Alterations in Cardiovascular Function

1. Alterations in Cardiovascular Function Ball & Bindler Donna Hills APN EdD

2. Blood Flow

3. Transition from fetal to pulmonary circulation • the umbilical cord is cut • systemic vascular resistance is increased • pressure in the L side of the heart increases • foramen ovale closes • breathing is initiated • pulmonary vascular resistance falls • blood that was shunted through the PDA now goes to the lungs.

4. FIGURE 26–1 Fetal circulation. Blood leaves the placenta and enters the fetus through the umbilical vein. The ductus venosus, the foramen ovale, and the ductus arteriosus allow the blood to bypass the fetal liver and lungs. After circulating through the fetus, the blood returns to the placenta through the umbilical arteries. From Ladewig, P. W., London, M. L., Moberly, S., & Olds, S. B. (2002). Contemporary Maternal-Child Nursing Care (8th ed,. p. 51 ). Upper Saddle River, NJ: Prentice Hall. Jane W. Ball and Ruth C. BindlerChild Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc.Upper Saddle River, New Jersey 07458All rights reserved.

5. FIGURE 26–2A, Fetal (prenatal) circulation. B, Pulmonary (postnatal) circulation. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle. Jane W. Ball and Ruth C. BindlerChild Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc.Upper Saddle River, New Jersey 07458All rights reserved.

6. Ductus Arteriosus • an opening in fetal circ. between the pulmonary artery (PA) and aorta (Ao). • in fetal circulation, most of the blood bypasses the lungs and returns to systemic circulation by way of the PDA (PA to Ao). • In transition to pulmonary circulation, the PDA constricts over 10-15hrs; permanent closure should occur by 3wks of age, UNLESS SATURATION REMAINS LOW

7. FIGURE 26–3 Normal pressure gradients and oxygen saturation levels in the heart chambers and great vessels. The ventricle on the right side of the heart has a lower pressure during systole than the left ventricle because less pressure is needed to pump blood to the lungs than to the rest of the body. Jane W. Ball and Ruth C. BindlerChild Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc.Upper Saddle River, New Jersey 07458All rights reserved.

8. Hypoxemia in the infant • below 95% pulse oximetry. • cyanosis results from hypoxemia • perioral cyanosis indicates central hypoxemia • acrocyanosis does not.

9. Response to Hypoxemia • acute: HR increases • chronic: bone marrow produces more RBC to increase the amount of Hgb available for oxygen transport. • Hct>50 is called polycythemia. • increased blood viscosity increases risk of thromboembolism.

10. Cardiac Functioning • 02 requirements are high the first few weeks of life • normally, HR increases to provide adequate oxygen transport • infant has little cardiac output reserve capacity • cardiac output depends almost completely on HR until the heart is fully developed (age 5 yr).

11. Compliance in the infant • in infancy, muscle fibers are less developed and organized • results in less functional capacity or less compliance • less compliance means the infant is unable or less able to distend or expand the ventricles to achieve an increase stroke volume in order to compensate for increased demands.

12. Severe Hypoxemia • children respond with bradycardia • cardiac arrest generally results from prolonged hypoxemia related to respiratory failure or shock • in adults, hypoxemia usually results from direct insult to the heart. • therefore, in children, bradycardia is a significant warning sign of cardiac arrest. • approp Rx for hypoxemia reverses brady.

13. Case Study • Dylan is a 3 mo old with Down Syndrome and VSD, admitted for CHF. His birth weight was 7 lb 9 oz; a week ago he weighed 12 lb at the pediatrician’s office and now weighs 12.10 lb. He is breathing 72 bpm with a HR of 190 and a sat of 91%. He is diaphoretic and is not taking his usual 3 oz formula every 3-4 hours. He has had 4 moderately wet diapers in the past 24 hrs.

14. Study questions for case study • Identify abnormal assessment data for Dylan • What other data would you collect? (Hx and assessment) • What is your priority nursing action? • What other nursing interventions would you do for him? For his mother?

15. Down Syndrome • A trisomy genetic abnormality; ;usually on chromo 21. • Classic characteristics: • Some degree of mental retardation with variable functional deficit • Microcephaly, flattened forehead, wide short neck. Epicanthal eye folds, simian palmar crease, protruding tongue, low set ears, short broad hands, hearing loss, hypotonia. • Increased incidence of DM, CHD and Leukemia

16. What aspects of Down Syndrome have an affect on his ability to maintain optimal health? • Protruding tongue • Hypotonia • Slower to reach milestones, compounded by hypotonia

17. Pulmonary Artery Hypertension • irreversible condition that results from R sided heart circulation being overloaded and therefore shunting excessive blood to the lungs. • overloads the R side of the heart, overloads the pulmonary system causing increased pulmonary vascular resistance (life threatening).

18. Obstructive Congenital Defects • due to abnormally small pulmonary vessels • which restrict flow of blood, so the heart hypertrophies to work harder to provide the blood flow to organs. • however, CO increases initially but eventually hypertrophied muscle becomes ineffective. • initially R sided failure, progressing to L sided and eventual bilateral failure

19. Congestive Heart Failure • cardiac output is inadequate to meet the body’s needs • may result from: • congenital heart defect that causes increased pulmonary blood flow or obstruction of blood outflow tract • problems with heart contractility • pathology that requires a high cardiac output (severe anemia, acidosis, respiratory disease).

20. CHF in the infant • can be subtle • good assessment skills are a must • tires easily, especially during feeding • (initial) weight loss • diaphoresis, irritability, frequent infection.

21. FIGURE 26–4 Jooti is receiving intravenous fluids and oxygen. Her condition is being continuously monitored for congestive heart failure. Jane W. Ball and Ruth C. BindlerChild Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc.Upper Saddle River, New Jersey 07458All rights reserved.

22. CHF in older children • exercise intolerance • dyspnea • abdominal pain or distention • peripheral edema.

23. Symptoms of progressive disease • tachycardia, tachypnea, pallor or cyanosis, F/G/R, cough, crackles. • fluid volume overload: periorbital and facial edema, JVD, hepatomegaly, ascites. • not mentioned in the book: increased weight gain, bounding pulses, edema of dependent body parts.

24. FIGURE 26–4 Jooti is receiving intravenous fluids and oxygen. Her condition is being continuously monitored for congestive heart failure. Jane W. Ball and Ruth C. BindlerChild Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc.Upper Saddle River, New Jersey 07458All rights reserved.

25. FIGURE 26–5 Infants with cardiac conditions often require supplemental feedings to provide sufficient calories for growth and development. The parents of this infant girl have been taught how to give her nasogastric feedings at home. Jane W. Ball and Ruth C. BindlerChild Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc.Upper Saddle River, New Jersey 07458All rights reserved.

26. Cardiomegaly • occurs at the heart attempts to maintain CO • if CHF is not adequately treated, precursors of Cardiogenic Shock arise: cyanosis, weak peripheral pulses, cool extremities, hypotension, heart murmurs • clarification: not all heart murmurs are heralding cardiogenic shock.

27. Clinical diagnosis • based upon clinical assessment: tachycardia, respiratory distress, crackles. • cxray could show cardiac enlargement, venous congestion, PE, atelectasis. • cardiac echo: defects or dysfunction • EKG: tachycardia, bradycardia, ventricular hypertrophy

28. Goals of Management • make the heart work efficiently • remove excess fluid • improve systemic circulation without overloading the pulmonary circulation

29. Medication therapy • positive inotropic effect and afterload -reducing agents • Digitalis • Digoxin • ACE inhibitors (Angiotensin-converting enzyme inhibitors) • Lisinopril • Beta Blockers • Indural (Propranolol) • Diuretics: Lasix, HCThiazide, aldactone.

30. Supportive treatment • oxygen • fluids, as indicated( in CHF, fluids may be restricted). • increased calories or concentrated formula(prescribed) • air way support/management • rest and spacing of activity/rest periods

31. Surgical treatment • cardiac catheterization, which may include procedural treatment in the cath lab • valve replacement • conduit placement • cardiac transplant

32. FIGURE 26–6 Interventional catheterization, balloon valvuloplasty to open the pulmonary valve. Jane W. Ball and Ruth C. BindlerChild Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc.Upper Saddle River, New Jersey 07458All rights reserved.

33. Developmental Assessment • the child may be unable to reach developmental milestones until CHF is adequately controlled • Taylor activity to child’s ability. • Energy must be adequate for motor milestones to improve. • Dev. Assessment: DDST II: followed Q 2-3mos in infancy/toddler. • limit contact with other children: risk of inf.

34. Congenital Heart Disease(CHD) • refers to a defect in the heart, great vessels or persistence of a fetal structure • occurs in 1% live births • higher incidence in still births and aborted fetuses • incidence has declined over past 25 yrs d/t techno advances in intrauterine assessment, surgical techniques and intensive care

35. Factors that increase risk for having a child with CHD • family hx of CHD • maternal age >35yr • coexisting maternal disease: DM, collagen vascular disease, PKU • exposure to teratogens or rubella infection

36. CHD • most CHD develop during first 8 wks of gestation • usually result of combined genetic and environmental interaction • fetal exposure to drugs:phenytoin & lithium • maternal viral infections:rubella • maternal metabolic disorders: DM, PKU • maternal complic of preg ie incr age, antepartal bleeding

37. CHD etiologies cont. • genetic factors: familial patterns • chromosomal abnormalities: most common is Down’s syndrome with 40% occurrence rate of CHD. • defects are divided into cyanotic and acyanotic (in pure form).

38. Acyanotic Heart Defects • constitutes the majority of heart defects in children • two types: obstructive and non-obstructive • obstructive: PS, AoS, Coarc. • non-obstructive:PDA, ASD, AV canal (endocardial cushing defect), VSD.

39. Cyanotic Heart Defects • generally caused by a valvular or vascular formation • ex: Tetralogy of Fallot, Transposition, hypoplastic LV, tricuspid atresia, pulmonary atresia, truncus arteriosus, and total anomalous venous return.

40. Acyanotic; non-obstructive lesions • PDA • ASD • AV canal • VSD

41. Pathophysiology of Acyanotic, non-obstructive CHD • openings in the septal wall cause a L to R shunt • oxygenated blood mixes with deoxygenated blood • volume overload to the pulmonary system • can cause CHF • PHT occurs d/t chronic volume overload to the lungs if uncorrected.

42. Patent Ductus Arteriosus • common; 9-12% of all CHD • persistant fetal structure • when the PDA remains open, blood is shunted from the Aorta to the Pulmonary artery, therefore increasing blood flow to the lungs: L to R. • bounding pulses, dyspnea, tachypnea, FTT. • at risk for freq URI and endocarditis, CHF. • continuous systolic murmur and thrill palp.

43. Treatment of a PDA • surgical ligation; transcatheter closure >18mos of age. • Indomethacin may stimulate closure in premies • Prostaglandin helps to keep the PDA open until surgical correction is optimal. • left untreated, LVH, pulmonary hypertension (PHT) and vascular obstructive disease develop.

44. Atrial Septal Defect; ASD • opening in the atrial shunting • L to R shunting • accounts for 6-10% of CHD • small to moderate size may go undiagnosed until preschool years or later • sx of large ASD: CHF, tiring easily, poor growth • soft systolic murmur heard in pulmonic space; wide S2 split.

45. Treatment of ASD • Echo shows RV overload and shunt size • cxray and EKG may be normal unless a large shunt • surgery to close or a patch via catheter during Cardiac Cath. • atrial arrhythmias can be a late sx or associated with a large ASD involving conduction system in the septum

46. FIGURE 26–7A, Septal occluder used to close an atrial septal defect (ASD) and less commonly to close a ventricular septal defect (VSD). B, Coil used to close a patent ductus arteriosus (PDA). The coil of wire covered with tiny fibers occludes the ductus arteriosis when a thrombus forms in the mass of fabric and wire. Jane W. Ball and Ruth C. BindlerChild Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc.Upper Saddle River, New Jersey 07458All rights reserved.

47. FIGURE 26–8 A child with atrial septal defect repair. Surgery is performed with this type of defect to prevent pulmonary vascular obstructive disease as an adult. Jane W. Ball and Ruth C. BindlerChild Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc.Upper Saddle River, New Jersey 07458All rights reserved.

48. Atrioventricular Canal: Endocardial Cushing Defect • accounts for 4-5% of CHD • partial or complete ASD/VSD with some degree of involvement of mitral/tricuspid valves variable • associated with Down’s syndrome • severity of sx depends on degree of mitral regurgitation. • sx in infants: CHF, tachypnea, tachycardia, FTT, incr URI, systolic murmur (LLSB)

49. Treatment of AV Canal • surgery during infancy to prevent PHT • patches placed over septal defects; mitral valve replacement • arrhythmias and mitral valve insufficiency occur post/op • no difference between short term survival rates in infants with or without Down’s syndrome.

50. Ventricular Septal Defect; VSD • opening in the ventricular septum • shunts L to R; increases pulmonary bld flow • most common: accounts for 20% CHD • only 15% large enough to generate symptoms: tachypnea, dyspnea,, FTT, reduced fluid intake, CHF, PHT. • systolic murmur ; LLSB • most small VSD close spontaneously