ST segment elevation in all leads except aVR and V1 (Fig. 28 A).
3. Spicy cor pulmonale, spontaneous pneumothorax, myocarditis, disorders cerebral circulation.
4. Transmural ischemia, the “damage” phase of myocardial infarction, dyskinesia or left ventricular aneurysm.
Changes in the ST segment and/or T wave (the so-called “primary changes”) are often recorded both in patients with cardiovascular diseases or extracardiac pathology, and in practically healthy individuals. The same changes can be the result of a wide variety of reasons. In practice, changes in the ST segment and T wave are most often considered signs of ischemia or small focal myocardial infarction. Indeed, with appropriate clinical picture, for example during the appearance pain V chest, registration of changes in the ST segment and T wave increases the likelihood of ischemia or myocardial infarction. However, in all other cases, it is impossible to determine from the ECG whether ST segment depression or the appearance of negative T waves are a consequence of myocardial ischemia. All others must be excluded possible reasons ECG changes using additional research methods. Differential diagnosis between ischemia and small-focal infarction is carried out on the basis of analysis of laboratory data, primarily on the degree of increase in the level of troponins and enzyme activity (reliable intravital diagnosis of small-focal infarction became possible only after the introduction of clinical practice methods for determining the activity of cardiac-specific isoenzymes, there was even such a term - “MV-CPK confirmed small-focal myocardial infarction”, in our time we can say “myocardial infarction without a Q wave, confirmed by an increase in troponin levels”).
When identifying long-lasting changes in the ST segment and T wave of unknown etiology in individuals without signs of organic heart disease, pharmacological tests may be useful. The most informative test is with isoproterenol (intravenous drip at a rate of 2-6 mcg/min for 0.5-4 minutes). Normalization of the ECG is a sign of the “functional” nature of repolarization changes. The cause of ECG changes in these cases is probably a violation of neurovegetative regulation. You can use a test with β-blockers (obzidan, 5-15 mg IV or 80 mg orally). Normalization of the ECG against the background of the action of obzidan also indicates a violation of neurovegetative regulation. The diagnostic value of a potassium test is much lower, since its results are difficult to interpret. A test with nitroglycerin is also uninformative. It should be noted that conducting pharmacological tests in individuals with an initially altered ECG is only of auxiliary value. The main role is played by a routine clinical examination with the use, if indicated, of additional research methods.
Painless “negative” ECG dynamics, most often the appearance of negative T waves, in the absence of other clinical, instrumental and laboratory signs, in most cases is not a sign of ischemia. Often the cause of “negative” ECG dynamics is the presence of arterial hypertension with myocardial hypertrophy, but without voltage signs of hypertrophy on the ECG. To clarify the diagnosis in such cases, it is also advisable to carry out functional tests, including samples from physical activity, transesophageal cardiac stimulation in combination with echocardiography (“stress echocardiography”) or with myocardial scintigraphy (see section “Coronary heart disease”).
A. Myocardial damage. In several leads - elevation of the ST segment with a convexity upwards with a transition to the T wave. In reciprocal leads - depression of the ST segment. The Q wave is often recorded. The changes are dynamic; the T wave becomes negative before the ST segment returns to baseline.
b. Pericarditis. ST segment elevation in many leads (I-III, aVF, V 3 -V 6). Absence of ST depression in reciprocal leads (except aVR). Absence of the Q wave. Depression of the PQ segment. Changes are dynamic; the T wave becomes negative after the ST segment returns to baseline.
V. Left ventricular aneurysm. ST segment elevation, usually with a deep Q wave or a form of the ventricular complex - QS type. Changes in the ST segment and T wave are permanent.
d. Early ventricular repolarization syndrome. Raising the ST segment with a convex downward transition to a concordant T wave. A notch on the descending knee of the R wave. A wide symmetrical T wave. Changes in the ST segment and T wave are permanent. Variant of the norm.
d. Other causes of ST segment elevation. Hyperkalemia, acute cor pulmonale, myocarditis, heart tumors.
2. Depression of the st segment
A. Myocardial ischemia. Horizontal or downward ST depression.
b. Repolarization disorder. Oblique depression of the ST segment with convexity upward (with left ventricular hypertrophy). Negative T wave. Changes are more pronounced in leads V 5, V 6, I, aVL.
V. Glycoside intoxication. Trough-shaped depression of the ST segment. Biphasic or negative T wave. Changes are more pronounced in the left precordial leads.
d. Nonspecific changes in the ST segment. Observed normally, with mitral valve prolapse, taking certain medications (cardiac glycosides, diuretics, psychotropic drugs), with electrolyte disturbances, myocardial ischemia, left and right ventricular hypertrophy, bundle branch block, WPW syndrome, tachycardia, hyperventilation, pancreatitis, shock.
I. T wave
1. Tall T wave. T wave amplitude > 6 mm in limb leads; V chest leads> 10-12 mm (in men) and > 8 mm in women. It is noted normally, with hyperkalemia, myocardial ischemia, in the first hours of myocardial infarction, with left ventricular hypertrophy, CNS lesions, anemia.
2. Deep negative T wave. A wide, deep negative T wave is recorded with lesions of the central nervous system, especially with subarachnoid hemorrhage. Narrow deep negative T wave - with ischemic heart disease, hypertrophy of the left and right ventricle.
3. Nonspecific changes in the T wave. Flattened or slightly inverted T wave. Observed normally, when taking certain medications, with electrolyte disturbances, hyperventilation, pancreatitis, myocardial ischemia, left ventricular hypertrophy, bundle branch block. Persistent juvenile type of ECG: negative T wave in leads V 1 -V 3 in young people.
K. QT interval
1. Prolongation of the QT interval. QT c > 0.46 for men and > 0.47 for women; (QT c = QT/RR).
A. Congenital prolongation of the QT interval: Romano-Ward syndrome (without hearing impairment), Ervel-Lange-Nielsen syndrome (with deafness).
b. Acquired QT prolongation: taking certain medications ( quinidine, procainamide, disopyramide, amiodarone, sotalol, phenothiazines, tricyclic antidepressants, lithium), hypokalemia, hypomagnesemia, severe bradyarrhythmia, myocarditis, mitral valve prolapse, myocardial ischemia, hypothyroidism, hypothermia, low-calorie liquid protein diets.
2. Shortening of the QT interval. QT< 0,35 с при ЧСС 60-100 мин –1 . Наблюдается при гиперкальциемии, гликозидной интоксикации.
L. Prong U
1. Increase in the amplitude of the U wave. U wave amplitude > 1.5 mm. Observed with hypokalemia, bradycardia, hypothermia, left ventricular hypertrophy, taking certain medications (cardiac glycosides, quinidine, amiodarone, isoprenaline).
2. Negative U wave. Observed with myocardial ischemia and left ventricular hypertrophy.
Electrocardiograms, one of the most important parameters that we, doctors, always pay attention to is the S-T segment. On the one hand, its dynamics may be an early objective sign of acute ischemic myocardial damage, including infarction; on the other hand, low specificity of changes S-T segment serves common cause diagnostic errors, which may result in unnecessary hospitalizations and medical procedures. Especially high clinical significance is given to the rise (elevation) of the S-T segment. And this is quite fair, since acute thrombotic obstruction of the coronary artery is almost always accompanied by a characteristic topical elevation of the S-T segment. Thus, S-T segment elevation is a potentially dangerous clinical ECG pattern until proven otherwise.
Without begging for medical and social significance coronary disease heart and one of its terrible complications - myocardial infarction, it should be emphasized that S-T segment elevation is a very common ECG phenomenon outside of coronary atherosclerosis. The correct interpretation of this phenomenon serves as a starting point for resolving the issue of further medical tactics.
5. Acute cor pulmonale (of course, first of all we are talking about pulmonary embolism). Concordance of S-T segment elevations in the “lower” standard and “anterior” chest leads is a highly specific ECG sign of acute overload of the right heart:
Fig.37
6. Acute pericarditis. The rises are concordant, plateau-shaped or obliquely ascending with a convexity downward; S-T elevation in pericarditis is never too high:
Fig.38
7. Stroke. With stroke, a slight plateau-like elevation of the S-T segment may appear in the chest leads. Often, this causes incorrect diagnosis of the “cerebral” form of myocardial infarction. I will give 3 examples (in all cases, the diagnosis of stroke was confirmed using SCT of the brain):
Fig.39 
Fig.40 
Fig.41
8. WPW syndrome. Despite the obviousness of electrocardiographic signs of ventricular preexcitation, the possibility of S-T segment elevation is often forgotten:
Fig.42 
Fig.43
9. Brugada syndrome. The “saddle-shaped” nature of the rise with upward convexity in leads V1-V3 is considered diagnostic:
Fig.44
10. Right ventricular hypertrophy. Along with the “textbook” types of right ventricular hypertrophy (S-type, R-type, rSR-type), you can occasionally see a small isolated plateau-like elevation of the S-T segment in the “anterior” precordial leads:
Fig.45
11. Takotsubo cardiomyopathy. The ECG picture is indistinguishable from acute myocardial infarction. Coronary angiography and cardiac ultrasound help to make the correct diagnosis:
Fig.46
12. Secondary (non-thrombotic) myocardial infarction. We are talking about a heart attack that occurs under conditions of “stressful” hemodynamics. For example, prolonged high tachysystole or severe arterial hypertension. In any case, with such infarctions, there are chronic stenoses or occlusions in the cardiac arteries:
Fig.47 
Fig.48
13. Other cases of segment elevation S-T:
Fig.49 
Fig.50
Fig.52
In emergency cardiology, detection of S-T segment elevation on an ECG is primarily suspicious for acute myocardial infarction, thromboembolism pulmonary artery or pericarditis. However, as practice shows, this ECG pattern is very common and is often detected in a variety of clinical circumstances, “mimicking” coronary pathology. Remember this! Good luck with your diagnostics!
Highly probable signs of “pre-scar” IHD include ST segment displacements: rise (elevation) and decrease (depression). With Holter monitoring, these changes are visible as a deviation of the ST trend from the zero level of “peaks” and “beards”.
The fact of the death of all layers of the myocardium on the ECG is reflected by the pathological Q wave (it is wide and its amplitude is more than a quarter of the height of the R wave in the same lead).
ST elevation and the presence of Q are included in the diagnosis formulations: ST-segment elevation AMI and Q-forming myocardial infarction.
ST elevation can also be observed in other conditions, remember this (early repolarization syndrome - characterized by notching on the descending knee of the R wave and the duration of this condition on the holter, pericarditis - changes in it are present in all or almost all leads). ST depression can also occur with an overdose of glycosides, but the shape of the segment is very characteristic and resembles a “trough”.
The remaining options for changing the QRS complex are considered possible (i.e., a diagnosis cannot be made based on them). Most often this is a negative T wave. If you are dealing with a patient with acute pain in the chest and any changes on the ECG, remember a simple rule: it is better to hospitalize ten patients without a heart attack than not to hospitalize one heart attack patient. Don't worry, the ambulance doctors will treat you with understanding.
Ischemic depression of the ST segment on ECG and Holter:
↓ST segment position trend in ischemic depression: “beards” are visible during ischemic episodes.
↓Picture from the same Holter ECG recording: in the leads characterizing the lower wall of the LV myocardium (II, III, AVF), reliable depression of the ST segment is visible (horizontal red lines pass through the beginning of the Q wave).
Ischemic ST segment elevation on ECG and Holter:
↓Trend of ST segment position during ischemic elevation: high “peaks” are visible at the time of ischemic attacks.
↓The beginning of the ischemic episode: in the leads characterizing the anterolateral areas of the LV myocardium (I, V3-V5), ST elevation began. Reciprocal ST depression begins in lead AVR.
↓Development of an ischemic episode: ST segment elevation increases, changes begin in previously “quiet” leads. In the middle chest leads, the complex takes on the shape of a “cat’s back”, characteristic of acute myocardial infarction.
↓Peak of the ischemic episode: ST segment elevation is maximum, in V4-V6 the QRS complex has taken on the character of a monophasic curve, in lead AVR the curve is also monophasic, but directed downwards (reciprocal changes). Interestingly, the patient came to the outpatient clinic for holter removal on his own feet, although with a mention in his diary of handfuls of nitrates taken. After decryption, he was hospitalized by ambulance.
Scar Q is a sign of the death of a section of the myocardium:
↓In leads V1-V4, a deep (more than a third of the height of the R wave) and fairly wide Q is visible. This is a sign of a previous myocardial infarction of extensive localization - the anterior wall, septum, part of the lateral wall of the left ventricle.
In addition, there is complete blockade right bundle branch (the left R wave disappeared behind the scar Q), as well as a complex rhythm disturbance - the NVES-VES pair triggered a jog of supraventricular tachycardia.
ECG changes in angina pectoris and chronic coronary heart disease occur not due to disruption of the coronary arteries themselves, but due to increasing myocardial anoxia 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 the results of functional tests.
- 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 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;
- Various disturbances of rhythm and intracardiac conduction are often observed;
- various disorders of intraventricular conduction, manifested by splitting of the QRS complex;
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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.
Coronary artery insufficiency and decreased flow to the myocardium arterial blood 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 early diagnostic sign development of ischemic heart 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:
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, carry out differential diagnosis 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.
It is necessary to differentiate negative T waves during ischemia and during dynamic changes without organic damage to the myocardium. To do this, a Valsalva maneuver, a test with hyperventilation, potassium, obsidan, orthostatic test and if with them the negative T wave turns into a positive one, then this indicates 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:
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.
