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Diagnosis and Management of
Supra-ventricular Tachycardia
Dr. D. Khanra
SR3
LPS Institute of Cardiovascular Sciences
GSVM Medical College, Kanpur
1
SVT in a nut-shell
Onset
Termination
2
AVNRT AVRT AT
AFLAVNRT
Regular Narrow QRS Tachycardia
Visible P Waves AF / AT /AFL
A >V
AFL /AT ? RP Interval
Short Long
< 70 ms > 70 ms
AVNRT
AVRT / AVNRT /
AT
AT / PJRT /
Atypical AVNRT
Yes No
Yes No
Yes
No
Pattern recognition vs Physiological approach
Wide freeways but narrow viewpoints
3
Breaking complexity with complexity
Differentials
• AT
• AFL
• Afib
• AVNRT
• AVRT
• JT
• VT
‘’Game Plan’’
• What’s the ‘drill’? eg. NCT vs WCT
• Eyeballing morphology? eg. VT criteria
• ‘Smoking gun’? eg. PR prolongation
• Pre test prob? eg. Patient profile, age, MI
• Absolute vs probable? eg. Termination with P
• Having a ‘tool box’! eg. P, delta, PR/ RP, axis, BBB
• ‘Big picture’ working diagnoses Be Open-minded
Beginning + tachycardia + termination = SVT
4
Hunt for P
Look at the Ts
Seek for the
midpoint
High to low P
(anterograde)
Low to high P
(retrograde)
5
ST: high to low: warm up usually present
No P at al: AVNRT> JT
Low to high P: AT/ AFL (non sinus), PR short
if retrograde: very long RP: atypical AVNRT
Pseudo q pattern in 4% of AVNRT
Pseudo S: AVNRT
Rarely, JT with VA conduction
RP short: AVNRT
AVRT may be possible
RP longer: AVRT (<50% of RR)
Atypical AVNRT if RP >50% of RR
Variable P + PR+ RR = MAT
AV dissociation
JT > VT
Myriads of P
6
Think physiologically
VV dictates AA
Ventricular participation +ve
AT ruled out, can be VT/ AVRT
AA dictates VV
Atrial participation +ve
VT ruled out, can be AT/ AVNRT
No PR prolongation
So no AVN involvement
Can not be AVNRT/ o-AVRT
PR prolongation
So AVN involvement
AVNRT/ o-AVRT 7
Do not miss ‘The End’
Ends with P
Can not be AT
Can be AVNRT/ AVRT/ VT/JT
Ends with no P
Can be anything
VAV (not AT)
vs VAAV (AT)
AT
8
AVRT caught red-handed!
RR alternans
ITS NOT AF
BBB normalises: Ipsilateral AP
9
LBBB + Right axis (discordant): VT likely
North west axis: VT likely
Axis helps
Axis changes
With onset of tachy
Or after termination
VT is likely
10
No RS in precordial lead: VT
Absolute vs probable
Sudden transition is V3: AP/ VT 11
AV dissociation: VT (may be in JT also)
Capture/ fusion: VT (may be in a-AVRT also)
‘The smoking gun’
12
Localising AP
-ve Delta
1. In I: left lat AP (most common)
2. In II: CS AP (adenosine sensitive)
3. In V1: Septal AP (DD AVNRT)
4. Rest: right lat AP
13
QRS transition AP localisation
At or before V1 Left sided pathways
b/w V1 – V2 or at V2 Mostly Right sided pathway
Lead 1: R>S Right sided pathway
Lead 1: R<S left sided pathway
b/w v2-v3 Right septal pathway
After v4 Right lateral pathway
Onset of LBBB prolong TCL: left sided AP
Onset of RBBB prolong TCL: Right sided AP
ECG mimicking IWMI: CS or post-septal AP
Fitzpatrick’s algorithm
AP: benign or malignant?
14Late coupled PAC renders AP to refractory Even prolonged PR did not start AVRT
Different level of fusion depending on prematurityBenign
His-refractory VPC
Long RP
BUT >50% of RR
BUT NOT atypical AVNRT
A advanced by his refractory VPC
SA – VA < 85 ms suggests AP
PPI – TCL <115 ms suggests AP
TCL PPI
NO Reset
AVNRT 15
Capture & Reset
= AVRT
Identifying Focus of AT
16
Focus of AT P in Limb leads P in Precordial leads
High Crista Terminalis (MC) Inf leads –ve
AVR +ve
-ve to +ve
Coronary sinus (Adenosine) Inf leads +ve
AVR -ve
+ve to -ve
Pulm veins (RSPV MC) I, AVL -ve All +ve
(large to small)
LA (LAA Mostly) least of all I, AVL -ve
Or flat
All –ve
Or flat
Zhi Young’s algorithm
Clin EP 2011
Short PR is not synonymous to AP
 Anterograde AP PR (<50ms)
 AT near to AVN PR (>50 ms) (low to high P)
 AFL near to CS (low to high P) (baseline undulating)
 JT with non conducted P (high to low P) (structural heart dis)
17
RP and PR
PR RP Diagnosis
const const ST
varies varies AVNRT
Varies const AVRT
const varies AT
RP is religiously fixed: AVRT
PR is religiously fixed: AT
Typical AVNRT: PR>RP
Atypical AVNRT: RP>PR
AVNRT:
Pseudo R in v1
Pseudo S in inf leads
Also pseudo q in 4% 18
AVRT:
Long RP
Distorts ST/ T
Mostly Left lat AP
Ugly BBB
LBBB
Rapid & steady descent
SVT
Slow & stuttered descent
VT
RBBB
later peak taller
SVT
First peak taller
VT
Bizarre BBB also in a-AVRT, ischemia
19
Looks are deceptive!
Morphology Criteria
Not very reliable
However,
the best
20
Grey Matter wins over ICD algorithms
21
22
Mechanism of arrhythmia?
Warm up and cool down
Rate <200
TCL variation >30ms
P anterograde
VAAV
Abrupt onset & offset
Rate >200
TCL variation <30ms
P retrograde
VAV
Rare
Precipitating factors
Eg QT long
Slow
velocity
Cut
Propagation
No overdrive
Suppression
Overdrive
Modify
Physical
milieu
How to manage?
23
Scenario Management
AVN involved in tachycardia
O-AVRT AVNRT JT
AVN blocker
(Adenosine, Diltiazem)
Long term: Diltiazem/ Verapamil in AVNRT
Sotalor for AVRT (blocks AVN and AP)
AVN not involved in tachycardia
A-AVRT with AF AFL
AVN blockers contraindicated
Amiodarone increases ERP of AP
May be terminated with Adenosine if near CS
Long term: Amiodarone
AT AFL Diltiazem blocks AVN
Reduces FVR
May be terminated with adenosine If near CS
Long term: beta blockers/ CCB
If hemo-dynamically unstable DC shock
(Heparin)
If recurrent AVNRT: RFA of slow pathway
AVNRT: RFA of AP
What we have learned?
24
 Be careful with the Ps
 Do not miss the beginning and the end
 Old ECG records are valuable for any axis change or BBB
 Ectopic activity during tachycardia is a gift
 Short PR doe not always mean WPW
 Long RP does not always mean AVRT
 Bizarre BBB does not always mean VT
 AV dissociation/ capture does not always mean VT
 Looks can be deceptive. Spinal reflexes are not wise
 So, think physiologically. And be logical & open-minded
Who have
NOT ARGUED
over a diagnosis of tachycardia
their colleagues?
25
QUIZ ECG # 1
26
If o-AVRT (LL AP), why no early transition in V1-V2?
How come varying degree of capture at same rate?
ANS: recurrent VPCs (‘’R on P’’)
27
QUIZ ECG # 2
APC (within T) prolongs PR and starts o-AVRT
With the resolution of LBBB TCL shortens
ANS: o-AVRT (Left lateral pathway)
28
QUIZ ECG # 3A
Regular WCT with LBBB morphology
Low to high P (retrograde), RP short
Axis normal, transition at V5
In V1, descent of QRS is little staggered
What would you do next?
29
QUIZ ECG # 3B
Post Diltiazem
ANS: AFL 1:1 converted to 2:1
30
QUIZ ECG # 4
A C C
F F F
A A A
NCT retrograde P long RP normal axis
Atypical LBBB, sudden transition in V3
Capture/ Fusion/ AV dissociation (so NOT AVRT)
ANS: VT
31
QUIZ ECG # 5
Long RP, RP less than 50% of RR, BUT PP dictates RR (so no AVRT)
Terminates with P (not AT), RP<PR and RP,PR both variable
ANS: AVNRT (? Atypical)

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Supraventricular tachycardia: ECG recognition and diagnosis

  • 1. Diagnosis and Management of Supra-ventricular Tachycardia Dr. D. Khanra SR3 LPS Institute of Cardiovascular Sciences GSVM Medical College, Kanpur 1
  • 2. SVT in a nut-shell Onset Termination 2 AVNRT AVRT AT AFLAVNRT
  • 3. Regular Narrow QRS Tachycardia Visible P Waves AF / AT /AFL A >V AFL /AT ? RP Interval Short Long < 70 ms > 70 ms AVNRT AVRT / AVNRT / AT AT / PJRT / Atypical AVNRT Yes No Yes No Yes No Pattern recognition vs Physiological approach Wide freeways but narrow viewpoints 3
  • 4. Breaking complexity with complexity Differentials • AT • AFL • Afib • AVNRT • AVRT • JT • VT ‘’Game Plan’’ • What’s the ‘drill’? eg. NCT vs WCT • Eyeballing morphology? eg. VT criteria • ‘Smoking gun’? eg. PR prolongation • Pre test prob? eg. Patient profile, age, MI • Absolute vs probable? eg. Termination with P • Having a ‘tool box’! eg. P, delta, PR/ RP, axis, BBB • ‘Big picture’ working diagnoses Be Open-minded Beginning + tachycardia + termination = SVT 4
  • 5. Hunt for P Look at the Ts Seek for the midpoint High to low P (anterograde) Low to high P (retrograde) 5
  • 6. ST: high to low: warm up usually present No P at al: AVNRT> JT Low to high P: AT/ AFL (non sinus), PR short if retrograde: very long RP: atypical AVNRT Pseudo q pattern in 4% of AVNRT Pseudo S: AVNRT Rarely, JT with VA conduction RP short: AVNRT AVRT may be possible RP longer: AVRT (<50% of RR) Atypical AVNRT if RP >50% of RR Variable P + PR+ RR = MAT AV dissociation JT > VT Myriads of P 6
  • 7. Think physiologically VV dictates AA Ventricular participation +ve AT ruled out, can be VT/ AVRT AA dictates VV Atrial participation +ve VT ruled out, can be AT/ AVNRT No PR prolongation So no AVN involvement Can not be AVNRT/ o-AVRT PR prolongation So AVN involvement AVNRT/ o-AVRT 7
  • 8. Do not miss ‘The End’ Ends with P Can not be AT Can be AVNRT/ AVRT/ VT/JT Ends with no P Can be anything VAV (not AT) vs VAAV (AT) AT 8
  • 9. AVRT caught red-handed! RR alternans ITS NOT AF BBB normalises: Ipsilateral AP 9
  • 10. LBBB + Right axis (discordant): VT likely North west axis: VT likely Axis helps Axis changes With onset of tachy Or after termination VT is likely 10
  • 11. No RS in precordial lead: VT Absolute vs probable Sudden transition is V3: AP/ VT 11
  • 12. AV dissociation: VT (may be in JT also) Capture/ fusion: VT (may be in a-AVRT also) ‘The smoking gun’ 12
  • 13. Localising AP -ve Delta 1. In I: left lat AP (most common) 2. In II: CS AP (adenosine sensitive) 3. In V1: Septal AP (DD AVNRT) 4. Rest: right lat AP 13 QRS transition AP localisation At or before V1 Left sided pathways b/w V1 – V2 or at V2 Mostly Right sided pathway Lead 1: R>S Right sided pathway Lead 1: R<S left sided pathway b/w v2-v3 Right septal pathway After v4 Right lateral pathway Onset of LBBB prolong TCL: left sided AP Onset of RBBB prolong TCL: Right sided AP ECG mimicking IWMI: CS or post-septal AP Fitzpatrick’s algorithm
  • 14. AP: benign or malignant? 14Late coupled PAC renders AP to refractory Even prolonged PR did not start AVRT Different level of fusion depending on prematurityBenign
  • 15. His-refractory VPC Long RP BUT >50% of RR BUT NOT atypical AVNRT A advanced by his refractory VPC SA – VA < 85 ms suggests AP PPI – TCL <115 ms suggests AP TCL PPI NO Reset AVNRT 15 Capture & Reset = AVRT
  • 16. Identifying Focus of AT 16 Focus of AT P in Limb leads P in Precordial leads High Crista Terminalis (MC) Inf leads –ve AVR +ve -ve to +ve Coronary sinus (Adenosine) Inf leads +ve AVR -ve +ve to -ve Pulm veins (RSPV MC) I, AVL -ve All +ve (large to small) LA (LAA Mostly) least of all I, AVL -ve Or flat All –ve Or flat Zhi Young’s algorithm Clin EP 2011
  • 17. Short PR is not synonymous to AP  Anterograde AP PR (<50ms)  AT near to AVN PR (>50 ms) (low to high P)  AFL near to CS (low to high P) (baseline undulating)  JT with non conducted P (high to low P) (structural heart dis) 17
  • 18. RP and PR PR RP Diagnosis const const ST varies varies AVNRT Varies const AVRT const varies AT RP is religiously fixed: AVRT PR is religiously fixed: AT Typical AVNRT: PR>RP Atypical AVNRT: RP>PR AVNRT: Pseudo R in v1 Pseudo S in inf leads Also pseudo q in 4% 18 AVRT: Long RP Distorts ST/ T Mostly Left lat AP
  • 19. Ugly BBB LBBB Rapid & steady descent SVT Slow & stuttered descent VT RBBB later peak taller SVT First peak taller VT Bizarre BBB also in a-AVRT, ischemia 19
  • 20. Looks are deceptive! Morphology Criteria Not very reliable However, the best 20
  • 21. Grey Matter wins over ICD algorithms 21
  • 22. 22 Mechanism of arrhythmia? Warm up and cool down Rate <200 TCL variation >30ms P anterograde VAAV Abrupt onset & offset Rate >200 TCL variation <30ms P retrograde VAV Rare Precipitating factors Eg QT long Slow velocity Cut Propagation No overdrive Suppression Overdrive Modify Physical milieu
  • 23. How to manage? 23 Scenario Management AVN involved in tachycardia O-AVRT AVNRT JT AVN blocker (Adenosine, Diltiazem) Long term: Diltiazem/ Verapamil in AVNRT Sotalor for AVRT (blocks AVN and AP) AVN not involved in tachycardia A-AVRT with AF AFL AVN blockers contraindicated Amiodarone increases ERP of AP May be terminated with Adenosine if near CS Long term: Amiodarone AT AFL Diltiazem blocks AVN Reduces FVR May be terminated with adenosine If near CS Long term: beta blockers/ CCB If hemo-dynamically unstable DC shock (Heparin) If recurrent AVNRT: RFA of slow pathway AVNRT: RFA of AP
  • 24. What we have learned? 24  Be careful with the Ps  Do not miss the beginning and the end  Old ECG records are valuable for any axis change or BBB  Ectopic activity during tachycardia is a gift  Short PR doe not always mean WPW  Long RP does not always mean AVRT  Bizarre BBB does not always mean VT  AV dissociation/ capture does not always mean VT  Looks can be deceptive. Spinal reflexes are not wise  So, think physiologically. And be logical & open-minded
  • 25. Who have NOT ARGUED over a diagnosis of tachycardia their colleagues? 25
  • 26. QUIZ ECG # 1 26 If o-AVRT (LL AP), why no early transition in V1-V2? How come varying degree of capture at same rate? ANS: recurrent VPCs (‘’R on P’’)
  • 27. 27 QUIZ ECG # 2 APC (within T) prolongs PR and starts o-AVRT With the resolution of LBBB TCL shortens ANS: o-AVRT (Left lateral pathway)
  • 28. 28 QUIZ ECG # 3A Regular WCT with LBBB morphology Low to high P (retrograde), RP short Axis normal, transition at V5 In V1, descent of QRS is little staggered What would you do next?
  • 29. 29 QUIZ ECG # 3B Post Diltiazem ANS: AFL 1:1 converted to 2:1
  • 30. 30 QUIZ ECG # 4 A C C F F F A A A NCT retrograde P long RP normal axis Atypical LBBB, sudden transition in V3 Capture/ Fusion/ AV dissociation (so NOT AVRT) ANS: VT
  • 31. 31 QUIZ ECG # 5 Long RP, RP less than 50% of RR, BUT PP dictates RR (so no AVRT) Terminates with P (not AT), RP<PR and RP,PR both variable ANS: AVNRT (? Atypical)