1. Cardiac Conditions in Children
Nursing Assessment and
Interventions
Kathryn Kushto-Reese

2. Leading Causes of Infant
Deaths
2006

3. Anatomy/Physiology Overview
 Chambers
 Valves
– AV (tricuspid & mitral)
– Semilunar (pulmonic &
aortic)
 Flow
 Saturations

4. Normal Blood Flow
Dexoygenated blood returns from the body
through the SVC/IVC → RA → tricuspid
valve → RV → pulmonic valve → pulmonary
artery → then to the lungs where blood gets
oxygenated.
This blood then returns via pulmonary veins
→ LA → mitral valve → LV → aortic valve
→ and out the aorta to the body.

5. NORMAL HEART

6. Newborn Physiology
 Pulmonary vs. Systemic Pressures
 In Utero
 At Birth
 Fetal Shunts
– Ductus arteriosus (conduit from pulmonary
artery to aorta)
– Foramen ovale (flapped opening between right
and left atria)
– Ductus venosus (bypass liver)

7. Pulmonary and Systemic
Pressures
 In utero – ↑ pulmonary pressure
 before birth: due to lungs being a fluid filled
system, the lungs are a higher pressure
system than the systemic circulation
 After birth – ↑ systemic pressure
 now that the lungs are filled with air, the
lungs are a lower pressure system than the
systemic circulation
 The blood will follow the path of least
resistance

9. Assessment: Cardiac Function
 Inspect chest/Palpate
 Heart Sounds: murmurs
 Quality of Pulses/Central
 Respiratory: effort and quality of
respirations
 Pulses: Extremities (peripheral)
– Cyanosis (central also)
– Capillary refill time
– Temperature /color

10. ASSESSMENT

11. Assessment: Cardiac Function
(continued)
 Renal
– Urine output, edema, hepatomegaly
 Vital Signs
– Heart rate, quality and symmetry, BP
– Peripheral pulses, check for symmetry
 Neurological
 Restless, irritable, decreased response
to environment

12. ASSESSMENT

13. Congestive Heart Failure
 A condition in which the heart is unable to
provide adequate cardiac output to meet the
circulatory and metabolic requirements of
the body.
 Failure may initially be right- or left-sided but
if left untreated, the entire heart will fail

14. Congestive Heart Failure (CHF)
 Causes:
– Heart muscle dysfunction
– Structural abnormalities
– Pulmonary abnormalities
– Systemic disease
– Infections
– Syndromes

15. Examples
 Obstructive lesions in heart
 Dysrhythmias
 Increased blood flow to lungs (VSD)
 Myocarditis
 Chemotherapy drugs
 Sepsis
 Respiratory failure

16. CHF Symptoms
Systemic Venous Congestion (rt sided)
Hepatomegaly
Peripheral edema, ascites
Pulmonary Venous Congestion (left sided)
Tachypnea
Central cyanosis
Dyspnea, ↑ WOB, rales, wheezing, nasal
flaring , grunting, cough
Others: lethargy, irritability, altered LOC

17. CHF Symptoms
 Decreased Myocardial Function
 Cardiomegaly
 Tachycardia
 Extremities cool, ↓ capp refill, etc…
 Failure to thrive, difficulty feeding , poor
weight gain
 Peripheral cyanosis/mottling
 Diaphoresis

18. ASSESSMENT

19. CHF Management
 Increase oxygen supply
– Oxygen therapy, raise HOB
– Correct anemia
 Decrease oxygen demand
– Remove “work” (breathing, feeding, teach
parents feeding techniques ( NG/GT feeds)
– Rest, group cares, emotional support

20. CHF Management
 Decrease oxygen demand
– Treat fever
– Treat dysrhythmias (Digoxin, Adenosine, B-
blockers)

21. CHF Management
 Increase cardiac output
– Increasing stroke volume
 Digoxin - ( mcg/kg/24hr.)
 Increase in force of myocardial contraction and
decreases conduction through SA and AV nodes (+
inotropic / - chronotropic)
 Inotropic support
– Dopamine * Dobutamine
– Milrinone * Epinephrine

22. CHF Management
 Increase cardiac output by:
– Decreasing afterload
 ACE Inhibitors such as Captopril/Enalapril
– Blocks conversion of angiotensin I to angiotensin II
(vasoconstrictor)
 Vasodilators
– IV (Nitroglycerine, Nitroprusside, Milrinone)
– Inhaled -- ?? (there are 2)

23. CHF Management
 Control fluid status
– Diuretics ( Lasix, Spironolactone
– Limit PO intake (initially) fluid/sodium
restrictions, daily ( bid) weights and maintain
nutritional status
 Address underlying disorder

24. Nursing Diagnoses
 Decreased cardiac output
 Altered tissue perfusion,
cardiopulmonary
 Fatigue
 Fluid volume excess
 Activity intolerance
 Impaired physical mobility
 Sleep pattern disturbance
 Anxiety
 Altered growth and development

25. Congenital Heart Defects
ETIOLOGY
GENETIC FACTORS/ CHROMOSOMAL
ABNORMALITIES
TERATROGENS
MATERNAL INFECTIONS
ENVIRONMENTAL EXPOSURES
PREMATURITY
ADVANCED MATERNAL AGE
PREGANCY COMPLICATIONS

26. Congenital Heart Defects
Defects that increase pulmonary
blood flow
– Patent Ductus Arteriosus (PDA)
– Atrial Septal Defect (ASD)
– Ventricular Septal Defect (VSD)
– Atrioventricular Canal Defect (AVC)

27. Ventricular Septal Defect (VSD)
 Most Common
 Most small /close spontaneously
 Symptoms of congestive heart failure
may occur/ especially if significant size
 Child has failure to thrive/ fatigue,
respiratory s/s, pulmonary hypertension
 Murmur ( turbulent flow through
abnormal or obstructive openings

28. VSD

29. ?? Increased Pulmonary Blood Flow

30. VSD Repair

31. Post -op

32. Obstructive Defects
 Coarctation of the Aorta
 Aortic Stenosis

33. Coarctation of
Aorta

34. Chest x ray

35. Obstructive Defects
 Coarctation of Aorta , Incidence
 Pathophysiology: obstruction of
systemic blood flow at the narrowed or
strictured part.
– Symptoms: high blood pressure and bounding
pulses in arms
 weak or absent femoral pulses, cool lower
extremities ↓ blood pressure in lower extremities
 CHF in infants
– Surgical treatment: Timing

36. Congenital Heart Defects
(continued)
Defects That Decrease
Pulmonary Blood Flow
–Tetralogy of Fallot
–Pulmonary Stenosis
–Pulmonary Atresia

37. Tetralogy of Fallot has 4 defects
1.Right Ventricular Hypertrophy
2.Overriding Aorta
3.Ventricular Septal defect
4.Pulmonic Stenosis

40. Tetralogy of Fallot (TOF)
 Symptoms: cyanosis, systolic murmur,
 Metabolic acidosis , poor growth,
clubbing, severe hypoxia (“tet spells”)
 Surgical treatment: palliative shunts and
complete repair

41. Abby with TOF

42. Clubbing of fingers

43. Hyper cyanotic or Tet Spells
 Occur most frequently in 1st yr of life
 May be preceded by feeding, crying or
defecation, fever, dehydration. ↑stress
 Characterized by profound hypoxemia,
blue extremities, circumoral cyanosis,
increased hgb and hct counts.
 Require prompt assessment and
treatment to prevent brain damage or
death.

44. “TET SPELL “

45. Treatment: “Tet Spells”
 Place infant in knee-chest position
 Older child will instinctively squat
 Maintain a calm comforting
approach
 Administer 100% oxygen
 Administer Morphine
 Administer fluids
 Propanolol for frequent Tet spells

47. Modified Blalock-Taussig

48. Final Repair

49. Mixed Defects

50. HLHS ( Hypoplastic Left Heart
Syndrome
 Structures on left side of heart
underdeveloped
 Mitral and Aortic valves closed or small
 Left ventricle non functional
 4th most common Congenital heart
defect

51. HLHS
 Right side of heart is the working part
 Blood lungs → left Atrium through an
ASD to right side of heart.
 Right ventricle pumps blood to lungs and
also to systemic circulation through a PDA.
 Few days – weeks ductus closed death
results.

52. HLHS

53. Symptoms
 Bluish/ Cyanotic
 Rapid pulse, murmur and ↑RR
 Cold hands and feet
 Lethargic
 Decreased pulses in extremities, ↓ pulse ox
 Poor sucking and feeding
 Increased respiratory effort and WOB
 Organomegaly

54. Treatment /Prognsis
 Prostaglandins in newborn to keep PDA
open
 Multiple Stage surgical repair
 Blalock-Taussig shunt
 Glenn procedure
 Fontan Procedure ( final )
 Chronic Health problems , earliest survivors
in 30’s→ Heart Transplant

55. Diagnostic Tools
 Chest X-ray
 ECG
 Echocardiogram
– Transesophageal echocardiogram
 Cardiac Catheterization
– Done under conscious sedation
– Can be diagnostic or interventional
– Post procedural care

56. Treatments
 Surgical Intervention
 Surgical repair/corrective surgery
 Palliative surgery/ temporary
 Interventional Cardiac
Catheterization
1. Open narrowed passages
2. Closure of openings pp. 907 text ,
table 26-7.

57. Chest x ray

58. Echocardiogram of VSD

59. Purpose of a Cath
 Diagnostic  Interventional Cath
– Define anatomy – Close PDA, ASD/PFO, VSD
– Measure pressures – Close collateral vessels
– Measure O2 content – Balloon dilate narrowed
– Calculate shunts, resistance, vessels or valves
CO – Place stents in narrowed
– All of above is frequently vessels
done off and on oxygen,
then on NO

60. Angioplasty/ dilation of Coarctation of
Aorta during cardiac catheterization

62. PDA Closure

63. Cardiac Cath procedure
 Assess for :
 Circulation: cool extremities,
↓ pedal pulses, capp refill
> 3 sec., decreased
Sensation and mobility
 Complications: bleeding,
arrhythmias, hematoma,
thrombus, and infection.

64. Post Procedure
 VS are q 15” x 4; q 30” x 2; q 1h x 2 then
IMC routine
 Stay on boards/supine x 2 hours
 With each set of V/S and prn, monitor:
– Perfusion (arterial and venous) to distal
extremity (pulses, color, CRT, temp)
– Bleeding/hematoma formation at site
 If no bleeding at site and palpable distal
pulse, may come off boards/sit up after
designated time

65. Post Procedure Management
 Antibiotics (Ancef 25mg/kg) x 2 doses
 Aspirin (3-5mg/kg) to start same night for
device placement
 CXR next morning if ASD or PDA device
placed
 Echo next morning if ASD or PDA device
placed
 “Discomfort” Control - acetaminophen

66. Going Home
 May go home 4-5 hours after a diagnostic
cath
 Will stay overnight and get d/c’d in AM after
most interventions
 Will return to school 2-3 days after
procedure
 PE class/sports participation may be limited
based on intervention

67. Potential Complications
 Miscellaneous
– Thromboembolism
– Infection
 Retroperitoneal Bleeds
 Pressure Sores
 Brachial Plexus Injury
 Effusion / tamponade

68. Surgery: Post Operative Care
 Monitoring and assessment
– Vital signs, arrhythmias, decreased
cardiac output, hypoxia, infection, S/S
CHF, respiratory compromise
– Arterial / venous pressure
– Fluids
– Neurological changes
 Provide rest and comfort
 Pain control
 Support family

69. Cardiac Transplant
 Improved CHD Management
 New Surgical Techniques
 Transplant
 Improved Survival of Transplant
 ECMO