Supraventricular Tachycardias
David Melvin, MD
10/1/2003
Introduction
Pathophysiology
Diagnosis
Treatment
Acute
Chronic
Excluding Atrial Fibrillation and Flutter
Epidemiology
Common problem presenting ED’s
Prevalence 2.25/1000
Orejarena, J AM Coll Card. 1998;31:150-7
Mean age of onset 57 years
Ranging from infancy to 90 years old
In this study, younger patients (mean of 37) were more likely to present to the ED and less likely to have structural heart disease(69%)
Mechanisms
Two basic mechanisms leading to all Tachyarrhythmias
Impaired impulse initiation
problems of abnormal automaticity
Abnormal impulse conduction
Re-entrant impulses
Location of disorder
SVT is any arrhythmia arising from AV node or above
Impulses can be transmitted from several loci
Sinus Node
Atrium
AV Node
Point of origin has implications for treatment
AV Node
There are two basic forms of SVT’s arising from the AV node
Atrioventricular Node Reciprocating Tachycardia(AVNRT)
Atrioventricular Reciprocating Tachycardia(AVRT)
Both are dependent on the AV node for maintenance of the Reentry circuit
Reentry Circuits
Mines in 1913 first described reentry as a mechanism of cardiac arrhythmias
Need a ring of conduction with unidirectional block in one branch
AVNRT
Accounts for more than half of the cases of PSVT’s
Fast and slow conducting fibers from the atrium to the AV node make up reentry circuit
Fast fibers have a long refractory period
Slow fibers have a shorter refractory period
AVNRT(cont)
Cycle is started by a PAC
Fast fibers are still refractory from previous impulse
Impulse conducted down Slow fibers and retrogradely up fast fibers
This slow-fast mechanism accounts for 90% of AVNRT’s
AVNRT(cont.)
From Schilling, Heart 2002;87:299–304
AVRT
Dependent on an accessory pathway
Wolf-Parkinson-White syndrome
Can have either Orthodromic or Antidromic conduction through the AV node
Most common is Orthodromic with retrograde conduction through the accessory pathway
AVRT(cont.)
From Schilling, Heart 2002;87:299–304
AVRT(cont.)
Reentry is precipitated by a PAC or PVC
Dependent on AV node for continued reentry
Both AVNRT and AVRT arise due to reentrant mechanism
Both are dependent on the AV node for their maintenance
Drugs that work on the AV node should break the circuit
Atrial Tachycardias
Unifocal atrial tachycardia
Single P wave morphology
May be due to either abnormal automaticity or reentry mechanisms
Sometimes mistaken for Flutter although rate is usually less than 250
Rare
Atrial Tachycardias(cont.)
Multifocal atrial tachycardia
Due to increased automaticity
Multiple atrial sites of impulse initiation
Usually not Paroxysmal
More common than unifocal
Atrial Tachycardias(cont.)
Atrial tachycardias are not dependent on the AV node for their propagation
AV blocking agents will slow conduction through the AV node but not break them
Sinus Tachycardias
Physiologic Sinus Tachycardia
Inappropriate Sinus Tachycardia
Reentrant Sinus Tachycardia
Micro reentry circuit within the SA node
Diagnosis
History
Physical Exam
EKG
EKG
Despite careful analysis of EKG 20% of SVT’s are incorrectly diagnosed
Certain features can lead to the diagnosis of particular SVT’s
Atrial Tachycardias
Unifocal
Atrial Rate usually <250 helping to distinguish from A. Flutter
Regular Rhythm
Positive P waves in inferior leads before each QRS if high atrial origin
P wave will have different morphology from Sinus P waves
Rhythm terminates with QRS complex
Sinus Rhythm
Atrial Tachycardia
Atrial Tachycardias
Multifocal
Irregular rhythm
Generally slower rates than other SVT’s
Generally more incessant in nature
Requires 3 distinct P wave morphologies with isoelectric periods between them.
AVNRT
Rapid rate 150-180
Regular
P waves generally hidden within the QRS complex
May see a pseudo r’ in V1 or pseudo S in inferior leads
pseudo r’: sens. 58%, spec. 91%
pseudo S: sens. 14%, spec. 100%
J. Am. Coll. Card 1993;21(1):85-9
AVRT
Fast
Regular
May see widened QRS if antegrade conduction down accessory pathway or signs of preexcitation in sinus (delta wave)
retrograde P waves follow QRS
QRS alternans
Orthodromic
Antidromic
Goals of Treatment
Acute
Break reentry circuit
Control rate
Chronic
Prevent recurrences
Acute
If unstable DC Cardiovert
Vagal Maneuvers
Diagnostic and Therapeutic
63% responded in a series by Mehta with younger patients more likely to respont
Lancet 1988, May:1181-5
30% response in series by Muller
Am J of Card 1994;74:500-503
Adenosine
Began to be investigated in the 1980’s
Became the first line treatment in the early 1990’s
Multicenter placebo-controlled trial by DiMarco showed that Adenosine was equally effective to Verapamil with better side effect profile
Annals of Internal Med 1990;113:104-110
Adenosine(cont.)
Blocks Adenosine receptors causing hyperpolarization of the cell
Extremely short half life limits side effects
Maybe ineffective in patients taking methylxanthines
Has replaced Ca channel blockers that had previously been the first line treatment
Will break most reentrant SVT’s dependent on the AV node
Chronic Treatment
Dependent on the severity and frequency of symptoms
Drug Therapy
Ca Channel blockers, Beta blockers, Dig, Flecainide, Propafenone
Not entirely effective and side effects
Catheter Ablation
Catheter Ablation
Has become the treatment of choice for persistently symptomatic patients
Those with WPW may be referred for ablation even without persistent symptoms
Success rates of about 96% have been reported
About 1% risk of 2nd or 3rd degree AV Block
Summary
Mechanism and Location of SVT has implications for treatment
EKG holds clues for the type of SVT, although 20% will not be discernable by the EKG
Adenosine is the mainstay of Acute tx.
Catheter Ablation is preferred for chronic management