Monthly Archive December 2018

ECG in sinus tachycardia of the heart

ECG in sinus tachycardia of the heart

Sinus tachycardia is defined as sinus rhythm with a frequency higher than 100 beats / min. The cause of sinus tachycardia may be physical exertion, emotional stress, or any other condition leading to the activation of the sympathetic nervous system.

Sometimes sinus tachycardia may be inadequate. A possible cause is hyperthyroidism, but often the cause remains unclear. Most often this is observed in young women. A high heart rate is usually constant and shows an additional excess increase in response to physical exertion arising immediately after its onset.

Less commonly, inadequate sinus tachycardia occurs as a result of primary disturbances in the sinus node itself (re-entree of the sinus node).

Since sinus tachycardia is usually a physiological response, it rarely needs special treatment. However, if sinus tachycardia is inadequate, the heart rate can be reduced with the help of BAB or ivabradine, which is a selective inhibitor of the automatic function of the sinus node.

If the patient does not have a serious disease, then the heart rate at rest rarely exceeds 100 beats / min. Therefore, when detecting apparent sinus tachycardia at rest, the likelihood of a different heart rhythm, such as atrial tachycardia or atrial flutter (TP), should be considered.

Signs of reciprocal AV-node tachycardia on ECG

Signs of reciprocal AV-node tachycardia on ECG

P teeth are layered on QRS complexes and therefore not visible. The QRS complex is narrow, the frequency of contractions of the ventricles is 150-200 per minute.

This form of supraventricular tachycardia occurs mainly in young people suffering from vascular dystonia. In people with heart disease, this form of heart rhythm disorder is quite rare.

The most common form of supraventricular tachycardia is reciprocal AV nodal tachycardia; A focus that initiates and maintains tachycardia is located above the level of the ventricles, in particular in the AV node.

It is believed that in the AV node, as a result of the so-called longitudinal dissociation, two pathways of excitation are formed: a slowly conducting, or alpha, path with a short refractory period and a fast conducting, or beta, with a long refractory period. Such splitting allows circular movement of the excitation wave when the excitation propagates from one path (alpha path) to another (beta path) and performs a fast circular motion.

At the analysis of an electrocardiogram the narrow QRS complexes, quickly following one after another, attract attention. The frequency of ventricular contractions is usually 120-220 per minute.

P teeth, although recorded, are negative and, due to the high frequency of contractions, are not visible or are not clearly visible. This results from the fact that teeth P are layered on the QRS complexes or are registered immediately after these complexes. The QRS and ST-T complexes do not initially change. Only with aberrant ventricular conduction, QRS complexes can be broadened, as in the blockade of the bundle of the His bundle (PG).

Accurately determining the boundaries of the P wave is sometimes difficult. Therefore, they used to speak simply about “supraventricular tachycardia”, making no distinction between atrial and AV-nodal tachycardia.

It is noteworthy that this tachycardia often occurs in young people, especially in girls, suddenly, for no apparent reason or after exercise, and also stops suddenly. These features have important clinical significance. Reciprocal AV-nodal tachycardia can also occur in patients with a heart condition. However, in most cases, the general condition of the patients, despite the rapid reduction of the ventricles, remains relatively satisfactory, since the blood pressure, as well as the stroke and minute volumes of the heart, decrease slightly.

It is known that after an attack of reciprocal AV-nodal tachycardia, there is often abundant urination due to the release of atrial natriuretic peptide.

Treatment of reciprocal AV-node tachycardia often begins with carotid sinus massage, the patient is asked to strain (Valsalva maneuver), give him cold water to drink, if necessary, intravenously, verapamil, cardiac glycosides, beta-adrenergic receptor blockers or flecainide, and if there is no effect from These measures address the issue of catheter ablation. Differential diagnosis and treatment of tachycardia with normal ventricular complexes are presented in the figure below.

Clinical manifestations of supraventricular tachycardias

Clinical manifestations of supraventricular tachycardias

Supraventricular tachycardia (SVT) can cause serious symptoms, such as syncopal or presynopal conditions (especially at the onset of an attack), marked palpitations, angina pectoris (even in the absence of coronary artery disease), shortness of breath, feeling of fatigue and polyuria due to the release of atrial natriuretic peptide.

Other patients may simply feel the arrhythmia without experiencing a pronounced heartbeat, or not feel any symptoms at all.

Patients may experience discomfort not only from symptoms caused by tachycardia, but also from the unpredictability of arrhythmias. Some people live in fear of waiting for the next attack and are afraid to travel or even leave the house for fear of a repetition of tachycardia.

In many patients, organic heart disease is absent, however, they fear that the arrhythmia may be a precursor of a severe heart attack or other serious cardiac catastrophe. It is necessary to convince these patients that they have “electrical” heart disease, and not circulatory disorders or structural cardiac pathology.

Stable supraventricular arrhythmia, occurring at a high frequency, can lead to the development of heart failure. In such cases, the term “tachycardiomyopathy” is used. At the same time, restoration of a normal rhythm is accompanied by regress of heart failure.

Sometimes in patients without coronary artery disease, tachycardia can lead to pronounced ECG changes characteristic of myocardial ischemia. It is well known that an increase in serum troponin levels is considered as a sign of acute MI.

However, a slight increase in troponin concentration can be observed in patients with a long-existing tachycardia, in whom angiography shows no signs of coronary disease or whose age and degree of coronary risk make the presence of coronary pathology unlikely. A slight increase in troponin levels in patients with supraventricular tachycardia (SVT) should not be considered a sign of MI.

ECG for reciprocal tachycardias from AV-connection (AVRT, AVURT)

ECG for reciprocal tachycardias from AV-connection (AVRT, AVURT)

There are two main types of supraventricular tachycardia (SVT): AV re-entry tachycardias with AV involvement and atrial tachyarrhythmias. (In the Russian-language literature for tachycardia, based on the re-entry mechanism, or “re-entry of the excitation wave”, the term “reciprocal tachycardia” is often used.)

When reciprocal tachycardias involving the AV connection between the atria and the ventricles, there is an additional electrical connection. In this case, the impulse can repeatedly and at high speed circulate between the atria and the ventricles in a circle consisting of a normal AV connection and an additional AV connection. As a rule, from the atria to the ventricles the impulse is conducted through the AV node, and then returns from the ventricles to the atria through an additional connection.

There are two types of additional connections between the atria and the ventricles.

Additional conductive path. In atrioventricular reciprocal (re-entree) tachycardia (AVRT), the additional connection is represented by a bundle of myocardial fibers, which, like a bridge, spreads through the atrioventricular sulcus and thus “bypasses” the AV node. If this additional AV route is able to conduct impulses from the atria to the ventricles, then the patient has WPW syndrome.

In atrioventricular nodal reciprocal (re-entree) tachycardia (AVRT), the AV node and the atrial tissue adjacent to it are functionally dissociated into fast and slow paths, so there are two pathways in the AV node itself. With this tachycardia, AV conduction from the atria to the ventricles is carried out along the slow path, and conduction from the ventricles to the atria through the rapid path.

Atrial tachyarrhythmias. The second group of supraventricular tachycardias (SVT) includes arrhythmias caused by frequent abnormal electrical activity within the atria: AF, TP, and atrial tachycardia. The mechanism underlying this type of tachycardia is limited to atrial tissue.

Unlike tachycardia of the first group, with atrial tachyarrhythmias, the AV node is not part of the mechanism of tachycardia, but only conducts (partially or fully) atrial impulses on the ventricles. Atrial tachyarrhythmias are often associated with diseases of the myocardium, valvular apparatus of the heart, or with extracardiac pathology, while reciprocal tachycardias involving AV compounds are due to the existence of abnormal electrical

Classification of supraventricular tachycardias (SVT)

Classification of supraventricular tachycardias (SVT)

Some tachycardias occur in the atria or the AV connection and, therefore, are supraventricular in origin. In this case, the ventricles are activated through the His-Purkinje fast-conducting system, as a result of which narrow ventricular complexes are usually formed. There are two main types of supraventricular tachycardias (SVT).

The first type is reciprocal tachycardias involving the AV connection. They involve an additional electrical connection between the atria and the ventricles.
In this case, the impulse can circulate repeatedly and at high speed between the atria and the ventricles in a circle consisting of a normal AV connection and an additional AV connection. As a rule, such tachycardia is not associated with any other pathology of the heart.

The second type is atrial tachyarrhythmias, due to frequent pathological electrical activity within the atria (ie, AF, TP, and atrial tachycardia). At the same time, the AV-node is not an integral part of the tachycardia mechanism, but only transmits (partially or completely) impulses from the atria to the ventricles. Tachycardias of this type are often associated with various heart diseases.

Some tachycardias occur in the atria or the AV connection and, therefore, are supraventricular in origin. All of them have one common feature: since they arise above the level of the bundle of the His branch, the ventricles are activated by impulses propagating through a specialized intraventricular rapidly conducting system, and therefore ventricular complexes are usually normal and narrow.

However, it is very important to realize and take into account that there are significant differences in the mechanisms of development, ECG signs and approaches to the treatment of various forms of supraventricular tachycardias (SVT). It is necessary to determine the type of tachycardia, and not just treat all tachycardias with narrow QRS complexes as supraventricular tachycardias (SVT).

The appearance of extrasystoles on an ECG in a teenager

The appearance of extrasystoles on an ECG in a teenager

Another predisposing factor to the appearance of extrasystoles on an adolescent ECG is an overload of the heart muscle during puberty. The fact is that different elements of the cardiovascular system develop at a given time at a different speed – as a rule, the heart grows much faster and more actively than blood vessels, which leads to an increase in blood pressure. This can be easily understood by imagining how a powerful pump tries to pump as much fluid as possible through a narrow opening. Increased load on the myocardium leads to increased excitability of its contractile elements, which facilitates the occurrence of extrasystoles. In adolescents with such a heart overload, extraordinary contractions are not observed at rest, but during exercise, the child may complain of heartbeat and interruptions in heart function. In addition, high blood pressure during this period can cause dizziness, headaches and flickering flies before the eyes. This state also disappears without a trace after puberty, when the work of the heart and the volume of the circulatory system begin to match each other.

If an adolescent 12-14 years old on an ECG, extrasystoles were found without other signs of organic heart damage (for example, congenital defects or consequences of a rheumatic attack), then such a child is simply sent for a second analysis after two weeks. If the conclusion “extrasystolic arrhythmia” is confirmed, then the adolescent is put on record in the cardiologic dispensary. There is nothing terrible in this, it just means that every six months the child will be examined by a cardiologist, moreover, such children are exempted from physical education, since physical exertion can provoke more severe heart rhythm disturbances. As a rule, after adolescence, the extrasystoles on the ECG disappear and the young person is removed from the register without consequences. If the arrhythmia remains unchanged, then they try to find its cause and begin drug therapy.

Although adolescents who have an irregular heartbeat, and require more careful medical attention, parents should treat this as part of the maturing of the young body, as a temporary condition that passes completely a couple of years. There is no specific treatment for this transient pathology, it is recommended only a high vitamin ration, especially rich in such vitamins as C and E – the main antioxidants of the body. It is also necessary to monitor the balance of inorganic ions, especially magnesium and potassium – in conditions and diseases accompanied by loss of fluid (taking diuretics, diarrhea, loss of electrolytes and sweat in hot weather) it is necessary to bring products rich in potassium (dried apricots, baked potatoes) into the diet and adequately compensate for the loss of minerals (for example, by taking Regidron solution in case of diarrhea). The lack of these ions in adolescents with extrasystoles and arrhythmias may result in more severe heart rhythm disturbances.

Extrasystoles on the ECG in a teenager – what is it and treatment recommendations

Extrasystoles on the ECG in a teenager – what is it and treatment recommendations

The most tireless organ of our body, no doubt, is the heart. It is reduced in the normal 60-70 times per minute, pumping huge amounts of blood. In view of the enormous importance of this organ, the work of the heart is regulated both from the outside (through the effect of hormones and the autonomic nervous system on the myocardium) and from the inside (the system of self-regulation and automatic heart function). However, this is also a kind of “Achilles’ heel” of the heart – sometimes these two systems work in isolation, leading to various heart rhythm disorders.

Many healthy children and adolescents in the period of 12-14 years for the first time go to a study such as electrocardiography – registration of changes in the electric field of the heart. This study is carried out as part of a routine medical examination, and often it records a heart rhythm disorder such as beats, an extraordinary, sudden contraction of the heart. Extrasystoles are the most common cause of arrhythmias in people of different ages. For many adolescents, this condition does not manifest itself with absolutely no symptoms, only a few note periodic interruptions in the work of the heart and heartbeat. Parents often start to panic when they see such an ECG conclusion, thinking that their child has a serious pathology. However, such results of electrocardiography in adolescence are quite common and temporary.

The heart of an adult and the heart of a child differ in many ways from each other, in addition to the size of the differences relate to the distribution of muscle mass and frequency of contractions. In adolescence, there is a rapid change in the entire cardiovascular system, the body matures and needs a different blood supply to the organ. Already these rapid changes in themselves lead to the emergence of extrasystoles – during the growth of the heart, special, excitable elements arise among its cells, capable for one reason or another to generate a nerve electrical impulse that causes a contraction of cardiomyocytes – myocardial cells. The structure of the myocardium, especially the fact that absolutely all cardiomyocytes are interconnected in a single three-dimensional network, therefore, the electrical impulse that has arisen in one place very quickly spreads to the whole heart and causes its contraction – this is the extrasystole. As a rule, after the end of adolescence and puberty, the excitable myocardial cells are already regulated by both intracardiac and intracardiac factors, so extrasystoles no longer arise.

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.