The document provides a comprehensive overview of neonatal electrocardiography (ECG), discussing various conditions such as atrial and ventricular hypertrophy, conduction disturbances, and specific syndromes like Wolff-Parkinson-White. It outlines the criteria for diagnosing different forms of heart block and the significance of specific ECG patterns in neonates. Additionally, the document highlights the challenges in interpreting ECG results in infants, emphasizing the importance of age-related norms and clinical context.

1. Neonatal EKG
Dr.Vinayak Vijay Kodur
3rd year DM Neonatology Resident
L.T.Municipal Medical College,Mumbai

2. Atrial Hypertrophy
• As the impulse begins in
RA, initial part of “p” wave
is formed by RA and later
by LA.
• RA= p pulmonale
LA= p mitrale
• LA is posteriorly placed
structure as compared to
RA so p wave is biphasic
in V1. LAH more negative
than positive deflection in
V1.

3. Atrial Hypertrophy
• RAH
1. P wave amplitude > 2.5mm in
Lead 2
2. p wave(initial part) >1.5mm
in V1
3. P wave axis >60
• ASD, TAPVC, PAPVC,
Tricuspid atresia, TR, Ebstein`s
anomaly, PPHN, Pulmonary
stenosis.
• LAH
• P wave duration >2.5mm
(0.10sec) lead 2
• Lead 2 inter peak distance
>o.o4sec.
• L to R shunt VSD, PDA, MR,
MS.

4. LV and RV forces
• LV versus RV forces in hexaxial and precordial leads
system.

5. Ventricular Hypertrophy Versus Ventricular Conduction
Disturbances
• Are not always easy to distinguish; both present with increased
QRS amplitudes.
• An accurate measurement of the QRS duration is essential.

6. RBBB Vs RVH

7. Volume vs Pressure overload: RVH

8. RVH criteria
• QR complex in V1
• An upright T wave in V1(normal in the first week of
life),
• Increased R wave amplitude in V1, and increased S wave
amplitude in V6 for the babies age.(according to the
Davignon criteria).
• Sensitivity and specificity has not been tested in the
neonate.

9. LVH criteria
• The performance of the ECG in recognition of left ventricular
hypertrophy is poorer than generally recognised and has not
been specifically tested in neonates.
• Left ventricular hypertrophy is expected to produce increased
left sided voltages.
• Garson described the most helpful ECG signs in children as
being T wave abnormalities in leads V5 and V6, increased R
wave amplitude in V1, increased S wave amplitude in V6
(according to the Davignon criteria), and a combination of these
last two variables.

10. LVH
• Left to right shunt lesions may result in left ventricular
hypertrophy, but this may be in association with right
ventricular hypertrophy and manifested as biventricular
hypertrophy.
• Left ventricular hypertrophy in the newborn may be attenuated
by the normal right-sided predominance of the newborn.
• The normal premature heart may not have developed the right-
sided predominance, especially if <28 weeks gestation, and left
ventricular predominance may be present.

11. LVH

12. Ventricular Conduction Disturbances
• Conditions that are grouped together as ventricular conduction
disturbances have abnormal prolongation of the QRS duration
in common. Ventricular conduction disturbances include the
following:
1. BBB, right and left
2. Preexcitation (e.g., WPW-type preexcitation)
3. Intraventricular block

13. Ventricular Conduction Disturbances
• In BBBs (and ventricular rhythms), the prolongation is in the
terminal portion of the QRS complex (i.e., “terminal slurring”).
• In preexcitation, the prolongation is in the initial portion of the
QRS complex (i.e., “initial slurring”), producing “delta” waves.
• In intraventricular block, the prolongation is throughout the
duration of the QRS complex.
• Normal QRS duration varies with age; it is shorter in infants than
in older children or adults.
• Prolonged QRS duration >0.10 sec in adults and infants >0.08 sec.

14. Ventricular Conduction Disturbances
• By far the most commonly encountered form of ventricular
conduction disturbance is RBBB.
• WPW preexcitation is uncommon, but it is a well-defined entity
that deserves a brief description.
• LBBB is extremely rare in children, although it is common in
adults with ischemic and hypertensive heart disease.

15. Ventricular Conduction Disturbances
• A= Normal
• B= BBB
• C= WPW
• D= Intra-
ventricular
block

16. BBB
• The classical ECG in Ebstein’s anomaly of the tricuspid valve
displays a prolonged PR interval and a wide RBBB.
• Left anterior fascicular block is found atrio-ventricular canal
defects and tricuspid atresia.
• In severe cardiomyopathy, interruption of the left bundle, which
results from the involvement of the left ventricle and/or its
conduction system, has been reported and carries a poor prognosis.
• Hereditary bundle branch block is an autosomal dominant
(chromosome 19q). Affected individuals can have RBBB, left or
right QRS axis deviation or AV block.

17. RBBB
• In RBBB, delayed conduction through the right bundle branch
prolongs the time required for a depolarization of the RV.
• When the LV is completely depolarized, RV depolarization is
still in progress. This produces prolongation of the QRS
duration, involving the terminal portion of the QRS complex,
called “terminal slurring” , and the slurring is directed to the
right and anteriorly because the RV is located rightward and
anteriorly in relation to the LV.

18. RBBB
• In a normal heart, synchronous depolarisation of the opposing
electromotive forces of the RV and LV cancels out the forces to
some extent, with the resulting voltages that we call normal.
• In RBBB (and other ventricular conduction disturbances),
asynchronous depolarisation of the opposing electromotive forces
may produce a lesser degree of cancellation of the opposing forces
and thus results in greater manifest potentials for both ventricles.
• Consequently, abnormally large voltages for both RV and LV may
result even in the absence of ventricular hypertrophy.
• Therefore, the diagnosis of ventricular hypertrophy in the presence
of BBB (or WPW preexcitation or intraventricular block) is
insecure.

19. RBBB
• In adults, when the QRS duration is longer than 0.12 second it is
called complete RBBB, and when the QRS duration is between
0.10 and 0.12 second, it is called incomplete right bundle branch
block (IRBBB).
• Normal QRS duration is shorter in infants and children.
• Therefore, dividing RBBB into complete and incomplete is
generally arbitrary and is particularly meaningless in children.

20. Criteria for Right Bundle Branch Block
1. RAD, at least for the terminal portion of the QRS complex. (The initial QRS
force is normal.)
2. The QRS duration clearly longer than the upper limit of normal for the
patient’s age. When the prolongation of the QRS duration is only mild, it could
be called incomplete RBBB.
3. Terminal slurring of the QRS complex that is directed to the right and usually,
but not always, anteriorly:
A. Wide and slurred S waves in leads I, V5, and V6
B. Terminal, slurred R′ in aVR and the right precordial leads (V4R, V1, and
V2).
4. ST-segment shift and T-wave inversion are common in adults but not in infants

21. Right Bundle Branch Block

22. RBBB
• Two paediatric conditions commonly associated with RBBB are
ASD and conduction disturbances after open heart surgery involving
right ventriculotomy.
• Ebstein’s anomaly, coarctation of the aorta in infants younger than 6
months of age, endocardial cushion defect, and partial anomalous
pulmonary venous return; it is also occasionally seen in normal
children. Rarely, RBBB is seen in myocardial diseases
(cardiomyopathy, myocarditis).
• The significance of RBBB in children is different from that in adults.
In several paediatric examples of RBBB, the right bundle is intact. In
ASD, the prolonged QRS duration is the result of a longer pathway
through a dilated RV rather than an actual block in the right bundle.

23. RBBB
• Right ventriculotomy for repair of VSD or tetralogy of Fallot
disrupts the RV subendocardial Purkinje network and causes
prolongation of the QRS duration without necessarily injuring
the main right bundle, although the latter may occasionally be
disrupted.

24. RBBB
• Although the RSR′ (or rSr′ ) pattern in V1 is unusual in adults,
this pattern is a normal finding in infants, toddlers, and children.
• From vectorcardiographic points of view, in order for a newborn
ECG pattern to change to the adult pattern, it has to go through a
stage in which rSr′ or RsR′ pattern appears. It is almost
impossible for a newborn ECG to change to an adult pattern
without going through the rSr′ (or rsR′ ) stage.
1. An rsR′ pattern in V1 is normal if it is associated with
normal QRS duration and normal QRS voltage.

25. RBBB
2. If the rSr′ pattern is associated with only slightly prolonged
QRS duration (not to satisfy the criterion of RBBB), it is
then incomplete RBBB. The QRS voltage may be slightly
increased in some cases for the same reason as discussed
under RBBB.
3. If the rsR′ pattern is associated with slightly prolonged
QRS duration and an abnormal QRS voltage, it is still
IRBBB, not ventricular hypertrophy.
4. RVH is justified only if an abnormal QRS voltage is
present in the presence of normal QRS duration.

26. LBBB
• LBBB is extremely rare in children.
• In LBBB, the duration of the QRS is prolonged for age, and the slurred
terminal portion of the QRS is directed leftward and posteriorly.
• A Q wave is absent in V6. A prominent QS pattern is seen in V1, and a
tall R wave is seen in V6.
• Associated with cardiac disease or surgery in the LV outflow tract,
septal myomectomy, and replacement of the aortic valve.
• Rarely associated with LBBB include LVH, myocarditis,
cardiomyopathy, MI, aortic valve endocarditis, and premature
ventricular contractions (or ventricluar tachycardia [VT]) originating in
the RV outflow tract.

27. LBBB

28. Intraventricular Block
• In, the prolongation is throughout the duration of the QRS
complex.
• This usually suggests serious conditions such as metabolic
disorders (e.g., hyperkalemia), diffuse myocardial diseases (e.g.,
myocardial fibrosis, systemic diseases with myocardial
involvement), severe hypoxia, myocardial ischemia, or drug
toxicity (quinidine or procainamide).

29. Wolf–Parkinson–White syndrome
• Normally impulse
generated in SA node can
only pass down to
ventricles is via the
conduction system as atria
and ventricles are separated
electrochemically by the
fibrous tissue in between
them.
• If there is some pathway of
conduction intact then can
result in WPW syndrome.

30. Wolf–Parkinson–White syndrome
• The anatomical substrate of preexcitation in Wolff–Parkinson–
White (WPW) syndrome is a direct muscular connection
between the atria and ventricles.
• Since accessory pathways rarely show decremental conduction,
the electrical impulse is conducted prematurely to the ventricles
resulting in a short PR interval.
• Conduction through the atrioventricular node and the accessory
pathway results in collision of two electrical wavefronts at the
ventricular level causing a delta wave and a fusion QRS
complex with prolonged duration.

31. Wolf–Parkinson–White syndrome
• Intermittent pre excitation is not uncommon in newborns and
infants.
• High prevalence of WPW syndrome is seen in newborns when
two of the four following characteristics are noted:
1. PR interval <0.10s,
2. QRS complex duration >0.08s,
3. lack of a Q wave in V6
4. left axis deviation

32. Wolf–Parkinson–White syndrome

33. Wolf–Parkinson–White syndrome
• Depending on the location of the accessory pathway as well as
the conduction properties of the atrioventricular node, even
continuous preexcitation may be subtle and only detected in the
mid-precordial leads.
• A common cause of a short PR interval in a normal heart is a
low right atrial pacemaker. The P wave is negative in lead aVF
and positive or isoelectric in lead I. The intraatrial conduction
time from the high to low right atrium is eliminated and
therefore the PR interval may be up to 40 ms less than normal.
• Ebstein`s anomaly, l-TGA, hypertrophic cardiomyopathy and
cardiac tumours - increased prevalence.

34. Wolf–Parkinson–White syndrome

35. Complete (third degree) atrioventricular
block
• Complete AV block implies complete absence of conduction from
atrium to ventricle.
• ECG shows normal atrial activation and slower dissociated regular
QRS complexes.
• 1: 15 000 to 20 000 live births
• maternal connective tissue disease anti Ro/SSA and La-SSB
antibodies.
• However, only 2 to 5% of women with known antibodies will
have a first child with AV block.

36. Complete (third degree) atrioventricular
block
• Acquired complete AV block is rare in neonates. It is mainly
infective (viral myocarditis, HIV infection) or may be related to
tumours.
• Recurrence rate in SLE / Sjogren`s syndrome is 18%.
• Mortality rate in patients with neonatal AV block is still high,
especially during the first 3 months of life.
• In spite of different treatment modes including the use of high
doses of betablockers and pacing, there is still significant
mortality.

37. Complete (third degree) atrioventricular
block

38. First and second degree atrioventricular
block
• Heart block associated with prolonged QT interval has been
described in neonates and infants receiving cisapride.
• Second degree AV block due to QT interval prolongation has
been also reported with the use of other agents such as
doxapram in premature infants.
• Neonates may present with first or second degree AV block and
rare reports exist demonstrating progression to complete AV
block after birth in children with and without antibody mediated
conduction disorders.

39. First and second degree atrioventricular
block
• First degree: Prolonged PR interval but each p wave is followed
by a QRS complex.
• Second degree
• Mobitz Type 1: Wenckebach periodicity, is almost always a
disease of the AV node.
• With each p is followed by a QRS with progressively increasing
PR interval until a beat is dropped, After the dropped QRS
complex, the PR interval resets and the cycle repeats.

40. First and second degree atrioventricular
block
• Is almost always a disease of the distal conduction system (His-
Purkinje System).
• Mobitz II heart block is characterized on a surface ECG by
intermittently nonconducted P waves not preceded by PR
prolongation and not followed by PR shortening.
• There is usually a fixed number of non-conducted P waves for every
successfully conducted QRS complex, and this ratio is often
specified in describing Mobitz II blocks.
• For example, Mobitz II block in which there are two P waves for
every one QRS complex may be referred to as "2:1 Mobitz II block"

41. 2nd Degree Heart Block Mobitz type 1
P wave not followed by QRS
P wave followed by QRS with increasing PR interval

42. 2nd degree block Mobitz type 2

43. Long QT syndrome

44. Long QT syndrome
• Prevalence 1:3000–5000
• Characterized by the occurrence of syncopal episodes due to
torsades de points ventricular tachycardia (VT) and by a high
risk for sudden cardiac death among untreated patients.
• 12% - sudden death is the first manifestation (4% infancy)
• Mutations of genes encoding ionic (potassium or sodium)
channels involved in the control of ventricular repolarization.
• Approximately 30% of cases are due to ‘de novo’ mutations.

45. Long QT syndrome
• Several members of the same family are gene-carriers. Disease
has low penetrance (gene-carriers may not show the clinical
phenotype and may have a normal QT interval.)
• Therefore a normal QT in the parents does not rule out familial
LQTS.
• Beta-blockers are the first choice therapy in LQTS and are
effective in preventing recurrences in 80% of already
symptomatic patients.

46. Long QT syndrome

47. Wondering Pacemaker

48. Sinus Arrhythmias

49. Premature atrial beats.
• Premature atrial beats usually have a different morphology and
mean vector from sinus P waves.
• In regular sinus rhythm at a normal rate, a P wave that occurs before
the next expected P wave is a premature atrial beat.
• A premature atrial beat may be conducted to the ventricles
normally, or with ventricular aberration or not conducted or
‘blocked’.
• In infants, since the refractory periods of the bundle branches are
similar, premature atrial beats may be conducted with either RBBB
or left bundle branch.

50. Premature atrial beats.
• Blocked premature atrial beats occur in a bigeminal sequence,
so-called ‘blocked atrial bigeminy’.
• This rhythm simulates sinus bradycardia; it is important to
examine the T waves carefully for blocked P waves.
• The distinction is important since blocked atrial bigeminy is
most often benign while severe sinus bradycardia may
accompany systemic illness.

51. Premature atrial beats.

52. Tachyarrthymias

53. Supraventricular tachycardia.
• A rapid regular tachyarrhythmia, which results from an
abnormal mechanism originating proximal to the bifurcation of
the bundle of His and does not have the morphology of atrial
flutter.
• The usual infant with SVT has an extremely regular R-R interval
after the first 10–20 beats, most often at rates greater than 230
beats/min and usually 260–300 / min.
• In 60% of cases, the P waves are visible, but the P waves almost
always have a different morphology from sinus.
• In over 90% of infants and children with SVT, the QRS complex
is narrow.

54. SVT paper speed of 25mm/sec
• Rapid narrow complex tachycardia at around 300 bpm.

55. SVT paper speed of 50mm/sec
• Same patient. There are no visible P waves this is an AVNRT.

56. SVT reverted back to normal
• Same patient, after reverting SVT back to sinus rhythm.

57. Supraventricular tachycardia.
• It is important to document SVT with a 12-lead ECG before
attempting conversion of the rhythm unless the infant is
critically ill.
• After sinus rhythm is achieved, the WPW pattern should be
sought on a 12-lead ECG.
• An echocardiogram is indicated to determine ventricular
function or the presence of congenital heart disease.
• Adenosine (0.1mg/kg) can be both diagnostic and therapeutic in
SVT.

58. SVT- Adenosine
• Half life: <1.5 seconds: transient AV nodal block as well as
sinus node block, negative chronotrope, ionotope.
• Side effects: flushing, nausea, dyspnea, bronchospasm are short
lived.
• Give 0.1/kg rapidly into a large vein. Repeat after 2 minutes with
0.25mg/kg.
• Maximum total dose 12mg.

59. Supraventricular tachycardia.

60. Atrial Flutter
• Characterized by a rapid,regular form of atrial depolarization:
the ‘flutter wave’.
• The picket fence morphology is similar to adults. However, the
flutter wave durations are generally 0·09 to 0·18 s with atrial
rates in infants between 300–500 beats/min.
• There is variable AV conduction from 1:1 to 4:1 yielding an
irregular ventricular rate.
• The QRS complex is usually the same as in sinus rhythm
although there may be occasional aberrancy.

61. Atrial Flutter
• Flutter waves, sawtooth p waves in lead 2, 3 avF (inferior leads)
• In neonate classic flutter waves might be absent.
• Positive and more discrete p waves in lead V1.
• Atrial rates of 300-600 with various degrees of aberrancy (BBB)
and physiological AV block.
• After conversion to sinus rhythm, recurrence of flutter is rare in
neonates with structurally normal heart.

62. Other Tachyarrhythmias
• Other types of supraventricular arrhythmias such as atrial
fibrillation or multifocal tachycardia are extremely rare in the
neonate.

63. Premature ventricular beats
• A premature abnormal QRS (not similar to the sinus QRS complex) that
is not preceded by a premature P wave.
• In infants, the QRS duration may be normal or slightly prolonged but if
the complex has a different morphology from the sinus, and is not
preceded by a premature P wave, the diagnosis is a premature
ventricular beat.
• The relationship between morphology and the site of origin is not exact
enough to be able to predict which ventricle is causing the arrhythmia.
• The QT interval should be measured carefully.
• 24-h Holter monitoring may be worthwhile.

64. Premature ventricular beats

65. Ventricular tachycardia
• It is a series of three or more repetitive complexes that originate from
the ventricles.
• The complexes are therefore different from the patient’s normal QRS;
usually, the QRS duration is prolonged for the age of the patient
(0·09 s or more in infants).
• ‘wide QRS’ tachycardia, the rate of VT 200–500 bpm.
• There may be a slight variation in the R-R interval over several beats.
There may be sinus P waves continuing unrelated to VT (AV
dissociation), retrograde P waves or no visible P waves.

66. Ventricular tachycardia

67. Potassium
• Potassium levels and changes in ECG:

68. Hyperkalemia
• Serum potassium > 5.5 mEq/L is associated with repolarization
abnormalities:
• Peaked T waves (usually the earliest sign of hyperkalaemia)
• Serum potassium > 6.5 mEq/L is associated with progressive
paralysis of the atria:
• P wave widens and flattens
• PR segment lengthens
• P waves eventually disappear

69. Hyperkalemia
• Serum potassium > 7.0 mEq/L is associated with conduction
abnormalities and bradycardia:
• Prolonged QRS interval with bizarre QRS morphology
• High-grade AV block with slow junctional and ventricular escape
rhythms
• Any kind of conduction block (bundle branch blocks, fascicular
blocks)
• Sinus bradycardia or slow AF
• Development of a sine wave appearance (a pre-terminal rhythm)

70. Hyperkalemia
• Serum potassium level of > 9.0 mEq/L causes cardiac
arrest due to:
• Asystole
• Ventricular fibrillation
• Pulseless Electrical Activity with bizarre, wide complex
rhythm.

71. Hypokalemia
• Hypokalaemia is defined as a potassium level < 3.5 mmol/L
• Moderate hypokalaemia is a serum level of < 3.0 mmol/L
• Severe hypokalaemia is defined as a level < 2.5 mmol/L
• Changes appear when K+ falls below about 2.7 mmol/l

72. Hypokalemia
• Increased amplitude and width of the P wave
• Prolongation of the PR interval
• T wave flattening and inversion
• ST depression
• Prominent U waves (best seen in the precordial leads)
• Apparent long QT interval due to fusion of the T and U waves
(= long QU interval)

73. Hypokalemia
• On worsening of Hypokalemia.
• Frequent supraventricular and ventricular ectopics
• Supraventricular tachyarrhythmias: AF, atrial flutter,
atrial tachycardia
• Potential to develop life-threatening ventricular
arrhythmias, e.g. VT, VF and Torsades de Pointes

74. Calcium
• Calcium disorders and changes in ECG:

75. Hypercalcemia
• The main ECG abnormality seen with hypercalcaemia
is shortening of the QT interval
• In severe hypercalcaemia, Osborn waves (J waves) may
be seen
• Ventricular irritability and VF arrest has been reported
with extreme hypercalcaemia

76. Hypocalcemia
• Hypocalcaemia causes QTc prolongation primarily by
prolonging the ST segment.
• The T wave is typically left unchanged.
• Dysrhythmias are uncommon, although atrial fibrillation
has been reported.
• Torsades de pointes may occur, but is much less common
than with hypokalaemia or hypomagnesaemia.

77. Thank You