CONGENITAL HEART DISEASES
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This document provides information about acyanotic heart defects, including definitions, causes, pathophysiology, clinical manifestations, diagnosis, management, and complications. It discusses several types of acyanotic heart defects such as atrial septal defect (ASD), ventricular septal defect (VSD), atrioventricular canal defect, patent ductus arteriosus (PDA), coarctation of the aorta, and aortic stenosis. For each condition, it outlines the definition, incidence, types if applicable, pathophysiology that occurs due to the structural abnormality, associated signs and symptoms, diagnostic evaluation, treatment options including medical management and surgery, and potential complications.
CONGENITAL HEART DISEASES
- 1. MRS.JEBAKUMARI SUTHA.A ASSOCIATE PROFESSOR HOD,PAEDIATRIC DEPARTMENT GANGA COLLEGE OF NURSING COIMBATORE-22
- 3. LEARNING OBJECTIVES The students will be able to •define Acyanotic heart defects •list down the causes of Acyanotic heart defects •explain the pathophysiology of Acyanotic heart defects •enlist the clinical manifestations of Acyanotic heart defects •mention the diagnostic findings of Acyanotic heart defects •elaborate on the management of Acyanotic heart defects •formulate nursing diagnosis for the child with Acyanotic heart defects
- 4. INTRODUCTION A congenital heart defect (CHD), also known as a congenital heart anomaly and congenital heart disease, is a defect in the structure of the heart or great vessels that is present at birth. Signs and symptoms depend on the specific type of defect.
- 6. DIFFERENCE BETWEEN ADULT /FETAL BLOOD CIRCULATION Placenta Umbilical vein Fetal Liver DV/IVC Right atrium FO Left atrium Left ventricle Ascending Aorta Upper part of body SVC Right atrium- Right ventricle PA DA Lungs D- Aorta other parts of body UA
- 7. AFTER BIRTH……. • Closure of umblical arteries-immediately after cutting the cord • Functional closure takes abt 2-3 months • Distal part form the umblical ligament • Proximal remains open as vesicle arteries
- 8. CONT….. • Closure of umblical veins takes latterthan arteries • Umblical vein form the ligamentam teres after complete obleteration • The ductus venosus collapses and becomes ligamentaum venosum ,the blood flow from which dissappears by the 7th dayof neonatal life
- 9. • Foramen ovale closes due to increased pressure in the left atrium and decreased pressure in the right atrium,it happens due to expansion of the lung • The anatomical closure takes about one month to year. CONT…..
- 10. CONGENITAL HEART DISEASES • DEFINITION • Congenital heart disease is the structural malformations of the heart or great vessels present at birth. • INCIDENCE CHD in children is generaly believed to be 5-8%/1000 live births.about 2-3 in 1000 infnts will be symptomatic during the first year of life.chd is the major cause of death in the first year of life.although there are more than 35 well regognized defects ,the most common heart anomaly is vsd
- 11. ETIOLOGY • The exact cause of chd is unknown about 90% of cases. • Heriditory and consanguinous marriage are important etiologigal factors. • Genitic disorder • Chromosomal aberration • Trisomy, turner syndrome • Factors • Fetal and maternal infection
- 12. CLASSIFICATION OF CHD ACYANOTIC CHD INCREASED PULMONERY OBSTRUCTION TO BLOOD FLOW BLOOD FLOWFROM VENTRICLE ASD COARCTATION OF AORTA VSD AORTIC STENOSIS PDA PULMONIC STENOSIS AVCANAL
- 13. ACYANOTIC HEART DEFECT ASD DEFINITION Abnormal opening between the atria allowing blood from the higher pressure( Left atrium) to flow into the lower pressure( right atrium)
- 14. INCIDENCE 8% -9% all infants born with congenital heart defects. CAUSES Unknown reason TYPES 1. OSTIUM PRIMUM DEFECTS 2. OSTIUM SECUNDRUM DEFECTS 3. SINUS VENOSUS DEFECTS
- 18. PATHOPHYSIOLOGY Flow of oxygenated blood from higher pressure left atrium to the lower pressure right atrium across the ASD Volume overload to right & left ventricular dilation Increased blood flow to the lungs Elevated pulmonary artery pressure
- 19. CLINICAL MANIFESTATION • Asymtomatic • Murmur • Atrial dysrrythmias • Pulmonary hypertension • Excessive tiredness • Frequent chest infection • May develop CHF
- 20. DIAGNOSTIC EVALUATION • Chest x –ray • ECG • ECO TREATMENT Direct suture or A patch of pericardium or Dacron patch closure
- 21. COMPLICATION • Arrhythmias • Frequently SVT • Sinus tachycardia • Paroxysmal atrial tachycardia • Atrial fibrillation • Atrio ventricular conduction disturbances
- 22. VENTRICULAR SEPTAL DEFECT DEFINITION Abnormal opening between the right and left ventricle.
- 23. INCIDENCE 33% Of all children born with VSD CAUSES The ventricular septum form before 8th` week of fetal life and require downward growth from endocardial cushion and the bulbar ridge seperating PA &Aorta. Failure of these structures to grow correctly will result VSD TYPES • Supra cristal or doubly committed defects • Peri membranous or subcristal defects • Canal type defects • Muscular defects
- 24. PATHOPHYSIOLOGY Flow of the oxygenated blood from high pressure left ventricle to low pressure right ventricle through the VSD Increased right ventricular & pulmonary arterial pressure Pulmonary over circulation
- 25. Increased venous return to the left heart results in left heart dilation Change in pulmonary arterial bed –increased pulmonary vascular resistance Reverse the shunt from right to left
- 26. CLINICAL MANIFESTATION Small VSD may be asymptamatic Pansystolic murmur Moderate breathing difficulty -slow to gain weight Respiratory infection Sign of Lv failure Mid systolic murmur Large VSD Hepatomegaly &oliguria Systolic murmur with thrill Failure to thrive Biventricular hypertrophy and CCF
- 27. DIAGNOSTIC EVALUATION History of illness Physicalexamination Chest x-ray ECG ECO Two dimentional echo cardiogram with doppler study
- 28. MANAGEMENT MEDICAL MANAGEMENT Management of heart failure( lasix ,digoxin) SURGICAL MANAGEMENT PALLIATIVE Pulmonary artery banding COMPLETE REPAIR Small defects – purse string approach Large defects-knilled dacron patch
- 29. NONSURGICAL Device closure during cardiac catheterization COMPLICATION Arrythmias Right ventricular failure Pulmonery complication-pneumonia,enlarged LA, left lobe collapsed Residual VSD Pulmonery hypertension Pulmonery stenosis Failure to thrive
- 30. ATRIOVENTRICULAR CANAL DEFECT • DEFINITON Incomplete fusion of endocardial cushion consists of a low ASD and continuous with high VSD and cleft of mitral and tricuspid valves creating large central Av valve that allows blood to flow between all four champers of the heart.
- 31. • INCIDENCE Approximately 5% of all children born with congenital heart lesion. CAUSES Failure of development of Av canal involves formation of mitral tricuspid valves. • Ostium primum ASD • Isolated mitral valve cleft • Partial and complete Av canal defect.
- 32. TYPES • PARTIAL Either VSD and ASD with cleft in anterior leaflet of the mitral valve. COMPLETE OP ASD plus VSD plus common Av valve. The mitral and tricuspid valves have incomplete valves ring.
- 33. PATHOPHYSIOLOGY When blood passes through both the ASD and VSD from the left side of the heart to the right side then a larger volume of blood than normal must be handled by the right side of the heart. This extra blood then passes through the pulmonary artery into the lungs,
- 34. PATHOPHYSIOLOGY cont.. causing higher pressure than normal in the blood vessels in the lungs. As pressure builds up in the lungs, the flow of blood from the left side of the heart to the right side and on to the lungs will diminish. Blood flow within the heart goes from areas where the pressure is high to areas where the pressure is low. If the septal defects are not repaired, and lung disease begins to occur, pressure in the right side of the heart will eventually exceed pressure in the left.
- 35. CLINICAL MANIFESTATION Dyspnea Murmur Mild cyanosis Poor feeding Slow weight gain
- 36. History illness Physical examination Chest X Ray ECG ECO DIAGNOSTIC EVALUATION
- 37. TREATMENT MEDICAL TREATMENT Management of heart failure and respiratory infection SURGICALTREATEMENT PALLIATIVE Pulmonary artery banding COMPLETE REPAIR COMPLICATION Heart bolck CHF Regurgitation Dysarrythmias
- 38. PATENT DUCTUS ARTERIOSUS • DEFINITION Failure of the fetus ductus arteriosus to close with in first week. INCIDENCE Approximately 7% of all infants CAUSES Unknown
- 39. PATHOPHYSIOLOGY In PDA,there is left to right shunt as blood flows from aorta(higher pressure) to pulmonary artery(lower pressure) Pulmonary overload Oxygenated blood of systemic circulation flows back to pulmonary circulation
- 40. Increased vascular pressure in the pulmonary tree &volume overload on left heart Pulmonary vascular disease &pulmonary hypertension
- 41. CLINICALMANIFESTATION • Asymptamatic • Tachypnea • Murmur • Bounding pulse • Feeding difficulties • Repeated respiratory infection. • Pericardial pain • Horseness of voice
- 42. DIAGNOSTIC EVALUATION History Physical examination Chest X Ray ECG ECO
- 43. MEDICAL MANAGEMENT Indomethocin 0.1-0.25 mg /kg /dose IV over 30 mts Antiprostoglandin agents Asprin Mefinamic acid TREATMENT
- 44. • SUPPORTIVE CARE • Rest • Adequate calory intake • Emotional support • SURGICAL MANAGEMENT • Division or ligation of PDA • Visual –assisted thorocoscopy surgery(VATS) • NONSURGICAL TREATEMENT • Use a coil to occlude the PDA
- 45. COMPLICATION • CCF • Infective endocarditis • Pulmonary hypertention • Thromboembolism • RHD
- 46. OBSTRUCTION OF BLOOD FLOW FROM VENTRICLES • COARCTATION OF AORTA • DEFINITION • It is localizsed narrowing near the insertion of Ductus arteriosus resulting in increased pressure proximal to the defect and decreased pressure distal to the obstruction. • INCIDENCE • Approximately 6% of all infants
- 47. CAUSES Extention of ductal tissue in to the neighbouring area in the aorta. TYPES PREDUCTAL The narrowing occurs proximal to the ductus arteriosus JUXTA DUCTAL T occurs opposite to the ductus POSTDUCTAL It occurs distal to the ductus
- 48. Narrowed aorta Produces increased left ventricular pressure Left ventricular hypertrophy ccf PATHOPHYSIOLOGY
- 49. CLINICALMANIFESTATION Neonates Severe CCF Poor perfusion Tachypnea Acidosis and absent femoral pulses OLDER CHILDREN May be asymptomatic Over growth of upper limbs Hypertension in the upper extremities
- 50. OTHER MANIFESTATION • Fatigue • Cramps • Headache • dyspnea • Breathlessness • Systolic murmur
- 51. Chest Xray ECG ECO Barrium swollow DIAGNOSTIC EVALUATION
- 52. MEDICAL Prostoglandin (PGE1 Antibiotics Correct acidosis Monitor 4 limb BP TREATMENT
- 53. SURGICAL& NON TREATMENT • SURGICAL MANAGEMENT • Direct end to end anastomosis • -Gore-tex or Dacron graft • Subclavion flab repair • Percutanious balloon angioplasty • NON SURGICAL TREATEMENT • Balloon angioplasty
- 54. COMPLICATION Post operative hypertension Residual hypertension Bacterial endocarditis Re coarctation Aortic aneurism Mild retardation of left arm COMPLICATION OF UN TREATED Bacterial endocarditis Aortic stenosis dessection Myocardial infarction CVA
- 55. AORTIC STENOSIS • DEFINITION • Narrowing or stricture of the aortic valve causing resistance to blood flow in the left ventricle,decresed cardiac output ,left ventricular hupertrophy ,pulmonary vascular congestion. • INCIDENCE • Appproximately 6% of all infants
- 56. CAUSES • Imperfect formation of the cusps of the aortic valve • In growth of muscle tissue above or below the level of the valve
- 57. TYPES 1.VALVULAR TYPES Malformation of the valve cusps 2.SUBAORTIC (SUBVALVULAR) Fibro membranous narrowing or hypertrophy of the ventricular septum with narrowing of the whole subaortic region (a tunnel effect)
- 58. • SUPRAVALVULAR TYPES • Fibro membranous narrowing of the left ventricular out flow tract occurs immediately above the aortic valve and may or may not extent in to the aortic arch
- 59. Valve obstructions Increased intraventricular pressure Left ventricular hypertrophy Increase preload dependence Sub endocardial ischemia Ventricular dilatation Contractile dysfunction Ischemia, arrhythmia PATHO PHYSIOLOGY
- 60. CLINICALMANIFESTATION Asymptomatic Exercise intolerance Dizziness and syncope Murmur NEONATES Severe CCF Tachypnea Poorperfusion Poor capillary refill Cold skin Poor feeding and metabolic acidosis
- 61. • OLDER CHILDREN • Chest pain on exertion • Decreased exercice tolerence • dyspnea • Pulmonary edema • Shortness of breath, • Syncope • Sudden death CLINICALMANIFESTATION cont…
- 62. DIAGNOSTIC EVALUATION Chest Xray ECG ECO Serial catheterization angiography TREATEMENT MEDICALTREATEMENT Treatement of heart failure PGE1 infusion Ventilatory support with intubation Aortic balloon valvuloplasty
- 63. SURGICALTREATEMENT VALVULAR AORTIC STENOSIS Aorticvalvotomy Vavle replacement may required at 2nd` procedure Homograft Ross procedure NON SURGICAL TREATEMENT Dilating narrowed valve with balloon angioplasty in the catheterization laboratory SUBVALVULAR AORTIC STENOSIS May involve incising membrane if one exists or cutting the fibromucular ring Patch may required to enlarge the entire Lvout flow tract and replace aortic valve known as Konno procedure
- 64. COMPLICATION • Low cardiac output • CCF • Arrhythmias
- 65. PULMONIC STENOSIS • DEFINITION • Narrowing at the entrance to the PA resistanse to blood flow causes Rvhypertrophy and decreased pulmonary blood flow • INCIDENCE • Approximately8% of all children • CAUSES • Unknown
- 66. TYPES 1. VALVULAR STENOSIS In this type the valve cusps are not correctly formed,and valve is dome-shaped with an anterior orifice. 2.LOCALIZED INFUNDIBULAR OBSTUCTION In this type below the valve is obstructed 3.GENERALIZED INFUNIBULAR NARROWING Whole valve is narrowed 4.SUPRAVALULAR OBSTRUCTION
- 67. Back flow to the right atrium Right atrium enlargement and hypertrophy Venous return.increase blood flow to systemic circulation Hepatomegaly,ascitis PATHOPHYSIOLOGY
- 68. CLINICALMANIFESTATION • Asymptomatic • Mild cyanosis or CHF • Murmur • Moonface • decreased cardiac output • Peripheral cyanosis • Dyspnea on exertion • Decreased exercice tolerence • Cold perpheries • Angina and syncope • Widely split second heart rate
- 69. DIAGNOSTIC EVALUATION • History of illness • Physical examination • Chest xray • ECG • ECO • TREATEMENT • SURGICALTREATMENT • In infants , trans ventricular (closed) valvotomy. • In children ,pulmonary valvotomy with cardio pulmonary bypass
- 70. NONSURGICALTREATMENT Balloon angioplasty PGE1 infusion Children with Noonens’ syndrome –patch anuloplasty..reconstruction of the incompetent cardiac valve NON SURGICAL MANAGEMENT
- 71. CCF Low cardiac output Arrhythmias Pulmonary valve insufficiency Right ventricular dysfunction. COMPLICATIONS
- 72. NURSING MANAGEMENT • Improving cardiac output by uninterrupted rest, minimum exercise. • Monitoring vital signs of the child. • Providing adequate nutrition-the child should be provided with small frequent feeding. • The older children may require high calorie diet. • Monitor the weight of the child daily • Maintain intake and output chart
- 73. NURSING MANAGEMENT • Preventing infections by avoiding exposure to infections and infected persons. • Early detection and treatment of upper respiratory tract infections. • Teach the parents and family members about health maintenance and follow up.
- 74. NURSING DIAGNOSIS • Risk for infection related to chronic illness • Fear and anxiety related to life threatening illness • Knowledge deficit related to long term problems and prevention of complications.
- 75. CONCLUSION • Acyanotic heart defects are congenital cardiac malformations that affect the atrial or ventricular walls, heart valves, or large blood vessels. Common causes include • genetic defects (e.g., trisomies), maternal infections (e.g., rubella), or maternal consumption of drugs or alcohol during
- 76. • Hockenberry - Wong’s nursing care of infants and children,2007,Elsevier. • Parul datta – Text book of pediatric nursing, 3rd edition, Jaypee brother publishers. • Marlow –Text book of pediatric nursing 1996,Elsevier. • Potts- Pediatric nursing 2007,Thomas learning. • Nelson –Textbook of pediatrics 2007,Elsevier. • Ghai- Essential pediatrics 2009,CBS. REFERENCES