ECG Side Wall Myocardial Infarction. Myocardial infarction

Electrocardiogram (ECG) with myocardial infarction is an affordable, high-precision and rapid diagnostic method. Timely carrying out such a instrumental method will allow in the shortest possible time to make the correct diagnosis and provide emergency assistance to the patient, save its life. If necessary, the doctor prescribes additional instrumental and laboratory methods to clarify and expand the diagnosis of "myocardial infarction".

Indications for the cardiogram, the capabilities of the technique

The cardiogram is a schematic image that allows you to accurately determine the features of the work of the heart muscle. The technique is easy to execute. It is performed using a special instrument - an electrocardiograph, which registers due to the degradation sensors, the processes of abbreviation and relaxation of various myocardial departments, including in different pathologies. Myocardial infarction is a frequent reason for the purpose of the electrocardiogram. This is due to the fact that even the early signs of myocardial infarction on ECG are visible quite clearly.

The states that are predecessors or symptoms of such a state as a myocardial infarction, in which the ECG is required:

• pain in the heart of different intensity;
• respiratory disorders;
• heart rate disorders;
• pallor and skin sinusiness;
• trembling limbs;

• severe dizziness;
• dyspnea;
• the forced position of the body in which the symptoms fade;
• the presence of chronic heart and vascular pathologies as a planned survey, as well as in developing on their background of the indicated signs.

The electrocardiographic curve in the form of alternating teeth makes it possible to identify such deviations and violations:

• features of the heart rhythm;
• pulse;
• violations of exchange processes in the heart muscle;
• miocardial necrosis sites. ECG allows you to determine the presence and indicative dimensions of dead tissues, which makes it possible to estimate the scale of pathology and assign proper treatment;
• the presence of dead areas of myocardium, which appeared earlier (with the hidden form of heart attack and other pathologies);
• chronic degenerative changes of the heart muscle;
• the thickness of the muscular walls of the heart, sections with hypo-or hypertrophy;
• the correct functioning of the pacemaker.

How to study with heart attack

To perform a cardiogram with myocardial infarction, both stationary and portable cardiographs can be used, which will allow you to perform a study in the ambulance car on the road to the office. Myocardial infarction is always a sudden pathological condition, so standard procedures for research preparation are not conducted. Do not worry about distorting results. Infarction on ECG in most cases is easily determined.

The main stages of the study:

1. Remove clothes above the belt and free the lower limbs to fix the electrodes.
2. Put a patient. If the patient has a forced sedent position, then you can remove the half-sidia cardiogram.
3. Special tool to lubricate the places of attaching the electrodes to the patient's body surface.
4. Fixation of electrodes on the body of the patient. In order to make a clear cardiogram with a heart attack, it is important to impose electrodes for 12 standard assignments: to the upper and lower limbs and the chest area.
5. If possible, ensure the patient's immobility.
6. Remove the cardiogram using the device, get a graphic image of the work of the heart on paper and monitor.

The study is short-time in time, which allows you to put the correct diagnosis of "myocardial infarction" as soon as possible and provide urgent assistance to the victim.

Normal cardiogram performance

There are such standard teeth:

• P - displays the pulse in atrium;
• Q - indicates the conduct of a pulse in the interventricular space;
• R - characterizes the conducting and distribution of the pulse in the ventricles;
• S - displays the final stage of the residual pulse through the ventricles;
• T - characterizes the process of relaxing ventricles before the following reduction;
• U is a weakly expressed prong, which indicates the state of the conductive system in the ventricles of the heart.

Normal images of the main teeth on the cardiogram:

• the P should be directed up from the axis (positive);
• qog q on a normal ECG is directed down from the axis (negative);
• tusk R is always sharply directed up. It is highlighted in size among the remaining teeth;
• teeth S in the absence of pathological processes in myocardium negative;
• tusk T - positive, small sizes, smooth;
• tusk U is a low-rise positive.

Important information carry intervals between the teeth:

1. S-T - indicates myocardial ischemia.
2. P-Q - Displays the presence of rhythm disorders.
3. P-P - is an important way to diagnose the rhythm of the heart muscle.
4. Q-S - displays the duration of the excitation period in the ventricles.
5. Q-T - shows the duration of the reduction of ventricles.
6. Q-R-S - indicates the presence of heart blocks.
7. P-R - displays the processes of abbreviation and relaxation in atria.
8. T-P - indicates the state of relaxation processes in the ventricles.

An experienced doctor will always evaluate the cardiogram indicators in a certain order not to miss important details.

Change cardiograms with heart attack

When developing a heart attack on an ECG, unlike other pathologies, the changes are manifested in a short time, which makes it possible to carry out accurate and rapid diagnosis of the disease at any stage.

The electrocardiograph for this pathology gives a clear idea of \u200b\u200bsuch pathological processes:

• places of education of necrosis;
• depth and vastness of necrosis;
• stages of disease and severity of manifestations;
• the presence of scarves on myocardium, which remained from past heart attacks or chronic ischemia.

Main ECG signs of myocardial infarction are as follows:

1. Deepening of the teeth Q.
2. Extension of the segment (interval) S-T.
3. S-T smoothing interval.
4. S-T segment lift.
5. Different deformations of the priest R.
6. The emergence of negative teeth T.
7. Unchanged Q-S-T complex.

Changes to ECG are often different at different stages of the disease.

Acute and acute periods of myocardial infarction are characterized by such changes:

• smoothing (disappearance) of Tusque T;
• the rise of the S-T segment is above the axis;
• smoothing Tong P.

At the subacute stage during the diagnosis of "myocardial infarction", on which the final scarring occurs, such deviations to the ECG are noted:

• lowering the S-T interval to the axis;
• the appearance of the negative teeth T.

The post-infarction period of myocardial infarction is characterized by the following changes to the ECG:

• the location of the S-T interval on the axis;
• preservation of negative teeth t;
• the appearance of a distinct teeth Q, which in previous stages can be smoothed in some cases.

The reasons for this are different. In particular, the pathology of blood vessels is atherosclerosis. At the same time, plaques are formed, which are narrowed, and over time and overlap the clearance of the vessel. Causes of atherosclerosis - smoking, obesity, increased blood pressure, passive lifestyle. Often - problems with metabolic processes in the body.

Sometimes circulation problems arise when inflammation of the main heart arteries. In this case, the arteritis develops. The disease is rare, but possible with a heart attack. There is infectious or non-infectious nature.

Ears are also able to lead to myocardial infarction, especially penetrating. Dangerous in terms of infarction is considered closed injuries, as they lead to serious damage, the contusion of the heart, which provokes a blood coagulation disorder. In addition, after bruises, thrombus are formed, which often cause acute myocardial infarction.

Thickening of the walls of the vessels due to the metabolism disorder - this process develops slowly, but it is irreversible. In this case, the front-part-based extensive myocardial infarction occurs very often.

It is rare, but it happens that the heart attack of the anterior wall is the result of the operation on the heart. Doctors are not always guilty, because it is almost impossible to predict complications.

The reasons for this are different. In particular, the pathology of blood vessels is atherosclerosis. At the same time, plaques are formed, which are narrowed, and over time and overlap the clearance of the vessel. Causes of atherosclerosis - smoking, obesity, increased blood pressure, passive lifestyle. Often - problems with metabolic processes in the body.

Pathogenesis

Distinguish the steps:

1. Ischemia
2. Damage (necrobiosis)
3. Necrosis
4. Scarring

Ischemia may be a predictor of heart attack and lasts for quite a long time. The basis of the process is a violation of myocardial hemodynamics. Usually, the narrowing of the artery of the heart is considered to be clinically significant when limiting myocardial blood supply can no longer be compensated.

Most often, this occurs when the artery is narrowing by 70% of its cross-section. When the compensatory mechanisms are evaluated, there is a damage when the metabolism and the myocardial function suffers, but the changes may be reversible (ischemia).

The stage of damage lasts from 4 to 7 hours. Necrosis is characterized by irreversibility of damage. After 1-2 weeks after the heart attack, the necrotic section begins to be replaced by a scar cloth. The final formation of the scar occurs after 1-2 months.

Causes causing ischemic heart disease

With the inability of the coronary arteries to provide the needs of myocardium in oxygen, the center of ischemia arises, and then necrosis. Infarctal etiological factors:

• Atherosclerosis with a predominant aorta defeat and coronary arteries of the heart.
• Hypertensive disease, cardiac shape.
• Thrombosis and embolism of coronaryov associated with blood hypercoagulation.
• Vasculitis (arteritis), leading to the proliferation of intravascular epithelium and sclerosis of the wall.
• Strong physical or psycho-emotional tension.
• Overweight, bad habits, hypodynamia, error in food.

Acute circular infarction - transmural large-scale heart damage associated with the obliteration of the envelope of the artery. Leads to severe complications, up to death from cardiogenic shock or myocardial rupture. Clinically manifests:

• acute compressing pain behind the sternum;
• feeling of panic fear;
• hyperiodosis - increased sweating;
• harsh weakness;
• collaptoid state;
• lack of air;
• feeling heartbeat and ripples.

Damage to the heart muscle proceeds in 4 stages:

• Double infarction (acute stage) is characterized by the greatest risk of severe complications. It is represented by the necrobiasis of muscle fibers with a weak cell reaction along the periphery.
• The acute stage lasts 1 week, the focus of necrosis is clearly formed, permeated by segmentation-nuclear leukocytes, around it is a "hemorrhagic whisk" (zone of point hemorrhage). The patient's condition is severe, but stable.
• The granulation tissue is growing into the graining area - a subacted stage. It lasts up to the month, the patient's condition gradually improves, the work of the heart is restored.
• The graded stage continues within 2 months. Myocardial infarction at the scarring stage germinates with a connective tissue, a scar is formed.

If in the period up to 2 months a new focus of myocardial necrosis appeared, they talk about recurrence. Repeat refer to the infarction that developed the field of grappling stage.

With a circular myocardial infarction, necrosis applies to the entire thickness of the left ventricular wall, leads to severe violations in the heart of the heart:

• acute heart failure with swelling of the lungs;
• arrhythmias and blockades with damage to the conductive heart system;
• cardiogenic shock with the development of DVS syndrome;
• multiple hemorrhages with reduced blood coagulation;
• migratory venous thrombosis as a result of the subsequent gain of coagulation;
• client intracardiac thrombosis;
• runner walls with hemotamponade cardiac shirt leading to death.

The stop of the coronary blood circulation can be caused by several reasons. It:

• Atherosclerosis. Chronic arterial disease, which is characterized by the formation of dangerous thrombov. If you do not interfere with their development, they will increase in the amount and eventually block the artery and blood supply.
• Sharp spasm coronary arteries. This can occur from cold or exposure to chemicals (poisons, drugs).
• Embolia. This pathological process, in which particles appear in lymph or blood, which should not be there, which leads to a violation of local blood supply. The reason for the acute myocardial infarction most often becomes fat embolism, when the fat droplets fall into the blood.
• Launched anemia. In this state, there is a sharp decrease in the hemoglobin in the blood, therefore, the transport functions of the blood decrease, so oxygen does not flow in due.
• Cardiomyopathy. The sharp hypertrophy of the heart muscle is characterized by inconsistency in the level of blood supply with increased needs.
• Surgical interventions. During the operation there was a complete dissection of the vessel across or a bandage.

In addition to the main reasons, risk factors can also be distinguished - pathological conditions that can lead to a heart attack. These include:

• cardiovascular diseases (often ischemic heart disease);
• diabetes;
• previously suffered myocardial infarction;
• hypertonic disease;
• heart arythmy ;
• increased cholesterol;
• smoking or alcohol abuse;
• obesity;
• improper nutrition (salt and animal abuse);
• increased concentration in triglyceride blood;
• age older than 40 years;
• chronic stress.

The reasons for the development of the myocardial infarction of the front wall of the left ventricle, cause many disputes among doctors. Some believe that this is a separate ailment, the second, consider its body's response to pathological processes.

That is, it makes sense to consider non-factors that lead to the occurrence of the state, namely the causes of blood supply disorders.

Such an extensive (transmural) infarction of the front wall of the left ventricle occurs due to the fact that a large vessel that feeds the heart was blocked. In this case, the thrombus overlaps the clearance of the front interventricular branch of the left coronary artery.

This is a fairly large vessel, which, in addition to the front wall, nourishes other parts of the heart, namely:

• Front wall
• Top left ventricle
• Interventricular partition
• Side wall
• Poofer muscles

Therefore, often the myocardial infarction of the anterior wall is combined with the defeat of the top of the heart. In some cases, the headborne myocardial infarction is developing when the interventricular partition is also affected.

Etiology

Myocardial infarction develops as a result of the obstruction of the lumen of the vessel of blood supplying myocardium (coronary artery). The reasons may be (in the frequency of occurrence):

1. Atherosclerosis of the coronary arteries (thrombosis, obturation of the plaque) 93-98%
2. Surgical Obbituration (Gleaning Artery or Dissection for Angioplasty)
3. Embolization of the coronary artery (thrombosis in coagulopathy, fat embolism, etc.)
4. Spasm of coronary arteries

Separately identify a heart attack at heart defects (abnormal debit of coronary arteries from the pulmonary trunk)

Clinical picture

The main clinical sign is an intense pain for the sternum (anginal pain). However, pain may wear a variable character. The patient can complain about the feeling of discomfort in the chest, abdominal pain, throat, hand, shovel. Often the disease has a solemn character, which is characteristic of diabetes patients.

The pain syndrome is preserved more than 15 minutes (1 hour can last) and stopped after a few hours, or after the use of narcotic analgesics, nitrates are ineffective. It happens a profuse sweat.

In 20-30% of cases in large-scale lesions, signs of heart failure are developing. Patients celebrate shortness, unproductive cough.

Often there are arrhythmias. As a rule, these are various forms of extrasystole or atrial fibrillation. Often the only symptom of myocardial infarction is a sudden heart stop.

The predisposing factor is the physical activity, psycho-emotional tension, the state of fatigue, hypertensive crisis.

Classification

In development stages:

1. Promotional period (0-18 days)
2. The most acute period (up to 2 hours from the beginning)
3. Sharp period (up to 10 days from the beginning of them)
4. Subighteous period (from 10 days to 4-8 weeks)
5. Scarring period (from 4-8 weeks to 6 months)

According to the anatomy of the lesion:

1. Transmural
2. Intramural
3. Subendocardial
4. Subepicarordial

By volume of lesion:

1. Large-Quality (Transmural), Q-Infarction
2. Small-scale, not Q-infarction

• Localization of the focus of necrosis.
  1. Myocardial infarction left ventricle (front, side, bottom, rear).
  2. Heart top of myocardial heart attack isolated.
  3. Miocardial infarction interventricular partition (septal).
  4. Myocardial infarction right ventricle.
  5. Combined localization: rear-bottom, front-side and dr.

With the flow:

1. Monocyclic
2. Stretty
3. Recurrents (in the 1st coronary artery, a new focus of necrosis from 72 hours to 8 days)
4. Repeated to them (in dr. Cor. Art., New focus of necrosis in 28 days from the previous one)

• Spontaneous (type 1) associated with ischemia due to the primary coronary event, such as plaque erosion and / or destruction, cracking or bundle.
• Secondary (type 2) associated with ischemia caused by an increase in the lack of oxygen or its receipt, for example, with a coronary spa, coronary embolism, anemia, arrhythmias, hyper-or hypotension.
• Sudden coronary death (type 3), including a heart stop, often with the symptoms of the alleged myocardial ischemia with the expected new element of ST and the new blockade of the left leg of the GIS bundle, detecting fresh blood turbine artery during angiography and / or autopsy, which has come to obtain blood samples or Before increasing the concentration of markers.
• CCV-Associated by them (type 4a).
• It is associated with the thrombosis of the stent (type 4B), which is confirmed by angiography or autopsy.
• AKSH-Associated by them (type 5).

It should be borne in mind that sometimes in patients can occur several types of them simultaneously or sequentially. It should be noted that the term "myocardial infarction" is not included in the concept of "necrosis of cardiomyocytes" due to the performance of the AKSH (hole in the ventricle, manipulation with the heart) and the influence of the following factors: renal and heart failure, pacemakeling, electrophysiological ablation, sepsis, myocarditis, cardiotropic action poisons, infiltrative diseases.

Front heart attack can be finely or large-scale. It is also divided at the location of the localization on the front wall:

• front-partitioning infarction;
• front-windows;
• sideways myocardial infarction;
• front-top-top;
• isolated-side;
• transmural.

Stages

The development of acute myocardial infarction can be divided into four stages:

1. Phase Damage. The acute stage of the course of the disease. Duration - from 2 hours to days. It is during this period that the process of dying myocardium in the affected area occurs. According to statistics, most people die at this stage, so it is imperative that it is imperative to diagnose the disease in a timely manner!
2. Acute. Duration - up to 10 days. During this period there is an inflammatory process in the infarct zone. Phase is characterized increase body temperature.
3. Tajection. Duration - from 10 days to month or two. At this stage there is a scar.
4. Scarring phase or chronic. Duration - 6 months. Symptoms of heart attack are not manifested, however, the risk of developing heart failure, angina and repeated heart attack is preserved.

Anterior wall infarction has the same stage as any other:

• The pre-infarction state is the duration of it from several hours to a month. A characteristic feature is an increase in the number of angina attacks.
• The sharpest - continues from 30 minutes to two hours. For this phase, burning pain is characterized, cold sweat appears, hell drops. The frequency of heart abbreviations can decrease or increase.
• Acute - lasts 2-10 days. The area of \u200b\u200bdamage is drawn up, pain decreases, there is a violation of the heart rhythm and the temperature rises.
• Subacute - duration 4-5 weeks. Begins to form a scar on the necrosis site. For this period, the restoration of cardiac rhythm is characteristic. Pain syndrome decreases, pressure normalizes.
• Post-infarction period. It lasts 3-6 months. At this time, the scar cloths are compacted, the heart gets used to new conditions of operation.

If the myocardial infarction of the anterior wall managed to detect at the first two stages and provide medical care, then the prediction of recovery will be positive, and the damage for the organ is minimal.

If the myocardial infarction of the anterior wall managed to detect at the first two stages and provide medical care, then the prediction of recovery will be positive, and the damage for the organ is minimal.

Causes of disease development

Doctors call the anterior wall infarction to a greater extent "male" disease, although in the older age groups the number of the diagnosis of such a state increases in women. Often, the hereditary factor is clearly traced, and it is connected with impaired state of blood vessels.

Among the risk factors for the emergence of extensive damage to the front wall of the heart are:

1. harmful habits, in particular, smoking;
2. increased blood pressure;
3. diabetes;
4. increased lipid / lipoproteins in the patient's blood.

Symptoms

Like any other heart disease, acute myocardial infarction is characterized by pain in the heart. Among other symptoms can be allocated:

• strong compressive pain in the chest, which is periodic and reminds of itself several times a day, and it can be very intense and give to other places, without lying in one place;
• unbearable pain in the heart, which is impossible to remove nitroglycerin;

• pain in the left hand, blade, shoulder, neck or jaw;
• acute air shortage, which may be observed due to blood supply disorders;
• dizziness, weakness, increased sweating, nausea and even vomiting (these manifestations often accompany pain);
• the violation of the pulse, which carries a bruising or slow character.

The first and most important sign of the extensive heart attack of the myocardium of the front wall becomes pain. She felt behind the sternum. Maybe pulling, novel. Often patients complain of pain in the left side of the body - jaw, shovel, shoulder.

There are a number of possible symptoms for myocardial infarction of the front wall:

• cold in fingertips;
• breathing problems;
• general weakness;
• heartbeat instability;
• skin sinusiness;
• anxiety and panic;
• figure condition.

With an atypical infarction flow, there may be a sharp burning pain in the stomach, urge to vomiting, memory problems, the inability to focus.

This will show itself extensive, that is, the large-scale infarction. As for the small focal form, its symptoms are sometimes lubricated, fuzzy is expressed. The only sign that will definitely be present - the pain in the chest, anxiety.

The risk of developing an extensive heart attack in older people and diabetics increases. Their heart, vessels and other organs work with deviations. At the same time, the symptoms of acute heart attack are not manifested. Pain does not arise due to a decrease in sensitivity. Then it is worth paying attention to such symptoms:

• sharp attack of weakness;
• dyspnea;
• strong headache;
• increased blood pressure, and then its sharp decline;
• cold abundant sweat;
• dizziness, loss of consciousness, coordination violation.

Before talking about the symptoms of a sharp infarction, let's deal with what we mean by this term. The sharp period starts about 2 days. What develops immediately after the magnitude of the vessel in the first hours and day is called an acute period. However, we will analyze the clinical manifestations of heart attack from the first moments, including the most acute period.

So, the main symptoms of the disease are as follows:

1. • Duration of pain Over 15-20 minutes
2. Total weakness
3. Cold sweat
4. Dyspnea
5. "Clean legs"

An extensive myocardial infarction is a serious problem that is often worth the patient's life. Unfortunately, the number of infarction does not decrease over time.

All over the world there is an increase in cardiovascular disasters.

Acute transmural name

The acute large-scale myocardial infarction of the front wall of the left ventricle is a pathological condition at which the death (necrosis) of the entire thickness of the heart muscle on the front wall of the left ventricle occurs.

1. Pain is a symptom that has a lot of characteristics.

• Pain in the heart or sternum is extremely intense. With a transmural infarction, the whole chest can hurt
• Prevalence of pain in the right and left chest departments, neck, lower jaw, hands
• Wavely character of pain - episodes of rise and sneeze
• No effect from nitroglycerin
• The duration of pain is thrust

Interruptions, heartbeat attacks

Total weakness

Cold sweat

Dyspnea

"Clean legs"

Diagnostics

Successful diagnosis of myocardial infarction is a complex process that consists of several stages:

1. Collect anamnesis. The doctor finds out whether the attacks of pain of different frequencies and localization in the past. In addition, he conducts a survey to find out if the patient has a patient to the risk group, whether myocardial infarction has been in blood relatives.
2. Laboratory studies. In the analysis of blood on acute myocardia, an increase in the number of leukocytes and an increase in the rate of settlement of erythrocytes (ESO) is indicated. At the biochemical level, an increase in activity is revealed:

• aminotransferase enzymes (ALT, AST);
• lactate dehydrogenase (LDH);
• creatineineins;
• mioglobin.

1. Using instrumental research techniques. At the ECG (electrocardiography), a characteristic sign of heart attack is considered a negative teeth T and the pathological complex QRS, and on EchoCG (echocardiography) - a local violation of the reduction of the affected ventricle. Coronary angiography reveals a narrowing or overlap of the vessel that feeds myocardium.

1. Early:
   1. Electrocardiography
   2. Echocardiography
   3. Blood test for cardiotropic proteins (MB-KFK, AsaT, LDH 1, Troponin)
2. Delayed:
   1. Coronary art
   2. Myocardial scintigraphy

At the first signs, the patient should be called an ambulance. Upon arrival in the hospital, myocardial research is conducted - ECG. The cardiogram will show the development stage, which will help determine emergency measures and decide on the treatment scheme. In addition to ECG, a biochemical blood test is prescribed, an ultrasound of the heart.

The diagnosis of myocardial infarction is based on clinical data, laboratory and instrumental studies.

1. Laboratory diagnostics includes the definition of markers - substances, the level of which increases with it. With an extensive infarction, the levels of such enzymes increase significantly as:

• Troponins T and I
• Mioglobin
• Creatine phosphokinase-MV (KFK-MV)
• Lactate dehydrogenase-1 (LDH-1)

In addition to the definition of specific infarction markers, general and biochemical blood tests are performed.

• Common blood test: the leukocyte content increases, elaborates
• Biochemical blood test: increased the content of fibrinogen, serumcoide, haptoglobin, sialic acids, A2 globulin, gamma globulin, C-reactive protein.

2. ECG diagnostics - a mandatory method that allows you to determine the localization, the prevalence of the defeat, complications of the infarction. ECG is used to control the dynamics of the disease.

3. Heart ultrasound - diagnostic method, which allows you to evaluate the contractile ability of myocardium, reveal the clomes in the heart cavity, set the localization of damage

4. Coronoanhibition - Method of a contrast study of heart vessels. Reuses violations of vessels, sets the clombal localization.

5. Myocardial scintigraphy

6. Computer tomography

7. MRI - Magneticoresonance Tomography

8. Positron-emission tomography

Describe your problem and get a doctor's answer from Israel with treatment options and necessary diagnostics

Emergency can be attributed to the reception of nitroglycerin tablets (up to 3 pieces) and the immediate challenge "ambulance". The main activities for the treatment of acute heart attack can only be performed by the medical staff.

Allocate several principles of therapy:

1. Restoration of blood circulation in coronary arteries. After the patient's arrival in the cardiorean compartment, all necessary research is carried out to confirm the diagnosis. After this, the sharp need to quickly restore blood circulation in coronary arteries. One of the main methods is thrombolysis (the dissolution of the thrombus cells inside the vascular bed). As a rule, for 1.5 hours of thrombolytics dissolve the thrombus and restore normal blood circulation. The most popular means are considered:

• Alplaza;
• Relay;
• Ansrereza;
• Streptokinase.

1. Purchase syndrome. To eliminate pain, use:

• Nitroglycerin under the tongue (0.4 mg), however, nitrates are contraindicated at low arterial pressure;
• beta blockers that eliminate myocardium ischemia and reduce the infarct zone (usually prescribed 100 mg of metoprolol or 50 mg of atenolol);
• narcotic analgesics - in special cases, when nitroglycerin does not help, morphine intramuscularly introduces the patient.

1. Surgical intervention. It may be necessary to conduct stenting to restore blood flow. A metal structure is carried out with a thrombus, which expands and expands the vessel. Planned operations are carried out to reduce the zone of necrotic lesions. Also to reduce the risk of re-infarction is carried out an aortocortonary shunting.
2. Common events. The first few days of the patient is in the intensive care unit. The mode is a strict bed. It is recommended to exclude visits to relatives in order to protect the patient from the excitement. During the first week, he may gradually begin to move, but observing all the recommendations of the doctor by diet and physical exertion. As for the diet, it is necessary to eliminate sharp, salty and pended dishes in the first week, and the menu is enriched with fruits, vegetables, poured dishes.

Treatment in the early stages, if possible, is reduced to the elimination of pain, restoration of coronary blood flow (thrombolytic therapy, angioplasty coronary arteries, AKSH). With pronounced heart failure under the clinic, an intra-director balloon counterpulcation is possible.

In the event of a heart stop, you must immediately start cardiovascular resuscitation. The availability of automatic external defibrillators increases survival in such situations.

In addition to restoring blood flow, infarct treatment has a goal:

• Anesthesia
• Preventing the formation of thrombov
• Reducing the need of myocardium in oxygen
• Normalization of blood pressure
• Treatment of complications

The treatment of extensive myocardial infarction is not easy task. Difficulties in therapy arise due to frequent development of complications against the background of large necrosis areas. The treatment is necessarily carried out in the intensive care unit and intensive therapy.

The purpose of therapy with myocardial infarction is the restoration of blood flow in the affected vessel. It can be carried out by 2 methods:

1. Medical dissolution of thromboms.
2. Surgical reduction of blood flow. Can be carried out 2 ways:

• Installing the stent in the vessel, which expands its lumen and restores blood flow.
• Shunting operation is the creation of cooped paths of blood flow using vessels taken from other parts of the body.

Therapy

An extensive hearth wall infarction is treated only in stationary conditions. With such a defeat of the heart, the mortality rate is the highest. Moreover, cases of recovery less than lethal. At first, the patient provides full physical and psycho-emotional peace.

In order for the body in general, and the heart in particular did not overload, the doctor will write a special diet. In the first two days, the condition of all organs and systems is carefully monitored. It is during this period that there is an increased risk of patient's death.

Treatment scheme includes such drugs:

1. Means contributing to the restoration of blood circulation to the damaged area.
2. Package.
3. Preparations that help get rid of arrhythmias.
4. Anticoagulants to eliminate blood clots.
5. Thrombolytics for resorption of existing thrombus.

In some cases, surgical intervention is required. In this case, three methods can be implemented for the treatment of anterior wall myocardial infarction:

• Angioplasty coronary artery.
• Stenting a coronary vessel.
• Aorticoronary artery shunting.

Effects

Acute myocardial ischemia can even more complicate the following manifestations:

• Violation of heart rhythm. The flickering of ventricles with the transition to fibrillation may cause fatal outcome.
• Heart failure. A dangerous state can cause swelling of the lungs, cardiogenic shock.
• Thromboembolia of the pulmonary artery. May be caused by pneumonia or lung infarction.
• Tamponade heart. This happens when the heart muscle is breaking in the heart attack zone and blood breakthrough into the pericardia cavity.
• Acute heart aneurysm. At the same time, the state of the portion of the scar tissue occurs, if there was an extensive lesion of myocardium.
• Post-infarction syndrome. This can be reached by pericarditis, pleurisy, arthralgia.

The effects of myocardial mocardine heart attacks are serious. The disease provokes the blockades of myocardial of different types, which often have a disappointing treatment forecast.

Acute infarction implications:

• Heart failure - an left ventricular type develops. The damaged portion of the heart is poorly reduced, there are congestive processes in a small circle of blood circulation, which leads to an insufficient inflow of blood into the peripheral organs.
• Pulmonary edema. For him, the appearance of shortness of breath is characterized, dry cough arises. After some time, it becomes wet, frothy sputum appears.
• Arrhythmia.
• Thrombosis of the vessels of a large circle. This leads to the movement of blood clots in the brain vessels, which leads to a stroke.

Among other consequences:

• Wrong work of the left ventricle.
• Sinoatrial blockades.
• Pericarditis - inflammation of the serous shell of the heart.
• Violation of the functioning of other organs.
• Paralysis of the limbs.

The consequences or complications of acute transmural them are associated with the restructuring of myocardium. If the heart attack has also developed in the partition zone - it aggravates the unfavorable forecast. So, with an acute transmural infarction, the following complications may develop:

• Cardiogenic shock is a formidable complication that can develop in the first day from the beginning of the disease. In low blood pressure, blood begins to "save" vital organs, redistributing exactly there. Such authorities are brain, kidneys, liver. The remaining organs lack oxygen, resulting in a violation of their function.
• Acute heart failure is one of the most adverse consequences that can be observed in an acute transmural infarction.
• Heart breaks - constitute a group of fatal consequences of myocardial infarction. Unfortunately, such a complication in most cases leads to a deadly outcome. Blood is poured into the window-shaped bag and squeezes it outside. In such conditions, it cannot be reduced, and the circulatory stop comes.

• Aneurysm - complication of them in which myocardium loses elasticity and is pronounced at the place of defeat
• Rhythm and conductivity disorders
• Pleurrites - cluster of fluid in pleural cavity
• Pericarditis - accumulation of fluid in the cavity of the breakbag
• Early post-infarction angina
• Thrombembolism of the body's pulmonary vessels - pulmonary artery, branches of the abdominal artery, the vessels of the lower extremities
• Formation of blood clots in the cavity of the heart
• Ulcers and erosion of the stomach and 12-tupest intestine
• Delay urination
• Mental disorders in the form of delirium, varying degrees of loss of consciousness. Attention should be paid to one of the mental violations in the list of implications of infarction - depression. It can take weight of them and serves as a frequent cause of suicidal actions.

Risk factors

• Tobacco and Passive Smoking
• Air pollution
• Men are more likely to suffer from myocardial infarction than women
• Obesity
• Alcohol consumption
• Diabetes

Prevention of ischemic heart disease

1. Burn with overweight.
2. Refuse bad habits.
3. Follow the level of glucose and blood cholesterol.
4. Exercise.
5. Control blood pressure.

Remember the possible clinical manifestations of the heart attack, the atypical flow of it. The ambulance doctor will determine the myocardial infarction on the electrocardiogram. But the further course of the disease and completeness of the restoration of heart functions depends on your knowledge and skills.

• Antitrombotic therapy aspirin and / or clopidogrel reduces the risk of myocardial infarction relapse. The use of clopidogrel and aspirin reduces the risk of angry-vascular events, but at the same time increases the risk of bleeding.
• Beta blockers as metoprolol or carvedilol can be used to prevent myocardial infarction. These drugs are especially improving the forecast for the patients who have a violation of the left ventricular function. Beta blockers reduce mortality and morbidity.
• Therapy of statins after myocardial infarction reduces mortality.
• The use of polyunsaturated fatty acids can also improve the forecast.
• The use of heparin in persons with unstable angina may reduce the risk of myocardial infarction, but at the same time increase the possibility of small bleeding.
• ACE inhibitors are also used to prevent myocardial infarction.

I21.0 acute transmural hearth miocardial infarction
Transmural infarction (acute):
. Front (wall) BD
. Peredouerous
. Advanced
. Promotional

An extensive myocardial infarction of the anterior wall of the left ventricle is usually due to occlusion of the main trunk of the left coronary artery or more often its branch - anterior downward artery.
The myocardial infarction of the anterior wall is often complicated by the ventricular extrasystole or ventricular tachycardia, as well as various reductant rhythm disorders.
Violations of atrioventricular conduction during the front infarction are observed relatively rarely. However, if they appear, they usually develop suddenly. The total transverse blockade with an extensive myocardial infarction of the front wall sharply increases the mortality of patients (almost 4 times), while with a heart attack of the rear wall of the left ventricle with a complete transverse blockade, mortality increases only 2 times. Conductivity disorders in the forefront myocardial infarction are often characterized by persistence and persisted for a long period, as they are due to necrosis of the conductive system cells.

Classification

Select the following varieties:

- Common transmural infarctiont myocardium

Located with thrombosis of the general barrel of the left coronary artery. Symptoms characteristic of myocardial infarction are recorded in OBCs I, II, AVL, V 1 - V 5 (V 6) - Fig. 64.

The acute period proceeds with complications: a cardiogenic shock, an acute left-detecting deficiency, arrhythmia, is an acute and chronic aneurysm, a break and tamponade of the heart.

Miocardial front-part-part

Front interventric arterry is affected. Under this localization, infarction changes are recorded in from K 1 - V 2 (V 3), a Q of Q can appear in these leads, the magnitude of the qs is most often a jelly complex.

The anterior-partitioning infarction myocardial infarction is complicated by the intraventricular conductivity, blockades of the left or right leg of the Gis beam, necrosis of the interventricular partition with its defect, damage to the papillary muscles and the development of the lack of mitral valve.

Head-top myocardial infarction

The descending branch of the left coronary artery is affected, the in-person changes are determined in the leads V3 - V 4. Observed Syndrome RV4

Miocardial front-side

The envelope branch of the left coronary artery is affected, the in-person changes are localized in leads I, AVL, V 5 - V 6. With this localization there is a break and tamponade of the heart. With an iso-layered lateral infarction, changes in V 5 - V 6.

Etiology and pathogenesis

Direct reasonthe development of myocardial infarction (im) is acute the coming inconsistency of the coronary blood circulation by the requests of myocardium due to occlusion Occlusion is a violation of the patency of some hollow formations in the body (blood and lymphatic vessels, subparent spaces and tanks), due to the resistant closure of their lumen on any site.
Coronary artery or a sharp decrease in blood flow on it with subsequent ischemia and necrosis.

Myocardial infarction with pathological teeth Q (thrombotic occlusion of the coronary artery) is developing in 80% of patients with myocardial infarction and leads to a transmural myocardial necrosis and the appearance of Q to the ECG.

Myocardial infarction without pathological teeth q most often occurs when spontaneous recovery of perfusion Perfusion - 1) long-lasting injection of fluid (for example, blood) with therapeutic or experimental goal in the blood vessels of the organ, body parts or the whole organism; 2) the natural blood supply to some organs, such as kidneys; 3) artificial blood circulation.
or well-developed collaterals Collateral is an anatomical education connecting the structures bypassing the main path.
. The size of the heart attack in this case is less, the function of the left ventricle suffers less, the hospital mortality is lower. However, the frequency of myocardial infarction is higher than with myocardial infarction with pathological teeth Q, due to the fact that such myocardial infarction companies are "unfinished" (that is, myocardium remaining viable is supplied with an affected coronary artery); By the end of the first year, mortality is equal. Therefore, with myocardial infarction without pathological teeth q, a more active treatment and diagnostic tactics should be followed.

At the heart of the development they lie three pathophysiological mechanism:

1. The gap of an atherosclerotic plaques, provoked by a sudden increase in the activity of the sympathetic nervous system (a sharp increase in blood pressure, frequency and heart rate, amplification of coronary circulation).

2. Thrombosis on the spot torn or even intact An intact (lat. Intactus - untouched) - intact, not involved in any process.
Fuckers as a result of improving blood thrombogenic ability (by increasing aggregation Aggregation - the platelet property will be connected to each other.
platelets, activation of the coagulant system and / or inhibition of fibrinolysis Fibrinolysis (fibrin + Greek. Lysis - decay, decomposition) - the process of dissolving the fibrin bunch as a result of enzymatic reactions; In thrombosis of fibrinolysis leads to the sewage tomb.
).

3. Vasoconstriction Vasoconstriction is a narrowing of the lumen of blood vessels, especially arteries.
: Local (coronary artery site, where the plaque is located) or generalized (the entire coronary artery).

The first stage of the development of acute myocardial infarction (OIM), although it is not always obligatory - the gap of an atherosclerotic plaque, which may further have a different flow:

1. A favorable course - when after breaking the plaques, hemorrhage in the plaque, the so-called "internal-defimal" thrombus, which does not cause the development of myocardial infarction, but in the future it can contribute to the progression of a clinical picture of coronary heart disease (IBS).

2. An unfavorable course - with the formation of a thrombus, which completely or almost completely overlaps the clearance of the coronary artery.

Highlight three Stages of formation of thrombaFurious Obstrument is the closure of the lumen of the hollow organ, including a circulatory or lymphatic vessel, causing a violation of its passability.
Coronary artery:

1. Bloach hemorrhage.

2. Formation of intravascular non-conclusive thrombus.

3. Spreading the thrombus until the computing of the vessel.

Internal-defimal thrombus consists mainly of platelets. The formation of thrombus is key in the development of OIM.

Much less often, it does not arise as a result of atherotromability. The leading pathogenetic mechanism in this case is considered vazospasm Vasospasm is a narrowing of arteries or arteriole to the degree of decrease in tissue perfusion.
.

Myocardial infarction as a result of coronarripism Coronarospasm (Coronarospasmus; Corono- -Pasm) - a temporary narrowing of the enlightenment of the coronary arteries of the heart as a result of a tonic reduction of smooth muscle elements of the arterial wall; Manifested by the attack of angina.
It is often often observed in people accepting drugs, the so-called "cocaine" myocardial infarction.

Significantly less often myocardial infarction develops as a result of other reasons.

Morphological features

Heart attack - the disease is always acute and stadium. With myocardial infarction, it is noted that in the first day the infarct zone appearance does not differ from healthy myocardial sites. The infarct zone at this time wears a mosaic character, that is, among the dead cells, there are also partially or even fully operational myocytes. On the second day, the zone is gradually eliminated from a healthy tissue and a peripartic zone is formed between them.

Often, in the peripheartal zone, the zone of focal dystrophy is distinguished, bordering the necrotic zone, and the zone of reversible ischemia, adjacent to the unique myocardial sites.

All structural and functional changes in the focal dystrophy zone are in most cases to be recovered (partially or even completely).

In the zone of reversible ischemia, changes are completely reversible. After the infarction zone is gradually softening and dissolving the dead myocytes, elements of connective tissue, vessel sections, nerve endings.

With a large-scale myocardial infarction about the 10th day on the periphery of the necrosis, a young granulation tissue is already formed, from which the connecting fabric that performs the scar is formed in the future. The substitution processes go from the periphery to the center, so in the center of the hearth, there may still remain softening foci, and this is a plot that is able to stretch, forming the aneurysm of the heart or even break with a rough non-compliance with the motor regime or other violations. In place of necrosis, dense scar tissue is finally formed not earlier than 3-4 months.
In the small-scale myocardial infarction, the scar is sometimes formed in earlier time. Not only the size of the core of necrosis, but also the condition of the coronary blood circulation in myocardium, is influenced by the scarring rate, but also in the peripartic sections. In addition, the following factors are important:

The age of the patient;

Blood level;

Motor mode;

State of exchange processes;

Security patient with full amino acids, vitamins;

Adequacy of the treatment;

The presence of concomitant diseases.

All this determines the intensity of reducing processes in the body as a whole and in myocardium in particular.

Even a relatively small load during the formation of the primary scar can lead to the development of the aneurysm of the heart (to protrude the wall of the ventricle, the formation of a kind of bag), whereas a month later the same load turns out to be useful and even necessary to strengthen the heart muscle and forming a stronger scar.

Epidemiology

Today in developed countries the number of patients with coronary pathology is constantly growing, and a shift occurs in the direction of younger age, which makes the problem of diagnosis, treatment and prevention of ischemic disease socially significant.

The incidence of men is much higher than among women: an average of 500 per 100,000 men and 100 per 100,000 women, over the age of 70, this difference is leveled.

The age-related peak of the morbidity of myocardial infarction is 50-70 years.

In men, the peak of morbidity falls at the winter, in women - for autumn, the decline in the incidence in men and women occurs simultaneously during the summer period.

The most dangerous time of the day in men is considered the preliminary clock (4-8 in the morning), when the frequency of development reaches 23.9%; In women, the same indicator is 25.9% in the morning clock (8-12 hours). This frequency of development them, depending on seasonality and the time of day, coincides with the same indicators of "sudden death".

A sudden death usually happens in the morning when climbing the patient with bed, which is most likely due to the increase in the activity of the sympathetic nervous system during awakening. This causes an increase in blood viscosity and the aggregation activity of platelets with the release of vasoactive biological substances, for which the spasms of vessels and thrombosis, with the development of ischemic stroke or acute myocardial infarction (OIM).

Approximately one third of all cases of OIM (and more young patients even more often) ends with a fatal outcome in the prehospital stage, in most cases, after 1 hour after the appearance of sharp symptoms. Among the patients with Oim, who lived before entering the hospital, as a result of modern therapy, less mortality and longer survival were noted.

The death of the patients of OIM in the first 4 hours is associated with the advent of arrhythmias and the development of ventricular fibrillation (arrhythmogenic death), and in a later date - with an increase in acute heart failure (cardiogenic shock).

Risk factors and groups

The risk factors of the development of myocardial infarction (im) coincide with those with ischemic heart disease (IBS).

Unmodifable risk factors:

1. Heredity. It is considered to be burdened by IHD, if close relatives (parents, brothers, sisters, grandparents) were cases of CDS on the male line up to 55 years old, in the female up to 65 years.
2. Age. In different populations, a direct relationship between the age of a person and the frequency of the occurrence of IBS is revealed - the older than the person, the higher the incidence of IBS.

3. Paul. Men are much more likely to hurt the EBS. In women up to 50-55 years old (the age of the onset of menopause) of the IBS is extremely rarely diagnosed. The exceptions are women with early menopause and various hormonal disorders in aggravating circumstances: arterial hypertension, hyperlipidemia, diabetes mellitus. After the occurrence of menopause, the frequency of the occurrence of HRS in women begins to grow steadily, and after 70-75 years old, the likelihood of IBS develops in men and women is the same.

Modifiable Risk Factors:
1. Incorrect meals. Eating rich in saturated fats of animal origin, with a high content of cook salt and low food tissue.

2. Arterial hypertension. The value of increased blood pressure, as one of the risk factors, is proved by numerous studies around the world.

3. Hypercholesterolemia. Increased in the blood of general cholesterol, low-density lipoprotein cholesterol. High density lipoprotein cholesterol is considered as an anti-sliced \u200b\u200bfactor - the higher its level, the less the risk of the occurrence of IBS.

4. Weak physical activity or lack of regular physical exertion. In people leading a sedentary lifestyle, the likelihood of the occurrence of IBS is 1.5-2.4 higher than that of physically active.

5. Obesity. It is especially dangerous to obesity on abdominal type, when fat is postponed in the abdomen.

6. Tabacocoaching. Direct communication of smoking with the development and progression of atherosclerosis is well known and does not need comments.

7. Sugar diabetes. The relative risk of death is even in persons with a violation of glucose tolerance above 30%, and in patients with diabetes type 2 - by 80%.

8. Alcohol abuse. However, the anti-risk factor is to use up to 30 g of pure alcohol per day for men and 20 g - for women.

9. Worldwide is now paying attention to the study of such risk factors, such as chronic psycho-emotional stress, increased heart rate, violation of the coagulation system, homocysteinemia (increase in blood levels of homocysteine).

Scientists also established the dependence of the risk of developing myocardial infarction depending on the psycho-emotional type of person. So, cholerics have 2 times more chances to get the first heart attack and 5 times more - repeated, and the death rate from infarction is 6 times more often.

By provoking moments for the development of acute myocardial infarction (OIM) are intensive physical or psycho-emotional stress. For an hour, after a significant physical tension, the risk of developments of the OIM increases 6 times, and in persons leading a sedimentary lifestyle - 10.7 times, and in persons engaged in intense exercise, 2.4 times. Such effect has strong experiences. Within 2 hours after psycho-emotional overvoltage, the risk of developing OIM increases 2.3 times.

The frequency of development of OIM increases in the morning hours, during the first hour after awakening. This also applies to the frequency of development of sudden death, stroke, transient myocardial ischemia, according to Holter observation. Risk increases are associated with an increase in blood pressure and heart rate at this time, the strengthening of the aggregation properties of platelets and a decrease in the fibrinolytic activity of blood plasma, an increase in the level of catecholamines, ACTH, cortisol.

The cooling and change in atmospheric pressure also contribute to the risk of developing OIM. So, with a decrease in temperature by 10 ° C, compared with the average for this time of the year, the risk of development of the first increases by 13%, and the re-38%. Changes in atmospheric pressure, both in one and the other way, are accompanied by an increase in the development of them by 11-12%, and repeated - by 30%.

Clinical picture

Cymptoms, flow

Phases of acute myocardial infarction (Oim):

1. Promotional period (lasts up to 30 days may not be absent).

2. The most acute period (lasts up to 2 hours from the beginning of an anginal status).

3. A sharp period (lasts up to 10 days from the beginning of myocardial infarction).

4. Subighteous period (starts from 10 days and continues up to 1-2 months).

5. The scarring period (on average lasts from 2-3 months to six months, sometimes ends only after 2-3 years).

Depending on the stage of the disease, its manifestation varies greatly.

Promotional period

During this period, patients develop signs of unstable angina:

Pain in chest pain;

Pains appear with smaller physical exertion, and even alone at all;

Pains are worse removed by nitrates, it takes a large dose of nitrates so that the pain passes.

Acute coronary syndrome (OX) combines diseases such as unstable angina, acute myocardial infarction and sudden heartfelt death. At the heart of all these states, despite their different manifestations, there is one mechanism. Both with a heart attack and at an unstable angina, the integrity of one of cholesterol plaques in the coronary artery is disturbed. The body responds to the resulting defect, sending platelets into the focus and activating the coagulation system of blood. As a result, a thrombus is formed, overlapping blood flow. A short-term or incomplete overlap of the vessel lumen causes the development of symptoms of unstable angina. If the blockage is aggravated, a heart attack occurs.

In connection with these patients with unstable angina, it is necessary to emerge to hospitalize.

Ostive period

During this period, the highest mortality from myocardial infarction is observed. At the same time, the most oral period is the most favorable therapy in terms of therapy. There are preparations that destroy the resulting thrombus, thereby restoring the disturbed blood flow by the vessel. However, these medicines are effective only for the first 12 hours from the moment of the development of a heart attack, and the sooner they are applied, the better the result will be.

In the sharpest period angry status - Very intense pain that is localized either behind the sternum or in the left half of the chest. Patients describe the pain as a daggey, drilling or gone ("heart squeezed in vice"). Often, pain rolling the waves, can give to the left shoulder, hand, inter-opaque area, lower jaw. Sometimes it applies to the right half of the chest and in the upper half of the abdomen.

The pain in general is similar to that during the attack of angina, but its intensity is much higher, it does not pass after taking 2-3 nitroglycerin tablets and usually lasts from 30 minutes and longer.

In addition to pain, cold sweat is often observed, severe weakness. Blood pressure is more often declining as a result of a decrease in the reduction in the damaged heart abbreviations, less often increases, since the body in response to stress throws a large amount of adrenaline that has a stimulating effect on the work of the cardiovascular system. Almost always, with myocardial infarction, patients experience pronounced anxiety, fear of death.

It is important to know that in 20% of patients, the most acute period of heart attack flows a small-axipput (the so-called "non-cissy" form of myocardial infarction). Such patients note the unclear gravity in the chest ("heart longing"), pronounced fatigue, malaise, insomnia, "unprecedented" alarm.

A person else from patients with myocardial infarction can manifest themselves the development of rhythm and conductivity disorders. Such patients feel interruptions in the work of the heart, it is possible - sharp increase in, or, on the contrary, slowing the pulse. Dizziness, pronounced weakness, episodes of losing consciousness may appear.

Sometimes myocardial infarction can manifest suddenly breathing breath or pulmonary edema.

Symptomatics of clinical variants of the acute phase of myocardial infarction

Painful (Status Anginosus)	A typical clinical course, the main manifestation at which an anginal pain is not dependent on the poses and position of the body, from movements and respiration, resistant to nitrates. The pain has a pressure-seeking, burning or tearing character with localization of the sternum, in the entire front breast wall with possible irradiation in the shoulders, neck, arms, back, epigastal area. Characterized with a combination with hyperhydrosis, cutting overall weakness, poverty of skin cover, excitation, motor concern.
Abdominal (STATUS GASTRALGICUS)	It is manifested by a combination of epigastric pains with dyspeptic phenomena - nausea, not bringing relief to vomiting, isotic, exhaust, sharp bloating. Possible irradiation of pain in the back, the tension of the abdominal wall and pain in palpation in the epigastrium.
Atypical pain	The pain syndrome has an atypical nature of localization (for example, only in the zones of irradiation - throat and lower jaws, shoulders, hands, etc.) and / or by nature.
Asthmatic (Status AstMaticus)	The only sign is the attack of shortness of breath, which is a manifestation of acute congestive heart failure (cardiac asthma or pulmonary edema).
Arrhythmic	Rhythm disorders serve as the only clinical manifestation or prevail in the clinical picture.
Cerebrovascular	In a clinical picture, signs of brainwater disorders prevail (more often - dynamic): fainting, dizziness, nausea, vomiting. Possible focal neurological symptoms.
Maloshimptomatic (asymptomatic)	The most difficult option for recognition is often diagnosed retrospectively according to ECG.

Acute period

In this period, acute pain pokes, since the process of destruction of cardiomyocytes is completed, and necrotic tissues are not sensitive to pain. Most patients may noted the preservation of residual pains: deaf and constant, as a rule, localizing the sternum.

On the second day, enzymes from damaged cells and destroyed fabrics fall into the blood, causing a temperature reaction: fever can appear up to 39 ° C, as well as malaise, weakness, sweating.

The effect of stress hormones (adrenaline, norepinephrine, dopamine) subsides, as a result of which blood pressure decreases, sometimes very significantly.

During breast pains can appear during this period, increasing with breathing, which is a sign of the development of pleurropericarditis. In part of patients, intensive grave pains in the heart can resume - in this case, the post-infarction angina or relapse of myocardial infarction is diagnosed.

Since the scar has not yet been formed, and some of the muscular heart cells are destroyed, during this period it is very important to minimize physical activity, stress. If this rule fails to comply with these rules, the aneurysm of the heart may develop or step by death from the heartbroken.

Subighteous period
During this period, painful sensations are usually absent. Considering the fact that the contractile ability of the heart is reduced, since the method of myocardium is turned off from work, symptoms of heart failure may appear: shortness of breath, edema feet. In general, the patient's condition improves: the temperature is normalized, blood pressure stabilizes, the risk of developing arrhythmia decreases.

The scarring processes occur in the heart: the body eliminates the resulting defect, replacing the destroyed cardiomyocytes with a connective tissue.

Miocardial infarction period

During this period, the formation of a full-fiber connecting tissue scar is continued and completed. The patient's well-being depends on the magnitude of the area of \u200b\u200bthe defeat and the presence or absence of complications of myocardial infarction.

In general, the state is normalized. The pain in the heart is not either there is a stable angina of a specific functional class. Man gets used to new living conditions.

Diagnostics

The sign of myocardial myocardial infarction of the front wall of the left ventricle, however, as an infarction of any other region, is the pathological prong Q. The qog q is considered pathological if:

Its amplitude is equal to or exceeds a quarter of the amplitude of the prong of R in the same assignment;

The width of the tooth q exceeds 0.03 s;

The amplitude of the flap q exceeds 4 mm;

Tusk q is served or split;

Often the pathological teeth q is combined with a negative Tusten T;

At the same time, the rise of the ST segment is observed in the same assignment.

Myocardial infarction front

The myocardial infarction of the opposite region (front part of the interventricular septum) in most cases is due to the blockage of the headborne branch of the anterior downward artery. With such localization, necrosis, as a rule, does not apply to the front wall of the right ventricle.

Characteristic ECG changes in front infarct are shown in the figure:

In leads V1-V3, an ECG of type QS is registered;

ST Segment in leads V1-V3 is located above isolated in the form of a monophasic curve;

ST Segment in leads II, III, AVF is below the isolated.

In the presence of the QS teeth, in the right infants, it is often impossible to reliably determine the character of them (transmural or non-transmural). In favor of a transmural infarction, a long-lasting significant rise in the STV1-V3 segment is above isolateed.

Other characteristic features of the provisional region are:

The appearance of the qv1-V3 of small amplitude (ECG has the type of QRS) is typical for the curtain stage of them of the transcendal region;

Sometimes in breasts V7-V9 there are reciprocal changes (an increase in the teeth R; to the acute stage - a decrease in the ST segment and the appearance of high teeth T);

The disappearance of the qv5, V6 teeth, however, such a disappearance can be caused by the blockade of the left leg of the Gis beam (blockade of the front or rear branch of LLPG);

The presence of the use of the QRS complex in V1-V3 leads with the type of ECG QS speaks in favor of them;

If such changes in the QRS complex are combined with negative Tusten T and the ST of the ST segment, then it clearly indicates to them.

Miocardial infarction of the front wall of the left ventricle

The myocardial infarction of the anterior wall is often due to the blockage of the anterior downward artery (distal departments), departing from the left coronary artery. Diagnose such an infarction according to characteristic changes in the ECG in leads V3, V4, which has a kind of QS or QR (less often QRs, QR, QRS), as well as in Anterior assignment across the sky. The registration of KSV4 teeth reliably indicates a transmural (the presence of the QSV3 teeth is observed both during transmural and nontransmural).

With the front wall of the LV, reciprocal changes in leads III, AVF, DORSALIS (in the sky) may be observed, which are manifested by an increase in the river R, and at an acute stage - a decrease in the ST segment and an increase in T. T.

Myocardial infarction of the opposite region and the front wall of the left ventricle

Such a heart attack localization is usually due to the blockage of the left front descending artery. Diagnose such an infarction according to characteristic changes in ECG in V1-V4 leads and anetior assignment across the sky. In this case, it is observed (more often than in the scarsing stage) QV1-V3, low amplitude prigning (in these cases, the ECG has a kind of QRS). The register of the QSV4 teeth is a reliable sign of transmural. As a rule, the QSV1-V3 teeth are observed both at transmural and non-transmural.

In leads III, AVF, DORSALIS (in the sky), reciprocal changes can be observed in the acute stage of them, manifest themselves with a decrease in the ST segment and the appearance of a wicked positive "coronary" Tusque T. Also increases the amplitude of the R teeth R, which is maintained in the scars. The dynamics of reciprocal changes to the ECG to the acute stage them occurs faster than the changes in the ST segment and the Tel Tel in V1-V4 leads.

Myocardial Infarction side wall left ventricle

The side wall, as a rule, caused by the lesion of the diagonal artery or the posterior branches of the left envelope of the artery. The signs of such a heart attack are determined by the change in the ECG in leads V5, V6, I, II, AVL, INFERIOR (in the sky). Tusk q is considered pathological if:

QV5, V6\u003e 15% RV5, V6 or QV5, V6\u003e 2 mm;

QAVL\u003e 25% RAVL.

In the scarsing stage a sign of the side wall of the left ventricle serves:

Deep Teeth SV5, V6, while ECG in these leads has the kind of QRS, QRS, QRS;

A significant decrease in the amplitude of the RV5, V6 teeth;

The pronounced suspicion of the QRSV5, V6, I, II, AVL complex.

A reliable sign of transmural is the presence of KSV5, V6 teeth. Sometimes reciprocal changes in the leads V1, V2 are observed, in which it is observed to a decrease in the ST segment, the appearance of a high positive Tusque T, an increase in the amplitude of the Tusque R.

Miocardial hypartmental infarction

It is usually caused by the lesion of the envelope of the artery or anterior descending artery, which depart from the left coronary artery. Signs of such a heart attack are determined by the change in ECG in leads V3-V6, I, AVL, II, ANTERIOR, INFERIOR (in the sky). Reciprocal changes (increasing the amplitude of the Tusque R; to the acute stage - the decrease in the ST segment and an increase in the positive tissue T) are observed in leads III, AVF, DORSALIS (in the sky).

Characteristic signs of the front-windows (myocardial infarction of the front and side walls of the left ventricle):

The presence of deep SV4-V6, while the amplitude of the teeth increases from V4 to V6;

A sharp decrease in the amplitude of the RV4-V6 teeth;

Pronounced suspicion of the QRSV4-V6 complex;

Lack of increasing teeth RV3, V4;

The presence of the QSV4-V6 teeth significantly indicates a transmural of them in this area.

Heart attack left ventricle

The tops of the left ventricle are usually caused by the blockage of the final branches of the left front descending artery. You can talk about such a localization of the heart attack if the signs are noted in isolation in the V4 (less often V3-V5), Anterior (in the sky). The presence of QSV4 reliably indicates a transmural myocardial infarction.

High mobile myocardial infarction

It is generally associated with the lesion of the diagonal artery or the branch of the left envelope of the artery. You can talk about such a localization of a heart attack if the signs are registered in isolation in the AVL (AVL, I) assignment. Occasionally reciprocal changes (High Teeth RV1, V2, in the Oral phase - decrease in the STV1, V2 segment, and the appearance of a high positive TV1, V2, v2) in leads V1, V2 (less often III, AVF).

QAVL is considered pathological, if it is greater than or equal to the amplitude of the RAVL tooth in the amplitude.

If you suggest a heart attack of high departures of the front wall, it is recommended to make an ECG in V4-V6 leads to 1 and 2 intercostal higher levels. It must be borne in mind that such them is quite badly regulated on the ECG.

Extensive Hemocardine Infarction Front Wall

An extensive front wall is due to the blockage of the main trunk of the left coronary artery (more often its branches - anterior downward artery). Signs of extensive infarction of such localization are recorded in leads V1-V6, I (II), AVL, ANTERIOR, INFERIOR (in the sky). At the same time, reciprocal changes must be observed (increasing the rinse R; into the acute phase is a decrease in the ST segment, a high positive Tusk T) in leads III, AVF, DORSALIS (in the sky).

The decrease in the height (compared with the previous ECG) of the teeth RIII, AVF, or RIII, AVF is evidenced by the rear wall of the left ventricle.

With an extensive front wall of the left ventricle for a diagnosis, all the above features described for individual infarction localities are retained.

The anterior wall is often complicated by ventricular extrasystole or tachycardia, and various reductant rhythm disorders.

Radically increases the mortality rate (4 times) with the total transverse blockade in the extensive front wall. At the same time, such a blockade with the rear wall of the left ventricle increases the mortality only 2 times.

Laboratory diagnostics

Laboratory confirmationacute myocardial infarction (OIM) is based on identifying:

Non-specific indicators of fabric necrosis and inflammatory myocardial reactions;
- Hyperfermenia (enters the classical triad of signs of Oim: pain syndrome, typical changes in ECG, hyperfermenia).

Non-specific indicators of fabric necrosis and inflammatory myocardial reactions:
1. Leukocytosis, not exceeding usual 12-15 * 10 9 / l (usually detected by the end of the first day from the beginning of the disease and with the uncomplicated flow of infarction are stored in about a week).
2. Aneozinophilia.
3. A small stickyidal shift of the blood formula left.
4. Increased ESP (increases usually a few days from the beginning of the disease and may remain increased for 2-3 weeks and longer even in the absence of complications).
The correct interpretation of these indicators is possible only when compared with the clinical picture of the disease and ECG data.

Long preservation (more than 1 week) leukocytosis or / and moderate fever in patients with OIM testifies to the possible development of complications: (pneumonia, pleurisy Purrites - inflammation of the pleura (serous sheath, covering the lungs and lining walls of the thoracic cavity)
, pericarditis, thromboembolism of small branches of the pulmonary artery and others).

Hyperfermenia
The main reason for increasing the activity and content of serum enzymes in patients with OIM is the destruction of cardiomyocytes and the release of released cell enzymes in blood.

The most valuable for the diagnosis of OIM is to determine the activity of several serum enzymes:
- creatinophosphokinease (KFK) and especially its MB fraction (MV-KFK);
- lactate dehydrogenase (LDH) and its isoenzyme 1 (LDH1);
- Aspartataminotransferase (AST);
- troponin;
- Mioglobin.

Increasing the activity of the MB fraction of the KFC, mainly contained in myocardium, specific to damage to the heart muscle, first of all, for OIM. The MV fraction of the KFK does not respond to damage to skeletal muscles, brain and thyroid gland.

The dynamics of MV-KFK at OIM:
- after 3-4 hours, activity begins to increase;
- after 10-12 hours reaches a maximum;
- After 48 hours from the beginning of an anginal attack returns to source numbers.

The degree of increase in the activity of MV-KFK in the blood as a whole correlates well with the size of them - the greater the scope of the heart muscle, the higher the activity of MV-KFK 1.

Dynamics of KFK at OIM:
- by the end of the first day the level of the enzyme is 3-20 times higher than the norm;
- After 3-4 days from the beginning of the disease, it is returned to the initial values.

1 It should be remembered that any cardiac surgery (including coronougiography, the catheterization of the heart cavities and electrical thermal therapy) is usually accompanied by a short-term lifting of the activity of the MB fraction of the KFK.

In the literature, there are also indications of the possibility of increasing the level of MV-KFK in severe paroxysmal tachyarhythmia, myocardits and long-term attacks of the stenocardia of rest, regarded as a manifestation of unstable angina.
In some cases, with extensive myocardial infarction, the flushing of enzymes in the overall blood flow is slowed down, therefore the absolute value of the activity of MV-KFK and the speed of its achievement may be less than with the usual flushing of the enzyme, although in that, and in another case, the area under the curve "concentration Time "remains the same.

Lactate dehydrogenase
LDH's activity at OIM increases slower than KFK and MV-KFK, and the longer remains 2.
Dynamics of LDG under the OIM:
- after 2-3 days from the beginning of the heart attack, the peak of activity comes;
- By 8-14 days, a return to the initial level is returned.

2 It should be remembered that the activity of the total LDG also increases in diseases of the liver, shock, stagnation of circulatory insufficiency, erythrocyte hemolysis, and megaloblastic anemia, tel, myocardium, inflammation of any localization, coronaryogiography, electrical treatment, severe physical activity, etc.
LDG1 isoenzyme is more specific for heart lesions, although it is also present not only in the muscle of the heart, but also in other organs and tissues, including red blood cells.

Aspartataminotransferase
AST Dynamics at Oim:
- after 24-36 hours from the beginning of the heart attack relatively quickly comes the peak of increasing activity;
- After 4-7 days, the concentration of AST returns to the initial level.

AST Activity Changes in special specificity for OIM: The AST level together with the activity of ALT increases with many pathological conditions, including in the diseases of the liver 3 .

3 With lesions of the liver parenchyma, the activity of Alt increases to a greater extent, and in case of heart diseases, AST activity increases to a greater extent. With it, the AST / Alt ratio (coefficient de ritis) is greater than 1.33, and in case of liver diseases, the AST / Alt ratio is less than 1.33.

Troponin
The troponin is a universal structure of protein nature for a cross-striped musculature, which is localized on the thin myofilaments of the contracting device of myocardiocyte.

The troponin complex itself consists of three components:
- troponin C - responsible for the binding of calcium;
- troponin T - designed to bind tropomyosis;
- Triponin I - is intended to inhibit the above two processes.
Troponin T and I exist in the myocardium-specific isoforms, differing from the isoforms of skeletal muscles, and the absolute cardiospecificity of 4 is determined.

Dynamics of troponinov at Oim:
- 4-5 hours after the death of cardiomyocytes due to the development of irreversible necrotic changes, troponin enters peripheral blood flow and are determined in venous blood;
- In the first 12-24 hours from the moment of the occurrence of OEM, the peak of concentration is achieved.

Cardial isoforms of troponin continue to preserve their presence in peripheral blood:
- Troponin I is determined for 5-7 days;
- Troponin T is defined up to 14 days.
The presence of these isoforms of troponin in the patient's blood is detected by IFA ELISA - an immunoassimensional analysis - a laboratory immunological method of a qualitative or quantitative determination of various compounds, macromolecules, viruses, etc., based on a specific antigen antigen reaction.
Using specific antibodies.

4 It should be remembered that the troponins are not early Biomarkers of OIM, so in early patients with suspicion of acute coronary syndrome, with a negative primary result, it is necessary to repeatedly determine the content of troponins in peripheral blood. In this situation, even a minor increase in the level of troponinov testifies to an additional risk for the patient, since the existence of a clear correlation between the level of increase in blood troponin and the size of the myocardial damage zone is proved.

Numerous observations have been shown that the elevated level of troponin in the blood of patients with acute coronary syndrome can be considered as a reliable indicator of the patient of the OIM. At the same time, the low level of troponin in this category of patients testifies in favor of setting a softer diagnosis of unstable angina.

Mioglobin
Specificity of myoglobin for the diagnosis of OIM is about the same as KFK, but lower than MV-KFK.
The level of myoglobin may increase by 2-3 times after intramuscular injections, and the increase in 10 or more times is usually considered to be diagnostically significant.
The rise of the level of myoglobin in the blood begins even earlier than increasing the activity of KFK. The diagnostically significant level is often achieved after 4 hours and in most cases is observed 6 hours after a painful attack.
The high concentration of myoglobin in the blood is observed only for several hours, therefore, if you do not repeat the analysis every 2-3 hours, the peak of the concentration can be skipped. Measurement of mioglobin concentration can be applied only in cases of income into the hospital in less than 6-8 hours after the start of the pain.

Principles of enzymatic diagnosis of OIM

1. In patients received during the first 24 hours after an anginal attack, the activity of KFK in the blood is determined - this should be done even in cases where the diagnosis of myocardial infarction is no doubt about the clinical and electrocardiographic data, since the degree of increasing activity of KFK informs Doctor of myocardial infarction sizes and forecast.

2. If the activity of KFK is within the normal range or elevated slightly (2-3 times), or the patient has obvious signs of the lesion of a skeletal muscles or brain, then to clarify the diagnosis, the definition of MV-KFK activity is shown.

3. The normal values \u200b\u200bof the activity of KFK and MV-KFK, obtained by a single blood intake at the time of the patient's arrival in the clinic, are not sufficient to exclude the diagnosis of OIM. The analysis must be repeated at least 2 times after 12 and 24 hours.

4. If the patient sucked more than 24 hours after an anginal attack, but less than 2 weeks, and the level of KFK and MV-KFK is normal, it is advisable to determine the activity of LDH in the blood (preferably - the activity of LDH1 and LDH2), AST with Alt and the calculation of the de ritis coefficient.

5. If anginal pain is repeated in a patient after hospitalization, it is recommended to measure KFK and MV-KFK immediately after the attack and after 12 and 24 hours.

6. Myoglobin in the blood is advisable to determine only in the first hours after a painful attack, the increase in its level is 10 times and more indicates necrosis of muscle cells, but the normal level of myoglobin does not exclude a heart attack.

7. The definition of enzymes is inappropriate in asymptomatic patients with normal ECG. The diagnosis on the basis of the hyperfermenia alone cannot be put anyway - there must be clinical and (or) ECG signs indicating the possibility of them.

8. The control of the number of leukocytes and the SE value must be carried out at the patient's admission and then at least 1 time per week, so as not to miss the infectious or autoimmune complications of the OIM.

9. The study of the level of activity of KFK and MV-KFK is valid only for 1-2 days from the presumptive onset of the disease.

10. The study of the level of AST activity is advisable to conduct only within 4-7 days from the presumptive onset of the disease.

11. Improving the activity of KFK, MV-KFK, LDH, LDH1, AST is not strictly specific to OIM, although, with other things being equal, the activity of MV-KFK is characterized by higher informativeness.

12. Lack of hyperfermenia does not exclude the development of OIM.

Differential diagnosis

1. Allergic and infectious-toxic shock.
Symptoms: Zailed pain, shortness of breath, drop in blood pressure.
Anaphylactic shock may occur with any medicinal intolerance. The beginning of the disease is sharp, it is clearly dedicated to the causal factor (injection of the antibiotic, the vaccination in order to prevent the infectious disease, the introduction of anti-trust serum, etc.). In some cases, the disease begins 5-8 days from the moment of non-herogenous intervention, it develops according to the type of phenomenon of Artus, in which the heart acts as a shock body.
Infectious-toxic shock with myocardial lesions may occur with any serious infectious disease.
The clinically disease is very similar to the myocardial infarction (im), differing from it in etiological factors. Differentiation is hampered due to the fact that in allergic and infectious allergic shock, neuronogenic myocardial necrosis can occur with rude changes in ECG, leukocytosis, an increase in ECU, hyperfermenia AST, LDH, GDD, KFK, MV-KFK.
In contrast to the typical it, in these shocks, the ECG does not have a deep tooth Q and the QS complex, the discordability of changes in the final part.

2. Pericarditis (Miopericiditis).
Etiological factors pericarditis: rheumatism, tuberculosis, viral infection (more often - coking virus or echo), diffuse diseases of the connective tissue; Often - terminal CPN.
In acute pericardia, subepicardial myocardial layers are often involved in the process.

In a typical version, with dry pericardia, stupid, gullings (less often - sharp) pain in the precodal area without irradiation in the back, under the blade, in the left hand, characteristic of myocardial infarction.
Pericard friction noise is registered on the same days as an increase in body temperature, leukocytosis, an increase in ESP. The noise is resistant, listened for several days or weeks.
With it, the noise of fridge fridge short-term; Preceded fever and an increase in ESR.
If cardiac insufficiency appears in patients with pericarditis, then it is justifying or biventricular. It is characterized by left ventricular heart failure.
The differential diagnostic value of enzymological tests is small. Due to the lesion of subepicarordial layers of myocardium, hyperfermenia AST, LDH, LDH1, GDD, KFK, and Evenzima MV-KFK can be registered in patients with pericarditis.

In the correct diagnosis, ECG data help. When pericardia, there are symptoms of subpycardial damage in the form of elevation of ST interval in all 12 generally accepted leads (no discordant characteristic of them). Teeth Q with pericade, unlike them, is not detected. Teeth T with pericade may be negative, it becomes positive after 2-3 weeks from the beginning of the disease.
With the appearance of pericardial exudate, a sprouting picture becomes very characteristic.

3. Left-sided pneumonia.
In pneumonia, pain in the left half of the chest can appear, sometimes intense. However, unlike precordial pain with them, they are clearly connected with breathing and cough, do not have a typical irradiation for them.
For pneumonia, a productive cough is characteristic. The beginning of the disease (chills, temperature rise, fighting in the side, the noise of friction of the pleura) is absolutely not typical for them.
Physical and radiographic changes in the lungs help diagnose pneumonia.
ECG at pneumonia may vary (low tooth t, tachycardia), but never changes that resemble them with it.
As with it, with pneumonia, leukocytosis can be detected, an increase in ESR, hyperfermenia AST, LDH, but only when myocardial lesions increase the activity of the GDD, LDH1, MV-KFK.

4. Spontaneous pneumothorax.
With pneumothorax, there is a strong pain in the side, shortness of breath, tachycardia. Unlike them, the spontaneous pneumothorax is accompanied by a tympanic percussion tone on the side of the lesion, the reduction of breathing, radiographic changes (gas bubble, the collapse of the lung, the displacement of the heart and the mediastinum in a healthy side).
ECG indicators with spontaneous pneumothorax or normal, or a transient decrease in T. T.
Leukocytosis, increasing ESP at pneumothorax does not happen. The activity of serum enzymes is normal.

5. Chest injury.
As with it, severe chest pain occur, shock is possible. The concussion and injury injury leads to damage to the myocardium, which is accompanied by the element or depression of the interval of ST, the negativity of the teeth T, and in severe cases - even the appearance of pathological tooth Q.
In the formulation of the correct diagnosis, a decisive role is played by the history.
The clinical assessment of the chest injury with changes in the ECG should be quite serious, since the necrosis of myocardial necrosis is based on these changes.

6. Osteochondrosis of the thoracic spine with the root compression.
With osteochondrosis with root sinphs in the chest, the left can be very strong, unbearable. But, unlike pain with them, they disappear when the patient takes a fixed forced position, and sharply enhanced when the torso and breathing turns.
Nitroglycerin, osteochondrosis nitrates are completely not effective.
With breast "radiculitis", a clear local pain in the paravertebral points is determined, less often in the course of the intercreation.
The number of leukocytes, as well as the values \u200b\u200bof ESO, enzymological indicators, ECG within the normal range.

7. Shingles.
The claying clinic lingually reminds the described above (see the description of the symptoms of the root syndrome during the osteochondrosis of the spine in the thoracic).
In some patients, fever can register in combination with moderate leukocytosis, an increase in ESP.
ECG, enzyme tests, as a rule, often help to exclude the diagnosis to them.
The diagnosis of "Shingle" becomes reliable from 2-4 days of the disease, when characteristic bubble (vesicular) rash appears in the course of the intercreation).

8. Bronchial asthma.
The asthmatic version of them in its pure form is rare, more often choking with pain in the atrial region, arrhythmia, shock symptoms.

9. Outragia left-deceiving deficiency Completes the course of many diseases of the heart, including cardiomyopathy, valve and congenital heart defects, myocardits and others.

10. Acute cholecystopancatitis.
In acute cholecystopancathite, as in the gastralgic version, they occur with severe pain in the epigastric region, accompanied by weakness, sweating, hypotension. However, pain in acute cholecystopancreatite is localized not only in epigastrics, but also in the right hypochondrium, irradiate up and right, in the back, sometimes can be encircling. It is characteristic of the combination of pain with nausea, vomiting, and a mixture of bile is determined in the vomit masses.
Palparato is determined by the pain at the point of the gallbladder, the pancreatic projections, the positive symptom of Kera, the symptom of the Ortner, the symptom of Mussy, which is not typical for them.
Scotching, local voltage in the right upper quadrant is not typical for them.

Leukocytosis, an increase in SE, Hyperfermenia AST, LDHs may appear in both diseases. In cholecystopancathite, an increase in the activity of alpha-amylase serum and urine, LDH 3-5 is noted. If they should be focused on high rates of enzyme activity of KFK, MB-KFK, GDD.
ECG with acute cholecystopancathite: decreased ST interval in a number of devices, weakly negative or two-phase prong T.
The large-scale metabolic damage to myocardials significantly worsens pancreatitis forecast, is often the leading factor in the fatal outcome.

11. The soda ulcer of the stomach.
As with it, sharp pain in the epigastrics are characteristic. However, in the trim ulcer of the stomach, unbearable, "dweller" pains, the most pronounced at the time of vacuum, and then decrease in intensity, while the epicenter of pain is moving several to the right and down.
With a gastralgic version of them, the epigastric pain may be intense, but it is not characterized by such an acute, instantaneous beginning with a subsequent decline.
With the trimming ulcer of the stomach in 2-4 hours from the moment of speaking the symptoms varies. In patients with trimming gastroduodenal ulcers, symptoms of intoxication appear; The language becomes dry, the features of the face are sharpened; The stomach becomes drawn, tense; There are positive symptoms of irritation; Percussively determined the "disappearance" of hepatic stupidity; Radiologically detected air under the right dome of the diaphragm.
As with them, and when wearing ulcers, the body temperature may be subfebrile, there is a moderate leukocytosis during the first day.
It is typically an increase in the activity of serum enzymes (LDH, KFK, MV KFK).
ECG during the sample ulcer of the stomach during the first day, as a rule, does not change. The next day, changes in the final part are possible due to electrolyte violations.

12. Cancer Cardial Stomach Department.
When cancer, cardia often occurs intensive grave pains in the epigastrium and under the mild-shaped process, combined with transient hypotension.
Unlike them with cardi cancer, epigastric pains are naturally repeated daily, they are associated with food intake.
ESP increases with both diseases, but the dynamics of the activity of KFK enzymes, MV KFK, LDH, GDD is characteristic only for them.
To eliminate the gastralgic option, they need an ECG study. The ECG is detected changes in the interval ST (more often depression) and the T (isoelectric or weakly negative) in III, AVF leads, which serves as a reason for the diagnosis of small-scale rear them.
When Cardi cancer ECG "frozen", it fails to determine the speaker characteristic of them.
The diagnosis of cancer is clarified when carrying out FGDS, a radiological study of the stomach in various positions of the body under study, including in the antiodetasis position.

13. Food toxicoinfection.
As with it, pain in epigastria appear, blood pressure drops. However, in food toxicoinfection, the pain in the epigastria is accompanied by nausea, vomiting, hypothermia. Diarrhea is not always found in food toxicoinfection, but it never happens when it.
ECG for food toxicoinfection either does not change, or during the study, "electrolyte violations" are determined in the form of a trough-shaped offset of the ST interval, a weakly negative or isoelectric teeth of T.
Laboratory studies in food toxicoinfection show moderate leukocytosis, erythrocytosis (blood thickening), a slight increase in the activity of ALT, AST, LDH without significant changes in the activity of KFK, MV-KFK, GDD characteristic of them.

14. Acute disruption of mesenteral blood circulation.
Epigastric pain, the drop in blood pressure occurs in both diseases. The differentiation is complicated by the fact that the thrombosis of mesenteral vessels, like them, is striking, as a rule, elderly people with various clinical manifestations of IBS, with arterial hypertension.
If the blood circulation is violated in the system of mesenteral vessels, pain is localized not only in the epigastria, but also throughout the abdomen. The stomach can be moderately, auscultative does not reveal the sounds of intestines peristalists, it is possible to detect the symptoms of irritation of peritoneum.
To clarify the diagnosis, an overview radiography of the abdominal cavity is carried out and the presence or absence of intestinal peristals and gas accumulation in intestinal loops is determined.
Disruption of mesenterological blood circulation is not accompanied by changes in the ECG and enzyme indicators characteristic of them.
With difficulty in the diagnosis of thrombosis of mesenteral vessels, pathognomonic changes can be detected at laparoscopy and angiography.

15. Dislaiming aneurysm abdominal aorta department.
With the abdominal form of aortic aortic aneurysm, in contrast to the gastralgic version, the following features are characterized:
- Start of illness with chest pain;
- the wave-like nature of pain syndrome with irradiation in the lower back in the course of the spine;
- the appearance of tumor formation of elastic consistency, pulsating synchronously with a heart;
- the appearance of systolic noise over tumor formation;
- Angle anemia.

16. Non-monogenous myocardial necrosis These may occur with thyrotoxicosis, leukose and anemia, systemic vasculitis, hypo- and hyperglycemic states.
Clinically against the background of symptoms of the main disease, pain in the heart (severely), shortness of breath, are noted.
These laboratory studies are non-informative in differentiation of non-corona necrosis with atherosclerotic genesis. Hyperfermenimia LDH, LDH1, GDD, KFK, MV-KFK are caused by myocardial necrosis as such, regardless of their etiology.
On the ECG, changes in the final part - depression or, less often, elevation of ST interval, negative teeth, with subsequent dynamics corresponding to Non-Prommural Items are detected on the ecg.
The exact diagnosis is established on the basis of all symptoms of diseases. Only such an approach makes it possible to methodically correctly evaluate the heart pathology properly.

18. Tumors of the heart(primary and metastatic).
In the tumors of the heart, persistent intensive pains in the precodal region, resistant to nitrates, heart failure, arrhythmias can appear.
The ECG is noted by the pathological teeth q, the element of the ST interval, the negative teeth of T. Unlike them with a heart tumor, there is no typical ECG evolution, it is unfinished.
Heart failure, arrhythmia refractors for treatment. The diagnosis is specified with a thorough analysis of clinical and radiological and echo-kg data.

19. PostatahKardial syndrome.
Postatahcardial syndrome is called an ECG phenomenon, expressed in the transient myocardial ischemia (depression of the ST interval, negative TC) after the relief of tachyarhythmia. This symptom complex must be assessed very carefully.
Firstly, Tahiaritimia may be the beginning of them and ECG after her relief often only identifies infarctional changes.
Secondly, the attack of tachyrhythmia to such an extent violates hemodynamics and coronary blood flow, which can lead to the development of myocardial necrosis, especially with initially defective coronary blood circulation in patients with sampling coronary atherosclerosis. Consequently, the diagnosis of post-thagidial syndrome is reliable after careful observation of the patient, taking into account the dynamics of clinical, echocheg-, laboratory data.

20. Premature repolarization syndrome.
The syndrome is expressed in the elevation of the ST interval in Wilson leads starting from the point j, located on the downlink knee of the R.
This syndrome is registered with healthy people, athletes, patients with neurocirculatory dystonia.
For the setting of the correct diagnosis, it is necessary to know about the existence of an ECG phenomenon - premature repolarization syndrome. In this case, the syndrome does not have a clinic, it does not have an ECG speaker characteristic.

Note
In the interpretation of the symptom of "acute pain in the epigastria" in combination with a hypotension during a differential diagnosis, they need to bear in mind and more rare diseases: acute adrenal insufficiency; gap of liver, spleen or hollow organ during injury; a syphilitic dry for a spinal cord with tabetic gastric crises (anisocorium, ptosis, reflex motionability of eyeballs, atrophy of the optic nerve, ataxia, lack of knee reflexes); Abdominal crises in hyperglycemia, ketoacidosis in patients with diabetes mellitus.

Complications

Myocardial infarction complications groups(THEM):

1. Electric - Rhythm and conduction disorders:
- Branditahiarium;
- extrasystole;
- intraventricular blockades;
- Av-blockade.
These complications are almost constantly constantly found with large-scale them. Often arrhythmia are not threatening for life, but indicate serious disorders (electrolyte, continuing ischemia, vagal hyperactivity, etc.) requiring correction.

2. Hemodynamic complications:
2.1 Due to the violations of the pump function of the heart:
- acute left vehicles;
- acute referee failure;
- biventricular failure;
- cardiogenic shock;
- gastrochie aneurysm;
- Infarction expansion.
2.2 Due to the dysfunction of nobble muscles.
2.3 due to mechanical disorders:
- acute mitral regurgitation due to the breaking of the papillary muscles;
- breaks of the heart, free wall or interventricular partition;
- left ventricular aneurysms;
- Others of nobble muscles.
2.4 Due to the electromechanical dissociation.

3. Jet and other complications:
- epistenocardic pericarditis;
- thromboembolism of the vessels of the small and large circle of blood circulation;
- early post-infarction angina;
- Dressler syndrome.

By time appearance Complications are classified as:

1. Early complications arising in the first hours (often at the stage of transportation of the patient in the hospital) or in the most acute period (3-4 days):
- rhythm and conduction disorders (90%), up to fibrillation of ventricles and complete AV-blockada (the most frequent complications and the cause of mortality at the prehospital stage);
- sudden stop of the heart;
- acute insufficiency of the pump function of the heart - an acute left-oscillage deficiency and cardiogenic shock (up to 25%);
- Heart breaks - exterior, internal; slow and simultaneous (1-3%);
- acute dysfunction of nipple muscles (mitral regurgitation);
- Early epistenocardic pericarditis.

2. Late complications (arise in the 2-3rd week, during the period of active regime expansion):
- Postinfarctic Dressler Syndrome Dressler syndrome - a combination of Pericarditis with pleuritis, less often pneumonia and eosinophilia, developing on the 3-4th week from the moment of acute myocardial infarction; due to sensitization of the body to destructive modified myocardial proteins
(3%);
- Priest thromboendocarditis (up to 20%);
- chronic heart failure;
- neurotrophic disorders (shoulder syndrome, anterior breast wall syndrome).

Both in the early and later stages of the current, they may arise the following complications:
- acute pathology of the gastrointestinal tract (sharp ulcers, gastrointestinal syndrome, bleeding, etc.);
- mental changes (depression, hysterical reactions, psychosis);
- Heart aneurysms (in 3-20% of patients);
- thromboembolic complications: systemic (due to cloth thrombosis) and TEL (due to the deep veins thrombosis of the heads).
Thromboembolism is clinically detected in 5-10% of patients (on autopsy - in 45%). Often they have an asymptomatic flow and are the cause of death in a number of hospitalized patients with them (up to 20%).
Some older men with benign hypertrophy of the prostate gland develops an acute urinary bubble atony (its tone is reduced, there are no urges to urinate) with an increase in the volume of the bubble to 2 liters, the retention of urination against the background of beddown and drug treatment, atropine.

Treatment abroad

Ulyanovsk State University

Institute of Medicine, Ecology and Physical Culture

Medical faculty

Department of Therapy and Professional Diseases

Patient Medical Map

Diagnosis Main: IBS: Acute myocardial infarction without teeth q Nizhne-side localization. Hypertensive disease, III degree, stage III, risk 4.

Curator: Alyapyshev G.S.,

course LD 08/9

Curation: 02/13/12

Lecturer: Menzorov M.V.

Ulyanovsk, 2012

Data is a patient

General information about the patient (passport part):

hypertensive disease coronary syndrome

1.FULL NAME:

2.Female gender

.Year of birth / Age: 02.05.48 / 64

.Education: secondary technical education

.Address of residence: ul. Tupolev 28-74

.Place of work: Does not work (pensioner, disabled group II)

.Profession:

.Date of arrival in the hospital: 09/23/12 17-30

.The start date of the Curation: 09/26/12

.Date of statement:

.Who is directed by the patient: PSP number

.Diagnosis of guide institution: IBS: acute coronary syndrome.

.Pre-diagnosis:

Diagnosis Main: Ischemic heart disease. Acute coronary syndrome. Hypertensive disease, III degree, stage III, risk 4.

Complications of the main disease: CXN IIA, III FC.

14.Clinical diagnosis:

Diagnosis Main: IBS: Acute myocardial infarction without teeth q Nizhne-side localization. Hypertensive disease, III degree, stage III, risk 4.

Complications of the main disease: CXN IIA, III FC.

Related: type 2 diabetes, moderate severity, subcompensation. The consequences of ONMK. Obesity 3 art. Post-terrboflectric disease of the lower limbs.

Complaints for admission

Main: Complaints for graceful stubborn pains with irradiation into the left hand and blade, not binding nitroglycerin, general weakness, feeling of air shortage.

Additional: Complaints for shortness of breath with moderate physical exertion (when climbing the second floor). Complaints on the stubborn pain, the feeling of discomfort in the heart area with moderate physical exertion.

Complaints of thirst, dry mouth, frequent, abundant urination. Reduced sensitivity of the right half of the body. Pain, hyperpigmentation and swelling in the lower limbs.

Complaints on the Day of Curation

09.12 The health of the patient has improved a little. Pain syndrome decreased. Complaints on shortness of breath, feeling of air shortage in a horizontal position and during exercise. Complaints of thirst, dry mouth, frequent, abundant urban; Reduced sensitivity in the right half of the body. Complaints of pain and swelling in the lower limbs.

Anamnesis Morbi:

He considers himself a patient since 36 years (since 1976), when for the first time began to note the increase in blood pressure up to 140/90 mm RT Art, which was accompanied by a headache, the noise in the ears. In this regard, he turned to the therapist to the clinic at the place of residence. Received hypotensive therapy. Periodically held inpatient treatment. The pressure increased as much as possible to 250/110 mm RT Art. Against the background of hypotensive therapy, the blood pressure was kept at 150/90 mm RT Art. He began to celebrate hearing impairment, vision. In 1983, periodically began to celebrate the feeling of heartbeat.

12.01 Suddenly felt the deterioration of the state, nausea, vomiting, violation of speech, disturbance of the sensitivity of the right half of the body. It was recorded an increase in pressure to 280/110 mm RT Art. Relatives caused ambulance, was delivered to the PSO. A diagnosis was made: ischemic stroke in the LSMA basin with phenomena of right-hand hemiparesis. Began to note a violation of deep and superficial sensitivity, motility of the right half of the body; Violation of memory on current events. Observed at the neurologist. Received outpatient treatment.

In 2010, pains in the field of heart appeared with moderate physical exertion, irradiating to the left blade, stopping nitroglycerin. From the same time, he began to mark the appearance of shortness of shortness of breath with a moderate physical activity, which is enhanced in a horizontal position. Ambulatory took Concor, Hartil, Thrombo Ass, Nitrosorbide. Over the past year, notes the appearance of prudent pain and shortness of breath with less physical exertion.

In the past few years, he notes the appearance of thirst, dryness in the mouth, abundant urination. It was examined by an endocrinologist 20.08.12. There was a diagnosis: type 2 diabetes mellitus. Began to take glucophage; I complied with a diet.

This deterioration of the state 23.09.12 at 15-00, when there were burning stubborn pains that were not bought by the reception of nitrosorbide. Relatives caused ambulance. It was delivered to the receiving department of the Central TsGCB in 17-30. Easy to hospitalized in Cro.

Anamnesis Vitae:

Born on May 2, 1948, a healthy child. Grew and developed with age, respectively, did not leave the peers. I started studying from 7 years. Married.

Labor history: Received secondary technical education. Profession - seller.

Professional harm denies.

Heredity is -proofing along the Father line (AG, IBS, OIM).

Nutrition is regular - 3 times a day, full, diverse.

Material conditions are satisfactory.

Harmful habits denies.

Transferred diseases: ORVI, chickenpox, corrosive inflammation of the lower extremities; Acute thrombophlebitis of the lower extremities.

Tuberculosis, hepatitis, venereal diseases - denies.

The use of poor-quality products, the presence of intestinal dysfunctions over the past 3 weeks does not notice.

The presence of contacts with infectious and feverish patients, with rodents and insect denies.

There were no operations. The conduct of endoscopic manipulations and visits to the dentist for the last year was not.

Transfusion history: Hemotransfusion was not conducted.

Allergic history: the intolerance to drugs denies.

Consists of a dispensary accounting at the therapist, neurologist, cardiologist.

Status Praesens:

The general state of moderate severity. Consciousness is clear. The physique is hyperstenic. Height 168. Weight 130 kg. [BMI] \u003d 130 / 2.82 \u003d 46 (norm 18.5 - 24.9 kg / m2). Waist circle 112cm.

Body temperature: 36.6 C. Facial expression.

Skin dry, clean, ordinary color, moderate humidity. Tour skin is normal. There are no rashes. Outflow on the female type. Hyperpigmentation of the skin and the swelling of the lower extremities to the level of the upper third of the leg.

The mucous membranes: mucous eyes, nose, oral cavity, moderate humidity, pale pink, no rash.

Lymphatic nodes: submandibular, cervical, axillary nodes of soft-elastic consistency, are not soldered between themselves and the surrounding fiber, with a diameter of 3-6 mm, movable, painless.

The throat is not hyperemic, the almonds are not increased, there is no plaque.

Muscles: Muscular system is developed moderately; when palpation muscles painless; The strength of the muscles is reduced in the right upper and lower limb.

Bones: without deformation. When palpation is painless.

Sustaines: The joints are not limited in mobility, when palpation is painless, movements are preserved in full.

Respiratory system system:

Inspection: Nose form normal, breathing through the nose is not difficult. The voice is quiet.

Breast cell of the correct hypersthenic shape: Opper and connectible pits are pronounced normally. Intercostal gaps are not expanded. Epigastric angle of more than 90 degrees. The blades are moderately adjacent. With the breath of the movement of the blades asymmetric. When breathing, the right half of the chest is lagging behind. There is no participation of auxiliary muscles in the act of breathing. There is no curvature of the spine. Breathing of mixed type, rhythmic, not difficult. ChDD 20-21 / min.

Comparative percussion: sound is clear, easy, symmetrical.

Auscultation: Breathing Vezicular, weakened in the lower departments. In the revengery of the lungs, wet wipes are listened; Capital, the noise of friction is not listened. Bronchophony over symmetrical sites is moderately expressed.

Circulatory system system

Inspection: external jugular veins and carotid arterys unchanged.

When examining the heart area without changes, the heart hump is disappearing. The urgent push, the pulsation of the abdominal aorta is not defined. Chest in the heart area without deformation.

Palpation: The top push is shifted to the left (in the fifth intercostrine in the middle-hearth line), spilled, low, weak, positive; Cardiac tremors are not palpable.

The pulse is the same on both hands, 60oud / min, rhythmic, medium filling and voltage; Hell on the shoulder arteries of the right and left 150/90 mm RT Art. Pulse - 60 mm RT Art.

Percussion: it is difficult due to excessive development of subcutaneous fatty fiber.

Auscultation: Rhythmic heart tones, muffled. I tone weakened, deaf at the top, accent II tone over the aorta; Noise, extrasystoles, are not listened. Heart rate \u003d 60 ot / min, the rhythm is correct.

System of digestive organs

Inspection: The language is pink, wet, slightly covered with a white bloom, the nipples of the tongue are expressed moderately. Cracked, ulcers, teeth fingerprints around the edges. In the oral cavity there are carious and filled teeth. Gums pink, bleeding, breaking, no ulcers. Pink mucosa pink. Swallowing free, painless.

The belly of the correct configuration, symmetrical, is involved in the act of breathing. The navel is drawn. Pigment spots, scars, hernia, extended subcutaneous veins are not marked. There is no visible peristals of the stomach and intestines.

With surface approximate and comparative palpation: the stomach is soft, the local muscle voltage sections are not defined. The hernia do not define. Mendel's symptoms, brush-blubberg negative.

Deep palpation is difficult due to pronounced abdominal obesity.

The noise of the splash, the noise of the incident drop is not determined.

With percussion of the abdomen - moderate tympanite.

Auscultation: intestinal peristalsis active.

Hepatolyenal system

Right acromial, scaling point is painless. Symptoms of Kerra, Murphy, Frainian-symptom - negative.

The liver does not protrude due to the rib arc. The dimensions of the liver according to the percussion of the Kurlov: according to the right medium-free line - 9 cm, on the front median line - 8 cm, along the edge of the left edge arc - 7 cm.

The spleen is not palpable. The sizes of the spleen: a long on x edge: 6 cm, diameter - 4 cm.

System of urinary organs

Inspection: The skin of the face of corporal color, the turgor is normal, the pairbital edema is not detected; Lumbar region without deformations.

Palpation: the bladder is not palpable, the perform is not determined. Urination frequency is 4-5 times a day. With palpation, ureteral points are painless.

Percussion: The symptom of the Pasternatskom is negative.

ENDOCRINE SYSTEM

Secondary sexual signs are developed, respectively, sex and age. The thyroid gland during inspection and palpation is not determined. Pathological eye symptoms (Skrevag, Darmilple, Mebius, Gref, Kohler) are negative. Obesity 3st.

NERVOUS SYSTEM

The state of the psyche: Consciousness is clear. Oriented in time, space and situation. Intellect corresponds to the level of development.

Vision, rumor - reduced. The smell is normal. There is no violation of taste. The communal symptoms are not expressed. Sleep is not broken.

CHMN study: Obony analyzer - Nimesmia. The visual analyzer is reduced visual acuity. ColorProduction - normal. The convergence of eyeballs is normal. Diplopia is not observed. The movement of eyeballs in full. The reaction to the light is saved. Triple nerve: chewing muscles moderate stress. Soreness at the points of the triple nerve is absent.

The auditory analyzer and the vestibular function: complaints about a pronounced rumor reduction. Swallowing is normal. There is no subjectively to reduce taste sensitivity. Podium nerve: medium line language. Meningheal symptoms: the rigidity of the occipital muscles is not detected.

Motor sphere: Passive movements in the limbs in full. No muscular contractures. Muscular tone of the right half of the body is reduced. Hypercines were not detected. The seizures denies. Palcepan sample performs satisfactory. There are no limbs. Reflexes are saved. This is not broken. Sensitivity in the right half of the body is broken. Right-sided hemipesis. Vegetative nervous system: without features. Skin color is normal, the sweating is normal. ATTENTION SAVED. Memory is weakened. Brad and hallucinations do not mark. There is no frequent change of mood.

Preliminary diagnosis and its rationale

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Complications of the main disease: CXN IIA, III FC.

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Complications of the main disease: CXN IIA, III FC.

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Complications of the main disease: CXN IIA, III FC.

Related: type 2 diabetes, moderate severity, subcompensation. The consequences of ONMK. Obesity 3 art. Post-terrboflectric disease of the lower limbs.

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