14.09.2020

Negative P in lead I. On the ecg, a bifurcation of the r wave What does the p wave of the electrocardiogram mean

The left atrium later starts and later ends excitation. The cardiograph registers the total vector of both atria by drawing a 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 limb leads is determined by the direction of the atrial electrical axis (which 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.

Amplitude must be less than T wave amplitude

How to decipher an electrocardiogram?

In our time, diseases of the cardiovascular system occupy one of the leading positions among other pathologies. One of the methods for determining diseases is an electrocardiogram (ECG).

What is a cardiogram?

The cardiogram graphically shows the electrical processes occurring in the heart muscle, or rather, the excitation (depolarization) and restoration (repolarization) of muscle tissue cells.

I recently read an article that talks about Monastic tea for the treatment of heart disease. With the help of this tea, you can FOREVER cure arrhythmia, heart failure, atherosclerosis, coronary heart disease, myocardial infarction and many other diseases of the heart and blood vessels at home.

I was not used to trusting any information, but I decided to check and ordered a bag. I noticed the changes within a week: the constant pain and tingling in my heart that had tormented me before receded, and after 2 weeks they disappeared completely. Try it and you, and if anyone is interested, then below is a link to the article.

The impulse conduction occurs along the conduction system of the heart - a complex neuromuscular structure consisting of sinoatrial, atrioventricular nodes, legs and bundles of His, passing into Purkinje fibers (their location is shown in the figure). The cardiac cycle begins with the transmission of an impulse from the sinoatrial node, or pacemaker. It sends a signal 60-80 times per minute, which is equal to the normal heart rate in a healthy person, then to the atrioventricular node.

In pathologies of the sinoatrial node, the AV node takes on the main role, the pulse frequency of which is approximately 40 per minute, which causes bradycardia. Further, the signal passes into the bundle of His, consisting of the trunk, right and left legs, which, in turn, pass into the Purkinje fibers.

The conduction system of the heart provides automatism and the correct sequence of contraction of all parts of the heart. Pathologies of the conduction system are called blockades.

With the help of an ECG, many indicators and pathologies can be detected, such as:

Heart rate, their rhythm.
Damage to the heart muscle (acute or chronic).
Blockade in the conduction system of the heart.
General condition of the heart.
Violation of the metabolism of various elements (calcium, magnesium, potassium).

Detection of pathologies not related to the heart (for example, an embolism of one of the pulmonary arteries). What does this analysis consist of? There are several elements in the ECG: waves, segments and intervals. They show how an electrical impulse travels through the heart.

Also attached to the cardiogram is the determination of the direction of the electrical axis of the heart and knowledge of the leads. Teeth are convex or convex sections of the cardiogram, indicated by capital Latin letters.

Segment - part of the isoline, located between two teeth. Isoline - a straight line on the cardiogram. An interval is a tooth together with a segment.

As you can see from the figure below, an ECG consists of the following elements:

Prong P - reflects the spread of the impulse in the right and left atrium.
Interval PQ - the time of passage of the impulse to the ventricles.
QRS complex - excitation of the myocardium of the ventricles.
The ST segment is the time of complete depolarization of both ventricles.
T wave - ventricular repolarization.
The QT interval is ventricular systole.
TR segment - reflects the diastole of the heart.

Leads are an integral part of the analysis. Leads are the potential difference between the points that are needed for a more accurate diagnosis. There are several types of leads:

Standard leads (I, II, III). I - potential difference between the left and right hand, II - right hand and left foot, III - left hand and left foot.

Reinforced leads. A positive electrode is placed on one of the limbs, when the remaining two are negative (there is always a black electrode on the right leg - grounding).

There are three types of augmented leads - AVR, AVL, AVF - from the right hand, left hand and left leg, respectively.

For the treatment of cardiovascular diseases, Elena Malysheva recommends a new method based on Monastic tea.

It contains 8 useful medicinal plants that are extremely effective in the treatment and prevention of arrhythmia, heart failure, atherosclerosis, coronary artery disease, myocardial infarction, and many other diseases. In this case, only natural ingredients are used, no chemicals and hormones!

What do the teeth on the result mean?

The teeth are an important part of the cardiogram, according to which the doctor looks at the correctness and sequence of the individual elements of the heart.

Prong R. Denotes the excitation of both atria. Normally, it is positive (above the isoline) I, II, aVF, V2 - V6, its length is 0.07 - 0.11 mm, and the amplitude is 1.5-2.5 mm. A positive P wave is an indicator of sinus rhythm.

If the right atrium is enlarged, the P wave becomes high and pointed (characteristic of a "cor pulmonale"), with an increase in the left atrium, a pathological M-shaped is seen (split of the tooth with the formation of two peaks - often with pathologies of the bicuspid valve).

P.Q. Interval - the time it takes the signal to travel from the atria to the ventricles. It occurs due to a delay in the conduction of an impulse in the AV node. Normally, its length is from 0.12 to 0.21 seconds. This interval shows the state of the sinoatrial node, the atria and the atrioventricular node of the conduction system of the heart.

Its lengthening indicates an atrioventricular heart block, while its lengthening indicates Wolff-Parkinson-White and (or) Laun-Ganone-Levin syndrome.

QRS complex. Shows the conduction of the impulse through the ventricles. Can be broken down into the following steps:

Having studied the methods of Elena Malysheva in the treatment of HEART DISEASE, as well as the restoration and cleaning of VESSELS, we decided to bring it to your attention.

An integral part of ECG decoding is the determination of the electrical axis of the heart.

This concept denotes the total vector of its electrical activity, practically it coincides with the anatomical axis with a slight deviation.

Electrical axis of the heart

There are 3 axis deviations:

normal axis. Angle alpha from 30 to 69 degrees.
The axis is deflected to the left. Angle alpha 0–29 degrees.
The axis is deflected to the right. The alpha angle is 70–90 degrees.

There are two ways to define an axis. The first is to look at the amplitude of the R wave in the three standard leads. If the largest interval is in the second - the axis is normal, if in the first - to the left, if in the third - to the right.

This method is fast, but it is not always possible to accurately determine the direction of the axis. For this, there is a second option - a graphical definition of the alpha angle, which is more complex, and it is used in controversial and complex cases to determine the axis of the heart with an error of up to 10 degrees. Died tables are used for this.

ST segment. The moment of complete excitation of the ventricles. Normally, its duration is 0.09–0.19 s. A positive segment (more than 1 mm above the isoline) indicates myocardial infarction, and a negative segment (more than 0.5 mm below the isoline) indicates ischemia. The saddle segment is indicative of pericarditis.
Prong T. Means the process of restoring the muscle tissue of the ventricles. It is positive in leads I, II, V4-V6, its duration is normal - 0.16–0.24 s, amplitude is half the length of the R wave.
The U wave. It is located after the T wave in very rare cases, the origin of this wave is still not exactly defined. Presumably, it reflects a short-term increase in the excitability of the cardiac tissue of the ventricles after electrical systole.

What are false interferences on the cardiogram that are not associated with heart pathologies?

Three types of interference can be seen on an electrocardiogram:

Inductive currents - fluctuations with a frequency of 50 Hz (alternating current frequency).
"Floating" isoline - displacement of the isoline up and down due to loose application of electrodes to the patient's skin.
Muscle tremors - frequent irregular asymmetrical fluctuations are visible on the ECG.

In conclusion, we can say that the ECG is an informative and accessible method for detecting heart pathologies. It covers a large number of characteristics, which helps in making the correct diagnosis.

A deep study of all aspects of cardiogram decoding will help the doctor in the rapid and timely detection of diseases and the choice of the correct treatment tactics.

Do you often experience discomfort in the area of the heart (pain, tingling, squeezing)?
You may suddenly feel weak and tired...
Feeling high pressure all the time...
There is nothing to say about shortness of breath after the slightest physical exertion ...
And you have been taking a bunch of medications for a long time, dieting and watching your weight ...

Read better what Olga Markovich says about this. For several years she suffered from atherosclerosis, coronary artery disease, tachycardia and angina pectoris - pain and discomfort in the heart, heart rhythm disturbances, high blood pressure, shortness of breath even with the slightest physical exertion. Endless tests, trips to doctors, pills did not solve my problems. BUT thanks to a simple recipe, constant pain and tingling in the heart, high blood pressure, shortness of breath - all this is in the past. I feel great. Now my doctor is wondering how it is. Here is a link to the article.

Krasnoyarsk medical portal Krasgmu.net

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) The regularity of heart beats 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 spread 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 in 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 unaltered 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 to 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, having 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.

What state of the myocardium does the R wave reflect on the ECG results?

The state of the whole organism depends on the health of the cardiovascular system. When unpleasant symptoms occur, most people seek medical attention. 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 section is a 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 the possible signs of a 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 sagging 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!

General ECG decoding scheme

determining the position of the electrical axis of the heart in the frontal plane;
determination of rotations of the heart around the longitudinal axis;
determination of rotations of the heart around the transverse axis.

P waves in standard lead II are positive and precede the ventricular QRS complex;
the shape of the P waves in the same lead is the same.

if the ectopic impulse simultaneously reaches the atria and ventricles, there are no P waves on the ECG, merging with unchanged QRS complexes;
if the ectopic impulse reaches the ventricles and only then the atria, negative P waves in the II and III standard leads are recorded on the ECG, located after the usual unchanged QRS complexes.

the duration of the P wave, which characterizes the speed of conducting an electrical impulse through the atria (normally, no more than 0.1 s);
the duration of the P-Q (R) intervals in the II standard lead, reflecting the overall conduction velocity in the atria, the AV node and the His system (normally from 0.12 to 0.2 s);
the duration of the ventricular QRS complexes, reflecting the conduction of excitation through the ventricles (normally from 0.08 to 0.09 s).

The maximum positive or negative value of the algebraic sum of the QRS complex teeth is recorded in that electrocardiographic lead, the axis of which approximately coincides with the location of the electrical axis of the heart. The average resulting QRS vector is plotted on the positive or negative part of the axis of this lead.
The 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 with the axis perpendicular to the electrical axis of the heart.

measuring the amplitude of the P wave (normally no more than 2.5 mm);
measuring the duration of the P wave (normally no more than 0.1 s);
determination of the polarity of the P wave in leads I, II, III;
determination of the shape of the R wave.

assessment of the ratio of Q, R, S waves in 12 leads, which allows to determine the rotations of the heart around three axes;
measuring the amplitude and duration of the Q wave. The so-called pathological Q wave is characterized by an increase in its duration by more than 0.03 s and an amplitude of more than 1/4 of the R wave amplitude in the same lead;
assessment of the R waves with the measurement of their amplitude, the duration of the interval of internal deviation (in leads V1 and V6) and the determination of the splitting of the R wave or the appearance of a second additional R wave (r’) in the same lead;
assessment of S waves with measurement of their amplitude, as well as determining the possible expansion, serration or splitting of the S wave.

determine the polarity of the T wave;
evaluate the shape of the T wave;
measure the amplitude of the T wave.

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.

In routine practice and in the absence of special equipment for assessing exercise tolerance and objectifying the functional status of patients with moderate and severe heart and lung diseases, a 6-minute walk test can be used, corresponding to submaximal.

Electrocardiography is a method of graphic recording of changes in the potential difference of the heart that occur during the processes of myocardial excitation.

Video about rehabilitation sanatorium Upa, Druskininkai, Lithuania

Only a doctor can diagnose and prescribe treatment during an internal consultation.

Scientific and medical news about the treatment and prevention of diseases in adults and children.

Foreign clinics, hospitals and resorts - examination and rehabilitation abroad.

When using materials from the site, the active reference is obligatory.

Electrocardiogram (ECG of the heart). Part 2 of 3: ECG Transcription Plan

This is the second part of the cycle about the ECG (popularly - the ECG of the heart). To understand today's topic, you need to read:

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

The ratio of ECG intervals with the phases of the cardiac cycle (ventricular systole and diastole).

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

Elements of a normal ECG

Before moving on to deciphering the ECG, you need to figure out what elements it consists of.

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

TEETH is the bulges and concavities on the electrocardiogram.

The following teeth are distinguished on the ECG:

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

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

Teeth, segments and intervals on the ECG.

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

Waves of the QRS complex

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

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

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

Variants of the QRS complex.

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

ECG analysis

General ECG decoding scheme

Checking the correctness of ECG registration.
Heart rate and conduction analysis:
- assessment of the regularity of heart contractions,
- counting the heart rate (HR),
- determination of the source of excitation,
- conductivity rating.
Determination of the electrical axis of the heart.
Analysis of atrial P wave and P-Q interval.
Analysis of the ventricular QRST complex:
- analysis of the QRS complex,
- analysis of the RS-T segment,
- T wave analysis,
- analysis of the interval Q - T.
Electrocardiographic conclusion.

1) Checking the correctness of ECG registration

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

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

2) Heart rate and conduction analysis:

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

calculation of heart rate (HR)

Large squares are printed on the ECG film, each of which includes 25 small squares (5 vertical x 5 horizontal). For a quick calculation of heart rate with the correct rhythm, the number of large squares between two adjacent R-R teeth is counted.

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

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

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

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

With an irregular rhythm, the maximum and minimum heart rates are usually calculated according to the duration of the smallest and largest R-R interval, respectively.

determination of the source of excitation

In other words, they are looking for where the pacemaker is located, which causes contractions of the atria and ventricles. Sometimes this is one of the most difficult stages, because various disturbances of excitability and conduction can be very intricately combined, which can lead to misdiagnosis and incorrect treatment. To correctly determine the source of excitation on the ECG, you need to know the conduction system of the heart well.

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

The source of excitation is in the sinoatrial node. ECG signs:

in standard lead II, the P waves are always positive and are in front of each QRS complex,
P waves in the same lead have a constant identical shape.

P wave in sinus rhythm.

ATRIAL Rhythm. If the source of excitation is in the lower sections of the atria, then the excitation wave propagates to the atria from the bottom up (retrograde), therefore:

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

P wave in atrial rhythm.

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

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

Rhythm from the AV junction, P wave overlaying the QRS complex.

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

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

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

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

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

To correctly account for conductivity, the write speed is taken into account.

To assess conductivity, measure:

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

Measurement of the interval of internal deviation.

3) Determination of the electrical axis of the heart.

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

4) Analysis of atrial P wave.

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

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

Pathological deviations of the P wave:

Pointed high P waves of normal duration in leads II, III, aVF are characteristic of right atrial hypertrophy, for example, in cor pulmonale.
Split with 2 peaks, an extended P wave in leads I, aVL, V5, V6 is characteristic of left atrial hypertrophy, for example, with mitral valve defects.

P wave formation (P-pulmonale) in right atrial hypertrophy.

P-wave (P-mitrale) formation in left atrial hypertrophy.

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

AV blockade is 3 degrees:

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

5) Analysis of the ventricular QRST complex:

The maximum duration of the ventricular complex is 0.07–0.09 s (up to 0.10 s). The duration increases with any blockade of the legs of the bundle of His.

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

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

The S wave can be of very different amplitudes, but usually no more than 20 mm. The S wave decreases from V1 to V4, and may even be absent in V5-V6. In assignment V3 (or between V2 - V4) the "transitional zone" (equality of R and S teeth) is usually registered.

analysis of the RS-T segment

The ST segment (RS-T) is a segment from the end of the QRS complex to the beginning of the T wave. The ST segment is especially carefully analyzed in CAD, as it reflects a lack of oxygen (ischemia) in the myocardium.

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

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

T wave analysis.

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

analysis of the interval Q - T.

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

6) Electrocardiographic conclusion.

Rhythm source (sinus or not).
Rhythm regularity (correct or not). Usually sinus rhythm is correct, although respiratory arrhythmia is possible.
The position of the electrical axis of the heart.
The presence of 4 syndromes:
- rhythm disorder
- conduction disorder
- hypertrophy and/or congestion of the ventricles and atria
- myocardial damage (ischemia, dystrophy, necrosis, scars)

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

Sinus rhythm with heart rate 65. Normal position of the electrical axis of the heart. Pathology is not revealed.

Sinus tachycardia with a heart rate of 100. Single supragastric extrasystole.

The rhythm is sinus with a heart rate of 70 beats / min. Incomplete blockade of the right leg of the bundle of His. Moderate metabolic changes in the myocardium.

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

ECG interference

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

Three types of ECG interference (explained below).

Interference on the ECG in the lexicon of health workers is called a pickup:

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

b) "floating" (drift) of the isoline due to poor contact of the electrode with the skin;

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

Diagnosis of heart diseases is carried out by the method of registration and study of electrical impulses resulting from relaxation and contraction of the heart muscle over a certain time period - electrocardiography.

It captures impulses and converts them into a visual graph on paper (electrocardiogram) with a special device - an electrocardiograph.

Brief description of ECG elements

On the graphical image, the time is fixed horizontally, and the frequency and depth of changes are recorded vertically. Sharp corners displayed above (positive) and below (negative) of the horizontal line are called teeth. Each of them is an indicator of the state of one or another part of the heart.

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

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

The range between adjacent teeth is called a segment, there are three of them: ST, QRST, TP. The tooth and the segment together represent the interval - the time of passage of the pulse. For accurate diagnosis, the difference in the indicators of the electrodes (the electrical potential of the lead) fixed on the patient's body is analyzed. Leads are divided into the following groups:

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

The result of the study is deciphered by a qualified cardiologist

Having received a schematic picture of the work of the heart, the cardiologist analyzes the change in all indicators, as well as the time for which they are noted by the cardiogram. The main data for decoding are the regularity of muscle contractions of the heart, the number (number) of contractions of the heart, the width and shape of the teeth that reflect the excited state of the heart (Q, R, S), the characteristic of the P-wave, the parameters of the T wave and segments.

T wave values

Repolarization or recovery of muscle tissue after contractions, which reflects the T wave, on the graphic image has the following standards:

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

T wave changes

The transformation of the T wave on the electrocardiogram is due to changes in the work of the heart. Most often they are associated with a violation of the blood supply that has arisen due to damage to the vessels with atherosclerotic growths, otherwise, coronary heart disease.

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

An inverted (inverse) form indicates myocardial ischemia, a state of extreme nervous excitement, cerebral hemorrhage, an increase in the heart rate over (tachycardia). Aligned T is manifested in alcoholism, diabetes, low potassium concentration (hypokalemia), heart neurosis (neurocircular dystonia), abuse of antidepressants.

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

The wave displayed at the bottom (negative) is an indicator of the development of ischemia or the presence of severe excitement. If at the same time there is a change in the ST segment, the clinical form of ischemia - a heart attack should be suspected. Wave pattern changes without involvement of the adjacent ST segment are not specific. It is extremely difficult to determine a specific disease in this case.

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

Causes of a negative T-wave

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

pulmonary pathologies (difficulty breathing);
malfunctions in the hormonal system (hormone levels are higher or lower than normal);
violation of cerebral circulation;
overdose of antidepressants, heart drugs and drugs;
symptomatic complex of disorders of a part of the nervous system (VSD);
dysfunction of the heart muscle, not associated with coronary disease (cardiomyopathy);
inflammation of the heart sac (pericarditis);
inflammation in the inner lining of the heart (endocarditis);
mitral valve lesions;
expansion of the right parts of the heart as a result of hypertension (cor pulmonale).

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

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

What state of the myocardium does the R wave reflect on the ECG results?

Why is an electrocardiogram performed?

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

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

What does the ECG show

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

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

Definition of the axis of the heart

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.

ECG elements in normal and pathological conditions

The main characteristics of a normal ECG are presented in Table. 7. Prong R reflects the depolarization of the atria, and its initial part is the right, and the final part is the left atrium. As can be seen from the following

the frequency of changes in the instantaneous vectors of the electromotive force formed during depolarization of the atrial myocardium by an impulse from the sinus node (Fig. 32, L), the average wave vector R is ok directed to the left, down and forward. In the 6-axis coordinate system, Bailey in the frontal plane in most healthy individuals, his position varies between 30 and 60 °. Therefore, it is obvious that normally with a sinus pacemaker, the tooth R usually positive in all standard and unipolar limb leads except aVR, in which it is negative. Amplitude R< 2.5 mm duration< 0,1 с (см. рис. 23).

Pathological changes in the P wave include:

I. Absence of a tooth R. It is noted when the pacemaker of the atria and ventricles is not the sinus node, but other structures.

1. With the correct rhythm of the ventricles (the same intervals R-R) depending on its frequency R may be absent in AV junction rhythm or paroxysmal AV junction tachycardia (see below). In these cases, the atria are excited retrogradely by an impulse generated in specialized cells of the II order pacemaker, which simultaneously propagates to the ventricles via the His-Purkinje system. With an unchanged propagation velocity of the retrograde wave of excitation, depolarization of the working myocardium of the atria and ventricles occurs simultaneously, and the wave R, superimposed on a higher amplitude complex QRS, do not differentiate.

2. With an irregular ventricular rhythm, the absence of a tooth R observed with: a) extrasystole from the atrioventricular connection (see below); b) atrial fibrillation and flutter. However, instead of teeth R small frequent flicker waves "/" or higher and rarer flutter waves "/" are registered (see below).

I. Changes in the normal direction (polarity) of the teeth R. As well as their absence, they are noted with a non-sinus pacemaker.

1. Negative prong R in all leads that precede the complex QRS, characteristic of the rhythm of the atrioventricular junction, as well as paroxysmal nodal (atrioventricular) tachycardia and extrasystole in the presence of accelerated retrograde impulse conduction from the atrioventricular node through the atria. As a result, their depolarization occurs earlier than the ventricles, which have a large area. The formation of negative P waves is due to the orientation of the atrial excitation vector in directions directly opposite to the normal one. When retrograde conduction slows down, a negative wave R registered immediately after the complex QRS, on laying on a segment ST.

2. Changing the normal polarity of the tooth R, preceding complex QRSb a number of leads. characteristic of ectopic atrial rhythms. Its most common variant with the clearest electrocardiographic features is the so-called rhythm.

coronary sinus. This is a lower right atrial rhythm, in which the driver is located in the myocardial cells of the lower part of the right atrium near the coronary sinus. Formation of negative teeth Rv leads II, III and aVF with a mandatory positive wave R in lead aVR is due to a change in the normal orientation of the atrial depolarization vector, as a result of which most of the myocardium is excited in a retrograde way. Occasionally, you can find a left-atrial rhythm, the hallmark of which is a characteristic change in the tooth R in leads V, 2. The rounding of its initial part, reflecting the excitation of the left atrium, and the sharpening of the final part (excitation of the right atrium) give the Rvid tooth a "shield and sword". 3. "Instability" of polarity, as well as the shape of the tooth R with a change from one cardiac cycle to another in the same lead from normal, positive, to biphasic (+-) and negative, is typical for the migration of the pacemaker through the atria due to sinus node weakness syndrome. In this case, the value of the interval may also slightly fluctuate. R-Q.

III. Change in amplitude and (or) duration of a tooth R characteristic of atrial hypertrophy or overload.

1. High (> Zmm) teeth / most pronounced in leads II, III, aVF and V, (Fig. 33), with their unchanged duration, indicate an increase in the right atrium and are called "P-pulmonal e". At the same time, in lead Vj they can be biphasic with a more pronounced initial positive phase. In lead II, the teeth R pointed, shaped like an isosceles triangle.

2. Low, broadened (> 0.1 s) and two-humped teeth R in leads I, aVL and V 4 _ 6, biphasic in lead V, with a wide and deep final negative phase (see Fig. 33) indicate an increase in the left atrium and are called "P-mi t ha 1 e". These changes, however, are nonspecific and are also observed in atrial conduction disturbances.

Interval P-Q, or P-R, measured from the beginning of the tooth R before the start of the complex QRS(see fig. 23). Although during this interval the impulse from the minus node propagates throughout the specialized conducting system of the heart, reaching the working myocardium of the ventricles, a large part of the time is spent on conduction through the atrioventricular node in June N. As a result, it is considered that the value of the interval R

Q reflects the magnitude of the impulse conduction delay in the atrioventricular node, that is, atrioventricular conduction. Fine is fl 0.12 to 0.2 siv to a certain extent depends on the heart rate.

Rice. 34. Complex QRS fine (A) and with various pathologies; B- Wolff-Parkinson-White syndrome. 1->2 - delta wave due to changes in the initial part of the ventricular depolarization process; IN- blockade of the right leg of the bundle of His. 1->2 - violation of the final part of depolarization; G - blockade of the left leg of the bundle of His. 1->2 - violation of the middle and 2->3 - the final part of the depolarization; D- left ventricular hypertrophy. ]->2 - slight uniform depolarization slowdown; E - hyperkalemia ia. 1->2 - significant uniform depolarization deceleration; AND - large focal myocardial infarction. 1->2 - pathological tooth Q

Pathological changes in the interval P - Q include:

1) lengthening more than 0.2 s. It is characteristic of atrioventricular conduction disorders - atrioventricular blockades (see below).

2) shortening less than 0.12 s. It indicates the conduction of an atrial impulse to the ventricles bypassing the atrioventricular node through an additional atrioventricular pathway - the bundle of Kent, James or Maheim, which is characteristic of the syndrome of premature ventricular excitation.

Complex QRS reflects the sequence and duration of depolarization of the working ventricular myocardium. The predominant direction (polarity) of its teeth in standard and unipolar limb leads normally depends on the position of the electrical axis of the heart (see below). In most cases, it is positive in leads I and II and negative in lead aVR. In the chest leads, the normal graphics of the complex QRS(see Fig. 29) is more stable. The normal values of the amplitude and duration of the teeth are presented in Table. 7.

Pathological changes in the QRS complex are caused by diffuse or local impairment of the process of ventricular depolarization and include (Fig. 34):

I. Changes in the sequence and shape of the teeth. They are associated with a violation of the sequence of propagation of the excitation wave and are often accompanied by a change in the amplitude and an increase in the duration of the teeth. Celebrated at:

a) syndrome of premature excitation of the ventricles, for which

are characterized by changes mainly in the initial part of the process

depolarization with the appearance of a delta wave;

b) violations of the conduction along the legs of the bundle of His, that is, inside

ventricular blockade. At the same time, changes are observed mainly in the middle and final parts of the depolarization period;

c) excitation of the ventricles by an impulse that arose in the myocardium of one

from the ventricles with extrasystole and ventricular tachycardia;

d) ventricular hypertrophy or overload;

e) local macrofocal changes in the myocardium due to

horny or transferred heart attack.

II. Changes in the amplitude of the teeth of the complex QRS.

1. Increasing the amplitude of the tooth Q more than 25% of tooth height R, which

often accompanied by an increase in its duration, it is noted with:

a) macrofocal changes in the myocardium in acute or "old"

myocardial infarction. At the same time, always Q equal to or greater than 0.04 s;

b) hypertrophy or overload of the left and right ventricles;

c) blockade of the left leg of the bundle of His.

2. Increasing the amplitude of the teeth R and/or S , which is often accompanied

driven by an increase in their duration and expansion of the complex

sa QRS, noted at:

a) ventricular hypertrophy or overload;

b) blockade of the legs of the bundle of His.

3. Reducing the amplitude of the teeth of the complex QRS non-specific and may

be observed, in particular, with the so-called diffuse changes in mi

okard due to its defeat in a variety of diseases, as well as

exudative and constrictive pericarditis. Amplitude reduction

prong R in separate leads, in combination with other electrocardiograms

graphic changes, may occur with myocardial infarction.

III. Increasing the duration of the complex QRS:

1) tooth increase Q noted with macrofocal changes in the myocardium,

2) a significant (> 0.12 s) increase in the duration of the complex QRS in general, along with other changes in the ECG, it is noted with: complete blockade of the legs of the bundle of His; ventricular extrasystole and tachycardia; hyperkalemia.

Segment ST (see tab. 7), which reflects the preservation of the state of depolarization by the ventricles, is normally on the isoline or is displaced up to 1 mm.

Norm options are also:

a) segment lifting ST in the chest leads, especially the right ones, by more than 1 mm, which is accompanied by a rise in the transition point of the complex QRS into the segment ST(points J). This is typical for the so-called syndrome of early repolarization of the ventricles, which occurs more often at a young age (Fig. 35, L);

b) obliquely ascending segment depression ST from the J point, displaced up to 2-3 mm below the isoline in the chest leads with tachycardia. Represents a normal response to physical activity (Fig. 35.4).

Pathological changes in the ST segment(see fig. 35):

I. Segment lifting ST. It is noted with subepicardial (trans-

mural) damage and myocardial ischemia in cases of:

1) various forms of coronary artery disease - angina, especially Prinzmetal, acute myocardial infarction, acute and chronic aneurysm of the heart;

2) acute pericarditis.

II. Segment depression ST horizontal or oblique

cabbage soup form. Noted for:

1) subendocardial injury and myocardial ischemia in various forms of coronary artery disease, especially angina pectoris and acute myocardial infarction, as well as some other heart diseases;

2) overload of the myocardium of the ventricles (for example, in a hypertensive crisis);

3) the influence of toxic substances, for example, cardiac glycosides, and myocardial dystrophy.

Segment Offset ST from the isoline also occurs when the synchrony of the depolarization of the ventricles is disturbed due to their hypertrophy, as well as in the blockade of the legs of the His bundle and ectopic ventricular complexes (extrasystole, paroxysmal and non-paroxysmal tachycardia). At the same time, the direction of displacement of the VT segment is discordant to the direction of the main deviation (tooth) of the complex QRS. For example, if it is represented by a high prong R, then, segment ST is displaced under the isoline and has a slanting downward shape.

The G wave reflects the process of repolarization of the ventricular myocardium, which spreads from the epicardium to the endocardium. The direction of its instantaneous and average vectors is generally similar to the depolarization vectors (see Fig. 27, 32), as a result of which fine tooth polarity T in most cases it is similar (concordant) to the main deviation (prong) of the complex QRS(see Table 7).

Pathological changes in the T wave include (see fig. 35):

I. negative prongs T. are nonspecific and occur in

a wide variety of pathological processes in the myocardium, in particular

1) subepicardial, or transmural, ischemia in various forms of IVS and HeKOToj. other diseases;

2) myocardial dystrophy of coronarogenic and non-coronary genesis, in particular, with ventricular overload, intoxication, electrolyte imbalance (hypokalemia), etc.; myocardiosclerosis can also serve as its substrate.

II. High pointed teeth D. Also non-specific

and are observed, in particular, with: 1) subendocardial ischemia; 2) hy-

Both options for tooth changes T may be secondary and occur when: 1) violation of the normal sequence of repolarization of the ventricular myocardium due to their hypertrophy (the direction of repolarization of the hypertrophied ventricle changes to the opposite); 2) blockade of the legs of the bundle of His; 3) ectopic ventricular arrhythmias. In this case, the polarity of the tooth T concordant to the direction of segment displacement ST, the continuation of which is the G wave (see Fig. 35, #, CO-Interval duration Q-T- the so-called electrical systole of the ventricles - approximately corresponds to their refractory period. This interval is measured from the beginning of the complex QRS until the end of the G wave (see Fig. 23). Since its value depends on the heart rate, it is advisable to determine the corrected interval Q - T (Q - Tk) according to the Bazett formula, in which the correction for heart rate is made:

Interval Q -TK is considered to be elongated if it is equal to or greater than 0.4 s for men and 0.45 s for women.

Value changes Q-Tw Q-Tk are nonspecific and are caused by a number of physiological and pathophysiological factors and pharmacological effects. Their measurement is of particular importance in assessing the genesis of ventricular ectopic arrhythmias and correcting antiarrhythmic therapy.

Prong changes U are nonspecific and practically have no diagnostic value.

The electrical axis of the heart is the average direction of the vector of the electromotive force of the ventricles during the entire period of depolarization, which is the vector sum of instantaneous vectors (Fig. 36, L). Its direction in the frontal plane is characterized by the angle a, which it forms with the I axis of the standard lead (Fig. 36, B).

In healthy adults, the value of the angle a varies widely - from -30 to +110°, however, in the range from +90 to +110° it can also be pathological. Depending on the angle a, the following options for the position of the electrical axis of the heart are distinguished as norm options(rice. 36, B): 1) intermediate - from +40 to +70°; 2) horizontal - from 0 to +40°; 3) moderate deviation to the left - from 0 to -30°; 4) vertical - from +70 to +90°, 5) moderate deviation to the right - from +90 to + 120°.

The vertical position is usually noted in young people and asthenics, horizontal - in the elderly and hypersthenics. The position of the electrical axis of the heart to some extent depends on the presence of hypertrophy of one or another ventricle. So, with hypertrophy of the left ventricle, the angle a is usually (but not necessarily) within 0., And the right - from +90 to +120 °.

A sharp deviation to the left (more than -30°) and to the right (more than +120°) is pathological change position of the electrical axis of the heart.

Angle a is estimated according to the nature of the graphics of the complex QRS in various leads using the 6-axis Bailey coordinate system. When the electrical axis of the heart is oriented in a direction perpendicular or almost perpendicular to the axis of the lead, its projection on it approaches 0 and the value of the potential recorded in this lead, that is, the teeth of the complex QRS or their algebraic sum, is minimal. An example is lead III in Fig. 27, B. If the electrical axis is oriented almost parallel to the axis of the lead, then the potential recorded in it will have the maximum amplitude, as, for example, lead I in Fig. 27, B. Thus, in this example, the electrical axis of the heart is oriented perpendicular to the axis of lead HI and approximately parallel to the axis of lead I, that is, between 0° and +30°.

An exact calculation of the angle a is made using special tables, based on the values of the algebraic sum of the amplitude of the teeth of the complex QRS separately in leads I and III.

A similar approach is also applicable to determining the mean ventricular repolarization vector (wave 7), which is normally oriented approximately in the same way as the vector QRS.

Form of the complex QRS and the G wave in various leads, depending on the position of the electrical axis of the heart, is shown in fig. 27, A, B, C and demonstrates the diversity of their normal schedules.

ECG interpretation: P wave

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 later ends excitation. The cardiograph registers the total vector of both atria by drawing a 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 limb leads is determined by the direction of the atrial electrical axis (which will be discussed later).
Normal amplitude: P II>P I>P III.

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.

Amplitude must be less than T wave amplitude

What is junctional rhythm, negative P wave

The junctional rhythm (rhythm of the atrioventricular junction) occurs when the automatism of the sinoatrial node is suppressed and the impulse propagates retrogradely from the atrioventricular junction. As a result, a negative P wave is recorded on the ECG. It precedes the QRS complex, appears simultaneously with it or after it.

When is junctional rhythm observed?

Such a rhythm is more often recorded with organic pathology of the heart (myocarditis, coronary heart disease, myocardiopathy), as well as with intoxication with certain medications (glycosides, reserpine, quinidine, etc.). However, sometimes the nodal rhythm can be periodically observed in healthy individuals with severe vagotonia.

Nodal rhythm in patients with heart disease can exacerbate the severity of their condition. Healthy people usually do not notice it.

Diagnosis of nodal heart rhythm

The rhythm of the atrioventricular junction is diagnosed only according to ECG data, in the presence of three or more nodal impulses in a row. The pulse rate at this rhythm is within 1 min.

"What is junctional rhythm of the heart, negative P wave" and other articles from the Arrhythmia section

negative p wave on ecg

Questions and answers on: negative p wave on ecg

The following arrhythmias have been registered:

Moderately frequent polytopic PVCs total - 6959, from 0 to 964 per hour, maximum from 09:18 to 10:18;

Paired ZHES total-6;

With an increase in heart rate for more than a minute, a moderate depression of the ST segment is recorded in lead 1. During sleep, a negative T wave is periodically recorded in lead 3.

There were no diagnostically significant changes in the ST segment.

QT interval prolongation was not registered.

Circadian index 1.36 - normal circadian heart rate profile

Average daily hell 132/79

Average daily hell 134/84

Midnight hell 117/64

Hypertensive load was steadily increased in SBP during the day and in DBP at night.

Maximum daily SBP 173 mm Hg, DBP 128 mm Hg

Maximum nighttime hell 138/73 at 22.20 before sleep

The degree of nighttime decrease in blood pressure is sufficient in terms of SBP and DBP, the average nighttime blood pressure does not exceed the average daily blood pressure.

ECHO: ultrasound signs of NMC of the 1st degree, NTC of the 1st stage, prolapse of the MC of the 1st stage. The dimensions of the heart cavities are within the normal range. ; QRS=0.08; PQ=0.13; e-axis-n; illegible-v2v3. Before pregnancy, when undergoing fluorography, they said that I had a hypoevolutionary heart (small).

Will I be able to bear the child safely? Only half of the term has passed, and extrasystoles are very poorly tolerated, I'm nervous, I have no appetite. I will only go to the doctor in July, maybe I can drink something sedative that can reduce the rhythm or reduce the number of ES? Thank you in advance.

There was a lot of stress, my heart hurt a lot, I lay down, didn’t get up, took cardioment, advocard, validol. did not help. I got together and did an ECG in a paid clinic, so as not to stand in lines, for complacency. Result: Sinus rhythm, correct.

Q wave 0.08 s, more than 1/2 R wave in leads III and aVF

RV1-V3; RV5(max)=18mm;

QRS - 0.14; RR - 0.50; QT - 0.36; PQ - 0.20.

RS-T segment in III, aVF shifted upwards from the isoelectric line

In leads II, III, aVF, V5-V6 ST segment elution (+0.2; +0.1; +0.2; +0.1; +0.2)

RS-T depression and negative (coronary) T wave in leads III, aVF and II

Discontinuous changes along the anterior wall - high T in V1-V2, ST depression in V1-V3.

They told me to go to the hospital immediately. How serious is this and do you really need to see a doctor. The state of health is unimportant, severe shortness of breath, I don’t want to go somewhere again. Thank you.

sum of amplitudes R(V6)+S(V1)=3.98mV>3.5mV

in lead V5, the amplitude of the R wave (3.07 mV) exceeds 2.6 mV

negative P teeth V6

diffuse changes in the myocardium

negative T-teeth I AVL V4 V5 V6

Diagnosis: coronary artery disease, GB 3 ST, atrial fibrillation permanent form

Takes in the morning - Lorista H 100mg, Corvasan 12.5mg

in the morning and in the evening, trifas every other day, lorista 100 mg in the evening, cordarone 200 mg Should I replace corvasan with metoprolol

Look at the load ecg:

I must say right away that the heart rate is emotional at rest, perhaps I was worried during the examination, because in a normal situation the pulse is not more than 55. I measure it regularly.

PQ=0.136s P=0.103s QRS=0.085s QT=0.326s

in hole II AVF P+ >= 2.3 mm

The T wave is smoothed out. II, negative. III, weak-neg. AVF

Vertical position of the EOS

Increased electrical activity of the right atrium

Violation of the processes of repolarization of the myocardium of the posterior wall of the left ventricle,

There is a deterioration in the processes of repolarization of the myocardium of the posterior wall of the left ventricle:

the T wave became negative in lead II, deeper in lead III, AVF.

No diagnostically significant shift of the ST segment was registered.

Recovery of the pulse at the 7th minute of rest. The duration of the recovery

period is normal.

Conclusion: the test is negative. Load tolerance is low.

Features: nonspecific changes in the myocardium of the posterior wall of the left ventricle.

Sinus rhythm. Heart rate-78 beats per minute.

EOS deviation to the right 95 degrees.

The ECG voltage is reduced.

Myocardial changes in the anterior septal, anteroapical, apical anterolateral region of the left ventricle (differentiate metabolic disorders from coronary circulation disorders)

T wave negative in leads I V2 V3 V4 V5

Recently, due to nervous experiences, very often it began to hurt in the heart area, some kind of pressing pain and tingling. On the ECG - heart rate - 66 beats / min. Electrical axis of the heart 81 degrees, vertical position. Sinus rhythm. Short PQ interval (PQ interval = 105ms). Incomplete blockade of the right bundle branch block (in lead V1 or V2, the QRS shape corresponds to the RSR type. QRS duration \u003d 98ms. Negative T-teeth: V2 (up to -0.18mV) How serious is this? And is any treatment required.

Negative p wave on ecg

Edited by Academician E. I. Chazov

I. Determination of heart rate. To determine the heart rate, the number of cardiac cycles (RR intervals) in 3 seconds is multiplied by 20.

A. Heart rate< 100 мин –1: отдельные виды аритмий - см. также рис. 5.1.

1. Normal sinus rhythm. The correct rhythm with a heart rate of 60-100 min -1. The P wave is positive in leads I, II, aVF, negative in aVR. Each P wave is followed by a QRS complex (in the absence of AV block). PQ interval 0.12 s (in the absence of additional pathways).

2. Sinus bradycardia. Correct rhythm. heart rate< 60 мин –1 . Синусовые зубцы P. Интервал PQ 0,12 с. Причины: повышение парасимпатического тонуса (часто - у здоровых лиц, особенно во время сна; у спортсменов; вызванное рефлексом Бецольда-Яриша; при нижнем инфаркте миокарда или ТЭЛА); инфаркт миокарда (особенно нижний); прием лекарственных средств (бета-адреноблокаторов, верапамила, дилтиазема, сердечных гликозидов, антиаритмических средств классов Ia, Ib, Ic, амиодарона, клонидина, метилдофы, резерпина, гуанетидина, циметидина, лития); гипотиреоз, гипотермия, механическая желтуха, гиперкалиемия, повышение ВЧД, синдром слабости синусового узла. На фоне брадикардии нередко наблюдается синусовая аритмия (разброс интервалов PP превышает 0,16 с). Лечение - см. гл. 6, п. III.Б.

3. Ectopic atrial rhythm. Correct rhythm. Heart rate 50-100 min -1. The P wave is usually negative in leads II, III, aVF. The PQ interval is typically 0.12 s. It is observed in healthy individuals and with organic lesions of the heart. Usually occurs when sinus rhythm slows down (due to increased parasympathetic tone, medication, or sinus node dysfunction).

4. Migration of the pacemaker. Right or wrong rhythm. heart rate< 100 мин –1 . Синусовые и несинусовые зубцы P. Интервал PQ варьирует, может быть < 0,12 с. Наблюдается у здоровых лиц, спортсменов при органических поражениях сердца. Происходит перемещение водителя ритма из синусового узла в предсердия или АВ -узел. Лечения не требует.

5. AV-nodal rhythm. Slow regular rhythm with narrow QRS complexes (< 0,12 с). ЧСС 35-60 мин –1 . Ретроградные зубцы P (могут располагаться как до, так и после комплекса QRS, а также наслаиваться на него; могут быть отрицательными в отведениях II, III, aVF). Интервал PQ < 0,12 с. Обычно возникает при замедлении синусового ритма (вследствие повышения парасимпатического тонуса, приема лекарственных средств или дисфункции синусового узла) или при АВ -блокаде. Ускоренный АВ -узловой ритм (ЧСС 70-130 мин –1) наблюдается при гликозидной интоксикации, инфаркте миокарда (обычно нижнем), ревматической атаке, миокардите и после операций на сердце.

6. Accelerated idioventricular rhythm. Regular or irregular rhythm with wide QRS complexes (> 0.12 s). Heart rate 60-110 min -1. P waves: absent, retrograde (occur after the QRS complex), or not associated with QRS complexes (AV dissociation). Causes: myocardial ischemia, condition after restoration of coronary perfusion, glycoside intoxication, sometimes in healthy people. In slow idioventricular rhythm, the QRS complexes look the same, but the heart rate is 30–40 min–1. Treatment - see Ch. 6, p. V.D.

B. Heart rate> 100 min -1: certain types of arrhythmias - see also fig. 5.2.

1. Sinus tachycardia. Correct rhythm. Sinus P waves of the usual configuration (their amplitude is increased). Heart rate 100-180 min -1, in young people - up to 200 min -1. Gradual start and end. Reasons: physiological reaction to stress, including emotional, pain, fever, hypovolemia, arterial hypotension, anemia, thyrotoxicosis, myocardial ischemia, myocardial infarction, heart failure, myocarditis, pulmonary embolism, pheochromocytoma, arteriovenous fistulas, the effect of drugs and other drugs (caffeine , alcohol, nicotine, catecholamines, hydralazine, thyroid hormones, atropine, aminophylline). Tachycardia is not relieved by massage of the carotid sinus. Treatment - see Ch. 6, p. III.A.

2. Atrial fibrillation. The rhythm is "wrong wrong". Absence of P-waves, random large- or small-wave oscillations of the isoline. The frequency of atrial waves is 350-600 min -1. In the absence of treatment, the frequency of ventricular contractions is 100-180 min -1. Causes: mitral valve disease, myocardial infarction, thyrotoxicosis, PE, condition after surgery, hypoxia, COPD, atrial septal defect, WPW syndrome, sick sinus syndrome, drinking large doses of alcohol, can also be observed in healthy individuals. If, in the absence of treatment, the frequency of ventricular contractions is small, then one can think of impaired conduction. With glycoside intoxication (accelerated AV nodal rhythm and complete AV block) or against the background of a very high heart rate (for example, with WPW syndrome), the rhythm of ventricular contractions may be correct. Treatment - see Ch. 6, item IV.B.

3. Atrial flutter. Regular or irregular rhythm with sawtooth atrial waves (f) most pronounced in leads II, III, aVF or V 1 . Rhythm is often regular with AV conduction 2:1 to 4:1, but may be irregular if AV conduction changes. The frequency of atrial waves is 250-350 min -1 with type I flutter and 350-450 min -1 with type II flutter. Reasons: see Ch. 6, item IV. With 1:1 AV conduction, the ventricular rate can reach 300 min–1, while due to aberrant conduction, expansion of the QRS complex is possible. At the same time, the ECG resembles that of ventricular tachycardia; this is especially often observed when using class Ia antiarrhythmic drugs without the simultaneous administration of AV blockers, as well as in WPW syndrome. Atrial fibrillation-flutter with chaotic atrial waves of various shapes is possible with one atrial flutter and another. Treatment - see Ch. 6, p. III.G.

4. Paroxysmal AV-nodal reciprocal tachycardia. Supraventricular tachycardia with narrow QRS complexes. Heart rate 150-220 min -1 , usually 180-200 min -1 . The P wave usually overlaps or follows the QRS complex (RP< 0,09 с). Начинается и прекращается внезапно. Причины: обычно иных поражений сердца нет. Контур обратного входа волны возбуждения - в АВ -узле. Возбуждение проводится антероградно по медленному (альфа) и ретроградно - по быстрому (бета) внутриузловому пути. Пароксизм обычно запускается предсердными экстрасистолами. Составляет 60-70% всех наджелудочковых тахикардий. Массаж каротидного синуса замедляет ЧСС и часто прекращает пароксизм. Лечение - см. гл. 6, п. III.Д.1.

5. Orthodromic supraventricular tachycardia in WPW syndrome. Correct rhythm. Heart rate 150-250 min -1. The RP interval is usually short, but may be prolonged with slow retrograde conduction from the ventricles to the atria. Starts and stops suddenly. Usually triggered by atrial extrasystoles. Causes: WPW syndrome, hidden additional pathways (see Chapter 6, p. XI.G.2). Usually there are no other heart lesions, but a combination with Ebstein's anomaly, hypertrophic cardiomyopathy, mitral valve prolapse is possible. Carotid sinus massage is often effective. With atrial fibrillation in patients with an obvious accessory pathway, impulses to the ventricles can be carried out extremely quickly; the QRS complexes are wide, as in ventricular tachycardia, the rhythm is irregular. There is a risk of ventricular fibrillation. Treatment - see Ch. 6, item XI.G.3.

6. Atrial tachycardia (automatic or reciprocal intraatrial). Correct rhythm. Atrial rhythm 100-200 min -1 . Non-sinus P waves. The RP interval is usually prolonged, but may be shortened in 1st-degree AV block. Causes: unstable atrial tachycardia is possible in the absence of organic lesions of the heart, stable - with myocardial infarction, cor pulmonale, and other organic lesions of the heart. The mechanism is an ectopic focus or reverse entry of an excitation wave inside the atria. It accounts for 10% of all supraventricular tachycardias. Massage of the carotid sinus causes a slowing of AV conduction, but does not eliminate the arrhythmia. Treatment - see Ch. 6, p. III.D.4.

7. Sinoatrial reciprocal tachycardia. ECG - as with sinus tachycardia (see Chapter 5, paragraph II.B.1). Correct rhythm. RP intervals are long. Starts and stops suddenly. Heart rate 100-160 min -1. The shape of the P wave is indistinguishable from the sinus. Reasons: can be observed in the norm, but more often - with organic lesions of the heart. The mechanism is the reverse entry of the excitation wave inside the sinus node or in the sinoatrial zone. It accounts for 5-10% of all supraventricular tachycardias. Massage of the carotid sinus causes a slowing of AV conduction, but does not eliminate the arrhythmia. Treatment - see Ch. 6, p. III.D.3.

8. Atypical form of paroxysmal AV nodal reciprocal tachycardia. ECG - as in atrial tachycardia (see Chapter 5, paragraph II.B.4). QRS complexes are narrow, RP intervals are long. The P wave is usually negative in leads II, III, aVF. The contour of the reverse entry of the excitation wave is in the AV node. Excitation is carried out anterograde along the fast (beta) intranodal pathway and retrograde - along the slow (alpha) pathway. Diagnosis may require an electrophysiological study of the heart. It accounts for 5-10% of all cases of reciprocal AV nodal tachycardias (2-5% of all supraventricular tachycardias). Massage of the carotid sinus can stop the paroxysm.

9. Orthodromic supraventricular tachycardia with delayed retrograde conduction. ECG - as in atrial tachycardia (see Chapter 5, paragraph II.B.4). QRS complexes are narrow, RP intervals are long. The P wave is usually negative in leads II, III, aVF. Orthodromic supraventricular tachycardia with slow retrograde conduction along an accessory pathway (usually posterior). The tachycardia is often persistent. It can be difficult to distinguish it from automatic atrial tachycardia and reciprocal intra-atrial supraventricular tachycardia. Diagnosis may require an electrophysiological study of the heart. Massage of the carotid sinus sometimes stops the paroxysm. Treatment - see Ch. 6, item XI.G.3.

10. Polytopic atrial tachycardia. Wrong rhythm. Heart rate > 100 min -1 . Non-sinus P waves of three or more different configurations. Different PP, PQ and RR intervals. Reasons: in the elderly with COPD, with cor pulmonale, treatment with aminophylline, hypoxia, heart failure, after surgery, with sepsis, pulmonary edema, diabetes mellitus. Often misdiagnosed as atrial fibrillation. May progress to atrial fibrillation/flutter. Treatment - see Ch. 6, p. III.G.

11. Paroxysmal atrial tachycardia with AV block. Irregular rhythm with the frequency of atrial waves 150-250 min -1 and ventricular complexes 100-180 min -1. Non-sinus P waves. Causes: glycoside intoxication (75%), organic heart disease (25%). ECG usually shows atrial tachycardia with second-degree AV block (usually Mobitz type I). Massage of the carotid sinus causes a slowing of AV conduction, but does not eliminate the arrhythmia.

12. Ventricular tachycardia. Usually - the correct rhythm with a frequency of 110-250 min -1. QRS complex > 0.12 s, usually > 0.14 s. The ST segment and T wave are discordant to the QRS complex. Causes: organic heart damage, hypokalemia, hyperkalemia, hypoxia, acidosis, drugs and other drugs (glycoside intoxication, antiarrhythmic drugs, phenothiazines, tricyclic antidepressants, caffeine, alcohol, nicotine), mitral valve prolapse, in rare cases - in healthy individuals. AV dissociation (independent contractions of the atria and ventricles) may be noted. The electrical axis of the heart is often deviated to the left, confluent complexes are recorded. It may be nonsustained (3 or more QRS complexes but the paroxysm lasts less than 30 s) or persistent (> 30 s), monomorphic or polymorphic. Bidirectional ventricular tachycardia (with the opposite direction of the QRS complexes) is observed mainly with glycoside intoxication. Ventricular tachycardia with narrow QRS complexes has been described (< 0,11 с). Дифференциальный диагноз желудочковой и наджелудочковой тахикардии с аберрантным проведением - см. рис. 5.3. Лечение - см. гл. 6, п. VI.Б.1.

13. Supraventricular tachycardia with aberrant conduction. Usually - the right rhythm. The duration of the QRS complex is usually 0.12-0.14 s. There are no AV-dissociation and drain complexes. Deviation of the electrical axis of the heart to the left is not typical. Differential diagnosis of ventricular and supraventricular tachycardia with aberrant conduction - see fig. 5.3.

14. Pirouette tachycardia. Tachycardia with irregular rhythm and wide polymorphic ventricular complexes; a typical sinusoidal picture is characteristic, in which groups of two or more ventricular complexes with one direction are replaced by groups of complexes with the opposite direction. Occurs with prolongation of the QT interval. Heart rate - 150-250 min -1. Reasons: see Ch. 6, p. XIII.A. Attacks are usually short-lived, but there is a risk of transition to ventricular fibrillation. Paroxysm is often preceded by alternating long and short cycles of RR. In the absence of prolongation of the QT interval, such ventricular tachycardia is called polymorphic. Treatment - see Ch. 6, p. XIII.A.

15. Ventricular fibrillation. Chaotic irregular rhythm, QRS complexes and T waves are absent. Reasons: see Ch. 5, item II.B.12. In the absence of CPR, ventricular fibrillation quickly (within 4-5 minutes) leads to death. Treatment - see Ch. 7, item IV.

16. Aberrant conduction. It is manifested by wide QRS complexes due to delayed impulse conduction from the atria to the ventricles. This is most often observed when the extrasystolic excitation reaches the His-Purkinje system in the phase of relative refractoriness. The duration of the refractory period of the His-Purkinje system is inversely proportional to the heart rate; if, against the background of long RR intervals, an extrasystole occurs (short RR interval) or supraventricular tachycardia begins, then aberrant conduction occurs. In this case, excitation is usually carried out along the left leg of the bundle of His, and aberrant complexes look like blockade of the right leg of the bundle of His. Occasionally, aberrant complexes look like a left bundle branch block.

17. ECG with tachycardia with wide QRS complexes (differential diagnosis of ventricular and supraventricular tachycardia with aberrant conduction - see Fig. 5.3). Criteria for ventricular tachycardia:

b. Deviation of the electrical axis of the heart to the left.

B. Ectopic and replacement contractions

1. Atrial extrasystoles. Extraordinary non-sinus P wave followed by a normal or aberrant QRS complex. PQ interval - 0.12-0.20 s. The PQ interval of an early extrasystole may exceed 0.20 s. Causes: occur in healthy individuals, with fatigue, stress, smokers, under the influence of caffeine and alcohol, with organic heart disease, cor pulmonale. The compensatory pause is usually incomplete (the interval between the pre- and post-extrasystolic P waves is less than twice the normal PP interval). Treatment - see Ch. 6, p. III.B.

2. Blocked atrial extrasystoles. Extraordinary non-sinus P wave that is not followed by a QRS complex. Through the AV node, which is in the refractory period, atrial extrasystole is not carried out. The extrasystolic P wave sometimes overlaps the T wave and is difficult to recognize; in these cases, a blocked atrial extrasystole is mistaken for sinoatrial block or sinus node arrest.

3. AV nodal extrasystoles. Extraordinary QRS complex with retrograde (negative in leads II, III, aVF) P wave, which can be registered before or after the QRS complex, or superimposed on it. The shape of the QRS complex is normal; with aberrant conduction, it may resemble a ventricular extrasystole. Causes: occur in healthy individuals and with organic heart disease. The source of extrasystole is the AV node. The compensatory pause may be complete or incomplete. Treatment - see Ch. 6, p. V.A.

4. Ventricular extrasystoles. Extraordinary, wide (> 0.12 s) and deformed QRS complex. The ST segment and T wave are discordant to the QRS complex. Reasons: see Ch. 5, item II.B.12. The P wave may be unrelated to extrasystoles (AV dissociation) or be negative and follow the QRS complex (retrograde P wave). The compensatory pause is usually complete (the interval between the pre- and post-extrasystolic P waves is equal to twice the normal PP interval). Treatment - see Ch. 6, item V.B.

5. Substituting AV-nodal contractions. They resemble AV nodal extrasystoles, however, the interval to the replacement complex is not shortened, but lengthened (corresponding to a heart rate of 35–60 min–1). Causes: occur in healthy individuals and with organic heart disease. The source of the replacement impulse is a latent pacemaker in the AV node. Often observed when sinus rhythm slows down as a result of increased parasympathetic tone, medication (eg, cardiac glycosides), and sinus node dysfunction.

6. Replacement idioventricular contractions. They resemble ventricular extrasystoles, however, the interval to the replacement contraction is not shortened, but lengthened (corresponding to a heart rate of 20–50 min–1). Causes: occur in healthy individuals and with organic heart disease. The replacement impulse comes from the ventricles. Replacement idioventricular contractions are usually observed when the sinus and AV nodal rhythm slows down.

1. Sinoatrial blockade. The extended PP interval is a multiple of the normal one. Causes: some drugs (cardiac glycosides, quinidine, procainamide), hyperkalemia, sinus node dysfunction, myocardial infarction, increased parasympathetic tone. Sometimes there is a Wenckebach period (gradual shortening of the PP interval until the next cycle falls out).

2. AV blockade of the 1st degree. PQ interval > 0.20 s. Each P wave corresponds to a QRS complex. Causes: observed in healthy individuals, athletes, with an increase in parasympathetic tone, taking certain drugs (cardiac glycosides, quinidine, procainamide, propranolol, verapamil), rheumatic attack, myocarditis, congenital heart defects (atrial septal defect, patent ductus arteriosus). With narrow QRS complexes, the most likely level of block is the AV node. If the QRS complexes are wide, conduction disturbance is possible in both the AV node and the His bundle. Treatment - see Ch. 6, p. VIII.A.

3. AV blockade of the 2nd degree of the Mobitz type I (with Wenckebach's periodicals). Increasing lengthening of the PQ interval up to the loss of the QRS complex. Causes: observed in healthy individuals, athletes, when taking certain drugs (cardiac glycosides, beta-blockers, calcium antagonists, clonidine, methyldopa, flecainide, encainide, propafenone, lithium), with myocardial infarction (especially lower), rheumatic attack, myocarditis . With narrow QRS complexes, the most likely level of block is the AV node. If the QRS complexes are wide, the violation of impulse conduction is possible both in the AV node and in the bundle of His. Treatment - see Ch. 6, item VIII.B.1.

4. AV blockade of the 2nd degree of the Mobitz type II. Periodic prolapse of QRS complexes. The PQ intervals are the same. Causes: almost always occurs against the background of organic heart disease. The pulse delay occurs in the bundle of His. 2:1 AV block occurs in both Mobitz I and Mobitz II types: narrow QRS complexes are more typical for Mobitz I AV block, wide ones for Mobitz II AV block. In high-degree AV block, two or more consecutive ventricular complexes fall out. Treatment - see Ch. 6, item VIII.B.2.

5. Complete AV block. The atria and ventricles fire independently. The atrial contraction rate exceeds the ventricular rate. Same PP intervals and same RR intervals, PQ intervals vary. Causes: Complete AV block is congenital. The acquired form of complete AV blockade occurs with myocardial infarction, isolated disease of the conduction system of the heart (Lenegre's disease), aortic malformations, taking certain drugs (cardiac glycosides, quinidine, procainamide), endocarditis, Lyme disease, hyperkalemia, infiltrative diseases (amyloidosis, sarcoidosis ), collagenosis, trauma, rheumatic attack. Blockade of impulse conduction is possible at the level of the AV node (for example, with congenital complete AV blockade with narrow QRS complexes), the His bundle, or the distal fibers of the His-Purkinje system. Treatment - see Ch. 6, p. VIII.B.

III. Determination of the electrical axis of the heart. The direction of the electrical axis of the heart approximately corresponds to the direction of the largest total vector of depolarization of the ventricles. To determine the direction of the electrical axis of the heart, it is necessary to calculate the algebraic sum of the teeth of the QRS complex amplitude in leads I, II and aVF (subtract the amplitude of the negative part of the complex from the amplitude of the positive part of the complex) and then follow the table. 5.1.

A. Causes of deviation of the electrical axis of the heart to the right: COPD, cor pulmonale, right ventricular hypertrophy, blockade of the right leg of the His bundle, lateral myocardial infarction, blockade of the posterior branch of the left leg of the His bundle, pulmonary edema, dextrocardia, WPW syndrome. It happens in the norm. A similar picture is observed when the electrodes are applied incorrectly.

B. Causes of deviation of the electrical axis of the heart to the left: blockade of the anterior branch of the left leg of the His bundle, lower myocardial infarction, blockade of the left leg of the His bundle, left ventricular hypertrophy, atrial septal defect of the ostium primum type, COPD, hyperkalemia. It happens in the norm.

C. Causes of a sharp deviation of the electrical axis of the heart to the right: blockade of the anterior branch of the left leg of the His bundle against the background of right ventricular hypertrophy, blockade of the anterior branch of the left leg of the His bundle with lateral myocardial infarction, right ventricular hypertrophy, COPD.

IV. Analysis of teeth and intervals. ECG interval - the interval from the beginning of one wave to the beginning of another wave. An ECG segment is the gap from the end of one wave to the beginning of the next wave. At a writing speed of 25 mm/s, each small cell on the paper tape corresponds to 0.04 s.

A. Normal 12-lead ECG

1. P wave. Positive in leads I, II, aVF, negative in aVR, may be negative or biphasic in leads III, aVL, V 1 , V 2 .

3. QRS complex. Width - 0.06-0.10 s. Small Q wave (width< 0,04 с, амплитуда < 2 мм) бывает во всех отведениях кроме aVR, V 1 и V 2 . Переходная зона грудных отведений (отведение, в котором амплитуды положительной и отрицательной части комплекса QRS одинаковы) обычно находится между V 2 и V 4 .

4. ST segment. Usually on the isoline. In the leads from the extremities, a depression of up to 0.5 mm and an elevation of up to 1 mm are normally possible. In the chest leads, ST elevation up to 3 mm with a downward bulge is possible (syndrome of early repolarization of the ventricles, see Chapter 5, p. IV.3.1.d).

5. T wave. Positive in leads I, II, V 3 -V 6 . Negative in aVR, V 1 . May be positive, flattened, negative, or biphasic in leads III, aVL, aVF, V1, and V2. Healthy young people have a negative T wave in leads V 1 -V 3 (persistent juvenile type of ECG).

6. QT interval. Duration is inversely proportional to heart rate; usually fluctuates between 0.30-0.46 s. QT c \u003d QT / C RR, where QT c is the corrected QT interval; normal QT c 0.46 in men and 0.47 in women.

Below are some conditions, for each of which characteristic ECG signs are indicated. However, it must be borne in mind that ECG criteria do not have one hundred percent sensitivity and specificity, therefore, the listed signs can be detected separately or in different combinations, or absent altogether.

1. High pointed P in lead II: right atrial enlargement. P wave amplitude in lead II > 2.5 mm (P pulmonale). Specificity is only 50%, in 1/3 of cases P pulmonale is caused by an increase in the left atrium. It is noted in COPD, congenital heart defects, congestive heart failure, coronary artery disease.

2. Negative P in lead I

A. Dextrocardia. Negative P and T waves, an inverted QRS complex in lead I without an increase in the amplitude of the R wave in the chest leads. Dextrocardia can be one of the manifestations of situs inversus (reverse arrangement of internal organs) or isolated. Isolated dextrocardia is often associated with other congenital malformations, including corrected transposition of the great arteries, pulmonary artery stenosis, and ventricular and atrial septal defects.

b. The electrodes are incorrectly applied. If the electrode intended for the left hand is applied to the right hand, then negative P and T waves are recorded, an inverted QRS complex with a normal location of the transition zone in the chest leads.

3. Deep negative P in lead V 1: left atrial enlargement. P mitrale: in lead V 1, the end part (ascending knee) of the P wave is expanded (> 0.04 s), its amplitude is > 1 mm, the P wave is expanded in lead II (> 0.12 s). It is observed in mitral and aortic defects, heart failure, myocardial infarction. The specificity of these signs is above 90%.

4. Negative P wave in lead II: ectopic atrial rhythm. The PQ interval is usually > 0.12 s, the P wave is negative in leads II, III, aVF. See ch. 5, item II.A.3.

1. Prolongation of the PQ interval: AV blockade of the 1st degree. PQ intervals are the same and exceed 0.20 s (see Chapter 5, item II.D.2). If the duration of the PQ interval varies, then AV blockade of the 2nd degree is possible (see Chapter 5, p. II.D.3).

2. Shortening of the PQ interval

A. Functional shortening of the PQ interval. PQ< 0,12 с. Наблюдается в норме, при повышении симпатического тонуса, артериальной гипертонии, гликогенозах.

b. WPW syndrome. PQ< 0,12 с, наличие дельта-волны, комплексы QRS широкие, интервал ST и зубец T дискордантны комплексу QRS. См. гл. 6, п. XI.

V. AV - nodal or lower atrial rhythm. PQ< 0,12 с, зубец P отрицательный в отведениях II, III, aVF. см. гл. 5, п. II.А.5.

3. Depression of the PQ segment: pericarditis. Depression of the PQ segment in all leads except aVR is most pronounced in leads II, III, and aVF. Depression of the PQ segment is also noted in atrial infarction, which occurs in 15% of cases of myocardial infarction.

D. Width of the QRS complex

A. Blockade of the anterior branch of the left leg of the bundle of His. Deviation of the electrical axis of the heart to the left (from -30° to -90°). Low R wave and deep S wave in leads II, III, and aVF. High R wave in leads I and aVL. A small Q wave may be present. There is a late activation wave (R') in lead aVR. The shift of the transitional zone to the left in the chest leads is characteristic. It is observed in congenital malformations and other organic lesions of the heart, occasionally in healthy people. Does not require treatment.

b. Blockade of the posterior branch of the left leg of the bundle of His. Deviation of the electrical axis of the heart to the right (> +90°). Low R wave and deep S wave in leads I and aVL. A small Q wave may be recorded in leads II, III, aVF. It is noted in ischemic heart disease, occasionally in healthy people. Occurs infrequently. It is necessary to exclude other causes of deviation of the electrical axis of the heart to the right: right ventricular hypertrophy, COPD, cor pulmonale, lateral myocardial infarction, vertical position of the heart. Complete confidence in the diagnosis is given only by comparison with previous ECG. Does not require treatment.

V. Incomplete blockade of the left leg of the bundle of His. Serrated R wave or late R wave (R’) in leads V 5 , V 6 . Wide S wave in leads V 1 , V 2 . The absence of a Q wave in leads I, aVL, V 5 , V 6 .

d. Incomplete blockade of the right leg of the bundle of His. Late R wave (R’) in leads V 1 , V 2 . Wide S wave in leads V 5 , V 6 .

A. Blockade of the right leg of the bundle of His. Late R wave in leads V 1 , V 2 with slanting ST segment and negative T wave. Deep S wave in leads I, V 5 , V 6 . It is observed with organic lesions of the heart: cor pulmonale, Lenegra's disease, coronary artery disease, occasionally - normal. Masked blockade of the right bundle branch block: the form of the QRS complex in lead V 1 corresponds to the blockade of the right bundle branch block, however, in leads I, aVL or V 5 , V 6 the RSR complex is recorded. Usually this is due to the blockade of the anterior branch of the left leg of the His bundle, left ventricular hypertrophy, myocardial infarction. Treatment - see Ch. 6, p. VIII.E.

b. Blockade of the left leg of the bundle of His. Wide serrated R wave in leads I, V 5 , V 6 . Deep S or QS wave in leads V 1 , V 2 . The absence of a Q wave in leads I, V 5 , V 6 . It is observed with left ventricular hypertrophy, myocardial infarction, Lenegra's disease, coronary artery disease, sometimes normal. Treatment - see Ch. 6, p. VIII.D.

V. Blockade of the right leg of the bundle of His and one of the branches of the left leg of the bundle of His. The combination of two-beam block with 1st degree AV block should not be regarded as a three-beam block: prolongation of the PQ interval may be due to slow conduction in the AV node, and not blockade of the third branch of the His bundle. Treatment - see Ch. 6, p. VIII.G.

d. Violation of intraventricular conduction. Expansion of the QRS complex (> 0.12 s) in the absence of signs of blockade of the right or left bundle branch block. It is noted with organic heart disease, hyperkalemia, left ventricular hypertrophy, taking antiarrhythmic drugs of classes Ia and Ic, with WPW syndrome. Treatment usually does not require.

E. QRS complex amplitude

1. Low amplitude of teeth. Amplitude of the QRS complex< 5 мм во всех отведениях от конечностей и < 10 мм во всех грудных отведениях. Встречается в норме, а также при экссудативном перикардите, амилоидозе, ХОЗЛ, ожирении, тяжелом гипотиреозе.

2. High-amplitude QRS complex

A. Left ventricular hypertrophy

1) Cornell criteria: (R in aVL + S in V 3) > 28 mm in men and > 20 mm in women (sensitivity 42%, specificity 96%).

3) Sokolov-Lyon criteria: (S in V 1 + R in V 5 or V 6) > 35 mm (sensitivity 22%, specificity 100%, the criterion is valid for people over 40 years old).

4) There are no reliable criteria for the blockade of the right leg of the bundle of His.

5) With left bundle branch block: (S in V 2 + R in V 5) > 45 mm (sensitivity 86%, specificity 100%).

3. Tall R wave in lead V 1

A. Hypertrophy of the right ventricle. Deviation of the electrical axis of the heart to the right; R/S 1 to V 1 and/or R/S 1 to V 6 . Depending on the shape of the QRS complex in lead V 1, there are three types of right ventricular hypertrophy.

1) Type A. High R in lead V 1 (qR, R, rSR'), often with downsloping ST segment depression and negative T wave. Right ventricular hypertrophy, usually pronounced (with pulmonary artery stenosis, pulmonary hypertension, Eisenmenger).

2) Type B. Complex type RS or Rsr’ in lead V 1 ; observed with atrial septal defect, mitral stenosis.

3) Type C. Complex type rS or rSr' with a deep S wave in the left chest leads (V 5 , V 6). Most often - with COPD.

4. Complexes with changing amplitude: electrical alternation. Alternation of the QRS complex: alternation of complexes of different directions and amplitudes. It is observed in exudative pericarditis, myocardial ischemia, dilated cardiomyopathy and other organic lesions of the heart. Complete alternation: alternation of the P wave, QRS complex and T wave. Usually observed with exudative pericarditis, often against the background of cardiac tamponade.

1. Myocardial infarction. Width > 0.04 s (> 0.05 s in lead III). Amplitude > 2 mm or 25% of R wave amplitude (50% in lead aVL, 15% in leads V4-V6).

2. Pseudo-infarction curve. Pathological Q wave in the absence of myocardial infarction. Causes: organic heart disease (especially dilated cardiomyopathy and hypertrophic cardiomyopathy, amyloidosis, myocarditis), diseases of the musculoskeletal system, hypertrophy of the left or right ventricle, COPD, cor pulmonale, pulmonary embolism, pneumothorax, blockade of the left leg of the His bundle, blockade of the anterior branch of the left leg His bundle, WPW syndrome, CNS disease, hypercalcemia, shock, hypoxia, pancreatitis, surgery, heart injury.

1. Shift of the transition zone to the right. R/S > 1 in lead V 1 or V 2 . It occurs normally, with right ventricular hypertrophy, posterior myocardial infarction, Duchenne myopathy, right bundle branch block, WPW syndrome.

2. Shift of the transition zone to the left. The transition zone is shifted to V 5 or V 6 . R/S< 1 в отведениях V 5 , V 6 . Встречается в норме, при передне-перегородочном и переднем инфаркте миокарда, дилатационной кардиомиопатии и гипертрофической кардиомиопатии, гипертрофии левого желудочка, ХОЗЛ, легочном сердце, гипертрофии правого желудочка, блокаде передней ветви левой ножки пучка Гиса, синдроме WPW .

3. Delta wave (additional wave in the initial part of the ventricular complex): WPW syndrome. PQ< 0,12 с; расширенный комплекс QRS с дельта-волной. Лечение - см. гл. 6, п. XI.Ж. Локализацию дополнительного пути можно установить по отведениям, в которых зарегистрирована отрицательная дельта-волна:

A. II, III, aVF - posterior accessory path;

b. I, aVL - left side path;

V. V 1 with a deviation of the electrical axis of the heart to the right - the right anterior-septal path;

V 1 with a deviation of the electrical axis of the heart to the left - the right lateral path.

4. Notch on the descending knee of the R wave (Osborne tooth). Late positive wave in the terminal part of the ventricular complex. Observed with hypothermia (treatment - see Chapter 8, paragraph IX.E). As the body temperature decreases, the amplitude of the Osborn wave increases.

1. ST segment elevation

A. Myocardial damage. In several leads - the rise of the ST segment with a bulge upward with a transition to the T wave. In reciprocal leads - depression of the ST segment. A Q wave is often recorded. Changes are dynamic; the T wave becomes negative before the ST segment returns to the isoline.

b. Pericarditis. Elevation of the ST segment in many leads (I-III, aVF, V 3 -V 6). Absence of ST depression in reciprocal leads (except aVR). Lack of Q wave. Depression of the PQ segment. The changes are dynamic; the T wave becomes negative after the ST segment returns to the isoline.

V. Aneurysm of the left ventricle. Elevation of the ST segment, usually with a deep Q wave or a form of ventricular complex - type QS. ST segment and T wave changes are permanent.

d. Syndrome of early repolarization of the ventricles. Elevation of the ST segment with a convexity downwards with the transition to a concordant T wave. Notch on the descending knee of the R wave. Wide symmetrical T wave. Changes in the ST segment and T wave are permanent. Norm variant.

e. Other causes of ST segment elevation. Hyperkalemia, acute cor pulmonale, myocarditis, heart tumors.

2. ST segment depression

A. myocardial ischemia. Horizontal or oblique ST depression.

b. repolarization disorder. Sloping depression of the ST segment with a bulge upward (with left ventricular hypertrophy). Negative T wave. Changes are more pronounced in leads V 5 , V 6 , I, aVL.

V. Glycoside toxicity. Trough-shaped depression of the ST segment. Biphasic or negative T wave. Changes are more pronounced in the left chest leads.

d. Nonspecific changes in the ST segment. They are noted normally, with mitral valve prolapse, taking certain medications (cardiac glycosides, diuretics, psychotropic drugs), with electrolyte disorders, myocardial ischemia, left and right ventricular hypertrophy, blockade of the bundle branch block, WPW syndrome, tachycardia, hyperventilation, pancreatitis, shock.

1. Tall T wave. T wave amplitude > 6 mm in limb leads; in chest leads > 10-12 mm (in men) and > 8 mm in women. It is noted normally, with hyperkalemia, myocardial ischemia, in the first hours of myocardial infarction, with left ventricular hypertrophy, CNS lesions, anemia.

2. Deep negative T wave. A wide, deep negative T wave is recorded with CNS lesions, especially with subarachnoid hemorrhage. Narrow deep negative T wave - with coronary artery disease, left and right ventricular hypertrophy.

3. Nonspecific changes in the T wave. A flattened or slightly inverted T wave. It is noted normally, when taking certain drugs, with electrolyte disturbances, hyperventilation, pancreatitis, myocardial ischemia, left ventricular hypertrophy, bundle branch block. Persistent juvenile ECG type: negative T wave in leads V 1 -V 3 in young people.

1. Prolongation of the QT interval. QTc > 0.46 for men and > 0.47 for women; (QT c \u003d QT / C RR).

A. Congenital prolongation of the QT interval: Romano-Ward syndrome (without hearing loss), Ervel-Lange-Nielsen syndrome (with deafness).

b. Acquired prolongation of the QT interval: taking certain drugs (quinidine, procainamide, disopyramide, amiodarone, sotalol, phenothiazines, tricyclic antidepressants, lithium), hypokalemia, hypomagnesemia, severe bradyarrhythmia, myocarditis, mitral valve prolapse, myocardial ischemia, hypothyroidism, hypothermia, low-calorie liquid protein diets.

2. Shortening of the QT interval. QT< 0,35 с при ЧСС 60-100 мин –1 . Наблюдается при гиперкальциемии, гликозидной интоксикации.

1. Increased U-wave amplitude. U-wave amplitude > 1.5 mm. It is observed with hypokalemia, bradycardia, hypothermia, left ventricular hypertrophy, taking certain drugs (cardiac glycosides, quinidine, amiodarone, isoprenaline).

2. Negative U wave. It is observed in myocardial ischemia and left ventricular hypertrophy.

V. Ischemia and myocardial infarction

A. Myocardial ischemia on the ECG is usually manifested by ST segment depression (horizontal or oblique) and T wave changes (symmetrical, inverted, high peaked or pseudo-normal T wave). Pseudonormalization refers to the transformation of an inverted T wave into a normal one. Nonspecific ST segment and T wave changes (slight ST segment depression, flattened or slightly inverted T wave) may also be noted.

1. Dynamics of myocardial infarction

A. Minutes-hours. An increase in T wave amplitude (spiky T wave) is usually observed in the first 30 minutes. ST segment elevation in multiple leads. ST segment depression in reciprocal leads - for example, ST segment depression in leads V 1 -V 4 in inferior myocardial infarction; ST depression in leads II, III, aVF in anterior myocardial infarction. Sometimes an inverted T wave is seen.

b. Hours-days. The ST segment approaches the isoline. The R wave decreases or disappears. The Q wave appears. The T wave becomes inverted.

V. Weeks-years. Normalization of the T wave. Q waves are usually preserved, however, after a year after myocardial infarction, in 30% of cases, pathological Q waves are not detected.

2. Myocardial infarction with pathological Q waves and without pathological Q waves. The appearance of pathological Q waves correlates poorly with the presence of a transmural lesion. Therefore, it is better to talk not about transmural and non-transmural myocardial infarction, but about myocardial infarction with pathological Q waves and myocardial infarction without pathological Q waves.

4. Diagnosis of myocardial infarction in the blockade of the left leg of the bundle of His. Four criteria for myocardial infarction:

A. dynamics of the ST segment in the first 2-5 days of myocardial infarction;

b. ST segment elevation (> 2 mm concordant to the QRS complex or > 7 mm discordant to the QRS complex);

V. pathological Q waves in leads I, aVL, V 6 or III, aVF;

notch on the ascending knee of the S wave in leads V 3 or V 4 (Cabrera's sign).

The sensitivity of these criteria is not high (Cardiology Clinics 1987; 5:393).

5. ECG - diagnosis of some complications of myocardial infarction

A. Pericarditis. Elevation of the ST segment and depression of the PQ segment in many leads (see Chapter 5, p. IV.3.1.b).

b. Aneurysm of the left ventricle. Prolonged (> 6 weeks) elevation of the ST segment in the leads, in which pathological Q waves are recorded (see Chapter 5, p. IV.3.1.c).

V. Conduction disorders. Blockade of the anterior branch of the left leg of the bundle of His, blockade of the posterior branch of the left leg of the bundle of His, complete blockade of the left leg of the bundle of His, blockade of the right leg of the bundle of His, AV blockade of the 2nd degree and complete AV blockade.

A. Hypokalemia. Prolongation of the PQ interval. Expansion of the QRS complex (rare). Pronounced U wave, flattened inverted T wave, ST segment depression, slight QT prolongation.

1. Light (5.5-6.5 meq / l). High peaked symmetrical T wave, shortening of the QT interval.

2. Moderate (6.5-8.0 meq/l). Reducing the amplitude of the P wave; prolongation of the PQ interval. Expansion of the QRS complex, a decrease in the amplitude of the R wave. Depression or elevation of the ST segment. Ventricular extrasystole.

3. Heavy (9-11 meq/l). Absence of a P wave. Expansion of the QRS complex (up to sinusoidal complexes). Slow or accelerated idioventricular rhythm, ventricular tachycardia, ventricular fibrillation, asystole.

B. Hypocalcemia. Prolongation of the QT interval (due to lengthening of the ST segment).

G. Hypercalcemia. Shortening of the QT interval (due to shortening of the ST segment).

VII. The action of drugs

1. Therapeutic action. Prolongation of the PQ interval. Sloping ST segment depression, shortening of the QT interval, T wave changes (flattened, inverted, biphasic), pronounced U wave. Decrease in heart rate with atrial fibrillation.

2. Toxic effect. Ventricular extrasystole, AV block, atrial tachycardia with AV block, accelerated AV nodal rhythm, sinoatrial block, ventricular tachycardia, bidirectional ventricular tachycardia, ventricular fibrillation.

1. Therapeutic action. Slight prolongation of the PQ interval. QT prolongation, ST segment depression, T wave flattening or inversion, prominent U wave.

2. Toxic effect. Expansion of the QRS complex. Severe prolongation of the QT interval. AV block, ventricular extrasystole, ventricular tachycardia, pirouette ventricular tachycardia, sinus bradycardia, sinoatrial block.

B. Class Ic antiarrhythmics. Prolongation of the PQ interval. Expansion of the QRS complex. Prolongation of the QT interval.

G. Amiodarone. Prolongation of the PQ interval. Expansion of the QRS complex. Prolongation of the QT interval, pronounced U wave. Sinus bradycardia.

VIII. Selected heart diseases

A. Dilated cardiomyopathy. Signs of an increase in the left atrium, sometimes - the right. Low amplitude of the teeth, pseudo-infarction curve, blockade of the left leg of the bundle of His, the anterior branch of the left leg of the bundle of His. Nonspecific changes in the ST segment and T wave. Ventricular extrasystole, atrial fibrillation.

B. Hypertrophic cardiomyopathy. Signs of an increase in the left atrium, sometimes - the right. Signs of left ventricular hypertrophy, pathological Q waves, pseudoinfarction curve. Nonspecific changes in the ST segment and T wave. With apical hypertrophy of the left ventricle - giant negative T waves in the left chest leads. Supraventricular and ventricular arrhythmias.

B. Amyloidosis of the heart. Low amplitude of the teeth, pseudo-infarction curve. Atrial fibrillation, AV block, ventricular arrhythmias, sinus node dysfunction.

D. Duchenne myopathy. Shortening of the PQ interval. High R wave in leads V 1 , V 2 ; deep Q wave in leads V 5 , V 6 . Sinus tachycardia, atrial and ventricular extrasystole, supraventricular tachycardia.

D. Mitral stenosis. Signs of enlargement of the left atrium. There is hypertrophy of the right ventricle, deviation of the electrical axis of the heart to the right. Often - atrial fibrillation.

E. Mitral valve prolapse. T waves are flattened or inverted, especially in lead III; ST segment depression, slight prolongation of the QT interval. Ventricular and atrial extrasystole, supraventricular tachycardia, ventricular tachycardia, sometimes atrial fibrillation.

G. Pericarditis. Depression of the PQ segment, especially in leads II, aVF, V 2 -V 6 . Diffuse ST-segment elevation with upward bulge in leads I, II, aVF, V 3 -V 6 . Sometimes - depression of the ST segment in lead aVR (in rare cases - in leads aVL, V 1 , V 2). Sinus tachycardia, atrial arrhythmias. ECG changes go through 4 stages:

1. ST segment elevation, T wave normal;

2. the ST segment descends to the isoline, the amplitude of the T wave decreases;

3. ST segment on the isoline, T wave inverted;

4. ST segment on the isoline, T wave is normal.

Z. Large pericardial effusion. Low amplitude of the teeth, alternation of the QRS complex. The pathognomonic sign is a complete electrical alternation (P, QRS, T).

I. Dextrocardia. The P wave is negative in lead I. QRS complex inverted in lead I, R/S< 1 во всех грудных отведениях с уменьшением амплитуды комплекса QRS от V 1 к V 6 . Инвертированный зубец T в I отведении.

K. Atrial septal defect. Signs of an increase in the right atrium, less often - the left; prolongation of the PQ interval. RSR' in lead V 1 ; the electrical axis of the heart is deviated to the right with a defect of the ostium secundum type, to the left - with a defect of the ostium primum type. Inverted T wave in leads V 1 , V 2 . Sometimes atrial fibrillation.

L. Stenosis of the pulmonary artery. Signs of enlargement of the right atrium. Right ventricular hypertrophy with high R wave in leads V 1 , V 2 ; deviation of the electrical axis of the heart to the right. Inverted T wave in leads V 1 , V 2 .

M. Sick sinus syndrome. Sinus bradycardia, sinoatrial block, AV block, sinus arrest, bradycardia-tachycardia syndrome, supraventricular tachycardia, atrial fibrillation/flutter, ventricular tachycardia.

A. COPD. Signs of enlargement of the right atrium. Deviation of the electrical axis of the heart to the right, shift of the transition zone to the right, signs of right ventricular hypertrophy, low amplitude of the teeth; ECG type S I -S II -S III. T wave inversion in leads V 1 , V 2 . Sinus tachycardia, AV nodal rhythm, conduction disturbances, including AV block, intraventricular conduction delay, bundle branch block.

B. TELA. Syndrome S I -Q III -T III, signs of overload of the right ventricle, transient complete or incomplete blockade of the right leg of the His bundle, displacement of the electrical axis of the heart to the right. T wave inversion in leads V 1 , V 2 ; nonspecific changes in the ST segment and T wave. Sinus tachycardia, sometimes - atrial arrhythmias.

B. Subarachnoid hemorrhage and other CNS lesions. Sometimes - a pathological Q wave. High wide positive or deep negative T wave, elevation or depression of the ST segment, pronounced U wave, pronounced prolongation of the QT interval. Sinus bradycardia, sinus tachycardia, AV nodal rhythm, ventricular extrasystole, ventricular tachycardia.

G. Hypothyroidism. Prolongation of the PQ interval. Low amplitude of the QRS complex. Flattened T wave. Sinus bradycardia.

D. CRF. ST segment elongation (due to hypocalcemia), high symmetrical T waves (due to hyperkalemia).

E. Hypothermia. Prolongation of the PQ interval. A notch in the final part of the QRS complex (Osborn's tooth - see Chapter 5, item IV.G.4). Prolongation of the QT interval, T wave inversion. Sinus bradycardia, atrial fibrillation, AV nodal rhythm, ventricular tachycardia.

X. EX. The main types of pacemakers are described by a three-letter code: the first letter indicates which chamber of the heart is being stimulated (A - Atrium - atrium, V - Ventricle - ventricle, D - Dual - both the atrium and ventricle), the second letter - the activity of which chamber is perceived (A, V or D), the third letter indicates the type of response to the perceived activity (I - Inhibition - blocking, T - Triggering - launch, D - Dual - both). So, in the VVI mode, both the stimulating and sensing electrodes are located in the ventricle, and when spontaneous activity of the ventricle occurs, its stimulation is blocked. In DDD mode, both the atrium and the ventricle have two electrodes (stimulating and sensing). Response type D means that if spontaneous atrial activity occurs, its stimulation will be blocked, and after a programmed time interval (AV-interval), a stimulus will be given to the ventricle; if spontaneous ventricular activity occurs, on the contrary, ventricular pacing will be blocked, and atrial pacing will start after a programmed VA interval. Typical modes of a single chamber pacemaker are VVI and AAI. Typical two-chamber EKS modes are DVI and DDD. The fourth letter R (Rate-adaptive - adaptive) means that the pacemaker is able to increase the rate of stimulation in response to a change in motor activity or load-dependent physiological parameters (for example, QT interval, temperature).

A. General principles of ECG interpretation

1. Assess the nature of the rhythm (own rhythm with periodic activation of the stimulator or imposed).

2. Determine which chamber(s) is being stimulated.

3. Determine the activity of which chamber(s) is perceived by the stimulator.

4. Determine the programmed pacer intervals (VA, VV, AV intervals) by atrial (A) and ventricular (V) pacing artifacts.

5. Determine the EX mode. It must be remembered that ECG signs of a single-chamber pacemaker do not exclude the possibility of the presence of electrodes in two chambers: for example, stimulated contractions of the ventricles can be observed both with single-chamber and dual-chamber pacemakers, in which ventricular stimulation follows a certain interval after the P wave (DDD mode) .

6. Eliminate violations of imposition and detection:

A. imposition disorders: there are stimulation artifacts that are not followed by depolarization complexes of the corresponding chamber;

b. detection disturbances: There are pacing artifacts that should be blocked if atrial or ventricular depolarization is normally detected.

B. Separate EX-modes

1. AI. If the intrinsic rate falls below the programmed pacer rate, atrial pacing is initiated at a constant AA interval. With spontaneous atrial depolarization (and normal detection), the pacemaker time counter is reset. If spontaneous atrial depolarization does not recur after the set AA interval, atrial pacing is initiated.

2. VI. With spontaneous ventricular depolarization (and normal detection), the pacemaker time counter is reset. If spontaneous ventricular depolarization does not recur after a predetermined VV interval, ventricular pacing is initiated; otherwise, the time counter is reset again and the whole cycle starts over. In adaptive VVIR pacemakers, the rhythm rate increases with an increase in the level of physical activity (up to a given upper limit of heart rate).

3. DDD. If the intrinsic rate falls below the programmed pacer rate, atrial (A) and ventricular (V) pacing is initiated at the specified intervals between the A and V pulses (AV interval) and between the V pulse and the subsequent A pulse (VA interval). With spontaneous or forced ventricular depolarization (and its normal detection), the pacemaker time counter is reset and the VA interval begins. If spontaneous atrial depolarization occurs in this interval, atrial pacing is blocked; otherwise, an atrial impulse is delivered. With spontaneous or imposed atrial depolarization (and its normal detection), the pacemaker time counter is reset and the AV interval begins. If spontaneous ventricular depolarization occurs in this interval, then ventricular pacing is blocked; otherwise, a ventricular impulse is delivered.

B. Pacemaker dysfunction and arrhythmias

1. Violation of imposition. The stimulation artifact is not followed by a depolarization complex, although the myocardium is not in the refractory stage. Causes: displacement of the stimulating electrode, perforation of the heart, an increase in the stimulation threshold (with myocardial infarction, taking flecainide, hyperkalemia), damage to the electrode or violation of its insulation, disturbances in impulse generation (after defibrillation or due to depletion of the power source), as well as incorrectly set EKS parameters.

2. Violation of detection. The pacer time counter is not reset when self or imposed depolarization of the corresponding chamber occurs, resulting in an abnormal rhythm (imposed rhythm superimposed on own). Causes: low amplitude of the perceived signal (especially with ventricular extrasystoles), incorrectly set pacemaker sensitivity, as well as the reasons listed above (see Chapter 5, paragraph X.B.1). It is often enough to reprogram the pacemaker sensitivity.

3. Hypersensitivity of the pacemaker. At the expected time (after the appropriate interval) no stimulation occurs. T waves (P waves, myopotentials) are misinterpreted as R waves and the pacemaker time counter is reset. In case of erroneous detection of the T wave, the VA interval starts from it. In this case, the sensitivity or refractory period of detection must be reprogrammed. You can also set the VA interval to the T wave.

4. Blocking by myopotentials. Myopotentials arising from hand movements can be misinterpreted as potentials from the myocardium and block stimulation. In this case, the intervals between the imposed complexes become different, and the rhythm becomes incorrect. Most often, such violations occur when using unipolar pacemakers.

5. Circular tachycardia. Imposed rhythm with the maximum rate for the pacemaker. Occurs when retrograde atrial stimulation after ventricular pacing is sensed by the atrial lead and triggers ventricular pacing. This is typical for a two-chamber pacemaker with the detection of atrial excitation. In such cases, it may be sufficient to increase the refractory period of detection.

6. Tachycardia induced by atrial tachycardia. Imposed rhythm with the maximum rate for the pacemaker. It is observed if atrial tachycardia (eg, atrial fibrillation) occurs in patients with a dual-chamber pacemaker. Frequent atrial depolarization is sensed by the pacemaker and triggers ventricular pacing. In such cases, switch to VVI mode and eliminate the arrhythmia.

18035 0

The appearance of a deep wide Q wave is a classic sign of myocardial necrosis. The Q wave can be characterized as a wave - reflecting the absence of the R wave, that is, the local disappearance of endocardial or epicardial activation allows that the lead studying this or that area registers the negative part of the activation vector. The Q wave is a sign of irreversible necrosis, it becomes a constant element of the ECG after an acute episode (Table 1). However, it is likely that the mechanism of Q wave formation is more complex, as this wave may be transient during ischemia and may spontaneously disappear months or years after an acute coronary syndrome or surgical myocardial revascularization. Spontaneous disappearance of the Q wave is more common in inferior than in anterior infarcts.

Table 1

Diagnosis of myocardial infarction

Source (modified with permission): Thygesen K., Alpert J.S., White H.D., Joint ESC/ACCF/AHA/WHF Task Force for the redefinition of myocardial infarction. Universal definition of myocardial infarction // Eur. Heart J. - 2007. - Vol. 28. - P. 2525-2538.

Leads with a Q wave indicate an area of infarction, and ST segment elevation indicates an area of acute ischemia. According to this principle, MI can be classified into the following types: septal, anterior, inferior, lateral, inferolateral and posterolateral.

Inferior wall infarction most often accompanied by the appearance of a Q wave in leads III and aVF (Fig. 1), less often in lead II. The isolated presence of a Q wave in lead III is the least specific, but the presence of a wide and deep Q wave in lead aVF (≥40 ms and ≥25% of R wave amplitude) is a more significant sign of inferior MI. In some cases, a downstream septal activation vector will be seen as a small r wave in leads III and aVF, while a fully negative wave will be seen in lead II, confirming the diagnosis. It is not uncommon to find abnormal Q waves in leads V5-V6 in inferior MI, in which case the term “inferolateral MI” can be used (see Figure 1). Sometimes in leads V5 and V6, located relatively low, you can register changes above the lower wall.
Posterior wall infarction diagnosed in the presence of high R waves in leads V1-V2, as a reflection of the loss of the activation vector in the bulk of the posterior LV wall (see Fig. 1). Posterior MI is usually associated with inferior wall infarction and, if absent, must be differentiated from other causes of tall R waves in leads V1-V2, such as RV hypertrophy, positional changes (counterclockwise rotation), preexcitation, or RBBB.
Septal or anterior septal infarction recorded in the right precordial leads V1-V3, since the IVS, in fact, is the anterior wall of the left ventricle. Deep Q waves in these leads are considered diagnostic, but the presence of very small r waves (‹20 ms) in lead V2 may be an important feature in this regard. LV hypertrophy (see Fig. 2), LBBB (Fig. 2), and RV enlargement with clockwise rotation (see Fig. 1) can also be accompanied by the appearance of a Q wave or an rS complex in leads V1-V3, making it difficult in these cases of MI diagnosis.
Lateral and anterolateral infarction is determined in leads I and aVL, which register the potential of the upper and side walls of the left ventricle. Pathological Q waves in these leads serve as diagnostic features. The disappearance of the activation vector directed to the left and upwards can cause the electric axis to deviate to the right.
RV infarction is not accompanied by the appearance of a pathological Q wave on the ECG, but it often appears with infarcts of the lower wall. Diagnosis is based on the presence in the acute phase of ST-segment elevation in the right precordial leads (V4R), clinical low ejection syndrome, and increased RV pressure. Differential diagnosis should be made with acute cor pulmonale due to PE.

Abnormal Q waves may appear with hypertrophic cardiomyopathy, preexcitation, or LBBB. These states must be excluded, and not interpreted as an "old" (or current) MI. On the other hand, correlation data of biochemical markers and pathological changes in ECG data have shown that significant necrosis may not be accompanied by the presence of a Q wave, which has led to the definitions of "subendocardial", "non-transmural" or (most often) "non-Q" MI.

Rice. 1. Inferior posterior MI in a patient with VT. An enlarged image of the anatomy of the left ventricle and aorta, constructed by a computer-aided navigation system (NavX™), is superimposed on the torso image from the same angle to understand anatomical correlations. The color code reflects the time of activation (stimulated by the pancreas): red - early, blue and purple - later. The gray area surrounded by a yellow oval indicates an endocardial scar. Note the deep Q wave in leads II, III, aVF, V6 and the dominant R wave in leads V1-V2. The ST segment is slightly elevated in leads II, aVF, and V5-V6 (indicating past myocardial infarction), and there is T-wave inversion in the same leads (a sign of ischemia).

Rice. 2. ST-segment elevation in transmural ischemia in the presence of LBBB. Initial recording before ischemia. ST-segment elevation in leads II, III, aVF and accentuation of ST-segment depression in leads I and aVL (mirror image) in acute inferior wall MI

The combination of MI with BBB is a fairly common occurrence in cases where BBB was present before a heart attack, or in conduction disorders of ischemic origin.

With RBBB, the diagnostic criteria for MI are preserved, since with such a blockade, the activation vector does not change significantly. The response of the Q wave and the ST segment is the same as in patients with a normal QRS complex. In LBBB, the Q wave is uninterpretable, but ST-segment change can be a marker of acute transmural ischemia, especially in the inferior leads (see Figure 2). To confirm the ischemic nature of ST segment changes, it is necessary to record ECG data in dynamics. In patients with continuous electrical stimulation of the pancreas, transient ST changes are also significant for the diagnosis of acute MI.

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

Electrocardiography

Hypertrophy of the myocardium of the atria and ventricles of the heart develops in various diseases that cause chronic hemodynamic overload in the systemic and pulmonary circulation. This leads to an increase in muscle fibers and the entire mass of the myocardium of the heart, which in turn increases the electromotive force and deflects the increased vector of the heart towards the hypertrophied ventricle or atrium. In this regard, the corresponding R or P wave increases on the ECG. In addition, the hypertrophied section is excited for a longer time, and therefore the QRS complex or P wave is widened or deformed.

Left atrial hypertrophy. In the left atrium, excitation begins and ends later than in the right, therefore, when the total time of atrial excitation is increased and, accordingly, the width of the P wave is greater than the norm and is 0.11-0.15 s. Due to the increase in the electromotive force of the left atrium, the amplitude of the second (left atrial) phase of the P wave increases. The latter takes on a two-humped shape with a large second phase. Such a P wave is recorded in leads I, II, aVF or aVL. In the left chest leads, the P wave is double-humped, enlarged with approximately the same amplitude of both positive phases. In lead VI, the P wave is biphasic with a predominance of a deep and wide negative phase, which is a very common and reliable sign of left atrial hypertrophy.
Broadened two-humped prong P is usually called P-mitrale, since it is most often found on the ECG of patients with mitral heart disease.

Right atrial hypertrophy. Only with a large hypertrophy of the right atrium (with dystrophic and sclerotic changes in its myocardium), the width of the P wave can reach 0.11-0.13 s. In leads II, III, aVF, the P wave becomes high, sometimes with a pointed top, since the electromotive force of atrial excitation increases, and its duration remains the same. This form of tooth is called P-pulmonale, because it is most often observed from the limbs. The main sign of hypertrophy related to any of these types is a high R wave (above normal) in the lead, the axis of which is parallel to the electrical axis of the heart.

With horizontal position the electric axis has a high RI wave (RI > RII) and a pronounced S III wave, the amplitude of which is greater than the amplitude of the low r wave wave, with RaVF > SavF. One of the signs of left ventricular hypertrophy proposed by Sokolow and Lyon (1948) is RI amplitude >15 mm. Often the QRS complex widens (more than 0.1 s), and the ST segment will blend down from the isoline. The TI wave, aVL, sometimes the Tp wave become low isoelectric or negative. The negative T wave in left ventricular hypertrophy usually has an asymmetric shape, a sloping downward bend and a steep ascending one. The TaVR wave may be positive.

When the electrical axis deviates a high RI,avL wave (RaVL>11 mm) and a deep S and r wave are noted to the left. Often there is a widening of the QRS complex, a significant shift down from the isoelectric line of the S-TI, II, aVL segment and up from the isoline of the S-TIII, avF segment. The TI, II, aVL wave is low or negative, the TIII wave is positive.

Educational video of assessment of the P wave on the ECG in normal and pathological conditions

Table of contents of the topic "Identification of pathology of the heart on the ECG":

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

The general scheme for decoding the ECG is presented somewhat below.

Segments and teeth of a normal ECG.

Tooth R.

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.

Prong R.

S tooth.

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

Segment RS-T.

T wave.

Q-T Interval(QRST)

Analysis of the electrocardiogram.

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.

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.

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

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

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

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

Rhythm from the AV junction are 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 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.

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

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) measurement of P wave amplitude; 2) measurement of the duration of the P wave; 3) determination of the polarity of the P wave; 4) determination of the shape of the P wave.

IV.1) Analysis of the QRS complex includes: a) assessment of the Q wave: amplitude and comparison with 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) Atanalysis of 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 should: determine the polarity of T, evaluate its shape, measure the amplitude.

4) Q-T Interval Analysis: Duration measurement.

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;

Electrocardiogram for cardiac arrhythmias

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

1) Sinus tachycardia: increase in the number of heartbeats up to 90-160 (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: decrease in the number of heartbeats to 59-40 per minute (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) Syndrome of weakness of the sinoatrial node: 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 up to 140-250 per 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 up to 140-220 per minute while maintaining the correct rhythm; the presence in leads II, III and aVF of negative P′ waves located behind the QRS′ complexes or merging with them and not recorded on the ECG; normal unchanged ventricular QRS' complexes.

3) Ventricular paroxysmal tachycardia: suddenly starting and also suddenly ending attack of increased heart rate up to 140-220 per minute while maintaining the correct rhythm in most cases; deformation and 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 unaltered QRST complexes of sinus origin.

4. Atrial flutter: the presence on the ECG of frequent - up to 200-400 per minute - regular, similar atrial F waves, which have 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): absence in all leads of the P wave; 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 (up to 200-300 per minute) flutter waves, regular and identical in shape and amplitude, resembling a sinusoidal curve.

7. Flickering (fibrillation) of the ventricles: frequent (from 200 to 500 per minute), but irregular waves, differing 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 to 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: 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.

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 to 60-30 beats per 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 the leads from the limbs 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 block I, II or III degree; blockade of two branches of the bundle of His.

Electrocardiogram in atrial and ventricular hypertrophy.

1. Left atrial hypertrophy: 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, the P waves are high-amplitude, with a pointed apex (P-pulmonale); in leads V, the P wave (or at least its first, right atrial phase) is positive with a pointed apex (P-pulmonale); in leads I, aVL, V, the P wave is of low amplitude, and in aVL it may be negative (a non-permanent sign); the duration of the P waves does not exceed 0.10 s.

3. Left ventricular hypertrophy: an increase in the amplitude of the R and S waves. 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 of myocardial infarction characterized by rapid, within 1-2 days, the formation of a pathological Q wave or QS complex, displacement of the RS-T segment above the isoline and first positive and then 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 20-25th day. The RS-T segment is located on the isoline.

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

krasgmu.net

7.2.1. Myocardial hypertrophy

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

7.2.1.1. Left atrial hypertrophy

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

Rice. 6. ECG with left atrial hypertrophy

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

7.2.1.2. Right atrial hypertrophy

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

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

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

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

Hypertrophy of the right atrium is a sign of a change in the P wave in leads II, III, aVF, V1, V2.

7.2.1.3. Left ventricular hypertrophy

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

With ventricular hypertrophy, there are significantly more changes on the ECG than with atrial hypertrophy.

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

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

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

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

Deep S in leads V1, V2;

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

Shift of the S-T segment below the isoelectric line with a bulge upwards;

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

Rice. 8. ECG with left ventricular hypertrophy

Left ventricular hypertrophy is often observed in arterial hypertension, acromegaly, pheochromocytoma, as well as insufficiency of the mitral and aortic valves, congenital heart defects.

7.2.1.4. Right ventricular hypertrophy

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

Signs of hypertrophy (Fig. 9):

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

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

The height of the RV6 tooth is less than normal;

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

Deep S wave in lead V5 as well as V6;

S-T segment displacement below the isoline with a bulge upwards in the right III, aVF, V1 and V2;

Complete or incomplete blockade of the right leg of the bundle of His;

Shift of the transition zone to the left.

Rice. 9. ECG with right ventricular hypertrophy

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

7.2.2. Rhythm disturbances

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

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

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

Signs of normal sinus rhythm:

The frequency of the P waves is in the range from 60 to 90 (in 1 min);

The same duration of RR intervals;

Positive P wave in all leads except aVR.

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

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

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

7.2.2.1. Sinus tachycardia

Increased generation of impulses in the sinus node (more than 100 impulses per 1 min).

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

7.2.2.2. Sinus bradycardia

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

On the ECG, it is manifested by the presence of a regular P wave and a lengthening of the R-R interval.

It should be noted that at a rate of less than 30 bradycardia is not sinus.

As in the case of tachycardia and bradycardia, the patient is treated for the disease that caused the rhythm disturbance.

7.2.2.3. Irregular sinus rhythm

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

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

7.2.2.4. Idioventricular rhythm

Heterotopic arrhythmia, in which the pacemaker is either the legs of the bundle of His or Purkinje fibers.

Extremely severe pathology.

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

Occurs only in severe heart disease. A patient with such a disorder needs urgent care and is subject to immediate hospitalization in cardiological intensive care.

7.2.2.5. Extrasystole

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

Supraventricular (it is also called atrial) extrasystole is recorded on the ECG if the focus that causes extraordinary excitation (contraction) of the heart is located in the atria.

Ventricular extrasystole is recorded on the cardiogram during the formation of an ectopic focus in one of the ventricles.

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

We list the ECG signs of atrial extrasystole:

Changed in shape and amplitude P wave;

Shortened P-Q interval;

The prematurely registered QRS complex does not differ in shape from the normal (sinus) complex;

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

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

If an extrasystole is seen in a practically healthy person, then the treatment consists in prescribing valocordin, corvalol and ensuring complete rest.

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

Signs of ventricular extrasystole:

The P wave is absent;

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

Complete compensatory pause.

Ventricular extrasystole always indicates damage to the heart (CHD, myocarditis, endocarditis, heart attack, atherosclerosis).

With ventricular extrasystole with a frequency of 3-5 contractions per 1 min, antiarrhythmic therapy is mandatory.

Most often, intravenous lidocaine is administered, but other drugs can also be used. Treatment is carried out with careful ECG monitoring.

7.2.2.6. Paroxysmal tachycardia

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

With supraventricular tachycardia (in this case, impulses are formed in the atria or atrioventricular node), the correct rhythm is recorded on the ECG with a frequency of 180 to 220 contractions per 1 minute.

The QRS complexes are not changed or expanded.

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

Supraventricular tachycardia occurs in Wolff-Parkinson-White syndrome, less often in acute myocardial infarction.

The ventricular form of paroxysmal tachycardia is detected in patients with myocardial infarction, with coronary artery disease, and electrolyte disturbances.

7.2.2.7. Atrial fibrillation (atrial fibrillation)

A variety of supraventricular arrhythmias caused by asynchronous, uncoordinated electrical activity of the atria, followed by a deterioration in their contractile function. The flow of impulses is not conducted to the ventricles as a whole, and they contract irregularly.

This arrhythmia is one of the most common cardiac arrhythmias.

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

Signs of atrial fibrillation:

R-R intervals are different (arrhythmia);

P waves are absent;

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

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

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

7.2.2.8. atrial flutter

It is observed much less frequently than atrial fibrillation.

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

7.2.2.9. ventricular fibrillation

The most dangerous and severe violation of the rhythm, which quickly leads to circulatory arrest. It occurs with myocardial infarction, as well as in the terminal stages of various cardiovascular diseases in patients who are in a state of clinical death. Ventricular fibrillation requires immediate resuscitation.

Signs of ventricular fibrillation:

Absence of all teeth of the ventricular complex;

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

7.2.3. Conduction disorders

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

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

Sinoatrial III degree;

Atrioventricular I, II and III degrees;

Blockade of the right and left legs of the bundle of His.

7.2.3.1. Sinoatrial block III degree

Conduction disorder, in which the conduction of excitation from the sinus node to the atria is blocked. On a seemingly normal ECG, another contraction suddenly drops out (blocks), that is, the entire P-QRS-T complex (or 2-3 complexes at once). In their place, an isoline is recorded. Pathology is observed in those suffering from coronary artery disease, heart attack, cardiosclerosis, with the use of a number of drugs (for example, beta-blockers). Treatment consists in the treatment of the underlying disease and the use of atropine, izadrin and similar agents).

7.2.3.2. Atrioventricular block

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

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

Atrioventricular blockade II degree - incomplete blockade, in which not all impulses coming from the sinus node reach the ventricular myocardium.

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

Signs of blockade type Mobitz-1:

Constantly lengthening interval P

Due to the first sign, at some stage after the P wave, the QRS complex disappears.

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

Atrioventricular blockade of the III degree - a condition in which not a single impulse coming from the sinus node is conducted to the ventricles. On the ECG, two types of rhythm are recorded that are not interconnected; the work of the ventricles (QRS complexes) and the atria (P waves) is not coordinated.

Blockade of the III degree is often found in cardiosclerosis, myocardial infarction, improper use of cardiac glycosides. The presence of this type of blockade in a patient is an indication for his urgent hospitalization in a cardiological hospital. Treatment is with atropine, ephedrine, and, in some cases, prednisolone.

7.2.3.3. Blockade of the legs of the bundle of His

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

With the blockade of the right or left legs of the bundle of His, the path of the impulse changes and therefore the excitation of the corresponding ventricle is delayed.

It is also possible the occurrence of incomplete blockades and the so-called blockades of the anterior and posterior branches of the bundle of His bundle.

Signs of a complete blockade of the right leg of the bundle of His (Fig. 10):

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

Negative T wave in leads V1 and V2;

S-T segment offset from the isoline;

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

Rice. 10. ECG with complete blockade of the right leg of the bundle of His

Signs of a complete blockade of the left leg of the bundle of His:

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

Offset of the S-T segment from the isoline;

Negative T wave in leads V5 and V6;

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

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

These types of blockades are found in heart injuries, acute myocardial infarction, atherosclerotic and myocardial cardiosclerosis, with the incorrect use of a number of medications (cardiac glycosides, novocainamide).

Patients with intraventricular blockade do not need special therapy. They are hospitalized to treat the disease that caused the blockade.

7.2.4. Wolff-Parkinson-White Syndrome

For the first time such a syndrome (WPW) was described by the above-mentioned authors in 1930 as a form of supraventricular tachycardia, which is observed in young healthy people (“functional blockade of the bundle of His bundle”).

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

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

Signs of WPW syndrome type A:

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

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

Signs of WPW syndrome type B:

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

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

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

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

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

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

7.2.5. Early ventricular repolarization

This phenomenon occurs in 20% of patients with cardiovascular pathology (most often occurs in patients with supraventricular arrhythmias).

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

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

ST segment elevation;

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

High amplitude teeth;

Double-humped P wave of normal duration and amplitude;

Shortening of PR and QT intervals;

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

Rice. 11. ECG in early ventricular repolarization syndrome

7.2.6. Cardiac ischemia

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

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

These include:

Reducing the amplitude of the R wave;

S-T segment depression;

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

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

7.2.7. angina pectoris

With the development of an angina attack on the ECG, it is possible to detect a shift in the ST segment and changes in the T wave in those leads that are located above the zone with impaired blood supply (Fig. 12).

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

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

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

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

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

The occurrence of angina pectoris is accompanied by the appearance of typical pain behind the sternum, usually provoked by physical activity. This pain is of a pressing nature, lasts for several minutes and disappears after the use of nitroglycerin. If the pain lasts more than 30 minutes and is not relieved by taking nitropreparations, acute focal changes can be assumed with a high probability.

Emergency care for angina pectoris is to relieve pain and prevent recurrent attacks.

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

7.2.8. myocardial infarction

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

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

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

Options QS, QrS are possible. S-T shift (Fig. 13) and T wave inversion are observed.

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

Sometimes there is a shift in S-T without the presence of a pathological Q wave (small-focal myocardial infarction). Signs of a heart attack:

Pathological Q wave in leads located above the infarction area;

Displacement by an arc upward (rise) of the ST segment relative to the isoline in leads located above the infarction area;

Discordant shift below the isoline of the ST segment in leads opposite to the area of infarction;

Negative T wave in leads located above the infarction area.

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

There are four stages in the development of myocardial infarction:

Acute;

subacute;

Scarring stage.

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

Rice. 14. The sequence of ECG changes in myocardial infarction: 1 - Q-infarction; 2 - not Q-infarction; A - the most acute stage; B - acute stage; B - subacute stage; D - cicatricial stage (post-infarction cardiosclerosis)

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

The subacute stage of infarction lasts for 1–3 months and is characterized by cicatricial organization of the focus of necrosis. On the ECG at this time, the ST segment gradually returns to the isoline, the Q wave decreases, and the R amplitude, on the contrary, increases.

The T wave remains negative.

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

Such staging is often referred to as the regular ECG dynamics in myocardial infarction.

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

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

Table 6. Localization of myocardial infarction

Great difficulties arise in the diagnosis of re-infarction, when new changes are superimposed on an already changed ECG. Helps dynamic control with the removal of the cardiogram at short intervals.

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

There are also atypical forms of a heart attack:

Abdominal (pain in the heart and abdomen);

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

Arrhythmic (cardiac pain and rhythm disturbances);

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

Painless.

Treating a heart attack is a very difficult task. It is usually the more difficult, the greater the prevalence of the lesion. At the same time, according to the apt remark of one of the Russian zemstvo doctors, sometimes the treatment of an extremely severe heart attack goes unexpectedly smoothly, and sometimes an uncomplicated, simple micro-infarction makes the doctor sign his impotence.

Emergency care consists in stopping pain (narcotic and other analgesics are used for this), also eliminating fears and psycho-emotional arousal with the help of sedatives, reducing the infarct zone (using heparin), and eliminating other symptoms in turn, depending on the degree of their danger.

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

The final stage is a long-term observation in the clinic at the place of residence.

7.2.9. Syndromes in electrolyte disorders

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

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

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

The most well-studied changes in the ECG in violation of the exchange of potassium, as well as calcium (Fig. 15).

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

7.2.9.1. Hyperkalemia

Signs of hyperkalemia:

High pointed T wave;

Shortening of the Q-T interval;

Reducing the amplitude of R.

With severe hyperkalemia, intraventricular conduction disturbances are observed.

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

7.2.9.2. hypokalemia

Signs of hypokalemia:

Decrease in the S-T segment from top to bottom;

Negative or two-phase T;

The appearance of U.

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

Hypokalemia occurs with the loss of potassium salts in patients with severe vomiting, diarrhea, after prolonged use of diuretic, steroid hormones, with a number of endocrine diseases.

Treatment consists in replenishing the deficiency of potassium in the body.

7.2.9.3. Hypercalcemia

Signs of hypercalcemia:

Shortening of the Q-T interval;

Shortening of the S-T segment;

Expansion of the ventricular complex;

Rhythm disturbances with a significant increase in calcium.

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

7.2.9.4. hypocalcemia

Signs of hypocalcemia:

Increase in the duration of the Q-T interval;

S-T segment lengthening;

Decreased amplitude of T.

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

7.2.9.5. Glycoside intoxication

Cardiac glycosides have long been successfully used in the treatment of heart failure. These funds are indispensable. Their intake contributes to a decrease in heart rate (heart rate), more vigorous expulsion of blood during systole. As a result, hemodynamic parameters improve and manifestations of circulatory insufficiency decrease.

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

Rice. 16. ECG with an overdose of cardiac glycosides

Signs of glycoside intoxication:

Decreased heart rate;

Shortening of the electrical systole;

Decrease in the S-T segment from top to bottom;

Negative T wave;

Ventricular extrasystoles.

Severe intoxication with glycosides requires discontinuation of the drug and the appointment of potassium preparations, lidocaine and beta-blockers.

www.dom-spravka.info

Spanish Fly for two - how they affect libido in women and men

Contents Biologically active additive based on an extract obtained from a beetle with a fly (or fly...
Diet of Ekaterina Mirimanova: menu for every day in detail

Ekaterina MirimanovaSystem minus 60. Revolution System minus 60 with Ekaterina Mirimanova"System minus 60. Revolution"...
What can unpleasant bloating and heaviness in the stomach indicate?

Heaviness and bloating are the causes of both ordinary overeating and more serious problems with the digestive tract....
What are the features of the second positive blood group

The second blood type, Rh-negative, appeared many years ago, when a person stopped being a hunter, and ...
Psychology of anorexia Psychology of anorexia

PSYCHOLOGICAL ASPECTS OF THE PHENOMENON OF ANOREXIA (EXPERIMENTAL STUDY) T. V. Tarasova, E. V. Arsent'eva V...
red circles under eyes red circles under eyes

Contents Due to the fact that the skin in this area is thin, it is more prone to the appearance of various kinds of spots. Redness under...

2021-09-08 10:32:39

Vasileostrovskaya station was opened without a canopy Vasileostrovskaya after

vseslav Sat, 10/17/2015 - 20:50 Vasileostrovskaya station is one of the oldest stations...
2021-08-29 00:19:31

Is it possible to eat goat mushroom

Most often, the goat mushroom (Suillus bovinus) is referred to in the everyday speech of mushroom pickers as a goat. This tubular...

2021-08-09 19:46:08

Why dream of a fish in water

Every person has had dreams at least once in their life. Many do not attach any importance to them, but some ...
2021-07-30 05:58:40

History of moon exploration

Daedalus (crater). Diameter: 93 km Depth: 3 km (NASA photo) The moon has attracted people's attention since ancient times. In II...

2021-07-20 02:27:11

Weird facts about US presidents Franklin Pierce knocked down an old woman and got away with it

The United States celebrates President's Day on the third Monday in February. Until the 70s, the celebrations were timed to...
2021-07-20 02:27:11

Wishes for the last call to graduates in prose

On the day of the last call, I want to say just one word to my beloved head teacher: “Thank you.” But how much is...

2021-07-20 02:27:11

Are watermelon seeds healthy?

Watermelon is considered a tasty and healthy berry, its seeds are especially useful. Small, dark brown or...
2021-07-10 01:01:20

The development of coherent speech in older preschoolers

“The development of speech in children of 6 years old” A child is not born with an established speech. It is not possible to give a definitive answer to...

2021-07-10 01:01:20
What is the semantic core of a blog

What is the semantic core of the site? The semantic core of the site (hereinafter referred to as SN) is a set ...
2021-07-10 01:01:20
How to clear the cache in Mozilla Firefox - Step by step instructions!

Many Mozilla Firefox users accumulate quite a large browsing history over time...
2021-07-10 01:01:20
Why you can get banned in Yandex, fall under the Ags or foot filter, as well as ways to get out of these sanctions

07/09/2014 Today we will briefly talk about the AGS-40 filter (by the way, named after a grenade launcher), which ...
2021-07-10 01:01:20
The best ways to get subscribers to the VKontakte group

5 votes Good day, dear readers of my blog. The promoted Vkontakte group can ...
2021-06-29 01:28:57
Eight top-secret planes that are easily confused with UFOs Strong and directional signals

Sturgeon is a real delicacy, from which you can cook many delicious dishes! Find out interesting...
2021-06-18 09:05:42
How to play with a friend in Minecraft single player?

To play the Minecraft computer game with your friend, you can choose any convenient way for yourself, ...
18.06.2021
How to play together in "minecraft" on a local network or via the Internet

A new game is always great opportunities and bright emotions. Very cool to install it and go to the end, ...

08.06.2021

Russia for the first time was included in the rating of "fattest countries"

Although obesity in itself is not a specific disease, it becomes a breeding ground for ...
08.06.2021

What happens if a girl eats a lot of parsley

Parsley is a green plant with a spicy and rich aroma. The most common...

How to decipher an electrocardiogram?

What is a cardiogram?

What do the teeth on the result mean?

What are false interferences on the cardiogram that are not associated with heart pathologies?

Krasnoyarsk medical portal Krasgmu.net

Normal electrocardiogram

Segments and teeth of a normal ECG.

Tooth R.

P-Q(R) interval.

Ventricular QRST complex.

Q wave.

Prong R.

S tooth.

Segment RS-T.

T wave.

Q-T Interval(QRST)

Analysis of the electrocardiogram.

General scheme (plan) of ECG decoding.

Six-axis Bailey system.

Electrocardiogram for cardiac arrhythmias

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

2. Extrasystole.

Electrocardiogram for violations of the conduction function.

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

Electrocardiogram in atrial and ventricular hypertrophy.

Electrocardiogram in ischemic heart disease.

What state of the myocardium does the R wave reflect on the ECG results?

Why is an electrocardiogram performed?

What does the ECG show

Detailed interpretation of the electrocardiogram

Definition of the axis of the heart

Possible research errors

General ECG decoding scheme

Electrocardiogram (ECG of the heart). Part 2 of 3: ECG Transcription Plan

Elements of a normal ECG

Waves of the QRS complex

ECG analysis

ECG interference

Brief description of ECG elements

T wave values

T wave changes

Causes of a negative T-wave

What state of the myocardium does the R wave reflect on the ECG results?

Why is an electrocardiogram performed?

What does the ECG show

Detailed interpretation of the electrocardiogram

Definition of the axis of the heart

Possible research errors

ECG elements in normal and pathological conditions

ECG interpretation: P wave

What is junctional rhythm, negative P wave

When is junctional rhythm observed?

Diagnosis of nodal heart rhythm

negative p wave on ecg

Popular articles on the topic: negative p wave on ecg

Questions and answers on: negative p wave on ecg

Negative p wave on ecg

Educational video of assessment of the P wave on the ECG in normal and pathological conditions

Segments and teeth of a normal ECG.

Tooth R.

P-Q(R) interval.

Ventricular QRST complex.

Q wave.

Prong R.

S tooth.

Segment RS-T.

T wave.

Q-T Interval(QRST)

Analysis of the electrocardiogram.

Six-axis Bailey system.

Electrocardiogram for cardiac arrhythmias

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

2. Extrasystole.

Electrocardiogram for violations of the conduction function.

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

Electrocardiogram in atrial and ventricular hypertrophy.

Electrocardiogram in ischemic heart disease.

Random articles

Advertising

Low hemoglobin