2. what are the most common cardiac disorder are in
neonate?
Why?
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3. Aorta
Left atrium
Left ventricle
Pulmonary Artery
Superior vena cava
Right atrium
Right ventricle
Inferior vena cava
Cardiac Anatomy & Physiology
Normal Heart Anatomy
Image:www.AboutKidsHealth.ca
Brachiocephalic
Artery
Left Common Carotid Artery
Left Subclavian Artery
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4. Aortic valve
Left atrium
Mitral valve
Left ventricle
Intraventricular Septum
Pulmonary valve
Right atrium
Tricuspid valve
Right ventricle
Heart Valves
Image:www.AboutKidshealth.ca
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5. Gestational age and APGAR scores may be predictive of
CHD.
◦ Questions that should be asked include the following:
◦ were there concerns about fetal distress at birth?
◦ was the infant cyanotic at birth?
◦ was oxygen required at birth?
◦ How soon did the newborn get discharged after birth?
◦ Maternal infectious (ie. Cytomegalovirus, herpes virus, Rubella).
◦ Ask about family history of congenital or childhood heart disease, or
sudden death.
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6. 1. Prematurity
2. Low APGAR scores
3. A history of fetal distress
4. Cyanosis or oxygen required at birth
5. Delayed discharge because of poor feeding
6. Lethargy
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7. ◦ 8/1000 live births, 3-4/100 stillborn and 10-25/100 abortuses
◦ Structural or functional heart disease that present at birth.
◦ It is not static ,there is always a continuous anatomical or
physiological change
◦ Most congenital defects are well tolerated during fetal life.
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8. Exact cause of CHD is unknown in 90% of cases.
Associated factors for CHD include:
◦ Fetal or maternal infection during the first trimester
(rubella).
◦ Chromosomal abnormalities (trisomy 21, 18, 13).
◦ Maternal insulin-dependent diabetes.
◦ Systemic lupus erythematosis (SLE)
◦ Teratogenic effects of drugs and alcohol
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10. Lesions % of all Lesions
• Ventricular septal defect 25-30
• Atrial septal defect 6-8
• Patent ductus arteriosus 6-8
• Coarctation of aorta 5-7
• Tetralogy of Fallot 5-7
• Pulomnary Valve Sterosis 5-7
• Aortic Valve Stenosis 4-7
• d-Transposition of great arteries 3-5
• Hypoplastic left ventricle 1-3
• All Others 10-15%
11. 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
Nada’s Minor Criteria
- Systolic murmur without thrill
- Abnormal P2 (accentuated P2)
- Abnormal BP (hypo / hypertension)
- Abnormal CXR
- Abnormal ECG
12. CHD suspected in any child with:
Feeding difficulty
Recurrent attack of respiratory tract infection
Growth failure
Cyanosis unresponsive to 100% oxygen
Tachycardia
Respiratory distress
Rhythm disturbance
Murmur ( absence of murmur doesn't rule out or in CHD)
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13. 1.Left to Right Shunt Lesions
1.1 Atrial Septal Defect ASD
Defect occur in any portion of the atrium
Pathophysiology
◦ Left to right shunt
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17. Clinical Manifestations
◦ Most are asymptomatic
◦ Right ventricular lift
◦ Mid-diostolic murmur at tricuspid area
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18. Diagnosis
Clinical
CXR
◦ Right. Ventricular & Atrial enlargement
◦ Large pulmonary Artery
◦ ↑ed pulmonary vascularity
ECG - volume overload, Rt ventricle & atrium
Echocardiography
Complications - pulmonary Hypertension , Eismenger syndrome
◦ Infective endocarditis prophylaxis for 6 months after surgery
or atrial occlusion device is used
Treatment
◦ Surgery-for all symptomatic
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19. Most common CHD
Both sexes are equally
affected
Can be single or multiple
Can be associated with other
congenital heart diseases
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21. Types of VSD
70% membranous close to pulmonary valve and Pulmonary
artery
20% muscular
5% Aortic valve (sub aortic)
5% near junction of Mitral and tricuspid valve (A-V canal
defect)
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22. I) Asymptomatic:
Small VSD , the pulmonary pressure is normal
Loud harsh systolic murmur at LLSB, with thrill
X-ray is normal
EKG normal
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23. II ) Large defects:
Excessive pulmonary blood flow lead to pulmonary
hypertension
Dyspnea, feeding difficulty
Poor growth
Profuse perspiration
Recurrent pulmonary infection
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24. Prominence of the precordium
Palpable parasternal lift
Apical trust with systolic thrill
Diastolic murmur at the apex
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25. Severity depend on :
The size of the defect
Level of pulmonary resistance to systemic resistance.
Defects < 0.5 restrictive
> 1cm non restrictive
Majority closes spontaneously
Large defects lead to CHF at early age
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26. Small size
Reassurance
No surgical treatment
Maintain integrity of primary and permanent teeth
Give anti- infective endocarditis prophylaxis
Antibiotic prophylaxis before
dental visit
Tonsillectomy
instrumentation of GUT,GIT
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27. Large VSD:
Control CHF
Prevent development of Pulmonary vascular disease.
Surgical closure in the first year of life (6M-12M).
Device closure of the VSD
Avoid oxygen; oxygen is a potent pulmonary
vasodilator and will increase blood flow into
the PA.
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28. During foetal life blood from PA
shunted through the DA in to the
Aorta.
After birth closed functionally
Prematurity and hypoxia
predispose for patency
Commonly associated with rubella
of the mother
Isolated PDAs are common in
high altitude
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30. Blood flow from the aorta to the pulmonary
Extent of the shunt depend on
◦ size of the ductus
◦ ratio of pulmonary and systemic vascular resistance
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31. Depend on the :
Size of the defect and direction of flow
Small defects no symptom
Large defect result in Large left to right shunt
CHF
Growth Failure
Repeated RTI
Reversal of shunt ,(Eisenmengers ) result in dyspnoea and cyanosis
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32. Bounding pulse
Wide pulse pressure
Heave , thrill in the 2nd ics
Continuous machinery murmur 2nd ics
EKG: bi-ventricular hyperthrophy
X-ray: prominent PA, increases PA marking enlarged chambers
ECHO: size of the PDA, direction of flow, chamber size
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33. Medical therapy:
Congestive heart failure treatment
infective endocarditis prophylaxis
Surgical closure of the PDA (banding)
Closure of the PDA
◦ In the symptomatic premature neonate—indomethacin or
ibuprofen given I.V.
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43. Occurs at any point from transverse
arch to iliac bifurcation
98% below the origin of left sub
clavian at the origin of Ductus
Associated with:
Turner syndrome
Mitral valve abnormality
Sub aortic stenosis
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45. Collaterals develop to bypass the obstruction.
Hypertension of the aortic branch proximal to
coarctation
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46. Severe critical stenosis the neonate present with
evidence of CHF if not corrected surgically result in
death.
Post the neonatal period Usually asymptomatic
Older children:
Headaches
Epistaxis
cold feet
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47. Weak or absent femoral pulses
Increased B/P in the upper extremities
B/P difference between upper and lower extremities
Radio Femoral pulse delay ( Collaterals)
loud , systolic murmur
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48. Chest x_ray:
Dilated descending Aorta,
enlarged LV.
ECG: normal in childhood,
later LV hypertrophy.
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49. Neonatal: closure of the ductus lead to hypo perfusion
and acidosis, thus give infusion of prostaglandin to
reopen the ductus, after stabilization
surgical treatment.
Re -stenosis balloon angioplasty is safe.
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50. 1. Cyanotic lesions with decreased pulmonary blood
flow
1.1. Tetralogy of Fallot /TOF/
Common cyanotic congenital cardiac anomaly
Four anatomical components of TOF:
◦ VSD
◦ Overriding Aorta
◦ Right ventricular outflow obstruction
◦ Right ventricular hypertrophy
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52. • Severity directly proportional to the degree of RVOT
obstruction.
• Change in pulmonary and systemic vascular resistance
and the degree of RVOT obstruction affect degree of R-L
shunt.
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53. Variable depend on RVOT obstruction
◦ pink to cyanosis
◦ CHF is not a usual manifestation of TOF
◦ Squatting
◦ Dyspnoea on exertion
◦ Hypoxic spells
◦ Growth failure
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57. Medical management:
A) Neonatal period if pulmonary flow is dependent of DA, give
prostaglandin to prevent ductal closure
B)Recognition and treatment of hyper cyanotic spell.
◦ Knee chest positioning of the patient
◦ Administration of oxygen
◦ Volume expansion
◦ Correction of acidosis
◦ Sedation with morphine
C) Treat infective endocarditis
D) Anaemia should be corrected
E) Severe polycythemia correction with phlebotomy should be done.
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60. 1.2 Pulmonary Atresia
- With VSD - Extreme form of TOF
- Without VSD - No egress of blood from Rt ventricle.
- Shunt through foramen ovale to Lt atrium
Left ventricle
systemic circulation
Aorta
PDA pulmonic circulation
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63. Clinical Manifestation
- Cyanosis at birth
- Respiratory distress
- Single heart sound
Diagnosis
- CXR
- ECG
- Echocardiography
Treatment - PGE1
- Surgery
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64. 1.3 Tricuspid atresia
- No outlet from Right atrium to right ventricle .
- Systemic venous return
Rt atrium
Lt atrium
Left ventricule
systemic Pulmonic
(VSD, PDA)
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67. 2.1. Transpostion of the
Great Arteries
The great arteries arise
from morphologically
wrong ventricles. (The
aorta arise from the RV and
Pulmonary arises from LV
in the setting of a
concordant atrioventricular
connection.
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69. The RV pressure is systemic
The blood returning from the lung pass to the lung via PA
Systemic venous return passes back to the systemic circulation
via the aorta.
Both ventricles are volume overloaded.
The right ventricle also pressure overloads and result in CHF
Survival depend on associated Large ASD, VSD,PDA.
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70. ◦ Cyanosis detected 87% of the neonates immediately ; rest later at
the age of 1 to 3 month and is progressive.
◦ Clubbing
◦ Squatting only 20% of patients
◦ Dyspnoea
◦ Cardiac failure
◦ Precordial lift
Prognosis
Patient die of anoxia and or CHF in the first 6 month of life
if there is little communication.
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71. Medical management:
Prostaglandin to keep the DA open until palliation
done
Give oxygen
Treat metabolic acidosis with bicarbonate.
Surgical:
Palliative balloon septostomy creating /increasing
ASD Rash kind procedure.
Arterial Switch (Jaten Procedure)
Atrial switch ( Mustard procedure)
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72. 2.2 Truncus arteriosus
- Single arterial trunk for both pulmonary &
systemic circulation.
Clinical Manifestation
- Cyanosis
- CHF at 2-3rd m
- Systalic ejection murmur
Treatment - surgery
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75. Relieving Respiratory Distress
Position the child in a reclining, semi-upright position.
Identify target oxygen saturations and administer oxygen
Administer prescribed medications and document response to
medications (improved, no change, or worsening respiratory
status).
◦ Diuretics.
May need to change oral feedings to nasogastric feedings
because of increased risk of aspiration with respiratory distress.
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76. Organize nursing care and medication schedule to
provide periods of uninterrupted rest.
Administer diuretics (furosemide, spironolactone
Administer digoxin as prescribed.
Administer afterload-reducing medications (captopril
[Capoten], enalapril [Vasotec]) as prescribed.
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77. Place pulse oximeter probe (continuous monitoring or
measure with vital signs)
Administer oxygen as needed.
Titrate amount of oxygen to reach target oxygen
saturations.
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78. For the infant:
◦ Small, frequent feedings.
◦ Fortified formula or breast milk.
◦ Limit oral feeding time to 15 to 20 minutes.
◦ Supplement oral feeds with nasogastric feedings as needed to
provide weight gain
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79. ◦ Maintain routine childhood immunization schedule.
◦ Prevent exposure to communicable diseases.
◦ Good hand washing.
◦ Maintain the prophylaxis antibiotic accordingly
Educate the family.
Teach the family about the defect and its treatment.
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