111414 atelectasis and ARDS Flashcards
atelectasis
collapsed portion of or entire lung
types of atelectasis
resorption
compression
loss of surfactant (neonatal)
contraction
resorption atelectasis
COMPLETE airway obstruction in bronchi, subsegmental bronchi, or bronchioles
prevents air from reaching alveoli
resorption of air trapped in distal airspaces through pores of Kohn, leading to collapse
what is the most common cause of fever 24-36 hrs after surgery?
resorption atelectasis from mucus plug
findings for resorption atelectasis
ipsilateral deviation of trachea
ipsilateral diaphgramatic elevation
absent breath sounds and absent vocal vibratory sensation (tactile fremitus)
collapsed lung doesn’t expand on inspiration
compression atelectasis
air or fluid accumulation in pleural cavity–increased pres collapses underlying lung
findings for compression atelectasis
trachea and mediastinum shift away from the atelectatic lung
surfactant synthesis is moedulated by different hormones–give ex
cortisol and thyroxine: increase surfactant synthesis
insulin: decreases surfactant synthesis
neonatal atelactasis
respiratory distress syndrome in newborns
decreased surfactant in fetal lungs (prematurity, maternal diabetes, cesarean section)
histology findings for neonatal atelectasis
collapsed alveoli lined by hyaline membranes
clinical findings for neonatal atelectasis
respiratory distress within few hrs of birth
hypoxemia and respiratory acidosis
ground glass appearance on CXR
how does hyaline membrane develop in atelectasis?
hypoxemia and CO2 retention lead to acidosis, leading to pulm vasoconstriction, leading to pulm hypoperfusion, leading to endothelial damage and epithelial damage and plasma leaking into alveoli. fibrin and necrotic cells make hyaline membrane
contraction atelectasis
fibrotic changes in lung or pleura prevent full expansion
irreversible
acute lung injury
endothelial or epithelial injury, initated by numerous factors
manifestations of acute lung injury
pulmonary edema (less severe form) diffuse alveolar damage (acute respiratory distress syndrome)--more severe
pulmonary edema-two mechanisms
alterations in Starling pressure
microvascular or alveolar injury–increase in capillary permeability (infections, aspiration, drugs, trauma, high altitude)
ARDS
noncardiogenic pulmonary edema resulting from acute alveolar-capillary damage (can be direct or indirect lung injury)
risks for ARDS
gram negative sepsis
gastric aspiration
severe trauma
pulm infections, heroin, smoke inhalation
clinical findings of ARDS
dyspnea
severe hypoxemia NOT responsive to O2 therapy
respiratory acidosis
pathogenesis of ARDS
alveolar macrophages and other cells release cytokines (neutrophil chemotaxis, transmigration of neutrophils from capillaries to alveoli, leakage of protein/fibrin rich exudate forming hyaline membranes, damage to pneumocytes causing surfactant deficiency leading to atelectasis)
acute injury to alveolar epithelial or endothelial cells
if survive the above, get repair by type 2 pneumocytes
if survive further, then get progressive interstitial fibrosis
time line post injury for ARDS
edema-1-3 days post
hyaline membrane-1 day post and continues
these two are the exudative stage
proliferative stage:
insterstitial inflammation
interstitial fibrosis
