Nick Mark MD Profile picture
Nov 2 20 tweets 8 min read
More fun pulmonary physiology:

🤿A person takes a deep breath of ambient air & free dives (e.g. holds her breath without a SCUBA tank) in the ocean. At a depth of 40m an arterial blood gas is drawn.

Compared to an ABG drawn at the surface, the divers PaO2 at 40m is:
The answer is INCREASED.

We know because people have free-dived with an arterial line: mean PaO2 at 40m was 197 mmHg (after 45s of breath holding!)

ncbi.nlm.nih.gov/pmc/articles/P…

But why? Understanding requires a deep dive into the alveolar gas equation. A 🫁 pulm #physiology🧵.
2/ ImageImageImage
Before getting to the fun stuff, we should acknowledge that it’s *weird* for your PaO2 to increase while breath holding.

For comparison look how PaO2 DECREASES if you hold your breath on land: it plummets from 110 to 60 mmHg in just 35 seconds!

What makes diving different?
3/ Image
To understand this case, we need to review the alveolar gas equation:

PAO2 = (FiO2 x (Patm - PH2O)) - PaCO2 / RQ

Basically, the partial pressure of O2 in the alveolus depends on the FiO2, the atmospheric pressure (Patm), & the content of CO2 in arterial blood (PaCO2).

4/ Image
Sidebar: This is actually a *simplification*. Fortunately the assumptions that allow us to simplify apply in every case we'd actually encounter in the ICU, so we never need to worry about the complex version... phew!😅

🤓 If you're curious though:
journals.physiology.org/doi/pdf/10.115…

5/ ImageImageImageImage
If we plug some values into the simplified alveolar gas equation, we can see what the normal partial pressure of O2 is in our alveoli.

(I'm assuming you're are at sea level with an atmospheric pressure of 1 atm = 1000 mbar = 760 mmHg)

We get a PAO2 of ~100 mmHg
6/ Image
Be careful not to confuse:
- alveolar O2 pressure (PAO2) with
- arterial O2 pressure (PaO2)

PAO2 (I pronounce it "P big-A O2" to avoid confusion) is O2 is in the alveoli. We estimate it using the alveolar gas equation

PaO2 is O2 is in arterial blood. We measure on an ABG.
7/
It's crucial to differentiate alveolar (PAO2) from arterial (PaO2) oxygen pressure because we like to compare those values to see how efficiently O2 is getting from alveolus into the blood!

Aa difference (some all it "Aa gradient") is just PAO2 - PaO2

(more later I promise)
8/ Image
🤿 Now that we've mastered the alveolar gas equation, let's go back our diver, who held her breath & descended to 40m.

As we descend under water the barometric pressure increases by 1 atmosphere every 10m. What effect does this pressure have on the air in her lungs 🫁?

9/
Imagine she takes a balloon; as she descends the🎈is gonna be compressed by the rising water pressure.

Boyle's law tells us that the volume of the balloon is inverse to the pressure.
P ∝ 1 / V

If the pressure increases 5 fold, the🎈 volume has to decrease by 5 fold also!

10/
The same thing is going to happen to the divers lungs.

At the surface when she takes a breath she will be at total lung capacity (TLC) ≈ 6 liters

When she reaches a depth of 40m, her lungs will be at residual volume (RV) ≈ 1.2 liters

No wonder they call this "squeeze!"

11/
What is going to happen to the partial pressure of oxygen in her alveoli (PAO2)?

Let's use our new friend the alveolar gas equation to find out:

12/ Image
Wow! Her PAO2 went up to 738 mmHg! With that much partial pressure of oxygen in the alveoli it's going to drive a lot more O2 into her blood.

That's exactly what we saw in the art line study!

This phenomenon is called *hydrostatic induced hyperoxia*

13/ Image
But wait a second! If the PAO2 went up to >700 mmHg, why did the PaO2 *only* increase to ~ 200 mmHg.

Quick review of what we/ve learned: what is her Aa difference?
Free diving to 40m has massively increased her Aa difference! Why?

15/ Image
Exposing her lungs to 5 atm of pressure decreased her lung volume from ~6 liters at the surface to 1.2 liter at 40m, but it didn't *uniformly* shrink all her alveoli like the balloon. It caused some of her alveoli to collapse completely!

This is extreme atelectasis!
16/
Atelectasis can cause blood to flow past the alveoli without participating in gas exchange, causing right to left SHUNT.

This might seem confusing because she isn't hypoxemic. But remember that despite 5x increase in her PAO2, her PaO2 only doubled. That's a lotta shunt!

17/
🥤As an analogy, imagine a 2L bottle of your favorite carbonated beverage.

🫧 How do they get so much CO2 dissolved in there?

They apply 4 atmospheres of CO2 above the liquid. This forces more CO2 into solution. yum 😋

This is just like a higher PAO2 driving up PaO2!
18/ Image
We should talk about what happens when she ascends to the surface, but maybe it's better to save that for a future pulm physiology tweetorial.

19/
Bottom line: we learned
- to use the alveolar gas equation to calculate alveolar partial pressure of oxygen (PAO2)
- why comparing PAO2 & arterial oxygen (PaO2) with Aa difference can be useful
- some cool diving physiology like hydrostatic induced hyperoxia & lung squeeze
20/20

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More from @nickmmark

Nov 1
Here’s another pulmonary physiology question that *everyone* who gives O2 to patients ought to know:

What is the primary mechanism by which supplemental oxygen can increase PaCO2 in someone with severe COPD?

1/
This is a hard question! You probably learned that "its bad to give someone with COPD ‘too much’ O2 because they might stop breathing”

Turns out hypoxic respiratory drive causing apnea is a MYTH..but there is an important truth here:

A🧵on Oxygen induced hypercapnia!
2/ Image
Every myth has a little kernel of truth:

In the 80s it was shown that giving people with severe COPD (GOLD stage IV) high flow oxygen (15 lpm) made their minute ventilation (VE) drop then return (almost) to normal, but PaCO2 rose significantly.

Why?

ncbi.nlm.nih.gov/pmc/articles/P…
3/ Image
Read 15 tweets
Nov 1
What is #MedMastodon & why might we need it?

A short thread explaining what it is & why I think it’s time to consider moving to a free, self-moderated medical community as a #MedTwitter alternative.

med-mastodon.com/web/home

1/
Despite its flaws I think Twitter is a great platform for medicine/science.

It’s a fantastic way to follow breaking news & scientific pubs. It’s a great way to hear what brilliant people think. It can be an OK way to engage in debate.

I’m a better doc because of #MedTwitter
2/
Where else can you see the moment impactful research is published? Or hear the authors explain it & discuss with them?

Where else can you hear about the experience of colleagues around the world?

I’ve learned a lot and made some great friends IRL on here.
3/
Read 12 tweets
Oct 31
Hi #MedTwitter friends -

Hoped it wouldn’t come to this but I just setup med-mastodon.com as a #MedTwitter alternative.

Trying to create a free, open community for sharing & discussing medical topics. Join & create your own free verified account.
Some advantages of mastodon:
- open source, decentralized platform
- a small community that can moderate itself (that means no hate speech, no misinformation)
- 500 characters per "toot"
- built in content warnings & enhanced privacy settings
- cross platform compatible
- free
Read 5 tweets
Oct 30
A case everyone needs to know:

A man admitted for CHF exacerbation is normoxic on ambient air. POCUS shows bilateral pleural effusions.

He develops Afib w/ RVR (HR 150s). A med is given. Suddenly he develops hypoxemia (SpO2 84% on NC, 94% on NRB).

What med & what happened?
1/
Which medication was most likely given for Afib with RVR that could have *caused* this person to become hypoxemic?

2/
This is a textbook example of *loss of hypoxic pulmonary vasoconstriction* due to administration of a calcium channel blocker (diltiazem).

This is a surprisingly common cause of iatrogenic hypoxemia!

A 🧵 about hypoxic pulmonary vasoconstriction & why it really matters!
3/
Read 11 tweets
Oct 11
Want to see how PEEP recruits atelectatic lung?

Here’s a video I shot of pig lungs 🫁 connected to a ventilator. Watch as we increase the PEEP from 0 to 5 to 10 cmH2O.👇
Caveat: Normally the inward elastic recoil of the lungs (causing collapse) is balanced by the outward elastic recoil of the chest wall (causing expansion). At FRC these forces are at equilibrium.

When you have lungs without a chest wall👆, PEEP is essential to prevent collapse. Image
(Fortunately) the physiology of lungs without a chest wall doesn’t happen very often, but you can see this in people undergoing sternotomy:

pubmed.ncbi.nlm.nih.gov/8865383/ ImageImageImage
Read 4 tweets
Oct 2
In his latest effort to win the Dunning-Kruger award, VP is now opposed to lung cancer screening.

In order for VP to consider cancer screening “worthwhile” its not enough to prevent lung cancer mortality it must prevent death from literally anything (all cause mortality)
1/
For context, large RCTs have demonstrated the value of lung cancer cancer screening in high risk people: those who are older & with greater 🚬 exposure.

In particular, the NLST (2011) & NELSON (2020) trials found reduced lung cancer mortality with low dose CT screening.
2/
A recent meta-analysis of 9 lung cancer screening RCTs (that included almost 100,000 people) confirmed this finding: low dose CT scans reduce lung cancer mortality.

For every 265 people screened, 1 death from lung cancer is prevented.
pubmed.ncbi.nlm.nih.gov/32583338/

3/
Read 14 tweets

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