Vagal elevation of the st segment is more common. Causes and clinical significance of the ECG phenomenon of ST segment elevation. What is ST segment elevation

Assessment of ST segment elevation or depression Normally, the ST segment is located on an isoline. Normal segment elevation:

leads from the limbs up to 1 mm,
V1-V2 up to 3 mm,
V5-V6 up to 2 mm.

ST segment depression:

Normal in limb leads up to 0.5 mm
V1-V2 ≥ 0.5 mm – deviation from the norm

ST segment elevation
↓
Limb leads	Chest leads
ST elevation ≥ 1 mm in ≥2 contiguous leads	ST elevation ≥ 2 mm in ≥2 leads
↓
Acute myocardial infarction (probable infarction with the appearance of the Q wave)

ST segment depression ≥1.5 mm in two or more adjacent leads
↓
Test for troponin and/or MV CPK and/or myoglobin
↓
Yes	No
↓	↓
Myocardial infarction without Q wave	Myocardial ischemia

Differential diagnosis for changes in the ST segment: 1. Standard option:

Isolated elevation of the J point (early repolarization phenomenon): displacement of the ST segment at the J point by 1-4 mm above the isoline. Concave upward displacement of the ST segment, in the shape of a fishhook, in combination with high symmetrical T waves, predominantly in leads V2-V4.
Isolated J-point depression: upward elevation of the ST segment at the J-point, found in an apparently healthy person.
RSR` in lead V1:

normal duration of the RSR` complex;
amplitude of the first R wave<8 мм в отведении V1;
amplitude R`<6 мм;
R/S<1 во всех правых грудных отведениях.

Preservation of the juvenile T waveform: T wave inversion in leads V1 and V2 in an apparently healthy adult.

2. ST segment or T wave changes suspicious for acute or subacute myocardial infarction or left ventricular aneurysm:

Horizontal or concave elevation with or without T wave inversion.
Horizontal ST depression in combination with high T waves in leads V1-V2 (indicates posterior wall damage)

3. Changes in the ST segment and (or) T wave, in the presence of signs of acute MI, suspicious for reciprocal changes or myocardial ischemia:

horizontal or downward ST shift with or without T wave changes in leads opposite those in which there is ST segment elevation.

4. Changes in the ST segment and (or) T wave, in the absence of signs of acute MI, suspicious for myocardial ischemia:

horizontal or downward ST depression with or without T wave inversion in the absence of ST segment elevation.

5. Changes in the ST segment and (or) T wave associated with ventricular myocardial hypertrophy:

With left ventricular hypertrophy - depression of the ST segment of a convex shape with inversion of the T wave in V4-V6, often in a horizontal position of the EOS - in leads I, aVL, and in a vertical position - II, III, aVF
With right ventricular hypertrophy, there is depression of the ST segment of a convex shape with inversion of the T wave in V1-V3.

6. Changes in the ST segment and (or) T wave associated with intraventricular conduction disorders: QRS ≥ 120 ms +

With LBP blockade there is ST segment depression and T wave inversion in V4-V6.
With PNPG blockade, there is ST segment depression and T wave inversion in V1-V3.

7. Changes in the ST segment and (or) T wave, suspicious for the early stage of acute pericarditis: Diffuse elevation of the ST segment of a concave shape. It can be observed in all leads except aVR, but more often in I, II, V5-V6. The absence of reciprocal changes and simultaneous inversion of the T wave is a distinctive sign from MI. The T wave remains concordant with the ST shift characteristic of early pericarditis. 8. TELA 9. Acute myocarditis 10. HCM 11. Cocaine abuse 12. Non-specificchanges in the ST segment and (or) T wave:

mild ST segment depression, or isolated T wave inversion, or other disorders that are not caused by a specific pathology.

Dynamics of the ECG segment during myocardial infarction:

ST depression - ischemia
ST elevation – damage current
Q wave – necrosis (infarction)

Two terms are used to describe myocardial infarction:

Acute ST-segment elevation MI
Acute MI with ST segment depression

Criteria for diagnosing acute ST-segment elevation MI (probable Q-wave infarction):

Pathological ST segment elevation ≥ 1 mm in two or more adjacent limb leads
Pathological ST segment elevation ≥ 2 mm in two or more precordial leads
High R waves in leads V1 and V2 in combination with ST segment elevation in II, III, aVF or V 4R may indicate an associated posterior wall infarction. A posterior wall infarction is virtually always accompanied by an infarction of the inferior wall or right ventricle. Posterior MI must be confirmed with enzymes.

Additional signs confirming MI:

The presence of reciprocal depression. Helps confirm the diagnosis of MI, but does not have diagnostic value on its own. This sign is of particular importance, because ST segment elevation may be normal if it is not accompanied by reciprocal ST depression. In acute pericarditis, ST segment depression occurs only in lead aVR and sometimes in lead V1.
Appearance of Q waves. These waves become fully apparent 2-12 hours after the onset of clinical symptoms.
A decrease in the amplitude of the R waves in leads V2-V4, i.e. Poor rise of the R wave, especially if the R wave is present in leads V1 or V2 and disappears or decreases in V3 or V4.
Dynamics of ST and T are observed within 10-30 hours from the onset of a heart attack

Criteria for diagnosing acute MI with ST segment depression (probable Q wave infarction): In a patient experiencing discomfort in the chest, ST segment depression ≥1.5 mm in two or more leads, as well as pathological levels of troponin and/or CK MB and/or myoglobin, allows a diagnosis of MI in the absence of the Q wave. Myocardial ischemia ST segment depression indicating ischemia must meet the following criteria:

Depth > 1mm.
Present in two or more leads.
Occurs in two or more consecutive QRS complexes.
The shape is horizontal or oblique; T wave inversion is optional.
Abnormal ST segment arching in leads V1-V3 or V2-V4 in combination with T wave inversion; the terminal portion of the abnormal ST segment has a typical uplifted appearance.

Nonspecific ST segment changes ST segment changes should be considered nonspecific if the following signs are present:

ST segment depression.
Isoline offset.
The presence or absence of T wave inversion.
Often associated with small flat or slightly inverted T waves.

T waves should be ≥ 0.5 mm in amplitude in leads I and II.
Causes of nonspecific changes in the ST segment:

Minor ST segment depression ≤ 1 mm is often observed in healthy people.
Incorrect application (poor contact) of electrodes.
Ischemia.
Electrolyte disturbances.
KMP.
Myocarditis.
Pericarditis, incl. constrictive.
Violation of intraventricular conduction.
TELA.
Hyperventilation.
Drinking cold water.
Arrhythmias.
Use of medications (drugs).
Alcohol abuse.

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

Among cardiovascular diseases with a possible fatal outcome, acute myocardial infarction (MI), which is currently called STEMI, occupies an important place. This is the most severe form of ACS, short of sudden cardiac death.

Pathophysiology. Due to hemorrhage into the atherosclerotic plaque and gradually increasing thrombosis of the coronary artery, stenosis of its lumen occurs, resulting 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) showed that they have risk factors. The combination of these factors contributes to the acceleration of the atherosclerotic process and a manifold increase in the risk of myocardial infarction (MI). Currently known risk factors include smoking, high blood cholesterol, high blood pressure and diabetes.

In addition to the above four main risk factors, others are also known, in particular, excess body weight, stress, physical inactivity, and hereditary predisposition.

Symptoms of ST-segment 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, as a rule, is crucial for making a diagnosis. Already 1 hour after the onset of a typical painful attack, in most cases the ECG shows clear signs of MI. Therefore, diagnosing myocardial infarction is the most important task of electrocardiography.

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

The signs of MI must be clear. In most cases, ECG changes are so typical that a diagnosis can be made without further testing.

Other important diseases, especially in the acute stage, such as an attack of stable angina in a patient with coronary artery disease, pericarditis or myocarditis, should not be misinterpreted as MI. 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 be indicated, at least, whether it is an acute phase or an old infarction. 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 an infarction of the anterior wall of the LV from an infarction of its posterior wall. Depending on the location of the MI, it is possible to approximately 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 in the infarction zone, EDS does not occur. The resulting EMF vector is directed from the necrosis zone. Therefore, the ECG shows a deep and widened Q wave (Purdy's Q wave) in the 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 is therefore less excitable. Therefore, in the damage zone, a vector appears that corresponds to the ST segment and is directed from the electrically negative myocardium to the electrically less negative one, i.e. to the part of the myocardium that is relatively positively charged. Therefore, on the ECG corresponding to the damage zone, ST segment elevation is recorded.

3. Peaked 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 the outside to the inside. Therefore, in leads that normally show positive T waves, symmetrical peaked negative T waves (coronary Pardee T waves) now appear.

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

Appearance serum troponins reflects the formation of a blood clot 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 a standard test 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 us to judge its dynamics. Their significance is especially great in cases where ECG data is erased or masked by PG branch block or WPW syndrome. Diagnosis of myocardial infarction (MI) is also difficult in cases where the infarction is localized in the circumflex branch of the left coronary artery.

Currently in diagnosis of myocardial infarction(MI) both of these research methods are used: 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 research, 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 in the ECG, when carefully read, appear within 1 hour after the onset of ischemia and are reliable diagnostic signs, while increased levels of serum markers in many cases are not associated with ischemic myocardial damage.

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

If chest pain occurs, you should always register ECG. If MI is suspected, it is recommended to perform a monitoring 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 the MI, i.e. both with an infarction of the anterior wall and with a infarction of the posterior wall in the acute phase, a significant change in the ST segment occurs. Normally, there is no ST segment elevation, although sometimes slight elevation or depression is possible even in practically healthy people.

At acute myocardial infarction(MI) the first sign on the ECG is a distinct rise in the ST segment. This rise merges with the following positive T wave, and, unlike the norm, the boundary between them disappears. In such cases, they speak 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 appearance monophasic deformation of the ST segment upon careful analysis, extremely tall pointed T waves (so-called asphyxial T waves, or hyperacute T waves) can be noted, caused by acute subendocardial ischemia.

Sharp and wide Q wave can be registered already in the acute stage of MI, but this sign is not mandatory. A negative T wave may still be absent in the acute stage.

At "old" myocardial infarction(MI) the previously occurring ST segment elevation is no longer detected, but other changes appear affecting the Q and T waves.

IN normal Q wave not wide (0.04 s) and shallow, not exceeding in height the fourth part of the R wave in the corresponding lead. With “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, pointed and negative (coronary Purdy's T wave), in addition, ST segment depression is noted. 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 presented in the figure below is sufficient. The classification presented in the figure above allows you to more accurately assess the dynamics of MI.

In general, it is believed that the more leads, in which pathological changes are noted, the larger 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 for a formed scar in “old” MI. These changes disappear as the patient's condition improves. However, it is known that, despite clinical improvement and healing, signs of old infarction, especially the large Q wave, persist.

ST segment elevation with positive T wave, i.e. A monophasic ST segment deformity with a large Q wave that persists for more than 1 week and a transition of the ST segment to a slowly rising curve should raise suspicion of a cardiac aneurysm.

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

W. Brady et al. analyzed the results of emergency physicians' assessment of 448 ECGs with ST segment elevation. Erroneous assessment of the ECG in the form of overdiagnosis of acute myocardial infarction (MI) followed by thrombolytic therapy for patients was detected in 28% of cases with cardiac aneurysm (AC), in 23% with early ventricular repolarization syndrome (EVRS), in 21% with pericarditis and in 5% - with left bundle branch block (LBBB) without signs of MI.
The assessment of the ECG phenomenon, which consists of ST segment elevation, is complex and includes an analysis of not only the characteristics 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 main 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, therapeutic tactics for patients with ST segment elevation are different.
1. Norm
Elevation of the concave ST segment in the limb leads is acceptable up to 1 mm, in the 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 portion of the heart muscle that occurs as a result of absolute or relative insufficiency of 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 a pathological 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, as ischemia and damage spread to the 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 move to the next stage, with the formation of necrosis in the myocardium. Electrocardiographically, 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, ST segment elevation is noted 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. With SP, the characteristic features are cyclical attacks of pain, a monophasic appearance of the ECG curve and cardiac arrhythmias. If the spasm continues long enough, an MI develops. The cause of vasospasm of the coronary arteries is endothelial dysfunction.
ST segment elevation in SP and developing MI does not differ significantly, 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 condition and persistent thrombosis in the second (Fig. 3, 4).
Patients with SP are predominantly young women who do not have classical risk factors for coronary heart disease (CHD), excluding smoking. SP is associated with such manifestations of angiospastic conditions as Raynaud's syndrome and migratory headaches. What these syndromes have in common is the possibility of developing arrhythmia.
For the diagnosis of SP, tests with physical activity are not very informative. The most sensitive and specific provocative test is the intravenous administration of 50 mcg of ergonovine at 5-minute intervals until a positive result is obtained, while the total dosage of the drug should not exceed 400 mcg. A test with ergonovine is considered positive when an attack of angina and ST segment elevation on the ECG occur. To quickly relieve the symptoms of vasospasm caused by ergonovine, nitroglycerin is used. The dynamics of ST segment changes in SP can be monitored 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. Cardiac aneurysm (AC)
AS usually forms after transmural MI. Bulging of the ventricular wall causes stretching of adjacent 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, AS is characterized by a picture of transmural MI, and therefore QS, occasionally Qr, is observed in most ECG leads. 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 signs observed in stages II and III of ST-segment elevation MI (Fig. 5).
5. Early ventricular repolarization syndrome (EVRS)
SRR is an ECG phenomenon consisting of registration of ST segment elevation up to 2-3 mm with a convexity downward, usually in many leads, most significantly in the chest leads. The point of transition of the descending part of the R wave into the T wave is located above the isoline; often a notch or wave is determined at the place of this transition (“camel hump”, “Osborne wave”, “hat hook”, “hypothermic hump”, “J wave”) , the T wave is positive. Sometimes, as part of this syndrome, there is a sharp increase in the amplitude of the R wave in the chest leads, combined 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 (AP)
A characteristic ECG sign of pericarditis is a concordant (unidirectional with the maximum wave of the QRS complex) ST segment displacement in most leads. These changes are a reflection of damage to the subepicardial myocardium adjacent to the pericardium.
In the ECG picture of AP, a number of stages are distinguished:
1. Concordant ST shift (ST elevation in those 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, involvement of the atrium myocardium in the inflammatory process is observed, which is reflected on the ECG in the form of a displacement of the PQ segment (in most leads - PQ depression), the appearance of supraventricular arrhythmias. With 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 (ACP)
With ALS, the ECG shows signs of overload of the right side of the heart 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 - formation of a deep S wave in lead I and a deep (pathological in amplitude, but usually 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, combined 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 McGean-White sign - QIII-TIII-SI.
3. Deviation of the electrical axis of the heart (EOS) to the right, sometimes the formation of EOS type SI-SII-SIII.
4. Formation of a high pointed P wave (“P-pulmonale”) in leads II, III, aVF.
5. Right bundle branch block.
6. Block of the posterior branch of the left bundle branch.
7. Increase in the amplitude of the R wave 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, shift of the transition zone to the left.
9. Sudden appearance of supraventricular cardiac 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 permanent or transient right bundle branch block with ST segment elevation in the right precordial leads (V1-V3).
Currently, the following conditions and diseases that cause SB are described: fever, hyperkalemia, hypercalcemia, thiamine deficiency, cocaine poisoning, hyperparathyroidism, hypertestosteronemia, mediastinal tumors, arrhythmogenic right ventricular dysplasia (ARVD), pericarditis, MI, SP, mechanical obstruction of the right outflow tract ventricle 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 during treatment with sodium channel blockers, mesalazine, vagotonic drugs, α-adrenergic agonists, β-blockers, 1st generation antihistamines, antimalarials, sedatives, anticonvulsants, neuroleptics, tri- and tetracyclic antidepressants, and lithium drugs.
The ECG of patients with BS is characterized by a number of specific changes that can be observed in complete or incomplete combination:
1. Complete (in the classic version) or incomplete blockade of the right bundle branch.
2. Specific form of ST segment elevation in the right precordial leads (V1-V3). Two types of ST segment elevation have been described: “saddle-back type” and “coved type” (Fig. 9). The rise of the “coved type” 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. Increasing the duration of the PQ interval (PR).
5. The occurrence of paroxysms of polymorphic ventricular tachycardia with spontaneous cessation 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 often occurs at night or early in the morning, which makes it possible to associate their occurrence with activation of the parasympathetic component of the autonomic nervous system. ECG signs such as ST segment elevation and prolongation of the PQ interval may be transient. H. Atarashi proposed taking 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. Lengthening this interval to 0.08 s or more in combination with ST elevation in V2 more 0.18 mV is a sign of an increased risk of ventricular fibrillation (Fig. 10).
9. Stress cardiomyopathy
(tako-tsubo syndrome, SCM)
SCM is a type of non-ischemic cardiomyopathy that occurs under the influence of severe emotional stress, more often in elderly 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 sections, where it becomes “stunned.” EchoCG reveals hypokinesis of the apical segments and hyperkinesis of the basal segments of the left ventricle (Fig. 11).
In the ECG picture of SCM, a number of stages are distinguished:
1. Elevation of the ST segment in most ECG leads, absence of reciprocal depression of the ST segment.
2. The ST segment approaches the isoline, the T wave is smoothed 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 (ARVD)
ARVD is a pathology that is an isolated lesion of the right ventricle (RV); often familial, characterized by fatty or fibrofatty infiltration of the ventricular myocardium, accompanied by ventricular arrhythmias of varying severity, including ventricular fibrillation.
Currently, two morphological variants of ARVC are known: fatty and fibrofatty. 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 fibrofatty variant is associated with significant thinning of the pancreatic wall, and the process may involve the left ventricular myocardium. Also, with ARVD, moderate or severe dilatation of the pancreas, aneurysms, or segmental hypokinesia may be observed.
ECG signs:
1. Negative T waves in the precordial 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 precordial leads may exceed the duration of the ventricular complexes in the left precordial leads. The ratio of the sum of QRS durations in leads V1 and V3 to the sum of QRS durations in V4 and V6 has great diagnostic value (Fig. 12).
11. Hyperkalemia (HK)
ECG signs of increased potassium levels in the blood are:
1. Sinus bradycardia.
2. Shortening of the QT interval.
3. The formation of tall, pointed positive T waves, which in combination with a shortening of the QT interval creates the impression of ST elevation.
4. Widening of the QRS complex.
5. Shortening, with increasing hyperkalemia - prolongation of the PQ interval, progressive impairment of atrioventricular conduction up to complete transverse block.
6. Decreased amplitude, smoothing of the P wave. With an increase in potassium levels, the complete disappearance of the P wave.
7. Possible ST segment depression in many leads.
8. Ventricular arrhythmias (Fig. 13).
12. Left ventricular hypertrophy (LVH)
LVH occurs in arterial hypertension, aortic heart defects, mitral valve insufficiency, cardiosclerosis, and congenital heart defects (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. Right overload
and left ventricles
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 with excess blood volume or pressure, and changes in the ECG are permanent. One should think about overload when an acute situation occurs; changes on 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 conduction disorder in the main trunk of the left bundle branch before its division into two branches or simultaneous damage to two branches of the left bundle branch. Excitation spreads in the usual way to the RV and in a roundabout way, with a delay - to the LV (Fig. 15).
The ECG shows a widened, deformed QRS complex (more than 0.1 s), which in leads V5-V6, I, aVL looks like rsR’, RSR’, RsR’, rR’ (the R wave predominates in the QRS complex). Depending on the width of the QRS complex, left bundle branch block can be complete or incomplete (incomplete LBBB: 0.1 s 15. Transthoracic cardioversion (EIT)
Cardioversion may be accompanied by transient ST segment elevation. J. van Gelder et al. reported that 23 of 146 patients with atrial fibrillation or flutter after transthoracic cardioversion had ST segment elevation of more than 5 mm, and there were no clinical or laboratory signs 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-segment elevation after cardioversion have a lower ejection fraction than patients without ST-segment elevation (27% and 35%, respectively). The mechanism of ST segment elevation is not completely clear (Fig. 16).
16. Wolff-Parkinson-White syndrome (WWS)
SVPU - conduction of an impulse from the atria to the ventricles along the additional Kent-Palladino 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, caused by 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 waves predominate), except for WPW syndrome, type C.
3. Bundle branch block (widening of the QRS complex more than 0.1 s). In WPW syndrome, type A, the impulse from the atria to the ventricles is carried out through the left Kent-Palladino bundle, for this reason the excitation of the left ventricle begins earlier than the right, and the blockade of the right bundle branch is recorded on the ECG. In WPW syndrome, type B, the impulse from the atria to the ventricles is conducted along the right Kent-Palladino bundle. For this reason, excitation of the right ventricle begins earlier than the left, and the blockade of the left bundle branch is recorded 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-Palladino bundle, which leads to excitation of the left ventricle before the right, and the ECG shows right bundle branch block and a negative D-wave in leads V5- V6.
4. The P wave is of normal shape and duration.
5. Tendency to attacks of supraventricular tachyarrhythmia (Fig. 17).
17. Atrial flutter (AF)
Atrial fibrillation is an accelerated, superficial, but regular 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 functional atrioventricular block, most often 2:1 or 4:1, the frequency of ventricular contractions is significantly less than the frequency of atrial contractions.
ECG criteria for atrial flutter:
1. F-waves, located at equal intervals, with a frequency of 220-350 per minute, of the same height, width and shape. F waves are well expressed 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 shape of F waves is “sawtooth”. The ascending leg is steep, and the downward leg gradually descends gently and passes without an isoelectric interval into the steep ascending leg of the next wave F.
4. Partial AV block of varying degrees is almost always observed (usually 2:1).
5. QRS complex of normal shape. Due to the layering of F waves, the ST interval and T wave are deformed.
6. The R-R interval is the same with a constant degree of atrioventricular block (correct form of atrial flutter) and different with a changing degree of AV block (irregular form of atrial flutter) (Fig. 18).
18. Hypothermia (Osborne syndrome, HT)
Characteristic ECG criteria for HT are the appearance of waves in the area of the J point, called Osborne waves, ST segment elevation in leads II, III, aVF and left thoracic leads V3-V6. Osborne waves are directed in the same direction as the QRS complexes, and their height is directly proportional to the degree of HT. As body temperature decreases, along with the described ST-T changes, a slowdown in heart rate and prolongation of the PR and QT intervals (the latter mainly due to the ST segment) are detected. As body temperature decreases, the amplitude of the Osborne wave increases. At body temperatures below 32°C, atrial fibrillation is possible, and 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 HT as mild (at body temperature 34-35°C), moderate (30-34°C) and severe (below 30°C) (Fig. 19).
Thus, the Osborne wave (hypothermic wave) can be considered as a diagnostic criterion for severe central disorders. Osborne wave amplitude was inversely correlated with a decrease in body temperature. According to our data, the severity of the Osborne wave and the value of the QT interval determine the prognosis. Prolongation of the QT interval >500 ms and severe deformation of the QRST complex with the formation of the Osborne wave 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 in the absence of the dynamics of the ST segment and TT wave characteristic of a heart attack, as well as a decrease in the depth of the Q wave when recording an ECG at the height of inspiration or expiration.
Conclusion
Based on an 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 a practicing physician often has to carry out a differential diagnosis of many diseases, including rare ones.

Literature
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4. Zhdanov G.G., Sokolov I.M., Shvarts Yu.G. Intensive therapy of acute myocardial infarction. Part 1 // Bulletin of intensive care. - 1996. - No. 4. - P.15-17.
5. Isakov I.I., Kushakovsky M.S., Zhuravleva N.B. Clinical electrocardiography. - L.: Medicine, 1984.
6. Clinical arrhythmology / Ed. prof. A.V. Ardasheva - M.: Publishing House "Medpraktika-M", 2009. - 1220 p.
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8. Kushakovsky M.S., Zhuravleva N.B. Arrhythmias and heart block (atlas of electrocardiograms). - L.: Medicine, 1981.
9. Limankina I.N. On the issue of cerebrocardiac syndrome in mentally ill patients. Current issues in clinical and social psychiatry. - Ed. SZPD, 1999. - pp. 352-359.
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The most common cause of ST elevation on the resting ECG in healthy individuals is early ventricular repolarization syndrome (EVRS).

ST segment elevation must be differentiated depending on whether it is recorded against the background of a Q wave after myocardial infarction, or whether it appears in the absence of a Q wave. The mechanisms of its elevation in these cases are different. More often, ST elevation in the presence of a Q wave is observed in the anterior chest leads (V1 and V2).

ST segment elevation in leads with Q due to myocardial infarction. Previous myocardial infarction is the most common cause of ST elevation during exercise testing and is directly related to the existence of areas of left ventricular dyskinesia or aneurysm. Exercise-induced ST segment elevation is observed in approximately 50% of patients with anterior myocardial infarction when tested in the first 2 weeks after the onset of myocardial infarction and in 15% of those with inferior myocardial infarction, and by week 6 the incidence of ST segment elevation in these patients decreases. Individuals with documented ST elevation in such cases have a lower ejection fraction than patients with Q waves but without exercise-induced ST elevation. In most cases, exercise-induced ST segment elevation in leads with a pathological Q wave is not a sign of more severe CAD and rarely reflects myocardial ischemia.

It is believed that ST segment elevation in leads with Q in the case of ischemia is predominantly T-dominant in nature, while ST-dominant in the absence of ischemia, being a consequence of dyskinesia.

Initial myocardial damage (Q depth) has a greater influence on the degree of ST elevation than reflects the severity of myocardial dysfunction.

These changes may be the result of reciprocal ST depression, which reflects ischemia in the opposite leads and may indicate the emergence of new areas of ischemia. A simultaneous decrease and increase in ST in opposite leads during the test suggests the presence of multivessel coronary artery disease, and in patients with a Q-myocardial infarction caused by a single-vessel lesion (confirmed by coronary angiography) 6-8 weeks ago - a probable residual stenosis of the infarct-related artery .

ST segment elevation in the absence of a Q wave. In patients without a history of myocardial infarction (absence of a Q wave on the resting ECG), ST segment elevation (except for leads V1 and AVR) during exercise indicates severe transient ischemia due to significant proximal stenosis or spasm of the coronary artery. This phenomenon is rare - 1 in 1000 tests, and in patients with obstructive coronary artery disease - in 1% of cases. It localizes the site of ischemia: for example, ST segment elevation in leads V2–V4 indicates damage to the anterior interventricular artery; in the lateral leads - about damage to the circumflex artery or diagonal branches; in leads II, III, AVF - about damage to the right coronary artery.

Key Point: Severe transmural ischemia causes ST-segment elevation during exercise in individuals without prior myocardial infarction (or without a Q wave on the resting ECG). ST segment elevation in this case localizes the ischemic zone, in contrast to ST depression, which is a consequence of general subendocardial ischemia and does not specify the location of the coronary artery lesion.

In patients with variant (spastic) angina, ST segment elevation is recorded simultaneously with the onset of angina, often occurring at rest. During exercise, ST segment elevation in such patients is observed only in 30% of cases. Many patients with ST segment elevation have reciprocal ST depression in opposite leads. ST segment elevation during exercise is arrhythmogenic - with it, ventricular arrhythmias are more often recorded.

Zadionchenko V.S. Shekhyan G.G. Shchikota A.M. Yalymov A.A.

Relevance of differential diagnosis reasons elevation segment ST on the ECG is due to the high frequency and significance of the pathological conditions underlying it, as well as significant differences in therapeutic tactics and prognosis of diseases.

W. Brady et al. analyzed the results of emergency physicians’ assessment of 448 ECGs with elevation segment ST. Erroneous assessment of the ECG in the form of overdiagnosis of acute myocardial infarction (MI) followed by thrombolytic therapy for patients was detected in 28% of cases with cardiac aneurysm (AC), in 23% with early ventricular repolarization syndrome (EVRS), in 21% with pericarditis and in 5% - with left bundle branch block (LBBB) without signs of MI.

Assessment of the ECG phenomenon consisting of elevation segment ST, is complex in nature and includes an analysis of not only the characteristics of changes in ST and other ECG components, but also clinical pictures of the disease. In most cases, a detailed analysis of the ECG is sufficient to differentiate the main syndromes leading to elevation segment ST. ST changes can be a variant of a normal ECG, reflect non-coronarogenic changes in the myocardium and serve reason acute coronary pathology requiring emergency thrombolytic therapy. Thus, therapeutic tactics for patients with elevation segment ST is different.

Acceptable elevation the ST segment is concave in the limb leads up to 1 mm, in the 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 portion of the heart muscle that occurs as a result of absolute or relative insufficiency of 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 a pathological 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, as ischemia and damage spread to the 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 move to the next stage, with the formation of necrosis in the myocardium. Electrocardiographically, 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, ST segment elevation is noted 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. With SP, the characteristic features are cyclical attacks of pain, a monophasic appearance of the ECG curve and cardiac arrhythmias. If the spasm continues long enough, an MI develops. Reason vasospasm of the coronary arteries is endothelial dysfunction.

ST segment elevation in SP and developing MI does not differ significantly, 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 condition and persistent thrombosis in the second (Fig. 3, 4).

Patients with SP are predominantly young women who do not have classical risk factors for coronary heart disease (CHD), excluding smoking. SP is associated with such manifestations of angiospastic conditions as Raynaud's syndrome and migratory headaches. What these syndromes have in common is the possibility of developing arrhythmia.

For the diagnosis of SP, tests with physical activity are not very informative. The most sensitive and specific provocative test is the intravenous administration of 50 mcg of ergonovine at 5-minute intervals until a positive result is obtained, while the total dosage of the drug should not exceed 400 mcg. A test with ergonovine is considered positive when an attack of angina and ST segment elevation on the ECG occur. To quickly relieve the symptoms of vasospasm caused by ergonovine, nitroglycerin is used. The dynamics of ST segment changes in SP can be monitored 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. Cardiac aneurysm (AC)

AS usually forms after transmural MI. Bulging of the ventricular wall causes stretching of adjacent 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, AS is characterized by a picture of transmural MI, and therefore QS, occasionally Qr, is observed in most ECG leads. 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 signs observed in stages II and III of ST-segment elevation MI (Fig. 5).

5. Early ventricular repolarization syndrome (EVRS)

SRR is an ECG phenomenon consisting of registration of ST segment elevation up to 2-3 mm with a convexity downward, usually in many leads, most significantly in the chest leads. The point of transition of the descending part of the R wave into the T wave is located above the isoline; often a notch or wave is determined at the place of this transition (“camel hump”, “Osborne wave”, “hat hook”, “hypothermic hump”, “J wave”) , the T wave is positive. Sometimes, as part of this syndrome, there is a sharp increase in the amplitude of the R wave in the chest leads, combined 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 (AP)

A characteristic ECG sign of pericarditis is a concordant (unidirectional with the maximum wave of the QRS complex) ST segment displacement in most leads. These changes are a reflection of damage to the subepicardial myocardium adjacent to the pericardium.

In the ECG picture of AP, a number of stages are distinguished:

1. Concordant ST shift (ST elevation in those 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, involvement of the atrium myocardium in the inflammatory process is observed, which is reflected on the ECG in the form of a displacement of the PQ segment (in most leads - PQ depression), the appearance of supraventricular arrhythmias. With 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 (ACP)

With ALS, the ECG shows signs of overload of the right side of the heart for a short time (occurs with status asthmaticus, pulmonary edema, pneumothorax, the most common cause- thromboembolism in the pulmonary artery basin). The most characteristic ECG signs are:

1. SI-QIII - formation of a deep S wave in lead I and a deep (pathological in amplitude, but usually 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, combined 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 McGean-White sign - QIII-TIII-SI.

3. Deviation of the electrical axis of the heart (EOS) to the right, sometimes the formation of EOS type SI-SII-SIII.

4. Formation of a high pointed P wave (“P-pulmonale”) in leads II, III, aVF.

5. Right bundle branch block.

6. Block of the posterior branch of the left bundle branch.

7. Increase in the amplitude of the R wave 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, shift of the transition zone to the left.

9. Sudden appearance of supraventricular cardiac 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 permanent or transient right bundle branch block with ST segment elevation in the right precordial leads (V1-V3).

Currently, the following conditions and diseases that cause SB are described: fever, hyperkalemia, hypercalcemia, thiamine deficiency, cocaine poisoning, hyperparathyroidism, hypertestosteronemia, mediastinal tumors, arrhythmogenic right ventricular dysplasia (ARVD), pericarditis, MI, SP, mechanical obstruction of the right outflow tract ventricle 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 during treatment with sodium channel blockers, mesalazine, vagotonic drugs, α-adrenergic agonists, β-blockers, 1st generation antihistamines, antimalarials, sedatives, anticonvulsants, neuroleptics, tri- and tetracyclic antidepressants, and lithium drugs.

The ECG of patients with BS is characterized by a number of specific changes that can be observed in complete or incomplete combination:

1. Complete (in the classic version) or incomplete blockade of the right bundle branch.

2. Specific form of ST segment elevation in the right precordial leads (V1-V3). Two types of ST segment elevation have been described: “saddle-back type” and “coved type” (Fig. 9). The rise of the “coved type” 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. Increasing the duration of the PQ interval (PR).

5. The occurrence of paroxysms is a textbook on the geography of polymorphic ventricular tachycardia with spontaneous cessation or transition to ventricular fibrillation.

The last ECG sign mainly determines clinical symptoms of this syndrome. The development of ventricular tachyarrhythmias in patients with SB often occurs at night or early in the morning, which makes it possible to associate their occurrence with activation of the parasympathetic component of the autonomic nervous system. ECG signs such as ST segment elevation and prolongation of the PQ interval may be transient. H. Atarashi proposed taking 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. Lengthening this interval to 0.08 s or more in combination with ST elevation in V2 more 0.18 mV is a sign of an increased risk of ventricular fibrillation (Fig. 10).

9. Stress cardiomyopathy

(tako-tsubo syndrome, SCM)

SCM is a type of non-ischemic cardiomyopathy that occurs under the influence of severe emotional stress, more often in elderly 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 sections, where it becomes “stunned.” EchoCG reveals hypokinesis of the apical segments and hyperkinesis of the basal segments of the left ventricle (Fig. 11).

In the ECG picture of SCM, a number of stages are distinguished:

1. Elevation of the ST segment in most ECG leads, absence of reciprocal depression of the ST segment.

2. The ST segment approaches the isoline, the T wave is smoothed 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 (ARVD)

ARVD is a pathology that is an isolated lesion of the right ventricle (RV); often familial, characterized by fatty or fibrofatty infiltration of the ventricular myocardium, accompanied by ventricular arrhythmias of varying severity, including ventricular fibrillation.

Currently, two morphological variants of ARVC are known: fatty and fibrofatty. 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 fibrofatty variant is associated with significant thinning of the pancreatic wall, and the process may involve the left ventricular myocardium. Also, with ARVD, moderate or severe dilatation of the pancreas, aneurysms, or segmental hypokinesia may be observed.

ECG signs:

1. Negative T waves in the precordial 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 precordial leads may exceed the duration of the ventricular complexes in the left precordial leads. The ratio of the sum of QRS durations in leads V1 and V3 to the sum of QRS durations in V4 and V6 has great diagnostic value (Fig. 12).

11. Hyperkalemia (HK)

ECG signs of increased potassium levels in the blood are:

1. Sinus bradycardia.

2. Shortening of the QT interval.

3. The formation of tall, pointed positive T waves, which in combination with a shortening of the QT interval creates the impression of ST elevation.

4. Widening of the QRS complex.

5. Shortening, with increasing hyperkalemia - prolongation of the PQ interval, progressive impairment of atrioventricular conduction up to complete transverse block.

6. Decreased amplitude, smoothing of the P wave. With an increase in potassium levels, the complete disappearance of the P wave.

7. Possible ST segment depression in many leads.

8. Ventricular arrhythmias (Fig. 13).

12. Left ventricular hypertrophy (LVH)

LVH occurs in arterial hypertension, aortic heart defects, mitral valve insufficiency, cardiosclerosis, and congenital heart defects (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. Right overload

and left ventricles

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 with excess blood volume or pressure, and changes in the ECG are permanent. One should think about overload when an acute situation occurs; changes on 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 conduction disorder in the main trunk of the left bundle branch before its division into two branches or simultaneous damage to two branches of the left bundle branch. Excitation spreads in the usual way to the RV and in a roundabout way, with a delay - to the LV (Fig. 15).

The ECG shows a widened, deformed QRS complex (more than 0.1 s), which in leads V5-V6, I, aVL looks like rsR’, RSR’, RsR’, rR’ (the R wave predominates in the QRS complex). Depending on the width of the QRS complex, left bundle branch block can be complete or incomplete (incomplete LBBB: 0.1 s

15. Transthoracic cardioversion (EIT)

Cardioversion may be accompanied by transient ST segment elevation. J. van Gelder et al. reported that 23 of 146 patients with atrial fibrillation or flutter after transthoracic cardioversion had ST segment elevation of more than 5 mm, with no clinical or laboratory signs 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-segment elevation after cardioversion have a lower ejection fraction than patients without ST-segment elevation (27% and 35%, respectively). The mechanism of ST segment elevation is not completely clear (Fig. 16).

16. Wolff-Parkinson-White syndrome (WWS)

SVPU - conduction of an impulse from the atria to the ventricles along the additional Kent-Palladino 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, caused by 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 waves predominate), except for WPW syndrome, type C.

3. Bundle branch block (widening of the QRS complex more than 0.1 s). In WPW syndrome, type A, the impulse from the atria to the ventricles is carried out along the left Kent-Palladino bundle, along this reason excitation of the left ventricle begins earlier than the right, and the blockade of the right bundle branch is recorded on the ECG. In WPW syndrome, type B, the impulse from the atria to the ventricles is conducted along the right Kent-Palladino bundle. For this reason, excitation of the right ventricle begins earlier than the left, and the blockade of the left bundle branch is recorded 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-Palladino bundle, which leads to excitation of the left ventricle before the right, and the ECG shows right bundle branch block and a negative D-wave in leads V5- V6.

4. The P wave is of normal shape and duration.

5. Tendency to attacks of supraventricular tachyarrhythmia (Fig. 17).

17. Atrial flutter (AF)

Atrial fibrillation is an accelerated, superficial, but regular 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 functional atrioventricular block, most often 2:1 or 4:1, the frequency of ventricular contractions is significantly less than the frequency of atrial contractions.

ECG criteria for atrial flutter:

1. F-waves, located at equal intervals, with a frequency of 220-350 per minute. the same height, width and shape. F waves are well expressed 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 shape of F waves is “sawtooth”. The ascending leg is steep, and the downward leg gradually descends gently and passes without an isoelectric interval into the steep ascending leg of the next wave F.

4. Partial AV block of varying degrees is almost always observed (usually 2:1).

5. QRS complex of normal shape. Due to the layering of F waves, the ST interval and T wave are deformed.

6. The R-R interval is the same with a constant degree of atrioventricular block (correct form of atrial flutter) and different with a changing degree of AV block (irregular form of atrial flutter) (Fig. 18).

18. Hypothermia (Osborne syndrome, HT)

Characteristic ECG criteria for HT are the appearance of waves in the area of the J point, called Osborne waves, ST segment elevation in leads II, III, aVF and left thoracic leads V3-V6. Osborne waves are directed in the same direction as the QRS complexes, and their height is directly proportional to the degree of HT. As body temperature decreases, along with the described ST-T changes, a slowdown in heart rate and prolongation of the PR and QT intervals (the latter mainly due to the ST segment) are detected. As body temperature decreases, the amplitude of the Osborne wave increases. At body temperatures below 32°C, atrial fibrillation is possible, and 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 HT as mild (at body temperature 34-35°C), moderate (30-34°C) and severe (below 30°C) (Fig. 19).

Thus, the Osborne wave (hypothermic wave) can be considered as a diagnostic criterion for severe central disorders. Osborne wave amplitude was inversely correlated with a decrease in body temperature. According to our data, the severity of the Osborne wave and meaning QT interval determines prognosis. Prolongation of the QT interval >500 ms and severe deformation of the QRST complex with the formation of the Osborne wave 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 in the absence of the dynamics of the ST segment and TT wave characteristic of a heart attack, as well as a decrease in the depth of the Q wave when recording an ECG at the height of inspiration or expiration.

Conclusion

Based on an 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 a practicing physician often has to carry out a differential diagnosis of many diseases, including rare ones.

Literature

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2. Heart disease: A guide for doctors / Ed. R.G. Oganova, I.G. Fomina. - M. Litterra, 2006. - 1328 p.

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Heart block

Heart block is a condition in which the conduction of electrical impulses generated by the heart's natural pacemaker (sinoatrial node) is disrupted, resulting in the heart's ability to pump blood being impaired. With partial or incomplete heart block, the conduction of impulses between the atria and ventricles along the His bundle slows down (first degree heart block); If not all impulses pass from the atria to the ventricles, then the person has a second degree heart block. With third degree heart block or complete heart block, not a single impulse passes from the atria to the ventricles, and the latter begin to contract at their own slow speed of 20-40 beats per minute. Heart block can be congenital or develop as a result of various heart diseases, including myocardial infarction, myocarditis, cardiomyopathy, and heart valve disease. It is often observed in older people due to chronic degenerative cicatricial changes in the conduction system of the heart. Heart block can often be asymptomatic, but if the pulse and heart rate suddenly slow down, the patient may develop heart failure or Adams-Stokes syndrome. Symptoms of the disease can be eliminated by using an artificial heart pacemaker;

Found in 1034 questions:

cardiologist 28 minutes ago / Evgeniy / Tambov

Moderate diffuse changes in the myocardium. Incomplete blockade right legs of p. His. EchoCG is normal. The therapist diagnosed: Atherosclerotic disease hearts. And he prescribed it for life: bisoprolol 2.5 mg and cardiomagnyl 75 mg at night. Ya open

I decided to do an ECG. Conclusion: The rhythm is sinus, regular. Heart rate 103/min. Horizontal position of the electrical axis hearts. Incomplete blockade PVLNPG. About myself: 37 years old, height 178 cm, weight 96. Lifestyle - measured. Tell me on. open

He was treated in the hospital. At the moment the diagnosis is: Conduction disorder hearts. Infrequent episodes of pacemaker migration. Full blockade right bundle branch, as a consequence of the transferred. open

P in leads V1-V2), respiratory arrhythmia, normotachysystole. Normal position of the electrical axis hearts. Strengthening of the atrial component. Incomplete blockade right bundle branch. “What is all this. open

Day. The ECG showed changes in the inferolateral region of the left ventricle + incomplete blockade PNPG. What was not shown on cardiograms before. Diagnosis: myocardial dystrophy p. shortness of breath, nagging pain. I can't walk because hearts. forced to lie down a lot or do little housework. open

Supraventricular and 83 ventricular extrasystoles, ultrasound hearts without pathologies. The cardiologist prescribed it for me. I was afraid but I feel it stopping hearts and then it all starts immediately anaprilin. TODAY WE GAVE A CARDIOGRAM DECODED AND THERE: blockade LEFT BAND BAND, EOS. open (5 more messages)

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Good afternoon A 3-year-old child underwent an ECG after follicular tonsillitis: Sinus arrhythmia. No EOS was detected. The position is vertical. NBPNPG. open

illnesses hearts not described blockade could well have been like watching a sore throat

hearts blockade

11 months. he has HPS (hypoplastic lion syndrome) hearts) underwent 2 operations Norwood and Glenn. the last one in November '13. I didn’t catch the word, sorry) eos +31°. incomplete blockade right and right stomach (?). Hypertraphy of the right atrium and right stomach ultrasound. open

Hello, I’m pregnant, 33 weeks, I previously had an ECG, Holter and ultrasound hearts,was AB blockade 1 tbsp and PMK 1 tbsp. I did it now. heart rate 78, horizontal position EOS, AB blockade Stage 1, signs of hypertrophy of the lower ventricle, insignificant. open

Walking up stairs, sex, sports) hurts in the area hearts presses, tingles (burning) quite strongly, etc. it beats, I clearly feel every blow hearts. The pain radiates under the left shoulder blade and in. at heart there is PMK 1st, not complete blockade right bundle branch, tachycardia. open

Five years ago I started having arrhythmia. Interruptions in work hearts. extrasystole, fading. Attacks of extrasystole begin abruptly and increase. — sinus. A total of 103 blockades were identified (at night) sa blockade.Duration 1.5-2 Sec. 100 (Night) total 832 detected (. open

Hello. I'm sitting at work. My heart began to pound, for an hour it stabbed, pressed, gave pain under the left shoulder blade, left arm, neck, left hypochondrium, then subsided and again,... open (2 more messages)

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Mitral-tricumental valve prolapse grade 1, with regurgitation grade 0-1, incomplete blockade right bundle branch. The heart often hurts. Fear what. Before going to bed, it seems that they will stop breathing, and I will forget the rhythm hearts very slow 40-45 beats per minute, I'm afraid. look

Bundle branch block, heart block

1) I am 32 years old. An ECG revealed a blockade of the left bundle branch, which doctors assume happened at the time of the attack (short-term loss of consciousness). Before this, the heart had never hurt and there were no earlier cardiograms. I was diagnosed with myocardial infarction. But, apart from the blockade, there was no other confirmation of the diagnosis either on the ECG or in my state of health (the doctors said it was a massive heart attack, but I walked calmly and felt nothing except weakness). At the same time, the level of blockade decreased slightly, but did not disappear. Blood tests are normal, blood pressure is normal, heart rate is elevated about 100 per 1 m. Question: is it possible that I really suffered a heart attack so easily? Could such a blockade indicate another disease? What do you recommend?

You see, in principle, myocardial infarction can cause bundle branch block, and painless forms of infarction are not that uncommon. In addition, the first-time blockade of the left bundle branch is always suspicious for the presence of a heart attack. But, I repeat - for the first time ARISING, i.e. if there was no blockade on previous ECGs, and then it suddenly appeared. As far as I understand, your blockade has been IDENTIFIED for the first time. Therefore, it is premature to talk about a heart attack, to put it mildly. There are indirect criteria that, even using an ECG, sometimes make it possible to separate infarction blockade from congenital or acquired for another reason, not to mention much more informative and reliable studies (for example, the same radioisotope methods). You can contact me again, I will try to help you undergo an examination that can really clarify the nature of these disorders and establish a real diagnosis.

2) Please answer the question of how to treat blockade of the first anterior-superior branch of the His bundle with blockade of anastomoses in an elderly woman. In April 2000, there was a large-focal anteroposterior infarction of the left ventricle. Atherosclerosis of the coronary arteries. Cardiosclerosis Stage 3 hypertension. Left ventricular hypertrophy. Now I have pain all over my chest. The therapist said that the scar had healed. Pressure 14090; 10570; 12575. The blockade was installed in 1994. Currently prescribed medications: nitrosorbitol, aspirin, captopres

You know, there are signs of severe atherosclerosis and cardiosclerosis, and treating such forms of the disease is always very difficult. Pain throughout the chest can be not only anginal in nature, but also depend on a number of other reasons, for example, they are often associated with damage to the pericardial nerve plexuses (ganglia) that occur after a heart attack or against the background of severe atherosclerosis. As you understand, IHD is not a disease that can be treated in absentia. Therefore, I can only write that, in my opinion, beta blockers (obzidan, tenormin, visken), small doses of ibuprofen or diclofenac (they often help with such pain), metabolic therapy (riboxin, panangin) could be prescribed here. . In addition, keep in mind that nitrates quickly develop addiction (tolerance) and their effectiveness quickly decreases. Therefore, it is recommended to periodically change nitro drugs. But all specific prescriptions must be made by the doctor, taking into account the patient’s condition and all contraindications.

3) Firstly, I want to thank you for such a detailed and clear answer, and secondly, I would like to ask you to explain to me the essence of the weakness of the sinusoidal node and the violation of AV conduction according to Mobitz I-2.

The main function of the sinus node is to generate the heart rate. The sinus node (more precisely, the pacemaker cells that make up the sinus node) generate electrical impulses with a certain frequency (which depends on a number of factors), and then these impulses “scatter” through a special conduction system of the heart throughout the heart, causing it to contract. So, the essence of sick sinus syndrome is that, for certain reasons, the normal generation of impulses is disrupted.

This manifests itself either in the fact that impulses begin to be generated too rarely, or in the fact that the adequate response of the sinus node to changing environmental conditions is disrupted, or in the fact that in other, underlying parts of the conduction system, processes begin to appear that are suppressed under normal conditions sinus node and so on. So sick sinus syndrome is a complex concept; it includes various pathological processes that arise in the conduction system and, accordingly, various clinical manifestations. Its diagnosis is complex and at the present stage, the diagnosis of SSSU must necessarily include an electrophysiological study and Holter ECG monitoring.

As for the disturbance of AV conduction according to Mobitz, this means that the slowdown in conduction through the AV node (as well as through the sinus node) can be of three degrees: from the first, when this slowdown is manifested only by specific changes on the ECG and clinically does not affect the patient’s well-being in any way (except for the clinic caused by the underlying disease), until the third, when there is absolutely no conduction through the AV node (complete transverse block). The second degree is characterized by the periodic loss of any regular heartbeat, all this is accompanied by very characteristic changes on the ECG. This will be Mobitz II