Signs of a normal ecg. What does the t wave show on an ecg? Biphasic p on an ecg

Quick page navigation

Almost every person who has undergone an electrocardiogram is interested in the meaning of the different teeth and the terms written by the diagnostician. Although only a cardiologist can give a full interpretation of an ECG, everyone can easily figure out whether their heart cardiogram is good or if there are some abnormalities.

Indications for an ECG

A non-invasive study - an electrocardiogram - is performed in the following cases:

• The patient complains of high blood pressure, chest pain and other symptoms indicating cardiac pathology;
• Deterioration in the well-being of a patient with a previously diagnosed cardiovascular disease;
• Abnormalities in laboratory blood tests - increased cholesterol, prothrombin;
• In preparation for surgery;
• Detection of endocrine pathology, diseases of the nervous system;
• After severe infections with a high risk of heart complications;
• For prophylactic purposes in pregnant women;
• Examination of the health status of drivers, pilots, etc.

Decoding ECG - numbers and Latin letters

A full-scale interpretation of the cardiac cardiogram includes an assessment of the heart rhythm, the functioning of the conduction system and the condition of the myocardium. For this, the following leads are used (electrodes are installed in a certain order on the chest and limbs):

• Standard: I - left/right wrist on the hands, II - right wrist and ankle area on the left leg, III - left ankle and wrist.
• Strengthened: aVR - right wrist and combined left upper/lower limbs, aVL - left wrist and combined left ankle and right wrist, aVF - left ankle area and combined potential of both wrists.
• Thoracic (potential difference between the electrode with a suction cup located on the chest and the combined potentials of all extremities): V1 - electrode in the IV intercostal space along the right border of the sternum, V2 - in the IV intercostal space to the left of the sternum, V3 - on the IV rib along the left-sided parasternal line, V4 - V intercostal space along the left midclavicular line, V5 - V intercostal space along the anterior axillary line on the left, V6 - V intercostal space along the mid-axillary line on the left.

Additional pectorals - located symmetrically to the left pectoral with additional V7-9.

One cardiac cycle on the ECG is represented by the PQRST graph, which records electrical impulses in the heart:

• P wave - displays atrial excitation;
• QRS complex: Q wave - the initial phase of depolarization (excitation) of the ventricles, R wave - the actual process of ventricular excitation, S wave - the end of the depolarization process;
• T wave - characterizes the extinction of electrical impulses in the ventricles;
• ST segment - describes the complete restoration of the original state of the myocardium.

When deciphering ECG indicators, the height of the teeth and their location relative to the isoline, as well as the width of the intervals between them, are important.

Sometimes a U pulse is recorded behind the T wave, indicating the parameters of the electrical charge carried away with the blood.

Interpretation of ECG indicators - the norm in adults

On the electrocardiogram, the width (horizontal distance) of the teeth - the duration of the period of excitation of relaxation - is measured in seconds, the height in leads I-III - the amplitude of the electrical impulse - in mm. A normal cardiogram in an adult looks like this:

• Heart rate - normal heart rate is within 60-100/min. The distance from the tops of adjacent R waves is measured.
• EOS - the electrical axis of the heart is considered to be the direction of the total angle of the electrical force vector. The normal value is 40-70º. Deviations indicate rotation of the heart around its own axis.
• The P wave is positive (directed upward), negative only in lead aVR. Width (duration of excitation) - 0.7 - 0.11 s, vertical size - 0.5 - 2.0 mm.
• PQ interval - horizontal distance 0.12 - 0.20 s.
• The Q wave is negative (below the isoline). Duration 0.03 s, negative height value 0.36 - 0.61 mm (equal to ¼ of the vertical size of the R wave).
• The R wave is positive. What matters is its height - 5.5 -11.5 mm.
• S wave - negative height 1.5-1.7 mm.
• QRS complex - horizontal distance 0.6 - 0.12 s, total amplitude 0 - 3 mm.
• The T wave is asymmetrical. Positive height 1.2 - 3.0 mm (equal to 1/8 - 2/3 of the R wave, negative in the aVR lead), duration 0.12 - 0.18 s (longer than the duration of the QRS complex).
• ST segment - passes at the level of the isoline, length 0.5 -1.0 s.
• U wave - height indicator 2.5 mm, duration 0.25 s.

Abbreviated results of ECG interpretation in adults and the norm in the table:

During normal research (recording speed - 50 mm/sec), ECG interpretation in adults is carried out according to the following calculations: 1 mm on paper when calculating the duration of intervals corresponds to 0.02 sec.

A positive P wave (standard leads) followed by a normal QRS complex means normal sinus rhythm.

Normal ECG in children, interpretation

Cardiogram parameters in children are somewhat different from those in adults and vary depending on age. Interpretation of the ECG of the heart in children, normal:

• Heart rate: newborns - 140 - 160, by 1 year - 120 - 125, by 3 years - 105 -110, by 10 years - 80 - 85, after 12 years - 70 - 75 per minute;
• EOS - corresponds to adult indicators;
• sinus rhythm;
• tooth P - does not exceed 0.1 mm in height;
• length of the QRS complex (often not particularly informative in diagnosis) - 0.6 - 0.1 s;
• PQ interval - less than or equal to 0.2 s;
• Q wave - unstable parameters, negative values ​​in lead III are acceptable;
• P wave - always above the isoline (positive), the height in one lead may fluctuate;
• S wave - negative indicators of variable value;
• QT - no more than 0.4 s;
• The duration of the QRS and the T wave are equal, 0.35 - 0.40.

Example of an ECG with rhythm disturbance

Based on deviations in the cardiogram, a qualified cardiologist can not only diagnose the nature of the heart disease, but also record the location of the pathological focus.

Arrhythmias

The following cardiac rhythm disorders are distinguished:

1. Sinus arrhythmia - the length of the RR intervals fluctuates with a difference of up to 10%. It is not considered a pathology in children and young people.
2. Sinus bradycardia is a pathological decrease in the frequency of contractions to 60 per minute or less. The P wave is normal, PQ from 12 s.
3. Tachycardia - heart rate 100 - 180 per minute. In teenagers - up to 200 per minute. The rhythm is correct. With sinus tachycardia, the P wave is slightly higher than normal, with ventricular tachycardia, the QRS length indicator is above 0.12 s.
4. Extrasystoles are extraordinary contractions of the heart. Single ones on a regular ECG (on a 24-hour Holter - no more than 200 per day) are considered functional and do not require treatment.
5. Paroxysmal tachycardia is a paroxysmal (several minutes or days) increase in heart rate up to 150-220 per minute. It is characteristic (only during an attack) that the P wave merges with the QRS. The distance from the R wave to the P height of the next contraction is less than 0.09 s.
6. Atrial fibrillation is an irregular contraction of the atria with a frequency of 350-700 per minute, and of the ventricles - 100-180 per minute. There is no P wave, there are small-to-large undulating oscillations along the entire isoline.
7. Atrial flutter - up to 250-350 atrial contractions per minute and regular slow ventricular contractions. The rhythm may be correct; the ECG shows sawtooth atrial waves, especially pronounced in standard leads II - III and thoracic leads V1.

Deviation of EOS position

A change in the total EOS vector to the right (more than 90º), a higher value of the height of the S wave compared to the R wave indicate pathology of the right ventricle and His bundle block.

When the EOS is shifted to the left (30-90º) and there is a pathological ratio of the heights of the S and R waves, left ventricular hypertrophy and blockade of the bundle branch of His are diagnosed. Deviation of EOS indicates a heart attack, pulmonary edema, COPD, but it can also be normal.

Violation of the conduction system

The following pathologies are most often recorded:

• 1st degree of atrioventricular (AV) block - PQ distance more than 0.20 s. After each P, QRS naturally follows;
• Atrioventricular block, stage 2. - a gradually lengthening PQ throughout the ECG sometimes displaces the QRS complex (Mobitz type deviation 1) or a complete loss of QRS is recorded against the background of a PQ of equal length (Mobitz 2);
• Complete block of the AV node - the atrial heart rate is higher than the ventricular heart rate. PP and RR are the same, PQ are different lengths.

Selected heart diseases

The results of ECG interpretation can provide information not only about the heart disease that has occurred, but also about the pathology of other organs:

1. Cardiomyopathy - atrial hypertrophy (usually the left one), low-amplitude waves, partial blockade of the His, atrial fibrillation or extrasystoles.
2. Mitral stenosis - the left atrium and right ventricle are enlarged, the EOS is deviated to the right, often atrial fibrillation.
3. Mitral valve prolapse - flattened/negative T wave, some QT prolongation, depressed ST segment. Various rhythm disturbances are possible.
4. Chronic pulmonary obstruction - EOS is to the right of normal, low-amplitude waves, AV block.
5. Damage to the central nervous system (including subarachnoid hemorrhage) - pathological Q, wide and high-amplitude (negative or positive) T wave, pronounced U, long duration of QT rhythm disturbance.
6. Hypothyroidism - long PQ, low QRS, flat T wave, bradycardia.

Quite often, an ECG is performed to diagnose myocardial infarction. At the same time, each of its stages corresponds to characteristic changes in the cardiogram:

• ischemic stage - a pointed T with a sharp apex is recorded 30 minutes before the onset of necrosis of the heart muscle;
• stage of damage (changes are recorded in the first hours to 3 days) - ST in the form of a dome above the isoline merges with the T wave, shallow Q and high R;
• acute stage (1-3 weeks) - the worst cardiogram of the heart during a heart attack - preservation of the dome-shaped ST and the transition of the T wave to negative values, decreased R height, pathological Q;
• subacute stage (up to 3 months) - comparison of ST with the isoline, preservation of pathological Q and T;
• stage of scarring (several years) - pathological Q, negative R, smoothed T wave gradually comes to normal values.

There is no need to sound the alarm if you find pathological changes in the ECG issued to you. It should be remembered that some deviations from the norm occur in healthy people.

If an electrocardiogram reveals any pathological processes in the heart, you will definitely be scheduled for a consultation with a qualified cardiologist.

This is the second part of a series about ECG (popularly known as ECG of the heart). To understand today's topic you need to read:

An electrocardiogram reflects only electrical processes in the myocardium: depolarization (excitation) and repolarization (restoration) of myocardial cells.

Normally, depolarization leads to contraction of the muscle cell, and repolarization leads to relaxation. To simplify further, instead of “depolarization-repolarization” I will sometimes use “contraction-relaxation”, although this is not entirely accurate: there is the concept of “electromechanical dissociation”, in which depolarization and repolarization of the myocardium do not lead to its visible contraction and relaxation. I wrote a little more about this phenomenon earlier.

Elements of a normal ECG

Before moving on to decoding the ECG, you need to understand what elements it consists of.

It is curious that abroad the P-Q interval is usually called P-R.

Teeth are convex and concave areas on the electrocardiogram.

The following waves are distinguished on the ECG:

A segment on an ECG is a segment of a straight line (isoline) between two adjacent teeth. The most important segments are P-Q and S-T. For example, the P-Q segment is formed due to a delay in the conduction of excitation in the atrioventricular (AV) node.

The interval consists of a tooth (a complex of teeth) and a segment. Thus, interval = tooth + segment. The most important are the P-Q and Q-T intervals.

Waves, segments and intervals on the ECG.

Pay attention to large and small cells (more about them below).

QRS complex waves

Since the ventricular myocardium is more massive than the atrial myocardium and has not only walls, but also a massive interventricular septum, the spread of excitation in it is characterized by the appearance of a complex QRS complex on the ECG. How to correctly identify the teeth in it?

First of all, the amplitude (size) of individual waves of the QRS complex is assessed. If the amplitude exceeds 5 mm, the tooth is designated by a capital (capital) letter Q, R or S; if the amplitude is less than 5 mm, then lowercase (small): q, r or s.

The R wave (r) is any positive (upward) wave that is part of the QRS complex. If there are several waves, subsequent waves are designated by strokes: R, R', R", etc. The negative (downward) wave of the QRS complex, located before the R wave, is designated as Q (q), and after - as S (s) . If there are no positive waves at all in the QRS complex, then the ventricular complex is designated as QS.

Variants of the QRS complex.

Normally, the Q wave reflects the depolarization of the interventricular septum, the R wave - the bulk of the ventricular myocardium, the S wave - the basal (i.e. near the atria) sections of the interventricular septum. The R V1, V2 wave reflects the excitation of the interventricular septum, and R V4, V5, V6 - the excitation of the muscles of the left and right ventricles. Necrosis of areas of the myocardium (for example, during myocardial infarction) causes the Q wave to widen and deepen, so close attention is always paid to this wave.

ECG analysis

General scheme of ECG decoding

1. Checking the correctness of ECG registration.
2. Heart rate and conduction analysis:
   • assessment of heart rate regularity,
   • heart rate (HR) counting,
   • determination of the source of excitation,
   • conductivity assessment.
3. Determination of the electrical axis of the heart.
4. Analysis of the atrial P wave and P-Q interval.
5. Analysis of the ventricular QRST complex:
   • QRS complex analysis,
   • analysis of the RS - T segment,
   • T wave analysis,
   • Q-T interval analysis.
6. Electrocardiographic report.

1) Checking the correctness of ECG registration

At the beginning of each ECG tape there must be a calibration signal - the so-called control millivolt. To do this, a standard voltage of 1 millivolt is applied at the beginning of the recording, which should display a deviation of 10 mm on the tape. Without a calibration signal, the ECG recording is considered incorrect. Normally, in at least one of the standard or enhanced limb leads, the amplitude should exceed 5 mm, and in the chest leads - 8 mm. If the amplitude is lower, this is called reduced ECG voltage, which occurs in some pathological conditions.

Control millivolt on the ECG (at the beginning of the recording).

2) Heart rate and conduction analysis:

Rhythm regularity is assessed by R-R intervals. If the teeth are at an equal distance from each other, the rhythm is called regular, or correct. The spread of the duration of individual R-R intervals is allowed no more than ± 10% of their average duration. If the rhythm is sinus, it is usually regular.

heart rate (HR) counting

The ECG film has large squares printed on it, each of which contains 25 small squares (5 vertical x 5 horizontal). To quickly calculate heart rate with the correct rhythm, count the number of large squares between two adjacent teeth R - R.

At a belt speed of 50 mm/s: HR = 600 / (number of large squares).

At a belt speed of 25 mm/s: HR = 300 / (number of large squares).

On the overlying ECG, the R-R interval is approximately 4.8 large cells, which at a speed of 25 mm/s gives 300 / 4.8 = 62.5 beats/min.

At a speed of 25 mm/s, each small cell is equal to 0.04 s, and at a speed of 50 mm/s - 0.02 s. This is used to determine the duration of the teeth and intervals.

If the rhythm is abnormal, the maximum and minimum heart rate is usually calculated according to the duration of the shortest and longest R-R interval, respectively.

determination of the excitation source

In other words, they are looking for where the pacemaker is located, which causes contractions of the atria and ventricles. Sometimes this is one of the most difficult stages, because various disorders of excitability and conduction can be very confusingly combined, which can lead to incorrect diagnosis and incorrect treatment. To correctly determine the source of excitation on an ECG, you need to have a good knowledge of the conduction system of the heart.

SINUS rhythm (this is a normal rhythm, and all other rhythms are pathological).

The source of excitation is located in the sinoatrial node. Signs on the ECG:

• in standard lead II, the P waves are always positive and are located before each QRS complex,
• P waves in the same lead have the same shape at all times.

P wave in sinus rhythm.

ATRIAL rhythm. If the source of excitation is located in the lower parts of the atria, then the excitation wave propagates to the atria from bottom to top (retrograde), therefore:

• in leads II and III the P waves are negative,
• There are P waves before each QRS complex.

P wave during atrial rhythm.

Rhythms from the AV connection. If the pacemaker is located in the atrioventricular (atrioventricular node) node, then the ventricles are excited as usual (from top to bottom), and the atria are excited retrogradely (i.e. from bottom to top). At the same time, on the ECG:

• P waves may be absent because they are superimposed on normal QRS complexes,
• P waves can be negative, located after the QRS complex.

Rhythm from the AV junction, superimposition of the P wave on the QRS complex.

Rhythm from the AV junction, the P wave is located after the QRS complex.

The heart rate during the rhythm from the AV junction is less than the sinus rhythm and is approximately equal to beats per minute.

Ventricular, or IDIOVENTRICULAR, rhythm (from Latin ventriculus [ventrikulyus] - ventricle). In this case, the source of rhythm is the ventricular conduction system. Excitation spreads through the ventricles in the wrong way and is therefore slower. Features of idioventricular rhythm:

• QRS complexes are widened and deformed (they look “scary”). Normally, the duration of the QRS complex is 0.06-0.10 s, therefore, with this rhythm, the QRS exceeds 0.12 s.
• There is no pattern between QRS complexes and P waves because the AV junction does not release impulses from the ventricles, and the atria can be excited from the sinus node, as normal.
• Heart rate less than 40 beats per minute.

Idioventricular rhythm. The P wave is not associated with the QRS complex.

To properly account for conductivity, the recording speed is taken into account.

To assess conductivity, measure:

• the duration of the P wave (reflects the speed of impulse transmission through the atria), normally up to 0.1 s.
• duration of the P - Q interval (reflects the speed of impulse conduction from the atria to the ventricular myocardium); interval P - Q = (wave P) + (segment P - Q). Normally 0.12-0.2 s.
• duration of the QRS complex (reflects the spread of excitation through the ventricles). Normally 0.06-0.1 s.
• interval of internal deviation in leads V1 and V6. This is the time between the beginning of the QRS complex and the R wave. Normally in V1 up to 0.03 s and in V6 up to 0.05 s. It is used mainly to recognize bundle branch blocks and to determine the source of excitation in the ventricles in the case of ventricular extrasystole (extraordinary contraction of the heart).

Measuring the internal deviation interval.

3) Determination of the electrical axis of the heart.

In the first part of the ECG series, it was explained what the electrical axis of the heart is and how it is determined in the frontal plane.

4) Analysis of the atrial P wave.

Normally, in leads I, II, aVF, V2 - V6, the P wave is always positive. In leads III, aVL, V1, the P wave can be positive or biphasic (part of the wave is positive, part is negative). In lead aVR, the P wave is always negative.

Normally, the duration of the P wave does not exceed 0.1 s, and its amplitude is 1.5 - 2.5 mm.

Pathological deviations of the P wave:

• Pointed, tall P waves of normal duration in leads II, III, aVF are characteristic of hypertrophy of the right atrium, for example, with “cor pulmonale”.
• Split with 2 apexes, widened P wave in leads I, aVL, V5, V6 is characteristic of left atrium hypertrophy, for example, with mitral valve defects.

Formation of the P wave (P-pulmonale) with hypertrophy of the right atrium.

Formation of the P wave (P-mitrale) with left atrial hypertrophy.

An increase in this interval occurs when the conduction of impulses through the atrioventricular node is impaired (atrioventricular block, AV block).

There are 3 degrees of AV block:

• I degree - the P-Q interval is increased, but each P wave corresponds to its own QRS complex (there is no loss of complexes).
• II degree - QRS complexes partially fall out, i.e. Not all P waves have their own QRS complex.
• III degree - complete blockade of conduction in the AV node. The atria and ventricles contract at their own rhythm, independently of each other. Those. idioventricular rhythm occurs.

5) Analysis of the ventricular QRST complex:

The maximum duration of the ventricular complex is 0.07-0.09 s (up to 0.10 s). The duration increases with any bundle branch block.

Normally, the Q wave can be recorded in all standard and enhanced limb leads, as well as in V4-V6. The amplitude of the Q wave normally does not exceed 1/4 of the height of the R wave, and the duration is 0.03 s. In lead aVR, there is normally a deep and wide Q wave and even a QS complex.

The R wave, like the Q wave, can be recorded in all standard and enhanced limb leads. From V1 to V4, the amplitude increases (in this case, the r wave of V1 may be absent), and then decreases in V5 and V6.

The S wave can have very different amplitudes, but usually no more than 20 mm. The S wave decreases from V1 to V4, and may even be absent in V5-V6. In lead V3 (or between V2 - V4), a “transition zone” is usually recorded (equality of the R and S waves).

RS - T segment analysis

The S-T segment (RS-T) is a segment from the end of the QRS complex to the beginning of the T wave. The S-T segment is especially carefully analyzed in case of coronary artery disease, since it reflects the lack of oxygen (ischemia) in the myocardium.

Normally, the S-T segment is located in the limb leads on the isoline (± 0.5 mm). In leads V1-V3, the S-T segment may shift upward (no more than 2 mm), and in leads V4-V6 - downward (no more than 0.5 mm).

The transition point of the QRS complex to the S-T segment is called point j (from the word junction - connection). The degree of deviation of point j from the isoline is used, for example, to diagnose myocardial ischemia.

T wave analysis.

The T wave reflects the process of repolarization of the ventricular myocardium. In most leads where a high R is recorded, the T wave is also positive. Normally, the T wave is always positive in I, II, aVF, V2-V6, with T I > T III, and T V6 > T V1. In aVR the T wave is always negative.

Q-T interval analysis.

The Q-T interval is called electrical ventricular systole, because at this time all parts of the ventricles of the heart are excited. Sometimes after the T wave a small U wave is recorded, which is formed due to short-term increased excitability of the ventricular myocardium after their repolarization.

6) Electrocardiographic report.

1. Source of rhythm (sinus or not).
2. Regularity of rhythm (correct or not). Usually sinus rhythm is normal, although respiratory arrhythmia is possible.
3. Position of the electrical axis of the heart.
4. Presence of 4 syndromes:
   • rhythm disturbance
   • conduction disturbance
   • hypertrophy and/or overload of the ventricles and atria
   • myocardial damage (ischemia, dystrophy, necrosis, scars)

Examples of conclusions (not entirely complete, but real):

Sinus rhythm with heart rate 65. Normal position of the electrical axis of the heart. No pathology was identified.

Sinus tachycardia with heart rate 100. Single supraventricular extrasystole.

Sinus rhythm with heart rate 70 beats/min. Incomplete blockade of the right bundle branch. Moderate metabolic changes in the myocardium.

Examples of ECG for specific diseases of the cardiovascular system - next time.

ECG interference

In connection with frequent questions in the comments about the type of ECG, I will tell you about the interference that may be on the electrocardiogram:

Three types of ECG interference (explained below).

Interference on an ECG in the lexicon of health workers is called interference:

a) induction currents: network induction in the form of regular oscillations with a frequency of 50 Hz, corresponding to the frequency of alternating electric current in the outlet.

b) “swimming” (drift) of the isoline due to poor contact of the electrode with the skin;

c) interference caused by muscle tremors (irregular frequent vibrations are visible).

comment 73 to the note “Electrocardiogram (ECG of the heart). Part 2 of 3: ECG interpretation plan"

Thank you very much, it helps to refresh your knowledge. ❗ ❗

My QRS is 104 ms. What does this mean? And is this bad?

The QRS complex is a ventricular complex that reflects the time of propagation of excitation through the ventricles of the heart. Normally in adults it is up to 0.1 seconds. Thus, you are at the upper limit of normal.

If the T wave is positive in the aVR lead, then the electrodes are not applied correctly.

I am 22 years old, I did an ECG, the conclusion says: “Ectopic rhythm, normal direction ... (incomprehensibly written) cardiac axis...”. The doctor said that this happens at my age. What is this and what is it connected with?

“Ectopic rhythm” means a rhythm NOT from the sinus node, which is the source of excitation of the heart normally.

Perhaps the doctor meant that such a rhythm is congenital, especially if there are no other heart diseases. Most likely, the pathways of the heart have not formed entirely correctly.

I can’t say in more detail - you need to know where exactly the source of the rhythm is.

I am 27 years old, the conclusion says: “changes in repolarization processes.” What does it mean?

This means that the recovery phase of the ventricular myocardium after excitation is somehow disrupted. On the ECG it corresponds to the S-T segment and the T wave.

Is it possible to use 8 leads for an ECG instead of 12? 6 chest and I and II leads? And where can I find information about this?

Maybe. It all depends on the purpose of the survey. Some rhythm disturbances can be diagnosed by one (any) lead. In case of myocardial ischemia, all 12 leads must be taken into account. If necessary, additional leads are removed. Read books on ECG analysis.

What will aneurysms look like on an ECG? And how to identify them? Thank you in advance...

Aneurysms are pathological dilations of blood vessels. They cannot be detected on an ECG. Aneurysms are diagnosed using ultrasound and angiography.

Please explain what “...Sine” means. rhythm 100 per minute." Is this good or bad?

“Sinus rhythm” means that the source of electrical impulses in the heart is in the sinus node. This is the norm.

"100 per minute" is the heart rate. Normally, in adults it is from 60 to 90, in children it is higher. That is, in this case the frequency is slightly increased.

The cardiogram indicated: sinus rhythm, nonspecific ST-T changes, possibly electrolyte changes. The therapist said it didn't mean anything, did it?

Nonspecific are changes that occur in various diseases. In this case, there are slight changes on the ECG, but it is impossible to really understand what their cause is.

Electrolyte changes are changes in the concentrations of positive and negative ions (potassium, sodium, chlorine, etc.)

Does the fact that the child did not lie still and laugh during the recording affect the ECG results?

If the child behaved restlessly, then the ECG may show interference caused by electrical impulses from the skeletal muscles. The ECG itself will not change, it will just be more difficult to decipher.

What does the conclusion on the ECG mean - SP 45% N?

Most likely, what is meant is the “systolic indicator”. What is meant by this concept is not clearly explained on the Internet. Possibly the ratio of the duration of the Q-T interval to the R-R interval.

In general, the systolic indicator or systolic index is the ratio of minute volume to the patient’s body area. Only I have not heard of this function being determined by ECG. It is better for patients to focus on the letter N, which means normal.

The ECG shows a biphasic R wave. Is it considered pathological?

It's impossible to say. The type and width of the QRS complex in all leads is assessed. Particular attention is paid to the Q (q) waves and their proportions with R.

Jaggedness of the descending limb of the R wave, in I AVL V5-V6, occurs in anterolateral MI, but it makes no sense to consider this sign in isolation without others, there will still be changes in the ST interval with discrepancy, or the T wave.

Occasionally the R wave falls out (disappears). What does it mean?

If these are not extrasystoles, then the variations are most likely caused by different conditions for conducting impulses.

Now I’m sitting and re-analyzing the ECG, my head is a complete mess, what the teacher explained. What is the most important thing you need to know so as not to get confused?((((

I can do this. We have recently started the subject of syndromic pathology, and they are already giving patients ECGs and we must immediately say what is on the ECG, and here the confusion begins.

Yulia, you want to immediately be able to do what specialists learn throughout their lives. 🙂

Buy and study several serious books on ECG, watch various cardiograms more often. When you learn from memory to draw a normal 12-lead ECG and ECG variants for major diseases, you will be able to very quickly determine the pathology on film. However, you will have to work hard.

An unspecified diagnosis is written separately on the ECG. What does it mean?

This is definitely not the conclusion of an electrocardiogram. Most likely, the diagnosis was implied when sending for an ECG.

thank you for the article, it really helps to understand in the initial stages and Murashko is then easier to perceive)

What does QRST = 0.32 mean as a result of an electrocardiogram? Is this some kind of violation? What could this be connected with?

Length of the QRST complex in seconds. This is a normal indicator, do not confuse it with the QRS complex.

I found the results of an ECG from 2 years ago, in the conclusion it says “ signs of left ventricular myocardial hypertrophy". After that, I did an ECG 3 more times, the last time 2 weeks ago, in all three last ECGs in the conclusion there was not a word about LV myocardial hypertrophy. What could this be connected with?

Most likely, in the first case, the conclusion was made tentatively, that is, without compelling reasons: “signs of hypertrophy...”. If there were clear signs, the ECG would indicate “hypertrophy...”.

how to determine the amplitude of the teeth?

The amplitude of the teeth is calculated by millimeter divisions of the film. At the beginning of each ECG there should be a control millivolt equal to 10 mm in height. The amplitude of the teeth is measured in millimeters and varies.

Normally, in at least one of the first 6 leads, the amplitude of the QRS complex is at least 5 mm, but not more than 22 mm, and in the chest leads - 8 mm and 25 mm, respectively. If the amplitude is smaller, they speak of a reduced ECG voltage. True, this term is conditional, since, according to Orlov, there are no clear distinction criteria for people with different body types.

In practice, the ratio of individual teeth in the QRS complex, especially Q and R, is more important, because this may be a sign of myocardial infarction.

I am 21 years old, the conclusion says: sinus tachycardia with heart rate 100. Moderate diffusion in the myocardium of the left ventricle. What does it mean? is it dangerous?

Increased heart rate (normally 60-90). “Moderate diffuse changes” in the myocardium - a change in electrical processes throughout the entire myocardium due to its dystrophy (impaired cell nutrition).

The cardiogram is not fatal, but it cannot be called good either. You need to be examined by a cardiologist to find out what is happening to the heart and what can be done.

My report says “sinus arrhythmia,” although the therapist said that the rhythm is correct, and visually the teeth are located at the same distance. How can this be?

The conclusion is made by a person, so it can be somewhat subjective (this applies to both the therapist and the functional diagnostics doctor). As written in the article, with correct sinus rhythm “ the spread of the duration of individual R-R intervals is allowed no more than ± 10% of their average duration." This is due to the presence of respiratory arrhythmia, which is described in more detail here:

What can left ventricular hypertrophy lead to?

I am 35 years old. In conclusion it is written: “ the R wave grows weakly in V1-V3". What does it mean?

Tamara, with hypertrophy of the left ventricle, thickening of its wall occurs, as well as remodeling (rebuilding) of the heart - a violation of the correct relationship between muscle and connective tissue. This leads to an increased risk of developing myocardial ischemia, congestive heart failure and arrhythmias. More details: plaintest.com/beta-blockers

Anna, in the chest leads (V1-V6), the amplitude of the R wave should normally increase from V1 to V4 (i.e., each subsequent wave should be greater than the previous one). In V5 and V6 the R wave is usually smaller in amplitude than in V4.

Tell me, what is the reason for the deviation in the EOS to the left and what does this mean? What is a complete right bundle branch block?

Deviation of the EOS (electrical axis of the heart) to the left usually occurs due to hypertrophy of the left ventricle (i.e. thickening of its wall). Sometimes deviation of the EOS to the left occurs in healthy people if their diaphragm dome is located high (hypersthenic physique, obesity, etc.). For correct interpretation, it is advisable to compare the ECG with previous ones.

Complete blockade of the right bundle branch is a complete cessation of the propagation of electrical impulses along the right bundle branch (see here article on the conduction system of the heart).

hello, what does this mean? left type ecg, IBPBP and BPVPL

Left type of ECG - deviation of the electrical axis of the heart to the left.

IBPBP (more precisely: UBPBP) is an incomplete blockade of the right bundle branch.

LPBL - blockade of the anterior branch of the left bundle branch.

Tell me, please, what does the small growth of the R wave in V1-V3 indicate?

Normally, in leads V1 to V4, the R wave should increase in amplitude, and in each subsequent lead it should be higher than in the previous one. The absence of such an increase or a ventricular complex of the QS type in V1-V2 is a sign of myocardial infarction of the anterior part of the interventricular septum.

You need to redo the ECG and compare it with the previous ones.

Tell me, please, what does it mean “R increases poorly in V1 - V4”?

This means that it is growing either fast enough or not evenly enough. See my previous comment.

Tell me, where can a person who doesn’t understand this in his life get an ECG so that they can tell him everything about it in detail later?

I did it six months ago, but I still didn’t understand anything from the vague phrases of the cardiologist. And now my heart began to worry again...

You can consult another cardiologist. Or send me an ECG report, I’ll explain. Although, if six months have passed and something is bothering you, you need to do an ECG again and compare them.

Not all ECG changes clearly indicate certain problems; most often, a change can have a dozen reasons. Such as, for example, changes in the T wave. In these cases, everything must be taken into account - complaints, medical history, results of examinations and medications, the dynamics of ECG changes over time, etc.

The ECG shows diffuse nonspecific ST-T changes. They referred me to an endocrinologist. For what? Can gynecological problems cause such changes?

Various endocrinological diseases (pheochromocytoma, thyrotoxicosis, etc.) can affect the shape and duration of different ECG waves and intervals.

The final part of the ventricular complex (S-T segment and T wave) can change in women with various hormonal disorders and during menopause (these are the so-called dishormonal and climacteric myocardial dystrophy, or cardiopathy).

Please tell me whether breathing during an ECG reading affects the correctness of the ECG?

My son is 22 years old. His heart rate is from 39 to 149. What could this be? The doctors don't really say anything. Prescribed Concor

During the ECG, breathing should be normal. Additionally, after taking a deep breath and holding your breath, standard lead III is recorded. This is necessary to check for respiratory sinus arrhythmia and ECG positional changes.

If your resting heart rate ranges from 39 to 149, you may have sick sinus syndrome. In SSSS, Concor and other beta blockers are prohibited, since even small doses can cause a significant decrease in heart rate. My son needs to be examined by a cardiologist and have an atropine test done.

At the conclusion of the ECG it is written: metabolic changes. What does it mean? Is it necessary to consult a cardiologist?

Metabolic changes in the ECG conclusion can also be called dystrophic (electrolyte) changes, as well as a violation of repolarization processes (the last name is the most correct). They imply a metabolic disorder in the myocardium that is not associated with an acute disturbance of the blood supply (i.e., with a heart attack or progressive angina). These changes usually affect the T wave (it changes its shape and size) in one or more areas, lasting for years without the dynamics characteristic of a heart attack. They do not pose a danger to life. It is impossible to say the exact reason based on the ECG, because these nonspecific changes occur in a variety of diseases: hormonal imbalances (especially menopause), anemia, cardiac dystrophy of various origins, ion balance disorders, poisoning, liver disease, kidney disease, inflammatory processes, heart injuries, etc. But you need to go to a cardiologist to try to figure out what is causing the changes on the ECG.

The conclusion of the ECG says: insufficient increase in R in the chest leads. What does it mean?

This can be either a normal variant or a possible myocardial infarction. The cardiologist needs to compare the ECG with previous ones, taking into account the complaints and clinical picture, if necessary, prescribe an EchoCG, a blood test for markers of myocardial damage, and repeat the ECG.

hello, tell me, under what conditions and in which leads will a positive Q wave be observed?

There is no such thing as a positive Q wave (q), it is either there or it is not. If this tooth is directed upward, it is called R (r).

Question about heart rate. I bought a heart rate monitor. I used to work without it. I was surprised when the maximum heart rate was 228. There were no unpleasant sensations. I never complained about my heart. 27 years old. Bike. In a calm state, the pulse is about 70. I checked the pulse manually without loads, the readings are correct. Is this normal or should the load be limited?

The maximum heart rate during physical activity is calculated as “220 minus age.” For you = 193. Exceeding it is dangerous and undesirable, especially for a person with little training and for a long time. It is better to exercise less intensely, but longer. Aerobic load threshold: 70-80% of maximum heart rate (for you). There is an anaerobic threshold: 80-90% of maximum heart rate.

Since on average 1 inhalation-exhalation corresponds to 4 heartbeats, you can simply focus on the breathing frequency. If you can not only breathe, but also speak short phrases, then it’s fine.

Please explain what parasystole is and how it is detected on an ecg.

Parasystole is the parallel functioning of two or more pacemakers in the heart. One of them is usually the sinus node, and the second (ectopic pacemaker) is most often located in one of the ventricles of the heart and causes contractions called parasystoles. To diagnose parasystole, a long-term ECG recording is required (one lead is sufficient). Read more in V.N. Orlov’s “Guide to Electrocardiography” or in other sources.

Signs of ventricular parasystole on the ECG:

1) parasystoles are similar to ventricular extrasystoles, but the coupling interval is different, because there is no connection between sinus rhythm and parasystoles;

2) there is no compensatory pause;

3) the distances between individual parasystoles are multiples of the smallest distance between parasystoles;

4) a characteristic sign of parasystole is confluent contractions of the ventricles, in which the ventricles are excited from 2 sources simultaneously. The shape of the confluent ventricular complexes is intermediate between sinus contractions and parasystoles.

Hello, please tell me what a small increase in R means on the ECG transcript.

This is simply a statement of the fact that in the chest leads (from V1 to V6) the amplitude of the R wave does not increase quickly enough. The reasons can be very different; they are not always easy to determine using an ECG. Comparison with previous ECGs, dynamic observation and additional examinations help.

Tell me what could be causing the change in QRS, which ranges from 0.094 s to 0.132 on different ECGs?

A transient (temporary) disturbance of intraventricular conduction is possible.

Thank you for including the tips at the end. And then I received an ECG without decoding and when I saw solid waves on V1, V2, V3 as in example (a) - I felt uneasy...

Please tell me what do biphasic P waves in I, v5, v6 mean?

A wide double-humped P wave is usually recorded in leads I, II, aVL, V5, V6 with left atrial hypertrophy.

Tell me, please, what does the ECG mean in the conclusion: “Attention is drawn to the Q wave in III, AVF (leveled on inspiration), probably features of intraventricular conduction of a positional nature.”?

The Q wave in leads III and aVF is considered pathological if it exceeds 1/2 of the R wave and is wider than 0.03 s. In the presence of pathological Q(III) only in the III standard lead, a test with a deep breath helps: with a deep breath, the Q associated with myocardial infarction is preserved, while the positional Q(III) decreases or disappears.

Since it is not constant, it is assumed that its appearance and disappearance is not associated with a heart attack, but with the position of the heart.

Write your comment:

Powered by WordPress. Design by Cordobo (with modifications).

High r wave on ecg

7.2.1. Myocardial hypertrophy

The cause of hypertrophy, as a rule, is excessive load on the heart, either by resistance (arterial hypertension) or volume (chronic renal and/or heart failure). Increased work of the heart leads to an increase in metabolic processes in the myocardium and is subsequently accompanied by an increase in the number of muscle fibers. The bioelectrical activity of the hypertrophied part of the heart increases, which is reflected in the electrocardiogram.

7.2.1.1. Left atrial hypertrophy

A characteristic sign of left atrial hypertrophy is an increase in the width of the P wave (more than 0.12 s). The second sign is a change in the shape of the P wave (two humps with a predominance of the second peak) (Fig. 6).

Rice. 6. ECG for left atrial hypertrophy

Left atrial hypertrophy is a typical symptom of mitral valve stenosis and therefore the P wave in this disease is called P-mitrale. Similar changes are observed in leads I, II, aVL, V5, V6.

7.2.1.2. Right atrial hypertrophy

With hypertrophy of the right atrium, changes also affect the P wave, which acquires a pointed shape and increases in amplitude (Fig. 7).

Rice. 7. ECG for hypertrophy of the right atrium (P-pulmonale), right ventricle (S-type)

Hypertrophy of the right atrium is observed with atrial septal defect, hypertension of the pulmonary circulation.

Most often, such a P wave is detected in diseases of the lungs; it is often called P-pulmonale.

Right atrium hypertrophy is a sign of changes in the P wave in leads II, III, aVF, V1, V2.

7.2.1.3. Left ventricular hypertrophy

The ventricles of the heart are better adapted to stress, and in the early stages their hypertrophy may not appear on the ECG, but as the pathology develops, characteristic signs become visible.

With ventricular hypertrophy, the ECG shows significantly more changes than with atrial hypertrophy.

The main signs of left ventricular hypertrophy are (Fig. 8):

Deviation of the electrical axis of the heart to the left (levogram);

Shift of the transition zone to the right (in leads V2 or V3);

The R wave in leads V5, V6 is high and larger in amplitude than RV4;

Deep S in leads V1, V2;

Expanded QRS complex in leads V5, V6 (up to 0.1 s or more);

Displacement of the S-T segment below the isoelectric line with convexity upward;

Negative T wave in leads I, II, aVL, V5, V6.

Rice. 8. ECG for left ventricular hypertrophy

Left ventricular hypertrophy is often observed with arterial hypertension, acromegaly, pheochromocytoma, as well as mitral and aortic valve insufficiency, and congenital heart defects.

7.2.1.4. Right ventricular hypertrophy

Signs of right ventricular hypertrophy appear on the ECG in advanced cases. Diagnosis at the early stage of hypertrophy is extremely difficult.

Signs of hypertrophy (Fig. 9):

Deviation of the electrical axis of the heart to the right (pravogram);

Deep S wave in lead V1 and high R wave in leads III, aVF, V1, V2;

The height of the RV6 tooth is less than normal;

Expanded QRS complex in leads V1, V2 (up to 0.1 s or more);

Deep S wave in lead V5 and also V6;

Displacement of the S-T segment below the isoline with convexity upward in the right III, aVF, V1 and V2;

Complete or incomplete blockade of the right bundle branch;

Shift the transition zone to the left.

Rice. 9. ECG for right ventricular hypertrophy

Right ventricular hypertrophy is most often associated with increased pressure in the pulmonary circulation in pulmonary diseases, mitral valve stenosis, mural thrombosis and pulmonary stenosis and congenital heart defects.

7.2.2. Rhythm disorders

Weakness, shortness of breath, rapid heartbeat, frequent and difficult breathing, interruptions in heart function, a feeling of suffocation, fainting or episodes of loss of consciousness may be manifestations of heart rhythm disturbances due to cardiovascular diseases. An ECG helps confirm their presence, and most importantly determine their type.

It should be remembered that automaticity is a unique property of the cells of the conduction system of the heart, and the sinus node, which controls the rhythm, has the greatest automaticity.

Rhythm disturbances (arrhythmias) are diagnosed in cases where there is no sinus rhythm on the ECG.

Signs of normal sinus rhythm:

P wave frequency – ranging from 60 to 90 (per 1 min);

Identical duration of R-R intervals;

Positive P wave in all leads except aVR.

Heart rhythm disturbances are very diverse. All arrhythmias are divided into nomotopic (changes develop in the sinus node itself) and heterotopic. In the latter case, excitatory impulses arise outside the sinus node, that is, in the atria, atrioventricular junction and ventricles (in the branches of the His bundle).

Nomotopic arrhythmias include sinus brady and tachycardia and irregular sinus rhythm. Heterotopic - atrial fibrillation and flutter and other disorders. If the occurrence of arrhythmia is associated with a dysfunction of excitability, then such rhythm disturbances are divided into extrasystole and paroxysmal tachycardia.

Considering all the variety of types of arrhythmias that can be detected on an ECG, the author, in order not to bore the reader with the intricacies of medical science, allowed himself only to define the basic concepts and consider the most significant rhythm and conduction disorders.

7.2.2.1. Sinus tachycardia

Increased generation of impulses in the sinus node (more than 100 impulses per minute).

On the ECG it is manifested by the presence of a normal P wave and a shortening of the R-R interval.

7.2.2.2. Sinus bradycardia

The pulse generation frequency in the sinus node does not exceed 60.

On the ECG it is manifested by the presence of a normal P wave and a prolongation of the R-R interval.

It should be noted that with a contraction frequency of less than 30, bradycardia is not sinus.

In both cases of tachycardia and bradycardia, the patient is treated for the disease that caused the rhythm disturbance.

7.2.2.3. Irregular sinus rhythm

Impulses are generated irregularly in the sinus node. The ECG shows normal waves and intervals, but the duration of the R-R intervals differs by at least 0.1 s.

This type of arrhythmia can occur in healthy people and does not require treatment.

7.2.2.4. Idioventricular rhythm

Heterotopic arrhythmia, in which the pacemaker is either the bundle branches or the Purkinje fibers.

Extremely severe pathology.

A rare rhythm on the ECG (that is, 30–40 beats per minute), the P wave is absent, the QRS complexes are deformed and widened (duration 0.12 s or more).

Occurs only in severe heart pathology. A patient with such a disorder requires emergency care and is subject to immediate hospitalization in a cardiac intensive care unit.

Extraordinary contraction of the heart caused by a single ectopic impulse. Of practical importance is the division of extrasystoles into supraventricular and ventricular.

A supraventricular (also called atrial) extrasystole is recorded on an ECG if the focus causing extraordinary excitation (contraction) of the heart is located in the atria.

Ventricular extrasystole is recorded on the cardiogram when an ectopic focus is formed in one of the ventricles.

Extrasystole can be rare, frequent (more than 10% of heart contractions in 1 minute), paired (bigemeny) and group (more than three in a row).

Let us list the ECG signs of atrial extrasystole:

P wave changed in shape and amplitude;

The P-Q interval is shortened;

A prematurely recorded QRS complex does not differ in shape from the normal (sinus) complex;

The R-R interval that follows the extrasystole is longer than usual, but shorter than two normal intervals (incomplete compensatory pause).

Atrial extrasystoles are more common in older people against the background of cardiosclerosis and coronary heart disease, but can also be observed in practically healthy people, for example, if a person is very worried or experiencing stress.

If extrasystole is noticed in a practically healthy person, then treatment consists of prescribing Valocordin, Corvalol and ensuring complete rest.

When registering an extrasystole in a patient, treatment of the underlying disease and taking antiarrhythmic drugs from the isoptin group are also required.

Signs of ventricular extrasystole:

The P wave is absent;

The extraordinary QRS complex is significantly widened (more than 0.12 s) and deformed;

Full compensatory pause.

Ventricular extrasystole always indicates heart damage (ischemic heart disease, myocarditis, endocarditis, heart attack, atherosclerosis).

In case of ventricular extrasystole with a frequency of 3–5 contractions per 1 minute, antiarrhythmic therapy is mandatory.

Lidocaine is most often administered intravenously, but other drugs can also be used. Treatment is carried out with careful ECG monitoring.

7.2.2.6. Paroxysmal tachycardia

A sudden attack of hyper-frequent contractions, lasting from a few seconds to several days. The heterotopic pacemaker is located either in the ventricles or supraventricularly.

With supraventricular tachycardia (in this case, impulses are formed in the atria or atrioventricular node), the correct rhythm is recorded on the ECG with a frequency of 180 to 220 contractions per minute.

QRS complexes are not changed or widened.

In the ventricular form of paroxysmal tachycardia, the P waves can change their place on the ECG, the QRS complexes are deformed and widened.

Supraventricular tachycardia occurs in Wolff–Parkinson–White syndrome, less commonly in acute myocardial infarction.

The ventricular form of paroxysmal tachycardia is detected in patients with myocardial infarction, with ischemic heart disease, and disturbances of electrolyte metabolism.

7.2.2.7. Atrial fibrillation (atrial fibrillation)

A type of supraventricular arrhythmias caused by asynchronous, uncoordinated electrical activity of the atria with subsequent deterioration of their contractile function. The flow of impulses is not carried out entirely to the ventricles, and they contract irregularly.

This arrhythmia is one of the most common heart rhythm disturbances.

It occurs in more than 6% of patients over 60 years of age and in 1% of patients younger than this age.

Signs of atrial fibrillation:

R-R intervals are different (arrhythmia);

There are no P waves;

Flicker waves are recorded (they are especially clearly visible in leads II, III, V1, V2);

Electrical alternation (different amplitudes of the I waves in one lead).

Atrial fibrillation occurs with mitral stenosis, thyrotoxicosis and cardiosclerosis, and also often with myocardial infarction. Medical care is to restore sinus rhythm. Procainamide, potassium preparations and other antiarrhythmic drugs are used.

7.2.2.8. Atrial flutter

It is observed much less frequently than atrial fibrillation.

With atrial flutter, normal excitation and contraction of the atria are absent and excitation and contraction of individual atrial fibers are observed.

7.2.2.9. Ventricular fibrillation

The most dangerous and severe rhythm disorder, which quickly leads to cessation of blood circulation. Occurs during myocardial infarction, as well as in the terminal stages of various cardiovascular diseases in patients who are in a state of clinical death. In case of ventricular fibrillation, urgent resuscitation measures are necessary.

Signs of ventricular fibrillation:

Absence of all teeth of the ventricular complex;

Registration of fibrillation waves in all leads with a frequency of 450–600 waves per 1 min.

7.2.3. Conduction disorders

Changes in the cardiogram that occur in the event of a disturbance in the conduction of an impulse in the form of a slowdown or complete cessation of the transmission of excitation are called blockades. Blockades are classified depending on the level at which the violation occurred.

There are sinoatrial, atrial, atrioventricular and intraventricular blockades. Each of these groups is further subdivided. For example, there are sinoatrial blockades of I, II and III degrees, blockades of the right and left bundle branches. There is also a more detailed division (blockade of the anterior branch of the left bundle branch, incomplete block of the right bundle branch). Among conduction disorders recorded using ECG, the following blockades are of greatest practical importance:

Sinoatrial III degree;

Atrioventricular I, II and III degrees;

Blockade of the right and left bundle branches.

7.2.3.1. III degree sinoatrial block

A conduction disorder in which the conduction of excitation from the sinus node to the atria is blocked. On a seemingly normal ECG, the next contraction suddenly disappears (is blocked), that is, the entire P-QRS-T complex (or 2-3 complexes at once). An isoline is recorded in their place. The pathology is observed in those suffering from coronary artery disease, heart attack, cardiosclerosis, and when using a number of drugs (for example, beta blockers). Treatment consists of treating the underlying disease and using atropine, isadrin and similar agents).

7.2.3.2. Atrioventricular block

Impaired conduction of excitation from the sinus node through the atrioventricular connection.

Slowing of atrioventricular conduction is first degree atrioventricular block. Manifests itself on the ECG as a prolongation of the P-Q interval (more than 0.2 s) with a normal heart rate.

Second degree atrioventricular block is an incomplete block in which not all impulses coming from the sinus node reach the ventricular myocardium.

On the ECG, the following two types of blockade are distinguished: the first is Mobitz-1 (Samoilov-Wenckebach) and the second is Mobitz-2.

Signs of Mobitz-1 type blockade:

Constantly lengthening P interval

As a result of the first sign, at some stage after the P wave the QRS complex disappears.

A sign of Mobitz-2 type block is the periodic loss of the QRS complex against the background of an extended P-Q interval.

Third degree atrioventricular block is a condition in which not a single impulse coming from the sinus node is carried to the ventricles. The ECG records two types of rhythm that are not related to each other; the work of the ventricles (QRS complexes) and the atria (P waves) is not coordinated.

Third degree blockade often occurs in cardiosclerosis, myocardial infarction, and improper use of cardiac glycosides. The presence of this type of blockade in a patient is an indication for his urgent hospitalization in a cardiology hospital. Atropine, ephedrine and, in some cases, prednisolone are used for treatment.

7.2.Z.Z. Bundle branch blocks

In a healthy person, an electrical impulse originating in the sinus node, passing through the branches of the His bundle, simultaneously excites both ventricles.

When the right or left bundle branch is blocked, the path of the impulse changes and therefore the excitation of the corresponding ventricle is delayed.

It is also possible that incomplete blockades and so-called blockades of the anterior and posterior branches of the bundle branch may occur.

Signs of complete blockade of the right bundle branch (Fig. 10):

Deformed and widened (more than 0.12 s) QRS complex;

Negative T wave in leads V1 and V2;

Displacement of the S-T segment from the isoline;

Widening and splitting of the QRS in leads V1 and V2 in the form of RsR.

Rice. 10. ECG with complete block of the right bundle branch

Signs of complete blockade of the left bundle branch:

The QRS complex is deformed and widened (more than 0.12 s);

Offset of the S-T segment from the isoline;

Negative T wave in leads V5 and V6;

Expansion and splitting of the QRS complex in leads V5 and V6 in the form of RR;

Deformation and expansion of the QRS in leads V1 and V2 in the form of rS.

These types of blockades occur in cases of heart injury, acute myocardial infarction, atherosclerotic and myocardial cardiosclerosis, and in the incorrect use of a number of medications (cardiac glycosides, novocainamide).

Patients with intraventricular block do not need special therapy. They are hospitalized for treatment of the disease that caused the blockade.

7.2.4. Wolff-Parkinson-White syndrome

This syndrome (WPW) was first described by the above-mentioned authors in 1930 as a form of supraventricular tachycardia that is observed in young healthy people (“functional bundle branch block”).

It has now been established that in the body, sometimes, in addition to the normal path of impulse conduction from the sinus node to the ventricles, there are additional bundles (Kent, James and Mahaim). Along these pathways, excitation reaches the ventricles of the heart faster.

There are several types of WPW syndrome. If excitation enters the left ventricle earlier, then WPW syndrome type A is recorded on the ECG. With type B, excitation enters the right ventricle earlier.

Signs of WPW syndrome type A:

The delta wave on the QRS complex is positive in the right precordial leads and negative in the left (the result of premature excitation of part of the ventricle);

The direction of the main teeth in the chest leads is approximately the same as with blockade of the left bundle branch.

Signs of WPW syndrome type B:

Shortened (less than 0.11 s) P-Q interval;

The QRS complex is widened (more than 0.12 s) and deformed;

Negative delta wave for the right chest leads, positive for the left ones;

The direction of the main teeth in the chest leads is approximately the same as with blockade of the right bundle branch.

It is possible to register a sharply shortened P-Q interval with an undeformed QRS complex and the absence of a delta wave (Lown-Ganong-Levin syndrome).

Additional bundles are inherited. In approximately 30–60% of cases they do not manifest themselves. Some people may develop paroxysms of tachyarrhythmias. In case of arrhythmia, medical care is provided in accordance with the general rules.

7.2.5. Early ventricular repolarization

This phenomenon occurs in 20% of patients with cardiovascular pathology (most often found in patients with supraventricular heart rhythm disturbances).

This is not a disease, but patients with cardiovascular diseases who experience this syndrome are 2-4 times more likely to suffer from rhythm and conduction disturbances.

Signs of early ventricular repolarization (Fig. 11) include:

ST segment elevation;

Late delta wave (notch on the descending part of the R wave);

High amplitude teeth;

Double-humped P wave of normal duration and amplitude;

Shortening of PR and QT intervals;

A rapid and sharp increase in the amplitude of the R wave in the chest leads.

Rice. 11. ECG for early ventricular repolarization syndrome

7.2.6. Coronary heart disease

In coronary heart disease (CHD), the blood supply to the myocardium is impaired. In the early stages, there may be no changes in the electrocardiogram, but in later stages they are very noticeable.

With the development of myocardial dystrophy, the T wave changes and signs of diffuse changes in the myocardium appear.

These include:

Reduced amplitude of the R wave;

S-T segment depression;

Biphasic, moderately widened and flat T wave in almost all leads.

IHD occurs in patients with myocarditis of various origins, as well as dystrophic changes in the myocardium and atherosclerotic cardiosclerosis.

With the development of an attack of angina, the ECG can reveal a displacement of the S-T segment and changes in the T wave in those leads that are located above the area with impaired blood supply (Fig. 12).

Rice. 12. ECG for angina pectoris (during an attack)

The causes of angina are hypercholesterolemia, dyslipidemia. In addition, arterial hypertension, diabetes mellitus, psycho-emotional overload, fear, and obesity can trigger the development of an attack.

Depending on which layer of the heart muscle ischemia occurs, there are:

Subendocardial ischemia (over the ischemic area, the S-T displacement is below the isoline, the T wave is positive, of large amplitude);

Subepicardial ischemia (rise of the S-T segment above the isoline, T negative).

The occurrence of angina is accompanied by the appearance of typical chest pain, usually provoked by physical activity. This pain is pressing in nature, lasts several minutes and goes away after taking nitroglycerin. If the pain lasts more than 30 minutes and is not relieved by taking nitro drugs, acute focal changes can most likely be assumed.

Emergency care for angina pectoris involves relieving pain and preventing recurrent attacks.

Analgesics (from analgin to promedol), nitro drugs (nitroglycerin, sustak, nitrong, monocinque, etc.), as well as validol and diphenhydramine, seduxen are prescribed. If necessary, oxygen inhalation is carried out.

7.2.8. Myocardial infarction

Myocardial infarction is the development of necrosis of the heart muscle as a result of prolonged circulatory disorders in the ischemic area of ​​the myocardium.

In more than 90% of cases, the diagnosis is determined using an ECG. In addition, a cardiogram allows you to determine the stage of a heart attack, find out its location and type.

An unconditional sign of a heart attack is the appearance on the ECG of a pathological Q wave, which is characterized by excessive width (more than 0.03 s) and greater depth (a third of the R wave).

Possible options: QS, QrS. An S-T shift (Fig. 13) and T wave inversion are observed.

Rice. 13. ECG for anterolateral myocardial infarction (acute stage). There are cicatricial changes in the posteroinferior parts of the left ventricle

Sometimes an S-T displacement occurs without the presence of a pathological Q wave (small-focal myocardial infarction). Signs of a heart attack:

Pathological Q wave in leads located above the infarct area;

Displacement of the S-T segment by an arc upward (lifting) relative to the isoline in the leads located above the infarct area;

Discordant displacement below the isoline of the S-T segment in leads opposite to the area of ​​infarction;

Negative T wave in leads located above the infarct area.

As the disease progresses, the ECG changes. This relationship is explained by the stages of changes during a heart attack.

There are four stages in the development of myocardial infarction:

The most acute stage (Fig. 14) lasts several hours. At this time, the S-T segment rises sharply in the corresponding leads on the ECG, merging with the T wave.

Rice. 14. Sequence of ECG changes during myocardial infarction: 1 – Q-infarction; 2 – not Q-infarction; A – the most acute stage; B – acute stage; B – subacute stage; D – scar stage (post-infarction cardiosclerosis)

In the acute stage, a zone of necrosis forms and a pathological Q wave appears. The R amplitude decreases, the S-T segment remains elevated, and the T wave becomes negative. The duration of the acute stage is on average about 1–2 weeks.

The subacute stage of infarction lasts for 1–3 months and is characterized by a cicatricial organization of the necrosis focus. On the ECG at this time there is a gradual return of the S-T segment to the isoline, the Q wave decreases, and the R amplitude, on the contrary, increases.

The T wave remains negative.

The scarring stage can last for several years. At this time, the organization of scar tissue occurs. On the ECG, the Q wave decreases or disappears completely, S-T is located on the isoline, negative T gradually becomes isoelectric, and then positive.

This phasing is often called the natural dynamics of the ECG during myocardial infarction.

A heart attack can be localized in any part of the heart, but most often occurs in the left ventricle.

Depending on the location, infarction of the anterior lateral and posterior walls of the left ventricle is distinguished. The localization and extent of changes are revealed by analyzing ECG changes in the corresponding leads (Table 6).

Table 6. Localization of myocardial infarction

Great difficulties arise when diagnosing a recurrent infarction when new changes are superimposed on an already changed ECG. Dynamic monitoring with recording of a cardiogram at short intervals helps.

A typical heart attack is characterized by burning, severe chest pain that does not go away after taking nitroglycerin.

There are also atypical forms of heart attack:

Abdominal (pain in the heart and stomach);

Asthmatic (cardiac pain and cardiac asthma or pulmonary edema);

Arrhythmic (cardiac pain and rhythm disturbances);

Collaptoid (cardiac pain and a sharp drop in blood pressure with profuse sweating);

Treating a heart attack is an extremely difficult task. As a rule, the more difficult it becomes, the more widespread the lesion is. At the same time, according to the apt remark of one of the Russian zemstvo doctors, sometimes the treatment of an extremely severe heart attack goes unexpectedly smoothly, and sometimes an uncomplicated, simple micro-infarction makes the doctor sign of impotence.

Emergency care consists of relieving pain (for this, narcotic and other analgesics are used), also eliminating fears and psycho-emotional arousal with the help of sedatives, reducing the area of ​​the heart attack (using heparin), and sequentially eliminating other symptoms depending on the degree of their danger.

After completing inpatient treatment, patients who have had a heart attack are sent to a sanatorium for rehabilitation.

The final stage is long-term observation in a local clinic.

7.2.9. Syndromes due to electrolyte disturbances

Certain ECG changes make it possible to judge the dynamics of electrolyte content in the myocardium.

To be fair, it should be said that there is not always a clear correlation between the level of electrolytes in the blood and the content of electrolytes in the myocardium.

Nevertheless, electrolyte disturbances detected by ECG serve as a significant aid to the doctor in the process of diagnostic search, as well as in choosing the correct treatment.

The most well studied changes in the ECG are disturbances in potassium and calcium metabolism (Fig. 15).

Rice. 15. ECG diagnosis of electrolyte disorders (A. S. Vorobyov, 2003): 1 – normal; 2 – hypokalemia; 3 – hyperkalemia; 4 – hypocalcemia; 5 – hypercalcemia

Tall, pointed T wave;

Shortening of the Q-T interval;

Decreased R amplitude.

With severe hyperkalemia, intraventricular conduction disturbances are observed.

Hyperkalemia occurs in diabetes (acidosis), chronic renal failure, severe injuries with crushing muscle tissue, adrenal insufficiency, and other diseases.

Decreased S-T segment downwards;

Negative or biphasic T;

With severe hypokalemia, atrial and ventricular extrasystoles and intraventricular conduction disturbances appear.

Hypokalemia occurs when there is a loss of potassium salts in patients with severe vomiting, diarrhea, after prolonged use of diuretics, steroid hormones, and with a number of endocrine diseases.

Treatment consists of replenishing potassium deficiency in the body.

Shortening of the Q-T interval;

Shortening of the S-T segment;

Expansion of the ventricular complex;

Rhythm disturbances with a significant increase in calcium.

Hypercalcemia is observed with hyperparathyroidism, bone destruction by tumors, hypervitaminosis D and excessive administration of potassium salts.

Increasing the duration of the QT interval;

Lengthening the S-T segment;

Decreased T amplitude.

Hypocalcemia occurs with decreased function of the parathyroid glands, in patients with chronic renal failure, with severe pancreatitis and hypovitaminosis D.

7.2.9.5. Glycoside intoxication

Cardiac glycosides have long been successfully used in the treatment of heart failure. These tools are irreplaceable. Their intake helps to reduce heart rate (heart rate) and more vigorously expel blood during systole. As a result, hemodynamic parameters improve and manifestations of circulatory failure decrease.

In case of an overdose of glycosides, characteristic ECG signs appear (Fig. 16), which, depending on the severity of intoxication, require either dose adjustment or discontinuation of the drug. Patients with glycoside intoxication may experience nausea, vomiting, and interruptions in heart function.

Rice. 16. ECG in case of overdose of cardiac glycosides

Signs of glycoside intoxication:

Shortening of electrical systole;

Decreased S-T segment downwards;

Negative T wave;

Severe intoxication with glycosides requires discontinuation of the drug and the prescription of potassium supplements, lidocaine and beta blockers.

Prikhodko Valentin Ivanovich, Copyright ©18 E-mail: , Ukraine.

All materials on the site are provided for informational and educational purposes only.

P-Q interval is determined from the beginning of the P wave to the beginning of the Q wave. If the Q wave is absent, then the P-Q interval ends at the transition to the R wave. The P-Q interval (P-R) reflects the time of excitation of the atria, atrioventricular node, atrioventricular bundle, its branches and cardiac conducting myocytes. Thus, the P-Q interval indicates the time required for the impulse originating in the sinoatrial node to reach the ventricles (L.V. Danovsky, 1976), that is, the time of atrioventricular conduction.

P-Q interval in adults it ranges from 0.12 to 0.2 s. It varies depending on the frequency of the rhythm: the more frequent the rhythm, the shorter this interval and vice versa. An extension of the P-Q interval of more than 0.2 s with bradycardia of more than 0.22 s) indicates a slowdown in atrioventricular conduction.
Q, R, S waves are designated as a single QRS complex. They reflect the period of excitation propagation through the ventricles.

Q wave shows excitation of the interventricular septum. It is often recorded in standard leads I and II, less often in III. On a normal level, the Q wave may be absent in all three standard leads. A pronounced (slightly deepened) Q wave in standard lead I is recorded in people with a hypersthenic build, when the electrical axis of the heart is horizontal and the heart is rotated counterclockwise around the longitudinal axis, when an S wave is recorded in standard lead III, that is, an ECG type is recorded in standard leads qRI and RsIII.
On the right chest leads V1, 2 Q wave Normally it is not recorded, but a small q wave is recorded in the left chest leads V4, 5, 6.

Deep Q wave, no more than 0.03 s wide, can be recorded in standard lead III with the heart in a vertical position. At the same time, in lead aVF the Q wave is shallow.

R wave- the largest amplitude, recorded in standard II and in the left chest leads. It reflects the process of propagation of excitation along the Eerhuska of the heart, the anterior, lateral and posterior walls of the left and right ventricles. The height of the R wave varies widely in standard leads - from 2 to 20 mm, with an average of 7-12 mm. In the chest leads, the R wave gradually increases from V1 to V4 (sometimes to V5).

In leads V5,6 it decreases somewhat due to the removal of the active electrode from the potential source. The height of the R wave in standard leads I, II, III and lead aVF normally does not exceed 20 mm, and in aVL - 11 mm (S. Bober et al., 1974). With a vertical position of the electrical axis of the heart, hypertrophy of the right ventricle, blockade of the right leg of the atrioventricular bundle, the height of the R wave increases in leads III, aVF and right chest. Normally, the ratio of the R wave to the S wave in the right precordial leads (V1, 2) is less than one, in V3 it can be equal to one, in leads V5,6 it is more than one.

Any ECG consists of several waves, segments and intervals, reflecting the complex process of propagation of an excitation wave throughout the heart.

The shape of electrocardiographic complexes and the size of the teeth are different in different leads and are determined by the size and direction of the projection of the moment vectors of the cardiac EMF onto the axis of a particular lead. If the projection of the torque vector is directed towards the positive electrode of a given lead, an upward deviation from the isoline is recorded on the ECG - positive waves. If the projection of the vector is directed towards the negative electrode, a deviation downward from the isoline is recorded on the ECG - negative waves. In the case when the moment vector is perpendicular to the lead axis, its projection onto this axis is zero and no deviations from the isoline are recorded on the ECG. If during the excitation cycle the vector changes its direction relative to the poles of the lead axis, then the wave becomes biphasic.

The general scheme for decoding the ECG is presented below.

Segments and waves of a normal ECG.

Prong R.

The P wave reflects the process of depolarization of the right and left atria. In a healthy person, in leads I, II, aVF, V-V the P wave is always positive, in leads III and aVL, V it can be positive, biphasic or (rarely) negative, and in lead aVR the P wave is always negative. In leads I and II, the P wave has maximum amplitude. The duration of the P wave does not exceed 0.1 s, and its amplitude is 1.5-2.5 mm.

P-Q(R) interval.

The P-Q(R) interval reflects the duration of atrioventricular conduction, i.e. time of excitation propagation through the atria, AV node, His bundle and its branches. Its duration is 0.12-0.20 s and in a healthy person depends mainly on the heart rate: the higher the heart rate, the shorter the P-Q(R) interval.

Ventricular QRST complex.

The ventricular QRST complex reflects the complex process of propagation (QRS complex) and extinction (RS-T segment and T wave) of excitation throughout the ventricular myocardium.

Q wave.

The Q wave can normally be recorded in all standard and enhanced unipolar limb leads and in precordial leads V-V. The amplitude of the normal Q wave in all leads, except aVR, does not exceed the height of the R wave, and its duration is 0.03 s. In lead aVR in a healthy person, a deep and wide Q wave or even a QS complex may be recorded.

R wave

Normally, the R wave can be recorded in all standard and enhanced limb leads. In lead aVR, the R wave is often poorly defined or absent altogether. In the chest leads, the amplitude of the R wave gradually increases from V to V, and then decreases slightly in V and V. Sometimes the r wave may be absent. Prong

R reflects the spread of excitation along the interventricular septum, and the R wave - along the muscles of the left and right ventricles. The interval of internal deviation in lead V does not exceed 0.03 s, and in lead V - 0.05 s.

S wave

In a healthy person, the amplitude of the S wave in various electrocardiographic leads fluctuates within wide limits, not exceeding 20 mm. With a normal position of the heart in the chest in the limb leads, the S amplitude is small, except in lead aVR. In the chest leads, the S wave gradually decreases from V, V to V, and in leads V, V it has a small amplitude or is absent altogether. The equality of the R and S waves in the precordial leads (“transition zone”) is usually recorded in lead V or (less often) between V and V or V and V.

The maximum duration of the ventricular complex does not exceed 0.10 s (usually 0.07-0.09 s).

RS-T segment.

The RS-T segment in a healthy person in the limb leads is located on the isoline (0.5 mm). Normally, in chest leads V-V there may be a slight displacement of the RS-T segment upward from the isoline (no more than 2 mm), and in leads V - downward (no more than 0.5 mm).

T wave

Normally, the T wave is always positive in leads I, II, aVF, V-V, and T>T, and T>T. In leads III, aVL and V, the T wave can be positive, biphasic or negative. In lead aVR, the T wave is normally always negative.

Q-T interval(QRST)

The Q-T interval is called electrical ventricular systole. Its duration depends primarily on the number of heart contractions: the higher the rhythm frequency, the shorter the proper Q-T interval. The normal duration of the Q-T interval is determined by the Bazett formula: Q-T=K, where K is a coefficient equal to 0.37 for men and 0.40 for women; R-R – duration of one cardiac cycle.

Electrocardiogram analysis.

The analysis of any ECG should begin with checking the correctness of its registration technique. First, you need to pay attention to the presence of various interferences. Interference that occurs during ECG recording:

a - induction currents - network induction in the form of regular oscillations with a frequency of 50 Hz;

b - “swimming” (drift) of the isoline as a result of poor contact of the electrode with the skin;

c - interference caused by muscle tremor (irregular frequent vibrations are visible).

Interference occurring during ECG recording

Secondly, it is necessary to check the amplitude of the control millivolt, which should correspond to 10mm.

Thirdly, the speed of paper movement during ECG recording should be assessed. When recording an ECG at a speed of 50 mm, 1 mm on paper tape corresponds to a time period of 0.02 s, 5 mm - 0.1 s, 10 mm - 0.2 s, 50 mm - 1.0 s.

I.Heart rate and conduction analysis:

1) assessment of the regularity of heart contractions;

2) counting the number of heartbeats;

3) determination of the source of excitation;

4) assessment of the conductivity function.

II. Determination of heart rotations around the anteroposterior, longitudinal and transverse axes:

1) determination of the position of the electrical axis of the heart in the frontal plane;

2) determination of the rotation of the heart around the longitudinal axis;

3) determination of the rotation of the heart around the transverse axis.

III. Analysis of the atrial P wave.

IV. Analysis of the ventricular QRST complex:

1) analysis of the QRS complex,

2) analysis of the RS-T segment,

3) analysis of the Q-T interval.

V. Electrocardiographic report.

I.1) Heart rate regularity is assessed by comparing the duration of R-R intervals between successively recorded cardiac cycles. The R-R interval is usually measured between the tops of the R waves. Regular, or correct, heart rhythm is diagnosed if the duration of the measured R-R is the same and the spread of the obtained values ​​does not exceed 10% of the average R-R duration. In other cases, the rhythm is considered abnormal (irregular), which can be observed with extrasystole, atrial fibrillation, sinus arrhythmia, etc.

2) With the correct rhythm, heart rate (HR) is determined by the formula: HR=.

If the ECG rhythm is abnormal, in one of the leads (most often in standard lead II) it is recorded longer than usual, for example, for 3-4 seconds. Then the number of QRS complexes recorded in 3 seconds is counted and the result is multiplied by 20.

In a healthy person, the resting heart rate ranges from 60 to 90 per minute. An increase in heart rate is called tachycardia, and a decrease is called bradycardia.

Assessing the regularity of rhythm and heart rate:

a) correct rhythm; b), c) incorrect rhythm

3) To determine the source of excitation (pacemaker), it is necessary to evaluate the course of excitation in the atria and establish the ratio of the R waves to the ventricular QRS complexes.

Sinus rhythm characterized by: the presence in standard lead II of positive H waves preceding each QRS complex; constant identical shape of all P waves in the same lead.

In the absence of these signs, various variants of non-sinus rhythm are diagnosed.

Atrial rhythm(from the lower parts of the atria) is characterized by the presence of negative P, P waves and the following unchanged QRS complexes.

Rhythm from AV connection characterized by: the absence of a P wave on the ECG, merging with the usual unchanged QRS complex, or the presence of negative P waves located after the normal unchanged QRS complexes.

Ventricular (idioventricular) rhythm characterized by: slow ventricular rhythm (less than 40 beats per minute); the presence of widened and deformed QRS complexes; lack of a natural connection between QRS complexes and P waves.

4) For a rough preliminary assessment of the conduction function, it is necessary to measure the duration of the P wave, the duration of the P-Q(R) interval and the total duration of the ventricular QRS complex. An increase in the duration of these waves and intervals indicates a slowdown in conduction in the corresponding part of the conduction system of the heart.

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

Bailey's six-axis system.

A) Determining the angle by graphical method. The algebraic sum of the amplitudes of the QRS complex waves is calculated in any two leads from the limbs (standard leads I and III are usually used), the axes of which are located in the frontal plane.

a positive or negative value of an algebraic sum on an arbitrarily chosen scale is plotted on the positive or negative part of the axis of the corresponding lead in the six-axis Bailey coordinate system. These values ​​represent projections of the desired electrical axis of the heart onto axes I and III of standard leads. From the ends of these projections, perpendiculars to the axes of the leads are restored. The intersection point of the perpendiculars is connected to the center of the system. This line is the electrical axis of the heart.

b) Visual determination of the angle. Allows you to quickly estimate the angle with an accuracy of 10°. The method is based on two principles:

1. The maximum positive value of the algebraic sum of the teeth of the QRS complex is observed in that lead, the axis of which approximately coincides with the location of the electrical axis of the heart, and is parallel to it.

2. A complex of type RS, where the algebraic sum of the teeth is zero (R=S or R=Q+S), is written in the lead whose axis is perpendicular to the electrical axis of the heart.

With a normal position of the electrical axis of the heart: RRR; in leads III and aVL, the R and S waves are approximately equal to each other.

In a horizontal position or deviation of the electrical axis of the heart to the left: high R waves are fixed in leads I and aVL, with R>R>R; a deep S wave is recorded in lead III.

In a vertical position or deviation of the electrical axis of the heart to the right: high R waves are recorded in leads III and aVF, and R R> R; deep S waves are recorded in leads I and aV

III. P wave analysis includes: 1) measurement of P wave amplitude; 2) measurement of the duration of the P wave; 3) determination of the polarity of the P wave; 4) determination of the shape of the P wave.

IV.1) Analysis of the QRS complex includes: a) assessment of the Q wave: amplitude and comparison with the R amplitude, duration; b) assessment of the R wave: amplitude, comparing it with the amplitude of Q or S in the same lead and with R in other leads; duration of the interval of internal deviation in leads V and V; possible splitting of a tooth or the appearance of an additional one; c) assessment of the S wave: amplitude, comparing it with the R amplitude; possible widening, jagged or splitting of the tooth.

2) AtRS-T segment analysis necessary: ​​find connection point j; measure its deviation (+–) from the isoline; measure the amount of displacement of the RS-T segment, either the isoline up or down at a point located 0.05-0.08 s from point j to the right; determine the form of possible displacement of the RS-T segment: horizontal, obliquely downward, obliquely upward.

3)When analyzing the T wave should: determine the polarity of T, evaluate its shape, measure the amplitude.

4) QT interval analysis: Duration measurement.

V. Electrocardiographic conclusion:

1) source of heart rhythm;

2) regularity of heart rhythm;

4) position of the electrical axis of the heart;

5) the presence of four electrocardiographic syndromes: a) heart rhythm disturbances; b) conduction disorders; c) hypertrophy of the myocardium of the ventricles and atria or their acute overload; d) myocardial damage (ischemia, dystrophy, necrosis, scars).

Electrocardiogram for heart rhythm disturbances

1. Disorders of automatism of the SA node (nomotopic arrhythmias)

1) Sinus tachycardia: increase in the number of heartbeats to 90-160(180) per minute (shortening R-R intervals); maintaining correct sinus rhythm (correct alternation of the P wave and the QRST complex in all cycles and a positive P wave).

2) Sinus bradycardia: decrease in the number of heartbeats to 59-40 per minute (increase in the duration of the R-R intervals); maintaining correct sinus rhythm.

3) Sinus arrhythmia: fluctuations in the duration of R-R intervals exceeding 0.15 s and associated with the respiratory phases; preservation of all electrocardiographic signs of sinus rhythm (alternating P wave and QRS-T complex).

4) Sinoatrial node weakness syndrome: persistent sinus bradycardia; periodic appearance of ectopic (non-sinus) rhythms; presence of SA blockade; bradycardia-tachycardia syndrome.

a) ECG of a healthy person; b) sinus bradycardia; c) sinus arrhythmia

2. Extrasystole.

1) Atrial extrasystole: premature extraordinary appearance of the P′ wave and the following QRST′ complex; deformation or change in the polarity of the P′ wave of the extrasystole; the presence of an unchanged extrasystolic ventricular QRST′ complex, similar in shape to ordinary normal complexes; the presence of an incomplete compensatory pause after an atrial extrasystole.

Atrial extrasystole (II standard lead): a) from the upper parts of the atria; b) from the middle parts of the atria; c) from the lower parts of the atria; d) blocked atrial extrasystole.

2) Extrasystoles from the atrioventricular connection: premature, extraordinary appearance on the ECG of an unchanged ventricular QRS′ complex, similar in shape to other QRST complexes of sinus origin; negative P′ wave in leads II, III and aVF after the extrasystolic QRS′ complex or absence of P′ wave (fusion of P′ and QRS′); the presence of an incomplete compensatory pause.

3) Ventricular extrasystole: premature extraordinary appearance on the ECG of an altered ventricular QRS complex; significant expansion and deformation of the extrasystolic QRS complex; the location of the RS-T′ segment and the T′ wave of the extrasystole is discordant to the direction of the main wave of the QRS′ complex; absence of a P wave before the ventricular extrasystole; the presence in most cases of a complete compensatory pause after a ventricular extrasystole.

a) left ventricular; b) right ventricular extrasystole

3. Paroxysmal tachycardia.

1) Atrial paroxysmal tachycardia: a sudden onset and also suddenly ending attack of increased heart rate up to 140-250 per minute while maintaining the correct rhythm; the presence of a reduced, deformed, biphasic or negative P wave before each ventricular QRS complex; normal unchanged ventricular QRS complexes; in some cases, there is a deterioration in atrioventricular conduction with the development of first degree atrioventricular block with periodic loss of individual QRS′ complexes (non-constant signs).

2) Paroxysmal tachycardia from the atrioventricular junction: a sudden onset and also suddenly ending attack of increased heart rate up to 140-220 per minute while maintaining the correct rhythm; the presence in leads II, III and aVF of negative P' waves located behind the QRS' complexes or merging with them and not recorded on the ECG; normal unchanged ventricular QRS complexes.

3) Ventricular paroxysmal tachycardia: a sudden onset and also suddenly ending attack of increased heart rate up to 140-220 per minute while maintaining the correct rhythm in most cases; deformation and widening of the QRS complex more than 0.12 s with discordant location of the RS-T segment and T wave; the presence of atrioventricular dissociation, i.e. complete separation of the rapid ventricular rhythm and normal atrial rhythm with occasionally recorded single normal unchanged QRST complexes of sinus origin.

4. Atrial flutter: the presence on the ECG of frequent - up to 200-400 per minute - regular, similar atrial F waves, having a characteristic sawtooth shape (leads II, III, aVF, V, V); in most cases, correct, regular ventricular rhythm with equal F-F intervals; the presence of normal unchanged ventricular complexes, each of which is preceded by a certain number of atrial F waves (2:1, 3:1, 4:1, etc.).

5. Atrial fibrillation: absence of P waves in all leads; the presence of random waves throughout the cardiac cycle f, having different shapes and amplitudes; waves f better recorded in leads V, V, II, III and aVF; irregular ventricular QRS complexes – irregular ventricular rhythm; the presence of QRS complexes, which in most cases have a normal, unchanged appearance.

a) coarse-wavy form; b) finely wavy form.

6. Ventricular flutter: frequent (up to 200-300 per minute), regular and identical in shape and amplitude flutter waves, reminiscent of a sinusoidal curve.

7. Ventricular fibrillation: frequent (from 200 to 500 per minute), but irregular waves, differing from each other in different shapes and amplitudes.

Electrocardiogram for conduction dysfunction.

1. Sinoatrial blockade: periodic loss of individual cardiac cycles; the increase in the pause between two adjacent P or R waves at the time of loss of cardiac cycles is almost 2 times (less often 3 or 4 times) compared to the usual P-P or R-R intervals.

2. Intraatrial block: increase in the duration of the P wave by more than 0.11 s; splitting of the P wave.

3. Atrioventricular blockade.

1) I degree: increase in the duration of the P-Q(R) interval by more than 0.20 s.

a) atrial form: expansion and splitting of the P wave; QRS is normal.

b) nodal form: lengthening of the P-Q(R) segment.

c) distal (three-bundle) form: pronounced QRS deformation.

2) II degree: loss of individual ventricular QRST complexes.

a) Mobitz type I: gradual prolongation of the P-Q(R) interval followed by loss of QRST. After an extended pause, the P-Q(R) is again normal or slightly extended, after which the entire cycle is repeated.

b) Mobitz type II: loss of QRST is not accompanied by a gradual lengthening of P-Q(R), which remains constant.

c) Mobitz type III (incomplete AV block): either every second (2:1) or two or more ventricular complexes in a row are lost (block 3:1, 4:1, etc.).

3) III degree: complete separation of atrial and ventricular rhythms and a decrease in the number of ventricular contractions to 60-30 per minute or less.

4. Block of the legs and branches of the His bundle.

1) Block of the right leg (branch) of the His bundle.

a) Complete blockade: the presence in the right chest leads V (less often in limb leads III and aVF) of QRS complexes of the rSR′ or rSR′ type, having an M-shaped appearance, with R′ > r; the presence in the left chest leads (V, V) and leads I, aVL of a widened, often jagged S wave; increase in the duration (width) of the QRS complex by more than 0.12 s; the presence in lead V (less often in III) of depression of the RS-T segment with a convexity facing upward, and a negative or biphasic (–+) asymmetric T wave.

b) Incomplete blockade: the presence of a QRS complex of type rSr′ or rSR′ in lead V, and a slightly widened S wave in leads I and V; duration of the QRS complex is 0.09-0.11 s.

2) Blockade of the left anterior branch of the His bundle: sharp deviation of the electrical axis of the heart to the left (angle α –30°); QRS in leads I, aVL type qR, III, aVF, II type rS; the total duration of the QRS complex is 0.08-0.11 s.

3) Block of the left posterior branch of the His bundle: sharp deviation of the electrical axis of the heart to the right (angle α120°); the shape of the QRS complex in leads I and aVL is type rS, and in leads III, aVF it is type qR; the duration of the QRS complex is within 0.08-0.11 s.

4) Left bundle branch block: in leads V, V, I, aVL there are widened deformed ventricular complexes of type R with a split or wide apex; in leads V, V, III, aVF there are widened deformed ventricular complexes, having the appearance of QS or rS with a split or wide apex of the S wave; an increase in the total duration of the QRS complex by more than 0.12 s; the presence in leads V, V, I, aVL of a discordant relative to QRS shift of the RS-T segment and negative or biphasic (–+) asymmetric T waves; deviation of the electrical axis of the heart to the left is often observed, but not always.

5) Blockade of three branches of the His bundle: atrioventricular block I, II or III degree; blockade of two branches of the His bundle.

Electrocardiogram for atrial and ventricular hypertrophy.

1. Left atrial hypertrophy: bifurcation and increase in the amplitude of P waves (P-mitrale); an increase in the amplitude and duration of the second negative (left atrial) phase of the P wave in lead V (less often V) or the formation of a negative P; negative or biphasic (+–) P wave (non-constant sign); increase in the total duration (width) of the P wave – more than 0.1 s.

2. Right atrium hypertrophy: in leads II, III, aVF, the P waves are high-amplitude, with a pointed apex (P-pulmonale); in leads V, the P wave (or at least its first - right atrial phase) is positive with a pointed apex (P-pulmonale); in leads I, aVL, V the P wave is of low amplitude, and in aVL it can be negative (not a constant sign); the duration of the P waves does not exceed 0.10 s.

3. Left ventricular hypertrophy: an increase in the amplitude of the R and S waves. In this case, R2 25mm; signs of rotation of the heart around the longitudinal axis counterclockwise; displacement of the electrical axis of the heart to the left; displacement of the RS-T segment in leads V, I, aVL below the isoline and the formation of a negative or biphasic (–+) T wave in leads I, aVL and V; an increase in the duration of the interval of internal QRS deviation in the left precordial leads by more than 0.05 s.

4. Right ventricular hypertrophy: displacement of the electrical axis of the heart to the right (angle α more than 100°); an increase in the amplitude of the R wave in V and the S wave in V; the appearance of a QRS complex of type rSR′ or QR in lead V; signs of rotation of the heart around the longitudinal axis clockwise; downward displacement of the RS-T segment and the appearance of negative T waves in leads III, aVF, V; an increase in the duration of the interval of internal deviation in V by more than 0.03 s.

Electrocardiogram for coronary heart disease.

1. Acute stage of myocardial infarction characterized by the rapid, within 1-2 days, formation of a pathological Q wave or QS complex, displacement of the RS-T segment above the isoline and the first positive and then negative T wave merging with it; after a few days the RS-T segment approaches the isoline. At the 2-3rd week of the disease, the RS-T segment becomes isoelectric, and the negative coronary T wave sharply deepens and becomes symmetrical and pointed.

2. In the subacute stage of myocardial infarction a pathological Q wave or QS complex (necrosis) and a negative coronary T wave (ischemia) are recorded, the amplitude of which gradually decreases starting from the 20-25th day. The RS-T segment is located on the isoline.

3. Scar stage of myocardial infarction characterized by the persistence for a number of years, often throughout the patient’s entire life, of a pathological Q wave or QS complex and the presence of a weakly negative or positive T wave.

krasgmu.net

7.2.1. Myocardial hypertrophy

The cause of hypertrophy, as a rule, is excessive load on the heart, either by resistance (arterial hypertension) or volume (chronic renal and/or heart failure). Increased work of the heart leads to an increase in metabolic processes in the myocardium and is subsequently accompanied by an increase in the number of muscle fibers. The bioelectrical activity of the hypertrophied part of the heart increases, which is reflected in the electrocardiogram.

7.2.1.1. Left atrial hypertrophy

A characteristic sign of left atrial hypertrophy is an increase in the width of the P wave (more than 0.12 s). The second sign is a change in the shape of the P wave (two humps with a predominance of the second peak) (Fig. 6).

Rice. 6. ECG for left atrial hypertrophy

Left atrial hypertrophy is a typical symptom of mitral valve stenosis and therefore the P wave in this disease is called P-mitrale. Similar changes are observed in leads I, II, aVL, V5, V6.

7.2.1.2. Right atrial hypertrophy

With hypertrophy of the right atrium, changes also affect the P wave, which acquires a pointed shape and increases in amplitude (Fig. 7).

Rice. 7. ECG for hypertrophy of the right atrium (P-pulmonale), right ventricle (S-type)

Hypertrophy of the right atrium is observed with atrial septal defect, hypertension of the pulmonary circulation.

Most often, such a P wave is detected in diseases of the lungs; it is often called P-pulmonale.

Right atrium hypertrophy is a sign of changes in the P wave in leads II, III, aVF, V1, V2.

7.2.1.3. Left ventricular hypertrophy

The ventricles of the heart are better adapted to stress, and in the early stages their hypertrophy may not appear on the ECG, but as the pathology develops, characteristic signs become visible.

With ventricular hypertrophy, the ECG shows significantly more changes than with atrial hypertrophy.

The main signs of left ventricular hypertrophy are (Fig. 8):

Deviation of the electrical axis of the heart to the left (levogram);

Shift of the transition zone to the right (in leads V2 or V3);

The R wave in leads V5, V6 is high and larger in amplitude than RV4;

Deep S in leads V1, V2;

Expanded QRS complex in leads V5, V6 (up to 0.1 s or more);

Displacement of the S-T segment below the isoelectric line with convexity upward;

Negative T wave in leads I, II, aVL, V5, V6.

Rice. 8. ECG for left ventricular hypertrophy

Left ventricular hypertrophy is often observed with arterial hypertension, acromegaly, pheochromocytoma, as well as mitral and aortic valve insufficiency, and congenital heart defects.

7.2.1.4. Right ventricular hypertrophy

Signs of right ventricular hypertrophy appear on the ECG in advanced cases. Diagnosis at the early stage of hypertrophy is extremely difficult.

Signs of hypertrophy (Fig. 9):

Deviation of the electrical axis of the heart to the right (pravogram);

Deep S wave in lead V1 and high R wave in leads III, aVF, V1, V2;

The height of the RV6 tooth is less than normal;

Expanded QRS complex in leads V1, V2 (up to 0.1 s or more);

Deep S wave in lead V5 and also V6;

Displacement of the S-T segment below the isoline with convexity upward in the right III, aVF, V1 and V2;

Complete or incomplete blockade of the right bundle branch;

Shift the transition zone to the left.

Rice. 9. ECG for right ventricular hypertrophy

Right ventricular hypertrophy is most often associated with increased pressure in the pulmonary circulation in pulmonary diseases, mitral valve stenosis, mural thrombosis and pulmonary stenosis and congenital heart defects.

7.2.2. Rhythm disorders

Weakness, shortness of breath, rapid heartbeat, frequent and difficult breathing, interruptions in heart function, a feeling of suffocation, fainting or episodes of loss of consciousness may be manifestations of heart rhythm disturbances due to cardiovascular diseases. An ECG helps confirm their presence, and most importantly determine their type.

It should be remembered that automaticity is a unique property of the cells of the conduction system of the heart, and the sinus node, which controls the rhythm, has the greatest automaticity.

Rhythm disturbances (arrhythmias) are diagnosed in cases where there is no sinus rhythm on the ECG.

Signs of normal sinus rhythm:

P wave frequency – ranging from 60 to 90 (per 1 min);

Identical duration of R-R intervals;

Positive P wave in all leads except aVR.

Heart rhythm disturbances are very diverse. All arrhythmias are divided into nomotopic (changes develop in the sinus node itself) and heterotopic. In the latter case, excitatory impulses arise outside the sinus node, that is, in the atria, atrioventricular junction and ventricles (in the branches of the His bundle).

Nomotopic arrhythmias include sinus brady and tachycardia and irregular sinus rhythm. Heterotopic - atrial fibrillation and flutter and other disorders. If the occurrence of arrhythmia is associated with a dysfunction of excitability, then such rhythm disturbances are divided into extrasystole and paroxysmal tachycardia.

Considering all the variety of types of arrhythmias that can be detected on an ECG, the author, in order not to bore the reader with the intricacies of medical science, allowed himself only to define the basic concepts and consider the most significant rhythm and conduction disorders.

7.2.2.1. Sinus tachycardia

Increased generation of impulses in the sinus node (more than 100 impulses per minute).

On the ECG it is manifested by the presence of a normal P wave and a shortening of the R-R interval.

7.2.2.2. Sinus bradycardia

The pulse generation frequency in the sinus node does not exceed 60.

On the ECG it is manifested by the presence of a normal P wave and a prolongation of the R-R interval.

It should be noted that with a contraction frequency of less than 30, bradycardia is not sinus.

In both cases of tachycardia and bradycardia, the patient is treated for the disease that caused the rhythm disturbance.

7.2.2.3. Irregular sinus rhythm

Impulses are generated irregularly in the sinus node. The ECG shows normal waves and intervals, but the duration of the R-R intervals differs by at least 0.1 s.

This type of arrhythmia can occur in healthy people and does not require treatment.

7.2.2.4. Idioventricular rhythm

Heterotopic arrhythmia, in which the pacemaker is either the bundle branches or the Purkinje fibers.

Extremely severe pathology.

A rare rhythm on the ECG (that is, 30–40 beats per minute), the P wave is absent, the QRS complexes are deformed and widened (duration 0.12 s or more).

Occurs only in severe heart pathology. A patient with such a disorder requires emergency care and is subject to immediate hospitalization in a cardiac intensive care unit.

7.2.2.5. Extrasystole

Extraordinary contraction of the heart caused by a single ectopic impulse. Of practical importance is the division of extrasystoles into supraventricular and ventricular.

A supraventricular (also called atrial) extrasystole is recorded on an ECG if the focus causing extraordinary excitation (contraction) of the heart is located in the atria.

Ventricular extrasystole is recorded on the cardiogram when an ectopic focus is formed in one of the ventricles.

Extrasystole can be rare, frequent (more than 10% of heart contractions in 1 minute), paired (bigemeny) and group (more than three in a row).

Let us list the ECG signs of atrial extrasystole:

P wave changed in shape and amplitude;

The P-Q interval is shortened;

A prematurely recorded QRS complex does not differ in shape from the normal (sinus) complex;

The R-R interval that follows the extrasystole is longer than usual, but shorter than two normal intervals (incomplete compensatory pause).

Atrial extrasystoles are more common in older people against the background of cardiosclerosis and coronary heart disease, but can also be observed in practically healthy people, for example, if a person is very worried or experiencing stress.

If extrasystole is noticed in a practically healthy person, then treatment consists of prescribing Valocordin, Corvalol and ensuring complete rest.

When registering an extrasystole in a patient, treatment of the underlying disease and taking antiarrhythmic drugs from the isoptin group are also required.

Signs of ventricular extrasystole:

The P wave is absent;

The extraordinary QRS complex is significantly widened (more than 0.12 s) and deformed;

Full compensatory pause.

Ventricular extrasystole always indicates heart damage (ischemic heart disease, myocarditis, endocarditis, heart attack, atherosclerosis).

In case of ventricular extrasystole with a frequency of 3–5 contractions per 1 minute, antiarrhythmic therapy is mandatory.

Lidocaine is most often administered intravenously, but other drugs can also be used. Treatment is carried out with careful ECG monitoring.

7.2.2.6. Paroxysmal tachycardia

A sudden attack of hyper-frequent contractions, lasting from a few seconds to several days. The heterotopic pacemaker is located either in the ventricles or supraventricularly.

With supraventricular tachycardia (in this case, impulses are formed in the atria or atrioventricular node), the correct rhythm is recorded on the ECG with a frequency of 180 to 220 contractions per minute.

QRS complexes are not changed or widened.

In the ventricular form of paroxysmal tachycardia, the P waves can change their place on the ECG, the QRS complexes are deformed and widened.

Supraventricular tachycardia occurs in Wolff–Parkinson–White syndrome, less commonly in acute myocardial infarction.

The ventricular form of paroxysmal tachycardia is detected in patients with myocardial infarction, with ischemic heart disease, and disturbances of electrolyte metabolism.

7.2.2.7. Atrial fibrillation (atrial fibrillation)

A type of supraventricular arrhythmias caused by asynchronous, uncoordinated electrical activity of the atria with subsequent deterioration of their contractile function. The flow of impulses is not carried out entirely to the ventricles, and they contract irregularly.

This arrhythmia is one of the most common heart rhythm disturbances.

It occurs in more than 6% of patients over 60 years of age and in 1% of patients younger than this age.

Signs of atrial fibrillation:

R-R intervals are different (arrhythmia);

There are no P waves;

Flicker waves are recorded (they are especially clearly visible in leads II, III, V1, V2);

Electrical alternation (different amplitudes of the I waves in one lead).

Atrial fibrillation occurs with mitral stenosis, thyrotoxicosis and cardiosclerosis, and also often with myocardial infarction. Medical care is to restore sinus rhythm. Procainamide, potassium preparations and other antiarrhythmic drugs are used.

7.2.2.8. Atrial flutter

It is observed much less frequently than atrial fibrillation.

With atrial flutter, normal excitation and contraction of the atria are absent and excitation and contraction of individual atrial fibers are observed.

7.2.2.9. Ventricular fibrillation

The most dangerous and severe rhythm disorder, which quickly leads to cessation of blood circulation. Occurs during myocardial infarction, as well as in the terminal stages of various cardiovascular diseases in patients who are in a state of clinical death. In case of ventricular fibrillation, urgent resuscitation measures are necessary.

Signs of ventricular fibrillation:

Absence of all teeth of the ventricular complex;

Registration of fibrillation waves in all leads with a frequency of 450–600 waves per 1 min.

7.2.3. Conduction disorders

Changes in the cardiogram that occur in the event of a disturbance in the conduction of an impulse in the form of a slowdown or complete cessation of the transmission of excitation are called blockades. Blockades are classified depending on the level at which the violation occurred.

There are sinoatrial, atrial, atrioventricular and intraventricular blockades. Each of these groups is further subdivided. For example, there are sinoatrial blockades of I, II and III degrees, blockades of the right and left bundle branches. There is also a more detailed division (blockade of the anterior branch of the left bundle branch, incomplete block of the right bundle branch). Among conduction disorders recorded using ECG, the following blockades are of greatest practical importance:

Sinoatrial III degree;

Atrioventricular I, II and III degrees;

Blockade of the right and left bundle branches.

7.2.3.1. III degree sinoatrial block

A conduction disorder in which the conduction of excitation from the sinus node to the atria is blocked. On a seemingly normal ECG, the next contraction suddenly disappears (is blocked), that is, the entire P-QRS-T complex (or 2-3 complexes at once). An isoline is recorded in their place. The pathology is observed in those suffering from coronary artery disease, heart attack, cardiosclerosis, and when using a number of drugs (for example, beta blockers). Treatment consists of treating the underlying disease and using atropine, isadrin and similar agents).

7.2.3.2. Atrioventricular block

Impaired conduction of excitation from the sinus node through the atrioventricular connection.

Slowing of atrioventricular conduction is first degree atrioventricular block. Manifests itself on the ECG as a prolongation of the P-Q interval (more than 0.2 s) with a normal heart rate.

Second degree atrioventricular block is an incomplete block in which not all impulses coming from the sinus node reach the ventricular myocardium.

On the ECG, the following two types of blockade are distinguished: the first is Mobitz-1 (Samoilov-Wenckebach) and the second is Mobitz-2.

Signs of Mobitz-1 type blockade:

Constantly lengthening P interval

As a result of the first sign, at some stage after the P wave the QRS complex disappears.

A sign of Mobitz-2 type block is the periodic loss of the QRS complex against the background of an extended P-Q interval.

Third degree atrioventricular block is a condition in which not a single impulse coming from the sinus node is carried to the ventricles. The ECG records two types of rhythm that are not related to each other; the work of the ventricles (QRS complexes) and the atria (P waves) is not coordinated.

Third degree blockade often occurs in cardiosclerosis, myocardial infarction, and improper use of cardiac glycosides. The presence of this type of blockade in a patient is an indication for his urgent hospitalization in a cardiology hospital. Atropine, ephedrine and, in some cases, prednisolone are used for treatment.

7.2.Z.Z. Bundle branch blocks

In a healthy person, an electrical impulse originating in the sinus node, passing through the branches of the His bundle, simultaneously excites both ventricles.

When the right or left bundle branch is blocked, the path of the impulse changes and therefore the excitation of the corresponding ventricle is delayed.

It is also possible that incomplete blockades and so-called blockades of the anterior and posterior branches of the bundle branch may occur.

Signs of complete blockade of the right bundle branch (Fig. 10):

Deformed and widened (more than 0.12 s) QRS complex;

Negative T wave in leads V1 and V2;

Displacement of the S-T segment from the isoline;

Widening and splitting of the QRS in leads V1 and V2 in the form of RsR.

Rice. 10. ECG with complete block of the right bundle branch

Signs of complete blockade of the left bundle branch:

The QRS complex is deformed and widened (more than 0.12 s);

Offset of the S-T segment from the isoline;

Negative T wave in leads V5 and V6;

Expansion and splitting of the QRS complex in leads V5 and V6 in the form of RR;

Deformation and expansion of the QRS in leads V1 and V2 in the form of rS.

These types of blockades occur in cases of heart injury, acute myocardial infarction, atherosclerotic and myocardial cardiosclerosis, and in the incorrect use of a number of medications (cardiac glycosides, novocainamide).

Patients with intraventricular block do not need special therapy. They are hospitalized for treatment of the disease that caused the blockade.

7.2.4. Wolff-Parkinson-White syndrome

This syndrome (WPW) was first described by the above-mentioned authors in 1930 as a form of supraventricular tachycardia that is observed in young healthy people (“functional bundle branch block”).

It has now been established that in the body, sometimes, in addition to the normal path of impulse conduction from the sinus node to the ventricles, there are additional bundles (Kent, James and Mahaim). Along these pathways, excitation reaches the ventricles of the heart faster.

There are several types of WPW syndrome. If excitation enters the left ventricle earlier, then WPW syndrome type A is recorded on the ECG. With type B, excitation enters the right ventricle earlier.

Signs of WPW syndrome type A:

The delta wave on the QRS complex is positive in the right precordial leads and negative in the left (the result of premature excitation of part of the ventricle);

The direction of the main teeth in the chest leads is approximately the same as with blockade of the left bundle branch.

Signs of WPW syndrome type B:

Shortened (less than 0.11 s) P-Q interval;

The QRS complex is widened (more than 0.12 s) and deformed;

Negative delta wave for the right chest leads, positive for the left ones;

The direction of the main teeth in the chest leads is approximately the same as with blockade of the right bundle branch.

It is possible to register a sharply shortened P-Q interval with an undeformed QRS complex and the absence of a delta wave (Lown-Ganong-Levin syndrome).

Additional bundles are inherited. In approximately 30–60% of cases they do not manifest themselves. Some people may develop paroxysms of tachyarrhythmias. In case of arrhythmia, medical care is provided in accordance with the general rules.

7.2.5. Early ventricular repolarization

This phenomenon occurs in 20% of patients with cardiovascular pathology (most often found in patients with supraventricular heart rhythm disturbances).

This is not a disease, but patients with cardiovascular diseases who experience this syndrome are 2-4 times more likely to suffer from rhythm and conduction disturbances.

Signs of early ventricular repolarization (Fig. 11) include:

ST segment elevation;

Late delta wave (notch on the descending part of the R wave);

High amplitude teeth;

Double-humped P wave of normal duration and amplitude;

Shortening of PR and QT intervals;

A rapid and sharp increase in the amplitude of the R wave in the chest leads.

Rice. 11. ECG for early ventricular repolarization syndrome

7.2.6. Coronary heart disease

In coronary heart disease (CHD), the blood supply to the myocardium is impaired. In the early stages, there may be no changes in the electrocardiogram, but in later stages they are very noticeable.

With the development of myocardial dystrophy, the T wave changes and signs of diffuse changes in the myocardium appear.

These include:

Reduced amplitude of the R wave;

S-T segment depression;

Biphasic, moderately widened and flat T wave in almost all leads.

IHD occurs in patients with myocarditis of various origins, as well as dystrophic changes in the myocardium and atherosclerotic cardiosclerosis.

7.2.7. Angina pectoris

With the development of an attack of angina, the ECG can reveal a displacement of the S-T segment and changes in the T wave in those leads that are located above the area with impaired blood supply (Fig. 12).

Rice. 12. ECG for angina pectoris (during an attack)

The causes of angina are hypercholesterolemia, dyslipidemia. In addition, arterial hypertension, diabetes mellitus, psycho-emotional overload, fear, and obesity can trigger the development of an attack.

Depending on which layer of the heart muscle ischemia occurs, there are:

Subendocardial ischemia (over the ischemic area, the S-T displacement is below the isoline, the T wave is positive, of large amplitude);

Subepicardial ischemia (rise of the S-T segment above the isoline, T negative).

The occurrence of angina is accompanied by the appearance of typical chest pain, usually provoked by physical activity. This pain is pressing in nature, lasts several minutes and goes away after taking nitroglycerin. If the pain lasts more than 30 minutes and is not relieved by taking nitro drugs, acute focal changes can most likely be assumed.

Emergency care for angina pectoris involves relieving pain and preventing recurrent attacks.

Analgesics (from analgin to promedol), nitro drugs (nitroglycerin, sustak, nitrong, monocinque, etc.), as well as validol and diphenhydramine, seduxen are prescribed. If necessary, oxygen inhalation is carried out.

7.2.8. Myocardial infarction

Myocardial infarction is the development of necrosis of the heart muscle as a result of prolonged circulatory disorders in the ischemic area of ​​the myocardium.

In more than 90% of cases, the diagnosis is determined using an ECG. In addition, a cardiogram allows you to determine the stage of a heart attack, find out its location and type.

An unconditional sign of a heart attack is the appearance on the ECG of a pathological Q wave, which is characterized by excessive width (more than 0.03 s) and greater depth (a third of the R wave).

Possible options: QS, QrS. An S-T shift (Fig. 13) and T wave inversion are observed.

Rice. 13. ECG for anterolateral myocardial infarction (acute stage). There are cicatricial changes in the posteroinferior parts of the left ventricle

Sometimes an S-T displacement occurs without the presence of a pathological Q wave (small-focal myocardial infarction). Signs of a heart attack:

Pathological Q wave in leads located above the infarct area;

Displacement of the S-T segment by an arc upward (lifting) relative to the isoline in the leads located above the infarct area;

Discordant displacement below the isoline of the S-T segment in leads opposite to the area of ​​infarction;

Negative T wave in leads located above the infarct area.

As the disease progresses, the ECG changes. This relationship is explained by the stages of changes during a heart attack.

There are four stages in the development of myocardial infarction:

Acute;

Subacute;

Scarring stage.

The most acute stage (Fig. 14) lasts several hours. At this time, the S-T segment rises sharply in the corresponding leads on the ECG, merging with the T wave.

Rice. 14. Sequence of ECG changes during myocardial infarction: 1 – Q-infarction; 2 – not Q-infarction; A – the most acute stage; B – acute stage; B – subacute stage; D – scar stage (post-infarction cardiosclerosis)

In the acute stage, a zone of necrosis forms and a pathological Q wave appears. The R amplitude decreases, the S-T segment remains elevated, and the T wave becomes negative. The duration of the acute stage is on average about 1–2 weeks.

The subacute stage of infarction lasts for 1–3 months and is characterized by a cicatricial organization of the necrosis focus. On the ECG at this time there is a gradual return of the S-T segment to the isoline, the Q wave decreases, and the R amplitude, on the contrary, increases.

The T wave remains negative.

The scarring stage can last for several years. At this time, the organization of scar tissue occurs. On the ECG, the Q wave decreases or disappears completely, S-T is located on the isoline, negative T gradually becomes isoelectric, and then positive.

This phasing is often called the natural dynamics of the ECG during myocardial infarction.

A heart attack can be localized in any part of the heart, but most often occurs in the left ventricle.

Depending on the location, infarction of the anterior lateral and posterior walls of the left ventricle is distinguished. The localization and extent of changes are revealed by analyzing ECG changes in the corresponding leads (Table 6).

Table 6. Localization of myocardial infarction

Great difficulties arise when diagnosing a recurrent infarction when new changes are superimposed on an already changed ECG. Dynamic monitoring with recording of a cardiogram at short intervals helps.

A typical heart attack is characterized by burning, severe chest pain that does not go away after taking nitroglycerin.

There are also atypical forms of heart attack:

Abdominal (pain in the heart and stomach);

Asthmatic (cardiac pain and cardiac asthma or pulmonary edema);

Arrhythmic (cardiac pain and rhythm disturbances);

Collaptoid (cardiac pain and a sharp drop in blood pressure with profuse sweating);

Painless.

Treating a heart attack is an extremely difficult task. As a rule, the more difficult it becomes, the more widespread the lesion is. At the same time, according to the apt remark of one of the Russian zemstvo doctors, sometimes the treatment of an extremely severe heart attack goes unexpectedly smoothly, and sometimes an uncomplicated, simple micro-infarction makes the doctor sign of impotence.

Emergency care consists of relieving pain (for this, narcotic and other analgesics are used), also eliminating fears and psycho-emotional arousal with the help of sedatives, reducing the area of ​​the heart attack (using heparin), and sequentially eliminating other symptoms depending on the degree of their danger.

After completing inpatient treatment, patients who have had a heart attack are sent to a sanatorium for rehabilitation.

The final stage is long-term observation in a local clinic.

7.2.9. Syndromes due to electrolyte disturbances

Certain ECG changes make it possible to judge the dynamics of electrolyte content in the myocardium.

To be fair, it should be said that there is not always a clear correlation between the level of electrolytes in the blood and the content of electrolytes in the myocardium.

Nevertheless, electrolyte disturbances detected by ECG serve as a significant aid to the doctor in the process of diagnostic search, as well as in choosing the correct treatment.

The most well studied changes in the ECG are disturbances in potassium and calcium metabolism (Fig. 15).

Rice. 15. ECG diagnosis of electrolyte disorders (A. S. Vorobyov, 2003): 1 – normal; 2 – hypokalemia; 3 – hyperkalemia; 4 – hypocalcemia; 5 – hypercalcemia

7.2.9.1. Hyperkalemia

Signs of hyperkalemia:

Tall, pointed T wave;

Shortening of the Q-T interval;

Decreased R amplitude.

With severe hyperkalemia, intraventricular conduction disturbances are observed.

Hyperkalemia occurs in diabetes (acidosis), chronic renal failure, severe injuries with crushing muscle tissue, adrenal insufficiency, and other diseases.

7.2.9.2. Hypokalemia

Signs of hypokalemia:

Decreased S-T segment downwards;

Negative or biphasic T;

The appearance of U.

With severe hypokalemia, atrial and ventricular extrasystoles and intraventricular conduction disturbances appear.

Hypokalemia occurs when there is a loss of potassium salts in patients with severe vomiting, diarrhea, after prolonged use of diuretics, steroid hormones, and with a number of endocrine diseases.

Treatment consists of replenishing potassium deficiency in the body.

7.2.9.3. Hypercalcemia

Signs of hypercalcemia:

Shortening of the Q-T interval;

Shortening of the S-T segment;

Expansion of the ventricular complex;

Rhythm disturbances with a significant increase in calcium.

Hypercalcemia is observed with hyperparathyroidism, bone destruction by tumors, hypervitaminosis D and excessive administration of potassium salts.

7.2.9.4. Hypocalcemia

Signs of hypocalcemia:

Increasing the duration of the QT interval;

Lengthening the S-T segment;

Decreased T amplitude.

Hypocalcemia occurs with decreased function of the parathyroid glands, in patients with chronic renal failure, with severe pancreatitis and hypovitaminosis D.

7.2.9.5. Glycoside intoxication

Cardiac glycosides have long been successfully used in the treatment of heart failure. These tools are irreplaceable. Their intake helps to reduce heart rate (heart rate) and more vigorously expel blood during systole. As a result, hemodynamic parameters improve and manifestations of circulatory failure decrease.

In case of an overdose of glycosides, characteristic ECG signs appear (Fig. 16), which, depending on the severity of intoxication, require either dose adjustment or discontinuation of the drug. Patients with glycoside intoxication may experience nausea, vomiting, and interruptions in heart function.

Rice. 16. ECG in case of overdose of cardiac glycosides

Signs of glycoside intoxication:

Decreased heart rate;

Shortening of electrical systole;

Decreased S-T segment downwards;

Negative T wave;

Ventricular extrasystoles.

Severe intoxication with glycosides requires discontinuation of the drug and the prescription of potassium supplements, lidocaine and beta blockers.

www.dom-spravka.info

With the normal location of the e.o.s. R II >R I >R III .

• The R wave may be absent in augmented lead aVR;
• With a vertical position of the e.o.s. the R wave may be absent in lead aVL (on the ECG on the right);
• Normally, the amplitude of the R wave in lead aVF is greater than in standard lead III;
• In chest leads V1-V4, the amplitude of the R wave should increase: R V4 >R V3 >R V2 >R V1;
• Normally, the r wave may be absent in lead V1;
• In young people, the R wave may be absent in leads V1, V2 (in children: V1, V2, V3). However, such an ECG is often a sign of myocardial infarction of the anterior interventricular septum of the heart.

3. Q, R, S, T, U waves

The Q wave is not wider than 0.03 s; in lead III it is up to 1/3-1/4 R, in the chest leads - up to 1/2 R. The R wave is the largest, variable in size (5-25 mm), its amplitude depends on the direction of the electrical axis of the heart. In healthy people, splitting and notching of the R wave may occur in one or two leads. Additional positive or negative teeth are designated R', R" (r', r") or S', S" (s', s"). In this case, teeth of larger sizes (R and S greater than 5 mm, Q greater than 3 mm) are indicated in capital letters, and smaller ones - in lowercase letters. Splitting and jagged high R waves (especially at the apex) indicate a violation of intraventricular conduction. Splitting and jagged low-amplitude R waves are not regarded as pathological changes. The observed incomplete blockade of the right bundle branch (split R III, RV1, RV2), as a rule, is not accompanied by widening of the QRS complex.

If the sum of the amplitudes of the R waves in leads I, II, III is less than 15 mm, this is a low-voltage ECG, it is observed in obesity, myocarditis, pericarditis, nephritis. The S wave is negative, unstable, its size depends on the direction of the electrical axis of the heart, its width is up to 0.03-0.04 s. Splitting, notching of the S wave are assessed in the same way as the R wave. The T wave has a height of 0.5-6 mm (from 1/3-1/4 in standard leads to 1/2 R in chest leads), it is always positive in I , II, AVF leads. In leads III, AVD, the T wave can be positive, smoothed, biphasic, negative, in leads AVR it is negative. In the chest leads, due to the peculiar position of the heart, the T wave V1-V2 is positive, and TV1 can be negative. Both reduced and enlarged T waves are regarded as a sign of pathology (inflammation, sclerosis, dystrophy, electrolyte disturbances, etc.). In addition, the direction of the T wave is of important diagnostic importance. The U wave is unstable, stretched, flat, increases sharply with hypokalemia, after an injection of adrenaline, treatment with quinidine, and with thyrotoxicosis. A negative U wave is observed with hyperkalemia, coronary insufficiency, and ventricular overload. The duration ("width") of intervals and teeth is measured in hundredths of a second and compared with the norm; the P-Q, QRS, Q-T, R-R intervals are usually measured in the second lead (in this lead the teeth are clearest), the QRS duration if pathology is suspected is assessed in leads V1 and V4-5.

ECG for rhythm disturbances, conduction disorders, atrial and ventricular hypertrophy

Sinus bradycardia:

The ECG differs little from normal, with the exception of a rarer rhythm. Sometimes, with severe bradycardia, the amplitude of the P wave decreases and the duration of the P-Q interval slightly increases (up to 0.21-0.22).

Sick sinus syndrome:

Sick sinus syndrome (SSNS) is based on a decrease in the automatic function of the SA node, which occurs under the influence of a number of pathological factors. These include heart diseases (acute myocardial infarction, myocarditis, chronic ischemic heart disease, cardiomyopathies, etc.), leading to the development of ischemia, dystrophy or fibrosis in the area of ​​the SA node, as well as intoxication with cardiac glycosides, b-adrenergic receptor blockers, quinidine.

It is characteristic that during a test with dosed physical activity or after the administration of atropine, they do not have an adequate increase in heart rate. As a result of a significant decrease in the function of automatism of the main pacemaker - the SA node - conditions are created for the periodic replacement of sinus rhythm with rhythms from centers of automatism of the second and third order. In this case, various non-sinus ectopic rhythms arise (usually atrial, from the AV junction, atrial fibrillation and flutter, etc.).

Contractions of the heart each time are caused by impulses emanating from different parts of the conduction system of the heart: from the SA node, from the upper or lower parts of the atria, and the AV junction. Such migration of the pacemaker can occur in healthy people with increased vagal tone, as well as in patients with coronary heart disease, rheumatic heart disease, various infectious diseases, and weak joint syndrome.

Atrial extrasystole and its characteristic signs:

1) premature appearance of the cardiac cycle;

2) deformation or change in the polarity of the P wave of the extrasystole;

3) the presence of an unchanged extrasystolic ventricular QRST complex;

4) the presence of an incomplete compensatory pause after the extrasystole.

Extrasystole from AV connection:

Its main ECG signs are:

1) premature, extraordinary appearance on the ECG of an unchanged ventricular QRS complex;

2) negative P wave in leads I, III and AVF after the extrasystolic QRS complex or absence of the P wave;

3) the presence of an incomplete compensatory pause.

ECG signs of ventricular extrasystole:

1) premature, extraordinary appearance on the ECG of an altered ventricular QRS complex;

2) significant expansion and deformation of the extrasystolic QRS complex (0.12 s or more);

3) the location of the RS-T segment and the T wave of the extrasystole is discordant to the direction of the main wave of the QRS complex;

4) absence of a P wave before the ventricular extrasystole;

5) the presence in most cases of a complete compensatory pause after an extrasystole.

1) frequent extrasystoles;

2) polytopic extrasystoles;

3) paired or group extrasystoles;

4) early extrasystoles of type R on T.

ECG signs of atrial paroxysmal tachycardia:

The most characteristic are:

1) a sudden onset and ending attack of increased heart rate up to 140-250 per minute while maintaining the correct rhythm;

2) the presence of a reduced, deformed, biphasic or negative P wave before each ventricular QRS complex;

3) normal, unchanged ventricular QRS complexes.

AV-paroxysmal tachycardia:

The ectopic focus is located in the area of ​​the av junction.

The most characteristic signs:

1) a sudden onset and ending attack of increased heart rate up to 140-220 per minute while maintaining the correct rhythm;

2) the presence in leads II, III and AVF of negative P waves located behind the QRS complexes or merging with them and not recorded on the ECG;

3) normal unchanged ventricular QRS complexes.

Ventricular paroxysmal tachycardia:

As a rule, it develops against the background of significant organic changes in the heart muscle. Its most characteristic features are:

1) a sudden onset and ending attack of increased heart rate up to 140-220 per minute while maintaining the correct rhythm in most cases;

2) deformation and expansion of the QRS complex more than 0.12 s with a discordant location of the S-T segment and T wave;

3) sometimes “captured” ventricular contractions are recorded - normal QRS complexes, which are preceded by a positive P wave.

Signs of atrial flutter:

The most characteristic signs are:

1) the presence on the ECG of frequent - up to 200-400 per minute - regular, similar atrial F waves, having a characteristic sawtooth shape (leads II, III, AVF, V1, V2);

2) the presence of normal unchanged ventricular complexes, each of which is preceded by a certain (usually constant) number of atrial waves F (2: 1, 3: 1, 4: 1) - the correct form of atrial flutter.

Atrial fibrillation:

The most characteristic ECG signs of atrial fibrillation are:

1) absence of P wave in all leads;

2) the presence throughout the entire cardiac cycle of random f waves, having different shapes and amplitudes. F waves are better recorded in leads V1, V2, II, III and AVF;

3) irregularity of ventricular complexes - directed ventricular rhythm (R-R intervals of varying duration);

4) the presence of QRS complexes, which in most cases have a normal, unchanged rhythm without deformation or widening.

Ventricular flutter and fibrillation:

When ventricular flutter is detected on the ECG, a sinusoidal curve with frequent, rhythmic, rather large, wide waves is recorded (any elements of the ventricular complex cannot be distinguished).

ECG signs of incomplete sinoatrial block are:

1) periodic loss of individual cardiac cycles (P waves and QRST complexes);

2) an increase in the pause between two adjacent P or R waves at the time of loss of cardiac cycles by almost 2 times (less often, 3 or 4 times) compared to the usual P-P intervals.

ECG signs of incomplete intraatrial block are:

1) increase in the duration of the P wave by more than 0.11 s;

2) splitting of the P wave.

1st degree AV block:

Atrioventricular block of the first degree is characterized by a slowdown in atrioventricular conduction, which is manifested on the ECG by a constant prolongation of the P-Q interval to more than 0.20 s. The shape and duration of the QRS complex do not change.

2nd degree AV block:

It is characterized by periodically occurring cessation of individual electrical impulses from the atria to the ventricles. As a result, from time to time there is a loss of one or more ventricular contractions. At this moment, only the P wave is recorded on the ECG, and the following ventricular QRST complex is absent.

There are three types of 2nd degree atrioventricular block:

Type 1 - Mobitz type 1.

There is a gradual, from one complex to another, slowing down of conduction through the AV node up to a complete delay of one (rarely two) electrical impulses. The ECG shows a gradual lengthening of the P-Q interval followed by loss of the ventricular QRS complex. Periods of gradual increase in the P-Q interval followed by loss of the ventricular complex are called Samoilov-Wenckebach periods.

High-grade (deep-grade) AV block:

The ECG shows either every second (2:1) or two or more ventricular complexes in a row (3:1, 4:1). This leads to severe bradycardia, against the background of which disturbances of consciousness may occur. Severe ventricular bradycardia contributes to the formation of replacement (escaping) contractions and rhythms.

Atrioventricular block 3rd degree (complete AV block):

It is characterized by a complete cessation of impulse transmission from the atria to the ventricles, as a result of which they are excited and contract independently of each other. The frequency of contractions of the atria is 70-80 per minute, ventricles - 30-60 per minute.

Heart blocks:

Single-bundle blocks - damage to one branch of the His bundle:

1) right bundle branch block;

2) blockade of the left anterior branch;

3) blockade of the left posterior branch.

1) blockade of the left leg (anterior and posterior branches);

2) blockade of the right leg and left anterior branch;

3) blockade of the right leg and left posterior branch.

Right bundle branch block:

Electrocardiographic signs of complete right bundle branch block are:

1) the presence in the right precordial leads V1, V2 of QRS complexes of type rSR1 or rsR1, having an M-shape, with R1 > r;

2) the presence in the left chest leads (V5, V6) and leads I, AVL of a widened, often jagged S wave;

3) increase in the duration of the QRS complex to 0.12 s or more;

4) the presence in leads V1 of a negative or biphasic (– +) asymmetric T wave.

Block of the left anterior branch of the His bundle:

1) sharp deviation of the electrical axis of the heart to the left (angle a –30°);

2) QRS in leads I, AVL type qR, III, AVF, II - type rS;

3) the total duration of the QRS complex is 0.08-0.11 s.

Left posterior bundle branch block:

1) sharp deviation of the electrical axis of the heart to the right (a +120°);

2) the shape of the QRS complex in leads I, AVL type rS, and in leads III, AVF type gR;

3) the duration of the QRS complex is within 0.08-0.11 s.

1) the presence in leads V5, V6, I, AVL of widened, deformed ventricular complexes of type R with a split or wide apex;

2) the presence in leads V1, V2, AVF of widened deformed ventricular complexes, having the appearance of QS or rS with a split or wide apex of the S wave;

3) an increase in the total duration of the QRS complex to 0.12 s or more;

4) the presence in leads V5, V6, I, AVL of a discordant T wave in relation to the QRS. Displacement of the RS-T segment and negative or biphasic (– +) asymmetric T waves.

Blockade of the right leg and left anterior branch of the His bundle:

The ECG shows signs characteristic of right leg block: the presence in lead V of deformed M-shaped QRS complexes (rSR1), widened to 0.12 s or more. At the same time, a sharp deviation of the electrical axis of the heart to the left is determined, which is most typical for blockade of the left anterior branch of the His bundle.

Blockade of the right bundle branch and the left posterior branch of the His bundle:

The combination of right bundle branch block and blockade of the left posterior branch of the His bundle is evidenced by the appearance on the ECG of signs of blockade of the right branch of the His bundle mainly in the right precordial leads (V1, V2) and deviation of the electrical axis of the heart to the right (a = 120°), if there is no clinical evidence of presence of right ventricular hypertrophy.

Block of three branches of the His bundle (three-bundle block):

It is characterized by the presence of conduction disturbances simultaneously in three branches of the His bundle.

1) presence on the ECG of signs of atrioventricular block of 1, 2 or 3 degrees;

2) the presence of electrocardiographic signs of blockade of two branches of the His bundle.

1) WPW-Wolf-Parkinson-White syndrome.

a) shortening of the P-Q interval;

b) the presence of an additional excitation wave of a triangle wave in the QRS complex;

c) increased duration and slight deformation of the QRS complex;

Electrocardiogram (ECG) for atrial and ventricular hypertrophy:

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 the increased load experienced by one or another part of the heart in the presence of valvular heart defects (stenosis or insufficiency) or with increased pressure in the systemic or pulmonary circulation.

1) an increase in the electrical activity of the hypertrophied part of the heart;

2) slowing down the conduction of an electrical impulse through it;

3) ischemic, dystrophic, metabolic and sclerotic changes in hypertrophied cardiac muscle.

Left atrial hypertrophy:

It is more common in patients with mitral heart defects, especially mitral stenosis.

1) bifurcation and increase in the amplitude of the teeth P1, II, AVL, V5, V6 (P-mitrale);

2) an increase in the amplitude and duration of the second negative (left atrial) phase of the P wave in lead V1 (less often V2) or the formation of a negative P in V1;

3) increase in the total duration of the P wave - more than 0.1 s;

4) negative or biphasic (+ –) P wave in III (non-constant sign).

Right atrial hypertrophy:

Compensatory hypertrophy of the right atrium usually develops in diseases accompanied by increased pressure in the pulmonary artery, most often in chronic cor pulmonale.

1) in leads II, III, AVF, the P waves are high-amplitude, with a pointed apex (P-pulmonale);

2) in leads V1, V2, the P wave (or its first, right atrial phase) is positive, with a pointed apex;

3) the duration of the P waves does not exceed 0.10 s.

Left ventricular hypertrophy:

Develops in hypertension, aortic heart defects, mitral valve insufficiency and other diseases accompanied by prolonged overload of the left ventricle.

1) an increase in the amplitude of the R wave in the left chest leads (V5, V6) and the amplitude of the S wave in the right chest leads (V1, V2); in this case, RV4 25 mm or RV5, 6 + SV1, 2 35 mm (on the ECG of persons over 40 years old) and 45 mm (on the ECG of young persons);

2) deepening of the Q wave in V5, V6, disappearance or sharp decrease in the amplitude of the S waves in the left chest leads;

3) displacement of the electrical axis of the heart to the left. In this case, R1 15 mm, RAVL 11 mm or R1 + SIII > 25 mm;

4) with pronounced hypertrophy in leads I and AVL, V5, V6, a shift of the S-T segment below the isoline and the formation of a negative or biphasic (– +) T wave may be observed;

5) an increase in the duration of the interval of internal QRS deviation in the left precordial leads (V5, V6) by more than 0.05 s.

Right ventricular hypertrophy:

Develops with mitral stenosis, chronic cor pulmonale and other diseases that lead to prolonged overload of the right ventricle.

1) rSR1 type is characterized by the presence in lead V1 of a split QRS complex of type rSR1 with two positive teeth r u R1, the second of which has a large amplitude. These changes are observed with normal QRS complex width;

2) R-type ECG is characterized by the presence of a QRS complex of type Rs or gR in lead V1 and is usually detected with severe hypertrophy of the right ventricle;

3) S-type ECG is characterized by the presence in all chest leads from V1 to V6 of a QRS complex of type rS or RS with a pronounced S wave.

1) displacement of the electrical axis of the heart to the right (angle a more than +100°);

2) an increase in the amplitude of the R wave in the right chest leads (V1, V2) and the amplitude of the S wave in the left chest leads (V5, V6). In this case, quantitative criteria may be: amplitude RV17 mm or RV1 + SV5, 6 > 110.5 mm;

3) the appearance of a QRS complex of the rSR or QR type in leads V1;

4) displacement of the S-T segment and the appearance of negative T waves in leads III, AVF, V1, V2;

5) an increase in the duration of the interval of internal deviation in the right chest lead (V1) by more than 0.03 s.

What state of the myocardium is reflected by the R wave on the ECG results?

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

Why is an electrocardiogram performed?

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

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

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

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

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

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

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

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

What does an ECG show?

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

Changes reflected in the cardiogram may show the following conditions:

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

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

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

Detailed interpretation of the electrocardiogram

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

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

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

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

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

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

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

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

Determination of the heart axis

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

Possible errors in research

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

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

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

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

Electrocardiogram for conduction disorders

in limb leads (more than 0.11 s);

splitting or jagged P waves (not a permanent sign)

periodic disappearance of the left atrial (negative) phase of the P wave in lead V1

increase in the duration of the P-Q(R) interval by more than 0.20 s, mainly due to the P-Q(R) segment;

maintaining the normal duration of P waves (no more than 0.10 s); maintaining the normal shape and duration of QRS complexes

an increase in the duration of the P-Q(R) interval by more than 0.20 s, mainly due to the duration of the P wave (its duration exceeds 0.11 s, the P wave is split);

maintaining the normal duration of the P-Q(R) segment (no more than 0.10 s);

maintaining the normal shape and duration of QRS complexes

increase in the duration of the P-Q(R) interval by more than 0.20 s;

maintaining the normal duration of the P wave (no more than 0.11 s);

the presence of pronounced deformation and widening (more than 0.12 s) of QRS complexes like a two-bundle block in the His system (see below)

a gradual, from one complex to another, increase in the duration of the P-Q(R) interval, interrupted by the loss of the ventricular QRST complex (while maintaining the atrial P wave on the ECG);

after loss of the QRST complex, re-registration of a normal or slightly extended P-Q(R) interval, then a gradual increase in the duration of this interval with loss of the ventricular complex (Samoilov-Wenckebach period);

P and QRS ratio - 3:2, 4:3, etc.

regular (type 3:2, 4:3, 5:4, 6:5, etc.) or random loss of one, rarely biventricular and triventricular QRST complexes (while maintaining the atrial P wave in this place);

the presence of a constant (normal or extended) P-Q(R) interval; possible expansion and deformation of the ventricular QRS complex (non-constant sign)

P-Q(R) interval normal or extended;

with the distal form of blockade, expansion and deformation of the ventricular QRS complex is possible (non-permanent sign)

the presence of a constant (normal or extended) P-Q(R) interval in those complexes where the P wave is not blocked;

expansion and deformation of the ventricular QRS complex (non-permanent sign);

against the background of bradycardia, the appearance of interfering (slipping) complexes and rhythms (non-constant sign)

decrease in the number of ventricular contractions (QRS complexes) for up to a minute;

ventricular QRS complexes are not changed

decrease in the number of ventricular contractions (QRS complexes) for a minute or less;

ventricular QRS complexes are widened and deformed

atrial flutter (F);

ventricular rhythm of non-sinus origin - ectopic (nodal or

R-R intervals are constant (correct rhythm);

Heart rate does not exceed min.

the presence in the left chest leads (V5, V1) and in leads I, aVL of a widened, often jagged S wave;

increase in the duration of the QRS complex by more than 0.12 s;

the presence in lead V1 (less often in lead III) of depression of the RS-T segment with a convexity facing upward, and a negative or biphasic (“-” and “+”) asymmetric T wave

slight increase in the duration of the QRS complex to 0.09-0.11 s

the QRS complex in leads I and aVL, type qR, and in leads III, aVF and II - type rS;

total duration of ventricular QRS complexes 0.08-0.11 s

the QRS complex in leads I and aVL is of type rS, and in leads III and aVF is of type qR; total duration of ventricular QRS complexes 0.08-0.11 s

the presence in V1, V2, III, aVF of widened deformed S waves or QS complexes with a split or wide apex;

an increase in the total duration of the QRS complex by more than 0.12 s;

the presence in leads V5, V6, aVL of a discordant displacement of the RS-T segment with respect to the QRS and negative or biphasic (“-” and “+”) asymmetric T waves;

deviation of the electrical axis of the heart to the left (often observed)

the presence in leads III, aVF, V1, V2, of widened and deepened QS or rS complexes, sometimes with initial splitting of the S wave (or QS complex);

increase in QRS duration to 0.10-0.11 s;

deviation of the electrical axis of the heart to the left (non-permanent sign)

sharp deviation of the electrical axis of the heart to the left (angle α from 30 to 90°)

deviation of the electrical axis of the heart to the right (angle α is equal to or greater than +120°)

signs of complete blockade of two branches of the His bundle (any type of two-bundle block - see above)

ECG signs of complete two-fascicle blockade

the appearance of an additional excitation wave within the QRS complex - the D-wave;

long and slightly deformed QRS complex;

discordant to the QRS complex displacement of the RS-T segment and change in the polarity of the T wave (non-constant signs)

the absence of an additional excitation wave in the QRS complex - the D-wave;

presence of unchanged (narrow) and undeformed QRS complexes

Krasnoyarsk medical portal Krasgmu.net

To accurately interpret changes when analyzing an ECG, you must adhere to the decoding scheme given below.

General scheme for decoding an ECG: deciphering a cardiogram in children and adults: general principles, reading the results, an example of decoding.

Normal electrocardiogram

Any ECG consists of several waves, segments and intervals, reflecting the complex process of propagation of an excitation wave throughout the heart.

The shape of electrocardiographic complexes and the size of the teeth are different in different leads and are determined by the size and direction of the projection of the moment vectors of the cardiac EMF onto the axis of a particular lead. If the projection of the torque vector is directed towards the positive electrode of a given lead, an upward deviation from the isoline is recorded on the ECG - positive waves. If the projection of the vector is directed towards the negative electrode, a deviation downward from the isoline is recorded on the ECG - negative waves. In the case when the moment vector is perpendicular to the lead axis, its projection onto this axis is zero and no deviations from the isoline are recorded on the ECG. If during the excitation cycle the vector changes its direction relative to the poles of the lead axis, then the wave becomes biphasic.

Segments and waves of a normal ECG.

Prong R.

The P wave reflects the process of depolarization of the right and left atria. In a healthy person, in leads I, II, aVF, V-V the P wave is always positive, in leads III and aVL, V it can be positive, biphasic or (rarely) negative, and in lead aVR the P wave is always negative. In leads I and II, the P wave has maximum amplitude. The duration of the P wave does not exceed 0.1 s, and its amplitude is 1.5-2.5 mm.

P-Q(R) interval.

The P-Q(R) interval reflects the duration of atrioventricular conduction, i.e. time of excitation propagation through the atria, AV node, His bundle and its branches. Its duration is 0.12-0.20 s and in a healthy person depends mainly on the heart rate: the higher the heart rate, the shorter the P-Q(R) interval.

Ventricular QRST complex.

The ventricular QRST complex reflects the complex process of propagation (QRS complex) and extinction (RS-T segment and T wave) of excitation throughout the ventricular myocardium.

Q wave.

The Q wave can normally be recorded in all standard and enhanced unipolar limb leads and in precordial leads V-V. The amplitude of the normal Q wave in all leads, except aVR, does not exceed the height of the R wave, and its duration is 0.03 s. In lead aVR in a healthy person, a deep and wide Q wave or even a QS complex may be recorded.

R wave

Normally, the R wave can be recorded in all standard and enhanced limb leads. In lead aVR, the R wave is often poorly defined or absent altogether. In the chest leads, the amplitude of the R wave gradually increases from V to V, and then decreases slightly in V and V. Sometimes the r wave may be absent. Prong

R reflects the spread of excitation along the interventricular septum, and the R wave - along the muscles of the left and right ventricles. The interval of internal deviation in lead V does not exceed 0.03 s, and in lead V - 0.05 s.

S wave

In a healthy person, the amplitude of the S wave in various electrocardiographic leads fluctuates within wide limits, not exceeding 20 mm. With a normal position of the heart in the chest in the limb leads, the S amplitude is small, except in lead aVR. In the chest leads, the S wave gradually decreases from V, V to V, and in leads V, V it has a small amplitude or is absent altogether. The equality of the R and S waves in the precordial leads (“transition zone”) is usually recorded in lead V or (less often) between V and V or V and V.

The maximum duration of the ventricular complex does not exceed 0.10 s (usually 0.07-0.09 s).

RS-T segment.

The RS-T segment in a healthy person in the limb leads is located on the isoline (0.5 mm). Normally, in chest leads V-V there may be a slight displacement of the RS-T segment upward from the isoline (no more than 2 mm), and in leads V - downward (no more than 0.5 mm).

T wave

Normally, the T wave is always positive in leads I, II, aVF, V-V, and T>T, and T>T. In leads III, aVL and V, the T wave can be positive, biphasic or negative. In lead aVR, the T wave is normally always negative.

Q-T interval(QRST)

The Q-T interval is called electrical ventricular systole. Its duration depends primarily on the number of heart contractions: the higher the rhythm frequency, the shorter the proper Q-T interval. The normal duration of the Q-T interval is determined by the Bazett formula: Q-T=K, where K is a coefficient equal to 0.37 for men and 0.40 for women; R-R – duration of one cardiac cycle.

Electrocardiogram analysis.

The analysis of any ECG should begin with checking the correctness of its registration technique. First, you need to pay attention to the presence of various interferences. Interference that occurs during ECG recording:

a - induction currents - network induction in the form of regular oscillations with a frequency of 50 Hz;

b - “swimming” (drift) of the isoline as a result of poor contact of the electrode with the skin;

c - interference caused by muscle tremor (irregular frequent vibrations are visible).

Interference occurring during ECG recording

Secondly, it is necessary to check the amplitude of the control millivolt, which should correspond to 10mm.

Thirdly, the speed of paper movement during ECG recording should be assessed. When recording an ECG at a speed of 50 mm, 1 mm on paper tape corresponds to a time period of 0.02 s, 5 mm - 0.1 s, 10 mm - 0.2 s, 50 mm - 1.0 s.

General scheme (plan) for decoding the ECG.

I.Heart rate and conduction analysis:

1) assessment of the regularity of heart contractions;

2) counting the number of heartbeats;

3) determination of the source of excitation;

4) assessment of the conductivity function.

II. Determination of heart rotations around the anteroposterior, longitudinal and transverse axes:

1) determination of the position of the electrical axis of the heart in the frontal plane;

2) determination of the rotation of the heart around the longitudinal axis;

3) determination of the rotation of the heart around the transverse axis.

III. Analysis of the atrial P wave.

IV. Analysis of the ventricular QRST complex:

1) analysis of the QRS complex,

2) analysis of the RS-T segment,

3) analysis of the Q-T interval.

V. Electrocardiographic report.

I.1) Heart rate regularity is assessed by comparing the duration of R-R intervals between successively recorded cardiac cycles. The R-R interval is usually measured between the tops of the R waves. Regular, or correct, heart rhythm is diagnosed if the duration of the measured R-R is the same and the spread of the obtained values ​​does not exceed 10% of the average R-R duration. In other cases, the rhythm is considered abnormal (irregular), which can be observed with extrasystole, atrial fibrillation, sinus arrhythmia, etc.

2) With the correct rhythm, heart rate (HR) is determined by the formula: HR=.

If the ECG rhythm is abnormal, in one of the leads (most often in standard lead II) it is recorded longer than usual, for example, for 3-4 seconds. Then the number of QRS complexes recorded in 3 seconds is counted and the result is multiplied by 20.

In a healthy person, the resting heart rate ranges from 60 to 90 per minute. An increase in heart rate is called tachycardia, and a decrease is called bradycardia.

Assessing the regularity of rhythm and heart rate:

a) correct rhythm; b), c) incorrect rhythm

3) To determine the source of excitation (pacemaker), it is necessary to evaluate the course of excitation in the atria and establish the ratio of the R waves to the ventricular QRS complexes.

Sinus rhythm is characterized by: the presence in standard lead II of positive H waves preceding each QRS complex; constant identical shape of all P waves in the same lead.

In the absence of these signs, various variants of non-sinus rhythm are diagnosed.

Atrial rhythm (from the lower parts of the atria) is characterized by the presence of negative P, P waves and the following unchanged QRS complexes.

The rhythm from the AV junction is characterized by: the absence of a P wave on the ECG, merging with the usual unchanged QRS complex, or the presence of negative P waves located after the usual unchanged QRS complexes.

Ventricular (idioventricular) rhythm is characterized by: slow ventricular rhythm (less than 40 beats per minute); the presence of widened and deformed QRS complexes; lack of a natural connection between QRS complexes and P waves.

4) For a rough preliminary assessment of the conduction function, it is necessary to measure the duration of the P wave, the duration of the P-Q(R) interval and the total duration of the ventricular QRS complex. An increase in the duration of these waves and intervals indicates a slowdown in conduction in the corresponding part of the conduction system of the heart.

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

Bailey's six-axis system.

a) Determination of the angle by graphical method. The algebraic sum of the amplitudes of the QRS complex waves is calculated in any two leads from the limbs (standard leads I and III are usually used), the axes of which are located in the frontal plane. A positive or negative value of an algebraic sum on an arbitrarily chosen scale is plotted on the positive or negative part of the axis of the corresponding lead in the six-axis Bailey coordinate system. These values ​​represent projections of the desired electrical axis of the heart onto axes I and III of standard leads. From the ends of these projections, perpendiculars to the axes of the leads are restored. The intersection point of the perpendiculars is connected to the center of the system. This line is the electrical axis of the heart.

b) Visual determination of the angle. Allows you to quickly estimate the angle with an accuracy of 10°. The method is based on two principles:

1. The maximum positive value of the algebraic sum of the teeth of the QRS complex is observed in that lead, the axis of which approximately coincides with the location of the electrical axis of the heart, and is parallel to it.

2. A complex of type RS, where the algebraic sum of the teeth is zero (R=S or R=Q+S), is written in the lead whose axis is perpendicular to the electrical axis of the heart.

With a normal position of the electrical axis of the heart: RRR; in leads III and aVL, the R and S waves are approximately equal to each other.

In a horizontal position or deviation of the electrical axis of the heart to the left: high R waves are fixed in leads I and aVL, with R>R>R; a deep S wave is recorded in lead III.

In a vertical position or deviation of the electrical axis of the heart to the right: high R waves are recorded in leads III and aVF, and R R> R; deep S waves are recorded in leads I and aV

III. P wave analysis includes: 1) measurement of P wave amplitude; 2) measurement of the duration of the P wave; 3) determination of the polarity of the P wave; 4) determination of the shape of the P wave.

IV.1) Analysis of the QRS complex includes: a) assessment of the Q wave: amplitude and comparison with the R amplitude, duration; b) assessment of the R wave: amplitude, comparing it with the amplitude of Q or S in the same lead and with R in other leads; duration of the interval of internal deviation in leads V and V; possible splitting of a tooth or the appearance of an additional one; c) assessment of the S wave: amplitude, comparing it with the R amplitude; possible widening, jagged or splitting of the tooth.

2) When analyzing the RS-T segment, it is necessary to: find the connection point j; measure its deviation (+–) from the isoline; measure the amount of displacement of the RS-T segment, either the isoline up or down at a point located 0.05-0.08 s from point j to the right; determine the form of possible displacement of the RS-T segment: horizontal, obliquely downward, obliquely upward.

3) When analyzing the T wave, you should: determine the polarity of T, evaluate its shape, measure the amplitude.

4) Q-T interval analysis: duration measurement.

V. Electrocardiographic conclusion:

1) source of heart rhythm;

2) regularity of heart rhythm;

4) position of the electrical axis of the heart;

5) the presence of four electrocardiographic syndromes: a) heart rhythm disturbances; b) conduction disorders; c) hypertrophy of the myocardium of the ventricles and atria or their acute overload; d) myocardial damage (ischemia, dystrophy, necrosis, scars).

Electrocardiogram for heart rhythm disturbances

1. Disorders of automatism of the SA node (nomotopic arrhythmias)

1) Sinus tachycardia: increase in the number of heartbeats up to (180) per minute (shortening R-R intervals); maintaining correct sinus rhythm (correct alternation of the P wave and the QRST complex in all cycles and a positive P wave).

2) Sinus bradycardia: decrease in the number of heartbeats for up to a minute (increase in the duration of the R-R intervals); maintaining correct sinus rhythm.

3) Sinus arrhythmia: fluctuations in the duration of the R-R intervals exceeding 0.15 s and associated with the respiratory phases; preservation of all electrocardiographic signs of sinus rhythm (alternating P wave and QRS-T complex).

4) Sinoatrial node weakness syndrome: persistent sinus bradycardia; periodic appearance of ectopic (non-sinus) rhythms; presence of SA blockade; bradycardia-tachycardia syndrome.

a) ECG of a healthy person; b) sinus bradycardia; c) sinus arrhythmia

2. Extrasystole.

1) Atrial extrasystole: premature extraordinary appearance of the P′ wave and the following QRST′ complex; deformation or change in the polarity of the P′ wave of the extrasystole; the presence of an unchanged extrasystolic ventricular QRST′ complex, similar in shape to ordinary normal complexes; the presence of an incomplete compensatory pause after an atrial extrasystole.

Atrial extrasystole (II standard lead): a) from the upper parts of the atria; b) from the middle parts of the atria; c) from the lower parts of the atria; d) blocked atrial extrasystole.

2) Extrasystoles from the atrioventricular junction: premature extraordinary appearance on the ECG of an unchanged ventricular QRS′ complex, similar in shape to other QRST complexes of sinus origin; negative P′ wave in leads II, III and aVF after the extrasystolic QRS′ complex or absence of P′ wave (fusion of P′ and QRS′); the presence of an incomplete compensatory pause.

3) Ventricular extrasystole: premature, extraordinary appearance on the ECG of an altered ventricular QRS complex; significant expansion and deformation of the extrasystolic QRS complex; the location of the RS-T′ segment and the T′ wave of the extrasystole is discordant to the direction of the main wave of the QRS′ complex; absence of a P wave before the ventricular extrasystole; the presence in most cases of a complete compensatory pause after a ventricular extrasystole.

a) left ventricular; b) right ventricular extrasystole

3. Paroxysmal tachycardia.

1) Atrial paroxysmal tachycardia: a sudden onset and also suddenly ending attack of increased heart rate for up to a minute while maintaining the correct rhythm; the presence of a reduced, deformed, biphasic or negative P wave before each ventricular QRS complex; normal unchanged ventricular QRS complexes; in some cases, there is a deterioration in atrioventricular conduction with the development of first degree atrioventricular block with periodic loss of individual QRS′ complexes (non-constant signs).

2) Paroxysmal tachycardia from the atrioventricular junction: a sudden onset and also suddenly ending attack of increased heart rate for up to a minute while maintaining the correct rhythm; the presence in leads II, III and aVF of negative P' waves located behind the QRS' complexes or merging with them and not recorded on the ECG; normal unchanged ventricular QRS complexes.

3) Ventricular paroxysmal tachycardia: a sudden onset and also suddenly ending attack of increased heart rate for up to a minute while maintaining the correct rhythm in most cases; deformation and widening of the QRS complex more than 0.12 s with discordant location of the RS-T segment and T wave; the presence of atrioventricular dissociation, i.e. complete separation of the rapid ventricular rhythm and normal atrial rhythm with occasionally recorded single normal unchanged QRST complexes of sinus origin.

4. Atrial flutter: the presence on the ECG of frequent - up to a minute - regular, similar atrial F waves, having a characteristic sawtooth shape (leads II, III, aVF, V, V); in most cases, correct, regular ventricular rhythm with equal F-F intervals; the presence of normal unchanged ventricular complexes, each of which is preceded by a certain number of atrial F waves (2:1, 3:1, 4:1, etc.).

5. Atrial fibrillation: absence of P waves in all leads; the presence of random waves throughout the cardiac cycle f, having different shapes and amplitudes; waves f better recorded in leads V, V, II, III and aVF; irregular ventricular QRS complexes – irregular ventricular rhythm; the presence of QRS complexes, which in most cases have a normal, unchanged appearance.

a) coarse-wavy form; b) finely wavy form.

6. Ventricular flutter: frequent (up to a minute), regular and identical in shape and amplitude flutter waves, reminiscent of a sinusoidal curve.

7. Ventricular fibrillation (fibrillation): frequent (from 200 to 500 per minute), but irregular waves, differing from each other in different shapes and amplitudes.

Electrocardiogram for conduction dysfunction.

1. Sinoatrial block: periodic loss of individual cardiac cycles; the increase in the pause between two adjacent P or R waves at the time of loss of cardiac cycles is almost 2 times (less often 3 or 4 times) compared to the usual P-P or R-R intervals.

2. Intraatrial block: increase in the duration of the P wave by more than 0.11 s; splitting of the P wave.

3. Atrioventricular blockade.

1) I degree: increase in the duration of the P-Q(R) interval by more than 0.20 s.

a) atrial form: expansion and splitting of the P wave; QRS is normal.

b) nodal form: lengthening of the P-Q(R) segment.

c) distal (three-bundle) form: pronounced QRS deformation.

2) II degree: loss of individual ventricular QRST complexes.

a) Mobitz type I: gradual prolongation of the P-Q(R) interval followed by loss of QRST. After an extended pause, the P-Q(R) is again normal or slightly extended, after which the entire cycle is repeated.

b) Mobitz type II: loss of QRST is not accompanied by a gradual lengthening of P-Q(R), which remains constant.

c) Mobitz type III (incomplete AV block): either every second (2:1) or two or more ventricular complexes in a row are lost (block 3:1, 4:1, etc.).

3) III degree: complete separation of atrial and ventricular rhythms and a decrease in the number of ventricular contractions for a minute or less.

4. Block of the legs and branches of the His bundle.

1) Block of the right leg (branch) of the His bundle.

a) Complete blockade: the presence in the right precordial leads V (less often in limb leads III and aVF) of QRS complexes of the rSR′ or rSR′ type, having an M-shaped appearance, with R′ > r; the presence in the left chest leads (V, V) and leads I, aVL of a widened, often jagged S wave; increase in the duration (width) of the QRS complex by more than 0.12 s; the presence in lead V (less often in III) of depression of the RS-T segment with a convexity facing upward, and a negative or biphasic (–+) asymmetric T wave.

b) Incomplete blockade: the presence of a QRS complex of type rSr′ or rSR′ in lead V, and a slightly widened S wave in leads I and V; duration of the QRS complex is 0.09-0.11 s.

2) Blockade of the left anterior branch of the His bundle: a sharp deviation of the electrical axis of the heart to the left (angle α –30°); QRS in leads I, aVL type qR, III, aVF, II type rS; the total duration of the QRS complex is 0.08-0.11 s.

3) Blockade of the left posterior branch of the His bundle: sharp deviation of the electrical axis of the heart to the right (angle α120°); the shape of the QRS complex in leads I and aVL is type rS, and in leads III, aVF - type qR; the duration of the QRS complex is within 0.08-0.11 s.

4) Left bundle branch block: in leads V, V, I, aVL there are widened deformed ventricular complexes of type R with a split or wide apex; in leads V, V, III, aVF there are widened deformed ventricular complexes, having the appearance of QS or rS with a split or wide apex of the S wave; an increase in the total duration of the QRS complex by more than 0.12 s; the presence in leads V, V, I, aVL of a discordant relative to QRS shift of the RS-T segment and negative or biphasic (–+) asymmetric T waves; deviation of the electrical axis of the heart to the left is often observed, but not always.

5) Blockade of three branches of the His bundle: atrioventricular block of I, II or III degree; blockade of two branches of the His bundle.

Electrocardiogram for atrial and ventricular hypertrophy.

1. Hypertrophy of the left atrium: bifurcation and increase in the amplitude of the P waves (P-mitrale); an increase in the amplitude and duration of the second negative (left atrial) phase of the P wave in lead V (less often V) or the formation of a negative P; negative or biphasic (+–) P wave (non-constant sign); increase in the total duration (width) of the P wave – more than 0.1 s.

2. Hypertrophy of the right atrium: in leads II, III, aVF, the P waves are high-amplitude, with a pointed apex (P-pulmonale); in leads V, the P wave (or at least its first - right atrial phase) is positive with a pointed apex (P-pulmonale); in leads I, aVL, V the P wave is of low amplitude, and in aVL it can be negative (not a constant sign); the duration of the P waves does not exceed 0.10 s.

3. Left ventricular hypertrophy: increase in the amplitude of the R and S waves. In this case, R2 25mm; signs of rotation of the heart around the longitudinal axis counterclockwise; displacement of the electrical axis of the heart to the left; displacement of the RS-T segment in leads V, I, aVL below the isoline and the formation of a negative or biphasic (–+) T wave in leads I, aVL and V; an increase in the duration of the interval of internal QRS deviation in the left precordial leads by more than 0.05 s.

4. Right ventricular hypertrophy: displacement of the electrical axis of the heart to the right (angle α more than 100°); an increase in the amplitude of the R wave in V and the S wave in V; the appearance of a QRS complex of type rSR′ or QR in lead V; signs of rotation of the heart around the longitudinal axis clockwise; downward displacement of the RS-T segment and the appearance of negative T waves in leads III, aVF, V; an increase in the duration of the interval of internal deviation in V by more than 0.03 s.

Electrocardiogram for coronary heart disease.

1. The acute stage of myocardial infarction is characterized by the rapid, within 1-2 days, formation of a pathological Q wave or QS complex, displacement of the RS-T segment above the isoline and the first positive and then negative T wave merging with it; after a few days the RS-T segment approaches the isoline. At the 2-3rd week of the disease, the RS-T segment becomes isoelectric, and the negative coronary T wave sharply deepens and becomes symmetrical and pointed.

2. In the subacute stage of myocardial infarction, a pathological Q wave or QS complex (necrosis) and a negative coronary T wave (ischemia) are recorded, the amplitude of which gradually decreases starting from day 2. The RS-T segment is located on the isoline.

3. The cicatricial stage of myocardial infarction is characterized by the persistence for a number of years, often throughout the patient’s entire life, of a pathological Q wave or QS complex and the presence of a weakly negative or positive T wave.