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1. Pediatric Cardiac Disorders
UNIVERSTY OF GONDAR
COLLEGE OF MEDICINE AND HEALTH SCIENCE
DEPARTMENT OF NURSING
Nega Tezera

2. CARDIO VASCULAR DISEASE (CVS)
LEARNING OBJECTIVES:
At the end of this session the students will be able to:
 Explain the physiological change of CVS in newborn
 Describe congenital heart disease
 Discuss common CHD
 Discuss the nursing responsibilities of a patient with
CHD
 Explain the common acquired heart diseases
 Discuss the c/m and management of heart failure
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3. ASSESSMENT OF HEART DISORDERS
IN CHILDREN
 History
 Physical
assessment
 general
appearance
 pulse, blood
pressure, &
respirations

4. Fetal Circulation
Main Blood Flow
 Placenta  Umbilical
Vein  Liver  Ductus
Venosus  Inferior
Vena Cava
 Vena Cava  Right
Atrium Foramen
Ovale Left Atrium 
Left Ventricle 
 Aorta Body

5. Fetal Circulation
Secondary Route:
 Right Atrium 
 Right Ventricle 
 Pulmonary Artery 
 Ductus Arteriosus 
(so does not go to lungs)
 Aorta 
 Body

6. Transition from Fetal Circulation to
Pulmonary circulation
 The umbilical arteries and vein and the ductus
venosus become non-functional
 Decreased pulmonary vascular resistance and
increased pulmonary blood flow
 Increase in pressure of the left atrium, decrease
pressure in right atrium, causing closure of
foramen ovale.
 Pulmonary resistance is less than systematic
resistance so there is left-to-right shunting
resulting in closure of the ductus arteriosus.

7. A - Congenital Cardiac Defects

8. A. Congenital Heart Defects (CHD)
 Globally, CHD affects over one million live
births annually and is the leading cause of
infant mortality attributable to birth defects.
 Critical congenital heart disease (CCHD)
refers to lesions of the cardiovascular system,
present at birth, which if left undiagnosed it
will result in infant morbidity and mortality.
 Gross structural abnormality of the heart or
great vessels.
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9. CAUSE
 Mostly unknown
 Multifactorial: Genetic-environmental
interaction
– Genetic/chromosomal
– Environmental: CMV, maternal
hypoxia, hyperthermia, DM (10 ´ risk),
drugs: like, phenytoin and other
anticonvulsants, alcohol, thalidomide
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10. CLASSIFICATION
1. ACYANOTIC
 L to R shunt
stenotic lesions
ASD
VSD
PDA
pulmonic valve stenosis
aortic coarctation 10

11. VSD
11
•Most common congenital
lesion
•Large VSD’s may be silent
and become symptomatic
in first few weeks as
pulmonary resistance 
•SOB and diaphoresis w
feeds
•Poor weight gain
•Systolic murmur
•CXR demonstrates CHF

12. Classification
2. CYANOTIC
 R to L shunts
 Mixing lesions
 Tetralogy of Fallot
 Transposition of great vessels
 Tricuspid atresia
 Truncus arteriosus
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13. Evaluation for suspected congenital
heart disease
 At birth, Nada’s criteria are used to evaluate a
newborn and the presence of one Major or two
Minor Criteria indicates Presence of Congenital
Heart Disease.
Nada’s Major Criteria
 Systolic murmur with thrill
 Any diastolic murmur
 Cyanosis (central)
 Congestive cardiac failure
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14. Evaluation cont’d
Nada’s Minor Criteria
 Systolic murmur without thrill
 Abnormal P2 (accentuated P2)
 Abnormal BP (hypo / hypertension)
 Abnormal CXR
 Abnormal ECG
 If the Nada’s criteria are positive then, send the baby
where he can be definitely diagnose with
echocardiography and evaluated further.
 All babies suspected to have CHD should be managed
with cautions in IV fluid administration to avoid
congestion.
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15. Major components of Evaluation
1. Presence or absence of cyanosis, which can be determined by
physical examination aided by pulse oximetry.
- Heart sounds - the presence and character of any murmurs.
2. Chest radiograph- Less informative but helps to see the heart
size and shows evidence of increased, normal, or decreased
pulmonary vascular markings
3. Electrocardiogram – To look for the rate, rhythm and chamber
hypertrophy and axis. can be used to determine whether
right, left, or biventricular hypertrophy exists.
4. Echocardiography
 It’s a definitive diagnostic method to evaluate the heart
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16. Clinical evaluation
 History
 feeding difficulties
 tachypnea
 diaphoresis
 syncope
 cyanotic episodes
 failure to thrive
 Physical Examination
 colour: pink, blue, gray
 vitals: tachypnea,
tachycardia, BP
 symptoms suggestive of
infection
 palpation and auscultation
of precordium
 chest auscultation
 survey for organomegaly
 pulses in all extremities

17. Defects that increase pulmonary
blood flow
Patent Ductus Arterious
Atrial septal defects
Ventricle septal defects

18. Atrial Septal Defect
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

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

20. AMPLATZER Septal Occluder
implanted during a catheter-based
procedure
Heart with atrial septal
defect

22. 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
 Check for bleeding at insertion site
 Measure I&O

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

24. Ventricle Septal Defect
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

25. Treatment
Surgical repair with a patch inserted

26. 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

27. Patent Ductus Arteriosus
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

28. Treatment for PDA
 Medical Mangement
 Medication
 Indomethacin - inhibits prostaglandin's
which help keep the ductus arteriosus
open
 Surgery
Ligate the
ductus arteriosus

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

30. Pulmonic stenosis
Tetralogy of fallot
Transposition of the great arteries
Truncus arteriosus
Defects with decrease blood flow and
mixed defects

31. Pulmonic Stenosis
 Narrowing of entrance that
decreases blood flow
 Treatment:
 Cardiac Catheterization
 Baloon Valvuloplasty
 Surgery
 Valvotomy

32. Tetralogy of Fallot
Four defects are:
1. 2.
3.
4.

33. Signs and Symptoms
1. Failure to thrive
2. Squatting
3. Lack of energy
4. Infections
5. Polycythemia
6. Clubbing of fingers
7. Cerebral absess
8. Cardiomegaly

34. Treatment
 Surgical interventions
 Blalock – Taussig or Potts procedure –
increases blood flow to the lungs.
 Open heart surgery

35. 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

36. Truncus arteriosus
 A single arterial trunk
arises from both
ventricles that supplies
the systemic,
pulmonary, and
coronary circulations. A
vsd and a single,
defective, valve also
exist.
 Entire systemic
circulation supplied from
common trunk.

37. Defects obstructing Systemic blood
flow
• Aortic stenosis
• Coarctation of the Aorta

38. Coarctation of the Aorta
1. Narrowing ofAorta causing
obstruction of left
ventricular blood flow
2. Left ventricular hypertrophy
Signs and Symptoms
1.  B/P in upper extremities
2. B/P in lower extremities
3. Radial pulses full/bounding and
femoral or popliteal pulses weak
or absent
4. Leg pains, fatigue
5. Nose bleeds

39. Treatment
 Goals of management are to improve ventricular
function and restore blood flow to the lower body.
 Medical management with Medication
 A continuous intravenous medication,
prostaglandin (PGE-1), is used to open the ductus
arteriosus (and maintain it in an open state)
allowing blood flow to areas beyond the
coarctation.
 Baloon Valvoplasty

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

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

42. 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.

43. Ask Yourself ?
 Laboratory analysis on a child with Tetralogy
of Fallot indicates a high RBC count. The
polycythemia is a compensatory mechanism
for:
a. Tissue oxygen need
b. Low iron level
C. Low blood pressure
d. Cardiomegaly

44. 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.

45. B - Acquired Cardiac Diseases

46. I - Congestive heart failure
 The inability of the myocardium to circulate
enough oxygenated blood to meet the
demands of the body.
 When the heart fails, cardiac output is
diminished. Heart rate, preload,
contractitility, and afterload are affected.
 Peripheral tissue is not adequately
perfused.
 Congestion in lungs and periphery
develops.

47. Etiology and Pathophysiology
 Congenital defects – allow blood to flow from
the left side of the heart to the right so that
extra blood is pumped to the pulmonary
system rather than through the aorta when the
ventricle contracts.
 Obstructive congenital defects – restricts the
flow of blood so the heart hypertrophies to
work harder to force blood through the
narrowed structures. The hypertrophied
muscle becomes ineffective.
 Other defects which weaken the heart muscle.

48. Compensatory Mechanisms
 Stimulation of the sympathetic nervous system
which releases norepinephrine from the adrenals.
This stimulates blood vessels to constrict and an
increase in the heart rate.
 Tachycardia increases venous return to the heart
which stretches the myocardial fibers and
increases preload. Only successful for short
period of time.
 Increased renin and ADH secretion caused by
decrease renal perfusion. Resultant increase in
Na and H2O retention to increase fluid to the
heart and leading to edema

49. Signs and Symptoms
1. Tires easily during feeding
2. Periorbital edema, weight gain
3. Rales and rhonchi
4. Dyspnea, orthopnea, tachypnea
5. Diaphoretic / sweating
6. Tachycardia
7. Failure to gain weight

50. ROSS HEART FAILURE CLASSIFICATION FOR
CHILDREN for dx purpose. (IJP, 2009)
Class I
 Asymptomatic
Class II
 Mild tachypnea or diaphoresis with feeding in
infants
 Dyspnea on exertion in older children
Class III
 Marked tachypnea or diaphoresis with feeding
in infants
 Marked dyspnea on exertion
 Prolonged feeding times with growth failure
Class IV
 Symptoms such as tachypnea, retractions,
grunting, or diaphoresis at rest
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51. Medication therapy
 positive inotropic effect and afterload -reducing agents
 Digitalis – increases contractility and decreases heart rate.
 Digoxin
 ACE inhibitors (Angiotensin-converting enzyme inhibitors)
- arterial vasodilator / afterload reducing agent
 Lisinopril
 Beta Blockers - increases contractility
 Indural (Propranolol)
 Diuretics: - enhance renal secretion of sodium and water by
reducing circulating blood volume and decreasing preload.
Lasix, HCThiazide, aldactone.

52. Treatment of Congestive Heart Failure
 Diet – low sodium, small frequent feedings
(be sure you can pick the right foods for a low NA diet.
 Nursing care:
 Measure intake and output – weighing diapers
 Observe for changes in peripheral edema and
circulation
 If ascites present – take serial abdominal
measurements to monitor changes.
 Skin care
 Turning schedule

53. 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

54. II- RHEUMATIC HEART DISEASE (RHD)
Rheumatic fever (ARF) :- is an inflammatory disease
affecting the heart , joint & subcutaneous tissue.
 ARF remains an important preventable cause of cardiac
disease
 Usually follow 2-6 wks after hemolytic streptococcal
respiratory infection.
 A family history of rheumatic fever and lower
socioeconomic status are additional factors.
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55. Jones Criteria (Modified) for
Diagnosis of Rheumatic Fever.
Major manifestation
 Carditis
 Polyarthritis
 Chorea
 Subcutaneous nodules
 Erythema marginatum
-N.B Two major or one
major and two minor
manifestations (plus
supporting evidence of
streptococcal
infection) are needed
Minor manifestation
- Fever
--  ESR
-  WBC
- Anemia
- ECG abnormal
-Clinical Previous rheumatic
fever or rheumatic heart
disease
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56. MANAGEMENT
 All patients with acute rheumatic fever should be
placed on bed rest and monitored closely for
evidence of carditis.
 They can be allowed to ambulate as soon as the
signs of acute inflammation have subsided..
 ANTIBIOTIC THERAPY
 The patient should receive 10 days of orally
administered penicillin or erythromycin, or a single
intramuscular injection of benzathine penicillin to
eradicate GAS from the upper respiratory tract.
 After this initial course of antibiotic therapy, the
patient should be started on long-term antibiotic
prophylaxis
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57. Mgt cont…
 Anti-Inflammatory Therapy.
 The usual dose of aspirin is 100 mg/kg/day in 4
divided doses PO for 3–5 days, followed by 75
mg/kg/day in 4 divided doses PO for 4 wk.
 The usual dose of prednisone is 2 mg/kg/day in 4
divided doses for 2–3 wk followed by a tapering of
the dose that reduces the dose by 5 mg/24 hr every
2–3 days
 In the case of Sydenham Chorea Sedatives may be
helpful early in the course of chorea;
 phenobarbital (16–32 mg every 6–8 hr PO) is the
drug of choice.
 If phenobarbital is ineffective, then haloperidol
(0.01–0.03 mg/kg/24 hr divided bid PO) or
chlorpromazine (0.5 mg/kg every 4–6 hr PO) should
be initiated
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58. COMPLICATIONS
 The arthritis and chorea of acute rheumatic fever resolve
completely without sequelae.
 Therefore, the long-term squeal of rheumatic fever are
usually limited to the heart
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59. RHEUMATIC HEART DISEASE (RHD)
 RHD is damage of the heart, particularly the
valves by one or more attacks of RF.
 The valvular lesions begin as small verrucae
composed of fibrin and blood cells along the
borders of one or more of the heart valves.
 The mitral valve is affected most often,
followed in frequency by the aortic valve; right-
sided heart manifestations are rare.
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60. Assignment (5pts)
- Kawasaki Disease and Subacute Bacterial Endocarditis /
Ineffective Endocarditis:
- NB – Make 5 group
- - Assignment incorporate- Epidemiology ,risk
- factors, nursing interventions.