So we used a mean guy on twitter to spur a discussion on Oxygenation Physiology and talk about when PaO2s are necessary and you can't use the pulse ox (hint: not often). My discussant is Alex Yartsev.
Alex Yartsev
Alex Yartsev (BappSci(MRS), MClinED, MB.BS, FCICM) is an Intensivist from Westmead ICU in Sydney, where he leads the ICU education program. He also coordinates the Mechanical Ventilation unit of study at Sydney University and acts as a Second Part examiner for the College of Intensive Care Medicine.
He is also the creator of Deranged Physiology, a beautiful free resource on clinical physio.
The Oxygen Cascade from Lung to Mitochondria
PaO2 Builds the Sat and the Sat Oxygenates the Tissue
— Landsberg Manual (@LandsbergManual) April 20, 2023
Do We Need an ABG to assess the cause or severity of lung disorders
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3776410/
Does an ABG help assess tissue oxygenation when compared to pulse ox? What is the Best Representation of Tissue Oxygenation
-PaO2 of 90 mm Hg, but Hb of 4 g/dL
Do ABG Machines Measure Saturation or Calculate It?
The First Tweet
Hb sat is a by product, no cell in the body senses hb sat… pao2 is sensed, pco2 is sensed, pH is sensed. Those who target a Hb sat..plz explain?!#Anesthesiology #EmergencyMedicine #meded #MedTwitter #CriticalCare#pulmonary #Anesthesiology #cardiotwitter #EmergencyMedicine pic.twitter.com/RjUml9BZgW
— Landsberg Manual (@LandsbergManual) April 13, 2023
Image 1
CO2 is just a representation of Alveolar Ventilation in the Alveolar Gas Equation from David Story, MD
Image 2
Metabolic Alkalosis
Fails, b/c PaO2 doesn't save you if the PaO2 was a little higher, same horrible physiology which would go unnoticed, you need to understand severe alkalosis, not look at a PaO2
Tweet 2
3 reasons it's RIDICULOUS to say spo2 beats ABG
1) SpO2 estimates SaO2, often poorly
2) SaO2 is a product of PaO2 & pH, yet pH is tightly regulated NOT in relation to O2, so it can't be the true goal of O2 Rx
3) The brain senses and protects a pao2 of 60@emcrit @meded @crickets pic.twitter.com/cZH4mVmfhH— Landsberg Manual (@LandsbergManual) April 27, 2023
Tweet 3
Tweet 4 – These Tweets Speak for Themselves
Pulse Ox Fails
Melanin
See the IBCC Chapter on Pulse Ox/ABGs
Hypotension and Pulse Ox
Anemia
Additional New Information
More on EMCrit
Additional Resources
Now on to the Podcast
Professor
Nassau University Medical Center
No conflicts of interest (coi).
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Hey Scott, I loved this podcast and the references were gold. I did want to pick your brain on something that I run into CONSTANTLY in my CVTU. We Intensivist/Pulmonologists continue to harp on the fact that we should be following SpO2 and not PaO2 2/2 to the oxygen delivery formula above. However, the CV surgeons are adamant that we should be weaning FiO2 based on the PaO2 because of increased pulmonary resisitance caused by hypoxia and the concern that it could worsen right heart pressures in fresh transplants or LVAD patients. I have not found any data to support… Read more »
curious to hear what Alex has to say, but I see absolutely no reason that pulmonary hypertension can’t be prevented using SpO2. I know that is how I handle it in my crit care practice. I think they have the burden of presenting some evidence or rationale.
Guys, guys, I think I have an answer, and you’re not going to like it (the surgeons were right!). The specific thing which controls hypoxic pulmonary vasoconstriction is (probably) oxygen tension, not content. In 1952, Duke & Killick perfused some disembodied cat lungs with a dextran solution at different levels of anaemia, some diluted down to a haemoglobin concentration of less than 10g/L. Provided the tension of dissolved oxygen remained stable, the pulmonary vessels did not care. This is logical, as the pulmonary circulation has no input into the total oxygen-carrying capacity of the blood, only the gas exchange component of it –… Read more »
Alex, we need to have a chat so you can walk me through this. I read the Duke et al. paper you sent, and I am not sure it truly speaks to the issue. But then as I started down that rabbit hole, it made me rethink our suppositions about the role of hypoxemia in PH in general.
Yep, it is rather likely that I have misunderstood some vital aspect here, so would be nice to have a discussion on this! Also, surely there MUST be some evidence about this younger than the 1950s 🙂 Move over, I might need to get into that rabbit hole with you!
Thank you Gentlemen, Interested to here where the rabbit hole leads.
CO2 is just a representation of Alveolar Ventilation in the Alveolar Gas Equation from David Story, MD
This is so important. Thank you for referencing this so much. Too many don’t realize hypoventilation means one cannot meet their metabolic demands and fail to recognize illness severity because of this. Failure to understand this simple point has lead to 1000’s of in hospital cardiac arrests that could have been prevented.
CO2 is just a representation of Alveolar Ventilation in the Alveolar Gas Equation from David Story, MD
Thank you so much for sharing this. Story’s short letter probably influenced me as much as anything I’ve read. Too many don’t understand the relationship between metabolic demand (Vo2) and alveolar ventilation. Lack of understanding has lead to countless in hospital cardiac arrests. His explanation is simple, elegant, and clinically important. Since reading Story’s letter I’ve always taught the alveolar air equation with his substitutions. Much more clinically relevant than A-a gradients.
very interesting topic – i do agree with both of you that we do pay too much attention to PaO2 rather than SaO2…
for the question of hypoxemia from hypoventilation, law of partial pressures will dictate that drop in PaO2 will happen because of elevation in PaCO2; vapor pressure and PaN2 being the same. Instead of patient on vent, i think someone can easily prove this in an anesthetized animal (rather than humans :-))
We occasionally have patients with severe anemia (hgb 7 or less) that can’t be transfused for personal beliefs or antibodies prolonging wait times for blood. We place them on supplemental oxygen thinking that once the hgb drops below a certain level then the amount of dissolved oxygen in the blood becomes clinically significant for oxygen delivery to the tissues. At what level of anemia does placing them on 100% O2 (usually via HFNC) start to reliably contribute to the amount of oxygen delivered to the tissues?
you will get a small contribution at any level of Hb, but when severely anemic, that small contribution matters. As to when to start, the pt would need to be showing me signs of inadequate O2 deliv. to the tissues.
Comment regarding proning contraindications: Morbid obesity is not among them. It’s relative – labour intense, yes, but absolutely possible, and likely even more beneficial for thse patients. Source: https://pubmed.ncbi.nlm.nih.gov/23450309/