Bifurcation of the r wave on ekg. ECG interpretation: R wave

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

• The R wave may be absent in the enhanced lead aVR;
• With a vertical arrangement of the e.o.s. 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 the standard lead III;
• In the 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 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, notching of the R wave in one or two leads can occur. Additional positive or negative teeth are designated R’, R” (r’, r”) or S’, S” (s’, s”). In this case, teeth of a larger size (R and S more than 5 mm, Q more than 3 mm) are indicated in capital letters, and smaller ones in lower case. Splitting, notches of high R waves (especially at the apex) indicate a violation of intraventricular conduction. Splitting, notching of low-amplitude R waves are not regarded as pathological changes. The observed incomplete blockade of the right bundle branch of Giss (splitting of R III, RV1, RV2), as a rule, is not accompanied by a 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 value depends on the direction of the electrical axis of the heart, the width is up to 0.03-0.04 s. Splitting, notching of the S wave is evaluated 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 the chest), it is always positive in I , II, AVF leads. In III, AVD leads, the T wave can be positive, smoothed, biphasic, negative, in the AVR leads it is negative. In the chest leads, due to the peculiarity of the position of the heart, the T wave V1-V2 is positive, and TV1 may be negative. Both reduced and enlarged T wave are regarded as a sign of pathology (inflammation, sclerosis, dystrophy, electrolyte disturbances, etc.). In addition, the direction of the T wave is of great 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, ventricular overload. The duration ("width") of intervals and teeth is measured in hundredths of a second and compared with the norm; intervals P-Q, QRS, Q-T, R-R, as a rule, are measured in the second lead (the teeth are most clear in this lead), the duration of the QRS in case of suspected pathology is evaluated in leads V1 and V4-5.

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

Sinus bradycardia:

The ECG differs little from the 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 (SSS) is based on a decrease in the automatism 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, cardiomyopathy, 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 blockers, quinidine.

It is characteristic that during the 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 automatism function 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 II and III order. In this case, various non-sinus ectopic rhythms arise (more often atrial, from the AV connection, atrial fibrillation and flutter, etc.).

The 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 sections of the atria, the AV junction. Such migration of the pacemaker can occur in healthy people with an increase in tone. vagus nerve, as well as in patients with ischemic heart disease, rheumatic heart disease, various infectious diseases, weakness syndrome SU.

Atrial extrasystole and its characteristic features:

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 after the extrasystole of an incomplete compensatory pause.

Extrasystoles from the AV junction:

The main ECG signs of it are.

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

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

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

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) suddenly starting 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, two-phase or negative P wave in front of each ventricular QRS complex;

3) normal, unchanged ventricular QRS complexes.

av-paroxysmal tachycardia:

The ectopic focus is located in the region of the av-junction.

Most characteristics:

1) suddenly starting 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) suddenly starting 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 for more than 0.12 s with a discordant location segment S-T and T wave

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

Signs of atrial flutter:

The most characteristic features are.

1) the presence on the ECG of frequent - up to 200-400 per minute - regular, similar to each other atrial F waves, which have 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) - correct form atrial flutter.

Atrial fibrillation (fibrillation):

The most characteristic ECG signs of atrial fibrillation are:

1) the absence of the P wave in all leads;

2) the presence throughout the entire cardiac cycle of random waves f, 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 different duration);

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

Flutter and ventricular fibrillation:

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

ECG signs of incomplete sinoatrial blockade are:

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

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

ECG signs of incomplete intra-atrial blockade are:

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

2) splitting of the R wave.

1st degree AV block:

Atrioventricular blockade of the 1st degree is characterized by a slowdown in atrioventricular conduction, which on the ECG is manifested by a constant lengthening of the P-Q interval to more than 0.20 s. The shape and duration of the QRS complex does not change.

2nd degree AV block:

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

There are three types of atrioventricular blockade of the 2nd degree:

1 type - Mobitz type 1.

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

High-degree (deep) AV blockade:

On the ECG, either every second (2: 1), or two or more consecutive ventricular complexes (3: 1, 4: 1) falls out. This leads to a sharp bradycardia, against the background of which disorders of consciousness may occur. Severe ventricular bradycardia contributes to the formation of replacement (slip) contractions and rhythms.

3rd degree atrioventricular block (complete AV block):

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

Heart blocks:

Single-beam blockade - the defeat of one branch of the bundle of His:

1) blockade of the right leg of the bundle of His;

2) blockade of the left anterior branch;

3) blockade of the left back 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.

Blockade of the right leg of the bundle of His:

Electrocardiographic signs of complete blockade of the right leg of the bundle of His are:

1) the presence in the right chest leads V1, V2 of QRS complexes of the type rSR1 or rsR1, which have an M-shaped appearance, with R1 > r;

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

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

4) the presence in leads V1 of a negative or two-phase (- +) asymmetric T wave.

Blockade of the left anterior branch of the bundle of His:

1) a 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.

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

1) a 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) duration of the QRS complex within 0.08-0.11 s.

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

2) the presence in leads V1, V2, AVF of widened deformed ventricular complexes that look like QS or rS with a split or wide top of the S wave;

3) an increase in the total duration of the QRS complex up 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 bundle of His:

On the ECG, signs characteristic of the blockade of the right leg are fixed: the presence in lead V of deformed M-shaped QRS complexes (rSR1), broadened 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 characteristic of the blockade of the left anterior branch of the His bundle.

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

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

Blockade of the three branches of the bundle of His (three-beam blockade):

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

1) the presence on the ECG of signs of atrioventricular blockade 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 in the QRS complex of an additional wave of excitation triangle wave;

c) an increase in the duration and a slight deformation of the QRS complex;

Electrocardiogram (ECG) with atrial and ventricular hypertrophy:

Cardiac hypertrophy is a compensatory adaptive reaction of the myocardium, which is expressed in an increase in the mass of the heart muscle. Hypertrophy develops in response to an increased load experienced by one or another part of the heart in the presence of valvular heart disease (stenosis or insufficiency) or with an increase in pressure in the systemic or pulmonary circulation.

1) an increase in the electrical activity of the hypertrophied 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:

More common in patients with mitral defects heart, especially with 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 negative P in V1;

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

4) negative or two-phase (+ -) P wave in III ( non-permanent feature).

Hypertrophy of the right atrium:

Compensatory hypertrophy of the right atrium usually develops in diseases accompanied by an increase in pressure in 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 with hypertension, aortic heart disease, insufficiency mitral valve 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); while RV4 25 mm or RV5, 6 + SV1, 2 35 mm (on the ECG of people over 40 years old) and 45 mm (on the ECG of young people);

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 severe hypertrophy in leads I and AVL, V5, V6, a shift of the ST segment below the isoline and the formation of a negative or two-phase (- +) T wave can be observed;

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

Right ventricular hypertrophy:

It develops with mitral stenosis, chronic cor pulmonale and other diseases leading to prolonged overload of the right ventricle.

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

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

3) S-type ECG is characterized by the presence in all chest leads from V1 to V6 of the QRS complex of the rS or RS type 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 can be: amplitude RV17 mm or RV1 + SV5, 6 > 110.5 mm;

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

4) displacement segment S-T 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 does the R wave reflect on the ECG results?

From health of cardio-vascular system depends on the state of the whole organism. When unpleasant symptoms occur, most people seek medical care. Having received the results of an electrocardiogram in their hands, few people understand what is at stake. What does the p wave represent on an ECG? What alarming symptoms require medical supervision and even treatment?

Why is an electrocardiogram performed?

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

The cardiograph captures the passage of electrical impulses through the heart, registers the heart rate and can detect the development of serious pathologies. The waves on the ECG give a detailed idea 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 magnitude relative to the projection of the EMF vectors on the axis of assignment. The tooth can be positive or negative. If it is located above the isoline of cardiography, it is considered positive, if below - negative. A biphasic wave is recorded when, at the moment of excitation, the tooth passes from one phase to another.

Important! An electrocardiogram of the heart shows the state of the conducting system, which consists of bundles of fibers through which impulses pass. By observing the rhythm of contractions and the features of rhythm disturbance, various pathologies can be seen.

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

• sinoatrial node;
• atrioventricular;
• legs of the bundle of His;
• Purkinje fibers.

The sinus node, as a pacemaker, is the source of impulses. They form at a rate of once per minute. With various disorders and arrhythmias, impulses can be created more often or less often 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 the ECG show

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

Changes reflected in the cardiogram can show the following conditions:

• rhythm and heart rate;
• myocardial infarction;
• blockade of the conduction system of the heart;
• violation of the metabolism of important trace elements;
• blockage of large arteries.

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

Attention! In addition to the teeth, there are segments and intervals in the ECG picture. Knowing what is the norm for all these elements, you can make a diagnosis.

Detailed interpretation of the electrocardiogram

The norm for the P wave is the location above the isoline. This atrial wave can only be negative in leads 3, aVL and 5. It reaches its maximum amplitude in leads 1 and 2. The absence of a P wave may indicate serious violations in the conduction of impulses in 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, transmitted to the rest of the heart.

Splitting of the P wave, when two peaks form, indicates an increase in the left atrium. Often bifurcation develops with pathologies of the bicuspid valve. The 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 area is horizontal line, since there are no delays due to good conductivity.

The Q wave is normally narrow, its width is not 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 possible signs heart attack, but the indicator itself is evaluated only in combination with others.

The R wave is ventricular, so it is the highest. The walls of the organ in this zone are the most dense. 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 chest leads (V5 and 6). At the same time, it should not exceed 2.6 mV. Too high a tooth is a sign of left ventricular hypertrophy. This condition requires an in-depth diagnosis to determine the causes of the increase (CHD, arterial hypertension, valvular heart disease, cardiomyopathy). If the R wave drops sharply from V5 to V6, this may be a sign of MI.

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

Definition of the axis of the heart

Another step in deciphering the electrocardiogram is the determination of the axis of the heart. A normal tilt is an angle between 30 and 69 degrees. Smaller numbers indicate a deviation to the left, and large numbers indicate a deviation to the right.

Possible research errors

It is possible to obtain unreliable data from an electrocardiogram if, when registering signals, the cardiograph is affected by the following factors:

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

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

When an experienced cardiologist deciphers a cardiogram, you can get a lot of valuable information. In order not to start the pathology, it is important to consult a doctor when the first painful symptoms occur. So you can save health and life!

Electrocardiogram for conduction disorders

in limb leads (more than 0.11 s);

splitting or serration of the P waves (non-permanent)

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

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

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

an increase in the duration of the P-Q (R) interval of 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);

preservation of the normal shape and duration of QRS complexes

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

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

the presence of severe deformation and broadening (more than 0.12 s) of QRS complexes in the form of a two-fascicle blockade in the His system (see below)

gradual, from one complex to another, an 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 the prolapse of the QRST complex, re-registration of a normal or slightly prolonged P-Q (R) interval, then a gradual increase in the duration of this interval with the prolapse of the ventricular complex (Samoilov-Wenckebach periodical);

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

regular (by type 3:2, 4:3, 5:4, 6:5, etc.) or random prolapse of one, rarely biventricular and three-ventricular QRST complexes (while maintaining the atrial P wave at this place);

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

P-Q(R) interval is 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 occurrence of interfering (slip) complexes and rhythms (non-permanent 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

flutter (F) atrial;

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 broadened, often serrated S wave;

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

the presence in lead V1 (less often in lead III) of RS-T segment depression with an upward bulge and a negative or biphasic ("-" and "+") asymmetric T wave

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

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

QRS complex in leads I and аVL type rS, and in leads III, аVF - type qR; total duration of ventricular QRS complexes 0.08-0.11 s

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

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

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

deviation of the electrical axis of the heart to the left (common)

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

increase in QRS duration up to 0.10-0.11 s;

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

a 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 a complete blockade of two branches of the bundle of His (any kind of two-bundle blockade - see above)

ECG signs of complete bifascicular blockade

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

prolonged and slightly deformed QRS complex;

shift of the RS-T segment discordant to the QRS complex and a change in the polarity of the T wave (non-permanent signs)

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

the presence of unchanged (narrow) and undeformed QRS complexes

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For an error-free interpretation of changes in the analysis of the ECG, it is necessary to adhere to the scheme of its decoding given below.

The general scheme for deciphering the ECG: deciphering the cardiogram in children and adults: general principles, reading results, decoding example.

Normal electrocardiogram

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

The shape of the 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 EMF of the heart onto the axis of one or another lead. If the projection of the moment vector is directed towards the positive electrode of this lead, an upward deviation from the isoline is recorded on the ECG - positive teeth. If the projection of the vector is directed towards the negative electrode, the ECG shows a downward deviation from the isoline - negative teeth. In the case when the moment vector is perpendicular to the axis of abduction, its projection on this axis is equal to zero and no deviation from the isoline is recorded on the ECG. If, during the excitation cycle, the vector changes its direction with respect to the poles of the lead axis, then the tooth becomes two-phase.

Segments and teeth of a normal ECG.

Tooth 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 a 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. the time of propagation of excitation through the atria, AV node, bundle of His and its branches. Its duration is 0.12-0.20 s and in a healthy person it 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 through the ventricular myocardium.

Q wave.

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

Prong R.

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 muscle 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 tooth.

In a healthy person, the amplitude of the S wave in various electrocardiographic leads varies widely, not exceeding 20 mm. In the normal position of the heart in the chest, the S amplitude in the limb leads is small, except for the aVR lead. In the chest leads, the S wave gradually decreases from V, V to V, and in the leads V, V has a small amplitude or is completely absent. Equality of the R and S waves in the chest leads (“transitional 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).

Segment RS-T.

The RS-T segment in a healthy person in the limb leads is located on the isoline (0.5 mm). Normally, in the chest leads V-V, a slight displacement of the RS-T segment up from the isoline (no more than 2 mm) can be observed, and in leads V - down (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 may be positive, biphasic, or negative. In lead aVR, the T wave is normally always negative.

Q-T Interval(QRST)

The QT interval is called electrical ventricular systole. Its duration depends primarily on the number of heartbeats: the higher the rhythm rate, the shorter the proper QT interval. The normal duration of the Q-T interval is determined by the Bazett formula: Q-T \u003d K, where K is a coefficient equal to 0.37 for men and 0.40 for women; R-R is the duration of one cardiac cycle.

Analysis of the electrocardiogram.

The analysis of any ECG should begin with checking the correctness of the recording technique. First, it is necessary to pay attention to the presence of various interferences. Interferences that occur during ECG registration:

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

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

c - pickup due to muscle tremor (wrong frequent fluctuations are visible).

Interference during ECG registration

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

General scheme (plan) of ECG decoding.

I. Analysis heart rate and conductivity:

1) assessment of the regularity of heart contractions;

2) counting the number of heartbeats;

3) determination of the source of excitation;

4) evaluation of the conduction function.

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

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

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

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

III. Analysis of the atrial R 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 conclusion.

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

2) With the correct rhythm, the heart rate (HR) is determined by the formula: HR \u003d.

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

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

Evaluation of rhythm regularity and heart rate:

a) correct rhythm; b), c) wrong 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 R waves to 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.

The atrial rhythm (from the lower sections of the atria) is characterized by the presence of negative P and P waves followed by 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 rate (less than 40 beats per minute); the presence of extended and deformed QRS complexes; the absence of a regular connection of 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 section of the conduction system of the heart.

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

Six-axis Bailey system.

a) Determination of the angle by a graphical method. Calculate the algebraic sum of the amplitudes of the QRS complex teeth in any two limb leads (usually I and III standard leads are used), the axes of which are located in the frontal plane. The positive or negative value of the algebraic sum on an arbitrarily chosen scale is plotted on the positive or negative part of the axis of the corresponding assignment in the six-axis Bailey coordinate system. These values ​​are projections of the desired electrical axis of the heart on axes I and III of the standard leads. From the ends of these projections restore perpendiculars to the axes of the leads. 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 the lead, the axis of which approximately coincides with the location of the electrical axis of the heart, parallel to it.

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

In the 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.

With 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.

With 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, with R R> R; deep S waves are recorded in leads I and aV

III. P wave analysis includes: 1) P wave amplitude measurement; 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 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; the duration of the interval of internal deviation in leads V and V; possible splitting of the tooth or the appearance of an additional one; c) assessment of the S wave: amplitude, comparing it with the R amplitude; possible broadening, serration 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 displacement of the RS-T segment, then the isoline up or down at a point 0.05-0.08 s to the right from point j; determine the shape of the possible displacement of the RS-T segment: horizontal, oblique descending, oblique ascending.

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

4) Analysis of the Q-T interval: measurement of duration.

V. Electrocardiographic conclusion:

1) the source of the heart rhythm;

2) regularity of the heart rhythm;

4) the position of the electrical axis of the heart;

5) the presence of four electrocardiographic syndromes: a) cardiac arrhythmias; b) conduction disturbances; c) ventricular and atrial myocardial hypertrophy or their acute overload; d) myocardial damage (ischemia, dystrophy, necrosis, scarring).

Electrocardiogram for cardiac arrhythmias

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

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

2) Sinus bradycardia: a decrease in the number of heartbeats per minute (an increase in the duration of 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 respiratory phases; preservation of all electrocardiographic signs of sinus rhythm (alternation of the P wave and the QRS-T complex).

4) Sinoatrial node weakness syndrome: persistent sinus bradycardia; periodic appearance of ectopic (non-sinus) rhythms; the 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 QRST complex following it; 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 the usual normal complexes; the presence after an atrial extrasystole of an incomplete compensatory pause.

Atrial extrasystole (II standard lead): a) from the upper sections of the atria; b) from the middle sections 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 the rest of the QRST complexes of sinus origin; negative P' wave in leads II, III and aVF after 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 P wave before ventricular extrasystole; presence in most cases ventricular extrasystole complete compensatory pause.

a) left ventricular; b) right ventricular extrasystole

3. Paroxysmal tachycardia.

1) Atrial paroxysmal tachycardia: suddenly starting and also suddenly ending attack of increased heart rate for a minute while maintaining the correct rhythm; the presence of a reduced, deformed, biphasic or negative P wave in front of each ventricular QRS' complex; normal unchanged ventricular QRS complexes; in some cases, there is a deterioration in atrioventricular conduction with the development of atrioventricular block I degree with periodic loss of individual QRS' complexes (non-permanent signs).

2) Paroxysmal tachycardia from the atrioventricular junction: suddenly starting and also suddenly ending attack of increased heart rate for 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: suddenly starting and also suddenly ending attack of increased heart rate for a minute while maintaining the correct rhythm in most cases; deformation and expansion of the QRS complex for more than 0.12 s with a discordant arrangement of the RS-T segment and the T wave; the presence of atrioventricular dissociation, i.e. complete separation of the frequent rhythm of the ventricles and the normal rhythm of the atria with occasionally recorded single normal unchanged QRST complexes of sinus origin.

4. Atrial flutter: the presence on the ECG of frequent - dov minute - regular, similar to each other atrial waves F, having a characteristic sawtooth shape (leads II, III, aVF, V, V); in most cases, the correct, regular ventricular rhythm with the same intervals F-F; 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 (fibrillation): the absence of P wave in all leads; the presence of irregular waves throughout the entire 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 (dove minutes), regular and identical in shape and amplitude flutter waves, resembling a sinusoidal curve.

7. Blinking (fibrillation) of the ventricles: frequent (from 200 to 500 per minute), but irregular waves that differ from each other various form and amplitude.

Electrocardiogram for violations of the conduction function.

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

2. Intra-atrial blockade: an increase in the duration of the P wave more than 0.11 s; splitting of the R wave.

3. Atrioventricular blockade.

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

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

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

c) distal (three-beam) form: severe QRS deformation.

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

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

b) Mobitz type II: QRST prolapse 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 consecutive ventricular complexes (blockade 3:1, 4:1, etc.) drop out.

3) III degree: complete separation of the atrial and ventricular rhythms and a decrease in the number of ventricular contractions for a minute or less.

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

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

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

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

2) Blockade of the left anterior branch of the bundle of His: 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, type II rS; the total duration of the QRS complex is 0.08-0.11 s.

3) Blockade of the left posterior branch of the bundle of His: a 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 of the rS type, and in leads III, aVF - of the qR type; the duration of the QRS complex is within 0.08-0.11 s.

4) Blockade of the left leg of the bundle of His: in leads V, V, I, aVL widened deformed ventricular complexes of type R with a split or wide apex; in leads V, V, III, aVF widened deformed ventricular complexes, having the form of QS or rS with a split or wide top of the S wave; an increase in the total duration of the QRS complex more than 0.12 s; the presence in leads V, V, I, aVL of a discordant with respect to QRS displacement 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 the three branches of the His bundle: atrioventricular blockade of I, II or III degree; blockade of two branches of the bundle of His.

Electrocardiogram in atrial and ventricular hypertrophy.

1. Hypertrophy of the left atrium: bifurcation and increase in the amplitude of the teeth P (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-permanent sign); an 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, 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 may be negative (a non-permanent sign); the duration of the P waves does not exceed 0.10 s.

3. Hypertrophy of the left ventricle: an increase in the amplitude of the R and S waves. At the same time, 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 two-phase (–+) T wave in leads I, aVL and V; an increase in the duration of the internal QRS deviation interval in the left chest leads by more than 0.05 s.

4. Hypertrophy of the right ventricle: 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; appearance in lead V of a QRS complex of the rSR' or QR type; signs of rotation of the heart around the longitudinal axis clockwise; shift of the RS-T segment down and the appearance of negative T waves in leads III, aVF, V; increase in the duration of the interval of internal deviation in V more than 0.03 s.

Electrocardiogram in ischemic heart disease.

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

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

The R wave (the main ECG wave) is due to excitation of the ventricles of the heart (for more details, see "Excitation in the myocardium"). The amplitude of the R wave in standard and enhanced leads depends on the location of the electrical axis of the heart (e.o.s.).

• The R wave may be absent in the enhanced lead aVR;
• With a vertical arrangement of the e.o.s. 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 the standard lead III;
• In the 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.

/ Methodological guide for ecg

Absence of P wave before ventricular extrasystole;

The presence of a complete compensatory pause after a ventricular extrasystole.

1.6. Paroxysmal tachycardia.

Paroxysmal tachycardia is a suddenly starting and just as suddenly ending attack of increased heart rate for a minute while maintaining the correct regular rhythm in most cases. These transient seizures can be intermittent (non-persistent) lasting less than 30 seconds and sustained (persistent) lasting 30 seconds.

An important sign of paroxysmal tachycardia is the preservation during the entire paroxysm (except for the first few cycles) of the correct rhythm and constant heart rate, which, unlike sinus tachycardia, does not change after physical activity, emotional stress or after an injection of atropine.

Currently, there are two main mechanisms of paroxysmal tachycardia: 1) the mechanism of re-entry of the excitation wave (re-entry); 2) an increase in the automatism of the cells of the conducting system of the heart - ectopic centers of the II and III order.

Depending on the localization of the ectopic center of increased automatism or the constantly circulating return wave of excitation (re-entry), atrial, atrioventricular and ventricular forms of paroxysmal tachycardia are distinguished. Since, in atrial and atrioventricular paroxysmal tachycardia, the excitation wave propagates through the ventricles in the usual way, the ventricular complexes in most cases are not changed. Main hallmarks atrial and atrioventricular forms of paroxysmal tachycardia, detected on the surface ECG, are the different shape and polarity of the P waves, as well as their location in relation to the ventricular QRS complex. However, very often on the ECG recorded at the time of the attack, against the background of a pronounced tachycardia, it is not possible to identify the P wave. Therefore, in practical electrocardiology, atrial and atrioventricular forms of paroxysmal tachycardia are often combined with the concept of supraventricular (supraventricular) paroxysmal tachycardia, especially since drug treatment both forms are largely similar (the same drugs are used).

1.6.1. Supraventricular paroxysmal tachycardia.

Suddenly starting and also suddenly ending attack of increased heart rate for a minute while maintaining the correct rhythm;

Normal unchanged ventricular QRS complexes, similar to QRS complexes, recorded before an attack of paroxysmal tachycardia;

The absence of a P wave on the ECG or its presence before or after each QRS complex.

1.6.2. Ventricular paroxysmal tachycardia.

With ventricular paroxysmal tachycardia, the source of ectopic impulses is the contractile myocardium of the ventricles, the bundle of His, or Purkinje fibers. Unlike other tachycardias, ventricular tachycardia has a worse prognosis due to a tendency to turn into ventricular fibrillation or cause severe circulatory disorders. As a rule, ventricular paroxysmal tachycardia develops against the background of significant organic changes in the heart muscle.

Unlike supraventricular paroxysmal tachycardia with ventricular tachycardia the course of excitation through the ventricles is sharply disturbed: the ectopic impulse first excites one ventricle, and then, with a great delay, passes to the other ventricle and spreads through it in an unusual way. All these changes resemble those in ventricular extrasystole, as well as in the blockade of the legs of the bundle of His.

An important electrocardiographic sign of ventricular paroxysmal tachycardia is the so-called atrioventricular dissociation, i.e. complete disunity in the activity of the atria and ventricles. Ectopic impulses originating in the ventricles are not conducted retrograde to the atria and the atria are excited in the usual way due to impulses arising in the sinoatrial node. In most cases, the wave of excitation is not conducted from the atria to the ventricles because the atrioventricular node is in a state of refractoriness (exposure to frequent impulses from the ventricles).

A sudden onset and also a sudden ending attack of increased heart rate for up to a minute while maintaining the correct rhythm in most cases;

Deformation and expansion of the QRS complex for more than 0.12 s with a discordant location of the RS-T segment and the T wave;

The presence of atrioventricular dissociation, i.e. complete separation of the frequent ventricular rhythm (QRS complex) and the normal atrial rhythm (P wave) with occasionally recorded single normal unchanged QRST complexes of sinus origin (“captured” ventricular contractions).

2. Syndrome of impaired impulse conduction.

The slowdown or complete cessation of the conduction of an electrical impulse through any part of the conduction system is called heart block.

As well as the impulse formation disorder syndrome, this syndrome is included in the heart rhythm disorder syndrome.

The impulse conduction disorder syndrome includes atrioventricular blockades, blockades of the right and left legs of the His bundle, as well as intraventricular conduction disturbances.

According to their genesis, heart block can be functional (vagal) - in athletes, young people with autonomic dystonia, against the background of sinus bradycardia and in other similar cases; they disappear with exercise or intravenous administration 0.5-1.0 mg of atropine sulfate. The second type of blockade is organic, which occurs in the syndrome of heart muscle damage. In some cases (myocarditis, acute myocardial infarction), it appears in the acute period and disappears after treatment, in most cases, such a blockade becomes permanent (cardiosclerosis).

2.1. Atrioventricular block.

Atrioventricular blockade is a partial or complete violation of the conduction of an electrical impulse from the atria to the ventricles. Atrioventricular blocks are classified on the basis of several principles. First, take into account their stability; accordingly, atrioventricular blockades can be: a) acute, transient; b) intermittent, transient; c) chronic, permanent. Secondly, the severity or degree of atrioventricular blockade is determined. In this regard, there are atrioventricular blockade of the first degree, atrioventricular blockade of the second degree of types I and II, and atrioventricular blockade of the third degree (complete). Thirdly, it provides for determining the place of blocking, i.e. topographic level of atrioventricular blockade. If conduction is disturbed at the level of the atria, the atrioventricular node, or the main trunk of the bundle of His, one speaks of a proximal atrioventricular block. If the impulse conduction delay occurred simultaneously at the level of all three branches of the His bundle (the so-called three-bundle block), this indicates a distal atrioventricular block. Most often, a disturbance in the conduction of excitation occurs in the region of the atrioventricular node, when nodal proximal atrioventricular block develops.

2.1.1. Atrioventricular block I degree.

This symptom is manifested by a slowdown in the conduction of the impulse from the atria to the ventricles, manifested by a prolongation of the P-q (R) interval.

Correct alternation of the P wave and the QRS complex in all cycles;

P-q(R) interval more than 0.20 s;

Normal shape and duration of the QRS complex;

2.1.2. Atrioventricular block II degree. 2nd degree atrioventricular block is intermittent

the resulting cessation of individual impulses from the atria to the ventricles.

There are two main types of atrioventricular block II degree - Mobitz type I (with periods of Samoilov-Wenckebach) and Mobitz type II.

2.1.2.1. Mobitz type I.

Gradual lengthening of the P-q(R) interval from cycle to cycle, followed by prolapse of the ventricular QRST complex;

After the loss of the ventricular complex on the ECG, a normal or prolonged P-q (R) interval is again recorded, then the whole cycle is repeated;

The periods of gradual increase in the P-q(R) interval followed by prolapse of the ventricular complex are called the Samoilov-Wenckebach periods.

2.1.2.2. Mobitz type II.

R-R intervals of the same duration;

Absence of progressive prolongation of the P-q(R) interval before blocking the impulse (stability of the P-q(R) interval);

Prolapse of single ventricular complexes;

Long pauses are equal to twice the P-P interval;

2.1.3. Atrioventricular block III degree. Atrioventricular blockade of the III degree (complete atrioventricular

ricular block) is a complete cessation of impulse conduction from the atria to the ventricles, as a result of which the atria and ventricles are excited and contracted independently of each other.

Lack of relationship between P waves and ventricular complexes;

The intervals P-P and R-R are constant, but R-R is always greater than P-R;

The number of ventricular contractions is less than 60 per minute;

Periodic layering of P waves on the QRS complex and T waves and deformation of the latter.

If atrioventricular block I and II degree (Mobitz type I) can be functional, then atrioventricular block II degree (Mobitz type II) and III degree develop against the background of pronounced organic changes in the myocardium and have a worse prognosis.

2.2. Blockade of the legs of the bundle of His.

Blockade of the legs and branches of the bundle of His is a slowdown or complete cessation of the conduction of excitation along one, two or three branches of the bundle of His.

With the complete cessation of the conduction of excitation along one or another branch or leg of the bundle of His, they speak of a complete blockade. Partial slowing of conduction indicates an incomplete blockade of the leg.

2.2.1. Blockade of the right leg of the bundle of His.

The blockade of the right leg of the bundle of His is a slowdown or complete cessation of the conduction of an impulse along the right leg of the bundle of His.

2.2.1.1. Complete blockade of the right leg of the bundle of His.

Complete blockade of the right leg of the bundle of His is the termination of the impulse along the right leg of the bundle of His.

The presence in the right chest leads V1,2 of QRS complexes rSR "or rsR", having an M-shaped appearance, and R "> r;

The presence in the left chest leads (V5, V6) and in leads I, aVL of a broadened, often serrated S wave;

The increase in the time of internal deviation in the right chest leads (V1, V2) is more than or equal to 0.06 s;

An increase in the duration of the ventricular QRS complex is greater than or equal to 0.12 s;

The presence in lead V1 of depression of the S-T segment and a negative or biphasic (- +) asymmetric T wave.

2.1.2.2. Incomplete blockade of the right leg of the bundle of His.

Incomplete blockade of the right leg of the bundle of His is a slowdown in the conduction of an impulse along the right leg of the bundle of His.

The presence in lead V1 of a QRS complex of the rSr or rsR type;

The presence in the left chest leads (V5, V6) and in leads I of a slightly broadened S wave;

The time of internal deviation in lead V1 is not more than 0.06 s;

The duration of the ventricular QRS complex is less than 0.12 s;

The S-T segment and the T wave in the right chest leads (V1, V2, as a rule, do not change.

2.2.2. Blockade of the left leg of the bundle of His.

The blockade of the left leg of the bundle of His is a slowdown or complete cessation of the conduction of an impulse along the left leg of the bundle of His.

2.2.2.1. Complete blockade of the left leg of the bundle of His.

Complete blockade of the left leg of the bundle of His is the termination of the impulse along the left leg of the bundle of His.

The presence in the left chest leads (V5, V6), I, aVl of widened deformed ventricular complexes, type R with a split or wide apex;

The presence in leads V1, V2, III, aVF of widened deformed ventricular complexes that look like QS or rS with a split or wide top of the S wave;

The time of internal deflection in leads V5.6 is greater than or equal to 0.08 s;

The increase in the total duration of the QRS complex is greater than or equal to 0.12 s;

The presence in leads V5,6, I, aVL of a discordant shift of the R(S)-T segment with respect to the QRS and negative or two-phase (- +) asymmetric T waves;

2.2.2.2. Incomplete blockade of the left leg of the bundle of His.

Incomplete blockade of the left leg of the bundle of His is a slowdown in the conduction of an impulse along the left leg of the bundle of His.

The presence in leads I, aVL, V5.6 of high broadened,

sometimes split R waves (no qV6 wave);

The presence in leads III, aVF, V1, V2 of broadened and deep complexes of the QS or rS type, sometimes with the initial splitting of the S wave;

Time of internal deflection in leads V5.6 0.05-0.08

The total duration of the QRS complex 0.10 - 0.11 s;

Due to the fact that left leg is divided into two branches: anterior-superior and posterior-inferior, blockades of the anterior and posterior branches of the left leg of the bundle of His are isolated.

With the blockade of the anterior-upper branch of the left leg of the bundle of His, the conduction of excitation to the anterior wall of the left ventricle is impaired. Excitation of the myocardium of the left ventricle proceeds, as it were, in two stages: first, the interventricular septum and the lower sections of the posterior wall are excited, and then the anterior-lateral wall of the left ventricle.

A sharp deviation of the electrical axis of the heart to the left (the alpha angle is less than or equal to -300 C);

QRS in leads I, aVL type qR, in leads III, aVF type rS;

The total duration of the QRS complex is 0.08-0.011 s.

With the blockade of the left posterior branch of the His bundle, the sequence of excitation coverage of the myocardium of the left ventricle changes. Excitation is initially carried out without hindrance along the left anterior branch of the His bundle, quickly covers the myocardium of the anterior wall, and only after that, through the anastomoses of the Purkinje fibers, it spreads to the myocardium of the posterior-lower sections of the left ventricle.

A sharp deviation of the electrical axis of the heart to the right (the alpha angle is greater than or equal to 1200 C);

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

The duration of the QRS complex is within 0.08-0.11.

3. Syndrome of combined disorders.

This syndrome is based on a combination of impaired impulse formation, manifested by frequent excitation of the atrial myocardium, and impaired conduction of the impulse from the atria to the ventricles, which is expressed in the development of a functional blockade of the atrioventricular junction. This functional atrioventricular block prevents the ventricles from working too frequently and inefficiently.

As well as syndromes of impaired formation and conduction of an impulse, the syndrome of combined disorders is an integral part of the syndrome of cardiac arrhythmias. It includes atrial flutter and atrial fibrillation.

3.1. Symptom of atrial flutter.

Atrial flutter is a significant increase in atrial contractions (up to) per minute while maintaining the correct regular atrial rhythm. The direct mechanisms leading to very frequent excitation of the atria during their fluttering are either an increase in the automatism of the cells of the conducting system, or the mechanism of re-entry of the excitation wave - re-entry, when conditions are created in the atria for a long rhythmic circulation of a circular wave of excitation. In contrast to paroxysmal supraventricular tachycardia, when the wave of excitation circulates through the atria with a frequency of one minute, with atrial flutter this frequency is higher and is per minute.

Absence of P waves on the ECG;

The presence of frequent - dov minute - regular, similar to each other atrial waves F, having a characteristic sawtooth shape (leads II, III, aVF, V1, V2);

The presence of normal unchanged ventricular complexes;

Each gastric complex is preceded by a certain number of atrial F waves (2:1, 3:1, 4:1, etc.) in regular atrial flutter; with an irregular shape, the number of these waves may vary;

3.2. Symptom of atrial fibrillation.

Atrial fibrillation, or atrial fibrillation, is a heart rhythm disorder in which frequent (from 350 to 700) per minute random, chaotic excitation and contraction of individual groups of atrial muscle fibers are observed throughout the entire cardiac cycle. At the same time, excitation and contraction of the atrium as a whole is absent.

Depending on the size of the waves, large- and small-wave forms of atrial fibrillation are distinguished. With a coarse waveform, the amplitude of the waves f exceeds 0.5 mm, their frequency is per minute; they appear with relatively greater regularity. This form of atrial fibrillation is more common in patients with severe atrial hypertrophy, for example, with mitral stenosis. With a fine-wave form of atrial fibrillation, the frequency of waves f reaches a minute, their amplitude is less than 0.5 mm. The irregularity of the waves is more pronounced than in the first variant. Sometimes the f waves are not visible at all on the ECG in any of the electrocardiographic leads. This form of atrial fibrillation is often found in older people suffering from cardiosclerosis.

Absence in all electrocardiographic leads of the P wave;

The presence throughout the entire cardiac cycle of random waves f, having different shapes and amplitudes. Waves f are better recorded in leads V1, V2, II, III and aVF.

Irregularity of ventricular QRS complexes (R-R intervals of different duration).

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

Syndrome diffuse changes myocardium.

The ECG reflects various changes and damage to the myocardium, however, due to the complexity and individual variability of the structure of the myocardium and the extreme complexity of the chronotopography of excitation in it, it is not possible to establish a direct connection between the details of the process of propagation of excitation and their reflection on the ECG until now. The development of clinical electrocardiography along an empirical path, comparing the morphology of the curves with clinical and pathological data, nevertheless, made it possible to determine combinations of signs that allow diagnosing (assuming the presence) of diffuse myocardial lesions with a certain accuracy, monitoring the action of cardiac drugs, detecting disturbances in the metabolism of electrolytes, especially potassium and calcium.

It should be remembered that there are often cases in which, contrary to the obvious clinical picture, ECG abnormalities are not observed, or ECG abnormalities are obvious, but their interpretation is extremely difficult or even impossible.

III. SYNDROME OF ELECTRIC DOMINATION OF HEART DEPARTMENTS.

Myocardial hypertrophy is an increase in the muscle mass of the heart, manifested by an increase in the duration of its excitation and is reflected by a change in depolarization and repolarization. Changes in depolarization are expressed in an increase in the amplitude and duration of the corresponding elements (P or QRS). Changes in repolarization are secondary and are associated with a prolongation of the depolarization process. As a result, the direction of the repolarization wave changes (the appearance of negative T). In addition, changes in repolarization reflect dystrophic changes in the hypertrophied myocardium.

1. Hypertrophy of the ventricles.

For ventricular hypertrophy, general ECG criteria will be identified, these are:

Increased voltage of the QRS complex;

Widening of the QRS complex;

Deviation of the electric axis of the QRS complex;

Prolongation of the internal deflection time (VVO) in lead V1 for the right ventricle and in V4-5 for the left ventricle (this group of changes is associated with changes in the depolarization process);

Changes in the ST segment and T wave due to impaired repolarization processes in the hypertrophied myocardium.

1.1. Left ventricular hypertrophy.

With hypertrophy of the left ventricle, its EMF increases, which causes an even greater predominance of the vectors of the left ventricle over the right one, while the resulting vector deviates to the left and back, towards the hypertrophied left ventricle.

Horizontal position of the electrical axis of the heart or deviation to the left;

The time of internal deviation of the left ventricle in V5-V6> 0.05 s;

An increase in the qV5-V6 wave, but not more than 1/4R in this lead;

Depending on the position of the electrical axis of the heart, RII>18 mm, RI>16 mm, RaVF>20 mm, RaVL>11 mm.

Change in the terminal part of the ventricular complex in the left chest leads (downward downward ST shift, negative T, asymmetric in V5-6, decreased T wave amplitude (T<1/10RV5-6);

Shift of the transitional zone to the right (rotation of the left ventricle anteriorly). With advanced left ventricular hypertrophy, the transition zone shifts to the left with a rapid transition from deep S to high R (narrow transition zone). Left ventricular hypertrophy is observed with mitral valve insufficiency, aortic defects, arterial hypertension and is included in the load syndrome on the left heart.

1.2. Hypertrophy of the right ventricle.

Diagnosis of right ventricular hypertrophy is difficult, because. the mass of the left ventricle is much greater than that of the right.

There are several variants of right ventricular hypertrophy. The first (the so-called R-type of changes) is a pronounced

hypertrophy, when the mass of the right ventricle is greater than the mass of the left. With this option, direct signs of right ventricular hypertrophy are recorded.

RV1 tooth > 7 mm;

Prong SV1< 2 мм;

Ratio of teeth RV1/SV1>1;

The time of internal deviation of the right ventricle (lead V1)> 0.03-0.05 s;

al-

Signs of right ventricular overload with repolarization changes in leads V1-2 (decrease in the ST segment, negative TV1-2). This type of hypertrophy is more common in patients with congenital heart disease and is associated with long-term

load on the right side of the heart.

The second variant of the ECG changes is expressed in the formation of a picture of an incomplete blockade of the right leg of the His bundle. ECG signs of incomplete blockade of the right bundle branch block were described above.

The third variant of right ventricular hypertrophy (Stype of changes) is observed more often in chronic pulmonary pathology.

Rotation of the right ventricle anteriorly around the longitudinal axis, transition zone V5-6;

Rotation around the transverse axis with the apex of the heart posterior (axis type SI-SII-SIII);

Deviation of the electrical axis of the heart to the right (angle alpha>1100);

An increase in the terminal R wave in lead aVR> 5 mm, while it can become the main tooth;

In the chest leads, the rS complex is observed from V1 to V6, while SV5>5 mm.

1.3. Combined hypertrophy of both ventricles.

Diagnosis of combined ventricular hypertrophy is difficult and often impossible, because opposite EMF vectors are mutually compensated and can neutralize the characteristic signs of ventricular hypertrophy.

2. Atrial hypertrophy.

2.1. Hypertrophy of the left atrium.

With hypertrophy of the left atrium, its EMF increases, which causes the resulting vector of the P wave to deviate to the left and back.

Increase in the width of the PII tooth more than 0.10-0.12 s;

Deviation of the electric axis of the P wave to the left, while PI>>PII>PIII;

Deformation of the P wave in leads I, II, aVL in the form of an oncoming wave with a distance between the peaks of more than 0.02 s;

In the first chest lead, the negative phase of the P wave increases, which becomes deeper than 1 mm and longer than 0.06 s.

The atrial complex with left atrial hypertrophy is called "P-mitrale", most often observed in patients with rheumatic mitral stenosis and mitral valve insufficiency, less often - hypertension, cardiosclerosis.

2.2. Hypertrophy of the right atrium.

With hypertrophy of the right atrium, its EMF increases, which is reflected on the ECG in the form of an increase in amplitude and time parameters. The resulting atrial depolarization vector deviates downward and forward.

High peaked ("Gothic" form) P wave in II, III, aVF leads;

The height of the tooth in the II standard lead> 2-2.5 mm;

Its width can be increased to 0.11 s;

The electrical axis of the P wave is deviated to the right - РIII>РII>РI. In lead V1, the P wave becomes high, spiky,

equilateral or recorded as two-phase with a sharp predominance of the first positive phase.

Typical changes in right atrial hypertrophy are called "P-pulmonale", because. they are often seen in patients with chronic diseases lungs, with thromboembolism in the pulmonary artery system, chronic pulmonary heart, congenital heart defects.

The appearance of these changes after acute situations with rapid reverse dynamics is referred to as atrial overload.

2.3. Hypertrophy of both atria.

On the ECG with hypertrophy of both atria, signs of hypertrophy of the left (split and broadened teeth PI, II, aVL, V5-V6) and the right atrium (high peaked PIII, aVF) are recorded. The greatest changes are detected in the first chest lead. The atrial complex on the ECG in V1 is biphasic with a high, pointed positive phase and a deep broadened negative phase.

IV. SYNDROME OF FOCAL MYOCARDIAL DAMAGE.

A focal myocardial lesion is a local circulatory disorder in a certain area of ​​the heart muscle with a violation of the processes of depolarization and repolarization and is manifested by syndromes of ischemia, damage and necrosis.

1. Syndrome of myocardial ischemia.

The occurrence of ischemia leads to a lengthening of the action potential of myocardial cells. As a result, the final phase of repolarization is lengthened, which is reflected by the T wave. The nature of the changes depends on the location of the ischemic focus and the position of the active electrode. Local disorders of the coronary circulation can be manifested by direct signs (if the active electrode is facing the lesion) and reciprocal signs (the active electrode is located in the opposite part of the electric field).

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For an error-free interpretation of changes in the analysis of the ECG, it is necessary to adhere to the scheme of its decoding given below.

General ECG decoding scheme: cardiogram decoding in children and adults: general principles, reading results, decoding example.

Normal electrocardiogram

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

The shape of the 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 EMF of the heart onto the axis of one or another lead. If the projection of the moment vector is directed towards the positive electrode of this lead, an upward deviation from the isoline is recorded on the ECG - positive teeth. If the projection of the vector is directed towards the negative electrode, the ECG shows a downward deviation from the isoline - negative teeth. In the case when the moment vector is perpendicular to the axis of abduction, its projection on this axis is equal to zero and no deviation from the isoline is recorded on the ECG. If, during the excitation cycle, the vector changes its direction with respect to the poles of the lead axis, then the tooth becomes two-phase.

Segments and teeth of a normal ECG.

Tooth 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 a 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. the time of propagation of excitation through the atria, AV node, bundle of His and its branches. Its duration is 0.12-0.20 s and in a healthy person it 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 through the ventricular myocardium.

Q wave.

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

Prong R.

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 muscle 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 tooth.

In a healthy person, the amplitude of the S wave in various electrocardiographic leads varies widely, not exceeding 20 mm. In the normal position of the heart in the chest, the S amplitude in the limb leads is small, except for the aVR lead. In the chest leads, the S wave gradually decreases from V, V to V, and in the leads V, V has a small amplitude or is completely absent. Equality of the R and S waves in the chest leads (“transitional 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).

Segment RS-T.

The RS-T segment in a healthy person in the limb leads is located on the isoline (0.5 mm). Normally, in the chest leads V-V, a slight displacement of the RS-T segment up from the isoline (no more than 2 mm) can be observed, and in leads V - down (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 may be positive, biphasic, or negative. In lead aVR, the T wave is normally always negative.

Q-T Interval(QRST)

The QT interval is called electrical ventricular systole. Its duration depends primarily on the number of heartbeats: the higher the rhythm rate, the shorter the proper QT interval. The normal duration of the Q-T interval is determined by the Bazett formula: Q-T \u003d K, where K is a coefficient equal to 0.37 for men and 0.40 for women; R-R is the duration of one cardiac cycle.

Analysis of the electrocardiogram.

The analysis of any ECG should begin with checking the correctness of the recording technique. First, it is necessary to pay attention to the presence of various interferences. Interferences that occur during ECG registration:

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

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

c - pickup due to muscle tremor (wrong frequent fluctuations are visible).

Interference during ECG registration

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

General scheme (plan) of ECG decoding.

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) evaluation of the conduction function.

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

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

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

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

III. Analysis of the atrial R 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 conclusion.

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

2) With the correct rhythm, the heart rate (HR) is determined by the formula: HR \u003d.

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

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

Evaluation of rhythm regularity and heart rate:

a) correct rhythm; b), c) wrong 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 R waves to 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.

The atrial rhythm (from the lower sections of the atria) is characterized by the presence of negative P and P waves followed by 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 rate (less than 40 beats per minute); the presence of extended and deformed QRS complexes; the absence of a regular connection of 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 section of the conduction system of the heart.

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

Six-axis Bailey system.

a) Determination of the angle by a graphical method. Calculate the algebraic sum of the amplitudes of the QRS complex teeth in any two limb leads (usually I and III standard leads are used), the axes of which are located in the frontal plane. The positive or negative value of the algebraic sum on an arbitrarily chosen scale is plotted on the positive or negative part of the axis of the corresponding assignment in the six-axis Bailey coordinate system. These values ​​are projections of the desired electrical axis of the heart on axes I and III of the standard leads. From the ends of these projections restore perpendiculars to the axes of the leads. 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 the lead, the axis of which approximately coincides with the location of the electrical axis of the heart, parallel to it.

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

In the 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.

With 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.

With 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, with R R> R; deep S waves are recorded in leads I and aV

III. P wave analysis includes: 1) P wave amplitude measurement; 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 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; the duration of the interval of internal deviation in leads V and V; possible splitting of the tooth or the appearance of an additional one; c) assessment of the S wave: amplitude, comparing it with the R amplitude; possible broadening, serration 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 displacement of the RS-T segment, then the isoline up or down at a point 0.05-0.08 s to the right from point j; determine the shape of the possible displacement of the RS-T segment: horizontal, oblique descending, oblique ascending.

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

4) Analysis of the Q-T interval: measurement of duration.

V. Electrocardiographic conclusion:

1) the source of the heart rhythm;

2) regularity of the heart rhythm;

4) the position of the electrical axis of the heart;

5) the presence of four electrocardiographic syndromes: a) cardiac arrhythmias; b) conduction disturbances; c) ventricular and atrial myocardial hypertrophy or their acute overload; d) myocardial damage (ischemia, dystrophy, necrosis, scarring).

Electrocardiogram for cardiac arrhythmias

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

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

2) Sinus bradycardia: a decrease in the number of heartbeats per minute (an increase in the duration of 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 respiratory phases; preservation of all electrocardiographic signs of sinus rhythm (alternation of the P wave and the QRS-T complex).

4) Sinoatrial node weakness syndrome: persistent sinus bradycardia; periodic appearance of ectopic (non-sinus) rhythms; the 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 QRST complex following it; 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 the usual normal complexes; the presence after an atrial extrasystole of an incomplete compensatory pause.

Atrial extrasystole (II standard lead): a) from the upper sections of the atria; b) from the middle sections 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 the rest of the QRST complexes of sinus origin; negative P' wave in leads II, III and aVF after 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 P wave before ventricular extrasystole; the presence in most cases after a ventricular extrasystole of a complete compensatory pause.

a) left ventricular; b) right ventricular extrasystole

3. Paroxysmal tachycardia.

1) Atrial paroxysmal tachycardia: suddenly starting and also suddenly ending attack of increased heart rate for a minute while maintaining the correct rhythm; the presence of a reduced, deformed, biphasic or negative P wave in front of each ventricular QRS' complex; normal unchanged ventricular QRS complexes; in some cases, there is a deterioration in atrioventricular conduction with the development of atrioventricular block I degree with periodic loss of individual QRS' complexes (non-permanent signs).

2) Paroxysmal tachycardia from the atrioventricular junction: suddenly starting and also suddenly ending attack of increased heart rate for 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: suddenly starting and also suddenly ending attack of increased heart rate for a minute while maintaining the correct rhythm in most cases; deformation and expansion of the QRS complex for more than 0.12 s with a discordant arrangement of the RS-T segment and the T wave; the presence of atrioventricular dissociation, i.e. complete separation of the frequent rhythm of the ventricles and the normal rhythm of the atria with occasionally recorded single normal unchanged QRST complexes of sinus origin.

4. Atrial flutter: the presence on the ECG of frequent - dov minute - regular, similar to each other atrial waves F, having a characteristic sawtooth shape (leads II, III, aVF, V, V); in most cases, the correct, regular ventricular rhythm with the same intervals F-F; 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 (fibrillation): the absence of P wave in all leads; the presence of irregular waves throughout the entire 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 (dove minutes), regular and identical in shape and amplitude flutter waves, resembling a sinusoidal curve.

7. Blinking (fibrillation) of the ventricles: frequent (from 200 to 500 per minute), but irregular waves that differ from each other in different shapes and amplitudes.

Electrocardiogram for violations of the conduction function.

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

2. Intra-atrial blockade: an increase in the duration of the P wave more than 0.11 s; splitting of the R wave.

3. Atrioventricular blockade.

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

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

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

c) distal (three-beam) form: severe QRS deformation.

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

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

b) Mobitz type II: QRST prolapse 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 consecutive ventricular complexes (blockade 3:1, 4:1, etc.) drop out.

3) III degree: complete separation of the atrial and ventricular rhythms and a decrease in the number of ventricular contractions for a minute or less.

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

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

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

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

2) Blockade of the left anterior branch of the bundle of His: 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, type II rS; the total duration of the QRS complex is 0.08-0.11 s.

3) Blockade of the left posterior branch of the bundle of His: a 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 of the rS type, and in leads III, aVF - of the qR type; the duration of the QRS complex is within 0.08-0.11 s.

4) Blockade of the left leg of the bundle of His: in leads V, V, I, aVL widened deformed ventricular complexes of type R with a split or wide apex; in leads V, V, III, aVF widened deformed ventricular complexes, having the form of QS or rS with a split or wide top of the S wave; an increase in the total duration of the QRS complex more than 0.12 s; the presence in leads V, V, I, aVL of a discordant with respect to QRS displacement 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 the three branches of the His bundle: atrioventricular blockade of I, II or III degree; blockade of two branches of the bundle of His.

Electrocardiogram in atrial and ventricular hypertrophy.

1. Hypertrophy of the left atrium: bifurcation and increase in the amplitude of the teeth P (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-permanent sign); an 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, 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 may be negative (a non-permanent sign); the duration of the P waves does not exceed 0.10 s.

3. Hypertrophy of the left ventricle: an increase in the amplitude of the R and S waves. At the same time, 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 two-phase (–+) T wave in leads I, aVL and V; an increase in the duration of the internal QRS deviation interval in the left chest leads by more than 0.05 s.

4. Hypertrophy of the right ventricle: 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; appearance in lead V of a QRS complex of the rSR' or QR type; signs of rotation of the heart around the longitudinal axis clockwise; shift of the RS-T segment down and the appearance of negative T waves in leads III, aVF, V; increase in the duration of the interval of internal deviation in V more than 0.03 s.

Electrocardiogram in ischemic heart disease.

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

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

On this topic...

When the excitation impulse leaves the sinus node, it begins to be recorded by the cardiograph. Normally, excitation of the right atrium (curve 1) begins somewhat earlier than the left (curve 2) atrium. The left atrium later starts and ends later excitation. The cardiograph registers the total vector of both atria, drawing P wave: The rise and fall of the P wave is usually gentle, the apex is rounded.

• A positive P wave is an indication of sinus rhythm.
• The P wave is best seen in standard lead 2, in which it must be positive.
• Normally, the duration of the P wave is up to 0.1 seconds (1 large cell).
• The amplitude of the P wave should not exceed 2.5 cells.
• The amplitude of the P wave in the standard leads and in the leads from the extremities is determined by the direction of the electrical axis of the atria (they will be discussed later).
• Normal amplitude: P II>P I>P III.

The P wave may be serrated at the apex, with the distance between the teeth not exceeding 0.02 s (1 cell). The activation time of the right atrium is measured from the beginning of the P wave to its first peak (no more than 0.04 s - 2 cells). The activation time of the left atrium is from the beginning of the P wave to its second peak or to the highest point (no more than 0.06 s - 3 cells).

The most common variants of the P wave are shown in the figure below:

The table below describes how the P wave should look in different leads.