Diagnosis of heart disease is carried out by recording and studying electrical impulses arising as a result of relaxation and contraction of the heart muscle over a certain period of time - electrocardiography. A special device called an electrocardiograph records the impulses and converts them into a visual graph on paper (electrocardiogram).

Brief description of ECG elements

In the graphic image, time is recorded horizontally, and frequency and depth of changes are recorded vertically. Sharp angles displayed above (positive) and below (negative) from the horizontal line are called serrations. Each of them is an indicator of the condition of one or another part of the heart.

On the cardiogram, the waves are designated as P, Q, R, S, T, U.

• the T wave on the ECG reflects the recovery phase of the muscle tissue of the heart ventricles between myocardial contractions;
• wave P – indicator of depolarization (excitation) of the atria;
• teeth Q, R, S reflect the excited state of the ventricles of the heart;
• The U-wave determines the recovery cycle of distant areas of the cardiac ventricles.

The range between adjacent teeth is called a segment; there are three of them: ST, QRST, TP. The tooth and the segment together represent the interval - the time it takes for the impulse to pass. For accurate diagnosis, the difference in indicators of the electrodes (electric potential of the lead) attached to the patient’s body is analyzed. Leads are divided into the following groups:

• standard. I – difference in indicators on the left and right hand, II – ratio of potentials on the right hand and left leg, III – left hand and leg;
• reinforced. AVR – from the right hand, AVL – from the left hand, AVF – from the left leg;
• chest Six leads (V1, V2, V3, V4, V5, V6) located on the chest of the subject, between the ribs.

A qualified cardiologist interprets the results of the study.

Having received a schematic picture of the work of the heart, the cardiologist analyzes the changes in all indicators, as well as the time for which the cardiogram records them. The main data for decoding are the regularity of muscle contractions of the heart, the number (number) of heart contractions, the width and shape of the waves reflecting the excited state of the heart (Q, R, S), the characteristics of the P wave, the parameters of the T wave and segments.

T wave indicators

Repolarization or restoration of muscle tissue after contractions, which is reflected by the T wave, has the following standards in the graphic image:

• lack of serration;
• smoothness on the rise;
• upward direction (positive value) in leads I, II, V4–V6;
• strengthening the range values ​​from the first to the third lead to 6–8 cells along the graphic axis;
• downward (negative value) in AVR;
• duration from 0.16 to 0.24 seconds;
• predominance in height in the first lead in relation to the third, as well as in lead V6 compared to lead V1.

Deviation of the pattern from the norm indicates dysfunction of the ventricles of the heart after muscle contraction.

T wave changes

The transformation of the T wave on the electrocardiogram is due to changes in the functioning of the heart. Most often they are associated with impaired blood supply resulting from damage to blood vessels by atherosclerotic growths, otherwise known as coronary heart disease.

Deviation from the norm of lines reflecting inflammatory processes can vary in height and width. The main deviations are characterized by the following configurations.

An inverted (inverse) form indicates myocardial ischemia, a state of extreme nervous excitement, cerebral hemorrhage, and an increase in heart rate above (tachycardia). Leveled T manifests itself in alcoholism, diabetes, low potassium concentration (hypokalemia), cardiac neurosis (neurocircular dystonia), and abuse of antidepressants.

A high T-wave, displayed in the third, fourth and fifth leads, is associated with an increase in the volume of the walls of the left ventricle (left ventricular hypertrophy), pathologies of the autonomic nervous system. A slight rise in the pattern does not pose a serious danger; most often, it is associated with irrational physical activity. Biphasic T indicates excessive consumption of cardiac glycosides or left ventricular hypertrophy.

The wave shown below (negative) is an indicator of the development of ischemia or the presence of severe excitement. If a change in the ST segment is observed, the clinical form of ischemia – infarction – should be suspected. Changes in wave pattern without involvement of the adjacent ST segment are not specific. Determining a specific disease in this case is extremely difficult.

There are a significant number of etiological factors for changes in the T wave in pathology of the heart muscle

Causes of a negative T-wave

If, with a negative T wave value, additional factors are involved in the process, this is an independent heart disease. When there are no concomitant manifestations on the ECG, a negative T display may be due to the following factors:

• pulmonary pathologies (difficulty breathing);
• disruptions in the hormonal system (hormone levels are higher or lower than normal);
• cerebrovascular accident;
• overdose of antidepressants, heart medications and medications;
• a symptomatic complex of disorders of part of the nervous system (VSD);
• dysfunction of the heart muscle not associated with coronary disease (cardiomyopathy);
• inflammation of the heart sac (pericarditis);
• inflammatory process in the inner lining of the heart (endocarditis);
• mitral valve lesions;
• enlargement of the right side of the heart as a result of hypertension (cor pulmonale).

Objective ECG data regarding changes in the T wave can be obtained by comparing a cardiogram taken at rest and an ECG in dynamics, as well as the results of laboratory tests.

Since abnormal T-wave display may indicate CAD (ischemia), regular electrocardiography should not be neglected. Regular visits to a cardiologist and an ECG procedure will help identify pathology at the initial stage, which will significantly simplify the treatment process.

Electrocardiography is one of the most common and most informative methods for diagnosing a huge number of diseases. An ECG involves a graphical display of the electrical potentials that are formed in the beating heart. Indicators are taken and displayed using special devices - electrocardiographs, which are constantly being improved.

As a rule, during the study, 5 waves are recorded: P, Q, R, S, T. In some moments, it is possible to record a subtle U wave.

Electrocardiography allows you to identify the following indicators, as well as variants of deviations from reference values:

• Heart rate (pulse) and regularity of myocardial contractions (arrhythmias and extrasystoles can be detected);
• Disturbances in the heart muscle of an acute or chronic nature (in particular, with ischemia or heart attack);
• metabolic disorders of the main compounds with electrolytic activity (K, Ca, Mg);
• intracardiac conduction disorders;
• hypertrophy of the heart (atria and ventricles).

Note:When used in parallel with a cardiophone, the electrocardiograph makes it possible to remotely determine some acute heart diseases (the presence of areas of ischemia or heart attacks).

ECG is the most important screening technique for detecting coronary artery disease. Valuable information is provided by electrocardiography with the so-called. "stress tests".

Isolated or in combination with other diagnostic techniques, ECG is often used in the study of cognitive (thought) processes.

Important:An electrocardiogram must be taken during medical examination, regardless of the age and general condition of the patient.

ECG: indications for performance

There are a number of pathologies of the cardiovascular system and other organs and systems for which electrocardiographic examination is prescribed. These include:

• angina pectoris;
• myocardial infarction;
• reactive arthritis;
• peri- and myocarditis;
• periarteritis nodosa;
• arrhythmias;
• acute renal failure;
• diabetic nephropathy;
• scleroderma.

With right ventricular hypertrophy, the amplitude of the S wave in leads V1-V3 increases, which may be an indicator of symmetrical pathology on the part of the left ventricle.

With left ventricular hypertrophy, the R wave is pronounced in the left precordial leads and its depth is increased in leads V1-V2. The electrical axis is either horizontal or deviated to the left, but can often correspond to the norm. The QRS complex in lead V6 is characterized by a qR or R shape.

Note:This pathology is often accompanied by secondary changes in the heart muscle (dystrophy).

Left atrial hypertrophy is characterized by a fairly significant increase in the P wave (up to 0.11-0.14 s). It acquires a “two-humped” shape in the left chest leads and leads I and II. In rare clinical cases, some flattening of the wave is noted, and the duration of the internal deviation of P exceeds 0.06 s in leads I, II, V6. Among the most prognostically reliable evidence of this pathology is an increase in the negative phase of the P wave in lead V1.

Hypertrophy of the right atrium is characterized by an increase in the amplitude of the P wave (over 1.8-2.5 mm) in leads II, III, aVF. This tooth acquires a characteristic pointed shape, and the electrical axis P is installed vertically or has a slight shift to the right.

Combined atrial hypertrophy is characterized by parallel expansion of the P wave and an increase in its amplitude. In some clinical cases, changes such as sharpening of P in leads II, III, aVF and splitting of the apex in I, V5, V6 are noted. In lead V1, an increase in both phases of the P wave is occasionally recorded.

For heart defects formed during intrauterine development, a significant increase in the amplitude of the P wave in leads V1-V3 is more common.

In patients with a severe form of chronic pulmonary heart disease with emphysematous lung damage, as a rule, an S-type ECG is determined.

Important:combined hypertrophy of two ventricles at once is rarely detected by electrocardiography, especially if the hypertrophy is uniform. In this case, the pathological signs tend to compensate each other.

With “premature ventricular excitation syndrome” on the ECG, the width of the QRS complex increases and the PR interval becomes shorter. The delta wave, which affects the increase in the QRS complex, is formed as a result of an early increase in the activity of areas of the cardiac muscle of the ventricles.

Blockades are caused by the cessation of the electrical impulse in one of the areas.

Impairments in impulse conduction are manifested on the ECG by a change in the shape and increase in the size of the P wave, and with intraventricular block - an increase in QRS. Atrioventricular block can be characterized by loss of individual complexes, an increase in the P-Q interval, and in the most severe cases, a complete absence of connection between QRS and P.

Important:sinoatrial block appears on the ECG as a rather bright picture; it is characterized by the complete absence of the PQRST complex.

In case of heart rhythm disturbances, electrocardiography data is assessed based on the analysis and comparison of intervals (inter- and intra-cycle) for 10-20 seconds or even longer.

The direction and shape of the P wave, as well as the QRS complex, are of great diagnostic importance when diagnosing arrhythmias.

Myocardial dystrophy

This pathology is visible only in some leads. It is manifested by changes in the T wave. As a rule, its pronounced inversion is observed. In a number of cases, a significant deviation from the normal RST line is recorded. Pronounced dystrophy of the heart muscle is often manifested by a pronounced decrease in the amplitude of the QRS and P waves.

If a patient develops an attack of angina, then the electrocardiogram shows a noticeable decrease (depression) in RST, and in some cases, inversion of T. These changes in the ECG reflect ischemic processes in the intramural and subendocardial layers of the cardiac muscle of the left ventricle. These areas are the most demanding for blood supply.

Note:a short-term rise in the RST segment is a characteristic sign of a pathology known as Prinzmetal's angina.

In approximately 50% of patients, between attacks of angina, changes on the ECG may not be recorded at all.

In this life-threatening condition, an electrocardiogram provides information about the extent of the lesion, its exact location and depth. In addition, an ECG allows you to monitor the pathological process over time.

Morphologically it is customary to distinguish three zones:

• central (zone of necrotic changes in myocardial tissue);
• the zone of pronounced dystrophy of the heart muscle surrounding the lesion;
• peripheral zone of pronounced ischemic changes.

All changes that are reflected on the ECG change dynamically according to the stage of development of myocardial infarction.

Dishormonal myocardial dystrophy

Myocardial dystrophy, caused by a sharp change in the patient’s hormonal background, is usually manifested by a change in the direction (inversions) of the T wave. Depressive changes in the RST complex are much less common.

Important: The severity of changes may vary over time. Pathological changes recorded on the ECG are only in rare cases associated with clinical symptoms such as pain in the chest area.

To distinguish the manifestations of coronary artery disease from myocardial dystrophy against the background of hormonal imbalance, cardiologists practice tests using pharmacological agents such as beta-adrenergic receptor blockers and potassium-containing drugs.

Changes in electrocardiogram parameters while the patient is taking certain medications

Changes in the ECG pattern can be caused by taking the following drugs:

• drugs from the group of diuretics;
• drugs related to cardiac glycosides;
• Amiodarone;
• Quinidine.

In particular, if the patient takes digitalis preparations (glycosides) in recommended doses, then relief of tachycardia (rapid heartbeat) and a decrease in the Q-T interval are determined. “Smoothing” of the RST segment and shortening of T are also possible. An overdose of glycosides is manifested by such serious changes as arrhythmia (ventricular extrasystoles), AV block and even a life-threatening condition - ventricular fibrillation (requires immediate resuscitation measures).

The pathology causes an excessive increase in the load on the right ventricle, and leads to its oxygen starvation and rapidly increasing dystrophic changes. In such situations, the patient is diagnosed with “acute cor pulmonale.” In the presence of pulmonary embolism, blockade of the branches of the His bundle is not uncommon.

The ECG shows a rise in the RST segment in parallel in leads III (sometimes in aVF and V1,2). There is T inversion in leads III, aVF, V1-V3.

Negative dynamics increase rapidly (a matter of minutes pass), and progression is noted within 24 hours. With positive dynamics, the characteristic symptoms gradually disappear within 1-2 weeks.

Early repolarization of the cardiac ventricles

This deviation is characterized by an upward shift of the RST complex from the so-called isolines. Another characteristic sign is the presence of a specific transition wave on the R or S waves. These changes in the electrocardiogram have not yet been associated with any myocardial pathology, therefore they are considered a physiological norm.

Pericarditis

Acute inflammation of the pericardium is manifested by a significant unidirectional elevation of the RST segment in any leads. In some clinical cases, the displacement may be discordant.

Myocarditis

Inflammation of the heart muscle is noticeable on the ECG by deviations from the T wave. They can vary from a decrease in voltage to an inversion. If, in parallel, the cardiologist conducts tests with potassium-containing drugs or β-blockers, then the T wave remains negative.

P wave- formed as a result of excitation of two atria. It begins to register immediately after the impulse leaves the sinus node. The left atrium begins and ends its excitation later; as a result of the overlapping excitations of the left and right atrium, a wave is formed. The amplitude of the P wave is usually greatest in stage II. lead. Normally, the duration of P is up to 0.1 s, the amplitude should not exceed 2.5 mm. In lead aVR, the wave is always negative. The P wave may be serrated at the apex, but the distance between the serrations should not exceed 0.02 s.

PQ interval- from the beginning of the P wave to the beginning of the Q wave. It corresponds to the time of passage of excitation through the atria and the AV junction to the ventricular myocardium. It varies depending on the heart rate, age and body weight of the patient. Normally, the PQ interval is 0.12 - 0.18 (up to 0.2 s). Thus, the PQ interval includes the P wave and the PQ segment.

Makruz Index. This is the ratio of the duration of the P wave to the duration of the PQ segment. Normally -1.1 - 1.6. This index helps in diagnosing atrial hypertrophy.

QRS complex- ventricular complex. This is usually the largest deviation in the ECG. The width of the QRS complex is normally 0.06 - 0.08 s and indicates the duration of intraventricular conduction of excitation. With age, the width of the QRS complex. The amplitude of the QRS complex waves usually varies. Normally, in at least one of the standard leads or in the limb leads, the amplitude of the QRS complex should exceed 5 mm, and in the precordial leads - 8 mm. In any of the chest leads in adults, the amplitude of the QRS complex should not exceed 2.5 cm.

Q wave- the initial wave of the QRS complex. it is recorded during excitation of the left half of the interventricular septum. Registration of a q wave of even small amplitude in leads V1-V3 is a pathology. Normally, the width of the q wave should not exceed 0.03 s, and its amplitude in each lead should be less than 1/4 of the amplitude of the next R wave in this lead.

R wave- usually the main wave of the ECG. It is caused by ventricular excitation, and its amplitude in standard leads and in limb leads depends on the position of the electrical axis of the heart. With the normal position of the electrical axis and RII>RI>RIII. The R wave may be absent in lead aVR. In the chest leads, the R wave should increase in amplitude from V1 to V4.

S wave- mainly due to the terminal excitation of the base of the left ventricle. This tooth may be absent normally, especially in the limb leads. In the chest leads, the greatest amplitude of the S wave is in leads V1 and V2. The width S in any case should not exceed 0.03 s.

ST segment - corresponds to that period of the cardiac cycle when both ventricles are completely covered by excitation. The point where the QRS complex ends is designated as the ST junction, or point J. The ST segment directly passes into the T wave. The ST segment is normally located on the isoline, but may be slightly elevated or depressed. Normally, the ST segment can be located even 1.5 - 2 mm above the isoline. In healthy people, this is combined with a subsequent high positive T wave and has a concave shape. In cases where the ST segment is not located on an isoline, its shape is described as concave, convex or horizontal. The duration of this segment does not have much diagnostic significance and is usually not determined.

T wave. Recorded during ventricular repolarization. This is the most labile wave of the ECG. The T wave is normally positive. Normally, the T wave is not serrated. The T wave is usually positive in those leads where the QRS complex is mainly represented by the R wave. In leads. where mainly negative waves are recorded in this complex, there is a tendency to register negative S. In lead aVR T should always be negative. The duration of this wave is from 0.1 to 0.25 s, but it does not have much diagnostic value. The amplitude usually does not exceed 8 mm. Normally, TV1 is necessarily higher than TV6.

QT interval. This is the electrical systole of the ventricles. The QT interval is the time in seconds from the beginning of the QRS complex to the end of the T wave. Depends on gender, age and heart rate. Normally, the duration of the QT interval is 0.35 - 0.44 s. QT is a constant for a given rhythm frequency separately for men and women. There are special tables that present the standards for electrical ventricular systole for a given gender and rhythm frequency. To identify gross disturbances in the duration of the QT interval in a given patient, various formulas are presented, the most common in practical use is the Bazett formula. This formula compares the conditionally calculated QT interval with its duration in a given patient and with the duration of the cardiac cycle (the distance between two adjacent R waves in seconds).

Normally, the mass of the left ventricle is approximately 3 times greater than the mass of the right ventricle. With left ventricular hypertrophy, its predominance is even more pronounced, which leads to an increase in the EMF and the excitation vector of the left ventricle. The duration of excitation of the hypertrophied ventricle also increases due to not only its hypertrophy, but also the development of dystrophic and sclerotic changes in the ventricle.

Characteristic features of the ECG during the period of excitation of the hypertrophied left ventricle:

in the right chest leads V1, V2, an rS type ECG is recorded: the r wave of V1 is caused by the excitation of the left half of the interventricular septum; the S V1 wave (its amplitude is greater than normal) is associated with excitation of the hypertrophied left ventricle;

in the left chest leads V5, V6, an ECG of type qR (sometimes qRs) is recorded: the q wave V6 (its amplitude is higher than normal) is caused by the excitation of the hypertrophied left half of the interventricular septum; the R V6 wave (its amplitude and duration is higher than normal) is associated with excitation of the hypertrophied left ventricle; the presence of the s wave V6 is associated with excitation of the base of the left ventricle.

Characteristic features of the ECG during the period of repolarization of the hypertrophied left ventricle:

segment ST V1 is above the isoline;

the T wave V1 is positive;

the ST V6 segment is below the isoline;

tooth T V6 negative asymmetrical.

Diagnosis "left ventricular hypertrophy" placed on the basis of ECG analysis in the chest leads:

high waves R V5, R V6 (R V6 >R V5 >R V4 - a clear sign of left ventricular hypertrophy);

deep teeth S V1, S V2;

the greater the left ventricular hypertrophy, the higher R V5, R V6 and deeper S V1, S V2;

segment ST V5, ST V5 with an arc convex upward, located below the isoline;

the T V5, T V6 wave is negative asymmetric with the greatest decrease at the end of the T wave (the greater the height of the R V5, R V6 wave, the more pronounced the decrease in the ST segment and the negativity of the T wave in these leads);

segment ST V1, ST V2 with an arc convexly facing downward, located above the isoline;

tooth T V1, T V2 positive;

in the right precordial leads there is a fairly significant rise in the ST segment and an increase in the amplitude of the positive T wave;

The transition zone with left ventricular hypertrophy is often shifted to the right precordial leads, while the T V1 wave is positive and the T V6 wave is negative: T V1 > T V6 syndrome (normally, it’s the other way around). T V1 >T V6 syndrome is an early sign of left ventricular hypertrophy (in the absence of coronary insufficiency).

The electrical axis of the heart with left ventricular hypertrophy is often moderately deviated to the left or located horizontally (a sharp deviation to the left is not typical for isolated left ventricular hypertrophy). Less commonly observed is the normal position of the e.o.s.; even less often - a semi-vertical position of the e.o.s.

Characteristic ECG signs in limb leads with left ventricular hypertrophy (e.o.s. located horizontally or deviated to the left):

The ECG in leads I, aVL is similar to the ECG in leads V5, V6: it looks like qR (but the waves have a smaller amplitude); segment ST I, aVL is often located below the isoline and is accompanied by a negative asymmetric wave T I, aVL;

The ECG in leads III, aVF is similar to the ECG in leads V1, V2: it looks like rS or QS (but the waves have a smaller amplitude); segment ST III, aVF is often raised above the isoline and merges with the positive wave T III, aVF;

the T III wave is positive, and the T I wave is low or negative, so left ventricular hypertrophy is characterized by T III > T I (in the absence of coronary insufficiency).

Characteristic ECG signs in limb leads with left ventricular hypertrophy (e.o.s. located vertically):

in leads III, aVF there is a high R wave; as well as a decrease in the ST segment and a negative T wave;

in leads I, aVL there is an r wave of small amplitude;

in lead aVR the ECG looks like rS or QS; the T aVR wave is positive; the ST aVR segment is located on the isoline or slightly above it.

Exercise testing is used to identify hidden coronary insufficiency, for differential diagnosis of coronary heart disease with other diseases, assessment of coronary circulatory reserves, physical ability, identification of transient arrhythmias and conduction disorders and differentiation of their functional and organic nature, determination of disease prognosis, etc. . Physical activity increases the myocardium's need for oxygen and blood flow through the coronary vessels.

The standardized method is the Master's test. Taking into account the gender, age and body weight of patients.

A non-standardized method is based on determining the amount of load depending on the capabilities of the individual: Bicycle ergometer test and treadmill test.

SSSU, principles of treatment.

ECG diagnosis of sinus sinus syndrome In case of SA node dysfunction, electrocardiographic signs of sinus dysfunction can be recorded long before the onset of clinical symptoms. 1. Sinus bradycardia – slowing of sinus rhythm with heart rate less than 60 per minute. due to reduced automatism of the sinus node. In SSSS, sinus bradycardia is persistent, long-lasting, refractory to physical activity and the administration of atropine (Fig. 1). 2. Bradysystolic form of atrial fibrillation (AF, atrial fibrillation, atrial fibrillation, absolute arrhythmia, atrial fibrillation, vorhofflimmern, arrhythmia perpetua, delirium cordis, arrhythmia completa) - chaotic, fast and irregular fibrillation of individual fibers of the atrial muscle not coordinated with each other as a result of ectopic atrial impulses with a frequency of 350 to 750 per minute, causing complete disorder of ventricular contractions. In the bradysystolic form of AF, the number of ventricular contractions is less than 60 per minute. (Fig. 2). 3. Migration of the pacemaker through the atria (wandering rhythm, sliding rhythm, migrating rhythm, migration of the cardiac pacemaker, wandering pacemaker). There are several variants of the wandering (wandering) rhythm: a) wandering rhythm in the sinus node. The P wave is of sinus origin (positive in leads II, III, AVF), but its shape changes with different heart contractions. The PR interval remains relatively constant. Severe sinus arrhythmia is always present; b) wandering rhythm in the atria. The P wave is positive in leads II, III, AVF, its shape and size change with different heart contractions. Along with this, the duration of the PR interval changes; c) wandering rhythm between the sinus and AV nodes. This is the most common variant of the wandering rhythm. With it, the heart contracts under the influence of impulses that periodically change their location, gradually moving from the sinus node, along the atrial muscles to the AV junction, and again return to the sinus node. ECG criteria for migration of the pacemaker through the atria are three or more different P waves in a series of cardiac cycles, a change in the duration of the PR interval. The QRS complex does not change (Fig. 3 and 4). 4. Passive ectopic rhythms. Reduced activity of the sinus node or complete blockade of sinus impulses due to functional or organic damage to the sinus node causes the activation of automatic centers of the second order (cells of atrial pacemakers, AV junction), III order (His system) and IV order (Purkinje fibers, ventricular musculature ). Automatic centers of the second order produce unchanged ventricular complexes (supraventricular type), while centers of the third and fourth order generate dilated and deformed ventricular complexes (ventricular, idioventricular type). The following rhythm disturbances have a substitutive nature: atrial, nodal, migration of the pacemaker through the atria, ventricular (idioventricular rhythm), jumping contractions. 4.1. Atrial rhythm (slow atrial rhythm) is a very slow ectopic rhythm with foci of impulse generation in the atria (Table 2): a) right atrial ectopic rhythm - the rhythm of an ectopic focus located in the right atrium. The ECG shows a negative P’ wave in leads V1–V6, II, III, aVF. The P-Q interval is of normal duration, the QRST complex is not changed; b) coronary sinus rhythm (coronary sinus rhythm) - impulses to excite the heart come from cells located in the lower part of the right atrium and the coronary sinus vein. The impulse propagates through the atria retrogradely from bottom to top. This leads to the registration of negative P’ waves in leads II, III, aVF. The P'aVR wave is positive. In leads V1–V6, the P’ wave is positive or biphasic. The PQ interval is shortened and is typically less than 0.12 s. The QRST complex is unchanged. The coronary sinus rhythm may differ from the right atrial ectopic rhythm only by shortening the PQ interval; c) left atrial ectopic rhythm - impulses to excite the heart come from the left atrium. In this case, a negative P’ wave is recorded on the ECG in leads II, III, aVF, V3–V6. The appearance of negative P' waves in I, aVL is also possible; the P' wave in aVR is positive. A characteristic sign of left atrial rhythm is the P' wave in lead V1 with an initial rounded dome-shaped part, followed by a pointed peak - “shield and sword” (“dome and spire”, “bow and arrow”). The P' wave precedes the QRS complex with a normal PR interval of 0.12–0.2 s. Atrial rhythm frequency is 60–100 per minute, rarely below 60 (45–59) per minute. or above 100 (101–120) per minute. The rhythm is correct, the QRS complex is not changed (Fig. 5); d) lower atrial ectopic rhythm - the rhythm of an ectopic focus located in the lower parts of the right or left atrium. This leads to the registration of negative P’ waves in leads II, III, aVF and a positive P’ wave in aVR. The PQ interval is shortened (Fig. 6). 4.2. Nodal rhythm (AV rhythm, replacing AV nodal rhythm) is a heart rhythm under the influence of impulses from the AV junction with a frequency of 40–60 per minute. There are two main types of AV rhythm: a) junctional rhythm with simultaneous excitation of the atria and ventricles (junctional rhythm without P wave, junctional rhythm with AV dissociation without P wave): the ECG shows an unchanged or slightly deformed QRST complex, P wave absent (Fig. 7); b) junctional rhythm with different simultaneous excitation of the ventricles and then the atria (nodal rhythm with a retrograde P’ wave, isolated form of the AV rhythm): an unchanged QRST complex is recorded on the ECG, followed by a negative P wave (Fig. 8). 4.3. Idioventricular (ventricular) rhythm (intrinsic ventricular rhythm, ventricular automatism, intraventricular rhythm) - ventricular contraction impulses arise in the ventricles themselves. ECG criteria: widened and deformed QRS complex (more than 0.12 s), rhythm with heart rate less than 40 (20–30) per minute. The terminal idioventricular rhythm is very slow and unstable. The rhythm is often correct, but may be incorrect if there are several ectopic foci in the ventricles or one foci with varying degrees of impulse formation or exit block. If an atrial rhythm is present (sinus rhythm, atrial fibrillation/flutter, ectopic atrial rhythm), it is independent of the ventricular rhythm (AV dissociation) (Fig. 9). 5. Sinoauricular block (block of exit from the SA node, dissociatio sino-atriale, SA-block) - a violation of the formation and/or conduction of impulses from the sinus node to the atria. SA blockade occurs in 0.16–2.4% of people, mainly in people over 50–60 years of age, more often in women than in men. 5.1. Sinoauricular block of the first degree is manifested by slow formation of impulses in the sinus node or slow conduction of them to the atria. A conventional ECG is uninformative and is diagnosed using electrical stimulation of the atria or recording of sinus node potentials and based on changes in conduction time in the sinoauricular node. 5.2. Sinoauricular block of the second degree is manifested by partial conduction of impulses from the sinus node, which leads to loss of contractions of the atria and ventricles. There are two types of sinoauricular block of the second degree: Sinoauricular block of the second degree, type I (with the Samoilov-Wenckebach period): a) progressive shortening of the RR intervals (Samoilov-Wenckebach period), followed by a long pause of the RR; b) the greatest distance PP - during a pause at the moment of loss of heart contraction; c) this distance is not equal to two normal RR intervals and is less than their duration; d) the first PP interval after the pause is longer than the last PP interval before the pause (Fig. 10). Sinoauricular block of the second degree, type II: a) asystole – absence of electrical activity of the heart (P wave and QRST complex are absent), contraction of the atria and ventricles is lost; b) pause (asystole) is a multiple of one normal RR interval (PP) or equal to two normal RR periods (PP) of the main rhythm (Fig. 11). Advanced sinoauricular block of the second degree, type II. By analogy with AV blockade, prolonged SA blockade 4:1, 5:1, etc. should be called advanced SA blockade of the second degree, type II. In some cases, the pause (isoelectric line) is interrupted by slipping complexes (rhythms) from the atrial centers of automaticity or, more often, from the area of ​​the AV junction. Sometimes delayed sinus impulses meet (coincide) with AV escape impulses. On the ECG, sparse P waves are located in close proximity to the escape QRS complexes. These P waves are not directed to the ventricles. The emerging AV dissociation can be complete or incomplete with ventricular seizures. One of the variants of incomplete AV dissociation, when each escape complex is followed by capture of the ventricles by a sinus impulse, is called escape-capture-bigemini (bigeminy of the “slip-out-capture” type). 5.3. III degree sinoauricular block (complete sinoauricular block) is characterized by the absence of excitation of the atria and ventricles from the sinus node. Asystole occurs and continues until the automatic center of the 2nd, 3rd or 4th order begins to operate (Fig. 12). 6. Stopping the sinus node (sinus node failure, sinus arrest, sinus pause, sinus–inertio) – periodic loss of the sinus node’s ability to produce impulses. This leads to loss of excitation and contraction of the atria and ventricles. There is a long pause on the ECG, during which the P and QRST waves are not recorded and the isoline is recorded. The pause when the sinus node stops is not a multiple of one RR (PP) interval (Fig. 13). 7. Atrial arrest (atrial asystole, atrial standstill, partial asystole) is the absence of atrial excitation, which is observed during one or (more often) more cardiac cycles. Atrial asystole can be combined with ventricular asystole, in such cases complete cardiac asystole occurs. However, during atrial asystole, pacemakers of the II, III, IV order usually begin to function, which cause excitation of the ventricles (Fig. 14). There are three main options for atrial arrest: a) atrial arrest together with failure (stop) of the SA node: P waves are absent, as are the electrograms of the SA node; a slow replacement rhythm is recorded from the AV junction or from the idioventricular centers. A similar phenomenon can be encountered with severe quinidine and digitalis intoxication (Fig. 14); b) absence of electrical and mechanical activity (stop) of the atria while maintaining the automaticity of the SA node, which continues to control the excitation of the AV node and ventricles. This picture is observed with severe hyperkalemia (>9–10 mm/l), when a regular rhythm appears with widened QRS complexes without P waves. This phenomenon is called sinoventricular conduction; c) preservation of the automaticity of the SA node and the electrical activity of the atria (P waves) in the absence of their contractions. Syndrome electromechanical dissociation (uncoupling) in the atria can sometimes be observed in patients with dilated atria after their electrical defibrillation. Permanent arrest, or atrial paralysis, is a rare occurrence. There are reports in the literature of atrial paralysis in cardiac amyloidosis, widespread atrial fibrosis, fibroelastosis, fat infiltration, vacuolar degeneration, neuromuscular dystrophies, and end-stage heart disease. 8. Bradycardia/tachycardia syndrome (tachy/brady syndrome). With this option, a rare sinus or replacement supraventricular rhythm alternates with attacks of tachysystole (Fig. 15). Clinical assessment of the function of the sinus node of the sinus node should be considered as a probable diagnosis in patients with the symptoms described above. The most complex electrophysiological studies should be carried out only when the diagnosis of sinus node dysfunction raises certain doubts. Valsalva maneuver. The simplest vagal tests with holding the breath while taking a deep breath (including the Valsalva maneuver), performed alone or in combination with straining, sometimes reveal sinus pauses exceeding 2.5–3.0 s, which must be differentiated from pauses caused by disorders AV conduction. The detection of such pauses indicates increased sensitivity of the sinus node to vagal influences, which can occur in both VDS and SSSU. If such pauses are accompanied by clinical symptoms, an in-depth examination of the patient is required to determine tactics treatment . Carotid sinus massage. The carotid sinus is a small formation of the autonomic nervous system located at the beginning of the internal carotid artery above the branch of the common carotid artery. The carotid sinus receptors are connected to the vagus nerve. The carotid sinus reflex under physiological conditions causes bradycardia and hypotension due to irritation of the vagus nerve and the vascular regulatory center in the medulla oblongata. With a hypersensitive (hypersensitive) carotid sinus, pressure on it can cause sinus pauses exceeding 2.5–3.0 s, accompanied by a short-term disturbance of consciousness. Before massage of the carotid zones, such patients are advised to assess the state of blood flow in the carotid and vertebral arteries, because Massaging arteries with pronounced atherosclerotic changes can lead to dire consequences (severe bradycardia up to loss of consciousness and asystole!). It is important to emphasize that carotid sinus syndrome can, on the one hand, develop against the background of normal sinus node function, and on the other hand, it does not exclude the presence of CVS. Tilt test. The tilt test (passive orthostatic test) is considered today as the “gold standard” in the examination of patients with syncope of unknown etiology. Load testing (bicycle ergometry, treadmill test). Stress testing assesses the ability of the sinus node to increase its rhythm in accordance with an internal physiological chronotropic stimulus. Holter monitoring. Ambulatory Holter monitoring, when performed during normal daily activity, appears to be a more valuable physiologic method for assessing sinus node function than stress testing. The alternating occurrence of bradyarrhythmias and tachyarrhythmias in patients with SSSS is often not detected on a conventional resting electrocardiogram. Studying the function of the sinus node using the TEES method. An indicator of automatic activity of the sinus node is the duration of the sinus pause from the moment of termination of stimulation (the last artifact of the electrical stimulus) to the beginning of the first independent P wave. This period of time is called the time of recovery of sinus node function (RSFRU). Normally, the duration of this period does not exceed 1500–1600 ms. In addition to VVFSU, another indicator is calculated - the corrected time for recovery of sinus node function (CRVFSU), which takes into account the duration of the VVFSU indicator in relation to the initial frequency of sinus rhythm. Treatment SSSU At the beginning of SSSU therapy, all drugs that may contribute to conduction disturbances are discontinued. In the presence of Tachy-Brady syndrome, the tactics can be more flexible: with a combination of moderate sinus bradycardia, which is not yet an indication for the installation of a permanent pacemaker, and frequent brady-dependent paroxysms of atrial fibrillation, in some cases it is possible to test allapinin in a small dose (1/2 tablet . 3–4 r./day) with subsequent mandatory monitoring with Holter monitoring. However, over time, the progression of conduction disorders may require discontinuation of drugs followed by installation of a pacemaker. If bradycardia persists, simultaneous use of belloid 1 tablet is permissible. 4 rubles/day or teopeca 0.3 g, 1/4 tablet. 2–3 rubles/day. It is necessary to exclude hyperkalemia or hypothyroidism, in which the patient may be mistakenly referred for installation of a permanent pacemaker. If SSSS is suspected, one should refrain from prescribing sinus node-suppressing drugs until Holter monitoring and special tests are performed. The prescription of β-blockers, calcium antagonists (verapamil, diltiazem), sotalol, amiodarone, cardiac glycosides is inappropriate. In cases of acute development of SSSS, etiotropic treatment is carried out first of all. treatment. If its inflammatory genesis is suspected, the administration of prednisolone 90–120 mg IV or 20–30 mg/day is indicated. inside. In case of acute myocardial infarction, anti-ischemic drugs (nitrates), antiplatelet agents (acetylsalicylic acid, clopidogrel), anticoagulants (heparin, low molecular weight heparins), cytoprotectors (trimetazidine) are prescribed. Emergency treatment of SSSU itself is carried out depending on its severity. In cases of asystole and MAS attacks, resuscitation measures are necessary. Severe sinus bradycardia, worsening hemodynamics and/or provoking tachyarrhythmias, requires the administration of atropine 0.5–1.0 ml of 0.1% solution subcutaneously up to 4–6 times/day, infusion of dopamine, dobutamine or aminophylline under the control of a cardiac monitor . For prophylactic purposes, a temporary endocardial stimulator can be installed.

The table on the right shows the ECG (12 leads) of two patients: a healthy person and a patient diagnosed with " severe right ventricular hypertrophy"(bases: deviation of the EOS to the right; dominant R wave V1; inversion of the T wave in the right precordial leads V1, V2). ECG tape speed - 25 mm/s (1 horizontal cell = 0.04 s).

Quantitative signs of right ventricular hypertrophy

R V1 > 7 mm;

S V1,V2 ≤ 2 mm;

1. R V5,V6< 5 mm;

   R V1 +S V5(V6) > 10.5 mm;

   R aVR > 4 mm;

   negative T V1 with a decrease in ST V1,V2 (R V1 > 5 mm) in the absence of coronary insufficiency.

ECG conclusion

Right ventricular hypertrophy- if, with ECG signs of right ventricular hypertrophy, a high R wave V1,V2 is observed without changes in the ST segment V1,V2 and T wave V1,V2.

Right ventricular hypertrophy with overload- if the ECG shows signs of right ventricular hypertrophy, a high R wave V1,V2 is observed in combination with a decrease in the ST segment V1,V2 and a negative T wave V1,V2.

Hypertrophy of the right ventricle with its overload and pronounced changes in the myocardium- if a high R wave with a decrease in the ST segment and a negative T wave are observed not only in leads V1, V2, but also in other chest leads.

Systolic overload of the right ventricle is manifested by a spatial displacement of the QRS loop to the right and forward, and the T loop to the left and backward. The centripetal portion of the QRS loop moves anterior to the isoelectric point, resulting in a clockwise QRS loop in the horizontal plane.

“Diastolic” overload of the right ventricle is manifested by an increase in the final deviation of the QRS loop, directed to the right and upward (forward or backward), with no changes in the remaining parts of the QRS loop and the T loop.

ECG signs of extrasystoles:

premature ventricular QRST complex and/or P wave (main sign);

complete compensatory pause - a pause that occurs after a ventricular extrasystole, while the distance between two sinus complexes P-QRST is equal to twice the R-R interval of the main rhythm;

incomplete compensatory pause - a pause that occurs after an atrial extrasystole (extrasystoles from the atrioventricular junction), while the duration of the pause is slightly longer than the usual P-P interval of the main rhythm;

allorhythmia - correct alternation of extrasystoles and normal contractions:

• bigeminy - the occurrence of extrasystole after each normal contraction;

  trigeminy - after every two normal heartbeats;

  quadrigymenia - after every three normal contractions.

Treatment of supraventricular extrasystoles

adherence to a rational regimen: giving up smoking, alcohol, strong tea and coffee, creating a favorable psycho-emotional environment;

potassium diet and potassium salts;

sedatives (tinctures of valerian, motherwort, Corvalol - 20..30 drops 3-4 times a day);

antiarrhythmic drugs:

• beta blockers (propranolol 10 mg 4 times a day; metoprolol- 50 mg 2 times a day);

  calcium antagonists (verapamil- 40 mg 3-4 times a day);

  cardiac glycosides in case of heart failure ( digoxin, isolanide- 0.25 mg 2 times a day);

  Class Ia drugs (quinidine 0.25 g 1-3 times a day).

1. Normal sinus rhythm

Sinus rhythm is the rhythm emerging from the sinus node, which is a first-order automatic center (for more details, see “The conduction system of the heart”). In healthy people, the rhythm is always sinus. However, sinus rhythm can also be observed in patients. The rhythm frequency (heart rate - heart rate) normally lies in the range of 60-80 beats per minute.

Criteria for normal sinus rhythm are:

1. The presence of a p wave of sinus origin, which precedes the qrs complex:

the P wave must be positive in standard lead II and negative in lead aVR;

in other limb leads, the shape of the P wave may be different depending on the orientation of the electrical axis of the heart (e.o.s.) - in most cases, the P wave is positive in leads I, aVF;

in chest leads V1, V2 the P wave is usually biphasic;

in the remaining chest leads V3-V6, the P wave in normal sinus rhythm is usually positive, but there may be variations depending on the location of the e.o.s.

constant and normal (0.12-0.2 s) distance of the PQ interval (each P wave should be followed by a QRS complex and a T wave);

constant shape of the P wave in all leads (the shape of the P wave may change in some leads during breathing, in this case an ECG is recorded while holding the breath);

Heart rate within 60-80 beats per minute;

constant distance between teeth P (R) - differences in the distance between teeth should not exceed 10%.

1. With atrial fibrillation, frequent (350-700 per minute) disordered, chaotic excitation and contraction of individual groups of atrial muscle fibers are observed.

ECG signs:

Absence of P wave in all leads;

The presence throughout the entire cardiac cycle of random small waves f, having different shapes and amplitudes. Best in leads (V1, V2, II, III and aVF)

Irregularity of ventricular QRS complexes - irregular ventricular rhythm

The presence of QRS complexes, which in most cases have a normal, unchanged appearance without deformation or widening.

Drug therapy

The following areas of drug therapy for atrial fibrillation are distinguished: cardioversion (restoration of normal sinus rhythm), prevention of repeated paroxysms (episodes) of supraventricular arrhythmias, control of the normal frequency of contractions of the ventricles of the heart. Another important goal of drug treatment for MA is the prevention of complications - various thromboembolisms. Drug therapy is carried out in four directions.

Treatment with antiarrhythmics. It is used if a decision has been made to attempt drug cardioversion (restoring the rhythm with the help of drugs). Drugs of choice – propafenone, amiodarone.

Propaphenone is one of the most effective and safe drugs used to treat supraventricular and ventricular heart rhythm disorders. The action of propafenone begins 1 hour after oral administration, the maximum concentration in the blood plasma is reached after 2–3 hours and lasts 8–12 hours.

Heart rate control. If it is impossible to restore the normal rhythm, it is necessary to bring the atrial fibrillation back to normal form. For this purpose, beta-blockers, non-dihydropyridine calcium antagonists (verapamil group), cardiac glycosides, etc. are used.

Beta blockers. Drugs of choice for controlling heart function (frequency and strength of contractions) and blood pressure. The group blocks beta-adrenergic receptors in the myocardium, causing a pronounced antiarrhythmic (heart rate reduction) as well as hypotensive (blood pressure reduction) effect. Beta blockers have been shown to statistically increase life expectancy in heart failure. Contraindications for use include bronchial asthma (since blocking beta 2 receptors in the bronchi causes bronchospasm).

Anticoagulant therapy. To reduce the risk of thrombosis in persistent and chronic forms of AF, blood thinning drugs must be prescribed. Anticoagulants of direct (heparin, fraxiparin, fondaparinux, etc.) and indirect (warfarin) action are prescribed. There are regimens for taking indirect (warfarin) and so-called new anticoagulants - antagonists of blood clotting factors (Pradaxa, Xarelto). Treatment with warfarin is accompanied by mandatory monitoring of coagulation parameters and, if necessary, careful adjustment of the drug dosage.

Metabolic therapy. Metabolic drugs include drugs that improve nutrition and metabolic processes in the heart muscle. These drugs purport to have a cardioprotective effect, protecting the myocardium from the effects of ischemia. Metabolic therapy for MA is considered an additional and optional treatment. According to recent data, the effectiveness of many drugs is comparable to placebo. Such medicines include:

• ATP (adenosine triphosphate);

  K and Mg ions;

  cocarboxylase;

  riboxin;

  mildronate;

  preductal;

  Einthoven proposed to determine the angle between a horizontal line (parallel to the axis of lead I) drawn through the center of the triangle and the electrical axis - angle a to describe the location of Aqrs in the frontal plane. He designated the left end of the horizontal line (the positive pole of the axis of lead I) as 00, the right end as ± 180°. He designated the lower end of the perpendicular intersecting the horizontal line in the center as +90°, and the upper end -90°. Now, with a simple protractor placed along the horizontal axis, you can determine the angle a. In the example we gave, the angle a=+40°.

  The same method you can determine the position of the electrical axis (average vector) of ventricular repolarization (AT) - angle a. and the electrical axis of atrial excitation (Ar) - angle a in the frontal plane.

  Electric axis position can be determined using Diede's scheme. Preliminarily calculate the algebraic sum of the amplitude of the waves of leads I and III in millimeters. Then the obtained values ​​are laid off on the corresponding sides of the diagram. Intersections of the grid with radial lines indicate the magnitude of the angle a.

  For this purpose, the tables of R. Ya. Pismenny and others are also used.

  It is generally accepted normal position of the electrical axis in the segment from +30° to +69°. The location of the electrical axis in the segment from 0° to +29° is considered horizontal. If the electrical axis is located to the left of 0° (in the -1°-90° quadrant), it is said to deviate to the left. The location of the electrical axis in the segment from +70° to + 90° is considered vertical. They talk about the deviation of the electrical axis to the right when it is located to the right of +90° (in the right half of the coordinate system).

  Normal ECG reflects the correct sequence of excitation of the heart parts characteristic of sinus rhythm, the normal orientation of the EMF vectors of their excitation and, therefore, the standard relationship between the direction and amplitude of the waves in various leads. as well as the normal duration of intervals between cycles and within cycles.

  The figure shows ECG healthy woman G. 32 years old. The sinus rhythm is correct, heart rate is 62 per minute. (R - R = 0.95 sec.). P - Q = 0.13 sec. P = 0.10 sec. QRS = 0.07 sec. Q - T = 0.38 ex. RII>R>RIII. In the frontal plane, the location of AQRS=+52°. AT=+39°. QRS - T = 13°. AP=+50. P wave amplitude = 1.5 mm. PII>PI>PIII. The P wave is biphasic, the first (positive) phase is larger than the second (negative).

  QRS complex I, II, aVL type qRs. QRSIII type R, q, „ aVL and SI, II are small. R,u is slightly jagged on the descending knee. Complex QRSV1-V3 type RS(rS). QRSV4_v6 type qRs. SV2=18 mm > SV3 > SV5, tooth rv1 RV5>RV6. The QRS transition zone is between leads V2 and V3. Segment RS - TV1-V3 is shifted upward from the isoelectric line by 1 - 2 mm. Segment RS - T in other leads at the level of the isoelectric line. Wave TII>TI>TIII. The TV1 tooth is negative, TV2 is positive. TV2 TV4>TV5>TV6.

  Normal electrocardiogram

  The normal electrocardiogram, regardless of the lead system, consists of three upward (positive) waves P, R and T, two downward (negative) waves Q and S, and a variable, upward U wave.

  In addition, the ECG distinguishes between P-Q, S-T, T-P, R-R intervals and two complexes - QRS and QRST (Fig. 10).

  

  Rice. 10. Waves and intervals of a normal ECG

  P wave reflects atrial depolarization. The first half of the P wave corresponds to the excitation of the right atrium, the second half - to the excitation of the left atrium.

  P-Q interval corresponds to the period from the beginning of atrial excitation to the beginning of ventricular excitation. The P-Q interval is measured from the beginning of the P wave to the beginning of the Q wave, in the absence of a Q wave - to the beginning of the R wave. It includes the duration of atrial excitation (the P wave itself) and the duration of excitation propagation mainly through the atrioventricular node, where the physiological delay in impulse conduction occurs ( the segment from the end of the P wave to the beginning of the Q wave). During the passage of an impulse through a specifically conducting system, such a small potential difference arises that no reflections of it can be detected on an ECG taken from the surface of the body. The P-Q interval is located on the isoelectric line, its duration is 0.12-0.18 s.

  QRS complex reflects ventricular depolarization. The duration (width) of the QRS complex characterizes intraventricular conduction, which varies within normal limits depending on the heart rhythm (decreases with tachycardia, increases with bradycardia). The duration of the QRS complex is 0.06-0.09 s.

  Q wave corresponds to the excitation of the interventricular septum. Normally, it is absent in the right chest leads. A deep Q wave in lead III appears when the diaphragm is high, disappearing or decreasing with deep inspiration. The duration of the Q wave does not exceed 0.03 s, its amplitude is no more than 1/4 of the R wave.

  R wave characterizes the excitation of the bulk of the ventricular myocardium, the S wave - excitation of the posterosuperior parts of the ventricles and the interventricular septum. An increase in the height of the R wave corresponds to an increase in potential within the electrode. At the moment when the entire myocardium adjacent to the electrode is depolarized, the potential difference disappears and the R wave reaches the isoelectric line or passes into the S wave located below it (internal deviation, or internal deflexion). In unipolar leads, the segment of the QRS complex from the beginning of excitation (the beginning of the Q wave, and in its absence, the beginning of the R wave) to the apex of the R wave reflects the true excitation of the myocardium at a given point. The duration of this segment is called the internal deviation time. This time depends on the speed of propagation of excitation and the thickness of the myocardium. Normally, it is 0.015-0.035 s for the right ventricle, and 0.035-0.045 s for the left ventricle. The time lag of the internal deviation is used to diagnose myocardial hypertrophy, branch block and its localization.

  When describing the QRS complex, in addition to the amplitude of its constituent waves (mm) and duration (s), their letter designation is given. In this case, small teeth are designated in lowercase letters, large ones in capital letters (Fig. 11).

  Rice. 11. The most common forms of the complex and their letter designation

  The S-T interval corresponds to the period of complete depolarization when there is no potential difference, and therefore is on the isoelectric line. A variant of the norm may be a shift in the interval in standard leads by 0.5-1 mm. The duration of the S-T interval varies widely depending on heart rate.

  T wave is the final part of the ventricular complex and corresponds to the phase of ventricular repolarization. It is directed upward, has a flat ascending knee, a rounded top and a steeper descending knee, i.e. it is asymmetrical. The duration of the T wave varies widely, averaging 0.12-0.16 s.

  QRST complex(Q-T interval) corresponds in time to the period from the beginning of depolarization to the end of ventricular repolarization and reflects their electrical systole.

  The Q-T interval can be calculated using special tables. The duration of the QRST complex normally almost coincides with the duration of mechanical systole.

  To characterize the electrical systole of the heart, the systolic indicator SP is used - the ratio of the duration of the electrical systole Q-T to the duration of the cardiac cycle R-R, expressed as a percentage:

  

  An increase in systolic value by more than 5% above normal may be one of the signs of inadequate function of the heart muscle.

  U wave occurs 0.04 s after the T wave. It is small, with normal amplification it is not detected on all ECGs and is mainly in leads V2-V4. The genesis of this tooth is unclear. Perhaps it is a reflection of the trace potential in the phase of increased myocardial excitability after systole. The maximum amplitude of the U wave is normally 2.5 mm, duration is 0.3 s.

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  What does an ECG show?

  A typical electrocardiographic study includes recording of EMF in 12 leads:

  • standard leads (I, II, III);
  • enhanced leads (aVR, aVL, aVF);
  • chest leads (V1..V6).

  

  Each lead records at least 4 ECG complexes (full cycles). In Russia, the standard for belt speed is 50 mm/s (abroad - 25 mm/s). At a belt speed of 50 mm/s, each small cell located between adjacent vertical lines (distance 1 mm) corresponds to an interval of 0.02 s. Every fifth vertical line on the electrocardiographic tape is thicker. The constant speed of the tape and the millimeter grid on the paper make it possible to measure the duration of ECG waves and intervals and the amplitude of these waves.

  Due to the fact that the polarity of the axis of lead aVR is opposite to the polarity of the axes of standard leads, the cardiac EMF is projected onto the negative part of the axis of this lead. Therefore, normally in lead aVR the P and T waves are negative, and the QRS complex has the form QS (less often rS).

  Left and right ventricular activation time- the period from the beginning of excitation of the ventricles until the excitation reaches the maximum number of their muscle fibers. This is the time interval from the beginning of the QRS complex (from the beginning of the Q or R wave), to the perpendicular lowered from the top of the R wave to the isoline. The activation time of the left ventricle is determined in the left chest leads V5, V6 (the norm is no more than 0.04 s, or 2 cells). The activation time of the right ventricle is determined in the chest leads V1, V2 (the norm is no more than 0.03 s, or one and a half cells).

  

  ECG waves are designated by Latin letters. If the amplitude of a tooth is more than 5 mm, such a tooth is indicated by a capital letter; if less than 5 mm - lowercase. As can be seen from the figure, a normal cardiogram consists of the following sections:

  • P wave- atrial complex;
  • PQ interval— time of passage of excitation through the atria to the ventricular myocardium;
  • QRS complex- ventricular complex;
  • q wave- stimulation of the left half of the interventricular septum;
  • R wave— the main wave of the ECG, caused by excitation of the ventricles;
  • s wave- final excitation of the base of the left ventricle (non-permanent ECG wave);
  • ST segment- corresponds to the period of the cardiac cycle when both ventricles are excited;
  • T wave— recorded during ventricular repolarization;
  • QT interval- electrical ventricular systole;
  • u wave- the clinical origin of this wave is not known exactly (it is not always recorded);
  • TP segment- diastole of the ventricles and atria.

  The health of the entire body depends on the health of the cardiovascular system. When unpleasant symptoms occur, most people seek medical help. Having received the results of an electrocardiogram in their hands, few people understand what is at stake. What does the p wave reflect on an ECG? What alarming symptoms require medical monitoring and even treatment?

  Why is an electrocardiogram performed?

  After examination by a cardiologist, the examination begins with electrocardiography. This procedure is very informative, despite the fact that it is carried out quickly and does not require special training or additional costs.

  An electrocardiogram is always taken upon admission to the hospital.

  The cardiograph records the passage of electrical impulses through the heart, records the heart rate and can detect the development of serious pathologies. The waves on an ECG give a detailed picture of the different parts of the myocardium and how they work.

  The norm for an ECG is that different waves differ in different leads. They are calculated by determining the value relative to the projection of the EMF vectors onto the lead axis. The tooth can be positive or negative. If it is located above the cardiography isoline, it is considered positive, if below it is considered negative. A biphasic wave is recorded when, at the moment of excitation, the wave passes from one phase to another.

  Important! An electrocardiogram of the heart shows the state of the conduction system, consisting of bundles of fibers through which impulses pass. By observing the rhythm of contractions and the characteristics of rhythm disturbances, one can see various pathologies.

  The conduction system of the heart is a complex structure. It consists of:

  • sinoatrial node;
  • atrioventricular;
  • bundle branches;
  • Purkinje fibers.

  The sinus node, as a pacemaker, is a source of impulses. They are formed at a rate of 60-80 times per minute. With various disorders and arrhythmias, impulses may be created more often or less frequently than normal.

  Sometimes bradycardia (slow heartbeat) develops due to the fact that another part of the heart takes over the function of the pacemaker. Arrhythmic manifestations can also be caused by blockades in various zones. Because of this, the automatic control of the heart is disrupted.

  What does an ECG show?

  If you know the norms for cardiogram indicators, how the teeth should be located in a healthy person, you can diagnose many pathologies. This examination is carried out in a hospital setting, on an outpatient basis and in emergency critical cases by emergency doctors to make a preliminary diagnosis.

  Changes reflected in the cardiogram may show the following conditions:

  • rhythm and heart rate;
  • myocardial infarction;
  • blockade of the cardiac conduction system;
  • disruption of the metabolism of important microelements;
  • blockages of large arteries.

  Obviously, research using an electrocardiogram can be very informative. But what do the results of the data obtained consist of?

  Attention! In addition to waves, the ECG pattern has segments and intervals. Knowing what the norm is for all these elements, you can make a diagnosis.

  Detailed interpretation of the electrocardiogram

  The norm for the P wave is located above the isoline. This atrial wave can be negative only in leads 3, aVL and 5. In leads 1 and 2 it reaches its maximum amplitude. The absence of a P wave may indicate serious disturbances in the conduction of impulses through the right and left atrium. This tooth reflects the state of this particular part of the heart.

  The P wave is deciphered first, since it is in it that the electrical impulse is generated and transmitted to the rest of the heart.

  Splitting of the P wave, when two peaks are formed, indicates an enlargement of the left atrium. Often bifurcation develops with pathologies of the bicuspid valve. A double-humped P wave becomes an indication for additional cardiac examinations.

  The PQ interval shows how the impulse passes to the ventricles through the atrioventricular node. The norm for this section is a horizontal line, since there are no delays due to good conductivity.

  The Q wave is normally narrow, its width is no more than 0.04 s. in all leads, and the amplitude is less than a quarter of the R wave. If the Q wave is too deep, this is one of the possible signs of a heart attack, but the indicator itself is assessed only in conjunction with others.

  The R wave is ventricular, so it is the highest. The walls of the organ in this zone are the densest. As a result, the electric wave travels the longest. Sometimes it is preceded by a small negative Q wave.

  During normal heart function, the highest R wave is recorded in the left precordial leads (V5 and 6). However, it should not exceed 2.6 mV. A tooth that is too high is a sign of left ventricular hypertrophy. This condition requires in-depth diagnostics to determine the causes of the increase (ischemic heart disease, arterial hypertension, heart valve defects, cardiomyopathies). If the R wave decreases sharply from V5 to V6, this may be a sign of MI.

  After this reduction, the recovery phase begins. On the ECG this is illustrated as the formation of a negative S wave. After a small T wave comes the ST segment, which normally should be represented by a straight line. The Tckb line remains straight, there are no bent areas on it, the condition is considered normal and indicates that the myocardium is completely ready for the next RR cycle - from contraction to contraction.

  Determination of the heart axis

  Another step in deciphering the electrocardiogram is determining the axis of the heart. A normal tilt is considered to be between 30 and 69 degrees. Smaller indicators indicate a deviation to the left, and larger indicators indicate a deviation to the right.

  Possible errors in research

  It is possible to obtain unreliable data from an electrocardiogram if the following factors influence the cardiograph when recording signals:

  • alternating current frequency fluctuations;
  • displacement of the electrodes due to their loose application;
  • muscle tremors in the patient's body.

  All these points affect the obtaining of reliable data when conducting electrocardiography. If the ECG shows that these factors have taken place, the study is repeated.

  
  Timely consultation with a doctor will help diagnose pathologies in the early stages

  When an experienced cardiologist interprets a cardiogram, a lot of valuable information can be obtained. In order not to trigger the pathology, it is important to consult a doctor when the first painful symptoms occur. This way you can save your health and life!

  More:

  Causes of a negative T wave on an ECG, possible heart diseases and the degree of their influence on the indicator