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Narrow Complex Tachycardias

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1 Narrow Complex Tachycardias
Moritz Haager PGY-5

2 Objectives Develop an approach Review treatment options
Dispositon decisions

3 Perspective SVT Broad umbrella term for any tachycardia originating above the ventricles Variable underlying mechanisms but basically one Tx approach Ranges from physiological  pathological, and benign  dangerous Occurs in all age groups Clinical presentation from asymptomatic  shock / CHF When presented with an undifferentiated presentation with a broad DDx and variability in outcome you need an APPROACH

4 Why should we care? Morbidity & Mortality Patient discomfort & anxiety
Syncopal events (falls) ~15% Risk of sudden cardiac death w/ accessory pathway driven arrhythmias Tachycardia-mediated cardiomyopathy LV dilatation w/ impaired LV function

5 Approach to Tachycardia
Stable or unstable? Assess ABC’s, O2, IV, monitors, crash cart to bedside In general if unstable, give’m juice Narrow or wide QRS? Regular or irregular? Look at the P waves Relationship to QRS P wave axis / rate P wave morphology(ies) What is the trigger / underlying cause?

6 Step 1: Stable or Unstable?
Not always black & white Continuum from stable  compensated  decompensated  shock  arrest Stability determined by big picture: Symptoms, signs, & vitals Cardio-respiratory reserve Age Co-morbidities Be prepared Any dysrhythmia could potentially deteriorate All therapies are potentially pro-arrhythmic

7 Step 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)

8 Step 3: Regular or Irregular?
Use calipers or paper Irregularity can be subtle, esp at fast rates Generally Irregular rhythms originate ABOVE the AV node VT is almost never irregular

9 Step 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 aVR Is there >1 distinct P wave morhology?

10 Diagnostic Trick: 50 mm/s ECG Tracings
Comparsion study of 8 EP’s Given 45 ECG’s of NCT’s printed at 25 mm/s & asked to give Dx & Tx plan 2 wks later given same ECG’s printed at 25 & 50 mm/s & asked to give Dx & Tx Results 50 mm/s increased diagnostic accuracy from 63 to 71%, P=0.002 J Emerg Med 2002; 22: 123–126

11 Final Categorization Narrow Complex Tachycardias
Regular w/ P’s = sinus, a. flutter w/ constant block, Focal atrial tachycardia, AVNRT, junctional tachycardia Irregular w/ P’s = MAT, a. flutter variable block Regular, no P’s = AVRT, AVNRT Irregular, no P’s = a. fib Wide Complex Tachycardias  Tx w/ AV nodal blockers  Rate control +/- rhythm control

12 Step 5: Underlying Causes
HIS DEBTS H – Hypoxia I – Ischemia / infarction S – Sympathetic excess Hyperthyroid, CHF, pheochromocytoma, excercise D – Drugs Anti-arrhythmics, cocaine, amphetamines, caffeine, etc E – Electrolytes K+, Ca2+, Mg2+ B – Bradycardias Eg. Sick sinus syndrome T – Thyroid disease S – Stretch Hypertrophy / dilation of atria & ventricles (CHF, valvular Dz) Preciptants vary w/ age, sex, co-morbidities, etc

13 Clinical Presentations
Typical Sx Palpitations 96% “Dizziness” 75% Dyspnea 47% Fatigue 23% Chest pain 35% Diaphoresis 17% Nausea 13% Neck pounding said to be pathogonomonic Wood KA, Drew BJ, Scheinman, MM. Frequency of disabling symptoms in supraventricular tachycardia. Am J Cardiol 1997;79: 3. Martin A, Hoyo JF,Matamoroas H, et al. Reentrant supraventricular tachycardia in the emergency department: A prospective study of clinical presentation and sequential therapy. Ann Emerg Med 2000;35:S40.

14 Case 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?

15 Polyuria in PSVT Loss of AV synchronization
Atrial contraction against closed AV valves Elevated atrial pressure & atrial stretch Release of atrial natriuretic peptide  polyuria NB: This is trivia – absence of polyuria does NOT exclude Dx of PSVT and you should still check at least a urine for glucose

16 Case 3 mo F w/ dyspnea & wheeze T 40.5oC, P 190, RR 60, SpO2 88%
Mod resp distress on exam w/ wheezes & crackles bilaterally Is this just sinus tachycardia from her fever?

17 Tachycardia & Fever Prospective observational study of 490 infants <1 yo Measured HR & rectal temp in calm, quiet kids w/o evidence of serious illness Analyzed relationship b/w HR & temp w/ multivariate linear regression Results HR increased ~10 bpm for every 1oC rise in infants b/w mo Ann Emerg Med. 2004;43:

18 Tachycardias: Mechanism
Reentry 50-80% of NCT’s Abrupt on-/off-set Do well w/ electricity Enhanced automaticity Typically catecholamines, drugs, lytes, ischemia Gradual on-/off-set Not likely to respond to electricity; Tx underlying cause Triggered dysthythmias Interruption of repolarization by afterdepolarizations Ischemia, drugs, lytes, catecholamines Not likely to respond to electricity; Tx underlying cause E.g. Torsades  IV magnesium

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

20 Maximal sinus tach 220 – age = maximum HR 220 -80 = 140
Unlikey this is just sinus tach

21 Regular NCT: DDx P waves present: No P-waves Sinus tachycardia
Atrial Flutter AVNRT AVRT Focal Atrial Tachycardia No P-waves Junctional Tachycardia Consider under PSVT as can be impossible to differentiate on ECG; Tx generally the same

22 AVNRT vs. AVRT AV nodal reentrant tachycardia
Most common PSVT (>60%) Dual AV nodal physiology 2 separate conduction paths in AV node Fast pathway Slow pathway Allow for re-entry circuit w/in AV node Atrioventricular reentrant tachycardia accessory pathway(s) (AP) = Tracks of conducting tissue outside of AV node, connecting atria & ventricles Re-entry circuit formed by AP & AV node (WPW) 2 or more separate AP’s (bypass AV node completely)

23 AVNRT “Typical” AVNRT – = 90-95%
Anterograde conduction down slow pathway Retrograde conduction up fast pathway If P waves seen RP < PR interval ATRIA VENTRICLES “Atypical” AVNRT is the reverse of what is pictured here

24 AVRT 2 types of AP “concealed” = capable of retrograde conduction only
“manifest” = allow anterograde +/- retrograde conduction See “pre-excitation” on ECG

25 WPW

26 Preexcitation Syndromes
WPW (Wolf-Parkinson-White) PR <120 msec QRS >100 msec Delta waves in some leads LGL (Lown-Ganong-Levine) PR <120 msec

27 WPW & SVT Orthodromic SVT
Anterograde via AV & returns via accessory tract Uses normal conduction system therefore get narrow complex tachycardia Orthodromic makes up 90-95% of WPW SVT’s

28 WPW & SVT Antidromic SVT
Anterograde conduction from atria to ventricles via accessory path & retrograde flow through AV node Wide complex tachycardia Avoid AV nodal blockers Use procainamide or cardiovert (5-10% of WPW SVT)

29 WPW & A Fib Irregular Wide complex tachycardia
May see capture & fusion beats Common (~30% of WPW pts) & potentially life-threatening AP w/ short refractory period & anterograde conduction  near 1:1 conduction  VF 0.15 – 0.39% incidence of sudden cardiac death Do NOT block AV node Channels all impulses down AP & increases risk of VF Use Procainamide or cardioversion

30 Predictors of Sudden Cardiac Death in WPW
Shortest pre-excited R-R interval during atrial fib <250 ms Hx of symptomatic tachycardia Multiple accessory pathways Ebstein’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

31 AVNRT vs. AVRT: Can you tell them apart
Helpful ECG findings Pseudo R’ in V1 Pseudo S in II, III, aVF specific (but not sensitive) for AVNRT ST elevation in aVR RP >100 ms ST depression ≥2mm Suggest (not highly specific or sensitive) AVRT V1 Psudo r’  think AVNRT Inferior leads Psuedo S  think AVNRT ST up in AVR Think AVRT (but not only) 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

32 PSVT: Acute Treatment Summary
Unstable DC cardioversion Stable 1) 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; 42:1493–531 Blomström-Lundqvist et al. ACC/AHA/ESC Guidelines for Management of SVA JACC 2003; 42:1493–531

33 Cardioversion Sedation Energy Levels ?1 mg midaz + 100 mcg fentanyl
PSVT:- 50 Joules Atrial fibrillation: 200 Joules Atrial flutter: Joules Orthodromic WPW: 50 Joules Narrow Complex VT: Joules

34 Adenosine Actions T1/2 <10 sec; Duration of action 30-40 sec
Coronary vasodilator Transient SA & AV nodal blockade Outward K+ current  hyperpolarizes cells Reflex catecholamine release & sympathetic discharge T1/2 <10 sec; Duration of action sec

35 Adenosine: 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

36 Adenosine: Pro-arrhythmic Effects
Significant literature reports A fib, VF, Transient sinus arrest / asystole, Torsades de pointes Prospective observational ED study 160 consecutive pts given adenosine Overall 21 (13%) pts had pro-arrhythmic s/e Prolonged AV block (>4sec) 11 (7%) Atrial Fib 2 (1%) Non-sustained VT 8 (5%) All resolved spontaneously; no serious outcomes Interesting 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:

37 Pearls Adenosine CAN convert some VT,
giving it to “diagnose” SVT w/ aberrancy is misguided Wide & irregular – think WPW + A fib NO AV nodal blockers Amiodarone may not be ideal Procainamide is the drug of choice

38 Adenosine: Drug Interactions
Theophylline ↑’s dose requirement Dipyridamole ↓’s dose requirement Carbamazepine potentiates adenosine-induced heart block CCB’s / BB’s Potentiate hypotension & bradycardia

39 Adenosine Dosing DBRCT of 201 pts w/ PSVT:
Adenosine Dose Conversion Rate 3 mg % 6 mg % 9 mg % 12 mg % P<0.001 for all doses c/w placebo All administered through PIV DiMarco et al. Ann Intern Med 1990; 113:

40 Practical Pearl Adenosine administration
Want to get it in as fast as possible Use 2 syringes w/ 18g needles one w/ adenosine Other w/ 10 cc NS Put both needles into IV access port Push the adenosine w/ one hand and… …chase immediately w/ the NS w/ the other NB: want an IV in the AC if at all possible

41 Adenosine via Central Line
Appears to have increased success rate Observational study of 200 pts w/ PSVT induced in EP lab found 99% success rate w/ 12 mg via femoral line Strickberger et al. Ann Intern Med 1997; 127: Randomized Cross-over study of 30 pts given adenosine via PIV or central line success rate w/ 3 mg was 77% when given via central line vs. 37% via PIV McIntosh-Yellin et al. JACC 1993; 22:741–5 Case reports of more severe S/E via central line (felt to be dose-related)

42 Case 4 31 yo F w/ PSVT Vagal maneuvers fail 6 mg adenosine IV  no response 12 mg adenosine IV  slows down briefly What now? Would you give her 18 mg of adenosine?

43 High Dose Adenosine Background What about higher doses?
ACLS: 6 mg, then 12 mg x2 if unsuccessful FDA approves use up to 12 mg Literature reports of uses up to 25 mg What about higher doses? Randomized cross-over comparison of of 31 pts w/ AVNRT/AVRT in EP lab given 12 & 18 mg adenosine via PIV Non-significant increase in efficacy w/ 18 mg 25/31 (81%) vs. 29/31 (94%); P = 0.103) No significant increase in adverse effects may have been underpowered to find difference 25 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 :

44 Calcium Channel Blockers
2nd line agents in PSVT Verapamil 1st dose: 2.5 – 5 mg IV over 2 min 2nd 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 WPW Diltiazem 1st dose: 0.25 mg/kg IV over 2 min 2nd dose (15 min later): 0.35 mg/kg IV over 2 min followed by gtt of 5-15 mg/h Generally felt to be safer than Verapamil but same cautions apply

45 What about Verapamil? RCT of 122 pts w/ PSVT treated w/ either adenosine or Verapamil NS difference in conversion to NSR 86.0% (52/60) vs. 87.1% (54/62), p=NS Adenosine worked much faster 34.2 +/ sec vs / sec, P < Cheng KA Zhonghua Nei Ke Za Zhi 2003; 42(11): 773-6

46 Adenosine vs Verapamil
DBRCT of 70 pts w/ PSVT No sig differences after 2 doses DiMarco et al. Ann Intern Med 1990; 113:

47 Adenosine vs. Verapamil
Retrospective study of 106 pts w/ PSVT treated w/ adenosine or verapamil No sig difference in overall efficacy Logistic regression found Adenosine worked better w/ faster HR Verapamil had better success w/ slower HR Interesting study, but hypothesis-generating at most; needs prospective, randomized investigation Euro Heart J 2004; 25: 1310–1317

48 Case 78 yo F presents w/ NCT Hx of PSVT – ECG looks identical
Had severe side effects w/ adenosine previously & refuses repeat Does not want to be shocked either When you ask for Verapamil the nurse points out her pressure is only 88/65 What can you do?

49 Calcium pre-Tx to prevent CCB-induced hypotension
Verapamil = vasodilator + myocardial depressant Get some decrease in BP (5-40 mm Hg) in up to 75% pts when given via IV route No RCT’s looking at Ca2+ pre-Tx 6 trials totalling 322 pts suggest pre-Tx blunts Verapamil-induced decrease in BP Ca gluconate 1g IV over 5 min appears to be a reasonable choice Ann Pharmacother 2000; 34: NB: No studies exist on Ca2+ pre-Tx for IV Diltiazem

50 PSVT: Chronic Tx Pts w/ frequent episodes / severe Sx Drugs
CCB’s B-blockers Digoxin Other antirhythmics Pill-in-pocket approach Dilitiazem 120 mg PO + propranolol 80 mg PO appears to work best Rarely get hypotension or bradycardia Decreases ED visits Catheter ablation techniques in EP lab Curative in >90% of pts – becoming 1st line May be reasonable to start in ED, but need reliable F/U Better left to cardiology or EP

51 Pediatric PSVT Sx may go unnoticed  higher risk of M & M
Higher rate of structural heart Dz Should all have cardiac w/u Tx options are more age & lesion-dependant

52 Pediatric Sx Suggestive of SVT in Infants
Symptoms Abrupt onset of Sx Poor feeding / Vomiting Irritability Diaphoresis Pallor May present in CHF w/ prolonged (12-24h) Hx of tachycardia Signs HR >220 Minimal beat-beat variability Signs of CHF Pulmonary edema Cardiomegaly Hepatomegaly Tachycardia impairs diastolic filling leading to decreased cardiac output

53 Acute Tx of Peds PSVT Unstable Stable
Ketamine 1-2 mg/kg IV for sedation, then DC cardioversion w/ 1-2 J/kg Stable 1) Vagal maneuvers Dive reflex – ice to face Avoid carotid massage 2) Adenosine 0.1 mg/kg IVP; repeat mg/kg 3) Verapamil mg/kg IV over 2 min Contraindicated in <1yo (risk of EMD) 4) Amiodarone, propfenone, sotalol Paediatr Drugs 2000; 2 (3):

54 Chronic Tx of Peds PSVT Refer to cardiology for w/u Drug Tx
Order echo & holter Very young may need admission Drug Tx Esp young kids where recurrence may go unnoticed Drug choice depends on age, underlying rhythym, physician preference Digoxn, BB’s, sotalol, propafenone, flecainide etc Invasive EP Tx Catheter ablation is safe and highly effective (>90%) Becoming Tx of choice in older kids Paediatr Drugs 2000; 2 (3):

55 Disposition of NCT pts Peds Adults
Young, or hemodynamically compromised NCT’s  admit for monitoring, w/u, & Tx Older, stable  cardiology referral, echo, holter Adults ALL WPW pts (not previously w/u) Pts w/ severe Sx or instability Pts failing drug Tx for NCT Pts wanting drug-free lifestyle

56 Key Take Home Points PSVT is a heterogenous grouping of arrhythmias
Unstable pts get cardioverted Adenosine is the Tx of choice for stable PSVT Avoid AV blockers in any WCT or irregular rhythym WPW has a small but definite risk of sudden cardiac death Ablation techniques are curative in >90% of pts w/ severe, or recurrent arrythmias

57 Appendix A: Levels of Evidence
Level A (highest): derived from multiple randomized clinical trials Level 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.

58 Appendix 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.

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