Narrow Complex Tachycardias Moritz Haager PGY-5. Objectives Develop an approach Develop an approach...

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Narrow Complex Narrow Complex Tachycardias Tachycardias Moritz Haager PGY-5 Moritz Haager PGY-5

Transcript of Narrow Complex Tachycardias Moritz Haager PGY-5. Objectives Develop an approach Develop an approach...

Page 1: Narrow Complex Tachycardias Moritz Haager PGY-5. Objectives Develop an approach Develop an approach Review treatment options Review treatment options.

Narrow Complex Narrow Complex TachycardiasTachycardias

Moritz Haager PGY-5Moritz Haager PGY-5

Page 2: Narrow Complex Tachycardias Moritz Haager PGY-5. Objectives Develop an approach Develop an approach Review treatment options Review treatment options.

ObjectivesObjectives

Develop an approach Develop an approach Review treatment optionsReview treatment options Dispositon decisionsDispositon decisions

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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

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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

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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?

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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

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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)

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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

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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?

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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

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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

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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

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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

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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?

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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

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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?

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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

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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

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Case 2 80 yo F w/ Case 2 80 yo F w/ sepsis: Is this sinus sepsis: Is this sinus tachy?tachy?

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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

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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

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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)

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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

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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

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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

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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

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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)

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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

Page 30: Narrow Complex Tachycardias Moritz Haager PGY-5. Objectives Develop an approach Develop an approach Review treatment options Review treatment options.

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

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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)

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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?

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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

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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

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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

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Adenosine vs Adenosine vs VerapamilVerapamil

DiMarco et al. Ann Intern Med 1990; 113: 104-110

DBRCT of 70 pts w/ PSVT

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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

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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?

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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

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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

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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

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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

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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

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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

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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

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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

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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..

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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.