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Pediatrics > perfusion: alterations in pediatric cardiovascular function > Flashcards

perfusion: alterations in pediatric cardiovascular function Flashcards

1
Q

FETAL CIRCULATION STRUCTURES

A
  • 1 umbilical vein , 2 umbilical arteries
  • foramen ovale
  • ductus arteriosus
  • ductus venosus
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2
Q

CHANGES AT BIRTH

A
  • 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
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3
Q

A&P OF PEDIATRIC DIFFERENCES

A
  • 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
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4
Q

ANATOMOY AND PHYSIOLOGY OF PEDIATRIC DIFFERENCES

A
  • 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
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5
Q

CHD:ETIOLOGY

A
  • 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
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6
Q

ETIOLOGY : CHD

A
  • maternal metabolic disorders( hypercalcemia,DM,phenylketonuria)
  • advanced maternal age, maternal viral infection (rubella,coxsackle
  • genetic factors
  • chromosomal abnormalities- sydromes :turner, down, digeorge, marfan
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7
Q

CLASSIFICATION OF CHD

A
  • increased pulmonary blood flow
  • decreased pulmonary blood flow
  • obstructed systemic blood flow
  • mixed defects
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8
Q

INCREASED PULMONARY BLOOD FLOW DEFECTS

A
  • 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
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9
Q

DEFECTS THAT INCREASED PULMONARY BLOOD FLOW

A
  • patent ductus arteriosus PDA
  • atrial septal defect ASD
  • ventricular septal defect VSD
  • atrioventricular can defect AV CANAL
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10
Q

CLINICAL MANIFESTATIONS

A
  • tires during feeding
  • poor weight gain
  • tachypnea, tachycardia
  • murmur
  • CHF
  • diaphoresis
  • periorbital edema
  • freq. resp infections
  • crackles
  • cardiomegaly
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11
Q

PDA : PATENT DUCTUS ARTERIOSUS

A
  • 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
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12
Q

ASD

A
  • 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
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13
Q

VSD

A
  • 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

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14
Q

AV CANAL

A
  • 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
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15
Q

NURSING MANGNAGMENT

A

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
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16
Q

NURSING MANAGEMENT

A
  • maintain oxygenantion and myocardial function
  • administer and monitor prescribed medications
  • promote rest
  • foster development
  • provide adequate nutrition
  • provide emotional support
  • discharge planning and teaching
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17
Q

OUTCOMES OF NURSING CARE

A
  • the child’s pain is effectively managed
  • full lung expansion is achieved with spirometry exercises or chest physiotherapy
  • incision heals without infection
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18
Q

CLINICAL THERAPY FOR CHF

A

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 ?

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19
Q

CLINICAL THERAPY FOR CHF

A

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

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20
Q

DEFECTS THAT DECREASE PULMONARY BLOOD FLOW (CYANOTIC DEFECTS)

A
  • 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
21
Q

TOF

A
  • 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

22
Q

TOF CONTINUED

A

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

23
Q

NURSING MANAGEMENT FOR CHD’S THAT DECREASE PULMONARY BLOD FLOW

A
  • treat hypercyanotic episodes
  • provide post op care
  • assess vitals, pulse ox, perfusion, distal pulses
  • monitor I&O
  • support families
24
Q

MIXED DEFECTS

A
  • infants survival is dependent on mixing of syatemic and pulmonary blood
  • cause varying degrees of cyanosis and CHF
25
Q

TRANSPOSITION OF GREAT ARTERIES

A

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
26
Q

TGA

A
  • 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
27
Q

NURSING MANAGEMENT

A
  • monitor prostaglandin therapy
  • treat hypercyanitic episodes
  • surgery by 1 week of age
  • support families
  • provide post op care
28
Q

DEFECTS THAT OBSTRUCT SYSTEMIC BLOOD FLOW

A
  • 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
29
Q

COARCTATION OF THE AORTA (COA)

A

-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
30
Q

COARCTATION OF THE AORTA (COA)

A
  • 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
31
Q

NURSING MANAGMENT OF COA

A

-see nursing management of defects that increase pulmonary blood flow

32
Q

COMMON DIAGNOSTIC TESTS

A
  • echocardiogram
  • EKG/halter monitor
  • cardiac cath
  • chest x ray
  • CT scan
  • MRI
  • exercise testing
33
Q

COMMON LAB TESTS

A
  • ABG
  • CBC
  • Digoxin level
  • ASO titers
  • ESR,CRP
  • serum lipids
34
Q

NURSING CARE: POST OP OPEN HEART TEACHING

A
  • 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
35
Q

CARDIAC CATHERTERIZATION

A
  • 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

36
Q

CARDIAC CATH

A

-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

37
Q

RHEUMATIC FEVER

A

-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
38
Q

CLINICAL MANIFESTATIONS OF RHEUMATIC FEVER

A

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
39
Q

DIAGNOSIS(JONES CRITERIA)

A

need evidence of preceding strep infection and 2 major manifestations or 1 major and 2 minor

40
Q

MAJOR MANIFESTATIONS

A
  • carditis
  • polyarthritis
  • chorea(involuntary movements)
  • rash
  • subcutaneous nodules
41
Q

MINOR MANIFESTATIONS

A
  • fever
  • arthralgia
  • increased ESR
  • increased CRP
  • prolonged PR interval
42
Q

TREATMENT

A

-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
43
Q

RHEUMATIC FEVER: NURSING MANAGEMENT

A
  • prevention (throat cultures, completion of antibiotic regimen)
  • treatment of streptococcal tonsillitis/pharyngitis
  • monitor temperature
  • bed rest
  • administer medications
  • home teaching
44
Q

KAWASAKI DISEASE

A
  • 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
45
Q

DIAGNOSIS -

A

HIGH FEVER OVER 39c (102.2) FOR 5 DAYS OR LONGER PLUS 4 OUT OF 5 FOLLOWING SIGNS

  1. redness and edema of hands and feet , peeling of skin
  2. dry,cracked lips , strawberry tongue, pharyngeal erythema
  3. conjunctival redness without discharge
  4. macular popular rash on trunk and extremities
  5. cervical lymphadenopathy
46
Q

TREATMENT

A

-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
47
Q

NURSING MANAGEMENT

A
  • assess heart sounds
  • administer medications
  • regulate IVIG infusion- watch for reactions
  • passive ROM for joint movement
  • promote comfort
  • home teaching
48
Q

KAWASAKI DISEASE VS RHEUMATIC FEVER

A

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

Pediatrics (7 decks)

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