Professional Documents
Culture Documents
AND ITS
DISORDER IN
CHILDREN
INTRODUCTION
The
THE HEART
The
ANATOMY
The
CONTD
Two
ETIOLOGY: It
CLASSIFICATION OF COMMON
CONGENITAL HEART DISEASE
ACYANOTIC HEART
DISEASE:Left to right shunt
Obstructive lesions
1. Pulmonary stenosis(PS)
1. Co-arcation of aorta
CYANOTIC HEART
DISEASE
Decreased
pulmonary blood
flow
Increased pulmonary
blood flow
1. Tetrology of
fallot(TOF)
1. Transposition of great
vessels
1. Tricuspid atresia
1. Total anomalous
pulmonary venous
connection
VENTRICULAR SEPTAL
DEFECT(VSD)
An
HEMODYNAMICS:
The pressure in left ventricle is greater in right ventricle this promotes the flow of
oxygenated blood from the left ventricle to this right ventricle shunt. This results in
increased right ventricular pressure and increased blood flow in right ventricle.
The flow of blood from left ventricle to right ventricles starts early in systole.
When the defect is restrictive, a high pressure gradient is maintained between the two
ventricles throughout the systole.
The murmur starts early masking the first sound and continues throughout the systole
with almost the same intensity appearing a pansystolic murmur on auscultation. As a
thrill.
Pulmonary artery and lungs as the disease progress long standing pulmonary arterial
hypertension may result in increased pulmonary resistance.
These results in diminished blood flow to the blood flow through the pulmonary
artery and veins and markedly in this right ventricle pressure there by the right
ventricle. Pressure raised by left ventricle pressure.[ventricular pressure lower than
aortic pressure].
The increased blood volume in left atrium may result in left atrial enlargement.passing
through a normal mitral valve results in delayed diastolic murmur at the apex.
CONTD
Since left ventricle has two outlets, the aortic valve
allowing forward flow and the VSD result in backward
leak, since the ejection into the right ventricle and
pulmonary artery is increased because of left to right
shunt.
At this stage, the direction of shunt is reversed to right to
left shunt. Cyanosis appears due to mixing and
hypoxaemia. This condition results in eisenmenger
complex. This indicates poor prognosis.
CLINICAL MANIFESTATION
Palpitation
Weight gain
Failure to thrive
Tachycardia
Tachypnea
Feeding problems
Exsertional dyspnea
Seating excessive
COMPLICATION
Pulmonary
Diagnosis
DIAGNOSTIC EVALUATION
MANAGEMENT
If
MEDICAL MANAGEMENT
Administration
SURGICAL MANAGEMENT
Surgery
OPERATIVE TREATMENT
Consists
TYPES
The defect is located at the center of the atrial septum the site of foramen
ovale.
Ostium primumASD:-
There is a large gap at the base of atrial septum and associated with deformity
of mitral and tricuspid valve or a small or high VSD.
They are located in the central portion of atrial septum, in the position of
foramen ovale. These defects are amenable to closure in catheterization in
laboratory.
Sinus venosusASD-
They are located at junction of superior vena cava and right atrium. These
defects do not have a superior margin because superior vena cava straddles
the defect.these defect is associated with anomalous drainage of one or
more right pulmonary veins.
HEMODYNAMICS
The
CLINICAL MANIFESTATION
ASD
DIAGNOSTIC EVALUATION
On
MANAGEMENT
Spontaneous
PATENT DUCTUS
ARTERIOSIS(PDA)
PDA is
HEMODYNAMICS
During fetal life the ductus arteriosis allow most of the ventricular blood to
bypass by non direction lung by direct in blood from pulmonary artery to aiota.
After birth with the initiation of respiration the ductus arteriosis is no longer
needed.
It should functionally closed within several hrs after birth (24-72hrs) and
anatomically within several days after birth.
If ductus arteriosis remain patent, oxygenated blood from the higher systemic
cercube flows to the lower pressure pulmonary cercube flow through PDA.
This cause left to right shunt.{in premature infants ductus arteriosis may remain
open because of lower oxygen level resulting from respiratory distress after
birth}
*Because of transfer of blood from aiota to pulmonary artery through the ductus
systemic flow is compromised. The volume blood that the heart must pump
meet demands of the peripheral tissue is increased. On the other side a greater
volume burden is placed on the lungs and hence on the left side of the heart.
CLINICAL MANIFESTATION
Children
life.
Older children present effort intolerance, easy
fatiguability, dyspnea on exertion
Increase respiratory infection
Frequent chest infection
Heart rate per over 150/mt, gallop rhythm due to
rapid filling of ventricle.
Large defect may be associated with congestive heart
failure and pulmonary hypertension.
Pulse is high volume and bounding pulse pressure is
wide.
ASSESSMENT OF SEVERITY
Larger
DIAGNOSTIC EVALUATION
Chest
DIFFERENTIAL DIAGNOSIS
Coronary
arteriovenous fistula
Ruptured sinus of valsalva fistulae into
right side
Systemic arteriovenous fistula over the
chest.
Pulmonary arterialvenous fistula
Bronchial collateral murmur
MANAGEMENT
Medical management: Indomethazine or ibuprofen may be used to close the
ductus in small new born preterm newborn; if diagnosis
is made within 2 wks of life.
Indomethzine causes inhibition of prostaglandin
synthesis 12-18 hrs after medication, improvement in left
or right shunt.
Dose is 0.2 mg/l kg/dose, orally, every 12-24 hr for three
doses(second and third dose is at 0.1 mg/kg/dose for <48
hr old and 0.25 mg/kg/dose for>7 days old)
Side effect of indomethazine:- it reduces amount of
albumin bound serum bilirubin and may develop
hyperbilirubinemia also a danger of transient and
hyponetremia.
SURGICAL MANAGEMENT
Consist of ligation of PDA, now a days device coil
closure of PDA is possible without need of
surgery in children more than 5 kg.
Note: - since the right to left shunt through the
PDA flows down the descending aorta, cyanosis is
present in toes but not in fingers. This is called
differential cyanosis and is a characteristic of
PDA with pulmonary arterial hypertension and
right to left shunt.
OBSTRUCTIVE LESIONS
These
AIORTIC STENOSIS
There
HEMODYNAMICS
CLINICAL FEATURES
Dyspnea
on exertion
May have history of angina on effort and
syncope.
Cardiac size is normal unless left
ventricular failure is present.
Systolic thrill may be palpable at the
second right interspace, suprasternal notch
and carotid arteries.
DIAGNOSIS
Pulse
MANAGEMENT
If
PULMONARY STENOSIS
There
is an obstruction to flow of
blood from right ventricle to lungs. It
accounts for 8% of congenital heart
defect.
90% of the obstruction occurs at the
level of pulmonary valve other
outside subvavlvular and
supravalvular pulmonary stenosis.
CONTD..
CONTD..
Infundibular
stenosis can be
distinguished from pulmonary stenosis
by: absence of click
absence of post stenotic dilatation
Relatively lower point of maximum
intensity of systolic murmur in 3-4 th left
interspace
HEMODYNAMICS
Blood
CLINICAL MANIFESTATION
Child
is generally asymptomatic.
Poor exercise tolerance; child become fatigue
with exertional dysphagia, precordial pain.
Presence of murmur in mild stenosis, cyanosis
and cardiac failure may occur with the severe
defect with severe symptoms of severe stenosis.
Complication-anoxic spell in infant, bacterial
endocarditis, congestive heart failure and sudden
death.
DIAGNOSTIC EVALUATION
Auscultation
MANAGEMENT
Pre
COARCTATION OF AORTA.
It
is a narrowing or constriction of
aiorta at any point most commonly
the constriction is located distal to
origin of the left subclavin artery in
the vignity of the ductus arteriosis.
HEMODYNAMICS
In fetal life the portion of the aorta distal to the left subclavian and
before the portion where the ductus arteriosus join is called Isthmus. At
birth, isthmus is the narrowest part of the aorta.
Following closure of ductus arteriosus, the descending aorta must
receive its total supply from left ventricle via ascending aorta.
The exact mechanism for the production of systemic hypertension in
coarcation is not known.
The narrowing of aorta obstructs the blood flow through constricted
segment of aorta thus increasing left ventricle pressure and work load.
Collateral vessel develops arise in chiefly between the branches of
subclavin and intercostals artery by passing the coarcation segment of
aorta and subclavin circulation to the lower extremity.
Palpable collaterals are also felt at medial and inferior angel of scapula.
Because of the decompression of the upper segment by collaterals, the
resting blood pressure in upper extremity may even be normal, but rises
on exercise.
CLINICAL MANIFESTATION
Children
CONTD.
Severe
DIAGNOSTIC EVALUATION
Reversal
MANAGEMENT
Either
Fig 16 anastomosis
TETRALOGY OF FALLOT
It
HEMODYNAMICS
Due
CLINICAL MANIFESTATION
Clinical
CONTD..
Hypercyanotic
CONTD
Clubbing of fingers, toe nails occur by 2-4 yr of age.
Exercise cause severe dyspnea.
Infant take knee chest position rather than expanding their
extremities when they lie down.
Child assumes squatting position to increase pulmonary blood
flow squatting act by increasing systemic resistance and
defecating blood flow to relatively low resistance pulmonary
circuit.
Infant becomes cyanotic and gasp for breath, convulsion or
hemeparesis even death may present.
Slow weight gain, failure to thrive, associated with dyspnea on
exertion.
CONTD
Short episodes of unconsciousness followed by sleep
may persist.
Murmur shortens and cyanosis increased with increasing
severity of right ventricular outflow tract obstruction.
COMPLICATION
Infective
endocarditis
Cerebrovascular accidents
Paradoxical embolism
Anoxic infarction due to anoxic spell.
Brain abscess Polychythemia develops because of body
attempts to compensate for unoxygenated blood.
The resulting increase viscosity of the blood
causes slowing of the circulation and possibly
thrombophlebitis, embolism and cerebrovascular
defect may occur.
DIAGNOSTIC EVALUATION
Cyanosis,
clubbing, polychythemia
Chest X ray reveals heart size is normal and
shape like shoe(boot shaped heart)
Pulmonary segment appear small and concave.
Lung margin is diminished
ECG reveals right axis deviation and left
ventricular hypertrophy.
Lab investigation shows degree of
polychythemia, arterial oxygen desaturation.
MEDICAL MANAGEMENT
Child
spell.
Oral B-blocker helps to prevent cyanotic spells.
Maximally tolerated dose of propranol ranging
from 0.5-1.5 mg/kg/dose should be administered.
Treat for dehydration and anemia.
Iron supplementation.
Treatment for congestive heart failure
vigorously.
SURGICAL MANAGEMENT
Palliative
CONTD..
Anastomosis of upper descending aorta and left pulmonary
artery(potts procedure): The particular blood vessel i.e. used to create a systemic
pulmonary anastomosis depends on the childs size because
one i.e too large may result in congestive heart failure.
Fig 20 Anstomosis
CONTD
Mustard
TRICUSPID ATRESIA
Failure
CLINICAL MANIFESTATION
Left
DIAGNOSTIC EVALUATION
Chest
X-ray
ECG left ventricular hypertrophy.
Cardiac catheterization
PATHOPHYSIOLOGY
At
MANAGEMENT
In
SURGICAL MANAGEMENT
Palliative
MODIFIED FONTAN
PROCEDURE
In
TRANSPOSITION OF GREAT
VESSEL(TGA)
TGA occurs
HEMODYNAMICS
This
CONTD
Two
CLINICAL MANIFESTATION
These
COMPLICATION
Infective
endocarditis
Brain abscess
Cerebro vascular accident due to
thrombosis
Severe hypoxia.
DIAGNOSTIC EVALUATION
Chest
MEDICAL MANAGEMENT
Treating
SURGICAL TECHNIQUE
Palliative
CONTD
CONTD
Arterial
TOTAL ANOMALOUS
PULMONARY VENOUS
CONNECTION (TAPVC)
All
HEMODYNAMICS
CLINICAL FEATURE
Cyanosis
Failure
to thrive
Cardiomegaly
Hyperkinetic precordium normal or accentuated
pulmonic component. A grade two to four
pulmonary ejection systolic murmur and a
tricuspid flow murmur.tricuspid regurgitation
DIAGNOSTIC INVESTIGATION
ECG
MANAGEMENT
Operation
ETIOLOGY
This
PATHOPHYSIOLOGY
During
CLINICAL FEATURES(MAJOR
CLINICAL MANIFESTATION)
Fever(range
102-1040F)
Polyarthritis i.e. joints shows limited range of
motion, inflammation , tenderness,
swelling(generally in large
joints,knees,wrist,elbow,shoulder and hip)
Other chacteristics:-Migrating and reversible
nature of progress helps to differentiate from
other of arthritis.
CONTD..
Carditis-
CONTD
Stenosis-
CONTD
Chorea(syndenhens
CONTD
Subcutaneous
MINOR COMPLICATION
Low grade fever(high in afternoon)
Weakness, fatigue, weight loss, epistaxis with no
known cause and abdominal pain.
Prolonged PR interval in ECG
COURSE OF DISEASE
Cardiac
DIAGNOSTIC EVALUATION
ASO(antistreptolysin
ESSENTIAL CRITERIA
Increase
ASO titer
Scearlet fever
Positive throat culture
MEDICAL MANAGEMENT
Focus
MANAGEMENT
Start
CONTD
Penicillin: Give
NURSING MANAGEMENT
Bed
CONTD
Accident
CONTD
If
PREVENTION
Primary
SYMPTOMS
People
PATHOPHYSIOLOGY
Normal blood flow from the left atrium to the LV and,
subsequently, to the systemic circulation, is altered in mitral
regurgitation.
In the presence of mitral regurgitation, blood flows antegrade
from the LV into the aorta, and the regurgitant volume flows
retrograde from the LV into the left atrium.
This causes a proportionate increase in LV ejection volume. The
regurgitant fraction reenters the LV, producing left ventricular
volume overload.
The LV compensates via the Frank-Starling mechanism,
resulting in a greater ventricular stroke volume.
CONTD
The volume of the regurgitant fraction depends on
several factors, including size of the orifice allowing
regurgitation and the pressure gradient between the left
ventricle and left atrium.
This volume also depends on ventricular systolic
pressure; therefore, the regurgitant volume increases in
situations that increase afterload, such as hypertension or
aortic stenosis.
COMPLICATIONS
In
CONTD
Inotropic agents may improve systolic blood pressure.
Intra-aortic balloon counterpulsation or immediate
surgical intervention (valvuloplasty) may be necessary in
severe cases.
In patients who stabilize but remain symptomatic, early
semielective surgery should be considered to reduce the
risk of irreversible ventricular dysfunction.
Patients who become asymptomatic with medical
therapy can be treated in the same manner as those with
chronic mitral regurgitation.
SURGICAL CARE
CONTD
Quadrilateral resection of a prolapsing leaflet with sliding
annuloplasty may be helpful in cases with mitral valve
prolapsed
E-to-E mitral valve repair is help in some cases in which an
opposition suture in placed in the center of the anterior and
posterior leaflets producing a double orifice
Mitral valve replacement is the final option in the treatment of
mitral regurgitation. The choice of which valve to use
(mechanical vs bioprosthesis) can be difficult.
Bioprosthetic valves resolve the anticoagulation issue but raise
problems of their own. Bioprostheses may degenerate rapidly
and may become calcified and dysfunctional as early as 6
months after insertion.
MITRAL STENOSIS
Mitral
CAUSES
Mitral
SYMPTOMS
Chest discomfort that increases with activity and extends to the arm,
neck, jaw or other areas (This is rare)
Cough, possibly with bloody phlegm
Difficulty breathing during or after exercise, or when lying flat;
Waking up due to breathing problems (This is the most common
symptom)
Fatigue
Frequent respiratory infections, such as bronchitis
Feeling of pounding heart beat (palpitations)
Swelling of feet or ankles
In infants and children, symptoms may be present from birth (congenital).
It will almost always develop within the first 2 years of life. Symptoms
include:
Cough
Poor feeding, or sweating when feeding
Poor growth
Shortness of breath
TREATMENT
SURGICAL TREATMENT
Percutaneous mitral balloon valvotomy (also called
valvuloplasty). During this procedure, a tube (catheter) is
inserted into a vein, usually in the leg. It is threaded up
into the heart. A balloon on the tip of the catheter is
inflated, widening the mitral valve and improving blood
flow. This procedure may be tried instead of surgery in
people with a less damaged mitral valve.
Surgery to repair or replace the mitral valve.
Replacement valves can be made from different
materials. Some may last for decades, and others can
wear out and need to be replaced.
(PROGNOSIS)
POSSIBLE COMPLICATIONS
Atrial
TRICUSPID
REGURGITATION
The
ETIOLOGY
Infection,
SURGICAL MANAGEMENT
Fig 37 Anatomically correct design conforms to the 3-D tricuspid valve opening.
AORTIC REGURGITATION
Aortic
CONTD
Aortic
CAUSES
CONTD.
CONTD
CONTD
SYMPTOMS
TREATMENT
When
NURSING MANAGEMENT OF
A CHILD WITH HEART
DISORDER
NURSING ASSESSMENT
Complete thorough history of child and family should be taken.
Child growth and development pattern, exercise intolerance.
Observe childs skin, mucous membrane for colour and temperature
change.
Extremities-Are extremities cold? is their difference present between
upper and lower extremity, check quality of pulse in all limbs, check
edema in extremity.
Observe for clubbing increase in soft tissue around terminal phlenges
of finger especially thumb nail. This may occur in cyanotic children one
year of age.
Observe for any chest deformity and precordial pulse.
Auscultate apical pulse rate for full one minute.
Determine cardiac rhythm or any change
Record vital signs
Look for any other congenital defect, abnormal fascia or relevant history.
oxygen therapy.
Observe child response to oxygen.
Observe child response while weaned off
from oxygen.
SUMMARY