This document discusses pediatric cardiac arrhythmias. Some key points: - Arrhythmias are classified based on site of origin such as the sinus node, atria, AV node or ventricles. Common arrhythmias include sinus tachycardia, supraventricular tachycardia, and ventricular tachycardia. - Presentation of arrhythmias in children varies by age. Neonates may experience atrial flutter or ectopic atrial tachycardia. Older children may experience WPW syndrome or AV nodal re-entrant tachycardia. - Diagnosis involves analyzing the ECG for heart rate, QRS width, and P wave relationship to the

1. Pediatric Cardiac
Arrythmia
Presented by- Dr Anand Singh DCH DNB

2. • The frequency and clinical significance of arrhythmias are different in
children compared with adults. Although arrhythmias are relatively
infrequent in infants and children.
• The normal heart rate varies with age, The younger the child, the faster
the heart rate.
• Therefore, the definitions of bradycardia (<60 beats/min) and tachycardia
(>100 beats/min) used for adults do not apply to infants and children.
• Tachycardia is defined as a heart rate beyond the upper limit of normal
for the patient’s age and bradycardia is defined as a heart rate slower
than the lower limit of normal age.

5. Classification of arrythmia
• Arrhythmias are commonly classified based on the site of origin -
• 1. Rhythm of sinus node- sinus arrythmia/tachycardia/bradycardia/pause or
node dysfunction/sick sinus syndrome
• 2. Rhythm of atrium- PAC/ EAT / MAT/ Atrial flutter or fibrillation/ SVT
• 3. Rhythm of AV node – Junctional premature beats, JET
• 4. Rhythm of ventricles- PVC/ VT / VF / acclerated ventricular rhythm.
• Grossly any tachycardia with its origin above the His bundle is called
supraventricular tachycardia (SVT) and all the tachycardias that arise below the
His bundle are called ventricular tachycardia (VT).

6. Electrocardiographically, arrhythmias can be characterized as –
1. Tachycardias
2. Bradycardias
3. Extrasystoles
- Tachycardias can be further classified according to –
- anatomic level of origin as supraventricular or ventricular and
- functional mechanism reentry, automaticity or triggered activity.
- Bradycardias are further subdivided into the level of dysfunction i.e sinus node or atrioventricular
dysfunction.
-The behavior and management depends on the mechanism by which the arrhythmia is produced
-Three mechanisms commonly involved are –
1. Increased automaticity
2. Re entrant mechanism
3. Triggered activity

7. 1.Increased Automaticity
Normally, sinus node automaticity is higher than other cardiac tissues with
impulses at a rate varying between 60 to 200/min.
-If another automatic focus develops in the atrium that fires at a rate faster
than sinus rate, then it would result in ectopic atrial tachycardia (EAT).
- If there are multiple automatic foci, then the resulting tachycardia is
called as multifocal atrial tachycardia (MAT).
-If an automatic focus develops in the junctional tissue (near His bundle), it
would cause ‘junctional ectopic tachycardia’ (JET) and a similar focus in the
ventricle will result in automatic VT

8. 2. Re-entrant Mechanism –
-Here, an abnormal electrical circuit is formed where some portion of the circuit conducts
fast and the other portion conducts slowly.
- When an impulse encounters this circuit, it travels along both slow and fast pathways.
By the time the impulse passes through the slow pathway, the fast pathway is
repolarized and is ready to conduct the impulse retrogradely.
-The wave then returns down the slow pathway setting up a closed circuit that is self-
sustaining. The tachycardias caused by this mechanism and the associated re-entrant
circuits.

9. 3. Triggered Activity-
This occurs during the repolarization phase of the cardiac cycle.
- If the trigger occurs in phase 3 of ventricular depolarization, it is called early after
depolarization.
- If the trigger occurs in phase 4, it is called delayed after-depolarization.
- Long QT syndrome and digoxin toxicity related tachycardias are associated with this.
mechanism.

10. - There is no specific symptom or sign that would help the clinician to diagnose arrhythmia.
1. Heart rate inappropriate for the clinical condition. Many a times, tachycardia is
diagnosed on routine assessment while the child would be asymptomatic. Parent would
notice ‘excessive neck pulsations’ and bring the child for evaluation.
2. Unexplained heart failure:-
a. Common in infants and young children who have poor symptom expression. The
incessant arrhythmia would result in cardiac dilatation and heart failure and could be
wrongly labeled as dilated cardiomyopathy. The underlying tachycardia as the cause may
be easily missed and requires a high index of suspicion.
b. Recent worsening or onset of new symptoms in a child with CHD
3. Episodic pallor, sweating or lethargy
4. Infants- tachypnea,, poor feeding, vomitting, excessive crying or restlessness.
4. In older children and adolescents, present with Palpitations and chest discomfort.
PRESENTATION OF CARDIAC ARRHYTHMIAS

11. 5. Syncope, breath holding attacks or seizures- more common with
bradyarrhythmias and are uncommon with SVT. However, VT can present
with cardiovascular collapse.
-In a child with suspected tachyarrhythmia, the following history should be
obtained:
a. Is there any precipitating event like exercise or emotion?
b. How do the palpitations go off—spontaneously or by some maneuvers like
coughing, sneezing or induced vomiting?
- If these vagal maneuvers abort the tachycardia, that would indicate the
presence of AV nodal dependent tachycardia (AVNRT and AVRT).

12. c. Family history of syncope or sudden death can suggest inherited disorders associated with
arrhythmias like prolonged QT syndrome, arrhythmogenic right ventricular cardiomyopathy
or hypertrophic cardiomyopathy
d. Sensorineural deafness (prolonged QT syndrome)
e. Previous cardiac surgery
f. Drug intake: Certain drugs like macrolide antibiotics, Tricyclic antidepressants and
digoxin.
6. A child with VT can present with syncope or can be completely asymptomatic.

13. Common arrhythmias according to the Age
1. Neonatal period and early infancy: Atrial flutter, ectopic atrial tachycardia, AVRT
- These SVTs have 30% chance of complete resolution by 12 months and 50% of them
resolve by 18 to 24 months.
2. Infancy and early childhood: WPW syndrome , PJRT , AET
3. Older children and adolescents: WPW syndrome , AV nodal re-entrant tachycardia

14. • DIAGNOSIS AND MANAGEMENT OF TACHYARRHYTHMIAS

15. • A combined strategy that simultaneously addresses both diagnosis and
treatment is appropriate.
• Extreme hemodynamic instability is relatively rare in childhood
arrhythmias particularly in the absence of structural heart disease.
• Children tolerate a wide range of heart rate, may appear quite
comfortable with heart rates exceeding 240/min.
• In those who present with instability, synchronized DC cardioversion
should be performed at a dose of 0.5 to 2 Joules/kg.
• Unless there is hemodynamic compromise; the important initial step is to
record a 12 lead ECG and rhythm strip during tachycardia.

16. 1.Is the QRS Complex Narrow or Broad?
2. Is the Heart Rate Regular or Irregular?
3. Is the P Wave Seen?
4. If P Wave is Seen, What is its Relation with QRS?
5. What is the Effect of Vagal Maneuvers or Administration of Adenosine?

17. Heart Rate- Use lead II or the lead
with the least artifact.
Calculate the approximate heart rate
by counting the number of large boxes
between 2 consecutive R’s
1. Heart rate = 1500 ÷ number of
small boxes in RR interval
OR
2. Count the number of large boxes
between 2 QRS
Heart rate = 300 ÷ number of large
boxes between QRS

18. Sinus rhythm is present if :-
1. PR interval is consistent
throughout the tracing
2. P wave deflection is positive
in leads 1, II and aVF but
negative in aVR
-Sinus rhythm is not if 
1. P wave is –ve in lead 2 &
aVF
2. +Ve in aVR

19. TYPE Description Etiology Significance
Regular Sinus Rhythm
- Regular Rhythm
- Rate normal for age - - - - -
- Rhythm is normal at
any age
Sinus Tachycardia
-Rate is faster than the
upper limit of normal for
age
( > 170 Infant, > 140
children )
- Anxiety, fever, shock,
Anemia, CHF ,
Thyrotoxicosis
- Increased cardiac
work is well tolerated
by healthy myocardium
Sinus Arrhythmia
- Phasic variation due to
ANS ( increasing during
inspiration & decreasing
during expiration ).
- Normal phenomenon
and is caused by phasic
variation in the firing
rate of cardiac
autonomic nerves with
the phases of respiration
- No significance

20. PR interval- In infants & young children > or = 0.16 sec or 4 small boxes
In older children & adolescents > or = 0.2 sec or 1 big box
QRS :- Normal is 1 small box wide (0.04 sec )
Wide is 2 small box or more ( > or = 0.08 sec )

22. Sinus Node Dysfunction (Sick Sinus Syndrome)
• Description- In sinus node dysfunction, the sinus node fails to function as
the dominant pacemaker of the heart or performs abnormally slowly,
resulting in a variety of arrhythmias.
• ECG abnormality - sinus bradycardia, sinus pause or arrest, sinus node
exit block, atrial fibrillation & brady tachycardia syndrome.
• Brady Tachyarrhythmia occurs when bradycardia and tachycardia
alternate. When these arrhythmias are accompanied by symptoms such as
dizziness or syncope, sinus node dysfunction is referred to as sick sinus
syndrome.

23. Causes
1. Idiopathic
2. Injury to the sinus node caused by extensive cardiac surgery, particularly involving the atria
3. Myocarditis, pericarditis or rheumatic fever
4. Congenital heart defects (CHDs)
5. Secondary to antiarrhythmic drugs (e.g. digitalis, propranolol, verapamil, quinidine )
6. Hypothyroidism
Significance
Brady tachyarrhythmia is the most worrisome.
Profound bradycardia after a period of tachycardia can cause presyncope, syncope, and even death.

24. Supra Ventricular Tachyarrythmia
- Supraventricular tachycardia (SVT) is a general term that refers to any rapid heart rhythm
originating above the ventricular tissue.
AV Re-entrant tachycardia ( 73.2 % ) – most common mechanism of SVT in infants
2. AV Nodal re- enterant ( 12.5 % ) – increasing incidence of AVNRT in childhood and into
adolescence.
3. Primary atrial tachycardia ( 14.3 % )
- Atrial flutter and IART
- Ectopic atrial tacchycardia
- Chaotic or multifocal atrial tachycardia
- Atrial fibrillation
4. Junctional ectopic tachycardia

26. - Orthodromic accessory AVRT is the most common
AVRT in normal infants.
Antegrade conduction through the normal, slow
atrioventricular (AV) node produces a normal QRS
complex, and the retrograde conduction through the
bypass tract creates inverted P waves after the QRS
complex (with a short RP interval).
- In Antidromic accessory AVRT
-The antegrade conduction through the bypass tract
produces a pre existed wide QRS complex. Retrograde
P waves precede the wide QRS complex with a short
PR interval (and a long RP interval).

27. -When the accessory pathway conducts impulses in the antegrade direction (atrium to ventricle) two
parallel routes of AV conduction are possible:-
1. Delay through the AV node
2. Other occurs without delay through the accessory pathway and results in preexcitation of the
ventricle .
- The result is a characteristic ECG pattern during sinus rhythm consisting of a short PR interval,
"delta wave" (both of which reflect preexcitation), and a widened QRS complex due to the delta wave.
This ECG pattern is referred to as the Wolff-ParkinsonWhite (WPW) pattern.
Wide
QRS
Complex

28. In orthodromic nodal RAVT
The retrograde P waves are usually
concealed in the QRS complex of normal
duration.
The ECG is similar to that of orthodromic
accessory RAVT.
In antidromic nodal RAVT (uncommon)
narrow QRS complexes are preceded by
retrograde P waves, with a short PR
interval.

29. Causes
1. WPW preexcitation (10% to 20% of cases)
2. Idiopathic in young infants than in older children
3. Patients with some CHDs (e.g., Ebstein’s anomaly, single ventricle, congenitally corrected
transposition of the great arteries) are more prone to this arrhythmia
4. After cardiac surgeries
Significance
1. Many infants tolerate SVT well. If the tachycardia is sustained for 6 to 12 hours, signs of CHF
usually develop in infants. Clinical manifestations of CHF include irritability, tachypnea, poor
feeding, and pallor. When CHF develops, the infant’s condition can deteriorate rapidly.
2. Older children may complain of chest pain, palpitation, shortness of breath and fatigue.
- A pounding sensation in the neck (i.e., neck pulsation) is fairly unique to the reentrant-type SVT
and considered to be the result of cannon waves, when the atrium contracts against a simultaneously
contracting ventricle.

30. 1. Infants - Placing an ice-water bag on the face (for up to 10 seconds)- Prroduces diving reflex
- Can be reapplied after 1 minute
Older children- Vagal stimulatory maneuvers (unilateral carotid sinus massage, pressure on eyeball
- Pressure is applied towards vertebral column, posteromedially and not more than 5 sec.
2. If the vagal maneuver is ineffective, Adenosine is considered the drug of choice.
-It has a very short duration of action (half-life <10 seconds)
-A/E apnea/ bronchospasm, acclerated or prolonged Ventricular rhythm can lead to VF.
- Adenosine is given by rapid IV bolus followed by a saline flush, starting at 50 μg/kg, increasing in
increment of 50 μg/kg, every 1 to 2 minutes. The usual effective dose is 100 to 150 μg/kg with
maximum dose of 250 μg/kg. Adenosine is 90% to 100% effective.
Treatment
- New syringes and new 3 way need to taken for every push.

31. 3. If the infant is in severe CHF and adenosine is not readily available, emergency treatment is
directed at immediate cardioversion. The initial dose of 0.5 joule/kg is increased in steps up to 2
joule/kg.
4. IV administration of propranolol may be used to treat SVT in the presence of WPW syndrome.
-IV verapamil should be avoided in infants younger than 12 months of age because it may produce
extreme bradycardia and hypotension in infants.
5. IV amiodarone can be tried as bolus followed by continious infusion to maintain effect.
S/E- Severe hypotension, acute fulminant liver failure, cardiogenic shock
5. Overdrive suppression (by transesophageal pacing or by atrial pacing) may be effective in children
who have been digitalized.

33. Prevention of Recurrence of SVT
1. In infants without WPW preexcitation, oral propranolol, atenolol for 12 months is effective.
2. Verapamil can also be used but it should be used with caution in patients with poor LV function
and in young infants.
- In the presence of WPW preexcitation, digoxin or verapamil may increase the rate of antegrade
conduction of the impulse through the accessory pathway and therefore should be avoided.
4. For children who have infrequent episodes of SVT - vagal maneuvers .
-If not effective, adenosine is used to correct the rhythm.
- Alternatively, the use of a beta-blocker or calcium channel blocker can be effective in slowing and
terminating the SVT.
5. If medical management fails or frequent recurrences occur- Radiofrequency catheter ablation or
surgical interruption of accessory pathway.
- Ablation therapy is controversial for asymptomatic patients with WPW preexcitation. Ablation is
not recommended in infants 1 to 2 years of age because of a possibility of spontaneous resolution of
SVT.

34. Atrial Tachycardia (AT)
- Atrial tachycardia (AT) is a subset of SVT originating entirely from atrial tissue and does not require
the atrioventricular (AV) junction, accessory pathways, or ventricular tissue for initiation and
maintenance of the elevated heart rate.
- Atrial fibrillation and atrial flutter, although fulfilling this definition, are usually not included in the
designation of AT and are typically identified as specific entities.
- Atrial ectopic tachycardia (AET) represents 10-20% of SVT in pediatric population. Its an
automatic arrhythmia that presents as an incessant rhythm . In addition arrhythmia has been
associated with chronic cardiomyopathy.
- Focal atrial tachycardia (FAT), also due to a single focus, behaves in a paroxysmal manner, starting
and stopping abruptly. Microreentry or triggered activity are thought to be the most common cause.
- Multifocal Atrial tachycardia (MAT) or chaotic atrial rhythm is defined by 3 or more P-wave
morphology, atrial rate >400 and ventricular rate of 150-250/min

36. Multifocal Atrial tachycardia (MAT) or chaotic atrial rhythm is defined by 3 or more P-wave
morphology, atrial rate >400 and ventricular rate of 19 150-250/min

37. Treatment of AET/MAT
- Atrial ectopic tachycardia is generally responsive to medical therapy and there are high chances of
spontaneous resolution.
- Medical treatment involves Digoxin which decreases ventricular response rate by slowing AV
conduction but has no effect on ectopic focus.
- Other drugs that can be used are amiodarone and propafenone.
- In patients with chronic or frequently recurrent conditions who unresponsive to medical therapy,
ablation therapy is suggested.
- Multifocal atrial tachycardia resolves completely after six months and the prognosis for long-term
outcome is excellent in children.
- In some cases, MAT is seen in patients with structural heart disease and the outcome is dependent
upon the underlying condition .
- Medical therapy is therapy is directed at controlling the ventricular response rate with a
combination of oral digoxin, beta blocker, and calcium channel blocker

39. - The pacemaker lies in an ectopic focus, and “circus movement” in the atrium is the mechanism of
this arrhythmia.
- Typical atrial flutter is characterized by an atrial rate (F wave with “sawtooth” configuration) of
about 300 (ranges, 240–360) beats/min, and normal QRS complexes , a ventricular response with
varying degrees of block (e.g., 2:1, 3:1, 4:1 )
ATRIAL FLUTTER

41. - Atrial fibrillation (AF) is the most common arrhythmia seen in adults but it is rare in children.
- AF is characterized by an extremely fast atrial rate (f wave at a rate of 350–600 beats/min) and
an “irregularly irregular” ventricular response with narrow QRS complexes.
ATRIAL FIBRILLATION

42. Ventricular Tachycardia
Description :-
1. VT is a series of three or more PVCs with a heart rate of 120 to 200 beats/min. QRS complexes
are wide and bizarre.
2. VT may be classified in various ways by its onset, duration, and morphology.
a. The onset may be paroxysmal (sudden) or nonparoxysmal.
b. By duration, VT may be (1) nonsustained VT (a duration of <30 seconds), (2) sustained VT (longer
than 30 seconds)
c. By morphology, it may be (1) monomorphic (one dominant QRS form), (2) polymorphic (a beat-
to-beat change in the QRS shape),
3. Torsades de pointes (meaning “twisting of the points”) is characterized by a paroxysm of VT with –
- progressive changes in the amplitude and polarity of QRS complexes separated by a narrow
transition QRS complex. It is a distinct form of polymorphic VT, occurring in patients with marked
QT prolongation.
4. Differentiating VT from SVT with aberrant conduction is sometimes difficult. However, in children,
almost all wide QRS tachycardias are VT. They should be treated as such until proven otherwise.

46. Causes
1. In patients with structural heart diseases such as tetralogy of Fallot (TOF), aortic stenosis,
hypertrophic or dilated cardiomyopathy, or MVP.
2. Postoperative CHDs (e.g., TOF, dextrotransposition of the great arteries, or doubleoutlet RV).
3. Myocarditis, cardiomyopathies, Chaga’s disease (trypanosomiasis in South America), myocardial
tumors, myocardial ischemia, and infarction
4. Pulmonary hypertension
5. Metabolic causes include hypoxia, acidosis, hyperkalemia, hypokalemia, and hypomagnesemia.
6. Mechanical irritation from an intraventricular catheter
7. Pharmacologic and chemical causes include catecholamine infusion, digitalis toxicity,
cocaine, and organophosphate insecticides.
8. Most antiarrhythmic drugs (especially classes IA, IC, and III) are also proarrhythmic.

47. Significance
1. VT may cause of sudden cardiac death.
2. Presenting symptoms may be dizziness, syncope, palpitation, or chest pain.
- The family history may be positive for ventricular arrhythmia or sudden death.
3. With a fast heart rate, cardiac output may decrease notably and the rhythm may deteriorate to
ventricular fibrillation (VF) in which effective cardiac output does not occur.
4. Chronic low rate VT may lead to a tachycardia-mediated cardiomyopathy.
5. Polymorphic VTs are more significant than monomorphic ones.
6. Those associated with abnormal cardiac structure (pre and postoperative) or function are more
significant than those seen in patients with structurally and functionally normal hearts.
7. VTs associated with certain forms of cardiomyopathy (arrhythmogenic RV dysplasia, hypertrophic
or dilated cardiomyopathy) and genetic electrical heart diseases (LQTS ) can be a cause of sudden
death.

49. BRADY - ARRYTMIAS

50. - Occurs due to disorder either affecting impulse formation or conduction -
1. Disorder of impulse formation-
- Sick sinus syndrome ( sinus pause or arrest )
- Familial, hypothyroidism
- Cong heart disease associated with isomerism
- Postoperative ( following a senning operation )
2. Disorder of impulse conduction-
- Sinus node conduction abnormality
- AV block
- Diphtheric myocarditis
- Hyperkalemia
- Drugs like calcium channel blocker, Beta blocker

51. Sinus Bradycardia
- Heart rate is slower than
the lower limit of normal
for the age
( < 80 in newborn
< 60 in children )
- Normal individuals,
trained athletes,
increased ICP,
hypothyroidism,
hypothermia
- In some patients,
marked bradycardia
may not maintain
normal cardiac
output.
Sinus Pause/ Arrest -Sinus node pacemaker
momentarily ceases activity
- Sinus arrest is of longer
duration and usually results
in an escape beat.
- Absence of the P wave
and QRS complex for a
relatively short time.
-Sinus pause of < 2
seconds are normal.
- No hemodynamic
significance but may
reduce cardiac output
in patients with
frequent and long
period of sinus pause
Sino Atrial Exit
Block
- An impulse
formed within the sinus
node fails to propagate
normally to the atrium.
- P wave is absent from
the normally expected P
wave, resulting in a long
RR interval.
- usually transient and
has no hemodynamic
significance

54. Atrioventricular (AV) block is defined as a delay or interruption in the transmission of an atrial
impulse to the ventricles.
- Heart block is divided into three catogeries.
1. First-degree AV block occurs when the PR interval is greater than the upper limits of normal for
age.

55. 2. Second-degree AV block is further divided into two categories based on ECG findings, Mobitz type 1
and type 2.
- In Mobitz type 1 block (also referred to as Wenckebach block), there is progressive prolongation of
the PR-interval until a P wave fails to be conducted.

56. In Mobitz type 2 block, the PR interval remains unchanged prior to the P wave that suddenly
fails to conduct to the ventricles.

57. 3.Third-degree AV block is also referred to as complete heart block.
On ECG, there is complete dissociation of the atrial and ventricular activity

59. Management
1.When detected in utero, steroid therapy may be applied if associated with
anti-Ro/SSA and anti-La/SSB.
2. Atropine or isoproterenol is indicated in symptomatic children until
temporary ventricular pacing is secured.
3. Transvenous ventricular pacemaker
- Problems may arise after a pacemaker is placed in children.
- Stress placed on the lead system by the linear growth of the child,
fracture of the lead system in a physically active child, electrode malfunction
(scarring of the myocardium around the electrode, especially in infants) and
the limited life span of the pulse generator require follow up of children with
an artificial pacemaker.

60. 1. QRS Complex
Narrow complex ( < 0.12 sec ) Wide complex ( > 0.12 sec )
-It is suggestive of SVT
-Most common in children
-Narrow means normal conduction above HIS bundle
- Origin below HIS bundle
( mostly in ventricles )
Ex – VT ( can be narrow complex in
neonates/ infants )
-Rarely SVT with bundle branch block
( sp. after cardiac surgery )
2. RR Interval ( heart rate )

61. RR Interval
Regular
Irregular
Ex – Atrial fibrillation
-Multifocal atrial tachycardia
-Atrial tachycardia with variable
conductionP wave visible / not visible
visible
Not visible
1. Increase ECG tracing from 25 mm to 50 mm
2. Transesophageal recording by ECG electrode placed
in esophagus
If still Not visible

62. Not visible P wave
AVNRT / JET
( P wave is submerged with QRS wave )
Give Adenosine ( both diagnostic & therapeutic )
If tachycardia breaks down with Adenosine , its AVNRT
Other causes of not visible P wave-
1. Can be superimposed on T wave , tall T Wave
2. Replaced with fibrillatory waves in AF
3. P wave appear as saw tooth appearance as in
Atrial flutter
Visible P wave

63. P wave & QRS Ratio
( no of P wave with no of QRS complex )
P/QRS Ratio < or = 1
( Atrial rate < or = Ventricular rate )
P/QRS Ratio > 1
( Atrial rate > Ventricular rate )
Atrial Tachycardia or Flutter
measure RP interval & PR interval

64. Measure RP interval & PR interval
RP interval > PR interval RP interval < PR interval
1. Atrial tachycardia
2. PJRT
3. Atypical AVNRT
( indicates short RP interval subgroup )
RP interval < 0.7 second RP interval > 0.7 seconds
AVNRT AVRT / AVNRT / Atrial tachycardia

65. Wide QRS Complex ( > 0.12 seconds )
- Any tachycardia with wide QRS is ventricular in origin unless proved otherwise.
- VT incidence is less than 5 percent in children.
- Incidence is more after surgery, drugs, metabolic and myocarditis.
Relationship between P wave & QRS
No relation
Classical VT
P / QRS Ratio 1:1
1. SVT with aberrancy
2. SVT with BBB
3. AVRT in WPW syndrome
4. VT with retrograde atrial
conduction

67. Take Home Message
• Artifacts , mechanical problems due to central line and electrolyte
problems (potassium, calcium and magnesium related) must be thought of
in all cases of arrhythmias in PICU .
• Rhythm problems once confirmed need to be urgently categorized into
two categories : stable or unstable.
• A twelve lead EKG should be attempted and a rhythm strip printed.
• Always remember that first principle in managing arrhythmias is to treat
the patient rather than the electrocardiogram.

68. - Evaluation heart rate and rhythm quickly and assessing the level of
significance in terms of hemodynamic alterations, blood pressure and
peripheral perfusion.
- If the patient loses consciousness or becomes hemodynamically unstable in
the presence of a tachyarrhythmia, prompt electrical cardioversion is
indicated.
- If the patient loses consciousness or becomes hemodynamically unstable in
the presence of a bradyarrhythmia, prompt medical therapy or cardiac
pacing(external or internal) is indicated.
- If heart rate is below 60 in a newborn or infant, cardiac compression
must be instituted in addition to ongoing treatment.

69. REFERENCES
1. Park text book of pediatric cardiology 6th edition
2. Nelson text book of pediatrics 20th edition
3. IAP text book of pediatric cardiology 2013 edition
4. PG text book of pediatrics by Dr Piyush Gupta 2nd edition
5. Journal of pediatric critical care april- june 2014
6. PALS allogrhythm 2010
7.KHAN academy ( for video’s )