ECG with slipping complexes

ECG with slipping complexes

ECG with slipping complexes

Slipping complexes can occur in the AV-connection or ventricles on the background of sinus bradycardia or the stop of the sinus node. In contrast to the extrasystoles, the coherence interval of a sliding complex is always greater than the cycle length of the main rhythm.

Slipping complexes of AV-compounds have the same configuration as the complexes resulting from the normal conduct of atrial impulses, while the form of slipping complexes of ventricular origin resembles ventricular extrasystoles. Slipping complexes and rhythms themselves do not require any treatment. If treatment is necessary, then it is aimed at increasing the frequency of the base rhythm.

Against the background of sinus bradycardia or with the inability of the sinus node to generate impulses from secondary sources of the specialized cardiac conduction system, slipping complexes may occur.

In contrast to extrasystoles, slip complexes always appear late, i.e. the adhesion interval is always greater than the cycle length of the dominant rhythm. It is important to distinguish between slipping and extrasystolic complexes, because the first indicates a violation of the function of the sinus node.

Vyskopzvayuschie complexes and rhythms themselves do not require any treatment. If treatment is necessary, then it is aimed at increasing the frequency of the base rhythm. Slipping complexes usually occur in the AV compound; less commonly, their source is localized in the ventricles. Ventricular complexes of slipping contractions from the AV connection are similar to those occurring at a normal rhythm, since the impulse is conducted in the usual way – through the bundle of His and his legs.

As with extrasystoles from an AV connection, the focus located in the AV connection can activate both the atria and the ventricles, which leads to the appearance of a retrograde P wave (ie, a negative P wave in leads II, III, aVF). In this case, the retrograde P wave can either precede the QRS complex, or be recorded after it or merge with it, depending on the ratio of the velocities of the impulse from the AV connection to the ventricles and atria. Ventricular slip complexes in their configuration are similar to ventricular extrasystoles.

Causes of ventricular premature beats and its significance

Causes of ventricular premature beats and its significance

Ventricular premature beats are a very common phenomenon, and the frequency of its detection in the general adult population increases with age. Causes of ventricular premature beats include acute myocardial infarction or myocardial ischemia, arterial hypertension; myocardial damage due to previous myocardial infarction, myocarditis or cardiomyopathy; mitral valve prolapse, valvular heart disease, digitalis intoxication. However, often no signs of heart disease are found.

In patients with symptomatic and / or frequent ventricular extrasystoles, its cause should be sought using non-invasive examination methods, including a thorough analysis of the 12-lead ECG, echocardiography and, if necessary, an exercise test.

Single ventricular extrasystoles registered on a normal ECG, and even complex forms of extrasystoles (i.e., extrasystoles frequent, multifocal, “R on T” or salvo) recorded during outpatient ECG monitoring, can be detected by chance in people with a healthy heart and necessarily are pathologies or have any predictive value.

On the other hand, in some observational studies involving adults (mostly men) who underwent physical exercise testing, it was shown that the occurrence of frequent ventricular extrasystole during exercise and especially immediately after its termination is associated with an increase in mortality times) over the next 5-15 years.

In patients with irreversible structural myocardial damage due to coronary heart disease (CHD), there is a correlation between the severity of the damage and the frequency of ventricular extrasystoles. According to the latest data, ventricular premature beats should be considered as an additional and independent risk factor, however there is no evidence that its suppression with antiarrhythmic therapy improves the prognosis.

Indeed, some antiarrhythmic drugs have been shown to increase mortality in patients with ventricular extrasystole after myocardial infarction.

Usually extrasystoles are asymptomatic. Nevertheless, some patients still experience discomfort. They may be concerned about the sense of heart failure due to its premature contraction or the subsequent compensatory pause, as well as the feeling of “heavy blows” caused by the increased strength of the post-extrasystolic contraction.

Patients may be worried that the irregularity of the heart activity is a precursor to a heart attack or other serious heart problems.

In some cases, patients with a structurally healthy heart, experiencing discomfort due to ventricular extrasystole, it is difficult to clarify the situation and calm them down. In such situations, therapy may be required to reduce symptoms. BABs can be effective, especially in the treatment of patients whose symptoms are associated with exercise.

For patients with a structurally normal heart and no signs of coronary artery disease, flekainid may be useful. It is generally recommended to avoid caffeine, but this is rarely effective.

Atrial activity of ventricular extrasystoles

Atrial activity of ventricular extrasystoles

The manifestation of atrial activity after the ventricular extrasystole depends on whether the ventricular impulse is conducted in the retrograde direction, i.e. through the AV connection to the atria. If this happens, an inverted P wave is formed, which often overlaps the ventricular ectopic complex itself and can be hidden by it.

In those cases where the AV-compound does not conduct a ventricular impulse on the atria, the atrial activity continues regardless of ventricular activity; only in these cases, after the ventricular extrasystoles, can you see a complete compensatory pause (when the interval between the pre-and post-extrasystolic sinus complexes is equal to twice the duration of the sinus cycle).

Sometimes the ventricular impulse can “penetrate” into the AV compound only partially. In this situation, the next sinus impulse can reach the AV compound, when it is still partially refractory, which will slow down the conduction and lengthen the PR interval. This phenomenon of “hidden retrograde conduction” often occurs after interpolated ventricular extrasystoles.

The time of occurrence of ventricular extrasystoles

The time of occurrence of ventricular extrasystoles

Ventricular ectopic complexes, which occur very early in the cardiac cycle, may be superimposed on the T wave of the previous contraction and are referred to as extrasystoles “R on T”. Most episodes of ventricular fibrillation (VF) and many episodes of ventricular tachycardia (VT) are initiated by extrasystoles “R on T”, although this does not mean that extrasystoles “R on T” always cause these forms of arrhythmia.

Ventricular extrasystoles occurring in the cardiac cycle only slightly prematurely, may accidentally occur immediately after the P wave caused by the normal activity of the sinus node: the P wave, thus, unlike the atrial extrasystoles, will not be premature. Such ventricular extrasystoles are called end-dia-table.

Usually, there is a pause after the ventricular extrasystoles. When such a pause is absent and the extrasystole, thus, looks “sandwiched” between two normal complexes, the extrasystole is called interpolated.

Frequency of ventricular extrasystoles

When extrasystoles are followed after each sinus complex, the term “bigeminy” is used. If extrasystoles follow after a couple of normal complexes, this is “trigeminia.” When two ectopic complexes follow in succession, they are referred to by the term “pair beats,” or “couplet.” “Zalpom” refers to more than two consecutive ectopic complexes.

ECG for ventricular extrasystoles

ECG for ventricular extrasystoles

Ventricular ectopic impulse is carried out through the ventricles not through the His-Purkinje system, but through a relatively slowly conducting myocardium. Changing the sequence and slowing down the activation of the ventricles causes the forming ventricular complexes to become deformed and broadened.

The complexes are premature, wide (<0.12 s), deformed and, unlike atrial extrasystoles, they are never preceded by a premature R-wave.

ECG characteristics of ventricular extrasystoles: – QRS complex of ventricular extrasystoles: Premature Wide (> 0.12s) Changed in shape (deformed) It is not preceded by a premature P wave. Several terms are used to describe the location of the source, time of occurrence and number of ventricular extrasystoles.

Characteristic source (focus) of ventricular premature beats

Ectopic complexes of the same form, following with the same intervals of adhesion, occur in the same focus. They are called “monofocal”, “monomorphic”, “monotopic”. Different in shape and adhesion intervals, ventricular complexes suggest the presence of more than one focus. Such extrasystoles are called “multifocal”, “polytopic”, “polymorphic”.

Ventricular extrasystole

Ventricular extrasystole

The clinical significance of ventricular premature beats depends on how often extrasystoles appear and whether they are single, paired or group. Under the group understand several extrasystoles, following each other. Next, you should also consider the configuration of extrasystoles. If extrasystoles have the same configuration, then they come from the same focus and are called monomorphic or monotopic, if extrasystoles are different in configuration, then we are talking about polymorphic or polytopic extrasystole.

In ventricular premature beats, unlike atrial beats, there is always a compensatory pause. This means that the total duration of 2 contractions (before and after extrasystoles) is equal to twice the RR interval of normal contractions. Under the interval RR understand, as mentioned earlier in the chapter on atrial extrasystoles, the distance from one R wave to the adjacent R wave.

The compensatory pause is explained as follows: the excitability of the sinus node and the atria during ventricular extrasystole is not disturbed. Since the excitation from the sinus node reaches the ventricles in the absolute refractory period associated with the extrasystole, the excitation of the ventricles is impossible. Only with the arrival of the next excitation wave from the sinus node is a normal contraction of the ventricles possible.

In ventricular arrhythmia, due to the pathological propagation of the excitation wave, a secondary violation of repolarization also appears in the form of ST segment depression and a negative T wave.

For the treatment of ventricular premature beats, a doctor has various antiarrhythmic drugs, such as beta-adrenergic receptor blockers and propafenone (prescribed only for severe clinical symptoms). Due to the arrhythmogenic effect inherent in all antiarrhythmic drugs (the frequency of heart rhythm disturbances caused by them is on average 10%), the attitude towards them is currently more restrained and they are prescribed with greater caution.

Features ECG with ventricular extrasystoles:

• Premature appearance of the QRS complex
• The broadening of the QRS complex, the configuration of which resembles the blockade of the corresponding PG leg
• Presence of compensatory pause
• Sometimes found in healthy people, but more often in people with heart disease.
• Treatment is indicated only when clinical symptoms appear. Assign beta-adrenergic receptor blockers, propafenone, amiodarone

Signs of ventricular extrasystoles on ECG

Signs of ventricular extrasystoles on ECG

• For ventricular extrasystoles, premature appearance of a wide and deformed QRS complex is characteristic.
• Unlike the atrial extrasystoles, there is always a compensatory pause before the ventricular one.
• Ventricular extrasystole – a frequent disturbance of the heart rhythm. It can be observed both in healthy people, without being accompanied by any other symptoms, or in people with a heart condition.

Ventricular extrasystole is a frequent disturbance of the heart rhythm, which can be observed in healthy people, without being accompanied by any other symptoms, but more often in people with various heart diseases, in particular, coronary heart disease, heart defects, cardiomyopathies, myocarditis. The cause of ventricular premature beats is an ectopic focus of excitation in the pancreas or LV.

Under the ventricular extrasystole understand the premature contraction of the ventricles, caused by a focus of excitation, which is located in the ventricles themselves. Using electrocardiography, it is easier to recognize ventricular premature beats than supraventricular (atrial premature beats). For ventricular extrasystoles, premature broad (more than 0.11 s) and deformed QRS complexes are characteristic, which by their configuration resemble the blockade of PG feet.

So, when extrasystoles occur in the right ventricle (RV), it is excited earlier than the left ventricle (LV), therefore a wide QRS complex is recorded on the ECG, resembling the blockade of LNPH in configuration, as LV excitement occurs late. If the center of extrasystole is in the LV, then the configuration of the QRS complex resembles the blockade of PNPG.

ECG with extrasystole from AV connection

ECG with extrasystole from AV connection

The extrasystoles arising in AV connection were called “nodal” earlier. It is now recognized that at least part of the AV node does not have automatic (pacemaker) activity and is not able to generate pulses, and that extrasystoles arising in the AV node cannot be distinguished from those whose source is in the His bundle.

In this connection, the more general term “extrasystoles from an AV connection” is used. Extrasystoles from the AV connection are less common atrial and ventricular. The need for treatment is rare.

Electrocardiographic manifestations. About an ekstrasistoliya from an AV-connection speak, if on the electrocardiogram the premature QRS complex having the same configuration, as sinus complexes is found.

The focus located in the AV junction can activate both the atria and the ventricles, which leads to the appearance of a retrograde P wave (ie, a negative P wave in leads II, III, aVF).

At the same time, the retrograde P wave can either precede the QRS complex, or be recorded after it or merge with it, depending on the ratio of the speeds of the premature pulse from the AV connection to the ventricles and the atria.

ECG for atrial extrasystole

ECG for atrial extrasystole

Atrial ectopic impulse leads to the appearance of a premature R wave. The place of its occurrence and, consequently, the direction of propagation of the atrial activation wave will differ from those during sinus rhythm, so that the premature R wave will differ in shape from the P wave of sinus origin.

Because atrial ectopic teeth P are premature, they can overlap the T wave of the anterior ventricular complex and thus deform it. Careful analysis of the ECG plays a key role in identifying ectopic P waves; Often the most appropriate for such an analysis is lead V1.

Atrioventricular and intraventricular conduction. Usually, a premature atrial impulse is conducted through the AV connection and along the legs of the His bundle in the same way as if the atria were activated by the sinus node. Therefore, the PR interval and the QRS complex atrial extrasystoles are similar to those of sinus rhythm.

If the QRS complex of sinus origin is deformed due to the blockade of the legs, then the QRS complex of the atrial beats will be the same.

However, sometimes atrial extrasystoles, especially those that occur very early in the cardiac cycle, can reach the AV connection or the bundle of the His bundle at a time when their conductivity has not yet recovered after the previous atrial impulse and which thus remain partially or completely refractory to arousal.

Partial or complete refractoriness of an AV connection will lead to a prolongation of the PR interval or blockage of the atrial extrasystole, respectively. The ECG pattern observed in cases where the atrial extrasystoles are not carried out on the ventricles can be mistakenly interpreted as an indication for an EKS!

Partial or complete refractoriness of one or another of the bundle of His (usually the right leg) may be accompanied by the appearance of signs of a partial or complete blockade of the leg, respectively. This phenomenon of functional blockade of the bundle of the His bundle is called “phase aberrant intraventricular conduction”.

As a result, QRS complexes of atrial extrasystoles become wide and, thus, if the premature P wave preceding the ventricular complex cannot be detected, atrial extrasystoles can be mistaken for ventricular ones.

Value. Atrial extrasystoles occur in many heart diseases, but are also common in people with a healthy heart, especially in the elderly. Usually they are benign, however, frequent atrial premature beats can be a precursor of atrial fibrillation (AF) or atrial tachycardia.

Signs of atrial arrhythmia on ECG

Signs of atrial arrhythmia on ECG

• Typically early appearance of a slightly deformed R-wave. There is no compensatory pause.
• The frequency of atrial beats in IHD is increased. Relatively often, atrial extrasystoles appear in vegetative-vascular dystonia.

Normally, people with a healthy heart have sinus rhythms. This means that normal physiological arousal occurs automatically in the sinus node and the heart contracts in time with the pulses generated in the sinus node. This phenomenon is called the automaton heart.

At a sinus rhythm normal teeth P and the QRS complexes are registered through identical intervals of time.

Heart rate is normal, as already mentioned, is about 60-80 beats per minute. In sinus bradycardia, the heart contracts with a frequency of less than 60 beats per minute, and in sinus tachycardia, the heart contracts with a frequency of more than 100 beats per minute.

Atrial premature beats are characterized by the premature appearance of individual atrial contractions. Since atrial extrasystoles appear as a result of pathological excitation in some part of the atrium wall, the P wave, which reflects the onset of pathological atrial excitation, is deformed and has not a semilunar shape inherent in it, but a pointed or bizarre and is located above the isoline (positive) ; sometimes the P wave is biphasic.

The remaining intervals and the teeth on the ECG are normal, in particular the atrial extrasystoles, do not affect QRS complexes, since the conduction of arousal from the atria to the ventricles is not disturbed. Only with very early atrial extrasystoles, some deformation of the QRS complexes is possible due to aberrant excitation in the ventricular myocardium.

Another feature of atrial premature beats is that the total duration of the RR interval before and after the extrasystoles is less than twice the RR interval. The RR interval is the time interval between two teeth of R. In atrial extrasystoles, unlike ventricular, there is no compensatory pause. This is due to the fact that the excitation of the sinus node is suppressed in the retrograde direction by the atrial extrasystole and premature atrial excitation occurs.

With very early extrasystoles, the AV node may be still in the period of absolute refractoriness, and the conduction of arousal into the ventricles is blocked. In this case, the P wave is recorded, which, however, is not followed by the ventricular QRS complex (blocked atrial extrasystoles). This is a special form of atrial arrhythmia.

Frequent atrial premature beats, especially with polymorphic P wave, often turns into atrial fibrillation.

Single atrial extrasystoles can also be recorded in people with a healthy heart, especially in vegetative dystonia, while frequent atrial extrasystoles are a sign of pathology (for example, IHD, cardiomyopathy, heart defects).

ECG features in atrial arrhythmia:

• Premature appearance of the P wave on the ECG
• Easy deformation of the P wave
• Lack of compensatory pause
• Background heart disease: vascular dystonia and ischemic heart disease
• Therapy: beta-adrenergic receptor blockers, verapamil, quinidine