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 observed 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 transition point 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 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 preparations.

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 ARVD 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 the potassium level, 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 wave predominates), 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-Paladino 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 pronounced 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.

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3. Janashia P.Kh. Kruglov V.A. Nazarenko V.A. Nikolenko S.A. Cardiomyopathies and myocarditis. - M. 2000. - P. 66-69.

4. Zhdanov G.G. Sokolov I.M. Schwartz 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.

7. Kushakovsky M.S. Cardiac arrhythmias. - St. Petersburg. Hippocrates, 1992.

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.

10. Mravyan S.R. Fedorova S.I. ECG phenomenon of ST segment elevation, its causes and clinical implications meaning// Clinical medicine. - 2006. - T. 84, No. 5. - P. 12-18.

11. Orlov V.N. Guide to electrocardiography. - M. Medical Information Agency, 1999. - 528 p.

12. Guide to electrocardiography / Ed. honorable activities sciences of the Russian Federation, prof. Zadionchenko V.S. - Saarbrucken, Germany. Publisher: LAP LAMBERT Academic Publishing GmbH&Co. KG, 2011. - P. 323.

13. Sedov V.M. Yashin S.M. Shubik Yu.V. Arrhythmogenic dysplasia/cardiopathy of the right ventricle // Bulletin of Arrhythmology. - 2000. - No. 20. - P. 23-30.

14. Topolyansky A.V. Talibov O.B. Emergency cardiology: Directory / Ed. ed. prof. A.L. Vertkina. - M. MEDpress-inform, 2010. - 352 p.

15. Antzelevitch C. Brugada P. Brugada J. et al. Brugada syndrome: 1992-2002: a historical perspective // ​​J Am Coll Cardiol 2003; 41: 1665-1671.

16. Atarashi H. Ogawa S. Harumi K. et al. Characteristics of patients with right bundle branch block and ST-segment elevation in right precordial leads // Am J Cardiol 1996; 78: 581-583.

17. Brugada R. Brugada J. Antzelevitch C. et al. Sodium channel blockers identify risk for sudden death in patients with ST-segment elevation and right bundle branch block but structurally normal hearts // Circulation 2000; 101:510-515.

18. Duclos F. Armenta J. Permanent Osborn wave in the absence of hypothermia // Rev Esp Cardiol 1972 Jul-Aug; Vol. 25 (4), pp. 379-82.

19. Durakovic Z.; Misigoj-Durakovic M.; Corovic N. Q-T and JT dispersion in the elderly with urban hypothermia // Int J Cardiol 2001 Sep-Oct; Vol. 80 (2-3), pp. 221-6.

20. Eagle K. Osborn waves of hypothermia // N Engl J Med 1994; 10: 680.

21. Fazekas T. Liszkai G. Rudas L.V. Electrocardiographic Osborn wave in hypothermia. // Orv Hetil 2000 Oct 22; Vol. 141(43), pp. 2347-51.

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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. 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)

Last 5:

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. 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)

Last 5:

Mitral tricumentary 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 advise?

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 of which is accompanied by very characteristic changes on the ECG. This will be Mobitz II

I thought for a long time about how to write this section for non-cardiologists and came to the conclusion that the most important thing would be to learn not to miss the signs of a heart attack. I believe that this will be a greater achievement than bothering oneself with such concepts as: endocardial, epicardial ischemia and the mechanisms of their development, how the stages of infarction of various walls occur, which arteries are responsible for this or that part of the heart, and so on. Let's leave these “aerobatic maneuvers” to cardiologists; our goals are more earthly.

So let's start with the most important thing - Myocardial infarction with ST elevation. Such a heart attack is accompanied by a very high mortality rate and requires urgent treatment; it is advisable to open the artery within the first 60-90 minutes. Therefore, missing it is an unforgivable mistake. Any doctor at all costs must learn to find ST elevation on an ECG. You may not know how to determine rhythm and blocks, but you need to know ST-elevation infarction in person.

From now on, we will get acquainted with the “pink ECGs” that you are used to seeing every day. As always, I will try to use high quality ECGs, but during a heart attack and/or when the patient is tossing around in bed with chest pain, “exemplary ECGs” are rarely obtained.

ST elevation and ST elevation infarction

In order to correctly assess the degree of elevation, you need to know where to measure it.

Look at the picture, where will you measure the elevation here? If you take it to the left, it will be less, if you take it to the right, it will be more.

In order to standardize measurements, a technique was introduced into practice for determining the j-junction point, which is located at the place where the S wave ends (if there is no S, then R) and the ST segment begins. If you step back 0.04 s from point j (that is, 2 mm at a belt speed of 50 mm/sec), then you will find point i at which you need to measure the height of elevation or depression.

Normally, elevation does not exceed 1 mm, but in leads V2-V3 it can be up to 2 mm or even 2.5 mm in people under 40 years of age. There are various figures, including those for point i, but I recommend that you use these indicators, even if you are “over-excited” someday, but it’s better than missing it.

Let's see what it looks like in life.

This is what the measurements look like. You can see at least 2 mm of elevation in lead III and almost 1.5 mm in lead AVF

Hover your cursor to enlarge the picture

Now, regarding ST elevation infarction

The most important criterion, along with elevation, is reciprocal changes - ST depression in leads opposite to the area of ​​infarction. That is, if there is elevation somewhere, then somewhere nearby there must be depression. In rare cases, reciprocal changes occur in those areas that are not visible on regular ECGs, but let’s agree right away - you send all patients with ST elevation and related complaints to hospitalization immediately or present them to a cardiologist.

Situations in which you can solve the problem yourself are limited to cases when you have an ECG on hand for comparison. That is, you can say with 100% confidence that the ECG looked like this before, for example: cases with post-infarction changes or early repolarization syndrome - we’ll talk about this later.

Now let's go back to the previous ECG. This is a heart attack.

ECG No. 1

Elevation is highlighted in red, and depression, which is reciprocal, is green. Such an ECG in 99.9999% of cases indicates an acute infarction in the area of ​​the lower wall (III, aVF). Remember, to talk about the presence of a heart attack, you need to have changes in the adjacent leads. For example (III, aVF or I, aVL or two adjacent chest leads).

ECG No. 2

Let's look at another ECG with an inferior infarction. Do not pay attention to the small tremor in leads V1-V2 - these are artifacts and they do not mean anything.

Area highlighted in red elevation, green - reciprocal depression . Yellow is also a reciprocal change, but due to the presence of a complete block of the right bundle branch (I hope you noticed it), this statement can be disputed.

ECG No. 3

Well, another ECG with a lateral wall infarction (I, AVL, usually there is also V5-V6, but not always), I think the explanations are unnecessary.

ECG No. 4

And the last ECG with anterolateral infarction. There is some isoline drift here, so I chose the most “clean” area for measurements.

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ECG remains a key method for diagnosing myocardial ischemia, especially with repeated studies that record changes in repolarization and depolarization over time. Transient changes in the ST segment and T wave, together with the clinical picture, even in the absence of anginal symptoms, are early and sensitive signs of myocardial ischemia. Changes in the QRS complex are often permanent, but can also be transient. At the same time, the information provided by the ECG is quite important: it indicates the localization of ischemia, its extent and helps in determining the indications for invasive myocardial revascularization. In this section we will try to summarize information about the ability to detect ischemic changes using ECG data.

When severe and sufficiently long-term (within minutes) ischemia occurs, the myofibrils completely or partially die, their polarity changes so that the ischemic area becomes electronegative, and a damage current occurs, which determines the rise of the ST segment, indicating severe ischemia. The vector created by ischemia is active only when the myocardium is repolarized (TP segment) and paradoxically disappears during the ST segment when the myocardium is depolarized (Figs. 1 and 2). With transmural ischemia, the ECG shows a negative deviation during the main course of the cardiac cycle, which becomes isoelectric only in the ST segment, leading to its elevation (see Fig. 1). In the case of subendocardial ischemia, on the contrary, the main potential is positive, and the ST segment shifts below the isoline (see Fig. 2). Local changes in action potential amplitude also determine ST segment displacement during ischemia. The nature of transient ST shifts observed over a period of minutes or hours is strictly due to an ischemic cause, further emphasizing the importance of studies of ECG data over time.

Rice. 1. The role of limited depolarization of the damaged area in the occurrence of ST segment elevation in transmural ischemia. The potential difference disappears after the entire myocardium is depolarized and reappears in healthy myocardium after its repolarization.

Rice. 2. Development of ST segment depression into T wave inversion in acute coronary syndrome. A - upon admission to the hospital, depression of the ST segment was registered in leads I, II, aVF and V4-V6. B - after 24 hours, there is no longer ST segment elevation, while inverted T waves are observed in the same leads

Determining the leads in which ST segment elevation is present and those leads where ST segment depression is simultaneously observed allows, with a certain degree of error, to localize the site of ischemia and obstruction of the corresponding branch of the coronary artery. ST segment elevation will be observed in those leads that are located above the ischemic epicardium, and the places where a tendency to ST depression is recorded are located on the opposite side of the heart (Table 1).

Table 1

ST segment elevation in acute ischemia depending on the obstructed coronary artery

Obstructed artery				II, III, aVF
Proximal LAD/LA		↓ ≥1 mm	- ≥1 mm	↓ ≥1 mm
Distal part of the LAD		- ≥1 mm
Proximal part of the PVA			↓ ≥0.5 mm	- ≥1.5mm
Distal part of the PVA	↓ ≥1 mm	- ≥1 mm	↓ ≥0.5 mm	- ≥1.5mm
Proximal part of OA LVA	↓ ≥1 mm		- ≥1 mm
Distal part of OA LVA		- ≥1 mm
RVA occlusion plus (three-vessel disease)		↓ ≥1 mm

Notes: LVA OA - circumflex branch of the left coronary artery; LDA - left anterior descending branch of the left coronary artery; LA - main trunk of the left coronary artery; RVA - right coronary artery; - - ST segment elevation; ↓ - ST segment depression.

The values ​​presented indicate the relative severity of ST deviation in each case. Sometimes ST segment displacement may not be present in all of the specified leads or group of leads.

Leads II, III, and aVF will show ST segment elevation over the ischemic inferior wall (Figs. 3 and 4), which most often occurs with SVA obstruction, but in some cases due to LVA OA obstruction. If the apical-lateral wall is ischemic, then ST segment elevation will also appear in the left precordial leads V5-V6. ST depression appears in leads I and aVL if the PVA is affected, rather than LVA OA. Leads V1-V3 demonstrate ST segment depression in cases of posterolateral wall ischemia (see Fig. 4). With obstruction of the proximal part of the SVA before the origin of the right ventricular branch, RV ischemia is manifested by ST elevation in leads V4R (symmetrical to lead V4 on the right side of the chest). ST segment depression in leads V5-V6, observed simultaneously with ST elevation in leads from the inferior wall, is an indicator of three-vessel disease.

Rice. 3. ST segment elevation during anterior wall infarction involving the pancreas. A - the gray arrow shows the direction of the ST vector. Note ST elevation in leads III and aVF with reciprocal inversion in leads I, aVL and V2. ST segment elevation in the right precordial leads V3R and V4R as a result of transmural ischemia/infarction of the RV. The magnetic resonance image of the LV is placed in a model of the chest. B - the zone of localization of the lower MI is highlighted in yellow. The horizontal plane with the zone of anterior RV MI is highlighted in yellow

Rice. 4. Subacute transmural ischemia of the inferior wall (including the MI site) is manifested by ST segment elevation. In this case, there is depression of the ST segment in leads aVL and V2-V3, which indicates the addition of ischemia of the posterior wall with a mirror image of the changes. The T wave is negative in leads II, III, aVF and V5-V6, demonstrating the development of ischemia

Obstruction of the left descending branch of the left coronary artery will be accompanied by ST segment elevation in the right precordial leads V1-V3, which remove the potential from the IVS (Fig. 5 and 6), as well as in leads V3-V6 in the case of anterior apical ischemia (see Fig. 5 ). In leads I and aVL, ST segment elevation will appear during ischemia in the upper basal parts of the LV, and in leads from the inferior wall II, III and aVF, ST depression may be observed as manifestations of reciprocal changes (Fig. 7, see Fig. 5). ST segment depression in leads V5-V6 with ST elevation in aVR is an additional sign of proximal obstruction of the left anterior descending branch of the main trunk of the left coronary artery.

Rice. 5. Acute anterolateral transmural ischemia. Magnetic resonance image of the LV with the ischemic zone marked in yellow (A). Pay attention to the superior location of the so-called “front” wall, which is the reason for recording its potential with lead aVL. In the horizontal plane (B), a pronounced zone of ischemia in the septal and anterior apical regions is shown in yellow.
ST segment elevation is recorded in leads I, aVL and V1-V6, indicating fairly widespread ischemia, possibly due to proximal damage to the left anterior descending branch. Note the reciprocal ST segment depression in leads III and aVF. The gray arrow indicates the direction of the ST vector. Note the superior and inferior positions of the so-called "anterior" and "posterior" papillary muscles

Rice. 6. New RBBB in acute anterior MI. The earlier recording (A) shows ST segment elevation in leads V1-V5, indicating transmural anteroseptal ischemia, and in leads II, III, and aVF, it indicates transmural inferior wall ischemia. There is also a pathological Q wave in leads V1-V4 (B). A few hours later, ST segment elevation increased significantly in leads V3-V5, with continued elevation in leads II, III, and aVF. The QRS complex widened with a wide R′ wave in leads V1-V3 and an S wave in lead I, as a manifestation of RBBB. Please note that the presence of this block does not make it difficult to record a pathological Q wave in leads V1-V3

Rice. 7. Anterolateral acute MI. Note ST segment elevation in leads I, aVL, and V5-V6 with reciprocal, mirror image ST segment depression in leads III and aVF. A pathologically wide Q wave was recorded in lead aVL and a small (or lack thereof) r wave in V2-V3, indicating a high lateral and anteroseptal infarction. Note: The T wave has a wide base in leads V2-V6 associated with slight ST segment elevation. This is often the only sign of ischemia in the very early stages of transmural ischemia/infarction.

Obstruction of the proximal part of the left OA leads to ischemia of the posterolateral wall with ST segment elevation in leads I and aVL or ST depression in the right precordial leads V1-V3. Distal obstruction of OA of the left artery is accompanied by ST elevation in leads II, III and aVF, more pronounced in lead III compared to II, sometimes in combination with ST elevation in V4-V6, but without ST depression in leads I and aVL.

Ischemic ST segment elevation, usually transient even with MI, spontaneously returns to baseline in less than 24 hours and within a few minutes after myocardial reperfusion. The presence of ST segment elevation for more than 24 hours indicates a poor prognosis and the development of a serious impairment of contraction of the affected myocardial segment.

ST segment depression is a common manifestation of ischemia, observed both at rest and during stress and exercise (see Fig. 2), although the ability to localize the ischemic zone with depression is lower than with ST segment elevation. The presence of ST depression at rest indicates severe CAD, especially when there is ST elevation in lead aVR. Diagnosis of ischemia becomes more accurate when dynamic changes occur spontaneously within minutes or hours or as a result of treatment. The ST segment displacement may completely disappear, and in cases of severe ischemia, T wave inversion in the same leads is possible (see Fig. 2).

In "early repolarization" syndrome or in cases of pericarditis, the ST segment may be persistently elevated or depressed even in the absence of acute ischemia. In the search for diagnostic signs, only dynamic ECG helps. Persistent ST elevation is characteristic of patients with ventricular aneurysm; in this case, as a rule, a pathological Q wave (see QRS changes: Q wave) will be recorded in the leads where ST segment elevation is detected. With pericarditis or myocarditis, there is a tendency for ST elevation to become more common; Thus, it occurs in the leads from the upper and lower extremities, as well as in the precordial leads and persists for many days. Normally, persistent ST depression of ‹0.1 mV in the left precordial leads is sometimes encountered, especially in women. ST segment depression can be caused by hyperventilation, especially with MVP, electrolyte disturbances, and when digitalis is used in therapeutic doses. In light of this, when forming an ECG conclusion for such findings, it is necessary to take into account all clinical information. In patients with a healthy heart and patent coronary arteries, significant ST segment depression is possible with paroxysms of SVT, narrow QRS complexes and tachycardia.

Francisco G. Cosío, José Palacios, Agustín Pastor, Ambrosio Núñez

Electrocardiography

Reflects the spread of the excitation wave to the basal sections of the interventricular septum, right and left ventricles.

1. The optional negative wave following the R wave may be absent in the limb leads and V5-6.

2. If there are several teeth, it is designated S respectively,

S`, S``, S```, etc.

3. Duration less than 0.04 sec, amplitude in chest

leads is greatest in leads V1-2 and gradually decreases towards V5-6.

ST segment

Corresponds to the period when both ventricles are completely covered by excitation, measured from the end of S to the beginning of T (or from the end of R in the absence of an S wave).

1. The duration of ST depends on the pulse rate.

2. Normally, the ST segment is located on the isoline, ST depression

no more than 0.5 mm (0.05 mV) is allowed in leads V2-3 and no more than 1 mm (0.1 mV) in other leads.

3. Its rise should not exceed 1 mm in all leads except V2-3.

4. In leads V2-3, ST segment elevation ≥2 mm (0.2 mV) should be considered pathological in persons over 40 years old, in persons under 40

years ≥2.5 mm (0.25 mV) in men and ≥1.5 (0.15 mV) in women, respectively.

T wave

Reflects the processes of ventricular repolarization. This is the most labile tooth.

1. Normally, the T wave is positive in those leads where the QRS complex is represented predominantly by the R wave.

2. With a normal position of the heart, the T wave is positive in leads I, II, III, aVL and aVF, negative in lead aVR.

3. T III can be reduced, isoelectric, slightly negative when the electrical axis of the heart deviates to the left.

4. In lead V 1, the T wave with the same frequency can be negative, isoelectric, positive or

biphasic, in lead V2 it is often positive, in leads V3-6 it is always positive.

In a qualitative description, a low T wave should be identified if its amplitude is less than 10% of the amplitude of the R wave in a given lead; flattened with an amplitude from -0.1 to 0.1 mV; inverted T wave in leads I, II, aVL, V2 -V6, if its amplitude is from -0.1 to -0.5 mV; negative at an amplitude of -0.5 mV or more.

QT interval (QRST)

Reflects the electrical systole of the heart. Measured from the beginning of the Q wave (or R if there is no Q) to the end of the T wave.

1. The duration depends on gender, age, and rhythm frequency. Normal QT value (corrected QT; QTc)

2. Normal QT values ​​range between 0.39–0.45 sec.

3. If measurements are made in different leads, as a basis

the highest value is taken (usually in leads V2 - V3).

4. QT interval prolongation is considered to be 0.46 seconds or more in women, 0.45 seconds or more in men, and shortening is 0.39 seconds or less.

U wave

An unstable, small amplitude (1–3 mm or up to 11% of the amplitude of the T wave) wave, concordant (unidirectional) to the T wave, following it after 0.02–0.04 sec. Most pronounced in leads V2-V3, more often with bradycardia. Clinical significance is unclear.

TR segment

Reflects the diastole phase of the heart. Measured from the end of the T wave (U) to the beginning of the P wave.

1. Located on an isoline, the duration depends on the rhythm frequency.

2. With tachycardia, the duration of the TR segment decreases, with bradycardia it increases.

RR interval

Characterizes the duration of a complete cardiac cycle - systole and diastole.

1. To determine your heart rate, divide 60 by the RR value expressed in seconds.

IN in cases where the rhythm frequency in one patient differs in a short period of time (for example, with atrial fibrillation),

the maximum and minimum rhythm frequencies should be determined from the largest and smallest RR values, or the average rhythm frequency should be calculated from 10 consecutive RRs.

When problems with the cardiovascular system begin, the most reasonable solution is to contact a cardiologist. In a hospital department, doctors can provide qualified assistance and conduct appropriate diagnostics. What happens to the heart if the electrocardiogram shows depression of the st segment on the ECG? What are the reasons for deviation from the norm? Is any therapy needed? Is there a risk to human life and health?

Why do an ECG?

Analysis of the state of the CT segment in the electrocardiogram remains a very relevant method of modern diagnostics. Using an ECG, you can detect cardiac pathologies in the early stages and begin their therapy. Therapeutic practice shows that the treatment and prognosis of many of these diseases depend on the stage of pathology at which they are diagnosed.

Timely diagnosis of cardiac pathologies will protect against serious complications

It is possible to assess how strongly the CT segment has shifted only in combination with other cardiac parameters. Depression or elevation in itself does not necessarily indicate pathology; it may be part of the norm.

When considering the results of electrocardiography, one cannot ignore the symptoms that appear. Displacement of the CT segment may be associated with non-coronarogenic changes in the myocardium.

Important! In rare cases, segment displacement may be a sign of acute coronary syndrome. This requires emergency medical attention.

General information about segment offset

When a person is healthy, his ECG is normal. Elevation of the st segment (rise) or decrease may indicate pathologies within the body. Normally, the st segment is located on an isoline, although there is a certain range of acceptable values.

ST depression is acceptable in limb leads up to 0.5 mm. Indicators greater than or equal to 0.5 in leads V1-V2, 0.5 are considered a deviation.

St segment elevation in the limb leads should be less than 1 mm. For leads V1-V2, the norm is up to 3 mm, and for V5-V6 – up to 2 mm.

The cardiogram is analyzed only by a doctor

Where does this information apply?

Knowing the norm of st segment elevation on an ECG helps in diagnosing some serious cardiac pathologies: myocardial infarction, coronary heart disease, myocardial hypertrophy, LV aneurysm, pericarditis, myocarditis, PE, etc.

Thus, during heart attacks there is no decrease in the st segment. This indicator can increase to 2-3 mm when the norm is up to 1. In addition to the growth of the CT segment, a pathological Q wave may appear on the electrocardiogram picture.

It is effective to use a troponin test when a heart attack is suspected. When a significant displacement of the CT segment occurs, the latest analysis allows us to clarify the diagnosis. If the test is negative, the patient has not had a heart attack, and acute ischemic disease requires treatment.

To correctly establish a diagnosis and prescribe effective treatment, it is important for a cardiologist to carefully read the electrocardiogram. There are some rules, taking into account which you can help the patient efficiently.

How he reads the ECG and what treatment he chooses depends on the experience of the cardiologist.

First of all, the ability of the heart to conduct electrical impulses is analyzed. The frequency and rhythm of the pulse are calculated, and the regularity of heart contractions is assessed. The cardiologist then pays attention to the work of the pacemaker and determines how well the impulses travel along the conduction pathways of the heart.

After these studies, the cardiologist evaluates the position of the electrical axis and examines the rotation of the heart around the longitudinal, transverse and anteroposterior axis. At the same stage, the P wave is assessed.

The next stage of deciphering the electrocardiogram is to consider the state of the QRS-T complex. When assessing the ST segment, the J point (the moment the S wave transitions to the ST segment) is important.

The shape of the arc that the J point forms to the end of the ST segment determines the presence of pathology. If it is concave, then the deviation is benign. Convex is a sign of myocardial ischemia.

Causes of cardiac changes

Myocardial infarction and other serious cardiovascular pathologies do not develop overnight. Perhaps the person neglected the alarming symptoms for some time, or did not follow the recommendations of the attending physician. Some did not take such a diagnosis as coronary artery disease seriously, underestimating the risks of the pathology.

Abnormalities in electrocardiogram results may appear for various reasons. Most often, this study provides a reliable picture of the work of the heart muscle. Although errors do occur, they are very rare.

Important! ST segment depression symptoms sometimes appear even in healthy people. If, in addition to changes in the ECG, there are no negative symptoms, we can talk about the physiological norm. Although periodic visits to a cardiologist and monitoring of heart condition should not be neglected.

Deviations from the norm in the electrocardiogram picture may appear if the procedure is performed incorrectly. This situation is possible if the electrodes are applied incorrectly. In this case, there is not enough contact, and the device records unreliable data.

Other non-cardiac causes of ECG abnormalities:

• electrolyte disturbances;
• hyperventilation;
• abuse of medications, including narcotic drugs;
• frequent drinking of alcohol;
• drinking cold water.

The development of any pathology can be stopped subject to timely diagnosis and proper treatment. To do this, if the slightest unpleasant symptoms appear in the heart area, it is recommended to visit a therapist to get a referral for examination. This way you can prevent the development of serious and dangerous pathologies.

More:

How to decipher an ECG analysis, norms and deviations, pathologies and diagnostic principles