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Alveolar Gas Equation for the USMLE Step 1? Diuretics? You Probably Won’t Guess the Connection.

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by Alec Palmerton, MD in Cheat Sheet

By the end of this USMLE Step 1 lesson, you will be able to answer the following questions:

  1. What is the treatment for altitude sickness? Explain this using acid/base chemistry?
  2. General anesthesia/narcotic drugs dulls the patient’s hypoxic/hypercapnic respiratory drives (they may still be present, but you would need a greater degree of hypoxia/hypercapnia to increase respiratory drive). When patients are coming out of anesthesia, what do anesthesiologists often do to increase the patient’s own respiratory drive?
  3. People with COPD may be a “chronic retainer” of CO2, meaning that instead of having the typical PACO2 of ~40 mmHg, it may be much higher (e.g. 60 mmHg or even higher!). What respiratory drive are they more dependent on?
  4. What negative effect can happen to someone w/ an exacerbation of COPD is given high O2? Why?
  5. Assuming constant water vapor, what would be the PAO2 if you had 100% O2 inhalation at 2 atm, w/ a PACO2 of 40 mmHg?

Ready for the recall-type USMLE Step 1 questions?

What does the alveolar gas equation tell us? What is the equation itself?

Alveolar O2 partial pressure (basically the amount of O2 molecules in the alveolus)

PAO2 = PIO2 – PACO2/R,

where PIO2 = partial pressure of O2 in inspired air, and PACO2 is the partial pressure of CO2 in the alveolus

What is the PIO2 in the alveolar gas equation at sea level? Why?

When air enters in your respiratory tract, it is humidified, so the water vapor displaces some of the gas molecules. This humidification value is typically 47 mmHg.

PIO2 = (760-47) * 0.21 = 150, where 47 = partial pressure of H2O vapor, and 21% = percentage of O2 in the air

Thus, the alveolar gas equation at 1atm becomes:

PAO2 = 150 – PACO2/R

What is the difference between PAO2 and PaO2?

PAO2 is the partial pressure of alveolar O2, whereas PaO2 is the partial pressure of O2 in the arterial blood

What is hypoxemia?

Low PaO2

What is hypoxia?

Low O2 in tissues

Why do you become hypoxemic when going to high altitudes?

Atmospheric pressure is lower, THUS the partial pressure of O2 is lower. In other words, if O2 is 21% at sea level (760 mmHg), then the PIO2 = 760*0.21 = 150 mmHg. However, if the atmospheric pressure were 0.5 atm (380 mmHg), then PIO2 = (380 – 47)*0.21 = 70 mmHg.

NOTE: the PERCENTAGE of O2 is THE EXACT SAME (it is a common misconception that the percentage of O2 is lower at higher altitudes).

How does your body compensate for this? Use the alveolar gas equation to explain.

Body compensates by hyperventilating. Blow off excess CO2 → PAO2 ↑

PAO2 = PIO2 – PACO2/R

There is a fixed # of air particles you can fit into your alveolus. If I have more CO2, there is LESS ROOM for O2, and vice-versa. Thus, if I decrease CO2, I will increase PAO2.

What is a respiratory alkalosis / acidosis?

PACO2 is too low

Vs.

PACO2 is too high

What is a metabolic alkalosis / acidosis?

HCO3- is too high

Vs.

HCO3- is too low

If I have a respiratory acidosis, what will my body do to compensate if I can’t control my breathing?

HCO3- reabsorption ↑ → metabolic alkalosis

Generally, a change in respiratory/metabolic status will lead to a compensatory response in the other category. In other words, if I have a metabolic alkalosis, my body will try to respond with a respiratory acidosis.

What is the basis for altitude sickness?

Hypoxemia, from low PAO2 from low atmospheric pressure (recall that hypoxemia from high altitude is due to low partial pressure, and NOT lower O2 percentage in the air)

House fire – worry about what toxins?

CO + cyanide poisoning

What is the treatment for CO poisoning? Why does this make sense?

100% O2, and if available expose them to a higher atmospheric pressure → higher PAO2

What would be the PAO2 if you had 100% O2 inhalation at 1atm, w/ a PACO2 of 40 mmHg?

PAO2 = (760-47) – 40/0.8 = 713-50 = 663 mmHg

Wait!

It is strongly recommended that you attempt to answer the final questions by yourself first, before looking at the answers.  Remember, the USMLE Step 1 exam will test your ability to make connections on the spot, the more practice you have, the higher your score!  Then, when you think you might know the answer (or are completely stumped), look at the answers below!

Ready for the answers?

What is the treatment for altitude sickness? Explain this using acid/base chemistry?

Acetazolamide – carbonic anhydrase inhibitor → blocks HCO3- reabsorption → increase HCO3- loss → metabolic acidosis

Body will compensate with respiratory alkalosis (hyperventilation) → PACO2 ↓, which will increase PAO2 → help relieve hypoxemia from low atmospheric pressure.

General anesthesia dulls the patient’s hypoxic/hypercapnic respiratory drives (they may still be present, but you would need a greater degree of hypoxia/hypercapnia to increase respiratory drive). When patients are coming out of anesthesia, what do anesthesiologists often do to increase the patient’s own respiratory drive?

To increase the patient’s respiratory drive, anesthesiologists will often decrease the patient’s ventilatory support, either by decreasing the respiratory rate (if the ventilator is breathing for the patient) or by decreasing the amount of pressure by which the ventilator augments the patient’s breath. In either case, the goal is to increase the patient’s PaCO2, so that their own respiratory drive will increase

People with COPD may be a “chronic retainer” of CO2, meaning that instead of having the typical PACO2 of ~40 mmHg, it may be much higher (e.g. 60 mmHg or even higher!). What respiratory drive are they more dependent on?

Normally, people are MUCH more dependent on their hypercapnic respiratory drive than their hypoxic drive.

However, in “chronic retainers”, because their body has adapted to high levels of CO2, they are no longer as reliant on their hypercapnic drive, and are instead MORE RELIANT ON THEIR HYPOXIC DRIVE. In other words, they will breathe automatically when they are hypoxic, and will stop breathing when they are no longer hypoxic.

What negative effect can happen to someone w/ an exacerbation of COPD is given high O2? Why?

People with COPD may be a “chronic retainer” of CO2, meaning that instead of having the typical PACO2 of ~40 mmHg, it may be much higher (e.g. 60 mmHg or even higher!), suppressing their hypercapnic drive and forcing them to rely on their hypoxic drive.

Many of these COPD patients will normally have O2 saturation near 90% on room air (healthy people have nearly 100%). Thus, when you give them O2, they can PARADOXICALLY STOP BREATHING AS MUCH, thus becoming HYPERCAPNEIC.

Assuming constant water vapor, what would be the PAO2 if you had 100% O2 inhalation at 2 atm, w/ a PACO2 of 40 mmHg?

PAO2 = (1520-47) – 40/0.8 = 1473-50 = 1423 mmHg

So in other words, LOTS more O2 molecules in high-pressure O2

What should you do next?

  1. Turn the narrative, “Pathogenesis to Presentation” questions into Anki cards by copy/pasting the question/answer into the “Front” and “Back” fields in Anki.  Do the same for the fundamental facts that you were unfamiliar with, to maximize your chances of USMLE Step 1 success!  Remember: the USMLE is a test of understanding, so the better you can understand these questions, the better your score!
  2. Add reverse cards when appropriate to your Anki cards
  3. Re-word the questions/explanations as desired, and BOLD the important text to make it easier to review in the future
  4. Learn something new?  Something unclear?  Comment below!
  5. If you liked this post, please consider sharing it on Facebook/Twitter!  I judge the utility of these posts by the number of comments / shares they receive, so if you’d like more, or would like a particular topic addressed, please let us know!

6 Comments
  1. oluwatosin ayanjoke says:

    Hi, Alec. Thanks to responses. I came across a question in uworld, but I do not understand the explanation given, i would really appreciate it if you could explain to me.
    In uworld, it says that hyperoxia leads to hypercapnia, one of the explanations given is that hyperoxia causes vasodilation, which I agree with, and vasodilation leads to increase physiological dead space-this I do not understand.

    1. Yousmle says:

      Physiologic dead-space is where blood reaches an alveolus that is poorly-/un-ventilated. You have hypoxic pulmonary vasoconstriction which helps to avoid this phenomenon, however when you give someone supplemental oxygen, you cause an increase in blood going to poorly ventilated areas → physiologic dead-space ↑.

      1. Mashhood Arif says:

        deadspace is ventilation without perfusion no ?

  2. oluwatosin ayanjoke says:

    oh, thanks i understand. its the CO2 in the venous system that is increased because of the CO2 from the tissues.

  3. oluwatosin ayanjoke says:

    I think you should check the formula of alveolar O2 because in FA,its PaCO2 not PACO2

    1. Yousmle says:

      Those are equivalent. There should not be a gradient between PACO2 and PaCO2 unless there is perfusion defect.

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Want FREE Cardiology Flashcards?

Cardiology is key for impressive USMLE scores. Master cardiology from a Harvard-trained anesthesiologist who scored USMLE 270 with these 130+ high-yield flash cards. You’ll be begging for cardio questions - even if vitals make you queasy.

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