Transcript Narrow Complex Tachycardias - Calgary Emergency Medicine

Narrow Complex
Tachycardias
Moritz Haager PGY-5
Objectives
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Develop an approach
Review treatment options
Dispositon decisions
Perspective
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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
Why should we care?
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Morbidity & Mortality
– Patient discomfort & anxiety
– Syncopal events (falls) ~15%
– Risk of sudden cardiac death w/
accessory pathway driven arrhythmias
– Tachycardia-mediated cardiomyopathy
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LV dilatation w/ impaired LV function
Approach to Tachycardia
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Stable or unstable?
– Assess ABC’s, O2, IV, monitors, crash cart to bedside
– In general if unstable, give’m juice
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Narrow or wide QRS?
Regular or irregular?
Look at the P waves
– Relationship to QRS
– P wave axis / rate
– P wave morphology(ies)
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What is the trigger / underlying cause?
Step 1: Stable or Unstable?
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Not always black & white
– Continuum from stable  compensated 
decompensated  shock  arrest
– Stability determined by big picture:
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Symptoms, signs, & vitals
Cardio-respiratory reserve
Age
Co-morbidities
Be prepared
– Any dysrhythmia could potentially deteriorate
– All therapies are potentially pro-arrhythmic
Step 2: Narrow or wide?
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Measure widest QRS on ECG
– Adults: wide = >0.12 sec (3 small boxes)
– Kids <8yo: wide = >0.08 sec (2 boxes)
Step 3: Regular or
Irregular?
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Use calipers or paper
– Irregularity can be subtle, esp at fast
rates
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Generally
– Irregular rhythms originate ABOVE the AV
node
– VT is almost never irregular
Step 4: Look at the P
waves
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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?
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Is the P wave coming from the SA?
– N axis: upright in II, negative in aVR
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Is there >1 distinct P wave morhology?
Diagnostic Trick: 50
mm/s ECG Tracings
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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
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Results
– 50 mm/s increased diagnostic accuracy
from 63 to 71%, P=0.002
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J Emerg Med 2002; 22: 123–126
Final Categorization
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Narrow Complex Tachycardias
– Regular w/ P’s
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= sinus, a. flutter w/ constant block, Focal atrial
tachycardia, AVNRT, junctional tachycardia
– Irregular w/ P’s
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= MAT, a. flutter variable block
– Regular, no P’s
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= AVRT, AVNRT
– Irregular, no P’s
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= a. fib
 Tx w/ AV nodal blockers
 Rate control +/- rhythm control
Wide Complex Tachycardias
Step 5: Underlying Causes
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HIS DEBTS
– H – Hypoxia
– I – Ischemia / infarction
– S – Sympathetic excess
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Hyperthyroid, CHF, pheochromocytoma, excercise
– D – Drugs
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Anti-arrhythmics, cocaine, amphetamines, caffeine, etc
– E – Electrolytes
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K+, Ca2+, Mg2+
– B – Bradycardias
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Eg. Sick sinus syndrome
– T – Thyroid disease
– S – Stretch
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Hypertrophy / dilation of atria & ventricles (CHF, valvular Dz)
Preciptants vary w/ age, sex, co-morbidities, etc
Clinical Presentations
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Typical Sx
–
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–
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Palpitations
96%
“Dizziness”
75%
Dyspnea
47%
Fatigue
23%
Chest pain
35%
Diaphoresis
17%
Nausea
13%
Neck pounding said to be pathogonomonic
Case
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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?
Polyuria in PSVT
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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
Case
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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?
Tachycardia & Fever
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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
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Results
– HR increased ~10 bpm for every 1oC rise
in infants b/w 2 -12 mo
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Ann Emerg Med. 2004;43:699-705
Tachycardias: Mechanism
1.
2.
3.
Reentry
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50-80% of NCT’s
Abrupt on-/off-set
Do well w/ electricity
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Typically catecholamines, drugs, lytes, ischemia
Gradual on-/off-set
Not likely to respond to electricity; Tx underlying cause
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Interruption of repolarization by afterdepolarizations
Ischemia, drugs, lytes, catecholamines
Not likely to respond to electricity; Tx underlying cause
E.g. Torsades  IV magnesium
Enhanced automaticity
Triggered dysthythmias
Case 2 80 yo F w/ sepsis:
Is this sinus tachy?
Maximal sinus tach
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220 – age = maximum HR
– 220 -80 = 140
– Unlikey this is just sinus tach
Regular NCT: DDx
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P waves present:
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–
–
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–
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Sinus tachycardia
Atrial Flutter
AVNRT
AVRT
Focal Atrial Tachycardia
No P-waves
– AVRT
– AVNRT
– Junctional Tachycardia
Consider under PSVT as
can be impossible to
differentiate on ECG; Tx
generally the same
AVNRT vs. AVRT
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AV nodal reentrant
tachycardia
– Most common PSVT
(>60%)
– Dual AV nodal
physiology
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2 separate conduction
paths in AV node
– Fast pathway
– Slow pathway
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Allow for re-entry circuit
w/in AV node
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Atrioventricular
reentrant tachycardia
– accessory pathway(s)
(AP)
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= 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)
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
AVRT
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2 types of AP
– “concealed” = capable
of retrograde conduction
only
– “manifest” = allow
anterograde +/retrograde conduction
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See “pre-excitation” on
ECG
Preexcitation Syndromes
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WPW (WolfParkinson-White)
– PR <120 msec
– QRS >100 msec
– Delta waves in
some leads
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LGL (Lown-GanongLevine)
– PR <120 msec
WPW & SVT
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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
WPW & SVT
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Antidromic SVT
– Anterograde conduction
from atria to ventricles
via accessory path &
retrograde flow through
AV node
– Wide complex
tachycardia
– Avoid AV nodal blockers
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Use procainamide or
cardiovert
(5-10% of WPW SVT)
WPW & A Fib
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Irregular Wide complex
tachycardia
– May see capture & fusion
beats
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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
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Do NOT block AV node
– Channels all impulses down AP
& increases risk of VF
– Use Procainamide or
cardioversion
Predictors of Sudden
Cardiac Death in WPW
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Shortest pre-excited R-R interval
during atrial fib <250 ms
Hx of symptomatic tachycardia
Multiple accessory pathways
Ebstein’s anomaly*
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Blomström-Lundqvist et al. ACC/AHA/ESC Guidelines
for Management of SVA ACC 2003; 42:1493–531
*= abnormal tricuspid valve  regurgitation & RA enlargement
AVNRT vs. AVRT: Can you
tell them apart
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Helpful ECG findings
– Pseudo R’ in V1
– Pseudo S in II, III, aVF
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specific (but not
sensitive) for AVNRT
– ST elevation in aVR
– RP >100 ms
– ST depression ≥2mm
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Suggest (not highly
specific or sensitive)
AVRT
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
Summary
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Unstable
– DC cardioversion
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Stable
–
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1)
2)
3)
4)
5)
6)
Vagal maneuvers (Class I/ level A)
Adenosine (Class I/ level A)
CCB’s (Class I/ level A)
BB’s (Class IIb/ level C)
Amiodarone (Class IIb/ level C)
Digoxin (Class IIb/ level C)
Blomström-Lundqvist et al. ACC/AHA/ESC Guidelines for Management of SVA
JACC 2003; 42:1493–531
Cardioversion
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Sedation
– ?1 mg midaz + 100 mcg fentanyl
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Energy Levels
– PSVT:- 50 Joules
– Atrial fibrillation: 200 Joules
– Atrial flutter: 25-50 Joules
– Orthodromic WPW: 50 Joules
– Narrow Complex VT: 50-100 Joules
Adenosine
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Actions
– Coronary vasodilator
– Transient SA & AV nodal blockade
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Outward K+ current  hyperpolarizes cells
– Reflex catecholamine release &
sympathetic discharge
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T1/2 <10 sec;
Duration of action 30-40 sec
Adenosine: Adverse
Effects
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Hot flash / flushing
Dizziness
Chest pain / pressure
Dyspnea
Feeling of impending doom
Pro-arrhythmia / blocks
~25%
~20-50%
~20-40%
~10-25%
~10%
~10%
>75% of pts will experience side effects w/ adenosine
Adenosine: Pro-arrhythmic
Effects
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Significant literature reports
– A fib, VF, Transient sinus arrest / asystole,
Torsades de pointes
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Prospective observational ED study
– 160 consecutive pts given adenosine
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Overall 21 (13%) pts had pro-arrhythmic s/e
– Prolonged AV block (>4sec)
– Atrial Fib
– Non-sustained VT
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11 (7%)
2 (1%)
8 (5%)
All resolved spontaneously; no serious outcomes
Euro J Emerg Med 2001; 8: 99-105
Pearls
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Adenosine CAN convert some VT,
– giving it to “diagnose” SVT w/ aberrancy
is misguided
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Wide & irregular – think WPW + A fib
– NO AV nodal blockers
– Amiodarone may not be ideal
– Procainamide is the drug of choice
Adenosine: Drug Interactions
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Theophylline
– ↑’s dose requirement
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Dipyridamole
– ↓’s dose requirement
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Carbamazepine
– potentiates adenosine-induced heart block
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CCB’s / BB’s
– Potentiate hypotension & bradycardia
Adenosine Dosing
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DBRCT of 201 pts w/ PSVT:
– Adenosine Dose
– 3 mg
– 6 mg
– 9 mg
– 12 mg
Conversion Rate
35.2%
62.3%
80.2%
91.4%
P<0.001 for all doses c/w placebo
 All administered through PIV
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DiMarco et al. Ann Intern Med 1990; 113: 104-110
Practical Pearl
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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
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– Put both needles into IV access port
Push the adenosine w/ one hand and…
 …chase immediately w/ the NS w/ the other
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– NB: want an IV in the AC if at all possible
Adenosine via Central
Line
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Appears to have increased success rate
– Observational study of 200 pts w/ PSVT induced
in EP lab
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found 99% success rate w/ 12 mg via femoral line
– Strickberger et al. Ann Intern Med 1997; 127: 417-422
– Randomized Cross-over study of 30 pts given
adenosine via PIV or central line
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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)
Case 4
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31 yo F w/ PSVT
– Vagal maneuvers fail
– 6 mg adenosine IV  no response
– 12 mg adenosine IV  slows down briefly
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What now? Would you give her 18 mg
of adenosine?
High Dose Adenosine
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Background
– ACLS: 6 mg, then 12 mg x2 if unsuccessful
– FDA approves use up to 12 mg
– Literature reports of uses up to 25 mg
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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
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Non-significant increase in efficacy w/ 18 mg
– 25/31 (81%) vs. 29/31 (94%); P = 0.103)
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No significant increase in adverse effects
– may have been underpowered to find difference
Weismueller et al. Deutsche Med Wochenschrift 2000. 125: 961-69
Calcium Channel Blockers
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2nd line agents in PSVT
– Verapamil
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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
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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
What about Verapamil?
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RCT of 122 pts w/ PSVT treated w/
either adenosine or Verapamil
– NS difference in conversion to NSR
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86.0% (52/60) vs. 87.1% (54/62), p=NS
– Adenosine worked much faster
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34.2 +/- 19.5 sec vs. 414.4 +/- 191.2 sec, P
< 0.0001
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Cheng KA Zhonghua Nei Ke Za Zhi 2003;
42(11): 773-6
Adenosine vs Verapamil
DBRCT of 70 pts w/ PSVT
DiMarco et al. Ann Intern Med 1990; 113: 104-110
Adenosine vs. Verapamil
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Retrospective study of
106 pts w/ PSVT
treated w/ adenosine
or verapamil
– No sig difference in
overall efficacy
– Logistic regression
found
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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
Case
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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?
Calcium pre-Tx to prevent
CCB-induced hypotension
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Verapamil = vasodilator + myocardial
depressant
– Get some decrease in BP (5-40 mm Hg) in up to
75% pts when given via IV route
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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: 622-9.
NB: No studies exist on Ca2+ pre-Tx for IV Diltiazem
PSVT: Chronic Tx
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Pts w/ frequent episodes / severe Sx
– Drugs
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CCB’s
May be reasonable to start in
ED, but need reliable F/U
B-blockers
Digoxin
Other antirhythmics
Better left to cardiology or EP
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
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Curative in >90% of pts – becoming 1st line
Pediatric PSVT
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Sx may go unnoticed  higher risk of
M&M
Higher rate of structural heart Dz
– Should all have cardiac w/u
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Tx options are more age & lesiondependant
Pediatric Sx Suggestive of
SVT in Infants
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Symptoms
– Abrupt onset of Sx
– Poor feeding /
Vomiting
– Irritability
– Diaphoresis
– Pallor
– May present in CHF
w/ prolonged (1224h) Hx of
tachycardia
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Signs
– HR >220
– Minimal beat-beat
variability
– Signs of CHF
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Pulmonary edema
Cardiomegaly
Hepatomegaly
Acute Tx of Peds PSVT
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Unstable
– Ketamine 1-2 mg/kg IV for sedation, then DC
cardioversion w/ 1-2 J/kg
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Stable
– 1) Vagal maneuvers
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Dive reflex – ice to face
– Avoid carotid massage
– 2) Adenosine
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0.1 mg/kg IVP; repeat 0.20-0.25 mg/kg
– 3) Verapamil
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0.1-0.3 mg/kg IV over 2 min
Contraindicated in <1yo (risk of EMD)
– 4) Amiodarone, propfenone, sotalol
Paediatr Drugs 2000; 2 (3): 171-181
Chronic Tx of Peds PSVT
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Refer to cardiology for w/u
– Order echo & holter
– Very young may need admission
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Drug Tx
– Esp young kids where recurrence may go unnoticed
– Drug choice depends on age, underlying rhythym,
physician preference
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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): 171-181
Disposition of NCT pts
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Peds
– Young, or hemodynamically compromised NCT’s
 admit for monitoring, w/u, & Tx
– Older, stable  cardiology referral, echo, holter
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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
Key Take Home Points
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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
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.
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.
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
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.