Hypoxemia, ARDS, ventilator management Flashcards
1
Q
Hypoxia vs Hypoxemia
A
- Hypoxemia means that O2 carriage (CaO2) is low
- Hypoxia means that O2 delivery (DO2) is low
2
Q
Determination of SpO2, CaO2, DO2
A
- SpO2 is proportional to PaO2 is proportional to [AxDx(P1-P2)]/T
- A is surface area, D is diffusion coefficient, pressure difference, and thickness of alveoli
- CaO2 depends mostly on [Hb] and O2 sat (SpO2), and dissolved O2 (PO2) only matters when there is CO poisoning (decreases functioning Hb)
- DO2 depends on CaO2 and CO
3
Q
Various oxygenation states and their causes
A
- Normoxemic hypoxia: tissues aren’t getting O2 but the SpO2 and Hb are normal
- Seen in heart failure (decreased CO) and embolisms (obstruction)
- Nomoxemic hypoxia w/ normal DO2: tissues are getting O2 but can’t utilize it due to problem w/ oxidative phosphorylation in mitochondria
- Seen in sepsis or cyanide poisoning
- All other causes of hypoxia are hypoxemic hypoxia: problem can be anywhere in the pathways
- Hypoxemic normoxic: anemia, pts arent hypoxic but they have low Hb, or CO poisoning
- They increase CO and therefore DO2 to compensate for the decreased CaO2
4
Q
A-a gradient
A
- Difference btwn alveolar O2 and arterial O2
- Under normal circumstances, PAO2 (alveolar) is 100, and PaO2 (arterial) is 80-100 so a normal A-a difference is 0-20 (depends on age: age+4/4)
- PAO2= 150- (PACO2/.8)
- The 150 depends on atm pressure (760 mmHg), inhaled O2% (FiO2, room air is 21%), and H2O partial pressure (47 mmHg)
- 150= (760-47)x.21
- PACO2 is normally 40, but depends on RR
5
Q
Causes of low PaO2 (hypoxemic hypoxia)
A
- Altitude: normal A-a gradient
- Hypoventilation: normal A-a gradient
- V/Q mismatch (V/Q MM): elevated A-a gradient, responds to supplemental O2
- R-L shunt: elevated A-a gradient, does not respond to supplemental O2
- Diffusion impairment: elevated A-a gradient, responds to supplemental O2
6
Q
Altitude and hypoventilation
A
- There is low inspired O2 b/c the atm pressure is reduced (decreases both PaO2 and PAO2), normal A-a
- In hypoventilation the increase in PCO2 will prevent the PO2 in alveoli from building up
- Therefore there is both low PAO2 and PaO2 in hypoventilation so the A-a gradient is normal
- There is hypercapnia in hypoventilation
7
Q
V/Q MM 1
A
- Can either be no perfusion of a well ventilated zone (increase in dead space, Q problem) or no ventilation in a well perfused zone (increase in shunting, V problem)
- The body responds to this mismatch of blood flow to air flow by vasoconstricting the areas not receiving air and dilating the areas that are receiving air
- This however doesn’t fully rectify the problem since the Hb in capillaries undergoing gas transfer are already saturated
- Therefore there is little compensation by hypoxic pulmonary vasoconstriction
- This means the PO2 will be difference than the PaO2 and the A-a gradient will be widened
8
Q
V/Q MM 2
A
- This gradient will improve when pts are given supplemental O2
- Shunting causes hypoxemia (can’t pick up O2), dead space causes hypercapnia (can’t drop off CO2), pulmonary embolism causes both
- Can indirectly measure dead space by comparing end tidal CO2 to PaCO2 (larger difference means more dead space)
- Hypoxemia from V/Q MM due to decreased SpO2, PaO2, and thus CaO2
9
Q
R-L shunt
A
- Cardiac defect where oxygenated blood from L side passes into the R heart and mixes w/ deoxygenated blood
- The A-a gradient will be widened, since the PO2 will be normal but the PaO2 will be low
- Supplemental O2 will not improve the A-a gradient
- -Hypoxemia from shunting due to decreased SpO2, PaO2, and thus CaO2
10
Q
Diffusion impairment
A
- Normal O2 diffusion takes .25 sec, and an RBC takes .75 sec going thru a pulmonary capillary
- Thus the alveolar wall must be very thick for diffusion to limit gas exchange
- This means that diffusion impairment (i.e. IPF) is usually seen during exercise when the HR is increased
- In the case of diffusion limited hypoxemia, there is a widened A-a gradient and it is improved by giving supplemental O2 (looks like V/Q MM)
11
Q
A-a gradient cutoff
A
- Path of O2 delivery: alveolar ventilation -> diffusion -> CaO2 -> DO2
- A problem in alveolar ventilation will lead to hypoxemia w/ normal A-a gradient (hypoventilation, high altitude)
- Any problem after alveolar ventilation will increase the A-a gradient, since PAO2 is normal but PaO2 is low
- Answer is usually V/Q MM if A-a gradient is widened
12
Q
Pulmonary edema
A
- Fluid extravasates into the alveolar space due to high hydrostatic pressure (cardiogenic), low osmotic pressures (hypoalbuminemia), or increased permeability
- The fluid in alveolar space leads to hypoxemia by V/Q MM and/or diffusion limited mechanisms
13
Q
Cardiogenic pulmonary edema
A
- Usually due to L sided HF, where the pressure backs up into pulmonary capillaries since the L heart can’t expel blood properly
- This is pulmonary venous HTN
14
Q
Non-cardiogenic pulmonary edema
A
- One cause is hypoalbuminemia leading to decreased oncotic pressure
- Another cause is increased capillary permeability
- This is usually accompanied by some level of increased pulmonary venous pressure
- Most common cause for non-cardiogenic pulmonary edema is ARDS (acute respiratory distress syndrome)
15
Q
ARDS
A
- Acute onset of bilateral pulmonary infiltrates (pulm edema on CXR), normal capillary hydrostatic pressure, and a lowered PaO2:FiO2 ratio
- Normal PaO2:FiO2 ratio is 500, and 18 then the pulm edema is due to L sided HF and it is not ARDS
- Damage is to lungs usually in lower lobes
