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Congenital Heart Disease

Congenital Heart Disease. Tammy L. Schena, RN, MSN, CCRN. Fetal Heart Development. Formation begins during 2nd week embryonic life Contractions by 8th week Sinus rhythm by 16th week. Epidemiology. 0.8% of all live births Correlating factors: chromosomal abnormalities (5-8%)

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Congenital Heart Disease

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  1. Congenital Heart Disease Tammy L. Schena, RN, MSN, CCRN

  2. Fetal Heart Development • Formation begins during 2nd week embryonic life • Contractions by 8th week • Sinus rhythm by 16th week

  3. Epidemiology • 0.8% of all live births • Correlating factors: • chromosomal abnormalities (5-8%) • teratogenic factors (1%) • family history: • one parent with CHD = 2-4%  risk • mother with CHD may increase risk by 25%

  4. Fetal Circulation • Oxygenation occurs in placenta • Fetal lungs bypassed • Fetal hypoxemia without tissue hypoxia • Very low SVR, very high PVR • fluid-filled alveoli

  5. Circulatory Changes at Birth • Closure of foramen ovale • LA Pressure > RA Pressure • Closure of ductus arteriosus • rise in paO2 • decrease in endogenous prostaglandins

  6. Circulatory Changes • Pulmonary vascular resistance: • breathing causes expansion of alveoli • alveolar hypoxia eliminated, rapid fall in PVR • pulmonary blood flow increases by 450% with onset of breathing

  7. Factors contributing to vasoconstriction: hypoxia acidosis hypothermia Factors contributing to vasodilation: alveolar oxygenation alkalosis analgesia Pulmonary Circulation

  8. Normal Heart Physiology • Saturations: • SVC, IVC, Coronary, Right atrium • Right heart filling pressures (CVP) • Left heart filling pressures • Coronary arteries

  9. Cardiac Output • Cardiac Output = stroke volume x heart rate • stroke volume  contractility • infants are heart rate dependent • Oxygen delivery = cardiac output x O2 content • O2 content  Hgb, saturation

  10. Cardiac Output (cont.) • Preload • amount of myocardial fiber stretch just before contraction • Starling’s Law • Afterload • pressure against which the ventricle must pump • A change in pressure or volume on one side of the heart has an effect on the other side

  11. Preload: Fluid (CVP) Diuretics Increased airway pressure Pericardial tamponade SVT Afterload: Hypoxia Acidosis Vasoactive infusions Increased SVR Increased PVR Coarctation Contributing Factors

  12. Congenital Heart Defect • A cardiac or extra-cardiac anatomic abnormality creating a disruption in the normal adaptation process • Heart or great vessels • Certain defects provide “transitional circulation”

  13. CHD Classification • Lesions producing obstruction • atrial • ventricular • Lesions producing shunts: • cyanotic • acyanotic

  14. Hemodynamics • What type of defect is present? • obstructive • cyanotic • acyanotic • How is cardiac output affected? • too high • too low

  15. Patent Ductus Arteriosus (PDA) • Fetal vessel connecting PA to aorta • Usually closes by 5 - 7 days of age • PDA: blood flows from aorta to pulmonary artery

  16. PDA Management • Indomethacin (Indocin) • Transcatheter closure (coil) • Surgical ligation • PDA may be life saving in some infants (“transitional circulation”)

  17. Atrial Septal Defect (ASD) • Improper development of atrial septum • Communication between right & left atria • LA to RA shunt produces RV volume overload and increased pulmonary blood flow

  18. ASD Management • Closure recommended • Open heart surgery by 4 - 6 years of age • sutured or patched • Transcatheter closure • “clamshell”

  19. Ventricular Septal Defect (VSD) • Abnormal opening between ventricles • LV to RV shunt: increased blood flow to RV, PA, lungs • Prolonged increased pulmonary blood flow: irreversible pulmonary vascular disease

  20. VSD Variations • Small: • pulmonary to systemic blood flow: 1.5 : 1 • Moderate: • pulmonary to systemic blood flow: 1.5 - 2 : 1 • Large: • pulmonary to systemic blood flow: > 2 : 1

  21. Why are large VSDs bad? • Pulmonary blood flow under high pressure • RVP = LVP: biventricular hypertrophy • Congestive heart failure • Eisenmenger’s Syndrome

  22. VSD Management • Pulmonary artery banding • reduce pulmonary blood flow • prevent pulmonary hypertension • Open heart surgery with Dacron patch • Via RA through tricuspid valve • Right ventriculotomy • Rarely left ventriculotomy

  23. Atrioventricular Canal Defect • Malformation of endocardial cushion: atrial septum, ventricular septum and AV valves • Usually acyanotic: • produces increased pulmonary blood flow

  24. AV Canal management • Medical management of CHF • Digoxin • Lasix • Surgical correction • Dacron patches • valvuloplasties

  25. Tetralogy of Fallot • 4 defects: • VSD, PS, RVH, overriding aorta • Cyanosis proportional to degree of PS • Minimal cyanosis until PDA closes

  26. Tet Management • Infancy • Blalock-Taussig (BT) shunt • Modified B-T shunt • CHF management (digoxin and diuretics) • Surgical correction at 8 mos to 3 years • VSD closure • RVOT reconstruction (patch)

  27. Blalock-Taussig Shunt

  28. Modified B-T Shunt

  29. Transposition of Great Arteries (TGA) • Aorta arises from RV • Pulmonary artery arises from LV • Must have septal defect or PDA for shunting • Extreme cyanosis

  30. TGA Management • IV Prostaglandin for patency of PDA • Balloon atrial septostomy (Rashkind) if no ASD present • Arterial Switch procedure • proximal aorta and PA transected & reattached • coronary arteries transposed to new ascending aorta position

  31. Arterial Switch

  32. Truncus Arteriosus • Entire pulmonary, systemic & coronary circulations supplied from one common trunk • Large VSD • RV & LV function as single ventricle

  33. Truncus Management • Management of CHF with digoxin & diuretics • Surgical correction • right ventriculostomy for VSD closure • common trunk becomes aorta • conduit with valve from RV to PA (Rastelli procedure)

  34. Tricuspid Atresia • Complete obstruction of blood flow from RA to RV • Blood flow: • RA to LA via PFO • Systemic & pulmonary blood mix in LA • Through VSD to PA

  35. Tricuspid Atresia Management • Must be immediately palliated • Surgeries done in multiple stages with final procedure Fontan (right atrial to pulmonary artery conduit)

  36. Tricuspid Atresia (cont.) • 1. Glenn Anastomosis • initial step in preparation for Fontan • goal is to separate systemic from pulmonary blood flow • SVC detached from RA and sutured to right PA (~40% of venous blood delivered to PA) • advantages:  cyanosis,  LV blood • disadvantage: SVC syndrome

  37. Glenn Shunt

  38. Tricuspid Atresia (cont.) • 2. Fontan • final operative procedure • IVC removed from RA, oversewn, joined to PA via homograft • complete extra-cardiac conduit • systemic venous return directly to lungs • passive flow of blood through PA

  39. Fontan

  40. Fontan (cont.) • Used for any “single ventricle” physiology • tricuspid atresia • hypoplastic left heart syndrome • severe pulmonary atresia • Modified Fontan: • conduit joining RA to RV to PA • Avoid variables that cause increases in PVR

  41. Total Anomalous Pulmonary Venous Return (TAPVR) • Failure of pulmonary veins to empty into LA • Oxygenated blood returns to the right heart • ASD present • paO2 will be the same on either side of the heart

  42. TAPVR Management • Control of CHF: prevention of pulmonary vascular disease • Surgical correction: • dissect and reattach pulmonary veins to left atrium • potential for attachment site obstruction

  43. Coarctation of the Aorta • Narrowing of aorta ranging from mild to severe • Bicuspid aortic valve • Extreme version: interrupted arch • Preductal or postductal

  44. Coarctation of the Aorta

  45. Coarctation Management • IV Prostaglandin E1 • Preductal coarctation: descending aorta flow dependent on PDA • Surgical resection, any age, depends on severity • subclavian artery flap, Dacron patch • end-to-end anastomosis • post-operative complications increase with increased age

  46. Hypoplastic Left Heart Syndrome • Severe hypoplasia of left ventricle • Usually includes mitral or aortic stenosis/atresia, coarctation • ASD present

  47. HLHS Management • IV Prostaglandin E1 • PDA for blood flow to aorta and coronaries • Three options • comfort measures only • cardiac transplantation • surgical palliation: Norwood

  48. HLHS (cont.) • Norwood: • PA transected from RV • Aorta created with homograft and sewn to RV, essentially creating a “truncus” • B-T shunt created for pulmonary blood flow • ASD/PFO maintained for unrestricted LA to RA blood flow

  49. Pearls • Goal of treatment is adequate CO and vital organ oxygenation • A change in pressure or volume on one side of the heart will have an effect on the other • The magnitude of a shunt is dependent on pressure gradient which determines flow

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