SVT

1. CASE SCENARIO
• 22 day old male neonate was brought to the ER with c/o
lethargy
poor feeding
reduced urine output
palpitations as felt by mother
Since morning

2. C: irritable
B: Rapid breathing, retractions (+)
C: No cyanosis, pallor (+)
Airway: clear
Breathing: Rate: 74/min
SCR, ICR (+)
No added sounds
Spo2 : 94% on RA

3. • Circulation HR: 336/min
Rhythm: Tachycardia- Narrow
complex (QRS) on ECG monitor with
absent p waves
Pulses: ++/+++
CFT: <3 sec
BP: 84/46mmhg

4. • Disability Baby irritable
B/L pupils RTL
• Exposure Temperature- Normal

5. • History: Uneventful antenatal and early neonatal period. 2nd
born by SVD in virudhachalam PVT hosp with birth wt of
2.5kg. Current weight 3.06kg.
• Breast feeding was established immediately, no feeding
issues since birth, no cyanosis since birth
• No h/o previous sibling death in family.

6. • Managed according to pals. Tachyarrhythmia confirmed to
be SVT by rhythm strip.
• As baby was hemodynamically stable, first dose adenosine
given 0.1mg/kg.
No response on ECG
Second dose 0.2mg/kg given

7. No response on ECG
Synchronized cardioversion given
with 0.5J/kg
No response on ECG
Synchronized cardioversion given
with 1J/kg
Sinus rhythm (+)

9. Synchronized cardioversion
• Sync button on defibrillator machine
• Synchronizes with the cardiac cycle so that shock is
delivered at the R wave of the cycle
Defibrillation is unsynchronized shock- delivers any time of
cycle, used in VF
IF unsynchronized shock is given for VT with pulse or SVT,
shock may be delivered during T wave- cardiac repolarization-
precipitation of VF

10. • ECHO done in casualty showed small PFO with L to R
shunt, LV function- good
• Baby shifted to NICU for further management.
• In NICU after one hour of stabilization, recurrence of SVT (+),
pulses well felt.
• Adenosine 0.2mg/kg given IV in central line with saline flush
• Reverted to sinus rhythm with Synchronized cardioversion of
2J/kg
• Loading dose of amiodarone 5mg/kg given IV over 20
minutes.
• In view of recurrence and worsening sensorium, not
maintaining spo2 on RA, Baby was intubated and connected
to mechanical ventilator with minimal settings.

11. • At 5 hours of admission, tachycardia settled, but perfusion
was poor. Peripheral pulses were absent and central pulses
were feeble. Hypotension (+)
• VBG showed acidosis :7.06 ph with bicarbonate of 10
• Hence baby started on ionotropes- Dobutamine 10mcg/kg/min
( suspected cardiogenic cause)
• As perfusion did not improve and poor femoral pulses with
unrecordable BP despite starting dobutamine, adrenaline
started suspecting myocardial dysfunction (0.2mcg/kg/min)
• Hemodynamic monitoring continued

12. • Case discussed with cardiology team:
Advised to discontinue amiodarone, and to consider on oral
propranolol
ECHO was repeated- showed Small PFO with L to R shunt
and Poor LV function
Adviced to continue adrenaline infusion

13. • Clinical dilemma:
- Whether amiodarone can be used for all forms of SVT
- Whether adenosine aborts all AV nodal pathway.
- In SVT refractory to adenosine, what drug to be followed
next apart from shock
- Amiodarone vs procainamide vs propanolol

14. • In between baby threw multiple episodes of seizures in the
form of posturing of all 4 limbs was loaded with
phenobarbitone
• After 7 hours of admission, baby’s perfusion only slightly
improved, sensorium worsened, tachypnoea (+) and
gasping (+)
• Possibilities :
- Severe metabolic acidosis
?Severe refractory cardiogenic hypotensive shock
? Amiodarone gasping syndrome

15. • In view of persisting acidosis on VBG , worsening PH- 6.9
with bicarbonate of 6, ‘Rescue Therapy’ bicarbonate
1meq/kg given as bolus and half correction initiated
• Usually not recommended for acidosis secondary to
hypoxia and shock. Here given since effect of acidosis on
cardiac contractility was uncertain and shock was refractory
to fluids and vasoactive agents.

17. AMIODARONE GASPING SYNDROME
• Ampoules of amiodarone contain benzyl alcohol. Large
amounts of benzyl alcohol in neonates have been
associated with “gasping syndrome” particularly preterms.
• Potentially fatal condition characterised by metabolic
acidosis, respiratory distress, gasping respirations,
convulsions, intracranial haemorrhage, hypotension
and cardiovascular collapse.

19. • Queries :
- Duration between amiodarone administration and
development of gasping episodes
- Whether this is dose dependant?
- Whether all the symptoms of hemodynamic compromise
was caused by amiodarone or underlying LV function

20. • By 12 hours of admission baby went into Ventricular
Tachycardia. Pulses well felt at that time
Possiblities:
- Ventricular tachycardia
- SVT with abberancy
• Reverted with synchronized cardioversion 2J/kg.
• Within 1 hour baby went into multiple episodes of VT. Pulses
felt throughout the episodes, all reverted with synchronized
cardioversion 2J/kg
• Adenosine not tried as previous 2 attempts were unsuccessful

21. • Ventricular Tachycardia
- Wide complex tachyarrhythmia generated within the
ventricle
• SVT with abberancy
- Occurs as a result of rate related BBB within the ventricle or
preexsiting BBB
- Impulse generated from atria to ventricle through accessory
pathway rather than AV node

22. • Difficult to differentiate SVT with abberancy from VT
- Both cause hemodynamic instability, similar heart rate and
both have wide QRS complex
- Sometimes can be differentiated with R-R interval and QRS
morphology
Clinician should assume the initial wide complex rhythmn is
VT unless proved to have pre existing abberancy
If RR interval is regular, with normal QRS morphology and
hemodynamically stable- may attempt one dose of adenosine-
SVT with abberancy will respond, VT will not. (PALS- 2010-11)

24. • Although underlying hemodynamic compromise was (+) a/w
poor LV function,
Adrenaline could have triggered the VT, hence adrenaline was
stopped following which there was no VT episodes
Dobutamine was tapered and stopped within 2 hours.
• Discussed with cardiology: Told possible VT triggered by
adrenaline, still amiodarone role not clear
• Possibility of WPW syndrome discussed- only contradicting
evidence is response to adenosine

25. • Rationale behind amiodarone
- Used in all forms of SVT and atrial tachycardia
• Amiodarone 5mg/kg 2nd loading given over 20 minutes, and
infusion started at 5mg/kg/day ( 5mcg/kg/min)

26. • Dobutamine was stopped at 13 hours of life. Amiodarone
infusion was continued.
• Overall sensorium was poor
• VBG post bicarbonate correction improved.
• No further arrhythmias were present. Amiodarone infusion
tapered to 2.5mg/kg/day
• Parents were requesting to go to higher centre for further
management, hence baby was referred at 36 hours of
admission to MMM chennai.

27. DIAGNOSIS AT DISCHARGE
• SVT- AVRT ? WPW syndrome
• Atrial Tachycardia

28. Dr. Amrutha Venkateswaran
SUPRA VENTRICULAR
TACHYARRYTHMIAS IN NEWBORN

29. SINUS RHYTHM
• Normal rhythm of the heart
• Characterized by P waves followed by QRS complexes
• Normal PR interval for that age
REFRACTORY PERIOD
This is the time during which another stimulus given to the
muscle (no matter how strong) will not lead to a second action
potential

30. ARRHYTHMIA
• Abnormal electrical activity
• Too fast or too slow
• Regular or irregular
Sinus Arrhythmia:
Physiological variation of heart rate due to respiratory
influence on the autonomic nervous system.

31. CARDIAC ELECTRICAL ANATOMY

32. NORMAL WAVEFORMS IN ECG
• P wave: Atrial depolarization
• Wave through AV node/ His bundle- isoelectric
• Q wave- Septal depolarization
• R/S wave: Ventricular depolarization
• T wave: Ventricular repolarization
• U wave: Mechanoelectric phenomenon

33. • Normal PR interval for age:
• Short PR interval: WPW preexcitation, Lown-Ganong-levine
Syndrome, Pheochromocytoma, DMD
• Long PR interval: Myocarditis, digitalis toxicity,
hyperkalemia

34. SUPRAVENTRICULAR TACHYCARDIA
• Commonest symptomatic arrhythmia in children and
infants.
• Tachycardia that originates proximal to the bundle of His (
above the ventricular level).
• Usually not a/w hemodynamic compromise- if (+)
- Congenital heart disease
- Cardiomyopathy
Underlying LV
function is impaired

35. EFFECT ON CARDIAC OUTPUT
• Increased HR leads to increased Output.
Further increase
Duration of diastole decreases
Reduction in stroke volume
Decreased Cardiac Output
Impaired coronary perfusion
Increased Oxygen demand
Myocardial dysfunction
CCF

36. • Often asymptomatic, episodic and paroxysmal in young
infants.
- Irritability
- Poor feeding, lethargty
- Breathlesness, palpitations felt by mother

37. ECG CHANGES
HEART RATE No beat to beat variability
Usually > 220/ min in infants
Usually >180/min in children
P WAVES Absent or Abnormal
P R INTERVAL Cannot be determined as P waves
are absent. Short PR in cases of
ectopic atrial tachycardia
R R INTERVAL Often constant
QRS COMPLEX Narrow

38. CHARACTERISTICS ST SVT
HISTORY Gradual Onset
H/O fever, pain,
hemorrhage,
dehydration
Abrupt onset,
cessation
Symptoms of CHF
PHYSICAL EXAM Signs of underlying
cause of ST
Signs of CHF
HEART RATE Usually < 220/ min Usually >220/min
MONITOR Variability in Heart
Rate
Minimally varying rate
with changes I activity
ECG P waves present/
Normal
P waves absent or
abnormal – inverted
in II, III, aVF
CHEST XRAY Usually normal heart
and lungs
Signs of CHF

39. TYPES OF SVT
• Mechanisms that produce SVT are classified as
Automaticity Re- Entry
JET-junctional
Ectopic Tachy
AET- atrial
Ectopic tachy
AVRT-
Atrioventricular
Reentry Tachy
AVNRT-
Atrioventricular
Nodal Reentry Tachy

40. AVRT- ATRIOVENTRICULAR REENTRY TACHY
• Most common type of SVT in children
*Paroxysmal Atrial Tachycardia (PAT)
• Two pathways are involved-
- Av node ( Slow )
- Accessory pathway ( Fast )

41. ORTHODROMIC REENTRANT TACHYCARDIA
• Commonest form of AVRT
• Impulse from atria goes through a close circuit formed by
an accessory pathway
• Direction is through the AV node- antegrade transmission,
and retrograde transmission from the ventricles through the
accessory pathway

42. Normal QRS complex- Antegrade conduction through a
normal AV node (slow)
Inverted P wave following a QRS- retrograde transmission
through the bypass tract

43. ANTEDROMIC REENTRANT TACHYCARDIA
• Less common
• Impulse goes through the faster bypass tract- antegrade
transmission
• Retrograde transmission through the slower AV nodal
pathway

44. Wide QRS complex- Due to antegrade transmission
through the fast bypass tract
Inverted P wave preceeding the QRS complex

45. Normally impulse
generated from the
SA node
Impulse reaches
the AV node
Impulse travels
through the septum
and reaches ventricle

46. In AVRT- acceossory
pathway is present
Impulse can travel
from atria through the
accessory pathway in
antegrade
Impulse can travel in
retrograde direction
Closed circuit-
tachyarrhythmia

47. WOLFF-PARKINSON-WHITE SYNDROME
Accessory pathway (+)
Impulse from SA node
reaches AV node
Impulse from SA node
also goes through the
accessory path-
Reaches ventricle faster
and causes
preexcitation

48. Impulse that travels
through slow pathway
reaches pre excited
ventricles
Gets masked by the
impulse from the
accesory path- so
travels in a retrograde
manner – in the
refractory period
Closed circuit for every
beat

49. ECG CHANGES
• Short PR interval – Preexcited ventricle
• Slow rising R wave due to prolonged ventricular
stimulation- delta wave
• Dominant R wave in V1 lead

50. MANAGEMENT
• Acute Treatment
- Vagal maneuvers
- Adenosine- Drug of choice
Administered as a rapid bolus with saline flush, very short half
life- <5 to 10 sec (needs to reach heart before that)
Transient AV block, slows ventricular rate
CI in AF, VT, Heart block

52. SVT REFRACTORY TO ADENOSINE
• Amiodarone- prolongs the refractory period of AV node,
atria and ventricle
• Used in almost all Supraventricular tachyarrhythmias
• Adverse effects- hypotension, bradycardia
• IV dose- loading of 5mg/kg over 20 minutes followed by
continuous infusion of 5-20mg/kg/day

53. • Procainamide- Slows conduction within myocardium
• Potential adverse effects- hypotension, acute hemodynamic
compromise, prolongation of QT interval
• Hence avoided in young children, infants
• IV dose- 15mg/kg over 30 minutes , followed by continuous
infusion of 10-20mcg/kg/min

54. • Verapamil- Slows AV nodal conduction
• Used in older children
• Causes apnoea, hypotension and cardiovascular collapse
• CI in CCF and WPW

55. • Beta Blockers- In SVT which does not respond to
adenosine and the rhythm is well tolerated
• IV propranolol and IV esmolol are commonly used
• Dose- 0.5 to 1mg/kg/dose
• Esmolol- IV loading of 100 to 500 mcg/kg slow push
followed by 25 to 100mcg/kg/min
Digoxin- Not used routinely- Delay in achieving therapeutic
levels

56. PREVENTION OF RECURRENCE
• Infrequent episodes of SVT without hemodynamic
compromise- observation, taught vagal maneuvers- if not
effective beta or calcium channel blockers can be used
Rationale behind observation- children <5 years outgrow their
SVT and may not require chronic therapy

57. • Choice of drug in infancy
- Propranolol- oral 2to 4mg/kg/day divided in 4 doses
• Older children
- Longer acting atenolol 1 to 2mg/kg/day orally
Older children with adequate LV function- verapamil can be
tried

58. INTERVENTION
• SVT without symptoms and proven WPW
- Evaluated with HOLTER monitor
- Persistent preexcitation are at increased risk for sudden
death- offered Electrophysiological studies (EPS)
<5 Years- Do not need EPS routinely

59. • RFA- Radiofrequency Ablation
>5 years and >15kg
Performed as a part of electrophysiological study
Identification of the accessory pathway and termination
Complications:
- Perforation
- Pericardial effusion, emboli
- Brachial plexus injury

60. • Indications
- WPW syndrome after abortion of sudden cardiac death
- WPW at risk for sudden death
- Recurrent or chronic SVT a/w LV dysfunction
- SVT which doesn’t respond to oral therapy for more than 5
years

61. • Cryoablation
- Catheter based cryoablation
- Short term efficacy> RFA
- Recurrence rate higher
• Surgery
- Repeated failed attempts of RFA
- Underlying cardiac condition requires surgery

62. • Mortality-
SVT with underlying heart disease- risk is higher