ARDS

Question 1

What happens to respiration in airspace filling diseases in general?

Answer 1

(similar to atelectasis - collapsed alveoli)

• Dec airspace that can actually participate in gas exchange = smaller effective volumes (dec FVC and TLC)
• Less ventilation –> low V/Q areas (SHUNT) –> low PaO2, inc A-a gradient, hypoxemia
• High V/Q area always co-occur (DEAD SPACE) & limited Vt = higher VD/VT
• Compensate by inc RR (if weak muscles, fatigue, cannot comp –> hypercapnia)
• Dec compliance (requires more pressure for same change in vol) - higher lung elastic forces
• Inc work of breathing

Question 2

ARDS Diagnosis (4)

Answer 2

• 1- Bilateral alveolar opacities on chest X-ray
• 2- Resp failure not explained by cardiogenic pulmonary edema (do echo - rule out CHF)
• 3- Dec PaO2/FIO2 ratio < 300 (so dec oxygen transfer)
• 4- ACUTE onset w/ apparent trigger (w/in 1 wk of clinical insult)

Question 3

ARDS Risk Factors (6)

Answer 3

• Pneumonia (**most common)
• Extra-pulmonary sepsis
• Aspiration of gastric contents (acid in airway or vomit –> aspirate)
• Severe, acute pancreatitis
• Major trauma/ burn
• Emergency surgery

Question 4

3 Phases of ARDS (+histo of ea)

Answer 4

• Exudative Phase - (acute) - capillary endothelial injury/alveolar endothelium injury, inc permeability, inflammatory cels and protein-rich edema in alveoli and interstitium, hyaline membranes (homogenous, eosinophilic and right on alveolar septa - fibrin and RBC debris)
  
  • “DAD” - diffuse alveolar damage (all 3 layers - not all alveoli)
  • NO NEUTROPHILS
• Proliferative Phase - (sub-acute) - cellular repair type II cells proliferate (see hyperplasia), fibroblasts and collagen deposition
• Chronic Phase - (late) - resolution of acute inflammation; alveolar macrophages replace neutrophils, fibroblast proliferation FIBROSIS (+/-)
  
  • If fibrosis - then see honeycomb lung, traction bronchiectasis, possible bronchial squamous metaplasia

Question 5

ARDS Prognosis

Answer 5

• Usually recover baseline spirometry @ 6 mo but may not recover physical function
• Gas diffusion impairments for 12 mo + if fibrosis
• <50% return to work after 1 yr

Question 6

Pathophysiology of ARDS

Answer 6

• Non-hydrostatic edema in some alveoli and some atelectasis (surfactant protein damage) –> V/Q mismatch (shunt) –> hypoxemia
• Unaffected areas of lung become high V/Q areas (dead space) - inc VD/VT
  
  • If cannot comp w/ inc RR –> hypercapnia
• Interstitial edema and surface tension - dec compliance

Question 7

How does mechanical vent affect ARDS?

Answer 7

• Mech Vent - Inc FIO2
  
  • Improves low V/Q areas of partially affected lung
  • Does not improves areas of complete shunt (cannot accept any air)
• PEEP - open atelectasis and dec fraction of lung w/ low V/Q
  
  • Pros - targeting the partially affected lung; recruit more alveoli for gas exchange by opening more alveoli previously collapsed; less V/Q mismatch and less VD/VT
  • Cons - barotrauma of normal lung areas (too much pressure) and can inc dead space here b/c more ventilation than perfusion here AND dec CO b/c less venous return

Question 8

How do you deal w/ hypercarbia in ARDS?

Answer 8

• Normally one would inc VT or inc RR but evidence of trauma from repeated opening–closing (inc mortality if high vent tidal volumes)
• “permissive hypercapnea” - prioritize maintaining low tidal vol to correcting acidemia

Question 9

4 Non-Vent Strategies for ARDS

Answer 9

• 1- Neuromuscular Blockade (paralysis) to dec oxygen consumption; more venous oxygen content –> inc PaO2 for oxygen delivery to critical tissues
• 2- Prone Position - put pt on stomach to change perfusion distribution - more blood flow to anterior/upper lobes
  
  • Makes sense b/c lower lobes have most shunt
• 3- Fluid Restriction - avoid adding hydrostatic edema to already existing non-hydrostatic edema
• 4- If severe … ECMO (extracorpeal membrane oxygenation) bypass