Mild depression of the st segment v3. ST segment depression - what is it? Treatment. Causes of cardiac changes

For various heart disorders, the most common diagnostic method remains (electrocardiogram). This is a simple, quick and painless way to determine whether there are problems with the heart.

A separate specialist will decipher the cardiogram. It is a graph divided into segments. The ST segment is an important indicator, so deviations in this case may indicate serious illnesses of cardio-vascular system or life-threatening conditions.

ST segment - what is it and what is it responsible for?

As you know, only a doctor should decipher a cardiogram. It is very difficult for an untrained person to understand graphs. The ECG procedure itself is carried out very quickly, but at the same time it is quite informative.

It shows heart rhythm, ventricular contractions, etc. The entire graph consists of various lines and segments, each of which performs its own function. It is worth remembering that it is necessary to evaluate the result completely; information solely on one segment will not yield much.

ST segment depression is not a disease, but an abnormality in the cardiogram. There may be several reasons for this condition and it is difficult to determine them without further examination.

The peculiarity of this segment is as follows:

The segment is located between points S and T, and the S wave is always negative, that is, it is below the isoelectric line. The T wave is usually located higher.
This segment is assessed holistically, but in most cases it shows how well the myocardium is saturated with oxygen.
The size of the segment depends on the heart rate. The more often the heart contracts, the shorter this section is.
The ST segment reflects the period of heart activity when both ventricles are in a state of excitation.
The ST section is always horizontal and located approximately at the level of the isoelectric line. However, if it is slightly higher (a couple of cells), then this is also considered normal.

Particular attention is paid to this area during diagnosis. coronary disease and suspected myocardial infarction.

A segment is said to be depressed if it has dropped below the isoelectric line by more than half a millimeter.

However, further examination of the heart, etc. is required to make a diagnosis and determine the causes. In some cases, even depression of a segment may be a sign of normality. Not only the depth of the segment’s depression relative to the isoelectric line is taken into account, but also its displacement, the location of the teeth, curvature, slope, and the location of other teeth.

Causes of ST segment depression

If the ECG shows a phenomenon such as ST segment depression, it is necessary to identify the reasons that led to this. They can be both physiological and pathological.

As a rule, strong deviations from the norm indicate the presence of pathology in the body. Such cases cannot be neglected; further examination of the body is necessary.

Among the causes of ST segment depression are:

Myocardial ischemia. Ischemic damage to the myocardium means cessation of blood supply to part of it due to pathological narrowing of blood vessels or arteries, blockage of their lumen. Coronary heart disease usually occurs in parallel with. This is a life-threatening condition. The threat directly depends on the degree of myocardial damage and the amount of dead tissue.
Hyperventilation of the lungs. This syndrome occurs with frequent shallow breathing when tissues are oversaturated with oxygen and the level of carbon dioxide in the blood drops. This phenomenon can also lead to electrocardiogram abnormalities. The cause of this condition may be fear, stress, or strong emotional shock.
Hypokalemia. As you know, potassium is an important element for heart function. Potassium supports normal muscle contractile function. Potassium deficiency occurs due to poor nutrition, metabolic disorders.
. This is a disease of the vegetative nervous system, which is accompanied by a whole range of symptoms. Dystonia affects heart function and blood pressure. Diseases may be the cause endocrine system, hormonal imbalances, severe stress.
Pregnancy. During pregnancy, the load on the cardiovascular system increases significantly. A common occurrence is tachycardia in pregnant women. Due to increased heart rate, deviations from the norm may appear on the cardiogram.

Only a doctor can determine the degree of deviation. It must be remembered that before the examination, the doctor is informed about all medications taken. Some medications can affect the functioning of the heart and heart rate, which can lead to abnormalities in the cardiogram.

What symptoms accompany the deviation?

The clinical picture may differ depending on what disease led to the ST segment depression

Manifestations may be cardiac or non-cardiac. For example, such disorders are often accompanied by signs of real depression, a disorder of the nervous system, which can be both a consequence and a cause of the condition.

Among the common clinical manifestations highlight:

Pain in chest. Pain does not always appear. With minor deviations, the disease is painless. Severe pain in the chest, radiating to the back and arm, may be signs of incipient pain. Often heart pain disappears after taking a nitroglycerin tablet.
. ST segment depression is accompanied by heart rate disturbances, most often palpitations. Tachycardia may occur with various diseases of cardio-vascular system.
Difficulty in physical activity. If you have heart problems, heavy loads become impossible. During active sports, shortness of breath, tachycardia, chest pain and other unpleasant symptoms appear.
. A feeling of shortness of breath may occur after physical exercise, and at rest. The second is a more alarming sign and indicates a deterioration in the blood supply to the lung tissue.
Headache. Diseases of the cardiovascular system often occur against the background of hypertension. Elevated levels lead to vasospasm and migraines. Usually the pain is localized in the occipital region.

When contacting a cardiologist, it is very important to correctly and completely describe the existing symptoms. Taking an anamnesis will help in making a diagnosis. It is necessary to clarify when and after what symptoms appear, how intense they are and when they disappear.

You should also pay attention to symptoms such as cough. At first glance, it is not associated with heart disease, but coughing attacks can be caused by insufficient nutrition of the lung tissue.There may also be a feeling of tightness in the chest area, which is a sign of angina and needs to be examined.

Features of treatment and prognosis

The doctor will prescribe treatment after accurately determining the causes of the disorders. First of all, when heart problems and a tendency to ischemia appear, doctors recommend changing your lifestyle: giving up bad habits, watch your diet, do not neglect feasible physical activity, spend more time in the fresh air.

Therapy may include:

Antiplatelet agents. These are drugs containing acetylsalicylic acid, intended for . They reduce the risk of blood clots, prevent heart attacks, and. The drugs have a number side effects, for example, increase the risk of bleeding, so the duration of the course needs to be adjusted.
Nitrates. This primarily includes Nitroglycerin. These drugs dilate blood vessels and ensure normal blood flow to the heart muscle, saturating it with oxygen. Nitrates are indispensable for acute heart attack myocardium.
Adrenergic blockers. The group of these drugs includes Metoprolol, Atenolol. They help normalize and restore abnormal heart rhythm. Often prescribed for coronary heart disease and.
Statins. Ischemia is usually caused by cholesterol plaques that block the lumen of blood vessels. Statins reduce levels. These include Simvastatin, Atorvastatin. It is also believed that these drugs reduce pain and prevent myocardial infarction.

More information about ECG can be found in the video:

Can lead to cardiac ischemia and other cardiac pathologies excess weight, therefore, first of all, it is necessary to normalize body weight. A normal work and rest schedule is also recommended. For the functioning of the cardiovascular system big influence causes stress and constant overwork.

You should not prescribe treatment for yourself without consulting a doctor. Uncontrolled use of drugs can lead to the opposite effect and provoke new complications. The prognosis depends on the timeliness of treatment. In the early stages it is usually favorable.

ECG changes with angina pectoris and chronic coronary heart disease, they arise not due to disruption of the coronary arteries themselves, but due to increasing anoxia of the myocardium due to lack of blood supply. The symptoms of this condition are nonspecific and may be present in other diseases. Therefore, a clear diagnosis is made based on a complex of ECG signs in combination with clinical symptoms and results functional tests.

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ECG phenomena in angina pectoris and ischemic heart disease

With ischemic heart disease The ECG shows characteristic changes in the ST segment and T wave.

Insufficiency of the coronary arteries and a decrease in the flow of arterial blood to the myocardium usually cause depression and a change in the shape of the ST segment, which normally smoothly, gently passes into the ascending knee of the T wave. IHD (coronary heart disease) is accompanied by a clear and steep transition of the ST segment into the T wave. This is an early diagnostic sign of the development of coronary artery disease in a patient. Further progression of the disease will be combined with depression of the ST segment below the isoline, which is associated with subendocardial damage due to myocardial ischemia and characteristic changes in the T wave.

ST segment changes

There are 5 types of ST segment depression:

1. Horizontal displacement of the ST segment. It is manifested by its displacement almost parallel to the isoline. The ST segment can transform into a positive or negative, isoelectric or biphasic T wave.
2. Oblique downward displacement of the ST segment. As it extends downward from the isoelectric line and away from the QRS complex, the degree of ST segment depression gradually increases. Sometimes this shift is called from R to T. Next, the segment turns into a positive or negative, isoelectric or biphasic T wave.
3. Displacement of the ST segment downward from the isoline with the arc convexly facing upward. The decline of the segment is expressed unequally throughout its entire length; its shape resembles an arc, with its convexity facing upward. The ST segment turns into a positive or negative, isoelectric or biphasic T wave.
4. Oblique upward displacement of the ST segment. The greatest depression with this option is recorded immediately after the QRS complex. After this, the segment smoothly rises to the isoelectric line and turns into a positive or biphasic T wave.
5. Trough-shaped displacement of the ST segment. This type is shaped like an arc, with its convexity facing downwards, and turns into a positive, isoelectric or biphasic T wave.

The most common occurrence of angina pectoris is horizontal and oblique downward displacement of the ST segment.

The severity of ST segment displacement is directly proportional to the severity of ischemic changes and coronary insufficiency. Its displacement downward from the isoline by 1 mm or more in the chest leads, more than 0.5 mm in standard leads, reliably indicates the presence of myocardial ischemia. A slight depression of up to 0.5 mm also occurs in healthy people.

With angina pectoris and coronary artery disease, elevation (rise) of the ST segment can also be observed. Usually in shape it resembles an arc with a convexity facing downwards. The ST segment in this case turns into a positive or isoelectric T wave. A diagnostically significant elevation of the ST segment should be at least 1 mm. In this case, a differential diagnosis is made with myocardial infarction.

ST changes characteristic of angina pectoris and coronary artery disease are most often localized in the left chest leads V4-V6 and leads II, III, aVF, I, aVL.

In acute myocardial infarction and acute coronary insufficiency, similar ST segment phenomena occur. Difference chronic course IHD and angina pectoris will have no changes in dynamics, stability for a long time.

T wave changes

The most specific change in the T wave in angina and ischemic heart disease is the “coronary” T wave (characterized by a pointed, symmetrical shape), often negative. This tooth shape is associated with the development of transmural myocardial ischemia. Negative T waves, characteristic of ischemic heart disease, are often deep, with an amplitude of 5 mm or more.

Sometimes myocardial ischemia manifests itself as giant positive T waves - a tall “coronary” T wave. This change also occurs in other diseases (hyperkalemia, pericarditis) and is not pathognomonic.

And also with ischemic heart disease and angina pectoris, two-phase T waves can be recorded: +- or -+. More often, such waves are recorded when the recording electrode is located peripherally from the ischemic zone.

In chronic ischemic heart disease and angina, a smoothed, reduced, isoelectric T wave is sometimes recorded. More often, a decrease occurs in most of the main leads.

Another sign of coronary heart disease is the ratio of T V1> T V6 and T I< T III.

Most often, pathological T waves are recorded in the left precordial leads, in leads I, aVL, and also in leads III, aVF. In the right chest leads V1-V2, changes in the T wave during angina pectoris are observed much less frequently.

Negative T waves should be differentiated during ischemia and dynamic changes without organic damage myocardium. To do this, a Valsalva test, a test with hyperventilation, potassium, obsidan, an orthostatic test are performed, and if with them a negative T wave turns positive, then this indicates against the presence of angina pectoris and ischemic heart disease.

An ECG conclusion is not a diagnosis. The final verdict is made by a cardiologist based on clinical symptoms, ECG signs, as well as the results of functional tests and studies.

Additional ECG symptoms

These symptoms may not always occur or may be combined with other diseases not related to ischemic heart disease and angina pectoris. Based on these signs alone, it is impossible to assume the presence or absence of the disease; they are only additional markers to the main ECG symptoms of IHD.

Signs indicating the probable presence of ischemic heart disease and angina include:

the presence of a negative or biphasic U wave;
a slight increase in the duration of the P wave;
increase in the QT interval due to prolongation of the electrical systole of the ventricles;
a sharp deviation between the electrical axes of the QRS complex and the T wave;
often observed various disorders rhythm and intracardiac conduction;
various disorders of intraventricular conduction, manifested by splitting of the QRS complex;

ECG changes during an angina attack

During the onset of an attack of heart pain due to angina pectoris, the ECG may show depression of the ST segment, combined with inversion of the T wave. But usually these are incoming changes that are not always possible to register due to their short duration. After the attack ends, the ECG usually returns to its original form. Changes in the myocardium during the onset of pain are associated with diffuse myocardial hypoxia.

Typically, an angina attack is provoked by physical activity, emotional outburst, or stress.

Features of Prinzmetal's angina

This is a special type of angina in which the attack occurs at rest or during normal daily activities and is not associated with any stress.

The ECG is characterized by the presence of ST elevation with a transition to a positive T wave. As a result, a monophasic curve is recorded. On the opposite wall of the myocardium there will be reciprocal changes (reverse to the existing ones), i.e. a decrease in the ST segment.

Changes in Prinzmetal's angina last for some time, and then return to the original level. It is assumed that this occurs due to incoming spasm of the coronary arteries.

During prolonged high-frequency attacks of tachycardia, ST segment depression and T wave negativity may occur as a result of myocardial ischemia. Such changes are more common in to a greater extent observed in patients with coronary atherosclerosis, but they can also be found in young people with a healthy heart. Anginal pain may be absent.

ST segment depression

Electrolyte imbalance, particularly hypokalemia, also plays a role in these changes.

In approximately 20% of cases, after the cessation of an attack of tachycardia, a decrease in the ST segment, negation of the T wave and prolongation of the QT interval can be observed within hours, days and weeks as an expression of myocardial ischemia after tachycardia. Long-term ECG changes give reason in some cases to assume the presence of small focal infarctions. T wave inversion usually has the characteristic of coronary T waves. According to some authors, hypokalemia has pathogenetic significance.

Description:

Symptoms of Depression:

Patients note a decrease in the ability to concentrate and pay attention, which is subjectively perceived as difficulty remembering and decreased success in learning. This is especially noticeable in adolescence and youth, as well as in people engaged in intellectual work. Physical activity also reduced to lethargy (even stupor), which can be perceived as laziness. In children and adolescents, depression can be accompanied by aggressiveness and conflict, which mask a kind of self-hatred. Everything can be divided depressive states into syndromes with and without an anxiety component.

The rhythm of mood changes is characterized by a typical improvement in well-being in the evening. Self-esteem and self-confidence decrease, which looks like specific neophobia. These same sensations distance the patient from others and increase his sense of inferiority. With long-term depression after the age of 50, this leads to deprivation and a clinical picture resembling dementia. Ideas of guilt and self-deprecation arise, the future is seen in gloomy and pessimistic tones. All this leads to the emergence of ideas and actions associated with auto-aggression (self-harm, suicide). The rhythm of sleep/wakefulness is disrupted, insomnia or lack of a sense of sleep is observed, and dark dreams predominate. In the morning the patient has difficulty getting out of bed. Appetite decreases, sometimes the patient prefers carbohydrate foods to protein foods, appetite may be restored in the evening. The perception of time changes, which seems endlessly long and painful. The patient stops paying attention to himself, he may have numerous hypochondriacal and senestopathic experiences, depressive depersonalization appears with a negative image of his own self and body. Depressive derealization is expressed in the perception of the world in cold and gray tones. Speech is usually slow with talking about one's own problems and past. Concentration is difficult and the formulation of ideas is slow.

During examination, patients often look out the window or at a light source, gesturing towards the own body, pressing hands to the chest, with anxious depression to the throat, a pose of submission, a Veragut fold in facial expressions, downturned corners of the mouth. In case of anxiety, accelerated gesture manipulation of objects. The voice is low, quiet, with long pauses between words and low directiveness.

Symptoms such as dilated pupils and tachycardia may indirectly indicate a depressive episode. constipation, decreased skin turgor and increased fragility of nails and hair, accelerated involutive changes (the patient seems older than his age), as well as somatoform symptoms, such as psychogenic shortness of breath. syndrome restless legs, dermatological hypochondria, cardiac and pseudorheumatic symptoms, psychogenic dysuria. somatoform disorders gastrointestinal tract. In addition, with depression, sometimes weight does not decrease, but increases due to cravings for carbohydrates; libido may also not decrease, but increase, since sexual satisfaction reduces anxiety levels. Other somatic symptoms include vague headaches, amenorrhea and dysmenorrhea, chest pain and, especially, a specific sensation of “stone, heaviness on the chest.”

Causes of Depression:

1. Genetic causes may include abnormalities in chromosome 11, although the existence of polygenic forms of the disorder is assumed.

2. The biochemical cause is a disturbance in the activity of neurotransmitter metabolism: deficiency of serotonin and catecholamines.

3. Neuroendocrine causes are expressed in disruption of the rhythmic functioning of the hypothalamic-pituitary, limbic system and pineal gland, which is reflected in the rhythm of the release of releasing hormones and melatonin. These processes are associated with photons daylight. This indirectly affects the overall rhythm of the body, in particular the rhythm of sleep/wakefulness, sexual activity, and eating.

Risk factors include age 20-40 years, lower social class, divorce in men, family history suicides, loss of relatives after 11 years of age, personality traits with traits of anxiety, diligence and conscientiousness, stressful events, homosexuality, problems of sexual satisfaction, the postpartum period, especially in single women. In the pathogenesis of depression, along with genetic factors that determine the level of neurotransmitter systems, the cultivation of helplessness in the family during periods of stress, which forms the basis of depressive thinking, and the loss of social contacts are important.

DIAGNOSIS OF MYOCARDIAL ISCHEMIA BY METHOD OF HOLTER ECG MONITORING.

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The issues of diagnosing myocardial ischemia during Holter monitoring, the significance of “silent” ischemia, and the causes of errors in the automatic measurement of ST segment displacement are considered.

In the more than 30 years since Holter used a portable device for extended ECG recording, advances in computer technology have led to the emergence of a new method for recording long-term ECG recordings—Holter monitoring (HM).

When using this method, doctors faced many hitherto unexplored problems. The most important among them was the definition: “What is a normal ECG in the conditions of normal human activity?”

Prominent American cardiologist White said: “The normal limits for the heart remain today in cardiovascular physiology one of the most difficult problems in accurate assessment and diagnosis. cardiovascular diseases, one of the most important and often neglected quantities." Studying a group of apparently healthy people aged 16 to 65 years, Clarke et al. found that 12 percent of these patients have rhythm disturbances in the form of sudden bradyarrhythmias or tachycardias with ventricular ectopies. Among 100 men and women examined by Kostis, ventricular extrasystoles were detected in 46%, 20% of them had more than 10 ventricular extrasystoles, and 5% had more than 100. It turned out that the usual standards for determining the heart rhythm as normal can be significantly exceeded, especially in young subjects. The issue of monitoring duration is another problem that needs to be addressed.

How long should I install the monitor? Bigger et al. believes that the number of detected extrasystoles is not linear dependence on the duration of monitor observation. It has been established that the largest number of ventricular extrasystoles, including paired ones, R on T is detected in the first 6-12 hours of observation. On the contrary, rhythm disturbances such as ventricular tachycardia are detected during longer observation and are linearly dependent on the duration of monitoring. In the presence of syncope or fainting conditions, to identify their causes, it is necessary to monitor the ECG for a longer period of time, more than 24 hours. It is reported that when monitoring increases to 3 days, the percentage of detection of atrioventricular and sinoatrial blocks increases three times.

The number of electrodes used depends on the objectives of the study and is determined by the lead system used. The two most commonly used modified leads are V1 and V5. However, to diagnose myocardial ischemia, the number of leads can be increased. Currently, a transition is being made to a three-axis ECG lead system. Three ECG recording channels are formed by 7 electrodes according to the type of orthogonal Frank leads (X, Y, Z).

The information content of various lead systems for detecting myocardial ischemia during HM ECG has been assessed by a number of researchers. Thompson et.al. (1995), when examining 110 patients with coronary artery disease with silent ischemia, compared the results obtained when recording 2 and 12 leads. The number of ischemic episodes was 16 and 44, and their total duration was 273 and 879 minutes. respectively. In a study by Lanza et. al. (1994) when diagnosing ischemia in 223 patients, the sensitivity of CM5 was 89%, CM5+CM3 - 91%, CM5+CMY - 94%, CM5+CM3+CMY - 96%. Langer et. al. (1995) when comparing the registration of 12 leads, 3 Frank leads, VCG and leads V2+V5+avF in 1067 patients did not reveal differences in their information content. Jiang et. al. (1995) when comparing the sensitivity of leads CM5, II and CM5+II in 60 patients, obtained values of 13, 71 and 96%, respectively. Osterhues et. al. (1994) during an examination of 54 patients determined the sensitivity of leads CM2+CM5 (43%) and CM2+CM5+D (61%).

ST-T analysis.

ST segment shifts as a possible sign of ischemic changes in the myocardium are assessed with particular care. ST segment analysis is associated with significant technical difficulties and the clinician should almost always not rely on automated measurements of ST segment changes without clinical control of reference points. There are two main approaches to analyzing ST shifts:

1) determination of the displacement of point j relative to the isolevel;

2) determination of the ST segment slope.

The equipment used usually provides two graphs of changes in the ST segment: the displacement below the isolevel and a graph of the ST slope relative to the J point, as well as a tabular representation of the same data.

In addition to these parameters, changes in the ST segment can be characterized by various additional criteria, for example, the ST integral - the area between the ST contour and the isoelectric level, the STx index - a decrease in ST at the “ischemic point”, the STn index, indicating that a fixed interval was used between points J and ST (for example, J+65 ms), index STj. indicating that measurements are taken at point J.

When analyzing ST segment shifts, much attention is paid to determining basic level, i.e. reference level of segment shifts. The baseline is usually represented by a straight line connecting the end of the P wave and the beginning of the wave T. A. Dambrowski et al. the reduction of the ST segment is assessed taking into account the configuration of the PQ segment: with an anchor-shaped PQ configuration, the ST displacement is assessed as a jump in relation to the last point of the PQ contour. Often the average value of the J point is taken as the baseline value.

Biagini et. al. (1983) in experiments with microspheres when studying local blood flow, they established a hemodynamic disturbance caused by critical stenosis of the coronary artery or pathological increase blood pressure in the left ventricle. Both of these factors cause a redistribution of blood flow with the development of ischemia always in the subendocardial layers. In the subepicardial layers, isolated ischemia according to Biagini et. al. never developed. Consequently, with the development of myocardial ischemia, it is localized in the inner layers of the ventricular wall, or all layers of the myocardium are involved in the ischemia process, i.e. it is transmural in nature.

Under experimental conditions, a few seconds after vessel occlusion, the amplitude of the T wave increases and a rise in the ST segment occurs, which quickly passes after blood flow is restored. Along with ST elevation, changes in the amplitude of the QRS complex are possible in the absence of an increase in ventricular volume. Transient Q waves may appear.

Electrocardiographic signs of transmural ischemia

1. Elevation of the ST segment in the area supplied by the stenotic artery.

2. Pseudonormalization of negative T waves.

3. Increase in T amplitude - peaking T (not always transmural ischemia!).

4. U-wave and T peaking.

5. Changes in the QRS complex.

6. No ECG changes.

Electrocardiographic signs of subendocardial ischemia.

1. ST segment depression.

2. Negative T wave (characteristic of long-term subendocardial ischemia or transmural ischemia).

3. Tall positive peaked T wave.

4. No ECG changes.

Ischemia criteria for Holter ECG monitoring.

(Data from Kodama, 1995, monitoring studies of 12 thousand patients from 1980 to 1993)

1. Horizontal or downward decrease in the ST segment by 0.1 mV at a point 80 ms from j, lasting 1 minute. For men, sensitivity is 93.3%, specificity is 55.6%, for women it is 66.7% and 37.5%, respectively.

2. Elevation of the ST segment by 0.1 mV lasting 80 ms from point j.

3. Episodes of ST segment elevation and ST segment depression.

An example of ischemic ST segment depression is shown in Fig. 1. As follows from the figure, myocardial ischemia is assessed by the position of point j. When automatically analyzing ST in Holter systems, instead of point j, a point is assessed at a certain distance from the beginning of the QRS complex, for example, 80 or 60 ms, and another point falling on the T wave. The last point helps to determine the slope of the ST segment.

Rice. 1. Example of ischemic depression of the ST segment.

A few words about physiological significance ST segment changes. In the transmembrane action potential, point j corresponds to the peak of the transmembrane potential (phase 1). At this time, the process of myocardial excitation ends and the repolarization phase begins. Thus, the position of this point clearly distinguishes between the processes of de- and repolarization. The shift of point j reflects the presence of damage current in the subendocardial or subepicardial direction.

If the ST segment is inclined obliquely downward or horizontally depressed, then the ischemic nature of the shifts is suspected. With an obliquely ascending position of the ST segment, even in the presence of a pronounced decrease in the j-point, which, as a rule, accompanies tachycardia, the rhythm-dependent nature of changes in the segment is diagnosed. The exception is when the area of ST reduction reaches 2 mm x 80 ms.

In practical work, ST shifts are studied using ST trends with their confirmation on the ECG page opening at moments of depression. To study the ST segment, three-channel ECG recording has advantages when trying to take into account changes in the ST vector in three directions - approximately sagittal, vertical and horizontal (Fig. 2).

Rice. 2. Assessment of changes in QRS and ST vectors.

When assessing ST and QRS vectors, Lundin suggests using the following methodology. The initial complex for which changes in dynamics will be compared is selected as the average complex for the first 2 minutes of observation. The current complex, obtained within several hours of recording, is superimposed on the reference complex. The QRS vector difference (QRS-VD) is defined as the difference in the areas of the reference and current complex. It is designated for each plane as Ax (horizontal axis), Ay (vertical axis), Az (sagittal axis). Next, the difference in the integral QRS vector is calculated as the square root of the sum of the squares of the differences. The ST vector (its magnitude or mode) ST-VM is the deviation of the ST segment from the baseline, measured at a point 60 ms from point j. The change in the ST vector - STC-VM (C - change) is determined relative to the ST vector in the reference complex. Ischemic episodes are compared with the initial position of the ST vector.

Association of ST-T changes with pain.

Depression or elevation (most often with myocardial infarction or post-infarction scar) ST appears after a painful attack or during it. Most often, pain appears a few minutes after the detection of a decrease in the ST segment, but it can appear simultaneously with these changes and in the final phase of an episode of depression. Pain usually disappears faster than ST segment changes, but sometimes ST segment changes are recorded before the onset of complaints. In such cases, performed too late, although still during pain, the ECG may be unchanged.

Deanfield et al. paid attention to episodes of ST depression that were not accompanied pain syndrome. These depressions have been called “silent” myocardial ischemia. It has now been proven that “silent” ischemia has a poor prognosis for the disease. Attention is drawn to the fact that it is precisely from these episodes that the effectiveness of treatment of coronary disease can be assessed. It has been established that in patients with unstable angina and chronic coronary insufficiency up to 80% of all ischemic episodes are silent.

Working group National Institute Health has defined “silent” ischemia as typical if the formula 1x1x1 is followed, which means a horizontal or oblique decrease in the ST segment of 1 mm or more, measured at a distance of 60-80 ms from point j, lasting 1 minute and separated from other episodes by 1 minute and more. This criterion can be considered specific for ischemia, but there is no specificity in determining the beginning and end of an ischemic episode. Many researchers define the duration of depression as the total time from its onset until the moment of return to the baseline. The beginning should be taken as a depression reaching 1 mm, and the end of ischemia should be a decrease in depression of less than 1 mm.

How reliable is the definition of “silent ischemia” based on ST segment depression? It all depends on what is taken as the standard. If we consider stress tests as a standard study in determining ischemia, then 96% of the HM results are consistent with the treadmill data. However, it should be understood that the stress test has its limitations in sensitivity and specificity. It is known that 30-40% of healthy people have a positive stress test.

Pathophysiology of myocardial ischemia.

The pathophysiological mechanisms of transient ischemia involve a decrease in coronary blood flow. This statement is contradicted by the fact that with a slight increase in heart rate for 5-15 minutes during normal life, ischemic episodes occur. The same changes occur in the same patients with dosed physical activity with a significantly greater increase in heart rate and with an increase in systolic pressure. This allows some researchers to postulate that increased oxygen demand is unlikely to cause ischemia, i.e. the mechanisms that form the oxygen balance during the day in patients with coronary artery disease are more complex. These include: 1) variability in the tension of the poststenotic part of the vessel, 2) lack of balance between the daily variability of the oxygen demand of the heart muscle and the threshold of oxygen deficiency, as well as 3) mechanisms regulating coronary blood flow. The latter include the state of the erythrocyte membrane and vasoreception sensitivity. As a result, a daily rhythm of myocardial ischemia variability is formed with a peak in the morning and afternoon hours. A certain circadian dependence is also noted in the appearance of “silent” ischemia. A large multicenter study of 306 patients with coronary artery disease with 48-hour monitoring showed that transient “silent” ischemia is recorded from 9 to 10 am and has a second peak at 20 pm. This circadian rhythm is similar to the circadian development of acute myocardial infarction and sudden death, which indicates the relationship between these phenomena.

Episodes of silent ischemia are preceded by positive results load tests. At negative tests“silent” ischemia develops rarely, and ischemia during exercise in patients with “silent” ischemia occurs already at the first stages of exercise. Speaking about the poor prognosis of “silent” ischemia, we should mention the data that it is these patients who need surgical treatment. Ischemia lasting more than 60 minutes increases the risk of AMI, and it is these patients who require surgery. When ischemia is less than 60 minutes, there is no difference in the incidence of AMI in individuals without “silent” and with “silent” ischemia.

It should be especially emphasized that it is necessary to take a more balanced approach to the diagnosis of silent ischemia in various cardiovascular pathologies, for example, with arterial hypertension, because, as shown, “silent” ischemia is akin to angina at rest, when pronounced lesions of the coronary vessels are detected.

Circadian changes in the terminal part of the ventricular complex should also include saddle-shaped ST elevation at night during sleep. Very often this ST elevation is mistaken for spastic reactions of the coronary vessels. For differential diagnosis It should be remembered that Prinzmetal's angina is a rapidly passing phenomenon, accompanied, as a rule, by rhythm disturbances and tachycardia (Fig. 3). Vagal ST shifts during sleep accompany the entire period of sleep and are replaced by the normal position of the segment with a tendency to decrease during awakening. In addition, with vagal reactions, a rare heart rate is noted.

Rice. 3. Prinzmetal's angina.

Errors in automatic measurement of ST shifts.

The criteria for myocardial ischemia have already been mentioned. They are quite definite with a visual assessment of the ECG. However, when automatically analyzing the ECG during chemotherapy, errors in the diagnosis of ischemia are common. Errors are inevitable when automatically measuring ST shifts. They come in several genera.

Errors due to poor recording quality. These errors occur both during automatic analysis by a computer and during visual analysis of the ECG by a doctor. In particular, they arise in cases where each subsequent complex is recorded at a new level, and the entire ECG takes on the appearance of a wave-like curve. There is no clear connection with breathing.

Such errors are often identified during physical activity during HM. An extremely noisy ECG is recorded, for example, when the electrode is removed or when a radiotelephone is used, when the level of artifacts is very high.

Computer errors associated with the ST segment analysis technique. When the shape of the ventricular complex changes, the starting point of the ST begins to change abruptly. Unstable determination of point j with a changing ST shape is most often associated with changes in heart rate. The ST segment displacement is estimated using the rule j + 60 or 80 ms. Relative to the isoline, this point can be very unstable, since any change in the shape of the ST and the S wave leads to a change in the angle between the S wave and the ST segment, which immediately affects the location of point j. In practice, most often, 40 ms are retreated from the vertex R and this point is taken as the starting point for the ST shift. The duration of ST in ms depends on the heart rate. In tachycardia, it is almost impossible to determine the end of the ventricular complex (T wave). One way to overcome this difficulty is to use a formula, such as Bazett's, to find the end of the ventricular complex. With this definition, the duration of ST segment depression is some specified part of the ECG section from R + 40 ms to the end of the T wave, for example, a part from 1/8 to 1/4 of this section. With tachycardia, the duration of ST segment depression is within 50-70 ms, and with bradycardia - 70-90 ms from the end of the QRS.

Error associated with binding point j to the top of the R wave. When the shape of the ventricular complex dynamically changes, for example, from a complex with a high R wave to a complex with a small r or QS wave, finding point j becomes impossible, since its binding is carried out at the top of the maximum positive or along the top of the maximally negative wave of the ventricular complex. Most often, such errors occur during positional changes.

Isoline measurement errors. It is customary to take the segment T-P as the isoline. With tachycardia, the T wave often “runs over” the P wave, the reference point, and therefore ends up on the P wave, or this point “runs over” the subsequent QRS complex on the Q or R wave, which makes it impossible to correctly navigate relative to the reference level of the initial isoelectric point. Persistent errors appear in the isoline measurement. As a consequence, the magnitude of the ST shift is determined incorrectly. The ST trend almost always contains an error of this kind. With tachycardia, even in the absence of a real ST shift, its decrease is detected. The reference level on the trend is taken to be the shift of position j relative to the reference level taken as the isoline. In such cases, the zero point is either on the T wave or on the P wave. Both increase the positive value of the reference point and lead to an apparent depression of the ST segment.

Another situation is also possible when the reference point falls on the Q wave, and then the isolevel will be lower, which will lead to a statement of ST segment elevation. Therefore, when assessing the ST segment, dynamic observation of the angle of inclination of the segment is important. In assessing ST segment elevation, an increase in point j with a downward tilt of the segment indicates an error of this kind.

Literature

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The most common important changes in the ST segment and T wave include those that are characteristic of myocardial ischemia and infarction. Since ventricular repolarization depends on myocardial perfusion, patients with coronary disease often exhibit reversible changes in the ST segment and T wave during transient myocardial ischemia.

Let us remember that pathological Q waves serve as indicators of myocardial infarction, but do not allow us to distinguish an acute one from one that occurred a week or a year ago. But during acute myocardial infarction, a series of characteristic changes in the ST segment and T wave occur, allowing one to differentiate between acute and non-acute myocardium (Fig. 4.24). In acute Q wave myocardial infarction, ST segment elevation is the first to appear, often accompanied by a tall T wave. At this early stage, myocardial cells are still viable and Q waves are not yet recorded. 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 several days, the ST segment returns to the baseline, but the T waves remain negative.

Weeks and months after a heart attack, the ST segment and T waves become normal, but abnormal Q waves remain, which is an invariable sign of myocardial infarction. If the ST segment remains elevated after several weeks, then there is a possibility of formation 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 leads located on opposite side. For example, in acute anterior septal MI, ST segment elevation in precordial 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 heart ventricle.

The mechanism of ST segment elevation during acute MI is not yet completely clear. 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 does not allow them to fully repolarize (Fig. 4.25). As a result, in a state of rest, partial depolarization of such cells causes the appearance of forces directed away from the damaged segment, causing a downward shift of the isoline. Due to the fact that the electrocardiograph records only the relative, and not the absolute, voltage value, the deviation of the isoline is not captured. As all myocardial cells, including those in the affected area, become completely depolarized, the resulting electrical potential of the heart actually becomes zero. However, due to a pathological downward displacement of the isoline, the ST segment appears to be located above the isoline. During the process of repolarization, the damaged cells return to an abnormal state of increased permeability in diastole, and the ECG again displays an abnormal shift in the basal line due to the presence of abnormal forces directed away from the electrode. Thus, the magnitude of ST segment elevation during MI is influenced to a certain extent by the relative displacement of the isoelectric line.

With non-transmural myocardial infarction, in the leads crossing the area of the infarction, there is a decrease in the ST segment, not its elevation. In this situation, the diastolic permeability of damaged cells adjacent to the infarct area causes the appearance of electrical forces directed from the endocardium to the epicardium and, therefore, towards the ECG electrodes. Thus, the basal line of the ECG is shifted upward (Fig. 4.25). After complete depolarization of the heart, its electrical potential returns to its true zero value, but relative to the abnormal basal line creates an apparent depression of the ST segment.

Rice. 4.25. Theoretical explanation for the occurrence of ST abnormalities during acute MI. Upstairs. Ion leakage causes partial depolarization of the cell of the damaged myocardium before the process of propagation of electrical excitation begins, which causes the appearance of forces directed away from the affected area and a decrease in the basal line of the ECG. But this process is not displayed on the ECG, since it records the relative, not the absolute, voltage value. While the heart is completely depolarized, the true voltage is zero, but there is an apparent ST segment elevation relative to the 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 depolarization ends, the voltage is indeed zero, but the ST segment appears slightly depressed relative to the upwardly shifted basal line

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

If the myocardium experiences a significant or critical oxygen deficiency, a cascade of biochemical changes occurs as a result of which certain changes appear on the ECG - ST segment depression.

Such changes in most cases should be regarded as acute until proven otherwise. But sometimes depression persists on the ECG for years, even in people who have no problems with coronary arteries. Only clinical picture will allow you to resolve the issue of patient management tactics, but we will not talk about the clinic.

And so, first of all, let's look at where this ST segment is located on the ECG.

On the left you see a schematic representation of an individual complex and ST segment. If you draw an imaginary line (ISOLINE) from the beginning to the end of the complex, then it will just pass through the ST segment. That is, there is no elevation or depression here - this is the norm. If the segment were below the isoline it would be called “depression”, if on the contrary, above the isoline it would be called “elevation”.

It should be noted that elevation or depression are not always pathological, it depends on their severity

Normal at rest

in the chest leads depression should be less than 0.5 mm.

in limb leads depression should be less than 0.5-1 mm.

Let's look at a fragment of the ECG

First you need to draw an isoline; the accuracy of the measurement depends on the correctness of this step. Usually, using a ruler, they find a more or less even section of the isoline between two complexes and draw a line through them. This will be the isoline. Somehow like this.

Now it is clearly visible that the ST segment is located under the isoline. But what to do now, where to measure this very depression? It is clear that you need to place the ruler vertically and measure from the isoline to the line of the segment itself, but where to do this?

Here you can see that if you choose a place arbitrarily, you can get completely different values of depression. How to proceed? The answer is simple, the measurement should be carried out as follows. You need to find the point (j) where the S wave ends, or if there is no S wave, then the point of intersection of the downward leg R with the isoline. Then set aside 0.08 s (4 mm) from this point and measure the depression (this will be point i) exactly at it. Some foreign authors recommend setting aside 0.04 s. (2 mm). But if there is derpessia, then it is there at 0.04 and at 0.08

In our case the situation will look like this

Thus, we can say that in lead V5 there is a depression of up to 0.5 mm (this is normal), and in lead V6 there is about 0.8 mm, which is beyond the normal range, but does not always indicate true ischemia. In such cases, such depression should be described in custody. And the clinician will already be wondering what to do about it; a detailed clinical interpretation is beyond the scope of this course.

The next topic is the most important in the entire section “ISCHEMIA”,