CARDIAC SURGERY
Lec: 3
Congenital Heart Diseases:-
Atrial Septal Defect
: - An opening in the interatrial septum which leads to
mixing of blood from pulmonary and systemic circulation. It is common and
represents 7% of all congenital heart diseases; female to male is 3 to 1. It can
occur alone or together with other congenital heart diseases. It may be essential
for life and sometimes created surgically.
Anatomical Classification:-
1. Ostium Secondom ASD :-in which the defect lies in the region of fossa
ovalis, it represents 85% of ASDs.
2. Ostium Primum ASD :- in which the atrial communication is just above
the mitral and Tricupid valve orifices and they are usually associated
with a cleft in the mitral valve.
3. Sinus venosus ASD: - represent 10% of ASDs usually associate with
anomalies of pulmonary venous return.
Natural History:-depends on 1.Type of defect, 2.Size of shun
3. Associated anomalies.
Pathophsiology:- ASD result in shunt of blood from left to right atrium
under low pressure producing excess pulmonary blood flow and increase
cardiac work load ,this will lead to gradual increase in right side pressure till it
becomes equal to left side pressure and bidirectional shunt develop through
different phases of cardiac cycle.
Clinical features:-
The child is usually smaller than normal otherwise they
are asymptomatic, as patient grow old they complain from palpitation,
tachypnea, On auscultation a fixed splitting of second heart sound and ejection
systolic murmur can be heard in pulmonary area.
Diagnosis:-By echo which shows the type of defect and the direction of
intracardiac shunt.
Manegement:-Spontaneous closure of ASD may occur but it is uncommon after
6 month age. Closure can be done either by surgery through median
sternotomy and cardiopulmonary bypass using synthetic patch or by
catheratization using umberella devise, usually this is better to be done for
children at pre-school age.
PATENT DUCTUS ARTERIOSUS:
Is a congenital anomaly caused by failure of
closure of the duct which connects between the pulmonary artery and the aorta
after birth, this will lead to excess flow of blood from aorta to pulmonary artery
after reduction of high fetal level of pulmonary vascular resistance, symptoms
depend on the size of duct, age at presentation and associated anomalies.
Clinical feature: In full term infant symtoms start at 6-8 weeks of life after
reduction of pulmonary vascular resistance(PVR) which leads to shunt, while in
premature infants symptoms begin in the 1
st
week of life due to presence of less
smooth muscles in the pulmonary arterioles which lead to earlier reduction in
PVR, commonest presentations are:-
1. Hyperactive pericardium and hyperdynamic circulation.
2. Bounding peripheral pulses with normal systolic BP and decreased
diastolic BP.
3. Continuous machinary murmur in the pulmonary area .
4. In severe cases heart failure may develope and galloping rythm can be
heard over pericardium
Diagnosis:By ECHO which shows the PDA and the associated anomalies.
MANEGEMENT:- Depends on age of patient and the presence of symptoms.
1. In premature infant prostaglandin inhibitor (indomethacin ) may be used
with70 % success rate.
2. In full term symptomatic infant closure of the duct must be done , this is
either done by catheterization or by surgery through left posterolateral
thoracotomy through 4
th
intercostals space.
3. In full term asymptomatic infant closure of the duct can be delayed till 5
years old.
VENTRICULAR SEPTAL DEFECT:
A hole in the interventricular septum may be
single or multiple and it represent about 40% of all congenital heart diseases, it
causes shunt of blood from left ventricle to right ventricle under high pressure.
Anatomical classification of VSDs depends on the site of the defect in the
interventricular septum which is of two main kinds:
1. Perimemberanous VSD occurs in the membranous part of ventricular
septum.
2. Muscular VSD occur in the muscular part of ventricular septum.
Clinical features: - depends on the size of VSD.
1. Small VSD may be asymptomatic or associate with few symptoms with small
amount of left to right shunt of blood.
2. Moderate size VSD usually asymptomatic at early life then they develop
tachycardia, tachypnea, inability to feed with more left to right shunt of blood.
3. large size VSD .infant usually develop congestive heart failure and failure to
thrive with recurrent chest infection ,they may die at one year age, the huge left
to right shunt will lead to increase in right side pressure which will end with
pulmonary hypertension if it is not treated .
On Auscultation: apansystolic murmur is heard over the apex of the heart.
If right side pressure increases, right to left shunt may develope and the patient
become cyanotic, here the intensity of murmur may decrease or may disappear.
Diagnosis: - By ECHO which shows the size and site of VSD, demonstrate the
direction of intracardiac shunt and give idea about pressure difference between
the two ventricles.
MANEGEMENT: VSD may be closed spontaneously the percentage of
spontaneous closure is inversely related to the age at which the patient is
diagnosed.
1. Small asymptomatic VSD may be observed up to 10 year age waiting for
spontaneous closure if not it must be closed surgically.
2. Moderate size VSD can be observed till 4 year age for spontaneous closure
if not it must be closed.
3. Large VSD with huge shunt must be closed before 2 year age.
Closure is done by surgery through median sternotomy and cardiopulmonary
bypass, usually the Right atrium is opened and the VSD is closed by a synthetic
patch
TETRALOGY OF FALLOT:-
Is congenital heart disease which presents with
ventricular septal defect, overriding of the aorta to Right ventricle, hypertrophy
of Right ventricle muscles and Right ventricle outflow tract obstruction, it may
occur alone or with other conginetal heart diseases. symtoms depends on
severity of malformation.
Infant usually present with cyanosis, tachypnea, they are usually small for age.
on auscultation ejection systolic murmur can be heard over pulmonary area.
In sever cases cyanotic spells may develope and infant try to sequate to increase
pulmonary blood flow
DIAGNOSIS:
1. Chest film shows narrow shadow of grate vessel in the superior
mediastinum with classical boot shape heart .
2. ECHO can diagnose the anomaly and show direction of the right to left shunt
MANEGEMENT:
It is better to repair the anomaly as early as possible before two year age, the
urgency of operation is determined by the age and severity of symptoms at
presentation, in severe cases prostaglandin E1 can be used to keep ductus
arteriosus open to increase pulmonary blood flow
Surgery is done by median sternotomy , cardiopulmonary bypass and total
correction by closing the VSD and enlargement of right ventricle out flow tract
together with resection of part of hypertrophied Right ventricle muscles.
Coarctation of Aorta:
mean the presence of narrowing of the aortic arch usually distal to
the site of insertion of ductus arteriosus and origin of left subclavian artery which leads to
blood flow obstruction in the descending thoracic aorta., it represents 5-10% of congenital
heart diseases, male > female.
Clinical Features:
Symtoms usually develop after closure of ductus arteriosus, infants
present with irritability, poor feeding, tachypnea while older children and adults present
with symtoms of unexplained high blood pressure in the head and upper limbs in
comparison to lower part of body, symtoms like headache, epistaxis, visual field
disturbance may be present,
O/E- 1. asystolic murmur can be heard over left pericardium and in between the
scapulae posteriorly. 2. arm-leg systolic BP gradient may be present. 3. Diminished
femoral pulse with delayed upstroke.
4.bruit of enlarged collateral vessels around the coarctation may be heard at the
infrascapular region.
Dx: 1. Chest film can show Cardiomegaly + Nothed ribs from enlarged
tortuous intercostals arteries.
2. Angiography can show the site and extent of narrowing and collateral vessels.
3.Echo to exclude presence of other cardiac anomalies.
Mx: Is by Left Posteriolateral thoracotomy through 4
th
intercostal space, the narrow
segment is resected and an appropriate size synthetic graft is used to bridge the defect.