Cardiogram after a heart attack. Diagnosis of myocardial infarction: clinical and ECG signs, photos with interpretation. Damage to the back wall

Used for practical purposes in the 70s of the 19th century by the Englishman A. Waller, the device that records the electrical activity of the heart continues to faithfully serve humanity to this day. Of course, over almost 150 years it has undergone numerous changes and improvements, but the principle of its operation, based on recordings of electrical impulses propagating in the heart muscle, remained the same.

Now almost every ambulance team is equipped with a portable, lightweight and mobile electrocardiograph, which allows you to quickly take an ECG, not waste precious minutes, diagnose and quickly transport the patient to the hospital. For large-focal myocardial infarction and other diseases that require emergency measures, minutes count, so an urgently taken electrocardiogram saves more than one life every day.

Deciphering an ECG for a cardiology team doctor is a common thing, and if it indicates the presence of acute cardiovascular pathology, then the team immediately turns on the siren and goes to the hospital, where, bypassing the emergency room, they will deliver the patient to the intensive care unit for emergency care. The diagnosis has already been made using an ECG and no time has been lost.

Patients want to know...

Yes, patients want to know what the strange teeth on the tape left by the recorder mean, so before going to the doctor, patients want to decipher the ECG themselves. However, everything is not so simple and in order to understand the “sophisticated” record, you need to know what the human “motor” is.

The heart of mammals, which includes humans, consists of 4 chambers: two atria, endowed with auxiliary functions and having relatively thin walls, and two ventricles, which bear the main load. The left and right parts of the heart are also different. Providing blood to the pulmonary circulation is less difficult for the right ventricle than pushing blood into the systemic circulation with the left. Therefore, the left ventricle is more developed, but also suffers more. However, regardless of the difference, both parts of the heart must work evenly and harmoniously.

The heart is heterogeneous in its structure and electrical activity, since contractile elements (myocardium) and non-contractile elements (nerves, vessels, valves, fatty tissue) differ from each other in varying degrees of electrical response.

Typically, patients, especially older ones, worry about whether there are signs of myocardial infarction on the ECG, which is quite understandable. However, to do this you need to learn more about the heart and the cardiogram. And we will try to provide this opportunity by talking about waves, intervals and leads and, of course, about some common heart diseases.

Heart Abilities

We first learn about the specific functions of the heart from school textbooks, so we imagine that the heart has:

Automatically, caused by the spontaneous generation of impulses, which then cause its excitation;
Excitability or the ability of the heart to activate under the influence of exciting impulses;
or the “ability” of the heart to ensure the conduction of impulses from the place of their origin to the contractile structures;
Contractility, that is, the ability of the heart muscle to contract and relax under the control of impulses;
Tonicity, in which the heart does not lose its shape in diastole and ensures continuous cyclic activity.

In general, the heart muscle in a calm state (static polarization) is electrically neutral, and biocurrents(electrical processes) are formed in it under the influence of exciting impulses.

Biocurrents in the heart can be recorded

Electrical processes in the heart are caused by the movement of sodium ions (Na+), which are initially located outside the myocardial cell, into it and the movement of potassium ions (K+), rushing from inside the cell to the outside. This movement creates the conditions for changes in transmembrane potentials throughout the entire cardiac cycle and repeated depolarizations(excitation, then contraction) and repolarizations(transition to the original state). All myocardial cells have electrical activity, but slow spontaneous depolarization is characteristic only of the cells of the conduction system, which is why they are capable of automatism.

Excitement spreading through conducting system, sequentially covers the parts of the heart. Starting in the sinoatrial (sinus) node (the wall of the right atrium), which has maximum automaticity, the impulse passes through the atrial muscles, the atrioventricular node, the bundle of His with its legs and is directed to the ventricles, stimulating parts of the conduction system even before the manifestation of its own automaticity .

Excitation that occurs on the outer surface of the myocardium leaves this part electronegative in relation to areas not affected by excitation. However, due to the fact that body tissues have electrical conductivity, biocurrents are projected onto the surface of the body and can be recorded and recorded on a moving tape in the form of a curve - an electrocardiogram. The ECG consists of waves that are repeated after each heartbeat, and through them shows the disorders that exist in the human heart.

How is an ECG taken?

Many people can probably answer this question. Doing an ECG, if necessary, will also not be difficult - there is an electrocardiograph in every clinic. ECG technique? It only seems at first glance that it is so familiar to everyone, but meanwhile, only medical workers who have undergone special training in taking an electrocardiogram know it. But we hardly need to go into details, since no one will allow us to do such work without preparation anyway.

Patients need to know how to properly prepare: that is, it is advisable not to overeat, not to smoke, not to drink alcoholic beverages and medications, not to get involved in heavy physical labor and not to drink coffee before the procedure, otherwise you can fool the ECG. It will certainly be provided, if nothing else.

So, a completely calm patient undresses to the waist, frees his legs and lies down on the couch, and the nurse will lubricate the necessary places (leads) with a special solution, apply electrodes from which wires of different colors go to the device, and take a cardiogram.

The doctor will decipher it later, but if you are interested, you can try to figure out your teeth and intervals yourself.

Teeth, leads, intervals

This section may not be of interest to everyone, in which case you can skip it, but for those who are trying to understand their ECG on their own, it may be useful.

The waves in the ECG are designated using Latin letters: P, Q, R, S, T, U, where each of them reflects the state of different parts of the heart:

P – atrial depolarization;
QRS wave complex – ventricular depolarization;
T – ventricular repolarization;
A weak U wave may indicate repolarization of the distal portions of the ventricular conduction system.

To record an ECG, 12 leads are usually used:

3 standard – I, II, III;
3 reinforced unipolar limb leads (according to Goldberger);
6 reinforced unipolar chest (according to Wilson).

In some cases (arrhythmias, abnormal location of the heart), there is a need to use additional unipolar chest and bipolar leads according to Neb (D, A, I).

When interpreting the ECG results, the duration of the intervals between its components is measured. This calculation is necessary to assess the rhythm frequency, where the shape and size of the teeth in different leads will be an indicator of the nature of the rhythm, the electrical phenomena occurring in the heart and (to some extent) the electrical activity of individual sections of the myocardium, that is, the electrocardiogram shows how our heart works at that time. or another period.

Video: lesson on ECG waves, segments and intervals

ECG analysis

A more rigorous interpretation of the ECG is made by analyzing and calculating the area of the teeth when using special leads (vector theory), however, in practice, they mainly make do with such an indicator as electrical axis direction, which is the total QRS vector. It is clear that everyone’s chest is structured differently and the heart does not have such a strict arrangement, the weight ratio of the ventricles and the conductivity inside them are also different for everyone, therefore, when deciphering, the horizontal or vertical direction of this vector is indicated.

Doctors carry out ECG analysis in a sequential order, determining the norm and violations:

Assess the heart rhythm and measure the heart rate (with a normal ECG - sinus rhythm, heart rate - from 60 to 80 beats per minute);
Intervals (QT, norm – 390-450 ms) are calculated, characterizing the duration of the contraction phase (systole) using a special formula (I often use Bazett’s formula). If this interval lengthens, then the doctor has the right to suspect. Hypercalcemia, on the contrary, leads to a shortening of the QT interval. The conductivity of the pulses reflected through the intervals is calculated using a computer program, which significantly increases the reliability of the results;
they begin to calculate from the isoline according to the height of the teeth (normally R is always higher than S) and if S exceeds R and the axis deviates to the right, then they think about disturbances in the activity of the right ventricle, if on the contrary - to the left, and the height of S is greater than R in II and III leads – left ventricular hypertrophy is suspected;
The QRS complex is studied, which is formed during the conduction of electrical impulses to the ventricular muscle and determines the activity of the latter (the norm is the absence of a pathological Q wave, the width of the complex is not more than 120 ms). If this interval shifts, then we speak of blockades (full or partial) of the bundle branches or conduction disturbances. Moreover, incomplete blockade of the right bundle branch is an electrocardiographic criterion of right ventricular hypertrophy, and incomplete blockade of the left bundle branch may indicate left ventricular hypertrophy;
They describe the ST segments, which reflect the period of restoration of the initial state of the heart muscle after its complete depolarization (normally located on the isoline) and the T wave, which characterizes the process of repolarization of both ventricles, which is directed upward, asymmetrical, its amplitude is lower than the wave in duration and is longer than the QRS complex.

The decoding work is carried out only by a doctor, however, some ambulance paramedics perfectly recognize common pathologies, which is very important in emergency cases. But first, you still need to know the ECG norm.

This is what the cardiogram of a healthy person looks like, whose heart works rhythmically and correctly, but not everyone knows what this record means, which can change under various physiological conditions, such as pregnancy. In pregnant women, the heart takes a different position in the chest, so the electrical axis shifts. In addition, depending on the duration, the load on the heart is added. An ECG during pregnancy will reflect these changes.

The cardiogram indicators in children are also excellent; they will “grow” with the baby, and therefore will change according to age; only after 12 years, the child’s electrocardiogram begins to approach the ECG of an adult.

The most disappointing diagnosis: heart attack

The most serious diagnosis on the ECG, of course, is, in the recognition of which the cardiogram plays the main role, because it is she (the first!) that finds areas of necrosis, determines the localization and depth of the lesion, and can distinguish an acute infarction from the scars of the past.

The classic signs of myocardial infarction on the ECG are the registration of a deep Q wave (OS), segment elevationST, which deforms R, smoothing it, and the subsequent appearance of a negative pointed isosceles tooth T. This elevation of the ST segment visually resembles a cat’s back (“cat”). However, a distinction is made between myocardial infarction with and without the Q wave.

Video: signs of a heart attack on an ECG

When there's something wrong with your heart

Often in ECG conclusions you can find the expression: “”. As a rule, such a cardiogram is obtained by people whose hearts have had an additional load for a long time, for example, due to obesity. It is clear that the left ventricle has a hard time in such situations. Then the electrical axis deviates to the left, and S becomes greater than R.

hypertrophy of the left (left) and right (right) ventricles of the heart on the ECG

Video: cardiac hypertrophy on ECG

One of the presenters will answer your question.

The questions in this section are currently answered by: Sazykina Oksana Yurievna, cardiologist, therapist

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In questions about interpreting the ECG, be sure to indicate the patient’s gender, age, clinical data, diagnoses and complaints.

Myocardial infarction (necrosis of cardiac muscle tissue) can have varying severity, occurring both asymptomatically and with pronounced characteristic pain.

In most cases, this disease at any stage is detected during routine examinations with an electrocardiograph.

This device, which has been used in cardiology for accurate diagnosis for over a hundred years, can provide information about the stage of the disease, its severity, as well as the location of the damage.

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Description of the technique

An electrocardiograph is a device that is capable of recording electrical impulses. Human organs emit currents of very low voltage, therefore, to recognize them, the device is equipped with an amplifier, as well as a galvanometer that measures this voltage.

The resulting data is sent to a mechanical recording device. Under the influence of currents emitted by the human heart, a cardiogram is constructed, on the basis of which the doctor can make an accurate diagnosis.

The rhythmic functioning of the heart is ensured by a special tissue called the cardiac conduction system. It is a specially innervated degenerated muscle fiber that transmits commands to contract and relax.

Acute transmural myocardial infarction of the inferior wall of the left ventricle, complicated by type II degree AV block

Cells in a healthy heart receive electrical impulses from the conduction system, the muscles contract, and the electrocardiograph records these weak currents.

The device picks up impulses that have passed through the muscle tissue of the heart. Healthy fibers have a known electrical conductivity, while in damaged or dead cells this parameter is significantly different.

The electrocardiogram shows areas from which information is distorted and abnormal, and it is they that carry information about the course of a disease such as a heart attack.

Main ECG signs of myocardial infarction

Diagnosis is based on measuring the electrical conductivity of individual areas of the heart. This parameter is affected not only by the state of muscle fibers, but also by electrolytic metabolism in the body as a whole, which is disrupted in some forms of gastritis or cholecystitis. In this regard, there are often cases when the ECG results make an erroneous diagnosis of the presence of a heart attack.

There are four distinct stages of a heart attack:

Acute transmural anteroseptal myocardial infarction with possible transition to the apex of the heart

In each of these periods, the physical structure of the cell membranes of muscle tissue, as well as their chemical composition, are different, so the electrical potential also differs significantly. ECG interpretation helps to accurately determine the stages of a heart attack and its size.

Most often, the left ventricle is susceptible to infarction, so the type of section of the cardiogram that displays the Q, R and S waves, as well as the S-T interval and the T wave itself is of diagnostic importance.

The teeth characterize the following processes:

Electrodes are fixed on various parts of the body, which correspond to the projection of certain areas of the heart muscle. For the diagnosis of myocardial infarction, the indicators obtained from six electrodes (leads) V1 – V6 installed on the chest on the left are important.

Developing myocardial infarction on the ECG is most clearly manifested by the following signs:

increase, change, absence or suppression of the R wave over the infarction area;
pathological S wave;
change in the direction of the T wave and deviation of the S – T interval from the isoline.

When a necrosis zone forms, the heart muscle cells are destroyed and potassium ions, the main electrolyte, are released.

The electrical conductivity in this area changes sharply, which is reflected in the cardiogram from the lead that is located directly above the necrotic area. The size of the damaged area is indicated by how many leads record the pathology.

Developing large-focal myocardial infarction of the inferior wall of the LV

Indicators of recency and frequency

Diagnosis of an acute infarction occurs in the first 3-7 days, when the active formation of a zone of dead cells, a zone of ischemia and damage occurs. During this period, the electrocardiograph records the maximum affected area, some of which will later degenerate into necrosis, and some will completely recover.

At each stage of a heart attack, it has its own specific diagram pattern from the leads located directly above the heart attack:

At the acute stage, that is, when the disease is 3–7 days old, the characteristic signs are:

the appearance of a high T wave, while the S – T interval may have a significant deviation from the isoline in the positive direction;
reversing the direction of the S wave;
a significant increase in the R wave in leads V4 – V6, which indicates hypertrophy of the ventricular walls;
the border of the R wave and the S – T section is practically absent; together they form a curve of a characteristic shape.

A change in the directions of the teeth indicates that the walls of the ventricle are greatly hypertrophied, so the electric current in them does not move upward, but inward, towards the interventricular septum.

At this stage, with proper treatment, it is possible to minimize the area of damage and the future area of necrosis, and if the area is small, it can be completely restored.

The stage of formation of the necrotic area occurs on days 7–10 and has the following characteristic picture:

the appearance of a wide and deep Q wave;
a decrease in the height of the R wave, which indicates weak excitation of the walls of the ventricle, or rather a loss of potential due to the destruction of cell walls and the release of electrolyte from them.

At this stage, treatment is aimed at stabilizing the condition and relieving pain, since it is impossible to restore dead areas. The compensatory mechanisms of the heart are activated, which separate the damaged area. The blood washes away the products of death, and the tissues that have undergone necrosis are replaced by connective fibers, that is, a scar is formed.

The last stage is characterized by a gradual restoration of the ECG pattern, but characteristic signs remain above the scar:

the S wave is absent;
the T wave is directed in the opposite direction.

This type of cardiogram appears because the connective tissue of the scar is not able to be excited and restored; accordingly, the currents characteristic of these processes are absent in these areas.

Large-focal anteroseptal-apical-lateral myocardial infarction, complicated by complete block of the right bundle branch, AV block of the first degree and sinus arrhythmia

Determining the location of the circulatory disorder

You can localize the area of damage to the heart muscle by knowing which parts of the organ are visible in each lead. Electrode placement is standard and provides detailed examination of the entire heart.

Depending on which lead records the direct signs described above, the location of the infarction can be determined:

Not all affected areas are shown here, since infarction can occur in both the right ventricle and the posterior parts of the heart. When diagnosing, it is very important to collect as much information as possible from all leads, then the localization will be as accurate as possible. For a confident diagnosis, information must be confirmed by data from at least three leads.

Extensiveness of the outbreak

The extent of the source of damage is determined in the same way as its location. Conventionally, the lead electrodes “shoot” the heart in twelve directions, intersecting in its center.

If the right side is examined, then six more directions can be added to these 12 directions. To make a diagnosis of myocardial infarction, convincing data from at least three sources is required.

When determining the size of the focus of damage, it is necessary to carefully study the data from the leads located in the immediate vicinity of the focus of necrosis. Around the dying tissue there is a zone of damage, and around it there is a zone of ischemia.

Each of these areas has a characteristic ECG pattern, so their detection may indicate the size of the affected area. The true size of the infarction is determined during the healing stage.

Transmural anteroseptal-apical myocardial infarction with transition to the lateral wall of the LV

Depth of necrosis

Various areas may be susceptible to dieback. Necrosis does not always occur throughout the entire thickness of the walls; more often it is deviated towards the inner or outer side, sometimes located in the center.

On the ECG one can confidently note the nature of the location. The S and T waves will change their shape and size depending on which wall the affected area is attached to.

Cardiologists distinguish the following types of necrosis location:

Possible difficulties

Although ECG for myocardial infarction is considered an effective diagnostic method, certain difficulties arise in its use. For example, it is very difficult to correctly diagnose overweight people, since the location of their heart muscle is changed.

If there is a violation of electrolyte metabolism in the body or diseases of the stomach and gallbladder, distortion in the diagnosis is also possible.

Some heart conditions, such as scarring or an aneurysm, make new damage barely noticeable. The physiological features of the structure of the conduction system also make it impossible to accurately diagnose infarctions of the interventricular septum.

Acute large-focal myocardial infarction of the lower wall of the LV with transition to the septum and apex of the heart, the lateral wall of the LV, complicated by atrial fibrillation and right bundle branch block

Type of pathology

Depending on the size and location of the lesion, characteristic patterns are noted on the cardiograph tape. Diagnosis is carried out on days 11–14, that is, at the healing stage.

Large-focal

The following picture is typical for this type of damage:

Subendocardial

If the damage has affected the tissue from the inside, then the diagnostic picture is as follows:

Intramural

For heart attacks located deep in the ventricular wall and not affecting the lining of the heart muscle, the ECG graph is as follows:

To determine the presence of a heart attack, its location and the stage of destruction of the heart muscle, the most reliable and accessible method is an ECG. The first signs appear after the third hour from the onset of the attack, increase in the first day and remain after the formation of the scar. To make a diagnosis, the depth of myocardial destruction and the extent of the process are taken into account, since the severity of the patient’s condition and the risk of complications depend on this.

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ECG signs of myocardial infarction

The electrocardiogram in acute disturbance of coronary blood flow reflects the failure of dead tissue to function and changes in cell excitability due to the release of potassium. Due to the fact that part of the functioning myocardium dies during a heart attack, the electrode over this zone cannot record the passage of the electrical signal.

Therefore, there will be no R on the recording, but a reflected impulse from the opposite wall will appear - a pathological Q wave, which has a negative direction. This element is present normally, but it is extremely short (less than 0.03 seconds), and when it becomes deep and long.

Due to the destruction of cardiomyocytes, intracellular potassium stores are released from them and concentrated under the outer lining of the heart (epicardium), causing electrical damage. This disrupts the process of recovery (repolarization) of the heart muscle and changes the ECG elements in this way:

above the necrosis zone, ST increases, and on the opposite wall it decreases, that is, the infarction is manifested by discordant (inconsistent) ECG abnormalities;
T becomes negative due to disruption of muscle fibers in the area of destruction.

Localization of pathology: anterior, posterior, lateral

If at the first stage of the analysis it is necessary to detect 5 signs of a heart attack (no R or low, Q has appeared, ST has increased, there is a discordant ST, negative T), then the next task is to search for leads where these disorders appear.

Front

When this part of the left ventricle is damaged, characteristic disturbances in the shape and size of the teeth are noted in:

leads 1 and 2, from the left hand – deep Q, ST is elevated and merges with positive T;
3, from the right leg – ST reduced, T negative;
chest 1-3 – R, QS wide, ST rises above the isoelectric line by more than 3 mm;
chest 4-6 – T flat, ST or slightly below the isoline.

Rear

When the focus of necrosis is localized along the posterior wall, the ECG can be seen in the second and third standard and enhanced leads from the right leg (aVF):

deepened and extended Q;
increased ST;
T positive, fused with ST.

Side

Infarction of the lateral wall leads to typical changes in the electrocardiogram in the third, from the left arm, 5th and 6th thoracic:

in-depth, significantly expanded Q;
increased ST;
T merges with ST into one line.

The first standard lead and chest lead record ST depression and negative, deformed T.

Stages during examination

ECG changes are not static when the heart muscle is destroyed. Therefore, it is possible to determine the duration of the process, as well as residual changes after suffering an acute myocardial malnutrition.

Sharp and spicy

It is very rare that a heart attack can be detected in the first minutes (up to 1 hour) after its occurrence. At this time, ECG changes are either completely absent or there are signs of subendocardial ischemia (ST elevation, T deformation). The acute stage lasts from an hour to 2 - 3 days from the onset of development of cardiac muscle necrosis.

This period is characterized by the release of potassium ions from dead cells and the occurrence of damage currents. They can be seen on the ECG as an increase in ST above the site of the infarction, and due to fusion with this element it ceases to be detected.

Subacute

This stage continues until approximately the end of the 20th day from the moment of the attack. Potassium is gradually washed out from the extracellular space, so ST slowly approaches the isoelectric line. This contributes to the appearance of the outlines of the T wave. The end of the subacute phase is considered to be the return of ST to its normal position.

Scarring

The duration of the recovery process and replacement of the site of necrosis with connective tissue can be about 3 months. At this time, a scar is formed in the myocardium, it partially grows with blood vessels, and new cardiac muscle cells are formed. The main ECG sign of these processes is the movement of T towards the isoline, its transition from negative to positive. R also gradually increases, and pathological Q disappears.

Rescheduled

Residual effects after a heart attack manifest themselves in the form of post-infarction cardiosclerosis. have different shapes and locations, they cannot participate in myocardial contraction and impulse conduction. Therefore, various blockades and arrhythmias arise. The ECG of patients who have had a heart attack reveals deformations of the ventricular complexes and incomplete return of ST and T to normal.

Variants of heart attack on the ECG

Depending on the extent, cardiac muscle infarction can be large-focal or. Each of them has its own ECG features.

Large-focal, q infarction: transmural and subepicardial

Large focal infarction, transmural (necrosis involving all layers of the myocardium)

Intramural infarction occurs when the source of damage is localized within the wall of the ventricle itself. In this case, there is no pronounced change in the direction of movement of the bioelectric signal, and potassium does not reach the inner or outer layers of the heart. This means that of all the signs, only negative T remains, which gradually changes its direction. Therefore, it is possible to diagnose intramural infarction only within 2 weeks.

Atypical options

All signs of myocardial necrosis in most cases can be detected on the ECG, with the exception of special location options - basal (anterior and posterior) at the point of contact of the ventricles with the atria. There are also certain diagnostic difficulties with simultaneous bundle branch block and acute coronary insufficiency.

Basal infarcts

High anterior myocardial necrosis (anterobasal infarction) is manifested only by a negative T wave in the left arm lead. In such a situation, it is possible to recognize the disease if you install the electrodes 1 - 2 intercostal spaces higher than usual. Posterobasal infarction does not have any typical signs. An exceptional increase in the amplitude of the ventricular complex (especially R) in the right precordial leads is possible.

Watch the video about ECG during myocardial infarction:

Bundle block and infarction

If the conduction of the signal along the ventricle is disrupted, then the impulse through the ventricle does not move along the conduction paths, this distorts the entire picture of the heart attack on the cardiogram. Only indirect symptoms in the chest leads can help with diagnosis:

abnormal Q in 5 and 6 (normally it is not there);
there is no increase in R from the first to the sixth;
positive T at 5 and 6 (usually it is negative).

Myocardial infarction on the ECG is manifested by a violation of the height of the teeth, the appearance of abnormal elements, displacement of segments, and a change in their direction relative to the isoline. Since all these deviations from the norm have a typical localization and sequence of appearance, using an ECG it is possible to establish the location of destruction of the heart muscle, the depth of damage to the heart wall and the time that has passed from the onset of a heart attack.

In addition to typical signs, in some situations you can focus on indirect violations. After a heart attack, scar tissue forms in the muscle layer instead of functioning cells, which leads to inhibition and distortion of the conduction of cardiac impulses and arrhythmia.

DEFINITION

Myocardial infarction is an emergency clinical condition caused by necrosis of an area of the heart muscle as a result of disruption of its blood supply.

MAIN CAUSES AND PATHOGENESIS

Developing as part of coronary heart disease, it is the result of coronary artery disease. The direct cause of myocardial infarction is most often occlusion or subtotal stenosis of the coronary artery, which almost always develops as a result of rupture or splitting of an atherosclerotic plaque with the formation of a thrombus, increased platelet aggregation and segmental spasm near the plaque.

CLASSIFICATION

From the point of view of determining the volume of required drug therapy and assessing the prognosis, three classifications are of interest.

A. According to the depth of the lesion (based on electrocardiographic data):

1. Transmural and large-focal (“Q-infarction”) - with ST segment elevation in

The first hours of the disease and the formation of the Q wave subsequently.

2. Small-focal (“not Q-infarction”) - not accompanied by the formation of a Q wave, but

Manifested by negative T waves

B. According to the clinical course:

1. Uncomplicated myocardial infarction.

2. Complicated myocardial infarction (see below).

B. By localization:

1. Left ventricular infarction (anterior, posterior or inferior, septal)

2. Right ventricular infarction.

CLINICAL PICTURE

According to the symptoms of the acute phase of myocardial infarction, the following clinical variants are distinguished:

Painful (status anginosus)	- a typical clinical course, the main manifestation of which is anginal pain, independent of posture and body position, movements and breathing, resistant to nitrates; the pain has a pressing, suffocating, burning or tearing nature with localization behind the sternum, throughout the entire anterior chest wall with possible irradiation to the shoulders, neck, arms, back, epigastric region; Characterized by a combination with hyperhidrosis, severe general weakness, pallor of the skin, agitation, and restlessness.
Abdominal (status gastralgicus)	- manifests itself as a combination of epigastric pain with dyspeptic symptoms - nausea, which does not bring relief with vomiting, hiccups, belching, and severe bloating; Possible irradiation of pain in the back, tension in the abdominal wall and pain on palpation in the epigastrium.
Atypical pain	- in which the pain syndrome is atypical in localization (for example, only in areas of irradiation - throat and lower jaw, shoulders, arms, etc.) and/or in nature.
Asthmatic (status asthmaticus)	- the only symptom in which is an attack of shortness of breath, which is a manifestation of acute congestive heart failure (cardiac asthma or pulmonary edema).
Arrhythmic	- in which rhythm disturbances are the only clinical manifestation or predominate in the clinical picture.
Cerebrovascular	- the clinical picture of which is dominated by signs of cerebrovascular accident (usually dynamic): fainting, dizziness, nausea, vomiting; focal neurological symptoms are possible.
Low-symptomatic (asymptomatic)	- the most difficult option to recognize, often diagnosed retrospectively using ECG data.

DIAGNOSTIC CRITERIA

At the prehospital stage of medical care, the diagnosis of acute myocardial infarction is made based on the presence of the following:

a) clinical picture

b) changes in the electrocardiogram.

A. Clinical criteria.

For painful infarction d have diagnostic value:

- intensity (in cases where similar pains have occurred previously, during a heart attack they are unusually intense),

- duration (unusually prolonged attack, lasting more than 15-20 minutes),

- patient behavior (excitement, motor restlessness),

- ineffectiveness of sublingual administration of nitrates.

Table 2.

List of questions required when analyzing pain syndrome in case of suspected acute myocardial infarction

Question	Note
When did the attack start?	It is advisable to determine as precisely as possible.
How long does the attack last?	Less than 15, 15-20 or more than 20 minutes.
Have there been any attempts to stop the attack with nitroglycerin?	Was there at least a short-term effect?
Does pain depend on posture, body position, movements and breathing?	During a coronary attack it does not depend.
Have you had similar attacks in the past?	Similar attacks that do not result in a heart attack require differential diagnosis with unstable angina and non-cardiac causes.
Did attacks (pain or suffocation) occur during physical activity (walking), did they force you to stop, how long did they last (in minutes), how did you react to nitroglycerin?	The presence of angina pectoris makes the assumption of acute myocardial infarction very likely.
Does the present attack resemble the sensations that arose during physical activity in terms of location or nature of the pain?	In terms of intensity and accompanying symptoms, an attack during myocardial infarction is usually more severe than during angina pectoris.

In any case auxiliary diagnostic value are:

Hyperhidrosis,

Sharp general weakness,

Pallor of the skin,

Signs of acute heart failure.

The absence of a typical clinical picture cannot serve as evidence of the absence of myocardial infarction.

B. Electrocardiographic criteria - changes that serve as signs:

Damage	- arcuate elevation of the ST segment with convexity upward, merging with a positive T wave or turning into a negative wave T (possible arcuate depression of the ST segment with convexity downward);
Large focal or Transmural infarction	- the appearance of a pathological Q wave and a decrease in the amplitude of the R wave or the disappearance of the R wave and the formation of QS;
Small focal infarction	- the appearance of a negative symmetrical T wave;

Notes: *1. An indirect sign of myocardial infarction, which does not allow determining the phase and depth of the process, is an acutely occurring bundle branch block (if there is an appropriate clinic).* *2. Dynamic electrocardiographic data have the greatest reliability, so electrocardiograms should be compared with previous ones whenever possible.*

In case of anterior wall infarction, similar changes are detected in standard leads I and II, enhanced lead from the left arm (aVL) and the corresponding chest leads (V1, 2, 3, 4, 5, 6). With high lateral myocardial infarction, changes can be recorded only in lead aVL and to confirm the diagnosis it is necessary to remove high chest leads. In case of infarction of the posterior wall (lower, diaphragmatic), these changes are detected in the II, III standard and enhanced leads from the right leg (aVF). In case of myocardial infarction of the high parts of the posterior wall of the left ventricle (posterior-basal), changes in standard leads are not recorded; the diagnosis is made on the basis of reciprocal changes - high R and T waves in leads V 1 -V 2 (Table 3).

Rice. 1. The most acute phase of transmural anterior myocardial infarction.

Table 3. Localization of myocardial infarction according to ECG data

Type of infarction by location	Standard leads		Chest leads
		III
Septal
Perioseptal
Front
Spread front
Anterolateral
Side
High side
Posterolateral
Posterior diaphragmatic
Posterobasal

TREATMENT OF MYOCARDIAL INFARCTION

Emergency therapy has several interrelated goals:

1. Relief of pain syndrome.

2. Restoration of coronary blood flow.

3. Reducing heart function and myocardial oxygen demand.

4. Limiting the size of myocardial infarction.

5. Treatment and prevention of complications of myocardial infarction.

The drugs used for this are presented in Table 3.

Table 3.

The main directions of therapy and drugs used in the acute stage of uncomplicated myocardial infarction

Medicine	Directions of therapy
Morphine intravenously in fractions	Adequate pain relief, reduction of pre- and afterload, psychomotor agitation, and myocardial oxygen demand	2-5 mg intravenously every 5-15 minutes until pain is completely eliminated or side effects appear
Streptokinase (streptase)	Restoration of coronary blood flow (thrombolysis), pain relief, limiting the size of myocardial infarction, reducing mortality	1.5 million IU IV over 60 minutes
Heparin intravenous bolus (if thrombolysis is not performed)	Prevention or limitation of coronary thrombosis, prevention of thromboembolic complications, reduction of mortality	10000-15000 IU intravenous bolus
Nitroglycerin or isosorbide dinitrate intravenous drip	Relieving pain, reducing the size of myocardial infarction and mortality	10 mcg/min. with an increase in speed by 20 mcg/min every 5 minutes under the control of heart rate and blood pressure
Beta blockers: propranolol (obzidan)	Reducing myocardial oxygen demand, relieving pain, reducing the size of necrosis, preventing ventricular fibrillation and left ventricular rupture, repeated myocardial infarction, reducing mortality	1 mg/min every 3-5 minutes for a total dose of 10 mg
Acetylsalicylic acid (aspirin)	Relief and prevention of processes associated with platelet aggregation; when prescribed early(!), it reduces mortality	160-325 mg chew;
Magnesium sulfate (cormagnesin)	Reducing myocardial oxygen demand, relieving pain, reducing the size of necrosis, preventing cardiac arrhythmias, heart failure, reducing mortality	1000 mg magnesium (50 ml 10%, 25 ml 20% or 20 ml 25% solution) intravenously over 30 minutes.

ALGORITHM FOR PROVIDING MEDICAL CARE TO PATIENTS WITH ACUTE MYOCARDIAL INFARCTION AT THE PREHOSPITAL STAGE

A. Uncomplicated myocardial infarction

B. Uncomplicated myocardial infarction ormyocardial infarction complicated by persistent pain syndrome

B. Complicated myocardial infarction

1. Pain relief

in acute myocardial infarction, this is one of the most important tasks, since pain, through activation of the sympathoadrenal system, causes an increase in vascular resistance, frequency and strength of heart contractions, that is, it increases the hemodynamic load on the heart, increases the myocardial oxygen demand and aggravates ischemia.

If preliminary sublingual administration of nitroglycerin (repeatedly 0.5 mg in tablets or 0.4 mg in aerosol) does not relieve pain, therapy with narcotic analgesics begins, which, in addition to analgesic and sedative effects, have an effect on hemodynamics: due to their vasodilating properties, they provide hemodynamic unloading of the myocardium, primarily reducing preload. At the prehospital stage, the drug of choice for relieving pain during myocardial infarction is morphine, which has not only the necessary effects, but also a duration of action sufficient for transportation. The drug is administered intravenously in fractional doses: 1 ml of a 1% solution is diluted with physiological sodium chloride solution to 20 ml (1 ml of the resulting solution contains 0.5 mg of the active substance) and 2-5 mg are administered every 5-15 minutes until the pain syndrome is completely eliminated or until side effects (hypotension, respiratory depression, vomiting). The total dose should not exceed 10-15 mg (1-1.5 ml of 1% solution) of morphine (at the pre-hospital stage, the dose should not be exceeded 20 mg).

For unexpressed pain, in elderly and debilitated patients, narcotic analgesics can be administered subcutaneously or intramuscularly. It is not recommended to administer more than 60 mg of morphine subcutaneously within 12 hours.

To prevent and relieve side effects of narcotic analgesics such as nausea and vomiting, intravenous administration of 10-20 mg of metoclopramide (Reglan) is recommended. For severe bradycardia with or without hypotension, the use of atropine at a dose of 0.5 mg (0.5 ml of 0.1% solution) intravenously is indicated; the fight against a decrease in blood pressure is carried out according to the general principles of correcting hypotension during myocardial infarction.

Insufficient effectiveness of pain relief with narcotic analgesics is an indication for intravenous infusion of nitrates. If the effectiveness of nitrates is low in combination with tachycardia, an additional analgesic effect can be obtained by administering beta-blockers. Pain can be relieved with effective thrombolysis.

Persistent intense anginal pain is an indication for the use of mask anesthesia with nitrous oxide (which has a sedative and analgesic effect) mixed with oxygen. Start with oxygen inhalation for 1-3 minutes, then use nitrous oxide (20%) with oxygen (80%) with a gradual increase in the concentration of nitrous oxide to 80%; after the patient falls asleep, they switch to a maintenance gas concentration of 50´ 50 %. On the positive side, nitrous oxide does not affect left ventricular function. The occurrence of side effects - nausea, vomiting, agitation or confusion - is an indication for reducing the concentration of nitrous oxide or discontinuing inhalation. When recovering from anesthesia, pure oxygen is inhaled for 10 minutes to prevent arterial hypoxemia.

To resolve the issue of the possibility of using narcotic analgesics, a number of points should be clarified:

- make sure that typical or atypical pain syndrome is not a manifestation of an “acute abdomen”, and ECG changes are a specific manifestation of myocardial infarction, and not a nonspecific reaction to a catastrophe in the abdominal cavity;

- find out whether there is a history of chronic diseases of the respiratory system, in particular bronchial asthma;

- clarify when the last exacerbation of broncho-obstructive syndrome occurred;

- establish whether there are currently signs of respiratory failure, what they are, and what the degree of its severity is;

- find out whether the patient has a history of convulsive syndrome, when was the last seizure.

2. Restoration of coronary blood flow in the acute phase of myocardial infarction,

reliably improving the prognosis, in the absence of contraindications, is carried out through systemic thrombolysis.

A). Indications for thrombolysis are the presence of ST segment elevation of more than 1 mm in at least two standard ECG leads and more than 2 mm in two adjacent precordial leads or acute complete block of the left bundle branch within a period that has passed since the onset of the disease, more than 30 minutes, but not exceeding 12 hours. The use of thrombolytic agents is possible later in cases where ST segment elevation persists, pain continues and/or unstable hemodynamics are observed.

Unlike intracoronary thrombolysis, systemic thrombolysis (carried out by intravenous administration of thrombolytic agents) does not require any complex manipulations or special equipment. Moreover, it is quite effective if started in the first hours of the development of myocardial infarction (optimally at the prehospital stage), since the reduction in mortality directly depends on the timing of its onset.

In the absence of contraindications, the decision on performing thrombolysis is based on an analysis of the time factor: if transportation to the appropriate hospital may be longer than the period before the start of this therapy by a specialized ambulance team (with an expected transportation time of more than 30 minutes or if in-hospital thrombolysis is delayed for more than than 60 minutes), the administration of thrombolytic agents should be carried out at the prehospital stage of medical care. Otherwise, it should be postponed until the hospital stage.

The most commonly used is streptokinase. Method of intravenous administration of streptokinase: administration of streptokinase is carried out only through peripheral veins; attempts to catheterize central veins are unacceptable; before infusion, it is possible to administer intravenously 5-6 ml of 25% magnesium sulfate, or 10 ml of Cormagnesin-200 intravenously in a stream, slowly (over 5 minutes); a “loading” dose of aspirin (250-300 mg - chew) is always given, except in cases where aspirin is contraindicated (allergic and); 1,500,000 units of streptokinase are diluted in 100 ml of isotonic sodium chloride solution and administered intravenously over 30 minutes.

Simultaneous administration of heparin when using streptokinase is not required - it is assumed that streptokinase itself has anticoagulation and antiaggregation properties. It has been shown that intravenous administration of heparin does not reduce mortality and the frequency of recurrences of myocardial infarction, and the effectiveness of its subcutaneous administration is questionable. If heparin was administered earlier for some reason, this is not an obstacle to thrombolysis. It is recommended to prescribe heparin 4 hours after stopping the streptokinase infusion. The previously recommended use of hydrocortisone for the prevention of anaphylaxis was found not only ineffective, but also unsafe in the acute stage of myocardial infarction (glucocorticoids increase the risk of myocardial rupture).

Main complications of thrombolysis

1). Bleeding (including the most serious - intracranial) - develops as a result of inhibition of blood coagulation processes and lysis of blood clots. The risk of stroke during systemic thrombolysis is 0.5-1.5% of cases; stroke usually develops on the first day after thrombolysis. To stop minor bleeding (from the puncture site, from the mouth, nose), compression of the bleeding area is sufficient. For more significant bleeding (gastrointestinal, intracranial), an intravenous infusion of aminocaproic acid is necessary - 100 ml of a 5% solution is administered over 30 minutes and then 1 g/hour until the bleeding stops, or tranexamic acid 1-1.5 g 3-4 once a day intravenously; In addition, transfusion of fresh frozen plasma is effective. However, it should be remembered that when using antifibrinolytic drugs, the risk of coronary artery reocclusion and reinfarction increases, so they should be used only for life-threatening bleeding.

2). Arrhythmias that occur after restoration of coronary circulation (reperfusion). Slow nodal or ventricular rhythms (with a heart rate of less than 120 per minute and stable hemodynamics) do not require intensive care; supraventricular and ventricular extrasystole (including allorhythmic); atrioventricular block I and II (Mobitz type I) degrees. Ventricular fibrillation requires emergency treatment (defibrillation and a set of standard resuscitation measures are required); bidirectional fusiform ventricular tachycardia of the “pirouette” type (defibrillation, intravenous bolus administration of magnesium sulfate are indicated); other types of ventricular tachycardia (use lidocaine administration or perform cardioversion); persistent supraventricular tachycardia (stopped by intravenous jet administration of verapamil or procainamide); atrioventricular block II (Mobitz type II) and III degree, sinoatrial block (atropine is injected intravenously in a dose of up to 2.5 mg, if necessary, emergency cardiac pacing is performed).

3). Allergic reactions. Rash, itching, periorbital edema occur in 4.4% of cases, severe reactions (anaphylactic shock) - in 1.7% of cases. If an anaphylactoid reaction is suspected, the streptokinase infusion should be immediately stopped and a bolus of 150 mg prednisolone administered intravenously. In case of severe hemodynamic depression and the appearance of signs of anaphylactic shock, 1 ml of a 1% solution of adrenaline is administered intravenously, while continuing the administration of steroid hormones intravenously. For fever, aspirin or paracetamol is prescribed.

4). Recurrence of pain after thrombolysis is controlled by intravenous fractional administration of narcotic analgesics. With an increase in ischemic changes on the ECG, intravenous drip administration of nitroglycerin is indicated or, if the infusion has already been established, an increase in the rate of its administration.

5). For arterial hypotension, in most cases it is sufficient to temporarily stop the thrombolytic infusion and elevate the patient's legs; if necessary, the blood pressure level is adjusted by administering fluids, vasopressors (dopamine or norepinephrine intravenously drip until systolic blood pressure stabilizes at 90-100 mm Hg).

Rice. 2. Reperfusion arrhythmia in transmural posterior myocardial infarction: an episode of junctional rhythm with independent restoration of sinus rhythm.

Clinical signs of restoration of coronary blood flow:

- cessation of anginal attacks 30-60 minutes after administration of the thrombolytic,

- stabilization of hemodynamics,

- disappearance of signs of left ventricular failure,

- rapid (within several hours) ECG dynamics with the ST segment approaching the isoline and the formation of a pathological Q wave, a negative T wave (a sudden increase in the degree of ST segment elevation followed by its rapid decrease is possible),

- the appearance of reperfusion arrhythmias (accelerated idioventricular rhythm, ventricular extrasystole, etc.),

- rapid dynamics of CF-CK (a sharp increase in its activity by 20-40%).

To resolve the issue of the possibility of using thrombolytic agents, a number of points should be clarified:

- make sure there are no acute internal bleedings during the previous 10 days - gastrointestinal, pulmonary, uterine, with the exception of menstrual bleeding, hematuria, etc. (pay attention to their presence in the anamnesis) or surgical interventions and injuries with damage to internal organs;

- exclude the presence of acute cerebrovascular accident, surgery or injury to the brain or spinal cord within the previous 2 months (pay attention to their presence in the anamnesis);

- exclude suspicion of acute pancreatitis, dissecting aortic aneurysm, as well as cerebral artery aneurysm, brain tumor or metastatic malignant tumors;

- establish the absence of physical signs or anamnestic indications of pathology of the blood coagulation system - hemorrhagic diathesis, thrombocytopenia (pay attention to hemorrhagic diabetic retinopathy);

- make sure that the patient does not receive indirect anticoagulants;

- to clarify whether there were any allergic reactions to the corresponding thrombolytic drugs, and in relation to streptokinase, whether it was previously administered within a period of 5 days to 2 years (during this period, due to the high titer of antibodies, the administration of streptokinase is unacceptable);

- in case of successful resuscitation measures, make sure that they were not traumatic and long-lasting (in the absence of signs of post-resuscitation injuries - rib fractures and damage to internal organs, pay attention to the duration exceeding 10 minutes);

- achieve stabilization of high blood pressure at a level of less than 200/120 mm Hg. Art. (pay attention to levels exceeding 180/110 mmHg)

- pay attention to other conditions that are dangerous for the development of hemorrhagic complications and serve as relative contraindications to systemic thrombolysis: severe liver or kidney diseases; suspicion of chronic cardiac aneurysm, pericarditis, infectious myocarditis, presence of a blood clot in the cardiac cavities; thrombophlebitis and phlebothrombosis; varicose veins of the esophagus, peptic ulcer in the acute stage; pregnancy;

- keep in mind that a number of factors that are not relative or absolute contraindications to systemic thrombolysis may increase its risk: age over 65 years, body weight less than 70 kg, female gender, arterial hypertension.

Systemic thrombolysis is possible in the elderly and senile, as well as against the background of arterial hypotension (systolic blood pressure less than 100 mm Hg) and cardiogenic shock.

In doubtful cases, the decision to conduct thrombolytic therapy should be deferred until the inpatient stage of treatment. Delay is indicated for atypical development of the disease, nonspecific ECG changes, long-standing bundle branch block and undoubted previous myocardial infarction masking typical changes.

B). The absence of indications for thrombolytic therapy (late periods, the so-called small-focal or non-Q-infarction), the impossibility of thrombolysis for organizational reasons, as well as its delay until the hospital stage or some contraindications to it, which are not a contraindication to the use of heparin, serve as an indication ( in the absence of own contraindications) to anticoagulant therapy. Its goal is to prevent or limit thrombosis of the coronary arteries, as well as to prevent thromboembolic complications (especially common in patients with anterior myocardial infarction, low cardiac output, and atrial fibrillation). To do this, at the prehospital stage (by the line team), heparin is administered intravenously in a dose of 10,000-15,000 IU. If thrombolytic therapy is not carried out in a hospital setting, then switch to a long-term intravenous infusion of heparin at a rate of 1000 IU/hour under the control of activated partial thromboplastin time. An alternative, apparently, is the subcutaneous administration of low molecular weight heparin in a “therapeutic” dose. The administration of heparin at the prehospital stage does not serve as an obstacle to thrombolysis in a hospital setting.

Despite the higher safety of heparin therapy compared to systemic thrombolysis, due to its significantly lower effectiveness, a number of contraindications to its implementation are much more stringent, and some relative contraindications to thrombolysis turn out to be absolute for heparin therapy. On the other hand, heparin can be prescribed to patients with some contraindications to the use of thrombolytic agents.

To resolve the issue of the possibility of prescribing heparin, the same points should be clarified as for thrombolytic agents:

- exclude a history of hemorrhagic stroke, brain and spinal cord surgery;

- make sure there is no tumor and peptic ulcer of the stomach and duodenum, infective endocarditis, severe damage to the liver and kidneys;

- exclude suspicion of acute pancreatitis, dissecting aortic aneurysm, acute pericarditis with a pericardial friction rub heard for several days (!) (danger of developing hemopericardium);

- establish the absence of physical signs or anamnestic indications of pathology of the blood coagulation system (hemorrhagic diathesis, blood diseases);

Find out if the patient has hypersensitivity to heparin;

- achieve stabilization of high blood pressure at a level of less than 200/120 mm Hg. Art.

IN). From the first minutes of myocardial infarction, all patients, in the absence of contraindications, are prescribed small doses of acetylsalicylic acid (aspirin), the antiplatelet effect of which reaches its maximum after 30 minutes and the timely initiation of use of which can significantly reduce mortality. The greatest clinical effect can be obtained by using acetylsalicylic acid before thrombolysis. The dose for the first dose at the prehospital stage is 160-325 mg, chew (!). Subsequently, at the inpatient stage, the drug is prescribed once a day, 100-125 mg.

To resolve the issue of the possibility of prescribing acetylsalicylic acid, only a small part of the restrictions for thrombolytic drugs are important; needs to be clarified:

Does the patient have erosive and ulcerative lesions of the gastrointestinal tract in the acute stage;

Whether there was a history of gastrointestinal bleeding;

Does the patient have anemia?

- does the patient have the “aspirin triad” (, nasal polyposis,

Aspirin intolerance);

Is there hypersensitivity to the drug?

3. Reducing heart work and myocardial oxygen demand

In addition to complete pain relief, it is provided by the use of

a) vasodilators - nitrates,

b) beta-blockers and

c) means of complex action - magnesium sulfate.

A. Intravenous administration of nitrates in acute myocardial infarction, it not only helps relieve pain, left ventricular failure, and arterial hypertension, but also reduces the extent of necrosis and mortality. Nitrate solutions for intravenous administration are prepared ex tempore: every 10 mg of nitroglycerin (for example, 10 ml of a 0.1% solution in the form of the drug perlinganite) or isosorbide dinitrate (for example, 10 ml of a 0.1% solution in the form of the drug isoket) is diluted in 100 ml physiological solution (20 mg of the drug - in 200 ml of physiological solution, etc.); Thus, 1 ml of the prepared solution contains 100 mcg, and 1 drop - 5 mcg of the drug. Nitrates are administered dropwise under constant monitoring of blood pressure and heart rate at an initial rate of 5-10 mcg/min, followed by an increase in speed by 20 mcg/min every 5 minutes until the desired effect is achieved or the maximum injection rate is 400 mcg/min. Typically the effect is achieved at a speed of 50-100 mcg/min. In the absence of a dispenser, the prepared solution containing 100 mcg of nitrate in 1 ml is administered under careful control (see above) at an initial rate of 6-8 drops per minute, which, subject to stable hemodynamics and persistence of pain, can be gradually increased up to the maximum speed - 30 drops per minute. The administration of nitrates is carried out by both linear and specialized teams and continues in the hospital. The duration of intravenous administration of nitrates is 24 hours or more; 2-3 hours before the end of the infusion, the first dose of nitrates is given orally. Overdose of nitrates, causing a drop in cardiac output and a decrease in systolic blood pressure below 80 mm Hg. Art., can lead to a deterioration in coronary perfusion and an increase in the size of myocardial infarction.

To resolve the issue of the possibility of prescribing nitrates, it is necessary to clarify a number of points:

- make sure that systolic blood pressure is above 90 mm Hg. Art. (for short-acting nitroglycerin) or above 100 mm Hg. st (for longer-acting isosorbide dinitrate);

- exclude the presence of aortic stenosis and hypertrophic cardiomyopathy with outflow tract obstruction (auscultation and ECG data), cardiac tamponade (clinical picture of venous congestion in the systemic circulation with minimal signs of left ventricular failure) and constrictive pericarditis (Beck’s triad: high venous pressure, ascites, “small quiet heart”);

- exclude intracranial hypertension and acute cerebral dyscirculation (including as manifestations of stroke, acute hypertensive encephalopathy, recent traumatic brain injury);

- exclude the possibility of nitrates provoking the development of small output syndrome due to damage to the right ventricle during infarction or ischemia of the right ventricle, which may accompany the posterior (lower) localization of left ventricular infarction, or with pulmonary embolism with the formation of acute cor pulmonale;

- make sure by palpation examination that there is no high intraocular pressure (with angle-closure glaucoma);

- determine whether the patient has nitrate intolerance.

B. Intravenous administration of beta-blockers

just as the use of nitrates helps relieve pain; by weakening the sympathetic influences on the heart (these influences are enhanced in the first 48 hours of myocardial infarction due to the disease itself and as a result of the reaction to pain) and reducing the myocardial oxygen demand, they help reduce the size of myocardial infarction, suppress ventricular arrhythmias, reduce the risk of myocardial rupture and thus increase thus patient survival. It is very important that beta-blockers, according to experimental data, can delay the death of ischemic cardiomyocytes (they increase the time during which thrombolysis will be effective).

In the absence of contraindications, beta-blockers are prescribed to all patients with acute myocardial infarction. At the prehospital stage, indications for their intravenous administration are for the linear team - corresponding rhythm disturbances, and for the specialized team - persistent pain syndrome, tachycardia, arterial hypertension. In the first 2-4 hours of the disease, fractional intravenous administration of propranolol (obzidan) 1 mg per minute every 3-5 minutes is indicated under the control of blood pressure, heart rate and ECG until the heart rate reaches 55-60 beats/min or until the total doses 10 mg. In the presence of bradycardia, signs of heart failure, AV block and a decrease in systolic blood pressure less than 100 mm Hg. Art. propranolol is not prescribed, and if these changes develop during its use, the administration of the drug is stopped.

To resolve the issue of the possibility of prescribing beta-blockers, it is necessary to clarify a number of points:

- make sure there is no acute heart failure or circulatory failure stage II-III, arterial hypotension;

- exclude the presence of AV block, sinoatrial block, sick sinus syndrome, bradycardia (heart rate less than 55 beats per minute);

- exclude the presence of bronchial asthma and other obstructive respiratory diseases, as well as vasomotor rhinitis;

- exclude the presence of obliterating vascular diseases (or endarteritis, Raynaud's syndrome, etc.);

B) Intravenous infusion of magnesium sulfate

carried out in patients with proven or probable hypomagnesemia or long QT syndrome, as well as in case of complications of myocardial infarction by certain types of arrhythmias. In the absence of contraindications, magnesium sulfate can serve as a definite alternative to the use of nitrates and beta-blockers if their administration is impossible for some reason (contraindications or absence). According to the results of a number of studies, it, like other drugs that reduce heart function and myocardial oxygen demand, reduces mortality in acute myocardial infarction, and also prevents the development of fatal arrhythmias (including reperfusion ones during systemic thrombolysis) and post-infarction heart failure. In the treatment of acute myocardial infarction, 1000 mg of magnesium (50 ml of 10%, 25 ml of 20% or 20 ml of 25% magnesium sulfate solution) is administered intravenously over 30 minutes in 100 ml of isotonic sodium chloride solution; Subsequently, intravenous drip infusion is carried out during the day at a rate of 100-120 mg of magnesium per hour (5-6 ml of 10%, 2.5-3 ml of 20% or 2-2.4 ml of 25% magnesium sulfate solution).

To resolve the issue of indications for prescribing magnesium sulfate, it is necessary to clarify a number of points:

- identify clinical and anamnestic signs of possible hypomagnesemia - hyperaldosteronism (primarily in congestive heart failure and stable arterial hypertension), hyperthyroidism (including iatrogenic), chronic alcohol intoxication, convulsive muscle contractions, long-term use of diuretics, glucocorticoid therapy;

- diagnose the presence of long QT syndrome using an ECG.

To resolve the issue of the possibility of prescribing magnesium sulfate, it is necessary to clarify a number of points:

- make sure there are no conditions manifested by hypermagnesemia - renal failure, diabetic ketoacidosis, hypothyroidism;

- exclude the presence of AV block, sinoauricular block, sick sinus syndrome, bradycardia (heart rate less than 55 beats per minute);

Rule out the presence of myasthenia gravis in the patient;

- determine whether the patient is intolerant to the drug.

4. Limiting the size of myocardial infarction

is achieved by adequate pain relief, restoration of coronary blood flow and a decrease in cardiac work and myocardial oxygen demand.

The same purpose is served by oxygen therapy, which is indicated for all patients with acute myocardial infarction due to the frequent development of hypoxemia, even with an uncomplicated course of the disease. Inhalation of humidified oxygen, carried out, if it does not cause excessive inconvenience, using a mask or through a nasal catheter at a rate of 4-6 l/min, is advisable during the first 24-48 hours of the disease (starts in the prehospital stage and continues in the hospital).

5. Treatment and prevention of complications of myocardial infarction.

All of the above measures, together with ensuring physical and mental rest and hospitalization on a stretcher, serve to prevent complications of acute myocardial infarction. Treatment in case of their development is carried out differentiated depending on the type of complications: pulmonary edema, cardiogenic shock, cardiac arrhythmia and conduction disturbances, as well as prolonged or recurrent pain attack.

1). In case of acute left ventricular failure with the development of cardiac asthma or pulmonary edema, simultaneously with the administration of narcotic analgesics and nitroglycerin, 40-120 mg (4-12 ml) of a solution of furosemide (Lasix) is injected intravenously, the maximum dose at the prehospital stage is 200 mg.

2). The basis for the treatment of cardiogenic shock is to limit the area of damage and increase the volume of functioning myocardium by improving the blood supply to its ischemic areas, for which systemic thrombolysis is performed.

Arrhythmic shock requires immediate restoration of an adequate rhythm by performing electrical pulse therapy, electrical cardiac stimulation; if this is impossible, drug therapy is indicated (see below).

Reflex shock relieved after adequate analgesia; for initial bradycardia, opioid analgesics should be combined with atropine at a dose of 0.5 mg.

True cardiogenic shock (hypokinetic type of hemodynamics) serves as an indication for IV drip administration of non-glycoside cardiotonic (positive inotropic) agents - dopamine, dobutamine, norepinephrine. This should be preceded by correction of hypovolemia. In the absence of signs of congestive left ventricular failure, the bcc is corrected by jet injection of 0.9% sodium chloride solution in a volume of up to 200 ml over 10 minutes, with repeated administration of the same dose in the absence of effect or complications.

Dopamine at a dose of 1-5 mcg/kg/min has a predominantly vasodilating effect, 5-15 mcg/kg/min has a vasodilating and positive inotropic (and chronotropic) effect, 15-25 mcg/kg/min has a positive inotropic (and chronotropic) effect. and peripheral vasoconstrictive effects. The initial dose is 2-5 mcg/kg/min with a gradual increase to the optimal dose.

Dobutamine, unlike dopamine, does not cause vasodilation, but has a powerful positive inotropic effect and a less pronounced increase in heart rate and arrhythmogenic effect. The drug is prescribed at a dose of 2.5 mcg/kg/min, increasing every 15-30 minutes by 2.5 mcg/kg/min until an effect, side effect is obtained, or a dose of 15 mcg/kg/min is achieved.

A combination of dopamine and dobutamine in maximum tolerated doses is used if there is no effect from the maximum dose of one of them or if it is impossible to use the maximum dose of one drug due to side effects (sinus tachycardia more than 140 bpm or ventricular arrhythmia).

A combination of dopamine or dobutamine with norepinephrine given at a dose of 8 mcg/min.

Norepinephrine (norepinephrine) is used as monotherapy when it is impossible to use other pressor amines. It is prescribed in a dose not exceeding 16 mcg/min, in mandatory combination with an infusion of nitroglycerin or isosorbide dinitrate at a rate of 5-200 mcg/min.

3). Ventricular extrasystole in the acute stage of myocardial infarction may be a harbinger of ventricular fibrillation. The drug of choice for the treatment of ventricular arrhythmias, lidocaine, is administered intravenously as a bolus at a rate of 1 mg/kg, followed by a drip infusion of 2-4 mg/min. The previously used prophylactic administration of lidocaine is not recommended for all patients with acute myocardial infarction (the drug increases mortality due to asystole). Patients with congestive heart failure and liver diseases are administered at a dose reduced by half.

For ventricular tachycardia, atrial flutter and atrial fibrillation with high heart rate and unstable hemodynamics, defibrillation is the treatment of choice. In case of atrial fibrillation and stable hemodynamics, (anaprilin, obzidan) is used to reduce heart rate.

With the development of atrioventricular block II-III degree, 1 ml of 0.1% atropine solution is administered intravenously; if trial therapy with atropine is ineffective and fainting occurs (Morgagni-Edams-Stokes attacks), temporary cardiac pacing is indicated.

COMMON THERAPY ERRORS.

The high mortality rate in the first hours and days of myocardial infarction makes it necessary to prescribe adequate drug therapy, starting from the first minutes of the disease. Losing time significantly worsens the prognosis.

A. Errors caused by outdated recommendations, which are partially preserved in some modern standards of medical care at the prehospital stage.

The most common mistake is the use of a three-stage analgesic regimen: if there is no effect from sublingual administration of nitroglycerin, the transition to narcotic analgesics is carried out only after an unsuccessful attempt to relieve pain using a combination of a non-narcotic analgesic (metamizole sodium - analgin) with an antihistamine (diphenidramine - diphenhydramine). Meanwhile, the loss of time when using such a combination, which, firstly, as a rule, does not allow you to obtain full analgesia, and secondly, unlike narcotic analgesics, it is not capable of providing hemodynamic unloading of the heart(the main goal of pain relief) and reduce the myocardial oxygen demand, leads to aggravation of the condition and worsening prognosis.

Much less frequently, but still used, myotropic antispasmodics (as an exception, the previously recommended papaverine is used, which was replaced by drotaverine - no-shpa), which do not improve the perfusion of the affected area, but increase the myocardial oxygen demand.

It is not advisable to use atropine for the prevention (this does not apply to relief) of the vagomimetic effects of morphine (nausea, vomiting, effect on heart rate and blood pressure), since it can increase the work of the heart.

The recommended prophylactic administration of lidocaine to all patients with acute myocardial infarction without taking into account the real situation, preventing the development of ventricular fibrillation, can significantly increase mortality due to the onset of asystole.

B. Errors due to other reasons.

Very often, for the purpose of pain relief for anginal status, the combined drug metamizole sodium with fenpiverine bromide and pitofenone hydrochloride (baralgin, spasmalgin, spazgan, etc.) or tramadol (tramal) is unjustifiably used, which have virtually no effect on the work of the heart and oxygen consumption by the myocardium, and therefore not shown in this case (see above).

In case of myocardial infarction, the use of dipiradamole (chimes) as an antiplatelet agent and “coronary lytic”, which significantly increases the myocardial oxygen demand, is extremely dangerous.

A very common mistake is the prescription of potassium and magnesium aspartate (asparkam, panangin), which does not affect the external functioning of the heart, the myocardial oxygen consumption, coronary blood flow, etc.

INDICATIONS FOR HOSPITALIZATION.

Acute myocardial infarction is a direct indication for hospitalization in the intensive care unit (unit) or cardiac intensive care unit. Transportation is carried out on a stretcher.

Electrocardiography (ECG) is a widely used method for diagnosing cardiovascular diseases. During the examination, the difference in electrical potentials that arise in the cells of the heart during its operation is recorded.

During myocardial infarction, a number of characteristic signs appear on the ECG, which can be used to predict the time of onset of the disease, the size and location of the lesion. This knowledge allows you to make a timely diagnosis and begin treatment.

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Cardiogram is normal

The ECG reflects the potential difference that occurs when the parts of the heart are excited during its contraction. Pulses are recorded using electrodes installed on different parts of the body. There are certain leads that differ from each other in the areas from which the measurement takes place.

Chest leads

Typically, a cardiogram is taken in 12 leads:

I, II, III - standard bipolar from the limbs;
aVR, aVL, aVF - reinforced unipolar from the limbs;
V1, V2, V3, V4, V5, V6 - six unipolar chest ones.

In some situations, additional leads are used - V7, V8, V9. In the projection of each positive electrode there is a certain part of the muscular wall of the heart. Based on changes in the ECG in any of the leads, it can be assumed in which part of the organ the source of damage is located.

ECG is normal, waves, intervals and segments

When the heart muscle (myocardium) relaxes, a straight line is recorded on the cardiogram - an isoline. The passage of excitation is reflected on the tape in the form of teeth, which form segments and complexes. If the tooth is located above the isoline, it is considered positive, if below it is considered negative. The distance between them is called the interval.

The P wave reflects the process of contraction of the right and left atria, the QRS complex registers the increase and decrease of excitation in the ventricles. The RS-T segment and the T wave show how the myocardium relaxes.

ECG for myocardial infarction

Myocardial infarction is a disease in which death (necrosis) of part of the muscle tissue of the heart occurs. The cause of its occurrence is an acute disturbance of blood flow in the vessels supplying the myocardium. The development of necrosis is preceded by reversible changes - ischemia and ischemic damage. Signs characteristic of these conditions can be recorded on an ECG at the onset of the disease.

ECG fragment with ST segment elevation, coronary T

During ischemia, the structure and shape of the T wave and the position of the RS-T segment change on the cardiogram. The process of restoring the original potential in the cells of the ventricles when their nutrition is disrupted proceeds more slowly. In this regard, the T wave becomes taller and wider. It is called "coronary T". It is possible to register a negative T wave in the chest leads, depending on the depth and location of the lesion in the heart muscle.

A prolonged absence of blood flow in the myocardium leads to ischemic damage. On the ECG this is reflected in the form of a displacement of the RS -T segment, which is normally located on the isoline. With different localizations and volumes of the pathological process, it will either rise or fall.

Heart muscle infarction develops in the walls of the ventricles. If necrosis affects a large area of the myocardium, they speak of a large-focal lesion. If there are many small foci - small focal. Deterioration in performance when interpreting the cardiogram will be detected in leads whose positive electrode is located above the site of cell death. In opposite leads, mirror-reciprocal changes are often recorded.

Large focal infarction

The dead area of the myocardium does not contract. In the leads recorded above the area of necrosis, changes in the QRS complex are detected - an increase in the Q wave and a decrease in the R wave. Depending on the location of the lesion, they will be recorded in different leads.

A large-focal process can cover the entire thickness of the myocardium or its part located under the epicardium or endocardium. Total damage is called transmural. Its main sign is the appearance of the QS complex and the absence of the R wave. With partial necrosis of the muscle wall, pathological Q and low R are detected. The duration of Q exceeds 0.03 seconds, and its amplitude becomes more than 1/4 of the R wave.

During a heart attack, three pathological processes are observed at once, which exist simultaneously - ischemia, ischemic damage and necrosis. Over time, the infarction zone expands due to the death of cells that were in a state of ischemic damage. When blood flow is restored, the ischemic area decreases.

The changes recorded on the ECG film depend on the time of development of the infarction. Stages:

1. Acute - the period from several hours to two weeks after a heart attack.
2. Subacute - a period of up to 1.5–2 months from the onset of the disease.
3. Cicatricial - stage during which damaged muscle tissue is replaced by connective tissue.

Acute stage

Changes in the ECG during a heart attack by stage

15–30 minutes after the onset of a heart attack, a zone of subendocardial ischemia is detected in the myocardium - a disturbance in the blood supply to the muscle fibers located under the endocardium. High coronary T waves appear on the ECG. The RS-T segment shifts below the isoline. These initial manifestations of the disease are rarely recorded; as a rule, patients do not yet seek medical help.

A few hours later, the damage reaches the epicardium, the RS-T segment moves upward from the isoline and merges with the T, forming a flat curve. Further, in the sections located under the endocardium, a focus of necrosis appears, which quickly increases in size. A pathological Q begins to form. As the infarction zone expands, the Q deepens and lengthens, the RS-T drops to the isoline, and the T wave becomes negative.

Subacute stage

The area of necrosis is stabilized, the area of ischemic damage is reduced due to the death of some cells and the restoration of blood flow in others. The cardiogram shows signs of infarction and ischemia - pathological Q or QS, negative T. RS-T is located on the isoline. Gradually, the ischemic zone decreases and the amplitude of T decreases, it smoothes out or becomes positive.

Scar stage

The connective tissue that replaced the dead muscle tissue does not participate in excitation. Electrodes located above the scar record the Q wave or QS complex. In this form, the ECG is stored for many years or the entire life of the patient. RS-T is on the isoline, T is smoothed or weakly positive. Negative T waves are also often observed over the replaced area.

Small focal infarction

Signs of infarction at different depths of myocardial damage

Small areas of damage in the heart muscle do not disrupt the excitation process. Pathological Q and QS complexes will not be detected on the cardiogram.

In small-focal infarction, changes on the ECG film are caused by ischemia and ischemic damage to the myocardium. A decrease or increase in the RS-T segment is detected, negative T waves are recorded in the leads located next to the necrosis. Biphasic T waves with a pronounced negative component are often recorded. With the death of muscle cells located in the posterior wall, only reciprocal changes are possible - coronary T in V1-V3. Leads V7-V9, onto which this area is projected, are not included in the diagnostic standard.

Widespread necrosis of the anterior part of the left ventricle is evident in all chest leads, I and aVL. Reciprocal changes - a decrease in RS-T and a high positive T, are recorded in aVF and III.

The upper sections of the anterior and lateral walls are outside the recorded leads. In this case, the diagnosis is difficult; signs of the disease are found in I and aVL or only in aVL.

Damage to the back wall

Posterior phrenic, or infarction of the inferior wall of the left ventricle, is diagnosed by leads III, aVF and II. Reciprocal signs are possible in I, aVL, V1-V3.

Posterobasal necrosis is less common. Ischemic changes are recorded when additional electrodes V7-V9 are applied from the back. An assumption about a heart attack of this localization can be made in the presence of mirror manifestations in V1-V3 - high T, increased amplitude of the R wave.

Damage to the posterolateral portion of the ventricle is seen in leads V5, V6, II, III, and aVF. In V1-V3 reciprocal signs are possible. In a widespread process, changes affect III, aVF, II, V5, V6, V7 -V9.

Index	1997	1998	1999
Number of calls to patients with MI
Uncomplicated	16255	16156	16172
Complicated	7375	7383	7318
Total	23630	23539	23490
% of the total number of patients with cardiovascular diseases
Hospitalized patients
Uncomplicated MI	11853	12728	11855
Complicated MI	3516	1593	3623
Total	15369	16321	15478
% of hospitalized patients to the number of calls
Uncomplicated MI	79,9	78,8	73,3
Complicated MI	47,6	48,7	49,5
Total	65,0	69,3	65,9