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Sequelae of Bed Rest
4-5% muscle strength loss each week
Tachycardia, decreased SV, CO, peak O2 uptake, orthostatic tolerance after 24 hours of bed rest
Shift towards fast twitch glycolytic
Insulin resistance, hypertriglyceremia, ectopic fat storage, decreased HDl cholesterol
Increased risk of delirium, CIPNM, and weakness
Benefits of early mobilization
earlier DC, improved respiratory function, reduced wasting/re-admission and mortality
CI for therapy for those with mechanical ventilation
MAP <65 or >120
Brady/tachycardia
RR <5 or >40
SpO2 <88%
ICP >20
Active GI blood loss, MI, procedure, insecure airway, agitation longer than 30m
Adaptations in fetal CVP
Placenta pools oxygenated blood and umbilical vein brings O2 towards but bypasses liver via the ductus venosus into the IVC
Alveoli are filled with fluid (low o2) which leads to hypoxic pulmonary vasoconstriction (increase resis in lungs, pulmonary arterial pressure, RV pressure, RA pressure)
Blood can enter LA from RA via foramen ovale
Ductus arteriosus blood from pulmonary artery → descending aorta →internal iliac arteries → umbilical arteries → placenta (low resistance pathway)
Surfactant
at 22wks, production occurs and is stored into lung cells
Endocrine adaptations
At birth, catecholamines (BP increase) increase and ventilation causes alveolar stretch
Cortical progressively increases from 30-36wks and rapid increase at birth to activate sodium pump to clear fetal lung fluid
What occurs during post-delviery
Placenta removed and lungs take in air
Umbilical cord is cut (increases resistance)
Lungs change from fluid to air (sodium pump allows for fluid to enter interstitial space; arterioles near alveoli dilate due to increased O2 → decreased RV/RA/pulmonary artery pressure and increased LA pressure, foramen ovale closes) (ductus arteriosus constricts due to lack of PGE from placenta; fully closed by 2-3wks)
What happens to adaptations post birth
Umbilical vein → ligamentum teres hepatis
Ductus venosus → ligamentum venosum
Foramen ovale → fossa ovalis
Umbilical Arteries → medial umbilical ligaments
Ductus arteriosus → ligamentum arteriosum
Patent Ductus Arteriosus
S/S: tachycardia, ejection systolic murmur, bounding pulse, increased respiratory distress, poor weight
Persistent opening of aorta
Patent Foramen Ovale
Venous thrombus may cross PFO into LA and enter systemic circulation (paradoxical embolism)
Present in 25% of adults; problem if clot forms
Endocardial Cushion Defect (ECD)
walls of chambers of heart are poorly formed/absent
Malformation of atrioventricular valves
Complete: involves atrial septal defect (ASD) and ventricular septal defect (VSD) - one large valve present
Partial: only an ASD or VSD - two valves but one is clefted
Surgery req <1y
Tetrology of Fallot
VSD, RV outflow obstruction, RV hypertrophy, aortic override → mixing of oxy and deoxy blood in LV via VSD and preferential flow of mixed blood through aorta because of obstruction to pulmonary valve
Cyanosis and crying/agitated
Pharm to maintain patency of ductus arteriosus to incre pulmonary BF
Respiratory Distress Syndrome
Due to lung immaturity, insufficient # of alveoli or surfactant (increased work of breathing and failure)
Most common in premie
Bronchopulmonary Dysplasia (BPD)
develops after chronic inury to lung with insufficiency healing (o2 toxicity and damage from mechanical ventilation) → inflammation, pulmonary edema, fibrosis
long term O2 therapy, decreased growth, increase neuro sequelae
Meconium aspiration syndrome
Respiratory distress in full term neonate born through meconium stained amniotic fluid (gasping prior to delviery or postnatal breaths)
→Peripheral airway blocked (atelectasis, pneumothorax, pulmonary HTN, BPD)
Cystic Fibrosis
Complex autosomal recessive disorder
S/S: chronic productive cough, abnormal x-ray, viscous mucus and impaired mucociliary transport, nasal polyps, digital clubbing, Na loss
→ chronic lung infections, fibrosis/bronchiectasis, nocturnal hypoxia
Cerebral Palsy
Altered respiratory mechanics, hypoventilation, clearing secretions, increased WOB, impaired phonation, aspiration, low physical activity
Down’s
1/3-1/2 have ECD, VSD, ASD, or tetralogy of fallot
Hypotonia (trunk tone reduced clearance; medullary compression from AA instability), delay in motor skills, hearing loss, cognition
Muscular Dystrophy
Duchenne’s: respiratory weakness and increased cardiac involvement with age (cardiomyopathy, arrhythmias, ECG, sudden death)
Becker’s: cardiac involvement earlier in life
Spinal Muscular Atrophy (SMA)
degeneration of anterior horn cells (LMN and progressive muscular atrophy)
ASD and VSD present
Weakness, contractures, fasciculations, scoliosis
Intervention Considerations
Elongation may not occur after physiological flexion and diaphragm may be impaired
Avoid Trendelenburg with reflux
Percussion with one hand for small children
With impaired ventilation (posterior pelvic tilt enhances diaphragm whereas prone improves ventilation to posterior lobe segments)