It's the height of COVID pandemic. A patient rolls into your ER, calm, walking and talking. Then, in full and complete sentences without any increased work of breathing, they proceed to tell you how they ate dinner indoors in an enclosed space with 12 of their relatives, and how their cousin had a “cold.” Now 10 or so days later, the patient develops a “little cough” and comes in “just to get checked out.” You throw a pulse ox on, and it reads 78%. Then, they finally pop the question,
“Doc, do you think I have COVID?”
Before you break the bad news (almost certainly yes, prepare for some fun contact tracing and isolation), you take a moment to ponder...
“How are you so hypoxic without showing the faintest hint of respiratory distress?”
Recently, we were forwarded an article that tackles this question(see citation below for full text). As fate would have it, COVID is not some mystical disease but it does require a trip back to physiology class from second year of med school. For my medics out there, this may be new for you, but here at MedicineWithout, we are here to make it simple for everyone.
Reasons why COVID patients can be hypoxic and not show it (IE the proverbial “happy hypoxic”):
1. Dyspnea (sensation of respiratory difficulty) is more about the CO2 than the O2
Recall that high carbon dioxide (CO2) levels (hypercarbia) produce more dyspnea than low oxygen levels (hypoxia).
Consider this, an increase of just 10mm Hg in PaCO2 (carbon dioxide tension) produces a large increase in minute ventilation (Ve) an intolerable sense of dyspnea. By contrast, a drop in PaO2 (oxygen tension) from 90 mm Hg to 60mm Hg will produce hardly any change in minute ventilation and therefore hardly any change in dyspnea. Any further dip than that though, will produce a large increase in minute ventilation as the ventilatory response to hypoxia follows a hyperbolic curve.
2. People are different.
There is broad variation in respiratory drive between individuals which can vary between 300-600% !!!!
3. People are old.
In response to hypoxia, elderly people (>65 years old) have a 50% decreased ventilatory response to hypoxia.
4. People are diabetic.
Much like the elderly, diabetics have a 50% decreased response to hypoxia as well.
5. People have fever.
I know this one is gonna give some people nightmares digging back to that hemoglobin dissociation curve, but we are gonna keep it simple. Higher temperature -> right shift-> more hemoglobin dissociation -> lower SaO2 at constant PaO2.
In English, fever-> lower pulse ox.
6. Pulse Oximeters are not as good as we think they are.
Recall what a pulse oximeter does. It measures the SpO2 by illuminating skin which is an estimation of true oxygen saturation or SaO2 which is measured with a co-oximeter. The difference between these two values can be +/- 4%, but when the SaO2 drops below 80%, the difference can be much more profound. In experimental settings using a hypobaric chamber at a PaO2 of 21.6-27.8 mm Hg, the difference between SpO2 and true SaO2 was -5.8 +/- 16%. Pulse oximetry readings are further affected by critical illness and also by black skin. In fact, in black skin, it can be 2.45 x less accurate at detecting a 4% difference between SpO2 and SaO2 in blacks compared to whites.
Bottom line, what does this all mean? It means that that COVID patient with the SpO2 so low that it seems incompatible with life may have a higher SaO2 than you think that allows them to be talking to you rather then well...dead.
So there you have it folks. COVID causes “happy hypoxia” by relatively sparing CO2 levels, causing fever, and taking advantage of individual variation in respiratory drive, the elderly, diabetics, and of the limitations of our measuring tools.
Thank you Tobin et al!
Stay safe out there!
Reference:
Tobin MJ, Laghi F, Jubran A. Why COVID-19 Silent Hypoxemia Is Baffling to Physicians. Am J Respir Crit Care Med. 2020;202(3):356-360. doi:10.1164/rccm.202006-2157CP