Segment elevation st v2 v3 offset. Normal ECG: ST segment

The most common important changes in the ST segment and the T wave are those that are characteristic of myocardial ischemia and infarctions. Because ventricular repolarization is dependent on myocardial perfusion, patients with coronary disease often show reversible ST-segment and T-wave changes with transient myocardial ischemia.

Recall that abnormal Q waves serve as indicators of myocardial infarction, but do not distinguish acute from one that occurred a week or a year ago. But in acute myocardial infarction, a series of characteristic changes in the ST segment and the T wave occurs, which make it possible to differentiate acute and non-acute myocardium (Fig. 4.24). In acute Q-wave myocardial infarction, ST-segment elevation appears first, often accompanied by a tall T wave. At this early stage, myocardial cells are still viable, and Q waves are not yet registered. However, after a few hours, the death of myocytes leads to a decrease in the amplitude of the R wave and the appearance of pathological Q waves in the ECG leads located above the infarction zone. In the first two days from the onset of a heart attack, the ST segment rises, the T wave becomes negative, and the Q wave deepens. After a few days, the ST segment returns to the isoline, but the T waves remain negative.

Weeks and months after an infarction, the ST segment and T waves become normal, but abnormal Q waves remain, which is an invariable sign of MI. If the ST segment remains elevated after several weeks, then there is a possibility of a bulging fibrous scar (ventricular aneurysm) at the site of the infarction. A similar evolution of changes in the QRS complex, ST segment and T waves is recorded using leads located above the infarction zone (Table 4.3). In this case, as a rule, reciprocal changes are observed in the leads located on the opposite side. For example, in acute anterior septal MI, ST elevation in chest leads x and V2 is accompanied by reciprocal changes (ST depression) in leads II, III, and aVF, i.e., in leads lying above the opposite (lower) wall of the ventricle of the heart.

The mechanism of ST-segment elevation during acute MI is not yet fully understood. However, there is an opinion that such changes occur from damaged myocardial cells located directly near the infarction zone; they excite abnormal systolic and diastolic currents. Objecting to this explanation, others believe that such cells are not capable of depolarization, but have an abnormal permeability that prevents them from fully repolarizing (Fig. 4.25). As a result, at rest, partial depolarization of such cells causes the appearance of forces directed away from the damaged segment, causing a downward displacement of the isoline. Due to the fact that the electrocardiograph registers only the relative, and not the absolute value of the voltage, the deviation of the isoline is not captured. As all the cells of the myocardium, including the cells of the affected area, completely depolarize, the resulting electrical potential of the heart really becomes zero. However, due to the pathological downward displacement of the isoline, the ST segment appears to be located above the isoline. During repolarization, the damaged cells return to an abnormal hyperpermeable state in diastole, and the ECG again displays an abnormal baseline shift due to the presence of abnormal forces directed away from the electrode. Thus, the relative displacement of the isoelectric line has a certain effect on the amount of ST segment elevation in MI.

In non-transmural myocardial infarctions, ST-segment depression occurs in leads that cross the area of infarction, rather than its elevation. In this situation, the diastolic permeability of damaged cells adjacent to the infarcted area causes the appearance of electrical forces directed from the endocardium to the epicardium and, consequently, towards the ECG electrodes. Thus, the basal line of the ECG is shifted upwards (Fig. 4.25). After complete depolarization of the heart, its electrical potential returns to its true zero value, but in relation to the abnormal basal line, it creates an apparent decrease in the ST segment.

Rice. 4.25. Theoretical explanation for the occurrence of ST deviations during acute MI. Upstairs. Leakage of ions causes partial depolarization of the damaged myocardial cell before the start of the process of propagation of electrical excitation, which causes the appearance of forces directed away from the affected area and a decrease in the baseline of the ECG. But this process is not displayed on the ECG, since it registers the relative, and not the absolute value of the voltage. While the heart has completely depolarized, the true voltage value is zero, but there is an apparent ST-segment elevation compared to an abnormally low baseline. At the bottom. In non-transmural MI, the process proceeds in a similar way, but ion leakage occurs from the subendocardial tissue, so that the partial depolarization preceding excitation is directed towards the recording electrode; therefore, the basal line is elevated. After the end of the depolarization, the voltage is indeed zero, but the ST segment seems to be slightly reduced in relation to the upshifted basal line.

Other common causes of ST segment and T wave changes associated with impaired cardiomyocyte repolarization are described in Fig. 4.26.

Synonyms: ST elevation myocardial infarction, acute myocardial infarction (MI), acute transmural infarction, myocardial infarction (MI) with Q wave.

Acute myocardial infarction (MI), now referred to as STEMI, occupies an important place among cardiovascular diseases with a possible fatal outcome. This is the most severe form of ACS apart from sudden cardiac death.

Pathophysiology. Due to hemorrhage into the atherosclerotic plaque and gradually increasing thrombosis of the coronary artery, stenosis of its lumen occurs with an outcome in occlusion. This leads to ischemia of the myocardium supplied by the affected coronary artery, and its necrosis.

Careful perennial epidemiological studies patients with myocardial infarction (MI) have shown that they have risk factors. The combination of these factors contributes to the acceleration of the atherosclerotic process and a multiple increase in the risk of myocardial infarction (MI). Currently known risk factors include smoking, elevated blood cholesterol levels, high blood pressure and diabetes mellitus.

In addition to the above four main risk factors, others are known, in particular, overweight, stress, physical inactivity, hereditary predisposition.

Symptoms of ST Elevation Myocardial Infarction (STEMI):
Severe anginal pain lasting more than 15 minutes
ST segment elevation on ECG
Positive blood test results for creatine kinase, its MB fraction, troponins (I or T)

Diagnosis of myocardial infarction with ST segment elevation (STEMI)

ECG is usually critical to the diagnosis. Within 1 hour after the onset of a typical pain attack, in most cases, clear signs of MI are noted on the ECG. Therefore, the diagnosis of MI is the most important task of electrocardiography.

When analyzing ECG in patients with myocardial infarction (MI), attention should be paid to the following features.

Signs of IM should be unambiguous. In most cases, ECG changes are so typical that a diagnosis can be made without resorting to further examination.

Other important diseases, especially in the acute stage, such as an attack of stable angina pectoris in a patient with coronary artery disease, pericarditis or myocarditis, should not be misinterpreted as myocardial infarction. For example, with pericarditis, there are no clear signs of MI on the ECG.

In the process of diagnosing MI, it is also necessary to establish the stage of MI, i.e. it should at least indicate whether it is an acute phase or an old infarct. This is important, since the treatment of MI has its own characteristics depending on the stage of the disease.

The diagnosis should also reflect the location of the MI. In particular, it is necessary to differentiate the infarction of the anterior wall of the left ventricle from the infarction of its posterior wall. Depending on the location of the MI, it is possible to roughly determine which coronary artery is affected.

Interpretation of individual ECG indicators in myocardial infarction (MI)

1. Large Q wave (necrosis zone). Due to myocardial necrosis, EMF does not occur in the infarction zone. The resulting EMF vector is directed away from the necrosis zone. Therefore, the ECG records a deep and widened Q wave (Purdy's Q wave) in leads that are located directly above the MI zone.

2. ST segment elevation. The zone of myocardial necrosis is surrounded by a zone of damage. Damaged tissue, compared to healthy tissue at the end of ventricular depolarization, carries a smaller negative charge, and therefore is less excitable. Therefore, a vector appears in the damage zone, which corresponds to the ST segment and is directed from the electrically negative myocardium to the electrically less negative one, i.e. to the portion of the myocardium that is relatively positively charged. Therefore, on the ECG corresponding to the damage zone, ST segment elevation is recorded.

3. Spiked negative T wave. The ECG of the ischemic zone detects changes in the repolarization phase. The repolarization vector is directed from the ischemic zone to the healthy myocardium. When the epicardial layers of the myocardium are damaged, the EMF vector is directed from outside to inside. Therefore, in leads that normally have positive T waves, symmetrical, spiked negative T waves (Purdy's coronary T waves) now appear.

The results of the study become positive 2-6 hours after the development of ischemia.

Appearance troponins in blood serum reflects the formation of a thrombus in the coronary artery. Therefore, a blood test for troponins, due to its high sensitivity (90% when performed after 6 hours) and specificity (approximately 95%), is the standard study in the emergency diagnosis of acute myocardial infarction (MI).

Definition serum markers of myocardial necrosis plays an important role not only in the diagnosis of acute myocardial infarction (MI), but also allows you to judge its dynamics. Their importance is especially great in cases where ECG data is erased or masked by blockade of the PG leg or WPW syndrome. It is also difficult to diagnose myocardial infarction (MI) in those cases when the infarction is localized in the basin of the circumflex branch of the left coronary artery.

Currently in diagnosis of myocardial infarction(IM) use both of these research methods: ECG and blood test for serum markers of myocardial necrosis. Moreover, they do not compete, but complement each other.

Despite this, as shown earlier completed In our study, the predictive value of the ECG is higher compared to a blood test for serum markers of myocardial necrosis, since in most cases of acute MI, changes on the ECG, when carefully read, appear already within 1 hour after the onset of ischemia and are reliable diagnostic signs, while an increase in the level of serum markers in many cases is not associated with ischemic myocardial damage.

In addition, a significant advantage ECG It also consists in the fact that it can be performed as many times as necessary without causing the patient any inconvenience.

When chest pain occurs, in all cases, register ECG. If MI is suspected, it is recommended to perform a control ECG at least every 3 days in combination with a blood test for serum markers of myocardial necrosis.

On ECG in acute myocardial infarction(MI) the following changes appear: regardless of the location of MI, i.e. in both anterior wall infarction and posterior wall infarction in the acute phase, there is a significant change in the ST segment. Normally, there is no ST segment elevation, although sometimes slight elevation or depression is possible even in apparently healthy people.

At acute myocardial infarction(MI) The first sign on the ECG is a distinct ST segment elevation. This rise merges with the positive T wave following it, and, unlike the norm, the border between them disappears. In such cases, one speaks of monophasic deformation of the ST segment. Such a monophasic deformity is pathognomonic for the acute phase, i.e. for "fresh" MI.

Differential diagnosis of myocardial infarction with ST segment elevation(STEMI) with a positive T wave is shown in the figure below.

Shortly before the advent monophasic deformation of the ST segment upon careful analysis, extremely high peaked T waves (the so-called asphyxic T waves, or hyperacute T waves) due to acute subendocardial ischemia can be noted.

Sharp and broad Q wave can be registered already in the acute stage of MI, but this feature is not mandatory. Negative T wave in the acute stage may still be absent.

At "old" myocardial infarction(MI) the previous ST segment elevation is no longer detectable, but there are other changes affecting the Q and T waves.

IN normal Q wave narrow (0.04 s) and shallow, not exceeding the height of the fourth part of the R wave in the corresponding lead. With the "old" MI, the Q wave is wide and deep.

T wave is normally positive and is at least 1/7 of the height of the R wave in the corresponding lead, which distinguishes it from the T wave in MI after the acute stage (i.e., in the early phase of stage II), when it becomes deep, peaked and negative (coronary Purdy's T wave), in addition, there is depression of the ST segment. However, sometimes the T wave is located on the isoline and is not reduced.

Usually for determining the ECG stage of myocardial infarction(IM) the classification shown in the figure below is sufficient. The classification shown in the figure above makes it possible to more accurately assess the dynamics of MI.

In general, it is believed that the more leads, in which pathological changes are noted, the more extensive is the zone of myocardial ischemia.

Changes ECG, namely a large Q wave (a sign of necrosis, Purdy's Q wave) and a negative T wave with or without ST segment depression are typical of the formed scar in "old" MI. These changes take place as the patient's condition improves. However, it is known that, despite clinical improvement and healing, signs of an old infarction, especially a large Q wave, persist.

ST segment elevation with positive T wave, i.e. Monophasic ST segment deformity with a large Q wave persisting for more than 1 week and transition of the ST segment into a slowly rising arch should raise suspicion of a cardiac aneurysm.

Further tactics after the diagnosis of myocardial infarction with ST elevation (STEMI) is the same as for myocardial infarction without ST segment elevation (NSTEMI).

W. Brady et al. analyzed the results of evaluation by emergency physicians of 448 ECGs with ST segment elevation. An erroneous assessment of the ECG in the form of overdiagnosis of acute myocardial infarction (MI) with subsequent thrombolytic therapy in patients was detected in 28% of cases with heart aneurysm (AS), in 23% - with early ventricular repolarization syndrome (ERVR), in 21% - with pericarditis and in 5% - with blockade of the left leg of the His bundle (LBBB) without signs of MI.
The assessment of the ECG phenomenon, which consists in ST segment elevation, is complex and includes an analysis of not only the features of ST changes and other ECG components, but also the clinical picture of the disease. In most cases, a detailed analysis of the ECG is sufficient to differentiate the underlying syndromes leading to ST-segment elevation. ST changes can be a variant of a normal ECG, reflect non-coronary changes in the myocardium and cause acute coronary pathology requiring emergency thrombolytic therapy. Thus, the therapeutic tactics in relation to patients with ST segment elevation is different.
1. Norma
Concave ST segment elevation is acceptable in limb leads up to 1 mm, in chest leads V1-V2, sometimes V3 up to 2-3 mm, in leads V5-V6 up to 1 mm (Fig. 1).
2. Myocardial infarction
with ST segment elevation (MI)
MI is necrosis of a section of the heart muscle, resulting from absolute or relative insufficiency of the coronary circulation. Electrocardiographic manifestations of ischemia, damage and necrosis of the myocardium depend on the location, depth of these processes, their duration, and the size of the lesion. It is believed that acute myocardial ischemia manifests itself mainly by changes in the T wave, and damage - by displacement of the ST segment, necrosis - by the formation of an abnormal Q wave and a decrease in the R wave (Fig. 2, 4).
The ECG of a patient with MI undergoes changes depending on the stage of the disease. At the stage of ischemia, which usually lasts from several minutes to 1-2 hours, a high T wave is recorded above the lesion. Then, when ischemia and damage spread to subepicardial regions, ST segment elevation and T wave inversion are detected (from several hours to 1-3 days .). The processes occurring at this time can be reversible, and the ECG changes described above may disappear, but more often they pass to the next stage, with the formation of necrosis in the myocardium. Electro-cardiographically, this is manifested by the appearance of a pathological Q wave and a decrease in the amplitude of the R wave.
3. Prinzmetal's Angina (SP)
With the development of spasm of the epicardial artery and subsequent transmural damage to the myocardium, there is an increase in the ST segment in the leads, reflecting the affected area. In SP, the spasm is usually short-lived, and the ST segment returns to baseline without subsequent myocardial necrosis. In SP, the characteristic features are the cyclicity of pain attacks, the monophasic type of the curve on the ECG, and cardiac arrhythmias. If the spasm continues long enough, MI develops. The cause of angiospasm of the coronary arteries is endothelial dysfunction.
Elevation of the ST segment in SP and developing MI does not have significant differences, since it is a reflection of one pathophysiological process: transmural ischemia due to occlusion of the epicardial artery caused by transient spasm in the first state and persistent thrombosis in the second (Fig. 3, 4).
Patients with SP are predominantly young women who do not have classic risk factors for coronary heart disease (CHD), except for smoking. SP is associated with such manifestations of angiospastic conditions as Raynaud's syndrome and migratory headaches. Combines these syndromes with the possibility of developing arrhythmia.
For the diagnosis of SP, tests with physical activity are uninformative. The most sensitive and specific provocative test is the intravenous administration of 50 micrograms of ergonovine with a 5-minute interval until a positive result is obtained, while the total dosage of the drug should not exceed 400 micrograms. The test with ergonovine is considered positive when an attack of angina pectoris and a rise in the ST segment on the ECG occur. For the rapid relief of symptoms of angiospasm caused by ergonovine, nitroglycerin is used. The dynamics of changes in the ST segment in SP can be traced by long-term ECG recording using the Holter method. In the treatment of SP, vasodilators are used - nitrates and calcium antagonists, b-blockers and high doses of acetylsalicylic acid are contraindicated.
4. Aneurysm of the heart (AS)
AS usually develops after transmural MI. The bulging of the ventricular wall causes stretching of neighboring areas of the myocardium, which leads to the appearance of a zone of transmural damage in the surrounding areas of the myocardium. On the ECG for AS, a picture of transmural MI is characteristic, and therefore QS is observed in most ECG leads, occasionally Qr. For AS, a “frozen” ECG is specific, which does not undergo dynamic changes in stages, but remains stable for many years. This frozen ECG has features observed in II, III stages of MI with ST segment elevation (Fig. 5).
5. Syndrome of early repolarization of the ventricles (ERVR)
SRW is an ECG phenomenon consisting in the registration of ST-segment elevation up to 2-3 mm with a downward bulge, as a rule, in many leads, most significantly in the chest. The transition point of the descending part of the R wave into the T wave is located above the isoline, often at the place of this transition a notch or wave is determined (“camel hump”, “Osborne wave”, “hat hook”, “hypothermic hump”, “J wave”) , the T wave is positive. Sometimes, within the framework of this syndrome, there is a sharp increase in the amplitude of the R wave in the chest leads, in combination with a decrease and subsequent disappearance of the S wave in the left chest leads. ECG changes may decrease during exercise testing and regress with age (Fig. 6).
6. Acute pericarditis (OP)
A characteristic ECG sign of pericarditis is a concordant (unidirectional with a maximum QRS wave) shift of the ST segment in most leads. These changes are a reflection of damage to the subepicardial myocardium adjacent to the pericardium.
In the ECG picture of OP, a number of stages are distinguished:
1. Concordant ST shift (ST elevation in leads where the maximum wave of the ventricular complex is directed upward - I, II, aVL, aVF, V3-V6, and ST depression in leads where the maximum wave in the QRS is directed downward - aVR, V1, V2, sometimes aVL), turning into a positive T wave (Fig. 7).

4. Normalization of the ECG (smoothed or slightly negative T waves can persist for a long time). Sometimes, with pericarditis, there is involvement in the inflammatory process of the atrial myocardium, which is reflected on the ECG in the form of a shift in the PQ segment (in most leads - PQ depression), the appearance of supraventricular arrhythmias. In exudative pericarditis with a large amount of effusion on the ECG, as a rule, there is a decrease in the voltage of all teeth in most leads.
7. Acute cor pulmonale (ACC)
In ALS, ECG signs of overload of the right heart are recorded for a short time (occurs with status asthmaticus, pulmonary edema, pneumothorax, the most common cause is thromboembolism in the pulmonary artery basin). The most characteristic ECG signs are:
1. SI-QIII - the formation of a deep S wave in lead I and a deep (pathological in amplitude, but, as a rule, not widened) Q wave in lead III.
2. Elevation of the ST segment, turning into a positive T wave (monophasic curve), in the "right" leads - III, aVF, V1, V2, in combination with depression of the ST segment in leads I, aVL, V5, V6. In the future, the formation of negative T waves in leads III, aVF, V1, V2 is possible. The first two ECG signs are sometimes combined into one - the so-called sign of McGene-White - QIII-TIII-SI.
3. Deviation of the electrical axis of the heart (EOS) to the right, sometimes the formation of an EOS of the SI-SII-SIII type.
4. Formation of a high pointed P wave (“P-pulmonale”) in leads II, III, aVF.
5. Blockade of the right leg of the bundle of His.
6. Blockade of the posterior branch of the left leg of the bundle of His.
7. Increased R wave amplitude in leads II, III, aVF.
8. Acute signs of right ventricular hypertrophy: RV1>SV1, R in lead V1 more than 7 mm, RV6/SV6 ratio ≤ 2, S wave from V1 to V6, displacement of the transition zone to the left.
9. Sudden onset of supraventricular arrhythmias (Fig. 8).
8. Brugada Syndrome (SB)
SB is characterized by syncope and episodes of sudden death in patients without organic heart disease, accompanied by ECG changes, in the form of a permanent or transient right bundle branch block with ST segment elevation in the right chest leads (V1-V3).
Currently, the following conditions and diseases that cause SB are described: fever, hyperkalemia, hypercalcemia, thiamine deficiency, cocaine poisoning, hyperparathyroidism, hypertestosteroneemia, mediastinal tumors, arrhythmogenic right ventricular dysplasia (ARVC), pericarditis, MI, SP, mechanical obstruction of the outflow tract of the right ventricle ventricular tumors or hemopericardium, pulmonary embolism, dissecting aortic aneurysm, various anomalies of the central and autonomic nervous system, Duchenne muscular dystrophy, Frederick's ataxia. Drug-induced SB has been described in the treatment of sodium channel blockers, mesalazine, vagotonic drugs, α-adrenergic agonists, β-blockers, 1st generation antihistamines, antimalarials, sedatives, anticonvulsants, antipsychotics, tri- and tetracyclic antidepressants, lithium preparations.
The ECG of patients with SB is characterized by a number of specific changes that can be observed in full or incomplete combination:
1. Complete (in the classic version) or incomplete blockade of the right leg of the bundle of His.
2. Specific form of ST segment elevation in the right chest leads (V1-V3). Two types of ST segment elevation have been described: "saddle-back type" ("saddle") and "coved type" ("arch") (Fig. 9). The “coved type” rise significantly prevails in symptomatic forms of SB, while the “saddle-back type” is more common in asymptomatic forms.
3. Inverted T wave in leads V1-V3.
4. Increase in the duration of the PQ (PR) interval.
5. The occurrence of paroxysms of polymorphic ventricular tachycardia with spontaneous termination or transition to ventricular fibrillation.
The last ECG sign mainly determines the clinical symptoms of this syndrome. The development of ventricular tachyarrhythmias in patients with SB occurs more often at night or early morning hours, which makes it possible to associate their occurrence with the activation of the parasympathetic link of the autonomic nervous system. ECG signs such as ST segment elevation and PQ prolongation may be transient. H. Atarashi proposed to take into account the so-called "S-terminal delay" in lead V1 - the interval from the top of the R wave to the top of the R wave. The lengthening of this interval to 0.08 s or more in combination with ST elevation in V2 is more 0.18 mV is a sign of an increased risk of ventricular fibrillation (Fig. 10).
9. Stress cardiomyopathy
(tako-tsubo syndrome, SKMP)
SKMP is a type of non-ischemic cardiomyopathy that occurs under the influence of severe emotional stress, more often in older women without significant atherosclerotic lesions of the coronary arteries. Damage to the myocardium is manifested in a decrease in its contractility, most pronounced in the apical regions, where it becomes "stunned". Echocardiography reveals hypokinesis of the apical segments and hyperkinesis of the basal segments of the left ventricle (Fig. 11).
In the ECG picture of SKMP, a number of stages are distinguished:
1. ST segment elevation in most ECG leads, no reciprocal ST segment depression.
2. The ST segment is approaching the isoline, the T wave is smoothing out.
3. The T wave becomes negative in most leads (except aVR where it becomes positive).
4. Normalization of the ECG (smoothed or slightly negative T waves can persist for a long time).
10. Arrhythmogenic dysplasia/
right ventricular cardiomyopathy (ARVC)
ARVH - pathology, which is an isolated lesion of the right ventricle (RV); often familial, characterized by fatty or fibrous-fatty infiltration of the ventricular myocardium, accompanied by ventricular arrhythmias of varying severity, including ventricular fibrillation.
Currently, two morphological variants of ARVD are known: adipose and fibro-fatty. The fatty form is characterized by almost complete replacement of cardiomyocytes without thinning of the ventricular wall; these changes are observed exclusively in the pancreas. The fibro-fatty variant is associated with a significant thinning of the pancreatic wall; the left ventricular myocardium may be involved in the process. Also, with ARVD, moderate or severe dilatation of the pancreas, aneurysms, or segmental hypokinesia can be observed.
ECG signs:
1. Negative T waves in chest leads.
2. Epsilon (ε) wave behind the QRS complex in leads V1 or V2, which sometimes resembles incomplete RBBB.
3. Paroxysmal right ventricular tachycardia.
4. The duration of the QRS interval in lead V1 exceeds 110 ms, and the duration of the QRS complexes in the right chest leads may exceed the duration of the ventricular complexes in the left chest leads. Of great diagnostic value is the ratio of the sum of QRS durations in leads V1 and V3 to the sum of QRS durations in V4 and V6 (Fig. 12).
11. Hyperkalemia (HK)
ECG signs of increased potassium in the blood are:
1. Sinus bradycardia.
2. Shortening of the QT interval.
3. The formation of high, spiked positive T waves, which, in combination with a shortening of the QT interval, gives the impression of ST elevation.
4. Expansion of the QRS complex.
5. Shortening, with increasing hyperkalemia - prolongation of the PQ interval, progressive impairment of atrioventricular conduction up to complete transverse blockade.
6. Decrease in amplitude, smoothing of the P wave. With an increase in the level of potassium, the complete disappearance of the P wave.
7. Possible depression of the ST segment in many leads.
8. Ventricular arrhythmias (Fig. 13).
12. Left ventricular hypertrophy (LVH)
LVH occurs in arterial hypertension, aortic heart disease, mitral valve insufficiency, cardiosclerosis, and congenital heart disease (Fig. 14).
ECG signs:
1. RV5, V6>RV4.
2. SV1+RV5 (or RV6) >28 mm in persons over 30 years of age or SV1+RV5 (or RV6) >30 mm in persons under 30 years of age.
13. Overload right
and left ventricle
The ECG with LV and RV overload looks identical to the ECG with hypertrophy, however, hypertrophy is a consequence of prolonged overstrain of the myocardium by excess blood volume or pressure, and changes on the ECG are permanent. An overload should be considered in the event of an acute situation, changes in the ECG gradually disappear with the subsequent normalization of the patient's condition (Fig. 8, 14).
14. Left bundle branch block (LBBB)
LBBB is a violation of conduction in the main trunk of the left branch of the His bundle before it splits into two branches, or the simultaneous defeat of two branches of the left leg of the His bundle. Excitation in the usual way spreads to the pancreas and roundabout, with a delay - to the left ventricle (Fig. 15).
On the ECG, a widened, deformed QRS complex (more than 0.1 s) is recorded, which in leads V5-V6, I, aVL has the form rsR ', RSR ', RsR ', rR ' (the R wave predominates in the QRS complex). Depending on the width of the QRS complex, left bundle branch block is either complete or incomplete (incomplete LBBB: 0.1 s 15. Transthoracic cardioversion (TIT)
Cardioversion may be accompanied by transient ST elevation. J. van Gelder et al. reported that 23 of 146 patients with atrial fibrillation or flutter after transthoracic cardioversion had ST-segment elevation greater than 5 mm and no clinical or laboratory evidence of myocardial necrosis. Normalization of the ST segment was observed on average within 1.5 minutes. (from 10 s to 3 min.). However, patients with ST elevation after cardioversion have a lower ejection fraction than patients without ST elevation (27% and 35%, respectively). The mechanism of ST segment elevation is not fully understood (Fig. 16).
16. Wolff-Parkinson-White Syndrome (SVPU)
SVPU - conducting an impulse from the atria to the ventricles along the additional Kent-Paladino bundle, bypassing the normal conduction system of the heart.
ECG criteria for SVPU:
1. Shortened PQ interval to 0.08-0.11 s.
2. D-wave - an additional wave at the beginning of the QRS complex, due to the excitation of the "non-specialized" ventricular myocardium. The delta wave is directed upward if the R wave predominates in the QRS complex, and downward if the initial part of the QRS complex is negative (Q or S wave predominates), except for WPW syndrome, type C.
3. Blockade of the bundle branch of His (widening of the QRS complex for more than 0.1 s). In WPW syndrome, type A, the conduction of the impulse from the atria to the ventricles is carried out along the left Kent-Paladino bundle, for this reason, the excitation of the left ventricle begins earlier than the right one, and the blockade of the right branch of the His bundle is recorded on the ECG. In WPW syndrome, type B, the impulse from the atria to the ventricles is conducted along the right Kent-Paladino bundle. For this reason, the excitation of the right ventricle begins earlier than the left, and the blockade of the left leg of the His bundle is fixed on the ECG.
In WPW syndrome, type C, the impulse from the atria to the lateral wall of the left ventricle goes along the left Kent-Paladino bundle, which leads to excitation of the left ventricle before the right one, and the ECG shows right bundle branch block and a negative D-wave in leads in V5- V6.
4. P wave of normal shape and duration.
5. Tendency to attacks of supraventricular tachyarrhythmia (Fig. 17).
17. Atrial flutter (AF)
TP is accelerated, superficial, but the correct rhythm of atrial contraction with a frequency of 220-350 per minute. as a result of the presence of a pathological focus of excitation in the atrial muscles. Due to the appearance of a functional atrioventricular block, most often 2:1 or 4:1, the frequency of ventricular contractions is much less than the atrial rate.
ECG criteria for atrial flutter:
1. F-waves, spaced at equal intervals, with a frequency of 220-350 per minute, of the same height, width and shape. F waves are well defined in leads II, III, aVF, often superimposed on the ST segment and imitate its elevation.
2. There are no isoelectric intervals - flutter waves form a continuous wave-like curve.
3. The typical F waveform is "sawtooth". The ascending leg is steep, and the descending leg descends gradually gently downward and passes without an isoelectric interval into the steep ascending leg of the next wave F.
4. Almost always there is a partial AV block of varying degrees (usually 2:1).
5. QRS complex of the usual form. Due to the layering of the F waves, the ST interval and the T wave are deformed.
6. The R-R interval is the same with a constant degree of atrioventricular blockade (correct form of atrial flutter) and different - with a changing degree of AV blockade (irregular form of atrial flutter) (Fig. 18).
18. Hypothermia (Osborne syndrome, GT)
Characteristic ECG criteria for HT are the appearance of teeth in the J-point region, called Osborne waves, ST-segment elevation in leads II, III, aVF, and left chest V3-V6. Osborne's waves are directed in the same direction as the QRS complexes, while their height is directly proportional to the degree of GT. As the body temperature decreases, along with the described changes in ST-T, slowing of the heart rate, lengthening of the PR and QT intervals (the latter - mainly due to the ST segment) are detected. As the body temperature decreases, the amplitude of the Osborn wave increases. At a body temperature below 32 ° C, atrial fibrillation is possible, ventricular arrhythmias often occur. At a body temperature of 28-30°C, the risk of developing ventricular fibrillation increases (the maximum risk is at a temperature of 22°C). At a body temperature of 18 ° C and below, asystole occurs. HT is defined as a decrease in body temperature to 35°C (95°F) or below. It is customary to classify GT as mild (at a body temperature of 34-35°C), moderate (30-34°C) and severe (below 30°C) (Fig. 19).
Thus, the Osborn wave (hypothermic wave) can be considered as a diagnostic criterion for severe central disorders. The amplitude of the Osborne wave was inversely correlated with a decrease in body temperature. According to our data, the severity of Osborn's wave and the value of the QT interval determine the prognosis. Prolongation of the QT interval c >500 ms and severe deformation of the QRST complex with the formation of Osborn's tooth significantly worsen the life prognosis.
19. Positional changes
Positional changes in the ventricular complex sometimes mimic signs of MI on the ECG. Positional changes differ from MI by the absence of the ST segment and TT wave dynamics characteristic of a heart attack, as well as by a decrease in the depth of the Q wave during ECG registration at the height of inhalation or exhalation.
Conclusion
Based on the analysis of domestic and foreign literature, as well as our own data, I would like to emphasize that ST segment elevation does not always reflect coronary pathology, and the practitioner often has to make a differential diagnosis of many diseases, including rare ones.

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Cardiovascular diseases, in particular coronary heart disease (CHD), are the leading cause of death in the Russian Federation. In 2007, 1.2 million people died from diseases of the circulatory system.

Currently, there are highly effective methods of treatment that can not only reduce mortality from myocardial infarction, but also reduce the likelihood of developing heart failure, heart rhythm disturbances and other complications leading to disability.

The effectiveness of treatment depends on the timeliness of diagnosis of myocardial infarction. This article presents modern criteria for the electrocardiographic diagnosis of acute forms of coronary artery disease. They can be used by emergency physicians, whose tasks include intensive care in patients with acute coronary syndrome (ACS) and ensuring their transportation to the hospital.

Dynamics of electrocardiographic signs of ACS

The development of myocardial ischemia in ACS is primarily manifested T wave change. With complete occlusion of the coronary arteries, a high and wide T wave is formed, on average, 30 minutes after the development of clinical manifestations of ACS.

When analyzing the ECG of a patient with ACS, it is important to consider not only the size and presence of T-wave inversion, but also its shape. Options for changing the T wave in the first hours of penetrating myocardial infarction are shown in Fig. 1.

Rice. 1. Variants of T wave changes as a sign of prolonged myocardial ischemia, characteristic of the most acute phase of AMI: A - T wave in V4 is very high and wide, exceeds the QRS complex in size; B - lead V3 - depression of the ST segment at point j and a wide high T wave; C- wide high T, much larger than the QRS complex; D- very high peaked T wave, shaped like that of hyperkalemia (this variant is less common)

In AMI with ST segment elevation, the T wave, on average, after 72 hours from the onset of the disease, becomes negative, but not deeper than 3-5 mm. In the future, as a rule, after a month, the shape of the T wave normalizes; if this happens earlier, then recurrent MI with “pseudonormalization” of the T wave should be excluded.

With incomplete occlusion of the coronary artery, T-wave inversion occurs, it becomes negative in those leads where it should be (or was when compared with the previous ECG) positive. More details on the criteria for changing the T wave against the background of ischemia without ST segment elevation are presented below.

the T wave should be positive in leads I, II, V3–6;
the T wave should be negative in lead aVR;
the T wave can be negative in III, aVL, aVF, V1, less often in V1, and with a vertical arrangement of the electrical axis of the heart in young people and in lead II;
with persistent juvenile ECG, the T wave may be negative in V1, V2, and V

the depth of the negative T wave exceeds 1 mm;
T-wave inversion is recorded in at least two adjacent leads;
the depth of the T wave in leads V2-4, exceeding 5 mm, in combination with an increase in the corrected Q-T interval to 0.425 s or more in the presence of the R wave, may be the result of spontaneous reperfusion and develop as a result of ACS with ST elevation.

Formation pathological Q wave may begin 1 hour after the development of coronary vessel occlusion and end 8-12 hours after the onset of symptoms of ACS. Below are the characteristics of the pathological Q wave, depending on the lead in which the ECG is recorded:

in lead V2, any Q wave is considered abnormal;
in lead V3, almost any Q wave indicates the presence of disorders;
in lead V4, the Q wave is deeper than 1 mm or wider than 0.02 sec, or deeper (wider) than the Q wave in lead V5 is not normally recorded;
in lead III, the Q wave should not exceed 0.04 s in width and be more than 25% of the size of the R wave;
in other leads, the Q wave should normally not be wider than 0.03 s;
the exceptions are leads III, aVR, and V1, where non-pathological wide and deep Q waves can normally be recorded, as well as lead aVL, where the Q wave can be wider than 0.04 s or deeper than 50% of the size of the R wave in the presence of a positive P wave in this assignment.

ST segment elevation with complete occlusion of the coronary artery, it develops rapidly and stabilizes by 12 hours from the onset of symptoms.

When analyzing the ECG, assessing the magnitude of ST segment elevation, it is important to take into account not only the degree of its rise, but also the form of its elevation. On fig. 2 shows the characteristic dynamics of changes in the ST segment in the emerging penetrating myocardial infarction.

Rice. 2. Dynamics of changes in repolarization against the background of ACS with ST segment elevation. The initially normal ST segment at 07:13 has a concave shape, at 07:26 it straightened (a straight line from point j to the T apex), then acquired a convex shape, and at 07:56 ST segment elevation increased, which is typical for AMI with elevation ST segment

Thus, if the ST segment acquires a convex shape, and its elevation has not yet reached a critical level, these changes should be regarded as subepicardial damage, which should be treated with reperfusion thrombolytic therapy.

However, changes in repolarization do not always begin with a change in the shape of the ST segment. In some cases, this segment remains concave and elevation is formed against the background of ongoing ischemia. This variant of ST segment elevation is diagnostically more favorable, since the area of myocardial damage in this case is significantly less than with a convex form of ST.

Occasionally, the shape of the ST segment remains concave, and its rise is so slight that signs of a heart attack may not be noticed, in this case, analysis of the shape of the T wave helps.

When interpreting, the presence of an “ischemic” T wave, characteristic of the most acute phase of AMI, reciprocal changes in the form of ST segment depression, ECG dynamics (comparison with the initial and during observation), the shape (bulge) of the ST segment, as well as the presence of a pathological wave Q.

Criteria for assessing ST segment elevation in ACS

The degree of ST segment elevation is estimated by the location of point j (the place where the QRS complex passes into the ST segment) relative to the upper level of the P-R interval. In this case, changes should be recorded in at least two consecutive leads.

For men over 40 years of age, ST-segment elevation of 2 mm or more in chest leads V2–3 and 1 mm or more in leads I, II, III, aVR, aVL, aVF, V1, and V4–6 is considered abnormal.

For men younger than 40 years, ST-segment elevation greater than 2.5 mm in leads V2–3 and 1 mm or more in leads I, II, III, aVR, aVL, aVF, V1, and V4–6 is considered abnormal.

In women, ST-segment elevation greater than 1.5 mm in leads V2–3 and 1 mm in leads I, II, III, aVR, aVL, aVF, V1, and V4–6 is considered abnormal.

At low voltage, a less pronounced ST segment elevation (0.5 mm or more) can be considered diagnostically significant.

In accessory leads V7–9, an elevation of 0.5 mm is diagnostically significant.

In accessory leads V3–4, a rise in R of 0.5 mm is considered pathological.

ST segment elevation can be transient, with spontaneous thrombolysis occurring in 20% of cases.

Lateral myocardial infarction secondary to complete occlusion of the left circumflex artery or diagonal branch of the anterior interventricular coronary artery can lead to penetrating MI with no ST elevation or very little ST elevation in lead aVL alone. Sidewall potentials are the worst reflected in standard ECG recording.

The degree of depression is assessed at point j and correlates with the lower level of the P-R interval.

Depression is pathological only if it is registered in at least two consecutive leads.

ST segment depression cannot be a sign of subendocardial infarction if it is reciprocal.

ST segment depression of 0.5 mm or more recorded in leads V2–3 and/or 1 mm or more in leads I, II, III, aVR, aVL, aVF, V1, and V4–6 is considered a sign acute subendocardial infarction (damage) of the myocardium.

The appearance of depression with a depth of 0.5 mm, not being a sign of subendocardial infarction, indicates an increased risk of its development. If it persists despite the use of the entire arsenal of appropriate therapy, it is advisable to perform coronary anatomy within 48 hours.

ST segment depression greater than 2 mm, recorded in three or more leads, indicates a poor prognosis. The risk of death is 35% within the next month and 47% within 4 years if coronary anatomy is not performed.

ST-segment depression in eight or more leads, combined with elevation in leads aVR / V1, is a sign of damage to the main trunk of the left coronary artery or damage to several large coronary arteries if it reaches 1 mm.

It should be borne in mind that the criteria for ischemic changes on the ECG are not used to detect myocardial infarction if the patient has intraventricular conduction disturbances with pronounced changes in repolarization, Wolff-Parkinson-White syndrome, ventricular replacement rhythm, and an artificial pacemaker that stimulates the ventricles. In these cases, there are initial violations of repolarization and changes in the ventricular complex.

Signs of ventricular hypertrophy, pulmonary embolism, and electrolyte disturbances make it difficult to diagnose ACS. In these cases, the clinical manifestations of the disease should be taken into account first of all.

Determination of markers of myocardial necrosis (troponin or CPK MB-fraction) and echocardiography performed in the hospital during the observation process will help to verify the diagnosis.

In some cases, ST segment elevation is detected in patients without acute coronary syndrome; thus, in young men, ST-segment elevation can reach 3 mm in the right chest leads. In addition, with early repolarization syndrome, an ST segment elevation is recorded, which has a concave shape and is most pronounced in lead V4; examples of such changes are shown in fig. 3.

Rice. 3. Variants of ST segment elevation in the norm: a- typical for males, more often recorded in young people; b- early repolarization syndrome; c- non-specific changes in repolarization, manifested by a concave rise in the ST segment, inversion of the T wave, a characteristic feature is a short Q-T interval

Features of ECG changes depending on the location of MI

When analyzing the ECG, it is important to take into account the features of the changes characteristic of various variants of the localization of ischemic damage.

Acute ST elevation myocardial infarction may present with reciprocal depression in certain leads. In some cases, when registering an ECG in 12 standard leads, reciprocal changes are more pronounced than direct signs of myocardial damage. Sometimes, based on the presence of reciprocal depression, in order to identify direct signs of myocardial infarction, it is necessary to remove additional leads in order to diagnose ST-elevation ACS.

Much depends on the type of occlusion of the coronary arteries (the anatomical location of the coronary arteries is shown in the figure).

For persistent occlusion main trunk of the left coronary artery, as a rule, cardiogenic shock develops with a fatal outcome. The ECG reveals signs of an extensive anterior-septal infarction with the capture of the side wall.

With subtotal occlusion of the main trunk of the left coronary artery, the ECG reveals ST segment depression over 1 mm in 8 or more leads in combination with ST segment elevation in leads aVR and (or) V1.

If occlusion anterior interventricular artery occurred distally to the origin of the diagonal branch, then anterior myocardial infarction develops, which is manifested by the formation of infarct changes in leads V2-4, with such localization of AMI, reciprocal changes are usually not detected.

Violation of blood flow in the anterior interventricular coronary artery (AIAC) proximal to the origin of the diagonal branch leads to the development of anterolateral AMI. The presence of signs of anterior MI is associated with ST elevation in lead aVL, 0.5 mm elevation is a highly sensitive sign of MI, and 1 mm is a highly specific sign of proximal LAD occlusion. With this variant of occlusion, reciprocal changes are recorded in lead III.

In the complete absence of blood flow in the LAD (occlusion proximal to the origin of the septal branch), changes appear not only in V2–4, but also in leads aVR, aVL, and V1.

ST-segment elevation in V1 is not a specific sign of AMI and is often normal, however, ST-segment elevation exceeding 2.5 mm is a reliable criterion for damage to the septum and (or) anterior basal sections, which was established by comparing EchoCG data with electrocardiography data .

Reciprocal changes in the form of ST segment depression are recorded in leads II, III, aVF and V5. ST-segment elevation in aVR, reciprocal ST-segment depression in lead III greater than ST-segment elevation in aVL, ST depression in V5, and right bundle branch block are predictors of LAJ occlusion proximal to the origin of the septal branch.

With occlusion lateral branch of the left circumflex coronary artery or diagonal branch of the LJCA develops lateral wall infarction. Such a heart attack in approximately 36% of cases is manifested by ST elevation in lead aVL, usually not exceeding 1 mm. Only in 5% of cases ST elevation reaches 2 mm. In 1/3 of patients with lateral AMI, there are no ECG changes, in 2/3 of cases there is some elevation or some depression of the ST segment.

The most reliable sign of ST-elevation AMI is reciprocal changes in the form of ST-segment depression in leads II, III, and aVF. With occlusion of the LAD or RCA, lateral infarction is manifested by ST elevation much more often - in 70-92% of cases. In CVLCA occlusion, lateral wall infarction is often associated with posterior MI.

In approximately 3.3-8.5% of cases, myocardial infarction, confirmed by the results of biochemical analysis (MB-CPK and troponin test), has a posterior localization. Since ST elevation changes are not detected on standard 12-lead ECG, isolated posterior wall MI may go undiagnosed.

It is possible to identify AMI of the posterior wall by reciprocal changes in the right chest leads. Changes will be manifested by ST segment depression in leads V1-4 (sometimes only in V2-4 if there was initially slight elevation within normal limits in lead V1, and sometimes only in V1).

In addition, a high reciprocal R wave is often recorded in the right chest leads as a result of the formation of a Q wave in leads characterizing posterior wall potentials. In some cases, it is not easy to identify reciprocal depression in the right chest leads, since many patients initially have a slight ST elevation in V2–3 and reciprocal depression will be less distinct, therefore, ECG evaluation over time is important.

To confirm posterior MI, an ECG should be taken in additional leads V7–9 (fifth intercostal space, posterior axillary line - V7, vertical line from the angle of the left scapula - V8, left paravertebral line - V9). Routine analysis of accessory leads in all patients with chest pain is not used, since the presence of reciprocal changes in the right precordial leads is a rather sensitive sign of posterior AMI.

Blood supply to the lower wall of the left ventricle in 80% of cases is carried out right coronary artery(PCA), in 20% - the envelope branch (OB) of the LCA.

RCA occlusion is the most common cause of inferior myocardial infarction. With proximal occlusion of the RCA, above the branch of the right ventricle, the development of a lower infarction is combined with the formation of a right ventricular infarction.

On the ECG, inferior wall infarction is manifested by the formation of ST-segment elevation in leads II, III, and aVF and is almost always accompanied by the presence of reciprocal depression in lead aVL.

If the cause of inferior infarction is occlusion envelope branch of the LCA, then the ECG shows signs of damage not only to the lower, but also to the posterior, as well as to the lateral walls of the left ventricle.

Since, with a combination of inferior and lateral infarction, reciprocal depression in aVL, which is a consequence of inferior infarction, is leveled by ST segment elevation, which is a sign of lateral infarction, no changes are recorded in lead aVL. However, in leads V5-6, ST-segment elevation, as a sign of lateral myocardial infarction, should be detected. If there is no reciprocal ST-segment depression in aVL and there are no signs of lateral infarction in V5–6, then ST elevation in leads II, III, and aVF can be considered pseudoinfarction.

Proximal RCA occlusion leads to the development of AMI of the right ventricle (RV) against the background of inferior AMI. Clinically, such a heart attack is manifested by the development of hypotension, deterioration of well-being from the use of nitrates and improvement of well-being against the background of intravenous administration of solutions. The short-term prognosis is characterized by a high probability of developing complications with fatal outcomes.

On the ECG, RV AMI is manifested by ST-segment elevation in leads V1–3 and simulates anterior septal myocardial infarction. A characteristic feature of right ventricular infarction is the severity of ST segment elevation in V1–2, in contrast to AMI of anterior septal localization, in which the maximum ST segment elevation is observed in leads V2–3.

To verify right ventricular infarction, it is necessary to remove additional right chest leads: V4R (the electrode for recording chest leads should be placed at a point located in the fifth intercostal space along the midclavicular line on the right) and V3R (registered in the area located between the locations of the electrodes for recording leads V1 and V4R).

Elevation of the ST segment in leads V3-4R by 0.5 mm or more is considered diagnostically significant. An ECG in accessory leads V3–4R should be taken when the ECG shows changes consistent with inferior myocardial infarction.

When combined with severe right ventricular hypertrophy, ST elevation in the chest leads can be significant and resembles an anterior infarction even in the presence of elevation in leads II, III, and aVF.

In conclusion, it is important to note that, in general, the sensitivity of ECG diagnostics of myocardial infarction, according to foreign cardiologists and emergency medical specialists, is only 56%, therefore, in 44% of patients with acute myocardial infarction, electrocardiographic signs of the disease are absent.

In this regard, in the presence of symptoms characteristic of acute coronary syndrome, hospitalization and observation in a hospital are indicated, the diagnosis will be established on the basis of other methods of examination.

However, it is the ECG that is the method that allows you to determine the presence of indications for thrombolytic therapy. According to the recommendations of the All-Russian Scientific Society of Cardiology, with complete occlusion of the coronary artery, it is advisable to perform thrombolysis in order to restore blood supply to the myocardium.

In this regard, when ST segment elevation is detected on the ECG in a patient with clinical signs of acute coronary syndrome, emergency hospitalization is indicated in the same hospital where thrombolytic therapy is possible. In other cases, hospitalization with a diagnosis of ACS without ST elevation is recommended in any hospital where there is an intensive care unit.

O. Yu. Kuznetsova, T. A. Dubaikaitis

ST segment measurement rules

The ST segment is measured 60 ms (one and a half small cells) from the J point.
Point J is the place where the S wave passes into the ST segment (or the S wave crosses the isoline).
Normally, leads V1-V3 may show ST elevation with a maximum in V2 up to 0.25 mV.
In other leads, elevation of 0.1 mV or more is considered pathological.

ST segment elevation

ST-segment elevation can take many forms, depending on the cause that caused it. The most common causes of ST elevation:

ST elevation myocardial infarction
Early ventricular repolarization syndrome (ERVR)
Pericarditis
Postinfarction aneurysm
Brugada syndrome
Complete left bundle branch block (LBBB)
Left ventricular hypertrophy
Variant angina (Prinzmetal's angina)

Shown below are examples of ST elevation in the conditions listed above. Look at each of the complexes, find the J point and calculate the ST elevation 60 milliseconds away. Then check the correct answer:

In the absence of d other signs of myocardial injury (eg, Q wave or deep negative T waves)curved ST elevation is usually benign, while oblique or convex ST elevation is usually abnormal and associated with myocardial ischemia.

There is a good "reminder" for concave and convex ST elevation:

ECG Criteria for Pathological ST Elevation in STEMI

New ST elevation in two or more adjacent leads is considered pathological:

≥2.5 mm in V2-V3 and ≥1 mm in other leads in men under 40
≥2.0 mm in V2-V3 and ≥1 mm in other leads in men over 40
≥1.5 mm in V2-V3 and ≥1 mm in other leads among women
≥0.5mm in V7-V9
≥0.5mm in V3R-V4R
If the patient has a complete blockade of LBBB or a pacemaker is installed, the modified Sgarbossa criteria should be used.
Use Smith's formula to distinguish between LAD STEMI and early ventricular repolarization syndrome (ERS).

ST segment depression

ST segment depression can be of three types:

Ascending ST depression often occurs against the background of tachycardia (for example, during exercise) and disappears with a decrease in heart rate. Such depression is a variant of the norm. Ascending depression, turning into high-amplitude "coronary" T waves, may mean the most acute stage of extensive myocardial infarction (the so-called De Winter's T-waves).

Horizontal and downward sloping ST depression, depth ≥0.5 mm in two adjacent leads is a sign of myocardial ischemia (all four examples above).

Always note that ST depression may be reciprocal of elevation in "mirror" leads. Most often, acute posterior myocardial infarction is manifested by horizontal V1-V3 depression and minimal elevation in V6 (to check in such cases, it is necessary to record leads V7-V9), and high lateral infarction - ST depression in II, III, aVF and subtle elevation in aVL (to check, you need to record V4-V6 two intercostal spaces above).

To recap: ST elevation and depression

Remember that both ST elevation and ST depression can be normal.
Before accepting such changes as a variant of the norm, exclude all possible pathological causes.
If you see both ST depression and ST elevation on the same ECG, then suspect STEMI and evaluate the elevation first, as it is much more dangerous. Then analyze the ST depression - it may be reciprocal changes.