Deciphering the ECG in a heart attack. Signs and stages of myocardial infarction on ekg. Transmural infarction ECG

An ECG for myocardial infarction displays the stages and possible complications in the heart. With the help of this study, the size of ischemia, depth and location are determined. The cause of a heart attack is 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.

Localization of ischemic foci on the ECG

ECG diagnostics allows you to determine the localization of the focus of ischemia. For example, it can appear in the walls of the left ventricle, on the anterior walls, septa, or side walls.

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

Localization of a heart attack by ECG:

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

What is cardiac ischemia

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

The absence 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. Gaps in blood vessels are provoked by blood clots - solid blood clots that clog capillaries, veins and arteries.

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

Changes and interpretation of results

Everyone knows what an ECG looks like, how to decipher it - units.

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

• Р — polarization of auricles;
• Q, R, S - polarization of the ventricles;
• T - repolarization of the ventricles;
• U - functioning of the distal parts of the ventricle.

The teeth stretching upwards are called "positive" by experts, and "negative" downwards. At healthy person Q, S are always negative, and R is always positive.

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

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

ECG signs a heart attack is diagnosed by Q, S, T, R. If you add their indicators together, you get something like a small hump, vaguely resembling a cat's arched back. Left ventricular hypertrophy is defined by R and S, where R is extended and S is deviated to the left.

Blockade right leg His is diagnosed by R and S, where R decreases and S expands. In the case of blockade of the right leg of His, both teeth expand - R and S.

Video

stages

Specialists distinguish 4 stages of myocardial infarction according to the ECG:

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

   O serious damage heart says ST elevation of 5 millimeters or more. Indicators characterize cardiac ischemia. Ends in death.

2. acute stage. Development period: 2 - 3 weeks. It is characterized by an expansion of the necrosis zone and an increase with subsequent expansion of Q. The T wave indicators tend to the mark of “negative” indicators, that is, it gradually decreases.
3. Non-acute stage. Development period: from 3 months to six months. It is characterized by an elongated T wave. The more acute 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 the final stage, as a result of which a scar is created. Its presence is determined by the scar Q. The scar remains in place until the last heartbeat. Scars may heal or grow.

   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, with a decrease - in the negative direction. If the scar does not show its activity, then the “T” indicator is gradually smoothed out.

Transmural infarction ECG

The stage of transmural infarction is divided into 4 stages:

• The most acute stage, which lasts from a minute to several hours;
• The acute stage, which lasts from an hour to 2 weeks;
• Non-acute stage, which lasts from 2 weeks to 2 months;
• Cicatricial stage, which occurs after 2 months.

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

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

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

ECG in a heart attack is of great importance for its diagnosis, in particular for the diagnosis of localization, the amount of necrosis, for differential diagnosis with an unclear picture, pains of a different nature and for prognosis.

Typical ECG changes in a heart attack are:

• a sharp shift in the RS-T interval (discordant) up and down in I and III standard leads;
• a rapid decrease in the amplitude of the QRS complex or the formation of Q, QS waves;
• rapid development of inversion and deformation (discordant in leads) of the T wave.

Changes in the QRS complex on the ECG during a heart attack

According to relatively recent studies, the positive QRS complex recorded in standard leads is a mirror image of the normally occurring negative potential of the inner layers of the myocardium (i.e., its intracavitary surface). If during this movement of excitation between the inner and outer layers a non-functioning, “dead” tissue arises, which loses its polarization property, negative deviations of the electrocardiogram are perceived from the outer layers of the heart. In this case, the intracavitary negative potential is transmitted either unchanged (negative QRS complex) or in the form of a positive, but reduced or deformed QRS complex (due to partial loss of depolarization function by the myocardium). The localization and size of the inactive, damaged ("dead") area, respectively, affect the ECG during a heart attack. This theory explains the main ECG deviations in a heart attack.

When the entire thickness of the myocardial wall is damaged (necrotized), QS teeth appear on the ECG with the disappearance of the P wave, which means that the negative potential passes through the “hole” (i.e., the area of ​​dead tissue) to the epicardium. With such "end-to-end" necrosis, "cavity-type" complexes are transmitted, emanating directly from the genetic system (as is known, it is located in the form of branchings of the hys bundle and Purkinje fibers subendocardially). With partial damage to the myocardium with the preservation of part of the living muscle tissue in the area of ​​damage (in the form of “inclusions”), the negative QS potential will be conducted to the outer layers, but there will be modifications on the ECG during a heart attack due to depolarization, manifested by the preserved areas of the myocardium.

Changes in the S-T segment and T wave on the ECG with a heart attack

Electrocardiograms acquire the so-called mural type with a sharp shift segment S-T. The displacement down and up from the isoline depends on whether this zone passes closer to the endocardium or the epicardium.

It is clinically accepted that the shift of the S-T line in coronary atherosclerosis is also a reflection of the degree of ischemia of the corresponding myocardium.

The T wave was previously considered an indicator of the process of restoring the bioelectrical capacity of the heart after systole. It is widely believed that this wave reflects the state of myocardial metabolism associated with the expenditure and replenishment of myocardial energy resources caused by its contraction. The metabolic and functional basis of this electrocardiographic indicator did not raise doubts among clinicians due to the fact that T wave changes were characteristic of a very wide range of physiological and pathological conditions(the tooth becomes altered not only with necrotic, inflammatory or sclerotic changes in the heart, but also with inhalation of a mixture poor in oxygen during hard work). In the experiment, the inversion of the T wave was obtained when the heart was exposed to heat, cold. Of all the changes that are observed in coronary atherosclerosis and other myocardial lesions, changes in the direction and wave of the T wave are the most frequent on the ECG during a heart attack, detectable already at weak degrees defeat and most reversible. The dynamic, temporary nature of the changes in this tooth is one of the proofs of the metabolic nature of the changes underlying it.

The question arises, what are chemical changes myocardium, leading to disruption of the course of electrical potentials and pathological ECG in a heart attack? An important prerequisite for clarifying this issue was the experience of M. G. Udelnov, which consists in the following. A piece of dead muscle tissue (taken from any animal) was applied to the heart of a cold-blooded (frog) or warm-blooded (rabbit) in situ (in vivo). As soon as a piece of dead tissue is applied to the heart, the electrocardiogram changes from normal to monophasic. As soon as a piece of tissue is removed from the surface of the heart, the electrocardiogram becomes normal. Similar experience has shown that to obtain a monophasic electrocardiogram, it is not necessary to apply a ligature to the coronary artery. Obviously, changes in the electrocardiogram under these conditions are due to some chemical products, which pass from a piece of dead tissue attached to the heart into the heart muscle.

In favor of the significance of changes in the composition of electrolytes in the myocardium during a heart attack (in the sense of the electrocardiographic picture), some clinical data also speak. So, during catheterization of the heart in patients with a heart attack in the blood of the coronary sinus, an increase in the content of potassium was noted. In the acute phase of the disease, hyperkalemia is observed (with a simultaneous decrease in the content of other electrolytes, in particular sodium). An excess of potassium in the blood is the result of its transition from the left ventricle affected by a heart attack.

In severe heart attacks, the ECG usually shows the entire electrocardiographic triad (change in the ST segment, QRS complex, T wave); with limited necrosis that does not cover the entire thickness of the heart wall, a monophasic curve on the ECG during a heart attack is not observed, but there is only a decrease in the S-T interval and inversion (or other changes) of the T wave.

Changes in I and II standard leads on the ECG during a heart attack indicate lesions localized in the anterior wall of the heart, and changes in III and II standard leads of the electrocardiogram indicate a lesion localized in the posterior wall of the heart.

Changes in chest leads

With the introduction into practice of ECG in thoracic infarction, the boundaries of topical diagnosis of foci of myocardial damage (and, of course, the diagnostic possibilities in general) have expanded significantly. Usually use six chest assignments, but their number can be increased if necessary; in fact, each point on the surface of the chest wall can serve to lead one of the electrodes. It is possible to draw up, using multiple chest leads, a kind of topographic map of the location of changes in the myocardium and, at the same time, to assess the degree of their massiveness (size). Of course, chest leads are suitable for recognizing focal lesions of the anterior and partly lateral walls of the heart. With extensive lesions of the anterior and anterolateral walls of the heart, changes in the electrocardiogram are noted both in standard I and II, and in all chest leads.

Undoubted advantages for topical and early diagnosis using ECG in infarction are given by unipolar leads according to Wilson or Goldberger. Changes on the ECG during a heart attack in leads V1-V2 indicate the localization of the lesion in the anterior part of the interventricular septum. Changes in the ECG during a heart attack in leads V5-V6 are characteristic of lesions in the outer (lateral) part of the left ventricle. Isolated changes indicate damage to the anterior wall in the area adjacent to the interventricular septum (with partial involvement) and the apex.

As you know, changes in the T wave in lead III are sometimes found in healthy individuals, but at the same time they can also indicate the presence of foci of necrosis in the posterior wall. To differentiate a negative T wave caused by organic changes from similar changes in this wave not associated with myocardial diseases (but depending on the position of the heart, high standing of the diaphragm, cardiac hypertrophy), unipolar lead aVF can be used. When the posterior wall is affected (usually due to coronary atherosclerosis, especially with infarctions of this localization), a deep Q wave, a negative T wave is observed both in standard lead III and in lead aVF, while in people without myocardial damage, in whom these changes are found in III standard lead, in aVF the Q wave is normal, and the T wave is positive.

An ECG with a heart attack allows you to determine atrial necrosis (although they are rarely isolated); in these cases, atrial P waves change and shift P-Q interval, With a left atrial infarction, a change in the P wave in the form of broadening, splitting or inversion in lead I, and the P-Q interval shifts down; with right atrial infarction, changes in the P wave and a downward shift in the P-Q interval are noted. Significance for the diagnosis of atrial infarction have electrocardiographic signs of atrioventricular blockade, atrial form paroxysmal tachycardia, atrial extrasystole and atrial fibrillation.

ECG for myocardial infarction

One of the key topics in electrocardiography is the diagnosis of myocardial infarction. Let's take a look at this important topic in the following order:

Information related to "ECG in myocardial infarction"

Introduction Causes of myocardial infarction Symptoms of myocardial infarction Forms of infarction Factors in the development of myocardial infarction Prevention of myocardial infarction Probability of developing complications of myocardial infarction Complications of myocardial infarction Diagnosis of acute myocardial infarction Urgent care in case of myocardial infarction Help before the arrival of the ambulance in case of myocardial infarction Should be able to resuscitate

Rice. 99. Intramural myocardial infarction In this type of myocardial infarction, the myocardial excitation vector does not change significantly, potassium effluent from necrotic cells does not reach the endocardium or epicardium and does not form damage currents that can be displayed on the ECG tape as a shift of the ST segment. Consequently, from the ECG signs of myocardial infarction known to us, there remained

The above listing of ECG signs of myocardial infarction allows us to understand the principle of determining its localization. So, myocardial infarction is localized in those anatomical regions of the heart, in the leads from which the 1st, 2nd, 3rd and 5th signs are recorded; 4th sign plays a role

A consistent change in the ECG in myocardial infarction, depending on the stage of this disease, is strictly natural (see Chapter VII.3). However, in practice, situations sometimes arise when ECG signs of an acute or subacute stage of myocardial infarction persist. long time and do not go into the stage of scarring. In other words, the elevation of the S-T segment above is recorded on the ECG for a rather long time.

Rice. 98. Subendocardial myocardial infarction In this myocardial infarction, the magnitude of the myocardial excitation vector does not change, since it originates from the conduction system of the ventricles, laid under the endocardium, and reaches the intact epicardium. Therefore, the first and second ECG signs of a heart attack are absent. Potassium ions during necrosis of myocardiocytes pour out under the endocardium, forming

Rice. 97. Large-focal myocardial infarctions The figure shows that the recording electrode A, located above the area of ​​the transmural infarction, will not record the R wave, since the entire thickness of the myocardium has died and there is no excitation vector here. Electrode A will register only the pathological Q wave (opposite wall vector display). In case of subepicardial

On fig. 89 schematically shows the myocardium of the ventricles. Rice. 89. Excitation of normal myocardium Vectors of excitation of the ventricular myocardium spread from the endocardium to the epicardium, they are directed to the recording electrodes and will be graphically displayed on the ECG tape as R waves (vectors between the ventricular septum are not considered for ease of understanding). When

At its core, myocardial infarctions are divided into two large groups: large-focal and small-focal. This division is focused not only on the volume of necrotic muscle mass but also on the peculiarities of myocardial blood supply. Rice. 96. Features of myocardial blood supply Nutrition of the heart muscle is carried out through the coronary arteries, anatomically located under the epicardium. By

Myocardial infarction is dangerous in many ways, due to its unpredictability and complications. The development of complications of myocardial infarction depends on several important factors: 1. the magnitude of damage to the heart muscle, the larger the area affected by the myocardium, the more pronounced the complications; 2. localization of the zone of myocardial damage (anterior, posterior, lateral wall of the left ventricle, etc.), in most cases it occurs

Sometimes, when registering an ECG in patients during an anginal attack or immediately after it, the signs characteristic of the acute or subacute stage of myocardial infarction are determined on the electrocardiogram, namely, the horizontal rise of the ST segment above the isoline. However, this segment elevation persists for seconds or minutes, and the electrocardiogram quickly returns to normal, unlike a heart attack.

Myocardial infarction clinic. ECG for myocardial infarction

The condition that determines results of myocardial infarction therapy. is his early diagnosis and an adequate assessment of the patient's condition for timely interventions, since all etiopathogenetic therapy gives the main results within the "time window" lasting up to 6 hours.

generally accepted criteria diagnosis of myocardial infarction are character pain syndrome, ECG changes, enzyme disorders. The consequences appear later than 6 hours, and therefore they do not play a special role for early intervention.

For early ECG diagnostics of myocardial infarction it is necessary to dwell on modern data on the ECG picture of MI in the acute phase. The most common classification of myocardial infarction was based on the identification of electrocardiographic and anatomical features. So, MI is divided into transmural and non-transmural, large- and small-focal. It has now been established that ECG signs and morphology are not identical, that is, MI with a pathological Q wave will not necessarily be end-to-end and vice versa. A new classification of MI according to ECG signs was adopted based on their comparison with the clinic, course and prognosis. According to it, MI is divided into a heart attack with a Qr wave on the ECG (the presence of pathological Q in at least 2 leads) and a heart attack without a Q wave with changes only in the final part of the ventricular ST segment elevation complex, the presence of an “ischemic” T wave.

From the analysis of clinical data it follows that a heart attack with a Q-wave on the ECG has a more severe prognosis in the acute period, however, heart attacks without a Q-wave on the ECG, in turn, give a number of adverse consequences in the first year after their development.

The difference in early and long-term forecasts is associated with morphofunctional characteristics of myocardial infarction with a pathological Q-wave on the ECG and without it. Q-wave MI usually develops as a result of rapid complete occlusion of a relatively large coronary artery (CA). The infarction process is quickly completed. The prognosis is determined by the magnitude of MI and the state of the myocardium. MI without a Q-wave is the result of incomplete closure of the CA, often smaller. A significant number of patients have a previous lesion of the coronary artery with the development of collaterals. All this determines the best prognosis. acute period. However, partial thrombosis in the future can turn into complete, and the presence of previous atherosclerotic changes in the CA creates conditions for progression in some patients. Hence the worsening of the late prognosis in MI without a pathological Q-wave.

ECG also does not provide an opportunity to distinguish from the group of patients with MI without a Q-wave on the ECG of individuals with "small-focal" MI. This purely anatomical representation cannot be accurately verified either by ECG or clinically.

It is well known that the heavier anterior myocardial infarctions. However, among diaphragmatic (posterior) MI, there are also severe forms. These include those in which the septal zone is involved with the development of severe arrhythmias and blockades, involvement of the right ventricle, as well as diaphragmatic MI with the appearance of a decrease in ST in the V1-3 chest leads and an increase in the R wave in these positions, which is associated with involvement in the posterior MI. -high areas of the myocardium. The prognosis for these patients is relatively worse. For the diagnosis of right ventricular MI, leads VR2-4 are used.

Availability clinical electrocardiographic syndrome The path of development of myocardial infarction allows in the first hours to make the correct diagnosis and start intensive causal therapy.

To resolve the issue about the scope medical measures it is also necessary, especially if several hours have passed since the onset of the pain attack, to determine the severity of the patient's condition, his immediate prognosis.

This is the last and most difficult part of my EKG cycle. I will try to tell it in an accessible way, taking as a basis " Guide to Electrocardiography» V. N. Orlova (2003).

heart attack(lat. infarcio - stuffing) - necrosis (necrosis) of the tissue due to the cessation of blood supply. The reasons for stopping blood flow can be different - from blockage (thrombosis, thromboembolism) to sharp spasm vessels. A heart attack may occur in any organ, for example, there is a cerebral infarction (stroke) or a kidney infarction. In everyday life, the word "heart attack" means exactly " myocardial infarction”, i.e. death of the muscle tissue of the heart.

In general, all heart attacks are divided into ischemic(more often) and hemorrhagic. With an ischemic infarction, the flow of blood through the artery stops due to some kind of obstacle, and with a hemorrhagic infarction, the artery bursts (ruptures) with the subsequent release of blood into the surrounding tissues.

Myocardial infarction affects the heart muscle not randomly, but in certain places. The fact is that the heart receives arterial blood from the aorta through several coronary (coronary) arteries and their branches. If using coronary angiography to find out at what level and in which vessel the blood flow stopped, it is possible to foresee which part of the myocardium suffers from ischemia(lack of oxygen). And vice versa.

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

Coronary angiography is a study of the patency of the coronary arteries of the heart by introducing a contrast agent into them and performing a series of x-rays to assess the rate of distribution of the contrast.

Since school, we remember that the heart has 2 ventricles and 2 atria, therefore, logically, all of them should be affected by a heart attack with the same probability. Nonetheless, It is always the left ventricle that suffers from a heart attack., because its wall is the thickest, is subjected to enormous loads and requires a large blood supply.

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

Isolated atrial and right ventricular infarctions- a huge rarity. Most often, they are affected simultaneously with the left ventricle, when ischemia passes from the left ventricle to the right or to the atria. According to pathologists, the spread of infarction from the left ventricle to the right is observed in 10-40% all patients with a heart attack (the transition usually occurs along the back wall of the heart). Transition to the atria occurs in 1-17% cases.

Stages of myocardial necrosis on the ECG

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

Type of ECG is normal.

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

1. ISCHEMIA: This is the initial myocardial injury 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 cycle, two opposite processes sequentially occur on the cell membranes of nerve and muscle cells: depolarization(excitement) and repolarization(recovery of the potential difference). Depolarization is a simple process, for which it is only necessary to open ion channels in the cell membrane, through which ions will run due to the difference in concentrations outside and inside the cell. Unlike depolarization, repolarization is an energy intensive process which requires energy in the form of ATP. ATP synthesis requires oxygen, therefore, with myocardial ischemia, the process of repolarization begins to suffer first of all. Impaired repolarization is manifested by changes in the T wave.

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

   With myocardial ischemia, the QRS complex and ST segments are normal, and the T wave is changed: it is expanded, symmetrical, equilateral, increased in amplitude (range) and has a pointed apex. In this case, the T wave can be both positive and negative - this depends on the location of the ischemic focus in the thickness of the heart wall, as well as on the direction of the selected ECG lead. Ischemia - reversible phenomenon, over time, metabolism (metabolism) is restored to normal or continues to deteriorate with the transition to the stage of damage.

2. DAMAGE: it deeper damage myocardium, in which determined under a microscope an increase in the number of vacuoles, swelling and degeneration of muscle fibers, disruption of the structure of membranes, mitochondrial function, acidosis (acidification of the environment), etc. Both depolarization and repolarization suffer. The damage is thought to primarily affect the ST segment. The ST segment may move above or below the isoline, but its arc (this is important!) when damaged bulges in the direction of displacement. Thus, in case of myocardial injury, the ST segment arc is directed towards displacement, which distinguishes it from many other conditions in which the arc is directed towards the isoline (ventricular hypertrophy, blockade of the bundle pedicles, etc.).

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

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

3. NECROSIS: myocardial death. The dead myocardium is unable to depolarize, so the dead cells cannot form an R wave in the ventricular QRS complex. For this reason, when transmural infarction(myocardial death in a certain area across the entire thickness of the heart wall) in this ECG lead of the wave no R at all., and is formed ventricular complex type QS. If necrosis has affected only part of the myocardial wall, a complex of the type QRS, in which the R wave is reduced, and the Q wave is increased compared to the norm.

   Variants of the ventricular QRS complex.

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

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

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

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

The formation of teeth on the ECG is normal.

Next, consider the drawing improved by me from V.N. necrosis zone, along its periphery - damage zone, and outside - ischemia zone. Along the wall of the heart are the positive ends of the electrodes (from No. 1 to 7).

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

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

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

Here is another picture for you to analyze on your own (“Practical electrocardiography”, V. L. Doshchitsin).

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

Stages of development of a heart attack on the ECG

The meaning of the stages of development of a heart attack is very simple. When blood supply is completely cut off in any part of the myocardium, then in the center of this area, muscle cells die quickly (within several tens of minutes). At the periphery of the focus, cells do not die immediately. Many cells gradually manage to “recover”, the rest die irreversibly (remember, as I wrote above, that the phases of ischemia and damage cannot exist for too long?). All these processes are reflected in the stages of development of myocardial infarction. There are four of them: acute, acute, subacute, cicatricial. Next, I give the typical dynamics of these stages on the ECG according to Orlov's guidance.

1) Acute stage of myocardial infarction (damage stage) has an approximate duration from 3 hours to 3 days. Necrosis and its corresponding Q wave may or may not be present. If the Q wave is formed, then the height of the R wave in this lead decreases, often up to complete disappearance (QS complex in transmural infarction). The main ECG feature of the most acute stage of myocardial infarction is the formation of the so-called monophasic curve. The monophasic curve consists of ST segment elevation and high upright T wave that merge together.

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

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

2) Acute stage lasts up to 2-3 weeks(to make it easier to remember - up to 3 weeks). Areas of ischemia and damage begin to decrease. The area of ​​necrosis is expanding the Q wave also expands and increases in amplitude. If the Q wave does not appear in the acute stage, it forms in the acute stage (however, there are infarcts and without Q wave, about them below). ST segment due to damage zone limitation begins to gradually approach the isoline, a T wave becomes negative symmetrical "coronary" due to the formation of a zone of transmural ischemia around the area of ​​damage.

3) Subacute stage lasts up to 3 months, occasionally longer. The damage zone disappears due to the transition to the ischemia zone (therefore, the ST segment comes close to the isoline), the area of ​​necrosis stabilizes(so about the true size of the infarct are judged at this stage). In the first half of the subacute stage, due to the expansion of the ischemic zone, negative the T wave broadens and grows in amplitude up to gigantic. In the second half, the ischemia zone gradually disappears, which is accompanied by the normalization of the T wave (its amplitude decreases, it tends to become positive). The dynamics of changes in the T wave is especially noticeable on the periphery ischemic areas.

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

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

Stages of myocardial infarction.

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

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

There are no zones of damage and ischemia in the cicatricial stage, so the ST segment is on the isoline, and the T wave can be up, down, or flattened. However, in some cases, in the cicatricial stage, it is still recorded small negative T wave, which is associated with constant irritation of adjacent healthy myocardium by scar tissue. In such cases, the T wave in amplitude should not exceed 5 mm and should not be longer than half of the Q or R wave in the same lead.

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

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

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

Differential diagnosis of a heart attack on an ECG

In the third year while studying pathological anatomy and physiology every medical student must learn that all the reactions of the body to the same effect in different tissues at the microscopic level proceed the same type. Sets of these complex sequential reactions are called typical pathological processes . Here are the main ones: inflammation, fever, hypoxia, tumor growth, dystrophy etc. With any necrosis, inflammation develops, which results in the formation of connective tissue. As I stated above, the word heart attack came from lat. infarcio - stuffing, which is due to the development of inflammation, edema, migration of blood cells into the affected organ and, consequently, its seal. At the microscopic level, inflammation occurs in the same way anywhere in the body. For this reason infarct-like ECG changes there are also with heart injuries and tumors of the heart(metastases in the heart).

Not every "suspicious" T wave, ST segment deviated from the isoline, or suddenly appeared Q wave is due to a heart attack.

Normal amplitude T wave ranges from 1/10 to 1/8 of the amplitude of the R wave. A high positive symmetrical "coronary" T wave occurs not only with ischemia, but also with hyperkalemia, increased vagal tone, pericarditis(see ECG below), etc.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

By 2 main features.

1) characteristic ECG dynamics. If the ECG shows changes in the shape, size and location of the teeth and segments typical of a heart attack over time, it is possible to speak with a high degree of confidence about myocardial infarction. In the infarction departments of hospitals EKG done daily. To make it easier to evaluate the dynamics of a heart attack on the ECG (which is the most pronounced on the periphery of the affected area), it is recommended to apply marks for placement of chest electrodes so that subsequent hospital ECGs are completely identical in chest leads.

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

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

The principle is this:

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

.
Direct signs are visible in II, III and aVF leads, reciprocal- in V1-V4.

Reciprocal ECG changes in some situations are the only for which a heart attack can be suspected. For example, with posterior basal (posterior) infarction myocardium, direct signs of a heart attack can be recorded only in the lead D (dorsalis) by Sky[read e] and in accessory chest leads V7-V9, which are not included in the standard 12 and are performed only on demand.

Accessory chest leads V7-V9.

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

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

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

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

Types of heart attacks

A couple of decades ago they shared transmural infarcts(ventricular complex type QS) and non-transmural macrofocal infarcts(such as QR), but it soon became clear that this does not give anything in terms of forecast and possible complications. For this reason, heart attacks are currently simply divided into Q-heart attacks(Q-wave myocardial infarctions) and non-Q infarcts(myocardial infarctions without Q wave).

Localization of myocardial infarction

The ECG report must indicate infarct zone(for example: anterolateral, posterior, inferior). To do this, you need to know in which leads ECG signs appear. various localizations heart attack.

Here are a couple of ready-made schemes:

Diagnosis of myocardial infarction by localization.

Topical diagnosis of myocardial infarction
(elevation- rise, from English. elevation; depression- decrease, from English. depression)

Finally

If you do not understand anything from what is written, do not worry. Myocardial infarctions and in general ECG changes in coronary artery disease - the most difficult topic in electrocardiography for students medical school. At the Faculty of Medicine, ECG begins to be studied from the third year on propaedeutics of internal diseases and study for another 3 years before receiving a diploma, but few of the graduates can boast of stable knowledge on this topic. I had a friend who (as it turned out later) after the fifth year was specially assigned to the obstetrics and gynecology department in order to meet less with ECG tapes that were incomprehensible to her.

If you want to more or less understand the ECG, you will have to spend many dozens of hours for thoughtful reading teaching aids and view hundreds of ECG tapes. And when you can draw an ECG from memory of any heart attack or rhythm disturbance, congratulate yourself - you are close to the goal.

Prevalence cardiovascular disease has grown to alarming proportions in recent decades. Myocardial infarction has become the main cause of death in developed countries, the numbers continue to grow, the disease is rapidly getting younger, especially among men.

What is a myocardial infarction?

A heart attack in the language of specialists is necrosis of the heart muscle, which occurs due to insufficient blood supply to the organ.

Preceding an acute condition ischemic disease caused by a lesion or blockage coronary arteries atherosclerotic plaques.

If one of the areas of the myocardium does not receive oxygen within 20 minutes, tissue necrosis occurs. The number of dead cells depends on the size of the blocked artery. The infarction develops rapidly, accompanied by severe pain behind the sternum, which can not be removed with medicines.

Symptoms

Not so long ago, a heart attack was considered an age-related disease, but now it often happens in thirty-year-old men. Women get sick less often because they are protected by the hormone estrogen before menopause, which prevents plaque formation. Although women are less susceptible to a heart attack, they endure the disease more severely.

The main symptoms of a heart attack:

• Severe sudden pain in chest. Pressive and compressive pain radiating to the back and shoulder. Unlike angina pectoris, signs of a heart attack appear without apparent causes and stress. Often the attack begins at rest.
• Taking pills does not bring relief.
• Loss of consciousness and difficulty in breathing may occur.
• Acute heart attack is accompanied by arrhythmia, increased blood pressure and body temperature up to 38 ° C, increased heart rate.

heart attack in women

Symptoms of a heart attack in women can be washed out. In about a month, the disease is manifested by a breakdown, insomnia, unreasonable anxiety, swelling, discomfort in the abdomen, shortness of breath and aching pain.

The attack begins with severe pain in the chest, but since women are able to patiently endure discomfort they often ignore danger signals. The pain spreads to the neck and left arm, the jaw and teeth may hurt. Often there is severe nausea with heartburn and vomiting, dizziness, pain in the back of the head, loss of consciousness, cold sweat and stiffness in the body.

Heart attack in men

The preinfarction state is rarely manifested by fatigue and anxiety. Usually the only signal of impending trouble is pain in the heart area. Sometimes the attack begins with nausea, the upper back hurts, there are unpleasant sensations in the elbows, arms and legs, less often in the jaw. Choking, burning in the throat, heartburn, hiccups, pallor and a sharp loss of strength often develop.

Men rarely ignore the disease, so they receive help in a timely manner and death due to myocardial infarction is less common than in women.

The difference in manifestations is explained by physiological features:

• A man's heart is larger than a woman's.
• Different heart rate in men and women.

To the question: "Is it possible to determine a heart attack by the first signs?" - There is only an affirmative answer. From timeliness medical care depends on the prognosis for recovery. ambulance should be promptly called when several signs of an attack appear simultaneously.

Symptoms of a heart attack before diagnosis

Any of these symptoms should be a signal for urgent medical attention.

Diagnostics

If a heart attack is suspected, an ECG is done necessarily and as early as possible. If abnormalities in the work of the heart are detected, the decoding of the cardiogram will show the characteristic signs of ischemia or acute infarction, and will also allow you to determine the type of damage and take adequate measures.

What does the electrocardiogram show (photo with transcript)?

The figure shows what the ECG section looks like:

• R- excitation of the atria. A positive value indicates sinus rhythm.
• PQ interval- the time of passage of the excitatory impulse through the atrial muscle to the ventricles.
• QRS complex- electrical activity of the ventricles.
• Q- an impulse in the left side of the interventricular septum.
• R- excitation of the lower cardiac chambers.
• S- completion of excitation in the lower left chamber.
• ST segment- the period of excitation of both ventricles.
• T– restoration of the electrical potential of the lower chambers.
• QT interval- the period of contraction of the ventricles. For the rhythm frequency characteristic of gender and age, this value is constant.
• TR segment- a period of electrical passivity of the heart, relaxation of the ventricles and atria.

Types of heart attack

With a heart attack, tissue necrosis and cicatricial changes can occur in different parts of the myocardium.

Localization at the site of damage differs as follows:

• Transmural infarction

Damages all layers of the myocardium. On the cardiogram, a penetrating lesion is reflected in a characteristic curve and is called a Q infarction. A Q wave is formed, indicating the absence of electrical activity in the scar tissue.

The Q wave forms within hours or days after a heart attack and persists for a long time. With timely medical intervention and providing enough oxygen to the heart, damage can be prevented.

The absence of Q waves on the cardiogram does not exclude a heart attack.

• Mini heart attack

With this type of lesion, point injuries are noted. Necrosis does not interfere with the work of the heart muscle and is often carried on the legs.

A change in the state of the tissues is often detected on the ECG after some time. After a mini-infarction, a Q-wave does not form.

• subepicardial, subendocardial or non-wave infarction

The center of damage is located in the left ventricle on the inner layer. ST-segment depression is reflected in the ECG. The cardiogram does not show a Q wave, and smoothing of the ST segment becomes evidence of violations.

Similar conditions can be caused by anginal attacks or provoked by taking medications for arrhythmias.

A subendocardial infarction is said to occur when the T segment shows horizontal or oblique depression. At physical activity a decrease of more than 1 mm or an oblique ascent of the curve is considered a sign of illness.

• intramural

The middle section of the muscle is damaged, and the outer and inner shells do not suffer. In the description of the ECG, the doctor will include a T-wave inversion that is negative for up to 2 weeks. The ST segment does not become flat.

With the help of an ECG, the doctor determines the localization of the lesion.

After a heart attack, disorders can be located on:

• Front baffle
• Anterior wall of the left ventricle (in the endocardium, epicardium, or transmurally)
• On the back wall (subendocardial or transmural)
• side
• In the lower section
• Combined arrangement possible

The most severe consequences are observed after anterior septal infarction and damage to the anterior wall of the left ventricle. The prognosis for this form of the disease is negative.

Isolated violation of the right ventricle is extremely rare, usually combined with the lower lesion of the left ventricle. Suffering predominantly back wall right ventricle, sometimes - anterior lateral. On the ECG, it is determined with an additional description of the indicators in the right side of the sternum.

Stages of development

With any localization, the development of a heart attack takes place in several stages. Whatever layers of the heart are affected by a heart attack, its development can be tracked in several stages. After the ECG study, the doctor receives a photo with a transcript. The stages of the disease look like this:

Types of infarction by area affected

macrofocal

Transmural infarcts, which are characterized by the following ECG indicators:

• Electrode A registers the Q wave
• Electrode B - tooth R

The amplitude of the teeth allows you to judge the depth of the lesion.

Small focal

• subendocardial infarction. The ECG shows a shift segment S-T below the isoelectric line, but the Q wave is not recorded.
• Intramural infarction is characterized by necrosis of the myocardial wall and preservation of the endocardium and epicardium.

Why is a heart attack dangerous?

Modern medicine knows how to eliminate the danger acute heart attacks, but even after the treatment course, the disease is dangerous with complications:

• Acute heart failure;
• The likelihood of myocardial rupture;
• Discoordination of contractions of the heart muscle (fibrillation);
• Arrhythmia;
• Aneurysm of the left ventricle;
• thrombosis of the heart.

In addition, the application medicines can cause ulcers and bleeding in gastrointestinal tract, hemorrhagic strokes, a steady decrease in blood pressure to the level of hypotension.

ECG: importance for the diagnosis and treatment of heart attacks

The importance of the ECG study lies not only in the diagnosis of heart attacks, but also in the ability to differentiate diseases with similar symptoms.

So, in acute conditions associated with problems in the abdominal cavity, hernia of the diaphragm, blockage of the pulmonary artery, angina pectoris, pericarditis in the acute stage and other diagnoses, the disease manifests itself with pain, the localization of which allows the likelihood of a heart attack.

At the same time, altered cardiogram indicators do not in all cases indicate problems in the work of the heart, and the absence of alarming indicators does not guarantee well-being in relation to cardiac activity.

Early diagnosis can reduce mortality from heart attacks, since it is possible to isolate the site of necrosis only in the first six hours after the first symptoms.

Video: ECG diagnosis of myocardial infarction

Myocardial infarction on the ECG has a number characteristic features, which help to differentiate it from other conduction and excitability disorders 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 focus. Therefore, the cardiogram is removed, if possible, even 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 of such a study, one can obtain comprehensive information about the work 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 the deformation of the QRST complex, in particular, a significant decrease in the R wave or its complete absence.

The classic ECG picture consists of several sections 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 well-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. The lengthening of this interval indicates a violation of conductivity.
3. QRST complex- the 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 axis of the ECG that does not have teeth), with pathologies capable of falling 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 the heart tissue. In the case of a heart attack - with necrosis, that is, the necrosis of myocardial cells, followed by their replacement with connective tissue. The stronger and deeper the damage, the larger the area of ​​necrosis, the more noticeable the changes on the ECG will be.

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

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

Further, the changes affect the Q wave - it becomes pathologically deep, which indicates a disruption in the work of pacemakers - nodes from special cells in the thickness of the myocardium, which begin to contract the ventricles.

The ST segment also changes - normally it is on the isoline, but with a heart attack it can rise higher or fall lower. In this case, they speak of segment elevation or depression, which is a sign of ischemia of the heart tissues. By 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 opposite leads.

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

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

The tape can move at a speed of 50 and 25 mm per second, a lower speed with better detail has a greater diagnostic value. When making a diagnosis of a heart attack, not only changes in leads I, II and III are taken into account, but also in enhanced ones. If the device allows you to record 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 stage of scarring, 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 the 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) related to development acute insufficiency circulation in the tissues of the heart. This stage does not last long, so they rarely have time to register it on a cardiogram tape, but its diagnostic value is quite high. The T wave at the same time increases, sharpens - they talk about 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 extends into the deeper layers of the heart. Reciprocal changes are possible.
2. Acute stage (stage of necrosis) 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 teeth. 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. Rhythm disturbances are characteristic - arrhythmias, extrasystoles.
3. Recognize the onset of the subacute stage it is possible to stabilize the ST segment. When it returns to the baseline, the infarction no longer progresses due to ischemia, the recovery process begins. Highest value in this period has a comparison of the existing size of the T wave with the original. It can be either positive or negative, but will slowly return to the isoline in sync with the healing process. The secondary deepening of the T wave in the subacute stage indicates inflammation around the necrosis zone and lasts, with the right drug therapy, not for long.
4. In the stage of scarring, the R wave rises again to its characteristic indicators, and T is already on the isoline. In general, the electrical activity of the heart is weakened, because part of the cardiomyocytes died and was replaced connective tissue, which does not have the ability to conduct and reduce. Pathological Q, if present, normalizes. 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 focus.

The main types of heart attack on the ECG

In the clinic, a heart attack is classified depending on the size and location of the focus. 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 a circulatory disorder has occurred in a large coronary vessel, and a large amount of tissue is affected. The main feature is a deep and wide Q, 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, deep T is observed in the subacute period. 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 has developed in the areas fed by the terminal branches of the coronary arteries; this type of disease has a more favorable prognosis. In intramural infarction (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. With subendocardial infarction (center at the inner shell), T is normal, and ST is depressed.

Depending on the location, determine the following types heart attack:

1. Anterior septal Q-infarction- noticeable changes in 1-4 chest leads, where there is no R in the presence of a wide QS, ST elevation. In standard I and II - pathological Q, classical for this type.
2. Lateral Q-infarction- identical changes affect 4-6 chest leads.
3. Posterior, or diaphragmatic Q-infarction, aka lower- pathological Q and high T in leads II and III, as well as increased from the right leg.
4. ventricular septal infarction- in standard I, deep Q, ST elevation and high T. In 1 and 2 chests, pathologically high R, A-V blockade is also characteristic.
5. Anterior non-Q infarction- in I and 1-4 chest T is higher than the preserved R, and in II and III, a decrease in all teeth along with ST depression.
6. Posterior non-Q infarction- in standard II, III and chest 5-6 positive Т, decrease in R and ST depression.

Video

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