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cyanotic heart disease.pptx

CONGENITAL HEART DEFECT

1 of 39
cyanotic heart disease.pptx
Cyanotic
Heart
Defect
Cyanotic Heart Defect is a
group-type of congenital
heart defect (CHD) that
occurs due to
deoxygenated blood entering
the systemic circulation.
Tetralogy of Fallot
cyanotic heart disease.pptx
cyanotic heart disease.pptx
cyanotic heart disease.pptx

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cyanotic heart disease.pptx

  • 2. Cyanotic Heart Defect Cyanotic Heart Defect is a group-type of congenital heart defect (CHD) that occurs due to deoxygenated blood entering the systemic circulation.
  • 7. Initial defect in TOF is a narrowing of the right ventricular outflow tract into the pulmonary artery . (Pulmonary Stenosis) Prevents deoxygenated blood from entering the pulmonary circuit In response to this outflow obstruction RV pressure is high as the LV, a right to left shunt appear (VSD) VSD allows shunting of blood between ventricles
  • 8. the aorta overrides the VSD, Mixed blood immediately exit the heart Severity and clinical consequences of TOF is the degree of right ventricular outflow obstruction.
  • 9. Clinical Manifestation Cyanosis, tet spell Clubbing of the fingers and toes The child starts crying, becomes bluer than before and may lose consciousness Slow weight gain (Poor growth) Dyspnoea on exertion
  • 10. Management Oxygen administration for cyanosis Maintain nutrition by small and frequent Give rest and allow only minimum activities for the child Oral beta blockers help prevent cyanotic spells Iron supplements is recommended for all the infant. Planning for surgical correction of defects should be done as soon as the child starts having spells. Neonates with severe TOF may be benefited from Prostaglandin E1 which causes dilation of the ductus and allows adequate pulmonary blood flow
  • 11. Surgical Management The preferred procedure is the modified blalock –taussing shunt, which provides blood flow to the pulmonary arteries from the left or right subclavion artery. Alternative include balloon dilation of the pulmonary valve.
  • 13. Pott’s procedure : The upper descending aorta is anastomosed with left pulmonary artery Brock’s procedure :Pulmonary valvotomy done to correct PS
  • 15. Tricuspid Atresia • Congenital absence of the tricuspid valve is called tricuspid atresia. • There is an absence of right atrioventricular connection. • The right ventricle is hypoplastic (undersized or absent). • This condition is associated with PS and PDA. • There is complete mixing of unoxygenated and oxygenated blood in the left Atrium and so have a mandatory ASD. • A PDA or VSD is necessary for PBF and survival.
  • 17. Effects ATRESIA OF TRICUSPID VALVE No communication between RA AND RV RV is underdeveloped. Systemic venous blood received by RA and Enters to LA through PFO or ASD
  • 18. Mixing of systemic and pulmonary blood Enters LV Modest Blood enters RV through VSD From RV and PDA blood enters Pulm trunk
  • 19. CLINICAL MANIFESTATION • Cyanosis • Children have signs of Chronic hypoxemia with clubbing
  • 20. Therapeutic Management • For the neonate whose pulmonary blood flow depend on the patency of the ductus arteriosus a continuous infusion of prostaglandin E is started until surgery can be arranged.
  • 21. Surgical Management • Palliative treatment is the placement of a shunt (systemic to pulmonary artery) to increase blood flow to the lungs. If the ASD is small, an atrial septostomy is done during cardiac catheterization. • initial subclavian artery-to-pulmonary shunt ( blalock-taussing procedure) • Fonton procedure. These surgery direct systemic venous return directly to the pulmonary ateries. (During the Fontan procedure, the surgeon: Disconnects the inferior vena cava (IVC) from the heart and connects it to the pulmonary artery using a conduit (tube).)
  • 24. TRANSPOSITION OF THE GREAT ARTERIES • Transposition of great vessels (TGA) is defined as aorta arising from the right ventricle and pulmonary artery from the left ventricle with no communication between the systemic and pulmonary circulation. • 5% of CHD
  • 26. Sign & Symptoms • Cyanosis • Fatigue • Slow weight gain • Clubbing of the finger • Rapid breathing
  • 27. Effects In patient with TGA the oxygenated pulmonary venous blood recirculates in the lungs whereas the systemic venous blood recirculates in the systemic circulation. The pulmonary artery saturation is thus higher than aortic saturation. Survival depends on the mixing available between the two circulation The patient with intact ventricular septum, the mixing site is the atrial communication through PFO and this being small, the mixing is very poor
  • 28. Presence of a VSD of adequate size results in good mixing as well as equalizes pressures between the ventricles and the great arteries
  • 29. Therapeutic management ( to provide intracardiac mixing) • The administration of intravenous prostaglandin E1 may be initiated to keep the ductus ateriosus open to temporarily increase blood mixing and provide an oxygen saturation. • During cardiac catheterization or under echocardiographic guidance , a balloon atrial septostomy ( Rashkind procedure) may also be performed to increase mixing by opening the atrial septum.
  • 31. • The arterial switch operation is now established as the treatment of choice for TGA. In this operation, the pulmonary artery and aorta are transected. The distal aorta is anastomosed to the proximal pulmonary stump and pulmonary artery to the proximal aortic stump.
  • 33. TRUNCUS ARTERIOSUS Truncus atreriosus results from the failure of separation of the truncus during the first 3-4 weeks of gestation. ( failure of the separation of the embryonic bulbar trunk into the aorta and pulmonary artery) • Usually accompanied by a ventricular septal defect • Truncus arteriosus is a birth defect of the heart. It occurs when the blood vessel coming out of the heart in the developing baby fails to separate completely during development, leaving a connection between the aorta and pulmonary artery.
  • 36. Total anomalous pulmonary venous return (TAPVR) • Rare defect characterized by failure of the pulmonary veins to join the left atrium. The pulmonary veins are abnormally connected to the systemic venous circuit via the right atrium such as the SVC and IVC
  • 38. Hypoplastic Left Heart Syndrome (HLHS) Hypoplastic left heart syndrome occurs when parts of the left side of the heart (mitral valve, left ventricle, aortic valve, and aorta) do not develop completely. The left ventricle is nonfunctional. Thus, the left side of the heart is completely unable to supply blood to the systemic circulation