2Objectives Develop an approach Review treatment options Dispositon decisions
3PerspectiveSVTBroad umbrella term for any tachycardia originating above the ventriclesVariable underlying mechanisms but basically one Tx approachRanges from physiological pathological, and benign dangerousOccurs in all age groupsClinical presentation from asymptomatic shock / CHFWhen presented with an undifferentiated presentation with a broad DDx and variability in outcome you need an APPROACH
4Why should we care? Morbidity & Mortality Patient discomfort & anxiety Syncopal events (falls) ~15%Risk of sudden cardiac death w/ accessory pathway driven arrhythmiasTachycardia-mediated cardiomyopathyLV dilatation w/ impaired LV function
5Approach to Tachycardia Stable or unstable?Assess ABC’s, O2, IV, monitors, crash cart to bedsideIn general if unstable, give’m juiceNarrow or wide QRS?Regular or irregular?Look at the P wavesRelationship to QRSP wave axis / rateP wave morphology(ies)What is the trigger / underlying cause?
6Step 1: Stable or Unstable? Not always black & whiteContinuum from stable compensated decompensated shock arrestStability determined by big picture:Symptoms, signs, & vitalsCardio-respiratory reserveAgeCo-morbiditiesBe preparedAny dysrhythmia could potentially deteriorateAll therapies are potentially pro-arrhythmic
7Step 2: Narrow or wide? Measure widest QRS on ECG Adults: wide = >0.12 sec (3 small boxes)Kids <8yo: wide = >0.08 sec (2 boxes)
8Step 3: Regular or Irregular? Use calipers or paperIrregularity can be subtle, esp at fast ratesGenerallyIrregular rhythms originate ABOVE the AV nodeVT is almost never irregular
9Step 4: Look at the P waves P waves present?Is there a P before every QRS?What is the relationship b/w the P and the QRS?What is the P wave rate? Ventricular rate?Is the P wave coming from the SA?N axis: upright in II, negative in aVRIs there >1 distinct P wave morhology?
10Diagnostic Trick: 50 mm/s ECG Tracings Comparsion study of 8 EP’sGiven 45 ECG’s of NCT’s printed at 25 mm/s & asked to give Dx & Tx plan2 wks later given same ECG’s printed at 25 & 50 mm/s & asked to give Dx & TxResults50 mm/s increased diagnostic accuracy from 63 to 71%, P=0.002J Emerg Med 2002; 22: 123–126
11Final Categorization Narrow Complex Tachycardias Regular w/ P’s= sinus, a. flutter w/ constant block, Focal atrial tachycardia, AVNRT, junctional tachycardiaIrregular w/ P’s= MAT, a. flutter variable blockRegular, no P’s= AVRT, AVNRTIrregular, no P’s= a. fibWide Complex Tachycardias Tx w/ AV nodal blockers Rate control +/- rhythm control
13Clinical Presentations Typical SxPalpitations 96%“Dizziness” 75%Dyspnea 47%Fatigue 23%Chest pain 35%Diaphoresis 17%Nausea 13%Neck pounding said to be pathogonomonicWood KA, Drew BJ, Scheinman, MM. Frequency of disabling symptomsin supraventricular tachycardia. Am J Cardiol 1997;79:3. Martin A, Hoyo JF,Matamoroas H, et al. Reentrant supraventriculartachycardia in the emergency department: A prospective study of clinicalpresentation and sequential therapy. Ann Emerg Med 2000;35:S40.
14Case 27 yo M w/ palpitations & dyspnea NCT at 160 on ECG c/w PSVT Also tells you he has been “pissin’ like a racehorse”Does he have diabetes?
15Polyuria in PSVT Loss of AV synchronization Atrial contraction against closed AV valvesElevated atrial pressure & atrial stretchRelease of atrial natriuretic peptide polyuriaNB: This is trivia – absence of polyuria does NOT exclude Dx of PSVT and you should still check at least a urine for glucose
16Case 3 mo F w/ dyspnea & wheeze T 40.5oC, P 190, RR 60, SpO2 88% Mod resp distress on exam w/ wheezes & crackles bilaterallyIs this just sinus tachycardia from her fever?
17Tachycardia & FeverProspective observational study of 490 infants <1 yoMeasured HR & rectal temp in calm, quiet kids w/o evidence of serious illnessAnalyzed relationship b/w HR & temp w/ multivariate linear regressionResultsHR increased ~10 bpm for every 1oC rise in infants b/w moAnn Emerg Med. 2004;43:
18Tachycardias: Mechanism Reentry50-80% of NCT’sAbrupt on-/off-setDo well w/ electricityEnhanced automaticityTypically catecholamines, drugs, lytes, ischemiaGradual on-/off-setNot likely to respond to electricity; Tx underlying causeTriggered dysthythmiasInterruption of repolarization by afterdepolarizationsIschemia, drugs, lytes, catecholaminesNot likely to respond to electricity; Tx underlying cause E.g. Torsades IV magnesium
20Maximal sinus tach 220 – age = maximum HR 220 -80 = 140 Unlikey this is just sinus tach
21Regular NCT: DDx P waves present: No P-waves Sinus tachycardia Atrial FlutterAVNRTAVRTFocal Atrial TachycardiaNo P-wavesJunctional TachycardiaConsider under PSVT as can be impossible todifferentiate on ECG; Tx generally the same
22AVNRT vs. AVRT AV nodal reentrant tachycardia Most common PSVT (>60%)Dual AV nodal physiology2 separate conduction paths in AV nodeFast pathwaySlow pathwayAllow for re-entry circuit w/in AV nodeAtrioventricular reentrant tachycardiaaccessory pathway(s) (AP)= Tracks of conducting tissue outside of AV node, connecting atria & ventriclesRe-entry circuit formed byAP & AV node (WPW)2 or more separate AP’s (bypass AV node completely)
23AVNRT “Typical” AVNRT – = 90-95% Anterograde conduction down slow pathwayRetrograde conduction up fast pathwayIf P waves seen RP < PR intervalATRIAVENTRICLES“Atypical” AVNRT is the reverse of what is pictured here
24AVRT 2 types of AP “concealed” = capable of retrograde conduction only “manifest” = allow anterograde +/- retrograde conductionSee “pre-excitation” on ECG
26Preexcitation Syndromes WPW (Wolf-Parkinson-White)PR <120 msecQRS >100 msecDelta waves in some leadsLGL (Lown-Ganong-Levine)PR <120 msec
27WPW & SVT Orthodromic SVT Anterograde via AV & returns via accessory tractUses normal conduction system therefore get narrow complex tachycardiaOrthodromic makes up 90-95% of WPW SVT’s
28WPW & SVT Antidromic SVT Anterograde conduction from atria to ventricles via accessory path & retrograde flow through AV nodeWide complex tachycardiaAvoid AV nodal blockersUse procainamide or cardiovert(5-10% of WPW SVT)
29WPW & A Fib Irregular Wide complex tachycardia May see capture & fusion beatsCommon (~30% of WPW pts) & potentially life-threateningAP w/ short refractory period & anterograde conduction near 1:1 conduction VF0.15 – 0.39% incidence of sudden cardiac deathDo NOT block AV nodeChannels all impulses down AP & increases risk of VFUse Procainamide or cardioversion
30Predictors of Sudden Cardiac Death in WPW Shortest pre-excited R-R interval during atrial fib <250 msHx of symptomatic tachycardiaMultiple accessory pathwaysEbstein’s anomaly*Blomström-Lundqvist et al. ACC/AHA/ESC Guidelines for Management of SVA ACC 2003; 42:1493–531*= abnormal tricuspid valve regurgitation & RA enlargement
31AVNRT vs. AVRT: Can you tell them apart Helpful ECG findingsPseudo R’ in V1Pseudo S in II, III, aVFspecific (but not sensitive) for AVNRTST elevation in aVRRP >100 msST depression ≥2mmSuggest (not highly specific or sensitive) AVRTV1Psudo r’ think AVNRTInferior leadsPsuedo S think AVNRTST up in AVRThink AVRT (but not only)Bottom line = 12-lead lacks 100% accuracy but important to look because AVRT more serious DxSee Adam Osters talk July 22, 2004 for more detailed explanation
32PSVT: Acute Treatment Summary UnstableDC cardioversionStable1) Vagal maneuvers (Class I/ level A)2) Adenosine (Class I/ level A)3) CCB’s (Class I/ level A)4) BB’s (Class IIb/ level C)5) Amiodarone (Class IIb/ level C)6) Digoxin (Class IIb/ level C)Blomström-Lundqvist et al. ACC/AHA/ESC Guidelines for Management of SVA JACC 2003; 42:1493–531Blomström-Lundqvist et al. ACC/AHA/ESC Guidelines for Management of SVAJACC 2003; 42:1493–531
34Adenosine Actions T1/2 <10 sec; Duration of action 30-40 sec Coronary vasodilatorTransient SA & AV nodal blockadeOutward K+ current hyperpolarizes cellsReflex catecholamine release & sympathetic dischargeT1/2 <10 sec;Duration of action sec
35Adenosine: Adverse Effects Hot flash / flushing ~25%Dizziness ~20-50%Chest pain / pressure ~20-40%Dyspnea ~10-25%Feeling of impending doom ~10%Pro-arrhythmia / blocks ~10%>75% of pts will experience side effects w/ adenosine
36Adenosine: Pro-arrhythmic Effects Significant literature reportsA fib, VF, Transient sinus arrest / asystole, Torsades de pointesProspective observational ED study160 consecutive pts given adenosineOverall 21 (13%) pts had pro-arrhythmic s/eProlonged AV block (>4sec) 11 (7%)Atrial Fib 2 (1%)Non-sustained VT 8 (5%)All resolved spontaneously; no serious outcomesInteresting thing about this study is that they gave adenosine to both NCT & WCT: 16% had WCT – the only adverse effect were 3/26 (11%) cases of prolonged AV block and adenosine was 69% efficacy in either terminating (7/26 or 27%) or diagnosing (11/26 or 42%) the rhtyhm.Euro J Emerg Med 2001; 8:
37Pearls Adenosine CAN convert some VT, giving it to “diagnose” SVT w/ aberrancy is misguidedWide & irregular – think WPW + A fibNO AV nodal blockersAmiodarone may not be idealProcainamide is the drug of choice
39Adenosine Dosing DBRCT of 201 pts w/ PSVT: Adenosine Dose Conversion Rate3 mg %6 mg %9 mg %12 mg %P<0.001 for all doses c/w placeboAll administered through PIVDiMarco et al. Ann Intern Med 1990; 113:
40Practical Pearl Adenosine administration Want to get it in as fast as possibleUse 2 syringes w/ 18g needlesone w/ adenosineOther w/ 10 cc NSPut both needles into IV access portPush the adenosine w/ one hand and……chase immediately w/ the NS w/ the otherNB: want an IV in the AC if at all possible
41Adenosine via Central Line Appears to have increased success rateObservational study of 200 pts w/ PSVT induced in EP labfound 99% success rate w/ 12 mg via femoral lineStrickberger et al. Ann Intern Med 1997; 127:Randomized Cross-over study of 30 pts given adenosine via PIV or central linesuccess rate w/ 3 mg was 77% when given via central line vs. 37% via PIVMcIntosh-Yellin et al. JACC 1993; 22:741–5Case reports of more severe S/E via central line (felt to be dose-related)
42Case 431 yo F w/ PSVTVagal maneuvers fail6 mg adenosine IV no response12 mg adenosine IV slows down brieflyWhat now? Would you give her 18 mg of adenosine?
43High Dose Adenosine Background What about higher doses? ACLS: 6 mg, then 12 mg x2 if unsuccessfulFDA approves use up to 12 mgLiterature reports of uses up to 25 mgWhat about higher doses?Randomized cross-over comparison of of 31 pts w/ AVNRT/AVRT in EP lab given 12 & 18 mg adenosine via PIVNon-significant increase in efficacy w/ 18 mg25/31 (81%) vs. 29/31 (94%); P = 0.103)No significant increase in adverse effectsmay have been underpowered to find difference25 of the 31 patients (81%) the tachycardia was terminated by 12 mg adenosine. In 29 of the 31 patients (94%)Weismueller et al. Deutsche Med Wochenschrift :
44Calcium Channel Blockers 2nd line agents in PSVTVerapamil1st dose: 2.5 – 5 mg IV over 2 min2nd dose (30 min later): 2.5 – 10 mg IV over 2 min (to max of 20 mg)NB: CONTRAINDICATED in <1yo (risk of EMD), wide QRS, or hypotensive pts, CHF, or WPWDiltiazem1st dose: 0.25 mg/kg IV over 2 min2nd dose (15 min later): 0.35 mg/kg IV over 2 min followed by gtt of 5-15 mg/hGenerally felt to be safer than Verapamil but same cautions apply
45What about Verapamil?RCT of 122 pts w/ PSVT treated w/ either adenosine or VerapamilNS difference in conversion to NSR86.0% (52/60) vs. 87.1% (54/62), p=NSAdenosine worked much faster34.2 +/ sec vs / sec, P <Cheng KA Zhonghua Nei Ke Za Zhi 2003; 42(11): 773-6
46Adenosine vs Verapamil DBRCT of 70 pts w/ PSVTNo sig differences after 2 dosesDiMarco et al. Ann Intern Med 1990; 113:
47Adenosine vs. Verapamil Retrospective study of 106 pts w/ PSVT treated w/ adenosine or verapamilNo sig difference in overall efficacyLogistic regression foundAdenosine worked better w/ faster HR Verapamil had better success w/ slower HRInteresting study, but hypothesis-generating at most; needs prospective, randomized investigationEuro Heart J 2004; 25: 1310–1317
48Case 78 yo F presents w/ NCT Hx of PSVT – ECG looks identical Had severe side effects w/ adenosine previously & refuses repeatDoes not want to be shocked eitherWhen you ask for Verapamil the nurse points out her pressure is only 88/65What can you do?
49Calcium pre-Tx to prevent CCB-induced hypotension Verapamil = vasodilator + myocardial depressantGet some decrease in BP (5-40 mm Hg) in up to 75% pts when given via IV routeNo RCT’s looking at Ca2+ pre-Tx6 trials totalling 322 pts suggest pre-Tx blunts Verapamil-induced decrease in BPCa gluconate 1g IV over 5 min appears to be a reasonable choiceAnn Pharmacother 2000; 34:NB: No studies exist on Ca2+ pre-Tx for IV Diltiazem
50PSVT: Chronic Tx Pts w/ frequent episodes / severe Sx Drugs CCB’sB-blockersDigoxinOther antirhythmicsPill-in-pocket approachDilitiazem 120 mg PO + propranolol 80 mg PO appears to work bestRarely get hypotension or bradycardiaDecreases ED visitsCatheter ablation techniques in EP labCurative in >90% of pts – becoming 1st lineMay be reasonable to start in ED, but need reliable F/UBetter left to cardiology or EP
51Pediatric PSVT Sx may go unnoticed higher risk of M & M Higher rate of structural heart DzShould all have cardiac w/uTx options are more age & lesion-dependant
52Pediatric Sx Suggestive of SVT in Infants SymptomsAbrupt onset of SxPoor feeding / VomitingIrritabilityDiaphoresisPallorMay present in CHF w/ prolonged (12-24h) Hx of tachycardiaSignsHR >220Minimal beat-beat variabilitySigns of CHFPulmonary edemaCardiomegalyHepatomegalyTachycardia impairs diastolic filling leading to decreased cardiac output
53Acute Tx of Peds PSVT Unstable Stable Ketamine 1-2 mg/kg IV for sedation, then DC cardioversion w/ 1-2 J/kgStable1) Vagal maneuversDive reflex – ice to faceAvoid carotid massage2) Adenosine0.1 mg/kg IVP; repeat mg/kg3) Verapamilmg/kg IV over 2 minContraindicated in <1yo (risk of EMD)4) Amiodarone, propfenone, sotalolPaediatr Drugs 2000; 2 (3):
54Chronic Tx of Peds PSVT Refer to cardiology for w/u Drug Tx Order echo & holterVery young may need admissionDrug TxEsp young kids where recurrence may go unnoticedDrug choice depends on age, underlying rhythym, physician preferenceDigoxn, BB’s, sotalol, propafenone, flecainide etcInvasive EP TxCatheter ablation is safe and highly effective (>90%)Becoming Tx of choice in older kidsPaediatr Drugs 2000; 2 (3):
55Disposition of NCT pts Peds Adults Young, or hemodynamically compromised NCT’s admit for monitoring, w/u, & TxOlder, stable cardiology referral, echo, holterAdultsALL WPW pts (not previously w/u)Pts w/ severe Sx or instabilityPts failing drug Tx for NCTPts wanting drug-free lifestyle
56Key Take Home Points PSVT is a heterogenous grouping of arrhythmias Unstable pts get cardiovertedAdenosine is the Tx of choice for stable PSVTAvoid AV blockers in any WCT or irregular rhythymWPW has a small but definite risk of sudden cardiac deathAblation techniques are curative in >90% of pts w/ severe, or recurrent arrythmias
57Appendix A: Levels of Evidence Level A(highest): derived from multiple randomized clinical trialsLevel B(intermediate): data are on the basis of a limited number of randomized trials, nonrandomized studies, or observational registries;Level C(lowest): primary basis for the recommendation is expert consensus.
58Appendix B: Classes of Recommendations Class I:Conditions for which there is evidence for and/or general agreement that the procedure or treatment is useful and effective.Class II:Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment.Class IIa: The weight of evidence or opinion is in favor of the procedure or treatment.Class IIb: Usefulness/efficacy is less well established by evidence or opinion.Class III:Conditions for which there is evidence and/or general agreement that the procedure or treatment is not useful/effective and in some cases may be harmful.