Applying Applied Physiology to COVID: Silent Hypoxia and The Work of Breathing

Enough time has passed and enough clinical experience with the behavior of COVID gained that we can now apply some applied physiology to our understanding of this aweful illness.  I don't have the answers any more than the next person, but I do know that whatever the behavior of COIVD, it can be viewed through the lens of what we do know about applied lung physiology, and some inferences can be made.  This post will be about that physiology and those inferences, using the frameworks in these lectures about applied physiology.

One of the striking early observations about patients presenting with COVID was their apparent lack of distress despite very low oxygen saturations.  This was termed "silent hypoxia" at some point, and I leave it to internet sleuths to trace its origins.  It led to a policy of early intubation of some COVID patients:

“Never in my life have I had to ask a patient to get off the telephone because it was time to put in a breathing tube,” said Dr. Richard Levitan, who recently spent 10 days at Bellevue Hospital Center in Manhattan.

There are two simple explanations for the observed phenomenon of silent hypoxia: first is that hypoxia is not nearly as potent a stimulus of respiration as is hypercarbia, as I took great pains to explain in the Applied Physiology lectures, using the example of shallow water breath hold divers who do not pre-oxygenate and emerge with sats on the order of 50%, the same as climbers on Mt Everest.  (See also this post on the boy in the wheel well, unpressurized, from California to Hawaii.)  I thank Matt Wong (@EM_phile on Twitter) for pointing me to this video which provides a striking illustration of lack of dyspnea with sudden and severe hypoxemia.  This video is compulsory viewing:

Dyspnea is driven far more by ventilation demands and the work of breathing than it is by hypoxia alone.  This is underrecognized.  I wager this stems in part from the fact that in most diseases that cause hypoxia, there is significantly elevated work of breathing because of parenchymal disease/infiltration (elastic loads) and airway secretions (resistive loads), combined with minute ventilation loads from high CO2 production, dead space ventilation (Vd/Vt) and metabolic acidosis.  If COVID does not have all of those loads, patients may not experience substantial subjective dyspnea despite low oxygen.

Limits of the Possible: Clinical Reasoning of a Harrowing Extubation

"The only way of discovering the limits of the possible is to venture a little way past them into the impossible."  -  Clark's Second Law

In prior posts here and on the Medical Evidence Blog (here, here, here, and here), I have outlined my position that the only way you can really know if a patient can breathe on their own is to let them try - a "trial of extubation".  Prediction equations get you published, but their signal to noise ratio is often poor and ignored, to patients' peril.  Indeed the reason I'm obsessed with extubation is because I think being intubated unnecessarily is one of the worst things a patient can endure, and the best thing I can do as an intensivist is identify the earliest moment when a patient can breathe on his own and extubate him.

I faced a very harrowing extubation decision recently, and I admitted to the medical students that it was the most nail-biting of my career.  But I think analyzing it, both before and after the fact can be very instructive.