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Dr.Azad A Haleem AL.Brefkani
University Of Duhok
Faculty of Medical Science
School Of Medicine
Pediatrics Department
azad8...
Classification
CHD
Acyanotic Cyanotic
Left-to-right
shunts
Outflow
obstruction
- Ventricular Septal Defect
(VSD)
- Persist...
Ventricular Septal Defect (VSD)
Ventricular Septal Defects (VSD)
• Most Common CHD.
• Three important things with VSD:
• Location
• Size
• pulmonary vascu...
Location of VSD
• Location of the VSD – prognostic and repair
approach.
• The VSDs are subdivided according to the part of...
pulmonary vascular resistance.
• At birth, the pulmonary vascular resistance is
normally elevated, thus, even large VSDs a...
Size of VSD
Small (< 3 mm in
diameter)
Moderate (3-5 mm in
diameter)
Large (6-10 mm in
diameter)
-hemodynamically
insignif...
Pathophysiology
• VSD permits a left-to-right shunt to occur at the
ventricular level with 3 adverse hemodynamic
consequen...
Clinical features
• Symptoms:
 Small VSD: Asyptomatics
 Large VSD:
 Heart failure with breathlessness
 failure to thri...
Physical signs
• Clinical findings (murmur)
– Grade II-IV/VI,
– medium- to high-pitched,
– harsh
– pansystolic murmur
– he...
Investigations
• Echocardiography
 Demonstrates the anatomy defect, haemodynamic effects and severity of
pulmonary HPT.
•...
X-Ray chest PA View
There is cardiomegaly, prominent main pulmonary artery segment and right
pulmonary artery. Enlarged le...
Small VSD
• Management
– Most will close spontaneously. Ensure by the
disappearance of the murmur, normal ECG on
follow up...
Large VSD
• Initial treatment (Medical) – diuretics and ACI
(captopril) or digoxin.
• Continued poor growth or pulmonary H...
Complications
• Pulmonary Hypertension
• Heart Failure.
• Growth delay.
• Eisenmenger complex
• Secondary aortic insuffici...
Atrial Septal Defects (ASD)
Atrial Septal Defects (ASD)
• Due to failure of septal growth or excessive reabsorption of tissue.
• are the most common c...
Pathophysiology
• Shunting across an atrial septal defect is left to right
• The degree of this shunting is dependent on;
...
Symptoms
-Asymptomatic (commonly)
-breathlessness, tiredness on
exertion
- Recurrent chest infections/wheeze
- Heart failu...
Management
• If significant shunt is present at around 3
y/o, closure is recommended.
• Cardiac catheterization with inser...
Prognosis & Complications
• ASDs detected in term infants may close
spontaneously. Secundum ASDs are well tolerated
during...
Endocardial cushion defects
Endocardial cushion defects
• also referred to as atrio-ventricular canal defects,
• may be complete or partial .
• The de...
Clinical Manifestations
• The symptoms of CHF usually develop as the pulmonary
vascular resistance decreases over the firs...
• Imaging Tests:
o The diagnosis usually is made with echocardiography.
o A chest radiograph reveals cardiomegaly with
enl...
Patent Ductus Arteriosus
Patent Ductus Arteriosus (PDA)
• The ductus arteriosus allows blood to flow from the
pulmonary artery to the aorta during ...
Pathophysiology
• Higher aortic pressure, blood shunts left to right through
the ductus
• The magnitude of the excess pulm...
Symptoms
-Depend on size of PDA
- Small – asymptomatic
- Moderate to larger shunts –
symptoms of CHF or even pulmonary
HPT...
Coarctation of the aorta
Coarctation of the aorta
• It is almost always juxtaductal in position.( the
part near where the ductus arteriosus
attache...
Clinical Manifestations
• Timing of presentation depends primarily on
the severity of obstruction and associated
cardiac d...
• Classically the femoral pulses are weaker and
delayed compared with the radial pulses.
• The blood pressure in the lower...
• The murmur of coarctation is typically best heard
in the left interscapular area of the back.
• If significant collatera...
Classification
CHD
Acyanotic Cyanotic
Left-to-right
shunts
Outflow
obstruction
- Ventricular Septal Defect
(VSD)
- Persist...
 Imaging Studies: Echocardiography shows the
site of coarctation and associated lesions.
• In older children, the ECG and...
Cyanosis
• Cyanosis:A bluish discoloration of skin and
mucous membrane due to excessive
concentration of reduced hemoglobi...
Central vs peripheral
• Central cyanosis:
– Seen on tongue as blue colour
– Associated with a fall in arterial blood O2 te...
Tetralogy of Fallot (TOF)
Tetralogy of Fallot (TOF)
• Tetralogy of Fallot is the most common cyanotic
congenital heart defect.
• Anatomically, there...
Clinical Manifestations
• The degree of cyanosis depends on the
amount of pulmonary stenosis.
• Infants initially may be a...
• A pulmonary stenosis murmur is the usual initial
abnormal finding.
• If the pulmonary stenosis is more severe, or as it
...
• Hypoxic spells/ paroxysmal hypercyanotic
attacks (1st 2years of life)
– Severe hypoxia tissue acidosis breathlessness
...
Imaging Studies
• The ECG usually has right axis deviation and right
ventricular hypertrophy.
• The classic chest x-ray fi...
Treatment
• The natural history of tetralogy of Fallot is progression of
pulmonary stenosis and cyanosis.
 Treatment of h...
Transposition of the Great
Arteries(TGA)
Clinical Manifestations
• Cyanosis is always present
• Finger clubbing
• Quiet tachypnea
• Single S2
• Usually no murmur
•...
Transposition of the Great Arteries
• It is the most common cyanotic lesion to present in the
newborn period .
• TGA is ve...
Imaging Studies
• ECG findings typically include right axis
deviation and right ventricular hypertrophy.
• The chest x-ray...
Treatment
• Simple (TGA) with intact ventricular septum:
– IV Prostaglandin E1 infusion
– Early Balloon arterial septostom...
cyanotic and acyanotic Congenital heart disease for undergraduated student uod 2015
cyanotic and acyanotic Congenital heart disease for undergraduated student uod 2015
cyanotic and acyanotic Congenital heart disease for undergraduated student uod 2015
cyanotic and acyanotic Congenital heart disease for undergraduated student uod 2015
cyanotic and acyanotic Congenital heart disease for undergraduated student uod 2015
cyanotic and acyanotic Congenital heart disease for undergraduated student uod 2015
cyanotic and acyanotic Congenital heart disease for undergraduated student uod 2015
cyanotic and acyanotic Congenital heart disease for undergraduated student uod 2015
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cyanotic and acyanotic Congenital heart disease for undergraduated student uod 2015

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cyanotic and acyanotic Congenital heart disease for undergraduated student uod 2015

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cyanotic and acyanotic Congenital heart disease for undergraduated student uod 2015

  1. 1. Dr.Azad A Haleem AL.Brefkani University Of Duhok Faculty of Medical Science School Of Medicine Pediatrics Department azad82d@gmail.com 2015
  2. 2. Classification CHD Acyanotic Cyanotic Left-to-right shunts Outflow obstruction - Ventricular Septal Defect (VSD) - Persistent Ductus Arteriosus (PDA) - Atrial Septal Defect (ASD - Pulmonary Stenosis - Aortic Stenosis -Coarctation of aorta  Teralogy of Fallot  transposition of the great arteries
  3. 3. Ventricular Septal Defect (VSD)
  4. 4. Ventricular Septal Defects (VSD) • Most Common CHD. • Three important things with VSD: • Location • Size • pulmonary vascular resistance. • The amount of flow crossing a VSD depends on the size of defect and the pulmonary vascular resistance.
  5. 5. Location of VSD • Location of the VSD – prognostic and repair approach. • The VSDs are subdivided according to the part of the septum they occur in : • Muscular, • perimembranous (adjacent to the tricuspid valve), • inlet, • outlet
  6. 6. pulmonary vascular resistance. • At birth, the pulmonary vascular resistance is normally elevated, thus, even large VSDs are not symptomatic at birth. • Over the first 6-8 weeks of life, pulmonary vascular resistance normally decreases. • More blood flows through the lung and into the left atrium. • However, in VSD, the amount of shunt increases, and symptoms may start to develop. • The size of the VSD affects the clinical presentation.
  7. 7. Size of VSD Small (< 3 mm in diameter) Moderate (3-5 mm in diameter) Large (6-10 mm in diameter) -hemodynamically insignificant -Between 80% and 85% of all VSDs -All close spontanously -Muscular close sooner than membranous -Least common group of children (3-5%) -Without evidence of CHF or pulmonary hypertension, may be followed until spontaneous closure occurs - develop CHF and FTT by age 3-6 months -Usually requires surgery.
  8. 8. Pathophysiology • VSD permits a left-to-right shunt to occur at the ventricular level with 3 adverse hemodynamic consequences: 1. left ventricular (LV) volume overload, 2. increased pulmonary blood flow, 3. compromise of systemic cardiac output.
  9. 9. Clinical features • Symptoms:  Small VSD: Asyptomatics  Large VSD:  Heart failure with breathlessness  failure to thrive.  Recurrent chest infections
  10. 10. Physical signs • Clinical findings (murmur) – Grade II-IV/VI, – medium- to high-pitched, – harsh – pansystolic murmur – heard best at the lower left sternal border with – radiation over the entire precordium
  11. 11. Investigations • Echocardiography  Demonstrates the anatomy defect, haemodynamic effects and severity of pulmonary HPT. • Small VSD: – Chest X-ray & ECG - normal • Large VSD:  Chest X-ray • Cardiomegaly • Enlarged pulmonary arteries • ↑ Pulmonary vascular markings • Pulmonary oedema  ECG : Biventricular hypertrophy and signs of pulmonary HPT  right ventricular enlargement and hypertrophy(if not treated)
  12. 12. X-Ray chest PA View There is cardiomegaly, prominent main pulmonary artery segment and right pulmonary artery. Enlarged left pulmonary artery shadow is seen below the left cardiac border, within the cardiac silhouette. The enhanced vascular markings are visible on the right side whereas it is obscured by the cardiac shadow on the left side cardiomegaly Increased pulm markings Enlarged pulm arteries
  13. 13. Small VSD • Management – Most will close spontaneously. Ensure by the disappearance of the murmur, normal ECG on follow up, normal echocardiogram. – While the VSD is present, for prevention of bacterial endocarditis : • Maintain good dental hygiene • Antibiotic prophylaxis before dental extraction or any operation where there’ll be bleeding – Surgical closure may not be required
  14. 14. Large VSD • Initial treatment (Medical) – diuretics and ACI (captopril) or digoxin. • Continued poor growth or pulmonary HPT requires closure of the defect. • Most VSDs are treated by surgery. But muscular defects by devices placed at cardiac catheterization. • Surgery is usually done at 3-6 months of age for : • Managing heart failure and failure to thrive. • Prevent permanent lung damage from pulmonary HPT and high blood flow.
  15. 15. Complications • Pulmonary Hypertension • Heart Failure. • Growth delay. • Eisenmenger complex • Secondary aortic insufficiency &Aortic regurgitation . • Infective endocarditis
  16. 16. Atrial Septal Defects (ASD)
  17. 17. Atrial Septal Defects (ASD) • Due to failure of septal growth or excessive reabsorption of tissue. • are the most common congenital cardiac lesion presenting in adults. • Classification: – Secundum ASD (80%) – Primum ASD or partial atrioventricular septal defect • Ostium primum ASDs may occur in isolation but most commonly present with a cleft in the anterior leaflet of the mitral valve(partial atrioventricular septal defect ) – Sinus venosus defect (least common) • occurs in the upper atrial septum • Associated with anomalous pulmonary venous return
  18. 18. Pathophysiology • Shunting across an atrial septal defect is left to right • The degree of this shunting is dependent on; - the size of the defect - the relative vascular resistance in the pulmonary and systemic circulations. • Resistance in the pulmonary vascular bed is commonly normal in children with ASD, and increase in volume load is usually well tolerated • The chronic significant left-to-right shunt can alter the pulmonary vascular resistance leading to pulmonary arterial hypertension, even reversal of shunt and Eisenmenger syndrome (if not treated)
  19. 19. Symptoms -Asymptomatic (commonly) -breathlessness, tiredness on exertion - Recurrent chest infections/wheeze - Heart failure -Arrhytmias (4th decade onwards) Physical Signs -A fixed and widely split 2nd heart sound -An ejection systolic murmur (soft), upper left sternal edge -Partial AVSD – apical pansystolic murmur from AV valve regurge. Chest X-ray - Usually normal - Cardiomegaly - enlarged pulmonary arteries -increased pulmonary vascular markings Echocardiography - Documents type, size and direction of shunt - The mainstay of diagnostic investigations ECG -provide strong diagnostic clue: -Both: right bundle branch block -secundum ASD – right axis deviation -partial AVSD – left axis deviation (superior axis)
  20. 20. Management • If significant shunt is present at around 3 y/o, closure is recommended. • Cardiac catheterization with insertion of an occlusion device (closure device). Secundum ASDs • Prophylaxis for subacute bacterial endocarditis. • Surgical correction at 3-5 y/o to prevent right heart failure and arrhythmias in later life. Primum ASD
  21. 21. Prognosis & Complications • ASDs detected in term infants may close spontaneously. Secundum ASDs are well tolerated during childhood, and symptoms do not usually appear until the 3rd decade or later. • Complications: − Congestive heart failure − Arrhythmias − Pulmonary hypertension − Infective endocarditis − Surgery may be associated with a long-term risk of atrial fibrillation or flutter. The risk of infective endocarditis exists during the first 6 months after surgery.
  22. 22. Endocardial cushion defects
  23. 23. Endocardial cushion defects • also referred to as atrio-ventricular canal defects, • may be complete or partial . • The defect occurs as the result of abnormal development of the endocardial cushion tissue, resulting in failure of the septum to fuse with the endo-cardial cushion; this results in abnormal atrioventricular valves as well. • The complete defect results in a primum ASD, Inlet VSD, and cleft in leaflet of mitral and cleft leaflet of the tricuspid valves. • In addition to left-to-right shunting at both levels, there may be atrioventricular valvular insufficiency.
  24. 24. Clinical Manifestations • The symptoms of CHF usually develop as the pulmonary vascular resistance decreases over the first 6 to 8 weeks of life. • Pulmonary hypertension resulting from increased pulmonary circulation often develops early; this results in a prominent S2. • The presence of murmurs varies depending on the balance of flows.  If intracardiac dynamics are balanced, there is little shunting and no significant murmur.  If dynamics are less balanced, murmurs consistent with an ASD, VSD, or valvular insufficiency may be heard.  Growth is usually poor.  Many children with Down syndrome have complete endocardial cushion defects.
  25. 25. • Imaging Tests: o The diagnosis usually is made with echocardiography. o A chest radiograph reveals cardiomegaly with enlargement of all chambers and the presence of increased vascularity. • The ECG reveals left axis deviation and combined ventricular hypertrophy and may show combined atrial enlargement. Treatment:  Initial treatment (Medical) – diuretics and ACI (captopril) or digoxin diuretics for treatment of CHF.  Surgical repair of the entire defect ultimately is required.
  26. 26. Patent Ductus Arteriosus
  27. 27. Patent Ductus Arteriosus (PDA) • The ductus arteriosus allows blood to flow from the pulmonary artery to the aorta during fetal life. This changes to the opposite after birth. • In term infants, it normally closes shortly after birth. Failure of the normal closure of it by a month post term is due to a defect in the constrictor mechanism of the duct. • In preterm infants, the PDA is not from CHD but due to prematurity.
  28. 28. Pathophysiology • Higher aortic pressure, blood shunts left to right through the ductus • The magnitude of the excess pulmonary blood flow depends on: − The internal diameter PDA. − The length PDA − Relationship of the pulmonary vascular resistance to the systemic vascular resistance. • If the PDA is large, pulmonary artery pressure may be elevated to systemic levels during both systole and diastole. Extremely high risk for the development of pulmonary vascular disease if left unoperated.
  29. 29. Symptoms -Depend on size of PDA - Small – asymptomatic - Moderate to larger shunts – symptoms of CHF or even pulmonary HPT Physical findings - Continuous machinery murmur beneath the left clavicle - Widened pulse pressure  collapsing or bounding pulse Chest X-ray & ECG - Usually normal unless the PDA is large and symptomatic - Features seen are indistinguishable from VSD - Duct should be readily identified by echocardiography Management - Small PDA – closure is recommended due to the risk of bacterial endocarditis - Moderate and large PDA – initially diuretics & digoxin, but eventually closure - Closure is with a coil or occlusion device introduced via cardiac catheter at abuot 1 y/o
  30. 30. Coarctation of the aorta
  31. 31. Coarctation of the aorta • It is almost always juxtaductal in position.( the part near where the ductus arteriosus attaches. ) • During development of the aortic arch, the area near the insertion of the ductus arteriosus fails to develop correctly, resulting in a narrowing of the aortic lumen.
  32. 32. Clinical Manifestations • Timing of presentation depends primarily on the severity of obstruction and associated cardiac defects. • Symptoms and Signs: SEVERE : Shock MODERATE : CHF, MILD : leg discomfort with exercise, headache, or epistaxis.
  33. 33. • Classically the femoral pulses are weaker and delayed compared with the radial pulses. • The blood pressure in the lower extremities is lower than that in the upper extremities • hypertension (upper extremity),
  34. 34. • The murmur of coarctation is typically best heard in the left interscapular area of the back. • If significant collaterals have developed, continuous murmurs may be heard throughout the chest. • An abnormal aortic valve is present approximately 50% of the time, causing a systolic ejection click and systolic ejection murmur of aortic stenosis.
  35. 35. Classification CHD Acyanotic Cyanotic Left-to-right shunts Outflow obstruction - Ventricular Septal Defect (VSD) - Persistent Ductus Arteriosus (PDA) - Atrial Septal Defect (ASD - Pulmonary Stenosis - Aortic Stenosis -Coarctation of aorta  Teralogy of Fallot  transposition of the great arteries
  36. 36.  Imaging Studies: Echocardiography shows the site of coarctation and associated lesions. • In older children, the ECG and chest x-ray usually show left ventricular hypertrophy and a mildly enlarged heart. • CXR: Rib notching may also be seen in older children (>8 years old) with large collaterals. Treatment:  Balloon angioplasty or surgical repair of the coarctation are most commonly performed.
  37. 37. Cyanosis • Cyanosis:A bluish discoloration of skin and mucous membrane due to excessive concentration of reduced hemoglobin (deoxygenated) in the blood.
  38. 38. Central vs peripheral • Central cyanosis: – Seen on tongue as blue colour – Associated with a fall in arterial blood O2 tension. – Clinically: • reduced(deoxygenated) Hb >5g/dL • SpO2= <85% by pulse oximetry test. • Peripheral cyanosis: – Blueness of hand and feet – Due to cold or circulatory disorder (e.g: DVT) – Can also occur in severe central cyanosis
  39. 39. Tetralogy of Fallot (TOF)
  40. 40. Tetralogy of Fallot (TOF) • Tetralogy of Fallot is the most common cyanotic congenital heart defect. • Anatomically, there are four structural defects: VSD, pulmonary stenosis, overriding aorta and right ventricular hypertrophy. • Tetralogy of Fallot is believed to be due to abnormalities in the septation of the truncus arteriosus into the aorta and pulmonary arteries that occur early in gestation (3 to 4 weeks).
  41. 41. Clinical Manifestations • The degree of cyanosis depends on the amount of pulmonary stenosis. • Infants initially may be acyanotic. • Older children+ long standing cyanosis+ not undergone surgery – Dusky blue skin – Grey sclerae with engorged blood vessel – Marked clubbing of fingers and toes
  42. 42. • A pulmonary stenosis murmur is the usual initial abnormal finding. • If the pulmonary stenosis is more severe, or as it becomes more severe over time, the amount of right- to-left shunting at the VSD increases, and the patient becomes more cyanotic. • With increasing severity of pulmonary stenosis, the murmur becomes shorter and softer. • single S2 and right ventricular impulse(heave) at the left sternal border are typical findings. • hypoxic ("Tet") spells • Independent of hypoxic spells, patients with tetralogy are at increased risk for cerebral thromboembolism and cerebral abscesses resulting in part from their right-to-left intracardiac shunt.
  43. 43. • Hypoxic spells/ paroxysmal hypercyanotic attacks (1st 2years of life) – Severe hypoxia tissue acidosis breathlessness and pallor – Rapid increase in cyanosis – Restless and agitated – Inconsolable crying – An ambulatory toddler may squat – Severe spells: • Prolonged unconsciousness and convulsions • Hemiparesis • OR death
  44. 44. Imaging Studies • The ECG usually has right axis deviation and right ventricular hypertrophy. • The classic chest x-ray finding is a boot-shaped heart : – Small heart – Uptilted apex (boot shaped) – pulmonary artery ‘bay’= concavity of L heart border – Oligaemic lung fields • Echocardiography: The diagnosis usually is made with echocardiography.
  45. 45. Treatment • The natural history of tetralogy of Fallot is progression of pulmonary stenosis and cyanosis.  Treatment of hypoxic spells consists of • oxygen administration, • placing the child in the knee-chest position (to increase venous return), • and giving morphine sulfate (to relax the pulmonary infundibulum and for sedation). • If necessary, the systemic vascular resistance can be increased acutely through the administration of an α-adrenergic agonist (phenylephrine). • β-adrenergic antagonists (propranolol) decrease muscular spasm.  Complete surgical repair with closure of the VSD and removal or patching of the pulmonary stenosis can be performed in infancy.  Subacute bacterial endocarditis prophylaxis is indicated.
  46. 46. Transposition of the Great Arteries(TGA)
  47. 47. Clinical Manifestations • Cyanosis is always present • Finger clubbing • Quiet tachypnea • Single S2 • Usually no murmur • Signs of CHF in children with transposition and a large VSD.
  48. 48. Transposition of the Great Arteries • It is the most common cyanotic lesion to present in the newborn period . • TGA is ventriculoarterial discordance secondary to abnormalities of septation of the truncus arteriosus. • In TGA, the aorta arises from the right ventricle, anterior and to the right of the pulmonary artery, which arises from the left ventricle. • This transposition results in desaturated blood returning to the right heart and being pumped back out to the body, while well-oxygenated blood returning from the lungs enters the left heart and is pumped back to the lungs. • Without mixing of the two circulations, death occurs quickly. • Mixing can occur at the atrial (ASD), ventricular (VSD), or great vessel (PDA) level.
  49. 49. Imaging Studies • ECG findings typically include right axis deviation and right ventricular hypertrophy. • The chest x-ray reveals increased pulmonary vascularity, and the cardiac shadow is classically an egg on a string created by the narrow superior mediastinum. • Echocardiography shows the transposition of the great arteries, the sites and amount of mixing, and any associated lesions.
  50. 50. Treatment • Simple (TGA) with intact ventricular septum: – IV Prostaglandin E1 infusion – Early Balloon arterial septostomy (BAS) – Surgery: arterial switch procedure (2-4weeks of age) • TGA with VSD: – No treatment during neonatal period, but may develop heart failure 1-2months age – Elective one-stage arterial switch operation + VSD closure before three months of age.

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