This document discusses fetal circulation and several congenital heart defects that can occur, including their pathophysiology, clinical presentation, and treatment. It begins by describing the normal fetal circulation, where oxygenated blood from the placenta travels through the umbilical vein, ductus venosus, and foramen ovale to supply the fetus. It then covers several defects: atrial septal defect, ventricular septal defect, patent ductus arteriosus, pulmonary stenosis, aortic stenosis, and coarctation of the aorta. For each, it provides an overview of how blood flow is disrupted, typical signs and symptoms, and treatment approaches like surgery, catheterization, or medication management.

1. By
Hidayat khan
MSN, BSN, RN and DPHN
Pediatric Cardiology

2. Fetal Circulation
 Before birth, blood from the placenta,
about 80% saturated with oxygen, returns
to the fetus by way of the umbilical vein.
 On approaching the liver, most of this
blood flows through the ductus venosus
directly into the inferior vena cava,
bypassing the liver.
 After a short course in the inferior vena
cava, where placental blood mixes with
deoxygenated blood returning from the
lower limbs, it enters the right atrium.

3. Fetal Circulation
 Here it is guided toward the oval foramen by
the valve of the inferior vena cava, and most
of the blood passes directly into the left
atrium.
 From the left atrium, where it mixes with a
small amount of desaturated blood returning
from the lungs, blood enters the left ventricle
and ascending aorta.
 Since the coronary and carotid arteries are
the first branches of the ascending aorta, the
heart musculature and the brain are supplied
with well-oxygenated blood.

4. Fetal Circulation
 A small amount from the IVC is prevented
from entering the left atrium and remains
in the right atrium.
 It mixes with desaturated blood returning
from the head and arms by way of the
superior vena cava.
 Desaturated blood from the superior vena
cava flows by way of the right ventricle
into the pulmonary trunk.

5. Fetal Circulation
 During fetal life, resistance in the
pulmonary vessels is high, such that most
of this blood passes directly through the
ductus arteriosus into the descending
aorta, where it mixes with blood from the
proximal aorta.
 After coursing through the descending
aorta, blood flows toward the placenta by
way of the two umbilical arteries.
 The oxygen saturation in the umbilical
arteries is approximately 58%.

6. Fetal Circulation
N.B.
A. A small amount of blood enters the liver sinusoids
and mixes with blood from the portal circulation.
B. A sphincter mechanism in the ductus venosus,
close to the entrance of the umbilical vein, regulates
flow of umbilical blood through the liver sinusoids.
This sphincter closes when a uterine contraction
renders the venous return too high, preventing a
sudden overloading of the heart.
 During its course from the placenta to the organs of
the fetus, blood in the umbilical vein gradually loses
its high oxygen content as it mixes with desaturated
blood.

7. Fetal Circulation
 Theoretically, mixing may occur in the following
places :
1) In the liver by mixture with a small amount of
blood returning from the portal system.
2) In the inferior vena cava which carries
deoxygenated blood returning from the lower
extremities, pelvis, and kidneys.
3) In the right atrium by mixture with blood returning
from the head and limbs.
4) In the left atrium by mixture with blood returning
from the lungs.
5) At the entrance of the ductus arteriosus into the
descending aorta.

9. Congenital heart disease (CHD)
Congenital heart disease is a defect in the
structure of the heart and
great vessels which is present at birth
• CHD are the main cause of defect-related deaths
• Incidence is 8-9/1000 live births
• More common in premature infants
• May be associated with a significant musculoskeletal
defect
(e.g. diaphragmatic hernia, tracheo-oesophageal fistula,
imperforate anus)

10. Congenital heart disease (CHD)
• Causes are multifactorial and
include maternal illness
(diabetes mellitus,
phenylketonuria, and systemic
lupus erythematosus),
maternal infections (Rubella),
drugs (lithium, thalidomide),
known teratogens, harmful
habits (alcohol, hydantoin)
and associations with
chromosomal abnormality or
other recognized patterns of
malformation or syndrome; Trisomy 18
100% have CHD

11. Central cyanosis
• noted in the trunk, tongue, mucous membranes
• due to reduced oxygen saturation
Peripheral cyanosis
• noted in the hands and feet, around mouth
• due to reduced local blood flow
Recognition of Cyanosis

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

14. Acyanotic Congenital Heart Disease
Left-to-Right Shunt Lesions
 Atrial Septal Defect (ASD)
 Ventricular Septal Defect (VSD)
 Atrioventricular Septal Defect (AV Canal)
 Patent Ductus Arteriosus (PDA)

15. Atrial Septal Defect
 ASD is an opening in the atrial septum permitting
free communication of blood between the atria.
Seen in 10% of all CHD.

16. Atrial Septal Defect
Clinical Signs & Symptoms
 Rarely presents with signs of CHF or other
cardiovascular symptoms.
• Most are asymptomatic but may have easy
fatigability or mild growth failure.
• Cyanosis does not occur unless pulmonary HTN
is present.

17. Atrial Septal Defect pathophysiology
1. Oxygenated blood is shunted
from left to right side of the heart
via defect
2. A larger volume of blood
than normal must be
handled by the right side of
the heart hypertrophy
3. Extra blood then passes
through the pulmonary
artery into the lungs,
causing higher pressure
than normal in the blood
vessels in the lungs 
congestive heart failure

18. Treatment
 Medical Management
 Medications – digoxin
 Cardiac Catheterizaton -
 Amplatzer septal occluder
 Open-heart Surgery

19. Atrial Septal Defect
Treatment:
 Surgical or catherization laboratory closure is
generally recommended.
• Closure is performed electively between ages 2 &
5 yrs to avoid late complications.
• Surgical correction is done earlier in children w/
CHF or significant Pulm HTN.

20. Treatment
 Device Closure – Amplatzer septal occluder
During cardiac catheterization the occluder is placed in the
Defect

21. Cardiac Catheterization
 Pre-care:
 History and Physical
 Lab work – EKG, ECHO cardiogram, CBC
 NPO
 Preprocedural teaching
 Post Care:
 Monitor vital signs
 Monitor extremity distal to the catheter instertion,
 Keep leg immobilized
 Vital signs
 Check for bleeding at insertion site
 Measure I&O

22. Ventricular Septal Defect
 VSD – is an abnormal opening in the ventricular
septum, which allows free communication
between the Rt & Lt ventricles. Accounts for 25%
of CHD.

23. Ventricular Septal Defect
Hemodynamics
 The left to right shunt occurs secondary to
PVR being < SVR, not the higher pressure in
the LV.
 This leads to elevated RV & pulmonary
pressures & volume hypertrophy of the LA &
LV.

24. Ventricular Septal Defect
Clinical Signs & Symptoms
• Small - moderate VSD, 3-6mm, are usually
asymptomatic and 50% will close
spontaneously
by age 2yrs.
• Moderate – large VSD, almost always have
symptoms and will require surgical repair.

25. Ventricular Septal Defect
Clinical Signs & Symptoms
• Prominent , Diastolic murmur.
• CHF, FTT, Respiratory infections, exercise intolerance.
Symptoms develop between 1 – 6
months

26. Ventricle Septal Defect
pathophysiology
1. Oxygenated blood is shunted
from left to right side of the
heart via defect
2. A larger volume of blood
than normal must be
handled by the right side of
the heart hypertrophy
3. Extra blood then passes
through the pulmonary
artery into the lungs,
causing higher pressure
than normal in the blood
vessels in the lungs 
congestive heart failure

27. Ventricular Septal Defect
Treatment
• Small VSD - no surgical intervention, no
physical restrictions, just reassurance and
periodic follow-up and endocarditis prophylaxis.
• Symptomatic VSD - Medical treatment
initially with afterload reducers & diuretics.

28. Ventricular Septal Defect
Treatment
 Indications for Surgical Closure:
 Large VSD with medically uncontrolled
symptomatology & continued FTT.
 Ages 6-12 mo with large VSD & Pulm. HTN

29. Treatment
Surgical repair with a patch inserted

30. Patent Ductus Arteriosus
 PDA – Persistence of the normal fetal vessel
that joins the PA to the Aorta.
 Normally closes in the 1st wk of life.
 Accounts for 10% of all CHD, seen in 10% of
other congenital hrt lesions and can often play
a critical role in some lesions.
 Female : Male ratio of 2:1
 Often associated with coarctation & VSD.

31. Patent Ductus Arteriosus
Hemodynamics
 As a result of higher aortic pressure, blood
shunts L to R through the ductus from Aorta
to PA.
 Extent of the shunt depends on size of the
ductus & PVR:SVR.
 Small PDA, pressures in PA, RV, RA are
normal.

32. Patent Ductus Arteriosus
Clinical Signs & Symptoms
 Small PDA’s are usually asymptomatic
 Large PDA’s can result in symptoms of CHF,
growth restriction, FTT.
 Bounding arterial pulses
 Widened pulse pressure
 Enlarged heart, prominent apical impulse
 Classic continuous machinary systolic murmur
 Mid-diastolic murmur at the apex

33. Patent Ductus Arteriosus pathophysiology
1. Blood shunts from
aorta (left) to the
pulmonary artery
(right)
2. Returns to the
lungs causing
increase pressure
in the lung
3. Congestive heart
failure

34. Patent Ductus Arteriosus
Treatment
 Indomethacin, inhibitor of prostaglandin synthesis
can be used in premature infants.
 PDA requires surgical or catheter closure.
 Closure is required treatment heart failure & to
prevent pulmonary vascular disease.
 Usually done by ligation & division or intra
vascular coil.
 Mortality is < 1%

35. Treatment for PDA
 Surgery
Ligate the
ductus arteriosus

36. Treatment for PDA
 Cardiac Catheterization
 Insert coil – tiny fibers
occlude the ductus
arteriosus when a
thrombus forms in the
mass of fabric and wire

37. Nursing Care:
 Pre-op
 Patient/parent teaching
 Assess for infection
 Obtain lab values for chart
 Post-op
 ABCs
 Rest
 Hydration/nutrition
 Prevent complications
 Discharge teaching

38. Pulmonary Stenosis
 Pulmonary Stenosis is
obstruction in the region of
either the pulmonary valve or
the subpulmonary ventricular
outflow tract.
 Accounts for 7-10% of all
CHD.
 Most cases are isolated
lesions
 Maybe biscuspid or fusion of
2 or more leaflets.
 Can present w/or w/o an
intact ventricular septum.

39. Pulmonary Stenosis
Hemodynamics
 RV pressure hypertrophy  RV failure.
 RV pressures maybe > systemic pressure.
 Post-stenotic dilation of main PA.
 W/intact septum & severe stenosis  R-L shunt
 cyanosis.
 Cyanosis is indicative of Critical PS.

40. Pulmonary Stenosis
Clinical Signs & Symptoms
 Depends on the severity of obstruction.
 Asymptomatic w/ mild PS < 30mmHg.
 Mod-severe: 30-60mmHg, > 60mmHg
 Prominent jugular wave.
 Split 2nd hrt sound w/ a delay
 Heart failure & cyanosis seen in severe cases.

41. Pulmonary Stenosis
Treatment
 Mild PS no intervention required, close follow-
up.
 Mod-severe – require relieve of stenosis.
 Balloon valvuloplasty, treatment of choice.
 Surgical valvotomy is also a consideration.

42. Pulmonic Stenosis
 Treatment:
 Medications – Prostaglandins to keep the PDA open
 Cardiac Catheterization
 Baloon Valvuloplasty
 Surgery
 Valvotomy

43. Aortic Stenosis
 Aortic Stenosis is an obstruction to the
outflow from the left ventricle at or near the
aortic valve that causes a systolic pressure
gradient of more than 10mmHg. Accounts for
7% of CHD.
 3 Types
 Valvular – Most common.
 Subvalvular(subaortic) – involves the left
outflow tract.
 Supravalvular – involves the ascending aorta
is the least common.

44. Aortic Stenosis
Hemodynamics
 Pressure hypertrophy of the LV and
LA with obstruction to flow from the
LV.
 Mild AS 0-25mmHG
 Moderate AS 25-50mmHg
 Severe AS 50-75mmHg
 Critical AS > 75mmHg

45. Aortic Stenosis
Clinical Signs & Symptoms
 Mild AS may present with exercise
intolerance, easy fatigabiltity, but usually
asymptomatic.
 Moderate AS – Chest pain, dypsnea on
exertion, dizziness & syncope.
 Severe AS – Weak pulses, left sided heart
failure, Sudden Death.
 LV thrust at the Apex.
 Systolic thrill @ rt base/suprasternal notch

46. Aortic Stenosis
Treatment
 Balloon valvuloplasty is the standard of
treatment. Aortic insufficiency & re-stenosis is
likely after surgery and may require valve
replacement.
 Activity should not be restricted in Mild AS.
 Mod-severe AS, no competitive sports.

47. Coarctation of the Aorta
 Coarctation- is narrowing of the aorta at
varying points anywhere from the transverse
arch to the iliac bifurcation.
 98% of coarctations are juxtaductal
 Male: Female ratio 3:1.
 Accounts for 7 % of all CHD.

48. Coarctation of the Aorta
Hemodynamics
 Obstruction of left ventricular outflow  pressure
hypertrophy of the LV.

49. Coarctation of the Aorta
Clinical Signs & Symptoms
 Classic signs of coarctation are diminution or
absence of femoral pulses.
 Higher BP in the upper extremities as compared
to the lower extremities.
 90% have systolic hypertension of the upper
extremities.
 Pulse discrepancy between rt & lt arms.

50. Coarctation of the Aorta
Clinical Signs & Symptoms
 With severe coarc LE hypoperfusion, acidosis,
HF and shock.
 Differential cyanosis if ductus is still open
 Cardiomegaly, rib notching on X-ray.
 absence of femoral pulses
1. Radial pulses full/bounding and femoral or
popliteal pulses weak or absent
2. Leg pains, fatigue
3. Nose bleeds

51. Coarctation of the Aorta

52. Coarctation of the Aorta
Treatment
 With severe coarctation maintaining the
ductus with prostaglandin E is essential.
 Surgical intervention, to prevent LV
dysfunction.
 Angioplasty is used by some centers.
 Re-coarctation can occur, balloon angioplasty
is the procedure of choice.

53. Surgery for Coarctation of Aorta
1.
Resect
narrow
area
2. Anastomosis

54. Cyanotic heart disease

55. 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.

56. 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.

57. 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.

58. 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.

59.  Tetralogy of Fallot’s
 Tetralogy of Fallot
 Four anomalies
 Pulmonary stenosis
 VSD
 Dextroposition of the
aorta
 Hypertrophy of right
ventricle

60. Clinical manifestation of TOF
Symptoms are variable depending of
degree of obstruction
 Cyanosis
 Digital clubbing and hyperpnea at rest are
directly related to the degree of cyanosis
 Tachycardia
 Mental retardation
 Retarded growth and development
 RV heave
 Systolic ejection murmur is heard along the left
sternal border

61.  Polycythemia
 Paroxymal dyspnea
 Severe dyspnea on exertion
 Squatting position for the relief of dyspnea
caused physical effort,
 “Blue” spells, paroxysmal hypercyanotic attacks
– infant becomes hyperpnea, restless, cyanosis
increases, gasping respirations, syncope

62. Hypercyanotic Spells/Blue Spells/Tet
Spells
Clinical Manifestations
‫٭‬ Most often occurs in morning after feedings,
defecation, or crying
‫٭‬ Acute cyanosis
‫٭‬ Hyperpnea
‫٭‬ Inconsolable crying
‫٭‬ Hypoxia which leads to acidosis

63. Chest X-Ray
• Decreased
pulmonary
vascular marking
• “Boot-shaped
heart”

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

65. 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.

66. 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.

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

68. 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.

69. Treatment of the Child with TOF
 Decrease cardiac workload
 Prevention of intercurrent infection
 Prevention of hemoconcentration
 Surgical repair – palliative or corrective surgery

70. Balloon Dilatation
of Pulmonic Valve

71. Nursing Care:
 Monitor VS
 I&O
 Medications
 Position
 Metabolic rest
 Assess and document child/family
interactions
 Parent teaching

72. Transposition of Great Vessels
 Aorta arises from the right
ventricle, and the pulmonary
artery arises from the left
ventricle - which is not
compatible with survival
unless there is a large
defect present in ventricular
or atrial septum.
artery
aorta

73. d-Transposition of the Great Arteries

74. Transposition of the Great Arteries
 Pathophysiology
 Cyanosis due to failure of delivery of pulmonary venous
blood to the systemic circulation
 Two parallel circulations with no mixing
 Open atrial septum (fossa ovalis) allows some left-to-right
shunt, enhanced by a left-to-right ductus arteriosus shunt
 Presence of ventricular septal defect facilitates mixing

75. Transposition of the Great
Arteries
 Aorta from right ventricle, pulmonary artery from
left ventricle.
 Cyanosis from birth, hypoxic spells sometimes
present.
 Heart failure often present.
 Cardiac enlargement and diminished pulmonary
artery segment on x-ray.

76. Transposition of the Great
Arteries
 Anatomic communication must exist between
pulmonary and systemic circulation, VSD, ASD,
or PDA.
 Untreated, the vast majority of these infants
would not survive the neonatal period.

77. Transposition of the Great Arteries
Clinical Manifestations
 Cyanosis, tachypnea are most often recognized
within the 1st hrs or days of life.
 Hypoxemia is usually moderate to severe,
depending on the degree of atrial level shunting and
whether the ductus is partially open or totally closed.
 Physical findings, other than cyanosis, may be
remarkably nonspecific.
 Murmurs may be absent, or a soft systolic ejection
murmur may be noted at the midleft sternal border.

78. Transposition of the Great Arteries
 Chest film
 Oval-shaped heart
 Narrow mediastinum
 Normal or increased pulmonary vascular markings

79. D-Transposition of the Great Arteries
This condition is a medical emergency,
and only early diagnosis and appropriate intervention can
avert the development of prolonged severe hypoxemia and
acidosis,

80. Treatment
When transposition is suspected, an infusion of prostaglandin
E1 should be initiated immediately to maintain patency of the
ductus arteriosus and improve oxygenation.
 Endotracheal intubation
 Infants who remain severely hypoxic or acidotic despite
prostaglandin infusion should undergo Rashkind balloon atrial
septostomy
 A Rashkind atrial septostomy is also usually performed in all
patients in whom any significant delay in surgery is necessary.

81. Preventing Birth
Defects
 Stop smoking
 Avoid drinking alcohol while pregnant
 Take a daily vitamin containing folic acid
 Antenatal to make sure any medication (over-the-
counter or prescription) is safe to take during
pregnancy
 Stop use of any illegal or "street" drugs

82. Nursing interventions pre and post
cardiac catheterization
 Assessment pre-op for baselines
 Assessment post-op:
 Vital signs (which ones are priority?)
 Extremities
 Activity
 Hydration
 Medications
 Comfort measures

83. Teaching after cardiac catheterization
 Parental teaching
 Watch for s/s of bleeding, bruising at site
 Loss of sensation in foot on side of cath
 When to call the physician
 If any of above s/s noted within 1st 24 hrs

84. 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
 migratory polyarthritis, subcutaneous nodules,
fevers, chorea movements.

85.  Rheumatic fever
 S/S
 Systolic murmur
 Chorea (sudden involuntary movement of the limbs)
 Macular rash on the trunk
 Swollen and tender joints, Subcutaneous nodules
 Positive ASO titer and increased ESR and C-reactive protein
 Fever
 Lethargy/general malaise
 Anorexia
 Splenomegaly
 Retinal hemorrhages

86. Treatment for Rheumatic Fever
 antibiotics to treat the strept infection: pcn,
erythromycin
 Analgasic for joint pain and fever
 monitored by cardiac echo (serial)
 steroids for severe carditis with CHF
 long term antibiotics until adulthood
 1x/mo IM (Pen G)
 Bedrest
 Prognosis depends on how much heart involvement

87. Principles that apply to all cardiac
conditions:
 Encourage normal growth and
development
 Counsel parents to avoid overprotection
 Address parents’ concerns and anxieties
 Educate parents about conditions, tests,
planned treatments, medications
 Assist parents in developing ability to
assess child’s physical status

88. Rheumatic heart disease
Rheumatic heart disease is a condition
in which the heart valves have been
permanently damaged by rheumatic
fever. The heart valve damage may start
shortly after untreated or under-treated
streptococcal infection such as strep
throat or scarlet fever. An immune
response causes an inflammatory
condition in the body which can result in
on-going valve damage

89. Sign and symptoms
THEORITICAL
 These are the most common
sign and symptoms of
Rheumatic fever:
• Fever
• Swollen, tender, red and
extremely painful joints —
particularly the knees and
ankles
• Nodules (lumps under the skin)
• Red, raised, lattice-like rash,
usually on the chest, back, and
abdomen
• Shortness of breath and chest
discomfort
CLINICAL
 Carditis
 Arthritis
 Chorea
 Erythema marginatum
 Arthralgia

90. CONTI
THEORITICAL
• Uncontrolled movements of
arms, legs, or facial
muscles
• Weakness
 Symptoms of Rheumatic
heart disease depend on
the degree of valve
damage and may include:
• Shortness of breath
(especially with activity or
when lying down)
• Chest pain
• Swelling
CLINICAL
 Subcutaneous
nodules


91. DIAGNOSIS
THEORITICAL
 History
 Physical examination
 Tests.
chest x ray
ECG
ECHO
Cardiac MRI
Blood test
CLINICAL
 Elevated ESR ,
 Elevated C reactive
protein and leukocytosis
 ECG P-R interval
prolong
 Chest X rays shows
enlarged heart

92. TREATMENT
THEORITICAL
 Treatment depends in
large part on how
much damage has
been done to the
heart valves. In
severe cases,
treatment may include
surgery to replace or
repair a badly
damaged valve.
CLINICAL
 Benzyle penicillin
 Aspirin
 Erythromycin

93. TREATMENT
THEORITICAL
 Prevention through
antibiotics for strep
throats to prevention
rheumatic fever .
 Anti inflammatory
drugs
aspirin ,steroids
and non
steroidal.
CLINICAL

94. COMPLICATIONS
THEORY
 Some complications of rheumatic heart
disease include:
• Heart failure. This can occur from either
a severely narrowed or leaking heart
valve.
• Bacterial endocarditis. This is an
infection of the inner lining of the heart,
and may occur when rheumatic fever has
damaged the heart valves.
• Complications of pregnancy and
delivery due to heart damage. Women
with rheumatic heart disease should
discuss their condition with their
healthcare provider before getting
pregnant.
• Ruptured heart valve. This is a medical
emergency that must be treated with
surgery to replace or repair the heart
valve.
CLINICAL
 Atrial hypertension
 Heart failure
 Atrial fibrillation
 Recurrence of acute
rheumatic fever
 Endocarditis

95. Nursing management
Assess the child’s pain perception using an
appropriate scale every 2 to 3 hours
. Provides information about the pain level
of the child.
Assess changes in behavior, such as high-
pitched cry, irritability , restlessness, refusal to
move, facial grimace, aggressive or
dependent behavior.

96. Nonverbal pain descriptions that are age-related
as child or infant may be unable to describe pain;
fear and anxiety associated with pain cause
changes in behavioral responses.
Examine affected joints, degree of joint pain, level
of joint movement.