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CONGENITAL
HEART DISEASE
    (CHD)
CONGENITAL HEART DISEASE (CHD)

They are typically arise in the 3rd–8th week of
  gestation.
The incidence of significant cardiac abnormalities is
  8:1000 live births.
In neonates and children with CHD, 15% will have
  more than one cardiac abnormality and 15% will
  have another extra-cardiac abnormality.
There are approximately nine 'common'
  congenital heart defects that make up about 90%
  of all cases of congenital heart disease; the
  remaining 10% are rare complex cardiac defects.
CONGENITAL HEART DISEASE (CHD)
                    Aetiology :

There is often no obvious aetiology; most would
  appear to be multifactorial with both genetic and
  environmental influences:
Maternal (environmental) factors
  Infection
  Rubella Disease
  DM, Maternal DM ,Drugs/medications Alcohol
  abuse,
Genetic factors
  Marfan syndrome
  Trisomy 21 , trisomy 18 (Edwards syndrome)
  Turner syndrome,
CONGENITAL HEART DISEASE (CHD)
              Classifications:
Congenital heart disease can be broadly
 classified according to the presence or
 absence of   cyanosis,
The presence of central cyanosis,
 blueness of the trunk and mucous
 membranes, is due to > 3-5 g/dl of
 deoxygenated haemoglobin in the
 arterial circulation.
CONGENITAL HEART DISEASE (CHD)
              Classifications:
I.   Cyanotic congenital heart diseases
       make up 1/3 of cases, and are usually
       more complex:
1.    A right to-left shunt resulting in decreased
      pulmonary blood flow.
     Many of these lesions consist of a septal
      defect in con-junction with a right-sided
      obstructive lesion, producing an obligatory
      right-to-left shunt.
     The most common type
     Tetralogy of Fallot (TOF).
CONGENITAL HEART DISEASE (CHD)
         Classifications:


2. Parallel systemic and
 pulmonary blood flow rather
 than in series.
 This is incompatible with life if there is no
 mixing, so typically neonates have a
 patent foramen ovale that allows some
 mixing of the two circulations at this
 level.
    The most common example of this is
   Transposition of the Great Arteries
                 (TGA).
CONGENITAL HEART DISEASE (CHD)
            Classifications:


3. Defects in the connections to the
  heart
 where there is mixing of the systemic and
  pulmonary flows.
An example of such a complex lesion is
  Total Anomalous Pulmonary Venous
  Drainage
CONGENITAL HEART DISEASE (CHD)
            Classifications:
II. Acyanotic congenital heart
   diseases represent : 2/3 of the cases
1. Left-to-right shunt with increased
   pulmonary blood flow:
which causes an increase in volume work
   on the heart e.g. patent ductus
   arteriosus (PDA), atrial septal defect
   (ASD) and ventricular septal defect
   (VSD).
CONGENITAL HEART DISEASE (CHD)
            Classifications:


2. An obstruction of the blood flow
  across a heart valve on the left
  heart:
such as aortic stenosis or in the aorta
  itself as occurs with coarctation of the
  aorta, leading to an increase and work
  of the heart.
I. Cyanotic CHD
Fallot's tetralogy
This is the most common cyanotic
  congenital heart disease and accounts for
  about 4-6% of all congenital heart
  diseases.
The four intracardiac lesions originally are:
   1. Pulmonary (typically infundibular or
      subpulmonary) stenosis;
   2. Right ventricular hypertrophy
   3. VSD;
   4. Overriding aorta
Fallot's tetralogy




                Four abnormalities
Clinical features:
The degree of cyanosis depends on the degree of pulmonary
   stenosis.
If there is significant pulmonary stenosis to virtual pulmonary
   atresia, presentation is in the neonatal period because of duct
   dependency.
As pulmonary stenosis progresses, cyanosis typically develop with
   in the first year of life.
Classically, hypercyanotic spells are thought to be due to
   infundibular or subpulmonary muscle spasm.
Squatting is an adaptation by the child to such hypoxic spells. This
   increases systemic vascular resistance and the venous return to
   the head.
Physical examination: moderate systolic ejection murmur which
   may disappear during a spell.
Continuous murmurs may be found in patients with
   aortopulmonary collaterals .
Clubbing develops in older children, usually after 6 months of age.
Investigations:
   ECG : right atrial and right ventricular
  hypertrophy.
 Chest x-ray: 'boot-shaped' heart with
  poorly developed lung vasculature.
 The Echocar-diography is diagnostic .

 Cardiac catheterization prior to
  surgery.
Indications for surgery

These are based on clinical
  progression include:
 Severe cyanosis ( oxygen
  saturation < 80% on room air),
 Hypercyanotic spells,

 Dyspnoea on effort,

 Syncopal attacks and

 Polycythaemia.
Surgical options (Curative)
        When the infant becomes symptomatic, a complete
         primary repair may be performed as a first
         procedure, or
        if asymptomatic, elect for total primary repair early,
         ideally with in the first 6 months, but usually within
         the first 3 years.
        This approach has the advantage of reducing the
         number of operations, restores normal oxygen
         saturation earlier in life and so helps development
         and, by repairing the defect early, leads to less right
         ventricular hypertro-phy, which may reduce the
         frequency of late arrhythmias.
Surgical options (Curative)




•Reapire of VSD

Enlagement of
the pulmonary
trunk
Surgical options (Palliative)
   Such palliative procedures divert systemic blood into the
    pulmonary circulation and may be used to improve
    oxygenation.
   Many types of systemic-to-pulmonary artery shunts have
    been described such as left subclavian to pulmonary
    artery shunt (Blalock-Taussig) or other modifications.
   The results of surgery are good with late survival at 5-10
    years following correction of tetralogy is 95%, with an
    operative mortality for a repair of between 5% and 10%,
    and an incidence of reoperation following tetralogy repair
    of 5-10%.
Surgical options (Palliative)
Transposition of great arteries
                  (TGA)

Is the second most common CHD, making up 2.5-5% of all
   congenital heart disease, and is the most common cause
   of cyanosis from a congenital cardiac defect discovered in
   the new-born period.
Clinical features

   Severe central cyanosis presenting in the first 48
    hours of life, with the cyanosis progressing in the
    first week.

   If there is a large atrial septal defect or ventricular
    septal defect there may be minimal cyanosis
    initially.

Investigations:
 The chest radiograph: pulmonary plethora, with the
  heart having an 'egg on its side' appearance, with a
  small pedicle (aorta in front of pulmonary artery).

   Cardiac catheterization and echocardiography
    confirm the diagnosis and delineate the anatomy.
Indications for surgery


   The outcome for infants with TGA in the
    first year of life without some form of
    intervention to increase systemic and
    pulmonary venous admixture is death in
    80-90% of cases.
   Initial palliation is by percutaneous
    (Rashkind) balloon atrial septostomy, or
    alternatively intravenous prostaglandin to
    keep the ductus open.
   Definitive repair is usually the Total Arterial
    Switch procedure, which has replaced the
    atrial switch or baffle (Mustard or Senning)
    operation because of reduced long-term
    complications
Cardiac Surgery


II. Acyanotic CHD
I. Patent ductus arteriosus
Accounts for 8-12% of congenital
  heart disease.
The ductus arteriosus, a normal
  fetal communication, facilitates
  the transfer of oxygenated blood
  from the pulmonary artery to the
  aorta shunting blood away from
  the lungs.
Normally, functional closure of the
  ductus occurs within a few hours
  of birth; it is abnormal if it
  persists beyond the neonatal
  period
Patent ductus arteriosus
                     Clinical features

 Small shunts usually causing no symptoms, and few signs
  apart from a continuous machinery murmur in the left
  sec-ond intercostal space.
 Larger ducts cause cardiac failure and can uncommonly
  lead to shunt reversal with cyanosis and clubbing.
Investigations :
   Echocardiography with Doppler colour flow.
   Cardiac catheterisation is performed only if additional
  lesions are suspected.
Indications for surgery:
 After 6 months of age, spontaneous closure of PDA is
  rare. Most should be closed by the preschool age.
 In the adult, surgical treatment is indicated if there is a
  persistent left to right shunt, even in the presence
  pulmonary hypertension.
Patent ductus arteriosus


Surgical options
   In the premature infant, pharmacological closure
    of the patent ductus arteriosus with indomethacin
    is generally successful.
   If medical treatment to close the ductus is
    unsuccessful, the lesion may be treated by
    interventional cardiology, using an umbrella or
    coil duct occlusion device inserted
    percutaneously.
   Surgical closure via a left thoracotomy, if the
    lesion is very large or the patient very small is
    preferred.
   This can be accomplished by either ligation or
    division of the patent ductus arteriosus.
II. Coarctation of the aorta


   This accounts for 6-7% of
    congenital heart disease
    and is defined as a
    haemodynamically
    significant narrowing of
    the aorta, usually in the
    descending aorta just
    distal to the left
    subclavian artery, around
    the area of the ductus
    arteriosus
III. Coarctation of the aorta

                       Pathophysiology
   The upper body is well perfused but
    the lower body, including the
    kidneys, is poorly perfused leading
    to fluid overload, excess renin
    secretion and acidosis.

   Children with coarctation are
    usually male and, if it occurs in
    females, it is suggestive of Turner
    syndrome.
   There are several common
    associated lesions, including
    bicuspid aortic valve, ventricular
    septal defect.
Coarctation of the aorta
              Clinical features
   The child may appear well in the first few days
    of life because the coarctation is bypassed
    by the ductus arteriosus and oxygenated
    blood reaches the entire systemic circulation.
   As the ductus closes, the child becomes
    progressively more unwell.
   Hypertension is a common presenting
    problem in older children, often just upper
    body hypertension with development of
    enormous collateral vessels that may cause
    ribnotching and flow murmurs over the scapula.
   Other symptoms include prominent pulsation
    in the neck, tired legs or intermittent
    claudication on exercise.
III. Coarctation of the aorta
 Indications for surgery


   Neonate with severe failure, operation
    indicated at time of diagnosis
   If cardiac failure delay 3-6 months
   Increased incidence of recurrent
    stenosis if operated at less than 3
    months
   Increased incidence of hypertesion if
    coarctation is repaired beyond infancy
III. Coarctation of the aorta
Surgical options
 Operative options include
  resection of the coarctation and
  end-to-end anastomosis or the
  use of the left subclavian artery
  as an onlay flap.
 In the older patient, th
  subclavian flap opration is not
  feasible and resection with end-
  to-end anastomosis,
  interposition graft or a 'jump'
  graft are preferred.
 Percutaneous balloon dilatation
  is an alternative procedure in
  older children and adults and, in
  particular, for recoarctation.
IV. Atrial Septal Defect (ASD)

   ASD is a defect in the
    septum between the left
    and right atria leading to
    a left-to-right shunt.
   It accounts for
    approximately 6-7% of
    all congenital heart
    disease and is more
    common in females.
   There are three
    commonly recognised
    atrial septal defects.
IV. Atrial Septal Defect (ASD)
                Symptoms and Signs

   Most small ASDs are asymptomatic.
   Larger shunts may cause exercise intolerance,
    dyspnea during exertion, fatigue, and atrial
    arrhythmias sometimes with palpitations.
   Passage of microemboli from the venous
    circulation across the ASD (paradoxical
    embolization), often associated with arrhythmias,
    may lead to cerebral or systemic thromboembolic
    disorders.
   Auscultation typically reveals midsystolic (or
    ejection systolic) murmur and a widely split, fixed
    S2 at the upper left sternal border in children.
IV. Atrial Septal Defect (ASD)
          Investigations:

Echocardiography will
 define the anatomy and
 any other abnormalities
 including the direction
 of the shunt.
Indications for surgery

   For primum & secundum ASD that fail close to spontaneously
    close treatment is aimed at closing the defect if a left-to-
    right shunt of 1.5:1 or more is present.
   Closure is performed during the first decade, most small
    ostium secundum ASDs (< 3 mm) close spontaneously;
    about 80% of those between 3 mm and 8 mm close
    spontaneously by age 18 months.
   Asymptomatic children with a small shunt require annual
    echocardiography.
   Because these children are at risk of paradoxical systemic
    embolization, some centers recommend a catheter-delivered
    closure device (eg, Amplatzer Septal Occluder, Cardio-Seal
    device) even for small ASDs.
   However, these devices are not suitable for primum or sinus
    venosus defects because these defects are near important
    structures.
Surgical options


   The traditional method of closure
    involves open-heart surgery with
    cardiopulmonary bypass (CPB) and
    closure of the defect either directly
    with sutures, as with most secundum
    defects or, if the defect is large,
    using a pericardial or synthetic patch.
   Operative mortality for isolated atrial
    septal defect repairs is < 1%, with
    excellent prognosis.
V. Ventricular septal defects
                      (VSD)
   These account for 20-30% of congenital heart
    disease and affect approximately 2 in 1000 live
    births.
   A defect in the interventricular septum that
    allows a left-to-right shunting of blood.
   This may occur in isolation or as part of a more
    complex set of cardiac abnormali-ties (e.g.
    tetralogy of Fallot, complete atrioventricular
    canal defect)
   Four major anatomical types of ventricular septal
    defect are described, based on the anatomical
    subsections of the interventricular septum:
Ventricular septal defects
               Investigations
   Chest radiography: may show
    cardiomegaly and pulmonary
    congestion,
   ECG showing evidence of biventricular
    hypertrophy.
   Echocardiography confirms the
    diagnosis and can estimate the degree
    of shunting across the defect.
   Cardiac catheterisation can quantify the
    various pressures within the cardiac
    chambers and so assess degree of
    pulmonary hypertension.
Ventricular septal defects
              Clinical features
Small defects may close or cause little
  systemic disturbance.In the first 5 years,
  up to 30-50% of ventricular septal defects
  close spontaneously. Clinically, a loud
  pansystolic murmur can be detected at
  the left sternal border due to high
  pressure flow between thé ventricles.
Large defects typically present with
  congestive cardiac failure in the first 2
  months of life. There is a preceding
  history of dyspnoea on exertion, failure to
  thrive, poor feeding and recurrent chest
  infections.
Indications for surgery:

  Approximately one-third of defects close in the first year of
   life; a further one-third become relatively smaller in relation
   to the growing heart.
 In clinically small defects with a good response to medical
   management, it may be appropriate in the infant to 'watch
   and wait', although there is a risk of endocarditis.
 Generally, surgical closure is indicated for large defects,
   failure to respond to medical therapy,
     left-to-right shunts > 2:1, signs of increasing pulmonary
   vascular résistance and the presence of complications of
   ventric-ular septal defect.
These include
    (1) aortic regurgitation, which occurs in about 5% of defects;
    (2) infundibular stenosis, which tends to be progressive and
   leads to shunt reversal; and
    (3) infective endocarditis.
Surgical options


   If the infant is severely symptomatic,
    the defect should be closed urgently,
    otherwise elective repair is advised
    between 1 and 3 years of age in the
    asymptomatic patient.
   Most now advocate a primary total
    correction, usually at the onset of
    symptoms or by 1 year in the
    asymptomatic patient.
   Operative mortality for isolated
    ventricular septal defect closure is 2-
    4%, with long-term prognosis.
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surgery.Congenital heart disease.(dr.aram)

  • 2. CONGENITAL HEART DISEASE (CHD) They are typically arise in the 3rd–8th week of gestation. The incidence of significant cardiac abnormalities is 8:1000 live births. In neonates and children with CHD, 15% will have more than one cardiac abnormality and 15% will have another extra-cardiac abnormality. There are approximately nine 'common' congenital heart defects that make up about 90% of all cases of congenital heart disease; the remaining 10% are rare complex cardiac defects.
  • 3. CONGENITAL HEART DISEASE (CHD) Aetiology : There is often no obvious aetiology; most would appear to be multifactorial with both genetic and environmental influences: Maternal (environmental) factors  Infection  Rubella Disease  DM, Maternal DM ,Drugs/medications Alcohol abuse, Genetic factors  Marfan syndrome  Trisomy 21 , trisomy 18 (Edwards syndrome)  Turner syndrome,
  • 4. CONGENITAL HEART DISEASE (CHD) Classifications: Congenital heart disease can be broadly classified according to the presence or absence of cyanosis, The presence of central cyanosis, blueness of the trunk and mucous membranes, is due to > 3-5 g/dl of deoxygenated haemoglobin in the arterial circulation.
  • 5. CONGENITAL HEART DISEASE (CHD) Classifications: I. Cyanotic congenital heart diseases make up 1/3 of cases, and are usually more complex: 1. A right to-left shunt resulting in decreased pulmonary blood flow. Many of these lesions consist of a septal defect in con-junction with a right-sided obstructive lesion, producing an obligatory right-to-left shunt. The most common type Tetralogy of Fallot (TOF).
  • 6. CONGENITAL HEART DISEASE (CHD) Classifications: 2. Parallel systemic and pulmonary blood flow rather than in series. This is incompatible with life if there is no mixing, so typically neonates have a patent foramen ovale that allows some mixing of the two circulations at this level. The most common example of this is Transposition of the Great Arteries (TGA).
  • 7. CONGENITAL HEART DISEASE (CHD) Classifications: 3. Defects in the connections to the heart where there is mixing of the systemic and pulmonary flows. An example of such a complex lesion is Total Anomalous Pulmonary Venous Drainage
  • 8. CONGENITAL HEART DISEASE (CHD) Classifications: II. Acyanotic congenital heart diseases represent : 2/3 of the cases 1. Left-to-right shunt with increased pulmonary blood flow: which causes an increase in volume work on the heart e.g. patent ductus arteriosus (PDA), atrial septal defect (ASD) and ventricular septal defect (VSD).
  • 9. CONGENITAL HEART DISEASE (CHD) Classifications: 2. An obstruction of the blood flow across a heart valve on the left heart: such as aortic stenosis or in the aorta itself as occurs with coarctation of the aorta, leading to an increase and work of the heart.
  • 11. Fallot's tetralogy This is the most common cyanotic congenital heart disease and accounts for about 4-6% of all congenital heart diseases. The four intracardiac lesions originally are: 1. Pulmonary (typically infundibular or subpulmonary) stenosis; 2. Right ventricular hypertrophy 3. VSD; 4. Overriding aorta
  • 12. Fallot's tetralogy Four abnormalities
  • 13. Clinical features: The degree of cyanosis depends on the degree of pulmonary stenosis. If there is significant pulmonary stenosis to virtual pulmonary atresia, presentation is in the neonatal period because of duct dependency. As pulmonary stenosis progresses, cyanosis typically develop with in the first year of life. Classically, hypercyanotic spells are thought to be due to infundibular or subpulmonary muscle spasm. Squatting is an adaptation by the child to such hypoxic spells. This increases systemic vascular resistance and the venous return to the head. Physical examination: moderate systolic ejection murmur which may disappear during a spell. Continuous murmurs may be found in patients with aortopulmonary collaterals . Clubbing develops in older children, usually after 6 months of age.
  • 14. Investigations:  ECG : right atrial and right ventricular hypertrophy.  Chest x-ray: 'boot-shaped' heart with poorly developed lung vasculature.  The Echocar-diography is diagnostic .  Cardiac catheterization prior to surgery.
  • 15. Indications for surgery These are based on clinical progression include:  Severe cyanosis ( oxygen saturation < 80% on room air),  Hypercyanotic spells,  Dyspnoea on effort,  Syncopal attacks and  Polycythaemia.
  • 16. Surgical options (Curative)  When the infant becomes symptomatic, a complete primary repair may be performed as a first procedure, or  if asymptomatic, elect for total primary repair early, ideally with in the first 6 months, but usually within the first 3 years.  This approach has the advantage of reducing the number of operations, restores normal oxygen saturation earlier in life and so helps development and, by repairing the defect early, leads to less right ventricular hypertro-phy, which may reduce the frequency of late arrhythmias.
  • 17. Surgical options (Curative) •Reapire of VSD Enlagement of the pulmonary trunk
  • 18. Surgical options (Palliative)  Such palliative procedures divert systemic blood into the pulmonary circulation and may be used to improve oxygenation.  Many types of systemic-to-pulmonary artery shunts have been described such as left subclavian to pulmonary artery shunt (Blalock-Taussig) or other modifications.  The results of surgery are good with late survival at 5-10 years following correction of tetralogy is 95%, with an operative mortality for a repair of between 5% and 10%, and an incidence of reoperation following tetralogy repair of 5-10%.
  • 20. Transposition of great arteries (TGA) Is the second most common CHD, making up 2.5-5% of all congenital heart disease, and is the most common cause of cyanosis from a congenital cardiac defect discovered in the new-born period.
  • 21. Clinical features  Severe central cyanosis presenting in the first 48 hours of life, with the cyanosis progressing in the first week.  If there is a large atrial septal defect or ventricular septal defect there may be minimal cyanosis initially. Investigations:  The chest radiograph: pulmonary plethora, with the heart having an 'egg on its side' appearance, with a small pedicle (aorta in front of pulmonary artery).  Cardiac catheterization and echocardiography confirm the diagnosis and delineate the anatomy.
  • 22. Indications for surgery  The outcome for infants with TGA in the first year of life without some form of intervention to increase systemic and pulmonary venous admixture is death in 80-90% of cases.  Initial palliation is by percutaneous (Rashkind) balloon atrial septostomy, or alternatively intravenous prostaglandin to keep the ductus open.  Definitive repair is usually the Total Arterial Switch procedure, which has replaced the atrial switch or baffle (Mustard or Senning) operation because of reduced long-term complications
  • 24. I. Patent ductus arteriosus Accounts for 8-12% of congenital heart disease. The ductus arteriosus, a normal fetal communication, facilitates the transfer of oxygenated blood from the pulmonary artery to the aorta shunting blood away from the lungs. Normally, functional closure of the ductus occurs within a few hours of birth; it is abnormal if it persists beyond the neonatal period
  • 25. Patent ductus arteriosus Clinical features  Small shunts usually causing no symptoms, and few signs apart from a continuous machinery murmur in the left sec-ond intercostal space.  Larger ducts cause cardiac failure and can uncommonly lead to shunt reversal with cyanosis and clubbing. Investigations : Echocardiography with Doppler colour flow. Cardiac catheterisation is performed only if additional lesions are suspected. Indications for surgery:  After 6 months of age, spontaneous closure of PDA is rare. Most should be closed by the preschool age.  In the adult, surgical treatment is indicated if there is a persistent left to right shunt, even in the presence pulmonary hypertension.
  • 26. Patent ductus arteriosus Surgical options  In the premature infant, pharmacological closure of the patent ductus arteriosus with indomethacin is generally successful.  If medical treatment to close the ductus is unsuccessful, the lesion may be treated by interventional cardiology, using an umbrella or coil duct occlusion device inserted percutaneously.  Surgical closure via a left thoracotomy, if the lesion is very large or the patient very small is preferred.  This can be accomplished by either ligation or division of the patent ductus arteriosus.
  • 27. II. Coarctation of the aorta  This accounts for 6-7% of congenital heart disease and is defined as a haemodynamically significant narrowing of the aorta, usually in the descending aorta just distal to the left subclavian artery, around the area of the ductus arteriosus
  • 28. III. Coarctation of the aorta Pathophysiology  The upper body is well perfused but the lower body, including the kidneys, is poorly perfused leading to fluid overload, excess renin secretion and acidosis.  Children with coarctation are usually male and, if it occurs in females, it is suggestive of Turner syndrome.  There are several common associated lesions, including bicuspid aortic valve, ventricular septal defect.
  • 29. Coarctation of the aorta Clinical features  The child may appear well in the first few days of life because the coarctation is bypassed by the ductus arteriosus and oxygenated blood reaches the entire systemic circulation.  As the ductus closes, the child becomes progressively more unwell.  Hypertension is a common presenting problem in older children, often just upper body hypertension with development of enormous collateral vessels that may cause ribnotching and flow murmurs over the scapula.  Other symptoms include prominent pulsation in the neck, tired legs or intermittent claudication on exercise.
  • 30. III. Coarctation of the aorta Indications for surgery  Neonate with severe failure, operation indicated at time of diagnosis  If cardiac failure delay 3-6 months  Increased incidence of recurrent stenosis if operated at less than 3 months  Increased incidence of hypertesion if coarctation is repaired beyond infancy
  • 31. III. Coarctation of the aorta Surgical options  Operative options include resection of the coarctation and end-to-end anastomosis or the use of the left subclavian artery as an onlay flap.  In the older patient, th subclavian flap opration is not feasible and resection with end- to-end anastomosis, interposition graft or a 'jump' graft are preferred.  Percutaneous balloon dilatation is an alternative procedure in older children and adults and, in particular, for recoarctation.
  • 32. IV. Atrial Septal Defect (ASD)  ASD is a defect in the septum between the left and right atria leading to a left-to-right shunt.  It accounts for approximately 6-7% of all congenital heart disease and is more common in females.  There are three commonly recognised atrial septal defects.
  • 33. IV. Atrial Septal Defect (ASD) Symptoms and Signs  Most small ASDs are asymptomatic.  Larger shunts may cause exercise intolerance, dyspnea during exertion, fatigue, and atrial arrhythmias sometimes with palpitations.  Passage of microemboli from the venous circulation across the ASD (paradoxical embolization), often associated with arrhythmias, may lead to cerebral or systemic thromboembolic disorders.  Auscultation typically reveals midsystolic (or ejection systolic) murmur and a widely split, fixed S2 at the upper left sternal border in children.
  • 34. IV. Atrial Septal Defect (ASD) Investigations: Echocardiography will define the anatomy and any other abnormalities including the direction of the shunt.
  • 35. Indications for surgery  For primum & secundum ASD that fail close to spontaneously close treatment is aimed at closing the defect if a left-to- right shunt of 1.5:1 or more is present.  Closure is performed during the first decade, most small ostium secundum ASDs (< 3 mm) close spontaneously; about 80% of those between 3 mm and 8 mm close spontaneously by age 18 months.  Asymptomatic children with a small shunt require annual echocardiography.  Because these children are at risk of paradoxical systemic embolization, some centers recommend a catheter-delivered closure device (eg, Amplatzer Septal Occluder, Cardio-Seal device) even for small ASDs.  However, these devices are not suitable for primum or sinus venosus defects because these defects are near important structures.
  • 36. Surgical options  The traditional method of closure involves open-heart surgery with cardiopulmonary bypass (CPB) and closure of the defect either directly with sutures, as with most secundum defects or, if the defect is large, using a pericardial or synthetic patch.  Operative mortality for isolated atrial septal defect repairs is < 1%, with excellent prognosis.
  • 37. V. Ventricular septal defects (VSD)  These account for 20-30% of congenital heart disease and affect approximately 2 in 1000 live births.  A defect in the interventricular septum that allows a left-to-right shunting of blood.  This may occur in isolation or as part of a more complex set of cardiac abnormali-ties (e.g. tetralogy of Fallot, complete atrioventricular canal defect)  Four major anatomical types of ventricular septal defect are described, based on the anatomical subsections of the interventricular septum:
  • 38. Ventricular septal defects Investigations  Chest radiography: may show cardiomegaly and pulmonary congestion,  ECG showing evidence of biventricular hypertrophy.  Echocardiography confirms the diagnosis and can estimate the degree of shunting across the defect.  Cardiac catheterisation can quantify the various pressures within the cardiac chambers and so assess degree of pulmonary hypertension.
  • 39. Ventricular septal defects Clinical features Small defects may close or cause little systemic disturbance.In the first 5 years, up to 30-50% of ventricular septal defects close spontaneously. Clinically, a loud pansystolic murmur can be detected at the left sternal border due to high pressure flow between thé ventricles. Large defects typically present with congestive cardiac failure in the first 2 months of life. There is a preceding history of dyspnoea on exertion, failure to thrive, poor feeding and recurrent chest infections.
  • 40. Indications for surgery:  Approximately one-third of defects close in the first year of life; a further one-third become relatively smaller in relation to the growing heart.  In clinically small defects with a good response to medical management, it may be appropriate in the infant to 'watch and wait', although there is a risk of endocarditis.  Generally, surgical closure is indicated for large defects, failure to respond to medical therapy, left-to-right shunts > 2:1, signs of increasing pulmonary vascular résistance and the presence of complications of ventric-ular septal defect. These include (1) aortic regurgitation, which occurs in about 5% of defects; (2) infundibular stenosis, which tends to be progressive and leads to shunt reversal; and (3) infective endocarditis.
  • 41. Surgical options  If the infant is severely symptomatic, the defect should be closed urgently, otherwise elective repair is advised between 1 and 3 years of age in the asymptomatic patient.  Most now advocate a primary total correction, usually at the onset of symptoms or by 1 year in the asymptomatic patient.  Operative mortality for isolated ventricular septal defect closure is 2- 4%, with long-term prognosis.