginaB. CHD. Acute myocardial infarction posterior wallV. CHD. Acute myocardial infarction side wall of the left ventricle *G. CHD. Acute myocardial infarction of the anterior-septalII. What changes in laboratory parameters are possible:A neutrophilic leukocytosis, accelerated erythrocyte sedimentation rate, hyperenzymemia *B. anemia, neutrophilic leukocytosis, eosinophilia.V. leukocytosis, accelerated SOE, fibrinopeniaH. Leukopenia, anemia

7. Methods of testing practical skills and theoretical knowledge.          1. Professional examination and questioning of the patient with myocardial infarctionPurpose:- Information necessary for diagnosis;- Assessment of the likelihood of disease;- The identification of other sources of information (relatives, other doctors, etc.);

- Establishing trust relationships with patients;- Assessment of a patient's personality and his attitude to the disease (the internal picture of disease);- Assess the state of consciousness and mental status of the patient, his position, general appearance, state of the external cover and some parts of the body.Uses: survey is mandatory for all patients in mind, survey conducted in all patients.Equipment: well-lit chambers, doctors' offices, fluorescent lighting.Conditions of performance: the absence of unauthorized persons, confidential atmosphere.Performed steps (stages):

№ action not fulfilled Fully implemented correctly

1 Inquire passport data 0 52 collection complaints 0 153 Medical history of the disease 0 204 Medical history of life 0 155 Epidemiological, allergic history 0 56 An objective examination of the patient 0 57 Compilation of survey 0 58 Correct diagnosis 0 59 differential diagnosis 0 2010 Treatment plan 0 5

Total: 0 100

2. Compilation of dietary recommendations and treatment programs.

Purpose: Treatment and prevention of disease complications.

№ action not fulfilled Fully implemented correctly

1 The study of the characteristics of medical tables on Pevsner

0 10

2 The right choice of dietary table in accordance with the diagnosis

0 10

3 Assessment of usefulness of the diet 0 204 In accordance with the diagnosis, disease severity and

stage of the appointment of primary therapy0 20

5 In accordance with the diagnosis, disease severity and stage of the appointment of primary therapy.

0 20

6 preventive measures 0 20Total: 0 100

Tests

1. The greatest risk of fatal myocardial infarction is associated with the development of:A pulmonary edemaB. AneurysmV. cardiogenic shock *

G. paroxysm of atrial fibrillation2. The acute period of myocardial infarction on ECG is characterized by:A high T-wave *B. ST-segment depressionV. arcuate lifting ST intervalG. barb deep Q3. What is the most characteristic feature of transmural myocardial infarctionA pronounced tooth QB. negative T wavesV. tooth formation QS *G. R-wave amplitude decrease4. Increased sedimentation rate in myocardial infarction is usually marked:A. in the first hoursB. On the second dayV. 3-4 daysBy the end of first week *5. At what stage of myocardial infarction is characterized by the formation of pathologic wave Q:A. sharpest* B. acuteV. subacuteG. scar6. Which of the biochemical changes in the early hours of acute myocardial infarction:A. ALT AST *B. thymol testV. reduction of fibrinogenG. increase CPK, LDH7. By the early complications of myocardial infarction are notA pulmonary edemaB. Cardiogenic shockV. cardiac tamponadeMr. Dressler's syndrome *8. What does the symptom of scissors in myocardial infarction:A decrease in ALT and LDH-1 increasedB. reduction of LDH-1 and increased ALT levels during the first weekV. reduction of leukocytosis and increased ESR in the first week *G. lowering ESR, and leukocytosis growth during the first week

8. Criteria for evaluating the current control

The level of student knowledge Progress in% and the score

evaluation

A student on the major issues and themes for students' independent work::Summarizes and makes decisions

96-100 5

creative thinkingindependently analyzedInto practiceShows high activity, a creative approach to the conduct of interactive gamesCorrectly solves the case studies with full justification for the answerUnderstands the subject matterKnows, says confidentHas a faithful representationPrepares informative modern visual aids or abstracts of high quality using data from the recent literature of 7-10 sources and the Internet.

A student on the major issues and themes on the SIW:creative thinkingindependently analyzedInto practiceShows high activity, a creative approach to the conduct of interactive gamesCorrectly solves the case studies with full justification for the answerUnderstands the subject matterKnows, says confidentHas a faithful representationPrepares informative modern visual aids or abstracts of high quality using data from the recent literature of 4-6 sources and the Internet.

91-95

5

A student on the major issues and themes on the SIW:independently analyzedInto practiceShows high activity, a creative approach to the conduct of interactive gamesCorrectly solves the case studies with full justification for the answerUnderstands the subject matterKnows, says confidentHas a faithful representationPrepares informative modern visual aids or abstracts of high quality using data from the recent literature of 3-5 sources and the Internet.

86-90

5

A student on the major issues and themes on the SIW:Into practiceShows high activity, a creative approach to the conduct of interactive gamesCorrectly solves the case studies with full justification for the answerUnderstands the subject matterKnows, says confidentHas a faithful representationPrepares informative modern visual aids or abstracts of high quality using data from the recent literature of 3-5 sources and the Internet.

81-85

4

A student on the major issues and themes on the SIW:Shows high activity during the interactive gamesCorrectly solve situational problems, but the justification for an incomplete answerUnderstands the subject matter

76-80 4

Knows, says confidentHas a faithful representationPrepares modern visual aids or abstracts using the recent literature data of 1-2 sources.

A student on the major issues and themes on the SIW:Correctly solve situational problems, but the justification for an incomplete answerUnderstands the subject matterKnows, says confidentHas faithful representations orA student on the major issues and themes on the CDS:Mistakes in solving situational problemsKnows, says uncertainlyHas a faithful representation of some issues topicPrepares informative modern visual aids or abstracts of high quality using data from the recent literature of 7-10 sources and the Internet.Prepares modern visual aids or abstracts of high quality using data from the recent literature of 4-6 sources and the Internet.

71-75

4

A student on the major issues and themes on the SIW:Understands the subject matterCorrectly solve situational problems, but can not justify a responseKnows, says confidentHas a faithful representation of some issues topic

66-70

3

A student on the major issues and themes on SIW:Mistakes in solving situational problemsKnows, says uncertainlyHas a faithful representation of some issues topic

61-65

3

A student on the major issues and themes on SIW:Knows, says uncertainlyHas a partial view

55-60

3

A student on the major issues and themes on SIW:It does not accurately representDo not know

Less then 55

2

9. Chronological map of classes.

№ Stages of the practice session forms of Expectancy at

employment (minutes)

270

1. Introduction by the teacher (study subjects). 10

2. Discussion topics practical training, testing students' knowledge base with new teaching technologies, demonstration material (slides, audio - video tapes, x-rays, EKG, etc.).

Poll.explanations.

60

3. Conclusion of the discussion. 20

4. The distribution of tasks for students to perform the practical part of training. Guidance and clarification on the requirements for practical tasks. Self-Supervision.

50

5. Mastering by the teacher of practical exercises (case-patient Supervision).

Medical history, interactive games, case studies.

40

6. Interpretation of laboratory and instrumental methods of investigation of the thematic patient, differential diagnosis, treatment plan and prevention, prescription, etc.

Working with clinical and laboratory equipment.

40

7. Discussion of the theoretical and practical knowledge of students, their reinforcement and assessment of the group in achieving the goal classes.

Oral questioning, test, discussion, checking the results of practical work.

30

8. Conclusion of the teacher on the passed lesson, evaluation of each student and the announcement of the results. Development tasks to prepare for the next session (a collection of questions).

Questions for homework.

20

10. Questions for the control of knowledge

1. The etiology of myocardial infarction2. The pathogenesis of myocardial infarction

3. Classification of myocardial infarction4. Clinical variants of myocardial infarction5. The clinical course of myocardial infarction6. Laboratory Methods of myocardial infarction7. ECG signs of myocardial infarction 8. Differential diagnosis of acute myocardial infarction.

9. Basic principles of treatment and rehabilitation of myocardial infarction.  10. Complications of myocardial infarction.

11. Recommended Reading              Summary:1. AI Martynov, NA Mukhin et al, "Internal Medicine" textbook in two volumes. Moscow: GEOTAR Media, 2009. 1227str.2. NA Mukhin, VS Moiseev, AI Martynov, "Internal Medicine"     textbook in two volumes. Moscow: GEOTAR Media, 2006. 1272str.

Optional:1. Therapy. Allen R., MD Meyrs Moscow, Medicine GEOTAR 1997. 1024str.2. Differential diagnosis of internal diseases. R. Helgin.,Trans. German ed. Tareeva, MA, Medicine 1993.3. Diagnosis and treatment of internal diseases. Guidelines for doctors in 3 volumes. Under the general editorship. Kosarev FI M., Medicine 1991.4. Roitberg GE, Strutynsky AV "Internal Medicine:The cardiovascular system. " 856 p. Moscow, 2007.5. Okorokov AN "Diagnosis of diseases of internal organs." V.6. Diagnosis of diseases of the heart and blood vessels. Moscow, 2003, 464 pages6. Okorokov AN "The treatment of diseases of internal organs." V.3,kn.1. Treatment of diseases of the heart and vessels. Moscow, 2005 464 pages                   Sites: www.TMA.uz., http://www.meddean.luc.edu,                                http://www.embbs.com

REVIEW

for a teaching manual on integrated learning associate E.R. Juraev assistant F.K. Ziyaeva, G.T. Bekenova on "Myocardial infarction".

Submitted by the authors of educational textbook devoted to an important topic in cardiology, namely, myocardial infarction, which is one of the most common causes of death and disability in the populationIn recent years, the increase in the incidence of myocardial infarction, particularly among

young and middle age. Despite the widespread reduction in hospital mortality from myocardial infarction, overall mortality from this disease remains high, reaching 30-50% of the total number of cases.

A teaching manual is designed for students of 4th year on the subject of Faculty Therapy, contains basic information on the etiology, pathogenesis, classification, clinical presentation, diagnosis and differential diagnosis, as well as the treatment of myocardial infarction. Educational tools built on the principle of the integral. A distinctive feature of this handbook is the presence of a diagnostic algorithm that represents the student-oriented framework for recognition of the disease. This approach can provide substantial assistance in the preparation of general practitioners, as well as in the formation of clinical thinking in students.

Head of the Department Clinical Pharmacology medical and medico-pedagogical TMA Faculty, Professor A.B. Yakubov