ECG changes in acute myocardial infarction. Types of myocardial infarction by location on ECG

I. Mogelwang, M.D. Cardiologist of the intensive care unit of the Hvidovre Hospital 1988

Coronary heart disease (CHD)

The main cause of IHD is obstructive damage to the main coronary arteries and their branches.

The prognosis for IHD is determined by:

number of significantly stenotic coronary arteries

functional state of the myocardium

The ECG provides the following information about the state of the myocardium:

potentially ischemic myocardium

ischemic myocardium

acute myocardial infarction (MI)

previous myocardial infarction

MI localization

MI depth

MI sizes

Information that is relevant for treatment, control and prognosis.

Left ventricle

In IHD, the myocardium of the left ventricle is primarily affected.

The left ventricle can be divided into segments:

Septal segment

Apical segment

Lateral segment

Posterior segment

Lower segment

The first 3 segments make up the anterior wall, and the last 3 segments make up the posterior wall. The lateral segment may thus be involved in anterior wall infarction as well as posterior wall infarction.

SEGMENTS OF THE LEFT VENTRICLE

ECG LEADS

ECG leads can be unipolar (derivatives of one point), in which case they are designated by the letter “V” (after the initial letter of the word “voltage”).

Classic ECG leads are bipolar (derivatives of two points). They are designated by Roman numerals: I, II, III.

A: reinforced

V: unipolar lead

R: right (right hand)

L: left (left hand)

F: leg (left leg)

V1-V6: unipolar chest leads

ECG leads reveal changes in the frontal and horizontal planes.

	Hand to hand	Lateral segment, septum
	Right hand -> left foot
	Left hand -> left foot	Lower segment
	(Enhanced unipolar) right hand	Attention! Possible misinterpretation
	(Enhanced unipolar) left hand	Lateral segment
	(Enhanced unipolar) left leg	Lower segment
	(Unipolar) at the right edge of the sternum	Septum/Posterior segment*
	(Unipolar)
	(Unipolar)
	(Unipolar)	Top
	(Unipolar)
	(Unipolar) along the left middle axillary line	Lateral segment
* - V1-V3 mirror image of changes in the posterior segment

ECG leads in the frontal plane

ECG leads in the horizontal plane

MIRROR IMAGE(with a specific diagnostic value detected in leads V1-V3, see below)

Cross section of right and left ventricles & Left ventricle segments:

Relationship between ECG leads and left ventricular segments

Depth and dimensions

QUALITATIVE ECG CHANGES

QUANTITATIVE ECG CHANGES

LOCALIZATION OF INFARCTION: ANTERIOR WALL

LOCALIZATION OF INFARCTION: POSTERIOR WALL

V1-V3; COMMON DIFFICULTIES

Infarction and bundle branch block (BBB)

LBP is characterized by a wide QRS complex (0.12 sec).

Right bundle branch block (RBB) and left bundle branch block (LBB) can be distinguished by lead V1.

RBP is characterized by a positive wide QRS complex, and LBP is characterized by a negative QRS complex in lead V1.

Most often, the ECG does not provide information about a heart attack in LBBB, unlike in LPN.

ECG changes in myocardial infarction over time

Myocardial infarction and silent ECG

Myocardial infarction can develop without the appearance of any specific changes on the ECG in the case of LBBB, but also in other cases.

ECG options for myocardial infarction:

subendocardial MI

transmural MI

without specific changes

ECG for suspected coronary heart disease

Specific signs of coronary heart disease:

Ischemia/Infarction?

In case of a heart attack:

Subendocardial/transmural?

Localization and sizes?

Differential diagnosis

ECG DIAGNOSTICS KEY FOR CORONARY HEART DISEASE

PD KopT - suspicion of KopT

States:

ECG symbols:

1. Anterior segment ischemia 2. Ischemia of the lower segment 3. Subendocardial inferior MI 4. Subendocardial infero-posterior MI 5. Subendocardial infero-posterior-lateral MI 6. Subendocardial anterior infarction (common) 7. Acute inferior MI 8. Acute posterior MI 9. Acute anterior MI 10. Transmural inferior MI 11. Transmural posterior MI 12. Transmural anterior MI (widespread) (septal-apical-lateral) * The mirror pattern (zer) of ST G is visible not only with posterior MI, in this case it is called reciprocal changes. For simplicity, this is released in context. The mirror image of ST G and ST L cannot be distinguished.

Myocardial infarction: general principles of ECG diagnosis.

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

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

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

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

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

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

Let us remind you that healthy person in leads reflecting the potential of the left ventricle (V5-6, I, aVL), a physiological q wave can be recorded, reflecting the excitation vector of the heart septum. The 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 formula QS, 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. Moreover, the larger this functioning layer, the higher the R wave. The Q wave in 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.

The 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: Q waves that are bifurcated or jagged are most often pathological and reflect necrosis (myocardial infarction).

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

Ischemia:

Damage:

Necrosis:

So, the main question for diagnosing myocardial necrosis (infarction) has been answered: with transmural necrosis, the electrocardiogram in the leads that are located above the necrosis zone has the formula of the gastric complex QS; with non-transmural necrosis, the ventricular complex has the appearance of Qr or QR.

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

Localization of infarction.

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

Below is a table for diagnosing different localizations of myocardial infarction using 12 leads included in the standard electrocardiographic study.

+ Treatments

Myocardial infarction

Various ECG leads in topical diagnosis of focal myocardial changes. At all stages of ECG development, starting with the use of three classical (standard) leads by W. Einthoven (1903), researchers sought to provide practitioners with a simple, accurate and most informative method for recording biopotentials cardiac 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 Einthoven triangle, the angles of which are formed by three limbs: the right and left arms and the left leg. Each side of the triangle forms an abduction 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 hand and left leg, the third (III) - between the electrodes of the left hand and left leg.

Using standard leads, it is possible to 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 either do not reveal even gross changes in the myocardium at all, or changes in the lead graph lead to erroneous diagnosis of focal changes. In particular, changes in the basal-lateral sections of the left ventricle are not always reflected in lead I, and in the basal-posterior sections - in lead III.

A deep Q wave and a negative T wave in lead III may be normal, but during inspiration these changes disappear or decrease and are absent in additional leads such as avF, avL, D and Y. A negative T wave can be an expression of hypertrophy and overload, in connection with which the conclusion is given based on the totality of changes detected 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 after the standard ones they began to use.

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

Especially long time CR leads were used in practical medicine. In this case, one electrode was placed on the right hand (indifferent), and the other (different, recording) in the chest area in positions from 1 to 6 or even to 9 (CR 1-9). In the first position, the 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 - to the fifth intercostal space along the midclavicular 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 midscapular and paravertebral lines at the level of the 4th position . These positions, as will be seen below, have been preserved to this day and are used for recording ECG according to Wilson.

However, it was later found that both the indifferent electrode itself and its location on different limbs influence 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 resistance of 5000 Ohms. The creation of such an indifferent electrode with a “zero” potential allowed F. Wilson to develop unipolar (unipolar) leads from the chest and limbs. The principle of registration of these leads is that the above-mentioned 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 arm (VR ), left hand(VL) and left leg (VF).

Using Wilson chest leads, you can determine the location of myocardial lesions. Thus, 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 lateral wall, V 6 - in the lateral 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 waves. Wilson's limb abduction has not found practical application due to the low voltage of the teeth.

In 1942, Wilson's limb leads were modified by E. Golberger, who proposed using a wire from two limbs combined into one assembly without additional resistance as an indifferent electrode, and a free wire from the third limb is used as an indifferent electrode. With this modification, the amplitude of the waves increased by one and a half times compared to the Wilson leads of the same name. In this regard, leads according to Golberger began to be called enhanced (a - augmented - enhanced) unipolar leads from the limbs. The principle of recording leads is that the indifferent electrode is alternately applied to one of the limbs: right arm, left arm, left leg, and the wires from the other two limbs are combined into one indifferent electrode. When a trim electrode is applied to the right arm, lead aVR is recorded, lead avL is recorded on the left arm, and lead avF is recorded on the left leg. The introduction of these leads into practice has significantly expanded the diagnostic capabilities of electrocardiography 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. Lead avL is also important for diagnostics focal changes in the basal-lateral sections of the left ventricle, lead avF - in the posterior wall, in particular in its diaphragmatic part.

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

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

More widely used additional leads include bipolar chest leads according to Neb. The technique he proposed for recording leads 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 projection of the apex hearts(V 7), the electrode from the left leg is at the site of the apical impulse (V 4). When installing the lead switch, lead D (dorsalis) is registered on pin I, lead A (anterior) is registered on pin II, and lead I (inferior) is registered on pin III. These leads achieve not a flat, but a topographic display of the potentials of the three surfaces of the heart: posterior, anterior and inferior.

Approximately, lead D 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 segment of the left ventricle.

According to V. Neb, in diagnosing 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 Wilson's chest leads in diagnosing 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 normally and with a horizontal position of the heart, the presence of a positive T wave in lead D excludes pathology.

According to our data, regardless of position hearts registration of lead D is mandatory 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 similar changes in avF. Lead avF reflects predominantly the posterodiaphragmatic parts of the left ventricle, and lead D reflects the posterior diaphragmatic (basal-lateral) sections. Therefore, minor 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) is recorded by the thoracic lead, but with the installation of a trim electrode in the area of ​​the xiphoid process. The lead reflects focal changes in the septal region. It is used for unclear changes in leads V 1-2.

Diagnosis of limited focal changes in the basal-lateral sections 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 is worth considering semisagittal abduction according to the Slapak a - Portilla method. Since these leads are a modification of lead D according to Neb, the indifferent electrode from the left hand is placed in position V 7. and the trim electrode from the right hand moves along a line connecting two points: one in the second intercostal space to the left of the sternum, the second in the second intercostal space along the anterior axillary line.

The 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 pin I. These leads record focal changes in the basal-lateral sections of the left ventricle. Unfortunately, the graphics of these leads are somewhat dependent 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 begun to be used in practical electrocardiography.

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

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

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

Leads are registered in the position of the lead switch on the I contact.

Approximately, lead X corresponds to leads I, avL V 5-6 and reflects the anterolateral steak of the left ventricle. Lead V corresponds to leads III and avF and reflects the posterior wall. Lead Z corresponds to lead V2 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 location, in the left ventricle orthogonal leads always react with appropriate graphics, while with small-focal myocardial lesions, especially in the basal sections of the left ventricle, changes in these leads are often absent. In such cases, Slapak-Portilla leads and chest leads from 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 orthogonal leads according to Frank, the electrodes are placed as follows: electrode E - on the sternum at the level between the fourth and fifth intercostal space, electrode M - posteriorly at the level of electrode E, electrode A - along the left mid-axillary line at the level of electrode E, electrode C - at an angle of 45° between electrodes A and E, i.e. in the middle of the line connecting the points of electrodes A and E, electrode F - along the right midaxillary line at the level of electrode E, electrode H - on the back of the neck and electrode F - on the left leg. On right leg a grounded electrode is installed. Thus, according to the Frank system, electrodes E, M, A, C, I are placed around the body at the level of attachment of the 5th rib to the sternum.

In practical medicine, corrected leads are rarely used.

Other additional leads 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 attached to determining the size of focal myocardial damage using 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 area of ​​ischemic damage. For this purpose, an electrocardiotopogram is recorded. In this case, it is 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 ones (along the right and left parasternal lines, the middle of the distance between the left parasternal and left midclavicular lines, along the left midclavicular, anterior, middle and posterior axillary lines). ECG recording is performed according to Wilson using a chest electrode. Based on the idea that the leads in which elevations of the S-T segment are recorded correspond to the peri-infarction zone, as an indicator of the size of the zone of ischemic damage to the myocardium, P. R. Magoko et al (1971) proposed the NST index (the number of leads with elevation of the S-T segment more than 1.5 mm), as an indicator of the severity of damage - the quotient of dividing the sum of S-T rises in mm by NST (ST = ΣST/NST). The number of ECG leads in which 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 by a square with an area of ​​1 cm2 (G. V. Ryabinina, 3. 3. Dorofeeva, 1977) . Of course, the magnitude 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 actual sizes of the corresponding zones of myocardial damage.

The disadvantage of the electrocardiotopogram method is that it can only be used for localization heart attack myocardium in the area of ​​the anterior and lateral walls in the absence of significant disturbances of intraventricular conduction (bundle branch block) and pericarditis.

Thus, at present, there are various lead systems and individual ECG leads, which are of great diagnostic value for determining 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 Holberger, six thoracic according to Wilson, three according to Neb and three uncorrected orthogonal.

In unclear cases, depending on the location 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 spaces above and below the fifth.

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Determination of the localization of myocardial infarction. Topography of myocardial infarction according to ECG

Before we begin the description various ECG variants of infarction. determined by differences in anatomical location, 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 picture shows diagram of various QRS loops for various localizations of infarction in accordance with the classification used at the Cardiology Clinic of the University of Barcelona. It should be noted that electrocardiographic, angiographic and pathological studies have shown that while the ECG is relatively specific in predicting the location of infarction, especially in isolated infarction (ie, the Q wave in certain leads correlates fairly well with pathological findings), its sensitivity is quite low (pathological infarction is often observed in the absence of an abnormal Q tooth on the ECG).

Generally sensitivity 12 lead ECG in the diagnosis of a previous heart attack is about 65%, and specificity varies from 80 to 95%. There are certain 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 extent. The sensitivity of individual criteria is very low, but increases in combination with several other techniques. As will be evident from the further presentation when various types heart attack, VKG sometimes has more sensitive criteria. For example, the transition of an infarction from the anterior wall to the lateral or inferior wall often goes unnoticed. VKG can expand diagnostic capabilities, as, for example, with questionable Q waves, and reveal the presence of several necrotic areas.

Doctor must try to assess the localization of the infarction using the ECG, even though there is not always a relationship between the ECG and pathomorphological changes. It is also obliged to The lower wall is essentially the upper section of the rear wall. Infarction can be classified as transmural or nontransmural depending on the depth of the wall involvement; apical or basal depending on high or low localization; posterior, anterior, septal or lateral, depending on the area of ​​the wall affected.

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

Heart attack usually involves either the anteroseptal (usually due to occlusion of the anterior descending coronary artery) or inferoposterior zone (due to occlusion of the circumflex and/or right coronary artery) of the left ventricle. The lateral 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, keep the following generalizations in mind:

a) the infarction usually does not affect the basal part of the anterolateral 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 may change the configuration of the terminal part of the loop;

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

G) Bottom part basal half of the posterior wall is an area that corresponds to a classic posterior wall infarction (high R in leads V1, V2), in the form of a mirror image in the dorsal leads, an infarction of the posterior wall is usually not isolated, but affects the apical part of the posterior wall (lower or diaphragmatic).

I would like to tell you about the main diagnostic method - ECG for myocardial infarction. Using a cardiogram, you will learn to determine the degree of damage to your heart by pathologies.

Nowadays, myocardial infarction is a very common dangerous disease. Many of us may confuse the symptoms of a heart attack with acute angina, which can lead to tragic consequences and death. With this diagnostic method, cardiologists can accurately determine the condition of the human heart.

If you notice the first symptoms, you should urgently do an ECG and consult a cardiologist. In our article you can find out how to prepare yourself for this procedure and how it will be deciphered. This article will be useful to everyone, since no one is immune from this pathology.

ECG for myocardial infarction

Myocardial infarction is necrosis (tissue death) of part of the heart muscle, which occurs due to insufficient oxygen supply to the heart muscle due to circulatory failure. Myocardial infarction is the main cause of mortality today and disability of people around the world.

ECG for myocardial infarction is the main tool for its diagnosis. If symptoms characteristic of the disease appear, you should immediately visit a cardiologist and undergo an ECG test, since the first hours are very important.

You should also undergo regular examinations to early diagnosis deterioration of heart function. Main symptoms:

• dyspnea;
• chest pain;
• weakness;
• rapid heartbeat, interruptions in heart function;
• anxiety;
• heavy sweating.

The main factors due to which oxygen poorly enters the blood and blood flow is disrupted are:

• coronary stenosis (due to a blood clot or plaque, the opening of the artery is acutely narrowed, which becomes the cause of large-focal myocardial infarction).
• coronary thrombosis (the lumen of the artery is suddenly blocked, causing large-focal necrosis of the walls of the heart).
• stenosing coronary sclerosis (the lumens of some coronary arteries, which causes small focal myocardial infarctions).

Myocardial infarction quite often develops against the background of arterial hypertension, diabetes mellitus and atherosclerosis. It can also occur due to smoking, obesity and a sedentary lifestyle.

Conditions that provoke myocardial infarction, due to which oxygen supply decreases, can be:

• constant anxiety;
• nervous tension;
• excessive physical activity;
• surgical intervention;
• changes in atmospheric pressure.

An ECG during myocardial infarction is carried out using special electrodes that are attached to an ECG machine and which record the signals sent by the heart. For a regular ECG, six sensors are enough, but for the most detailed analysis Twelve leads are used to determine the functioning of the heart.

Cardiac pathology can acquire various shapes. Electrocardiographic diagnosis of myocardial infarction can detect the following types of disease:

• transmural;
• subendocardial;
• intramural.

Each disease is characterized by a specific state of zones of necrosis, damage, and ischemia. Transmural myocardial infarction has signs of large-focal necrosis, which affects from 50% to 70% of the walls of the left ventricle. The vector of depolarization of the opposite wall helps to detect signs of myocardial infarction of this type.

The difficulty of diagnosis lies in the fact that a significant part of the myocardium does not demonstrate the changes occurring in it and only vector indicators can indicate them. Subendocardial myocardial infarction does not belong to small focal forms of the disease.

It almost always occurs extensively. The greatest difficulty for doctors in examining the condition of an internal organ is the blurring of the boundaries of the affected myocardium.

When signs of subendocardial damage are detected, doctors observe the time of their manifestation. Signs of myocardial infarction of the subendocardial type can be considered full confirmation of the presence of pathology if they do not disappear within 2 days. Intramural myocardial infarction is considered rare in medical practice.

It is detected quite quickly in the first hours of its occurrence, since the vector of myocardial excitation on the ECG indicates changes in the heart metabolic processes. Potassium leaves cells affected by necrosis. But the difficulty in detecting pathology is that potassium damage currents are not formed, because it does not reach the epicardium or endocardium.

To identify this type of myocardial infarction, even longer monitoring of the patient's condition is required. An ECG must be performed regularly for 2 weeks. One transcript of the analysis results is not a full confirmation or denial preliminary diagnosis. It is possible to clarify the presence or absence of a disease only by analyzing its signs in the dynamics of their development.

Depending on the symptoms, there are several types of myocardial infarction:

• Anginal is the most common option. It manifests itself as severe pressing or squeezing pain behind the sternum that lasts more than half an hour and does not go away after taking medication (nitroglycerin). This pain can radiate to the left side of the chest, as well as to the left arm, jaw and back. The patient may experience weakness, anxiety, fear of death, and severe sweating.
• Asthmatic – a variant in which there is shortness of breath or suffocation, strong heartbeat. Most often there is no pain, although it may be a precursor to shortness of breath. This variant of the development of the disease is typical for older age groups and for people who have previously suffered a myocardial infarction.
• Gastralgic is a variant characterized by an unusual localization of pain that manifests itself in the upper abdomen. It can spread to the shoulder blades and back. This option is accompanied by hiccups, belching, nausea, and vomiting. Due to intestinal obstruction, bloating is possible.
• Cerebrovascular - symptoms associated with cerebral ischemia: dizziness, fainting, nausea, vomiting, loss of orientation in space. The appearance of neurological symptoms complicates the diagnosis, which can be absolutely correctly made in this case only with the help of an ECG.
• Arrhythmic - an option when the main symptom is palpitations: a feeling of cardiac arrest and interruptions in its work. Pain is absent or mild. Possible weakness, shortness of breath, fainting or other symptoms caused by a fall blood pressure.
• Low-symptomatic - an option in which detection of a previous myocardial infarction is possible only after taking an ECG. However, a heart attack can be preceded by mild symptoms such as causeless weakness, shortness of breath, and interruptions in heart function.

For any type of myocardial infarction, an ECG must be done for an accurate diagnosis.

Cardiac cardiogram

Human organs pass a weak current. This is precisely what allows us to make an accurate diagnosis using a device that records electrical impulses. The electrocardiograph consists of:

• a device that enhances weak current;
• voltage measuring device;
• recording device on an automatic basis.

Based on the cardiogram data, which is displayed on the screen or printed on paper, the specialist makes a diagnosis. There are special tissues in the human heart, otherwise called the conduction system, they transmit signals to the muscles indicating relaxation or contraction of the organ.

The electric current in the heart cells flows in periods, these are:

• depolarization. The negative cellular charge of the heart muscles is replaced by a positive one;
• repolarization. The negative intracellular charge is restored.

A damaged cell has lower electrical conductivity than a healthy one. This is exactly what the electrocardiograph records. Passing a cardiogram allows you to record the effect of currents that arise in the work of the heart.

When there is no current, the galvanometer records a flat line (isoline), and if the myocardial cells are excited in different phases, the galvanometer records a characteristic tooth directed up or down.

An electrocardiographic test records three standard leads, three reinforced leads and six chest leads. If there are indications, then leads are also added to check the posterior parts of the heart.

The electrocardiograph records each lead with a separate line, which further helps to diagnose cardiac lesions.
As a result, a complex cardiogram has 12 graphic lines, and each of them is studied.

On the electrocardiogram, five teeth stand out - P, Q, R, S, T, there are cases when U is also added. Each has its own width, height and depth, and each is directed in its own direction.

There are intervals between the teeth, they are also measured and studied. Interval deviations are also recorded. Each tooth is responsible for the functions and capabilities of certain muscular parts of the heart. Experts take into account the relationship between them (it all depends on the height, depth and direction).

All these indicators help to distinguish normal myocardial function from impaired, caused by various pathologies. The main feature of the electrocardiogram is to identify and record symptoms of pathology that are important for diagnosis and further treatment.

ECG diagnosis of myocardial infarction allows you to determine the localization of ischemia. For example, it may appear in the walls of the left ventricle, on the anterior walls, septa or lateral walls.

It is worth noting that myocardial infarction most rarely occurs in the right ventricle, therefore, to determine it, specialists use special chest leads in diagnosis.

Localization of myocardial infarction by ECG:

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

Preparation and procedure

Many people believe that the ECG procedure does not require special preparation. However, for a more accurate diagnosis of myocardial infarction, it is necessary to adhere to the following rules:

1. Stable psycho-emotional background, the patient must be extremely calm and not nervous.
2. If the procedure takes place in the morning, you should refuse to eat.
3. If the patient smokes, it is advisable to refrain from smoking before the procedure.
4. It is also necessary to limit fluid intake.

Before the examination, it is necessary to remove outerwear, and expose your shins. The specialist wipes the electrode attachment area with alcohol and applies special gel. Electrodes are placed on the chest, ankles and arms. During the procedure the patient is in horizontal position. The ECG takes approximately 10 minutes.

During normal operation of the organ, the line has the same cyclicity. The cycles are characterized by sequential contraction and relaxation of the left and right atria and ventricles. At the same time, complex processes occur in the heart muscle, accompanied by bioelectric energy.

Electrical impulses generated in different parts of the heart are evenly distributed throughout the human body and reach skin person, which is fixed by the device using electrodes.

Interpretation of ECG for myocardial infarction

Myocardial infarction is divided into 2 types - large focal and small focal. An ECG allows you to diagnose large focal myocardial infarction. The electrocardiogram consists of teeth (protrusions), intervals and segments.

On a cardiogram during a heart attack, the protrusions look like concave or convex lines. In medical practice, there are several types of teeth that are responsible for the processes occurring in the myocardium; they are designated by Latin letters.

The P protrusion characterizes the contractions of the atria, the Q R S protrusions reflect the state of the contractile function of the ventricles, and the T protrusion records their relaxation. The R wave is positive, the Q S waves are negative and directed downward. A decrease in the R wave indicates pathological changes in the heart.

Segments are straight line segments connecting the protrusions to each other. The ST segment located in the midline is considered normal. An interval is a specific area consisting of protrusions and a segment.

A large focal myocardial infarction is shown on the cardiogram as a modification of the complex of Q R S protrusions. The appearance of a pathological Q protrusion indicates the development of pathology. The Q indicator is considered the most stable sign of myocardial infarction.

An electrocardiogram does not always show signs that determine the development of pathology the first time, but only in 50% of cases. The first characteristic sign of the development of pathology is ST segment elevation.

What does a large heart attack look like on a cardiogram? The following picture is typical for large focal MI:

• R wave - completely absent;
• Q wave - significantly increased in width and depth;
• ST segment - located above the isoline;
• T wave - in most cases has a negative direction.

During the study, the following features and deviations are checked:

1. Poor circulation, which leads to arrhythmia.
2. Restriction of blood flow.
3. Failure of the right ventricle.
4. Thickening of the myocardium – development of hypertrophy.
5. Irregular heart rhythm as a result of abnormal electrical activity of the heart.
6. Transmural infarction of any stage.
7. Features of the location of the heart in the chest.
8. Heart rate regularity and activity intensity.
9. The presence of damage to the myocardial structure.

Normal indicators

All impulses heart rate are recorded in the form of a graph, where changes in the curve are marked vertically, and the time of declines and rises is calculated horizontally.

Teeth - vertical stripes are designated by letters Latin alphabet. Horizontal segments are measured that record changes - the intervals of each cardiac process (systole and diastole).

In adults, normal indicators of a healthy heart are as follows:

1. Before the contraction of the atria, the P wave will be indicated. It is a determinant of sinus rhythm.

It can be negative or positive, and the duration of such a marker is no more than a tenth of a second. Deviation from the norm may indicate impaired diffuse metabolic processes.

2. The PQ interval has a duration of 0.1 seconds.

It is during this time that the sinus impulse has time to pass through the artioventicular node.

3. The T wave explains the processes during repolarization of the right and left ventricles. It indicates the stage of diastole.
4. The QRS process lasts 0.3 seconds on the graph, which includes several teeth. This is a normal depolarization process during ventricular contraction.

ECG indicators during myocardial infarction are very important in diagnosing the disease and identifying its features. Diagnosis must be quick in order to find out the features of damage to the heart muscle and understand how to resuscitate the patient.

The location of the affected area can be different: death of the tissues of the right ventricle, damage to the pericardial sac, death of the valve.

The lower left atrium may also be affected, preventing blood from leaving this area. Transmural infarction leads to blockage of blood vessels in the area of ​​the coronary supply to the heart muscle. Defining points in diagnosing a heart attack:

• Exact localization of the site of muscle death.
• Period of effect (how long the condition lasts).
• Depth of damage. On ECG signs Myocardial infarction is easily detected, but it is necessary to find out the stages of the lesion, which depend on the depth of the lesion and the strength of its spread.
• Concomitant lesions of other areas of the heart muscles.

Important to consider. The indicators of the teeth are also in the case of blockade of the His bundle in the lower part, which provokes the onset of the next stage - transmural infarction of the left ventricular septum.

In the absence of timely treatment, the disease can spread to the area of ​​the right ventricle, since the blood flow is disrupted and necrotic processes in the heart continue. To prevent a deterioration in health, the patient is administered metabolic and diffuse drugs.

Stages of myocardial necrosis

Between healthy and dead (necrotic) myocardium, intermediate stages are distinguished in electrocardiography:

• ischemia,
• damage.

ISCHEMIA: this is the initial damage to the myocardium, in which there 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 series, on cell membranes In nerve and muscle cells, two opposite processes occur sequentially: depolarization (excitation) and repolarization (restoration of the potential difference). Depolarization is a simple process, for which you only need to open ion channels in the cell membrane, through which, due to the difference in concentrations, ions will flow outside and inside the cell.

Unlike depolarization, repolarization is an energy-intensive process that requires energy in the form of ATP. Oxygen is necessary for the synthesis of ATP, therefore, during myocardial ischemia, the repolarization process first begins to suffer. Impaired repolarization is manifested by changes in the T wave.

With myocardial ischemia, the QRS complex and ST segments are normal, but the T wave is changed: it is widened, symmetrical, equilateral, increased in amplitude (span) and has a pointed apex. In this case, the T wave can be either positive or 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 is a reversible phenomenon; over time, metabolism (metabolism) is restored to normal or continues to deteriorate with the transition to the damage stage.

DAMAGE: this is a deeper damage to the myocardium, in which an increase in the number of vacuoles, swelling and degeneration of muscle fibers, disruption of membrane structure, mitochondrial function, acidosis (acidification of the environment), etc. are determined under a microscope. Both depolarization and repolarization suffer. The injury is thought to primarily affect the ST segment.

The ST segment can shift above or below the isoline, but its arc (this is important!) when damaged is convex in the direction of displacement. Thus, when the myocardium is damaged, the arc of the ST segment is directed towards the displacement, which distinguishes it from many other conditions in which the arc is directed towards the isoline (ventricular hypertrophy, bundle branch block, etc.).

When damaged, the T wave can be of different shapes and sizes, which depends on the severity of concomitant ischemia. The damage also cannot exist for long and turns into ischemia or necrosis.

NECROSIS: death of the myocardium. Dead myocardium is unable to depolarize, so dead cells cannot form an R wave in the ventricular QRS complex. For this reason, during transmural infarction (death of the myocardium in a certain area along the entire thickness of the heart wall), there is no R wave at all in this ECG lead, and a QS-type ventricular complex is formed.

If necrosis has affected only part of the myocardial wall, a QrS type complex is formed, in which the R wave is reduced and the Q wave is increased compared to normal. Normally, the Q and R waves must obey a number 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.
• the R wave 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 r wave may normally be absent, then the ventricular complex has the appearance of QS. In people under 30 years of age, the QS complex can normally occasionally be in V1-V2, and in children - even in V1-V3, although this is always suspicious for an infarction of the anterior part of the interventricular septum.

Diagnosis in patients with bundle branch blocks

The presence of a blockade of the right leg does not prevent the detection of large-focal changes. And in patients with left leg block, ECG diagnosis of a heart attack is very difficult. Many ECG signs of large-focal changes against the background of left leg block have been proposed. When diagnosing acute MI, the most informative of them are:

1. The appearance of a Q wave (especially a pathological Q wave) in at least two leads from leads aVL, I, v5, v6.
2. Reduction of the R wave from lead V1 to V4.
3. Serration of the ascending limb of the S wave (Cabrera sign) in at least two leads from V3 to V5.
4. Concordant ST segment shift in two or more adjacent leads.

If any of these signs are detected, the probability of a heart attack is 90-100%, however, these changes are observed only in 20-30% of patients with MI due to blockade of the left leg (changes in the ST segment and T wave in dynamics are observed in 50%). Therefore, the absence of any ECG changes in a patient with left leg block does not in any way exclude the possibility of a heart attack.

For accurate diagnosis it is necessary to determine the activity of cardiac-specific enzymes or troponin T. Approximately the same principles for diagnosing MI in patients with ventricular pre-excitation syndrome and in patients with an implanted pacemaker (continuous ventricular stimulation).

In patients with blockade of the left anterior branch, signs of large-focal changes in the lower localization are:

1. Registration in lead II of complexes like QS, qrS and rS (wave r
2. The R wave in lead II is smaller than in lead III.

The presence of a blockade of the left posterior branch, as a rule, does not make it difficult to detect large-focal changes.

Transmural infarction ECG

Experts 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 two weeks;
• Non-acute stage, which lasts from two weeks to two months;
• The scar stage, which occurs after two months.

Transmural infarction refers to the acute stage. According to the ECG, it can be determined by the rising wave “ST” to “T”, which is in a negative position. At the last stage of transmural infarction, the formation of the Q wave occurs. The “ST” segment remains on the instrument readings from two days to four weeks.

If, upon repeated examination, the patient continues to rise in the ST segment, this indicates that he is developing a left ventricular aneurysm. Thus, transmural infarction characterized by the presence of a Q wave, a movement of “ST” towards the isoline and a “T” wave expanding in the negative zone.

Infarction of the posterior regions of the ventricle is quite difficult to diagnose using an ECG. In medical practice, in about 50% of cases, diagnostics do not show problems with the posterior regions of the ventricle. The posterior wall of the ventricle is divided into the following parts:

• The diaphragmatic region, where the posterior walls adjacent to the diaphragm are located. Ischemia in this part causes an inferior infarction (posterior phrenic infarction).
• The basal region (upper walls) adjacent to the heart. Cardiac ischemia in this part is called posterobasal infarction.

An inferior infarction occurs as a result of blockage of the right coronary artery. Complications are characterized by damage to the interventricular septum and posterior wall.

With lower infarction ECG indicators change as follows:

• The third Q wave becomes larger than the third R wave by 3 mm.
• The cicatricial stage of the infarction is characterized by a decrease in the Q wave to half R (VF).
• The expansion of the third Q wave to 2 mm is diagnosed.
• With a posterior infarction, the second Q wave rises above the first Q (in a healthy person these indicators are the opposite).

It is worth noting that the presence of a Q wave in one of the leads does not guarantee a posterior infarction. It can disappear and appear when a person breathes intensely. Therefore, to diagnose a posterior infarction, perform an ECG several times.

The difficulty is this:

1. Excess weight of the patient can affect the conduction of cardiac current.
2. It is difficult to identify new scars of myocardial infarction if there is already scarring on the heart.
3. Impaired conduction of complete blockade, in this case it is difficult to diagnose ischemia.
4. Frozen cardiac aneurysms do not record new dynamics.

Modern medicine and new ECG machines are able to easily carry out calculations (this happens automatically). Using Holter monitoring, you can record the work of the heart throughout the day.

Modern wards have cardiac monitoring and an audible alarm, which allows doctors to notice altered heartbeats. The final diagnosis is made by a specialist based on the results of an electrocardiogram and clinical manifestations.

The region of the myocardium in which MI develops depends on the location of the occluded coronary artery and the degree of collateral blood flow. There are two main blood supply systems to the myocardium, one supplies the right half of the heart, the other the left half.

The right coronary artery passes between the right atrium and the right ventricle and then curves onto the posterior surface of the heart. In most people, it has a descending branch that supplies the AV node.

The left coronary artery divides into the left descending and left circumflex arteries. The left descending artery supplies the anterior wall and most of the interventricular septum. The circumflex artery passes between the left atrium and the left ventricle and supplies the lateral wall of the left ventricle. In approximately 10% of the population, it has a branch that supplies blood to the AV node.

Localization of the infarction is important for prognostic and therapeutic purposes to determine the area of ​​necrosis.

The location of the infarction can be grouped into several anatomical groups. These are inferior, lateral, anterior and posterior myocardial infarctions. Combinations of these groups are possible, for example, anterolateral MI, which is very common.

Four main anatomical sites of MI.

Almost all myocardial infarctions involve the left ventricle. This is not surprising because the left ventricle is the largest chamber of the heart and experiences the most stress. Therefore, it is the most vulnerable area in case of disruption of the coronary blood supply. Some inferior MIs also involve part of the right ventricle.

Characteristic electrocardiographic changes of MI are recorded only in those leads that are located above or near the site of the lesion.

· Inferior MI involves the diaphragmatic surface of the heart. It is often caused by occlusion of the right coronary artery or its descending branch. Characteristic electrocardiographic changes may be seen in inferior leads II, III, and aVF.

· Lateral MI involves the left lateral wall of the heart. It often occurs due to occlusion of the left circumflex artery. Changes will occur in left lateral leads I, aVL, V5 and V6.

· Anterior MI involves the anterior surface of the left ventricle and is usually caused by occlusion of the left anterior descending artery. Any of the chest leads (V1 - V6) may show changes.

· Posterior MI involves the posterior surface of the heart and is usually caused by occlusion of the right coronary artery. Unfortunately, there are no leads that are located above the posterior wall. The diagnosis is therefore based on reciprocal changes in the anterior leads, especially V1. Reciprocal changes will be discussed later.

Note: The anatomy of the coronary arteries can vary markedly among individuals, making it impossible to accurately predict which vessel is affected.

Inferior infarcts

Inferior MI is usually the result of occlusion of the right coronary artery or its descending branch. Changes occur in leads II, III And aVF. Reciprocal changes may be noticeable in the anterior and left lateral leads.

Although most MI lesions retain abnormal Q waves throughout the patient's life, this is not necessarily true for inferior MIs. During the first six months, the criteria for pathological Q waves disappear in 50% of patients. The presence of small Q waves in the inferior leads may therefore suggest scarring after MI. Remember, however, that small inferior Q waves may also be noticeable normally.

Lateral infarctions

Lateral MI results from occlusion of the left circumflex artery. Changes may be noticeable in leads I, aVL, V5 And V6. Reciprocal changes are noted in the inferior leads.

Anterior infarcts

Anterior MI is the result of occlusion of the left anterior descending artery. Changes are noticeable in the chest leads ( V1 - V6). If the entire left coronary artery is affected, anterolateral MI is observed with changes in the precordial leads and in leads I and aVL. Reciprocal changes are noted in the inferior leads.

Anterior MI is not always accompanied by the formation of a Q wave. In some patients, the normal progression of the R wave in the precordial leads may only be disrupted. As you already know, normal chest leads show a progressive increase in the height of the R waves from V1 to V5. The amplitude of the R waves should increase by at least 1 mV in each lead from V1 to V4 (and often V5). This dynamic may be disrupted by anterior MI, an effect called delayed R wave progression. Even in the absence of abnormal Q waves, delayed R wave progression may indicate anterior MI.

Delayed R wave progression is not specific for the diagnosis of anterior MI. It may also be seen in right ventricular hypertrophy and in patients with chronic lung disease.

Posterior infarctions

Posterior MI is usually the result of right coronary artery occlusion. Since none of the normal leads lies above the posterior wall, the diagnosis is verified by reciprocal changes in the anterior leads. In other words, since we will not be able to find ST segment elevation and Q waves in the posterior leads (which are not there), we must look for ST segment depression and tall R waves in the anterior leads, especially in lead V1. Posterior MI is a mirror image of anterior MI on the ECG.

The normal QRS complex in lead V1 consists of a small R wave and a deep S wave; therefore, the presence of a high R wave, especially with ST segment depression, is easily noticeable. In the presence of clinical signs, an R wave of greater amplitude than the corresponding S wave indicates posterior MI.

Another useful tip. Since the inferior and posterior walls usually share a common blood supply, posterior MI is often accompanied by the formation of an inferior wall infarction.

One reminder: The presence of a large R wave greater than the amplitude of the S wave in lead V1 is also a criterion for the diagnosis of right ventricular hypertrophy. The diagnosis of right ventricular hypertrophy, however, requires the presence of a right axis deviation, which is absent in posterior MI.

What is the location of the infarction? Is it really spicy?

Non-Q myocardial infarction

Not all myocardial infarctions are accompanied by the appearance of a Q wave. Previously, it was believed that Q waves were recorded when the MI penetrated the entire thickness of the myocardial wall, while the absence of Q waves indicated the formation of an infarction only in the inner layer of the myocardial wall, called the subendocardium. These infarctions were called transmural or subendocardial.

However, studies have found that there is no clear correlation between the appearance of Q waves and the depth of myocardial damage. Some transmural MIs do not show Q waves, and some subendocardial MIs do not show Q waves. Therefore, the old terminology has been replaced by the terms “Q-wave infarction” and “non-Q-wave infarction.”

The only ECG changes seen in non-Q wave myocardial infarction are T wave inversion and ST segment depression.

It has been established that there is a lower mortality rate in non-Q MI and a higher risk of recurrence and mortality in Q MI.

Angina pectoris

Angina pectoris is a typical chest pain associated with coronary artery disease. A patient with angina may develop a myocardial infarction or angina may persist for many years. An ECG recorded during an attack of angina will show ST segment depression or T wave inversion.

Three examples of ECG changes that may accompany angina: (A) T wave inversion; (B) ST segment depression; and (C) ST segment depression with T wave inversion.

Important differences between ST segment depression in angina and non-Q-MI are the clinical picture and dynamics. In angina, the ST segments usually return to their base soon after the attack subsides. In non-Q MI, ST segments remain depressed for at least 48 hours. It may be useful to determine cardiac enzymes that will be increased during the formation of MI, and do not change with angina.

Prinzmetal's angina

There is one type of angina, which is accompanied by ST segment elevation. Unlike typical angina, which is usually provoked by exercise and is the result of progressive atherosclerotic disease of the coronary arteries, Prinzmetal's angina can occur at any time and in many patients is the result of coronary artery spasm. ST segment elevation appears to reflect reversible transmural damage. The contours of the ST segments often will not have the rounded, dome-shaped shape of an MI, and the ST segments will quickly return to the base after the attack has subsided.

Patients with Prinzmetal's angina are actually divided into two groups: without atherosclerosis of the coronary arteries, the pain is determined solely by spasm of the coronary artery, and with atherosclerotic lesions. ECG does not help distinguish between these two groups.

Summary

ST segment at coronary disease hearts

ST segment elevation

It may be noticeable with the development of transmural myocardial infarction or with Prinzmetal's angina.

ST segment depression

May be noticeable in typical angina or non-Q wave myocardial infarction.

The shape of the ST segment in patients with acute ischemic pain is the main determining factor in the choice of therapy. Patients with acute ST segment elevation on the ECG require immediate reperfusion therapy (thrombolysis or angioplasty). Patients with ST segment depression or no ST segment changes usually receive conservative therapy.

Limitations of ECG in the diagnosis of myocardial infarction

The electrocardiographic picture of developing myocardial infarction usually includes changes in the ST segment and the appearance of new Q waves. Any factors that mask these effects, distorting the ST segment and QRS complex, have Negative influence for electrocardiographic diagnosis of AMI. Two of these factors are WPW syndrome and left bundle branch block.

Rule: In case of left bundle branch block or Wolff-Parkinson-White syndrome, the diagnosis of myocardial infarction cannot be reliable by ECG. This rule includes patients with left bundle branch block on ECG due to ventricular pacing.

In patients with WPW syndrome, delta waves are often negative in the inferior leads (II, III, and aVF). These changes are often referred to as pseudoinfarcts because delta waves can resemble Q waves. A short PR interval is a major clue to distinguish WPW from AMI.

Exercise testing

Exercise testing is a noninvasive method for assessing the presence of CAD. This method is not perfect (false positives and false negatives are common), but it is one of the best screening methods available.

Exercise testing is usually performed by the patient on a treadmill with steady walking or on an exercise bike. The patient is connected to an ECG monitor and the rhythm strip is continuously recorded during the procedure. A complete 12-lead ECG is recorded at short intervals. Every few minutes, the speed and inclination of the walking belt are increased until the following conditions occur: (1) the patient is unable to continue the procedure for any reason; (2) achieving the patient's maximum heart rate; (3) appearance of cardiac symptoms; (4) the appearance of significant changes on the ECG.

The physiology of testing assessment is simple. The classified loading protocol causes a safe and gradual increase in the patient's heart rate and systolic blood pressure. The patient's blood pressure multiplied by the heart rate is a good indicator of myocardial oxygen consumption. If the myocardial oxygen demand exceeds the ability to deliver it, changes characteristic of myocardial ischemia may be recorded on the ECG.

Significant atherosclerotic damage to one or more coronary arteries restricts blood supply to the myocardium and limits oxygen consumption. Although the resting ECG may be normal, physical activity subclinical signs of ischemic heart disease may be recorded.

If the test for CAD is positive, the ECG will show ST segment depression. T wave changes are too vague to be of clinical significance.

If the ST segment is depressed during testing, especially if the changes persist for several minutes during the recovery period, there is a high probability of the presence of CAD and damage to the left coronary artery or several coronary arteries. The appearance of cardiac symptoms and a decrease in blood pressure are particularly important signs at which testing should be stopped immediately.

The rate of false positives and false negatives depends on the population being tested. A positive test in a young, healthy person without symptoms or risk factors for CAD is likely to be a false positive. On the other hand, a positive test in an elderly person with chest pain, a history of myocardial infarction, and arterial hypertension is highly likely to be a true positive. A negative test result does not exclude the possibility of CAD.

Indications for exercise testing are as follows:

Differential diagnosis of chest pain

Evaluating a patient with a recent MI to assess the prognosis of the patient and the need for further invasive testing, such as cardiac catheterization

· General assessment of patients over 40 years of age with risk factors for coronary artery disease.

Contraindications include any acute illness, severe aortic stenosis, decompensated congestive heart failure, severe hypertension, resting angina, and the presence of significant arrhythmia.

Mortality from the procedure is very low, but the equipment for cardiopulmonary resuscitation must always be available.

Joan L. is a 62-year-old executive. She is on an important business trip and spends the night in a hotel. Early in the morning she wakes up with shortness of breath and heaviness in the chest, which radiates to the lower jaw and left arm, moderate dizziness and nausea. She gets out of bed, but the pain does not go away. She calls the emergency department. Her complaints are relayed by telephone to the hotel doctor, who immediately orders an ambulance to take her to the local emergency room. She arrives there only 2 hours after the onset of her symptoms, which continue despite taking three nitroglycerin tablets.
In the emergency department, an ECG shows the following:
Does she have a myocardial infarction? If the answer is yes, can you tell if the changes are acute and what area of ​​the heart is affected?

Joan's prompt arrival in the emergency department, ST segment elevation, and absence of Q waves on the ECG mean that she is an excellent candidate for either thrombolytic therapy or acute coronary angioplasty. Unfortunately, she only got sick 1 month ago hemorrhagic stroke, has mild hemiparesis on the left, which prevents thrombolytic therapy. In addition, acute angioplasty surgery is not available in this small hospital, and the nearest major medical center is several hours away. Therefore, Joan was hospitalized in the cardiology department.

Late at night, one of the nurses notices specific contractions on her ECG:

Joan's ECG shows that the ventricular ectopies have been suppressed. It also shows the appearance of new Q waves in the anterior leads with subsequent complete development of anterior myocardial infarction.

Later in the day, Joan begins to experience chest pain again. A repeat ECG was taken: What has changed?

Joanna developed third degree AV block. Severe conduction blocks usually occur with anterior MI. Her dizziness is due to inadequate pumping function of the myocardium at a ventricular rate of 35 beats/min. Installation artificial driver rhythm is required.

Finishing touches

There are many medications, electrolyte disturbances, and other disorders that can significantly alter the normal ECG pattern.

In some of these cases, the ECG may be the most sensitive indicator of impending disaster. In others, even minor electrocardiographic changes may be early sign growing problem.

We will not dwell on the mechanisms of these changes in this chapter. In many cases, the reasons for ECG changes are simply not known. Topics we will cover include the following:

Electrolyte disturbances

Hypothermia

· Medicines

· Other cardiac disorders

Lung diseases

Diseases of the central nervous system

· The heart of an athlete.

Electrolyte disturbances

Changes in potassium and calcium levels can significantly alter the ECG.

Hyperkalemia

Hyperkalemia is accompanied by progressive ECG changes that can culminate in ventricular fibrillation and death. The presence of electrocardiographic changes is a more reliable clinical sign of potassium toxicity than serological potassium levels.

As potassium increases, T waves begin to increase in all 12 leads. This effect can be easily confused with peaked T waves in acute myocardial infarction. One difference is that changes in T waves in AMI are limited to those leads that lie above the infarction area, whereas in hyperkalemia, the changes are diffuse.

With a further increase in potassium, the PR interval lengthens, and the P wave gradually flattens and then disappears.

Subsequently, the QRS complex widens, then it merges with the T wave, forming sinusoidal complexes. Eventually ventricular fibrillation develops.

It is important to note that these changes do not always correspond to blood potassium levels. Progression from hyperkalemia to ventricular fibrillation can occur very quickly. Any ECG change due to hyperkalemia requires close clinical attention.

Hypokalemia

For hypokalemia, ECG may also be a better indicator of potassium toxicity than serum potassium levels. Three changes may be noticed, occurring in no particular order:

ST segment depression

T wave smoothing

· Appearance of a U wave.

The term U wave is given to the wave appearing after the T wave in the cardiac cycle. Its exact physiological significance is not fully understood. Although U waves are the most characteristic feature hypokalemia, they are not accurate diagnostic sign. U waves can sometimes be noticeable in normal conditions and when potassium levels are normal.

Calcium disorders

Changes in serum calcium levels primarily affect the QT interval. Hypocalcemia prolongs it; hypercalcemia reduces it. Do you remember the potentially fatal arrhythmia associated with QT prolongation?

Fusiform ventricular tachycardia, type ventricular tachycardia, observed in patients with prolongation of the QT interval.

Hypothermia

When body temperature drops below 30°C, several changes occur on the ECG:

· Everything slows down. Sinus bradycardia is common and all segments and intervals (PR, QRS, QT) may be prolonged.

· A distinctive and virtually diagnostic pattern of ST segment elevation may be seen. It consists of a sharp rise right at the J point and then a sudden decline back to the bottom. This configuration is called a J wave or Osborne wave.

· Ultimately, various arrhythmias may occur. Low heart rate atrial fibrillation is the most common, although almost any rhythm disorder can occur.

· Muscle tremors due to shaking may complicate ECG analysis. A similar effect may be seen in patients with Parkinson's disease. Do not confuse this with atrial flutter.

Interference from muscle tremors resembles atrial flutter.

Medicines

Cardiac glycosides

There are two categories of electrocardiographic changes caused by cardiac glycosides: those associated with therapeutic doses of the drug, and changes due to overdose (toxicity) of cardiac glycosides.

ECG changes associated with therapeutic doses of SG

Therapeutic doses of SG are characterized by changes in the ST segment and T wave in most patients. These changes are known as the digitalis effect, and consist of ST segment depression with flattening or inversion of the T wave. The reduction of the ST segments has an oblique downward shape, starting almost immediately at the R wave. This distinguishes the digitalis effect from the more symmetrical ST segment depression of ischemia. It is more difficult to differentiate the digitalis effect from ventricular hypertrophy from repolarization disorders, especially because SGs are often used in patients with congestive heart failure, who often have left ventricular hypertrophy.

The digitalis effect is usually most noticeable in leads with tall R waves. Remember: the digitalis effect is normal, expected, and does not require discontinuation of the drug.

ECG changes associated with overdose (toxicity) of cardiac glycosides

Toxic manifestations of FH may require clinical intervention. SG intoxication can manifest itself as conduction blocks and tachyarrhythmias, alone or in combination.

Suppression (suppression) of the sinus node

Even with therapeutic doses of SG, the sinus node can slow down, especially in patients with sick sinus syndrome. In case of overdose, sinoatrial blockades or complete depression of the sinus node may occur.

Blockades

SGs slow conduction through the AV node and can cause 1st, 2nd, and 3rd degree AV blocks.

The ability of cardiac glycosides to slow down AV conduction is used in the treatment of supraventricular tachycardia. For example, SGs may slow the ventricular rate in patients with atrial fibrillation; however, the ability of SG to slow heart rate is clearly noticeable in patients at rest, but disappears during exercise. Beta blockers such as atenolol or metoprolol also have a similar effect on AV conduction but may better control heart rate during exercise or stress.

Tachyarrhythmias

Since SG increases the automaticity of all cells of the conduction system, causing them to act as pacemakers, there is no tachyarrhythmia that they cannot cause. Paroxysmal atrial tachycardia and atrial premature contractions are the most common; Atrioventricular rhythms, atrial flutter and fibrillation are quite common.

Combinations

The combination of atrial tachycardia with second degree AV block is the most characteristic rhythm disorder in SG intoxication. Conduction block is usually 2:1, but may vary. This is the most common, but not the only, cause of AT with conduction block.

Sotalol and other drugs that prolong the QT interval

The antiarrhythmic drug sotalol increases the QT interval and therefore may, paradoxically, increase the risk of ventricular tachyarrhythmias. The QT interval should be monitored carefully in all patients taking sotalol. The drug should be discontinued if the QT interval increases by more than 25%.

Other drugs that may prolong the QT interval include other antiarrhythmics (eg, quinidine, procainamide, disopyramide, amiodarone, and dofetilide), tricyclic antidepressants, phenothiazines, erythromycin, quinolone antibiotics, and various antifungal medications.

Some patients taking quinidine may experience U waves. This effect does not require any intervention.

Several inherited repolarization disorders with QT prolongation have been identified and associated with specific chromosomal disorders. All individuals in these families should be tested for the presence of the genetic defect by recording resting and exercise ECGs. If the above changes are detected, it is recommended to prescribe beta blockers, and sometimes implantable defibrillators, since the risk is high sudden death. These patients should also be excluded from athletic competition and should never be prescribed medications that may prolong the QT interval.

Because the QT interval typically changes with heart rate, the corrected QT interval, or QTc, is used to assess the absolute length of the QT. QTc adjusts to fluctuations in heart rate, determined by dividing the QT interval by the square root R-R. QTc should not exceed 500 ms during therapy with any medicine which can prolong the QT interval (550 ms if there is interventricular block); Compliance with this rule reduces the risk of ventricular arrhythmias.

Other cardiac disorders

Pericarditis

Acute pericarditis can cause ST segment elevation and T wave flattening or inversion. These changes can easily be confused with developing AMI. Certain ECG features may be helpful in differentiating pericarditis from myocardial infarction:

· ST segment and T wave changes of pericarditis tend to be diffuse (but not always), involving many more leads than the limited changes of MI.

· In pericarditis, T wave inversion usually occurs only after the ST segments have returned to the base. In myocardial infarction, T wave inversion usually precedes ST segment normalization.

· In pericarditis, Q wave formation is not observed.

· Sometimes the PR interval decreases.

The formation of effusion in the pericardial cavity reduces the electrical power of the heart, which is accompanied by a decrease in voltage in all leads. ST segment and T wave changes may not be noticeable.

If the effusion is large enough, the heart actually floats freely within the pericardial cavity. This is accompanied by the phenomenon of electrical alternans, in which the electrical axis of the heart changes with each contraction. Not only the axis of the QRS complex can change, but also the P and T waves. A change in EOS is manifested on the ECG by a change in the amplitude of the waves from contraction to contraction.

Hypertrophic obstructive cardiomyopathy (HOCM)

We have already discussed hypertrophic obstructive cardiomyopathy, formerly known as idiopathic hypertrophic subaortic stenosis, in the case of patient Tom L. Many patients with HOCM have normal ECG, but left ventricular hypertrophy and left axis deviation are often observed. Occasionally, Q waves may be seen in the lateral and inferior leads, but they do not indicate MI.

Myocarditis

Any diffuse inflammatory process involving the myocardium can cause many changes on the ECG. The most common are conduction blocks, especially interventricular blocks and hemiblocks.

Lung diseases

Chronic obstructive disease lungs (COPD)

The ECG of a patient with long-standing pulmonary emphysema may show low voltage, right axis deviation, and slow progression of the R wave in the precordial leads. Low voltage is caused by the effect of increasing the residual air volume in the lungs. The deviation of the electrical axis to the right is caused by the expansion of the lungs, displacing the heart into a vertical position.

COPD can lead to chronic cor pulmonale and right ventricular congestive heart failure. The ECG in this case may show right atrium dilatation (P-pulmonale) and right ventricular hypertrophy with repolarization disorders.

Acute pulmonary embolism

Sudden massive embolism pulmonary artery can greatly change the ECG. Research results may include the following:

Right ventricular hypertrophy with repolarization changes due to acute right ventricular dilatation

Right bundle branch block

Myocardial infarction on the ECG has a number of characteristic signs that help differentiate it from other disorders of conduction and excitability of the heart muscle. It is very important to conduct an ECG diagnosis in the first few hours after an attack in order to obtain data on the depth of the lesion, the degree of functional heart failure, and the possible localization of the lesion. Therefore, if possible, the cardiogram is taken while still in the ambulance, and if this is not possible, then immediately upon the patient’s arrival at the hospital.

ECG signs of myocardial infarction

An electrocardiogram reflects the electrical activity of the heart - by interpreting the data from such a study, one can obtain comprehensive information about the functioning of the conduction system of the heart, its ability to contract, pathological foci of excitation, as well as the course of various diseases.

The first sign to look for is deformation of the QRST complex, in particular, a significant reduction in the R wave or its complete absence.

The classic ECG picture consists of several areas that can be seen on any normal tape. Each of them is responsible for a separate process in the heart.

1. P wave– visualization of atrial contraction. By its height and shape one can judge the state of the atria, their coordinated work with other parts of the heart.
2. PQ interval– shows the spread of the excitation impulse from the atria to the ventricles, from the sinus node down to the atrioventricular node. Prolongation of this interval indicates a conduction disorder.
3. QRST complex– ventricular complex, which provides complete information about the state of the most important chambers of the heart, the ventricles. Analysis and description of this part of the ECG is the most important part of diagnosing a heart attack; the main data is obtained from here.
4. ST segment– an important part, which is normally an isoline (a straight horizontal line on the main ECG axis, without teeth), with pathologies capable of descending and rising. This may be evidence of myocardial ischemia, i.e. insufficient blood supply to the heart muscle.

Any changes in the cardiogram and deviations from the norm are associated with pathological processes in cardiac tissue. In the case of a heart attack - with necrosis, that is, necrosis of myocardial cells with their subsequent replacement with connective tissue. The stronger and deeper the damage, the wider the area of ​​necrosis, the more noticeable the changes on the ECG will be.

The first sign to look for is deformation of the QRST complex, in particular, a significant reduction in the R wave or its complete absence. This indicates a violation of ventricular depolarization (the electrical process responsible for heart contraction).

Any changes in the cardiogram and deviations from the norm are associated with pathological processes in the cardiac tissue. In the case of a heart attack - with the necrosis of myocardial cells, followed by their replacement with connective tissue.

Further changes affect the Q wave - it becomes pathologically deep, which indicates a disruption in the functioning of pacemakers - nodes made of special cells in the thickness of the myocardium that begin contraction of the ventricles.

The ST segment also changes - normally it is on the isoline, but during a heart attack it can rise higher or fall lower. In this case, they speak of elevation or depression of the segment, which is a sign of ischemia of the heart tissue. Using this parameter, it is possible to determine the localization of the area of ​​ischemic damage - the segment is raised in those parts of the heart where necrosis is most pronounced, and lowered in the opposite leads.

Also, after some time, especially closer to the scarring stage, a negative deep T wave is observed. This wave reflects massive necrosis of the heart muscle and makes it possible to determine the depth of damage.

An ECG photo for myocardial infarction with interpretation allows you to consider the described signs in detail.

The tape can move at speeds of 50 and 25 mm per second; more low speed with better detail. When diagnosing a heart attack, not only changes in leads I, II and III are taken into account, but also in the reinforced ones. If the device allows you to record the chest leads, then V1 and V2 will display information from the right parts of the heart - the right ventricle and atrium, as well as the apex, V3 and V4 about the apex of the heart, and V5 and V6 will indicate the pathology of the left parts.

Closer to the scarring stage, a negative deep T wave is observed. This wave reflects massive necrosis of the heart muscle and allows you to determine the depth of damage.

Stages of myocardial infarction on ECG

A heart attack occurs in several stages, and each period is marked by special changes on the ECG.

1. Ischemic stage (damage stage, acute) associated with the development of acute circulatory failure in the tissues of the heart. This stage does not last long, so it is rarely recorded on a cardiogram tape, but its diagnostic value is quite high. At the same time, the T wave increases and becomes sharper - they speak of a giant coronary T wave, which is a harbinger of a heart attack. Then ST rises above the isoline; its position here is stable, but further elevation is possible. When this phase lasts longer and becomes acute, a decrease in the T wave can be observed, as the focus of necrosis spreads to the deeper layers of the heart. Reciprocal and reverse changes are possible.
2. Acute stage (necrosis stage) occurs 2-3 hours after the onset of the attack and lasts up to several days. On the ECG it looks like a deformed, wide QRS complex, forming a monophasic curve, where it is almost impossible to distinguish individual waves. The deeper the Q wave on the ECG, the deeper layers were affected by ischemia. At this stage, transmural infarction can be recognized, which will be discussed later. Characteristic rhythm disturbances are arrhythmias, extrasystoles.
3. Recognize the onset of the subacute stage possible by stabilizing the ST segment. When it returns to the baseline, the infarction no longer progresses due to ischemia, and the recovery process begins. Highest value in this period, there is a comparison of the existing T wave sizes with the original ones. It can be either positive or negative, but will slowly return to the baseline in sync with the healing process. Secondary deepening of the T wave in the subacute stage indicates inflammation around the necrosis zone and does not last long, with proper drug therapy.
4. In the scarring stage, the R wave rises again to its characteristic values, and T is already on the isoline. In general, the electrical activity of the heart is weakened, because some of the cardiomyocytes have died and been replaced by connective tissue, which does not have the ability to conduct and contract. Pathological Q, if present, is normalized. This stage lasts up to several months, sometimes six months.

It is very important to conduct an ECG diagnosis in the first few hours after an attack in order to obtain data on the depth of the lesion, the degree of functional heart failure, and the possible localization of the lesion.

Main types of heart attack on ECG

In the clinic, a heart attack is classified depending on the size and location of the lesion. This is important in the treatment and prevention of delayed complications.

Depending on the size of the damage, there are:

1. Large-focal, or Q-infarction. This means that the circulatory disorder occurred in a large coronary vessel, and a large volume of tissue was affected. The main sign is a deep and widened Q wave, and the R wave cannot be seen. If the infarction is transmural, that is, affecting all layers of the heart, the ST segment is located high above the isoline, in the subacute period a deep T is observed. If the damage is subepicardial, that is, not deep and located next to the outer shell, then R will be recorded, albeit small.
2. Small focal, non-Q infarction. Ischemia developed in areas supplied by the terminal branches of the coronary arteries; this type of disease has a more favorable prognosis. With an intramural infarction (the damage does not extend beyond the heart muscle), Q and R do not change, but a negative T wave is present. In this case, the ST segment is on the isoline. In subendocardial infarction (focus near the inner lining), T is normal and ST is depressed.

Depending on the location, the following types of heart attack are determined:

1. Anteroseptal Q-infarction– noticeable changes in 1-4 chest leads, where there is no R in the presence of wide QS, ST elevation. In standard I and II – pathological Q, classic for this type.
2. Lateral Q-infarction– identical changes affect chest leads 4-6.
3. Posterior or diaphragmatic Q-infarction, also known as inferior– pathological Q and high T in leads II and III, as well as intensified from the right leg.
4. Interventricular septal infarction– in standard I, deep Q, ST elevation and high T. In thoracic 1 and 2, R is pathologically high, and A-V block is also characteristic.
5. Anterior non-Q infarction– in thoracic I and 1-4 T is higher than the preserved R, and in II and III there is a decrease in all waves along with ST depression.
6. Posterior non-Q infarction– in standard II, III and chest 5-6 positive T, decreased R and depression ST.

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