week 8: caring for child and family w CVS, neuro, and MSK dysfunction Flashcards
(73 cards)
1
Q
what are the 2 types of cardiac defects
A
- congenital
- aquired
2
Q
what is congenital cardiac defects
A
anatomic: abnormal function
3
Q
what is acquired cardiac defects
A
disease process
- infection
- autoimmune response
- enviro factors
- familial tendencies
- meds
4
Q
describe congenital heart disease (CHD)
A
- 5 to 8 per 1000 live births
- about 2 or 3 are symptomatic in 1st year of life
- major cause of death in 1st yr of life (after prematurity)
- most common anomaly is ventricular septal defect (VSD)
- often children with CHD have another recognized anomaly (trisomy 21, 13, 18, +++)
5
Q
what are the 4 circulatory changes at birth that are normal
A
- umbilical vein; umbilical arteries
umbilical veins + arteries construct (CUT CORD)
low resistance to high resistance
no blood flowing = clotting - foramen ovale
foramen ovale closes so that blood can no longer move from R atrium to L atrium by-passing pulm arteries
baby lungs working so how blood entering L atrium and pulm arteries doing their job - ductus arteriosus
closes -> ligamentum arteriosus
so blood cannot bypass lungs
lungs in full swing - ductus venosus
b4 fuctus venous closed it was taking oxygenated blood thru umbilical vein (placenta) by passing liver
now blood from portal vein directed into liver -> blood filtered/metabolized
6
Q
for CHD what are the 2 altered hemodynamics
A
acyanotic and cyanotic
7
Q
what are the classification of CHD defects
A
- increased pulmonary blood flow
- decreased pulmonary blood flow
- obstruction to blood flow (out of the heart)
- mixed blood flow (saturated and desaturated blood mix within the heart)
8
Q
in CHD describe the defect of increased pulmonary blood flow defects
A
abnormal connection between 2 sides of heart
- septum or great vessels
- increased BV on R side of heart
- increased pulmonary blood flow
- decreased systemic blood flow
9
Q
what are examples of CHD caused by increased pulmonary blood flow defects
A
- atrial septal defect
- ventricular septal defect
- patent ductus arteriosus
10
Q
describe CHD in particular obstructive defects
A
- blood exiting heart meets area of anatomical narrowing (stenosis) causing obstruction to blood flow
- increased pressure proximal to defect
- decreased pressure distal to obstruction
- usually occurs near valve
11
Q
give examples for CHD caused by obstructive defects
A
- coarctation of aorta
- aortic stenosis
- pulmonic stenosis
12
Q
describe CHD caused by decreased pulmonary blood flow defects
A
- pulmonary blood flow obstructed AND anatomical defect (ASD or VSD) between R and L sides of the heart
blood has difficulty exiting R side of heart
- pressure on R side increases
- allows desat blood to shunt R to L
(results in desat in L side of heart and systemic circulation)
13
Q
give examples of decreased pulmonary blood flow defects causing CHD
A
- tetralogy of fallot
- tricuspid atresia
14
Q
describe CHD - mixed defects
A
fully saturated systemic blood flow mixes with desaturated pulmonary blood flow
- causing relative desat of systemic blood flow
- pulmonary congestion occurs
- CO decreased
15
Q
examples of CHD causing mixed defects
A
- transposition of great arteries or vessels
- total anomalous pulmonary venous connection
- truncus arteriosus
- hypoplastic L heart syndrome
16
Q
describe CHF
(congestive heart failure)
A
- inability of heart to pump adequate amount of blood into systemic circulation
- R or L sided failure
- heart muscle may become damaged if left untreated
17
Q
treatment goals for CHF
A
- relieve symptoms
- decrease morbidity (including risk of hospitalization)
- slow progression of heart failure
- improve pt survival and quality of life
18
Q
nursing care management for CHD
A
- assist in measures to improve cardiac function
- monitor afterload reduction
- decrease cardiac demands
- reduce rep distress
- maintain nutritional status
- prevent infections
- assist in measures to promote fluid loss
- support child and family
19
Q
hypoxemia
A
- can adversely affect every tissue in the body
- state where insufficient o2 to meet metabolic demands
- identified by decreased arterial o2 sat
(hypoxia, cyanosis, polycythemia, clubbing)
20
Q
describe a hypercyanotic episode
A
- severe cyanotic episode
- associated w TOF
- can be spontaneous
- can be precipitated by events associated w decreased systemic vascular resistance
- usually self-limiting
- knee-chest position (increases systemic vascular resistance)
21
Q
is endocarditis congenital or acquired
A
acquired
22
Q
describe endocarditis
1. what are the most common pathogens
2. caused by routine exposure to bacteremia associated w usual daily activities
A
- staphylococcus aureus, streptococcus, fungus
- dental work, invasive procedures involving resp tract; GI/GU tract, cardiac surgery, central lines, IV drug use
23
Q
how does endocarditis manifest clinical (s/s)
A
- unexplained fever, malaise, wt loss
- janeway lesions
- osler nodes
- roth spots
24
Q
describe janeway lesions
A
- nontender erythematous macules on palms and soles
- more common in acute
25
describe osler nodes
- tender subq violet nodules mostly on pads of fingers and toes
26
roth spots
exudative, edematous hemorrhagic lesions of the retina w pale centers
27
treatment of endocarditis
- antibiotics
- prophylaxis in high risk pt
- surgery
28
nursing care for endocarditis
- education
- med admin
- assessments
29
what is hypertrophic cardiomyopathy
- one of the most common forms of inherited cardiomyopathy
- hypertrophy of L ventricle
30
what is cardiomyopathy
refers to abnormalities of myocardium in which the ability of muscle to contract is impaired
- familial or genetic cause
- infection
- deficiency states
- metabolic abnormalities
- collagen vascular disease
- idiopathic
31
clinical manifestations of cardiomyopathy (how would they present to ER)
- s/s of HF - most common <1yr
- may be asymp
- may present w chest pain, syncope, palpitations, HF symptoms, and/or sudden cardiac arrest
- physical exam may be normal
32
cardiomyopathy diagnosis
ECG, exercise testing, cardiac MRI, genetic testing
33
cardiomyopathy treatment
- based on symptoms
- correct the cause; if unable, aim at managing CHF and dysrhythmias
- beta blockers - 1st line
- cautious use of diuretics
- implantable cardioverter/defib
- may need heart transplant
34
nursing care for cardiomyopathy
education + supportive care
35
systemic hypertension
1. primary
2. secondary
1. no identifiable cause
2. identifiable cause - may be curable
36
pediatrics systemic hypertension
hypertension generally secondary to structural abnormality or underlying pathology
- renal disease
- cardiovascular disease
- endocrine or neurological disorders
37
clinical manifestations of HTN
increased BP
sympt in children - headaches, dizziness or lightheadedness, fatigue, blurred vision, chest pain, nosebleeds, SOB
38
treatment of HTN
underlying cause
pharm and nonpharm
39
nursing care for HTN
education
monitoring
40
kawasaki disease + cause
- AKA - mucocutaneous lymph node syndrome
- acute systemic vasculitis affecting medium sized arteries, especially coronary arteries
- unknown cause: self limiting, w fever and manifestations of acute inflammation lasting for 12 days w/o therapy
41
what is the diagnostic criteria for Kawasaki Disease
requires > or equal days of fever plus > or equal of following 5 criteria:
- bilateral bulbar conjunctival injection
- oral mucous membrane changes, including injected or fissured lips, injected pharynx, or strawberry tongue
- peripheral extremity changes, including erythema of palms and soles, edema of hands and feet (acute phase), and periungual
- polymorphous rash
- cervical lymphadenopathy (> or equal 1 lymph node >1.5 cm in diameter)
42
kawasaki disease 3 phases
- acute: onest of high fever, unresponsive to antibiotics and antipyretics
- subacute: resolution of fever and lasts until all clinical signs disappear
- convalescent - clinical signs resolved but lab values are not normal
increased risk of coronary artery aneurysm long term
43
kawasaki disease treatment
treat disease within 10 days w appearance of sympt
- IVIG
- Aspirin
44
kawasaki disease nursing care
- monitor
- fluid balance
- nutrition
45
what are the 3 types of shock
- hypovolemic
- distributive
- cardiogenic
46
3 stages of shock
- compensated shock
- decompensated shock
- irreversible or terminal shock
47
3 managements for shock
ventilation
fluids
improvement of cardiac function
48
cerebral palsy
- group of permanent disorders of the development of movement and postures, causing activity limitations that are attributed to non-progressive disturbances that occured in the developing fetal or infant brain
- characterized by abnormal muscle tone and coordination
- 1.5-3 per 1000 live births
- most common permanent physical disability in childhood
- 15-60% of these children will also have epilepsy
49
etiology of CP
prenatal brain abnormalities
- 80% are caused by unknown brain abnormalities
- intrauterine exposure to chorioamnionitis
- 12% of infants born prior to 36 wks
- periventricular leukomalacia
- results of shaken baby syndrome
50
3 types of CP
1. spastic
2. dyskinetic
3. ataxic
51
spastic CP
increased muscle tone, poor control of posture, balance and coordinated movements
52
dyskinetic CP
- slow, worm-like movements of extremities, trunk, face, and tongue
53
ataxic CP
rapid repetitive movements; wide gait, unable to hold objects
54
diagnostic evaluation of CP
- infants @ risk warrant careful assessment during early infancy
- neurologic examination and history
- neuroimaging
- metabolic and genetic testing
55
possible signs of CP
- poor head control after age 3 mo
- stiff or rigid limbs
- arching back/pushing away
- floppy tone
- unable to sit w/o support at age 8 mo
- clenched fists after age 3 mo
56
possible behavioural signs of CP
- excessive irritability
- no smiling by age 3 mo
- feeding difficulties: persistent tongue thrusting, frequent gagging or choking w feeds
57
CP and IQ
- wide variation
- 30%-50% of CP pts are cognitively impaired
- difficult to assess
- rigid, atonic, and quadriparetic CP have highest incidence of profound impairment
58
Goals of therapy CP
- to establish locomotion, communication, and self-help skills
- to gain optimal appearance and integration of motor functions
- to correct associated defects as effectively as possible
- to provide educational opportunities adapted to the child's capabilities
- to promote socialization experiences
59
therapeutic management of CP
- ankle foot braces may be worn
- ortho surgery to correct spastic deformities
- pharma agents to treat pain related to spasms and seizures
- oral antispastic meds - general spasms
- botulinum A injections - localized spasticity
- baclofen - implanted pump - severely affected who have side effects w oral drugs
- dental hygiene
- physical/occupational therapy
60
nursing care for CP
- assist family
- med admin
- safety
- ADL assistance
- rec activities
61
what is spina bifida
- aka myelomeningocele
- failure of osseous spine to close
- commonly associated w hydrocephalus
62
2 types of spina bifida
1. spina bifida occulta
- not visible externally
2. spina bifida cystica
- visible defect
- saclike protrusion
63
describe muscular dystrophies in children
- largest group of muscular diseases in children
- all have genetic origin w gradual degeneration of muscle fibers, progressive weakness, and wasting of skeletal muscle
- all have increasing disability and deformity w loss of strength
64
Duchenne Muscular Dystrophy (DMD)
- aka pseudohypertrophic muscular dystrophy
- most severe and most common
- X-linked inheritance pattern; 1/3 are fresh mutations
- 1 in 3500 male births
65
characteristics of DMD
- onset btwn 2-7 yrs
- progressive muscle weakness, wasting, and contractures
- calf muscles hypertrophy in most pts
- progressive generalized weakness in adolesence
- death from resp or cardiac failure
66
5 diagnostic evals for DMD
1. creatine kinase
- elevated 1st 2 yrs of life (b4 clinical sympt)
2. EMG
- record electrical pattern in muscle when it is contracting
3. muscle biopsy
- most reliable way to dx DMD - shows what is happening inside the cell
4. DNA test
- leads to exact genetic info
5. display of usual characteristics of the disease
67
clinical manifestations of DMD
- waddling gait, frequent falls, gower sign
- lordosis
- enlarged muscles, especially thighs and upper arms
- profound muscular atrophy in later stages
- varying degrees of mild cognitive impairment
68
therapeutic management of DMD
- no effective treatment established
- primary goal: maintain function in unaffected muscles as long as possible
- ROM, bracing, performance of ADLs, surgical release of contractures prn
- physio
- keeping kid active
- genetic counseling for fam
69
nursing care management
- help child and fam cope w chronic, progressive, debilitating disease
- design program to foster independence and activity as long as possible
- teach kid self-help skills
- appropriate health assistance
70
describe spinal cord injuries
- usually from indirect trauma
- motor collisinos w/o child restraints
- vertebral compression from blows to the head or butt (diving, surfing, falls from horses)
- birth injuries from traction force on spinal cord during breech delivery
- surgeries
71
4 levels of spinal cord injuries
- higher injury: more extensive damage
- paraplegia: complete or partial paralysis of lower extremities
- tetraplegia: lacking functional use of all 4 extremities (formerly called quadriplegia)
- high cervical cord injury affects phrenic nerve, paralyzes diaphragm -> vent dependent
72
therapeutic management of spinal cord injury
stabilization and transport
functional electrical stim
73
nursing care management of spinal cord injury
- stabilization, careful assessment, prevention of complications, maintain max function
- rehab: evaluation and support
