This document discusses various types of supraventricular arrhythmias including sinus arrhythmia, premature atrial contractions, atrial flutter, atrial fibrillation, AV nodal reentry SVT, and AV reentry SVT. It provides details on the characteristics, mechanisms, and features seen on ECG for each type. Common arrhythmias in neonates such as premature atrial contractions, atrial flutter, and different forms of supraventricular tachycardia are also mentioned. The classification of tachycardias based on site of origin and rhythm is summarized.

1. Supra ventricular
arrhythmia
DR J P SONI
Division of Pediatric Cardiology
Professor and Head of the Department
Paediatrics
DR S N Medical College
Jodhpur
Doc_jpsoni@yahoo.com

2. Supraventricular tachycardia (SVT), by definition, includes all forms
of tachycardia that either arise above the bifurcation of the bundle
of His or that have mechanisms dependent on the bundle of His.

3. Supra – Ventricular Arrhythmia
A. Sinus arrhythmia
B. Premature Atrial Contractions (PACs)
C. Wandering Atrial Pacemaker
D. Multifocal atrial tachycardia
Atrial flutter
Atrial fibrillation (Afib)
E. AV nodal re entery SVT
F. AV re entery SVT
A B C D E F

5. Sinus Arrhythmia (SA)
SA is refers to the normal dencrease and increase in heart rate
that occurs during inspiration and expiration. This is a normal
response and is more accentuated in children than adults.

7. Sinus Tachycardia (ST)
ST refers to a fast heartbeat (tachycardia) because of rapid firing
of the sinoatrial (sinus) node. This occurs in response to exercise,
exertion, excitement, pain, fever excessive thyroid hormone, low
blood oxygen (hypoxia), stimulant drugs (such as caffeine)
Normal fetal heart rate
Tachycardia : T 13 and Tuner syndrome
Mild tachy cardia : T21
Bradycardia : T18 and Triploidy
5 weeks 100
10weeks 170
14 weeks 155

8. •PAC's can have three different outcomes depending on the degree of prematurity (i.e., coupling interval
from previous P wave), and the preceding cycle length.
•
•1. Not conducted (blocked); i.e., no QRS complex because the PAC finds AV node still refractory.
•2. conducted with AV node : short PR interval, normal QRS and incomplete compensatory pause.
• 3. Conducted with aberration; i.e., PAC makes it into the ventricles but finds one or more of the
conducting fascicles or bundle branches refractory. The resulting QRS is usually wide, and is
sometimes called an Ashman beat
Premature Atrial Contractions (PACs)

9. Atrial Premature Beats

10. Atrial Premature Beats

11. •
• The fate of a PAC depends on the coupling interval from the last P wave and
the preceding cycle length or heart rate -
•When the cycle length (i.e., PP interval) has increased (slower heart rate), this results in increased
refractoriness of all the structures in the conduction system (i.e., wider boxes).
•PAC can't get through the AV node and is not conducted.
• PAC is blocked in the right bundle branch and results in a RBBB QRS complex (aberrant conduction
•PAC is far enough away to conduct normally.

12. The benign premature ventricular contractions that occur occasionally do not interfere with the average
lifespan, but their frequent occurrence implies an ominous prognosis.
High VPB burden, that is greater than 10000 ectopic ventricular beats or greater than 10% of all beats
recorded on 24-hour ambulatory monitoring.
The characteristics of VPBs that confer poor prognosis include:-
•An "arrhythmic burden" with VPBs more than 500 in 24 hours on Holter monitoring
•VPBs morphologies with LBBB or RBBB
•VPBs with intermediate or superior axis and wide QRS complexes
•Short-coupled VPBs
•VPBs superimposed on preceding T-waves
•VPBs induced by adrenergic stimulation
Cardiomyopathy is more likely in patients whose ventricular premature beats have a very wide QRS
complex, the beats arise from the epicardium, or in patients with VPBs occurring higher than a quarter of
all beats on 24-hour Holter monitor (VPB burden of over 25%).
This cardiomyopathy is generally considered to be reversible after ablation; however, some degree of left
ventricular systolic dysfunction may rarely persist after the ablation of the ectopic focus.

14. The PVCs were defined as frequent when they were >60 beats/h.
PVCs, CPLTs and ventricular tachycardia were considered to have originated from the right ventricle when the
Q wave, R wave and S wave (QRS) morphology showed a left bundle branch block pattern (LBBB), and from the
left ventricle when it showed a right bundle branch block pattern (RBBB).
PVCs arising from the left ventricle (10%) have a right bundle branch block (RBBB) morphology (dominant R
wave in V1).
,
PVC arising from right ventricle (RVOT) have left bundle branch block (LBBB) the SR transition lead is V1
or V2, (100% specificity).
Ventricular tachycardia is diagnosed when three or more ventricular complexes occurred in sequence at a rate
at least 20% greater than the average sinus rate.
Episodes of ventricular tachycardia is defined as sustained when lasting >30 s; otherwise they were defined as
non‐sustained.

16. Ventricular PVC with aberrancy

18. Non sustained “ VT”

19. V1 = R suggestive of LVOT PVC

20. Frequent VPBs are often associated with complications if remained unattended, which include;
•Left ventricular dysfunction
•Dilated cardiomyopathy
•Sustained Ventricular tachycardia
•Sudden cardiac arrest

23. V1 = R suggestive of LVOT PVC

25. •Torsades de pointes is a polymorphic VT (Figure 7) and is often seen in the congenital or acquired long Q–T
syndromes. Other forms of polymorphic VT with normal Q–T include catecholaminergic polymorphic
ventricular tachycardia (CPVT) (genetic defect in the ryanodine receptor of the sarcoplasmic reticulum),
ischemia, or digitalis intoxication.
Brugada syndrome characterized with RBBB and ST elevation in leads V1-3
Right ventricular (RV) dysplasia VT (ARVC) is characterized by fatty infiltration of the RV free wall.
The VT shows a left bundle branch block (LBBB) pattern and the resting ECG in sinus may
show T inversion in V1-V3. Notching of the QRS, called epsilon waves, may be present.
Short Q–T syndrome is a genetic condition

26. beta-blockers are typically first-line therapy. Catecholamine-sensitive or exercise-induced VPBs have an
excellent response to the initiation of beta-blocker therapy.
The European Heart Rhythm Association/Heart Failure Association recommends that patients with heart
failure with reduced ejection fraction and a high burden of VPBs, defined as greater than 10000 VPBs/24
hours, should be aggressively treated with catheter ablation if they have failed, declined, or are intolerant to
antiarrhythmic therapy (especially if there is a single dominant VPB morphology)
The Lown Grading system for PVCs –
•Grade 0: No evidence of premature beats
•Grade 1: Occasional PVCs (less than 30/hour)
•Grade 2: Frequent PVCs (more than 30/hour)
•Grade 3: Multiform
•Grade 4: Repetitive PVCs (A-couplets, B-salvos of more than 3)
•Grade 5: R on T pattern

27. •Frequent premature ventricular contractions (PVCs), couplets and episodes of ventricular
tachycardia are extremely rare in the neonatal population.
•In general, asymptomatic ventricular arrhythmias in the absence of heart disease are
associated with a favourable prognosis.
•Frequent PVCs and couplets do not require treatment but do require careful follow‐up
•Sustained or high‐rate ventricular tachycardia even if asymptomatic must be treated
appropriately; the prognosis appears to be generally favourable.
•In conclusion, newborns with frequent monomorphic ventricular arrhythmia who are
asymptomatic and considered healthy on the basis of non‐invasive cardiological evaluation have a
good long‐term prognosis after diagnosis.
•Frequent PVCs and CPLTs do not require treatment, but require careful follow‐up. Conversely,
sustained and high‐rate asymptomatic monomorphic ventricular tachycardia must be treated
appropriately, but the prognosis appears to be generally favourable.

28. Classification of tachy-arrhythmia
based on site of abnormal focus in Heart
AV node & above Below AV node
SVT Ventricular tachycardia
Narrow
or
Wide Wide
QRS QRS

30. Classification of SVTs
Based on rhythm
• Based on Rhythm - Regular vs. irregular
– Regular: AVNRT, AVRT, AT, AF
– Irregular: AF, AT, MAT
• Based on RP interval -
- Short RP interval – AVNRT, AVRT, Atrial tachycardia
- Long RP interval - PJRT, Atypical AVNRT, Atrial tachycardia

31. Automatic atrial tachycardia
Atrial tachycardia is a form of supraventricular tachycardia,
originating within the atria but outside of the sinus node.
Both atrial flutter and multifocal atrial tachycardia are specific
types of atrial tachycardia.

32. Atrial tachycardia does not involve re-entry through the AV node or ventricle. It is caused by a focal area of
automaticity in the atrium. Atrial tissue adjacent to the crista terminalis in the right atrium or the ostia of
the pulmonary veins in the left atrium is particularly susceptible to the development of automaticity.
P waves are seen before the QRS complexes, although they can be hidden in the T wave with tachycardia.

33. Pathophysiology of atrial tachycardia
Usually due to single ectopic focus rarely due to multiple foci
The underlying mechanism can involve reentry, triggered activity or increased
automaticity.
May be paroxysmal or sustained.
Multiple causes including digoxin toxicity, atrial scarring, catecholamine excess,
congenital abnormalities; may be idiopathic.
Sustained atrial tachycardia may rarely be seen and can progress to tachycardia-
induced cardiomyopathy

34. Features of atrial tachycardia
Atrial rate > 100 bpm.
P wave morphology is abnormal when compared with sinus P wave due to ectopic origin.
There is usually an abnormal P-wave axis (e.g. inverted in the inferior leads II, III and aVF)
At least three consecutive identical ectopic p waves.
QRS complexes usually normal morphology unless pre-existing bundle branch block, accessory
pathway, or rate related aberrant conduction.
Isoelectric baseline (unlike atrial flutter).
AV block may be present — this is generally a physiological response to the rapid atrial rate, except
in the case of digoxin toxicity where there is actually AV node suppression due to the vagotonic
effects of digoxin, resulting in a slow ventricular rate (“PAT with block”).

36. Chaotic (multifocal) atrial tachycardia

37. Heart rate > 100 bpm (usually 100-150 bpm; may be as high as 250 bpm).
Rapid, Irregularly irregular rhythm with varying PP, multiple P wave morphology, PR and RR intervals. (best
seen in the rhythm strip).
At least 3 distinct P-wave morphologies in the same lead.
Isoelectric baseline between P-waves (i.e. no flutter waves).
Absence of a single dominant atrial pacemaker (i.e. not just sinus rhythm with frequent PACs).
Some P waves may be nonconducted; others may be aberrantly conducted to the ventricles.

39. ATRIAL FLUTTER “P” WAVE

41. ATRIAL FIBRILLATION

42. Summary of important dos and don'ts for antiarrhythmic medication
•DO monitor flecainide and digoxin concentrations
•DO NOT use β blocker with calcium channel blocker
•DO NOT use intravenous verapamil below 1 year of age
•DO monitor QT intervals with sotalol
•DO halve the dose of digoxin when given with amiodarone
Atrial Ectopic Tachycardia (AET)/Junctional Ectopic Tachycardia (JET):
AET and (JET) usually do not respond to typical treatments used for re-entrant tachycardia such as adenosine and
cardioversion (Allen, 2001).
The goal is to restore AV synchrony and reduce the ventricular response rate with drugs like amiodarone, digoxin or B -
blockers like esmolol. (Park, 2010). Treat hyperthermia aggressively by exposure to topical ice, actively cooling and muscle
relaxation. These rhythms respond to atrial overdrive pacing at a rate at about 10-20% above the ectopic rate (Grosse-
Wortmann; Schwartz, 2014). Provide sedation and reduce the catecholamine infusions providing the patient tolerates a
reduction in vasoactive drugs. Ensure patient is well sedated. Pull back invasive CV lines in the RA if they are contributing
to the arrhythmia reducing a potential source of irritation of the atrial wall (Schwartz, 2014). A combination of strategies
may slow the ectopic rate and improve hemodynamics.

43. Neonatal Arrhythmias ARE Common in neonates with
structurally normal hearts.
Following arrhythmias are seen in neonates –
Premature atrial contractions (PAC’s)
Atrial flutter
Atrioventricular reentry tachycardia (AVRT),
Permanent junctional reciprocating tachycardia (PJRT),
Ventricular tachycardia and
Heart block.
Neonatal heart block is associated with maternal autoimmune disease, i.e.
systemic lupus.

44. Paroxysmal Supraventricular tachycardia’s (PSVT) are common in infancy and childhood with an incidence
between 1:250 to 1:1,000.
In 90% of cases it is due to a re-entrant rhythm and usually occurs in children whose heart is otherwise
structurally normal. The predisposing conditions like congenital heart disease, medications and concomitant
infection was observed only in 15% of cases of arrhythmia.
30-40% of children presenting with new onset PSVT do so in the first few weeks after birth.
About 40% of all PSVTs in pediatric age occur during the 1st month of life, 10% in the 1st year, 15% between
1st to 6th years age.
Recurrence is 60% in patients presenting with SVT within the first 4-6 months of life. In them the PSVT tend to
disappear during the ensuing 6 months. If first episode of SVT occur after the 6th months of age, then they
have risk of recurrences for next one year, the 70% of them will have risk of recurrence in next 6 years.
There is an inverse relationship between age of the first SVT attack and likelihood of recurrence.
The 90% and 15% SVT infants have spontaneous resolution by 1 year of age if it occur before and after one
year of age, respectively.
Paroxysmal Supraventricular Tachycardia (SVT),

45. Most SVTs (AVRT, AVNRT, PJRT, AF) are due to re-entry.
AT and JET are caused by enhanced automaticity.
Atrial tachycardia, may be due to either re-entry or triggered activity

46. no p-wave
- AV node reentry
AVRT
AVNRT
Paroxysmal Supraventricular Tachycardias : Short RP vs. Long RP
RP < PR
- AV node reentry
- AV reentry using an
accessory pathway
RP > PR
- Atrial tachycardia
- AV reentry using a
decremental AP
ex. PJRT
- AV node reentry -
atypical/uncommon form
AT

47. Typical PSVT is classically characterized by abrupt onset and termination, narrow
QRS complexes, a regular RR interval, and absence of clearly discernible P waves
or a P wave is present within the T wave of all beats, then most likely diagnosis is
Orthodromic reciprocating tachycardia (AVRT).
This is because atrial activation is never simultaneous with ventricular
depolarization, but follows this with an interval of 70 msec accordingly and the P
wave occurs during ventricular repolarization and deforms the T wave.
ORT and AVNRT usually display a 1:1 AV relationship, distinguishing them from
atrial tachycardia, junctional ectopic tachycardia, and ventricular tachycardia.

48. Re-entry
2
Presence of anatomically defined circuit
Anti clock wise ARVT
Orthodromic : narrow QRS, No delta wave, retrograde p wave after QRS
Anti - Clockwise without re-entery tachycardia – ECG will have short PR intervale, wide
QRS – delata wave , No PR segment.

49. RP interval
PR interval < RP
PR interval
is smaller
than RP interval &
“P” POSITIVE
AVRT TACHYCARDIA
(Orthodromic)
JET
ATYPICAL AVNRT

53. PSVT - AVRT ORTHODROMIC

54. PSVT
PSVT - AVRT ORTHODROMIC

55. PSVT - AVRT ORTHODROMIC

56. PSVT - AVRT ANTIDROMIC

57. PSVT - AVRT ANTIDROMIC PR>RP

58. AVNRT is a form of SVT involving the region around the AV node. The Antegrade and retrograde
conduction occur over anatomically discrete atrial inputs into the AV node.
One pathway, the “fast” pathway, conducts more rapidly than the other pathway, the “slow”
pathway.
Tachycardia usually proceeds Antegrade down the “slow” pathway and retrograde up the “fast”
pathway. The RP (VA) interval in tachycardia is extremely short (70 msec), such that P waves are
essentially obscured by the QRS complex, because of more or less simultaneous atrial and
ventricular depolarization, in such a way that P wave is totally hidden within the QRS complex or,
less commonly, emerges from this as a pseudo-s wave (or pseudo-q wave) in the inferior leads and
pseudo-r’ wave in lead V1.
The presence of positive P waves in the inferior leads (a feature
that reveals a P wave axis pointing inferiorly) rules out both
AVNRT and AVRT.
The only SVT in which A-V dissociation is possible is junctional Tachycardia(JET). It is
characterized by, P waves independent of ventricular complexes and occurring with regular P-P
intervals.

59. In typical AVNRT (90%) the pathway with antegrade conduction is the slow pathway, whereas retrograde
Conduction is fast. Typical AVNRT occur when the atrial impulse reaches the AV node, when fast pathway
is refractory & slow pathway is excitable . The impulse is conducted through slow pathway and before it
leaves the AV node the fast pathway has recovered, such that the impulse may travel up via fast pathway and
circulate within AV node and re-entry circuit is established. This will emit impulse to the atria and ventricle
Simultaneously and P wave will be hidden in QRS.
In roughly 25% of slow-fast AVNRT atria will be activated slightly after ventricles, and P wave will be
Seen just at the end of QRS, fused P wave. P wave will be negative in II,III,AVF – pseudo “S” and positive in
V1 – pseudo r wave. Previous ECG is needed to confirm that these changes were not present previously.

62. “p” WAVE AFTER QRS, narrow RP interval
“p” WAVE AFTER QRS – Narrow RP interval PSVT
Responded to adenosine, AVNRT PSVT

63. ECG after adenosine, AXIS -60, V1 rsR pattern, suggestive of ostium primum defect

64. Clockwise re - entry AVRT
Antidromic : wide QRS complex with delta wave PSVT. “P”wave rarely
seen, if visible it is retrograde and occur just before the QRS.

68. If the patient is clinically stable, one should firstly attempt vagus nerve stimulation manoeuvres,
such as the “diving reflex”, obtained by applying ice for 15-20 seconds to the newborn’s face
(region of the mouth and nose) or carotid sinus massage or Valsalva manoeuvres.
The older cooperating children e.g. making them blow energetically into a straw, causing them to
vomit.
The eyeball compression is always contraindicated in paediatric age

69. The intravenous Adenosine is the drug of choice at all ages for tachycardia’s involving the atrioventricular
node. Its key advantage is its short half life and minimum or no negative inotropic effects. Its effectiveness in
re-entrant arrhythmias is in excess of 98%. Adenosine is a drug which causes a block at the level of the
sinoatrial node and of the atrio-ventricular node. It must be administered in a fast bolus either by intravenous
or intra-osseous route, followed by saline wash-out (2- 2.5 ml). The initial recommended dose is 0.1 mg/ kg; if
ineffective it can subsequently be increased to 0.2 mg/kg and up to a maximum of 0.5 mg/kg.
Carotid massage
Adenosine
Calcium Channel blocker
Beta blocker
All cause depolarization
of AV node and increase
Effective refractory
period.
ERP
Of ASV node and block
entry of impulse from
assessory path way and
allow
Sinu impulse to pass
through av node to
establish sinu rhythm.

70. Adenosine administration
5 cc
Undiluted
Adenosine 50-200
mcg/kg, fast push
Max 0.3mg/kg
Saline bolus,
fast push
Central line, ideally
Brachial line enough in
small children
Continuous ECG recording

72. Adenosine is a useful diagnostic tool in patients with broad or narrow QRS complex tachycardia; it
terminates arrhythmias dependent on the AV node.
Because atrial tachycardia is not dependent on the AV node, the adenosine treatments do not terminate the
arrhythmia but can be diagnostic by slowing the rate, allowing for better exposure of atrial activity on the
ECG. Adenosine infusion will unmasks other supraventricular mechanisms during transient AV block that is
Atrial tachycardia- AF or Flutter.
Adenosine is safe and effective for diagnosis and treatment in undifferentiated regular wide complex
tachycardia.
If the underlying rhythm is SVT with aberrancy, it will uncover a latent delta wave (Wolff-Parkinson-White
syndrome ).
If SVT is ventricular tachycardia (VT), the rhythm will likely be unaffected,
The adenosine test is also used for the diagnosis of sinus node dysfunction (DNS), and it has been described
that in patients with DNS, episodes of syncope or presyncope were associated with a more marked inhibition
of the sinus node (NS) after adenosine administration compared to normal subjects.

74. Stable Narrow QRS tachycardia
Adenosine bolus
Sudden
termination
AVNRT
AVRT
Slow and
unmask
Flutter,
ectopic atrial tachy
No
effect
Sinus tachy,
Junctional ectopic
tachycardia
VT

75. PSVT -> ADENOSINE

76. In neonates with the signs and symptoms of tachy-cardiomyopathy who do not respond to adenosine,
amiodarone may be useful as it has the greatest antiarrhythmic effect.
It should be given as Injection, in loading dose of 5 mg/kg over 20 minutes followed by an infusion of 10
mg/kg or 25-50 mcg /kg/min over the next 24 h with caution owing to the high incidence of side effect.
The main electrophysiological effect of amiodarone is to increase duration of the action potential and
the refractoriness of all cardiac cells. Amiodarone does not significantly affect myocardial contractility.
Patients with atrio-ventricular re-entrant PSVT can be treated effectively by class Ic drugs, such as
propaphenone and flecainide. but should be used with caution owing to the high incidence of side
effects .

77. The propaphenone or flecainide (class Ic drugs) are useful at a dose of 2 mg/kg intravenously in 20
minutes as first dose. A second bolus dose of 1 mg/kg in 20 minutes is administered if conversion to
sinus rhythm is not achieved after 8 hours.
The oral dose of flecainide in less than 1 month neonate is 2 mg/kg/day orally, in two divided dosages
every 12 hours and 1 to 3 mg/kg/day orally or 50 to 100 mg/m2/day orally in 3 divided doses in baby
more than one month age.
They are effective where the re-entry circuit is supported by an accessory pathway.
It should not be administered to patients who have organic heart disease or heart failure as it can
depress ventricle function further

78. If PSVT Patient is Haemodynamically stable and not responding to medical treatment, than choice of
treatment is intra venous temporary pacing through umbilical or femoral vein.
If PSVT patient is Haemodynamically unstable then treatment of choice is external synchronized DC
shock .
The temporary external anti-tachycardial pacing approach allows repeated termination of the
tachycardia at the bedside until an adequate therapeutic concentration of an effective drug regimen is
achieved and obviates repeated direct-current.
Digoxin can be administered in all forms of PSVT involving the atrio-ventricular node, except for
patients with Wolff-Parkinson-White syndrome below one year of age.

79. How long to continue Rx ?
Most (60–90%) infants with Wolff‐Parkinson‐White syndrome undergo
spontaneous resolution by 1 year of age.
Most infants with ectopic atrial tachycardia who present at <6 months of age
will be free of tachycardia after 12 months of antiarrhythmic therapy.
Simpson et al showed that 57% of babies who as fetuses had SVT and who
survived the neonatal period required long term treatment (median duration of
six months; range 1–60). For the hydropic infants, 79% of the survivors beyond
the neonatal period received maintenance drugs for a median duration of
10 months (range 1–10).

80. Antiarrhythmic prophylaxis of PSVT :
To prevent recurrence prophylaxis is usually recommended in the first year of life, because the
diagnosis of tachycardia may be delayed up to the appearance of symptoms.
Most (60-90%) infants with Wolff-Parkinson White syndrome undergo spontaneous resolution by 1
year of age.
Most infants with ectopic atrial tachycardia at < 6 months of age will be free from atrial tachycardia
after 12 months of antiarrhythmic therapy.
Patients under antiarrhythmic treatment should be monitored monthly to adapt the drug dosage to the
natural increase in body weight.

81. Antiarrhythmic prophylaxis of PSVT :
In patients with re-entrant PSVT, antiarrhythmic treatment can be stoped after the first 8-12 months of
therapy.
In these cases it may be useful to perform trans-esophageal atrial stimulation during the therapeutic
wash-out to assess the inducibility of tachycardia. If tachycardia is still inducible, the physician should
consider whether to resume treatment.
Parents should be trained to measure HR at the chest or wrist, using the stethoscope or finger
technique respectively.

82. Diagnostic Evaluation:
The diagnostic tests that should be considered in order to ensure an accurate diagnosis and impact of
arrhythmia.
1. Document the rhythm disturbance by a 12 or 15 lead paediatric electrocardiogram. Paediatric 15 Lead ECG
includes right sided leads V4R, V5R, V6R. This can be invaluable in accurate identification of the type of
arrhythmia. The patient should be monitored continuously.
2. A Holter electrocardiogram may be of value in identification of the arrhythmia events.
3. Perform an atrial electrocardiogram using the atrial pacing wire in post cardiac surgical patients, where P-
waves cannot be clearly identified. It can be helpful to capture electrical evidence of termination of the
tachycardia on a 15 lead ECG or rhythm strip.
4. Test blood levels of K + , Ca++, Mg++; thyroid function tests; complete blood count, toxicology screen
(Hanash, 2010). Electrolyte imbalances are often associated with rhythm disturbances. If suspicious of
myocarditis or with worsening cardiac function check viral etiologies (Hanash, 2010). Lab testing may include
cardiac enzymes: troponin levels and CPK-MB – markers of myocardial injury.
5. A chest X-ray may demonstrate enlargement of the heart.
6. ECHO: Echo provides a qualitative and quantitative evaluation of cardiac function to rule out underlying
structural heart disease, thrombus formation and ventricular dysfunction. A quantitative value of ejection
fraction can be reported.
7. Use of pharmacological agents such as adenosine and procainamide can assist with diagnosis of arrhythmias
8. Exercise testing may be used to provoke and diagnose arrhythmias and associated symptoms.
9. A catecholamine challenge or transoesophageal pacing can also be used to provoke arrhythmias in a
controlled environment. Invasive electrophysiology studies with cardiac catheterization help to identify
ectopic foci and accessory pathways which can be mapped and ablated (Curley, 2001).

83. Aortic Arch with VSD JET (Zampi 2012).
Severe Aortic Stenosis Aortic Valve Surgery - Conduction abnormalities and complete heart block may be seen post surgical
resection of sub-aortic obstructive tissue (May, 2005). junctional tachycardia may occur (Grosse- Wortmann, 2010). Prone to VT
(Shaddy, 2011).
Atrial Septal Defect (ASD) - Sinus node dysfunction and transient atrial arrhythmias, atrial flutter, atrial
fibrillation, ventricular tachycardias (Brugada, 2013; Hanash, 2010).
Atrio-ventricular Septal Defect (AVSD) Transient and permanent sinus node dysfunction, supraventricular arrhythmias
(Keane, 2006); JET . Grosse-Wortmann et al found that complete AV block .
cc-TGA /L-TGA) Ventricular ectopy. Congenital AV block may preexist due to intrinsic structural
malformation (Wals2007).
Cor–Triatriatum Sinus bradycardia, atrial tachyarrhythmias, AV conduction disturbances (May, 2015)
D-TGA- Sinus bradycardia, sinoatrial block, junctional rhythm, JET, PVC, Mobitz 1, VT
(Brugada, Decker 2012; Zampi 2012; Aziz 2013). Prone to VT if repaired with atrial level switch procedures, Senning or
Mustard (Shaddy, 2011). 50% of patients have serious arrhythmias (Williams, 2005).
Ebstein’s Anomaly of the Tricuspid Valve Common to have rhythm disturbances related to atrial and ventricular dilatation and
conduction disturbances (May, 2005): accessory pathways (Huh, 2010); WPW and VT (Curley, 2001), SVT, atrial fibrillation, atrial
flutter (Hanash, 2010); 1 st degree heart block and rarely 3rd degree heart block (Park, 2006). Congenital accessory pathways such
as WPW may preexist due to intrinsic structural malformation (Walsh, 2007).
Pulmonary Atresia with Intact Rare rhythm disturbances observed (May, 2005). Ventricular arrhythmias if coronary sinusoids with
ischemia.
Ventricular Septum Pulmonary Atresia with a VSD Sometimes AV conduction abnormalities observed (M

84. Wide QRS tachycardia
Stable Unstable
DC shock
➢If 1:1 P-QRS relation,
try adenosine
➢If AV dissociation, IV
Lignocaine 1 mg/kg or IV
amiodarone 5 mg/kg
➢If no response, DC
shock
CPR

86. Wide QRS complex tachycardias should be assumed to be VT in pediatric patients. However, SVT with
aberrancy, SVT with the presence of an underlying bundle branch block or ventricular preexcitation, or
SVT in an antidromic tachycardia circuit can result in wide QRS complex tachycardias.
VT is rare in the neonatal period. It is defined as three or more PVCs in a row at a rate faster than 120
bpm/min and has a wide QRS complex with AV dissociation during the tachycardia. Capture beats or fusion
beats are diagnostic markers in VT.
Nonsustained VT is defined as three or more consecutive PVCs with a duration of <30 seconds.
There are 2 benign forms of VT according to the bundle branch block pattern of QRS morphology that
suggests the origin of VT;
right ventricular outflow tract VT (left bundle branch block pattern with inferior axis) and
idiopathic fascicular VT (right bundle branch block pattern QRS morphology with superior axis).

92. Ventricular tachycardia refractory to Adenosine