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Pulmonology Quiz 2c

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eem8u's version from 2016-11-15 11:19

Pulmonary Edema & ARDS

Question Answer
Starling Forces (F)F= K(Pc - Pis) - σ (COPc - COPis) , σ is reflection coefficient (correction factor
pulmonary capillary pressure(7 mm Hg)
peripheral tissue capillary pressure17 mm Hg
interstitial fluid P in lungs, compare to periphery- 8mmHg (more negative)
colloid osmotic P of IS, compare to periphery15 mmHg (double that of periphery)
normal net starling forces & volumeOUTWARD FILTRATION 20mL/h
normal colloid osmotic pressure of capillary28
interstitial fluid prevented from > alveolus viaTIGHT Jx
outward movement is -/+?POSITIVE
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Causes of Pulmonary Edema
Question Answer
increased Pc viaL-sided heart failure/mitral valve disease
cardiogenicL-sided heart failure (pc increase)
increase Kbarriers broken down /increased permeability = “noncardiogenic”
decreased COPc(maintain build inwards) via hypoalbuminemia
why is hypoalbuminemia more likely to cause edema in the peripheryb/c pulm capillaries are more permeable — low COPc is also low COPic
decreased lymph drainage caused byincrease central venous pressure (backup) or obstruction (e.g lymphangitis carcinomatosis)
how does COPis fx as an edema safety measure (and when is this compromised)COPis decreases w/ filtration (protein becomes more dilute )— comp. when permeability increased
***edema begins at Left atrial pressure of20-25 mmHg
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Acute Respiratory Distress Syndrome (ARDS)
Question Answer
4 main characteristicsNoncardiogenic (increased permeability) edema, hypoxemia, lung inflammation, decreased lung compliance
4 diagnostic criteriatiming, chest imaging, hypoxemia, origin
timingwithin one week of precipitant
****chest imaging shows, CXR vs CTBILATERAL opacity (not fully explained by effusions/lung collapse or NODULE) - CT will show HETEROGENEITY
***hypoxemia - Pao2/Fio2 ratioPaO 2 /FIO 2 ratio < 300 mm Hg with PEEP (positive end-­‐expiratory pressure) ≥ 5 cm H 2 0
origin of edemaNot explained by cardiac failure or fluid overload >> absence of left atrial HTN no longer req'd for diagnosis
P:F ratio measuresgas exchange (lower - worse) Pao2/Fio2 ratio
Pao2/fio2 ratio of mild/moderate/severe≤ 300 mm Hg but > 200 mg Hg (mild) — ≤ 200 mm Hg but > 100 mg Hg (moderate) — PaO 2 /FIO 2 ≤ 100 mm Hg
risk range and explanation of hyperoxiaFio2 > 0.7 b/c generation for free radicals/superoxide
toxic inhalation agentssmoke, chlorine, ammonia, phosgene
most common cause ARDSsepsis
clinic symptoms 4TACHYPNEA = RESPIRATORY DISTRESS / possible cough/chest pain / cyanosis / rales
Tx1) underlying disorder 2) gas exchange support while lungs are healing 3) supportive care (esp for sepsis)
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Pathogenesis/Patholophysiology of ARDS
Question Answer
4 pro-inflammatory cytokines released upon injuryTNF, IL1 / 6 / 8
ARDS & surfactantfunction lost - 1) injury to type II and 2) leaked proteins interfere with function
hyaline membrane developmentendothelium damage > passage of cells > membrane on the inside of the alveolus
****histologic patter of ARDSDAD (diffuse alveolar damage)
exudative stage (timing, histology, fea.)5-7 days, HYALINE membrane (protein rich edema) / neutrophils & fibrin in interstitium & air space / hemorrhage /
proliferative stage (timing, histology, fea.) 7-14 days, type II hyperplasia /obliterations of pulmonary vessels /less neutrophils/ FIBROBLASTs (indicating proliferation)
fibrotic stage (timing, histology, fea.)> 14 days, **FIBROSIS /scar tissue >> reorganization & thrombi (some people do not progress here)
hyaline membrane comprised ofplasma proteins/ fibrin / cellular debris
process of edema removalNa+/Cl- active transport across epithelial ion channels (I and II pneumoncytes) / Na+ also through Na/K ATPase (type II) >> water follows through aquaporins / protein through diffusion & endocytosis / macrophages
****hypoxemia results fromSHUNT — low v/q due to alveolar flooding
possible sequelae of inactived/insufficient surfactantatelectasis/ alveolar collapse
****risk of positive airway pressureVASCULAR compression (pulmonary HTN) > exacerbate
compliance hysteresis FRC in ARDScompliance decreased, hysteresis increased, FRC decreased (b/c of alveoli collapse)
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Mechanical Ventilation
Question Answer
calculate PLPl = Palv- Pol (expand lungs>> breathing by increasing Palv or decreasing Pol)
negative pressure breathing occurs, Palv levelsNORMALly - when Ppl becomes more negative w/ inspiration (Palv = o at end of inspiration and expiration)
positive pressure breathing occurs, Palv levelsEndo tube - Palv + at end of inspiration (prevent alveoli collapse)
volutrama and prevention(ventilator-induced injury) - overdistenion of lung, pv w/ low Vt
barotrauma and prevention(ventilator-induced injury) “causing things to pop”, pv by limiting airway pressures
atelectrauma and prevention(ventilator-induced injury) SHEAR STRESS of repeated opening/closing of acinus, pv with PEEP
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Neonatal RDS
Question Answer
differentiation of type II pneumocytes begins at20 weeks
****surfactant stored inlamellar bodies (seen first at 20 weeks)
surfactant expressed at3rd trimester/ 24-26 weeks
2 causes of surfactant-related RDdecreased production / reduced activity (b/c of different composition)
signs of respiratory distress (5)tachypnea /nasal flaring (decreases resistance), grunting, retractions, cyanosis
Txantenatal corticosteroids for preterm risk, PPventilation, exogenous surfactant
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