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Acynotic heart defects
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  1. 1. PRESENTOR Anjani Walia Msc Nursing Student CON, AIIMS
  2. 2. Objectives  Explain fetal circulation.  Define CHD & its risk factors.  Classify congenital heart disease.  Explain acyanotic heart disease & classify it.  Explain VSD, its clinical manifestation, diagnostic criteria & management in detail.  Explain ASD, its clinical manifestation, diagnostic criteria & management in detail.
  3. 3.  Explain PDA, its clinical manifestation, diagnostic criteria & management in detail.  Explain aortic stenosis, its clinical manifestation, diagnostic criteria & management in detail.  Explain pulmonary stenosis, its clinical manifestation, diagnostic criteria & management in detail.  Explain coarctation of aorta, its clinical manifestation, diagnostic criteria & management in detail.  Explain nursing management for acyanotic disease.
  4. 4. Fetal circulation
  5. 5. Congenital Heart Disease  CHD refers to structural heart defects that are present at birth.  CHD accounts for nearly one-third of all major congenital anomalies.  The prevalence of CHD in infancy is estimated at 6-8 per 1000 live births  25% are life threatening & require early intervention.
  6. 6. Risk Factors Gestational diabetes Febrile illness in first trimester Rubella Phenylketonuria Lupus
  7. 7. Vitamin deficiency Teratogens Exposure to organic solvents Herbicides, pesticides, ionizing radiation
  8. 8. Acyanotic heart disease  An acyanotic heart defect, also known as non- cyanotic heart defect, is a class of congenital heart defects.  In these, blood is shunted from the left side of the heart to the right side of the heart due to a structural defect in the septum.
  9. 9. Ventricular Septal Defect  VSD is a developmental defect of the interventricular septum, wherein communication between the cavities of the two ventricles is observed.
  10. 10. Pathophysiology  A defect in the interventricular septum allows communication between the systemic & pulmonary circulations.  As a result, flow moves from a region of high pressure to a region of low pressure—i.e. from the L-to-R shunt.
  11. 11. Left-to-right shunt Has 3 hemodynamic consequences:  Increased LV volume load  Excessive pulmonary blood flow  Reduced systemic cardiac output
  12. 12. Clinical manifestation Small VSDs  Mild or no symptoms.  Murmur is detected during routine examination. Feeding or weight gain usually is not affected. Moderate VSDs  Excessive sweating, especially notable during feeds.  Fatigue with feeding  Lack of adequate growth  Frequent respiratory infections
  13. 13. Large VSDs  Symptoms & signs are similar to, but more severe  Poor weight gain & frequent respiratory infections are common Eisenmenger syndrome  At rest, patients may have no symptoms with mild systemic desaturation.  With exercise, symptoms include exertional dyspnea, cyanosis, chest pain, syncope, & hemoptysis.
  14. 14. Diagnostic evaluation Radiography  Chest radiography may reveal the size of VSDs, heart size, pulmonary vascularity. Echocardiography  To determine the size & location of virtually all VSDs.  Doppler echocardiography provides additional physiologic information (eg, RV pressure, PA pressure & interventricular pressure difference).
  15. 15. Magnetic Resonance Imaging  Infrequently required for the diagnosis of VSDs.  As a rule, it is employed only when USG is not feasible or when USG findings are not diagnostic. Electrocardiography  With moderate-sized VSDs & with moderate or large left-to-right shunts with volume overload in the LV, LV hypertrophy is the rule.  In patients with large VSDs & equal ventricular pressures, RV hypertrophy is demonstrated as a dominant R wave in the right precordial leads & upright T waves in younger patients.
  16. 16. MANAGEMENT Medical Management of Symptomatic CHF  Increased caloric density.  Diuretics – Furosemide (1-3 mg/kg/d divided in 2 or 3 doses)  ACE inhibitors (eg, captopril & enalapril)
  17. 17. Intracardiac Repair of Defect  Direct surgical repair using cardiopulmonary bypass is preferred  PA banding, part of a 2-stage procedure, is largely reserved for critically ill infants with multiple VSDs or for those with associated anomalies.  Reported complications have included aortic & tricuspid regurgitation, device embolization, complete heart block, transient left bundle-branch block (LBBB), hemolysis, small residual shunts, & perforation.
  18. 18. Arterial Septal Defect  Defect in the inter atrial septum  Allowing pulmonary venous return from the left atrium to pass directly to the right atrium.
  19. 19. Types  Ostium secundum ASD: This type of ASD results from incomplete adhesion between the flap valve associated with the foramen ovale & the septum secundum after birth.  Ostium primum ASD: These defects are caused by incomplete fusion of septum primum with the endocardial cushion. The defect lies immediately adjacent to the atrioventricular (AV) valves, either of which may be deformed & incompetent.
  20. 20.  Sinus venosus ASD: Abnormal fusion between the embryologic sinus venosus & the atrium causes these defects. In most cases, the defect lies superior in the atrial septum near the entry of superior vena cava.  Coronary sinus ASD: The coronary sinus defect is characterized by unroofed coronary sinus & persistent left superior vena cava that drains into the left atrium. A dilated coronary sinus often suggests this defect.
  21. 21. Clinical manifestations  Palpable pulsation of the Pulmonary Artery  Ejection click can be detected because of a dilated pulmonary artery.  S1 is typically split  S2 is often widely split & fixed  Murmur is heard in the 2nd ICS at the upper left sternal border  Patients with large left-to-right shunts often have a rumbling middiastolic murmur at the lower left sternal border
  22. 22.  In patients with an ostium primum defect & an associated cleft of the mitral valve, an apical systolic regurgitant murmur of mitral regurgitation may be present.  In the rare case of severe pulmonary arterial hypertension, atrial shunt reversal (Eisenmenger syndrome) may occur, leading to cyanosis & clubbing.
  23. 23. Diagnostic evaluation  Routine laboratory studies  Complete blood cell (CBC) count, Type & screen, Metabolic profile or chemistry panel, Coagulation studies (prothrombin time [PT] & activated partial thromboplastin time [aPTT])
  24. 24. Chest radiography  Show cardiomegaly because of dilatation of the right atrium & right ventricular chamber.  The pulmonary artery is prominent  Pulmonary vascular markings are increased in the lung fields.
  25. 25. Transthoracic echocardiography  An uncertain diagnosis can be clarified with transthoracic 2-D echocardiography, which provides direct noninvasive visualization of most types of ASDs including evaluation of the RA, RV & PA as well as other associated abnormalities. MRI  A major advantage of MRI is the ability to quantify RV size, volume & function along with the ability to identify the systemic & pulmonary venous return.
  26. 26. Electrocardiography  Characteristic findings in patients with secundum ASD are a normal sinus rhythm, right-axis deviation, an interventricular conduction delay or right bundle branch block.
  27. 27. Cardiac catheterization  May be useful if the clinical data are inconsistent, if clinically significant pulmonary arterial hypertension is suspected, or if concurrent coronary artery disease must be assessed in patients older than 40 years.  Catheterization is also a viable alternative for intervention for secundum ASD.
  28. 28. MANAGEMENT Surgical management  Direct closure of the defect by using an open approach with extracorporeal support. Minimally invasive approaches  Size of the incision is simply decreased with different approaches to cardiopulmonary bypass. Examples include partial or full submammary skin incision, hemisternotomy, & limited thoracotomy.
  29. 29. Percutaneous transcatheter closure  In recent times, secundum ASD have been closed by using a variety of catheter-implanted occlusion devices rather than by direct surgical closure with cardiopulmonary bypass.  These devices are placed through a femoral venous approach & are deployed like an umbrella to seal the septal defect.  These devices work best for centrally located secundum defects.
  30. 30. Complications  Long-term risk of atrial fibrillation or flutter  Risk of infective endocarditis exists during the first 6 months after surgery.  Congestive heart failure  Arrhythmias  Pulmonary hypertension  Paradoxical embolization  Stroke
  31. 31. Patent Ductus Arteriosus  Persistent communication between the descending thoracic aorta & the pulmonary artery  Results from failure of normal physiologic closure of the fetal
  32. 32. Symptoms  The typical child with PDA is asymptomatic.  At times, the patient may report decreased exercise tolerance or pulmonary congestion in conjunction with a murmur.  Tachypnea, diaphoresis, inability or difficulty with feeding & weight loss or no weight gain.  A ductus arteriosus with a moderate-to-large L to R shunt may be associated with a hoarse cry, cough, lower respiratory tract infections, atelectasis or pneumonia.
  33. 33.  With large defects, the patient may have a h/o feeding difficulties & poor growth during infancy, described as FTT.  Adults whose PDA has gone undiagnosed may present with s/s of heart failure, atrial arrhythmia, or even differential cyanosis limited to the lower extremities, indicating shunting of unoxygenated blood from the pulmonary to systemic circulation.
  34. 34. DIAGNOSIS  Based on careful clinical evaluation, including physical examination showing the characteristic murmur, typical ECG abnormalities, radiographic changes, & echocardiographic/Doppler findings.  ECG is the primary diagnostic study used to evaluate & diagnose PDA.  CBC & metabolic panel
  35. 35. Doppler Echocardiography  The echocardiographic findings are typically diagnostic for PDA.  High velocity jets of turbulent flow in the pulmonary artery can be reliably detected by color flow Doppler imaging; this technique is sensitive in detecting even the small PDA. Chest Radiography  Cardiomegaly may be present with or without CHF.  If significant L-to-R shunt through the PDA is present, the PA , PV , LA & LV are enlarged on chest films. Also, the ascending aorta may be prominent.
  36. 36. Electrocardiography  In the neonate, especially the premature neonate with a large PDA, T-wave inversion & ST segment depression may be present, suggesting ischemia or a supply-demand mismatch.
  37. 37. Cardiac Catheterization & Angiography  Color-flow Doppler mapping is more sensitive than cardiac catheterization in detecting a small PDA.  However, cardiac catheterization may be required for confirmation of clinical diagnosis in children with pulmonary hypertension and/or associated congenital cardiovascular malformations.  Selective angiography is the definitive tool for determining the presence & size of the ductus.  Angiography is also used to define the intracardiac anatomy when other defects are suspected.
  38. 38. MANAGEMENT Medical management  If medical therapy is ineffective, urgent intervention to close the structure should be undertaken.  CHF is an indication for closure of PDA in infancy.
  39. 39.  All PDA should be closed because of the risk of bacterial endocarditis associated with the open structure.  Closure of the PDA is stimulated by administration of prostaglandin synthesis inhibitors, such as indomethacin or aspirin, which is effective in premature infants.  Indomethacin (0.1 mg/kg) is administered orally at 8-hour intervals.  This treatment is particularly valuable in premature infants presenting with respiratory distress syndrome complicated by left-to-right shunting through the ductus.
  40. 40. Conservative Management  Until the patency of the ductus is corrected, administer antibiotics in patients during instances of high exposure to bacteremia (eg, instrumentation, dental procedures), as recommended by the American Heart Association for the prevention of bacterial endocarditis.  In infants who present with CHF, the standard treatment of digoxin & diuretic therapy usually palliates the condition.
  41. 41. Cardiac Catheterization  The use of the percutaneous route to close the PDA is becoming more common.  Transcatheter occlusion is an effective alternative to surgical intervention & is becoming the treatment of choice for most cases of PDA in children & adults.  Typically, complete occlusion is achieved at catheterization.  Occasionally, a tiny residual left-to-right shunt remains at the end of the procedure, which closes by thrombus formation over the following days or weeks.
  42. 42. Surgical Ligation  Remain the standard treatment of large PDA that require treatment in infancy.  Indications for surgical treatment include the failure of indomethacin treatment, Contraindications to medical therapy (eg, thrombocytopenia, renal insufficiency), Signs & symptoms of CHF, PDA found in an older infant
  43. 43. COMPLICATIONS  Bacterial endocarditis  Late CHF  Development of pulmonary vascular obstructive disease.
  44. 44. Research input Res Dev Disabil. 2015 Oct-Nov;45-46:58-68. Neurodevelopmental outcome after surgery for acyanotic congenital heart disease. Sarrechia, Miatton, François, Gewillig, Meyns , Vingerhoets, De Wolf This study was designed to objectify the neuropsychological profile & evaluate associations with medical data. Patients with a corrected atrial or ventricular septal defect, ASD-II or VSD & a matched control group were submitted to an intelligence test (Wechsler Intelligence Scale for Children, third edition, Dutch version) & evaluated with a neuropsychological test battery (Developmental Neuropsychological Assessment, second edition, Dutch version).
  45. 45. Hospitalization variables were retrieved to evaluate associations with cognitive outcome. Parents completed a behavioral checklist (Achenbach Child Behavior Checklist for Children aged 6-18). RESULTS: ASD-II patients showed lower scores in domains of visuospatial processing, language, attention, & social perception. VSD patients displayed subtle problems in attention & visuospatial information processing. Only few perioperative medical factors, but also socioeconomic variables were associated with cognitive outcomes. Parents of ASD-II patients reported more school problems when compared to controls.
  46. 46. CONCLUSIONS: After treatment for aCHD, subtle cognitive difficulties can present in domains of visuospatial information processing, language, attention, & social perception. These shortcomings might hamper school performances, as is suggested by lower school competence ratings. Ongoing follow-up & cognitive screening is warranted to promote developmental progress, in which both parents & clinicians share responsibility.
  47. 47. Research input J Med Assoc Thai. 2012 Dec;95(12):1501-8. Comparison of renal function between cyanotic & acyanotic congenital heart disease in children & adolescent. Amornchaicharoensuk Y et.al. OBJECTIVE: To evaluate the prevalence renal dysfunction & to compare glomerular & tubular function between cyanotic & acyanotic CHD in children & adolescent. Correlations among clinical factors, urinary glomerular & tubular markers for kidney injury were also determined.
  48. 48. MATERIAL & METHOD: Renal function was determined by estimated GFR, urine protein/creatinine, urine microalbumin /creatinine, FE Na+, FE Mg2, & urine NAG/creatinine in children & adolescent with CHD. RESULTS: 46 patients, 15 cyanotic (group 1) & 31 acyanotic CHD (group 2), were studied. Only the differences of urine NAG/creatinine, FE Mg2+, & urine protein/creatinine between the two groups were statistically significant. Significantly higher prevalence of abnormal biochemical markers in group 1 compared to those of group. The authors found moderate correlation between hemoglobin & functional class of the patients & highly negative correlation between oxygen saturation & functional class .
  49. 49. CONCLUSION: Cyanotic CHD patients had more prevalence & higher abnormal biochemical markers for renal dysfunction than those of acyanotic CHD. Their urine protein/creatinine, FE Mg2 & urine NAG/creatinine were higher than those of acyanotic CHD. Only low correlation among biochemical markers was found.
  50. 50. Pulmonic stenosis  Refers to a dynamic or fixed anatomic obstruction to flow from the right ventricle (RV) to the pulmonary arterial vasculature.  Isolated valvular PS comprises approximately 10% of all congenital heart disease.  Except for critical stenosis in neonates, survival is the rule in congenital PS.  A slight female predominance exists.
  51. 51. Pathophysiology Valvular pulmonic stenosis • The valve commissures are partially fused & the 3 leaflets are thin & pliant, resulting in a conical or dome-shaped structure with a narrowed central orifice. Subvalvula r pulmonic stenosis • Occurs as a narrowing of the infundibular or subinfundibular region, often with a normal pulmonic valve. Present in individuals with TOF & can also be associated with a VSD. Peripheral pulmonary stenosis • Cause obstruction at the level of the main pulmonary artery, at its bifurcation, or at the more distal branches. May occur at a single level, but multiple sites of obstruction are more common.
  52. 52. CLINICAL MANISFESTATION  Those with severe PS may experience exertional dyspnea & fatigue.  In extremely rare cases, patients present with exertional angina, syncope, or sudden death.  Peripheral edema & other typical symptoms occur with right heart failure.  Cyanosis is present in those with significant R to L shunt via a patent foramen ovale, ASD or VSD.
  53. 53. DIAGNOSIS Plain Chest Radiography Prominence of the main, right, or left pulmonary arteries caused by post stenotic dilatation. Echocardiography Definitive confirmation of the diagnosis of PS. Using 2-D imaging, thickening of the valves, characteristic of nondysplastic valves, RV hypertrophy can be noted readily.
  54. 54. Cardiac Catheterization & Pulmonary Angiography Generally is not needed except when a significant discrepancy is noted between clinical findings & echocardiographic findings. Can diagnose PS by a pressure gradient from the pulmonary artery to the RV on "pull-back" of the pulmonary artery catheter. In the case of isolated PPS, pulmonary angiography may be needed to establish the diagnosis.
  55. 55. Electrocardiography  The degree of RV hypertrophy on the ECG is largely correlated directly with the severity of PS.  With mild PS, 50% of patients have a normal ECG tracing or only mild right-axis deviation.  With moderately severe PS, right-axis deviation & increased R-wave amplitude in V1 are seen.  Severe PS is associated with extreme right-axis deviation, a dominant R wave in AVR, & a prominent R wave (>20 mm) in V1.
  56. 56. Management  Traditionally, PS was treated by surgical valvotomy.  Pulmonary artery balloon angioplasty with or without placement of an expandable metal stent can be used to treat supravalvular PS & PPS.  Expandable metal stents can overcome an obstruction successfully  However, the need for stent reexpansion as the individual grows remains problematic.
  57. 57. Aortic stenosis  The obstruction of blood flow across the aortic valve.  Among symptomatic patients with medically treated moderate-to-severe aortic stenosis, mortality from the onset of symptoms is approximately 25% at 1 year & 50% at 2 years.  Symptoms of aortic stenosis usually develop gradually after an asymptomatic latent period of 10- 20 years.
  58. 58. Signs & symptoms Chest pain: Typically precipitated by exertion & relieved by rest Heart failure: Paroxysmal nocturnal dyspnea, orthopnea, dyspnea on exertion, & shortness of breath Syncope: Occurs upon exertion when systemic vasodilatation in the presence of a fixed forward stroke volume causes the arterial systolic blood pressure to decline
  59. 59. Soft or normal S1 Systolic hypertension Paradoxical splitting of the S2 Pulsus alternans Systolic murmur Prominent S4 Ejection click
  60. 60. DIAGNOSIS Echocardiography  Two-dimensional transthoracic echocardiography can confirm the clinical diagnosis of aortic stenosis  Provide specific data on LV function.  The structure & function of the other heart valves can also be assessed. Chest Radiography  Cardiac size often is normal, with rounding of the LV border & apex. Post stenotic dilatation of the ascending aorta is common.
  61. 61. Cardiac Catheterization & Coronary Arteriography  An accurate measure of aortic stenosis  Exclusion of CAD by coronary angiography is important in all patients >35 years who are being considered for valve surgery.  Coronary angiography should also be performed in patients <35 years if they have LV systolic dysfunction, s/s suggestive of CAD, or 2 or more risk factors for premature CAD, excluding gender.
  62. 62. Radionuclide Ventriculography  Evaluate myocardial perfusion at rest & during exertion & exercise may be considered as part of the complete workup of aortic stenosis. Exercise Stress Testing  Contraindicated in symptomatic patients with severe aortic stenosis  May be considered in asymptomatic patients with severe aortic stenosis.  Closely monitored exercise stress testing may be of value to assess exercise capacity in asymptomatic patients.
  63. 63. Management  Treated supportively with oxygen, cardiac & oximetry monitoring, IV access, loop diuretics, nitrates, morphine & noninvasive or invasive ventilatory support .  Patients with severe heart failure due to aortic stenosis that is resistant to medical management should be considered for urgent surgery.  Angina pectoris requires monitoring. Measures may include nitrates, oxygen, & morphine to relieve the chest discomfort.
  64. 64. Percutaneous Balloon Valvuloplasty  Used as a palliative measure  who are not surgical candidates or as a bridge to aortic valve replacement in critically ill patients.  The high rate of restenosis & the absence of a mortality benefit preclude its use as a definitive treatment method in adults with severe aortic stenosis.
  65. 65. Aortic Valve Replacement  Surgical treatment of choice.  If concomitant coronary disease is present, aortic valve replacement & coronary artery bypass graft (CABG) should be performed simultaneously.  Successful aortic valve replacement produces substantial clinical & hemodynamic improvement in patients with aortic stenosis
  66. 66. Ross procedure  Patient's own pulmonary valve & main pulmonary artery are transplanted to the aortic position.  A homograft is placed in the pulmonary position. Its durability may be better than tissue valves. Percutaneous transcatheter valve replacement  Not candidates for or are at high risk for complications with surgical replacement of the aortic valve.  Studies have suggested that this as a less invasive option for these high-risk patients.
  67. 67.  Beta-Adrenergic Receptor Blockers  Cardiac Glycoside  increasing vagal tone  pulmonary congestion may be treated with digoxin  control the ventricular rate in patients with atrial fibrillation.  Loop Diuretics  with uncontrolled heart failure should be treated supportively with loop diuretics.
  68. 68.  ACE Inhibitor  reduce angiotensin II levels & aldosterone secretion.  Opioid Analgesics  Morphine  Can also help patient anxiety, distress, & dyspnea.
  69. 69. Coarctation of the aorta  Defined as a constricted aortic segment that comprises localized medial thickening, with some infolding of the medial & superimposed neointimal tissue.  Coarctation is about twice as common in boys as it is in girls.  It is common in girls who have Turner syndrome.
  70. 70. CLASSIFICATION Preductal coarctation • Proximal to the ductus arteriosus. Blood flow to the aorta is dependent on the ductus arteriosus; therefore severe coarctation can be life- threatening. Ductal coarctation • At the insertion of the ductus arteriosus. This kind usually appears when the ductus arteriosus closes. Postductal coarctation • Distal to the insertion of the ductus arteriosus. Even with an open ductus arteriosus, blood flow to the lower body can be impaired
  71. 71. CLINICAL MANISFESTATION  Difficulty breathing  Poor appetite or trouble feeding, Failure to thrive  Dizziness or shortness of breath, faint or near- fainting episodes,  Chest pain, abnormal tiredness or fatigue, headaches, or nosebleeds  Arterial hypertension in the arms with low BP in the lower extremities is classic.  Weak pulses in the femoral arteries & arteries of the feet are found.
  72. 72. DIAGNOSIS Electrocardiography  with early onset of coarctation of the aorta may reveal RV rather than LV hypertrophy. Chest Radiography  May reveal cardiomegaly, pulmonary edema, & other signs of CHF
  73. 73. Echocardiography  Intracardiac anatomy & allows assessment of associated significant intracardiac anomalies.  Evaluation of the aortic arch to assess the transverse aortic arch, isthmus, & severity of coarctation MRI & CT  Useful in older or postoperative patients to assess residual arch obstruction, arch hypoplasia, or formation of aneurysms.
  74. 74. MANAGEMENT  Diuretics & inotropic drugs.  Prostaglandin E1 (0.05-0.15 mcg/kg/min) is infused intravenously to open the ductus arteriosus.  Ventilatory assistance  An umbilical artery catheter may be placed in neonates to assess the response to prostaglandin infusion with regard to improving lower-body blood flow.  Patients stabilized by the above interventions are better candidates for surgical or catheter intervention.
  75. 75. Surgical Care Balloon angioplasty & stenting  Balloon angioplasty is the treatment of choice for postsurgical recoarctations.  Vascular stenotic lesions can be opened with balloon angioplasty but because of the elastic recoil of the vessel wall, the vessel lumen may return to the predilation size following withdrawal of the balloon catheter.  Such recoil & vascular dissection following balloon dilatation can be circumvented with implantation of endovascular stents.
  76. 76. Nursing Management
  77. 77. Nursing management Decreased Cardiac Output r/t Structural factors of congenital heart defect Assess heart sounds for gallops (S3, S4), HR & BP. Note skin color, temperature, & moisture. Check for peripheral pulses, including capillary refill. Assess for reports of fatigue & reduced activity tolerance. Inspect fluid balance & weight gain. Weigh patient regularly.
  78. 78. Monitor ECG for rate, rhythm. Provide adequate rest periods. Position child in semi-Fowler’s position. Administer oxygen therapy as prescribed.
  79. 79. Activity Intolerance r/t Generalized weakness Assess level of fatigue, ability to perform ADL & other activities in relation to severity of the condition. Assess dyspnea on exertion, skin color changes during rest & when active. Allow for rest periods between care. Avoid allowing the infant to cry for long periods of time, use soft nipple for feeding; cross-cut nipple; if unable for infant to ingest sufficient calories by mouth, gavage-feed infant.
  80. 80. Provide neutral environmental temperature; keep the infant covered to prevent heat loss. Provide toys & games for quiet play & diversion appropriate for age of child. Assist parents to plan for care & rest schedule. Explain to parents need to conserve energy & encourage rest.
  81. 81. Risk for Injury r/t Cardiac function compromised by congenital defects & medication administration Assess for risk of drug toxicity Assist & support family’s feeling & decision regarding surgery. Prepare parents & child for diagnostic procedures and/or surgery Instruct in the administration of drugs, taking the apical pulse, when to withhold, to notify the low or irregular pulse, signs of toxicity. Teach actions to take if the child becomes cyanotic (knee-chest or squatting position, elevating head & chest), when to call the physician.
  82. 82. Risk for Infection r/t Chronic illness Assess temperature, IV site if present, increased WBC, increased pulse & respirations. Avoid allowing those with infections to have contact with infant/ child. Provide adequate rest & nutritional needs for age. Wash hands before giving care. Use sterile technique for IV maintenance if present. Administer antibiotics as ordered Instruct parents & child in maintaining personal hygiene
  84. 84. PREVENTION OF CHD Education of lay public on the risks associated with consanguinity, drugs & teratogens in the first trimester of pregnancy Immunization against rubella Fetal echocardiography is emerging as a modality for early diagnosis of CHD. Conditions that involve major chamber discrepancy (such as hypoplastic left heart syndrome), single ventricles & common AV canal can be identified by routine screening as early as 14-16 weeks gestation.
  85. 85. Summary & 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 pregnancy.  Acyanotic heart defects are characterized pathophysiologically by a left-to-right shunt, which causes pulmonary hypertension & right heart hypertrophy.
  86. 86. The symptoms depend on the extent of the malformation & the resulting impairment of cardiac function. Infants may be asymptomatic or present with exercise intolerance, failure to thrive, & symptoms of heart failure. Acyanotic heart defects requiring treatment are repaired via catheter procedures or surgery. Supportive medical therapy is needed in cases of heart failure (e.g., diuretics, inotropic agents) or if surgery cannot be performed (e.g., prostaglandin).
  87. 87. References  Altman CA, Fulton DR, Weisman LE, Armsby C. Diagnosis and Initial Management of Cyanotic Heart Disease in the Newborn. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/diagnosis- and-initial-management-of-cyanotic-heart-disease-in-the- newborn.  Ghai. Essential pediatric.8th ed . CBS Publishers;.Pp 400- 450.  Hurst JW, Fuster V, Walsh RA, Harrington RA, editors. Hurst’s the heart. 13th ed. New York: McGraw-Hill Medical; 2011. Pp 1900-1904
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Hinweis der Redaktion

  • the most severe complication of a large VSD. Fixed & irreversible pulmonary hypertension develops, resulting in reversal of the left-to-right shunt to a right-to-left shunt.
  • In patients with small VSDs, ECG findings are normal.
  • In Children with small VSDs neither medical therapy nor surgical therapy is indicated. Prophylactic antibiotic therapy against endocarditis is no longer indicated in most cases. Maintenance of good oral hygiene is of paramount importance in reducing the risk of endocarditis.
    to relieve pulmonary congestion
    These medications reduce both the systemic & pulmonary pressures, thereby reducing the left-to-right shunt
  • No specific or definitive medical therapy is available
  • crossed embolism, refers to an embolus which is carried from the venous side of circulation to the arterial side, or vice versa.
  • Spontaneous closure of the PDA is common. If significant respiratory distress or impaired systemic oxygen delivery is present, therapy is usually prudent.
  • These children can be treated until they are several years old & are good candidates for ductal closure. When medical treatment of congestive heart failure fails in infants, the patients are referred early for surgical closure of the structure.
  •  arterial pulse waveform showing alternating strong and weak beats
    just after the first heart sound. The sounds occur in the presence of a dilated aorta or pulmonary artery 
  • are limited in symptomatic patients with aortic stenosis who are not candidates for surgery.
  • In mild cases, children may show no signs or symptoms at first & their condition may not be diagnosed until later in life.
    In more severe coarctations, babies may develop serious problems soon after birth
  • Significant HTNor CHF is an indication
    Surgical relief of the aortic obstruction & catheter interventional techniques (balloon angioplasty & stents) are available alternatives.