Lecture 28 - Review and Clinical Cases Flashcards
(57 cards)
With V/Q imbalance (<1), what will be the arterial PaCO2? How come? What about PaO2?
Normal at 40 because signals to the brain will cause hyperventilation
PaO2 will rise a little, but still hypoxemia
Minute ventilation of V/Q imbalance?
High due to compensatory hyperventilation
How would the A-a gradient due to anatomic shunt vary if PiO2 is increased? Why?
Increased because the gradient represents a % of blood that is not coming in contact with working alveoli and the PaO2 will be much higher than 100 mmHg like at room air
How to distinguish between the 5 causes of hypoxemia?
- Low inspired PiO2
- Hypoventilation
- Diffusion limitations
- Shunt
- V/Q imbalance
- If PaCO2 is high then there HAS TO BE hypoventilation
- Calculate A-a gradient (normal in first 2 causes, elevated in last 3) - if normal, then the hypoventilation is the ONLY cause of the hypoxemia
- Check if putting patient on 100% O2 would allow raising the PaO2 above 500 mmHg
- If not, then it’s shunt. If it does work, then check DLCO to determine if it’s diffusion limitations or V/Q imbalance
Are both the amount of O2 bound to Hb and amount of O2 dissolved in blood dependent on PaO2?
YUP (Hb until it reaches 100% SaO2)
Which is more important for O2 delivery to tissues: PaO2 or Hb saturation?
Hb saturation
Is CO2 more perfusion or diffusion limited?
Perfusion limited
At rest, with a low FiO2 or low PAO2, will the blood be able to reach 100% saturation of Hb?
YUP
How will doubling the diffusion capacity in a normal person affect PaO2?
Normal because PaO2 will simply equilibrate with PAO2
How will doubling the diffusion capacity in a normal person affect max O2 uptake at extreme altitude? Explain.
Increase it because the PAO2 will be so low that increasing the diffusion capacity will help
What is the PcO2 in pulmonary capillary tension in a normal person at rest?
80 mmHg or more!
For 2/3 of capillary: 100 mmHg
For 1/3: 40 to 100 mmHg
Would increasing afterload increase SvO2 in a septic shock patient?
NOPE
3 ways to improve CO?
- Increase preload
- Reduce afterload
- Iniotropes
What does aspirin overdose cause?
TWO primary acid-base disorders:
- Metabolic acidosis due to salacylic acid to develop in blood
- Respiratory alkalosis due to hyperventilation caused by effect of salicylic acid on brain
How to calculate A-a gradient when given PaCO2 and PaO2?
PAO2 = 150 - PaCO2/0.8
A-a gradient: PAO2 pv - PaO2
If PaCO2 is high and it is due to respiratory acidosis, does that automatically mean hypoventilation?
YESSSSSS
If the A-a gradient is elevated and you have respiratory acidosis, what does this mean?
Means there is another one of these 3 happening with the hypoventilation:
- Diffusion limitations
- Shunt
- V/Q imbalance
Why would a decrease in alveolar space cause an increase in PaCO2?
Decrease alveolar minute ventilation
Why would someone with asthma have turbulent flow?
Gas velocity increase to a greater extent than the decrease in radius to maintain the same volume of gas incoming => Re increases
Why do the normal anatomical shunts not cause a PACO2-PaCO2 gradient?
Because CO2 is much more soluble in blood and the extra CO2 will simply diffuse and will not disturb the PaCO2
Can you have hypoxemia without hypoxia?
NOPE
Can you have hypoxia without hypoxemia?
YUP (like in anemia)
Why doesn’t CO poisoning cause reduced PaO2?
The PaO2 refers to the partial pressure of the gas in the blood. As there is no appreciable PaCO (carboxyhemoglobin) there is no effect on the PaO2
Why is PaCO2 normal in low V/Q?
Because the peripheral chemoreceptors will detect any rise in the PaCO2 and signal the brain stem to increase the minute ventilation to keep the PaCO2 at the normal range
