What is CLC syndrome? Chatelier syndrome ecg How does chatelier syndrome manifest on ecg

The operation of a pacemaker significantly changes the picture of the electrocardiogram (ECG). At the same time, a working stimulator changes the shape of the complexes on the ECG in such a way that it becomes impossible to judge anything from them.

In particular, the work of the stimulator can mask ischemic changes and myocardial infarction. On the other hand, since modern stimulators work “on demand”, the absence of signs of the stimulator on the electrocardiogram does not mean that it is broken. Although there are often cases when nursing staff, and sometimes doctors, without proper grounds, tell the patient “your stimulator is not working,” which greatly irritates the patient. In addition, the long-term presence of right ventricular stimulation also changes the shape of its own ECG complexes, sometimes simulating ischemic changes. This phenomenon is called “Chaterje syndrome” (more correctly, Chatterjee, named after the famous cardiologist Kanu Chatterjee).

Rice. 77. Artificial heart rate driver, heart rate = 75 per 1 min. The P wave is not detected; each ventricular complex is preceded by a pacemaker impulse. The ventricular complexes in all leads are deformed according to the type of blockade of the left bundle branch of His, i.e. excitation is imposed through the apex of the right ventricle.

Thus: interpretation of an ECG in the presence of a pacemaker is difficult and requires special training; if acute cardiac pathology (ischemia, heart attack) is suspected, their presence/absence should be confirmed by other methods (usually laboratory). The criterion for correct/incorrect operation of the stimulator is often not a regular ECG, but a test with a programmer and, in some cases, daily ECG monitoring.

Electrocardiographic syndromes and phenomena

I. Goethe: “Man sees only what he knows.” This expression of the German poet fits medical science perfectly. Medicine, being an inexact science, often relies on the intuitive-empirical component of the doctor’s knowledge. A medical diagnosis is not always postulated unambiguously; it is often probabilistic in nature. Electrocardiography is an example instrumental diagnostics, characterized by low specificity in many clinical situations, which leads to discrepancies in the interpretation of electrocardiograms. In such ambiguous situations, it should be considered optimal syndromic approach, allowing you to “model” treatment tactics even before nosological diagnosis. As is known, a syndrome is a set of symptoms united by a common etiology. In addition, the concept should be highlighted phenomenon, literally meaning - rare, unusual occurrence . In ECG diagnostics, the phenomenon forces the doctor to pay attention to a fact that makes it possible to assert with a high probability the presence of a cause-and-effect relationship. However, the ECG syndrome, like the ECG phenomenon, must be known by sight. This is what this section is dedicated to.

Koechker syndrome is a reversion of negative T waves in patients with acute myocardial infarction, as a manifestation of false-negative ECG dynamics.

Koechker syndrome occurs on the 2-5th day of myocardial infarction; is not associated with rethrombosis and the appearance (intensification) of clinical signs of left ventricular failure. In other words, this is not a relapse myocardial infarction. The duration of Koechker syndrome, as a rule, does not exceed 3 days. Subsequently, the ECG picture returns to its original one: the T wave becomes negative or isoelectric. The reasons for this ECG pattern are unknown. I am impressed by the point of view that it is a manifestation of episthenocarditis pericarditis; however, characteristic pericardial pain is not observed with this syndrome. Correct interpretation of Koechker's syndrome avoids unnecessary medical interventions: thrombolysis or PCI. Prevalence:

1 in 50 cases of myocardial infarction.

Chaterrier's phenomenon (synonym: memory phenomenon) is nonspecific changes in the final part of the ventricular complex (mainly the T wave) in spontaneous contractions, appearing during prolonged artificial (artificial) right ventricular stimulation.

Artificial stimulation of the ventricles is accompanied by a violation of the geometry of their contraction. With more or less long-term stimulation (from 2-3 months), changes in the QRS complex may appear in spontaneous contractions in the form of negative T waves in many ECG leads. Such dynamics simulate ischemic changes. On the other hand, in the presence of truly angina-like pain, this phenomenon makes it almost impossible to diagnose small-focal myocardial infarction. Correct interpretation of the Shaterrier phenomenon allows one to avoid unnecessary hospitalizations and unjustified medical interventions.

It is important to understand that the Shaterier phenomenon can appear not only against the background of prolonged artificial stimulation of the heart - this is the main reason, but not the only one. With chronic blockade of the bundle branch, with frequent ventricular extrasystole or with the WPW phenomenon, the final part of the ventricular complex in normal contractions can also change - negative or low-amplitude T waves are formed.

Thus, any long-term disturbances in the geometry of ventricular contraction due to abnormal conduction of the intraventricular impulse may be accompanied by the Shaterrier phenomenon.

VT1 ˃ VT6 syndrome. It was noticed that on the ECG healthy people the amplitude of the T wave in V6 is always approximately 1.5-2 times greater than the amplitude of the T wave in V1. Moreover, the polarity of the T wave in V1 does not matter. A violation of this relationship, when the amplitudes of the T waves in V1 and V6 “even out” or the T in V1 exceeds the T in V 6, is a deviation from the norm. This syndrome is most often observed when hypertension(sometimes this is the earliest sign of LV myocardial hypertrophy) and with various clinical forms IHD. It may also be an early sign of digitalis intoxication.

The clinical significance of this syndrome: allows one to suspect an “abnormality” and, if necessary, continue the diagnostic search “from simple to complex.”

Syndrome of insufficient growth of the R wave from V1 to V3. In most cases, the amplitude of the R wave in the “right” chest leads increases, and by lead V3 it reaches at least 3 mm. In situations where the amplitude of the R wave in V3 is less than 3 mm, it is reasonable to talk about the syndrome of insufficient growth of the R wave from V1 to V3. This syndrome can be divided into 2 categories:

1. There are no other abnormalities on the ECG.

Variant of the norm (more often with a hypersthenic constitution),

Sign of LV myocardial hypertrophy,

Incorrect placement of chest electrodes (V1-V3) on the intercostal space above.

2. There are other abnormalities on the ECG.

Typical for the following clinical situations:

Myocardial infarction in progress (in this case there will be ECG dynamics characteristic of a heart attack in leads V1 - V3),

Severe LV myocardial hypertrophy with other ECG criteria for hypertrophy,

Blockade of the LBP (complete or incomplete), blockade of the anterior branch of the LBP,

S-type of right ventricular hypertrophy (rare).

Difficulty in interpreting the syndrome of insufficient growth of the R wave from V1 to V3 arises, as a rule, if it is diagnosed as an independent, asymptomatic ECG pattern, and there are no other ECG abnormalities. With correctly applied chest electrodes and the absence of any cardiac history, its main cause is moderate hypertrophy of the LV myocardium.

The short-long-short phenomenon. As you know, premature contraction of the heart is called extrasystole. Extra excitation coupling interval is shorter ( short) interval between main contractions. This is followed by a compensatory pause ( long), which is accompanied by a prolongation of cardiac refractoriness and an increase in its dispersion (refractoriness dispersion). In this connection, immediately after a post-extrasystolic sinus contraction, there is a possibility of another extrasystole ( short) - the “product” of refractoriness dispersion. Mechanism of “repeated” extrasystole: re-enrty or early post-depolarization. Examples:

The short-long-short phenomenon in a patient with functional brady-dependent extrasystole, which in this case does not have any particular clinical significance:

The short-long-short phenomenon in a patient with severe sleep apnea syndrome, obesity and stage 3 hypertension. As we can see, after a compensatory pause, a paired polymorphic ventricular extrasystole appeared. In this patient, the short-long-short phenomenon can trigger polymorphic ventricular tachycardia and lead to sudden death:

The short-long-short phenomenon in a patient with long QT syndrome: triggering of VT of the “pirouette” type. Sometimes, with this syndrome, the short-long-short phenomenon is a prerequisite for the initiation of ventricular tachyarrhythmia:

In patients with functional extrasystole, the short-long-short phenomenon has no clinical significance; it only “facilitates” the occurrence of brady-dependent extrasystole. In patients with severe organic heart disease and channelopathies, this phenomenon can trigger life-threatening ventricular arrhythmias.

The phenomenon of "gap" in conduction. This term refers to a period in the cardiac cycle during which conduction of a premature impulse becomes impossible (or slowed), although impulses with less premature impulses are conducted. Differences in refractoriness at different levels of the cardiac conduction system provide the electrophysiological basis for this phenomenon.

On the first ECG we see an early atrial extrasystole carried out to the ventricles without aberration. On the second ECG, the coupling interval of the atrial extrasystole is longer, but the extrasystole is conducted to the ventricles with a delay (aberration).

Mostly, the “gap” phenomenon is encountered by specialists performing cardiac electrophysiology.

Ashman's phenomenon is a short-cycle aberration (3rd phase block) that occurs when the refractory period of the AV junction increases, due to a sudden prolongation of the interval between two previous contractions. The longer the interval between contractions, the higher the likelihood of aberrant conduction (or blocking) of the next supraventricular impulse.

A classic example of the Ashman phenomenon in atrial fibrillation:

Ashman's phenomenon, which arose after a post-extrasystolic compensatory pause:

Blocking of atrial extrasystole that occurs after spontaneous prolongation of the interval between sinus contractions:

Clinical significance of the Ashman phenomenon: its correct interpretation allows one to avoid overdiagnosis of a) ventricular extrasystole and b) organic disorders conduction at the AV junction.

The stop-and-restart phenomenon is a continuously relapsing course of paroxysmal atrial fibrillation, when after the end of one attack, after 1-2 sinus contractions, a new paroxysm starts.

Characteristic of vagus-dependent atrial fibrillation. On the one hand, the phenomenon reflects the high ectopic activity of the muscular couplings of the pulmonary veins, on the other hand, the high profibrillatory readiness of the atrial myocardium.

The phenomenon of hidden ventriculoatrial conduction. In addition to retrograde excitation of the atria, there is a possibility of penetration of the ventricular impulse into the AV junction to varying depths with its discharge (prolongation of refractoriness, blockade). As a result, subsequent supraventricular impulses (usually 1 to 3) will be delayed (aberrated) or blocked.

Hidden VA conduction due to PVCs, leading to stage 1 functional AV block:

Hidden VA conduction due to PVCs, leading to stage 2 functional AV block:

Hidden VA conduction due to PVCs, accompanied by a post-positioned (displaced) compensatory pause:

Clinical significance of hidden AV conduction: correct interpretation of this phenomenon allows us to distinguish between functional AV blockades and organic ones.

D association of the AV node. In most people, the AV node is homogeneous. In some, the AV node is electrophysiologically divided into a fast and slow conduction zone (dissociated). If a person is subjectively healthy, this phenomenon has no clinical significance. However, in some patients, dissociation of the AV node is accompanied by the development of paroxysms of nodal reciprocal AV tachycardia. The trigger for tachycardia is the supraventricular extrasystole, which is carried out along the fast path, and moves only retrograde along the slow path - the re-entry loop is closed. The phenomenon of AV node dissociation is reliably established by cardiac electrophysiology. At the same time, on regular ECG Sometimes you can find signs of dissociative illness.

Let's consider the following clinical case. A 30-year-old female patient complains of attacks of unmotivated palpitations. Daily ECG monitoring was performed.

Fragment of an ECG - normal variant:

ECG fragment - 1st stage AV block. against the background of sinus tachycardia - absolutely not typical for the norm:

ECG fragment - 2nd stage AV block, type 1. Note the “rapid” lengthening of the P-R interval followed by loss of the ventricular wave:

A sudden increase in the P-R interval by more than 80 ms makes one think about the dissociation of the AV node into zones with different impulse conduction speeds. This is what we see in this example. Subsequently, the patient underwent cardiac electrophysiology: AV nodal reciprocal tachycardia was verified. Ablation of the slow pathway of the AV node was performed with good clinical effect.

Thus, signs of AV node dissociation on a surface ECG (alternation of normal and extended P-R intervals; a one-time increase in the P-R interval in the Wenckebach period by more than 80 ms) in combination with an arrhythmic history make it possible to establish a diagnosis with a high probability even before cardiac electrophysiology.

The phenomenon of extrasystole from the Kent bundle. Despite the seemingly incredible nature of this phenomenon, it is not so rare. The Kent bundle not only serves as an additional pathway for conducting impulses from the atria to the ventricles, but is also capable of automaticity (spontaneous diastolic depolarization). Extrasystole from the Kent bundle can be suspected when signs of the WPW phenomenon are combined on the ECG with late diastolic ectopia, simulating ventricular extrasystole. In this case, the widened ventricular complex represents a continuous delta wave.

Consider the following clinical example. A 42-year-old woman complained of attacks of unmotivated palpitations. Two-day ECG monitoring was performed. On the first day of the study, about 500 “widened” ventricular complexes were recorded, appearing in late diastole and disappearing with increased heart rate. At first glance, a harmless functional ventricular extrasystole. However, late diastolic ventricular extrasystole, being calcium-dependent, mainly appears against the background of tachysystole or immediately after its end. In this case, late ventricular complexes are recorded when normal frequency heart rate and bradycardia, which in itself is strange.

The situation became completely clear on the second day of monitoring, when signs of intermittent ventricular preexitation appeared. It became clear that late-diastolic ventricular complexes are nothing more than extrasystole from the Kent bundle.

Clinical significance of extrasystole from the Kent bundle: correct interpretation of this phenomenon allows us to exclude the diagnosis of ventricular extrasystole and direct the diagnostic and treatment process in the necessary direction.

The phenomenon of hidden atrioventricular conduction. It is observed with supraventricular tachyarrhythmias, especially with atrial fibrillation. The essence of the phenomenon is that supraventricular impulses, arriving frequently and irregularly at the AV junction, penetrate it to different depths; discharge it without reaching the ventricles. As a result, 1) the conduction of subsequent supraventricular impulses slows down, 2) the replacement ectopic impulse slows down (drops out).

On a surface ECG, the phenomenon of hidden AV conduction can be indicated based on the following signs:

Alternation of short and long R - R intervals in atrial fibrillation:

Absence of escape complexes with excessively long R-R intervals in atrial fibrillation:

Absence of escape complexes during a multi-second pause when sinus rhythm is restored:

When regular atrial flutter transitions to irregular or atrial fibrillation:

Clinical significance of the phenomenon of hidden AV conduction: has mainly academic significance, allowing you to “understand the unknown.”

The phenomenon of stem extrasystole. Extrasystole from the distal parts of the AV junction (trunk of the His bundle) is a type of ventricular extrasystole and is called “trunk”. I designate this type of extrasystole as an arrhythmic phenomenon, firstly, due to its relative rarity, secondly, due to its external similarity with typical parietal ventricular extrasystole, and thirdly, due to its refractoriness to traditional antiarrhythmic drugs.

Clinical and electrocardiographic signs of truncal extrasystole: 1) the QRS complex often has a supraventricular appearance, or is slightly widened due to sporadic aberration or due to the proximity to the proximal part of one of the bundle branches; 2) retrograde activation of the atria is not typical; 3) the coupling interval is variable, since the brainstem localization of the extrasystolic focus suggests calcium-dependent depolarization - that is, abnormal automatism; 4) absolute refractory to class I and III antiarrhythmics.

With truncal extrasystole good clinical effect can only be obtained with long-term use of class II or IV antiarrhythmic drugs.

The phenomenon of supernormal conductivity is the conduction of an impulse instead of its expected blockade (aberration).

Probable mechanism: the atrial impulse caught the LAP in its supernormal phase.

Probable mechanism: the magnitude of the spontaneous diastolic potential in the His-Purkinje system is maximum immediately after the end of repolarization of “sinus” contractions (in our case they are expanded due to LBP blockade), therefore early atrial impulses have the greatest chance of “normal” conduction.

Example #3 (reverse Ashman phenomenon):

Probable mechanism: the phenomenon of a “gap” (failure) in conduction; shortening of refractoriness when the length of the previous cycle changes.

The phenomenon of sinus pause. Sudden sinus pauses on an ECG cannot always be interpreted unambiguously. Sometimes, for the correct interpretation of the phenomenon, in addition to a thorough analysis of the cardiogram itself, a comprehensive clinical and anamnestic assessment is necessary. Examples:

Pauses during sinus arrhythmia can be so pronounced that there is a misconception about the presence of SA blockade. It must be remembered that sinus arrhythmia is asymptomatic; typical mainly for young and middle-aged people, including subjectively healthy people; appears (intensifies) with bradycardia (usually at night); the pauses themselves are never too long, without thereby provoking the appearance of slipping complexes; cardioneurotic symptoms are a common clinical satellite.

2nd degree sinoatrial block:

It is necessary to find out what type of blockade: 1st or 2nd. This is a fundamental question, since the prognosis is different. SA blockade, stage 2, type 1, often occurs at rest (especially at night) in young healthy individuals; in classical cases, clinically and electrocardiographically it is preceded by Wenkibach's periodicals; as a rule, the pause length does not exceed twice the R-R interval of the previous contractions; the presence of slipping complexes is not typical; There is no history of syncope.

SA blockade, stage 2, type 2, appears suddenly without Wenkibach periodicity; there is often concomitant organic myocardial damage, detected instrumentally; in older people, without obvious changes in the heart during ECHO, the main cause is cardiosclerosis; the pause may be longer than twice the R-R interval of the previous contractions; slipping complexes often occur; Syncopal history or equivalent is typical.

Blocked atrial extrasystole:

As a rule, it causes difficulties in diagnosis only if the number of blocked extrasystoles is small, and the number of ordinary (unblocked) ones does not exceed the statistical norm - this dulls the doctor’s vigilance. Elementary care when analyzing the ECG will allow you to reliably verify a blocked atrial extrasystole. In my experience, an extremely early blocked ectopic P wave always deforms the T wave to some extent, which makes possible diagnostics of this phenomenon without EPI.

Hidden stem extrasystole:

Mentioning hidden extrasystole in this section, I pay tribute to the extreme unusualness of this phenomenon. We are talking about stem extrasystole, the conduction of which is blocked antero- and retrogradely. Thus, it is not visible on a surface ECG. Its diagnosis is possible only with His bundle electrocardiography. In the above figure, the stem extrasystole is provoked artificially: stimulus S. As we can see, S stimuli do not extend beyond the AV junction and are therefore not visible on the ECG. The third imposed stimulus causes transient 2nd degree AV block (“false” AV block). On an external ECG, a hidden brainstem extrasystole can be suspected if there is a combination of normal (wired) AV extrasystoles and sudden cardiac pauses like 2nd degree AV block.

The phenomenon of brady-dependent blockade (long cycle aberration, phase IV). Aberration with increasing prematurity does not surprise anyone - since it is associated with a rapid increase in heart rate, when refractoriness in the conduction system has not yet had time to shorten. The aberration looks much more unusual when the heart rate slows down, when it would seem that the refractory period is obviously over.

The basis for long cycle aberration is the ability of cells of the His-Purkinje system to spontaneous diastolic depolarization. Therefore, if there is a pause in the work of the heart, the membrane potential in some parts of the conduction system of the heart can reach the value of the resting potential (“critical hypopolarization”), which slows down or makes it impossible to conduct the next impulse. It is necessary to understand that such a situation almost always reflects an organic pathology of the conduction system, when initially the cells of the AV junction are in a state of hypopolarization (low value of the maximum diastolic potential). The phenomenon of brady-dependent blockade is not typical for a healthy heart and often precedes more severe conduction disorders.

The phenomenon of superfrequency suppression (“overdrive suppression”) literally means: suppression of pacemakers by more frequent impulses. This phenomenon is based on the hyperpolarization of automatic cells due to the fact that they undergo activation more frequent than their own excitation frequency. We can observe this physiological phenomenon on the ECG of any healthy person, when the sinus node subjugates all lower-level pacemakers. The higher the sinus rhythm frequency, the lower the likelihood of heterotopic impulses, including extrasystole. On the other hand, if the frequency of impulses of the ectopic focus exceeds the automaticity of the sinus node, then the sinus node itself will undergo superfrequency suppression. The latter fact often attracts medical attention, since the pause after restoration of sinus rhythm may be excessively long. For example:

With EPI, sinus node dysfunction is detected through the “overdrive suppression” phenomenon.

The phenomenon of early extrasystolic contraction. Early is called ventricular extrasystole type R on T and atrial extrasystole type P on T.

With all the likelihood of the appearance of such extrasystoles in a healthy person (especially atrial ones), it must be remembered that the shorter the prematureness of extraexcitation, the less typical it is for normal myocardium. Therefore, when encountering an early extrasystole for the first time, it is necessary to clinically and instrumentally assess the presence of variance in myocardial refractoriness - that is, the likelihood of triggering a tachyarrhythmia through an extrasystole. Early atrial extrasystole, originating from the muscular couplings of the mouths of the pulmonary veins, often begins to be detected in middle-aged people. Most often, it manifests itself through a reflex mechanism as part of an extracardiac disease due to an incorrect lifestyle. And if the cause of the arrhythmia is not eliminated, then sooner or later early atrial extrasystole begins to trigger atrial fibrillation. A combination of early atrial extrasystole, left atrial dilatation and hypertension (or latent arterial hypertension) is the most reliable clinical predictor of future atrial tachyarrhythmia. In elderly people, early atrial extrasystole is recorded in most cases.

Much greater responsibility falls on the shoulders of the doctor in the clinical analysis of early ventricular extrasystole - since life-threatening ventricular rhythm disturbances are almost always initiated by the R on T phenomenon. In a healthy person, early ventricular extrasystole can be recorded only against the background of a rapid rhythm; when it slows down, it becomes mid-diastolic:

An isolated R on T phenomenon against the background of normo- or bradycardia is always suspicious regarding its special electrophysiological origin: early afterdepolarization. As is known, in healthy myocardium there are no conditions for early post-depolarizations (especially in ventricular myocardium). Therefore, if the obvious causes of early ventricular extrasystole in the form of acute or chronic organic damage myocardium are rejected, it is necessary to exclude others - congenital ones. Let me remind you that with so-called electrical heart disease, early ventricular extrasystole can be the only manifestation of a hidden pathology for a long time.

U wave phenomenon on the ECG. There is still no consensus regarding the origin of the U wave. The question of its clinical significance remains debatable. There are several theories about its origin:

1) The U wave is caused by late potentials that follow their own action potentials.

2) The U wave is caused by potentials resulting from stretching of the ventricular musculature during the period of rapid ventricular filling in early diastole.

3) The U wave is caused by potentials induced by delayed late repolarization when the walls of the left ventricle are stretched during diastole.

4) The U wave is caused by repolarization of the papillary muscles or Purkinje fibers.

5) The U wave is caused by electrical oscillations caused by a mechanical wave of sufficient intensity at the mouths of the veins after the passage of a normal arterial pulse along a closed “artery-vein” circuit.

Thus, all theories are based on the existence of certain late oscillations, on a short time shifting the transmembrane potential of the myocardium at the time of early diastole towards hypopolarization. I am closer to theory No. 2. Moderately hypopolarized myocardium has increased excitability - as is known, the U wave on the ECG chronologically coincides with the so-called supernormal phase of the cardiac cycle, in which, for example, extrasystole easily occurs.

The clinical significance of the U wave is uncertain (and in my opinion insignificant). Normally, the U wave is a small (about 1.5-2.5 mm on the ECG), positive, gently sloping wave, following the T wave 0.02-0.04 seconds. It is best visualized in leads V3, V4. Often the U wave is not detected at all or is “layered” on the T wave. And, for example, at a heart rate of more than beats per minute, its detection is almost impossible due to the overlap with the atrial P wave. It is believed that normally it has the greatest amplitude in healthy young people age. However, theoretically it can occur in any clinical situation, increasing in amplitude during tachysystole:

It is believed that a negative U wave is absolutely not typical for the norm. Negative U-oscillation is almost always associated with some kind of pathology. Another thing is that the diagnostic value of such a reversion can be completely different:

The phenomenon of accelerated idioventricular rhythms. It is correct to talk about the replacing ("saving") role of the ventricular rhythm only in those cases when it appears against the background of cardiac arrest during "paroxysmal" SA or AV blockade, or during passive AV dissociation. In other situations, we are dealing with an accelerated idioventricular rhythm (AVR), appearing as if unmotivated (“active”). Its frequency does not exceed one minute, otherwise it is diagnosed ventricular tachycardia. There are several reasons for the appearance of UIR:

Reperfusion syndrome in acute myocardial infarction,

Known organic heart disease with reduced left ventricular systolic function (as part of potentially malignant Bigger ectopia),

Idiopathic cases in healthy individuals.

Most often, URIs appear during acute myocardial infarction at the time of complete or partial recanalization of the coronary artery. In such a situation, the stunned cardiomyocytes receive a large number of calcium, which shifts the transmembrane potential to the threshold level (cell hypopolarization); as a result, cardiomyocytes acquire the property of automaticity. It is important to know that URI is not a reliable criterion for successful reperfusion: recanalization may be partial or intermittent. However, together with other clinical signs the prognostic value of UIR, as a marker of restoration of coronary blood flow, is quite high. Cases of “reperfusion” ventricular fibrillation are very rare. Examples:

Reperfusion syndrome is encountered mainly by hospital doctors working in cardiac intensive care units; Clinic cardiologists or functional diagnostic doctors more often deal with other causes of URI.

Digitalis intoxication, as a cause of UID, occurs in last years less and less. You just have to remember it.

The identification of UIR in patients with organic heart disease against the background of left ventricular systolic dysfunction is of great clinical importance. Any ventricular ectopy in such a situation should be treated as potentially malignant - it certainly increases the risk of sudden cardiac death through the initiation of ventricular fibrillation, especially if it appears during the recovery period after exercise. Example:

Just a few years ago, when registering UID in people without organic heart disease, cardiologists rendered a verdict of an “uncertain” clinical prognosis - such subjects were under medical patronage. However, long-term observations of them have shown that URIs do not increase the risk of sudden cardiac death and in such cases are a “cosmetic” arrhythmia. Often, URI in healthy individuals is associated with other cardiac and non-cardiac anomalies: the WPW phenomenon, accessory chordae, early ventricular repolarization syndrome, manifestations of connective tissue dysplasia syndrome. The clinical significance of URI will be determined by the subjective tolerability of the arrhythmia and its effect on intracardiac hemodynamics (the likelihood of developing arrhythmogenic dilatation of the heart). Examples:

The doctor should not be confused by such URI parameters as frequency variability and polymorphism of ventricular complexes. The irregularity of the rhythm is determined by the internal automatism of the ectopic center or the blockade of the exit with Wenckebach periodicity. The apparent polytopic nature of ectopic complexes is, in fact, nothing more than an aberrant conduction of excitation. The general consensus is that the mechanism of URI in healthy individuals is abnormal automaticity.

In the differential diagnosis of accelerated ventricular rhythms, the Ashman phenomenon, the WPW phenomenon, and tachy- or brady-dependent bundle branch block should be excluded.

The phenomenon of myopotential inhibition is a variant of hypersensing of a pacemaker to the potentials of skeletal muscles chest, shoulder girdle, abdominal muscles or diaphragm. As a result, the detecting electrode, perceiving extracardiac signals, gives a command to inhibit the next artificial impulse - a cardiac pause occurs, which can result in fainting for the patient. As a rule, myopotential inhibition is provoked by some action, for example, active work with the hands. This phenomenon is typical for pacemakers with a monopolar electrode configuration; They have been implanted less and less in recent years. Examples:

Options for correcting myopotential inhibition: 1) reducing the sensitivity threshold of the electrode, 2) reprogramming the system to a bipolar version of sensing, 3) replacing the electrode with a new one, with a bipolar core.

The phenomenon of pseudo-delta wave (false ∆-wave). As is known, the delta wave is a specific sign of ventricular preexcitation, due to the presence of an additional antegrade conduction pathway without the impulse delay characteristic of the AV node. The familiar ECG picture in the form of a delta wave, widening the QRS complex and shortening the P-Q interval due to preexitation, is called the WPW phenomenon. However, sometimes there is a “temptation” to detect a delta wave where it actually does not exist, but where there is a ventricular extrasystole, the onset of which is very similar to pre-excitation. This is the so-called pseudo-delta wave. Such a ventricular complex imitates a continuous delta wave (synonyms: continuous antidromic conduction, extrasystole from the Kent bundle). A diagnostic difficulty occurs when a ventricular extrasystole with a pseudo-delta wave is recorded on a standard ECG. When analyzing long-term ECG monitoring, everything falls into place: the WPW phenomenon with extrasystole from the Kent bundle (solid delta wave) Always will be combined with the presence of ventricular complexes with a true delta wave. On the contrary, when registering ventricular extrasystole with a pseudo-delta wave, classical signs of the WPW phenomenon (including intermittent preexitation) will not be detected. Examples:

By the “width” of the pseudo-delta wave one can judge the localization of the extrasystolic focus: endocardial or epicardial. The algorithm is as follows: 1) if the pseudo-delta wave is more than 50 ms, then we can talk about the epicardial origin of the PVC, 2) if if the pseudo-delta wave is less than 50 ms, then pay attention to the shortest RS interval in the extrasystole on a 12-channel ECG : its duration of less than 115 ms indicates an endocardial localization of the focus, while with a duration of 115 ms or more they proceed to the third step: the presence of a q-wave in lead aVL, 3) the presence of a q-wave in lead aVL indicates the epicardial origin of the PVC, its absence - about endocardial. For example, in the ECG below, even according to the roughest calculations, the width of the pseudo-delta wave exceeds 50 ms:

The localization of the extrasystolic focus is of interest not only to invasive arrhythmologists: with frequent epicardial extrasystoles, the risk of developing arrhythmogenic dilatation of the heart is much higher.

Post-tachycardia syndrome. With a frequent heart rate, myocardial energy resources are mobilized. If an episode of tachysystole continues for too long or the heart rate is extremely high, then intracellular metabolism is disrupted (cannot cope with the load) - transient myocardial dystrophy is formed. In such a case, after the end of the tachycardia, nonspecific changes in repolarization, called post-tachycardia syndrome, can be detected on the ECG. Theoretically, after any tachycardia (sinus, supraventricular or ventricular) in the recovery period, manifestations of post-tachycardia syndrome may occur. In its classical form, it represents a transient reversal of the T wave in the precordial leads. However, practical experience shows that ECG changes following tachycardia can also affect the S-T segment. Therefore, in clinical practice the following manifestations of post-tachycardia syndrome are encountered:

Obliquely ascending depression S-T segment with upward convexity (like “systolic overload”),

- “slow” obliquely ascending depression of the S-T segment,

Negative T wave.

The duration of post-tachycardia syndrome is unpredictably variable: from several minutes to several days. With persistent sympathicotonia, manifestations of post-tachycardia syndrome can exist for months and years. Classic example serves as a juvenile type of ECG (negative T waves in leads V1-V3), characteristic of adolescents and young people with a labile psyche.

Let's briefly consider the options for post-tachycardia syndrome.

Oblique depression of the S-T segment with convexity upward after tachycardia, as a rule, is formed in individuals with initial manifestations of left ventricular myocardial hypertrophy; In such patients, the standard resting ECG has completely normal parameters. The most pronounced depression is observed in leads V5, V6. Its appearance is familiar to everyone:

As a rule, within no more than an hour after an episode of tachycardia, the ECG returns to normal. If myocardial hypertrophy progresses, then the normalization of the S-T segment is delayed for hours or even days, and subsequently the manifestations of systolic overload are “fixed” at rest.

"Slow" obliquely ascending depression of the S-T segment is rare. Most often it appears after tachycardia against the background functional disorders myocardium according to the NCD type.

A negative T wave is the most common variant of post-tachycardia syndrome. It's extremely non-specific. I will give three examples.

Negative T waves in the precordial leads in a 21-year-old boy (can be considered a juvenile type of ECG) against the background of persistent sympathicotonia:

Negative T waves in the precordial leads formed after ventricular tachycardia:

Negative T waves in the precordial leads formed after supraventricular tachycardia:

The clinical significance of post-tachycardia syndrome is great! He is common cause unnecessary hospitalizations and medical examinations. By imitating ischemic changes, especially in combination with cardialgia syndrome, post-tachycardia syndrome can “mimic” coronary pathology. Remember him! Good luck with your diagnostics!

B blockade of the median branch of the left bundle branch. In approximately 2/3 of people, the left bundle branch branches not into two branches, but into three: anterior, posterior and median. Along the median branch, electrical excitation extends to the anterior part of the IVS and part of the anterior wall of the left ventricle.

Its isolated blockade is an extremely rare occurrence. However, if it happens, then part of the IVS and the anterior wall of the left ventricle are excited abnormally - from the posterior and lateral walls of the left ventricle. As a result, in the horizontal plane the total electrical vector will be directed forward, and in leads V1-V3 the formation of high R waves (complexes of the qR, R or Rs type) is observed. This condition must be differentiated from:

Right ventricular hypertrophy

Posterobasal myocardial infarction,

Normal ECG of children in the first years of life, when for natural reasons the potentials of the right ventricle predominate.

Blockade of the median branch of the left bundle branch can occur both within functional impairment conductivity, and indirectly reflect, for example, atherosclerotic lesion anterior descending artery, being a subclinical ECG marker of coronary artery disease.

The author of these lines literally encountered this conduction disorder a couple of times during his professional career. I will give one such observation. In a patient with severe chest pain, the following ECG pattern was verified (Fig. A): oblique elevation of the S-T segment in leads aVL, V2 and V3; anterior superior semi-block and blockade of the median branch of the left bundle branch (high-amplitude R waves in leads V2, V3). Outside the attack, the ECG returned to normal (Fig. B).

Coronary angiography revealed a spasm of the anterior descending artery in the middle third of the patient, which resolved with intracoronary administration of nitrates; concentric coronary atherosclerosis was absent. Vasospastic angina was diagnosed. Thus, the blockade of the median branch appeared only at the time of an anginal attack, reflecting “deep” myocardial ischemia.

Pseudo-pacemaker syndrome. As is known, pacemaker syndrome can be triggered by a chronically existing violation of the normal sequence of contractions of the atria and ventricles, for example, due to ventriculoatrial conduction or an inappropriately long AV delay; or its manifestation is associated with hemodynamic nonequivalence of natural (own) heart contractions and forced ones. Pseudo-pacemaker syndrome is a hemodynamic disorder caused by the presence of ventriculoatrial conduction or severe 1st degree AV block with clinical manifestations similar to pacemaker syndrome, but in the absence of cardiac pacing. The development of this “pseudo-syndrome” is most often observed with long-term AV block of the 1st degree, exceeding when electrocardiographically the P wave begins to overlap the S-T interval of the preceding ventricular complex; in this case, atrial systole occurs against the background of a closed mitral valve.

I will give a literary observation. The patient was admitted to the clinic with symptoms of decompensated CHF 4 years after pacemaker implantation in DDDR mode with a base stimulation frequency of 50 per minute. The ECG revealed sinus rhythm with 1st degree AV block. lasting about 600 ms:

The overall percentage of atrial stimulation did not exceed 5%, ventricular - 7%. In dynamics, it was found that rare episodes of the imposed rhythm or P-synchronous stimulation of the ventricles were interrupted by ventricular extrasystole, which was again followed by sinus rhythm with pronounced AV block of the 1st degree:

The operating algorithm of this pacemaker was such that after any ventricular contraction, an atrial refractory period of 450 ms was triggered, and the P wave appeared approximately 200 ms after the ventricular complex - very early and therefore not detected. This led to almost complete inhibition of ventricular stimulation. In this case, it was necessary to either shorten the atrial refractory period or provoke the development of complete AV block. This patient, in addition to the basic treatment of heart failure, was prescribed high doses of Verapamil, which, by inhibiting AV conduction, led to ventricular contractions becoming 100% forced (P-synchronous stimulation). Drug AV blockade turned out to be a decisive factor - it made it possible to eliminate desynchronization in the contraction of the atria and ventricles, after which the symptoms of heart failure were stopped.

In this example, we see how long-term severe AV block of the 1st degree. may cause the development of heart failure.

Ventriculophasic sinus arrhythmia is a change in the length of the PR interval under the influence of ventricular contraction in the absence of ventriculoatrial conduction. It is traditionally believed that this arrhythmia occurs when the number of sinus waves P exceeds the number of ventricular QRS complexes - that is, with 2nd or 3rd degree AV block. In this case, the P-P interval, which contains the QRS complex, becomes shorter than the P-P interval free from ventricular contraction:

At the same time, ventriculophase sinus arrhythmia can be observed with ventricular extrasystole, artificial stimulation of the ventricles. For example:

The most likely mechanism for this phenomenon: stretching of the atria during ventricular systole, causing mechanical stimulation of the sinoauricular node.

7.2.1. Myocardial hypertrophy

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

7.2.1.1. Left atrial hypertrophy

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

Rice. 6. ECG for left atrial hypertrophy

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

7.2.1.2. Right atrial hypertrophy

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

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

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

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

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

7.2.1.3. Left ventricular hypertrophy

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

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

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

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

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

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

Deep S in leads V1, V2;

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

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

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

Rice. 8. ECG for left ventricular hypertrophy

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

7.2.1.4. Right ventricular hypertrophy

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

Signs of hypertrophy (Fig. 9):

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

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

The height of the RV6 tooth is less than normal;

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

Deep S wave in lead V5 and also V6;

Bias S-T segment below the isoline convex upward in the right III, aVF, V1 and V2;

Complete or incomplete blockade of the right bundle branch;

Shift the transition zone to the left.

Rice. 9. ECG for right ventricular hypertrophy

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

7.2.2. Rhythm disorders

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

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

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

Signs of normal sinus rhythm:

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

Identical duration of R-R intervals;

Positive P wave in all leads except aVR.

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

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

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

7.2.2.1. Sinus tachycardia

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

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

7.2.2.2. Sinus bradycardia

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

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

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

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

7.2.2.3. Irregular sinus rhythm

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

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

7.2.2.4. Idioventricular rhythm

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

Extremely severe pathology.

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

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

7.2.2.5. Extrasystole

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

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

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

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

Let us list the ECG signs of atrial extrasystole:

P wave changed in shape and amplitude;

The P-Q interval is shortened;

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

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

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

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

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

Signs of ventricular extrasystole:

The P wave is absent;

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

Full compensatory pause.

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

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

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

7.2.2.6. Paroxysmal tachycardia

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

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

QRS complexes are not changed or widened.

With ventricular form paroxysmal tachycardia P waves may change their location on the ECG, QRS complexes are deformed and widened.

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

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

7.2.2.7. Atrial fibrillation(atrial fibrillation)

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

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

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

Signs of atrial fibrillation:

R-R intervals different (arrhythmia);

There are no P waves;

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

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

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

7.2.2.8. Atrial flutter

It is observed much less frequently than atrial fibrillation.

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

7.2.2.9. Ventricular fibrillation

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

Signs of ventricular fibrillation:

Absence of all teeth of the ventricular complex;

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

7.2.3. Conduction disorders

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

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

Sinoatrial III degree;

Atrioventricular I, II and III degrees;

Blockade of the right and left bundle branches.

7.2.3.1. III degree sinoatrial block

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

7.2.3.2. Atrioventricular block

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

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

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

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

Signs of Mobitz-1 type blockade:

Constantly lengthening P interval

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

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

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

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

7.2.Z.Z. Bundle branch blocks

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

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

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

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

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

Negative T wave in leads V1 and V2;

Displacement of the S-T segment from the isoline;

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

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

Signs of complete blockade of the left bundle branch:

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

Offset of the S-T segment from the isoline;

Negative T wave in leads V5 and V6;

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

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

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

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

7.2.4. Wolff-Parkinson-White syndrome

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

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

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

Signs of WPW syndrome type A:

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

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

Signs of WPW syndrome type B:

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

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

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

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

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

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

7.2.5. Early ventricular repolarization

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

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

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

ST segment elevation;

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

High amplitude teeth;

Double-humped P wave of normal duration and amplitude;

Shortening of PR and QT intervals;

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

Rice. 11. ECG for early ventricular repolarization syndrome

7.2.6. Cardiac ischemia

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

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

These include:

Reduced amplitude of the R wave;

S-T segment depression;

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

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

7.2.7. Angina pectoris

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

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

The causes of angina are hypercholesterolemia, dyslipidemia. In addition, arterial hypertension, diabetes, psycho-emotional overload, fear, obesity.

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

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

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

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

Urgent Care for angina pectoris is to relieve pain and prevent recurrent attacks.

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

7.2.8. Myocardial infarction

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

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

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

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

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

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

Pathological Q wave in leads located above the infarction area;

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

Discordant displacement below the S-T segment isoline in leads opposite 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 stages of changes during a heart attack.

There are four stages in the development of myocardial infarction:

Acute;

Subacute;

Scarring stage.

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

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

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

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

The T wave remains negative.

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

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

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

Depending on the location, a distinction is made between anterior lateral and rear walls left ventricle. The localization and extent of changes are revealed by analyzing ECG changes in the corresponding leads (Table 6).

Table 6. Localization of myocardial infarction

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

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

Meet and atypical forms heart attack:

Abdominal (pain in the heart and stomach);

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

Arrhythmic (cardiac pain and rhythm disturbances);

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

Painless.

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

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

After finishing inpatient treatment Patients who have had a heart attack are sent to a sanatorium for rehabilitation.

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

7.2.9. Syndromes due to electrolyte disturbances

Certain ECG changes allow us to judge the dynamics of electrolyte content in the myocardium.

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

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

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

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

7.2.9.1. Hyperkalemia

Signs of hyperkalemia:

Tall, pointed T wave;

Shortening of the Q-T interval;

Decreased R amplitude.

With severe hyperkalemia, intraventricular conduction disturbances are observed.

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

7.2.9.2. Hypokalemia

Signs of hypokalemia:

Decreased S-T segment downwards;

Negative or biphasic T;

The appearance of U.

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

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

Treatment consists of replenishing potassium deficiency in the body.

7.2.9.3. Hypercalcemia

Signs of hypercalcemia:

Shortening of the Q-T interval;

Shortening of the S-T segment;

Expansion of the ventricular complex;

Rhythm disturbances with a significant increase in calcium.

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

7.2.9.4. Hypocalcemia

Signs of hypocalcemia:

Increasing the duration of the QT interval;

Lengthening the S-T segment;

Decreased T amplitude.

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

7.2.9.5. Glycoside intoxication

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

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

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

Signs of glycoside intoxication:

Decreased heart rate;

Shortening of electrical systole;

Decreased S-T segment downwards;

Negative T wave;

Ventricular extrasystoles.

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

WPW (VPW) - syndrome:

The main changes on the ECG with this syndrome include: shortening of the P - R interval, the presence of a D wave (delta wave), widening of the QRS complex.

The P-R interval is calculated from the beginning of the P wave to the beginning of the D wave, which is a thickening or notch (“ladder”) that deforms the beginning of the QRS complex.
It appears as a result of early premature excitation of the myocardium of one of the ventricles through an additional bundle. For most adults, the PD interval is 0.12 s, for children
The duration of wave D is 0.02-0.07 s, its height during sinus rhythm rarely exceeds 5 mm. The direction of the wave coincides with the direction of the QRS complex. The QRS complex in WPW syndrome has a confluent nature: it is expanded to 0.11-0.12 s in adults and to 0.10 s or more in children due to the addition of wave D to its initial part. The terminal portion of the QRS complex does not change. There are several types of WPW syndrome depending on the location of ventricular preexcitation.

Type A WPW syndrome:

In the right and left chest leads, the D wave and the QRS complex are directed upward. In leads V3 and V1, the QRS complex can look like R, RS, rS, rSr. The electrical QRS axis deviates to the right.

In lead I, wave D is more often negative, simulating an enlarged Q wave (QR complex); positive D wave (RS complex) is less common; in lead III, the D wave is usually positive. With this type of syndrome, the P - R interval sometimes exceeds 0.12 s (up to 0.14 s).

Type B WPW syndrome:

In the left precordial leads, the D wave and the QRS complex are directed upward. The electrical axis of the heart deviates to the left.

In lead I, the QRS complex is represented by a high R wave, wave D is positive, in lead III - the QRS complex, wave D is often negative and can enhance the Q wave. In this case, the Q wave sometimes imitates signs of lower myocardial infarction.

Type of AV syndrome WPW:

The electrical axis of the heart deviates to the left (as in type B): in lead I, the D wave and the QRS complex have a positive polarity, in lead III they are discordant.

Type C WPW syndrome:

The electrical axis of the heart deviates to the right; in leads I, AVL wave D is negative, in leads III, AVF it is positive.

The syndrome is recorded in approximately 0.2-0.3% of electrocardiographic studies and occurs at any age in both men and women.

Clinically, the syndrome is manifested by attacks of paroxysmal tachycardia, usually supraventricular.

Paroxysms of arrhythmia in WPW syndrome are caused by the effect of reverse excitation entry (re-entry), when a circular motion occurs through the AV junction - ventricles - Kent's bundle - atria - AV junction.

The impulse can be transmitted to the ventricles either through an additional bundle, returning through the AV connection (on the ECG: moderate and deformed ventricular complex), or “rotate” in the opposite direction (in this case, the QRS shape will be normal).

The frequency of paroxysms can reach up to 300 per minute, depending on the refractoriness of additional pathways.

Sometimes the syndrome is combined with paroxysms of atrial fibrillation, extrasystoles, and less often with atrioventricular blockades.

WPW syndrome is often recorded when congenital anomalies heart: atrial and ventricular septal defects, tetralogy of Fallot, Marfan syndrome, mitral valve prolapse.

Detection of WPW syndrome limits the patient's ability to choose or maintain a profession in which the sudden occurrence of an arrhythmia attack can lead to an accident at work.

Wood syndrome:

Gallaverdin syndrome:

Gonax - Ashman syndrome:

It can occur in a premature impulse, for example in an extrasystole, or persist in all complexes during tachycardia, since they depend on the relationship between the preceding diastole. With a shorter coupling interval, aberrance occurs at the same length of preceding diastole.

Supraventricular extrasystole confirms this rule (a long preceding diastole plus a short coupling interval leads to the appearance of Gonax-Ashman syndrome). This occurs because the long cycle is accompanied by a long transmembrane action potential, and the impulse following the end of the short cycle may still be in phase III repolarization upon reaching the right bundle branch due to the fact that the refractory period of the transmembrane action potential in the right bundle longer than on the left. As a result, the impulse will not be conducted along this leg, which creates a picture of a right bundle branch block. In supraventricular tachycardia, the first beat may be aberrant as a result of this mechanism, but subsequent beats are less likely to have an aberrant configuration due to the short duration of the preceding diastole.

Iervel-Lange-Nielsen syndrome:

The genesis of these conditions is not clear. Perhaps the development of arrhythmia plays a role.

At autopsy: the heart is of normal size. In most cases, microscopic examination of the heart does not reveal any pathology, in more rare cases - tortuosity and thickening coronary arteries due to hypertrophy of muscle fibers, changes in Purkinje fibers, and a decrease in the glycogen content in them. The prognosis of the disease is unfavorable. After intense physical exertion or stressful situations, syncope suddenly develops, leading to the death of patients.

The use of digitalis drugs during the intersyncope period has a positive effect in preventing the development of syncope. It has been noted that with age the number of syncope attacks in patients decreases.

The type of inheritance is autosomal recessive. In heterozygous carriers of the pathological gene, the ECG shows a slight prolongation of the QT interval.

Clerc - Levy - Cristesco syndrome (CLC syndrome):

Cossio syndrome II (post-tachycardia syndrome):

Dynamic monitoring of ECG changes and determination of serum enzyme activity are necessary. Cossio syndrome is most often observed in patients with coronary atherosclerosis, but can also occur in young people without evidence of organic heart disease.

Lown-Genong-Levine syndrome. See Clerk-Levy-Christesco syndrome.

Lev's syndrome (Lev's disease):

Conduction disorders (intraventricular block of the right or left bundle branch, complete transverse block) are caused by mechanical compression of the intraventricular conduction system.

In Lev's disease, the coronary vessels and ventricular myocardium are not changed. The disease occurs mainly in older people (usually women), but can also occur at the age of 40 years.

Diagnosis of the disease is based on the following criteria: the occurrence of progressive intraventricular block, more or less quickly ending in the formation of complete atrioventricular block; localization of complete atrioventricular block below the common trunk of the His bundle; absence of any organic heart disease; ECG signs of degenerative calcification (fibrosis) in the area of ​​the interventricular septum.

Lenegr syndrome:

Damage to the cardiac conduction system is associated with hyalinosis and interstitial fibrosis. The exact nature of the disease is not known. In most cases, the patient first develops a blockade of the right bundle branch, which is subsequently joined by a blockade of the anterior, less often the posterior branch of the left bundle branch, and finally a complete transverse block develops.

Less commonly, blockade of the anterior branch of the left leg precedes blockade of the right bundle branch. Lenegra's disease most often affects middle-aged men. There are isolated descriptions of the disease in men aged 19-21 years.

Mobitz syndrome (dissociation with interference, junctional rhythm type II):

The occurrence of the syndrome is not explained by complete inhibition of sinus impulses, but only by its sharp decrease with a relatively high level of excitability of the centers of the second order of automatism in the atrioventricular node system and severely hindered retrograde conduction of ectopic impulses to the sinus node. Under these conditions, the atria contract in the relatively slow rhythm of sinus impulses, and the ventricles contract in a slightly more rapid rhythm of impulses from the atrioventricular junction. In such cases of dissociation of atrial and ventricular contractions, the P waves and QRS complexes interfere with each other.

Morquio syndrome II (Morquio's disease):

Oppenheimer-Rothschild syndrome:

Most often, the electrocardiographic picture of arborization blockade is caused by minor local disturbances coronary circulation type of heart attacks.

The lower the voltage of the teeth in the picture of this blockade, the more careful the prognosis should be made, especially with the simultaneous lengthening of the P-Q interval.

Romano-Ward syndrome:

Samoilov-Wencchebach syndrome I:

Samoilov-Wenckebach blockade II:

Sick sinus syndrome (SSNS):

These include:
1) constant sinus bradycardia with a frequency of 45-50 beats per 1 minute at rest;
2) failure of the sinus node, long or short-term sinus pause (2-2.5 s);
3) repeated sinoatrial blockade or blockade of the exit from the sinus node (sinus pauses 2-2.5 s);
4) slow and unstable restoration of sinus node function after stopping an attack of supraventricular tachycardia;
5) repeated alternations sinus bradycardia(long pauses 2.5-3 s) with paroxysms of atrial fibrillation (flutter) or tachycardia (brady-tachycardia syndrome).

Partial or complete loss of the sinus node’s pacemaker role leads to the appearance of secondary arrhythmias: migration of the supraventricular pacemaker and replacement escape rhythms, which in turn can be complicated by atrioventricular dissociation. These disorders themselves are not included in the concept of SSSS, but they may indirectly reflect the inferiority of the sinus node if there is evidence of its organic damage. In addition to replacement rhythms, SSSS is characterized by combinations with distal arrhythmias and blockades.

The clinical manifestations of sick sinus syndrome are quite varied: along with the manifest forms, a latent variant is also found.

The main complaints in SSSU are fainting, dizziness, palpitations, shortness of breath and pain in the heart area.

Sometimes patients do not show any complaints, and SSSU is detected only during an electrocardiographic study. In genesis clinical manifestations manifest forms lies in the nature of arrhythmias, which lead to impaired blood circulation in organs and tissues as a result of severe bradycardia, tachybradyarrhythmia or periods of asystole. The most common and important is cerebral syndrome, which occurs with moderate or severe cerebral circulatory disorders.

With moderate impairment of cerebral blood flow, patients experience increased excitability, insomnia and memory loss. Severe disturbances of cerebral blood flow manifest themselves in the form of syncopal attacks, short-term paresis, aphasia, etc.

Long-term and persistent bradyarrhythmia often contributes to the development of heart failure, and the “bradycardia-tachycardia” syndrome leads to the formation of thromboembolism of various localizations.

The latent form of SSSS most often manifests itself during an exacerbation of the underlying disease or when medications are prescribed that inhibit the function of the sinus node.

Reasons for the sinus node losing its role as a pacemaker:

3) sclerodegenerative processes with damage to the sinus node and distal areas of the specialized conduction system, combined with intracardiac calcification. There are probably people with congenital or hereditary inferiority of the sinus node and the conduction system of the heart, which increases as they age;

4) regulatory dysfunctions of the sinus node are widespread, the cause of which in most cases is excessive influence vagus nerve or increased sensitivity of M-cholinergic receptors of the sinus node. In addition, there are other causes of reversible sinus node dysfunction, such as hypercalcemia and hyperkalemia;

5) medicinal or exogenous toxic effects on the sinus node. Substances that can disrupt the function of the sinus node include b-blockers, verapamil, cardiac glycosides, toxic doses of tricyclic antidepressants, lithium salts, cholinesterase blockers (including household insecticides). Severe damage to the sinus node caused by poisoning with poisonous mushrooms is known.

To assess the functional state of the sinus node and diagnose SSSS, the following methods are currently used: Holter monitoring for 24 hours or more; transesophageal electrical stimulation; electrophysiological methods for studying the function of the sinus node; physical activity test (bicycle ergometry); pharmacological tests (atropine, etc.).

Sandwich syndrome:

Frederic syndrome (Frederic phenomenon):

Atrial fibrillation and flutter may alternate. Impulses from the atria are not conducted to the ventricles.

The ventricles are excited by a pacemaker located in the atrioventricular junction or in the ventricles themselves. If the excitation comes from the atrioventricular junction, then the QRS complex is not changed.

With idioventricular rhythm, the QRS complex is widened and deformed and is similar in shape to the ECG with bundle branch block. The ventricular rhythm is regular and rare. Distances R-R are the same. The ventricular contraction frequency is usually 40-60 per minute. The ventricular rhythm in Frederick's syndrome can be disrupted by ventricular extrasystoles.

Eckl phenomenon (syndrome):

Inverse relationships are observed as a result of exposure to atropine. Small doses of it, reducing the intensity of this inhibition and thereby limiting its influence on a more sensitive node, lead to the manifestation of nodal automatism. Large doses of this alkaloid completely turn off the effect parasympathetic innervation both at the I and II centers. Under these conditions, the normal ratios of the frequency of impulse formation in them are restored again, and at the same time the dominance of the sinus node. Similar phase changes can be observed in athletes under conditions of intense physical activity.

El-Sherif syndrome (pacemaker allorhythmia):

Negative impact of loss of AV synchrony that occurs with single-chamber ventricular stimulation(VVI mode), most pronounced at rest or when the patient is in an upright position. The disappearance of timely atrial systole leads to a decrease in cardiac output to 1/3 of the initial value and can cause arterial hypotension, up to the development of syncope or presyncope. Other symptoms include weakness, dizziness and shortness of breath.

Hypotension is most likely and pronounced when you are patient in an upright position, the maximum severity of the manifestation is in the first seconds after the start of ventricular stimulation, when reflex vasoconstrictor compensatory mechanisms have not yet fully activated.

Thus, single-chamber ventricular pacing is most inappropriate for patients in whom sinus rhythm is persistently predominant and intermittently causes bradycardia at a rate less than the cycle length of the ventricular stimulator (for example, in patients with SSS or carotid sinus syndrome).

This has been demonstrated in ambulatory blood pressure monitoring in patients with implanted IVR operating in on-demand ventricular stimulation mode.

The onset of ventricular stimulation was accompanied by hypotension, which was more pronounced in patients who complained of syncope or presyncope.

Retrograde (ventricular-atrial) conduction from the complex imposed on the ventricle causes even more pronounced hemodynamic disturbances. The observed atrial expansion may be accompanied by a reflex vasodepressor reaction. Sequential atrioventricular pacing or atrial pacing can avoid these problems if AV conduction is not impaired.

Pacemaker syndrome is not observed in all patients with IVR operating in the VVI mode, but it does occur in a small proportion of patients, as has been shown in a number of clinical studies. Moreover, less severe forms This syndrome is probably simply underdiagnosed. Two-chamber allows you to avoid the development of the syndrome.

Training video for decoding an ECG with a pacemaker (artificial pacemaker)