111414 atelectasis and ARDS

Question 1

atelectasis

Answer 1

collapsed portion of or entire lung

Question 2

types of atelectasis

Answer 2

resorption
compression
loss of surfactant (neonatal)
contraction

Question 3

resorption atelectasis

Answer 3

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

Question 4

what is the most common cause of fever 24-36 hrs after surgery?

Answer 4

resorption atelectasis from mucus plug

Question 5

findings for resorption atelectasis

Answer 5

ipsilateral deviation of trachea
ipsilateral diaphgramatic elevation
absent breath sounds and absent vocal vibratory sensation (tactile fremitus)
collapsed lung doesn’t expand on inspiration

Question 6

compression atelectasis

Answer 6

air or fluid accumulation in pleural cavity–increased pres collapses underlying lung

Question 7

findings for compression atelectasis

Answer 7

trachea and mediastinum shift away from the atelectatic lung

Question 8

surfactant synthesis is moedulated by different hormones–give ex

Answer 8

cortisol and thyroxine: increase surfactant synthesis

insulin: decreases surfactant synthesis

Question 9

neonatal atelactasis

Answer 9

respiratory distress syndrome in newborns

decreased surfactant in fetal lungs (prematurity, maternal diabetes, cesarean section)

Question 10

histology findings for neonatal atelectasis

Answer 10

collapsed alveoli lined by hyaline membranes

Question 11

clinical findings for neonatal atelectasis

Answer 11

respiratory distress within few hrs of birth
hypoxemia and respiratory acidosis
ground glass appearance on CXR

Question 12

how does hyaline membrane develop in atelectasis?

Answer 12

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

Question 13

contraction atelectasis

Answer 13

fibrotic changes in lung or pleura prevent full expansion

irreversible

Question 14

acute lung injury

Answer 14

endothelial or epithelial injury, initated by numerous factors

Question 15

manifestations of acute lung injury

Answer 15

pulmonary edema (less severe form)
diffuse alveolar damage (acute respiratory distress syndrome)--more severe

Question 16

pulmonary edema-two mechanisms

Answer 16

alterations in Starling pressure
microvascular or alveolar injury–increase in capillary permeability (infections, aspiration, drugs, trauma, high altitude)

Question 17

ARDS

Answer 17

noncardiogenic pulmonary edema resulting from acute alveolar-capillary damage (can be direct or indirect lung injury)

Question 18

risks for ARDS

Answer 18

gram negative sepsis
gastric aspiration
severe trauma
pulm infections, heroin, smoke inhalation

Question 19

clinical findings of ARDS

Answer 19

dyspnea
severe hypoxemia NOT responsive to O2 therapy
respiratory acidosis

Question 20

pathogenesis of ARDS

Answer 20

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

Question 21

time line post injury for ARDS

Answer 21

edema-1-3 days post
hyaline membrane-1 day post and continues
these two are the exudative stage

proliferative stage:
insterstitial inflammation
interstitial fibrosis