Cardiac Arrhythmias with no Cardiac Causes. Who is to Blame?
The study of the possible cardiac arrhythmias, their electrocardiography identification and the bases of their medical treatment, are not possible without doing beforehand a brief summary of the cardiac electrogenesis and arrhythmogenesis physiology.
SPECIFIC INTRACARDIAC ELECTRICAL CONDUCTION SYSTEM
In the heart we can define two types of muscular fibers: the ones called banal, base of the myocardium muscles contraction; and the specific muscular fibers that are a particular modification of the muscular fiber, from which it depends the electric stimuli production and conduction.
One of the main characteristics of the heart is that is an organ with certain autonomy, because if it already has a series of important extern regulation and control mechanisms, also is capable of generating its own stimuli, with a determined rhythm and frequency depending on the specie, breed, sex, age and physical condition.
This cardiac electrical autonomy depends in an exclusive way of the specific myocardium fibers from the conduction system, that has a specialized tissue formed by the next elements:
a) Sinusal Node (SAN), sino-auricular, sino-atrial or Keith-Flack, who first discovered it in 1907. Is the physiologic pacemaker of the heart and is where the electric potential initiates. Is the structure with more rhythm, autonomy and chronotropism, that is why it rules the cardiac activity.
Anatomically it is localized in the "sulcus terminalis", in the angle formed by the cranial cava vein and its union with the right auricle.
It is formed by myocardial specialized fibers surrounded by a dense fibroelastic connective tissue and the cells in this fibers are rich in content of glycogen.
b) Auricular-Ventricular Node (NAV) or atrio-ventricular node or of Tawara, who discovered it in 1906. Is the one in charge of the conduction of electrical stimuli from the atriums to the ventricles and to modulate this impulse. This is the second element in charge of the rhythm and it can take the pacemaker role in pathologic situations when the rhythm goes up or when the rhythm of the sinusal node decreases under the acceptable limits.
It is localized above the tricuspid valve, in the right heart as the sinusal node, in the union of the caudal and ventral portions of the interauricular septum with the right auricle.
Is a structure integrated in the intrinsic system because it communicates with the sinusal node through the internode section that is formed by various conduction fibers and also is communicated with the bundle of His that conducts the stimuli to the ventricles.
This node is formed by fibers that resemble the ones of the sinusal node, with fewer myofibers than the banal myocardium muscular fibers.
c) Bundle of HIS described by His in 1893, is a structure that appears in the auricular-ventricular node and roams with a cranial and ventral direction, and later it bifurcates into left and right branches.
Its fibers are also rich in glycogen and have fewer connective tissue.
The left branch of the bundle of His divides rapidly forming the anterior left fascicle and posterior left fascicle and it is extended through the left side of the interventricular septum, to continue with the Purkinje fibers on the division of the medial and apical third of the interventricular septum's left side.
The right branch of the bundle of His descends through the right side of the interventricular septum to end and branch in the Purkinje Fibers, on the most apical zone of the right side of the interventricular septum.
d) Purkinje Fibers described by Purkinje in 1845, are the ones in charge of conducting the electrical stimuli to the banal muscular fibers so that at it reception these contract.
The Purkinje Fibers penetrate a third of the myocardium, taking as a reference the endocardium.
CARDIAC ACTIVATION AND ELECTROGENESIS
The study of the activation and generation of electrical cardiac system impulse is fundamental because without it, it is impossible to check the arrhythmias that we will see ahead. The so called electrogenesis must be understood as the mechanism or process for which there is development of the electrical cardiac generating activity of the waves detected in the electrocardiogram, waves that are registered in the exterior surface of the body.
The auricular activation begins in the sinusal node, placed, since we have already said, in the union of the cranial cava vein with the right auricle. This cellular formation is the habitual cardiac pacemaker and it has the aptitude to generate its own impulses, imposing its own rhythm, frequency and automatism in normal conditions to the rest of the myocardium both as for the auricles and as for the ventricles refers.
The normotrop stimulus that originates in the sinusal node, invades the banal auricular myofibers, propagating later to the whole auricular myocardium in the shape of concentric circles every time in major radios. This so special form of spread is due to the fact that in the auricles, the intrinsic specific system of conduction is different from that of the ventricles.
The trajectory crossed by the electrical impulse inside the auricles is the following: external face of the right auricle, anterior face of the right auricle, interauricular septum, anterior left face of the left auricle and finally, the most caudal and ventral part of the left auricle.
If we represent in vectors this auricle activation, the resultant vector of the same one or vector P is the sum of the partial vectors of the activation of the right auricle, interauricular septum and the left auricle, and it goes from above to below, from right side to left side and from ahead to behind. The sense comes marked by the top of this vector P.
The predominance of the forces of activation of the left auricle is the determinant of the caudal, ventral and left sense of the resultant vector. In the majority of the young animals, this vector is more caudal than in the adults.
In short, we can say that the auricle depolarization, and therefore the cardiac one, begins in the sinusal nodule, so that the right auricle is depolarized first and the end of the depolarization of the left auricle being the one that marks the end of the auricle global activation.
The electrocardiography consequence of the auricular activation is the inscription on the electrocardiography tracing of the P WAVE. The first part of the above mentioned wave, its initial slope, corresponds to the activation of the right auricle, the beginning of the activation of the left auricle and to the activation of the interauricular septum. The second half of the P wave corresponds basically to the terminal slope marked by the left auricle activation.
The duration of the P wave is according to the necessary time in order that the front of excitement spreads from the sinusal node up to the most distant parts of the auricles. The largeness of the P wave, is determined by the existing relation between the auricle myocardium activated and in rest (represented by a bipolar vector) and the spatial axes of the cardiac derivation that is explored in that moment.
As soon as the auricle activation was concluded, the wave of excitement comes to the auricular-ventricular node.
The electrical excitement proceeding from the sinusal node, is canalized obligatorily by the auricular-ventricular node, where it suffers a physiological delay for, later, fasten into the bundle of His.
The electrocardiography consequence of the auricular-ventricular conduction is the inscription in the electrocardiography tracing of a segment called PQ, which registers after the P wave.
Really, the P wave joins with the segment P-Q and there obtains the so called P-R Interval that includes the auricle activation and the auricular-ventricular conduction.
Though in the clinical practice it does not have too much importance, it is necessary to highlight that the endocavitary electrocardiography is the only skill that it would allow to detect and to register in an effective form the brief electrical phenomenon that reflects the step of excitement of the wave along the bundle of His, which would be the following step. This skill allows to detect and to locate auricular-ventricular blockages with enough accuracy.
The auricle repolarization determines a vector that has the same intensity and the same direction as the vector of depolarization, with the difference of which in the case that occupies us, the sense is opposite.
This vector does not have detectable consequences in the electrocardiography tracing since it remains superposed with the ventriculogram tracing that masks it; for this reason, only in certain pathological cases we will be able to appreciate it.
The ventricular activation include the set of electrical phenomena that they lead to the depolarization or ventricular contraction.
In order for this to take place, we have to bear in mind a series of special considerations inherent in the heart:
First it is necessary to emphasize the unequal distribution of the branches of the bundle of His; the right branch, which descends along the right face of the interventricular septum (IVth septum), is long and it ends next to the top of the right ventricle.
The left branch, passes through the opposite face of the septum, it is shorter and divides in the third half of the IVth septum in the anterior fascicle and the posterior fascicle; as consequence of this, the interventricular septum is the first portion of the ventricles that is activated, and chronologically the left branch is the first one in acting, leading the wave of depolarization to the left face of the interventricular septum.
Secondly, it is important to bear in mind the unequal thickness of the free ventricular walls since in an adult patient, the free wall of the left ventricle is thicker than that of the right ventricle, concerning two times its thickness.
Given that the largeness of the electrical potentials generated by the activation of a muscular wall is directly proportional to the thickness of the same one, the result is that the potentials proceeding from the ventricular left wall will be wider, than the ones originated from the depolarization of the free ventricular right wall and will register in a different way opposite to the left ventricle than opposite to the right.
The dog was included by Hamlin and Smith in 1965, according to its process of ventricular activation, in the so called group A, given that it has three general fronts of depolarization; in this group A are also classified the cat, the rat, the man and the monkey.
The ventricular activation in the dog begins with the initial septum activation, continues with the middle and parietal septum activation and ends with the activation of parietal and basal septum.
Since we have already said, the ventricular activation begins with the initial depolarization, during the first 5 milliseconds of the QRS complex of the electrocardiography tracing, of the apical third of the left face of the interventricular septum. This process is named Initial Septal Activation, being ventrocefalic the average direction of the electrical activity.
From this point, the electrical excitement spreads in the following 5 milliseconds to the crown that surrounds the top of the left ventricle, including portions of the endocardium septum and of the free wall of the left ventricle.
Simultaneously, the right interventricular septum is activated from the right ventricular endocardium, when the stimulus comes from the right branch of the bundle of His, more delayed, like we have already said in advance.
This phenomenon of initial activation of the septum and of the apex of the left ventricle, produces a vector, which spreads in cranial-caudal direction, towards the right and scantly dorsum-ventral, with its positive ahead and its negativity behind.
Later it takes place the parietal activation that is carried out by means of the Purkinje net, immediately after the initial septum activation, beginning in the deep subendocardiac layers, to spread after rapidly to the superficial epicardic layers.
The activation of the left ventricle takes place with a light anticipation with regard to the right ventricle and generates electrical potentials of major intensity.
We would be in the following 10 milliseconds of the QRS complex, where the third apical of the interventricular septum is depolarized completely, which is excited from both endocardic surfaces, the apical portions of the free walls of both ventricles being activated rapidly in a radial way from the endocardium towards the epicardium.
In following 3-5 milliseconds, the third half of the interventricular septum and the free ventricular walls are activated, in direction apic-basilar, staying only the basal third without exciting.
Since we already talked, the activation of the left ventricle always takes place with a light anticipation on the right ventricle.
These phenomena that we have seen, of medial septum and parietal activation, originate a resultant vector of activation, directed to the left side and caudally, responsible for the electropositivity of the QRS complex in the IInd derivation of the ECG.
In the final 15 milliseconds of a complex in the ECG, there is a septal and parietal activation, that is the last myocardiac zone that is depolarized, concluding with this the process of ventricular depolarization.
This process produces the last vectors of ventricular activity, of apical-basilar direction, lightly directed to the right. With it we will find the ventricles completely depolarized.
In short we can conclude that the initial septum and apex activation of the left ventricle produces an electronegative vector measured opposite to the left ventricle (aVF derivation).
The parietal and septum half activation produces an electropositive vector and the basal terminal activation produces an electronegative one, of apical-basilar direction and of scarce largeness.
The consequence of all this, is the inscription in the ECG of the QRS complex with different morphology depending on the electrocardiograph derivation that is in use.
The entire duration of the QRS complex, is the so called QRS Interval and it represents the required time in order that the process of excitement spreads over the most retired points from the Purkinje system to the whole ventricular myocardium and it constitutes a measurement of the grade of simultaneous activation of the individual myocardiac fibers.
The ventricular repolarization takes place after the depolarization.
The time that passes between both phenomena expresses in the electrocardiograph point of view as the ST Segment. It is usual for this repolarization to begin, in general, in the same place as the depolarization, in other way, the zones that first are depolarized are those that first repolarize.
The distribution vector of the different waves of the ECG reveals that the processes of depolarization and repolarization continue the same rules, and for this reason, the potentials generated during the repolarization are an opposite sign to the ones generated in the ventricular depolarization.
The electrocardiograph consequence of the process is the T Wave.
The process of repolarization is slow compared to the depolarization and because of this, the T wave is of major duration compared to the QRS complex.
The largeness and the form of the T wave is determined by the routes of repolarization and the dipoles without canceling the generation.
In many occasions, while in practice, it is possible to include the duration of the QRS complex (QRS interval) with the S-T segment and the duration of the T wave in the so called Q-T Interval.
As soon as the production, conduction, spread and consistent contraction of the physiological mechanisms of the heart were checked, we are going to remember in a very abridged way the different mechanisms by which an arrhythmia can appear, before entering squarely into the classification and the study of these.
ARRHYTHMIAS PRODUCTION MECHANISMS
1. Acceleration of an Automatic Normal Focus.
The typical example is the sinusal tachycardia.
2. Stop of an Automatic Normal Focus.
The typical example is the sinusal bradycardia.
3. Automatism Acquisition By A Cell That Was Not Possessing It.
The examples are the extrasystoles and the auricular-ventricular, auricular or ventricular tachycardias.
The extrasystoles by automatism of new appearance do not mate with the base rhythm in any sense.
4. Abnormal Secondary Automatisms.
They always depend on a previous stimulus that induces them.
They are changes on the membrane potential of the myocardiac fibers, that take place before the entire repolarization or after it. Many extrasystoles must be included in this group.
5. Anomalies in Impulses.
a. With anatomical injury of the myocardiac fibers of the intrinsic conduction system.
b. With electrophysiological alteration.
It is a question of the cardiac conduction blockades.
6. Simplification Excess in the Impulses Conduction.
a. Simplification excess with an anatomical cause: incidental routes between auricles and ventricles.
They are the syndromes of pre-excitement.
b. Simplification excess with an electrical cause.
It is a question of two electrophysiological concepts:
i. Phenomenon of addition: it takes place when two weak impulses come to a point and manage to overcome it because they take part simultaneously; if any of them was coming separately to this point, it would not be capable of crossing it and it would be blocked.
ii. Phenomenon of Wedensky: it is a phenomenon in which an impulse of lower intensity as for to cross a point of the conduction system, arrives at this point just after another impulse of greater intensity which is going to allow that, in this case, the impulse of lower intensity, which was too weak in normal conditions, can cross the difficult point by the simplification phenomenon of Wedensky.
This notion implies that an electrical impulse that originates in any point, manages to activate the heart completely and besides it, does not disappear later, but after a slow retrograde conduction, it activates the myocardium again that would be already in excitable period and a new contraction is generated. The typical example is constituted by the auricular fibrillations.
1. Bonagura, J.D., Ware,W.A.; Atrial fibrillation in the dog; clinical findings in 81 cases. J.Am.Med.Assoc.1986; 22:111-0.
2. Collet,M., LE Bobinnec,G.; Electro-cardiographie et rythmologie canines. Maison Alfort: Collection Médecine Vétérinaire, Ed. du Point Vétérinaire,1990.
3. Cornet,P.; Précis d' électrocardiographie canine. Maison Alfort: Ed. du Point Vétérinaire,1985.
4. Dimarco, J.P., Prystowsky, E.N.; Atrial arrhythmias. State of the Art. American Heart Association. Futura Publishing Co, Inc. NY, 1994.
5. Durrer,D., Van Der Tweel,L.H.; Excitation of the left ventricular wall of the dog and goat. Annal´s New York Academy of Sciences, pp. 779-803.
6. Edwards,N.J.: Bolton´s Handbook of canine and feline electrocardiography. 2 nd. Ed. Philadelphia: W.B. Saunders Co., 1987.
7. Fox,P.R., Sisson, D., Moïse, N.S.: Textbook of Canine and feline Cardiology. 2 nd. Ed. Philadelphia. W.B. Saunders Co. 1999.
8. Hamlin,R.L., Smith,R.; Anatomical and physiologic basis for interpretation of the electrocardiogram. Am.J.Vet.Res., 21, (701-708), 1960.
9. Hamlin,R.L., Smith,R.; Categorization of common domestic mammals based upon their ventricular activation process. Annals New York Academy of Sciences, pp. 195-203. 1965.
10. Kulbertus, H.E., Wellens, H.J.J., Bourgeois, I.M.G.P., Sutton, R. ; Atrial Fibrillation: Facts from yesterday-Ideas for tomorrow. Futura Publishing Co. Inc. NY, 1994.
11. Lunney,J., Ettinger,S.J.: Mexiletine administration for management of ventricular arrhythmia in 22 dogs.: J.A.A.H.A.1991; 27:597-600.
12. Muir,W.W.: Antiarrhythmic drugs. Treatment of cardiac arrhythmias. Vet.Clin.No.Am.: Small Anim.Pract.1991; 21 (5): 957-87.
13. Novotny,M.J., Adams,H.R.: New perspectives in cardiology: recent advances in antiarrhythmic drug therapy. J.A.V.M.A.; 1986; 189 (5): 533-9.
14. Tilley,L.P., Owens,J.M.: Cardiología de los pequeños animales. Barcelona: Salvat Editores, S.A.,1987.
15. Tilley, L.P.; Essentials of canine and feline electrocardiography. 3 rd. Ed. Philadelphia: Lea & Febiger. 1992.
16. Ynaraja Ramirez, E. ; Manual Clínico de Cardiología Básica en el perro y el Gato. Pulso Ediciones S.A. Barcelona. 1995.