Cardiovaskuler jurnal reading 26

228 Chapter 3. Pathophysiology of the cardiovascular system ( I.Hulın, F. Simko et al.)

In congestive cardiomyopathy it is possible to no-tice an abnormal conduction in the ventricles whichleads to some abnormalities in the QRS complex.We can notice the presence of some nonspecific STsegment and T wave changes as seen in other car-diomyopathies. In restrictive cardiomyopathies wecan notice a low voltage QRS complex and disap-pearance of progression in the precordium.

3.25.6.8 Electrocardiographic changesin metabolic and electrolytedisorders

The cardiac tissue is electrically active, and that iswhy the electrolyte changes can affect its electricalactivity.In hyperkalaemia the appearance of tall T waves

and a prolonged ventricular complex which becomesmated with the T wave to form one peak. P wave issmall and PR interval is prolonged.In hypokalaemia T waves become flattened or in-

verted. Whereas the U wave becomes very clear andthe QT interval is markedly prolonged. Its prolon-gation is partly due to the U wave which is matedinto the T wave. These signs signalize the possibleoccurrence of arrhythmias especially when digitalisor antiarrythmic drugs (group 1) are applied. TheECG changes in hypokalaemia are similar to thoseof hypocalcaemia. Hypocalcaemia prolongs the STinterval as well as the T wave, this will lead to QTinterval prolongation. Hypocalcaemmia on the otherside is not as dangerous as hypokalaemia in generat-ing cardiac arrhythmias. Non specific ECG changesoccur in hyperthyroidism, hypothyroidism, diabeticketoacidosis, and of course after the use of antiarry-thmic drugs. The prolongation of PR and QT in-terval as well as some non specific changes in STsegment and T wave are the most commonly seen.

3.26 The electrophysiologicalbasis in the generationof cardiac arrhythmias

The term arrhythmia constitutes all changes ofthe cardiac rhythm that render the rhythm differentfrom the normal sinus rhythm. The sinus rhythmis initiated in the SA node. The activation is pro-gressing then from the atria to the ventricles havinga normal PR interval that doesn’t exceed 0,20 s andthe heart rate in adults ranges between 60–100/min.The development of electrocardiology and espe-

cially the intracardial electrophysiological study andthe Holter monitoring could influence many opinionsabout cardiac arrhythmias. Many findings were usedto explain changes in the conventional electrocardio-graphy.From the histological and functional point of view

we can differentiate two types of cardiac cells: con-tractile cells, which duty is to provide the pumpingfunction of the heart and specialized cells for the for-mation and conduction of activation. The contractilecells have the ability to perform mechanical worksand conduct electrical impulses from cell to cell.The myocardial cells are connected to one another

by intercalated disks by which they form intercon-nected muscle fibers. The intercalated disks servethe conduction of mechanical energy, yet they haveelectrical characteristics which render the activationconduction from cell to cell much easier.The intercalated disks are formed by union of

plasma membranes of the neighboring cells. It isactually a doubled plasma membrane. The junctionis step, shaped with the alternation of areas orientedvertically and horizontally to the disk plane. Thisleads to an increment of the total surface area ofthe membranous contact. There are special junctionstructures in the intercalated disks being: The fasciaadherens, macula adherens (desmosom), and a nexus(gap). Fascia adherens is the most common struc-ture which form both plasmatic membranes whichare wavy and inserted to each other. They runin a parallel manner and are separated by a 20–30 nm wide slot. Fascia adherens on the other sideis the place where myofillaments are inserted. The

3.26. The electrophysiological basis in the generation of cardiac arrhythmias (I.Hulın) 229

desmosom or macula adherens is a structure having0,2–0,5 micrometer diameter in which the neighbor-ing plasma membranes are situated parallel to eachother. Nexus or the gap is a special structure whichis found in the longitudinal segments of the inter-calated discs. The electrochemical impulse spreadsthrough the gap from cell to cell. It is composedof tight junctions of the neighboring plasma mem-branes. The membrane is structurally different inthese areas. The gaps contain small channels 2–2,5nm in diameter through which small ions candiffuse from cell to cell. Gaps and desmosomes dopresent even in the lateral surfaces of the neighbor-ing cells.

According to other electrophysiological character-istics we can differentiate what is known as fast andslow cells. The fast cells are characterized by a largediameter and high speed of conduction. Their restingpotential is –90mV. The ascending edge of the actionpotential is very steep. On the action potential curvewe can see the overshoot to positive values and theplateau is very clear as well. Purkinje cells and func-tioning cells of the myocardium have the characteris-tics of the fast cells. The resting potential of the slowcells is between –50 and –70mV. Even the thresholdpotential is low (–30 till –40mV). The stimulationof slow cells starts endogenously by increasing themembrane potential (from –70 to –40mV) to reachthe threshold level. The ascending part of the ac-tion potential curve is not steep and there is no overshooting. There is no plateau on the action potentialcurve. These are the characteristics of both SA nodecells and AV node cells.

From the functional point of view we can find twotypes of cells, the myocardial functioning cells andcells of the cardiac conductive system. The mainfunction of the conductive system of the heart is thegeneration of impulses and their conduction form theSA node where they are usually generated to theatrial and ventricular myocardium. According tothe ultrastructure we can differentiate three types ofcells: the P cells, the transitional cells, and Purkinjecells.

P cells or the pacemaker cells present in largenumber in the AV junctional area. These cells gener-ate impulses and hence are marked as the automaticcells. Comparing those cells with the contractile cellsthey contain small number of mitochondria, and lessdeveloped sarcoplasmic reticulum. The slow conduc-

tion in the AV node is partially caused by the absenceof the intercalated disks.The transitional cells form a heterogeneous group

of cells which are present among the P cells, Purk-inje cell, and myocardial fibers. Purkinje cells aremainly present in the branches of His bundle and inthe Purkinje network. If we compare them with thecontractile cells we will find that they have less mito-chondria and linearly situated myofibrils. These cellsare also composed of many intercalated disks with asimple T system which might be absent. This systemmight be the basis of fast conduction of activation.From the conductive point of view the contractileelements are less effective. The Purkinje cells andsimilar contractile cells are on the other hand con-sidered to be electrophysiological.The basic electrophysiological characteristics of

the heart cells are automacity, excitability, and con-ductivity. Automacity is the ability of some cardiaccells to generate impulses which can spread to thesurrounding area. Excitability is the ability of all thecells in the heart to respond to an effective impulse.In case of repeated impulses these cells need a certaintime for recovery (refractory period). Conductivityis the ability of the cell to conduct impulses. The im-pulse conduction is related to the electrical phenom-ena of the transmembranous transmission but it isas well related to the heart as whole. The mentionedelectrophysiological characteristic could be disturbedand might lead into a disturbance of cardiac rhythm.This is the reason why we explain them in relationwith the generation of arrhythmia.

3.26.1 Automacity

Automatic cells (slow cells) are characterized by di-astolic transmembranous potential which is modifi-cated by spontaneous diastolic depolarization (grad-ual change in membrane potential in phase 4). Thediastolic transmembrane potential is not horizontalas in the contractile cells but is slow ascending, tillit reaches the threshold potential. In the contractilecells (fast cells) the formation of transmembrane ac-tion potential is the result of impulse affect, whichwas formed in the pacemaker cells.The impulse leads to an electrical flow which pro-

gresses across the cellular membrane. This electricalflow will reduce the diastolic transmembrane poten-tial of the regional contractile cells (in phase 4) tothe threshold potential. The change of the mem-


brane potential to the threshold potential and thebeginning of phase 0 will stimulate an electrical flowwhich spreads across the membranes and its originis in the automatic cells.The automatic cells have even with no external

interference the ascending phenomena in phase 4.This event proves that a slow diastolic depolarizationtakes place on the membranes. During diastole thecontinuous Na+ or Ca2+ flow is evident. It is markedas the IBi which is equalized by the K+ efflux IK2 orIP flow (see fig. 3.34 page 230).

Figure 3.34: Ascend phase 4th of transmembraneaction potential of an automatic cells

Inactivation of the potassium efflux explains theformation of transmembranous action potential,when sodium and calcium influx overwhelms or ex-ceeds the potassium efflux. IP inactivation is on theother hand responsible for the diastolic depolariza-tion of the SA node cells, and the IK2 inactivation isresponsible for diastolic depolarization of the Purk-inje cells. In normal conditions phase 4 is faster inthe SA node than in the Purkinje cells. The reason isthat the IP is inactivated faster than the IK2. Fromthe mentioned facts we can learn that automacity hasits origin in the changes of ionic flow. Automacityis produced when there is an excess in permeabilityand conductivity of K+, Na+, and Ca2+. Transmem-branous action potential (phase 0) in the automaticcells grows more slowly and reaches less values dueto its generation from lower values of the diastolictransmembrane potential.

The structures of the conducting system havethe duty of impulse conduction to other structures.Apart from this they have the ability to generate im-pulses which in certain conditions can be propagatedto the surrounding regions. Automacity can generatein the cells of A-V junctional area, but even in thebundle of His and Purkinje system where fast cellsare found. But this automacity is smaller (slower)and normally the sinus automacity is the dominantone.The automatic cells reach the threshold potential

fast. That is why cells which need the shortest timefor reaching the threshold potential dominate overothers and they become the center of impulses. Thetime taken by the diastolic depolarization to reachthe threshold potential is basically determined bythree factors.

1. The ascending speed of diastolic transmembranepotential (phase 4). The fast and soon reachedthreshold potential determines high automatic-ity

2. Level of the threshold potential. Whenmore negative level of the threshold potentialwith same ascending speed of diastolic trans-membrane potential the threshold potential isreached sooner. The final result is a faster auto-maticity meaning that a more negative thresh-old potential will increase the heart rate and viceversa.

3. Level of the diastolic transmembrane action po-tential (DTP). As this level is more negative onthe beginning of phase 4 more time is neededfor the spontaneous diastolic depolarization toreach the level of the threshold potential. Thespeed of impulse formation is hence decreased.Contraversly when the starting DTP is not verynegative the threshold potential is reached verysoon and the speed of impulse generation isfaster.

3.26.2 Automacity disturbances

Decrement of the SA node automaticity can happendue to the following causes:

1. Lowering of the DTP speed

2. Increment of the maximal diastolic potential(e.g.: due to hyperpolarisation)


3. Decrement of the threshold potential (reachingthe 0 level)

These causes can occur in combination (seefig. 3.35 page 232).

Increment of the SA node automaticity can hap-pen due to opposite causes of the mentioned above.

When the SA node automaticity is decreased itcould be compensated for by the automaticity ofthe AV junctional area and its frequency is only be-tween 20–40/min. If the automaticity in the AV areawas disturbed either, a pacemaker will generate inthe subjunctional area and its frequency is only be-tween 20–40/min. During certain structural condi-tions with slower activity the SA node automaticitycan not be interfered. These structures are depolar-ized with every excitation and they start to repeatthe cycle of renewing the membrane potential, whichstarts to get slower during any given disturbance.Impulses which start to generate as a result of thereduced automacity of the SA node, can be single orrepeated. These impulses from AV junctional areaor from the ventricles are referred to as escape im-pulses when they are repeated they may generate anindependent rhythm (escape rhythm).

In some case the ectopic, atrial, the AV junctional,or the ventricular automacity can increase so muchthat it exceeds the sinus rhythm. In these cases weare not dealing with a defensive but with a hyperac-tive rhythm. Impulses generating from an incrementof automacity can be isolated or can be repeated.Isolated impulses, which activate the heart do not de-pend on the original rhythm, they stimulate what isknown as parasystole. Isolated impulses which occurin relation with the original rhythm generate what isknown as extraxystole. Impulses can originate fromin one or more centers.

It was proved experimentally that depolarizationis sometimes incomplete or delayed. After reach-ing the membrane potential –50 till –70mV an earlypost potentials can occur and depolarization maystart again. Delayed post potentials (see fig. 3.36page 232) are the result of oscillating diastolic de-polarization. Arrhythmias caused by post potentialsare marked as trigger arrhythmias. They differ fromarrhythmias caused by a disturbance in the automac-ity. Trigger activity is noticed with arrhythmias thatoccur post acute coronary occlusion in its late stages(see fig. 3.36 page 232).

3.26.3 Excitability disturbances

Excitability is the ability of all cardiac cells to re-sponse on stimulus.Cardiac cells need a certain time to renew their

own excitability. The period needed for their ex-citability renewal corresponds with the final part ofthe TAP (voltage dependent excitability renewal).Slow cells need a longer period to renew theirexcitability (time dependent excitability renewal).This means that those cells don’t have their excitabil-ity renewed, when in phase 3 they reach a certainlevel of potential. Their excitability will be renewedafter some time of the TAP ends. Potential renewalof excitability corresponds with the transmembraneaction potential. The relation of excitability withTAP can be devided into 5 periods (phases) (seefig. 3.37 page 231):

Figure 3.37: Relationship of excitability to TAP

1. Complete refractory period. In this periodthe cellular membrane is absolute refractory to-wards any impulse. Absolute Refractory periodARP (see fig. 3.37 page 231)

2. Period of local response. It is a very short pe-riod in which some local changes of potential canoccur, yet the potential can not be propagated.The effective refractory period ERP consist ofthe ARP and a period of local response

3. Period of partial excitability. Consist of the lastpart of phase 3. The response is obtained only


Figure 3.35: Automacity decrease in SA node

Figure 3.36: Early and late postpotentials

by an above threshold stimulus and it can bepropagated. This phase is marked as the relativerefractory period (RRP)

4. Period of normal excitability. The cell respondsto any stimulus which has the threshold inten-sity.

5. Period of supernormal excitability. In this shortsection at the end of phase 3. The cell respondsto a sub threshold stimulus.

3.26.4 Conduction disorders

The impulse which generates in the SA node is prop-agated through a special conductive system to theatria and to the ventricles. The progress of acti-vation is basically an electrochemical change, whichtakes place on the cellular membranes. This is real-ized without chemical mediators, but the speed of theactivation progress can be changed by material whichusually affect the TAP (those are catecholamins,acetylcholin and anti arrythmic substances).

The cytoplasm of muscle fibers and interstitialfluid have a low resistance and are good electric


transmitters. Cellular membranes are structureswith high resistance and they seperate these 2 me-dia. The conduction is different in the fast and slowcells. For fast cells the regenerative conduction istypical. For slow cells in the junctional area, mainlythe AN and H ones the decremental conduction istypical. The speed of conduction in different cardiacstructures is:

• atria 1–2 m/s

• AV node 0,05 m/s

• His–Purkinje system 1,5–4 m/s

• Ventricles 0,3 m/s

The speed of conduction is determined by 2 basicfactors:

1. How fast the TAP level is reached (dV/dtphase 0)

2. Ultrastructural characteristics

Thin fibers (contractile and transitional cells) andthose not having intercalated disks (P cells) con-duct activation slowly. Thick fibers with intercalateddisks (Purkinje cells) conduct activation fast.In the sinoatrial junction and AV junction area the

activation is progressing slowly. This is caused by thepresence of large number of P cells and transitionalcells. In these structures conduction disturbancescan be in form of supernormal conduction, gap phe-nomena, slow conduction, and a hidden conductionand reentry mechanism.Conduction faster than normal. An early impulse

can be blocked during propagation. Sometimes anectopic impulse is created even earlier and this im-pulse could be propagated. On one side we are deal-ing with a supernormal excitability of the surround-ing cells but on the other hand there is a supernor-mal conduction. This could be the result of tran-sitional hyperpolarisation of cellular membranes. Itwas shown experimentally that a supernormal con-duction can be time or tension dependent. Duringpre- mature stimuli the supernormal conduction maylead to gap phenomena. Premature impulse slowsthe progression of activation. The earlier impulsecomes the slower. The activation reaches the distalzones outside of refractory period.

The result is that there is shortening of the com-plete activation progressing time. Another gap phe-nomen is noticed with antigrade and retrograde con-duction. Differentiation could only be obtained byintracardial electrocardiologic monitoring.

Conduction via abnormal pathways. These con-ductions are mainly shown in WPW (Wolf Parkin-son White) syndrome and in short PR interval syn-drome. It cold occur even with other disorders. Inthese cases the activation is progressing via unusualpathways which might or might not be histologicallyevident.

Slowing of conduction. There are many types ofslow conduction. It could only concern a certain partof conductive system of the heart. In the electrocar-diologic terminology we use the term block. We candistinguish many types of blocks. First degree heartblock. This term refers to a condition when impulsesare constantly created but their propagation is some-how a bit slower than normal.

Second degree heart block It is marked as Mob-itz I. A classic picture are Wenckebach periods dur-ing which the P-Q interval is gradually prolongingtill they reach a state where no impulse is propa-gated anymore. When the relation is not strong theblock is marked as Mobitz II.

Third degree heart block This type occurs whenno impulse is conducted to the ventricle. Atriaand ventricles have an independent activity on eachother. The AV dissociation can be caused by an ex-tremely long refractory period of the AV junction. Itcan be a picture of complete block. In this case noimpulse is transmitted from atria to ventricles. Incase of incomplete block and AV dissociation someimpulses can be conducted from atria to ventricles.In other cases it is possible that a fast activity in thejunctional area could be transmitted in a retrogradedirection back to the atria. There is formation ofAV dissociation with interference. Sinoatrial blockis a condition during which no impulse is conductedfrom the SA node to the atria. Usually in these casesthere is the formation of a substitute impulse in theAV–junctional area.

Aberrant Ventricular Conduction. Is formed asa result of differences in the refractory period be-tween some parts of the transitional abnormal dis-tribution of supra ventricular impulses. We can seeventricular complexes which have abnormal shapes.The condition can occur as a result of prolongation


of the refractory period in one of the branches orwhen the impulse reaches the ventricle through anaccessory pathway. In physiological conditions therefractory period is longer in the right arm. Theclassical aberrant conduction in ventricles dependsupon the length of diastole. It could be seen dur-ing extrasystolia or with tachycardia. Electrocardio-graphic picture of wide QRS with a supra–ventriculartachycardia may disappear with a certain drop in theheart rate. During fast heart rate the impulses inthe right branch of bundle of His are in the refrac-tory phase. The picture of aberrant conduction canoccur even when the cycle is prolonged. It is causedby an increased diastolic depolarization, or when thethreshold potential reaches near 0 levels, or by somehidden conductive pathway, or by a combination ofmany factors. Aberrant conduction occurs even withnormal cycle of an intermittent ventricular block. Itcan occur with incomplete depolarization in a cer-tain area of a conductive system of the heart or withincomplete production of TAP.Concealed Conduction Could be a partial depolar-

ization which can not be differentiated using the elec-trocardiogram. Concealed conduction is the cause ofa large number of phenomena in arrythmology. Usu-ally it is concerned with AV junction or branch ofbundle of His.Reentry disorders of conduction are sometimes

dealing with a certain area. We can talk about anextra bundle branch or local block. In the surround-ing tissue the activation can be conducted normally.A block in such a place could be unidirectional. Thismeans that activation can reach this area from theopposite side. In this case activation can spread re-peatedly via same pathways. The progress of activa-tion is slow.We are talking about classical reentry phenomena.

The obstacle of the spread of activation doesn’t haveto be an anatomical structure. When a circular ac-tivation is formed the conditions will be in favor ofslow progress of activation and of shortening the re-fractory period.

A. reentry with normal conductivity and uni-directional block

This type occurs in slow cells during some ab-normal conditions. In this case extrasystolies areformed. These extrasystolies have constant intervalafter the previous systole. Basically depending on

these facts three types of reentry can occur

1. enclosed conductive circle

2. unidirectional block

3. a proper speed for conducting activation.

An enclosed reentry circle can have many types.It can occur in the atria with or without participa-tion of the junctional area. In His-Purkinje systema vicious circle could occur either in the peripheralPurkinje fibers or at the level of junction of Purk-inje fibers with the contractile myocardium. In thiscase the vicious circle is very small. It is a typi-cal example of microreentery. It is usually the basicreason for ventricular extrasystolies and hyperactiveventricular rhythm. (see fig. 3.38 on page 235). Anenclosed circle could be formed in the branches andthe fascicles which have parallely situated fibers. Theproper conditions for the circle closure occur whentwo independent waves of activation are progressingsimultaneously. This condition is known as reentrywith summation of activation.A closed circle can happen in AV junctional area

(see fig. 3.39 on page 235). Reentry phenomenthen leads to the appearance of junctional reciprocaltachycardia. It is a regular supraventricular tachy-cardia. Reentry cycle can exist with the participa-tion of intranodal structures, or with the participa-tion of juxtanodal structures.Intranodal circle can have a pathway with a short

refractory period and a prolonged conduction, or itcan take the b pathway with a long refractory pe-riod and a shortened conduction. Sometimes theremight be formation of a pathway in the extranodalstructures which have the character of specialized ab-normal pathways. Reciprocal tachycardia with AVjunctional area participation can have:

1. slow antigrade and fast retrograde conduction

2. fast antigrade and slow retrograde conduction.

Unidirectional block. In this case the determinantis that a part of tissue can be activated from thetissue which is in the area of block. Overmore ifthe myocardium is not in the refractory period itcould be reexcited. A small circle could be formed,(a microreentery) or a large circle could be formed, amacroreentery, which has the character of intra andextra nodal circle. When it is intranodal it has the


Figure 3.38: Unidirectional block of one Purkinje fiber

Figure 3.39: Closed circuit in AV junctional region

characteristic of B pathways. The impulse can betransmitted form the atria via the A pathway to-wards the ventricles and can be transmitted retro-gradly back to the atria. The atria may be reacti-

vated. As a result of this the reentry continues withthe participation of both pathways.

When the cycle consist of atria, AV-junctionalarea, and ventricular myocardium it is very difficult


or even impossible to determine the exact place ofthe unidirectional block.A proper speed of conduction. When a reentry

of this type is formed the progress of activation cannot be very fast, otherwise it hits a zone which is inthe refractory period. It also can not be very slow.Because of the mentioned the atria would be thenactivated first by the SA node.

B. Reentery resulting from disturbance of re-fractory period

In this case some zones with shortened refractoryperiod may occur. In neighboring zones the refrac-tory period is prolonged or different (non homoge-nous). This situation usually occurs in areas whereslow and fast cells exist. During fibrillation theremay be a microreentery in different areas of the my-ocardium.

3.26.5 Sinoatrial node dysfunction

SA node is the dominant pacemaker of the heart be-cause it is the fastest one to reach the threshold po-tential level. The speed of diastolic depolarizationis under the control of vegetative nervous systemi.e. (autonomic nervous system). It is getting fastduring activation of the organism and slows downduring sleep and rest. The increment in impulse for-mation at rest is usually obtained by sympathetic ac-tivation via the B adrenergic receptors. Slowing onthe other hand is realized through the activation ofparasympathetic fibers via the muscarinic receptors.Sinus rhythm in the adults reaches a frequency be-tween 60–100beat/min. In children the frequency ishigher, in newborn it is about 120–140/min. Trainedindividuals (athletes) have a frequency which is be-low 50/min, most probably as a result of an incre-ment in parasympathetic tonus.The normal SA node function can be disturbed

due to decrement in the direct vascular supply ofthe SA node. This usually happens in coronarysclerosis, mainly the right coronary artery. An-other type of dysfunction is senile amyloidosis ofatrial myocardium. Sinus bradycardia occurs in hy-pothyroidism, hypothermia, liver diseases, brucel-losis, vasovagal syncope, hypoxia, hypercapnia, aci-dosis, acute hypertension, and in other conditions.If bradycardia occurs quickly, it can evoke haemo-dynamic changes, which are manifested as an acute

drop in the cardiac output. There might be no im-pulse formation in the SA node (sinus arrest) or theremight be a block of the SA node. Sometimes the SAnode dysfunction occurs together with AV dysfunc-tions. Elsewhere the SA node disfuction and arrestis manifested by syncope and a possible junctionalrhythm. Yet more often the SA dysfunction is shownas an inability to increase cardiac frequency duringsituations which are usually accompanied by tachy-cardia. The SA node dysfunction can appear afterthe use of pharmaceutics which usually don’t affectthe heart rate in healthy individuals.

Sick sinus syndrom has a very wide range of symp-toms. It is manifested by bradycardia, sinoatrialblock, or sinus arrest. Atrial tachyarhythmia aswell as fibrillation and flutter are usually joinedwith tachyarhythmia and bradyarrythmia. Sinoa-trial block of first degree presents a prolonged pro-gression of activation from the SA node to the sur-rounding tissue. When the atrial activation (P wave)is the first to be shown in the ECG, the first degreeblock can not be diagnosed from the electrocardio-gram. Only by a special examination being an in-tracardiac registration if possible.

Second degree sinuatrial block is a disorder, duringwhich some impulses from the SA bundle are nottransmitted to the surrounding tissue. It is expressedas the abscence of one P wave and the related QRScomplex.

Third degree sinuatrial block is actually a com-plete sinuatrial block. It cannot be differentiatedfrom sinus arrest on the ECG. This disorder couldbe registered by the use of intracardial registrationbradycardia.

Tachycardia syndrom is shown as tachyarhythmiaon the ECG. In this case the retrograde progressionof activation from the atria can lead to SA node sup-pression. The most important thing is to recognizethe relation between the SA node dysfunction andother symptoms from which the patient suffers.

Very important is the 24 hour monitoring of theelectrical function of the heart. By pharmacologicaltests it is possible to influence the autonomic nervoussystem, to find out if there is a primary error in theSA node. By using a complete chemical (pharma-cological) block of the autonomic nervous system itis possible to prove the SA node dysfunctions causedby the autonomic nervous system and to exclude pri-mary SA node dysfunction. An effective method is


the intracardiac registration with complete pharma-cological block, so that it is possible to measure therefractory time for the SA node. First we providethe atrial pacing and after that we notice how muchtime is needed for the activity of the node to oc-cur. The SA node recovery (refractory time) is lessthan 550 ms, its prolongation is a sign of SA nodedysfunction. The carotid sinus syndrom can be ver-ified by short massaging of this area and monitoringthe ECG. Patients with SA node dysfunction mayor may not have various symptoms in relation withthis dysfunction. In the asymptomatic SA dysfunc-tion it is not necessary to do the electrocardiologicalmonitoring or cause any trauma to the patients byother examinations. SA node dysfunction often oc-curs together with AV conduction defects. Here thehaemodynamic symptoms are mostly caused by theAV conduction disorder and not by the SA node dys-function alone. In these cases it is necessary to pro-vide a complete electrocardiographical examinationtogether with the electrocardiographic registrationof the His bundle and a programmed atria R andventricular stimulation. In patients with SA nodedysfunction, which is connected with haemodynamicoutcomes a permanent pacemaker is very likely thebest solution. In a disorder which is manifested onlyduring a paroxysm or during an attack it is betterto use ventricular or biventricular or even atrial ondemand pacemaker (this pacemaker paces only whenneeded).

3.26.6 Disturbances of AV conduc-tion

There is a morphologically defined structure betweenthe atria and ventricles. This structure provides thetransmission of activation from atria to ventricles.Apart from activation conduction the atrioventric-

ular junction shares in the cardiac action coordina-tion by slowing down the conduction of activation,so that to enable the atria and ventricles to work in acoordinate manner from the haemodynamical pointof view.The AV junction is composed of structures to-

gether known as the AV junctional area. It is com-posed of the AV compact node, which is suppliedby sympathetic and parasympathetic fibers. Theprogress of activation is influenced by the autonomicnervous system. Slow transmission of activation is

known to occur in trained individuals with a markedvagotonia. The AV junctional area as well as theAV node changes during many diseases. AV blockscan occur even as congenital defects. The progressof activation across the AV area can be changed inmyocardial infarction of the posterior wall or in rightcoronary artery spasm. The AV junction is affectedby many drugs, mainly digoxin, beta blockers, cal-cium blockers, and some toxic substances. The AVconduction disorders are seen in some viral infectionslike viral myocarditis, in rheumatic fever, infectiousmononucleosis, in amyloidosis, and in neoplastic dis-eases of the heart. AV block can occur simultane-ously with the bundle branch block. This usuallyoccur in sclerotic fibrosis of the cardiac skeleton, aor-tic and mitral valves. Sclerodegenerative changes ofthe AV junctional area can occur in an isolated man-ner. Hypertension and aortic or mitral stenosis arediseases, which usually accelerate the degeneration ofthe conductive system, or may cause its calcificationand fibrosis.

First degree AV block. Often marked as the pro-longation of AV conduction. There is prolongationof the PR interval for more than 0,20s on ECG. Thisinterval represents the progress of activation throughthe atria, AV bundle and His -Purkinje system. Theprolongation can occur in any of these parts. TheQRS complex is normal. When the PR interval ischanging the error usually lies in the AV bundle. Incase the error is more distal in the His-Purkinje sys-tem, it is always accompanied by QRS prolongation.Only by using the intracardiac electrography it ispossible to locate the exact place of the error.

Second degree AV block. Also known as the in-termittent AV block. In this case some impulses arenot conducted to the ventricles. On the ECG wecan notice a gradual prolongation of the PR inter-val, untill one ventricular systole doesn’t occur. Thisis also known as Mobitz 1 second degree AV block.Before this the disorder was known as Wenckebachperiods or Wenckebach block. The error is usuallylocalized in the AV node. The QRS complex is usu-ally unchanged. This block may occur in myocardialinfarction, in digitalis intoxication, post b blockersand calcium antagonists. The seriosity of this liesin the haemodynamic changes. When there are nohaemodynamic changes, the prognosis is excellent(see fig. 3.40 page 238).

Sometimes the impulse is not conducted to the


Figure 3.40: AV block of 2nd type, Mobitz type I.

ventricles without prolongation of the PR interval.This is known as Mobitz type 2 second degree heartblock. The primary error is usually localized in theHis-Purkinje system. Often there is prolongationof the QRS complex. The most important thing isto know whether the error progresses to a completeblock or not. It is usually found in the anteroseptalinfarct, or in sclerodegenerative or calcificating dis-orders of the fibrous skeleton of the heart. In what iscalled a higher degree block, two or more successiveimpulses are not expressed in the ventricles. If theresulting haemodynamics is affected a pacemaker isnecessary (see fig. 3.41 on page 238).

Figure 3.41: AV block of 2nd type, Mobitz type II.

Third degree heart block, also known as completeAV block. No impulse is transmitted from atriato ventricles. If there is a ventricular substitutiverhythm, the frequency reaches 40–55/min. Com-plete congenital AV block originates in the AV bun-dle. The main error is usually localized in the Hisbundle (see fig. 3.42 on page 238). This completeAV block causes syncope and ventricular arrest. Butusually this block is preceded by some mild dysfunc-tion. That is why it is important to define them,know their progression, and if possible determine theprobability of a substitutive rhythm occurrence dur-

ing the complete AV block. The last mentioned de-mand is the most important one. The resulting pic-ture of the complete AV block depends if there is orif there is not a substitutive rhythm, and the typeof this rhythm. In good conditions the substitutiverhythm can generate in His bundle. Here the fre-quency reaches 40–60/min. Because the progress ofactivation is usually normal, the ventricular complexis not deformed. Yet when the activation is gener-ated in distal parts of the conductive system e.g. inPurkinje fibers, the frequency is about 25–45/min.The progress of activation in the ventricles is abnor-mal, and shows itself as a wide QRS complex.

Figure 3.42: AV block of 3rd type

AV dissociation represents a disorder in which thecontrol of the ventricles is separated from the controlof the atria. This error doesn’t have to be combinedwith the complete AV block. AV dissociation canoccur in extreme sinus bradycardia. It can also oc-cur when there is an ectopic junctional or ventricu-

3.27. Tachyarhythmia (I.Hulın) 239

lar pacemaker that has a higher frequency of impulseformation than the SA node. Here an interference inthe rhythms can occur. This condition occurs in caseof accelerated junctional or ventricular rhythm, in is-chemic disease of the heart, in myocardial infarction,or after cardiac surgery.AV blocks that have haemodynamic symptomatol-

ogy can be solved by the use of pacemaker. Prior tothis it is necessary to perform an intracardiac electro-cardiographic examination. The obtained results en-able us to understand the pathophysiological mech-anism of the disorder. Valuable information are ob-tained from the electrocardiographic registration ofthe bundle of His, and from programmed stimula-tion. Electrocardiography is necessary in patientswith syncope and a bundle branch or a bifascicu-lar block the His bundle electrocardiography is nec-essary. If the HV interval is longer than 100 ms,this means that there is an infra–His disorder, whichshould be solved by pacemaker. In AV block weshould differentiate between the intra or infra–Hisblock, or finally if there is block in the His-PurkinjeSystem.It is possible to use a trans venous insertion of

catheter electrodes to the apex of the right ventri-cle with an external monitoring to handle a com-plicated case of atrioventricular conduction distur-bance. Electrodes for permanent pacing is usuallyplaced in the right atrium or right ventricle via thesubclavian vein. The source of power is fixed sub-cutaneously in the sub clavicular area. Epicardialelectrodes are used when, due to other reasons tho-racotomy is performed. The pacemaker can have afixed frequency or it can work on demand, it may alsobe rate adaptive. The electrodes can be connectedto atrium or ventricle or it can be connected to botharteries or ventricles. From the pathological pointof view it is not easy to simulate the optimal func-tion of the conductive system of the heart. Pacingcan cause haemodynamic changes in the atria andthe atrioventricular valves. Such change can mani-fest itself as marked difficulties for the patient. Thecombination of symptoms is known as the pacemakerSyndrom.

3.27 Tachyarhythmia

All kinds of tachyarhythmias can be devided intotwo types depending on their origin. A group oftachyarhythmias which cause are changes in thespread, and progression of activation. Another groupis caused by a defect in the formation of stimuli.The electrophysiological bases of conduction distur-bances were considered in the previous chapter. Thereentry mechanism is the most common of cardiacdysarhythmias. With no detailed electrophysiologi-cal differentiation it is shown that the following fourconditions are needed for the reentry to occur:

1. An electrophysiological nonhomogenesity of twoor more areas in the heart, which are activated,or can be activated following each other, andhence they can form a potentially morphologi-cal base for a close conductive circle. This non-homogenesity results from the difference in theconductivity of these structures or the differencein their refractory period.

2. A unidirectional block means, that there is partof the conductive loop that can be activatedfrom the neighboring area, which is part of theconductive loop and part of the block.

3. The refractory period should be shortened toa level that permits reexcitability on repeatedactivation.

4. Re excitation leads to the formation of loop ac-tivation.

The repeated circulation of an impulse can formthe basis for the formation of arrhythmia’s. Thesearrhythmia’s can be initiated repeatedly. Yet theycan end as an extra systole or as a fast stimulation.This characteristic renders them different from thetrigger arrhythmias.Arrhythmias that are generated from disturbance

in the impulse formation, can be further devidedinto, those caused by automacity change, and thoseresulting from triggered activation. Normally themyocardial cells lack the pacemaker action of theSA node, in other words this activity is very low inthem. The pacemaker activity is obtained due to the

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