室上性心动过速.ppt

Supraventricular TachycardiasDavid Melvin,MD10/1/2003IntroductionnPathophysiologynDiagnosisnTreatmentnAcutenChronicnExcluding Atrial Fibrillation and FlutterEpidemiologynCommon problem presenting EDsnPrevalence 2.25/1000nOrejarena,J AM Coll Card.1998;31:150-7nMean age of onset 57 yearsnRanging from infancy to 90 years oldnIn this study,younger patients(mean of 37)were more likely to present to the ED and less likely to have structural heart disease(69%)MechanismsnTwo basic mechanisms leading to all TachyarrhythmiasnImpaired impulse initiationnproblems of abnormal automaticitynAbnormal impulse conductionnRe-entrant impulsesLocation of disordernSVT is any arrhythmia arising from AV node or abovenImpulses can be transmitted from several loci nSinus NodenAtriumnAV NodenPoint of origin has implications for treatmentAV NodenThere are two basic forms of SVTs arising from the AV nodenAtrioventricular Node Reciprocating Tachycardia(AVNRT)nAtrioventricular Reciprocating Tachycardia(AVRT)nBoth are dependent on the AV node for maintenance of the Reentry circuitReentry CircuitsnMines in 1913 first described reentry as a mechanism of cardiac arrhythmiasnNeed a ring of conduction with unidirectional block in one branchAVNRTnAccounts for more than half of the cases of PSVTsnFast and slow conducting fibers from the atrium to the AV node make up reentry circuitnFast fibers have a long refractory periodnSlow fibers have a shorter refractory periodAVNRT(cont)nCycle is started by a PACnFast fibers are still refractory from previous impulsenImpulse conducted down Slow fibers and retrogradely up fast fibersnThis slow-fast mechanism accounts for 90%of AVNRTsAVNRT(cont.)From Schilling,From Schilling,Heart 2002;87:299304AVRTnDependent on an accessory pathwaynWolf-Parkinson-White syndromenCan have either Orthodromic or Antidromic conduction through the AV nodenMost common is Orthodromic with retrograde conduction through the accessory pathwayAVRT(cont.)From Schilling,From Schilling,Heart 2002;87:299304AVRT(cont.)nReentry is precipitated by a PAC or PVCnDependent on AV node for continued reentrynBoth AVNRT and AVRT arise due to reentrant mechanismnBoth are dependent on the AV node for their maintenancenDrugs that work on the AV node should break the circuitAtrial TachycardiasnUnifocal atrial tachycardianSingle P wave morphologynMay be due to either abnormal automaticity or reentry mechanismsnSometimes mistaken for Flutter although rate is usually less than 250nRareAtrial Tachycardias(cont.)nMultifocal atrial tachycardianDue to increased automaticitynMultiple atrial sites of impulse initiationnUsually not ParoxysmalnMore common than unifocalAtrial Tachycardias(cont.)nAtrial tachycardias are not dependent on the AV node for their propagationnAV blocking agents will slow conduction through the AV node but not break themSinus TachycardiasnPhysiologic Sinus TachycardianInappropriate Sinus TachycardianReentrant Sinus TachycardianMicro reentry circuit within the SA nodeDiagnosisnHistorynPhysical ExamnEKGEKGnDespite careful analysis of EKG 20%of SVTs are incorrectly diagnosednCertain features can lead to the diagnosis of particular SVTsAtrial TachycardiasnUnifocalnAtrial Rate usually 250 helping to distinguish from A.FlutternRegular Rhythm nPositive P waves in inferior leads before each QRS if high atrial originnP wave will have different morphology from Sinus P wavesnRhythm terminates with QRS complexSinus RhythmSinus RhythmAtrial TachycardiaAtrial TachycardiaAtrial TachycardiasnMultifocalnIrregular rhythmnGenerally slower rates than other SVTsnGenerally more incessant in naturenRequires 3 distinct P wave morphologies with isoelectric periods between them.AVNRTnRapid rate 150-180nRegularnP waves generally hidden within the QRS complexnMay see a pseudo r in V1 or pseudo S in inferior leadsnpseudo r:sens.58%,spec.91%npseudo S:sens.14%,spec.100%nJ.Am.Coll.Card 1993;21(1):85-9AVRTnFastnRegularnMay see widened QRS if antegrade conduction down accessory pathway or signs of preexcitation in sinus(delta wave)nretrograde P waves follow QRSnQRS alternansOrthodromicAntidromicGoals of TreatmentnAcutenBreak reentry circuitnControl ratenChronicnPrevent recurrencesAcutenIf unstable DC CardiovertnVagal ManeuversnDiagnostic and Therapeuticn63%responded in a series by Mehta with younger patients more likely to respontnLancet 1988,May:1181-5n30%response in series by MullernAm J of Card 1994;74:500-503AdenosinenBegan to be investigated in the 1980snBecame the first line treatment in the early 1990snMulticenter placebo-controlled trial by DiMarco showed that Adenosine was equally effective to Verapamil with better side effect profilenAnnals of Internal Med 1990;113:104-110Adenosine(cont.)nBlocks Adenosine receptors causing hyperpolarization of the cellnExtremely short half life limits side effectsnMaybe ineffective in patients taking methylxanthinesnHas replaced Ca channel blockers that had previously been the first line treatmentnWill break most reentrant SVTs dependent on the AV nodeChronic TreatmentnDependent on the severity and frequency of symptomsnDrug TherapynCa Channel blockers,Beta blockers,Dig,Flecainide,PropafenonenNot entirely effective and side effectsnCatheter AblationCatheter AblationnHas become the treatment of choice for persistently symptomatic patientsnThose with WPW may be referred for ablation even without persistent symptomsnSuccess rates of about 96%have been reportednAbout 1%risk of 2nd or 3rd degree AV BlockSummarynMechanism and Location of SVT has implications for treatmentnEKG holds clues for the type of SVT,although 20%will not be discernable by the EKGnAdenosine is the mainstay of Acute tx.nCatheter Ablation is preferred for chronic management