Narrow Complex Tachycardias Moritz Haager PGY-5. Objectives Develop an approach Develop an approach...
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Transcript of Narrow Complex Tachycardias Moritz Haager PGY-5. Objectives Develop an approach Develop an approach...
Narrow Complex Narrow Complex TachycardiasTachycardias
Moritz Haager PGY-5Moritz Haager PGY-5
ObjectivesObjectives
Develop an approach Develop an approach Review treatment optionsReview treatment options Dispositon decisionsDispositon decisions
PerspectivePerspective
SVTSVT– Broad umbrella term for Broad umbrella term for any tachycardia any tachycardia
originating above the ventriclesoriginating above the ventricles– Variable underlying mechanisms but Variable underlying mechanisms but
basically one Tx approachbasically one Tx approach– Ranges from physiological Ranges from physiological pathological, pathological,
and benign and benign dangerous dangerous– Occurs in all age groupsOccurs in all age groups– Clinical presentation from asymptomatic Clinical presentation from asymptomatic
shock / CHF shock / CHF
When presented with an undifferentiated presentation with a broad DDx and variability in outcome you need an APPROACH
Why should we care?Why should we care?
Morbidity & MortalityMorbidity & Mortality– Patient discomfort & anxietyPatient discomfort & anxiety– Syncopal events (falls) ~15%Syncopal events (falls) ~15%– Risk of sudden cardiac death w/ Risk of sudden cardiac death w/
accessory pathway driven accessory pathway driven arrhythmiasarrhythmias
– Tachycardia-mediated Tachycardia-mediated cardiomyopathycardiomyopathy
LV dilatation w/ impaired LV functionLV dilatation w/ impaired LV function
Approach to Approach to TachycardiaTachycardia Stable or unstable?Stable or unstable?
– Assess ABC’s, OAssess ABC’s, O22, IV, monitors, crash cart to , IV, monitors, crash cart to bedsidebedside
– In general if unstable, give’m juiceIn general if unstable, give’m juice Narrow or wide QRS?Narrow or wide QRS? Regular or irregular?Regular or irregular? Look at the P wavesLook at the P waves
– Relationship to QRSRelationship to QRS– P wave axis / rateP wave axis / rate– P wave morphology(ies)P wave morphology(ies)
What is the trigger / underlying cause?What is the trigger / underlying cause?
Step 1: Stable or Step 1: Stable or Unstable?Unstable? Not always black & whiteNot always black & white
– Continuum from stable Continuum from stable compensated compensated decompensated decompensated shock shock arrest arrest
– Stability Stability determined by big picturedetermined by big picture:: Symptoms, signs, & vitalsSymptoms, signs, & vitals Cardio-respiratory reserveCardio-respiratory reserve AgeAge Co-morbiditiesCo-morbidities
Be preparedBe prepared– Any dysrhythmia could potentially Any dysrhythmia could potentially
deterioratedeteriorate– All therapies are potentially pro-arrhythmicAll therapies are potentially pro-arrhythmic
Step 2: Narrow or Step 2: Narrow or wide?wide? Measure widest QRS on ECGMeasure widest QRS on ECG
– Adults: wide = >0.12 sec (3 small Adults: wide = >0.12 sec (3 small boxes)boxes)
– Kids <8yo: wide = >0.08 sec (2 Kids <8yo: wide = >0.08 sec (2 boxes)boxes)
Step 3: Regular or Step 3: Regular or Irregular?Irregular? Use calipers or paperUse calipers or paper
– Irregularity can be subtle, esp at fast Irregularity can be subtle, esp at fast rates rates
GenerallyGenerally– Irregular rhythms originate ABOVE Irregular rhythms originate ABOVE
the AV nodethe AV node– VT is almost never irregularVT is almost never irregular
Step 4: Look at the P Step 4: Look at the P waveswaves P waves present?P waves present? Is there a P before every QRS?Is there a P before every QRS? What is the relationship b/w the P and What is the relationship b/w the P and
the QRS? the QRS? – What is the P wave rate? Ventricular rate?What is the P wave rate? Ventricular rate?
Is the P wave coming from the SA?Is the P wave coming from the SA?– N axis: upright in II, negative in aVRN axis: upright in II, negative in aVR
Is there >1 distinct P wave morhology?Is there >1 distinct P wave morhology?
Diagnostic Trick: 50 Diagnostic Trick: 50 mm/s ECG Tracingsmm/s ECG Tracings Comparsion study of 8 EP’sComparsion study of 8 EP’s
– Given 45 ECG’s of NCT’s printed at 25 Given 45 ECG’s of NCT’s printed at 25 mm/s & asked to give Dx & Tx planmm/s & asked to give Dx & Tx plan
– 2 wks later given same ECG’s printed 2 wks later given same ECG’s printed at 25 & 50 mm/s & asked to give Dx at 25 & 50 mm/s & asked to give Dx & Tx& Tx
ResultsResults– 50 mm/s increased diagnostic 50 mm/s increased diagnostic
accuracy from accuracy from 63 to 71%, P=0.00263 to 71%, P=0.002 J Emerg Med 2002; 22: 123–126J Emerg Med 2002; 22: 123–126
Final CategorizationFinal Categorization
Narrow Complex TachycardiasNarrow Complex Tachycardias– Regular w/ P’s Regular w/ P’s
= sinus, a. flutter w/ constant block, Focal atrial = sinus, a. flutter w/ constant block, Focal atrial tachycardia, AVNRT, junctional tachycardiatachycardia, AVNRT, junctional tachycardia
– Irregular w/ P’s Irregular w/ P’s = MAT, a. flutter variable block= MAT, a. flutter variable block
– Regular, no P’s Regular, no P’s = AVRT, AVNRT= AVRT, AVNRT
– Irregular, no P’s Irregular, no P’s = a. fib= a. fib
Wide Complex TachycardiasWide Complex Tachycardias
Tx w/ AV nodal blockers
Rate control +/- rhythm control
Step 5: Underlying Step 5: Underlying CausesCauses HIS DEBTSHIS DEBTS
– H – HypoxiaH – Hypoxia– I – Ischemia / infarctionI – Ischemia / infarction– S – Sympathetic excessS – Sympathetic excess
Hyperthyroid, CHF, pheochromocytoma, excerciseHyperthyroid, CHF, pheochromocytoma, excercise– D – DrugsD – Drugs
Anti-arrhythmics, cocaine, amphetamines, caffeine, etcAnti-arrhythmics, cocaine, amphetamines, caffeine, etc– E – ElectrolytesE – Electrolytes
KK++, Ca, Ca2+2+, Mg, Mg2+2+
– B – BradycardiasB – Bradycardias Eg. Sick sinus syndromeEg. Sick sinus syndrome
– T – Thyroid diseaseT – Thyroid disease– S – StretchS – Stretch
Hypertrophy / dilation of atria & ventricles (CHF, valvular Hypertrophy / dilation of atria & ventricles (CHF, valvular Dz)Dz)
Preciptants vary w/ age, sex, co-morbidities, etc
Clinical PresentationsClinical Presentations
Typical SxTypical Sx– PalpitationsPalpitations 96%96%– ““Dizziness”Dizziness” 75%75%– DyspneaDyspnea 47%47%– FatigueFatigue 23%23%– Chest painChest pain 35%35%– DiaphoresisDiaphoresis 17%17%– NauseaNausea 13%13%– Neck pounding said to be pathogonomonicNeck pounding said to be pathogonomonic
CaseCase
27 yo M w/ palpitations & 27 yo M w/ palpitations & dyspneadyspnea
NCT at 160 on ECG c/w PSVTNCT at 160 on ECG c/w PSVT Also tells you he has been “pissin’ Also tells you he has been “pissin’
like a racehorse”like a racehorse” Does he have diabetes?Does he have diabetes?
Polyuria in PSVTPolyuria in PSVT
Loss of AV synchronizationLoss of AV synchronization Atrial contraction against closed Atrial contraction against closed
AV valvesAV valves Elevated atrial pressure & atrial Elevated atrial pressure & atrial
stretchstretch Release of atrial natriuretic Release of atrial natriuretic
peptide peptide polyuria polyuriaNB: This is trivia – absence of polyuria does NOT exclude Dx of PSVT and you should still check at least a urine for glucose
CaseCase
3 mo F w/ dyspnea & wheeze3 mo F w/ dyspnea & wheeze T 40.5T 40.5ooC, P 190, RR 60, SpOC, P 190, RR 60, SpO22 88% 88% Mod resp distress on exam w/ Mod resp distress on exam w/
wheezes & crackles bilaterallywheezes & crackles bilaterally Is this just sinus tachycardia from Is this just sinus tachycardia from
her fever? her fever?
Tachycardia & FeverTachycardia & Fever
Prospective observational study of Prospective observational study of 490 infants <1 yo490 infants <1 yo– Measured HR & rectal temp in calm, Measured HR & rectal temp in calm,
quiet kids w/o evidence of serious quiet kids w/o evidence of serious illnessillness
– Analyzed relationship b/w HR & temp w/ Analyzed relationship b/w HR & temp w/ multivariate linear regressionmultivariate linear regression
ResultsResults– HR increased ~10 bpm for every 1HR increased ~10 bpm for every 1ooC C
rise in infants b/w 2 -12 morise in infants b/w 2 -12 mo Ann Emerg Med. 2004;43:699-705Ann Emerg Med. 2004;43:699-705
Tachycardias: Tachycardias: MechanismMechanism1.1. ReentryReentry
50-80% of NCT’s50-80% of NCT’s Abrupt on-/off-setAbrupt on-/off-set Do well w/ electricityDo well w/ electricity
2.2. Enhanced automaticityEnhanced automaticity Typically catecholamines, drugs, lytes, ischemiaTypically catecholamines, drugs, lytes, ischemia Gradual on-/off-setGradual on-/off-set Not likely to respond to electricity; Tx underlying Not likely to respond to electricity; Tx underlying
causecause3.3. Triggered dysthythmiasTriggered dysthythmias
Interruption of repolarization by afterdepolarizationsInterruption of repolarization by afterdepolarizations Ischemia, drugs, lytes, catecholaminesIschemia, drugs, lytes, catecholamines Not likely to respond to electricity; Tx underlying Not likely to respond to electricity; Tx underlying
cause E.g. Torsades cause E.g. Torsades IV magnesium IV magnesium
Case 2 80 yo F w/ Case 2 80 yo F w/ sepsis: Is this sinus sepsis: Is this sinus tachy?tachy?
Maximal sinus tachMaximal sinus tach
220 – age = maximum HR220 – age = maximum HR– 220 -80 = 140220 -80 = 140– Unlikey this is just sinus tachUnlikey this is just sinus tach
Regular NCT: DDxRegular NCT: DDx
P waves present:P waves present:– Sinus tachycardiaSinus tachycardia– Atrial FlutterAtrial Flutter– AVNRTAVNRT– AVRTAVRT– Focal Atrial TachycardiaFocal Atrial Tachycardia
No P-wavesNo P-waves– AVRTAVRT– AVNRTAVNRT– Junctional TachycardiaJunctional Tachycardia
Consider under PSVT as can be impossible to differentiate on ECG; Tx generally the same
AVNRT vs. AVRTAVNRT vs. AVRT
AV nodal reentrant AV nodal reentrant tachycardiatachycardia– Most common PSVT Most common PSVT
(>60%)(>60%)– Dual AV nodal Dual AV nodal
physiologyphysiology 2 separate conduction 2 separate conduction
paths in AV nodepaths in AV node– Fast pathwayFast pathway– Slow pathwaySlow pathway
Allow for re-entry Allow for re-entry circuit w/in AV nodecircuit w/in AV node
Atrioventricular Atrioventricular reentrant tachycardiareentrant tachycardia– accessory pathway(s)accessory pathway(s)
(AP) (AP) = Tracks of conducting = Tracks of conducting
tissue outside of AV tissue outside of AV node, connecting atria node, connecting atria & ventricles& ventricles
Re-entry circuit formed Re-entry circuit formed by by
– AP & AV node (WPW)AP & AV node (WPW)– 2 or more separate 2 or more separate
AP’s (bypass AV node AP’s (bypass AV node completely)completely)
AVNRTAVNRT ““Typical” AVNRTTypical” AVNRT – = 90-95% – = 90-95%•Anterograde conduction down slow pathwayAnterograde conduction down slow pathway•Retrograde conduction up fast pathwayRetrograde conduction up fast pathway
•If P waves seen RP < PR intervalIf P waves seen RP < PR interval
““Atypical” AVNRTAtypical” AVNRT is the reverse of what is pictured here is the reverse of what is pictured here
VENTRICLES
ATRIA
AVRTAVRT
2 types of AP2 types of AP– ““concealed”concealed” = =
capable of retrograde capable of retrograde conduction only conduction only
– ““manifest”manifest” = allow = allow anterograde +/- anterograde +/- retrograde retrograde conductionconduction
See “pre-excitation” See “pre-excitation” on ECGon ECG
Preexcitation Preexcitation SyndromesSyndromes WPW (Wolf-WPW (Wolf-
Parkinson-White)Parkinson-White)– PR <120 msecPR <120 msec– QRS >100 msecQRS >100 msec– Delta waves in Delta waves in
some leadssome leads
LGL (Lown-LGL (Lown-Ganong-Levine)Ganong-Levine)– PR <120 msecPR <120 msec
WPW & SVTWPW & SVT
Orthodromic SVTOrthodromic SVT– Anterograde via Anterograde via
AVAV & returns via & returns via accessory tractaccessory tract
– Uses normal Uses normal conduction conduction system therefore system therefore get get narrow narrow complex complex tachycardiatachycardia
Orthodromic makes up 90-95% of WPW SVT’s
WPW & SVTWPW & SVT
Antidromic SVTAntidromic SVT– Anterograde Anterograde
conduction from atria conduction from atria to ventricles via to ventricles via accessory path & accessory path & retrograde flow retrograde flow through AV nodethrough AV node
– Wide complex Wide complex tachycardiatachycardia
– Avoid AV nodal Avoid AV nodal blockersblockers
Use procainamide or Use procainamide or cardiovertcardiovert
(5-10% of WPW SVT)
WPW & A FibWPW & A Fib
IrregularIrregular Wide complex Wide complex tachycardiatachycardia– May see capture & fusion May see capture & fusion
beatsbeats CommonCommon (~30% of WPW pts) (~30% of WPW pts)
& & potentially life-threateningpotentially life-threatening– AP w/ short refractory period AP w/ short refractory period
& anterograde conduction & anterograde conduction near 1:1 conduction near 1:1 conduction VF VF
– 0.15 – 0.39% incidence of 0.15 – 0.39% incidence of sudden cardiac deathsudden cardiac death
Do NOT block AV nodeDo NOT block AV node– Channels all impulses down Channels all impulses down
AP & increases risk of VFAP & increases risk of VF– Use Procainamide or Use Procainamide or
cardioversioncardioversion
Predictors of Sudden Predictors of Sudden Cardiac Death in WPWCardiac Death in WPW Shortest pre-excited R-R interval Shortest pre-excited R-R interval
during atrial fib <250 msduring atrial fib <250 ms Hx of symptomatic tachycardiaHx of symptomatic tachycardia Multiple accessory pathwaysMultiple accessory pathways Ebstein’s anomaly*Ebstein’s anomaly*
Blomström-Lundqvist et al. ACC/AHA/ESC Guidelines for Management of SVA ACC 2003; 42:1493–531
*= abnormal tricuspid valve *= abnormal tricuspid valve regurgitation & RA enlargement regurgitation & RA enlargement
AVNRT vs. AVRT: Can AVNRT vs. AVRT: Can you tell them apartyou tell them apart
Helpful ECG findingsHelpful ECG findings– Pseudo R’ in V1Pseudo R’ in V1– Pseudo S in II, III, aVFPseudo S in II, III, aVF
specific (but not specific (but not sensitive) for sensitive) for AVNRTAVNRT
– ST elevation in aVR ST elevation in aVR – RP >100 msRP >100 ms– ST depression ≥2mmST depression ≥2mm
Suggest (not highly Suggest (not highly specific or sensitive) specific or sensitive) AVRTAVRT
Bottom line = 12-lead lacks 100% accuracy but important to look because AVRT more serious Dx
See Adam Osters talk July 22, 2004 for more detailed explanation
PSVT: Acute Treatment PSVT: Acute Treatment SummarySummary UnstableUnstable
– DC cardioversionDC cardioversion StableStable
– 1) Vagal maneuvers (Class I/ level A)1) Vagal maneuvers (Class I/ level A)– 2) Adenosine (Class I/ level A)2) Adenosine (Class I/ level A)– 3) CCB’s (Class I/ level A)3) CCB’s (Class I/ level A)– 4) BB’s (Class IIb/ level C)4) BB’s (Class IIb/ level C)– 5) Amiodarone (Class IIb/ level C)5) Amiodarone (Class IIb/ level C)– 6) Digoxin (Class IIb/ level C)6) Digoxin (Class IIb/ level C)
Blomström-Lundqvist et al. ACC/AHA/ESC Guidelines for Management of SVA JACC 2003; 42:1493–531
CardioversionCardioversion
SedationSedation– ?1 mg midaz + 100 mcg fentanyl?1 mg midaz + 100 mcg fentanyl
Energy Levels Energy Levels – PSVT:- 50 JoulesPSVT:- 50 Joules– Atrial fibrillation: 200 JoulesAtrial fibrillation: 200 Joules– Atrial flutter: 25-50 JoulesAtrial flutter: 25-50 Joules– Orthodromic WPW: 50 JoulesOrthodromic WPW: 50 Joules– Narrow Complex VT: 50-100 JoulesNarrow Complex VT: 50-100 Joules
AdenosineAdenosine
ActionsActions– Coronary vasodilatorCoronary vasodilator– Transient SA & AV nodal blockadeTransient SA & AV nodal blockade
Outward KOutward K++ current current hyperpolarizes hyperpolarizes cellscells
– Reflex catecholamine release & Reflex catecholamine release & sympathetic dischargesympathetic discharge
TT1/21/2 <10 sec; <10 sec; Duration of action 30-40 secDuration of action 30-40 sec
Adenosine: Adverse Adenosine: Adverse EffectsEffects Hot flash / flushingHot flash / flushing ~25%~25% DizzinessDizziness ~20-50%~20-50% Chest pain / pressureChest pain / pressure ~20-40%~20-40% DyspneaDyspnea ~10-25%~10-25% Feeling of impending doomFeeling of impending doom ~10%~10% Pro-arrhythmiaPro-arrhythmia / blocks/ blocks ~10%~10%
>75% of pts will experience side effects w/ adenosine
Adenosine: Pro-Adenosine: Pro-arrhythmic Effectsarrhythmic Effects Significant literature reportsSignificant literature reports
– A fib, VF, Transient sinus arrest / asystole, A fib, VF, Transient sinus arrest / asystole, Torsades de pointesTorsades de pointes
Prospective observational ED studyProspective observational ED study– 160 consecutive pts given adenosine160 consecutive pts given adenosine
Overall 21 (13%) pts had pro-arrhythmic s/eOverall 21 (13%) pts had pro-arrhythmic s/e– Prolonged AV block (>4sec)Prolonged AV block (>4sec) 11 (7%)11 (7%)– Atrial FibAtrial Fib 2 (1%)2 (1%)– Non-sustained VTNon-sustained VT 8 (5%)8 (5%)
All resolved spontaneously; no serious outcomesAll resolved spontaneously; no serious outcomes
Euro J Emerg Med 2001; 8: 99-105
PearlsPearls
Adenosine CAN convert some VT, Adenosine CAN convert some VT, – giving it to “diagnose” SVT w/ giving it to “diagnose” SVT w/
aberrancy is misguidedaberrancy is misguided Wide & irregularWide & irregular – think WPW + A – think WPW + A
fibfib– NO AV nodal blockersNO AV nodal blockers– Amiodarone may not be idealAmiodarone may not be ideal– Procainamide is the drug of choiceProcainamide is the drug of choice
Adenosine: Drug Adenosine: Drug InteractionsInteractions
Theophylline Theophylline – ↑’↑’s dose requirements dose requirement
Dipyridamole Dipyridamole – ↓’ ↓’s dose requirements dose requirement
Carbamazepine Carbamazepine – potentiates adenosine-induced heart blockpotentiates adenosine-induced heart block
CCB’s / BB’sCCB’s / BB’s– Potentiate hypotension & bradycardiaPotentiate hypotension & bradycardia
Adenosine DosingAdenosine Dosing
DBRCT of 201 pts w/ PSVT:DBRCT of 201 pts w/ PSVT:– Adenosine DoseAdenosine Dose Conversion Conversion
RateRate– 3 mg3 mg 35.2%35.2%– 6 mg6 mg 62.3%62.3%– 9 mg9 mg 80.2%80.2%– 12 mg12 mg 91.4%91.4%
P<0.001 for all doses c/w placeboP<0.001 for all doses c/w placebo All administered through PIVAll administered through PIV
DiMarco et al. Ann Intern Med 1990; 113: 104-110
Practical PearlPractical Pearl
Adenosine administrationAdenosine administration– Want to get it in as fast as possibleWant to get it in as fast as possible– Use 2 syringes w/ 18g needlesUse 2 syringes w/ 18g needles
one w/ adenosineone w/ adenosine Other w/ 10 cc NSOther w/ 10 cc NS
– Put both needles into IV access portPut both needles into IV access port Push the adenosine w/ one hand and…Push the adenosine w/ one hand and… ……chase immediately w/ the NS w/ the otherchase immediately w/ the NS w/ the other
– NB: want an IV in the AC if at all NB: want an IV in the AC if at all possiblepossible
Adenosine via Central Adenosine via Central LineLine Appears to have increased success rateAppears to have increased success rate
– Observational study of 200 pts w/ PSVT Observational study of 200 pts w/ PSVT induced in EP lab induced in EP lab
found found 99% success rate w/ 12 mg via femoral line99% success rate w/ 12 mg via femoral line– Strickberger et al. Ann Intern Med 1997; 127: 417-Strickberger et al. Ann Intern Med 1997; 127: 417-
422422
– Randomized Cross-over study of 30 pts Randomized Cross-over study of 30 pts given adenosine via PIV or central linegiven adenosine via PIV or central line
success rate w/ 3 mg was success rate w/ 3 mg was 77%77% when given when given via via central linecentral line vs. vs. 37% via PIV37% via PIV
– McIntosh-Yellin et al. JACC 1993; 22:741–5McIntosh-Yellin et al. JACC 1993; 22:741–5
– Case reports of more severe S/E via central Case reports of more severe S/E via central line (felt to be dose-related)line (felt to be dose-related)
Case 4Case 4
31 yo F w/ PSVT31 yo F w/ PSVT– Vagal maneuvers failVagal maneuvers fail– 6 mg adenosine IV 6 mg adenosine IV no response no response– 12 mg adenosine IV 12 mg adenosine IV slows down slows down
brieflybriefly What now? Would you give her 18 What now? Would you give her 18
mg of adenosine?mg of adenosine?
High Dose AdenosineHigh Dose Adenosine
BackgroundBackground– ACLS: 6 mg, then 12 mg x2 if unsuccessfulACLS: 6 mg, then 12 mg x2 if unsuccessful– FDA approves use up to 12 mgFDA approves use up to 12 mg– Literature reports of uses up to 25 mgLiterature reports of uses up to 25 mg
What about higher doses?What about higher doses?– Randomized cross-over comparison of of Randomized cross-over comparison of of
31 pts w/ AVNRT/AVRT in EP lab given 12 31 pts w/ AVNRT/AVRT in EP lab given 12 & 18 mg adenosine via PIV& 18 mg adenosine via PIV
Non-significant increase in efficacy w/ 18 mgNon-significant increase in efficacy w/ 18 mg– 25/31 (81%) vs. 29/31 (94%); P = 0.103)25/31 (81%) vs. 29/31 (94%); P = 0.103)
No significant increase in adverse effectsNo significant increase in adverse effects– may have been underpowered to find differencemay have been underpowered to find difference
Weismueller et al. Deutsche Med Wochenschrift 2000. 125: 961-69
Calcium Channel Calcium Channel BlockersBlockers 22ndnd line agents in PSVT line agents in PSVT
– VerapamilVerapamil 11stst dose: 2.5 – 5 mg IV over 2 min dose: 2.5 – 5 mg IV over 2 min 22ndnd dose (30 min later): 2.5 – 10 mg IV over 2 dose (30 min later): 2.5 – 10 mg IV over 2
min (to max of 20 mg)min (to max of 20 mg) NB: CONTRAINDICATED in <1yo (risk of EMD), NB: CONTRAINDICATED in <1yo (risk of EMD),
wide QRS, or hypotensive pts, CHF, or WPWwide QRS, or hypotensive pts, CHF, or WPW– DiltiazemDiltiazem
11stst dose: 0.25 mg/kg IV over 2 min dose: 0.25 mg/kg IV over 2 min 22ndnd dose (15 min later): 0.35 mg/kg IV over 2 dose (15 min later): 0.35 mg/kg IV over 2
min followed by gtt of 5-15 mg/hmin followed by gtt of 5-15 mg/h Generally felt to be safer than Verapamil but Generally felt to be safer than Verapamil but
same cautions applysame cautions apply
What about What about Verapamil?Verapamil? RCT of 122 pts w/ PSVT treated w/ RCT of 122 pts w/ PSVT treated w/
either adenosine or Verapamileither adenosine or Verapamil– NS difference in conversion to NSRNS difference in conversion to NSR
86.0% (52/60) vs. 87.1% (54/62), p=NS86.0% (52/60) vs. 87.1% (54/62), p=NS
– Adenosine worked much fasterAdenosine worked much faster 34.2 +/- 19.5 sec vs. 414.4 +/- 191.2 34.2 +/- 19.5 sec vs. 414.4 +/- 191.2
sec, P < 0.0001sec, P < 0.0001 Cheng KA Zhonghua Nei Ke Za Zhi Cheng KA Zhonghua Nei Ke Za Zhi
2003; 42(11): 773-62003; 42(11): 773-6
Adenosine vs Adenosine vs VerapamilVerapamil
DiMarco et al. Ann Intern Med 1990; 113: 104-110
DBRCT of 70 pts w/ PSVT
Adenosine vs. Adenosine vs. VerapamilVerapamil Retrospective study Retrospective study
of 106 pts w/ PSVT of 106 pts w/ PSVT treated w/ adenosine treated w/ adenosine or verapamilor verapamil– No sig difference in No sig difference in
overall efficacyoverall efficacy– Logistic regression Logistic regression
foundfound Adenosine worked Adenosine worked
better w/ faster HR better w/ faster HR Verapamil had better Verapamil had better success w/ slower HRsuccess w/ slower HR
Interesting study, but hypothesis-generating at most; needs prospective, randomized investigation
Euro Heart J 2004; 25: 1310–1317
CaseCase
78 yo F presents w/ NCT78 yo F presents w/ NCT Hx of PSVT – ECG looks identicalHx of PSVT – ECG looks identical Had severe side effects w/ adenosine Had severe side effects w/ adenosine
previously & refuses repeatpreviously & refuses repeat Does not want to be shocked eitherDoes not want to be shocked either When you ask for Verapamil the nurse When you ask for Verapamil the nurse
points out her pressure is only 88/65points out her pressure is only 88/65 What can you do?What can you do?
Calcium pre-Tx to Calcium pre-Tx to prevent CCB-induced prevent CCB-induced hypotensionhypotension Verapamil = vasodilator + myocardial Verapamil = vasodilator + myocardial
depressantdepressant– Get some decrease in BP (5-40 mm Hg) in up Get some decrease in BP (5-40 mm Hg) in up
to 75% pts when given via IV route to 75% pts when given via IV route No RCT’s looking at CaNo RCT’s looking at Ca2+2+ pre-Tx pre-Tx 6 trials totalling 322 pts suggest pre-Tx 6 trials totalling 322 pts suggest pre-Tx
blunts Verapamil-induced decrease in BPblunts Verapamil-induced decrease in BP Ca gluconate 1g IV over 5 min appears Ca gluconate 1g IV over 5 min appears
to be a reasonable choiceto be a reasonable choice– Ann Pharmacother 2000; 34: 622-9.Ann Pharmacother 2000; 34: 622-9.
NB: No studies exist on Ca2+ pre-Tx for IV Diltiazem
PSVT: Chronic TxPSVT: Chronic Tx
Pts w/ frequent episodes / severe SxPts w/ frequent episodes / severe Sx– DrugsDrugs
CCB’sCCB’s B-blockersB-blockers DigoxinDigoxin Other antirhythmicsOther antirhythmics Pill-in-pocket approachPill-in-pocket approach
– Dilitiazem 120 mg PO + propranolol 80 mg PO Dilitiazem 120 mg PO + propranolol 80 mg PO appears to work bestappears to work best
Rarely get hypotension or bradycardiaRarely get hypotension or bradycardia Decreases ED visitsDecreases ED visits
– Catheter ablation techniques in EP labCatheter ablation techniques in EP lab Curative in >90% of pts – becoming 1Curative in >90% of pts – becoming 1stst line line
May be reasonable to start in ED, but need reliable F/U
Better left to cardiology or EP
Pediatric PSVTPediatric PSVT
Sx may go unnoticed Sx may go unnoticed higher higher risk of M & Mrisk of M & M
Higher rate of structural heart DzHigher rate of structural heart Dz– Should all have cardiac w/uShould all have cardiac w/u
Tx options are more age & lesion-Tx options are more age & lesion-dependantdependant
Pediatric Sx Pediatric Sx Suggestive of SVT in Suggestive of SVT in InfantsInfants SymptomsSymptoms
– Abrupt onset of Abrupt onset of SxSx
– Poor feeding / Poor feeding / VomitingVomiting
– IrritabilityIrritability– DiaphoresisDiaphoresis– PallorPallor– May present in May present in
CHF w/ prolonged CHF w/ prolonged (12-24h) Hx of (12-24h) Hx of tachycardiatachycardia
SignsSigns– HR >220HR >220– Minimal beat-Minimal beat-
beat variabilitybeat variability– Signs of CHFSigns of CHF
Pulmonary edemaPulmonary edema CardiomegalyCardiomegaly HepatomegalyHepatomegaly
Acute Tx of Peds PSVTAcute Tx of Peds PSVT
UnstableUnstable– Ketamine 1-2 mg/kg IV for sedation, then DC Ketamine 1-2 mg/kg IV for sedation, then DC
cardioversion w/ 1-2 J/kgcardioversion w/ 1-2 J/kg StableStable
– 1) Vagal maneuvers1) Vagal maneuvers Dive reflex – ice to faceDive reflex – ice to face
– Avoid carotid massageAvoid carotid massage– 2) Adenosine2) Adenosine
0.1 mg/kg IVP; repeat 0.20-0.25 mg/kg0.1 mg/kg IVP; repeat 0.20-0.25 mg/kg– 3) Verapamil3) Verapamil
0.1-0.3 mg/kg IV over 2 min0.1-0.3 mg/kg IV over 2 min Contraindicated in <1yo (risk of EMD)Contraindicated in <1yo (risk of EMD)
– 4) Amiodarone, propfenone, sotalol4) Amiodarone, propfenone, sotalol
Paediatr Drugs 2000; 2 (3): 171-181
Chronic Tx of Peds Chronic Tx of Peds PSVTPSVT Refer to cardiology for w/uRefer to cardiology for w/u
– Order echo & holterOrder echo & holter– Very young may need admissionVery young may need admission
Drug TxDrug Tx– Esp young kids where recurrence may go unnoticedEsp young kids where recurrence may go unnoticed– Drug choice depends on age, underlying rhythym, Drug choice depends on age, underlying rhythym,
physician preferencephysician preference Digoxn, BB’s, sotalol, propafenone, flecainide etcDigoxn, BB’s, sotalol, propafenone, flecainide etc
Invasive EP TxInvasive EP Tx– Catheter ablation is safe and highly effective (>90%)Catheter ablation is safe and highly effective (>90%)– Becoming Tx of choice in older kidsBecoming Tx of choice in older kids
Paediatr Drugs 2000; 2 (3): 171-181
Disposition of NCT ptsDisposition of NCT pts
PedsPeds– Young, or hemodynamically compromised Young, or hemodynamically compromised
NCT’s NCT’s admit for monitoring, w/u, & Tx admit for monitoring, w/u, & Tx– Older, stable Older, stable cardiology referral, echo, cardiology referral, echo,
holterholter AdultsAdults
– ALL WPW pts (not previously w/u)ALL WPW pts (not previously w/u)– Pts w/ severe Sx or instabilityPts w/ severe Sx or instability– Pts failing drug Tx for NCTPts failing drug Tx for NCT– Pts wanting drug-free lifestylePts wanting drug-free lifestyle
Key Take Home PointsKey Take Home Points
PSVT is a heterogenous grouping of PSVT is a heterogenous grouping of arrhythmiasarrhythmias
Unstable pts get cardiovertedUnstable pts get cardioverted Adenosine is the Tx of choice for stable PSVTAdenosine is the Tx of choice for stable PSVT Avoid AV blockers in any WCT or irregular Avoid AV blockers in any WCT or irregular
rhythym rhythym WPW has a small but definite risk of sudden WPW has a small but definite risk of sudden
cardiac deathcardiac death Ablation techniques are curative in >90% of Ablation techniques are curative in >90% of
pts w/ severe, or recurrent arrythmiaspts w/ severe, or recurrent arrythmias
Appendix A: Levels of Appendix A: Levels of EvidenceEvidence Level A Level A
– (highest): derived from (highest): derived from multiple multiple randomized clinical trialsrandomized clinical trials
Level B Level B – (intermediate): data are on the basis of a (intermediate): data are on the basis of a
limited numberlimited number of randomized trials, of randomized trials, nonrandomized studies, or nonrandomized studies, or observational registries;observational registries;
Level C Level C – (lowest): primary basis for the (lowest): primary basis for the
recommendation is recommendation is expert consensusexpert consensus..
Appendix B: Classes of Appendix B: Classes of RecommendationsRecommendations Class I: Class I:
– Conditions for which there is evidence for and/or general Conditions for which there is evidence for and/or general agreement that the procedure or agreement that the procedure or treatment is useful treatment is useful and effective.and effective.
Class II: Class II: – Conditions for which there is Conditions for which there is conflicting evidence conflicting evidence
and/or a divergence of opinionand/or a divergence of opinion about the about the usefulness/efficacy of a procedure or treatment.usefulness/efficacy of a procedure or treatment.
Class IIa: The weight of evidence or opinion is in favor of the Class IIa: The weight of evidence or opinion is in favor of the procedure or treatment.procedure or treatment.
Class IIb: Usefulness/efficacy is less well established by Class IIb: Usefulness/efficacy is less well established by evidence or opinion.evidence or opinion.
Class III: Class III: – Conditions for which there is evidence and/or general Conditions for which there is evidence and/or general
agreement that the procedure or agreement that the procedure or treatment is not treatment is not useful/effective and in some cases may be useful/effective and in some cases may be harmful.harmful.