Heart attack on ecg - signs and decoding. Features of ECG in myocardial infarction - procedure and signs of ECG disease in infarctions of different localization

Myocardial infarction: general principles ECG diagnostics.

With a heart attack (necrosis), muscle fibers die. Necrosis, as a rule, is caused by thrombosis of the coronary arteries or their prolonged spasm, or stenosing coronary sclerosis. The zone of necrosis is not excited and does not form EMF. The necrotic area, as it were, breaks through a window into the heart, and with transmural (to the entire depth) necrosis, the intracavitary potential of the heart penetrates into the subepicardial zone.

In the vast majority of cases in humans, the arteries supplying the left ventricle are affected, and therefore heart attacks occur in the left ventricle. Right ventricular infarction occurs incomparably less frequently (less than 1% of cases).

The electrocardiogram allows not only to diagnose myocardial infarction (necrosis), but also to determine its localization, size, depth of necrosis, stage of the process and some complications.

With a sharp violation of coronary blood flow in the heart muscle, 3 processes develop sequentially: hypoxia (ischemia), damage and, finally, necrosis (heart attack). The duration of the preliminary infarction phases depends on many reasons: the degree and speed of impaired blood flow, the development of collaterals, etc., but usually they last from several tens of minutes to several hours.

The processes of ischemia and damage are described in the previous pages of the manual. The development of necrosis affects the QRS segment of the electrocardiogram.

Above the site of necrosis, the active electrode registers a pathological Q wave (QS).

Recall that healthy person in the leads reflecting the potential of the left ventricle (V5-6, I, aVL), a physiological wave of q can be recorded, reflecting the excitation vector of the septum of the heart. Physiological q wave in any leads, except aVR, should not be more than 1/4 of the R wave with which it was recorded, and longer than 0.03 s.

When transmural necrosis occurs in the heart muscle above the subepicardial projection of necrosis, the intracavitary potential of the left ventricle is recorded, which has the QS formula, i.e. represented by one large negative tooth. If, along with necrosis, there are also functioning myocardial fibers, then the ventricular complex has the formula Qr or QR. and the larger this functional layer, the higher the R wave. The Q wave in the case of necrosis has the properties of a necrosis wave: more than 1/4 of the R wave in amplitude and longer than 0.03 s.

An exception is lead aVR, in which the intracavitary potential is normally recorded, and therefore the ECG in this lead has the formula QS, Qr or rS.

Another rule of thumb is that bifurcated or serrated Q waves are most often pathological and reflect necrosis (myocardial infarction).

Look at the animations of the formation of an electrocardiogram at three sequential processes: ischemia, damage and necrosis

Ischemia:

Damage:

Necrosis:

So, the main question of diagnosing myocardial necrosis (infarction) was answered: with transmural necrosis, the electrocardiogram in the leads that are above the necrosis zone has the formula of the gastric complex QS; with nontransmural necrosis, the ventricular complex looks like Qr or QR.

Another important regularity is characteristic of a heart attack: in the leads located in the zone opposite to the necrosis focus, mirror (reciprocal, discardant) changes are recorded - the Q wave corresponds to the R wave, and the r (R) wave is the s (S) wave. If the ST segment is raised with an arc upward above the infarction zone, then in opposite areas it is lowered downward in an arc (see figure).

Localization of myocardial infarction.

An electrocardiogram allows you to distinguish between infarction of the posterior wall of the left ventricle, septum, anterior wall, lateral wall, basal wall of the left ventricle.

Below is a table of diagnostics of different localization of myocardial infarction in 12 leads, which are included in the standard of electrocardiographic research.

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Myocardial infarction

Various ECG leads in topical diagnosis focal changes myocardium. At all stages of ECG development, starting with the use of three classical (standard) leads by V. Eynthoven (1903), the researchers sought to give practical doctors a simple, accurate and most informative method for recording biopotentials. hearty muscles. The constant search for new optimal methods for recording an electrocardiogram has led to a significant increase in leads, the number of which continues to increase.

The basis for recording standard ECG leads is the Eynthoven triangle, the angles of which form three limbs: the right and left arms and the left leg. Each side of the triangle forms a lead axis. The first lead (I) is formed due to the potential difference between the electrodes applied to the right and left hands, the second (II) —between the electrodes of the right arm and left leg, the third (III) —between the electrodes of the left arm and left leg.

Using standard leads, you can detect focal changes in both the anterior (I lead) and the posterior wall (III lead) of the left ventricle of the heart. However, as further studies have shown, standard leads in some cases, even gross changes in the myocardium are not detected at all, or changes in the lead schedule lead to an erroneous diagnosis of focal changes. In particular, changes in the basal-lateral parts of the left ventricle are not always reflected in lead I, basal-posterior - in lead III.

A deep Q wave and a negative T wave in lead III may be normal, however, on inspiration, these changes disappear or decrease, are absent in such additional leads as avF, avL, D and Y. A negative T wave can be an expression of hypertrophy and overload. in this connection, the conclusion is given on the totality of changes found in various leads of the electrocardiogram.

Since the recorded electrical potential increases as the electrodes approach the heart, and the shape of the electrocardiogram is largely determined by the electrode located on the chest, soon they began to use the standard ones.

The principle of registration of these leads is that the trim (main, recording) electrode is located in the thoracic positions, and the indifferent one - on one of the three limbs (on the right or left arm, or left leg). Depending on the location of the indifferent electrode, a distinction is made between chest leads CR, CL, CF (C - chest - chest; R - right - right; L - link - left; F - foot - leg).

Especially long time v practical medicine used CR-leads. In this case, one electrode was placed on the right hand (indifferent), and the other (trim, recording) in the chest area in positions from 1 to 6 or even up to 9 (CR 1-9). V 1st position a trim electrode was applied to the area of ​​the fourth intercostal space along the right edge of the sternum; in the 2nd position - on the fourth intercostal space along the left edge of the sternum; in the 3rd position - in the middle of the line connecting the 2nd and 4th positions; in the 4th position - on the fifth intercostal space along the mid-clavicular line; in the 5th, 6th and 7th positions - along the anterior, middle and posterior axillary lines at the level of the 4th position, in the 8th and 9th positions - along the mid-scapular and paravertebral lines at the level of the 4th position ... These positions, as will be seen below, have been preserved at the present time and are used for recording ECG according to Wilson.

However, later it was found that both the indifferent electrode itself and its location on various limbs affect the shape of the electrocardiogram.

In an effort to minimize the influence of an indifferent electrode, F. Wilson (1934) combined three electrodes from the limbs into one and connected it to a galvanometer through a 5000 Ohm resistance. The creation of such an indifferent electrode with a "zero" potential allowed F. Wilson to develop unipolar (unipolar) leads from chest and limbs. The principle of registration of these leads is that the aforementioned indifferent electrode is connected to one pole of the Galvanometer, and a trim electrode is connected to the other pole, which is applied in the above chest positions (V 1-9, where V is volt) or on the right hand (VR ), left arm (VL) and left leg (VF).

With the help of Wilsonian chest leads, it is possible to determine the localization of myocardial lesions. So, leads V 1-4 reflect changes in the anterior wall, V 1-3 - in the anteroseptal region, V 4 - in the apex, V 5 - in the anterior and partially in the side wall, V 6 - in the side wall, V 7 - in the lateral and partially in the posterior wall, V 8-9 —in the posterior wall and interventricular septum. However, leads V 8-9 are not widely used due to the inconvenience of applying electrodes and the small amplitude of the electrocardiogram teeth. They did not find practical application and abduction from the limbs according to Wilson due to the low voltage of the teeth.

In 1942, Wilson's leads from the limbs were modified by E. Golberger, who proposed using a wire from two limbs combined into one node without additional resistance as an indifferent electrode, and the free wire from the third limb is a trim electrode. With this modification, the amplitude of the teeth increased by one and a half times in comparison with the leads of the same name according to Wilson. In this regard, the Golberger leads began to be called enhanced (a - augmented) unipolar leads from the limbs. The principle of registration of leads It consists in the fact that a trim electrode is alternately applied to one of the extremities: right arm, left arm, left leg, and the wires from the other two extremities are combined into one indifferent electrode. When a trim electrode is applied to the right hand, lead aVR is recorded, on the left hand - avL and the left leg - avF. The introduction of these leads into practice has significantly expanded the possibilities of electrocardiography in the diagnosis of cardiovascular diseases. Lead avR best reflects changes in the right ventricle and atrium. Leads avL and avF are indispensable in determining the position of the heart. The avL lead is also important for diagnostics focal changes in the basal-lateral parts of the left ventricle, abduction avF - in the posterior wall, in particular in its diaphragmatic part.

Currently, it is mandatory to register an ECG in 12 leads (I, II, III, avR, avL, avF, V 1-6).

However, in some cases diagnostics focal changes in 12 conventional leads is difficult. This prompted a number of researchers to search for additional leads. So, sometimes they use the registration of chest leads in similar positions from the higher intercostal spaces. Then the leads are designated as follows: the intercostal space is indicated from above, and the position of the chest electrode (for example, V 2 2. Y 2 3 etc.), or from the right half of the chest cell V 3R —V 7R, is indicated below.

More widely used additional leads include bipolar chest leads according to Neb. The technique for recording leads proposed by him is that the electrode from the right hand is placed in the second intercostal space on the right at the edge of the sternum, the electrode from the left hand is placed along the posterior axillary line at the level of the apex projection hearts(V 7), the electrode from the left leg is at the site of the apical impulse (V 4). When the switch is installed on the I contact, lead D (dorsalis) is registered, on the II contact - A (anterior) and on the III contact I (inferior). These leads achieve not a flat, but a topographic display of the potentials of the three surfaces of the heart: posterior, anterior and inferior.

Lead D roughly corresponds to leads V 6-7 and reflects the posterior wall of the left ventricle; lead A corresponds to leads V 4-5 and reflects the anterior wall of the left ventricle; Lead I corresponds to leads U 2-3 and reflects the interventricular septum and partially the anterior left ventricular steak.

According to V. Neb, in the diagnosis of focal changes, lead D is more sensitive for the posterolateral wall than leads III, avF and V 7. and leads A and I are more sensitive than chest leads according to Wilson in the diagnosis of focal changes in the anterior wall. According to V.I.Petrovsky (1961, 1967), lead D does not respond to focal changes in the diaphragmatic region. With a negative T wave, which is found in lead III in normal and horizontal position of the heart, the presence of a positive T wave in lead D excludes pathology.

According to our data, regardless of the position hearts registration of lead D is required in the presence of a negative T wave, as well as a deep, not even widened Q wave in lead III and the absence of such changes in avF. Lead avF reflects mainly the posterior diaphragmatic parts of the left ventricle, and abscission D - posterior basal (basal-lateral). Therefore, chalk (I) changes in the basal parts of the left ventricle are reflected in lead D and may be absent in avF, and the combination of Changes in leads D and avF indicates a more widespread lesion of the posterior wall of the left ventricle.

Lead V E (E - ensiformis - septal), a thoracic lead is recorded, but when a trim electrode is installed in the area xiphoid process... Lead reflects focal changes in the septal region. It is used for fuzzy changes in leads V 1-2.

Diagnosis of limited focal changes in the basal-lateral parts of the left ventricle, when the process has not spread to the anterior and posterior walls, often becomes impossible when using 12 conventional leads. In these cases, registration deserves attention. semisagittal leads according to the Slapak a - Portilla technique... Since these leads are a modification of Neb lead D, an indifferent electrode from the left hand is placed in position V 7. and the trim electrode from the right hand moves along the line connecting two points: one is in the second intercostal space to the left of the sternum, the second is in the second intercostal space along the anterior axillary line.

ECG is recorded in the following positions:

S 1 - trim electrode in the second intercostal space to the left of the sternum;

S 4 - along the anterior axillary line at the level of S 1;

S 2 and S 3 - at an equal distance between the two extreme points (between S 1 and S 4).

The lead switch is installed on the I contact. These leads register focal changes in the basal-lateral parts of the left ventricle. Unfortunately, the timing of these leads depends to some extent on the shape of the chest and the anatomical position of the heart.

In the last two decades, orthogonal bipolar uncorrected and corrected leads have been used in practical electrocardiography.

The lead axes of the orthogonal electrocardiogram are directed in three mutually perpendicular planes: horizontal (X), frontal (G) and sagittal (Z).

Orthogonal bipolar uncorrected lead X is formed by two electrodes: a positive one (from the left hand), which is placed in position V 6. and negative (on the right hand) - to the V 6R position. Lead Z is recorded when the positive (from the left hand) electrode is in the V 2 position and the negative (from the right) electrode in the V 8R position.

Lead V is recorded when a positive electrode (on the left hand) is applied to the xiphoid process and negative (on the right hand) to the second intercostal space on the right at the sternum. Finally, lead R 0 approaches the given leads. which is registered when a positive (from the left hand) electrode is applied at position V 7. negative (on the right hand) - in position V1.

Leads are recorded in the position of the lead switch on pin I.

Lead X roughly corresponds to leads I, avL V 5-6 and reflects the anterolateral left ventricular steak. Leads V corresponds to leads III and avF and reflects the posterior wall. Lead Z corresponds to lead V 2 and reflects the interventricular septum. Lead Ro corresponds to leads V 6-7 and reflects the posterolateral wall of the left ventricle.

With large focal heart attack myocardium, regardless of its localization, in the left ventricle, the orthogonal leads always respond with the appropriate graphics, while with small focal lesions of the myocardium, especially in the basal parts of the left ventricle, changes in these leads are often absent. In such cases, the Slapak-Portilla leads and the chest leads from the higher intercostal spaces are used.

Corrected orthogonal leads are based on strict physical principles, taking into account the eccentricity and variability of the cardiac dipole, and therefore are insensitive to the individual characteristics of the chest and the anatomical position of the heart.

To register corrected orthogonal leads, various combinations of electrodes connected to each other through certain resistances have been proposed.

With the most commonly used corrected Frank orthogonal leads, the electrodes are placed as follows: electrode E - on the sternum at the level between the fourth to fifth intercostal space, electrode M - behind at the level of electrode E, electrode A - along the left middle axillary line at the level of electrode E, electrode C - at an angle of 45 ° between electrodes A and E, that is, in the middle of the line connecting the points of electrodes A and E, electrode F - along the right middle axillary line at the level of electrode E, electrode H - on the back of the neck and electrode F - on the left leg. A grounded electrode is placed on the right leg. Thus, according to Frank's system, electrodes E, M, A, C, I are placed in the circle of the body at the level of attachment of the V rib to the sternum.

In practical medicine, corrected leads are rarely used.

Other additional assignments are given in the literature: ZR according to Pescodor; Dm, Am, Im, CKR, CKL, CKF according to Gurevich and Krynsky; MCL, and MCL 6 by Marriott. However, they do not have significant advantages over those listed above and are not used in practical medicine.

Currently great importance is given to the determination of the size of focal myocardial damage by non-invasive methods, which is important both for the immediate and long-term prognosis of the disease, and for assessing the effectiveness of treatment methods aimed at limiting the zone of ischemic damage. For this purpose, an electrocardiotopogram is recorded. In this case, it was proposed to use a different number of precordial leads. The most widespread is a system of 35 leads with five horizontal rows from the second to the sixth intercostal space, inclusive, and seven vertical (along the right and left parasternal lines, the middle of the distance between the left parasternal and left mid-clavicular lines, along the left mid-clavicular, anterior, middle and posterior axillary lines). ECG recording is performed according to Wilson using a chest electrode. Proceeding from the idea that the leads in which elevations of the S-T segment are recorded correspond to the peri-infarction zone, Magoko et al. (1971) proposed the NST index (the number of leads with the elevation of the S-T segment more than 1.5 mm), as an indicator of the severity of the injury - the quotient of dividing the sum of the rise S — T in mm by NST (ST = ΣST / NST). The number of ECG leads, in which the elevations of the S-T segment and changes in the ventricular complex of the QS type were determined, are depicted using a cartogram, where each of the 35 leads is conventionally represented as a square with an area of ​​1 cm2 (G V. Ryabinina, 3. 3. Dorofeeva, 1977) ... Of course, the size of the peri-infarction zone and transmural myocardial damage expressed in this way due to the different thickness and configuration of the chest and position hearts cannot be completely identified with the real dimensions of the corresponding zones of myocardial damage.

The disadvantage of the electrocardiotopogram method is that it can only be used when localizing heart attack myocardium in the region of the anterior and lateral walls in the absence of significant violations of intraventricular conduction (blockade of the bundle of His) and pericarditis.

Thus, at present there are a variety of lead systems and individual ECG leads, which have a large diagnostic value to determine the nature and localization of focal changes in the myocardium. If such a lesion is suspected, registration of the following leads is mandatory: three standard, three reinforced from the extremities according to Golberger, six thoracic according to Wilson, three according to Neb and three uncorrected orthogonal ones.

In unclear cases, depending on the localization of the affected area, leads V 7-9 are additionally recorded. V E. R o. and sometimes also S 1 -4 according to Slapak-Portilla, V 3R -6 R and V 1-7 in the intercostal space above and below the fifth.

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Determination of the localization of myocardial infarction. ECG topography of myocardial infarction

Before proceeding with the description various ECG variants of myocardial infarction... determined by differences in anatomical localization, it is appropriate to recall what was briefly mentioned at the beginning of this chapter in relation to the affected areas and the coronary circulation.

The figure shows diagram of various QRS loops with different localizations of infarction in accordance with the classification used in the Cardiology Clinic of the University of Barcelona. It should be noted that electrocardiographic, angiographic and pathological studies have shown that if the ECG is relatively specific in predicting the localization of infarction, especially in isolated infarction (i.e., the Q wave in certain leads correlates quite well with pathological data), its sensitivity is rather low (pathological a heart attack is often observed in the absence of an abnormal Q tooth on the ECG).

Generally 12-lead ECG sensitivity in the diagnosis of a previously transferred heart attack is about 65%, and the specificity varies from 80 to 95%. There are some criteria that have low sensitivity (less than 20%), but high specificity. Moreover, despite the importance of the ECG in diagnosing a heart attack, it does not accurately determine its degree. The sensitivity of individual criteria is very low, but increases in combination with several other techniques. As will be evident from the subsequent presentation, for various types of infarction, VCG sometimes has more sensitive criteria. For example, the transition of an anterior wall infarction to a lateral or inferior wall often goes unnoticed. VCG can expand diagnostic capabilities, as, for example, with questionable Q waves, and reveal the presence of several necrotic zones.

Doctor must try to assess the localization of infarction by ECG, even though the relationship between the ECG and pathomorphological changes does not always take place. It is also obliged to the bottom wall is essentially, upper section back wall. A heart attack can be classified as transmural or non-transmural depending on the depth of the wall lesion; apical or basal, depending on high or low localization; posterior, anterior, septal or lateral, depending on the area of ​​damage to the wall.

Heart attack is not always limited solely to the septal, anterior, posterior, inferior, or lateral wall. Various combined lesions are much more common, generally depending on the zone of myocardial damage, which in turn is associated with occlusion of the coronary artery.

Heart attack usually involves either the anterior septal (usually due to occlusion of the anterior descending coronary artery) or the inferoposterior zone (due to occlusion of the circumflex and / or right coronary artery) of the left ventricle. The side wall of the heart can be damaged in any area. A heart attack may be more pronounced in one area or another. In any case, the following generalizations should be kept in mind:

a) the infarction usually does not affect the basal part of the antero-lateral septal region;

b) infarction of the highest part and the posterolateral, basal wall and / or interventricular septum is not accompanied by Q waves, indicating a lesion, but can change the configuration of the terminal part of the loop;

c) in 25% of cases, the infarction of the posterior wall of the left ventricle passes to the right ventricle;

G) Bottom part the basal half of the posterior wall is a zone that corresponds to the classic posterior wall infarction (high R in leads V1, V2), in the form of a mirror image in the leads on the back, posterior wall infarction is usually not isolated, but affects the apex of the posterior wall (inferior or diaphragmatic).

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

What is ECG

An electrocardiogram is a diagnostic technique that detects 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 that is approved for use during pregnancy and in childhood.

With the help of a cardiogram, it is determined:

• what is the state of the structure that contributes to the contraction of the myocardium;
• heart rate and rhythm;
• the work of the conducting paths;
• assess the quality of the supply of the heart muscle through the coronary vessels;
• reveal the presence of scars;
• pathology of the heart.

For more accurate information about the state of the organ, daily monitoring, exercise ECG, transesophageal ECG can be used. Thanks to these procedures, the development of pathological processes can be detected in a timely manner.

ECG for myocardial infarction displays the stages and possible complications in heart. With the help of this study, the size of ischemia, depth and location are determined. A heart attack is caused by ischemia (insufficient blood supply to the heart).

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Myocardial infarction is called the death of the heart muscle, as a result, it stops working.

ECG localization of ischemic foci

ECG diagnostics allows you to determine the localization of the ischemic focus. For example, it can manifest in the walls of the left ventricle, anterior walls, septa, or lateral walls.

It is least often found in the right ventricle, therefore, to determine it, experts use the chest leads in the diagnosis.

ECG localization of infarction:

• Anterior - LAP artery is affected. Indicators: V1-V4. Leads: II, III, aVF.
• Posterior - RCA artery is affected. Indicators: II, III, aVF. Leads: I, aVF.
• Lateral - the Circunflex artery is affected. Indicators: I, aVL, V5. Leads: VI.
• Basal - RCA artery is affected. Indicators: none. Leads V1, V2.
• Septal - the Septal performan artery is affected. Indicators: V1, V2, QS. Leads: absent.

What is heart ischemia

Myocardial infarction, or acute ischemia of the heart muscle, claims millions of lives every year. Ischemia occurs due to insufficient blood delivery to the heart.

Lack of blood circulation in one of the parts of the heart for more than 15 minutes leads to the death of this area.

As a result, necrosis (death) of heart cells occurs. Breaks in blood vessels triggered by blood clots - solid blood clots that clog the capillary, veins and arteries.

Under the strong pressure of the incoming blood, the vessel ruptures. Statistics note that more than half of people die instantly, the remaining 30% die in hospitals. About 15-20% of those affected survive.

Changes and interpretation of results

What an ECG looks like, everyone knows how to decipher it - only a few.

The teeth on the ECG are indicated by Latin letters: P, Q, R, S, T, U:

• P - polarization of the atria;
• Q, R, S - ventricular polarization;
• T - ventricular repolarization;
• U - the functioning of the distal parts of the ventricle.

The teeth stretching upward are called "positive" by experts, and "negative" downward. In a healthy person, Q, S always have a negative result, and R - a positive one.

To decipher the ECG, analyze the intervals of change between the waves and their components. The analysis allows you to establish the rhythm and heart rate.

The higher the tooth, the more actively the heart works. The lower, the slower.

ECG signs of a heart attack are diagnosed by Q, S, T, R. If you add their indicators together, you get something like a small hump, vaguely reminiscent of the bowed back of a cat. Left ventricular hypertrophy is defined by R and S, where R extends and S deviates to the left.

Right bundle branch block is diagnosed by R and S, where R decreases and S expands. In the case of a blockade of the right pedicle of His, both R and S teeth expand.

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Stages

Experts distinguish 4 stages of myocardial infarction by ECG:

1. The most acute stage. Development period: from 3 hours to 3 days. The decreasing length of the R wave speaks of the developing necrosis. The smaller its length, the greater the likelihood of necrosis of a part of the heart.

   Serious damage to the heart is indicated by a ST elevation of 5 millimeters or more. The indicators characterize cardiac ischemia. Ends in death.

2. Acute stage. Development period: 2 - 3 weeks. It is characterized by the expansion of the necrosis zone and an increase with subsequent expansion of Q. The T wave indicators tend to the level of "negative" indicators, that is, it gradually decreases.
3. Mild stage. Development period: from 3 months to six months. It is characterized by an elongated T-wave. The sharper the stage, the longer it is. At the second stage of the disease, its length stabilizes for several weeks, then "T" tends in the opposite direction, becoming positive.
4. The cicatricial stage is considered to be the end stage that results in a scar. Its presence is determined by the Q scar. The scar remains in place until the last heart beat. Scars can heal or enlarge.

   The activity of the scar is determined by the "T" wave. With an increase in the size of the scar, it moves in positive side, when decreasing - in the negative direction. If the scar does not show its activity, then the "T" indicator is gradually smoothed out.

Transmural infarction ECG

Specialists divide the stage of transmural infarction into 4 stages:

• The most acute stage, which lasts from a minute to several hours;
• Acute stage, which lasts from an hour to 2 weeks;
• Mild stage, which lasts from 2 weeks to 2 months;
• The cicatricial stage, which occurs after 2 months.

Transmural infarction refers to the acute stage. On the ECG, it can be determined by the rising wave of "ST" to "T", which is in a negative position. On the last stage it is formed Q. The "ST" segment remains on the indicators of devices from 2 days to 4 weeks.

If, during a second examination, the patient continues to rise of the "ST" segment, then he develops an aneurysm of the left ventricle.

With transmural infarction, a Q wave is found, "ST" moves towards the isoline, "T" expands in the negative zone.

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

Changes in the ECG in myocardial infarction depend on its shape, location and stage.

By electrocardiographic signs, first of all, one should distinguish between transmural and subendocardial myocardial infarctions.

Myocardial necrosis usually manifests itself in ECG changes complex QRS. The formation of a necrotic focus in the myocardium leads to the termination of the electrical activity of the affected area, which causes a deviation total vector QRS 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 revealed, which is typical for subendocardial large-focal infarctions. The deeper the necrosis, the more pronounced these changes.

In transmural myocardial infarction, a QS-type complex is recorded on the ECG in the leads from the epicardial side. Above the islet of intact myocardium, surrounded by a necrotic process, there is an upward notch on the QS wave. Subepicardial necrosis can manifest itself only by a decrease in the amplitude of the R wave without the formation of a pathological 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 the leads

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

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

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

The most acute stage of myocardial 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 injury, accompanied by an elevation of the ST segment, up to fusion with the T wave (monophasic curve). Necrosis and the corresponding Q wave may begin to form, but it may not be. 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 myocardial infarction - the formation of the so-called monophase curve ... The monophasic curve consists of ST segment elevation and a high positive T wave, which merge together.

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

An important feature of the acute, acute and subacute stages of a heart attack

myocardium are		reciprocal		changes in electrocardiographic
		segment			leads,	the respective
localization of myocardial necrosis, concomitant					his depression		in leads,
characterizing the opposite parts of the myocardium. V						the most acute
	acute stage similar			ratios can			to arise

applied to complex QRS and T.

Subacute stage lasts from 1 to 2 months. The zone of damage disappears due to the transition to the zone of ischemia (therefore, the ST segment is close to

half of the subacute stage due to the expansion of the ischemic zone, the negative T wave broadens and grows 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 at the periphery of the ischemic zone.

If the ST segment elevation has not returned to normal after 3 weeks after the infarction, it is necessary to exclude the formation of a cardiac aneurysm.

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

Problem number 1

Acute anterior, apex, with transition to the lateral wall Q-myocardial infarction

Problem number 2

Acute antero-septal, apex with transition to the lateral wall Q-myocardial infarction

Problem number 3

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

Problem number 4

Acute anterior, apex and lateral wall left ventricular myocardial infarction

Problem number 5

Acute stage of anterior widespread myocardial infarction

Problem number 6

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

Problem number 7

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

Problem number 8

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

Problem number 9

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

Problem number 10

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

Problem number 11

The most acute stage of myocardial infarction with ST segment elevation of the antero-septal, apex and lateral wall of the left ventricle

Problem number 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

Problem number 13

Anterior, apex and lateral wall myocardial infarction, acute stage

Problem number 14

Without Q myocardial infarction (intramural) anterolateral wall

Problem number 15

Acute lower Q-left ventricular myocardial infarction

Problem number 16

The most acute stage of myocardial infarction with ST segment elevation bottom wall left ventricle

Problem number 17

Sinus bradycardia.

Problem number 18

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

Problem number 19

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

Problem number 20

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

Problem number 21

Acute lower myocardial infarction

Problem number 22

Lower myocardial infarction, acute stage

Problem number 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

On an ECG with myocardial infarction, doctors clearly see signs of cardiac tissue necrosis. A cardiogram for a heart attack is a reliable diagnostic method and allows you to determine the degree of heart damage.

ECG interpretation for myocardial infarction

An electrocardiogram is a safe research method, and if a heart attack is suspected, it is simply irreplaceable. ECG in myocardial infarction is based on cardiac conduction disturbances, i.e. in certain areas of the cardiogram, the doctor will see abnormal changes that indicate a heart attack. To obtain reliable information, doctors use 12 electrodes when taking data. Cardiogram for myocardial infarction(photo 1) registers such changes based on two facts:

• with a heart attack in a person, the process of excitation of cardiomyocytes is disturbed, and this happens after cell death;
• in the tissues of the heart affected by a heart attack is disturbed electrolyte balance- potassium largely leaves the damaged tissue pathologies.

These changes make it possible to register lines on the electrocardiograph, which are signs of conduction disturbances. They do not develop immediately, but only after 2-4 hours, depending on the compensatory capabilities of the body. Nevertheless, a cardiogram of the heart with a heart attack shows the accompanying signs, which can be used to determine the violation of the work of the heart. A photo with a transcript is sent by the cardiological ambulance team to the clinic where such a patient will be admitted - cardiologists will be ready in advance for a serious patient.

Myocardial infarction on the ECG looks like this:

• complete absence of the R wave or its significant decrease in height;
• extremely deep, sinking Q wave;
• raised S-T segment above the isoline level;
• the presence of a negative T wave.

The electrocardiogram also shows the various stages of a heart attack. Heart attack on ECG(photo in gal.) can be subacute, when changes in the work of cardiomyocytes are just beginning to appear, acute, acute and at the stage of scarring.

Also, an electrocardiogram allows the doctor to evaluate the following parameters:

• diagnose the very fact of a heart attack;
• determine the area where pathological changes have occurred;
• establish the limitation of the changes that have arisen;
• decide on the tactics of treating the patient;
• predict the possibility of death.

Transmural myocardial infarction is one of the most dangerous and severe types of heart damage. It is also called macrofocal or Q-infarction. The cardiogram after myocardial infarction with large focal lesions shows that the zone of death of heart cells captures the entire thickness of the heart muscle.

Myocardial infarction

Myocardial infarction is a consequence of coronary heart disease. Most often, ischemia is caused by atherosclerosis of the heart vessels, spasm or blockage. Happen heart attack(photo 2) may also result from surgery, if an artery is ligated or angioplasty is performed.

Ischemic infarction goes through four stages of the pathological process:

• ischemia, in which the cells of the heart stop receiving the required amount of oxygen. This stage can last for a rather long time, since the body turns on all compensatory mechanisms to ensure the normal functioning of the heart. The immediate mechanism of ischemia is the narrowing of the cardiac vessels. Until a certain point, the heart muscle copes with such a lack of blood circulation, but when thrombosis narrows the vessel to a critical size, the heart is no longer able to compensate for the shortage. This usually requires a 70 percent or more narrowing of the artery;
• damage that occurs directly in cardiomyocytes, which begins within 15 minutes after the cessation of blood circulation in the damaged area. A heart attack lasts about 4-7 hours. This is where the patient begins characteristic signs heart attack - chest pain, heaviness, arrhythmia. Extensive heart attack is the most difficult outcome of an attack; with such damage, the zone of necrosis can be up to 8 cm wide;
• necrosis - death of heart cells and the termination of their functions. In this case, the death of cardiomyocytes occurs, necrosis does not allow them to perform their functions;
• scarring - the replacement of dead cells with connective tissue formations that are not able to take on the function of precursors. This process begins almost immediately after necrosis and little by little for 1-2 weeks a connective tissue scar of fibrin fibers forms on the heart at the site of injury.

Hemorrhagic cerebral infarction is a related condition in terms of mechanisms of damage, however, it is the release of blood from the vessels of the brain, which interfere with the functioning of cells.

Heart after a heart attack

Heart after myocardial infarction(photo 3) undergoes the process of cardiosclerosis. Connective tissue, which replaces cardiomyocytes, turns into a rough scar - it can be seen by pathologists when autopsy people who have had myocardial infarction.

The scar after myocardial infarction has a different thickness, length and width. All these parameters affect the further activity of the heart. Deep and large foci of sclerosis are called extensive infarction. Recovery from such a pathology is extremely difficult. With microsclerosis, the infarction, as well, can leave minimal damage. Often, patients do not even know that they have suffered such a disease, since the symptoms were minimal.

A scar on the heart after a heart attack does not hurt in the future and does not make itself felt for about 5-10 years after a heart attack, however, it provokes a redistribution of the cardiac load to healthy areas, which now have to do more work. After a certain time, the heart looks worn out after a heart attack - the organ cannot carry out the load, coronary heart disease in patients is aggravated, pains in the heart, shortness of breath appear, they quickly get tired, and constant drug support is required.

Myocardial infarction photo gallery