1. NURSING CARE OF THE CHILD WITH A CARDIOVASCULAR DISEASE

2. ASSESSMENT OF HEART DISORDERS IN CHILDREN History Physical assessment –general appearance –pulse, blood pressure, & respirations

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. Bindler Child Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved.

5. FIGURE 26–2 A, 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. Bindler Child Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All 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. Bindler Child Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All 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. ASSESSMENT OF HEART DISORDERS IN CHILDREN Diagnostic tests –Electrocardiogram –Radiography –Echocardiography –Phonocardiography & magnetic resonance imaging –Exercise testing –Laboratory tests

14. CONGENITAL HEART DISEASE Defects with increased pulmonary blood flow –Ventricular Septal Defect Opening between ventricles S/S –4-8 weeks, fatigue and harsh murmur Therapeutic management –Most close spontaneously, those that don’t require open heart surgery

15. 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

16. Treatment of VSD if no sx CHF or PHT, treatment is conservative surgical patching during infancy if FTT closure by transcatheter device during CC for some defects: Rashkind procedure. prophylaxis for infective endocarditis is required high risk for surgical repair in first few months of life

17. Defects with increased pulmonary blood flow –Atrial Septal Defect Opening between the atria S/S –Murmur, second heart sound splitting Management –Surgery

18. 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

19. FIGURE 26–7 A, 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. Bindler Child Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved.

20. 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. Bindler Child Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved.

21. –Patent Ductus Arteriosus Fetal structure that should begin closing with the first breath and should complete by 3 months S/S –Wide pulse pressure and continuous murmur Management –Administration of indomethacin –Cardiac Catheterization –Surgery

22. 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

23. NURSING CARE OF THE CHILD WITH A HEART DISORDER Obstructive defects –Pulmonic Stenosis Narrowing of the pulmonary valve or artery causing the right ventricle to hypertrophy S/S –Mild right sided heart failure –Cyanosis –SEM Therapeutic Management –Balloon angioplasty to relieve the stenosis

24. - Aortic Stenosis Stenosis of the aortic valve prevents blood from passing from the left ventricle into the aorta, leading to hypertrophy of the left ventricle S/S –Usually asymptomatic but with murmur –May have chest pain and even sudden death Therapeutic Management –Stabilization with a Beta Blocker or Calcium Channel Blocker –Balloon valvuloplasty –Valve replacement

25. –Coarctation of the Aorta Narrowing of the lumen of the aorta S/S –Absence of palpable femoral &/or brachial pulses; headache, vertigo, nosebleeds, CVA; leg pain Therapeutic Management –Surgery or angiography

26. Defects with decreased pulmonary blood flow –Tricuspid Atresia The tricuspid valve is closed, blood flows through the patent foramen ovale into the left atrium, bypassing the lungs. Then it is shunted back through a PDA into the lungs. When these structures close, cyanosis, tachycardia, and dyspnea occur. Surgery must correct. Treatment: IV infusion of PGE until surgery

27. Clinical Manifestations of Cyanotic Heart Disease chronic hypoxemia causes fatigue, clubbing, exertional dyspnea, delayed milestones, tire easily with feeding, reduced growth, CHF hypercyanotic (hypoxic) spells: incr rate and depth of respir, incr cyanosis, incr HR, pallor and poor perfusion, agitation and irritability.

28. FIGURE 26–13 Clubbing of the fingers is one manifestation of a cyanotic defect in an older child. What neurologic signs may be associated with such a defect? Jane W. Ball and Ruth C. Bindler Child Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved.

29. Cyanotic Spell most signif prob to develop in infants and toddlers with cyanotic heart disease brought on by crying, feeding, exercise, warm bath, or straining to defecate during a hypoxic spell, child will often squat knee to chest to decrease venous return (by incr systemic vascular resistance) from LE which decr CO and relieves the cyanotic spell.

30. Defects with decreased pulmonary blood flow –Tetralogy of Fallot Four anomalies –Pulmonary stenosis –VSD –Dextroposition of the aorta –Hypertrophy of right ventricle S/S –Cyanosis –Polycythemia (increase in number of RBC) –Dyspnea, growth restriction, clubbing of fingers Therapeutic Management –Surgery

31. Tetralogy of Fallot combination of four defects –pulmonary stenosis: degree determines severity –VSD –over-riding of the aorta –RVH accounts for 10% of CHD elevated R sided pressures: R to L shunt xray: boot shaped heart d/t RVH risk for metabolic acidosis and syncope.

32. Treatment of TOF total repair is done by 6 mo if cyanotic spells surgery is not necessarily currative, but most have improved quality of life and improved longevity residual problems: arrhythmias and RV dysfunction lifelong SBE required

33. FIGURE 26–9 This infant has a congenital heart defect with decreased blood flow. What is the prognosis for an infant who has either of the most common malformations—tetralogy of Fallot or transposition of the great vessels? Jane W. Ball and Ruth C. Bindler Child Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved.

34. FIGURE 26–10 A child with a cyanotic heart defect squats (assumes a knee–chest position) to relieve cyanotic spells. Jane W. Ball and Ruth C. Bindler Child Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved.

35. FIGURE 26–12 Place the infant who has a hypercyanotic spell in the knee–chest position. This position increases systemic vascular resistance in the lower extremities. Jane W. Ball and Ruth C. Bindler Child Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved.

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

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

38. ACQUIRED HEART DISEASE Congestive Heart Failure –S/S Tachycardia, tachypnea Right sided: increased venous pressure, hepatomegaly Left sided: dyspnea, crackles (rales), cyanosis, and, eventually, ride sided failure –Therapeutic management Reduce workload of the heart using diuretics, inotropics, and vasodilators

39. 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).

40. 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.

41. 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. Bindler Child Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved.

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

43. 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.

44. 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. Bindler Child Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved.

45. 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. Bindler Child Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved.

46. 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.

47. 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

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

49. 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.

50. 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

51. Rheumatic fever –S/S Systolic murmur Chorea (sudden involuntary movement of the limbs) Macular rash on the trunk Swollen and tender joints, SQ nodules on tendon sheaths Positive ASO titer and increased ESR and C-reactive protein –Therapeutic management Bedrest Antibiotics to eliminate Group A Beta hemolytic Strept Prognosis depends on how much heart involvement

52. Rheumatic Fever inflammatory connective tissue disorder that follows initial infection by group A beta-hemolytic streptococci may lead to permanent mitral or aortic valve damage sx: migratory polyarthritis, subcutaneous nodules, erythema marginatum, fevers, St. Vitus dance (chorea movements) dx: Jones criteria and an elevated ASO

53. Treatment for Rheumatic Fever antibiotics to treat the strept infection: pcn, erythromycin asa for joint pain and fever monitored by cardiac echo (serial) steroids for severe carditis with CHF SBE prophylaxis long term antibiotics until adulthood –daily oral or 1x/mo IM (Pen G)

54. Infective Endocarditis inflammation of the lining, valves, and arterial vessels of the heart caused by bacterial, enterococci and fungal infections significant M&M for children with CHD, prosthetic valves and shunts, and in immunocompromised children with long term central venous catheters.

55. SBE Prophylaxis Prophylaxis for infective bacterial endocarditis aka SBE prophylaxis ;systemic bacterial endocarditis prophylaxis see Table 14-4 p 489 in B&B commonly given before dental procedures to prevent oral bacteria from entering the blood stream and seeding in the area of defect, causing a bacterial endocarditis one large dose given 1 hr before a procedure requiring prophylaxis

56. Kawasaki disease –S/S (early) High fever that doesn’t respond to therapy Swollen hands and feet, enlarged joints Strawberry tongue, red lips, conjunctiva Enlarged cervical lymph nodes –S/S (late) Skin desquamation Platelet count increases aneurysms –Therapeutic management Administration of Ibuprofen for inflammation and platelet aggregation IV immunoglobulin to decrease immune response Most children recover fully but some will need heart surgery to repair damage

57. Kawasaki Syndrome acute systemic inflammatory disease aka mucocutaneous lymph node syndrome most common cause of acquired heart disease etiology unknown 3 stages: –acute, subacute and convalescent dx based upon clinical signs

58. Diagnostic Criteria for Kawasaki Syndrome fever > 102.2 x 5 days plus 4 of the following: bilateral conjunctivitis strawberry tongue; cracks/fissures of lips palmar/plantar erythema, induration,then desquamation maculopapular rash on trunk acute cervical lymphadenitis

59. FIGURE 26–14 This child shows many of the signs of the acute stage of Kawasaki syndrome. Jane W. Ball and Ruth C. Bindler Child Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved.

60. Treatment of Kawasaki Syndrome high dose ASA and IgG given early significantly decreases the risk of cardiac involvement greatest risks are coronary artery lesions and cardiac aneurysms monitor for cardiac involvement for months: aneurysms, early atherosclerosis, arrhythmias, CHF, coronary stenosis, MI and potential death.

61. FIGURE 26–15 This child has returned for one of her frequent follow-up visits to assess her cardiac status after treatment for Kawasaki syndrome. Notice the lips that show the inflammation and cracking. Jane W. Ball and Ruth C. Bindler Child Health Nursing: Partnering with Children & Families © 2006 by Pearson Education, Inc. Upper Saddle River, New Jersey 07458 All rights reserved.

62. Dyslipidemia fam hx incr risk of CAD d/t high levels of LDL and cholesterol total lipid panel, nutritional history and life style needs to be considered. children need fats to grow, metabolize vitamins and produce hormones high fat/sat fat diet is not recommended. long term studies of effect of childhood lipid levels on life span inconclusive

63. Hypertension 1-3% of the pedi population unknown cause = essential or primary HTN underlying kidney or cardiac disease=secondary HTN children’s BP in >90th at incr risk for adult HTN HTN in adol correlates with obesity and elevated serum lipid level

64. Shock in Children n A clinical syndrome characterized by prostration and insufficient perfusion to meet the metabolic demands of tissues n Hypotension is not part of the definition in children

65. Shock vs. Hypotension n Shock –State of insufficient perfusion to meet the metabolic demands of tissues n Hypotension –Physical sign characterized by a fall in systolic blood pressure (BP below normal values) –Hypotension is a late sign of shock in children and it’s presence in children implies profound cardiovascular compromise

66. Pathophysiology n Hypovolemic shock –Hemorrhage –Dehydration n Distributive shock –Neurogenic / Spinal –SIRS / Sepsis –Anaphylaxis n Cardiogenic –Pump failure –Obstructive

70. Help! n Excuse me, I believe that my child is in a state of inadequate tissue perfusion!

71. Recognition of shock n Early recognition is key –The longer you wait, the higher the mortality!!!! n Key parameters to assess: –L.O.C. –Respiratory rate –Heart rate –Peripheral perfusion Skin color and temp. Capillary refill

72. Heart Rate n Tachycardia –Above higher normal limit (age x 5 minus 150) –4yr X 5 = 20 – 150 = 130 Too fast –Infant > 220 –Child > 180 Too slow –< 60 –Sustained –Decompensated shock Slowing or Bradycardia

73. Level of Consciousness (L.O.C.) (Key) n Changes in L.O.C. occur early –Irritable –Does not interact with parents –Stares vacantly into space –Poor response to pain –Asleep/sleeping a lot Difficult to arouse –Unresponsive

74. Peripheral Perfusion (Key) n Decreased or bounding pulses n Volume discrepancy –Central vs peripheral pulses Poor or brisk capillary refill Cool or mottled or red and warm extremities Decreased urine output

75. Respiratory Rate n Compensated shock –Tachypnea Elevated for age “Quiet respirations” –Think of DKA or Hypovolemia Retractions –Sepsis Decompensated shock –Bradypnea or apnea

76. Compensated (Early) Shock n Vital organ function is maintained by intrinsic compensatory mechanisms; blood flow is usually normal or increased but generally uneven or maldistributed in the microcirculation.

77. Compensated (Early) Shock n Normal level of consciousness –Agitated n Quiet tachypnea n Tachycardia –Sustained –Difference between central and peripheral pulses n Normal or delayed capillary refill n Normal or elevated B/P

78. Decompensated Shock (with hypotension) n Efficiency of the CVS gradually diminishes, until perfusion in the microcirculation becomes marginal despite compensatory adjustments.

79. Decompensated Shock (with hypotension) n Altered level of consciousness –Painful stimulation or unresponsive n Delayed capillary refill –> 5 seconds n Hypotension n Weak central pulses, absent peripheral pulses n Bradycardia

80. Hypotension n Blood Pressure –Lowest acceptable systolic blood pressure Birth – 1 month: 60 mmhg 1 month – 1 year: 70 mmhg 1 year – 10 year: 70 + (2 X age in years) >10 years : 90 mmhg n Normal systolic –80 + (2 x age in years) –or fiftieth percentile

81. Irreversible (terminal) shock n Damage to vital organs such as the heart or brain of such magnitude that the entire organism will be disrupted regardless of therapeutic intervention. Death occurs even if CV measurements return to normal levels with therapy.

82. Hypovolemic shock n Hypovolemia is the usual cause of shock in the out of hospital setting –Most common cause is blood loss secondary to blunt force trauma –Vomiting and diarrhea is a second leading cause

83. Septic Shock n Most common form of distributive shock n Infectious organism or their byproducts (endotoxins) n Triggers an immune response –Vasodilation –Increase capillary permeability –Maldistribution of blood n Early stage –High cardiac output, low vascular resistance Tachycardia –Bounding pulses Flash capillary refill Flush, warm skin n Later stage –Just like hypovolemic shock

84. Neurogenic n Usually the result of either head or high spinal cord injury (T6) –Disrupts sympathetic nervous system innervention with blood vessels and heart –Uncontrolled vasodilation n Signs and symptoms –Hypotension with wide pulse pressure –Normal heart rate or bradycardia –Increased respiratory rate –Diaphragmatic breathing

85. Cardiogenic Shock n Usually a problem with stroke volume –Rate is either: Too fast –Inadequate time for ventricle filling –SVT, Atrial Fib Too slow –Bradycardia Or not at all –Asystole –PEA n Manifestations –Alteration in L.O.C. –Trouble breathing Crackles/rales –Trouble feeding or not feeding well –Large liver –S 3 gallop

86. Anaphylactic Acute multisystem allergic response n Can occur in seconds or minutes –Usually within 5 – 10 minutes of exposure n Venodilation n Systemic vasodilation n Pulmonary vasoconstriction Signs & symptoms n – Anxiety/agitation n – Nausea and vomiting n – Urticaria (hives) n – Angioedema n – Respiratory distress n – Hypotension n – Tachycardia

88. Nursing management n Dxs: –Ineffective breathing pattern R/T diminished oxygen needed for impaired tissue perfusion –Altered tissue perfusion R/T reduced blood flow, decreased blood volume, reduced vascular tone –Altered family process R/T a child in a life- threatening condition

89. Nursing management n Goals: n Inc O 2 to lungs –Adm O 2 as prescribed, position to maintain open airway, monitor artificial airway n Promote venous return and cardiac output –Position flat with legs elevated –Adm. IV fluids and plasma expander, vasopressor and cardiotonics –Maintain opt body tempr. Neck in neutral or “sniffing” position

90. The end. Q & A ?