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.