appraisal and reappraisal cardiac therapy

Appraisal and reappraisal of cardiac therapy Edited bv Arthur C. DeGraff and Julian Frieden Electrophysiology and pharmacology of cardiac arrhythmias. II. Relationship of normal and abnormal electrical activity of cardiac fibers to the genesis of arrhythmias B. Re-entry. Section I Andrew L. Wit, Ph.D.* Michael R. Rosen, M.D.* Brian F. Hoffman, M.D. New York, A! Y. I. The concept of re-entry Under physiological conditions the conducting impulse dies out after sequential activation of the atria and ventricles because it is surrounded by recently excited and thus refractory tissue. The heart then must await a new impulae, normally arising in the sinus node, for subsequent activation. The concept of re-entry implies that the pro- pagating impulse does not conduct throughout the heart and dies out after its complete activation but persists to re-excite the heart after the end of the refractory period. For this to happen the impulse must remain somewhere in the heart while the cardiac fibers it has excited regain excitability so that the impulse can re-enter and reactivate them. The effective refractory period of human cardiac fibers is long and ranges from about 150 msec. in the atrium to about 500 msec. in the ventricular specialized conducting 8ystem.l The impulse destined to re-enter or re-excite the heart therefore must survive for this period if it is to outlast the refractory period.2 However, it cannot remain stationary while awaiting the end of the refractory period but must continue to conduct over a pathway which is functionally iso- lated from the rest of the heart. Such a conduc- From the Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, N. Y. 10032. Received for publication June 20, 1974. Reprint requests to: Dr. Michael R. Rosen, Department of Pbarmacol- ogy, College of Physicians and Surgeons, 630 W. 168th St., New York, N. Y. 10032. *Drs. Wit and Rosen are Senior Investigators of the New York Heart Association. Dr. Rosen is a Research Fellow of the John Polachek Foundation. Dr. Wit is a Caree? Scientist of the Irma T. Hirsch1 Trust. tion pathway must provide a return route to the regions which previously have been excited and must be sufficiently long to permit propagation of the impulse during the refractory period. The cardiac impulse conducts at a velocity between 0.5 and 4 MJsec. in cardiac fibers other than those in the sinus and atrioventricular nodes. If it traveled at these speeds while waiting for the re- mainder of the heart to regain excitability it would have traveled in a pathway between 15 cm. and 1 M. long in order to survive.2 Cranefield and Hoffman2 have stated “that so long a path, however circuitous, could exist in functional isolation from the rest of the heart has never seemed likely.” Travel at a normal velocity is not the only way in which the impulse, destined to re-enter, might persist during the refractory period. Slowing of the conduction velocity obviates the necessity of such a long conduction pathway. For example, if conduction is slowed to 0.02 MJsec., the impulse would travel only 6 mm. during a refractory period of 300 msec.2 Pathways of this length are readily available in the heart. Conduction is slow enough to enable re-entry to occur in cardiac fibers with “slow response” action potentials- i.e., either in the normally slow fibers of the sinoatrial @A) and atrioventricular (AV) nodes, or in fibers whose normally fast response has been slowed by disease,3s 4 or other mechanisms such as drugs. Shortening of the refractory period also will facilitate the occurrence of re-entry by reducing the period of time during which the impulse must linger in the heart, awaiting the recovery of ex- 664 November, 1974, Vol. 88, No. 5, pp. 664-670

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Cardiac Theraphy

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Appraisalandreappraisalofcardiactherapy EditedbvArthurC.DeGraffandJulianFrieden Electrophysiologyandpharmacologyofcardiac arrhythmias.II.Relationshipofnormaland abnormalelectricalactivityofcardiacfibersto thegenesisofarrhythmiasB.Re-entry.SectionI AndrewL.Wit,Ph.D.* MichaelR.Rosen,M.D.* BrianF.Hoffman,M.D. NewYork,A!Y. I.Theconceptofre-entry Underphysiologicalconditionstheconducting impulsediesoutaftersequentialactivationofthe atriaandventriclesbecauseitissurroundedby recentlyexcitedandthusrefractorytissue.The heartthenmustawaitanewimpulae,normally arisinginthesinusnode,forsubsequentactiva- tion.Theconceptofre-entryimpliesthatthepro- pagatingimpulsedoesnotconductthroughout theheartanddiesoutafteritscompleteactiva- tionbutpersiststore-excitetheheartafterthe endoftherefractoryperiod.Forthistohappen theimpulsemustremainsomewhereintheheart whilethecardiacfibersithasexcitedregainex- citabilitysothattheimpulsecanre-enterand reactivatethem. Theeffectiverefractoryperiodofhumancar- diacfibersislongandrangesfromabout150 msec.intheatriumtoabout500msec.inthe ventricularspecializedconducting8ystem.lThe impulsedestinedtore-enterorre-excitethe heartthereforemustsurviveforthisperiodifit istooutlasttherefractoryperiod.2However,it cannotremainstationarywhileawaitingtheend oftherefractoryperiodbutmustcontinuetocon- ductoverapathwaywhichisfunctionallyiso- latedfromtherestoftheheart.Suchaconduc- FromtheDepartmentofPharmacology,CollegeofPhysiciansand Surgeons,ColumbiaUniversity,NewYork,N.Y.10032. ReceivedforpublicationJune20,1974. Reprintrequeststo:Dr.MichaelR.Rosen,DepartmentofPbarmacol- ogy,CollegeofPhysiciansandSurgeons,630W.168thSt.,NewYork, N.Y.10032. *Drs.WitandRosenareSeniorInvestigatorsoftheNewYorkHeart Association.Dr.RosenisaResearchFellowoftheJohnPolachek Foundation.Dr.WitisaCaree?ScientistoftheIrmaT.Hirsch1Trust. tionpathwaymustprovideareturnroutetothe regionswhichpreviouslyhavebeenexcitedand mustbesufficientlylongtopermitpropagationof theimpulseduringtherefractoryperiod.The cardiacimpulseconductsatavelocitybetween 0.5and4MJsec.incardiacfibersotherthan thoseinthesinusandatrioventricularnodes.Ifit traveledatthesespeedswhilewaitingforthere- mainderofthehearttoregainexcitabilityit wouldhavetraveledinapathwaybetween15 cm.and1 M.longinordertosurvive.2Cranefield andHoffman2havestatedthatsolongapath, howevercircuitous,couldexistinfunctional isolationfromtherestofthehearthasnever seemedlikely. Travelatanormalvelocityisnottheonlyway inwhichtheimpulse,destinedtore-enter,might persistduringtherefractoryperiod.Slowingof theconductionvelocityobviatesthenecessityof suchalongconductionpathway.Forexample,if conductionisslowedto0.02MJsec.,theimpulse wouldtravelonly6mm.duringarefractory periodof300msec.2Pathwaysofthislengthare readilyavailableintheheart.Conductionisslow enoughtoenablere-entrytooccurincardiac fiberswithslowresponseactionpotentials- i.e.,eitherinthenormallyslowfibersofthe sinoatrial@A)andatrioventricular(AV)nodes, orinfiberswhosenormallyfastresponsehas beenslowedbydisease,3s 4 orothermechanisms suchasdrugs. Shorteningoftherefractoryperiodalsowill facilitatetheoccurrenceofre-entrybyreducing theperiodof timeduringwhichtheimpulsemust lingerintheheart,awaitingtherecoveryofex- 664November,1974,Vol.88,No.5,pp.664-670

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