Week 1: Hypoxemic respiratory failure

Question 1

Hypoxemia vs hypoxia

Answer 1

• hypoxemia: low oxygen in the blood. Defined by Oxygen carriage
• hypoxia: lack of adequate oxygen at the tissue level

Question 2

oxygen carriage

Answer 2

CaO2=1.35[Hb] x SpO2+ 0.003x PaO2

• CaO2=carriage of O2 in blood (mL O2/mL blood)
• SpO2=% saturation of hb
• Adequate oxygen delivery when PaO2>60 and SpO2>90%

Question 3

Oxygen Delivery

Answer 3

DO2=CO x CaO2
CO=cardiac output=SVx HR
in units of ccO2/min

Question 4

Categories of hypoxia

Answer 4

1. normoxemic hypoxia with normal DO2 (normal carriage and delivery)
   - sepsis, salicylate toxicity, cyanide toxicity
2. Normoxemic hypoxia with low DO2
   - lower Cardiac output state, embolic phenomena
3. Hypoxemic hypoxia with low DO2
   - all else

Question 5

Causes of hypoxemia

Answer 5

1. High altitude
   - normal A-a gradient
   - decreased PinspO2, Patm lower
2. hypoventilation
   - normal A-a gradient
   - high PACO2 and low PAO2
3. diffusion abnormality
   - lower PaO2, higher T (membrane thickness)
   - will respond to suppO2
4. Shunt
   - high A-a gradient
   - supp O2 won’t improve b/c V:Q=0
5. Ventilation-perfusion (V/Q) mismatch
   - high A-a gradient
   - lower CaO2, SpO2, PaO2
   - pulmonary vasoconstriction tries to rectify by diverting bloodflow to better ventilated areas
   - can be overcome by SuppO2

Question 6

Hypoxemia algorithm

Answer 6

1. Elevated A-a gradient
   a. doesn’t correct with O2
   - shunt
   b. corrects with O2
   - CXR: patchy –V/Q mismatch
   - CXR: diffuse–diffusion impairment
2. normal A-a gradient
   a. no hypercapnia –high altitude
   b. yes hypercania–hypoventilation

Question 7

Pulmonary Edema

Answer 7

governed by Starling mechanism

1. Cardiogenic (increased Pc)
   - pulmonary venous hypertension, most commonly caused by problematic left heart
2. Non-cardiogenic
   - normal hydrostatic pressure
   - usually from increased capillary permeability
   - e.g. pregnancy-low oncotic pressure, slightly high hydrostatic pressure
   - ARDS

Question 8

3 characteristics of ARDS

Answer 8

1. Acute onset
2. bilateral pulmonary infiltrates on CXR
3. PaO2: FiO2 ratio<200 (normal ~500)

Question 9

Pathogenesis of ARDS

Answer 9

1. inhalation or toxic injuries
   - alveolar epithelial cells release cytokines that increase capillary permeability, cause exudation of fluid into alveolar spaces and chemotaxis of PMNs and fibroblasts
   - causes destruction and fibrosis
2. Endogenous: sepsis or pancreatitis
   - circulating humoral mediators increase endothelial cell permeability with resultant fluid exudation, cellular chemotaxis, alveolar epithelial damage with fibrosis
   - Il-1B, Il-6, Il-10, TNF-a, TGF-1

Question 10

Pathology of ARDS

Answer 10

1. Exudative phase
   - diffuse alveolar damage
   - hyaline membranes (collection of fluid, fibrin, cellular debris which line alveolar ducts and spaces)
   - Type I pneumocyte damage
2. Fibroproliferative phase (starts day 5-7)
   - cellular infiltrate (fibroblasts)
   - type II pneumocyte hyperplasia
   - collagen deposition

Question 11

Causes of ARDS

Answer 11

• pneumonia
• sepsis
• aspiration
• inhalation
• medications
• pancreatitis
• trauma
• idiopathic

Question 12

Treatment of ARDS

Answer 12

• supportive
• treat underlying cause
• high PEEP ventilation
• low tidal volume ventilation
• (prevent shear stress, volutrauma, barotrauma on ventilation)
• conservative fluid management