pediatric cardiac disorders it’s a worthwhile area to study!
TRANSCRIPT
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PEDIATRIC CARDIAC DISORDERS
It’s a worthwhile area to study!
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Cardiac Disorders in Peds
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
5 to 8 in 1000 live births Cause unknown
Multiple factors Genetics/family history Environment
Toxins Viruses
Maternal chronic illness (diabetes, seizure meds) Chromosomal abnormalities
Down syndrome DiGeorge syndrome Noonan or William syndrome Trisomy 13 or 18
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Older Classifications of CHD
Acyanotic “pink” NO unoxygenated blood goes to the
periphery Cyanotic
“blue” Unoxygenated blood is shunted to the
periphery May be pink
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Newer Classifications of CHD Hemodynamic characteristics
Increased pulmonary blood flowToo much to lungs; “pink”; pulmonary
edema Decreased pulmonary blood flow
Too little to lungs; “blue”; cyanotic Obstruction of blood flow out of the heart
Can’t get to lungs or body Mixed blood flow
Most common
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Comparison of CHD Classification Systems
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Background info/Hemodynamics Review fetal to neonatal circulation (also pp. 1342-1343
Hockenberry, 9th ed.)
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.
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Fetal circulation
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Fetal to Neonatal Circulation
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Normal Heart Pressures(Fig. 34-7 p.1351)
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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
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Tests of cardiac function
Prenatal ultrasound Chest x-ray Electrocardiogram
(ECG) Echocardiogram Cardiac
catheterization Stress test
(dobutamine or exercise)
Cardiac MRI
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Cardiac Catheterization
Invasive routine diagnostic procedure Benefits
Better visualization Actual pressures, sats, hemodynamic
values Risks:
Hemorrhage Fever N/V loss of a pulse transient dysrhythmias
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Nursing interventions for Cardiac
Catheterization (p.1348,9 9th ed. Hockenberry) Pre-procedure:
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
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Cardiac Catheterization
Post-procedure: √ 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.
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Cardiac Catheterization (cont’d) 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
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Cath lab
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Congestive heart failure (Fig. 34-8 p. 1353)
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Symptoms of CHF
Increased work of breathing
Tachycardia Decreased pulses Decreased urinary
output Poor weight gain Diaphoresis with
activity
Hepatomegaly Cold, cool
extremities, especially with stress or activity
JVD? Decreased BP is LATE
sign
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Defects with Increased Pulmonary Blood Flow
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
PDA, ASD, VSD Symptoms
Increased work of breathing
Rales/rhonchi and/or wheezing
Failure to thrive
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Patent Ductus Arteriosus
Ductus doesn’t close Common in preemies “machinery” murmur
audio Treatment
Indomethacin Cath lab Ligation
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Atrial Septal Defect
Hole between two atria of heart
Usually asymptomatic
If not treated, increased risk of atrial dysrhythmia or stroke
Usually close on own
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Ventricular Septal Defect
Hole between two ventricles of heart
Symptoms related to size & location of VSD and amount of pulmonary blood flow
Fix by patching with Goretex
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Atrioventricular Canal
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
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Nursing Management
AVOID OXYGEN!!!!!!!! Especially pre-op
Diuretics Monitor VS, I & 0, daily
wt. Encourage rest periods
to conserve energy Monitor labs: Hgb, Hct,
electrolytes Closely monitor
feedings May need higher calorie
feeds
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Obstructive Defects
Coarctation of the aorta, aortic stenosis, pulmonic stenosis
Symptoms dependent upon area of obstruction
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Coarctation of Aorta
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!!!!!!!
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Post-op Coarctation Care
Neuro checks Urine output Blood pressure
PAIN!!!!!!!
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Aortic stenosis
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
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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.
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Defects with Decreased Pulmonary Blood Flow and Mixed Defects
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
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Effects of Hypoxemia
Main clinical manifestations: Cyanosis Polycythemia
Thicker blood Clubbing Clotting abnormalities Delayed growth and development – can be
associated with any heart defect
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Hypoxemia Management
Prostaglandin E1 given if cyanosis shown as newborn
Assess for and treat tet spells Surgery
Corrective or palliative—often staged
Prevent dehydration AVOID OXYGEN!!!!!
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Tetralogy Of Fallot
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Hypercyanotic “tet spells”
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
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Knee-Chest Position
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Tet Repair
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.)
Complete repair—operative mortality <3%!
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Transposition of the Great Arteries
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
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Hypoplastic Left Heart Syndrome
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
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Management of Children with Mixed Defects
Medications Digoxin—KNOW!! pp.1354-
1358—good info on meds Improves contractility of heart Review dig toxicity—pulse
rates in infants & children Diuretics—furosemide
Watch for what ?? Ace-inhibitors (angiotensin
converting inhibitors—the PRIL’s) Reduce afterload on the heart
make heart pump more efficiently.
Beta-blockers—cause decreased heart rate, BP * vasodilatation
Decrease cardiac workload Meds-as stated Decrease stimulation Cluster care Maintain neutral thermal
environment Sedation for irritable child
Remove accumulated fluid & sodium Closely monitor I&O Restrict fluid in acute
phase Weigh daily if stable
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Continued management of CHF Nutrition
Smaller, more frequent feeds
High calorie formula Decrease respiratory
effort Rest Avoid colds, RSV Position with HOB Avoid crying and distress
Family support/education Keep them present,
holding, rocking, AMAP
Improve tissue oxygenation 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.
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Post-operative Care
PAIN!!!!!!!!!!!!!!!!!!! Cardiac monitoring
Heart rate Blood pressure Intracardiac pressures
Chest tube care Quantity & quality of
output Urine output
Minimum 1 ml/kg/hour
Neurological checks Move all extremities Back to baseline
Respiratory care Deep breathing IS
Rest & activity Up next day Ambulate
GI distress Avoid vomiting
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Care of the Family and Child with Congenital Heart Disease
Help family adjust to the disorder May be grieving loss of normal child
Educate family Help family cope with effects of the disorder Prepare child and family for surgery
Remember developmental level of child 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
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Kawasaki Disease
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)
(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
Symptoms of inflammation C reactive protein level ESR
Cardiac symptoms L ventricular function as seen on
Echocardiogram Children do NOT generally have sx of CHF
Other lab changes Anemia Leukocytosis with ‘L shift’
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Kawasaki continued
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 Here is a website with some good
information on the diagnosis and management of this disease: http://www.kdfoundation.org/
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Newburger, J. W. et al. Circulation 2004;110:2747-2771
From the American Heart Association
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Education of parents
Teach parents common signs of Aspirin toxicity while on high doses of ASA Tinnitus Headache Dizziness Confusion
Teach parents to report recurrence of fever
Teach parents CPR Inform parents that final cardiac sequelae
may not be known for some time.
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QUESTIONS