perfusion: alterations in pediatric cardiovascular function Flashcards
FETAL CIRCULATION STRUCTURES
- 1 umbilical vein , 2 umbilical arteries
- foramen ovale
- ductus arteriosus
- ductus venosus
CHANGES AT BIRTH
- umbilical cord cut= increase systemic vascular resistance
- increased blood and pressure in LA and LV causes foramen ovale to close
- ductus arteriosis constricts and closes in 10-15 hours after birth
A&P OF PEDIATRIC DIFFERENCES
- infants have increased metabolic and oxygen demands, so HR increases to maintain high cardiac output
- infants at increased risk for heart failure because heart is more sensitive to fluid overload
- muscle fibers of heart less developed
ANATOMOY AND PHYSIOLOGY OF PEDIATRIC DIFFERENCES
- decreased compliance- ventricles do not expand well
- stroke volume cannot increase much
- heart fully developed age 5 yrs
- ventricles same size at birth ,but by 2months of age LV is twice size of RV
CHD:ETIOLOGY
- defect in heart or great vessels
- persistence of fetal structure after birth
- most develop in first 8wks of gestation
- caused by exposure to drugs ,alcohol , secondary smoke
ETIOLOGY : CHD
- maternal metabolic disorders( hypercalcemia,DM,phenylketonuria)
- advanced maternal age, maternal viral infection (rubella,coxsackle
- genetic factors
- chromosomal abnormalities- sydromes :turner, down, digeorge, marfan
CLASSIFICATION OF CHD
- increased pulmonary blood flow
- decreased pulmonary blood flow
- obstructed systemic blood flow
- mixed defects
INCREASED PULMONARY BLOOD FLOW DEFECTS
- abnormal connection between two sides of heart
- blood shunts from left to right
- if untreated , pulmonary overcirculation leads to RV hypertrophy, CHF, pulmonary HTN, and eventually death
DEFECTS THAT INCREASED PULMONARY BLOOD FLOW
- patent ductus arteriosus PDA
- atrial septal defect ASD
- ventricular septal defect VSD
- atrioventricular can defect AV CANAL
CLINICAL MANIFESTATIONS
- tires during feeding
- poor weight gain
- tachypnea, tachycardia
- murmur
- CHF
- diaphoresis
- periorbital edema
- freq. resp infections
- crackles
- cardiomegaly
PDA : PATENT DUCTUS ARTERIOSUS
- fetal ductus arteriosus does not close
- common in preterm infants
- blood shunted from the aorta to the PAs and lungs
- may close spontaneously
- IV indomethacin or ibuprofen -10 -14 days of life
- can be closed during cardiac cath with coils and other devices, surgical ligation
- prognosis is god
ASD
- small or large opening in atrial septum
- closure: spontaneous , transcatherter device in cath lab, or surgery - age 4 to 5 years
- prognosis good is ASD is closed
- untreated adults - CHF,pulmonary HTN,atrial arrhythmias
VSD
- opening in ventricular septum
- increased PVR and RV enlargement with large VSD
Clinical closure therapy
-small VSD- may close spontaneously
surgery - patch
closure in cath lab
prognosis- highest risk if repair needed in first few months of life : good prognosis for older children
AV CANAL
- ASD+ VSD +tricuspid and mitral valve defects
- blood moves freely among the 4 chambers
- associated with down syndrome
-severity of symptoms depends on degree of mitral valve regurgitation
- repair: surgical -done in infancy
- may need O2 until surgery
- prognosis: mitral valve insufficiency and arrhythmias are common
NURSING MANGNAGMENT
pre op
-family education, psychosocial support
post op
monitor for complications, impaired perfusion, arrhythmias, infections
- heart sound -bradycardia ,irregular HR
- pulse ox , cap refill, LOC, urine output, pedal pulses
- monitor vital signs , inspect incision site
- assess respiratory system, breath sounds signs of distress , pneumonia
- pain assessment
- manage fluids and nutrition
NURSING MANAGEMENT
- maintain oxygenantion and myocardial function
- administer and monitor prescribed medications
- promote rest
- foster development
- provide adequate nutrition
- provide emotional support
- discharge planning and teaching
OUTCOMES OF NURSING CARE
- the child’s pain is effectively managed
- full lung expansion is achieved with spirometry exercises or chest physiotherapy
- incision heals without infection
CLINICAL THERAPY FOR CHF
GOAL: make heart work more efficiently and remove excess fluid
Diuretics: remove accumulated fluid and sodium
-monitor potassium
ACE inhibitors- lessen workload of heart by decreasing peripheral vascular resistance
-Iomotropics
Digoxin- improves contractility and increases cardiac output
Hold dig for ?
CLINICAL THERAPY FOR CHF
beta blockers
- improves cardiac function
- propananolol, carvedilol
oxygen
-improve tissue oxygenation
surgery or cardiac catheterization to correct CHD
supportive treatment - rest , fluid and dietary management
DEFECTS THAT DECREASE PULMONARY BLOOD FLOW (CYANOTIC DEFECTS)
- little or no blood reaches lungs to get oxygenated
- causes increased pressure on right side of heart, leading to right to left shunting if a septal opening exists
- polycythemia increased risk for thromboembolism
- cyanotic episodes with feeding ,crying ,exercise
TOF
- FOUR DEFECTS: pulmonary stenosis,right ventricular hypertrophy, VSD,overriding aorta
- PS impedes the flow of blood to the lungs
- elevated right heart pressure causes right to left shunt
- increase workload on the RV causes it to hypertrophy
The aorta receives blood from both the RV and LV
TOF CONTINUED
CLINICAL MANIFESTATIONS -depends on the size of the PS
-systolic murmur, cyanosis , polythemia, poor growth, clubbing of fingers and toes, exercise intolerance, squatting
CLINICAL THERAPY:
- repair- surgical by 6 months of age
- may have B-T shunt first to delay total repair
- management of hypercyanotic episodes
PROGNOSIS:
improve quality of life- may have arrhythmias and right ventricular dysfunction
NURSING MANAGEMENT FOR CHD’S THAT DECREASE PULMONARY BLOD FLOW
- treat hypercyanotic episodes
- provide post op care
- assess vitals, pulse ox, perfusion, distal pulses
- monitor I&O
- support families
MIXED DEFECTS
- infants survival is dependent on mixing of syatemic and pulmonary blood
- cause varying degrees of cyanosis and CHF
TRANSPOSITION OF GREAT ARTERIES
PARALLEL CIRCULATION
-life threatening at birth
- pulmonary artery leaves the L ventricle and the aorta exits from the R ventricle
- must have PDA or septal defect to permit blood flow
- clinical manifestations- cyanosis, hypoxia ,CHF, mumur,tachypnea, slow feeder
TGA
- prostaglandins E1 to maintain PDA
- ballon atrial septostomy to enlarge foramen ovale (creates ASD)
- arterial switch - resect and reanastomose great vessels (within first week of life)
- other procedures possible, depending on defect
- prognosis: survival impossible without surgery
- 97% survival age 20 years
- few complications with arterial switch,many problems like arrhythmias occur with old surgical procedures
NURSING MANAGEMENT
- monitor prostaglandin therapy
- treat hypercyanitic episodes
- surgery by 1 week of age
- support families
- provide post op care
DEFECTS THAT OBSTRUCT SYSTEMIC BLOOD FLOW
- increase workload on left ventricle of the heart, leading to decreased cardiac output
- low cardiac output leads to decrease pulses, decrease urine output, sluggish cap refill
- blood backs up into LA and then lungs -CHF
COARCTATION OF THE AORTA (COA)
-narrowing or constriction of the descending aorta, obstructing systemic blood flow
- clinical manifestations
- constriction is progressive; 20-30% develop CHF by 3 months
- blood pressure higher in arms than legs
- weak femoral or pedal pulses
- weakness in the legs after exercise
- systolic murmur
COARCTATION OF THE AORTA (COA)
- CLINICAL THERAPY -NBs may need prostaglandin
- may need to threat CHF before surgery
- repair: surgical reapir preferred over dilation with balloon during cardiac cath
- prognosis coarct may reoccur, persistent HTN is common, lifelong follow -up required
NURSING MANAGMENT OF COA
-see nursing management of defects that increase pulmonary blood flow
COMMON DIAGNOSTIC TESTS
- echocardiogram
- EKG/halter monitor
- cardiac cath
- chest x ray
- CT scan
- MRI
- exercise testing
COMMON LAB TESTS
- ABG
- CBC
- Digoxin level
- ASO titers
- ESR,CRP
- serum lipids
NURSING CARE: POST OP OPEN HEART TEACHING
- sternal precautions- do not lift child under the arms, one hand under head and one under hips
- car seat- protect incision with blanket
- sponge bathe until steri-strips off
- activity as tolerated ,no rough play
- no back packs
- antibiotic prohhlaxis if prosthetic heart valve
- no live vacines for 6 months , if RBC transfusion
CARDIAC CATHERTERIZATION
- catheterization used to create atrial septostomy or dilate narrowing (balloon)
- stent can keep PDA open
- coil used to close PDA or other vessels
-preop:
dental disease
respiratory illness
diaper rash
CARDIAC CATH
-post op : monitor for:
-perfusion, bleeding, arrhythmia, infection
-check under leg for bleeding
-maintain pressure dressing for 4 hours
-lie with leg straight for 6 hours (may need leg board)
-assess dressing
Q 5MIN x3
Q 15MN x4
Q 1 HR x 3-4
RHEUMATIC FEVER
-inflammatory disorder of connective tissue after infection by group A beta-hemolytic streptococci
example: post strep throat
- affects joints, skin,brain,serous surfaces, and heart
- rheumatic heart disease
- most common complication of RF
- damage to valves as result of RF
- may lead to permanent aortic or mitral valave damage
CLINICAL MANIFESTATIONS OF RHEUMATIC FEVER
may appear 1-3 weeks after an untreated strep in fection
- Heart - new murmur, carditis involving mitral or aortic valve, results in valve damage
- Joints- inflamed, painful (polyarthritis)
- Skin- rash with pink macules and blanching in the middle of the lesion (erythema marginatum)
- Brain- chorea
aimless movements of extremities , facial grimacing
DIAGNOSIS(JONES CRITERIA)
need evidence of preceding strep infection and 2 major manifestations or 1 major and 2 minor
MAJOR MANIFESTATIONS
- carditis
- polyarthritis
- chorea(involuntary movements)
- rash
- subcutaneous nodules
MINOR MANIFESTATIONS
- fever
- arthralgia
- increased ESR
- increased CRP
- prolonged PR interval
TREATMENT
-antibiotics to eradicate strep infection
penicillin G - IM x1
penicillin V- oral x 10 days
sulfa- oral x 10 days
erythromycin (if allergic to above)- oral x 10 days
- aspirin to treat carditis , joint inflammation, fever
- steroids
- long term antibiotic prophylaxis
- most children recover fully
RHEUMATIC FEVER: NURSING MANAGEMENT
- prevention (throat cultures, completion of antibiotic regimen)
- treatment of streptococcal tonsillitis/pharyngitis
- monitor temperature
- bed rest
- administer medications
- home teaching
KAWASAKI DISEASE
- acute febrile illness associated with systemic vasculitis
- unknown etiology affecting children younger than 5 yrs
- often preceded by an upper respiratory tract infection
- seen in all races but more common in Japanese
- serious complications include coronary artery dilation and aneurysms
DIAGNOSIS -
HIGH FEVER OVER 39c (102.2) FOR 5 DAYS OR LONGER PLUS 4 OUT OF 5 FOLLOWING SIGNS
- redness and edema of hands and feet , peeling of skin
- dry,cracked lips , strawberry tongue, pharyngeal erythema
- conjunctival redness without discharge
- macular popular rash on trunk and extremities
- cervical lymphadenopathy
TREATMENT
-intravenous immuniglobin (IVIG) ans aspirin reduces the incidence of coronary lesions by 5%
- standard therapy - a single dose of 2g/kg IVIG infused
- acute phase aspirin is administred as anti-inflammatory at 80 to 100mg/kg/day every 6 hours
- once fever has resolved aspirin is reduced to the anti -thrombotic dose of 3 to 5 mg/kg/day as a single daily dose
NURSING MANAGEMENT
- assess heart sounds
- administer medications
- regulate IVIG infusion- watch for reactions
- passive ROM for joint movement
- promote comfort
- home teaching
KAWASAKI DISEASE VS RHEUMATIC FEVER
KAWASAKI
-inflammatory process
-diagnosed by fever for 5 days plus 4/5 criteria
conjunctivitis, enlarged lymph nodes, swollen, peeling hand and feet, erythema of throat with strawberry tongue and cracked lips
- treated with IVIG
- affects coronary arteries
RHEUMATIC FEVER
- post strep infection
- diagnosed by jones criteria
- treated with antibiotics
- affects valves of the heart
