A bunch of maheim in the heart. Topic: physiological properties of the heart muscle
Bachman the bundle starts from the sinoatrial node, some of the fibers are located between the atria (interatrial bundle to the left atrial appendage), some of the fibers are directed to the atrioventricular node (anterior internodal tract).
Wenckebach the bundle starts from the sinoatrial node, its fibers are directed to the left atrium and to the atrioventricular node (middle internodal tract).
James the bundle connects one of the atria with the AV junction or passes within this junction; along this bundle, excitation can prematurely spread to the ventricles. The James bundle is important for understanding the pathogenesis of Lown–Guenon–Levine syndrome. The faster propagation of the impulse in this syndrome through the accessory pathway leads to a shortening of the PR (PQ) interval, but there is no widening of the QRS complex, since excitation spreads from the AV junction in the usual way.
Kenta bundle - accessory atrioventricular connection - an abnormal bundle between the left atrium and one of the ventricles. This bundle plays an important role in the pathogenesis of Wolff–Parkinson–White syndrome. Faster propagation of the impulse through this additional pathway leads to: 1) shortening of the PR interval (PQ); 2) earlier excitation of part of the ventricles - wave D occurs, causing expansion of the QRS complex.
Mahaima bundle (atriofascicular tract). The pathogenesis of Mahaim syndrome is explained by the presence of an additional pathway connecting the His bundle with the ventricles. When excitation is carried out through the Maheim bundle, the impulse propagates through the atria to the ventricles in the usual way, and in the ventricles part of their myocardium is excited prematurely due to the presence of an additional conduction pathway. The PR (PQ) interval is normal, and the QRS complex is widened due to the D wave.
Extrasystole- premature (extraordinary) contraction of the heart, initiated by excitation emanating from the myocardium of the atria, AV junction or ventricles. The extrasystole interrupts the dominant (usually sinus) rhythm. During extrasystole, patients usually experience interruptions in the functioning of the heart.
Property myocardial contractility provides the contractile apparatus of cardiomyocytes connected into a functional syncytium using ion-permeable gap junctions. This circumstance synchronizes the spread of excitation from cell to cell and the contraction of cardiomyocytes. An increase in the force of contraction of the ventricular myocardium - the positive inotropic effect of catecholamines - is mediated by β 1 - adrenergic receptors (sympathetic innervation also acts through these receptors) and cAMP. Cardiac glycosides also increase contractions of the heart muscle, exerting an inhibitory effect on Na+,K+ - ATPase in the cell membranes of cardiomyocytes.
Required initial level of knowledge:
1. Location and structural features of the automation nodes and conduction system of the human heart.
2. Membrane-ionic mechanisms of the origin of PP and PD in excitable structures.
3. Mechanisms and nature of information transfer in muscle tissue.
4. Ultrastructure of skeletal muscle tissue and the role of cellular-subcellular formations involved in contraction.
5. Structure and function of the main contractile and regulatory proteins.
6. Basics of electromechanical coupling in skeletal muscle tissue.
7. Energy supply for the process of excitation - contraction - relaxation in the muscles.
Lesson plan:
1. Introductory word from the teacher about the purpose of the lesson and the scheme of its implementation. Answers to student questions - 10 minutes.
2. Oral survey - 30 minutes.
3. Educational, practical and research work of students - 70 minutes.
4. Students complete individual control tasks - 10 minutes.
Questions for self-preparation for the lesson:
1. Physiological properties and characteristics of the heart muscle.
2. Automaticity of the heart muscle, its causes. Parts of the conduction system of the heart. The main pacemaker of the heart, the mechanisms of its rhythm-forming function. Features of the occurrence of PD in the cells of the sinus node.
3. Automatic gradient, the role of the atrioventricular node and other parts of the conduction system of the heart.
4. Action potential of working cardiomyocytes, its features.
5. Analysis of the spread of excitation throughout the heart.
6. Excitability of the heart muscle.
7. Contractility of the heart muscle. The “all or nothing” law. Homeo- and heterometric mechanisms of regulation of myocardial contractility.
8. The ratio of excitation, contraction and excitability during the cardiac cycle. Extrasystoles, mechanisms of its formation.
9. Age characteristics in children.
Educational, practical and research work:
Task No. 1.
Watch the video “Properties of the heart muscle.”
Task No. 2.
Look at the slides “Origin and propagation of excitation in the cardiac muscle.” Draw in a notebook (for memorization) the location of the main elements of the conduction system. Note the features of the propagation of excitation in it. Draw and remember the features of the action potential of working cardiomyocytes and pacemaker cells.
Task No. 3.
After studying the theoretical material and watching (slides, films), answer the following questions:
1. What is the ionic basis of the membrane action potential of myocardial cells?
2. What phases does the action potential of myocardial cells consist of?
3. How did the representation of myocardial cells develop?
4. What is the significance of diastolic depolarization and threshold potential in maintaining cardiac automaticity?
5. What are the main elements of the conduction system of the heart?
6. What are the features of the propagation of excitation in the conduction system of the heart?
7. What is refractoriness? What is the difference between periods of absolute and relative refractoriness?
8. How does the initial length of myocardial fibers affect the strength of contractions?
Task No. 4.
Analyze situational tasks.
1. The membrane potential of the pacemaker cell of the heart increased by
20 mV. How will this affect the frequency of automatic pulse generation?
2. The membrane potential of the pacemaker cell of the heart decreased by 20 mV. How will this affect the frequency of automatic pulse generation?
3. Under the influence of the pharmacological drug, phase 2 (plateau) of the action potentials of working cardiomyocytes was shortened. What physiological properties of the myocardium will change and why?
Task No. 5.
Watch videos introducing experimental techniques. Discuss what you saw with your teacher.
Task No. 6.
Perform experiments. Analyze and discuss your results. Draw conclusions.
1. Analysis of the conduction system of the heart by applying ligatures (Stannius ligatures), (see workshop, pp. 62-64).
2. Excitability of the heart, extrasystole and reaction to rhythmic stimulation. (see Workshop pp. 67-69).
1. Lecture material.
2. Human physiology: Textbook/Ed. V.M.Smirnova
3. Normal physiology. Textbook./ V.P. Degtyarev, V.A. Korotich, R.P. Fenkina,
4. Human physiology: In 3 volumes. Per. from English/Under. Ed. R. Schmidt and G. Tevs
5. Workshop on physiology / Ed. M.A. Medvedev.
6. Physiology. Fundamentals and functional systems: Course of lectures / Ed. K. V. Sudakova.
7. Normal physiology: Course of physiology of functional systems. /Ed. K.V. Sudakova
8. Normal physiology: Textbook / Nozdrachev A.D., Orlov R.S.
9. Normal physiology: textbook: 3 volumes. V. N. Yakovlev et al.
10. Yurina M.A. Normal physiology (educational manual).
11. Yurina M.A. Normal physiology (short course of lectures)
12. Human physiology / Edited by A.V. Kositsky.-M.: Medicine, 1985.
13. Normal physiology / Ed. A.V. Korobkova.-M.; Higher school, 1980.
14. Fundamentals of human physiology / Ed. B.I. Tkachenko.-St. Petersburg; 1994.
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The presence of additional conduction pathways (APP) connecting the atria with the ventricular myocardium or with elements of the conduction system is due to the incompleteness of heart formation in embryogenesis.
The main additional pathways include:
- Kent's bundle - atrioventricular (multiple options are possible). The Kent bundle can be either manifest (excitation is carried out in both antegrade and retrograde directions) and latent (has only retrograde conduction).
- Mahaim fibers - connecting the atrioventricular node to the right side of the interventricular septum or the right branch of the His bundle (less than the trunk of the His bundle with the right ventricle).
- The James tract is a bundle that connects the sinus node and the inferior part of the atrioventricular node.
- The Berschenmanche tract is a bundle connecting the right atrium and the common trunk of the His bundle.
In approximately 50% of cases, additional pathways are located in the free wall of the left ventricle, in 30% of cases in the interventricular septum and in 20% in the wall of the right ventricle.
The main consequence of the presence of an additional pathway is the syndrome of premature excitation of the ventricles, i.e. depolarization of part or all of the ventricular myocardium occurs earlier than along normal conduction pathways. In this case, the electrocardiogram records a shortening of the P-Q interval (less than 0.12 s) in combination with changes in the QRS complex (delta wave) or without it.
The peculiarity of impulse conduction along an additional conduction path is the ability to quickly conduct it at a constant speed, as long as the interval between impulses exceeds the refractory period of the additional conduction path. Unlike the additional conduction pathway, the atrioventricular node is characterized by decremental conduction, i.e. inverse relationship between conduction velocity and impulse frequency.
The most common form of premature ventricular excitation syndrome is Wolff-Parkinson-White syndrome, caused by the presence of the atrioventricular bundle of Kent. Its frequency is 0.15-0.2% in the general population. Wolff-Parkinson-White syndrome is quite often (about 30% of cases) combined with congenital heart defects and other stigmata of dysembryogenesis. Familial cases of Wolff-Parkinson-White syndrome have been reported, in which multiple bundles of Kent are more often detected. When electrocardiographic signs of premature ventricular excitation syndrome and paroxysms of tachycardia are combined, they speak of Wolff-Parkinson-White syndrome. The presence on the electrocardiogram of signs of premature ventricular excitation syndrome in the absence of tachycardia paroxysms is called the Wolf-Parkinson-White phenomenon. It should be noted that with age, the frequency of paroxysms of supraventricular tachycardia increases (20-39 years - 10%, over 60 years - 36%) and the Wolf-Parkinson-White phenomenon can transform into Wolf-Parkinson-White syndrome. If there are no signs of premature ventricular excitation syndrome on the electrocardiogram, but there are paroxysms of tachycardia with the participation of a hidden, retrograde conduction bundle of Kent, this condition is called hidden Wolff-Parkinson-White syndrome. In latent Wolff-Parkinson-White syndrome, the presence of an additional pathway can only be detected during an intracardiac electrophysiological study. In rare cases, the so-called intermittent Wolff-Parkinson-White syndrome is noted, when signs of premature ventricular excitation syndrome on the electrocardiogram may appear and disappear.
The Kent bundle is most often located in the free wall of the left ventricle (46-60% of cases), in 25% of cases - in the posteroseptal region and in the septal region, in 13-21% of cases - in the free wall of the right ventricle and in 2% - in the anteroseptal region areas. Approximately 13% of patients have more than one accessory pathway.
The severity of the syndrome of premature excitation of the ventricles can be different and depends on the speed of conduction along the Kent bundle and the speed of conduction along normal conduction pathways (Fig. 1).
Rice. 1. Factors influencing the severity of premature ventricular excitation (from H.J. Wellens, M. Conover).
A, B - electrocardiogram and intracardiac electrogram (HRA - upper right atrium, His - His bundle trunk, CS - coronary sinus). B - conduction time from the sinus node (SU) through normal pathways is 35+80+45=160 ms. The pulse propagation time from the control system to the left-sided additional conduction path is 65 ms and along the additional conduction path is 30 ms (total - 95 ms). Due to the short conduction time through the accessory pathway, a significant part of the left ventricular myocardium is excited prematurely, which is reflected in the electrocardiogram
in the form of P-Q shortening, the formation of a pronounced delta wave and a significant expansion of the QRS complex. D - lengthening of the conduction time from the SG to the beginning of the additional conduction path to 90 ms and slower conduction along the additional conduction path (35 ms) in combination with faster conduction through the atrioventricular node (60 ms) leads to the fact that a large
part of the left ventricular myocardium is excited through normal pathways and only a small part through an additional pathway. The electrocardiogram shows a normal P-Q interval and a narrow QRS complex.
Tachycardias associated with the existence of additional pathways are called reciprocal tachycardias (RT). In the most common form of RT, excitation propagates from the atria to the ventricles through the normal AV node, returning from the ventricles to the atria along an accessory pathway. As a result, tachycardia develops with a narrow QRS complex, in which P waves are recorded after this complex (PR > RP).
Tachycardias that develop during this course of the excitation wave are called orthodromic. Very rarely, conduction in the opposite direction is possible, resulting in the development of antedromic RT with a wide QRS complex. Additional pathways (eg, the bundle of Kent) connecting the atria to the ventricles, bypassing the AV node, are the cause of Wolff-Parkinson-White (WPW) syndrome. In this syndrome, arrhythmias are combined with a characteristic ECG pattern with a shortened PQ interval and an “erased” QRS complex. The shortening of the PQ interval and the appearance of the delta wave are associated with antegrade conduction along the accessory pathway, but retrograde conduction of excitation along these pathways plays a decisive role in the occurrence and maintenance of orthodromic RT. Thus, the arrhythmia may be maintained by a hidden accessory pathway (normal PQ interval, absence of delta wave in sinus rhythm).
In Lown-Ganong-Levine (LGL) syndrome, an accessory pathway connects the atrium to the His bundle, bypassing the AV node. On the ECG, the PQ interval is short (as in WPW syndrome), but the QRS complex is narrow. The type of arrhythmia in patients with LGL syndrome is the same as in WPW syndrome, and their drug treatment is similar.
Clinical picture
RT usually manifests itself in one of three age periods: in the first year of life, in adolescence and young adulthood (from 12-13 to 21-23 years) and in middle-aged people (45-60 years).
In children of the first year of life, with a prolonged attack of RT, signs of heart failure may be observed. In other cases, there are attacks of shortness of breath, lethargy, difficulty feeding, or symptoms of rapid pulsation in the precordial region.
RT may also first appear in adolescence or young adulthood. Typical attacks have a sudden onset and in many cases are associated with physical exertion. Paroxysms of RT can last from a few seconds to several hours (in rare cases, more than 12 hours). Young, otherwise healthy people tolerate RT surprisingly easily, and it is often almost asymptomatic. The transition of RT to MA is an alarming symptom, since it can lead to a sharp and potentially life-threatening increase in the frequency of ventricular contractions (more than 250/min).
It may seem strange that arrhythmias involving accessory pathways (i.e., innate structures) sometimes appear only in middle age. However, in the anamnesis of many patients there is no indication of arrhythmias. We know little about long-term changes in accessory pathway function, but this age group has more unilateral conduction pathways (ventricular to atrium only) than younger adults with arrhythmia symptoms. Thus, with unilateral conduction pathways, a higher incidence of clinical manifestations of RT can apparently be expected than with bilateral conduction. On the other hand, a more frequent occurrence of atrial and ventricular extrasystoles due to age is also possible.
Treatment
Often an attack can be stopped with the help of vagotonic procedures (Valsalva maneuver, immersing the face in ice water), which slow down conduction in the AV node and destabilize the recurrent excitation circuit.
In children under 10 years of age, MA is a rare complication. For the purpose of prevention at this age, digoxin can be successfully used, but when prescribing it during puberty, it should be taken into account that the use of digoxin during the maturation of the child’s body is unsafe due to its facilitating effect on additional pathways.
In all other cases, digoxin is contraindicated, as it can shorten the refractory period of the atrial myocardium and accessory pathways and contribute to the development of VF. The attack can sometimes be stopped with the help of vagotonic procedures, especially if they are carried out soon after the onset of symptoms. In other cases, it is possible to interrupt the circular motion of the excitation wave by slowing down conduction through the AV node with verapamil or adenosine. An alternative strategy is to slow conduction along accessory pathways, which are probably the weakest link in the reentrant circuit; All drugs of classes 1a and 1c cause such a slowdown.
Despite concerns about the proarrhythmic activity of Class 1c agents when used in the treatment of ventricular arrhythmias, there is no evidence that they produce similar effects in otherwise healthy individuals with accessory pathway arrhythmias. Flecainide, procainamide, or disopyramide given intravenously or orally are effective and safe as emergency treatments for attacks. In practice, after identifying tachycardia with a narrow QRS complex, most patients are prescribed intravenous verapamil, which usually stops the arrhythmia not by affecting additional pathways, but by temporarily blocking or slowing conduction through the AV node. Long-term prevention of attacks requires drugs that are exceptionally effective with low toxicity. Flecainide, encainide, propafenone and disopyramide meet these criteria. Procainamide and quinidine are rarely used in Europe, but in North America they are widely used for long-term prophylaxis.
Amiodarone is quite effective, but the risk of toxic effects forces it to be used only in exceptional circumstances (for example, when all other treatments have failed).
Ed. N. Alipov
“Tachycardias caused by additional pathways” - article from the section
If the development and differentiation of cells of the conduction system of the heart is disrupted, embryonic tracts may remain in the myocardium. These muscle fibers form additional bundles along which the impulse moves around the main direction. Premature excitation of the ventricles occurs, which can be an asymptomatic form of arrhythmia or lead to sudden cardiac arrest.
Diagnosis requires an ECG and EPI. Treatment is conservative or radio wave cauterization of the myocardium is used.
📌 Read in this article
What does an additional pathway in the heart mean?
The conduction of the cardiac impulse from the sinus to the atrioventricular node (AVN), its short delay and movement through the ventricles is considered normal.
But some people also have additional pathways that can bypass the atrioventricular node. They may be located between parts of the AVU and the atria, the septum, or the ventricles themselves.
Additional pathways are normal for the intrauterine period of development. They are needed to contract cardiac tissue until the 20th week of pregnancy, and then in the area of the atrioventricular ring all muscle fibers become thinner, contract, and fibrous tissue forms in their place. If this does not happen, then they remain and after the birth of the child can lead to the development of arrhythmia. Moreover, this anomaly can manifest itself at any age.
Familial forms of rhythm disturbance are especially difficult.
Often, the detection of additional bundles is combined with a violation of the structure of the valves, septum, dysplasia (pathology of formation) of connective tissue, etc.
Clinical manifestations occur with rheumatism, hyperthyroidism.
Types of additional pathways
- The following bundles of muscle fibers extend from the atria:
- James - goes to the terminal part of the AVN from the sinus node;
- Kenta-Palladino - connects the atria with the ventricles (there are right and left) bypassing the conduction system of the AVU;
Breschenmash - from the right atrium to the bundle of His.
The Mahaim bundle unites the His trunk and AVU, the right ventricle and the septum. Sometimes additional paths are called nodal shunts, since they help bypass the AVU; short fibers in the node itself also belong to this group. There are also options with multiple paths.
Clinical significance of the pathology
In the presence of an abnormal path in the myocardium, various disturbances in the rhythm of contractions occur, called the syndrome of premature excitation of the ventricles.
Patients often learn about the existence of congenital pathologies of the conduction tract only when they have concomitant heart disease.
The impulse is formed in the sinus node, goes to the AVN and then along the normal pathway to the ventricles. At the same time, the next one passes along the additional path. Both enter the ventricle, but the second one comes before the first. This leads to disruption of the shape of the ventricular complexes on the ECG and premature excitation along the accessory pathway (delta wave).
The greater the speed of signal movement along abnormal fibers, the more myocardium will be covered by early excitation.
Even in one patient, the severity of arrhythmia varies significantly depending on the tone of the autonomic system, stress factors, hormonal and electrolyte balance.
It is used to detect abnormal pathways.
It is characterized by accelerated conduction of impulses bypassing the AVU along the Kent, Breshenmache pathways or simultaneous movement along the James and Mahaim beams. It can be obvious and hidden (only in the opposite direction), constant or periodic. In the latter case, the signal passes normally, but if there is a significant delay, an additional path is switched on in the AVU.
The ECG reveals:
- short PQ up to 0.1;
- additional wave (delta);
- altered QRS complex;
- leg block;
- normal atrial waves;
- attacks of tachycardia or atrial fibrillation.
Clerk-Levy-Christesco syndrome
Associated with activation of the James beam. Most patients have no clinical manifestations. During physical or emotional stress, strong heart palpitations and shortness of breath may occasionally occur. On the ECG it appears as a shortening of the PQ interval, while the ventricular complex is of normal shape, there is no delta wave. In the absence of symptoms, it has a benign course.
Activating the Mahaim Beam
In this case, the impulse almost completely passes the atrioventricular node, but then quickly moves along an additional path to the His bundle.
This causes blockade of the right (more often) or left leg, widening of the QRS and formation of a delta wave. The atrial wave and the distance from it to the ventricular complex do not change. Patients often develop supraventricular tachycardia.
Conservative treatment
If patients do not have manifestations of rhythm disturbances (shortness of breath, fainting, heart pain, circulatory disorders), then specific treatment is not required.
Such patients require periodic examination (at least once a year) and prophylactic administration of drugs to improve metabolic processes in the myocardium (Panangin, Riboxin, Magne B6). Particular vigilance is needed in case of familial forms of arrhythmia, especially in cases of sudden cardiac arrest in close relatives, as well as persons whose professions involve physical (athletes) or neuro-emotional (drivers, pilots) overload. They first try to relieve an attack of arrhythmia by massaging the carotid sinus (near the angle of the lower jaw), pressing on the eyeballs, holding the breath while inhaling and straining, inducing a cough or gag reflex.
The use of medications from the group of calcium antagonists and beta blockers is contraindicated, as they improve conduction along the accessory pathway, which increases the frequency of ventricular contractions and the possibility of developing ventricular fibrillation.
Endovascular destruction of accessory pathways
To destroy additional pathways, laser radiation, cold cauterization, or electric current can be used. Radiofrequency acupressure on the myocardium is recognized as the most effective. Its advantages include:
- good tolerance;
- short rehabilitation period;
- the ability to refuse to take antiarrhythmic drugs that are highly toxic.
If there are additional conduction pathways, before surgery, in addition to the standard ECG and stress tests, it is necessary to conduct an electrophysiological study of the heart. Sometimes ultrasound with Doppler sonography and MRI are also required.
Indications and contraindications
Cauterization of the myocardium with radio waves is carried out when a patient has:
- attacks of loss of consciousness, vascular collapse;
- reduction in cardiac output;
- direct and reverse impulse conduction with paroxysmal tachycardia;
- latent form of Wolff-Parkinson-White syndrome with a burdened hereditary history, high occupational risk;
- poor tolerance to medications or resistance to them, the presence of contraindications;
- atrial fibrillation and flutter;
- reciprocal (associated with impulse circulation) tachycardia;
- several accessory pathways with complex rhythm disturbances.
Carrying out
A conductor is inserted through a puncture in the femoral vein or artery, through which an electrode is brought to the location of the abnormal bundle. It heats up to 70 degrees, which destroys the cells of the accessory tract. For control, EPI is performed. In the absence of pathological passage of impulses, the operation is considered effective. Some patients may require a cardioverter-defibrillator or .
The presence of additional pathways allows impulses to bypass the existing conduction system of the heart.
This leads to ventricular preexcitation syndromes, which is dangerous during attacks of supraventricular tachycardia and atrial fibrillation.
The patient may have no symptoms, but in a stressful situation the risk of sudden cardiac arrest is increased. For treatment, medications are prescribed or radio wave ablation (cauterization) of the myocardium is performed.
Correct and timely first aid for tachycardia can save lives. What can and should be done at home during an attack? How to provide emergency care for paroxysmal, supraventricular tachycardia?
It starts directly from the lower part of the atrioventricular node, there is no clear boundary between them. This bundle is supplied by the artery of the atrioventricular node. Nerve fibers of the vagus nerve reach the atrioventricular bundle, but it does not contain its ganglia. The trunk of this puchea is located on the right side of the connective tissue ring between the atrium and the ventricle. Then it passes to the posterior and lower edges of the membranous part of the interventricular septum and reaches its muscular part. The length of the atrioventricular bundle trunk is 10-20 mm, diameter 0.5 mm. It stretches in the interventricular septum towards the apex.
Atrioventricular bundle is divided into three branches: the right - a continuation of the common trunk - goes to the right ventricle, the left anterior - to the anterior and lateral walls of the left ventricle, the left posterior - to the posterior wall and most of the interventricular septum (left, posterior). The left branches in its upper part are located nearby. The main branches subsequently break up into smaller branches and then pass into a dense network of cardiac conductive myocytes. Between the left branches at the level of the papillary muscles there is a network of conductive fibers - anastomoses, through which excitation can quickly pass when one of these branches is blocked into the blocked area of the left ventricle.
Ramifications right and the left branches of the atrioventricular bundle end in an extensive network of pyriforms located subendocardially in both ventricles. An electrical impulse arriving along the intraventricular pathways reaches these neurons and passes from them directly to the contractile cells of the ventricles, causing excitation and then contraction of the myocardium. The network of cardiac conductive myocytes is fed with blood from the capillary network of arteries of the corresponding region of the myocardium. In a healthy heart, impulses originate in the sinoatrial node and pass through the atria to the atrioventricular node.
Then they arrive into the ventricles through the atrioventricular bundle and its right and left branches, a network of cardiac conductive myocytes and reach the contractile cells of the ventricular myocardium.
In addition to the described main cardiac pathways, there are additional tracts or pathways.
In past century Kent described a bundle of fibers connecting the right atrium to the right ventricle, then the same bundles were found between the left atrium and the left ventricle in patients with Wolff-Parkinson-White syndrome.
Another additional path described by Mahaim. These so-called paraspecific fibers (or bundle) connect the atrioventricular node or atrioventricular bundle with the basal part of the interventricular septum, bypassing the legs of this bundle. The passage of a sinus impulse through the Maheim bundle leads to premature excitation of the base of one or another ventricle, and therefore broadening is observed on the ECG due to the appearance of a delta wave.
Fibers, or bundle, James. They connect the sinoatrial node to the lower part of the atrioventricular node. Along the James bundle, the impulse bypasses a significant part of the atrioventricular node, which can cause premature excitation of the ventricles, that is, a shortening of the P-Q interval on the ECG.
Conducting an impulse through additional ways is considered the main cause of Wolff-Parkinson-White syndrome. This same fact is a prerequisite for the development of extra asystole and paroxysmal tachycardia.
