Rotate counterclockwise heart. Energy practice “Magic whirling”

Any change in the position of the heart is due to its rotation around three axes: anterior-posterior (sagittal), longitudinal (long) and transverse (horizontal). The size and direction of ECG waves in various leads determine the electrical positions of the heart (Fig. 16).

Rice. 16. Diagram of the rotation of the heart around various axes. The arrows show the direction of rotation of the heart: a - around the anterior-posterior axis; b - around the long axis; c - around the transverse axis.

When the heart rotates around the anterior-posterior axis (Fig. 16, a), the heart takes either a horizontal or vertical position, which is most clearly reflected in standard leads. The horizontal position of the heart causes its electrical axis to deviate to the left, and the vertical position - to the right. The horizontal and vertical position of the heart is also reflected in unipolar leads from the limbs (see above).

The rotation of the heart along the long (longitudinal) axis (Fig. 16, b) occurs both clockwise and in the opposite direction and also causes ECG changes in all leads. Such a turn is observed during a number of physiological processes: a change in body position, the act of breathing, physical stress, etc.

When the heart rotates around the transverse (horizontal) axis, the apex of the heart shifts either anteriorly or posteriorly (Fig. 16, c). The rotation of the heart around the transverse axis is reflected in the unipolar limb leads.

Wilson proposed to determine the electrical position of the heart by the teeth of unipolar chest leads and limb leads. Electrocardiography distinguishes 5 positions of the heart: vertical, semi-vertical, intermediate, semi-horizontal and horizontal.

When the electrical position of the heart is vertical (angle a is +90°), the shape of the QRS complex in the unipolar lead from the left arm is similar to that observed in the right positions of the chest leads, and the shape of the QRS complex in the unipolar lead from the left leg is similar to that observed in the left positions of the chest leads ( Fig. 17).

Rice. 17. Electrocardiogram of a person with a healthy heart in standard chest and enlarged unipolar limb leads with a vertical position of the heart in the chest (the designations are the same as in Fig. 11): 1 - right ventricle; 2 - left ventricle.

In a semi-vertical position (angle α is +60°), the shape of the QRS complex in the unipolar lead from the left leg is similar to that observed in the left positions of the chest leads.

In an intermediate position of the heart (angle a is 4-30°), the shape of the QRS complex in the unipolar lead from the left arm and left leg is similar to that observed in the left positions of the chest leads.

With a semi-horizontal position of the heart (angle a is 0°), the shape of the QRS complex in the unipolar lead from the left arm is similar to that observed in the left positions of the chest leads.

When the heart is in a horizontal position (angle α is -30°), the shape of the QRS complex in the unipolar lead from the left arm is similar to that observed in the left positions of the chest leads, and the shape of the QRS complex in the unipolar lead from the left leg is similar to that observed in the right positions of the chest leads (Fig. .18).

Rice. 18. Electrocardiogram of a person with a healthy heart in standard, chest and enlarged unipolar limb leads with a horizontal position of the heart (the designations are the same as in Fig. 11): 1 - right atrium; 2 - right ventricle; 3 - left ventricle.

In cases where there is no similarity between the unipolar chest leads and the unipolar limb leads, the electrical position of the heart is indeterminable. X-ray data have shown that the ECG does not always accurately reflect the position of the heart.

The ECG is usually recorded in a supine position.

Various positions of the subject (vertical, horizontal, on the right or left side), changing the position of the heart, cause changes in the ECG waves.

In a vertical position, the number of heart contractions increases, the electrical axis of the heart deviates to the right. This causes corresponding changes in the size and direction of ECG waves in standard and chest leads. The duration of the QRS complex decreases. The size of the T wave decreases, especially in leads II and III. The RS-T segment in these leads is slightly shifted downward.

When positioned on the right side, the electrical axis of the heart rotates around the long axis counterclockwise, and when positioned on the left side, it rotates clockwise with corresponding ECG changes.

The shape and direction of ECG waves in children differs from the ECG of an adult. In old age, the P and T waves are often reduced. The duration of the P-Q interval and QRS complex is usually at the upper limit of normal. With age, deviation of the electrical axis of the heart to the left is much more common. The systolic reading is often slightly higher than expected.

In women, the amplitude of the P, T waves and the QRS complex is slightly smaller in the standard and precordial leads. More often there is a displacement of the RS-T segment and a negative T wave in lead III.

The area of ​​the QRS complex waves is smaller. The ventricular gradient is smaller and deviated more to the left, the U wave is larger. The duration of the P-Q interval and QRS complex is on average shorter. The duration of electrical systole and systolic indicator are longer.

With the predominant effect on the heart of the parasympathetic division of the autonomic nervous system, the number of heart contractions decreases. The P wave decreases and occasionally increases slightly. The duration of the P-Q interval increases slightly. The question of the influence of the parasympathetic department on the T wave cannot be considered completely clarified. According to some data, the T wave decreases, according to others, it increases. The Q-T segment often decreases.

With a predominant effect on the heart of the sympathetic department of the autonomic nervous system, the number of heart contractions increases. The P wave usually increases, sometimes decreases. The duration of the P-Q interval decreases. The T wave, according to some data, increases, according to others, it decreases.

Positive emotions have little effect on the ECG. Negative emotions (fear, fright, etc.) cause increased heart rate, mostly an increase, and sometimes a decrease in the waves.

During a deep breath, due to the downward displacement of the diaphragm, the heart assumes a vertical position. Its electrical axis deviates to the right, which causes corresponding changes in the ECG. Affects the shape of ECG waves and increases the impact on the heart during inhalation of the sympathetic department of the autonomic nervous system. During deep exhalation, ECG changes are caused by elevation of the diaphragm, deviation of the electrical axis of the heart to the left and the predominant effect on the heart of the parasympathetic division of the autonomic nervous system.

During normal breathing, these ECG changes are insignificant.

Physical stress can cause ECG changes in various ways: it has a reflex effect on the depolarization and repolarization of the heart, a reflex and direct effect on the conduction system and contractile myocardium. Usually these paths are combined. ECG changes depend on the degree and duration of action of these factors.

Pronounced changes in ECG waves are observed after significant physical stress: an increase, and sometimes a mild broadening of the P wave; a decrease in the duration of the P-Q interval, and sometimes a downward shift due to layering of the P-Ta segment; a slight decrease in the duration of the QRS complex and often a deviation of the electrical axis of the heart to the right, as well as a downward shift of the RS-T segment; enlargement of the T wave; the decrease in the Q-T segment is proportional to the increase in heart rate; the appearance of an enlarged U wave.

Eating a large amount of food causes an increase in heart rate and a decrease in the T wave (occasionally significant, even becoming negative) in leads II and III. Sometimes there is a slight increase in the P wave, an increase in the Q-T segment and systolic indicator.

These ECG changes reach a maximum after 30-60 minutes. after eating and disappear after 2 hours.

ECG changes during the day in healthy people are insignificant and relate mainly to the T wave. The T wave reaches its maximum value early in the morning, and after breakfast its value is the smallest.

Electrocardiography (ECG) remains one of the most common methods for examining the cardiovascular system and continues to develop and improve. Based on the standard electrocardiogram, various modifications of the ECG have been proposed and are widely used: Holter monitoring, high-resolution ECG, tests with dosed physical activity, drug tests.

Leads in electrocardiography

The concept of “electrocardiogram lead” means recording an ECG when electrodes are applied to certain areas of the body that have different potentials. In practical work, in most cases, they are limited to recording 12 leads: 6 from the limbs (3 standard and 3 “unipolar reinforced”) and 6 thoracic leads - unipolar. The classic lead method proposed by Einthoven is the registration of standard limb leads, designated by Roman numerals I, II, III.

Enhanced limb leads were proposed by Goldberg in 1942. They record the potential difference between one of the limbs on which the active positive electrode of a given lead is installed (right arm, left arm or left leg), and the average potential of the other two limbs. These leads are designated as follows: aVR, aVL, aVF. The designations for augmented limb leads come from the first letters of English words: a - augmented (reinforced), V - voltage (potential), R - right (right), L - left (left), F - foot (leg).

Unipolar chest leads are designated by the Latin letter V (potential, voltage) with the addition of the position number of the active positive electrode, indicated in Arabic numerals:

lead V 1 - active electrode located in the fourth intercostal space along the right edge of the sternum;

V 2 - in the fourth intercostal space along the left edge of the sternum;

V 3 - between V 2 and V 4;

V 4 - in the fifth intercostal space along the left midclavicular line;

V 5 - in the fifth intercostal space along the anterior axillary line;

V 6 - in the fifth intercostal space along the midaxillary line.

Using the chest leads, you can judge the condition (size) of the heart chambers. If the usual program for recording 12 generally accepted leads does not allow one to reliably diagnose a particular electrocardiographic pathology, or clarification of some quantitative parameters is required, additional leads are used. These could be leads

V 7 - V 9, right chest leads - V 3R -V 6R.

Electrocardiogram recording technique

The ECG is recorded in a special room, remote from possible sources of electrical interference. The study is carried out after a 15-minute rest on an empty stomach or no earlier than 2 hours after a meal. The patient should be undressed to the waist, the lower legs should be freed from clothing. Electrode paste must be used to ensure good skin contact with the electrodes. Poor contact or the appearance of muscle tremors in a cool room can distort the electrocardiogram. The examination, as a rule, is carried out in a horizontal position, although nowadays examinations have also begun to be carried out in a vertical position, since in this case a change in autonomic support leads to a change in some electrocardiographic parameters.

It is necessary to record at least 6-10 cardiac cycles, and in the presence of arrhythmia, much more - on a long tape.

Normal electrocardiogram

On a normal ECG, 6 waves are distinguished, designated by the letters of the Latin alphabet: P, Q, R, S, T, U. The electrocardiogram curve (Fig. 1) reflects the following processes: atrial systole (P wave), artioventricular conduction (P-R interval or, as it was previously designated as the P-Q interval), ventricular systole (QRST complex) and diastole - the interval from the end of the T wave to the beginning of the P wave. All waves and intervals are characterized morphologically: the teeth - by height (amplitude), and the intervals - by time duration, expressed in milliseconds. All intervals are frequency-dependent quantities. The relationship between heart rate and the duration of one or another interval is given in the corresponding tables. All elements of a standard electrocardiogram have a clinical interpretation.

Electrocardiogram analysis

The analysis of any ECG should begin with checking the correctness of its recording technique: to exclude the presence of various interferences that distort the ECG curve (muscle tremors, poor contact of electrodes with the skin), it is necessary to check the amplitude of the control millivolt (it should correspond to 10 mm). The distance between the vertical lines is 1 mm, which corresponds to 0.02 s when the belt moves at a speed of 50 mm/s, and 0.04 s at a speed of 25 mm/s. In pediatric practice, a speed of 50 mm/s is preferable, since against the background of physiological age-related tachycardia, errors are possible when calculating intervals at a tape speed of 25 mm/s.

In addition, it is advisable to take an ECG with a change in the patient’s position: in the wedge- and orthoposition, since in this case a change in the nature of autonomic support can contribute to a change in some parameters of the electrocardiogram - a change in the characteristics of the pacemaker, a change in the nature of the rhythm disturbance, a change in heart rate, a change in characteristics conductivity

The general scheme of ECG analysis includes several components.

• Heart rate and conduction analysis:
  - determination of the source of excitation;
  - counting the number of heartbeats;
  - assessment of the regularity of heart contractions;
  - assessment of the conductivity function.
• Determination of heart rotations around the anteroposterior and longitudinal transverse axes:
  - position of the electrical axis of the heart in the frontal plane (rotations around the anteroposterior axis, sagittal);
  - rotation of the heart around the longitudinal axis;
  - rotations of the heart around the transverse axis.
• Analysis of the atrial P wave.
• Analysis of the ventricular QRST complex:
  - analysis of the QRS complex;
  - analysis of the RS-T segment;
  - T wave analysis;
  - analysis of the Q-T interval.
• Electrocardiographic report.

Heart rate and conduction analysis

The source of excitation is determined by determining the polarity of the P wave and its position relative to the QRS complex. Sinus rhythm is characterized by the presence in standard lead II of positive P waves preceding each QRS complex. In the absence of these signs, a non-sinus rhythm is diagnosed: atrial, rhythm from the AV junction, ventricular rhythms (idioventricular), atrial fibrillation.

Counting the number of heartbeats is carried out using various methods. The most modern and simplest method is counting using a special ruler. If this is not available, you can use the following formula:

Heart rate = 60 R-R,

where 60 is the number of seconds in a minute, R-R is the duration of the interval, expressed in seconds.

If the rhythm is incorrect, you can limit yourself to determining the minimum and maximum heart rate, indicating this spread in the “Conclusion”.

The regularity of heartbeats is assessed by comparing the duration of R-R intervals between successively recorded cardiac cycles. The R-R interval is usually measured between the tips of the R (or S) waves. The spread of the obtained values ​​should not exceed 10% of the average duration of the R-R interval. It has been shown that sinus arrhythmia of varying severity is observed in 94% of children. Conventionally, V degrees of sinus arrhythmia severity are distinguished:

I degree - there is no sinus arrhythmia or fluctuations in heart rate per 1 minute do not exceed 5 contractions;

II degree - mild sinus arrhythmia, rhythm fluctuations within 6-10 contractions per 1 minute;

III degree - moderately severe sinus arrhythmia, rhythm fluctuations within 11-20 contractions per 1 minute;

IV degree - pronounced sinus arrhythmia, rhythm fluctuations within 21-29 contractions per 1 minute;

V degree - pronounced sinus arrhythmia, rhythm fluctuations within 30 or more contractions per minute. Sinus arrhythmia is a phenomenon inherent in healthy children of all ages.

In addition to physiologically observed sinus arrhythmia, abnormal (irregular) heart rhythm can be observed with various types of arrhythmias: extrasystole, atrial fibrillation and others.

Assessing conduction function requires measuring the duration of the P wave, which characterizes the speed of conduction of the electrical impulse through the atria, the duration of the P-Q (P-R) interval (conduction speed through the atria, AV node and His system) and the total duration of the ventricular QRS complex (conduction of excitation through the ventricles). An increase in the duration of intervals and waves indicates a slowdown in conduction in the corresponding part of the conduction system of the heart.

The P-Q interval (P-R) corresponds to the time it takes for an impulse to travel from the sinus node to the ventricles and varies depending on age, gender and heart rate. It is measured from the beginning of the P wave to the beginning of the Q wave, and in the absence of a Q wave, to the beginning of the R wave. Normal fluctuations in the P-R interval are between 0.11-0.18 s. In newborns, the P-R interval is 0.08 s, in infants - 0.08-0.16 s, in older ones - 0.10-0.18 s. Slowing of atrioventricular conduction may be due to vagal influence.

The P-R interval may be shortened (less than 0.10 s) as a result of accelerated impulse conduction, innervation disorders, due to the presence of an additional fast conduction path between the atria and ventricles. Figure 3 shows one of the options for shortening the P-R interval.

This electrocardiogram (see Fig. 2) reveals signs of the Wolff-Parkinson-White phenomenon, including: shortening of the P-R interval to less than 0.10 s, the appearance of a delta wave on the ascending limb of the QRS complex, deviation of the electrical axis of the heart to the left. In addition, secondary ST-T changes may be observed. The clinical significance of the presented phenomenon lies in the possibility of the formation of supraventricular paroxysmal tachycardia by the re-entry mechanism (re-entry of the impulse), since additional pathways have a shortened refractory period and are restored to conduct the impulse faster than the main path.

Determination of the position of the electrical axis of the heart

Rotations of the heart around the anteroposterior axis. It is customary to distinguish three conventional axes of the heart, as an organ located in three-dimensional space (in the chest).

The sagittal axis is anteroposterior, perpendicular to the frontal plane, passing from front to back through the center of mass of the heart. Turning counterclockwise along this axis brings the heart to a horizontal position (displacement of the electrical axis of the QRS complex to the left). Rotate clockwise to a vertical position (displacement of the QRS electrical axis to the right).

The longitudinal axis anatomically runs from the apex of the heart to the right venous opening. When rotated clockwise along this axis (viewed from the apex of the heart), most of the anterior surface of the heart is occupied by the right ventricle; when rotated counterclockwise, the left ventricle is occupied.

The transverse axis passes through the middle of the base of the ventricles perpendicular to the longitudinal axis. When rotating around this axis, a displacement of the heart is observed with the apex forward or the apex backward.

The main direction of the electromotive force of the heart is the electrical axis of the heart (EOS). Rotations of the heart around the conventional anteroposterior (sagittal) axis are accompanied by deviation of the EOS and a significant change in the configuration of the QRS complex in standard and enhanced unipolar limb leads.

Rotations of the heart around the transverse or longitudinal axes are referred to as so-called positional changes.

The determination of EOS is carried out using tables. To do this, compare the algebraic sum of the R and S waves in standard leads I and III.

There are the following options for the position of the electrical axis of the heart:

• normal position when the alpha angle is from +30° to +69°;
• vertical position - alpha angle from +70° to +90°;
• horizontal position - alpha angle from 0° to +29°;
• axis deviation to the right - alpha angle from +91° to +180°;
• axis deviation to the left - alpha angle from 0° to - 90°.

The nature of the location of the heart in the chest, and accordingly, the main direction of its electrical axis, is largely determined by the characteristics of the physique. Children with asthenic physique have a vertical position of the heart. In children with a hypersthenic constitution, as well as with a high position of the diaphragm (flatulence, ascites), it is horizontal, with a deviation of the apex to the left. More significant turns of the EOS around the anteroposterior axis, both to the right (more than +90°) and to the left (less than 0°), are usually caused by pathological changes in the heart muscle. A classic example of deviation of the electrical axis to the right is the situation with a ventricular septal defect or tetralogy of Fallot. An example of hemodynamic changes leading to deviation of the electrical axis of the heart to the left is aortic valve insufficiency.

An easier way to roughly determine the direction of the EOS is to find the limb lead in which the R wave is the highest (without an S wave or with a minimal S wave). If the maximum R wave in lead I is a horizontal position of the EOS, if in lead II it is normal, if in lead aVF it is vertical. Registration of the maximum R wave in lead aVL indicates a deviation of the EOS to the left, in lead III - a deviation of the EOS to the right, but if the maximum R wave is in lead aVR, the position of the EOS cannot be determined.

Atrial P wave analysis

P wave analysis includes: change in P wave amplitude; measurement of P wave duration; determination of P wave polarity; determination of the shape of the P wave.

The amplitude of the P wave is measured from the isoline to the top of the wave, and its duration is measured from the beginning to the end of the wave. Normally, the amplitude of the P wave does not exceed 2.5 mm, and its duration is 0.10 s.

Since the sinus node is located in the upper part of the right atrium between the mouths of the superior and inferior vena cava, the ascending part of the sinus node reflects the state of excitation of the right atrium, and the descending part reflects the state of excitation of the left atrium, and it is shown that the excitation of the right atrium occurs before the left by 0. 02-0.03 s. The normal P wave is rounded in shape, gently sloping, with symmetrical rise and fall (see Fig. 1). The cessation of atrial excitation (atrial repolarization) is not reflected on the electrocardiogram, as it merges with the QRS complex. In sinus rhythm, the direction of the P wave is positive.

In normosthenics, the P wave is positive in all leads except lead aVR, where all electrocardiogram waves are negative. The largest value of the P wave is in standard lead II. In individuals of asthenic physique, the size of the P wave increases in standard III and aVF leads, while in lead aVL the P wave may even become negative.

With a more horizontal position of the heart in the chest, for example in hypersthenics, the P wave increases in leads I and aVL and decreases in leads III and aVF, and in standard lead III the P wave may become negative.

Thus, in a healthy person, the P wave in leads I, II, aVF is always positive, in leads III, aVL it can be positive, biphasic or (rarely) negative, and in lead aVR it is always negative.

Ventricular QRST analysis

The QRST complex corresponds to the electrical systole of the ventricles and is calculated from the beginning of the Q wave to the end of the T wave.

Components of the electrical systole of the ventricles: the QRS complex itself, the ST segment, the T wave.

The width of the initial ventricular QRS complex characterizes the duration of excitation transmission through the ventricular myocardium. In children, the duration of the QRS complex ranges from 0.04 to 0.09 s, in infants - no wider than 0.07 s.

The Q wave is the negative wave before the first positive wave in the QRS complex. The Q wave can be positive only in one situation: congenital dextracardia, when it is facing upward in standard lead I. The Q wave is caused by the spread of excitation from the AV junction to the interventricular septum and papillary muscles. This most variable ECG wave may be absent in all standard leads. The Q wave must meet the following requirements: in leads I, aVL, V 5, V 6, not exceed 4 mm in depth, or 1/4 of its R, and also not exceed 0.03 s in duration. If the Q wave does not meet these requirements, it is necessary to exclude conditions caused by a deficiency of coronary blood flow. In particular, in children, an abnormal origin of the left coronary artery from the pulmonary artery (ALCA from PA or Bluntd-White-Garland syndrome) often appears as a congenital pathology of the coronary vessels. With this pathology, the “coronary” Q wave is most often persistently detected in lead aVL (Fig. 3).

The presented electrocardiogram (see Fig. 3) reveals a deviation of the electrical axis of the heart to the left. In lead aVL, the Q wave is 9 mm, with its height R = 15 mm, the duration of the Q wave is 0.04 s. At the same time, in standard lead I, the duration of the Q wave is also 0.04 s, in the same lead there are pronounced changes in the final part of the ventricular complex in the form of depression of the S-T interval. The suspected diagnosis of anomalous origin of the left coronary artery from the pulmonary artery was confirmed by echocardiography and then by coronary angiography.

At the same time, in infants, a deep Q wave may be in lead III, aVF, and in lead aVR the entire ventricular complex may have a QS appearance.

The R wave consists of ascending and descending knees, is always directed upward (except in cases of congenital dextracardia), reflects the biopotentials of the free walls of the left and right ventricles and the apex of the heart. The ratio of the R and S waves and the change in the R wave in the chest leads are of great diagnostic importance. In healthy children, in some cases, different sizes of the R wave are observed in the same lead - electrical alternans.

The S wave, like the Q wave, is an unstable negative ECG wave. It reflects a somewhat late coverage of excitation of distant, basal areas of the myocardium, supraventricular crests, conus arteriosus, and subepicardial layers of the myocardium.

The T wave reflects the process of rapid repolarization of the ventricular myocardium, i.e., the process of restoration of the myocardium or cessation of excitation of the ventricular myocardium. The state of the T wave, along with the characteristics of the RS-T segment, is a marker of metabolic processes in the ventricular myocardium. In a healthy child, the T wave is positive in all leads except aVR and V 1. In this case, in leads V 5, V 6, the T wave should be 1/3-1/4 of its R.

The RS-T segment - the segment from the end of the QRS (the end of the R or S wave) to the beginning of the T wave - corresponds to the period of full coverage of the ventricles by excitation. Normally, displacement of the RS-T segment up or down is permissible in leads V 1 -V 3 no more than 2 mm. In the leads most distant from the heart (in standard and unipolar from the limbs), the RS-T segment should be on the isoline, with a possible upward or downward displacement of no more than 0.5 mm. In the left chest leads, the RS-T segment is recorded on the isoline. The transition point of the QRS to the RS-T segment is designated as the RS-T junction point j (junction).

The T wave is followed by a horizontal T-P interval, corresponding to the period when the heart is at rest (diastole).

The U wave appears 0.01-0.04 s after the T wave, has the same polarity and ranges from 5 to 50% of the height of the T wave. To date, the clinical significance of the U wave has not been clearly defined.

Q-T interval. The duration of ventricular electrical systole has important clinical significance, since a pathological increase in ventricular electrical systole may be one of the markers of the appearance of life-threatening arrhythmias.

Electrocardiographic signs of hypertrophy and overload of the heart cavities

Cardiac hypertrophy is a compensatory adaptive reaction of the myocardium, expressed in an increase in the mass of the heart muscle. Hypertrophy develops in response to increased stress in the presence of acquired or congenital heart defects or with increased pressure in the pulmonary or systemic circulation.

Electrocardiographic changes in this case are caused by: an increase in the electrical activity of the hypertrophied part of the heart; slowing down the conduction of an electrical impulse through it; ischemic, dystrophic and sclerotic changes in the altered heart muscle.

However, it should be noted that the term “hypertrophy” widely used in the literature does not always strictly reflect the morphological essence of the changes. Often, dilatation of the heart chambers has the same electrocardiographic signs as hypertrophy, with morphological verification of the changes.

When analyzing the ECG, the transition zone (Fig. 4) in the precordial leads should be taken into account.

The transition zone is determined by the lead in which the R and S waves, i.e., their amplitude on both sides of the isoelectric line, are equal (see Fig. 4). In healthy older children, the QRS transition zone is usually determined in leads V 3, V 4. When the ratio of vector forces changes, the transition zone moves towards their predominance. For example, with right ventricular hypertrophy, the transition zone moves to the position of the left precordial leads and vice versa.

Signs of atrial overload

Electrocardiographic signs of left atrium overload form an electrocardiographic complex of signs, called P-mitrale in the literature. Enlargement of the left atrium is a consequence of mitral regurgitation with congenital, acquired (due to rheumatic carditis or infective endocarditis), relative mitral regurgitation or mitral stenosis. Signs of left atrium overload are presented in Figure 5.

Enlargement of the left atrium (see Fig. 5) is characterized by:

• an increase in the total duration (width) of the P wave by more than 0.10 s;
• widened double-humped P wave in leads I, aVL, V 5 -V 6;
• the presence of a pronounced negative phase of the P wave in lead V 1 (more than 0.04 s in duration and more than 1 mm in depth).

Since the lengthening of the P wave can be caused not only by an increase in the left atrium, but also by intra-atrial blockade, the presence of a pronounced negative phase of the P wave in lead V 1 is more important when assessing overload (hypertrophy) of the left atrium. At the same time, the severity of the negative phase of the P wave in lead V 1 depends on the heart rate and on the general characteristics of the wave voltage.

Electrocardiographic signs of overload (hypertrophy) of the right atrium form a complex of signs called P-pulmonale, since it develops in pulmonary pathology, as well as in chronic pulmonary heart disease. However, these conditions are uncommon in children. Therefore, the main causes of enlargement of the right atrium are congenital heart defects, such as Ebstein's tricuspid valve anomaly, as well as primary changes in the pulmonary artery - primary pulmonary hypertension.

Signs of right atrium enlargement are presented in Figure 6.

Enlargement of the right atrium (see Fig. 6) is characterized by:

• a high-amplitude P wave with a pointed apex in leads II, III, aVF, this sign is required in lead V 1 or V 2;
• P wave duration not exceeding 0.10 s.

In Figure 6, in addition to signs of right atrium overload, there are also signs of right ventricular overload.

Signs of ventricular overload (hypertrophy)

Since the ECG normally reflects the activity of only the left ventricle, electrocardiographic signs of left ventricular overload emphasize (exaggerate) the norm. Where the R wave is normally high (in lead V 4, the position of which coincides with the left border of the heart), it becomes even higher; where the S wave is normally deep (in lead V 2), it becomes even deeper.

Many voltage criteria for overload (hypertrophy) of the left ventricle have been proposed - more than 30. The most well-known include the Sokolov-Lyon index: the sum of the amplitudes of the R wave in lead V 5 or V 6 (where it is greater) and S in lead V 1 or V 2 ( where more) more than 35 mm. However, the amplitude of the waves in the precordial leads is influenced by the gender, age and constitution of the patient. Thus, an increase in the voltage of the teeth can be observed in thin young people. Therefore, secondary changes in the final part of the ventricular complex are of great importance: displacement of the S-T interval and the T wave. As a sign of a relative deficiency of coronary blood flow, a deepening of the Q wave in leads V 5, V 6 is possible. But at the same time, the Q wave should not exceed more than 1/4 of its R and 4 mm in depth, since this sign indicates primary coronary pathology.

Predominant dilatation of the left ventricle has the following characteristics: R in V 6 is greater than R in V 5, greater than R in V 4 and more than 25 mm; sudden transition from deep S waves to high R waves in the precordial leads; shift of the transition zone to the left (towards V 4) (Fig. 7).

Signs of predominant hypertrophy of the left ventricular myocardium are depression (displacement below the isoline) of the S-T segment in lead V 6, possibly also in V 5 (Fig. 8).

Electrocardiographic signs of overload (hypertrophy) of the right ventricle appear when its mass increases by 2-3 times. The most reliable sign of right ventricular hypertrophy is the qR complex in lead V 1.

Additional signs are secondary changes in the form of displacement of the S-T segment and changes in the T wave. In some pathological conditions, in particular with an atrial septal defect, right ventricular hypertrophy is also demonstrated by incomplete blockade of the right bundle branch in the form of rsR in lead V 1 (Fig. 9) .

In conclusion, a standard electrocardiogram is very important for an adequate diagnosis, subject to several rules. This is, firstly, taking an electrocardiogram with a change in body position, which makes it possible to initially differentiate organic and inorganic damage to the heart. Secondly, this is the choice of the optimal shooting speed - for children 50 mm/s. Finally, the electrocardiogram should be analyzed taking into account the individual characteristics of the child, including his constitution.

For questions regarding literature, please contact the editor.

The editors apologize for typos

In the output of the article “Foot and Mouth Disease”, No. 8 2004, you should read:

A. E. Kudryavtsev, Candidate of Medical Sciences, Associate Professor,
T. E. Lisukova, Candidate of Medical Sciences, Associate Professor,
G. K. Alikeeva, Candidate of Medical Sciences
Central Research Institute of Epidemiology, Ministry of Health of the Russian Federation, Moscow

In the article by I. Yu. Fofanova “Some issues of the pathogenesis of intrauterine infections”, No. 10.2004. On page 33 in the 2nd column from left to right you should read: “In the second trimester (after clarification of the diagnosis), the use of antibacterial therapy is indicated, taking into account the sensitivity of antibiotics (penicillin or macrolides). Prescription of amoxiclav, augmentin, ranklav, azitrox, sumamed during pregnancy is possible only when the expected benefit to the mother outweighs the potential risk to the fetus or child. Despite the fact that experimental studies have not revealed the teratogenic effects of these drugs, their use during pregnancy should be avoided.”

E. V. Murashko,Candidate of Medical Sciences, Associate Professor, Russian State Medical University, Moscow

In the book "Eye of Revelation" Colonel Bradford indicates clockwise rotation:

“The First Ritual,” said the colonel, “is quite simple. It is intended to accelerate the movement of the Whirlwinds. As children, we used this in our games. Your actions: stand straight, with your arms extended horizontally along your shoulders. Begin to spin around your axis until you feel slight dizziness. One warning: you must rotate from left to right. In other words, if you place the watch on the floor with the dial facing up, your hands should move in the direction of the hands."

Note that Colonel Bradford defines the "clockwise" direction as the direction in which a person rotates from left to right, regardless of his location on the planet.

Given that Bradford was in the northern hemisphere when he wrote that you need to rotate from left to right (clockwise), some people wonder whether to adapt his instructions and rotate counterclockwise while in the southern hemisphere.

When I ask them: " Why do you think we should change the direction of rotation?"

Their answer is usually along the lines of " Water in the southern hemisphere swirls counterclockwise, while in the northern hemisphere it swirls clockwise.".

However, this concept itself is based on a popular misconception, and therefore the reason for the change in direction of rotation is also not convincing.

Alistair B. Fraser Ph.D., Professor Emeritus of Meteorology, Penn State University, USA, explains in detail:

"Compared to the rotations we see every day (car tires, CDs, sink drains), the Earth's rotation is almost imperceptible - only a revolution per day. Water in a sink rotates in a few seconds, so its rotation speed is ten thousand times higher than that of the Earth. This is not surprising, given that the Coriolis force is several orders of magnitude smaller than any of the forces involved in these everyday examples of rotation. The Coriolis force is so small that it affects the direction of rotation of water no more than the direction of rotation of a compact particle. disk.

The direction of rotation of the water in the sink drain is determined by how it was filled, or what turbulence was created in it during washing. The size of these rotations is small, but compared to the rotation of the Earth, it is simply huge."

It is difficult to describe the Coriolis effect in more detail without resorting to mathematical equations or complex concepts such as angular mechanics. First of all, our frame of reference is: “ What we see depends on where we are" This means that we are standing on a solid surface, when in fact this is not the case - after all, the earth is a rotating ball.

Coriolis effect

In physics Coriolis effect is the obvious deviation of moving objects when viewed from a rotating frame of reference. As an example, consider two children on opposite sides of a rotating carousel throwing a ball to each other (Figure 1). From these children's point of view, the ball's path is bent sideways by the Coriolis effect. From the thrower's perspective, this deflection is directed to the right as the carousel rotates counterclockwise (as viewed from above). Accordingly, when moving clockwise, the deflection is directed to the left.

If you are really interested in a detailed explanation of the Coriolis effect, enter “Coriolis effect” into a search engine and study this issue thoroughly.

Direction of chakra rotation

Peter Kalder did not describe the direction of movement of the vortices (chakras):

“The body has seven centers, which can be called Vortexes. They are a kind of magnetic centers. In a healthy body they rotate at high speed, and when their rotation slows down, this can be called old age, illness or decline. The fastest way to restore youth, health and vitality is to make these vortices spin again at the same speed. There are five simple exercises to achieve this goal. Any one of them is useful on its own, but all five are needed to get the best results. Lamas call them rituals, and I will treat them the same way.” - Peter Kalder, edited by Alina and Mikhail Titov, “The Eye of Revelation”, 2012.

I wonder if Calder deliberately avoided mentioning the counterclockwise direction? According to Barbara Ann Brennan, a former NASA scientist and authority on human energy, healthy chakras should rotate clockwise; and closed, unbalanced ones are counterclockwise.

In her successful book, Hands of Light, she says:

"When the chakras are functioning normally, each of them will be open and will rotate clockwise to absorb the specific energy needed from the global field. Rotating clockwise to receive energy from the Global Energy Field into the chakras is similar to the right hand rule in electromagnetism, which states, that a change in the magnetic field around a wire will cause a current in that wire.

When the chakras rotate counterclockwise, there is an outflow of energy from the body, causing metabolic disorders. In other words, when the chakra rotates counterclockwise, we do not receive the energy we need, which we perceive as psychological reality. Such a chakra is considered closed to incoming energy."

Possible influences of traditions

(a) Traditional Tibetan "trul-hor" yantra yoga

Chogal Namhai Norbu, one of the great masters of Dzogchen and Tantra, was born in Tibet in 1938. His book " Yantra Yoga: Tibetan Yoga of Movement"Published by the publishing house "Snow Lion".

"Trul-hor" means "magic wheel", says Alejandro Chaul-Reich, a faculty member at the Ligmincha Institute and an assistant professor at the University of Texas Medical School. He says:

"The characteristic trul-hor movements arose from the deep meditation practices of Tibetan yoga practitioners. Traditionally practiced in remote Himalayan caves and monasteries, trul-hor movements are now available to serious Western students. They are a powerful cleansing tool, balancing and harmonizing the subtle aspects of your energetic dimension."

Ryan Parker specialist in Five Tibetan Rituals, is currently conducting research comparing the Five Rituals and the Trul-Hor. According to Peter Kelder in The Eye of Revelation, the rituals, like the trul-khor, date back about 2,500 years.

In his latest Comparative Table he states:

"The Buddhist trul-hor suggests the existence of energy centers that rotate clockwise. The "trul-hor" is sometimes called a stimulus for the rotation of energy centers. Moreover, they begin to rotate in unison. Although this rotation can be caused in many ways, the rotation of the body is special associated with the stimulation of the centers. Clockwise rotation is considered beneficial, and is the suggested direction of rotation in the Buddhist "trul-hor."

(b) Pradakshina

Throughout history, Tibet and India exchanged ancient knowledge, and it is possible - but not proven - that the First Ritual may have been influenced by the practice of Pradakshina.

In Hinduism Pradakshina means the act of worship - walking clockwise around a holy place, temple, shrine. Dakshina means right, so you go to the left, with the spiritual object always on your right.

During Pradakshina, you walk clockwise around a temple, shrine, person, mountain, place or even yourself. Hindu temples even have special passages so that people can perform these movements around them in a clockwise direction.

The purpose of such circular movements is to focus or purify oneself, or to honor the object of worship.

Circling is so common that it is found in the cultures of the Greeks, Romans, Druids and Hindus. This is usually associated with a sacrifice or purification process. The interesting thing is that for all these cultures the direction of movement is always the same - clockwise!

Other interesting facts about clockwise rotation

During one of my classes, a dance teacher told me that children are initially taught to spin in a clockwise direction. Obviously, it's easier for them (although there are exceptions). He said it was well known among dance teachers - If you need to calm children down, make them spin counterclockwise. And so that activate them - let them circle clockwise!

This energetic effect is exactly what people experience when performing Ritual No. 1, as described by Colonel Bradford. It seems to me that if the lamas gave instructions to rotate clockwise, then this is how it should be!

Who practices counterclockwise rotation

However, I know a certain Marina who rotates counterclockwise due to a life-threatening health condition that she is trying to correct. She is very committed to meeting her body's needs, as you can read below:

"According to Qi Gong and Traditional Chinese Medicine, clockwise movement speeds up life processes by increasing the speed of movement of the chakras to the original. Counterclockwise movement slows down the chakras. Most of those who practice rituals want to speed up chakras that have slowed down due to age, weight and so on, because it is logical that they rotate clockwise. However, one day, during morning prayer, I realized that in my case, the acceleration of the chakras would only have negative consequences, since the chakra affecting my lungs was incapable of acceleration. So, I started spinning counterclockwise, and soon I noticed that it became easier to perform other rituals!”

To summarize, until documents or teachers are found, all attempts to understand the motives of Ritual No. 1 will only be theoretical. Therefore, you should do what you personally feel is good for you!

The position of the heart relative to the longitudinal axis, conventionally drawn through the apex and base of the heart, is assessed by the configuration of the QRS complexes in the chest leads, that is, in the horizontal plane. The following are used as visual references:

1) location of the transition zone,

2) the presence of Q and S waves in lead V6.

There are the following options for the position of the heart in the horizontal plane:

1. Normal position (Fig. 34).

Rice. 34. Normal position of the heart in the horizontal plane. Visual features: transition zone (ZZ) in V3; Q and S waves in V6.

2. Rotation of the heart around the longitudinal axis clockwise (Fig. 35).

Rice. 35. Rotation of the heart around its longitudinal axis clockwise. Visual features: transition zone in V4–V5; The q wave is absent in V6, the S wave is present in V6.

3. Rotation of the heart around the longitudinal axis counterclockwise (Fig. 36).

Rice. 36. Rotation of the heart around its longitudinal axis counterclockwise. Visual signs: transition zone in V1–V3, q wave present in V6, S wave absent in V6.

Determination of heart rotation around the transverse axis.

There are rotations of the heart around the transverse axis with the apex forward and backward. As visual signs, an assessment of the QRS complex in standard leads I, II, III is used, namely the presence of Q and S waves in it.

The position of the heart relative to the transverse axis may be normal, and anterior to posterior rotation of the apex of the heart is also noted.

1. Normal position of the heart relative to the transverse axis (Fig. 37).

Rice. 37. Configuration of the QRS complex in standard leads with a normal position of the heart relative to the transverse axis. Visual signs: the presence of small q and S waves in leads I, II, III or only in one or two of the three leads.

2. Rotation of the heart around the transverse axis with the apex anterior (Fig. 38).

Rice. 38. Configuration of the QRS complex in standard leads when the heart is rotated around the transverse axis with the apex anterior. Visual signs: the presence of q waves in standard leads I, II, III in the absence of an S wave in the same leads.

3. Rotation of the heart around the transverse axis with the apex posteriorly (Fig. 39).

Rice. 39. Configuration of the QRS complex in standard leads when the heart is rotated around the transverse axis with the apex posteriorly. Visual signs: the presence of S waves in standard leads I, II, III in the absence of a q wave in the same leads.

Select one or more correct answers.

1. LEAD WHEN ELECTRODES ARE POSITIONED ON THE FOREARMS IS DESIGNATED AS

2. LEAD WHEN ELECTRODES ARE POSITIONED ON THE RIGHT ARM AND LEFT LEG IS DESIGNATED AS

3. LEAD WHEN ELECTRODES ARE POSITIONED ON THE LEFT ARMS AND LEFT LEG IS DESIGNATED AS

4. REINFORCED SINGLE PLUS LIMBS LEAD ARE DESIGNATED AS

5. THE P WAVE ON THE ECG REFLECTS THE PROCESS

1) passage of excitation through the sinus node

2) passage of excitation from the sinus node to the right atrium

3) excitation of both atria

4) passage of excitation from the atria to the right ventricle

5) spread of excitation through the atria, AV node and ventricles

6. NORMAL P WAVE DURATION AND AMPLITUDE IS

1) 0.066-0.10 s and 0.5-2.5 mm

2) 0.10-0.14 s and 0.5-1 mm

2) 0.12-0.16 s and 2-3 mm

4) 0.16-0.20 s and 3-4 mm

7. P-Q INTERVAL ON ECG REFLECTS THE PROCESS

1) passage of excitation through the atria

2) spread of excitation along the interventricular septum

3) spread of excitation through the left ventricle

4) passage of excitation through the atria and AV junction

8. NORMAL P-Q DURATION IS

9. QRS COMPLEX ON ECG REFLECTS THE PROCESS

1) ventricular repolarization

2) excitation of both atria

3) propagation of excitation along the AV junction to the ventricles

4) spread of excitation through the right and left ventricles

10. ST SEGMENT ON ECG REFLECTS THE PROCESS

1) atrial repolarization

2) depolarization of both ventricles

3) ventricular repolarization

4) depolarization of the atria and ventricles

Chapter 3
Electrocardiogram for myocardial hypertrophy

Hypertrophy of the atria or ventricles develops with their prolonged hyperfunction. Hypertrophy of a particular part of the heart refers to an increase in the mass and number of muscle fibers. General patterns of ECG changes during hypertrophy include:

1) increase in EMF of the corresponding part of the heart;

2) an increase in the excitation time of the hypertrophied part of the heart, which is manifested by a slight increase in the impulse conduction time, i.e., conduction disturbance, which is facilitated by the associated dilatation of the heart;

3) impaired repolarization of the corresponding part of the heart due to relative coronary insufficiency, the development of dystrophy and sclerosis;

4) a change in the position of the heart in the chest due to a change in the direction of the excitation wave in the hypertrophied part of the myocardium.

Thus, with cardiac hypertrophy, ECG changes can be caused by one or several factors at once, the most important of which are:

1) hypertrophy itself;

2) dilation accompanying hypertrophy;

3) conduction disturbance due to hypertrophy and (or) dilatation;

4) change in the location of the heart in the chest cavity.

The lack of a clear correlation between ECG changes and the mass of the heart, including its parts, led to the use, along with the term “hypertrophy,” of the term “enlargement.” However, it is customary to prefer the term “hypertrophy”.

ATRIAL HYPERTROPHY

Atrial hypertrophy can be isolated, that is, affect only the left or RA, or combined.

RA hypertrophy

With RA hypertrophy, its EMF increases. The duration of excitation of the RA exceeds the norm, while the excitation of the LA remains within the latter. In Fig. Figure 40 shows a diagram of the formation of the P wave in normal conditions and with RA hypertrophy.

Rice. 40. Formation of P waves in normal conditions and with RA hypertrophy. Explanation in the text.

Normally, the P wave consists of two components, the 1st component is caused by excitation of the PP. The 2nd component occurs 0.02 s later than the first and is associated with LA excitation. Layering on top of each other, both components form a single P wave, where the ascending part reflects the excitation of the RA, and the descending part, respectively, the left one. A two-humped P wave is allowed, but the time between the peaks of individual components should not exceed 0.02 s.

With RA hypertrophy, the vector of excitation of this part of the heart increases, which leads to an increase in the amplitude and duration of the first component of the P wave. The second part of the P wave, associated with excitation of the LA, is not changed compared to the norm. As a result of the addition of the excitation vectors of the right and LA, a single pointed P wave is formed, which is usually called “P-pulmonale”. In this case, the total duration (width of the P wave) of atrial excitation does not exceed normal values.

In Fig. Figure 41 shows the mechanism of formation of the P wave in the right chest lead (V1) normally and with RA hypertrophy.

Fig.41. Formation of a biphasic P wave in lead V1 in normal conditions and with RA hypertrophy. Explanation in the text.

Normally, in the chest lead V1, the P wave is in most cases biphasic (+/–). Its first, positive, phase is due to the excitation of the RA, and the second, negative, phase is due to the excitation of the LP. This is due to the fact that when the RA is excited, the excitation vector is directed towards the positive electrode of a given lead, and when the LA is excited, towards the negative. In this case, the width and amplitude of both phases of the wave are the same.

With RA hypertrophy, the vector of its excitation increases, which leads to an increase in the amplitude of the first positive phase of the P wave. As a result, the latter becomes asymmetrical with a predominance of the first positive phase.

Thus, the most important sign of RA hypertrophy is the formation of a high-amplitude, pointed P wave (more than 2–2.5 mm) with its duration maintained (a slight increase to 0.11–0.12 s is allowed). This is most often found in leads II, III, aVF, and in the presence of a biphasic P wave in the right chest leads, its asymmetry with a predominance of the positive phase is revealed.

Other signs of RA hypertrophy include:

1) deviation of the electrical axis of the atria to the right, namely PIII > PII > PI (with normal PII > PI > PIII);

2) an increase in the activation time of the PP by more than 0.04 s (this indicator is measured by the time from the beginning of the P wave to its apex);

3) a decrease in the Macruse index to less than 1.1 (the Macruse index represents the ratio of the duration of the P wave to the duration of the PQ segment and is normally equal to 1.1–1.6);

4) an indirect sign is a violation of the relationship between the P and T waves in leads II, III, aVF according to the type: PI, III, aVF > TII, III, aVF (with PII normal , III, aVF< TII, III, aVF).

In Fig. 42 shows an ECG of a patient with RA hypertrophy.

Rice. 42. ECG for RA hypertrophy. High pointed tooth PII, III, aVF. In lead VI, the P wave is asymmetrical with a predominance of the positive phase.

“P-pulmonale” is most often noted with:

1) chronic specific and nonspecific lung diseases (chronic bronchitis, bronchial asthma, pneumosclerosis, emphysema, fibrosing alveolitis, tuberculosis, pneumoconiosis, etc.), leading to the development of chronic pulmonary heart disease;

2) pulmonary hypertension;

3) congenital and acquired heart defects with overload of the right parts;

4) repeated thromboembolism into the pulmonary artery system.

In cases where changes characteristic of RA hypertrophy appear on the ECG after an acute situation (acute pneumonia, an attack of bronchial asthma, pulmonary edema, myocardial infarction, pulmonary embolism), it is customary to use the term “overload” of the RA. Usually these signs disappear after acute clinical symptoms subside. It is also customary to talk about overload of the PP when we are talking about diseases in which hypertrophy of this part of the heart usually does not develop (chronic ischemic heart disease, thyrotoxicosis, diabetes mellitus, etc.).

LA hypertrophy

With LA hypertrophy, the EMF associated with the excitation of this part of the heart increases. This leads to an increase in the vector of excitation of the LA and the duration of its excitation while maintaining the magnitude and duration of excitation of the PP. As can be seen in Fig. 43, the first component of the P wave, associated with excitation of the PP, does not differ from the norm. The second part of the P wave, caused by the excitation of the hypertrophied LA, is increased in amplitude and duration. As a result, a double-humped wide P wave is formed. In this case, the second peak exceeds the first in amplitude. This wave is called “P-mitrale” because it is most often found in mitral stenosis.

Rice. 43. Formation of P waves in normal conditions and in LA hypertrophy.
Explanation in the text.

The formation of the P wave during LA hypertrophy in the right chest lead (VI), where a two-phase wave is usually normally formed, is shown in Fig. 44.

Rice. 44. Formation of a biphasic P wave in lead VI in normal conditions and with LA hypertrophy. Explanation in the text.

The LA excitation vector is directed from the V1 electrode towards its negative pole, which causes, following the positive phase of the P wave due to the excitation of the PP, the appearance of a deep and wide negative phase of this wave. As a result, a two-phase (+/–) PVI wave is formed with a sharp predominance of the second negative phase. The width of the second negative phase of the P wave is usually increased due to longer excitation of the LA.

Thus, the most significant sign of LA hypertrophy is the formation of a wide and double-humped P wave (P width exceeds 0.10–0.12 s), which is most pronounced in leads I, II, aVL, V5, V6. In the right chest leads, in the presence of a biphasic P wave, this pathology will be indicated by the predominance of the second negative phase.

Other signs of LA hypertrophy include:

1) deviation of the electrical axis of the atria to the left or its horizontal position, namely PI > PII > PIII (with the norm being PII > PI > PIII);

2) an increase in LA activation time of more than 0.06 s (this indicator is measured by the time from the beginning of the P wave to its second peak or the highest point of the P wave);

3) an increase in the Makruse index of more than 1.6.

In Fig. 45 shows an ECG of a patient with LA hypertrophy.

Rice. 45. ECG for LA hypertrophy. A wide double-humped P wave is recorded in leads I, II, V5, V6. V1 with a predominance of the negative phase. PaVR is wide and negative.

“P-mitrale” are most often noted with:

1) mitral stenosis;

2) mitral insufficiency;

3) aortic heart defects;

4) congenital heart defects with overload of the left parts;

5) hypertension;

6) cardiosclerosis.

When a wide double-humped P wave appears on the ECG after an acute situation (hypertensive crisis, myocardial infarction, acute left ventricular failure, etc.), it is interpreted as a sign of LA overload. It is believed that such changes disappear as the clinical manifestations of these disorders subside.

Hypertrophy of both atria

With hypertrophy of both atria, the excitation vectors of the right and left atria increase, which leads to the appearance on the ECG of signs of hypertrophy of both parts of the heart. RA hypertrophy is usually recorded in leads III and aVF in the form of a high, pointed P wave. LA hypertrophy is better reflected in leads I, aVL, V5, V6, where a wide double-humped P wave is recorded. With combined atrial hypertrophy, the duration of the P wave increases in all leads.

The ECG in lead V1 is of greatest importance for recognizing hypertrophy of both atria. As shown in Fig. 46, due to combined hypertrophy, the excitation vectors of the right and left at the same time increase. This leads to a pronounced increase in the first and second components of the P wave.

Rice. 46. Formation of the P wave in lead V1 in normal conditions and in hypertrophy of both atria. Explanation in the text.

As a result, a P wave is recorded in leads V1 or V2 and V3 with a pronounced first positive and second negative phase. The first positive, pointed, high-amplitude phase is caused by the excitation of the hypertrophied PP. The second negative, wide phase is associated with LA hypertrophy (Fig. 46).

Another sign of hypertrophy of both atria is an increase in the activation time of the right and LA (for the RA more than 0.04 s, for the LA - 0.06 s).

In practice, instead of the term “hypertrophy of both atria,” the concepts of “enlargement of both atria” or “combined atrial hypertrophy” can be used.

Hypertrophy of both atria is most often observed with:

1) mitral-tricuspid heart defects;

2) aortic-tricuspid heart defects;

3) congenital heart defects with overload of both halves;

4) a combination of chronic nonspecific lung diseases, accompanied by cor pulmonale and hypertension, ischemic heart disease, and cardiosclerosis.

In Fig. 47 shows an ECG with hypertrophy of both atria.

If after an acute situation (myocardial infarction, pulmonary edema, etc.) changes in the P wave appear on the ECG, characteristic of hypertrophy of both atria, they are usually designated by the term “overload of both atria.” This conclusion will be supported by the normalization of the ECG as the clinical manifestations subside.

Rice. 47. ECG with hypertrophy of both atria. PI, II, V4–V6 wide serrated. R aVR wide double-humped negative. In V1, the P wave has pronounced positive and negative phases. PIII, aVF, V2 - high pointed.

VENTRICULAR HYPERTROPHY

Just like atrial hypertrophy, ventricular hypertrophy can be isolated, that is, either the left or right ventricle, as well as combined.

LV hypertrophy

With LV hypertrophy, its mass more than normally prevails over the mass of the RV. All this leads to an increase in the EMF and the excitation vector of the LV. The duration of excitation of the hypertrophied ventricle also increases due not only to its hypertrophy, but mainly due to the development of dystrophic and sclerotic changes in it.

The course of LV excitation during its hypertrophy is conventionally divided into stages that make it possible to understand the essence of the occurring phenomena.

Stage I of excitation occurs in the same way as normally and is caused by excitation of the left half of the interventricular septum, which, due to its hypertrophy, has an even more pronounced predominance of EMF than normal, in relation to its right half. The direction of the excitation vector of the septum in the frontal plane is oriented from left to right (Fig. 48). As a result, a positive wave is recorded in the right chest leads , whereas in the left pectorals, on the contrary, there is a negative q wave. This is explained by the fact that the direction of this vector is oriented towards the right chest leads, i.e. towards the positive electrode, while in relation to the left chest electrodes the vector is directed in the opposite direction, namely towards their negative pole.

Rice. 48. The course of excitation of the ventricular myocardium in stage I with LV hypertrophy.

Due to hypertrophy of the left half of the interventricular septum, the vector of its excitation is greater than normal. Therefore, the q wave in the left chest leads, in particular in V6, has a greater amplitude than normal, but is not pathological.

Stage II of excitation is characterized by further excitation of the interventricular septum, which, however, becomes electrically neutral and at this stage no longer affects the total vector of excitation of the heart. The determining vector at this stage is the vector of excitation of the right and hypertrophied LV. In this case, naturally, the LV excitation vector predominates, which determines the direction of the resulting vector from right to left (Fig. 49).

Rice. 49. The course of excitation of the ventricular myocardium in stage II with LV hypertrophy.

On the ECG at this stage, a deeper than normal S wave is recorded in the right chest lead (V1), while in the left chest lead (V6) a higher R wave. This is explained by the fact that the resulting vector is directed from the right chest leads to the side left chest leads, i.e. in lead V1 it is projected onto the negative side of the axis, and in lead V6 - respectively, onto the positive side. In this case, the width of the S wave in V1 and R wave in V6 is slightly larger than normal, due to the longer period of excitation of the hypertrophied LV.

In most cases, the process of excitation during LV hypertrophy is limited to these two stages, the analysis of which allows us to draw the following conclusions.

1. With LV hypertrophy, an ECG in the form of rS is recorded in the right precordial leads (V1, V2). The r wave in V1 is caused by the excitation of the left half of the interventricular septum. The S wave in V1 has a larger amplitude than normal, is somewhat wider and is associated with excitation of the hypertrophied LV.

2. With LV hypertrophy in the left precordial leads (V5, V6), the ECG looks like qR or occasionally qRS. The q wave in V6 is caused by the excitation of the left half of the hypertrophied interventricular septum, and therefore it has a larger amplitude than normal. The R wave in V6 is associated with the excitation of the hypertrophied LV, so it is somewhat wider and its amplitude is greater than normal. Occasionally, an S wave is recorded in lead V6 and the ECG looks like qRS. The S wave in these cases, as well as normally, is caused by excitation of the base of the LV.

The process of repolarization during LV hypertrophy occurs in the right ventricle in the same way as normally, i.e., it spreads from the epicardium to the endocardium. On the contrary, in a hypertrophied LV, the repolarization process begins, in contrast to normal conditions, from the endocardium and spreads to the epicardium. This is due to the fact that the process of repolarization in the LV during its hypertrophy begins, in contrast to the norm, during a period when excitation in the epicardium has not yet ended. This, in turn, is associated with a longer propagation of the excitation wave in the hypertrophied myocardium. As a result, the repolarization vectors of the right and LV during hypertrophy of the latter have the same orientation from left to right (Fig. 50).

Rice. 50. The process of repolarization during LV hypertrophy. Explanation in the text.

As a result, with LV hypertrophy in lead V1, ST segment elevation will be noted, since at the moment of termination of excitation in the LV, repolarization vectors of both ventricles directed to the positive part of the axis of this lead will act on the V1 electrode. On the contrary, at the moment of the end of excitation in the LV, electrode V6 is acted upon by the repolarization vectors of both ventricles, whose direction is projected onto the negative side of this lead. This leads to a displacement of the ST segment below the isoelectric line. The direction of the RV repolarization vector towards the active electrode of lead V1, reinforced by the LV repolarization vector, which has a similar direction, leads to the registration of a larger than normal positive T wave in this lead. The LV repolarization vector during its hypertrophy is directed from the positive pole of lead V6, and therefore a negative T wave is recorded in this lead. The T wave in V6 is asymmetrical, the greatest amplitude of its decrease is located at the end of the T wave. This is explained by the fact that the repolarization wave is gradually approaching to electrode V6, exerting its maximum effect at the end of this process, when the reduction wave is located in the immediate vicinity of electrode V6.

LV hypertrophy is mainly diagnosed based on visual analysis of the precordial ECG. For this, the following diagnostic signs are used:

1. High R wave in leads V5, V6 (it should be high and larger in amplitude than RV4):

a) a clear sign of LV hypertrophy is the sign
RV6 > RV5 > RV4;

b) with moderate LV hypertrophy, a sign is noted
RV4< RV5 >RV6.

2. Deep S wave in leads V1 and V3.

3. Shift of the ST interval below the isoline with a negative asymmetric T wave in V5, V6 and a slight elevation of the ST segment in V1, V2 in combination with a positive T wave.

4. Shift of the transition zone towards the right precordial leads.

5. TV1 > TV6 syndrome (normally the opposite) in the absence of coronary insufficiency.

6. Deviation of the EOS to the left (optional sign).

7. An increase in the activation time of the left ventricle in the left precordial leads above 0.04 s (this indicator is measured by the time from the beginning of the ventricular complex to the apex of the R wave in the corresponding lead).

Quantitative signs of LV hypertrophy (Janushkevicius Z.I., Shilinskaite Z.I., 1973) include two groups of signs (A and B).

Group A

1) deviation of the EOS to the left;

2) R1 > 10 mm;

3) S(Q)aVR > 14 mm;

4) TaVR > 0 for S(Q)aVR > RaVR;

5) RV5, VV6 > 16 mm;

6) RaVL > 7 mm;

7)TV5, V6< 1 мм при RV5, V6 >10 mm and TV1–V4 > 0 in the absence of coronary insufficiency;

8) TV1 > TV6, when TV1 > 1.5 mm.

Group B

1) R1 + SIII > 20 mm;

2) reduction of the ST1 segment down > 0.5 mm with R1 > S1;

3) T1< 1 мм при снижении ST1 >0.5 mm at R1 > 10 mm;

4) TaVL< 1 мм при снижении STaVL >0.5 mm and with RaVL > 5 mm;

5) SV1 > 12 mm;

6) SV1 + RV5(V6) > 28 mm in persons over 30 years of age or SV1 + RV5(V6) > 30 mm in persons under 30 years of age (Sokolov-Lyon sign);

7) QV4–V6 > 2.5 mm at Q< 0,03 с;

8) decrease in STV5,V6 > 0.5 mm with elevation of STV2–V4;

9) ratio R/TV5,V6 > 10 with TV5,V6 > 1 mm;

10) RaVF > 20 mm;

11) RII > 18 mm;

12) activation time of the left ventricle in V5, V6 > 0.05 s.

LV hypertrophy is diagnosed in the presence of:

1) 2 or more signs of group A,

2) 3 or more signs of group B,

3) one characteristic from group A and one characteristic from group B.

Electrocardiographic findings for LV hypertrophy:

1. If a high R wave in leads V5, V6 is combined with a decrease in the ST segment and a negative or reduced T wave in these leads, then we speak of LV hypertrophy with its overload (Fig. 51).

Rice. 51. ECG for LV hypertrophy with overload.

2. If, with high R in V5, V6, there are no changes in the ST segment and T wave, then they speak of LV hypertrophy (Fig. 52).

Rice. 52. ECG for LV hypertrophy.

3. If, with LV hypertrophy, a decrease in the ST segment and negative T waves are detected not only in leads V5, V6, but also in other leads, for example from V3 to V6, then in conclusion they write about LV hypertrophy with severe overload (Fig. 53) .

Rice. 53. ECG for LV hypertrophy with severe overload.

4. With more pronounced changes in the ST segment and T wave in the precordial leads (the appearance of deep negative or symmetrical T waves in V1–V6), in conclusion, they speak of LV hypertrophy with a violation of its blood supply or with a violation of the coronary circulation. At the same time, the area of ​​the myocardium is indicated where the disturbance in the myocardial blood supply or coronary circulation is predominantly localized (Fig. 54).

Rice. 54. ECG for LV hypertrophy with impaired coronary circulation in the anteroseptal region of the LV.

Pancreatic hypertrophy

RV hypertrophy is diagnosed using an ECG with great difficulty, especially in its initial stages. With RV hypertrophy, the EMF of this part of the heart and the vector of its excitation increases. The duration of ventricular excitation is prolonged. Simultaneously with RV hypertrophy, the right half of the interventricular septum hypertrophies. The position of the heart in the chest cavity changes.

There are several ECG options for pancreatic hypertrophy:

1) pronounced RV hypertrophy, in which the RV is larger than the LV (R-type);

2) The RV is hypertrophied, but it is smaller than the LV. In this case, excitation in the RV flows slowly, longer than in the LV (rSR¢-type);

3) moderate hypertrophy of the RV, when it is significantly smaller than the LV (S-type).

Excitation of the myocardium with pronounced hypertrophy of the right ventricle, when it is larger than the left ventricle (variant I) can be represented in the form of several stages.

Stage I of excitation. Due to the sharp hypertrophy of the RV and the right half of the interventricular septum, the mass of which prevails over its left half, the resulting vector of excitation of the interventricular septum is directed opposite to that under normal conditions, i.e. from right to left (Fig. 55).

Rice. 55. The course of excitation with pronounced hypertrophy of the pancreas in the first stage of excitation of the interventricular septum. Explanation in the text.

As a result, a q wave is recorded in lead V1, since the total excitation vector is directed in the direction opposite to the positive electrode of this lead. In contrast, a small r wave is formed in lead V6 due to the propagation of the excitation wave to the positive pole of this lead.

In stage II, the myocardium of the right and left ventricles is excited. In this case, as normally, the RV vector is directed from left to right, and the left one is directed vice versa, i.e. from right to left. However, since the mass of the RV myocardium is greater than that of the left, the resulting vector is directed from left to right (Fig. 56). This direction of the resulting vector towards the positive pole of lead V1 and negative V6 causes the appearance of a pronounced R wave in the right chest lead and an S wave in the left.

Rice. 56. The course of excitation with pronounced pancreatic hypertrophy in stage II. Explanation in the text.

Consequently, with pronounced RV hypertrophy in lead V1, the ECG usually looks like qR or R. The q wave in V1 is associated with the excitation of the hypertrophied interventricular septum, its right half. If there is no noticeable predominance of the vector of the right half of the interventricular septum over the vector of its left half, for example, when both vectors are approximately equal, then the q wave in V1 may be absent. The R wave in V1 is associated with excitation of the hypertrophied pancreas. In lead V6, the ECG usually looks like rS or Rs, less often RS with a deep S wave. The r(R) wave in V6 is caused by excitation of the right half of the interventricular septum and the initial excitation of the LV. The s(S) wave in V6 is recorded during depolarization of the hypertrophied RV. The greater the pancreatic hypertrophy, the greater the height of R in V1 and the deeper the S in V6 and the less r in V6 and vice versa.

The process of repolarization in the LV during severe RV hypertrophy proceeds as normal, i.e., the repolarization vector is directed from the endocardium to the epicardium, from right to left. The repolarization wave in the RV differs from the norm in that it comes from the endocardium during the period when its excitation at the epicardium has not yet ended, and, therefore, just like in the LV, the vector is oriented from right to left (Fig. 57). At the moment of the end of excitation in the ventricles, the ST segment in V1, V6 will not be located on the isoline as normal, since the electrodes V1 and V6 will record during this period the electric field of the recovery that has already begun in the right and LV. In this case, in lead V1 the ST segment will be located below the isoline, since the repolarization vector is directed towards the negative pole of this electrode. On the contrary, the ST segment will be located above the isoline in lead V6, towards the positive pole of which the resulting repolarization vector will be directed.

Rice. 57. The process of repolarization with pronounced pancreatic hypertrophy. Explanation in the text.

A similar mechanism explains the formation of an asymmetric negative T wave in V1 and a positive T wave in V6.

The formation of an ECG during pancreatic hypertrophy, when it is smaller than the left one and its excitation occurs slowly, has its own characteristics (option 2). In this case, in stage I of excitation (Fig. 58), just as normally, the left half of the interventricular septum is excited, which determines the direction of the total depolarization vector from left to right.

Rice. 58. The course of excitation in stage I with RV hypertrophy, when it is smaller than the LV and the process of its excitation is slowed down. Explanation in the text.

On the ECG, under the influence of this vector, an r wave is formed in the right chest leads (V1), and a q wave in the left chest leads (V6), which is due to the orientation of the resulting vector towards the positive pole of the right and negative pole of the left chest leads.

Stage II of excitation (Fig. 59) covers the period of depolarization of the right and left ventricles. The excitation vector of the RV is directed from left to right, and that of the left - from right to left. The resulting vector, despite the hypertrophy of the pancreas, is also directed from right to left.

Rice. 59. The course of excitation in stage II with RV hypertrophy, when it is smaller than the LV and the process of its excitation is slowed down. Explanation in the text.

Under the influence of this resulting vector, projected onto the negative sides of the axes of the right chest leads, the S wave is recorded in V1. On the contrary, the orientation of the total excitation vector towards the positive electrodes of the left chest leads leads to the appearance of the R wave in V6.

Stage III excitation is associated with the final excitation of the hypertrophied RV, which continues after the end of LV depolarization. As a result, the final vector of RV excitation is directed from left to right (Fig. 60). Under the influence of this vector, directed to the positive pole of the right precordial leads, the R¢ wave is formed in lead V1. In this case, an S wave is formed in the left chest leads (V6), since the final excitation vector of the RV is oriented towards the negative sides of the electrodes. The peculiarity of the R¢ wave is that it is larger than the r wave preceding it, i.e. R¢ ​​in V1>r in V1. This is explained by the fact that the final excitation of the RV does not encounter opposition from the LV EMF, and also by the fact that the vector of the final excitation of the RV is close to the V1 electrode.

Rice. 60. The course of excitation in stage III with RV hypertrophy, when it is smaller than the LV and the process of its excitation is slowed down. Explanation in the text.

The third option is associated with moderate pancreatic hypertrophy, but it remains significantly smaller than the left one. Stage I of excitation (Fig. 61) proceeds similarly to the norm. The excitation vector of the left half of the interventricular septum is directed from left to right. Therefore, as normal, the r wave is recorded at electrode V1, and the q wave is recorded at electrode V6.

Rice. 61. Progression of excitation in stage I with moderate pancreatic hypertrophy. Explanation in the text.

Stage II of excitation reflects the course of depolarization in the right and left ventricles and proceeds in the same way as normally. Thus, the excitation vector of the RV is directed from left to right, and the LV is directed from right to left (Fig. 62). The total excitation vector is directed from electrode V1 to electrode V6, i.e. from right to left.

Rice. 62. The course of excitation in stage II with moderate pancreatic hypertrophy. Explanation in the text.

Under the influence of the total vector, an S wave is formed in lead V1, which is smaller than normal, and in lead V6 an R wave is formed, the amplitude of which is also reduced compared to the norm. This is due to the fact that the resulting vector of ventricular excitation, directed towards the left chest leads, will be significantly less due to the EMF of the hypertrophied RV.

Diagnostic signs of pancreatic hypertrophy

The diagnosis of pancreatic hypertrophy is made by ECG changes in the chest leads. The main sign of pancreatic hypertrophy is a high R wave in leads V1, V2, when RV1 > SV1. The appearance of a deep S wave in the left precordial leads (V5, V6) is also specific.

Along with these signs, you need to know that their severity depends on the type of pancreatic hypertrophy. In Fig. 63 presents the types of ventricular complexes in the chest leads with various types of RV hypertrophy.

Rice. 63. Variants of ECG waves in the right (V1, V2) and left (V5, V6) chest leads for various types of pancreatic hypertrophy.

Sharply expressed hypertrophy of the pancreas, when it is larger in mass than the left ventricle (R-type):

Severe hypertrophy of the RV, when it is smaller than the LV, and excitation in it proceeds slowly (rSR¢ type):

Moderate hypertrophy of the RV, when it is smaller than the LV (S-type):

Along with the indicated main signs of pancreatic hypertrophy, the following should be taken into account:

a) deviation of the EOS to the right or direction of the EOS type SI–SII–SIII;

b) the presence of a late R wave in lead aVR, due to which the ECG takes the form of QR or rSR¢;

c) increase in the activation time of the RV in V1, V2 by more than 0.03 s;

d) displacement of the transition zone towards the right chest leads (V1–V2).

Quantitative signs can also be used in recognizing pancreatic hypertrophy (Janushkevicius Z.I., Shilinskaite Z.I., 1973; Orlov V.N., 1983). These include:

1) RV1> 7 mm;

2) SV1, V2< 2 мм;

3) SV5 > 7 mm;

4) RV5,V6< 5 мм;

5)RV1 + SV5 or RV1 + SV6 > 10.5 mm;

6) RaVR > 4 mm;

7) Negative TV1 and decreased STV1, V2 with RV1 > 5 mm and absence of coronary insufficiency.

In addition to the above criteria, in the diagnosis of pancreatic hypertrophy, indirect signs can also be used, which may allow one to suspect this pathology, but since they are also found in practically healthy people, they require additional examination (clinical, radiological, echocardiographic, etc.):

1) R in V1, V2 is high and greater than S in V1, V2, and S in V5, V6 has a normal amplitude or is absent altogether. However, high R in V1, V2 is occasionally recorded in healthy people, especially in children;

2) S in V5, V6 is deep, and R in V1, V2 has a normal amplitude;

3) S in V5,V6 > R in V1, V2;

4) late RaVR, especially if more than 4 mm or RaVR > Q(S)aVR;

5) deviation of the EOS to the right, especially if Ð a > 110°;

6) EOS type SI–SII–SIII;

7) complete or incomplete blockade of PNPG;

8) ECG shows signs of RA hypertrophy;

9) ECG shows signs of LA hypertrophy;

10) large-wave form of MA;

11) RV activation time in V1 > 0.03 s;

12) the phenomenon TI > TII > TIII, often combined with a decrease in S in leads II and III.

Electrocardiographic findings for RV hypertrophy

1. If, in the presence of signs of pancreatic hypertrophy, a high R wave in leads V1, V2 is not combined with changes in the ST segment and T wave, then it is customary to draw a conclusion about pancreatic hypertrophy (Fig. 64).

Rice. 64. ECG for pancreatic hypertrophy.

2. If, with electrocardiographic signs of RV hypertrophy, a high R wave in leads V1, V2 is combined with a decrease in the ST segment and a negative T wave in the same leads, then they speak of RV hypertrophy with overload, less often the term RV hypertrophy with myocardial dystrophy is used (Fig. 65 ).

Rice. 65. ECG for RV hypertrophy with overload.

3. If, during RV hypertrophy, a high R in leads V1, V2 is combined with a decrease in the ST segment and a negative T wave not only in these leads, but also in others (for example, from V1 to V4), then they speak of RV hypertrophy with overload and pronounced changes myocardium (Fig. 66).

Rice. 66. ECG for pancreatic hypertrophy with overload and pronounced changes in the myocardium.

Hypertrophy of both ventricles

Electrocardiographic diagnosis of hypertrophy of both ventricles (combined hypertrophy) is very difficult. This is due to the fact that signs of hypertrophy of one ventricle are offset by signs of hypertrophy of the other. However, if you use the following electrocardiographic signs, you can recognize hypertrophy of both ventricles.

1. In leads V5, V6, a high R wave is recorded (often RV5,V6 > RV4) due to LV hypertrophy. In leads V1, V2, the R wave is also high and more than 5–7 cm, which indicates pancreatic hypertrophy.

2. With RV hypertrophy, the QRS complex in leads V1, V3 looks like rSR’ with a deep S wave, which is caused by excitation of the hypertrophied LV. It is often noted that RV5,V6 > RV4.

3. A clear picture of hypertrophy in leads V5, V6 in combination with signs of complete or incomplete blockade of PNPG in V1, V2.

4. A combination of clear signs of LV hypertrophy and deviation of the EOS to the right, which is usually associated with concomitant RV hypertrophy.

5. The combination of obvious signs of RV hypertrophy with deviation of the EOS to the left, which indicates the presence of LV hypertrophy.

6. With reliable RV hypertrophy, a pronounced q wave is recorded in V5, V6, which indicates hypertrophy of the left part of the interventricular septum and, consequently, concomitant LV hypertrophy. This symptom is often combined with a high R wave in V5, V6.

7. With reliable signs of severe RV hypertrophy with high R in V1 and V2, there are no S waves in the left precordial leads, which is characteristic of LV hypertrophy.

8. With severe LV hypertrophy with high R in the left chest leads, the S wave in the right chest leads has a small amplitude. This is often accompanied by an enlarged R wave in V1 and V2, which, together with the first sign, indicates pancreatic hypertrophy.

9. If there are clear criteria for LV hypertrophy, a deep S wave is observed in the left precordial leads.

10. With pronounced hypertrophy of the pancreas with high R in the right chest leads, a deep S wave is noted in the same leads. In this case, there is a normal or enlarged R wave in the left chest leads.

11. Large R and S waves of approximately the same amplitude in leads V3–V5.

12. With obvious signs of LV hypertrophy, there is a late R wave in lead aVR and the QRS complex takes the form QR,Qr , rSr¢, rSR¢.

13. Combination of signs of LV hypertrophy with “P-pulmonale” or “P-mitrale”.

14. With obvious electrocardiographic signs of RV hypertrophy, a decrease in the ST segment and a negative T wave in leads V5, V6 are observed, with positive T waves in V1, V2 and the absence of clinical signs of coronary insufficiency.

15. Clear signs of LV hypertrophy are accompanied by a decrease in the ST segment and a negative T wave in the right precordial leads. In this case, positive T waves are recorded in the left chest leads and there are no clinical manifestations of coronary insufficiency.

16. Negative U waves in all chest leads, as well as in standard leads I and II.

17. There is a combination of clear signs of pancreatic hypertrophy and the sum of the teeth RV5 or RV6 and SV1 or SV2 exceeding 28 mm in people over 30 years of age or 30 mm in people under 30 years of age.

18. The combination of an SV1 wave of very small amplitude with a deep SV2 wave in the presence of a small r wave in the same leads and a relatively high R wave in the left chest leads, along with a shift of the transition zone to the left.

19. Normal ECG in the presence of clinical evidence of enlarged ventricles of the heart.

Rice. 67 illustrates an ECG with signs of combined ventricular hypertrophy.

Rice. 67. ECG with hypertrophy of both ventricles.

Assignments in test form for self-control

In addition, the rotation of the heart occurs with severe kyphoscoliosis, pathological processes in the lungs, accompanied by a displacement of the heart and large vessels towards the pathological process. As a result of the rotation of the heart, the topography of the edge-forming arches of the heart changes, which in turn affects the configuration of the cardiovascular shadow (Fig. 1).

Rice. 1. Rotation of the heart (the dotted line indicates the contour of the superior vena cava):

1 - turn from right to left (posterior displacement of the left parts of the heart); 2 - rotation of the heart from left to right (the right ventricle is shifted to the right and is edge-forming).

Turning of the heart to the left is observed with severe isolated hypertrophy of the right ventricle (mitral stenosis, cor pulmonale, congenital heart defects with arterial hypertension in the lungs), enlargement of both cavities of the right heart (tricuspid insufficiency), and right-sided kyphoscoliosis. The degree of rotation of the heart to the left can reach 10-40°.

The cardiovascular shadow in the direct projection acquires a mitral configuration as a result of lengthening and bulging of the arch of the pulmonary trunk. The left atrial appendage and left ventricle are displaced posteriorly; the latter usually remains edge-forming only at the apex of the heart. With significant rotations, the right ventricle and conus arteriosus become edge-forming along the left contour of the heart.

Turning of the heart to the left is observed with a significant volumetric increase in the left ventricle (aortic stenosis, aortic insufficiency, hypertension), left-sided kyphoscoliosis. P.S. to the right, as a rule, occurs at a smaller angle than to the left (10-15°), and therefore changes in the topography of the heart are less significant. Cardiovascular shadow of the aortic configuration with an emphasized rounding of the enlarged left ventricular arch. The arch of the left atrium lengthens somewhat, the appendage of which is shifted anteriorly. The right atrium and superior vena cava are displaced posteriorly, the right ventricle becomes red-forming and the lower part along the right contour of the heart shadow.

Thus, when the heart turns to the right, both lower edge-forming arches are formed by the ventricles, and the upper ones by the corresponding atria. The vascular bundle is expanded as a result of the reversal of the aorta, so the shadow of the vascular bundle is a summary image of the ascending and descending aorta.

The rotation of the heart is approximately determined according to fluoroscopy, radiography and x-ray kymography in a direct projection. This sign is more reliably clarified by angiocardiography (the size of the cavity and displacement of the interventricular septum) or an angiogram of the coronary vessels (topography of the coronary vessels). The optimal projections are straight and both anterior oblique.

Determination of heart rotation around the transverse axis

Rotations of the heart around the transverse axis are usually associated with deviation of the apex of the heart forward or backward relative to its normal position. When the heart rotates around the transverse axis tip first the ventricular QRS complex in standard leads takes the form qR I qR II, qR III. On the contrary, when the heart rotates around the transverse axis tip back The QRS complex has the form rs I, rs II, rs III.

Atrial P wave analysis

Atrial P wave analysis includes:

1) measurement of the amplitude of the P wave (normally no more than 2.5 mm);

2) measurement of the duration of the P wave (normally no more than 0.1 s);

3) determination of the polarity of the P wave in leads I, II, III;

4) determination of the shape of the P wave.

In the normal direction of movement of the excitation wave along the atria (from top to bottom), the P waves I, II, III are positive, and in the direction of movement of the excitation wave from bottom to top, they are negative. Split waves with two apexes P I, aVL, V 5, V 6 are characteristic of pronounced hypertrophy of the left atrium, and pointed high-amplitude teeth P II, III, aVF are characteristic of hypertrophy of the right atrium (see below).

Analysis of the ventricular QRS complex includes:

1) assessment tooth ratio Q, R, S in 12 leads, which allows you to determine the rotation of the heart around three axes (see above);

2) measurement amplitude and duration of the tooth Q. A pathological Q wave is characterized by an increase in its duration of more than 0.03 s and amplitude of more than 1/4 of the amplitude of the R wave in the same lead;

3) measurement tooth amplitude R, determination of its possible splitting, as well as the appearance of a second additional tooth R’ (r’);

4) measurement amplitude of the S wave, determination of its possible widening, jaggedness or splitting.

When analyzing the state of the RS-T segment, you must:

1) measure positive (+) or negative (-) connection point deviation j from the isoelectric line;

2) measure the displacement of the RS-T segment at a distance of 0.08 c to the right of connection point j;

3) determine the form of displacement of the RS-T segment: horizontal, oblique-downward or oblique-ascending displacement.

When analyzing the T wave you should:

1) determine the polarity of the T wave,

2) evaluate its shape and

3) measure the amplitude of the T wave.

The Q-T interval is measured from the beginning of the QRS complex (Q or R wave) to the end of the T wave and compared with the proper value calculated using Bazett's formula:

The electrocardiographic report indicates:

1) main pacemaker: sinus or non-sinus rhythm;

2) regularity of heart rhythm: correct or incorrect rhythm;

3) number of heartbeats (HR);

4) position of the electrical axis of the heart;

5) the presence of four ECG syndromes: rhythm and conduction disturbances, hypertrophy of the ventricular and/or atrium myocardium, as well as myocardial damage (ischemia, dystrophy, necrosis, scars, etc.).

Turning the heart backwards - what is it?

When the heart rotates with its apex forward around its transverse axis, the average QRS vector deviates forward, the initial vector (Q) is directed more to the right and upward than usual (in the F plane). It is located parallel to the frontal plane and therefore clearly projects to the minus axes of all standard leads (I, II and III).

The ECG shows a pronounced wave QI, II, III. The final vector (S) deviates posteriorly and downward, perpendicular to the frontal plane and is not projected to minus on the axis of standard leads, therefore, the S wave is not recorded in leads I, II, III. Thus, when the heart rotates with its apex forward around the transverse axis on the ECG in leads I, II and III record the qR complex.

When the heart rotates with its apex backward around the transverse axis, the average QRS vector deviates backward (in the S plane), the final vector (S) deviates to the right and upward, giving a significant projection to the negative pole of the axes of leads I, II and III. The ECG shows a pronounced wave SI, II, III. The initial vector (Q) is directed downward and forward and therefore is not projected to the negative pole of the axes of standard leads. As a result, there is no Q wave in the ECG in leads I, II and III. The QRSI, II, III complex is represented by the RS type.

ECG of a healthy woman D., 30 years old. The sinus rhythm is regular, 67 per minute. P - Q=0.12 sec. P = 0.10 sec. QRS = 0.08 sec. Q - T = 0.38 sec. Ru>RI>Rir AQRS=+52°. Ap=+35°. At=+38°. Complex QRSI,II,III type qR. This shows that the initial vector (Q) is directed to the right and upward more than usual, and is therefore projected to the minus of all standard leads (wave qI, II, III). The final vector (S) deviates posteriorly and downward, perpendicular to the frontal plane and is not projected onto the axes of leads I, II, III (there is no S wave, cw). Such changes in the direction of the initial and final vectors may be due to the rotation of the heart with the apex forward. It should be noted that the QRS transition zone coincides with lead V2, which is the right border of its normal location. Complex QRSV5V6 type RS, which reflects a simultaneous slight rotation clockwise around the longitudinal axis. The P and T waves and the RS-T segment are normal in all leads.

Conclusion. A variant of a normal ECG (rotation of the heart with the apex forward around the transverse axis and clockwise around the longitudinal axis).

ECG of a healthy man K., 37 years old. Severe sinus bradycardia, 50 per 1 min. Interval P - Q=0.15 sec. P = 0.11 sec. QRS=0.09 sec. Q - T=0.39 sec. RII>RI>RIII. AQRS = +50°. Ar=+65°. At=+50°. QRS angle - T=0°. Complex QRSI,II,III type qR. The Q wave is most pronounced in lead II, where its amplitude is 3 mm and its duration is slightly less than 0.03 sec. (normal sizes). The described QRS shape is associated with the heart turning its apex forward.

In the chest leads, the QRSV5, V6 complex is also of the qR type, and the RV1 wave is pronounced, but not enlarged (amplitude 5 mm). These QRS changes indicate a counterclockwise rotation of the heart around its longitudinal axis. The transition zone is located normally (between V2 and V3). The remaining ECG waves are normal. The RS segment - TII,III is elevated by no more than 0.5 mm, which may be normal.

Conclusion. Sinus bradycardia. Turning the heart counterclockwise and with the apex forward (a variant of a normal ECG).

ECG of a healthy woman K., 31 years old. The sinus rhythm is regular, 67 per minute. P - Q=0.16 sec. P=0.09 sec. QRS=0.08 sec. Q - T=0.39 sec. RII>RI>RIII. AQRS=+56°. At=+26°. QRS angle - T=30°. Ar=+35°.

Complex QRSI,II,III type Rs. Pronounced S in leads I, II, III indicates a significant deviation of the final vector (S) to the right and upward. The absence of the QI, II, III wave is associated with the direction of the initial QRS vector down and forward (towards the positive pole of the standard leads). This orientation of the initial and final QRS vectors may be due to the rotation of the heart with its apex backwards around its transverse axis (type SI, SII, SIII ECG). The remaining ECG waves are within the usual normal characteristics: QRSV6 type qRs. The QRS transition zone between V2 and V3, the RS segment - TV2 is shifted upward by 1 mm. In the remaining leads, RS-T is at the level of the isoelectric line, TIII is slightly negative, TaVF is positive, TV1 is negative, TVJ_V6 is positive, with a slightly larger amplitude in V2V3. The P wave is of normal shape and size.

Conclusion. Variant of normal ECG type SI, SII, SIII (rotation of the heart with the apex backwards around the transverse axis).

Training video for determining the EOS (electrical axis of the heart) using an ECG

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Rice. 4.21. The position of the electrical axis of the heart is horizontal (angle a * +15 *). There is also a rotation of the heart around the longitudinal axis counterclockwise (complex QRS in leads V 5 and V 6 types QR, transition zone (TZ) in lead V 2 .

Rice. 4.22. There is a rotation of the electrical axis of the heart to the right (angle a * +120°), as well as a rotation of the heart around the longitudinal axis clockwise PZ in lead V 6 (complex QRS in leads V 5 (V 6 type AS).

Determination of heart rotation around the transverse axis (apex forward or backward)

Less commonly, the ECG records rotations of the heart around its transverse axis, occurring in the anteroposterior (sagittal) plane (Fig. 4.23). Rotations of the heart around the transverse axis are usually associated with deviation of the apex of the heart forward or backward along

in relation to its usual position, which leads to a violation of the usual spatial arrangement of the three moment vectors of ventricular depolarization in the sagittal and frontal planes. Rotations of the heart around the transverse axis with the apex forward or backward are best recorded in three standard limb leads. Take a look at fig. 4.23. It depicts the familiar six-axis Bailey coordinate system, rotated at a certain angle to the observer, as well as the spatial arrangement of three moment vectors (0.02 s, 0.04 s and 0.06 s).

In most cases, with a normal position of the heart (Fig. 4.23, a), the initial torque vector (0.02 s) is oriented slightly up and to the right, and the final torque vector (0.06 s) is oriented up and to the left or right. Both vectors are spatially located at a certain angle to the frontal plane, with the 0.02 s vector oriented forward, and the 0.06 s vector backward. Both vectors are projected onto the negative parts of the axes of standard leads, as a result of which relatively small amplitude Q and Q waves can be recorded in these leads. S. It should be remembered that the teeth Q And S can be recorded only in one or two of three standard leads: in I and II or in II and III.

tip first(Fig. 4.23, b) the initial moment vector (0.02 s) shifts even more upward and slightly to the right, and therefore the tooth Q begins to be registered in all three standard leads and becomes more pronounced.

The final moment vector (0.06 s) deflects downwards and backwards, as a result of which it is now located almost perpendicular to the frontal plane. Therefore, its projection on the axes of all standard leads approaches zero, which leads to the disappearance of wave 5 in these leads.

When the heart rotates around the transverse axis tip back(Fig. 4.23, c) the initial moment vector (0.02 s) shifts forward and down so that its orientation in space turns out to be almost perpendicular to the frontal plane. Therefore, the projection of the 0.02 s vector on the axis of standard leads approaches zero, and the teeth themselves Q are not registered.

The final moment vector (0.06 s) shifts even more upward and begins to be projected onto the negative parts of the axes of all three standard limb leads, which leads to the appearance of fairly deep teeth S v S u And Sm.

Thus, to determine the rotation of the heart around the transverse axis, it is necessary to evaluate the configuration of the complex QRS in standard limb leads.

Atrial Wave Analysis R

After determining the rotation of the heart around the anteroposterior, longitudinal and transverse axes, proceed to the analysis of the atrial wave R. Prong analysis R includes: 1) measurement of tooth amplitude R, 2) tooth duration measurement R u 3) determination of tooth polarity R, 4) determination of tooth shape R.

Prong amplitude R is measured from the contour line to the top of the prong, and its duration is from the beginning to the end of the prong, as shown

in Fig. 4.24. Normal tooth amplitude R does not exceed 2.5 mm, and its duration is 0.1 s. Prong polarity R in leads I, II and III is the most important electrocardiographic sign, indicating the direction of movement of the excitation wave along the atria and, consequently, the localization of the source of excitation (pacemaker). As you remember, with normal movement of the excitation wave along the atria from top to bottom and to the left, the teeth are positive, and when the excitation is directed from bottom to top, they are negative. In this latter case, the pacemaker is located in the lower parts of the atria or in the upper part of the AV. node. With excitation emanating from the middle part of the right atrium, the depolarization wave is directed both upward and downward. Average vector R directed to the left, respectively, the tooth R increases, the tooth becomes larger Plv and the P wave ||(becomes negative and shallow.

Determining the tooth shape is of great practical importance R. Split with two apexes, widened tooth R in the left leads (I, aVL, V 5, V 6) is typical for patients with mitral heart defects and left atrial hypertrophy, and pointed high-amplitude teeth R in leads I, III, aVF are observed with hypertrophy of the right atrium in patients with cor pulmonale (for more details, see Chapter 7).

Ventricular complex analysis QRST

turning the heart upside down, what is it?

In the Children's Health section, answer the question ECG result. What does sinus rhythm mean and the heart turning its apex backwards? asked by the author Olimp Business the best answer is a variant of the norm

Normally, the rhythm is only sinus. and EOS depends on age and constitution.

Expensive! The heart rhythm is set by the sinus nerve node. Therefore, it is customary to evaluate the rhythm that does not have deviations from the norm - sinus. This is all, therefore, the norm. But turning the top back depends on a number of conditions. Features of the chest, muscle mass, lung condition, height of the diaphragm, etc. At least this is a variant of the norm and should not be complex about this. That's it.

Rotation of the heart by the left ventricle forward how to treat

ECG when the heart rotates around the longitudinal axis. An example of longitudinal rotation of the heart

The rotation of the heart around its longitudinal axis, drawn through the base and apex of the heart, according to Grant, does not exceed 30°. This rotation is viewed from the apex of the heart. The initial (Q) and final (S) vectors are projected onto the negative half of the lead V axis. Therefore, the QRSV6 complex has the shape of qRs (the main part of the QRS loop k + V6). The QRS complex has the same shape in leads I, II, III.

The clockwise rotation of the heart corresponds to the position of the right ventricle somewhat more anteriorly, and the left ventricle somewhat more posteriorly, than the normal position of these chambers of the heart. In this case, the interventricular septum is located almost parallel to the frontal plane, and the initial QRS vector, reflecting the electromotive force (EMF) of the interventricular septum, is oriented almost perpendicular to the frontal plane and to the axes of leads I, V5 and V6. It also tilts slightly up and to the left. Thus, when the heart is rotated clockwise around the longitudinal axis, the RS complex is recorded in all chest leads, and the RSI and QRIII complexes are recorded in standard leads.

ECG of a healthy man M, 34 years old. The rhythm is sinus, regular; heart rate - 78 per 1 min. (R-R = 0.77ceK.). Interval P - Q = 0.14 sec. P=0.09 sec. QRS=0.07 sec. (QIII=0.025 sec.), d -T= 0.34 sec. RIII RII RI SOI. AQRS=+76°. AT=+20°. AP=+43°. ZQRS - T = 56°. The wave PI-III, V2-V6, aVL, aVF is positive, not higher than 2 mm (lead II). The PV1 wave is biphasic +-) with a larger positive phase. Complex QRSr type RS, QRSIII type QR (Q pronounced, but not extended). Complex QRSV| _„ type rS. QRSV4V6 type RS or Rs. Transition zone of the QRS complex in lead V4 (normal). The RS segment - TV1 _ V3 is shifted upward by no more than 1 mm; in the remaining leads it is at the level of the isoelectric line.

The TI wave is negative. shallow. The TaVF wave is positive. TV1 is smoothed. TV2-V6 is positive, low and increases slightly towards leads V3, V4.

Vector analysis. The absence of QIV6 (type RSI, V6) indicates the orientation of the initial QRS vector forward and to the left. This orientation may be associated with the location of the interventricular septum parallel to the chest wall, which is observed when the heart is rotated clockwise around its longitudinal axis. The normal location of the QRS transition zone shows that in this case the hourly turn is one of the options for a normal ECG. A weakly negative TIII wave with a positive TaVF can also be regarded as normal.

Conclusion. Variant of a normal ECG. Vertical position of the electrical axis of the heart with clockwise rotation around the longitudinal axis.

The interventricular septum is almost perpendicular to the frontal plane. The initial QRS vector is oriented to the right and slightly downward, which determines the presence of a pronounced QI, V5V6 wave. In these leads there is no S wave (QRI, V5, V6 shape, since the base of the ventricles occupies a more posterior left position and the final vector is oriented back and to the left.

ECG of a healthy woman Z. 36 years old. Sinus (respiratory) arrhythmia. The number of contractions is 60 - 75 per minute. P-Q interval=0.12 sec. P=0.08 sec. QRS=0.07 sec. Q-T=0.35 sec. R, R1 R1II. AQRS=+44°. At=+30°. QRS angle - T=14°. Ar = +56°. Complex QRS1,V5,V6 type qR. QRSIII type rR's. The RV1 tooth is slightly enlarged (6.5 mm), but RV1 is SV1, and RV2 is SV2.

The described changes in the QRS complex are associated with a rotation of the initial vector to the right and the final vectors to the left, up and back. This position of the vectors is due to the rotation of the heart counterclockwise around the longitudinal axis.

Other ECG waves and segments are without deviation from the norm. Rp tooth (1.8 mm) P1 Rpg Vector P is directed downward, to the left along the axis of lead II. The average QRS vector in the horizontal plane (chest leads) is parallel to the axis of lead V4 (highest R in lead V4). TIII is smoothed, TaVF is positive.

Conclusion. A variant of a normal ECG (rotation of the heart around the longitudinal axis counterclockwise).

In the ECG analysis protocol, information about rotations around the longitudinal (as well as transverse) axis of the heart according to ECG data is noted in the description. It is not advisable to include them in the ECG conclusion, since they either constitute a variant of the norm, or are a symptom of ventricular hypertrophy, which should be written about in the conclusion.

When assessing the ECG, rotations of the heart around the longitudinal axis, passing from the base to its apex, are also distinguished. Rotation of the right ventricle forward shifts the transition zone to the left, and the S waves in leads V 3 deepen. V4. V5. V 6. the QS complex can be recorded in lead V 1. This rotation is accompanied by a more vertical position of the electrical axis, which causes the appearance of qR I and S III.

Anterior rotation of the left ventricle shifts the transition zone to the right, which causes enlargement of the R waves in leads V 3 . V 2. V 1 disappearance of S waves in the left precordial leads. This rotation is accompanied by a more horizontal arrangement of the electrical axis and registration of qR I and S III in the limb leads.

The third variant of heart rotation is associated with its rotation around the transverse axis and is designated as rotation of the apex of the heart forward or backward.

The forward rotation of the apex of the heart is determined by the registration of q waves in standard leads and lead aVF. which is associated with the exit of the depolarization vector of the interventricular septum into the frontal plane and its orientation upward and to the right.

Posterior rotation of the apex of the heart is determined by the appearance of S waves in standard leads and lead aVF. which is associated with the release of the depolarization vector of the posterior basal sections into the frontal plane and its orientation upward and to the right. The spatial arrangement of the vectors of the initial and final forces of ventricular depolarization has the opposite direction, and their simultaneous registration in the frontal plane is impossible. In three (or four) Q syndrome, there are no S waves in these leads. With three (or four) S syndrome, registration of q waves in the same leads becomes impossible.

The combination of the above rotations and deviations of the electrical axis of the heart makes it possible to determine the electrical position of the heart as normal, vertical and semi-vertical, horizontal and semi-horizontal. It should be noted that determining the electrical position of the heart is of more historical than practical interest, while determining the direction of the electrical axis of the heart makes it possible to diagnose intraventricular conduction disorders and indirectly determines the diagnosis of other pathological ECG changes.

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Electrocardiogram when the heart rotates around the longitudinal axis

When the heart rotates clockwise around its longitudinal axis (as viewed from the apex), the right ventricle moves forward and upward, and the left ventricle moves backward and downward. This position is a variant of the vertical position of the heart axis. In this case, a deep Q wave appears on the ECG in lead III, and occasionally in lead aVF, which can simulate signs of focal changes in the posterior phrenic region of the left ventricle.

At the same time, a pronounced S wave is detected in leads I and aVL (the so-called Q III S I syndrome). There is no q wave in leads I, V 5 and V 6. The transition zone may shift to the left. These changes also occur with acute and chronic enlargement of the right ventricle, which requires appropriate differential diagnosis.

The figure shows an ECG of a healthy 35-year-old woman with an asthenic build. There are no complaints about dysfunction of the heart and lungs. There is no history of diseases that could cause hypertrophy of the right heart. Physical and x-ray examination revealed no pathological changes in the heart and lungs.

The ECG shows the vertical position of the atrial and ventricular vectors. Â P = +75 . Â QRS = +80. Noteworthy are the pronounced q waves along with tall R waves in leads II, III and aVF, as well as S waves in leads I and aVL. Transition zone in V 4 -V 5. These ECG features could provide grounds for determining hypertrophy of the right heart, but the absence of complaints, anamnesis data, and the results of clinical and X-ray examinations made it possible to exclude this assumption and consider the ECG to be a normal variant.

The rotation of the heart around the longitudinal axis counterclockwise (i.e., with the left ventricle forward and upward), as a rule, is combined with deviation of the apex to the left and is a rather rare variant of the horizontal position of the heart. This variant is characterized by a pronounced Q wave in leads I, aVL and left chest along with pronounced S waves in leads III and aVF. Deep Q waves may mimic signs of focal changes in the lateral or anterior wall of the left ventricle. The transition zone with this option is usually shifted to the right.

A typical example of this variant of the norm is the ECG shown in the figure of a 50-year-old patient with a diagnosis of chronic gastritis. This curve shows a pronounced Q wave in leads I and aVL and a deep S wave in lead III.

Practical electrocardiography, V.L. Doshchitsin

A normal ECG with a horizontal position of the electrical axis of the heart must be distinguished from signs of left ventricular hypertrophy. When the electrical axis of the heart is vertical, the R wave has a maximum amplitude in leads aVF, II and III; in leads aVL and I, a pronounced S wave is recorded, which is also possible in the left chest leads. ÂQRS = + 70 – +90. Such#8230;

Posterior rotation of the heart is accompanied by the appearance of a deep S1 wave in leads I, II and III, as well as in lead aVF. A pronounced S wave may also be observed in all chest leads with a shift of the transition zone to the left. This variant of a normal ECG requires differential diagnosis with one of the ECG variants for right ventricular hypertrophy (S-type). The picture shows#8230;

Premature or early repolarization syndrome is a relatively rare variant of a normal ECG. The main symptom of this syndrome is ST segment elevation, which has a peculiar shape of a convex downward arc and begins from a highly located J point on the descending knee of the R wave or on the terminal part of the S wave. Notch at the point of transition of the QRS complex to the descending segment ST#8230;

Peculiar ECG changes are observed in individuals with dextrocardia. They are characterized by the opposite direction of the main teeth compared to the usual one. Thus, in lead I, negative P and T waves are detected, the main wave of the QRS complex is negative, and a QS type complex is often recorded. Deep Q waves may be observed in the precordial leads, which may give rise to erroneous diagnosis of large-focal changes#8230;

A variant of the norm may be an ECG with shallow negative T waves in leads V1-V3, in young people under 25 years of age (rarely older) in the absence of dynamics in them compared to previously recorded ECGs. These T waves are known as juvenile waves. Sometimes in healthy people on the ECG in leads V2 #8212; V4 is marked by tall T waves, which#8230;

Electrocardiogram when the heart rotates around the transverse axis

Posterior rotation of the heart is accompanied by the appearance of a deep S1 wave in leads I, II and III, as well as in lead aVF. A pronounced S wave may also be observed in all chest leads with a shift of the transition zone to the left. This variant of a normal ECG requires differential diagnosis with one of the ECG variants for right ventricular hypertrophy (S-type).

The figure shows an ECG of a healthy 16-year-old boy. Physical and x-ray examination revealed no signs of pathology. The ECG showed a pronounced S wave in leads I, II, III, aVF, V 1 – V 6, and a displacement of the transition zone to V 5. The Q wave and T wave inversion in lead aVL were also detected, which disappeared when recording the ECG during expiration.

When the heart turns its apex forward in leads I, II, III and aVF, a pronounced Q wave is recorded. The ventricular complex in these leads has a qR shape, and in some cases the depth of the Q wave can exceed 1/4 of the height of the R wave. Often this position of the axis is combined with turning the heart around its longitudinal axis counterclockwise. In such cases, a pronounced Q wave is also detected in the left chest leads.

The figure shows an ECG of a healthy 28-year-old man who had no anamnestic indications of cardiac pathology and its clinical signs. In leads I, II, III, aVF, V 3 – V 6, a pronounced Q wave is recorded, the depth of which does not exceed 1/4 of the amplitude of the R wave. These changes reflect the rotation of the heart with the apex forward and around the longitudinal axis counterclockwise.

“Practical electrocardiography”, V.L. Doshchitsin

In some cases, variants of a normal ECG associated with different positions of the heart axis are mistakenly interpreted as a manifestation of one or another pathology. In this regard, we will first consider the “positional” variants of a normal ECG. As mentioned above, healthy people may have a normal, horizontal or vertical position of the electrical axis of the heart, which depends on body type, age and...

A normal ECG with a horizontal position of the electrical axis of the heart must be distinguished from signs of left ventricular hypertrophy. When the electrical axis of the heart is vertical, the R wave has a maximum amplitude in leads aVF, II and III; in leads aVL and I, a pronounced S wave is recorded, which is also possible in the left chest leads. ÂQRS = + 70° – +90°. Such...

When the heart rotates clockwise around its longitudinal axis (as viewed from the apex), the right ventricle moves forward and upward, and the left ventricle moves backward and downward. This position is a variant of the vertical position of the heart axis. On the ECG, a deep Q wave appears in lead III, and occasionally in lead aVF, which can simulate signs...

Premature or early repolarization syndrome is a relatively rare variant of a normal ECG. The main symptom of this syndrome is ST segment elevation, which has a peculiar shape of a convex downward arc and begins from a highly located J point on the descending knee of the R wave or on the terminal part of the S wave. A notch at the point of transition of the QRS complex to the descending ST segment ...

Peculiar ECG changes are observed in individuals with dextrocardia. They are characterized by the opposite direction of the main teeth compared to the usual one. Thus, in lead I, negative P and T waves are detected, the main wave of the QRS complex is negative, and a QS type complex is often recorded. Deep Q waves may be observed in the chest leads, which may give rise to erroneous diagnosis of large-focal changes...

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