I am hoping to stimulate some discussion involving a simple question with complex pulmonary physiology.
2 questions involving a patient with COPD who is a known CO2 retainer (pCO2 around 50-60 with a preserved pH) at baseline:
1. Why can putting them on high flow oxygen (i.e. when they present to a Emergency with increased dyspnea) worsen their CO2 retention?
2. How do you know how much oxygen to give these individuals if they are truly hypoxemic?
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7 comments - CLICK HERE to read & add your own!:
I think there are two key components to your first question. The most basic one is why COPD patients get hypercapnic to begin with. Bart Celli has a nice paper on ERJ (1998 Sep;12(3):666-71) looking at central respiratory drive in COPD suggesting that at baseline Pts get hypercapnic mainly because of mechanic limitation and that their "central drive" is still preserved. Pts with worse function get hypercapnic because they have worse function...
The second component goes back to your question: so, once you have limited mechanics and are already hypercapnic, why does O2 make it worse?
I have found references to older studies suggesting that Pts with COPD (both eucapnic and hypercapnic at baseline) actually have a decreased central drive in response to CO2 when compared to healthy subjects:
Altose MD et al J Clin Invest 1977; 59: 500–507.
Light RW et al Chest 1988; 94: 61–67.
Bart Celli in the study I referenced on my previous comment tested their drive and found actually a slightly increased drive with intact CO2 response (he was not looking at O2 supplementation) in his COPD subjects. In the studies such as the two above drive was not directly measured or different methods had to be used.
Now moving to the O2 supplementation. I have been taught and read that part of the problem is like the hyperventilating diver: with the CO2 already high, the response to further increases is blunted and the chemoreceptor kicking in is the hypoxemia one. If O2 goes up there is no other drive to kick in. That has seemed oversimplified to me. It does not take into account the limited mechanics of the COPD to begin with nor that when Pts come to the ER and are placed on o2 they are (usually) sick and probably have even worse flow limitation.
Have you come across good data/studies on that mechanism?
I've seen no data on this. I was taught (as we all were) that this phenomenon has to do with loss of the central CO2-mediated respiratory drive, with subsequent dependence on a "hypoxic" drive. Thus, supplemental O2 can then remove the "hypoxic" drive, the patient stops breathing, and the CO2 rises.
Although I'm sure we all have some anecdotal experience with that, current thinking is that the described mechanism is mostly theoretical. On a more practical level, it is thought that supplemental oxygen can reverse the hypoxic vasoconstriction that occurs in patients with COPD, and thus worsen V/Q matching, with increased perfusion to poorly ventilated regions and, thus, a relative hypoventilation.
My approach is this: increased hypercapnea tends not to kill people, and we can usually address this (if need be) with NIPPV or mechanical ventilation. So, in a hypoxic patient with COPD, I give as much oxygen as is required to provide adequate oxygen delivery to tissues (i.e. accept an O2 sat of 88-90% or so, possibly higher if there is evidence of ischemia as well) regardless of the pCO2.
Great responses. The residents and I had this debate on rounds last month with a patient who essentially remained hypoxemic all night (mid 80's).
I firmly agree with JCH's approach and finally brow-beated the residents to do the same.
I think the main reason for the increased pCO2 is the V-Q mismatch. When patients receive oxygen, they reverse some hypoxic vasoconstriction in "diseased" areas and retain CO2 because of this.
Based upon Carlos' quoted studies (I found the same) I think the drive to breathe is unchanged/only slightly altered in most patients. This is represented in the ICU when patients on the vent attempt to blow their pCO2 to normal despite the best efforts of the intensive care team. I.e. as the work of breathing has decreased, the medulla wants the pCO2 normalized.
Again, great question Mike. I think your last statement in the comments sums it up. We have been taught to some degree that brains from COPD patients "don't want to breathe" when the truth is they just CAN'T breath because of all the extra work of breathing.
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