PAEDIATRIC CARDIAC
DISORDERS
Robyn Smith
Department of Physiotherapy, UFS, 2011
Dealing with a child with cardiac dysfunction
is often disconcerting and we are often unsure
of how to proceed this lecture aims to provide
an overview of common heart pathology in
children and the physiotherapy management
thereof
Background
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Congenital heart defects (CHD) occur in 1% of the live births
(6 of every 1 000)
Most common congenital abnormality seen
Approximately 1/3 of these children will require surgery,
whilst the rest of the cases resolve spontaneously or are
deemed haemodynamically insignificant
Early surgical intervention is recommended to limit CVS and
neurodevelopmental complications. Most children are
operated on before 1 year of age
Background
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Mortality for children with CHD has decreased
significantly ( ≤ 5 %) as a result of medical and
surgical advances, and many of these children are
surviving well into adulthood.
The decreasing mortality rates has resulted in the
shift in focus to the neurodevelopmental status of
these children and ways of addressing the
associated developmental delays
Background
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As PT’s we will encounter children with CHD in all
clinical settings we work in
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Acute care setting – pre/postoperatively
Sub-acute care setting in the ward
Out patient department
As PT’s we need to know:
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What CHD is
Types of cardiac disorders
How the child’s CVS system is affected during exercise
Prevalent complications associated CHD
Aetiology
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In most cases of CHD the aetiology is multi-factorial
and include
 genetic
inheritance (patterns not yet clear)
 Maternal conditions
 Environmental factors
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Above factors interact during the first 8-10 weeks
of gestation a critical development phase of the
heart
Cardiac Physiology in the infant
Normal foetal circulation
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Foetal heart in not dependant on the lungs for
respiration. Instead the placenta is used for gaseous
exchange.
The R and L ventricles exist in a parallel circuit
Blood travels through the umbilical vein through the
ductus venosus to the foetal heart via the IVC to the RA
and through the foramen ovale to the LA
The SVC leads to the RA to the RV to the pulmonary
artery to the lungs or ductus arteriosus bypassing the
lungs into the descending aorta to perfuse the lower
extremities and the body, travelling back to the
placenta via the umbilical arteries.
Normal foetal circulation
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The blood travelling through the left ventricle to the
aorta perfuses the upper extremities and the brain.
All of the blood flowing through the chambers of
the heart, arteries and veins is rich in Oxygen
The vessels for pulmonary circulation in the foetus
are vasoconstricted. All blood travelling in the
arteries to the lungs is oxygen rich and contributes
to the nourishment of the lung tissue
Changes in the circulatory system
at birth
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As the baby takes its first breath the lungs expand, causing
the lung P to fall. This allows the blood to move more easily
into the lung.
After reaching the lungs and being oxygenated the blood is
moved to the LA. The P on the L side of the atrial septum
becomes higher than on the R causing the foramen ovale to
gradually close (closed by 3/12)
Once the lungs are filled with air and the oxygen level in
the child’s blood rises the muscle wall of the ductus
arteriosus contracts no longer allowing blood to flow through
the ductus. The ductus arteriosus closes 10-15 hours after
birth.
Now child has separate oxygenated and de-oxygenated
blood and relies fully on the lungs for gaseous exchange
Normal circulation after birth
Common heart disease in children
Congenital heart defects
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At any point in the development of the cardiac
system problems can arise leading to congenital
heart disease.
CHD can be classified into two main groups:
lesions ( ↓O2 saturation in the blood)
 Acyanotic lesions (O2 saturation unaltered, but can
result in pressure or volume related issued)
 Cyanotic
Common cardiac conditions seen in children
Acyanotic Congenital Heart Defects
Classification of Acyanotic
heart lesions
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Coarctation of aorta
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Pulmonary stenosis
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Aortic stenosis
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Patent ductus arteriousus
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Atrial septal defects
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Ventral septal defects
increased pulmonary bloodflow
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Atrioventricular septal defects
with shunting O2 rich blood from
obstructive in nature
left to right
“PINK BABY”
Patent Ductus Arteriosus (PDA)
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The ductus arteriousus is the foetal vascular connection
between the main pulmonary trunk and the aorta which
under normal circumstances closes soon after birth (usually
within the first week of life).
If it stays open excessive blood shunts from the aorta ton the
lungs
Causing pulmonary oedema and in the long run pulmonary
vascular disease
Symptoms may vary from mild to severe depending on the
magnitude of the shunt
Very common in premature infants and may further
complicate weaning from the ventilator and result in CHF
Patent Ductus Arteriosus (PDA)
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clinical signs and symptoms of significant PDA
 Poor
feeding
 Failure to thrive (below weight for and height for age)
 Sweating with crying or play
 Persistent tachypnoea or breathlessness (dyspnoea)
 Easy tiring
 Tachycardia
 Frequent lung infections
 A bluish or dusky skin tone
 Developmental delay
Patent Ductus Arteriosus (PDA)
Patent Ductus Arteriosus (PDA)
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Management
Closing of PDA can be induced
using medication (indomethacin)
Surgically
Surgical correction is done via a thoracotomy
Atrial Septal Defect (ASD)
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An ASD is an opening or whole in the wall separating
the atria
This permits free communication of blood between the
two atria.
Seen in 10% of all congenital heart disease
Rarely presents with signs of congestive heart
failure or other cardiovascular symptom
Most are asymptomatic but may have easy
fatigability or mild growth failure. The right atrium
and ventricle may enlarge over time
Cyanosis does not occur unless pulmonary
hypertension is present.
Atrial Septal Defect (ASD)
Atrial Septal Defect (ASD)
Management:
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Surgical or catheterization closure is usually indicated
Closure is performed electively between ages 2 & 5 yrs
if the whole has not closed in order to avoid late
complications. Children may be on anticoagulant
therapy for 6 months to prevent clotting
Surgical correction is done earlier in children with
congestive heart failure or significant pulmonary
hypertension
Venticular Septal Defect (VSD)
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A VSD is an abnormal opening in the ventricular
septum, which allows free communication between the
right and left ventricles ventricles.
Oxygen rich blood in the left ventricle is then pumped
into the right ventricle through the opening instead of to
the body. In a large VSD excessive blood is pumped to
the lungs resulting in congestion and shortness of breath.
In return excessive amounts of blood are pumped back
from the lungs to the left heart overburdening and
enlarging it resulting in CHF
Venticular Septal Defect (VSD)
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In case of a small VSD most children are
asymptomatic and 50% will close spontaneously
by age 2yrs
In the case of a moderate or large VSD the child will
be symptomatic. This may include dyspnoea, feeding
difficulties, failure to thrive recurrent respiratory
infections and profuse sweating
Venticular Septal Defect (VSD)
Venticular Septal Defect (VSD)
Management
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In case of a small VSD 50% will close spontaneously
by age 2yrs
Large VSD’s are usually closed surgically
Atrioventricular Septal Defect
(AVSD)
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AVSD results from the incomplete fusion of the
tendocardial cushions, which help to form the lower
portion of the atrial septum, the membranous portion
of the ventricular septum and the septal leaflets of
the triscupid and mitral valves.
They account for 4% of all CHD
Commonly associated with chromosomal disorders
Down Syndrome
Clinical findings include CHF in infancy, recurrent
respiratory infections, failure to thrive, exercise
intolerance and easy fatigability.
Atrioventricular Septal Defect
(AVSD)
Atrioventricular Septal Defect
(AVSD)
Treatment
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Surgery is always required.
Prior to surgery congestive symptoms are treated.
Pulmonary banding maybe required in premature
infants or infants < 5 kg.
Correction is done during infancy to avoid irreversible
pulmonary vascular disease.
Pulmonary artery banding
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The primary is to reduce
excessive pulmonary
blood flow and protect
the pulmonary
vasculature from
hypertrophy and
irreversible (fixed)
pulmonary hypertension.
Truncus arteriosus
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Defect characterised by a
single arterial trunk arising
from both ventricles from
which the aorta and
pulmonary arteries arise
from a single semi-lunar
valve
Pulmonary hypertensive crisis
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Can be a severe complication post operatively
Children at risk of pulmonary hypertension are those with
excessive shunting of blood from left to right e.g. VSD, AVSD
This results in excessive bloodflow to the lungs resulting in
distension and damage to the pulmonary artery wall which
becomes muscularised
Unable to dilate and vulnerable to reactive vasoconstriction
Hypoxaemia, hypercapnea, metabolic acidosis as well as
relentless handling (including by the physiotherapist) and
tracheal suctioning may predispose the child to a
hypertensive crisis.
In children at risk physiotherapy should be indicated,
treatment must be quick and effective and vitals need to be
monitored. Effective sedation, paralysis and additional
oxygen may be required to avoid a crisis.
Pulmonary hypertensive crisis
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In the case of a crisis the
pulmonary arteries constrict
resulting in an increase in
pulmonary artery pressure
and CVP. The systemic blood
pressure will drop suddenly
resulting in cardiac arrest.
Treatment includes sedation,
paralysis and the
administration of Nitric Oxide
and 100% oxygen to try and
facilitate pulmonary
vasodilatation
Obstructive causes of CHD
Coarctation of the aorta
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Congenital narrowing of the aorta as it leaves the
heart anywhere from the transverse arch to the iliac
bifurcation.
Resulting in increased pressures in the arteries nearest
the heart, head and arms and decreased circulation
in lower extremities.
7 % of all CHD
Male: Female ratio 3:1
Coarctation of the aorta
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This is often not evident in the newborn until the
ductus arterious closes causing a constriction. The
blood in the left ventricle has then to be pumped
out against the constriction.
Child presents with symptoms of left ventricular
hypertrophy and left ventricular failure, with
congestive heart failure. Changing a healthy baby
into a baby that has hard breathing, is sweaty and
wheezing.
Coarctation of the aorta
Coarctation of the aorta
Coarctation of the aorta
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Management:
With severe coarctation maintaining the ductus with
prostaglandin E is essential
Early surgical repair and resection of the stenosis is
imperative
Simple coarctation repair have a extremely low
mortality but in complex cases mortality might be
higher
A rare complication of surgical repair is paraplegia
(longer cross clamping times during surgery)
In 18% of children undergoing surgery re-coarctation
occurs
Obstructive causes
Aortic Stenosis
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Is an obstruction to the
outflow from the left
ventricle at or near the
aortic valve.
Resulting in left ventricular
overload and hypertrophy
Pulmonary Stenosis
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Is obstruction in the region
of either the pulmonary
valve or the sub-pulmonary
ventricular outflow tract.
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Pulmonary circulation
decreased
Work of the RV increased
RV hypertrophy
↓ cardiac output
Accounts for 7% of CHD.
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Accounts for 7-10% of all
CHD.
Obstructive causes
Aortic Stenosis
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Asymptomatic in mild cases,
in more severe cases
fatigue, syncope and
dyspnoea
Treatment is surgical repair
Pulmonary Stenosis
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Symptoms include
dyspnoea, exercise
intolerance, fatigue CHF
and hypoxaemia
Treatment is surgical repair
Obstructive causes
Aortic Stenosis
Pulmonary Stenosis
Cyanotic Congenital Heart Defects
Classification of cyanotic
heart lesions
Cyanotic heart lesions include:
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Tetralogy of Fallot
Hypoplastic left heart
Trasposition of the great vessels
Tetralogy of Fallot (TOF)
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Most common cyanotic heart lesion
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Has 4 components:
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A high VSD
Pulmonary stenosis
Anomalous position aorta
RV hypertrophy
Results in a right to left shuntting of blood with low oxygen
levels in the artieires and in the body tissues
Resulting in cyanosis, easy fatigability, fainting and shock.
Clubbing may be observed
Tetralogy of Fallot (TOF)
Tetralogy of Fallot (TOF)
Tetralogy of Fallot (TOF)
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Early surgical intervention (TOF repair) is usually
required
Palliative care by means of anestomosis and
pulmonary valvotomy can be done
Hypoplastic Left Heart Syndrome
(HLHS)
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Most serious congenital heart malformation with the
poorest of prognosis
Means that the left ventricle is extremely small and
the mitral valve and aortic valves may be missing
Symptoms usually minimal until the ductus arteriosus
closes causing shock and multi-organ failure
Hypoplastic Left Heart Syndrome
(HLHS)
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Treatment prpstaglandin E1 until surgery
Initial palliative surgeries
Heart transplant is often the suggested option
Hypoplastic Left Heart Syndrome
(HLHS)
Other Congenital Heart Defects
Transposition of the great
vessels
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Aorta arises from the RV and the pulmonary
arteries arise from the LV
The 2 circulations namely the systemic and
pulmonary are in parallel instead of in series
Venous blood circulates around the body and
oxygenated blood around the lungs
May be dyspnoea, cyanosis and syncope
Transposition of the great
vessels
Transposition of the great
vessels
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Treatment
Palliative surgeries including pulmonary banding or
atrial septum excision
Corrective surgery
Non Congenital Heart Disease
Cardiomyopathy
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Primary heart muscle disease
Cardiomyopathy is a chronic and sometimes progressive
disease in which the heart muscle is abnormally
enlarged, thickened and/or stiffened.
The condition typically begins in the walls of the
ventricles and in more severe cases also affects the
walls of atria)
The actual muscle cells as well as the surrounding
tissues of the heart become damaged.
Hallmark is depressed cardiac functioning. Eventually,
the weakened heart loses the ability to pump blood
effectively and heart failure or irregular heartbeats
(arrhythmias or dysrhythmia) may occur.
Cardiomyopathy
Cardiomyopathy
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"primary cardiomyopathy" where the heart is
predominately affected and the cause may be due
to infectious agents or genetic disorders
"secondary cardiomyopathy" where the heart is
affected due to complications from another disease
affecting the body e.g. HIV, cancer, muscular
dystrophy or cystic fibrosis
Cardiomyopathy
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Cardiomyopathy can affect a child at any stage of
their life. It is not gender, geographic, race or age
specific.
Rare disease in infants and young children.
Cardiomyopathy continues to be the leading reason
for heart transplants in children.
Complications may include arrythmias, heart block,
blood clots, congestive heart faiulure, endocarditis
and sudden death
Organ Transplantation
Heart transplant
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Heart transplantation is used only as an option in end
stage heart failure in children with heart defects or
cardiomyopathies that are unresponsive to surgery or
medication
Heart failure may occur in children with CHD postoperatively due to the nature of their artificial
circulations
Individual units have their own transplant protocols
A heart transplant presents a ling risk of organ
rejection and infection
The transplant half life of children is estimated at 18
years
Heart transplant
Physiotherapy Assessment
Assessment of the child with
CHD
History
Will need to conduct an interview with
the family:
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Children often have a very long and
complicated medical and often surgical
history that has to be well document
Medications that the child is taking e.g.
blood thinners, and immunosuppressant
drugs
Social, economic and family
circumstsances need to be determined
(CHF highly stressful to the family unithigh divorce rate)
Developmental history –these children
often present with developmental
delays
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Is child receiving any early
intervention services e.g. physio/OT
Child’s general health
Sleeping patterns’
Current and previous level of
functioning
ADL – if child of schoolgoing age is
he attending school.
What is their chief complaint with the
child:
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Most common complaint from parent
with children awaiting surgery is
failure to thrive and poor feeding. I
In older children it is often lethargy,
fatigue
Assessment of the child with
CHD
Interview with paediatric
cardiologist
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Nature of the CHD
Intervention and treatment
planning
Precautions
Need for physiotherapeutic
intervention
Assessment of the child with
heart disease
Oxygenation –laboratory
results
Vital sign parameters
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Arterial blood gas values and
saturation monitor reading
are incredibly important when
assessing a patient with
cardiac dysfunction
Cyanotic lesions the ABG may
be reduced due to the mixing
of arterial and venous blood
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The following reading need to
be taken manually or read
off the monitor HR, RR, BP
prior to your assessment to
serve as baseline values
Important to retake vital signs
during assessment and after
as well
Assessment of the child
with heart disease
PaO2
60-80 mmHg
PaO2
40-60 mmHg
PaO2 ≤
40 mmHg
= SaO2 ≤ 60%
= SaO2 60-90%
= SaO2 90-95%
Mild hypoxaemia
Severe hypoxaemia
Assessment of the child with
heart disease
General observations
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Child’s LOC – is he sedated, on a
neuromuscluar blocker (paralysis)
in children where any movement
or position changing has a
negative impact on the CVS
function)
Equipment and indwelling
devices
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Pain
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Integrity of the skin
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Surgical sites and wounds e.g.
sternotomy/ thoracotomy
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Clubbing
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Oedema
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Capillary refill
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Cyanosis central and
peripheral
Assessment of the child with
heart disease
Respiratory system
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Chest shape
Chest deformities
Chest expansion
Thoracic mobility; flexion,
extension, lateral flexion,
rotation
Breathing pattern
Shoulder girdle tightness
and mobility
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Shortness of breath
(tachypnoea)
Dyspnoea and grade
Cough
Sputum
Auscultation
If ventilated –ventilator
settings
Assessment of the child with
heart disease
Musculoskeletal system
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Posture
ROM
Muscle strength
Functional ability &
ADL
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Functional and ADL
tasks appropriate for
age need to be
assessed in line with
the child’s condition
Assessment of the child with
heart disease
Aerobic capacity,
endurance and
exercise tolerance
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In younger children
observe during activity
and play- monitor HR
In older child can do
the 6 min. walk test
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Shortness of breath
can objectively be
monitored through the
ventilatory index in
older children
Can also use the
dyspnoea index or
Borg scale but it is
often subjective and
difficult in children
Ventilatory index
child must inhale deeply and count to 15 (8 seconds)
0
1
2
3
4
• Count aloud to 15 without taking a breath
• Count aloud to 15 taking 1 breath
• Count aloud to 15 taking 2 breaths
• Count aloud to 15 taking 3 breaths
• Count aloud to 15 taking 4 breaths
Dyspnoea Index
1
2
3
4
• Breathlessness barely noticeable
• Breathlessness moderately bothersome
• Breathlessness severe and very uncomfortable
• Most severe breathlessness ever experienced
Borg scale of perceived exertion
6-8
8-10
• Very, very light
• Very light
10-12
• Fairly light
12-14
• Somewhat hard
14-16
• Hard
16-18
• Very hard
18-20
• Very, very hard
Preoperative physiotherapy
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Seeing the child prior to surgery affords the physiotherapist
the opportunity to get to know the child and their family,
makes the post-operative period far easier.
Provides an opportunity to do a quick respiratory,
developmental and functional assessment
In other cases it might be a child you know well from
previous inpatient/out patient visits to adress recurrent
respiratory tract infections and neurodevelopmental delays
Explain the operation in simple terms and tell him/her and
the parents about the post operative stay in PICU (lines,
ventilator ,ET tubes etc.). Also indicate the post-operative
role of the physiotherapist.
Preoperative physiotherapy
aims
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Maintain joint ROM, circulation and function preoperatively
Correct posture and positioning in bed
CPT if indicated to clear secretions and breathing
exercises
Teach older child how to cough with wound/chest
support
Maintain functional abilities as cardiovascular status
allows
Postoperative physiotherapeutic
problems
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Pain –see child has adequate sedation
Decreased air entry
Retained secretions
Ineffective cough –must cough with wound support
Reduced UL movements
Decreased mobility
Family and caregiver education
Postoperative physiotherapy
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Avoid physiotherapy in the first few hours after surgery as
they are aiming to stabilise the child and achieve
haemodynamic stability
The exception to the rule here may be in the case of a
lobar collapse on the post-operative CXR or poor ABG. In
this case careful physiotherapy is to be done avoiding any
deterioration in haemodynamic status
Postoperative physiotherapy
When not to treat
Confidence in treating cardiothoracic patient only comes
with experience, but accurate assessment will reveal the
needs of the child:
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Treatment should be avoided in the following cases:
Haemodynamic instability
Tachycardia or bradycardia
Hyper/hyptensive
Child in a pulmonary hypetensive crisis
Postoperative physiotherapeutic
intervention
Intubated in the ICU
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Localised breathing exercises if child awake and of age
or tactile neurophysiological stimulation
Modified postural drainage positions are used as
the head down position may compromise cardiac
output and diaphragm functioning
Mechanical vibrations, gentle percussions (ensure
adequate analgesia) and suctioning to remove secretions
Must give chest support when coughing
Bilateral UL mobility above 90 degrees
Correct positioning for ventilation and posture
Postoperative physiotherapeutic
intervention
Extubated in the ICU
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Children are usually extubated quickly unless underlying
lung pathology or secondary infection.
Teach huffing & coughing with chest support
Localised and lateral basal breathing exercises or can
use blowing pin-wheel, bubbles, incentive spirometry
Manual CPT techniques if indicated
Functional activities e.g. teaching log rolling, coming up
into sitting
Active bed exercise programme
Older child can sit out in a chair in the unit
Postoperative physiotherapeutic
intervention
Ward
Exercise rehabilitation in paediatric patients
 Mobilisation can be start once inotropic drugs stopped
and some of drains removed
 Studies in children show an improvement in work capacity
& VO2 max following a 6-8 week rehabilitation exercise
programme
 Not much research has been done on rehabilitation
exercise programmes in children
Postoperative physiotherapeutic
intervention
Ward
Exercise rehabilitation in paediatric patients
An at risk group for exercise.....
 There is a small population of children who are at risk of
sudden death ( hypertrophic cardiomyopathy, coronary
artery anomalies, Marfan Syndrome, Aortic valve stenosis
and long QT syndrome)with physical activity and sport
participation.
 These children need to be identified and restriction placed
on competitive sport and high intensity physical activity
Postoperative physiotherapeutic
intervention
Ward
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Start with activity and endurance training
Allow older child to walk, cycle and stair climb (can be
taught to monitor own HR)
Smaller children uses play and functional activities
Pay attention to the following principles
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mode : walking, cycling
Duration (sick children shorter intensity e.g. 3-5 minutes
Frequency (3-5/wk)
Intensity: monitor exhaustion, dyspnoea and HR (not a rise of ≥
20 beats)
In older children where stress ECG can be done, the child can
exercise at 60 -65% of maximal HR
Postoperative physiotherapeutic
intervention
Ward and out patient basis
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Aerobic and endurance training
Not all patients e.g. Left to right shunt have impaired
exercise tolerance where in some cases children with
cyanotic heart lesions and severe abnormalities may
have impaired exercise tolerance due to the
hypoxemia
Exercise tolerance is also often affected by recurrent
hospitalisations, inactivity and periods of bed rest
Therefore post operatively there must be a
progressive exercise plan aiming to improve the
child’s cardiovascular fitness and endurance
Postoperative physiotherapeutic
intervention
Ward and out patient basis
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Aerobic and endurance training
Over time children that have had a complete defect repair
at an early age should have normal cardiovascular
functioning-with normal age expected exercise tolerance and
endurance
In cases where complete repair was not possible and cardiac
functioning still impaired the child have to monitor HR and
signs of fatigue can aim at improving endurance and at least
maintaining it where possible
Sporting activity in cases of impaired cardiac function needs
to be reviewed by the interdisciplinary team
Postoperative physiotherapeutic
intervention
Ward and out patient basis
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Strength training
General strength training may be undertaken preand postoperatively although there is a 6-8 week
postoperative restriction on lifting activities for
children
Important that children breathe correctly during
resistance training in order not to increase the
blood pressure
Postoperative physiotherapeutic
intervention
Ward and out patient basis
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Neurodevelopmental outcomes in children with heart disease:
CHD often has a significant impact on a child’s development
Cause of delays are often multifactorial
Child with CHD may have brain insults prior to surgery due
to prolonged hypoxaemia
Studies have found that children with CHD show delays in all
main areas of development as well as tonal abnormalities
(hypotonia), abnormal posture emotional and behavioural
difficulties
Following open heart surgery children may suffer from mild
hypotonia, motor problems and CMD may occur in 5% of
cases.
Postoperative physiotherapeutic
intervention
Ward and out patient basis
Neurodevelopmental outcomes in children with heart disease:
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language development also delayed in many cases. Even at
one year after surgery most children were still behind for
age. Delayed gross and fine motor development also
impacted negatively on perceptual skills.
Children often exhibited behavioural problems and greater
caregiver dependency
Postoperative physiotherapeutic
intervention
Ward and out patient basis
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Neurodevelopmental therapy
Age appropriate play is an important activity that can be
used in order to get a child to move
In cardiac patient it is often important to then try and get the
child accustomed to prone over towel enven on a caregivers
lap during awake, play time. Prone is an important
developmental position.
Nerodevelopmental assessment and therapy to aid the child
in catching up on his age appropriate milestones is often
essential post operatively especially in younger children who
were acutely ill and failed to thrive.
Regular developmental monitoring would also be
recommended
Family and caregiver support
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A family suffers huge amounts of anxiety and stress in
the case of having a child with CHD
The distress, frustration and reaction shown by the
mother may affect the relationship with the child
Often over-restriction and over-observation of children
with CHD by parents
The child’s reaction and adjustment to their illness is
largely related to the emotional and behavioural
reaction of the family
Physiotherapist can play an important role by providing
support and encouraging more positive interactions
within the family
References
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Ammani Prasad, S. & Main, E. Paediatrics in Physiotherapy for
respiratory and cardiac Problems. Adults and children 4th ed. Pryor,
J.A. & Ammani Prasad, S. (eds.)358-363
E-medicine. 2010. pulmonary artery banding.
Available online at:
http://emedicine.medscape.com/article/905353-overview
Hendon. K.L. Not dated. Congenital Heart Disease (slideshow)
Children’s Cardiomyopathy Foundation. 2010. About the disease.
Available online at:
http://www.childrenscardiomyopathy.org/site/description.php
References
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Pepper, J.R.; Anderson, J.M. & Innocenti, D.M. 1992. Cardiac surgery
in Cash’s Textbook of chest, Heart and Vascular disorders for
Physiotherapists. 4th ed. Downie, P.A. (ed). Mosby, london pp 407429
Bar-Or, O. & Rowland, T.W. 2004. Cardiovascular disease in
Paediatric exercise medicine. From physiological principles to
healthcare application. Human Kinetics, USA Pp177-217
Brossman, H. 2008. Cardiac disorders in Pediatric Physical Therapy.
4th ed. Telin, J.S. (ed.). Lippincott williams Wilkins, Baltimore pp 589609
References

Main, E. 1998. Paediatric Cardiothoracic Surgery in Paediatric
Management in Cardiovascular/Respiratory Physiotherapy.Smith,
M. & Ball,V. (eds.).Mosby, London pp291-298
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Image courstey of GOOGLE images (2010)