1. Cardiovascular Stressors and Adaptation

2. Common Cardiovascular Disorders in Children
Congenital Heart Defects
Congestive Heart Failure
Acquired Heart Disease

3. Review of Normal Circulation

4. How to Understand Congenital Defects
Think of blood as:
Red highly O2 saturated
Blue unsaturated
Purple medium O2 saturated (mixed)
Lavender- reduced volume of medium O2 saturated (mixed)
Pink Low O2 saturated
Light Blue Reduced volume of unsaturated

5. Fetal Circulation

6. Fetal Shunts
ductus venosus: accessory (extra) vein, carries oxygenated blood from umbilical vein into lower venous system
foramen ovale: shunts mixed blood from right atrium to left atrium (hole in the atrial septum)
ductus arteriosus: accessory (extra) artery, shunts mixed blood away from lungs to descending aorta

7. How does the fetus receive sufficient oxygen from the maternal blood supply?
Fetal hemoglobin carries 20-30% more oxygen than maternal hemoglobin
Fetal hemoglobin concentration is 50% greater than mother’s
Fetal heart rate bpm (increases cardiac output)

8. What happens to the shunts after birth?

9. Transition from intrauterine to extrauterine life
Cord is clamped, neonate initiated respirations
O2 levels rise = greater pressure in the left atrium, decreased pressure in the right atrium leading to an immediate closure of the foramen ovale

10. Transition from intrauterine to extrauterine life
After O2 circulates systemically, over 24 hours, the pressure in the left ventricle will become greater than the pulmonary artery and closes the ductus arterosis
The absent flow of blood through the umbilicus gradually closes the ductus venosus over 12 hr to 2 weeks

11. Cardiac Defects Either:
Ductal closure failure (no structural abnormality)
Structural abnormality

12. Diagnosis Assessment findings Results of diagnostic testing
Cardiac Catherization

13. Cardiac Catheterization
Primary method to measure extent of cardiac disease in children
Shows type and severity of the CHD
Insert tiny catheter through an artery in arm, leg or neck into the heart
Take blood samples and measure pressure, measure o2 saturation, and as an intervention
Sedation or anesthesia
Outpatient vs Hospital

14. Cardiac Catheterization-Post Op
Monitor closely (cardiac monitor, continuous pulse ox) VS q 15
Assess dressing at insertion site for infection, hematoma
Dressing must remain dry for 1st hrs
No blood drawn from extremity used
Palpate a pulse distal to the dressing to assure blood flow to extremity is not obstructed: keep extremity straight for 48 hrs after procedure

15. If Congenital Defect is suspected or confirmed,
Intervention is Important to Prevent CHF

16. Congestive Heart Failure
Heart doesn’t pump blood well enough –can not provide adequate cardiac output due to impaired myocardial contractility
Causes in children:
Defects
Acquired heart disease
Infections

17. Congestive Heart Failure
Most common cause in children is congenital heart defects
Increased volume load or increased pressure in heart
Excess volume and pressure builds up in lungs leading to labored breathing
Builds up in rest of body leading to edema

18. Congestive Heart Failure Symptoms
1st sign: tachycardia
tire easily
rapid, labored breathing
decreased urine output
fluid and sodium are retained
increased sweating, pallor
peripheral edema

19. CHF Diagnosis and Treatment
CXR- shows enlargement
Echocardiogram- dilated heart vessels, hypertrophy, increase in heart size
Tx-aimed at reducing volume overload, improve contractility
May require surgery

20. Congestive Heart Failure Medical Management
Digoxin- Helps strengthen the heart muscle, enables it to pump more efficiently
1st line tx
Dosing depends on wt and age
Digoxin toxicity: vomiting, bradycardia
Need HR, EKG, drug levels
check apical pulse first, don’t give if HR < 100 bmp in infants and < 70 bpm in children
Parent teaching

21. Congestive Heart Failure Medical Management
Diuretics- Helps the kidneys remove excess fluid from the body
Potassium sparing
Potassium wasting
Potassium supplements- given along with wasting diuretics
Lasix-1st agent for children-lose K esp. when taken with digoxin

22. Congenital Heart Disease
35 different types
Common to have multiple defects
Range from mild to life threatening and fatal
Genetic and environmental causes

23. Blood Flows From High to Low Pressure
Higher pressure
Lower Pressure

24. Types of CHD Acynotic defects- purple blood (too much to lungs)
Septal defects
VSD
ASD
PDA
Obstructive Cyanotic defects-reduced flow (lungs/body)
Pulmonic Stenosis light blue blood (lungs)
Coarctation of the aorta pink blood (body)
Cyanotic defects- from poor perfusion (lungs and body)
Tetrology of Fallot light blue & purple blood
Hypoplastic left heart lavender blood
Transposition of the greater vessels

25. Septal Defects- increased pulmonary blood flow
Left to right shunting (acyanotic defect)
Sends already sat blood back to lungs
Increased cardiac workload
Excessive pulmonary blood flow
Right ventricular strain, dilation, hypertrophy

26. Ventricular Septal Defect
Most common CHD
High Pressure in LV forces blood back to RV
Results in increased pulmonary blood flow (heart must pump extra blood), higher than normal artery pressure

27. Ventricular Septal Defect
S/S: vary with the size of the defect
4-8 weeks of age develop loud, harsh systolic heart murmur
Right ventricular hypertrophy
20-60% close spontaneously
cardiac cath shows: O2 level of RV higher than normal
large defects: develop CHF, poor feeding, failure to thrive

28. Ventricular Septal Defect
Treatment:
Small defects: followed by cardiologist, prophylactic ABX
Large defect: open heart surgery with cardiopulmonary bypass, will suture or patch hole closed
If child is not stable for open heart surgery: pulmonary artery banding: narrowing of pulmonary artery to reduce blood flow to lungs

29. VSD Medical Management
For infants not medically stable for surgery or awaiting surgery-
Digoxin: to improve cardiac output;
Oxygen

30. Atrial Septal Defect
Pressure in LA is greater than RA (blood flows left to right)
Oxygen rich blood leaks back to RA to RV and is then pumped back to lungs, results in ventricular hypertrophy
Few symptoms at birth, over time may experience fatigue and dyspnea on exertion

31. Atrial Septal Defect Clinical Presentation
Large defect may cause CHF
Harsh systolic murmur
Second heart sound is split: “fixed splitting” ** diagnostic of ASD
pulmonary valve closes later than aortic valve- risk for pulm edema
Echocardiogram: shows enlarged right side of heart, increased pulmonary circulation

32. ASD Management Nonsurgical management: prosthetic patch
Surgical management: open-heart with CP bypass, edges are sutured or will use patch to cover hole
Diuretics to control symptoms until repair is performed

33. Patent Ductus Arteriosus
Failure of ductus arteriosus to close completely at birth
Blood from the aorta flows into the pulmonary arteries to be reoxygenated in the lungs, returns to LA and LV
More common in preemies
H to L

34. Patent Ductus Arteriosus
Preterm infants: present with CHF and respiratory distress
Fullterm infants: may be asymptomatic with a continuous “machinery” type murmur
Tire easily, growth retardation (shorter, weigh less, less muscle mass), prone to frequent respiratory tract infections

35. Patent Ductus Arteriosus
Chest radiographs (x-ray) show enlarged LA and LV
Medical management: Indomethacin (prostaglandin inhibitor that stimulates ductus to constrict)
Surgical management: ductus is divided and ligated (usually performed in first year of life to decrease risk of bacterial endocarditis

36. Acyanotic Defects
VSD & ASD
Rt CHF
Pulm edema
Pulm htn
PDA

37. Obstructive Defects- decreased pulmonary blood flow
Right to left shunt
unsat blood into sat blood
Pulmonic Stenosis
Coarctation of the Aorta

38. Pulmonary Stenosis Obstruction of the right ventricular outflow tract
Decreased pulmonary blood flow

39. Pulmonary Stenosis Symptoms
Right ventricular hypertrophy
High ventricular pressure may cause blood to back up into right atrium and force foramen ovale to open to allow blood to flow from right to left atrium
Mild-Mod: Usually asymptomatic except for
Systolic ejection murmur with a palpable thrill
If Severe: right ventricular failure, CHF, if there is right to left shunting through the foramen ovale, mild to moderate cyanosis

40. Pulmonary Stenosis Medical Management:
If asymptomatic: cardiac follow-up
Prophylactic ABX
Surgical Management:
Pulmonary balloon valvuloplasty via cardiac cath
if unsuccessful: valvotomy

41. Coarctation of Aorta
Localized constriction of the aorta at or near the insertion site of the ductus arteriosus
Reduces cardiac output (impedes blood flow from heart to body=pink blood)
Aortic pressure is high proximal to the constriction and low distal to the constriction-CVA
Higher pressure
Pink Blood

42. Coarctation of Aorta
S/S: related to severity of the constriction and presence of associated cardiac defects
Mild: asymptomatic, sys. murmur, diminished pulses in lower ext
Severe: poor lower body perfusion, metabolic acidosis, CHF, systemic hypertension
In both: BP is 20mmHg higher in arms than in lower extremities

43. Coarctation of Aorta Diagnosis-clinical exam, echo
Treatment is based on severity

44. Treatment of Coarctation of Aorta
Symptomatic newborn treated with:
Digoxin
diuretics to manage CHF
may also receive PGE1 (prostaglandin) infusions to maintain ductal patency and improves perfusion to lower extremities- although will cause inc pulm flow
surgical repair within first 2 years

45. Cynaotic Defects
Decreased pulmonary blood flow (light blue blood to lungs)
Transposition of the greater vessels
Tetrology of Fallot
Hypoplastic left heart

46. Tetralogy of Fallot Consists of 4 Parts:
VSD
RV hypertrophy
Overriding aorta
Pulmonic Stenosis: impedes blood flow to the lungs, forces unoxygenated blood through the VSD & into aorta
Blood is purple
Blood is light blue

47. S/STetralogy of Fallot
The degree of pulmonic stenosis governs the onset and severity of symptoms.
Mild: little to no right to left shunting infant has “tet spells” hypercyanotic episodes
Mod-severe: some cyanotic at birth when PDA closes, other infants become increasingly cyanotic over the first few months of life

48. Tetralogy of Fallot
Tire easily especially with exertion, difficulty feeding and gaining weight,
Other signs: chronic hypoxemia

49. Management Tetralogy of Fallot
Over time may have hypercyanotic episodes (tet spells)
often preceded by crying, feeding or stooling, worsening cyanosis, increased respiratory rate, may lose consciousness
Treatment of tet spells:
knee-chest position then apply O2
Do not leave alone- cyanosis can cause LOC, death

50. Tetralogy of Fallot Medical management:
Symptomatic newborn: PGE1 infusion to maintain ductal patency
Older infants: close monitoring for worsening of hypoxia
Surgical management: done at 3-12 months of age, in stages
primary open-heart repair: close VSD, open pulmonary valve, remove obstructing muscle

51. Hypoplastic Left Heart Syndrome
pulmonary venous blood is shunted through foramen ovale into right atrium
mixed blood travels through the right ventricle to the pulmonary artery, patent ductus arteriosus
as ductus begins to close in first day of life infant becomes symptomatic
Palest pink L
Purple H

52. Hypoplastic Left Heart Syndrome
symptoms:
CHF
hypoperfusion, shock
grayish-blue color
dyspnea
hypotension
Diagnosis
Clinical presentation and echo (increased size in right side)

53. Hypoplastic Left Heart Syndrome
Medical Management:
PGE1 to keep ductus arteriosus open
Correct acid-base and electrolyte imbalances
Surgical management:
Heart transplant
Three-stage repair

54. Transposition of Great Arteries
Aorta is connected to RV (unoxygenated blood goes to body)
Pulmonary artery is attached to LV (oxygen rich blood is recirculated to lungs)
Survival depends on mixing these two circulations through the fetal structures (foramen ovale and ductus arteriosus)

55. Transposition of Great Arteries
Cyanosis apparent at birth or shortly after, no response to oxygen
Prompt diagnosis and treatment needed for survival
Arterial switch procedure: redirects blood flow, may be done in stages within 1st year

56. Caring for the Child with a Congenital Heart Defect
Nursing Care: taking infant home before corrective surgery
Provide parents with information about care
Review steps for follow-up care, emergency management (s/s respiratory distress, CPR)
Key: promote normalcy within the limits of the child’s condition

57. Caring for the Child with a Congenital Heart Defect
Preoperative:undergoing corrective surgery
Explain procedures to parents and child, assure understanding
Encourage child and parents to express fears
Prepare child for surgery and post-op, show models of equipment (chest tube)

58. Caring for the Child with a Congenital Heart Defect
Postoperative:
Monitor cardiac output
Support respiratory function
Maintain fluid and electrolyte balance
Promote comfort (IV morphine, sedatives)
Promote healing and recovery

59. Acquired Heart Diseae HTN Endocarditis Rheumatic Fever
Kawasaki Disease

60. Hypertension Primary HTN Secondary HTN Caused by increased body mass
Genetics
Secondary HTN
Cause is from an underlying condition such as kidney disease or heart defects

61. Hypertension No set systolic and diastolic number for diagnosis
Need to compare to child’s age, gender and height
If 3 different readings are above the 95th percentile for that child then diagnosis is confirmed

62. Hypertension Managed by eliminating the primary cause if possible
Exercise, life style modification
ACE inhibitors
ARBs
Beta-Blockers
Ca Channel Blockers

63. Infective Endocarditis
Inflammation of the lining of the valves and arteries
Caused by bacterial and fungal infections in the blood stream that infects an already existing injured endocardium
Children at risk: cardiac defects, severe valve disorders

64. Infective Endocarditis
Symptoms:
Fever, fatigue, headache, N/V, new or changed murmur, CHF, dyspnea
Treatment:
Antibiotics IV for 2-8 weeks, surgery to replace valves, treatment of CHF

65. Rheumatic Fever
Acute RF is leading cause of acquired heart disease (but has decreased in US b/c abx)
Inflammatory autoimmune condition
Seen in children age 5-15
Usually follows untreated strep A infection (pharyngitis)
Causes scarring of the mitral valves

66. Rheumatic Fever S/S: Tachycardia Polyarthritis Carditis Chorea
Erythema marginatum (nonpuritic)
Subcutaneous nodules

67. Rheumatic Fever
Diagnosis- clinical symptoms and +ASO titer

68. Rheumatic Fever Management: Treat infection Treat other symptoms
Streptococcal prophylaxis
PCN IM every month or
PCN PO BID (if allergic Sulfadiazine PO QD)

69. Kawasaki Disease Acquired heart disease in children under age 5
Boys>girls
Asian decent
Multisystem vasculitis (inflammation of blood vessels)
3 stages of illness
Affects the coronary arteries
Occurs due to antibody vascular injury post infection

70. Kawasaki Disease first stage day 1-14
Prolonged fever
Bilateral, nonpurulent conjunctivitis
Changes in mouth (erythema, fissures, crusting of lips, strawberry tongue)
Induration of hands and feet
Erythema of palms and soles
Erythemous rash
Enlarged cervical lymph nodes

71. Kawasaki Disease second stage day 15-25
Fever and most of the previous symptoms resolve
Extreme irritability develops
Anorexia
Lip cracking and fissuring
Desquamation of fingers and toes
Arthritis
Vascular changes in myocardium and coronary arteries

72. Kawasaki Disease Third phase- day 26-40
Lasts until erythrocyte sed rate returns to normal and all symptoms disappear

73. Management Prevent or reduce coronary artery damage
Gamma-globulin IV followed by
High dose aspirin therapy at same time (80-100mg/kg/day once daily), continued through weeks 6-8 of disease

74. Kawasaki Disease Nursing care: Administer meds Comfort measures
Hydration
Parental support

75. Practice Questions!

76. The indicated area on the diagram showed higher than anticipated oxygen level on cardiac catherization. The nurse concludes that is diagnostic for which CHD? (Select All that Apply)
1. PDA
2. VSA
3. Coartation of Aorta
4 ASD
5. Tetrology of Fallot

77. A parent of a toddler with Kawaski’s disease tells the nurse “I just don’t know what to do with my child. He’s never acted like this before.” The nurses best reply is:
Don’t worry. This type of behavior is typical for a toddler
Irritability is part of Kawasaki’s disease. Please don’t be embarrassed
Perhaps your child would benefit from stricter limits
You seem to be in need of a referral to our Child Guidance Center

78. When assessing a child for signs and symptoms of rheumatic fever, which symptoms should the nurse anticipate?
Tachycardia and joint pain
Bradycardia and swollen joints
Loss of coordination and pruritic rash
Poor weigh gain and fever

79. The nurse assessing a newborn and auscultates a split S2
The nurse assessing a newborn and auscultates a split S2. The nurse should further assess for:
Cyanosis
Crackles
Hypoxemia
Blood pressure differences in extremities

80. Which nursing intervention is most effective in preventing rheumatic fever in children?
Refer children with sore throats for a throat culture
Include an ECG in the child’s yearly physical examination
Assess the child for a change in the quality of the pulse
Assess the child’s blood pressure

81. A newborn with patent ductus arteriousus is scheduled to receive indomethacin. The nurse administers this medication to:
Open the ductus arteriosus
Close the ductus arteriosus
Enlarge the ductus arteriosus
Maintain the size of the ductus arteriosus

82. Which congenital heart defect necessitates that the nurse take upper and lower extremity blood pressure readings?
Coarctation of the aorta
Tetralogy of Fallot
Ventricular septal defect
Patent ductus arteriosus

83. An infant with ventricular septal defect develops congestive heart failure and is placed on digoxin therapy twice a day. The infant vomits the morning dose of digoxin. The most appropriate nursing intervention is to:
Notify the pediatrician as soon as possible
Take the infant’s pulse for 1 minute and repeat the dose of digoxin
Skip the dose and give twice the amount at the next dose
Repeat the dose and chart that the infant vomited the first dose

84. The parents of a newborn with small ventricular septal defect ask why their baby is being sent home instead of undergoing immediate open heart surgery. The nurse’s best response is:
Your baby’s condition is too serious for immediate open heart surgery
Ventricular septal defects are not repaired until the infant is older
Your baby has a small defect, and it is likely to close spontaneously
Your baby must be fully immunized before surgery

85. An infant with tetralogy of Fallot becomes hypoxic following a prolonged bout of crying. The nurse’s first action should be to:
Administer oxygen
Administer morphine
Place the infant in the knee-chest position
Comfort the infant