Pediatric Cardiology - for medical students

By: Asmaa Usama Nagi
Pediatric
Cardiology

1-Chromosomal & genetic factors As Down syndrome & Turner
2-Environmental factors CRS
Maternal diabetes
Drugs…
3-Hereditary factors If a parent or a sibling has CHD,
the risk is increased.

Classification
According to the physiology of the lesion.
Acyanotic
Stenotic lesions: AS, PS.
Shunt lesions: ASD, VSD.
Cyanotic
With ↑Pulmonary BF
With ↓ Pulmonary BF
VSD
ASD
PDA
PS
AS
CoA
TOF
TGA
Eisenmenger S

PS **infundibular type.
It causes severe ☒
Large VSD Of membranous type.
Beneath the aortic valve.
Together with PS  ↑↑ RV pressure.
Overriding aorta Receives blood from both ventricles.
Blood passes from RV to aorta to avoid PS
 Rt to Lt shunt & cyanosis.
Pulmonary aa. Become hypoplastic.
RVH Secondary to ☒ of right outflow tract.
Description

Cyanosis Develops over the next few weeks or
months after birth.
Clubbing of fingers & toes.
Dyspnea on exertion & easy fatigability.
Growth failure.
Squatting position: to ↓↓ return of unsaturated blood
from the LL to the heart.
☒ of femoral a. → ↑↑ aortic pressure ,thus
decreasing the RT to LT shunt.
Cyanotic spells Hypoxic, blue or tet spells.
Spasm of pulmonary infundibulum
±↓systemic VR → ↓Pulmonary BF
→episodes of deep cyanosis &
dyspnea.
The murmur of the PS disappears
during the spell.
Convulsions, unconsciousness &
even death.
RV heave but no
cardiomegaly.
Palpable thrill over the
pulmonary area.
Single S2
Harsh ejection systolic
murmur over the
pulmonary area due to
PS.
Or pansystolic murmur,
due to blood turbulence
over RV outflow tract.
Cyanosis is variable
~ absent (pink Fallot).
Clubbing of fingers &
toes.
Tachypnea.
Symptoms Signs

RV heave but no cardiomegaly.
P Palpable thrill.
Murmur of
PS
VSD murmur
Single S2
Harsh ejection systolic murmur.
Or pansystolic murmur
Cyanosis is variable
Tachypnea.
Signs

Chest X ray
Normal heat size.
Due to RVH Apex is raised above the diaphragm.
Characteristic “Cœur en sabot”
Or boot shaped heart.
Lung fields Oligemia
Aorta Large ascending aorta.
Right aortic arch (25% of cases)
Pulmonary
segment
Concavity.
ECG: RVH ± RA hypertrophy.
Echo Doppler: confirms the Dx.
Cardiac cath

DDx
Other causes of cyanotic CHD.
1-Pulmonary atresia.
2-Tricuspid atresia.
3-TGA
4-Truncus arteriosus.
5-TAPVR
5-Eisenmenger syndrome.

Complications
CHF Extremely rare
Cerebral thrombosis Due to polycythemia
May lead to hemiplegia or coma.
Bacterial endocarditis
Brain abscess Due to lack of filtering effect of
the pulmonary circulation
Death Due to cyanotic spells.

ttt
Cyanotic
spells
AKA: Hypoxic, blue or tet spells.
Convulsions, unconsciousness & even death.
The murmur of the PS disappears during the spell.
1- Put the child in knee-chest position.
2- O2 administration.
3- Morphine sulphate.
4- IV β blockers (Propranolol)
5- IV NaCHO3 if there’s acidosis;
6- IV fluid replacement & volume expansion.
~~ General anesthesia 
Prepare for surgery.

Surgical
Palliative Total correction
Systemic a. to PA shunt Closure of VSD &
resection of the RV
outflow and
enlargement of the
area with patch if
necessary.
Medical ttt
1-ttt of cyanotic spells
2-ttt of polycythemia. Repeated phlebotomy.
3- ttt of IDA Iron
4- β Blockers Oral,, to avoid spells.
5- IV PGE1 To keep the duct patent &
augment pulmonary flow.
Prophylactic ttt
As VSD

Description
• The aorta arises from the RV.
• PA arises from the LV.
Associated anomalies e.g. ASD, VSD, PDA & PS.
CHF
Differential
cyanosis

Systemic
(non-Oxygenated)
Blood is recirculated through the body
without oxygenation.
Pulmonary
(Oxygenated)
Blood is recirculated through the lungs.
A lesion that allows
mixing of systemic
& pulmonary blood.
e.g. ASD, VSD, PDA
Is necessary for survival.

Systemic
(non-Oxygenated)
Blood is recirculated through the body
without oxygenation.
Pulmonary
(Oxygenated)
Blood is recirculated through the lungs.
A lesion that allows
mixing of systemic &
pulmonary blood.
e.g. ASD, VSD, PDA
Is necessary for survival.
Symptoms
Cyanosis Shortly after birth.
Differential cyanosis if PDA is present.
RD, easy fatigability & feeding difficulties.
Polycythemia & hyperviscosity.
CHF *** if associated e VSD
Signs
Cyanosis Is marked
with small mixing lesions.
RV heave e RVH
Polycythemia **Older infants.
Soft flow murmur.
or pansystolic murmur (VSD).
Single S2
~Signs of pulmonary HTN

Chest X ray
Slight cardiomegaly
Cardiac base: narrow Due anteroposterior
arrangement of the great
arteries.
RVH
Characteristic “egg on its side” shape of the heart.
Lung fields Plethoric
ECG: RVH ± LVH.
Echo Doppler: demonstrates the
arterial transposition & detects
the degree of mixing.
Cardiac cath
TGA

Chest X ray
Slight cardiomegaly
Narrow cardiac base Due anteroposterior
arrangement of the great
arteries.
RVH
Characteristic “egg on its side” shape of the heart.
Lung fields Plethoric

DDx
Other causes of cyanotic CHD.
1-Pulmonary atresia.
2-Tricuspid atresia.
3-TOF
4-Truncus arteriosus.
5-TAPVR
5-Eisenmenger syndrome.

Complications
1. Hypoxemia & polycythemia.
2. Pulmonary HTN
3. CHF: occurs early
** if associated e VSD.

Surgical
Arterial switch
procedure
Arterial switch
procedure
With coronary a.
reimplantation.
……
Medical ttt
1-ttt of HF
3- ttt of IDA Iron
4- Correction of acidosis & electrolyte disturbances.
5- PGE1 infusion To keep the PDA opening to
help blood mixing.
Prophylactic ttt
As VSD & TOF
Catheter Balloon arterial septoplasty
By rupturing the arterial septum
in the catheterization lab.
To create an ASD to
help mixing of blood.

Medical ttt
1-ttt of HF
3- ttt of IDA Iron
4- Correction of acidosis & electrolyte disturbances.
5- PGE1 infusion To keep the PDA opening to
help blood mixing.
Catheter Balloon arterial septoplasty
By rupturing the arterial septum
in the catheterization lab.
To create an ASD to
help mixing of blood.

TGA Is marked
with small mixing lesions.
TOF Cyanosis is variable

Other cyanotic CHD
Hypoplastic LV
Hypoplastic RV
Single ventricle
Double outlet RV
 Truncus
arteriosus.
 TAPVR
 Tricuspid
atresia

Reverse or bidirectional shunt through
VSD, ASD, PDA or AV canal
as a result of Pulmonary vascular obstructive disease.
Anatomical defect → Lt to Rt shunt →Increased Pulmonary BF
→Pathological changes in the wall of small pulmonary
arterioles → thickening → increased pulmonary VR→
pulmonary HTN RT-to-Lt (reversed) or bidirectional shunt !!
Symptoms Signs
Onset: ** 2nd - 3rd decade.
Cyanosis becomes
apparent & progressive.
Symptoms of CHF.
Symptoms of LCOP.
RVH
S2: loud, closely split or single.
Diastolic shock over P
Graham Steel murmur,,
Due to functional PI.
Soft ejection systolic murmur followed by a
blowing early diastolic murmur

tttInv.
Prevention
ttt of extracardiac complications as
polycythemia, anemia, thromboembolism,
infections & growth failure.
Combined heart
lung transplantation
Single lung
transplantation.
Polycythemia.
Chest X ray:
Cardiomegaly (RVH & RAH)
Enlarged PA & hilar pulmonary
vessels.
Normal or slightly increased
pulmonary vasculature.
ECG: marked RVH.
Echocardiography.
Cardiac cath

Marked RVH
Enlarged PA
Increased
vasculature.

Definition
Symptoms Signs
tttInv
Hemodynamics

Incidence
Site of
defect
Description
The ** CHD.
25-30%
Membranous Muscular
Common
Single defect
Less common
Single or multiple.
Perimembranous
VSD????

Pathophysiology
Size of the defect.
Degree of pulmonary resistance.
Depends on
Symptoms
Signs
Small defect Large defect
1. Dyspnea on exertion then at rest.
2. Excessive sweating during feeding.
3. Repeat LRTI.
4. Failure to thrive.
Systolic thrill at LLSR.
Harsh pansystolic murmur at 3rd & 4th left ICS.
 Prominent precordium
 Cardiomegaly with laterally
displaced apex.
 Functional flow murmurs:
On mitral area; mid diastolic.
On pulmonary area: ejection systolic.

Symptoms
Small
defect
Large defect
1. Dyspnea on exertion then at rest.
2. Excessive sweating during feeding.
3. Repeat LRTI.
4. Failure to thrive.

Signs
Systolic thrill at LLSR.
Harsh pansystolic murmur at 3rd & 4th left ICS.
 Prominent precordium
 Cardiomegaly with laterally displaced
apex.
 Functional flow murmurs:
On mitral area; mid diastolic.
On pulmonary area: ejection systolic.

Chest X ray
1. Cardiomegaly.
2. Prominent pulmonary a.
3. Lung plethora.
ECG: Biventricular hypertrophy.
Echo: Demonstrates the size of the
defect & blood flow.
Cardiac
catheterization:
Necessary to assess size of the
shunt & pulmonary pressure.
VSD

Complications
Failure to thrive.
Repeated LRTI
HF
IE
Arrythmias.
Pulmonary HTN
~Eisenmenger syndrome .

DDx
Other causes of pansystolic murmur
MR
TR
PDA with pulmonary HTN.

Fate of VSD
Spontaneous closure Of small defects
>60% of cases ^^.
Relative closure ‫يكرب‬ ‫القلب‬ ‫ما‬ ‫لك‬ ‫جحمه‬ ‫بيقل‬
Pulmonary HTN & Eisenmenger S 

Surgical
In cases of large
defect
Before Pulmonary vascular
changes become irreversible
(Eisenmenger S).
Medical ttt
In case of small defect.
Follow-up & ttt of complications as HF & RTI…
Prophylactic ttt
Against IE.
Device closure of VSD through cardiac cath.
‫وجديدة‬ ‫أل‬ ‫حلوة‬

Device closure of VSD through
cardiac cath.

Incidence
Description
7-10 % of all CHD
Ostium
secundum
Ostium
premium
Sinus
venosus
early
surgery

Pathophysiology
The degree of left to right shunt
depends on the size of the defect.
Symptoms
Signs
No symptoms. 1. Dyspnea.
2. Easy fatigability.
3. Repeat chest infections.
4. Low weight gain.
 RVH; left parasternal lift!
 S2 over the pulmonary area:
characteristic sign of wide splitting
and fixed in inspiration & expiration..
 Soft ejection systolic murmur on the
pulmonary area.
Due to ↑↑ pulmonary blood flow.

Chest X ray
1. Enlarged RV.
2. Large pulmonary conus.
3. Lung plethora.
ECG: RV or Biventricular
hypertrophy.
±RBBB
Echo: It’s diagnostic…
Cardiac
catheterization:
ASD

Fate of ASD
Spontaneous closure Is rare 
HF occurs during infancy,
childhood or adulthood.
According to the type of ASD

Surgical
Should be done early in cases of
ostium premium defects.
Medical ttt
In case of small defect.
Prophylactic ttt
Against IE.
Device closure of ASD through cardiac cath
‫تاني‬

Device closure of ASD through
cardiac cath.

PDA is a persistent opening between the two major blood vessels.
The opening, called the ductus arteriosus, is a normal part of a
baby's circulatory system before birth that usually closes shortly
after birth
Pathophysiology
Thus, a (PDA) produces a left-to-right shunt. In other words, it allows blood to go from
the systemic circulation to the pulmonary circulation.
Therefore, pulmonary blood flow is excessive .
Pulmonary engorgement results with decreased pulmonary compliance.
The reaction of the pulmonary vasculature to the increased blood flow is unpredictable.

Symptoms
Signs
Small PDA Large PDA
No symptoms. 1. Failure to thrive.
2. Repeated chest infections.
3. LSHF in severe cases.
4. When pulmonary HTN develops, the
shunt is reversed to become right to left
& dyspnea & cyanosis develop.
Loud S2
Continuous (or systolic!)
machinery murmur
on 2nd left ICS ,
radiating to left clavicle & LSB.
Thrill continuous or systolic at P.
Pulse pressure: wide (low DBP).
in cases of big PDA. Cardiomegaly
with dynamic LV apex.

Signs
Pulse pressure: wide (low DBP).
In cases of big PDA. Cardiomegaly
with dynamic LV apex.
Thrill continuous or systolic at P.
Loud S2
Continuous (or systolic!)
machinery murmur
on 2nd left ICS ,
radiating to left clavicle & LSB.

Chest X ray
1. Enlarged LV.
2. Prominent pulmonary a.
3. Lung plethora.
ECG: Normal or shows:
LV or Biventricular
hypertrophy
Echo: Very useful in Dx
Cardiac
catheterization:
PDA

Fate of PDA
Spontaneous closure of big PDA
after the first few days of life
Is extremely rare  
Early
complications
In large PDA

DDx
Other causes of continuous murmur
A-V fistula
Double MV lesion
AP window

Surgical
Should be done very early to prevent complications.
Medical ttt
Indomethacin
Prophylactic ttt
Against IE.
Device closure of PDA using coils or devices
Is the preferred ttt in many centers.

Description
Valvular
stenosis
Infundibular
stenosis
Fused pulmonary
commissures.
Domed valve
With small central
opening.
Post stenotic dilatation of
the main pulmonary a.
Hypertrophy of the
muscular outflow tract of
the RV (infundibulum)
leading to ☒ of flow.

Infundibular stenosis
Hypertrophy of the muscular outflow
tract of the RV (infundibulum) leading
to ☒ of flow.

Pathophysiology
↑RV pressure to maintain COP.
~↑RA as well  right to left shunt across patent foramen ovale.

Symptoms
Signs
In most cases In severe cases
No symptoms. 1. Exertional dyspnea & fatigue.
2. Exertional chest pain.
3. RSHF.
PS
Systolic thrill & RV heave in severe cases.
Diminished P2 (single S2 in severe PS).
Ejection click & harsh ejection systolic murmur over P.
In critical PS, cyanosis & gallop rhythm develop.

Chest X ray
1. Post-stenotic dilatation of
pulmonary a. (in valvular type.)
2. Oligemic lung fields
3. ±Enlarged RV& RA.
ECG: RVH
Echo: Important for Dx
& measurement of
pulmonary valve gradient.
Cardiac
catheterization
PS

DDx
Other causes of ejection systolic murmur
 AS
 CoA
 ASD
 Pulmonary HTN

Prognosis
of PS
Mild degree Compatible with long life.
Severe degree HF before middle age. 

Surgical
Pulmonary valvotomy.
Medical ttt
~Propranolol in some cases with infundibular stenosis.
Follow-up & ttt of complications.
Prophylactic ttt
Against IE.
Catheter Balloon dilatation
If pulmonary valve gradient >60 mmHg
Is very successful and now considered standard ttt.

Description
Valvular Subvalvular Supravalvular
Aortic valve is bicuspid.
Cusps are fused at their
edges  stenosis.
Fibrous ring around the
LV outflow tract.
Narrowed ascending aorta
above the valve.
Echo

Description
Valvular Subvalvular Supravalvular
Aortic valve is bicuspid.
Cusps are fused at their
edges  stenosis.
Fibrous ring around the
LV outflow tract.
Narrowed ascending aorta
above the valve.
Aortic
valvotomy
Resection
of subaortic
membrane
Echo

Pathophysiology
↑LV pressure to maintain COP.
LVH occurs.

Symptoms
Signs
In most cases In severe cases
No symptoms. Few symptoms
1. Anginal pain.
2. Dizziness, fainting,
loss of consciousness on effort.
3.~CHF.
AS
Low SBP & pulse pressure.
Cardiomegaly with prominent LV impulse.
Systolic thrill palpable at the LLSB, suprasternal
notch & along neck veins.
A2:diminished & delayed
Harsh ejection systolic murmur On A1 or A2 .
Transmitted upwards to the neck.

PDA Wide pulse pressure low DBP
AS Low Pulse pressure. Low SBP

Chest X ray
1. Post-stenotic dilatation of aorta
(in valvular type.)
2.LVE
ECG: LVH
LV ischemia indicates
severe AS.
Echo: LVH
Bicuspid valve
Supravalvular or subaortic stenosis
Post stenotic dilatation.
Pressure gradient across the valve.
Cardiac
catheterization
Can detect site of obstruction
Accurate pressure gradient measurement.
Calculation of valve area.
AS
Exercise
ECG

DDx
Other causes of ejection systolic murmur
 PS
 CoA
 ASD
 Pulmonary HTN

Complications
HF
IE
Sudden death on vigorous exercise 

Surgical
Aortic
valvotomy
For valvular stenosis.
Resection
of subaortic membrane
For subaortic stenosis.
Medical ttt
In cases of HF.
Prophylactic ttt
As VSD
Avoidance of competitive sports.
Balloon dilatation in cardiac catheterization lab
May be successful.

Description
It’s a narrowing of a
segment of aorta, of
variable degrees.
Mostly (98%) located
below the origin of left
Subclavian a.,,
at the origin of ductus
arteriosus.

Pathophysiology
Coarctation is a mechanical ☒ between proximal & distal aorta.
The pressure in proximal aorta and LV is elevated,,
whereas that of distal aorta is decreases.
 Collateral vessels including internal mammary a. & intercostal
vessels develop in response to the pressure difference.

Symptoms
Signs
In most
cases
In severe cases
No symptoms. ~leg cramps, chest pain , headache.
HF 10%
May occur in the
1st few days of life.
May present with
a complication
Bacterial endocarditis
Rupture of intracranial
aneurysm
UL LL
Normal brachial pulse. Weak or absent femoral pulse.
BP is higher (~HTN) Lower BP
Collateral vessels. may be visible or palpable around the
scapula.
LVH with forcible apex beat.
Ejection systolic
murmur
over the A1 & A2 , also heard on suprasternal
notch & interscapular area.
HF may be the only presentation in neonates.

Reversed BP gradient in
Limbs at any age
+
Absent or weak femoral
pulse.
Dx of CoA

Chest X ray
Notching
1. Of aortic shadow at site of Coarctation &
post stenotic dilation of aorta.
2. Ribs :due to erosion by the dilated
intercostals.
3. Barium filled esophagus: by dilated aorta to
form an “E” shape.
ECG: Normal.
LVH.
Echo: LVH
Coarctation segment
Pressure gradient can be measured.
Other associated anomalies as bicuspid or MV
anomalies.
Cardiac
catheterization
Site of coarctation.
Accurate pressure gradient.
Adequacy of collateral vessels.
CoA

DDx
 Other causes of HTN.
 Other causes of HF in neonates.
 Other causes of ejection systolic murmur
e.g. AS, PS, ASD, HOCM.

Surgical
Resection with end-to-end anastomosis
or graft repair.
Medical ttt
ttt of HTN.
ttt of HF.
Prophylactic ttt
As VSD.
Balloon dilatation
In cardiac cath lab.
Successful with variable degrees..

Epidemiology
Rheumatic fever occurs at all ages except infancy but incidence peaks
between 5-15 years (when GAS infections are most frequent).
It is still the leading cause of acquired heart disease in children in the developing countries
Rheumatic fever is an inflammatory disease involving
mainly the heart& joints
and less frequently the CNS, the skin and SC tissue.
It is always potentially serious as it may lead to permanent cardiac damage
(chronic valvular disease).
Etiology
Both initial and recurrent attacks are non-suppurative complications of
group A β hemolytic streptococcal (GAS) URTI.
Skin infections usually lead to acute GN but rarely, if ever to ARF.

Low-Risk
populations:
High-Risk
populations:
Those with incidence ≤2 per
100,000 school-age children
per year or all-age rheumatic
heart disease prevalence of
≤1 per thousand population.
Those with incidence >2 per
100,000 school-age children
per year or all-age rheumatic
heart disease
Include virtually all of the
United States, Canada, and
Western Europe.
prevalence of >1 per thousand
population.
and most developing countries.

Diagnosis of RF
Evidence of a preceding GAS infection:
1- Positive throat culture for streptococci.
Or rapid antigen test.
2 - Elevated and/or rising ASO titer.
3- Raised other streptococcal antibodies: Antideoxyribonuclease B.
The Dx of acute rheumatic fever should not be made in those patients with
elevated or increasing streptococcal Ab titers who do not fulfill the Jones criteria.

anti-DNase b test
For Dx of streptococcal infection

A. For all patient populations with evidence of preceding GAS infection
Clinical manifestations and Dx
Initial ARF Recurrent ARF
2 major criteria,
1 major and 2 minor,
2 major,
Or 3 minor
Revised Jones Criteria for
diagnosis of Rheumatic Fever

Low risk populations Moderate and high-risk
populations
•Clinical and/or subclinical carditis
•Polyarthritis only
•Monoarthritis or polyarthritis
•Polyarthralgia
•Chorea
•Erythema marginatum
•Subcutaneous nodule.
Arthralgia Polyarthralgia Monoathralgia
Fever ≥38.5°C ≥38°C
ESR ESR ≥60 mm
in the first hour
ESR ≥30 mm/h
And/or CRP ≥3.0 mg/dL.
PR interval Prolonged PR interval,
after accounting for age variability
(unless Carditis is a major criterion).
B-MajorcriteriaMinorcriteria

Arthralgia Polyarthralgia Monoathralgia
Fever ≥38.5°C ≥38°C
ESR ESR ≥60 mm
in the first hour
ESR ≥30 mm/h
And/or CRP ≥3.0 mg/dL.
PR interval Prolonged PR interval,
after accounting for age variability
(unless Carditis is a major criterion)
C-Minor criteria

Subclinical Carditis indicates echocardiographic valvulitis as defined.
Polyarthralgia, which should only be considered as a major manifestation in
moderate-to-high-risk populations after exclusion of other causes.

N.B
 Additionally, joint manifestations can only be considered in either
the major or minor categories but not both in the same patient !
As in past versions of the criteria, erythema
marginatum and subcutaneous nodules are
rarely “stand-alone” major criteria.
• CRP value must be greater than ULNR for lab.
• Also, because ESR may evolve during the course of
ARF, peak ESR values should be used.

N.B
• ARF = acute rheumatic fever;
• CRP, C-reactive protein;
• ESR, erythrocyte sedimentation rate;
• and GAS, group A streptococcal infection.
*Low-risk populations are those with ARF incidence ≤2 per 100 000 school-
aged children or all-age rheumatic heart disease prevalence of ≤1 per 1000
population per year.

Rheumatic Carditis
Rheumatic Arthritis
Rheumatic Chorea
Subcutaneous nodules
Erythema marginatum
50-60%
75%
10-15%
<3%
<1%

• Occurs in about 50-60% of all cases of ARF.
• Pancarditis that involves the endocardium, myocardium and pericardium.
• Involvement of the endocarium is a must for rheumatic Carditis.
Rheumatic Carditis
Clinical Carditis

Murmurs in patients with carditis include:
A- Endocarditis
1-Pan systolic murmur
at the apex (MR)
Caused by mitral
valvulitis.
Blowing in character high
pitched, soft.
May be musical, localized over the apex.
Not associated with thrill.
Disappears within 6 months if not associated
with chronic organic MR.
2-Carey Coombs
murmur (MS)
A low-pitched mid diastolic murmur at the apex.
3-AR: Early diastolic murmur over the aortic area.
4- Appearance of new murmurs.
5- Change in character of existing murmurs.

Murmurs in patients with carditis include:
A- Endocarditis
1-Pan systolic murmur
at the apex (MR)
Caused by mitral valvulitis.
 Blowing in character high pitched, soft.
 May be musical, localized over the apex.
 Not associated with thrill.
Disappears within 6 months if not associated
with chronic organic MR.
2-Carey Coombs
murmur (MS)
A low-pitched mid diastolic murmur at the apex.
3- Early diastolic murmur over the aortic area.
4- Appearance of new murmurs.
5- Change in character of existing murmurs.

C- Pericarditis
1-Dry
pericarditis
Precordial pain and friction rub.
2-Pericarditis with mild to moderate effusion.
3-Pericarditis
with massive pericardial effusion:

1. Weak pulse.
2. Pulsus paradoxus
↓↓ pulse volume during inspiration caused by exaggeration
of the normal phenomenon of slight decrease in SBP during inspiration.
3. Congested non pulsating neck veins.
4. Apex beat is weak or impalpable.
5. Dullness outside the apex by percussion.
6. Heart sounds are distant and muffled.
7. Ewart’s sign:
compression of the left lung produces dullness
and bronchial breathing at the base posteriorly.
Manifestations of pericarditis with
massive pericardial effusion

Myocarditis
• Tachycardia
• S1 may be muffled.
• Arrhythmias
• Cardiac dilatation & HF
ECG
low voltage, prolonged P-R and Q-T intervals.
ST-T changes and arrhythmia.

Endocarditis Myocarditis Pericarditis
1. Pan systolic murmur
at the apex
2. Carey Coombs murmur.
3. Early diastolic murmur
over the aortic area.
4.Appearance of new
murmurs.
5.Change in character of
existing murmurs.
• Tachycardia
• S1 may be muffled.
• Arrhythmias
• Cardiac dilatation & HF
1-Dry pericarditis.
2-Pericarditis with mild to
moderate effusion.
3-Pericarditis with massive
pericardial effusion
ECG
low voltage,
prolonged P-R and Q-T
intervals.
ST-T changes and
arrhythmia.

• Other Causes of Carditis such as viral myocarditis.
• Other causes of pericarditis.
• IE
• CHD.
• MVP.
• Kawasaki disease.
DDx
Rheumatic Carditis

• Defined as Carditis without a murmur of valvulitis but with
echocardiographic evidence of valvulitis.
• The echocardiographic features of subclinical Carditis must meet those
included in the following in order to distinguish pathological from
physiological degrees of valve regurgitation.
Rheumatic Subclinical Carditis

Pathological
MR
Pathological
AR
Seen in at least 2 views
Jet length
(in at least 1 view)
≥2 cm ≥1 cm
Peak velocity
(m/s)
>3 >3
Pan-systolic jet in at least 1 envelope
(All 4 met)

• Occurs in 75% of patients with ARF.
• There is often an inverse relationship between the severity of arthritis
and the severity of cardiac involvement.
• In low risk population, only migratory polyarthritis is a major criterion.
• In high risk population, Polyarthralgia and aseptic Monoarthritis are also major criteria.
Rheumatic Arthritis
 • Arthritis does not result in chronic joint disease. ‫المفاصل‬ ‫بيلحس‬
• Following the initiation of anti-inflammatory therapy,
arthritis may disappear in 1-2 days.
If un ttt , it may persist for a 1-2 weeks.
• Arthralgia may occur in some joints and frank arthritis in others.
In low risk population In high risk population
Migratory polyarthritis,
Only.
Polyarthralgia and aseptic
Monoarthritis

Treatment of arthritis (Ant inflammatory)
Salicylates provide dramatic relief.
50-70 mg/kg/day in 4 divided doses PO for 3-5 days,
followed by 50 mg/kg/day in 4 divided doses PO for 3 wk.
½ that dose for another 2-4 wk.
Early administration of salicylates to a patient before Dx is
established may obscure the diagnosis.

Other causes of arthritis such as:
DDx
IE
Juvenile RA & other collagen diseases.
Malignancy as Leukemia.
SCD.
Septic arthritis.
TB arthritis.
Gonococcal infection.
Reactive arthritis (Salmonella & Shigella).
Rheumatic Arthritis

DDx
IE
Juvenile RA & other collagen diseases.
Malignancy as Leukemia.
SCD.
Septic arthritis.
TB arthritis.
Gonococcal infection.
Reactive arthritis (Salmonella & Shigella).
Rheumatic Arthritis

AKA Sydenham, St. Vitus Dance Chorea
Rheumatic Chorea
Occurs in about 10-15% of patients with ARF.
pure chorea Usually presents as:
Isolated, frequently subtle, neurological
behavioral disorder.
It may be associated with Carditis.
Rheumatic arthritis is a rare association.
Has long latent period 2-6 months

Rheumatic Chorea
Clinical manifestations:
Characterized by:
• Involuntary movements,
• Emotional liability & hypotonia.
The onset is usually insidious.

Purposeless or semi purposeful,
irregular, non repetitive, rapid,
jerking movement
of the limbs and face.
Face Limbs
Characteristic grimacing of the face. The child tends to drop things,
to spill from a cup
and handwriting deteriorates.
Exaggerated by emotional stress but disappear during sleep.
Speech ***slurred.
Hemichorea
Rare
Chorea that affects
one side of the body
1-Involuntary movements:

Semi purposeful,
irregular,
non repetitive,
rapid, jerking

Emotional disorders:
There is alteration of temperament with characteristic liability of emotions.
Emotional liability The child laughs and cries without
apparent reason.
Muscular
hypotonia
is common.
chorea mollis In some cases, the weakness of muscle
is severe enough to resemble
paralysis

Clinical tests
for detection of chorea
Marked fluctuation
in muscle tone
Dinner fork deformity
Felt by asking the patient to
squeeze the examiner’s hand.
• When the arms and hands are extended, there is a
characteristic deformity in which the wrist is flexed
and the fingers extended at both the IP & MCP
joints.
• When the tongue is protruded, it is rapidly
withdrawn to prevent being bitten by involuntary
jaw movements.

The knee jerk Pronation sign
** sustained
or “hung up”.
pendulum type
(due to hypotonia)
On elevation of the UL above the level
of the head, with the palms of hands
facing each other,
there is pronation in the forearms and
the limbs fall down gradually.
The hung up reflex appears when the
contraction of the muscle that occurs
after the struck of the hammer coincides
with involuntary movement.

In pure chorea, the ESR and ASOT are normal.
This is attributed to the long latent period (2-6 months).
Laboratory findings:
Prognosis
- Chorea is a self limited condition.
- Mild cases subside within few weeks but a course of 3 months is average.
- The disease may progress to become so severe as to require a padded cot.

LP: 2-6 months
OnsetofARF
Chorea
starts
Average: 3 months

••Degenerative chorea
(Huntington’s chorea)
Progressive course
Age incidence :30-50 years.
Post encephalitic
chorea
Past history of encephalitis
Regressive in course.
Tics
Collagen diseases e.g. SLE
Wilson disease.
Drugs,
cerebral palsy,
hyperactivity
should also be excluded.
DDx

ttt of Rheumatic Chorea
***Phenobarbital is the drug of
choice.
every 6-8 hr PO 16-32 mg
Haloperidol If phenobarbital
is ineffective,
divided bid PO 0.01-0.03
mg/kg/day
Chlorpromazine every 4-6 hr PO 0.5 mg/kg
Some patients may benefit from a few week course of corticosteroids

Erythema marginatum
Incidence occasionally (<3%).
Shape
The lesion begins as red, raised non pruritic macules
then extend outward to form (wavy lines or rings) with
pale centers
Coalesce forming irregular circinate patterns,
which vary in shape and site from hour to hour.
Changing in pattern and evanescent .
Site ***over the trunk
Spare the face.

.
Subcutaneous nodules
Incidence ≤1% of patients with ARF
When they occur, usually severe Carditis is present.
Shape Bilaterally symmetrical lesions, comprising firm nodules.
Size Vary in diameter from a few millimeters to a centimeter.
Site **over the bony prominences.
Movable, painless and not tender.
Best demonstrated by fully flexing the joint
and stretching the skin over the extensor surface.

Bilaterally symmetrical firm nodules.
Vary in diameter from a few millimeters to a centimeter.
**over the bony prominences.
Movable, painless and not tender.

Minor criteria
Fever Arthralgia
--It is completely
absent in patients
with pure chorea.
Low risk
population
at least 38.5° C Major Minor
polyarthritis arthralgia
(in the absence of
polyarthritis as a major
criterion)
Moderate/ High
risk population
at least 38.0° C Polyarthralgia Aseptic
monoathralgia

CRP ESR
Low risk population 3.0 mg/dl
[30 mg/L]
at least 60 mm/hr
Moderate/ High risk
population
at least 30 mm/hr
Elevated acute phase reactants

• Abdominal pain.
• Precordial pain.
• Epistaxis
• Rapid sleeping pulse rate
• Tachycardia out of proportion to fever
• Malaise.
• Anemia.
• Leukocytosis.
Associated
findings

Treatment of ARF
can be divided into three approaches
1. Treatment of GAS infection.
2. Bed Rest
3. Use of anti-inflammatory agents.
4. Therapy for complications, such as HF.
• Chronic valvular heart disease after an attack of rheumatic Carditis.
• Severe acute carditis is the commonest cause of death of rheumatic fever.
Complications

Primary Prevention of
Rheumatic Fever
Treatment of streptococcal throat infection

FrequencyRouteDose
OnceIM1,200,000 u
600,000 u
if wt. less than 28 kg
1-Benzathine
penicillin
10 days
twice
oral250 mgkgday2-Penicillin v
10 days
oral40 mg/kg/day3-Erythromycin
10 daysOral or IM50 mg/kg/day4-others:
ampicillin,
amoxicillin,
cephalexin
Don’t use tetracycline or sulfa drugs
Primary Prevention of
Rheumatic Fever

General Guidelines for Bed Rest
and Indoor Ambulation
Severe carditisModerate carditisMild carditisArthritis
alone
As long
as HF is present
4-6w3-4w1-2 wBed rest
2-3 mo.4-6w3-4w1-2wIndoor
ambulation
1-Arthritis alone.
2-Carditis
Mild Questionable cardiomegaly.
Moderate Definite but mild cardiomegaly.
Severe Marked cardiomegaly or HF.

Treatment of arthritis (Ant inflammatory)
Salicylates provide dramatic relief.
50-70 mg/kg/day
in 4 divided doses PO
for 3-5 days,
followed by 50 mg/kg/day for 3 wk.
½ that dose for another 2-4 wk.
Early administration of salicylates to a patient before Dx is established
may obscure the diagnosis.

Mild cases
without
evidence
of CHF
Salicylates
alone
50-70 mg/kg/day
4 divided doses PO
for 3-5 days
50 mg/kg/day
4 divided doses PO
For 3 wk.
25-35 mg/kg/day for another 2-4 wk.
Treatment of carditis

Prednisone
2 mg/kg/day
4 divided doses
for 2-3 wk.
1 mg/kg/day for another 2-3 wk.
Then When the patient responds
clinically & on lab tests (ESR, CRP)
tapering of the dose by
5 mg/day
every 2-3 days.
At the beginning of tapering steroid
dose, Salicylates
to prevent rebound of inflammation.
50 mg/kg/day
4 divided doses
for 6 wk.
Supportive therapies include
digoxin, fluid & salt restriction, diuretics, and O2
-The cardiac toxicity of digoxin is enhanced with myocarditis.
Moderate and severe cases
associated with cardiomegaly and/or HF

ttt of Rheumatic Chorea
***Phenobarbital 16-32 mg every 6-8 hr PO is the drug of
choice.
Haloperidol 0.01-0.03 mg/kg/day divided bid PO If phenobarbital is
ineffective,
Chlorpromazine 0.5 mg/kg every 4-6 hr PO
Some patients may benefit from a few week course of corticosteroids

Treatment of streptococcal URTI (within 9 days) to prevent an initial
attack of rheumatic fever.
Primary prophylaxis
(See table for ttt of group A streptococcal Infection..)

(Prevention of recurrences of rheumatic fever)
FrequencyRouteDoesAntibiotic
Every 2-3 wIM1,200,000 u
600,000 u
If wt. <28 kg
1-Benzathine penicillin
Twice dailyoral250 mg2-Penicillin V
Once dailyoral1gm3-Sulfadiazine
variableoralvariable4- Macrolide
or Azithromycin
Secondary prevention

DurationCategory
At least 10 yrs. since last episode,
and at least until age 40 yrs.,
sometimes lifelong prophylaxis..!
Rheumatic fever with carditis and residual
heart disease .
(Persistent valvular disease*)
10 yrs or well into adulthood
whichever is longer
Rheumatic fever with carditis but no
residual heart disease.
(no valvular disease clinically or by Echo *)
5 yrs or until age 21 yrs ,
whichever is longer
Rheumatic fever without carditis.
‫أساسًا‬
192
whicheverislonger
Duration of secondary prevention.

Prevention of IE in
rheumatic heart patients
• Maintenance of optimal oral healthcare.
• Those with a prosthetic valve or prosthetic material used in valve repair should
receive prophylaxis according to AHA recommendations.

Infection of the endocardial surface of the heart or the intimal surface
of arterial vessels (endarteritis).
The term includes acute and subacute endocarditis as well as non-
bacterial endocarditis caused by viruses, fungi and other microorganisms.
High Risk Groups
1. Patients with congenital or rheumatic heart diseases.
2. Patients with prosthetic valves.
3. Patients with previous cardiac surgery.
4. Patients without pre-existing heart disease who have
immune deficiency or chronic CVC.

Infective endocarditis
Susceptible Valves
1.Congenitally abnormal
valves.
2.Rheumatic heart valves.
3.Valves damaged by jet
streams of shunts as VSD.
Etiology
Bacteremia
which may originate from
1.Dental extraction
2.CVC.
3.Cardiac surgery.
4.Urinary or intestinal
procedures.
Causative organisms
Bacterial
1.Strept. viridans.
2.Staph. aureus.
3.Others as S Pneumoniae,
H influenza,
S Epidermidis.
Non bacterial
1. Viruses.
2. Fungi.
3. Chlamydia.
4. Rickettsia.

Etiology
Causative
Organisms
1. Viruses.
2. Fungi.
3. Chlamydia.
4. Rickettsia.
Strept. viridans.
Staph. aureus.
Strept. Pneumoniae,
Staph. Epidermidis.
H. influenza
Bacterial
Non bacterial

1. In damaged valves, the endothelium is
injured. Fibrin and platelets adhere to it.
2. In the presence of bacteremia,
microorganisms lodge and adhere to
endothelium causing IE.
3. Vegetations are formed and consist of
fibrin, platelets and microorganisms.
Infection is responsible for hemodynamic
manifestations while dislodgment of vegetations
is responsible for the embolic manifestations of
infective endocarditis.

1. Prolonged low grade fever, headache and malaise
2. Anorexia and easy fatigability
3. Arthralgia and myalgia.
4. Abdominal pain and weight loss.
5. Splenomegaly is common.
6. Clubbing of fingers (pale toxemic).
General manifestations

1. Tachycardia
2. New murmurs or changing character of
existing murmurs.
3. Arrhythmia
4. Acute CHF.
B. Cardiac manifestations
Petechiae in skin and mucous membranes
Cerebral embolism: hemiplegia, cerebral abscess, cranial nerve palsy.
Ocular embolism: blindness
Arthritis.
Meningitis
Pulmonary embolism: cough, dyspnea, chest pain, hemoptysis
C. Embolic Manifestations
Osler nodes: tender pea sized intradermal nodules in the pads of fingers and toes.
Janeway lesions: painless small erythematous or hemorrhagic lesions on the palms or soles.
Splinter hemorrhage: linear lesions beneath the nails
Mycotic aneurysm of vessel wall and hemorrhage.
Metastatic abscesses.

Osler’s nodes Tender
painful
Erythematous
nodules,
Pea sized
intradermal
On tips of
fingers & toes
Janeway
lesions
painless Erythematous
macules.
Or hemorrhagic
lesions.
On the palm &
sole

Petechiae in skin and mucous membranes
Cerebral embolism hemiplegia, cerebral abscess, cranial
nerve palsy.
Ocular embolism blindness
Pulmonary embolism cough, dyspnea, chest pain, hemoptysis
Arthritis.
Meningitis

1. Positive blood culture.
2. Elevated ESR and CRP.
3. Anemia and leucocytosis.
4. Hematuria and renal impairment.
Lab findings

1. Valve vegetations.
2. Myocardial abscess.
3. Prosthetic valve dysfunction.
4. New onset valve insufficiency.
Echocardiographic
Findings

INFECTIVE ENDOCARDITIS
 Changing or new heart murmurs.
 Prolonged fever.
 Positive blood culture.
 Elevated ESR.
 Leucocytosis.
Most Common Findings
 Cardiomegaly.
 Splenomegaly.
 Petechiae.
 Embolism.
Weight loss.

It is based on a high index of suspicion in the evaluation of an
infection in a child with an underlying contributory factor.
The critical information for appropriate ttt is obtained from
blood cultures.
All other laboratory data are secondary in importance.
Diagnosis

1. Positive blood cultures: 2 or more separate blood cultures.
2. Evidence of endocarditis in Echo.
Diagnosis
The Duke criteria help in the diagnosis
Major Criteria:

Predisposing conditions.
Fever.
Embolic vascular signs.
Immune complex phenomena e.g. G.N,
arthritis, Osler nodes,…
A single positive blood culture.
Serologic evidence of infection.
ECHO signs not meeting the major criteria.
Minor Criteria
2 major criteria,
5 minor criteria
-----suggest definite endocarditis.

Minor Criteria
Predisposing conditions.
Fever.
Embolic vascular signs.
Immune complex phenomena e.g. GN, arthritis, Osler nodes,…
A single positive blood culture.
Serologic evidence of infection.
ECHO signs not meeting the major criteria

The American Heart Association (AHA): Cardiac Conditions
Associated with the Highest Risk of an Adverse Outcome from
Infective Endocarditis for Which Prophylaxis with Dental
Procedures Is Reasonable
 Prosthetic cardiac valve or prosthetic material used for cardiac valve
repair
 Previous IE
 Congenital heart disease (CHD)
1. Unrepaired cyanotic CHD, including palliative shunts and conduits
Completely repaired CHD with prosthetic material or device, whether placed by
surgery or catheter intervention, during the 1st 6 mo. after the procedure†
2. Repaired CHD with residual defects at the site or adjacent to the
site of a prosthetic patch, or prosthetic device (which inhibit endothelialization)

Congenital heart disease (CHD)
Prosthetic cardiac valve,
or prosthetic material used for cardiac valve repair.
Previous IE.
Prophylaxis for patients undergoing cardiac surgery with
placement of prosthetic material.
Oral hygiene.
Vigorous ttt of sepsis and local infections and careful asepsis
during heart surgery and catheterization reduce the
incidence of IE.

• In contrast to prior recommendations, prophylaxis for GI or GU procedures is
no longer recommended in the majority of cases. Prophylaxis for patients
undergoing cardiac surgery with placement of prosthetic material is still
recommended.
• Continuing education regarding both oral hygiene and, in appropriate cases,
the need for prophylaxis is important, especially in teenagers and young
adults.
• Vigorous ttt of sepsis and local infections and careful asepsis during heart
surgery and catheterization reduce the incidence of IE.

A substantial reduction in the number of patients who require prophylactic ttt
and the procedures requiring coverage was recommended.
• The primary reasons for these revised recommendations were that
(1) IE is much more likely to result from exposure to the more frequent
random bacteremias associated with daily activities than from a dental or
surgical procedure;
(2) Routine prophylaxis may prevent a small number of cases.
(3) The risk of antibiotic-related adverse events exceeds the benefits of
prophylactic therapy.

In patients with pre-existing heart disease,
prophylaxis against IE is recommended before dental procedures or surgery.
Dental and URTI:
1.Oral amoxicillin 50mg/kg one hour before procedure. Or
2.Azithromycin 15mg/kg one hour before the procedure.
Prophylaxis

Oral amoxicillin 50 mg/kg 1 hour before
procedureAzithromycin 15 mg/kg

Prophylaxis
Ampicillin Vancomycin
50 mg/kg IV 20 mg/kg IV
PLUS
gentamicin
1.5 mg/kg
30 minutes before the procedure.
then additional ½ the dose
of ampicillin
6 hours after the initial dose.
GIT or genitourinary surgery on high risk patient

Medical Treatment
mg/kg/day Divided into
Penicillin G 300.000 unit/kg/day 4 equal doses.
Gentamicin 5-7 2 equal doses.
Cloxacillin 200 4 equal doses.
Or
Vancomycin
40-60 2 equal doses
If the organism is identified, If the organism is not yet known
specific therapy is instituted
immediately according to the
culture results.
therapy should start with 3 antibiotic
combinations.

Therapy should be continued for 4-6 weeks
to ensure complete organization of vegetations.
Bed rest, salt restriction, digitalis and diuretic therapy
should be used when CHF occurs.
Medical Treatment

1. Removal of vegetations and valve replacement:
indicated in infected prosthetic valve, recurrent emboli,
increasing vegetation size while receiving treatment,
intractable HF and fungal endocarditis.
2. Surgical repair of ruptured aortic sinus or mycotic
aneurysm.
Surgical Treatment

HEART FAILURE
• Heart failure means the inability of the heart to deal
with venous return and maintain the cardiac output.
• Heart Failure occurs when the COP does not meet the
metabolic needs of the body.
• CHF is increased venous pressure in pulmonary veins
(left HF) or systemic veins (right HF) or both.

Heart Failure
1. Congenital heart disease:
1. Coarctation of aorta.
2. TGA.
3. Severe AS or atresia.
4. HLHS.
5. TAPVR.
6. Left to right shunt lesions
as VSD and PDA.
2. Erythroblastosis fetalis.
3. Viral myocarditis
4. Asphyxia.
Newborns

1.Left to right shunt lesions as VSD and PDA.
2.TGA
3.Ostium primum ASD
4.Coarctation of aorta
5.TAPVR
3. Cardiomyopathy
4. Endocardial fibroelastosis
5. Arrhythmia
Infants
Heart Failure

1. Coarctation of aorta.
2. TGA.
3. Severe AS or atresia.
4. HLHS.
5. TAPVR.
6. Left to right shunt lesions
as VSD and PDA.
2. Erythroblastosis fetalis.
4. Asphyxia.
1.Left to right shunt lesions as VSD and PDA.
2.TGA
3. Ostium primum ASD
4.Coarctation of aorta
5.TAPVR
3. Cardiomyopathy
4. Endocardial fibroelastosis
5. Arrhythmia
InfantsNewborns

TGA
TAPVR
VSD & PDA
Coarctation
of aorta
Viral
myocarditis

HEART FAILURE
1. Rheumatic fever
2. HTN as GN.
3. Bacterial endocarditis
5. Arrhythmia
6. Cor pulmonale
7. Congenital heart defects
8. Hemosiderosis and severe anemia.
Older Children

1. Tachypnea on feeding and exertion.
2. Interrupted feeding and sweating.
3. Irritability, sleeplessness and weak cry.
4. Failure to gain weight.
Clinical Manifestations
1. Tachypnea, retractions.
2. Cyanosis or pallor.
3. Tachycardia.
4. Cardiomegaly.
5. Wheezy chest.
6. Hepatomegaly.
7. Edema is a late sign.
Symptoms
Signs
Newborns and Infants

Edema is a late sign
Signs
Tachypnea,
retractions
Wheezy chest
Cardiomegaly
Hepatomegaly
1. Cyanosis or pallor
2. Tachycardia

1. Onset may be sudden with rapid
progressive course or may be
gradual.
2. Dyspnea, orthopnea and PND.
3. Palpitation and sweating.
1. Tachycardia
2. Congested neck veins
3. Pallor or cyanosis.
4. Cardiomegaly
5. Gallop rhythm in most cases
6. Tender hepatomegaly
7. Generalized edema
8. Wheezy chest
Older Children

• The underlying cause of HF must be removed or alleviated if possible.
• If the cause is a congenital cardiac anomaly amenable to surgery, medical
ttt of the HF is indicated to prepare the patient for surgery.
• With today’s excellent outcomes of primary surgical repair of congenital
heart defects, even in the neonatal period, few children require aggressive
heart failure management to “grow big enough for surgery.” ❤❤❤
• In contrast, if the cause of HF is cardiomyopathy, medical mge provides
temporary relief from symptoms and may allow the patient to recover if
the insult is reversible (e.g. myocarditis).
• If the lesion is not reversible, heart failure management usually allows the
child to return to normal activities for some period and delay, sometimes
for months or years, the need for heart transplantation.

ttt
1. Bed rest.
2. Feeding.
3. O2 therapy.
4. Diuretics.
5. Digitalis.
6. After load reducing drugs.
7. ttt of pulmonary edema.
8. ttt of Cardiogenic shock.
9. ttt of the cause.

Bed rest:
Semi sitting position is preferred.
IV fluid (70% of amount) in early stages
with severe RD
because oral feeding
may be hazardous.
NGT feeding after few days if still RD.
Oral feeding is started as soon as condition allows.
In older children with mild HF, oral feeding is given from the start.
Feeding

Diuretics
Furosemide I.V 1 mg/kg/dose, or orally
2-3 mg/kg/day
rapid onset + short duration
Chlorothiazide oral 20-30 mg/kg/day in 2 doses slower onset + longer duration
Spironolactone oral 1-3 mg/kg/day in 2 doses potassium sparing
K+ serum level should be frequently monitored.
Potassium depletion in digitalized patients may be fatal.
Hypokalemia is treated with
oral KCl 0.5 gm twice daily

Digitalis
Action increases the force and velocity of ventricular contraction.
Loading
dose
Total dose:
0.04-0.05 mg/kg
in 3 doses
(½,
¼
then ¼ total dose).
Separated by
8 hour interval.
Maintenance
dose
0.01mg/kg or
¼ the total
loading dose
started 24 hours
after the first loading
dose.
2 divided doses

0.04-0.05
mg/kg
8 hr. 8 hr.8 hr.
½ ¼ ¼

N.B
Slow digitalization Potassium therapy
without loading dose can be used.
In this case only maintenance dose
is given without initial loading dose.
Full digitalization is achieved in
7-10 days.
Is usually needed in chronic use of
diuretics and digitalis.
Diuretics as Furosemide cause
potassium depletion.
Hypokalemia increases digitalis
toxicity.
7-10 days.

Treatment
1.Stop digitalis
2.Correction of Hypokalemia
3.Treatment of arrhythmia
Signs
Cardiac
arrhythmia,
depressed ST segment.
Extracardiac
nausea, vomiting, headache,
disturbed vision and seizures.
Digitalis toxicity is potentiated by
hypo K+
hypo Ca++
hypo Mg++
Myocarditis.
Digitalis toxicity

After load reducing drugs
They cause
arterial
dilatation and
decrease the
systemic vascular
resistance.
***Captopril Indication S/E
Used in severe HF. hypotension
0.5-3
mg/kg/day
ttt of pulmonary edema Diuretics
Mechanical ventilation.
ttt of cardiogenic shock
dopamine and dobutamine.
ttt of the cause

BP = COP x PVR
HTN: BP above the 95th percentile for age.
SBP DBP
0-2 years 85 55
2-6 years 100 60
6-10 years 105 65
10-15 years 115 70

Primary
(=essential)
HTN
Secondary
HTN
Ne identifiable cause can be
found.
HTN as a result of another
disease process.
Age **adolescents
Uncommon in
children <10 years
May occur at any age, even in
the neonatal period.
Weight Mild-moderate obesity Marked obesity with
adrenocortical diseases.
Level of BP Usually mild
Or slightly above 95th
Mild to extreme
Family history Of essential HTN Of renal disease
Premature CVS disease…
Manifestations of
underlying disease
None Present

Transient HTN Chronic HTN
Renal
Drugs & poisons
Neurological
Others:
 Hypercalcemia
 Chronic upper airway ☒
Renal
Vascular
Endocrine
Neurological
Essential HTN

Renal APIGN
HSP with nephritis
HUS
Pyelonephritis
Hypervolemia
Renal trauma
Drugs & poisons
Neurological ↑↑ICP
GBS
Encephalitis,
poliomyelitis
Burns
Posterior fossa lesions
Others:
Hypercalcemia
Chronic upper airway ☒
Transient HTN
1-Corticosteroids
2-Sympathomimetics
3-Anti HTN withdrawal:
methyl dopa ,
propranolol.
4-Cyclosporine
5-Vitamin D
intoxication.
Lead, mercury & cadmium

Chronic HTN
Renal 1-Chronic GN
2-CT diseases e.g. SLE
3-Chronic pyelonephritis
4-Congenital disorders;
MCKD & dysplastic kidney
Renal tumors & trauma
Ureteral & VUR
Vascular 1. Coarctation of aorta; thoracic or abdominal
2. Vasculitis
3. Renal a. stenosis, thrombosis or anuerysm.
4. Renal V. thrombosis.
5. Umbilical a. catheterization…..
Endocrine CAH
Cushing
Hyperthyroidism
Hyperparathyroidism
Pheochromocytoma
Neuroblastoma..
Neurological Intracranial mass or hge.
Brain injury.
Essential HTN

C/P of HTN
Asymptomatic
HTN
Discovered only on routine examination.
Symptoms of Headache,, dizziness, blurred vision,
Anorexia,
Epistaxis.
HTN encephalopathy Vomiting, hyperthermia
Ataxia, stupor,
seizures
Hypertensive HF.
Renal functions.
C/p of the underlying cause.
Careful measurement
of height & weight.
Detection of flank masses.

Dx
Repeated BP measurements to confirm HTN
Screening tests
CBC
Urinalysis
Urine culture
Uric acid
BUN & creatinine
Obstructive lesions  UTI….
Serum electrolytes
Calcium
Peripheral plasma
renin activity
↑↑ in ↓↓
Renal or renovascular
involvement.
Mineralocorticoid
excess.
Catecholamines
Steroids
In urine
In plasma & urine.

Renal
imaging
U/S
Radionuclide scan
Doppler U/S
Renal angiography
IVP

Essential HTN Transient secondary HTN Chronic secondary HTN
Most patients continue
to have HTN as adults.
Usually disappears
without after effects.
Treatable
cause
Untreatable
cause
Good
prognosis
Gradual deterioration of
cardiac & renal functions.
Death due to HTN
encephalopathy.
HF
Intracranial hge

Prevention
of HTN
Avoid risk factors: Obesity, elevated serum cholesterol, hish
dietary Na intake, sedentary lifestyle.
Increase in physical activity through school-based programme.

Arterial vasodilators Hydralazine 0.25-1 mg/kg/dose Every 6-8 hrs.
Adrenergic blockers propranolol 0.5-6 mg/kg/dose Every 6-8 hrs.
Renin-angiotensin
inhibitors
Captopril 0.1-0.5 mg/kg/dose Every 8-12 hrs.
CCBs nifedepine 0.25-0.5 mg/kg/dose Every 4-6 hrs.
Diuretics Furosemide 1-2 mg/kg/dose Every 6-12 hrs.
ttt
of HTN
Anti-hypertensive drugs

ttt of
Hypertensive crisis
Rapid control of BP through:-
Sublingual nifedepine
IV labetalol
Nitroprusside +IV furosemide
Percutaneous
transluminal
dilatation of renal a.
Nephrectomy
In case of renal artery stenosis. In case of uncontrolled HTN due
to renal or renovascular
disorders.
Surgical ttt

Keep on.
You are a hero.
Never give up!

Pediatric Cardiology - for medical students

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