Zones of myocardial infarction by ecg. Pathological changes on the ECG in myocardial infarction. How to recognize the exact site of necrosis

In this publication, I would like to talk about such a necessary and effective diagnostic method as ECG in myocardial infarction. After reading the information provided, everyone will be able to determine the heart attack on the ECG, as well as its stage, the degree of damage.

Many, faced with this kind of disease, increasingly understand that myocardial infarction is one of the terrible and popular pathologies of the heart, the consequences of which can lead to great health troubles in general, not excluding death.

During the onset of symptoms, many, having read information from many sources, often confuse the symptoms of a heart attack with angina pectoris. In order not to make self-made mistakes, you should go to the hospital at the first symptoms, where specialists can determine the exact condition of the heart using an ECG.

What is a heart attack and its types

Myocardial infarction is one of the clinical types of coronary artery disease, which occurs with the formation of ischemic necrosis of a myocardial area, subsequently leading to an absolute or relative insufficiency of its blood supply.

Important! ECG during a heart attack is one of the main types of diagnosis and identification of signs of the disease. At the first symptoms of myocardial infarction, you should immediately contact a cardiologist for an ECG test - a test in the first 60-120 minutes, which are very important!

The main reasons for visiting a doctor are:

• shortness of breath
• Pain syndromes behind the sternum,
• Malaise,
• Frequent pulse when listening, as well as unstable rhythms of the heart,
• Feeling of fear, with a strong sweating.

Should know! Myocardial infarction is the first sign of development against the background of arterial hypertension, a strong decrease or increase in glucose, as well as against the background of atherosclerosis, smoking, excess weight or a sedentary lifestyle.

The following factors provoke a heart attack:

• Frequent anxiety, depression, stress, anxiety,
• Work related to physical activity or sports activities (weightlifters),
• surgical interventions,
• Frequent changes in atmospheric pressure.

To ensure your health and your life, at the first signs, you should undergo a diagnosis. With the help of an ECG during the formation of a heart attack, the specialist will use special electrodes that are connected to the cardiogram machine, after which certain kinds of signals from the heart muscle will occur. To conduct a conventional ECG, 6 sensors should be used, in the case when it comes to determining a heart attack from an ECG, as many as 12.

Types of MI

Pathology of MI is possible in most forms, but an ECG in the study of this organ can reveal only the following:

• Transmural infarction (has indicators of macrofocal necrosis of the walls of the left ventricle of the heart, which can reach up to 55-70% of the lesion),
• Subendocardial (in 90% of cases it is extensive, ECG often shows blurred edges of the affected area of ​​the myocardium, which makes it difficult for the sonographer to see this problem),
• Intramural (considered one of the small-focal types of pathologies).

According to the identified symptoms, the following forms of MI can be distinguished:

• Anginal - one of the most common types of heart attack. It manifests itself as severe pain behind the chest, which often radiates to the left upper body (face, arm, hypochondrium). The patient feels unwell, lethargy, a sharp deterioration in general condition, sweating.
• Asthmatic - manifests itself as shortness of breath, lack of oxygen for inspiration. With these symptoms in adults and the elderly, this suggests that MI has already been experienced,
• Gastralgic - an unpleasant localization of pain in the upper abdomen. There may also be an unpleasant feeling of tightness in the shoulder blades, back. All this causes hiccups, a feeling of nausea, "bloating" of the abdomen, pain in some areas of the intestine.
• Cerebrovascular - manifests itself as dizziness, severe pain in the temples and the back of the head, nausea, vomiting. This type of diagnosis can only be determined by an ECG.
• Arrhythmic - a constant feeling that the pulse disappears, or is temporarily absent. There may be a fainting state, a severe headache, a sharp decrease in blood pressure.
• Asymptomatic - the localization of a heart attack lies in a sharp weakness and shortness of breath.

It should be remembered! For better recognition of these symptoms, an ECG should be taken immediately.

ECG in the study of myocardial infarction

ECG is an integral part in recognizing one or another symptom of MI, and its diagnostic method is simple and explains a lot, both for cardiologists and doctors. Thanks to the latest technologies, everyone has a chance to quickly and effectively diagnose the heart and identify pathologies of a heart attack, both at home and in specially designated institutions.

Any ECG performed is a direct proof of the existence of a particular disease in humans for doctors. MI is easily confused with pancreatitis, cholecystitis, so an electrocardiogram should be performed immediately.

Although the following fact should be noted - in almost 8-9% of this diagnosis, there may be incorrect data. Therefore, in order to more accurately identify a particular pathology, an ECG should be performed several times, as well as decoding.

Overview of infarct on ECG

Conducting an ECG with the development of an acute violation of blood flow in the myocardium is the very integral part of the study of the organ. The interpretation of diagnosis increases several times during the first few hours of the formation of MI, because it is at this time that the symptoms of this disease begin to manifest themselves.

On the film at the first stages of the development of the disease, one can observe only the initial disturbances in the blood supply, and then only if these disturbances were revealed during the production of the electrocardiogram. In the photo, this is expressed as changes in the S-T segment.

Let's present you visual indicators of changes in ECG waves:

This kind of deviation on the electrocardiogram is associated with 3 factors occurring in the infarction area, thereby subdividing into certain zones:

• Tissue necrosis - but only with the development of a Q-infarction,
• Violation of the integrity of cells, which subsequently threatens with necrosis,
• Insufficient amount of blood flow, which is quite recoverable.

There are certain signs that the description of the ECG revealed the development of MI:

• The R wave (zR) is small or completely absent,
• Q wave (zQ) deep,
• T wave (zT) negative,
• the S-T segment is lower than the isoline.

Temporary stages of development of a heart attack on a cardiogram

Name Time interval Signs according to ECGO The most acute stage From the first hours of development to three days, the S-T segment is much higher than the isoline, due to this location, it is difficult to see the T wave. completion of this stage

T wave negative

Scars on the heart From 3-4 days to 80-90 days Slow increase in the T wave to the isoline, and the Q wave slowly declines

Table of stages of IM formation

ECG signs depending on the size of the focus

Type of infarction Subtypes Signs of ECG Q-infarction Transmural (circular) - the lesion occurs throughout the heart wall No zR

zQ - deep

segment S - T is much higher than the isoline, merging with zT

during subacute type of infarction - ST negative

Subepicardial - the lesion occurs near the outer shell R wave - rather enlarged,

ST during this period becomes negative, being in the subacute stage

Intramural - the lesion occurs inside the cardiac muscle layer Pathologies do not occur in the R, Q waves

S-T segment without visible changes

ST negative

Subendocardial - a lesion near the inner sheath of the muscle Pathologies do not occur in the R, Q and T waves

segment S - T is below the isoline by at least 0.02 mV

ECG changes during different MI positions

In order to accurately establish the diagnosis, the specialist must use all twelve electrodes for the ECG. Imagine this as a photo:

And depending on the position of the lesion, the disease on the film is displayed in different ways. Consider the types of heart attacks.

Anterior septal Q infarction

Leads Signs of pathologies Standard. I, II and from the left hand from Q - deep

segment S - T slowly rises above the isoline

ZT - positive, while becoming close to the segment

Standard. III and from the right leg, the S-T segment slowly decreases above the zT isoline during this period becomes negative Thoracic I-III (during the transition to the top, IX chest) Without zR, and instead of it there is a QS segment S-T to be at least 1 above the isoline, 8-2.8 mm From the right hand and chest (IX-VI) ST - flat segment S - T is in the lower part of the isoline at least 0.02 mV is displaced

Lateral MI

Lead is the standard. III from the left arm, right leg and chest V-VI

Signs of pathologies - zQ - deep, extended, segment S - T slowly rises above the isoline.

Anterior-posterior Q-infarction

Lead is the standard. III from the left hand, right leg and chest III - VI

Signs of pathologies - zQ - deep, extended, the S-T segment rises significantly above the isoline, while zT is positive, merging with the segment.

Posterior diaphragmatic

AbductionSigns of pathologiesStandard. II, III from the right leg Q - deep, wide

segment S - T is much higher than the isoline, merging with zT (positive)

Standard I segment S - T slowly decreases above the isoline Thoracic I-VI (but not always) segment S - T is below the isoline, while zT is deformed to a negative value

Q-infarction anterior subendocardial

AbductionSigns of pathologiesStandard. I, and from the left hand, chest I-IVzT is positive, located below the R wave Standard. II-III segment S - T slowly decreases above the isoline, sT is negative Thoracic V-VIsT is 50% positive, and the remaining 50% are slightly below the isoline

Posterior subendocardial non-Q infarction

Lead standard. II, III, from the right leg, chest V-VI.

Signs of pathologies - s R - reduced, sT - positive, then there is a slight decrease in the segment, without a Q wave.

Difficulties in conducting an ECG

The location of the teeth and gaps can provoke the following factors:

• if the patient is overweight, the electrical position of the heart can be changed,
• scars on the heart with a previously transferred MI do not reveal new changes,
• it is almost impossible to identify IHD with conduction disorders in the form of a blockade along the left leg of the His bundle,
• A "frozen" ECG with aneurysm will not reveal new changes in the work of the heart.

With the help of an ECG, there is a chance to determine the localization of ischemia. Let's give you a table:

On the ECG, it manifests itself depending on the stage of development. This procedure is always carried out to determine the location and size of the focus of necrosis. This is a reliable study, the decoding of which helps to notice any pathological changes in the heart.

What is an EKG

An electrocardiogram is a diagnostic technique that captures malfunctions in the functioning of the heart. The procedure is performed using an electrocardiograph. The device provides an image in the form of a curve, which indicates the passage of electrical impulses.

This is a safe diagnostic technique, approved for use during pregnancy and in childhood.

With the help of a cardiogram determine:

• what is the state of the structure that promotes myocardial contraction;
• heart rate and rhythm;
• the work of pathways;
• evaluate the quality of supply of the heart muscle through the coronary vessels;
• reveal the presence of scars;
• heart pathology.

For more accurate information about the state of the organ, 24-hour monitoring, exercise ECG, and transesophageal ECG can be used. Thanks to these procedures, it is possible to detect the development of pathological processes in a timely manner.

With myocardial infarction, 3 zones are distinguished, each of which has its own ECG characteristic: 1) the necrosis zone, located in the center, is characterized by a change in the QRS complex (primarily an increase or the appearance of a pathological Q wave). 2) the zone of damage located around the zone of necrosis is characterized by a shift of the S-T segment. 3) the zone of ischemia, which is even further to the periphery around the zone of damage, is characterized by a change (inversion) of the T wave. influence each other, because of which there can be a rather diverse range of changes.

ECG changes in myocardial infarction depend on its form, location and stage.

According to electrocardiographic signs, first of all, it is necessary to distinguish between transmural and subendocardial myocardial infarctions.

Myocardial necrosis is usually manifested on the ECG by changes in the QRS complex. The formation of a necrotic focus in the myocardium leads to the cessation of the electrical activity of the affected area, which causes the deviation of the total QRS vector in the opposite direction. As a result, in leads with a positive pole above the necrotic zone, a pathologically deep and wide Q wave and a decrease in the amplitude of the R wave are detected, which is typical for subendocardial large-focal infarcts. The deeper the necrosis, the more pronounced these changes.

In transmural myocardial infarction, a QS complex is recorded on the ECG in leads from the epicardial side. Above the island of intact myocardium, surrounded by necrotic process, there is an upward notch on the QS wave. Subepicardial necrosis may be manifested only by a decrease in R wave amplitude without the formation of an abnormal Q wave. Finally, intramural infarction may not cause changes in the QRS complex at all. The ECG of a patient with myocardial infarction undergoes changes depending on the stage of the disease.

There are 4 main types of localization of myocardial infarction:

anterior - changes are recorded in leads V1-4;

lower (posterior diaphragmatic) - with direct changes in leads

lateral - with direct changes in leads I, AVL, V5-6;

posterior basal - in which there are no direct changes in the 12 generally accepted ECG leads, and reciprocal changes are recorded in leads V1-2 (high, narrow R wave, ST segment depression, sometimes high, pointed T wave). Direct changes can only be detected in accessory leads D, V7-9.

with right ventricular infarction, direct changes (ST segment elevation) are recorded only in additional (right chest) leads

Acute stage of infarction (stage of ischemia and damage ) has an approximate duration of up to several hours. It is manifested by the appearance of initially ischemia (usually subendocardial) with a transition to damage, accompanied by a rise in the ST segment, up to merging with the T wave (monophasic curve). Necrosis and its corresponding Q wave may or may not be present. If the Q wave is formed, then the height of the R wave in this lead decreases, often up to complete disappearance (QS complex in transmural infarction). home ECG feature the most acute stage of myocardial infarction - the formation of the so-called monophasic curve . The monophasic waveform consists of ST-segment elevation and a high upright T wave that merge into one.

In the acute stage, which lasts from 2 to 10 days, the damage zone is partially transformed into a necrosis zone (a deep Q wave appears, up to the QT complex), partially, along the periphery - into an ischemia zone (a negative T wave appears). The gradual decline of the ST segment to the isoline occurs in parallel with the deepening of the negative T waves.

An important feature of the most acute, acute and subacute stages of infarction

in relation to the QRS complex and the T wave.

Subacute stage lasts from 1 to 2 months. The damage zone disappears due to the transition to the ischemic zone (therefore, the ST segment closely

half of the subacute stage due to the expansion of the ischemic zone, the negative T wave broadens and increases in amplitude up to a giant one. In the second half, the ischemia zone gradually disappears, which is accompanied by the normalization of the T wave (its amplitude decreases, it tends to become positive). The dynamics of changes in the T wave is especially noticeable on the periphery of the ischemic zone.

If ST-segment elevation has not returned to normal after 3 weeks from the moment of infarction, it is necessary to exclude the formation of an aneurysm of the heart.

The cicatricial stage is characterized by the stability of the ECG signs that persisted by the end of the subacute period. The most constant manifestations are a pathological Q wave and a reduced R wave.

Task #1

Acute anterior, apices, with transition to the side wall Q-myocardial infarction

Task #2

Acute anterior-septal, apices with transition to the side wall Q-myocardial infarction

Task #3

Acute anterior with transition to the apex and side wall Q-myocardial infarction

Task #4

Acute anterior, apical and lateral wall myocardial infarction of the left ventricle

Task #5

Acute stage of anterior advanced myocardial infarction

Task #6

Acute stage of Q-myocardial infarction with ST segment elevation of the anterior septal and lateral wall of the left ventricle

Task #7

Acute stage of Q-myocardial infarction with ST segment elevation of the anterior septal and lateral walls of the left ventricle.

Task #8

Acute stage of Q-myocardial infarction with elevation of the ST segment of the anterior wall of the left ventricle.

Task #9

Acute stage of Q-myocardial infarction with ST segment elevation of the anterior septal, apex and lateral walls of the left ventricle

Task #10

Subendocardial ischemia of the anterior septal, apex and lateral walls of the left ventricle

Task #11

Acute stage of myocardial infarction with ST segment elevation of the anterior septal, apex and lateral wall of the left ventricle

Task #12

a b c Dynamics of ECG changes in Q-myocardial infarction of the anterior wall

a) 1 hour from the onset of myocardial infarction, b) 24 hours from the onset of myocardial infarction, c) 10 days from the onset of myocardial infarction

Task #13

Anterior, apex and lateral wall myocardial infarction, acute stage

Task #14

Without Q myocardial infarction (intramural) of the anterior-lateral wall

Task #15

Acute inferior Q-myocardial infarction of the left ventricle

Task #16

Acute stage of myocardial infarction with ST segment elevation of the inferior wall of the left ventricle

Task #17

sinus bradycardia.

Task #18

Acute stage of myocardial infarction with ST segment elevation of the inferior wall

Task #19

Acute stage of Q-myocardial infarction with ST-segment elevation of the inferior wall of the left ventricle.

Task #20

Acute stage of Q-myocardial infarction with ST-segment elevation of the inferior wall of the left ventricle.

Task #21

Acute inferior myocardial infarction

Task #22

Lower myocardial infarction, acute stage

Task #23

a b c Dynamics of ECG changes in Q-myocardial infarction of the lower wall

a) 1 hour from the onset of myocardial infarction, b) 24 hours from the onset of myocardial infarction, c) 3 weeks from the onset of myocardial infarction

heart attack(lat. infarcio - stuffing) - necrosis (necrosis) of the tissue due to the cessation of blood supply.

The reasons for stopping blood flow can be different - from blockage (thrombosis, thromboembolism) to a sharp vasospasm.

A heart attack may occur in any organ, for example, there is a cerebral infarction (stroke) or a kidney infarction.

In everyday life, the word "heart attack" means exactly " myocardial infarction”, i.e. death of the muscle tissue of the heart.

In general, all heart attacks are divided into ischemic(more often) and hemorrhagic.

With an ischemic infarction, the flow of blood through the artery stops due to some kind of obstacle, and with a hemorrhagic infarction, the artery bursts (ruptures) with the subsequent release of blood into the surrounding tissues.

Myocardial infarction affects the heart muscle not randomly, but in certain places.

The fact is that the heart receives arterial blood from the aorta through several coronary (coronary) arteries and their branches. If using coronary angiography to find out at what level and in which vessel the blood flow stopped, it is possible to foresee which part of the myocardium suffers from ischemia(lack of oxygen). And vice versa.

Myocardial infarction occurs when
blood flow through one or more arteries of the heart.

We remember that the heart has2 ventricles and 2 atria, therefore, logically, all of them should be affected by a heart attack with the same probability.

Nonetheless, It is always the left ventricle that suffers from a heart attack. , because its wall is the thickest, is subjected to enormous loads and requires a large blood supply.

Cross section of the chambers of the heart.
The walls of the left ventricle are much thicker than the right.

Isolated atrial and right ventricular infarctions- a huge rarity. Most often, they are affected simultaneously with the left ventricle, when ischemia passes from the left ventricle to the right or to the atria.

According to pathologists, the spread of infarction from the left ventricle to the right is observed in 10-40% all patients with a heart attack (the transition usually occurs along the back wall of the heart). Transition to the atria occurs in 1-17% cases.

Stages of myocardial necrosis on the ECG

Between healthy and dead (necrotic) myocardium in electrocardiography, intermediate stages: ischemia and injury.

Type of ECG is normal.

Thus, the stages of myocardial damage in a heart attack are as follows:

1) ISCHEMIA: is the initial myocardial injury in whichthere are no microscopic changes in the heart muscle yet, and the function is already partially impaired.

As you should remember from the first part of the cycle, two opposite processes sequentially occur on the cell membranes of nerve and muscle cells: depolarization(excitement) and repolarization(recovery of the potential difference).

Depolarization is a simple process, for which it is only necessary to open ion channels in the cell membrane, through which ions will run due to the difference in concentrations outside and inside the cell.

Unlike depolarization, repolarization is an energy intensive process which requires energy in the form of ATP.

ATP synthesis requires oxygen, therefore, with myocardial ischemia, the process of repolarization begins to suffer first of all. Impaired repolarization is manifested by changes in the T wave.

Options for changes in the T wave during ischemia:

a is the norm

b - negative symmetrical "coronary" T wave (occurs with a heart attack)
in - high positive symmetrical "coronary" T wave (with a heart attack and a number of other pathologies, see below),
d, e - biphasic T wave,
e - reduced T wave (amplitude less than 1/10-1/8 R wave),
g - smoothed T wave,
h - slightly negative T wave.

With myocardial ischemia, the QRS complex and ST segments are normal, and the T wave is changed: it is expanded, symmetrical, equilateral, increased in amplitude (range) and has a pointed apex.

In this case, the T wave can be both positive and negative - this depends on the location of the ischemic focus in the thickness of the heart wall, as well as on the direction of the selected ECG lead.

Ischemia - reversible phenomenon, over time, metabolism (metabolism) is restored to normal or continues to deteriorate with the transition to the stage of damage.

2) DAMAGE: this is deeper damagemyocardium, in whichdetermined under a microscopean increase in the number of vacuoles, swelling and degeneration of muscle fibers, disruption of the structure of membranes, mitochondrial function, acidosis (acidification of the environment), etc. Both depolarization and repolarization suffer. The damage is thought to primarily affect the ST segment.

The ST segment may move above or below the isoline , but its arc (this is important!) when damaged bulges in the direction of displacement.

Thus, in case of myocardial injury, the ST segment arc is directed towards displacement, which distinguishes it from many other conditions in which the arc is directed towards the isoline (ventricular hypertrophy, blockade of the bundle pedicles, etc.).

Options for displacement of the ST segment in case of damage.

T wave when damaged, it can be of different shapes and sizes, which depends on the severity of concomitant ischemia. Damage also cannot exist for a long time and passes into ischemia or necrosis.

3) NECROSIS: myocardial death. The dead myocardium is unable to depolarize, so the dead cells cannot form an R wave in the ventricular QRS complex. For this reason, whentransmural infarction(myocardial death in a certain area across the entire thickness of the heart wall) in this ECG lead of the waveno R at all., and is formed ventricular complex type QS. If necrosis has affected only part of the myocardial wall, a complex of the typeQRS, in which the R wave is reduced, and the Q wave is increased compared to the norm.

Variants of the ventricular QRS complex.

Normal teeth. Q and R must obey a set of rules , for example:

• the Q wave should always be present in V4-V6.
• the width of the Q wave should not exceed 0.03 s, and its amplitude should NOT exceed 1/4 of the amplitude of the R wave in this lead.
• prong R should increase in amplitude from V1 to V4(i.e., in each subsequent lead from V1 to V4, the R wave should howl higher than in the previous one).
• in V1, the normal r wave may be absent, then the ventricular complex looks like QS. In people under 30 years of age, the QS complex may occasionally be in V1-V2, and in children even in V1-V3, although this is always suspicious for anterior ventricular septal infarction.

What does an ECG look like depending on the zone of infarction

So, to put it simply, necrosis affects the Q wave and the entire ventricular QRS complex. Damage reflects on ST segment. Ischemia affects T wave.

The formation of teeth on the ECG is normal.

Along the wall of the heart are the positive ends of the electrodes (from No. 1 to 7).

To facilitate perception, I drew conditional lines, which clearly show the ECG from which zones is recorded in each of the indicated leads:

Schematic view of the ECG depending on the zone of infarction.

• Lead #1: located above the transmural infarct, so the ventricular complex appears as a QS.
• #2: non-transmural infarction (QR) and transmural injury (ST elevation with upward bulge).
• #3: transmural injury (ST elevation with upward convexity).
• No. 4: here in the original drawing it is not very clear, but in the explanation it is indicated that the electrode is above the zone of transmural damage (ST elevation) and transmural ischemia (negative symmetrical "coronary" T wave).
• No. 5: over the zone of transmural ischemia (negative symmetrical "coronary" T wave).
• No. 6: the periphery of the ischemic zone (biphasic T wave, i.e. in the form of a wave. The first phase of the T wave can be either positive or negative. The second phase is the opposite of the first).
• No. 7: away from the ischemic zone (lowered or flattened T wave).

Here's another picture for you to parse

Another diagram of the dependence of the type of ECG changes on the zones of infarction.

Stages of development of a heart attack on the ECG

The meaning of the stages of development of a heart attack is very simple.

When blood supply is completely cut off in any part of the myocardium, then in the center of this area, muscle cells die quickly (within several tens of minutes). At the periphery of the focus, cells do not die immediately. Many cells gradually manage to “recover”, the rest die irreversibly (remember, as I wrote above, that the phases of ischemia and damage cannot exist for too long?).

All these processes are reflected in the stages of development of myocardial infarction.

There are four of them:

acute, acute, subacute, cicatricial.

1) The most acute stage of a heart attack (damage stage) has an approximate duration from 3 hours to 3 days.

Necrosis and its corresponding Q wave may or may not be present. If the Q wave is formed, then the height of the R wave in this lead decreases, often up to complete disappearance (QS complex in transmural infarction).

The main ECG feature of the most acute stage of myocardial infarction is the formation of the so-called monophasic curve. The monophasic curve consists of ST segment elevation and high upright T wave that merge together.

Shift of the ST segment above the isoline by 4 mm and above in at least one of the 12 conventional leads indicates the severity of heart damage.

Note. The most attentive visitors will say that myocardial infarction cannot begin precisely with stages of damage, because between the norm and the damage phase there should be the above-described ischemic phase! Right. But the ischemic phase lasts only 15-30 minutes, so the ambulance usually does not have time to register it on the ECG. However, if this succeeds, the ECG shows tall positive symmetrical "coronary" T waves, characteristic for subendocardial ischemia. It is under the endocardium that the most vulnerable part of the myocardium of the heart wall is located, since there is increased pressure in the cavity of the heart, which interferes with the blood supply to the myocardium (“squeezes out” the blood from the heart arteries back).

2) Acute stage lasts up to 2-3 weeks(to make it easier to remember - up to 3 weeks).

Areas of ischemia and damage begin to decrease.

The area of ​​necrosis is expanding the Q wave also expands and increases in amplitude.

If the Q wave does not appear in the acute stage, it forms in the acute stage (however, there are infarcts and without Q wave, about them below). ST segment due to damage zone limitation begins to gradually approach the isoline, a T wave becomes negative symmetrical "coronary" due to the formation of a zone of transmural ischemia around the area of ​​damage.

3) Subacute stage lasts up to 3 months, occasionally longer.

The damage zone disappears due to the transition to the ischemia zone (therefore, the ST segment comes close to the isoline), the area of ​​necrosis stabilizes(so about the true size of the infarct are judged at this stage).

In the first half of the subacute stage, due to the expansion of the ischemic zone, negative the T wave broadens and grows in amplitude up to gigantic.

In the second half, the ischemia zone gradually disappears, which is accompanied by the normalization of the T wave (its amplitude decreases, it tends to become positive).

The dynamics of changes in the T wave is especially noticeable on the periphery ischemic zones.

If ST segment elevation does not return to normal 3 weeks after infarction, it is recommended to do echocardiography (EchoCG) to exclude heart aneurysms(saccular expansion of the wall with slow blood flow).

4) Cicatricial stage myocardial infarction.

This is the final stage, in which a strong tissue is formed at the site of necrosis. connective tissue scar. It is not excited and does not contract, therefore it appears on the ECG in the form of a Q wave. Since the scar, like any scar, remains for the rest of life, the cicatricial stage of a heart attack lasts until the last contraction of the heart.

Stages of myocardial infarction.

What kind ECG changes are in the cicatricial stage? The scar area (and hence the Q wave) may to some extent decrease due to:

1. contractions ( seals) scar tissue, which brings together intact areas of the myocardium;
2. compensatory hypertrophy(increase) adjacent areas of healthy myocardium.

There are no zones of damage and ischemia in the cicatricial stage, so the ST segment is on the isoline, and the T wave can be up, down, or flattened.

However, in some cases, in the cicatricial stage, it is still recorded small negative T wave, which is associated with constant irritation of adjacent healthy myocardium by scar tissue. In such cases, the T wave in amplitude should not exceed 5 mm and should not be longer than half of the Q or R wave in the same lead.

To make it easier to remember, the duration of all stages obeys the rule of three and increases incrementally:

• up to 30 minutes (ischemia phase),
• up to 3 days (acute stage),
• up to 3 weeks (acute stage),
• up to 3 months (subacute stage),
• the rest of life (cicatricial stage).

In general, there are other classifications of stages of a heart attack.

Differential diagnosis of a heart attack on an ECG

All reactions of the body to the same effect in different tissues at the microscopic level proceed the same type.

Sets of these complex sequential reactions are called typical pathological processes.

Here are the main ones: inflammation, fever, hypoxia, tumor growth, dystrophy etc.

With any necrosis, inflammation develops, which results in the formation of connective tissue.

As I stated above, the word heart attack came from lat. infarcio - stuffing, which is due to the development of inflammation, edema, migration of blood cells into the affected organ and, consequently, its seal.

At the microscopic level, inflammation occurs in the same way anywhere in the body.

For this reason infarct-like ECG changes there are also with heart injuries and tumors of the heart(metastases in the heart).

Not every “suspicious” T wave, deviated ST segment, or sudden Q wave is caused by a heart attack.

Normal amplitude T wave is from 1/10 to 1/8 of the amplitude of the R wave.

A high positive symmetrical "coronary" T wave occurs not only with ischemia, but also with hyperkalemia, increased vagal tone, pericarditis etc.

ECG for hyperkalemia(A - normal, B-E - with increasing hyperkalemia).

T waves may also look abnormal when hormonal disorders(hyperthyroidism, climacteric myocardial dystrophy) and with changes in the complex QRS(for example, with blockades of the bundle of His bundle). And that's not all the reasons.

Features of the ST segment and T wave
in various pathological conditions.

ST segment maybe rise above the contour not only in myocardial injury or infarction, but also in:

• heart aneurysm,
• PE (pulmonary embolism),
• Prinzmetal angina,
• acute pancreatitis,
• pericarditis,
• coronary angiography,
• secondarily - with blockade of the bundle of His bundle, ventricular hypertrophy, early ventricular repolarization syndrome, etc.

ECG option for PE: McGene-White syndrome
(deep S wave in lead I, deep Q and negative T wave in lead III).

ST segment depression cause not only a heart attack or myocardial damage, but also other causes:

• myocarditis, toxic myocardial damage,
• taking cardiac glycosides, chlorpromazine,
• post tachycardia syndrome,
• hypokalemia,
• reflex causes - acute pancreatitis, cholecystitis, stomach ulcer, hiatal hernia, etc.,
• shock, severe anemia, acute respiratory failure,
• acute disorders of cerebral circulation,
• epilepsy, psychosis, tumors and inflammation in the brain,
• hunger or overeating
• carbon monoxide poisoning,
• secondarily - with blockade of the bundle of His bundle, ventricular hypertrophy, etc.

Q wave most specific for myocardial infarction, but it can also temporarily appear and disappear in the following cases:

• cerebral infarctions (especially subarachnoid hemorrhages),
• acute pancreatitis,
• coronary angiography,
• uremia (the end stage of acute and chronic renal failure),
• hyperkalemia,
• myocarditis, etc.

As I noted above, there are non-Q wave infarcts on the ECG. For example:

1. when subendocardial infarctionwhen a thin layer of myocardium near the endocardium of the left ventricle dies. Due to the rapid passage of excitation in this zonethe Q wave does not have time to form. On the ECG reduced R wave height(due to the loss of excitation of part of the myocardium) andthe ST segment descends below the isoline with a downward bulge.
2. intramural infarctionmyocardium (inside the wall) - it is located in the thickness of the myocardial wall and does not reach the endocardium or epicardium. Excitation bypasses the infarction zone on both sides, and therefore there is no Q wave. But around the zone of infarction is formedtransmural ischemia, which manifests itself on the ECG as a negative symmetrical "coronary" T wave. Thus, intramural myocardial infarction can be diagnosed by the appearancenegative symmetrical T wave.

It must also be remembered that ECG is just one of the research methods when establishing a diagnosis, although a very important method. In rare cases (with atypical localization of the necrosis zone), myocardial infarction is possible even with a normal ECG! I will dwell on this below.

How do heart attacks differ from other pathologies on an ECG?

According to 2 main features.

1) characteristic ECG dynamics.

If the ECG shows changes in the shape, size and location of the teeth and segments typical of a heart attack over time, it is possible to speak with a high degree of confidence about myocardial infarction.

In the infarction departments of hospitals EKG done daily.

To make it easier to evaluate the dynamics of a heart attack on the ECG (which is the most pronounced on the periphery of the affected area), it is recommended to apply marks for placement of chest electrodes so that subsequent hospital ECGs are completely identical in chest leads.

An important conclusion follows from this: if a patient had pathological changes in the past on a cardiogram, it is recommended to have a “control” copy of the ECG at home so that the ambulance doctor can compare a fresh ECG with an old one and draw a conclusion about the age of the detected changes. If the patient has had a previous myocardial infarction, this recommendation becomes iron rule. Each patient with a previous heart attack should receive a control ECG at discharge and keep it where he lives. Take it with you on long trips.

2) the presence of reciprocity.

Reciprocal changes are "Mirror" (relative to the isoline) ECG changes on the opposite wall left ventricle. Here it is important to consider the direction of the electrode on the ECG. The center of the heart (the middle of the interventricular septum) is taken as the “zero” of the electrode, therefore one wall of the heart cavity lies in the positive direction, and the opposite wall lies in the negative direction.

The principle is this:

• for the Q wave, the reciprocal change will be R wave enlargement, and vice versa.
• if the ST segment is displaced above the isoline, then the reciprocal change will be ST offset below the isoline, and vice versa.
• for a high positive "coronary" T wave, the reciprocal change would be negative T wave, and vice versa.

ECG in posterior diaphragmatic (lower) myocardial infarction.
Directsigns are visible in II, III and aVF leads,reciprocal- in V1-V4.

Reciprocal ECG changesin some situations are the onlyfor which a heart attack can be suspected.

For example, with posterior basal (posterior) infarctionmyocardium, direct signs of a heart attack can be recorded only in the leadD (dorsalis) by Sky[read e] and in accessory chest leads V7-V9, which are not included in the standard 12 and are performed only on demand.

Accessory chest leads V7-V9.

Concordance ECG elements - unidirectionality with respect to the isoline of the same ECG teeth in different leads (that is, the ST segment and the T wave are directed in the same direction in the same lead). Happens with pericarditis.

The opposite concept discordance(diversity). The discordance of the ST segment and the T wave with respect to the R wave is usually implied (ST deviated to one side, T to the other). It is characteristic of complete blockades of the bundle of His.

ECG at the onset of acute pericarditis:
no Q wave and reciprocal changes, characteristic
concordant ST segment and T wave changes.

It is much more difficult to determine the presence of a heart attack, if there is intraventricular conduction disorder(bundle branch block), which itself unrecognizably changes a significant part of the ECG from the ventricular QRS complex to the T wave.

Types of heart attacks

A couple of decades ago they shared transmural infarcts(ventricular complex type QS) and non-transmural macrofocal infarcts(type QR), but it soon became clear that this does not give anything in terms of prognosis and possible complications.

For this reason, heart attacks are currently simply divided into Q-heart attacks(Q-wave myocardial infarctions) and - rise, from English. elevation ; depression - decrease, from English.depression )