Transcript Pediatric Cardiac Disorders

PEDIATRIC CARDIAC
DISORDERS
It’s a worthwhile area to study! 
Cardiac Disorders in Peds
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Two major groups of disorders:
 Congenital
Aka “born with”
 Most structural defects

 Acquired
Develop later in life
 Bacterial endocarditis
 Rheumatic fever
 Kawasaki disease
 Systemic HTN
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Incidence & Causes
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5 to 8 in 1000 live births
Cause unknown
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Multiple factors
 Genetics/family history
 Environment
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Toxins
Viruses
Maternal chronic illness (diabetes, seizure meds)
 Chromosomal abnormalities
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Down syndrome
DiGeorge syndrome
Noonan or William syndrome
Trisomy 13 or 18
Older Classifications of CHD
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Acyanotic
 “pink”
 NO
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unoxygenated blood goes to the periphery
Cyanotic
 “blue”
 Unoxygenated
 May
be pink
blood is shunted to the periphery
Newer Classifications of CHD
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Hemodynamic characteristics
 Increased
 Too
pulmonary blood flow
much to lungs; “pink”; pulmonary edema
 Decreased
 Too
pulmonary blood flow
little to lungs; “blue”; cyanotic
 Obstruction
 Can’t
 Mixed
of blood flow out of the heart
get to lungs or body
blood flow
 Most
common
Comparison of CHD Classification Systems
Background info/Hemodynamics
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Review fetal to neonatal circulation (also pp. 1342-1343
Hockenberry, 9th ed.)
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Blood flows from area of high pressure to one of low
pressure (Fig. 34-7 p. 1351 Hockenberry, 9th ed.)
The greater the pressure gradient, the greater the rate
of flow.
The greater the resistance, the lower the rate of flow
In the NORMAL HEART, pressures on the R side are less
than the L side, and the resistance in the pulmonary
circulation is less than that in the systemic circulation.
Fetal circulation
Fetal to Neonatal Circulation
Normal Heart Pressures(Fig. 34-7 p.1351)
The proposed pulse-oximetry monitoring protocol based on results from the right hand (RH)
and either foot (F).
Kemper A R et al. Pediatrics 2011;128:e1259-e1267
©2011 by American Academy of Pediatrics
Tests of cardiac function
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Prenatal ultrasound
Chest x-ray
Electrocardiogram (ECG)
Echocardiogram
Cardiac catheterization
Stress test (dobutamine or
exercise)
Cardiac MRI
Cardiac Catheterization
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Invasive routine diagnostic procedure
Benefits
 Better visualization
 Actual pressures, sats, hemodynamic values
Risks:
 Hemorrhage
 Fever
 N/V
 loss of a pulse
 transient dysrhythmias
Nursing interventions for Cardiac Catheterization
(p.1348,9 9th ed. Hockenberry)
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Pre-procedure:
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Complete a thorough hx & physical exam
Check for allergies to iodine and shellfish
age appropriate teaching & preparation
 Don’t forget the parents
NPO 4-6 hrs before procedure; sedation~ IV or po
Monitor VS, SaO2, Hgb, Hct, coags, BMP
Mark pedal pulses—before procedure to ensure correct palpation
afterwards.
Determination the amount of sedation based on the child’s age, condition
& type of procedure
Cardiac Catheterization
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Post-procedure:
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√ for bleeding at site of insertion of catheter in groin
√ pulses esp. distal to site of insertion, temp & color of extremities,
VS q 15
 Remember the 5 P’s (pain, pallor, pulse, paresthesia, paralysis)
OR CMTS—circulation, mobility, temperature, sensation
√ heart rate for one full minute, for signs of dysrhythmias or
bradycardia
Prevent bleeding by keeping leg immobilized for 4-8 hrs
I & O, especially O. Fluids may be offered po starting with clear
liquids.
√ Labs; infants are at risk for hypoglycemia—monitor blood glucose as
child may need IV with dextrose
Encourage the child to void to promote excretion of contrast medium.
Cardiac Catheterization (cont’d)
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Potential cardiac catheterization complications:
 Nausea
&/or vomiting
 Low-grade fever
 Loss of pulse in catheterized extremity
 Transient dysrhythmias
 Acute hemorrhage from entry site
 apply
direct continuous pressure at 2.5cm above the catherter
entry site to localize pressure over the location of the vessel
puncture.
 Keep child flat and notify the physician
 Prepare for possible administration of additional fluids prn
Cath lab
Congestive heart failure (Fig. 34-8 p. 1353)
Symptoms of CHF
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Increased work of
breathing
Tachycardia
Decreased pulses
Decreased urinary output
Poor weight gain
Diaphoresis with activity
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Hepatomegaly
Cold, cool extremities,
especially with stress or
activity
JVD?
Decreased BP is LATE sign
Defects with Increased Pulmonary
Blood Flow
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Abnormal connection between
two sides of heart leads to
 Increased blood volume on
right side of heart
 Increased pulmonary blood
flow
 Decreased systemic blood
flow
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PDA, ASD, VSD
Symptoms
 Increased
work of
breathing
 Rales/rhonchi and/or
wheezing
 Failure to thrive
Patent Ductus Arteriosus
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Ductus doesn’t close
Common in preemies
“machinery” murmur
audio
Treatment
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Indomethacin
Cath lab
Ligation
Atrial Septal Defect
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Hole between two atria of
heart
Usually asymptomatic
If not treated, increased
risk of atrial dysrhythmia
or stroke
Usually close on own
Ventricular Septal Defect
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Hole between two
ventricles of heart
Symptoms related to size &
location of VSD and
amount of pulmonary
blood flow
Fix by patching with
Goretex
Atrioventricular Canal
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ASD, VSD, and affected
mitral & tricuspid valves
Associated with Down
syndrome
Symptoms related to size
of holes, degree of
valvular involvement, & size
of ventricles
Often accompanied with
pulmonary hypertension
Nursing Management
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AVOID OXYGEN!!!!!!!!
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Especially pre-op
Diuretics
Monitor VS, I & 0, daily wt.
Encourage rest periods to
conserve energy
Monitor labs: Hgb, Hct,
electrolytes
Closely monitor feedings
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May need higher calorie
feeds
Obstructive Defects
Coarctation of the
aorta, aortic stenosis,
pulmonic stenosis
 Symptoms dependent
upon area of
obstruction
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Coarctation of Aorta
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Narrowed aorta leads to
decreased systemic blood
flow
May not present until early
childhood
Bounding upper extremity
pulses, weak to absent
lower extremity pulses
HYPERTENSION!!!!!!!
Post-op Coarctation Care
Neuro
checks
Urine output
Blood pressure
PAIN!!!!!!!
Aortic stenosis
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Obstructs blood flow to
body
Leads to left ventricle
hypertrophy
Asymptomatic often
Chest pain with exercise
Sometimes see sudden
death
Repair with ballooning,
repair, or replacement of
valve
Pulmonary Stenosis and Catheter Placement
Leads to right ventricular hypertrophy
which may lead to reopening of the
foramen ovale. If severe, my lead to
congestive heart failure.
Defects with Decreased Pulmonary
Blood Flow and Mixed Defects
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May or may not be cyanotic (usually are)
Tetralogy of Fallot
Transposition of Great Arteries
Truncus Arteriosus
Hypoplastic Left Heart Syndrome (HLHS)
LOTS of other defects that are uncommon, book
discusses them
Effects of Hypoxemia
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Main clinical manifestations:
 Cyanosis
 Polycythemia
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Thicker blood
 Clubbing
 Clotting
abnormalities
 Delayed growth and development – can be associated
with any heart defect
Hypoxemia Management
Prostaglandin E1 given if cyanosis shown
as newborn
 Assess for and treat tet spells
 Surgery
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Corrective
or palliative—often staged
Prevent dehydration
 AVOID OXYGEN!!!!!
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Tetralogy Of Fallot
Hypercyanotic “tet spells”
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Acutely cyanotic
↓ pulm. blood flow & ↑ right to left shunting
Prompt tx to prevent brain damage &/or death
 Calm
infant/child
 Place in knee chest position
 Toddler will get in “squatting” position to compensate
for hypoxia
 Give oxygen
 Morphine/fentanyl/versed given
Knee-Chest Position
Tet Repair
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Complicated
Dependent on how big RV
is, how stenotic pulmonic
valve is, and how big the
VSD is
Either fly or die
Palliative shunt: modified
Blalock-Taussig shunt
(p.1364, Table 34-4, 9th ed.)
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Complete repair—operative
mortality <3%!
Transposition of the Great Arteries
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NOT GOOD!
Cath lab initially
Prostaglandins
Surgery at 6-7 days old—
arterial switch of pulmonary
artery and aorta, but also
coronary arteries are switched
and re-anastomosed.
Long term prognosis very good
Hypoplastic Left Heart Syndrome
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VERY VERY VERY BAD!! Mortality rates range from 10-30% (2002-04)
Can not correct easily
3 staged surgeries: Norwood, Mod Blalock Taussig, & Glenn procedure
vs. transplant
Long-term data not in yet, will probably need transplant
Management of Children with Mixed
Defects
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Medications
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Digoxin—KNOW!! pp.1354-
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1358—good info on meds
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Improves contractility of heart
Review dig toxicity—pulse rates in
infants & children
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Watch for what ??
Ace-inhibitors (angiotensin
converting inhibitors—the
PRIL’s)
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Diuretics—furosemide
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Reduce afterload on the heart
make heart pump more efficiently.
Beta-blockers—cause
decreased heart rate, BP *
vasodilatation
Decrease cardiac workload
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Meds-as stated
Decrease stimulation
Cluster care
Maintain neutral thermal
environment
Sedation for irritable child
Remove accumulated fluid
& sodium
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Closely monitor I&O
Restrict fluid in acute phase
Weigh daily if stable
Continued management of CHF
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Nutrition
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Decrease respiratory effort
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Smaller, more frequent
feeds
High calorie formula
Rest
Avoid colds, RSV
Position with HOB
Avoid crying and distress
Family support/education
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Keep them present, holding,
rocking, AMAP
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Improve tissue oxygenation
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Meds assist with this by
increasing efficiency of the
heart
Oxygen may be added with
appropriate order,
especially if there is
pulmonary edema, or lower
respiratory infection.
Post-operative Care
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PAIN!!!!!!!!!!!!!!!!!!!
Cardiac monitoring
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Chest tube care
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Heart rate
Blood pressure
Intracardiac pressures
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Quantity & quality of output
Minimum 1 ml/kg/hour
Deep breathing
IS
Rest & activity
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Move all extremities
Back to baseline
Respiratory care
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Urine output
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Neurological checks
Up next day
Ambulate
GI distress
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Avoid vomiting
Care of the Family and Child with
Congenital Heart Disease
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Help family adjust to the disorder
 May be grieving loss of normal child
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Educate family
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Help family cope with effects of the disorder
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Prepare child and family for surgery
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Remember developmental level of child
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Pain, scars, IS, activity
Refer to support group with families who have already been through the
experience
 TOUCH is the IL Assoc. This link opens a broad site, then click on IL.
 Support group with lots of links for families and persons with CHD
Website: From Cincinnati Children’s Hospital
Kawasaki Disease
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Multisystem disorder involving vasculitis & may
progress to coronary arteries causing aneurysm
formation
Leading cause of acquired heart dz in US
Etiology still unknown
3 phases:
acute
 subacute
 convalescent
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Criteria for KD (must meet 5 out of 6)
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(Box 34-10, p. 1388, Hockenberry (9th ed)
fever > 5 days
 conjunctival infection without exudate
 oral changes: erythema, “strawberry tongue,
fissured lips
 extremities changes: peripheral edema, erythema of palms
and soles, peeling of hands & feet
 erythematous rash
 cervical lymphadenopathy
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Other manifestations
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Symptoms of inflammation

C reactive protein level
  ESR
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Cardiac symptoms

L ventricular function as seen on Echocardiogram
 Children do NOT generally have sx of CHF
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Other lab changes
 Anemia
 Leukocytosis
with ‘L shift’
Kawasaki continued
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Tx best within first 7- 10 days. :
 ASA
80-100mg/kg/day initially.
This is one dx that requires use of high doses of aspirin
even in children. Dose is decreased to 3-5 mg/kg/day
once afebrile 48-72 hrs.
 IVIG 2 g/kg over 8-12 hr
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Here is a website with some good information on
the diagnosis and management of this disease:
 http://www.kdfoundation.org/
From the
American Heart
Association
Newburger, J. W. et al. Circulation 2004;110:2747-2771
Education of parents
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Teach parents common signs of Aspirin toxicity while
on high doses of ASA
 Tinnitus
 Headache
 Dizziness
 Confusion
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Teach parents to report recurrence of fever
Teach parents CPR
Inform parents that final cardiac sequelae may not
be known for some time.
QUESTIONS