This document provides an overview of heart failure in infants and children. It defines congestive heart failure and describes the pathophysiology, including compensatory responses. Signs and symptoms are outlined. Causes of heart failure are discussed by age, including common congenital heart defects and other etiologies like anemia or arrhythmias. Diagnosis, classification systems, and management options are also mentioned. The goal is to help medical professionals understand, identify, and treat heart failure in pediatric patients.

1. HEART FAILURE IN INFANCY A
ND CHILDHOOD
P2 Lecture
BY
Dr Arodiwe Ijeoma
29/10/16
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2. Outline
1. Definition
2. Pathophysiology
3. Signs and symptoms
4. Causes by age
5. Management – Various options
6. Communication
7. Summary
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3. Learning Objectives
1. Understand what HF is.
2. Identify a child with ccf
3. Apply the best treatment opti
on
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4. Definition
1. Congestive heart failure (CHF) refers to an
inability of the heart to pump as much blood as
required for the adequate metabolism of the
body tissues leading to a clinical state of
systemic and pulmonary congestion
2. Complex clinical syndrome.
Structural or functional cardiac disorder that impai
rs the ability of the ventricle to fill with or eject bl
ood
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5.  Clinical picture of CHF results from a combinatio
n of “relatively low output” and compensatory re
sponses to increase it
 It is a medical emergency that should be looked
for in every acutely ill child.
 The cardinal manifestations
1. Dyspnea and fatigue.
2. Fluid retention: Pulmonary/peripheral
edema.
3. Cardiomegaly
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6. Cardiac insufficiency state.
 Prof. Eichna in 1959.
Distinction between Circulatory Congestion (CC) &
CCF
CC is 2° to Noncardiac causes and CCF is 2° Cardi
ac causes (Myocardial failure).
 CC is the Hemodynamic disturbance associated with
CCF;
Removal of the Congestion relieves the symptoms.
: Includes so-called high output failure; Aneamia, Th
yrotoxicosis, Infections
Shock vs CCF??
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7. Cardiac insufficiency state.
 The term CCF is reserved for Circulato
ry congestion in which there is myocardial
failure.”
Basically
The implication is that in heart failure th
ere must be something structurally or func
tionally abnormal with the heart.
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8.  CCF a clinical diagnosis.
 There is no “gold standard” laboratory test
.
 A careful history is how one makes the di
agnosis.
 There should be some direct evidence of s
tructural heart disease.
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9. 1. Duration
- Acute or Chronic HF
2. Ventricular involvement
-RV HF, LV HF
or Biventricular (congestive) HF.
The latter is the commonest in infants and
young children.
3. Cardiac function affectation
- Systolic HF or Diastolic HF
Classification
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10. CLASSIFICATION
 NYHA Heart Failure Classification is not
applicable
 Ross Heart Failure Classification was
developed for global assessment of heart
failure severity in infants
 Modified to apply to all pediatric ages
 Modified Ross Classification incorporates
1. Feeding difficulties
2. Growth problems
3. Symptoms of exercise intolerance
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11. MODIFIED ROSS HEART FAILURE CLAS
SIFICATION FOR CHILDREN
Class I
 Asymptomatic
Class II
 Mild tachypnea or diaphoresis with feeding in infants
 Dyspnea on exertion in older children
Class III
 Marked tachypnea or diaphoresis with feeding in infants
 Marked dyspnea on exertion
 Prolonged feeding times with growth failure
Class IV
 Symptoms such as tachypnea, retractions, grunting, or diaphoresis
at rest
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12. Stages of Heart Failur
e
•This newer staging sch
eme is very clinically ori
ented.
•Target therapy in a mor
e focused manner towar
d specific subsets of pati
ents.
• Patients only progress
forward in this schema,
although occasionally pa
tients may go from D to
C.
Stages Definition
Stage A. Patients at risk of CCF.
Eg: HTN, DM, CAD.
Stage B Pt has structural heart disease ass
ociated with the development of C
CF but asymptomatic.
Eg CHD, DCM. Asymptomatic valv
ular heart disease.
Stage C Pts has current or prior sympt of
CCF associated with underlying str
uctural heart disease.
Stage D Marked symptoms of heart failure
at rest despite maximal medical th
erapy and who require specialized
interventions. Eg: Mechanical circ
ulatory device
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13. • Class 1- asymptomatic.
No limitation to ordinary physical
activity.
• Class 11- mild limitation of physical activity.
Unable to climb up stairs.
• Class 111- moderate/marked limitation.
Shortness of breath on walking on flat
surface.
• Class IV- severe limitation. Orthopnoea,
breathlessness even at rest. No
physical activity possible.
NYHA Functional classification
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14. What is the Path
ophysiology CC
F?
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15. Pathophysiology
 The Frank-Starling law,
With ↑ Preload (LV EDV), healthy heart ↑ C
OP until a max. is reached and cardiac output
can no longer be augmented (Fig. 1 ).
There is ↑ SV in the failing heart with ↑ed prelo
ad
But not the same level of maximal COP as N h
eart
At this point, Pulmonary Congestion develop
s: Tachypnea and dyspnea
and Systemic congestion: Hepatomegaly. I
ncr JVP, Leg oedema
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16. There are three major determinants of Heart function
1. Preload – Volume of blood stretching the LV just pri
or to contraction . A measure of this Left Ventricular End Diastoli
c Volume (LVEDV) is left ventricular filling pressure. (LVFP)
According to the Starlins law of the heart, with incre
asing LVFP, stroke volume increases until the critical LVFP (25m
mHg) is reached, beyond which stroke volume will no longer incr
ease. ( Fig 1 )
S. V.
FIG. 1∙
25 mmHg LVFP
Pathophysiology of HF
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17. 2. Afterload:
This is the resistance or impedance against which t
he heart must contract. A measure of this is the peripher
al vascular resistance (PVR). Stroke volume decreases wi
th increasing PVR , unlike with preload.
SV
PVR
FIG II
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18. 3. Contractility or inotropic state of the heart
This refers to the intrinsic ability of the heart mu
scle to contract independently of its external loa
d.
 Positive inotropic agents - digitalis. Isoproterenol
Adrenalin.
 Negative inotropic agents- propranolol. cardiac i
nsult, hypoxia, hypercapnia , acidosis
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19. Pathophysiology Contd
 In response to increased load
 Hypertrophy occurs that tends to normalize the lo
ad per cell.
 Myocytes elongate only and rarely divides.
 Reprogramming of the cardiac myocytes occurs, r
esulting in a more fetal-like response leading to an
increase in the size of the cardiac myocyte,
- Renders the surviving myocytes a short-
term structural and functional advantage.
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20. Compensatory Responses (C
R)
The failing heart activation 2 important neuro
hormonal mechanisms:
1. The Sympathetic Nervous System (SNS) .
2. The Renin-Angiotensin-Aldosterone System
(RAAS).
Attempt to preserve COP and thus are benefic
ial initially,
However Chronic stimulation is injurious to
myocardial function.
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21. Highlights on CR
 1. SNS:
↑ in sympathetic tone: 2° to ↑ adrenal secreti
on Epinephrine and ↑ neural release of Norepin
ephrine.
Initial beneficial effects
↑ HR and myocardial contractility with resulting
↑ in COP.
However chronic stimulation leads to adverse
myocardial effects,
Eg :↑ afterload, Hypermetabolism, Arrhythmoge
nesis, and Direct myocardial toxicity
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22. Catecholamines Toxicity
 Possible Mechanism
1. Produce calcium overload
2. Inhibition of the synthesis of contractile proteins.
3. High levels depletes β-adrenergic receptors on Myocar
dial surface.
→ functional loss of the catecholamine-mediated
positive inotropic response.
Clinically,
Reduction of adrenergic stimulation by the use of β-ad
renergic blockers
Leads to Improvement
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23. RAAS
 ↓ blood flow to the kidneys
1. ↑ in Renin
2. ↑ Angiotensin II/ Aldosterone.
3. Reabsorption of both water and salt
from the renal tubules.
4. Angiotensin II may cause a trophic res
ponse in vascular smooth muscle (va
soconstriction) and myocardial hypertro
phy.
5. Angiotensin II also promotes myocardial
fibrosis..
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24. RAAS
 Although
Adaptive by attempting to restore w
all stress to normal.
 In CHF Angiotensin II plays a malada
ptive role by initiating fibrosis and alt
ering ventricular compliance.
Thus,
Using β-adrenergic blockers and (ACE)
inhibitors in the treatment of CHF are to block
its maladaptive roles
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25.  When these determinants are deranged adaptive mech
anisms are called into play.
 These include :
1. Adrenergic mechanisms.
2. Renal mechanism and Atrial natriuretic protein.
(ANP & BNP).
3. Stimulation of IGF and GH
4. Ventricular dilatation/hypertrophy
ANP and BNP are hormones secreted by the heart/Brain in
response to volume and pressure overload that increas
e vasodilation and diuresis
Prevent inflammation, cardiac fibrosis and hypertrophy
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26. But when these fail, myocardial decompensa
tion result.
In the decompensation;
- Stroke volume is decreased
- LVEDP is increased
- Atrial pressure increased
- Systemic venous congestion &
- Pulmonary venous congestion occurs
Pathophysiology cont
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27. 29 October 2023 27
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28. 10 Disease or
Ineffective R
Effective Remodeling
Fig III- Scheme of pathophysiological
mechanisms leading to HF.
Impaired myocardial
contractility
Excessive work-load on heart
Adaptive or com
pensatory
response
Myocyte Loss
Myocardial Injury
Con
gestive Heart Failure
Remodeling of the Heart
Compensated state
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29. 29 October 2023 29
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30. CARDIAC REMODELING?
 Maladaptive cardiac hypertrophy
 Expansion of the Myofibrillar components of individual
myocytes (new cells rarely form)
 An increase in the myocyte/capillary ratio
 Activation and proliferation of abundant nonmyocyte
cardiac cells, some of which produce cardiac scarring
 Produce a poorly contractile and less compliant heart
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31. What is the Eti
ology of CCF?
(Causes by age)
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32. Etiology in Cong. Heart Dz
CCF by itself is not a diagnosis but a manifestation of an underlying
anatomical or pathological cause affecting the heart.
 AT BIRTH /NEONATES
1. Arrhythmia (SVT, VT, CHB)
2. Critical MS, TA,HLHS.
 INFANTS
A. Ventricular Volume Overload
Eg: ASD, ECD, PDA, VSD , TGA , TAPVR.
B. Systemic outflow obstruction (Pressure overload)
Eg: PS, AS, CoA.
C. Systemic inflow obstruction
Eg: MS, Pulm Veins obst, Cor-triatriatum
 CHILDHOOD.
RHD (AR, MR, MS,) Pulm Veins obst.
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33. Etiology in Normal Heart
 AT BIRTH /NEONATES
Eg: Anaemia, Asphyxial Cardiomyopathy & Large AV fistula
 INFANTS
Eg: Anaemia, Infection / Sepsis, Fluid Overload,
Hypoglyceamia, Hypothyroidism,
DCM, Carnitine Deficiency, Hypertension, Arrhythmia,
AV fistula.
 CHILDHOOD
Eg: RF/RHD, IE, Anaemia, Arrhythmia, Renal failure
Cardiomyopathy, Hypertension. Kawasaki synd
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34. Summary causes;- Severe anaemia*
- Severe pneumonia*
- Septicemia *
- CHD- ECD, VSD, PDA, TGA, TA *
- Acute hypertension e.g. AGN
- Supra ventricular tachycardia
(Tachyarrhythmias)
- Congenital heart block
- Endocrine disorders e.g.
hypothyroidism, hyperthyroidism
- Arterio-venous fistulae.
*commonest underlying causes in Nigeria and most parts of the tropics.
Aetiology of CCF cont
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35. CAUSES OF HF IN CHILDREN
CARDIAC
CHD
● Excessive Preload
● Excessive Afterload
● Complex CHD
NO STRUCTURAL ANOMALIES
● Cardiomyopathy
● Myocarditis
● Acquired valve disorders
● Hypertension
● Kawasaki syndrome
● Arrhythmia
(Bradycardia or tachycardia
NONCARDIAC
● Anemia
● Sepsis
● Hypoglycemia
● Diabetic ketoacidosis
● Hypothyroidism
● Other endocrinopathies
● Arteriovenous fistula
● Renal failure
● Muscular dystrophies
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36. Highlights on Etiology: CHD
 Onset of CCF varies predictably with the type of
defect
1. Vol. OL lesions
Eg: VSD, PDA, and ECD. causes of CHF in the fi
rst 6 mo.
NOT before 6 to 8 wks because the ↑PVR.
2. ASD rarely causes CHF , BUT OP ASD may caus
es CHF in adolescent.
3. TOF do not cause CHF unless they have receiv
ed a large a Gore-Tex interposition shunt (modi
fied Blalock-Taussig shunt).
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37. Highlights on Etiology: AHD
 The age at onset of CHF is not as predictable as with
CHD, but the following generalities apply:
1. Viral myocarditis tends to be more com < 1 year.
occasionally in the NB period, with a fulminating
clinical course with poor prognosis.
3. Kawasaki disease is seen in 1 - 4 yrs.
4. Acute Rheumatic Carditis causes CCF school-
age children.
5. RHD usually Vol OL lesions MR,AR cause CHF in
older children and adults.
These diseases are uncommon in industrialized
countries.
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38. Anaemia & DCM
 At any age, Low conc. of Hb may lead to a re
lative inability to degrade nitric oxide (NO) h
ypoxia
leading to the vasodilation that is so t
ypical of high-output heart failure.
 Low blood pressure may in turn activate neu
roendocrine activity.
DCM may cause CHF at any age.
Cause is idiopathic.
Others: Infectious, Endocrine, or Metabolic
disorders or Antineoplastic treatment (e.g., A
nthracycline & Doxo).
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39. What are the clinical m
anifestations (signs & s
ymptoms) of CCF?
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40. Clinical presentations
 Age dependent
 In neonates, the earliest clinical
manifestations may be subtle
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41. CLINICAL MANIFESTATIONS IN INFANT
S WITH HF
 Feeding difficulties
 Rapid respirations*
 Tachycardia*
 Cardiac enlargement*
 Gallop rhythm (S3)
 Hepatomegaly*
* common in older children
 Pulmonary rales
 Peripheral edema*
 Easy fatigability.*
 Sweating
 Irritability
 failure to thrive.
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42. 1. Significant tachycardia – resting HR, no fever
> 160/min in infancy
> 140/min at 2 years
> 120/min at 4 years
> 100/ min at 6 years and above.
2. Significant Tachypnoea –resting RR, no fever
> 60 cycles/min, 0- 1 month
> 40 “ >1mth- 24 mths
>30 “ >2-5 years
> 28 “ > 5-10 years
>25 “ >10 years
DIAGNOSTIC CRITERIA FOR CCF
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43. 3. Cardiomegaly.
• Displaced AB in the presence of a normally located trachea. Norm
al location of AB-4th left intercostal space, mid-
clavicular line in < 4yrs
--5th LICS, MCL in > 4yrs
• Cardio-thoracic ratio above the upper limit of normal for age
– 60% for children under 5 years
– 50% for children over 5 years.
4 Tender hepatomegaly of at least 3cm below the right subcostal m
argin in the mid- clavicular line.
• N.B—A clinical diagnosis of CCF can be made on the basis of presen
ce of at least 3 of the criteria, one of which must be criterion 3.
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44. • Systemic venous congestion results in:
- elevated jugular venous pulsation
- Hepatomegaly - tender and rapidly enlarging.
- Pedal oedema usually absent in infants and yo
ung children . Why?
- Peripheral cyanosis
• Pulmonary venous congestion result in:
- cough, tachypnoea, dyspnoea, grunt/ wheeze if se
vere , basal crepitations , recurrent apnoea in the ne
wborn
Clinical Features of HF
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45. • Low cardiac output and increased adrenergic driv
e leads to :
- tachycardia, apnoeic spells in new born,
- restlessness, cold extremities, cloudy sensorium
- Poor peripheral pulses / pulses alternans
• Fluid retention causes
-abnormal weight gain
- decreasing urinary output
Clinical Features cont
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46. Feeding difficulties & increased fatigabilit
y
Important clue in detecting CHF in infants
 Often it is noticed by mother
 Interrupted feeding (suck- rest -suck cycles)
 Infant pauses frequently to rest during feedings
 Inability to finish the feed, taking longer to finish each feed
(> 30 minutes)
 Forehead sweating during feeds –due to activation of
sympathetic nervous system –a very useful sign
 Increasing symptoms during and after feedings
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47. Tachycardia
 Rate is difficult to evaluate in a crying or moving child
 Tachycardia in the absence of fever or crying when
accompanied by rapid respirations and is
Cardiomegaly is indicative of HF
 Persistently raised heart rate > 160 bpm in infants
 > 100 bpm in older children.
 Consider SVT if heart rate > 220 bpm in infants and >
180 bpm in older children.
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48. Cardiomegaly
Consistent sign of impaired cardiac function,
secondary to ventricular dilatation and/or
hypertrophy.
On CXR a CT ratio of > 60% in the newborn and >
55% in older infants with CHF is the rule.
 May be absent in early stages, especially with
myocarditis, arrhythmias, restrictive disorders.
Noted as a displaced AB
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49. 29 October 2023 49
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50. Chest X ray
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51. Hepatomegaly
 Lower edge of the liver is palpable 1 to 2 cms
below right costal margin normally in infancy
 In the presence of respiratory infection increased
expansion of the lungs displace liver caudally
 Usually in such circumstances the spleen is
palpable
 Tender Hepatomegaly is a sign of CHF
 Decrease in size is an excellent criterion of
response to therapy
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52. Pulmonary crepitations (rales)
 Of not much use in detecting CHF in infants
 Rales may be heard at both lung bases
 When present difficult to differentiate from
those due to the pulmonary infection which
frequently accompanies failure
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53. Peripheral edema
 Edema is a very late sign of failure in infants and
children
 Presacral and posterior chest wall edema in young
infants
 It indicates a very severe degree of failure.
 Daily wt monitoring is useful in neonates -- rapid
increase in wt > 30 gm /day may be a clue to CCF and
is useful in monitoring response to treatment.
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54. Severe CCF
 Cold extremity, low blood pressure, skin mottling
are signs of impending shock
 Pulsus alternans (alternate strong and weak
contractions of a failing myocardium)
 Pulsus paradoxus (decrease in pulse volume and
blood pressure with inspiration) are frequently
observed in infants with severe CHF
54
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55. 1. PCV. WBC total and differential - baseline
- exclude anaemia and
sepsis possibly.
2. Electrolyte and urea - baseline and to exclude
hypokalaemia
3 Serum calcium - to exclude hypercalcemia
4. Chest radiograph - probably diagnostic
e.g. from
typical heart shape
- Underlying lung
pathology, Cardiomegaly
Investigations
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56. Investigation Cont’d
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57. What is Management principles of
CCF?
– Various options
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58. Aim of treatment is to reduce the load on the failing heart
and to restore myocardial contractility to normal.
A. To reduce preload
– Diuretics : fast acting diuretics e.g. frusemide. Ethacry
nic acid plus
supplemental potassium, if more than one dose of diuret
ic required.
– Reduce water intake 2/3 maintainance.
B. To reduce after load – only in intractable cases
– arteriolar vasodilator e.g. hydralazine,
– ACEI: Enalapril 0.1-0.5 mg/kg/day
– Captopril 6 mg/kg/day in divided doses.
Principles of Treatment of HF
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59. C. To improve cardiac performance
-Digitalis: Prototype of which is Digoxin: +Ionotropi
c & Neg Chronotropic
Note: Safety precautions and side effects
:ECG features of effect and of toxicity.
:NOT indicated in Anaemia HF?
- Dopamine preferred in infants with severe distr
ess or those with renal compromise
- Recently, low-dose β-adrenergic blockers has
been added, with encouraging results.
D. Treat specific underlying cause(s) e.g pneu
monia, Aneamia, or CHD
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60. MOA: DIGITALIS
 Special role in heart failure by
 ↑ contractility & depress SA node & AV no
de. Interacts with Calcium channels
 Its half-life of 36hrs, so given once or twic
e daily
 Initial effect can be seen within 30min aft
er oral administration and within 15min aft
er IV.
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61.  Digitalis
 oral: 0.04-0.06 mg/kg/day
 I.V.: 70-80% of oral dose
 Rapid/Slow (48hrs) digitalization
 May be performed over 12-24 hours.
 Calculate TDD administer 1/2 of TDD, followed
by 1/4, then 1/4 of TDD 6- 12 hours apart
 Maintenance digoxin is approximately 1/4 of TD
D, divided b.i.d., or 0.01 mg/kg per dose b.i.d.
 Case example: patient weight is 5.5
kg. What is the TDD
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62. Effiel Tower at Dusk
HELLO people are we
still on the same page
?
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63. Digitalis effect
 Prolongation of PR
 shortening of QTc
 sagging of ST segment
 slowing of heart rate
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64. Digoxin toxicity
 GI symptoms are common presenting symptoms: nausea
, vomiting, anorexia, colour blindness (older child)
 Most common sign of cardiac toxicity is arrhythmia: brad
ycardia, AV block, PVCs
 Treatment includes withholding doses.
 Atropine for sinus bradycardia.
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65. 29 October 2023
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Digoxin toxicity
- sinus bradycardia
- 2nd degree heart block
- supraventricular arrhythmias
- ventricular bigeminy/ trigeminy
(rare in children)
- premature ventricular
contractions
- ventricular tachycardia
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66. medications dosages
 Diuretics
 Furosemide (Lasix); 0.5- 4.0 mg/kg/dose
 Chlorothiazide (Diuril); 20-50 mg/kg/day
 Spironolactone (Aldactone); 2-4 mg/kg/day
 Afterload reduction
 Captopril (Capoten); 1-6 mg/kg/dose t.i.d.
 Enalapril (Vasotec); 0.1 – 0.5 mg/kg/day
 Beta-blocker
 Propranolol 2-4mg/kg/day
 Carvediolol 3.125-6.25mg/day
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67. E. Provide general supportive measures
- Bed rest in A cardiac position semiupright po
sition to relieve respiratory distress.
- Intranasal oxygen and 40-50% humidity.
Oxygen tents are ideal and far more
effective than nasal catheters.
- Daily weighing?
- Nasogastric tube feeding of fortified feeds
- Prostaglandin EI- to ensure patency of PDA
in duct-dependent CHD e.g. HLHS, CoA.
When surgically feasible, OHS for underlying
CHD and valvular heart disease is the best appr
oach for complete cure.
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68. SURGICAL AND DEVICE THERAP
Y
 Pacemaker and implantable defibrillator
therapy
 Biventricular pacing
 Ventricular assist devices
 Heart transplantation

69. GENERAL MEASURES: Calories
 Adequate calories should be provide
d to permit appropriate weight gain.
 Infants in CHF need significantly hig
her caloric intakes than recommende
d for average children.
 The required caloric intake may be a
s high as 150 - 160 kcal/kg/day for i
nfants in CHF.
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70. ?? Adequate calories
 cannot take in needed calories: tachypnea,
 increased work of breathing,
 diminished strength of sucking,
 and difficulty with coordination of sucking and s
wallowing.
a. Increasing caloric density with
fortification of feeding
b. Frequent small feedings are better
tolerated than large feedings in infants.
c. If oral feedings are not well tolerated cont
inuous (NGT) feeding is indicated.
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71. Communication
 In dealing with parents, it is preferable to
use words like “pulmonary congestion”, “li
ver congestion” rather than ‘heart failure”,
since “heart failure”, is likely to be misund
erstood by the parents and this may hamp
er useful interaction.
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72. Depends on
1. The underlying cause(s). Acute HF due to
severe Anaemia or Pneumonia if well trea
ted has a better prognosis than that in a child
with CHD/AHD which tends to recur.
2. Early diagnosis and treatment.
Non-recognition or delayed diagnosis of HF
is associated with increased mortality in eme
rgency paed units.
Prognosis
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73. Summary
 Heart failure is a complex clinical syndrome b
ut relatively straightforward to diagnose.
 Heart failure implies underlying structural an
d functional changes in the heart that contrib
ute importantly to the clinical syndrome.
 The pathophysiologic principles such as reduc
ed preload, afterload and augmentation of
contractility is employed in its treatment.
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74. 1. Oluwatoyin Ogunkunle. Heart failure in Childhoo
d in Paediatrics and Child health in a Tropical regi
on
2.Jaiyesimi F. Heart failure in infancy and early child
hood med digest 1981: 7 : 13-23
3. Olowu A.O. Studies on Heart Failure in Sagamu
NJP 1993: 20(2): 29-34
4. Jaiyesimi: Congestive Cardiac Failure in emergen
cy Paediatrics practice in Nigeria. Trop Cardiol 197
7: 3:9-14
References
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75. Review Questions
1a. List 6 possible causes of heart failure in
childhood.
b. Outline the pathophysiology of heart
failure.
c. Discuss the management of heart failure
in an 18mo old child.
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76. Doonu Ndi Banyi
God Bless You
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77. Cardiac Dysrrythmias
P2 Lecture
by
Dr Arodiwe ijeoma
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78. OUTLINE
 Introduction
 Brief review of ECG
 Abnormality of Rate
 Abnormality of Rhythm
 Conduction abnormality
 Summary
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79. Learning Objectives
 Recognize common pediatric cardiac arrhythmias
 Recognize early signs of clinical decompensation/
hemodynamic instability
 Initiate management of arrhythmias in the inpatie
nt setting
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80. Introduction
Arrhythmias
Abnormality of Rate, Rhythm & Conduction
of the electrical activity of the heart
Can be
- Physiological or Pathological,
- Congenital (WPW) or Acquired,
- Self-limited or life threatening.
For all of which ECG is essential in the diag
nosis ( Physiology of conduction system)
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81. Categories
 Arrhythmias
1. Sinus node (Rate) disorders:
Sinus arrhythmia, Sinus Brady & Sinus Tac
hy
2. Disorders of Rhythm: Ectopic Premature
beat (PAC, PVC)
Atrial flutter, Atrial Fib & Ventricular Fib
3. Conduction disorders: Heart blocks (1st -3
rd degree)
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82. CONVENTIONAL LEADS
1. Limb leads (frontal plane):
I, II, III, aVR, aVL, aVF
2. Chest (Precordial) Leads (horizontal
plane):
 Adults: V1, V2, V3, V4, V5 and V6.
 Children: V1 to V6, + V3R and/or V4R
82
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83. PLACEMENT OF ECG LEADS
83
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84. Placement of precordial leads:
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85. 29 October 2023
85
Placement of precordial leads:
 V1 : 4th R intercostal space, parasternal
 V2 : 4th L “ “ “
 V3 : exactly mid way between V2 and V4
 V4 : 5th L intercostal space, MCL
 V5 : same transverse level as V4, AAL
 V6 : “ “ “ “ “ V4, MAL
 V3R : corresponds to V3 on the Right side
 V4R : “ “ V4 “ “ Right side
 V1, V2, V3R and V4R - R ventricular activity
 V3, V4 (transitional) - septal activity
 V5, V6 - L ventricular activity
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86. 29 October 2023
86
COMPONENTS OF THE STANDARD ECG
In the standard ECG recording:
 Paper speed = 25mm/sec
 1 small square (horizontal) = 0.04 sec
 1 large square (horizontal) = 0.2 sec
 10mm (vertical) = 1 mV
 (Standardization)
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87. STANDARD ECG RECORDING
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88. 2
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89. 3
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90. 29 October 2023
90
COMPONENTS OF THE STANDARD ECG
R
Isoelectric lin
e
Height of R
Depth of S
QRS
QT
S
P
Q
T
PR
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91. 91
COMPONENTS OF ECG
 P wave = atrial depolarisation
 QRS complex = ventricular depolarisatio
n
 T wave = ventricular repolarisation
 PR interval = atrioventricular (AV)
conduction
 QRS interval = ventricular depolarisation
time
 QT interval = duration of ventricular
systole
(depolarisation + repolarisation)
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92. ECG analysis for arrhythmias
Analyse for
 1. Rate
 2. Rhythm
 3. PR Interval
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93. What are the Sinus node (Rate)
disorders?
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94. Normal ranges of HR
AGE Range(beat/min )
Birth 120 - 180
1-6mos 120 - 140
6-12mos 110 - 130
1-5years 100 - 120
6-10 years 90 - 120
10 – 15 years 60 -100
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95. 29 October 2023
95
RATE :
Age dependent – faster at birth, gradually slowin
g with increasing age thereafter.
How do we Calculate Rate?
1. Divide 300 by the number of large squares in s
uccessive R – R interval.
2. Divide 1500 by the nos of small squares
3. Multiply the number of R-R cycles in 6 large squ
ares (1.2 sec.) by 50.
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96
SINUS RHYTHM
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97. Sinus arrhythmia
 Most common irregularity of heart rhythm
seen in children
 Normal variant of beat to beat variation.
 Reflects healthy interaction between auton
omic, respiratory and cardiac control activ
ity in CNS
 Heart rate increases during inspiration and
decreases during respiration.
 It requires no treatment.
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98. 29 October 2023
98
SINUS ARRHYTHMIA
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99. Sinus Bradycardia - Symptoms
 HR is lower than the expected for age
 Normal in Athletes/during sleep
 General: Fatigue, lightheadedness, dizzines
s, syncope
 Hemodynamic instability: Hypotension, poor
end-organ perfusion, respiratory distress/fai
lure, sudden collapse/death
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100. Sinus bradycardia - Causes
1º Abnormal pacemaker/conduction system
(congenital or postsurgical injury), cardio
myopathy, myocarditis
2º: Reversible Hs & Ts:
 Hypoxia – Hypotension – H+ ions (acidosis)
 Hypothyroidism – Hypothermia – Hyperkalem
ia
 Trauma (head) ↑ ICP
 Toxins/drugs (Ca++ channel blockers, β-adrenergic bloc
kers, digoxin, opioids)
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101. Sinus Bradycardia
Sinus bradycardia
 Asymptomatic: No treatment
 Symptomatic: Chronotropic drugs
- Atropine 0.1 – 0.5ug/kg
- Isoproterenol
- Cardiologist evaluation
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102. 29 October 2023 102
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103. Sinus Tachycardia (ST)
 HR > upper limit for age but not more 220
bpm (SVT)
 Causes –
- Physiological compensation rapid
discharge from S.A: Crying, Pain, Anx
iety and Exercise.
- Pathological events: Fever, shock,
fever, , hypoxia, H.F. , anemia
-Drugs: Atropine, adrenaline or the
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104. ST
 ECG shows a discernable P wave followed
by a QRS. While in SVT the P wave is not
recognizable.
 Treatment is directed towards the cause.
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105. 29 October 2023 105
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106. Supraventricular tachycardia: SVT
 Most common in pediatric practice
Requiring treatment. HR > 220bpm
Commonest has an assessory pathway in the atri
a. (Retrograde activation of the atria)
 Impulse comes from above the ventricles and co
nducted normally
 Presentation: 1st Infancy , 2nd peaks @ in adole
scense
 Rapid, regular, normal narrow QRS, P wave not
discernable but 1:1 with QRS.
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107. SVT
Figure 5-42 Supraventricular tachycardia. Note a normal QRS complex tac
hycardia at a rate of 214 beats/minute without visible P waves.
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108. SVT
 Causes: Unknown
 WPW Syndrome
 CHD: Eg Ebstein”s anomaly, cTGA
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109. SVT: Symptoms
 Older kids can describe a sensation of a fa
st heart rate, palpitations, or chest tightne
ss. Rarely present in CHF?
 Infancy: Poor feeding, irritability, tachypne
a excessive sweating, CHF.
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110. SVT - Treatment
Goal: identify unstable patient and terminate the rhyth
m
Options
1. Trial of Vagal maneuvers in stable patients: Mass
age of carotid sinus (one side at a time), Gag reflex
or using ice park on the face 15-20s. Parasympat
hetic stimulation ↓ HR
2. DOC: IV Adenosine
 Stop conduction through AV node
 0.1 mg/kg (max 6 mg), repeat 0.2 mg/kg ( max 12 m
g) with Saline flush
 Digoxin give TDD stat. IV preferable (Slow onset)
3. Critically ill: DC Cardioversion with 1-2 j/kg
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111. SVT - Treatment
 WPW syndrome ( 25 % pts with SVT)
 Radiofrequency catheter ablation of the accessory pa
thway
 Frontline treatment, Very effective (total cure)
 Cutoff points usually are 5 yrs and 15 kg, unless severe SV
T
 Long term Medications
1. Digoxin 0.05mg /kg for about 1 yr. and beta blockers as
first line
 Amiodarone
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112. Electrophysiology(EPs)/PMs
Arrhythmias. Unresponsive to drug
1 1°or 2°(postop) arrhythmias.
2. SVT: High-frequency ablations
of aberrant /Automatic
ectopic atrial foci.
3. Highly sophisticated miniaturized
PMs with long life span: for the
smallest infants with heart block.

113. What are disorders of Rhythm
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114. Disorders of Rhythm
 Ectopic (Premature) beat: Originate from
other site other than the SA. Occur earlier
than expected on ECG.
 Presents as regular irregular/ irregular irre
gular beat
 Types
 a. Premature atrial contraction (PAC)
b. Premature Vent. contraction (PVC)
c. Atrial flutter/ d. Atrial Fibrillation
e. Ventricular Fibrillation
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115. Ectopic (Premature) beat
a. PAC
1. P wave is different from a
sinus P wave followed by a
normal PR & QRS complex
2. Benign: Stop with exercise.
3. Some caused by structural
heart dz (SHD)/ Digoxin
4. No treatment needed
except caused by SHD
b. PVC
 No P wave with Abnormally
wide ORS and inverted T
wave.
 Unifocal or Multifocal.
Unifocal has same ORS
morphology.
 Bigeminy: Sinus beat
followed by PVC, repeating
as a pattern
 Treatment: Unifocal
requires none. Multifocal
 IV Lidocaine, Propranolol
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116. Isolated PAC/ PVC

117. 10/29/2023

118. 4

119. Review Question
 1. which of these is a rate disorder.
a. PAC,
b. Atrial flutter
c. Sinus bradycardia
d. Ventricular fibrillation
e Heart block.
2. Cardiac arrthythmia can be benign. Justif
y these statement with examples. How will
you manage PAC.
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120. Rhythm Disorders: Atrial flutter
 Atrial rate 200-300bpm, with regular and undul
ating wave forms stimulating “sawtooth”
 Variable AV conduction 2:1,3:1,4:1 block resultin
g in slow ventriclar
 Causes: DCM, Myocarditis, Digoxin toxicity Post
Surgery: Fontan, Atrial Switch (TGA)
 Treatment: Digoxin (toxicity) Withhold drug use
DC cardioversion to NSR
Add Propranolol after TDD.
Maintain with Digoxin
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121. 29 October 2023
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122. Rhythm Disorders: Atrial fibrillation
 Rare in children.
 Atrial rate so fast > 450bpm irregular irre
gular.
 The P wave is not easy to discern but the
ORS complex is normal
 Causes: Severe MS with Dilated LA, & Hyp
ertrophic subaortic stenosis
 Treatment: Digoxin Add Propranolol after
TDD. Maintain with Digoxin
 DC cardioversion to NSR
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123. 29 October 2023
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124. Rhythm Disorders: Ventricular Fibrillation
 Bizarre ORS Complexes. With waxy lines of vary
ing sizes.
Rapid Rate with no palpable peripheral pulses: Te
rminal event in patient with cardiac arrest Cause
s: long QT syndrome, Brugada syndrome – inher
ited Arrhythmia, Autosomal Dominant.
Child goes into V-fib, faints, sudden dea
th
Cardiomyopathies, SHD causing ventricular dysf
unction.
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125. 29 October 2023 125
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126. V-fib
Treatment: Immediate DC Defibrillation,
Cardioversion to NSR.
Start CPR
IV Lidocaine or Procainamide
Careful screening
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127. What are the conduction disorder
s? (CDs)
Heart blocks (1st -3rd degree)
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128.  CDs there is a Delay or Interruption
in transmitting the impulse from the SA
node to the AV – node or to the termin
al branches
ECG: Prolonged PR interval
1st degree heart block
2nd degree heart block
- Mobitz type I (Wenckebach).
- Mobitz type II
3rd degree (complete) heart block
(AV Dissociation)
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129. PR INTERVAL
a. The normal is age and heart rate depen
dent.
Usually
0.08 – 0.16 sec Infancy - 1 year of age
ECG = (2- 4 small squares)
0.10 - 0.18 sec older child
ECG = 2.5 – 4.5 small sq
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130. First degree Block
 PR interval > normal for age.
 The ECG is otherwise normal, No heamod
ynamic consequence.
 Causes: ARF, Myocarditis, CHD: ASD, Ebs
tein’s anomaly and digoxin toxicity
 Treatment: Resolves with treating the cau
se.
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131. First degree block:
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132. 2ND Degree HB
1. Mobitz I (Wenckebach Phenomenon)
2. Mobitz II.
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133. Mobitz 1: There is a progressive prolongation PR,
Untill the P wave is not conducted = dropped ventr
icular beat. Benign
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134. 10/29/2023 OO OGUNKUNLE 134

135.  Mobitz type II:
 There is an unpredictability about the dro
pped P wave.
 So called “All or none” phenomenon
-The ECG has normal PR interval & - QRS complex
or it is completely block
 It is serious than type one and can progress to
3rd dgr
Rare in children & needs Cardiologist
evaluation
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136. Mobitz Type II
10/29/2023 OO OGUNKUNLE
136

137. 3rd Degr HB
 Complete HB
 There is a complete dissociation between the P
wave and the QRS complex.
 The atrial rate and the ventricular rate are regul
ar but different with the latter being slower
 Causes: L-TGA, Infant of mother with SLE, Surgi
cally induced HB,
 Presentation: Asymptomatic or in CCF
 Treatment: Treat the cause
Epicardial/Transvenous Pacemaker
insertion
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138. 10/29/2023 OO OGUNKUNLE 138

139. References /WEBSITES
1. Okoroma EO. Cardiac Arrhythmias in Paediatrics and
Child health in a tropical region. Eds Azubuike and
Nkanginieme 2007
2. ECG Interpretation. Donna Thomas http://www.ceufa
st.com/courses/viewcourse.asp?id=239
. 3. Pediatric EKG Interpretation
http://www.utmb.edu/pedi_ed/core/cardiology/page_
04.htm
4. Okoroma EO, Aghaji MAC. Congenital complete hea
rt block, treatment by pacemaker implantation in a thr
ee mo old Nigeria child. Cardiol Trop. 1987.
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140. ALL THE GRACE OF GOD
& THANK YOU FOR LISTENING!
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