Hey All - I'm an EMT student at the moment, and was randomly inspired to investigate the possible problem with giving O2 to a COPD patient - I've been staling these forums for a bit now, and was hoping maybe somebody could bring me out of the dark.
Let me preface this by saying that I konw you're supposed to give high flow O2 if indicaed, regardles of COPD status, and just be ready for any problems - that isn't the source of my confusion....but I got curious about exactly what is going on with COPD patients who have transitioned to a hypoxic respiratory drive.
From what I gather the transition to hypoxic drive from CO2 controled respiration occurs because of some combination of at least two things. Namely
1. The down-regulation or degredaditon of chemoreceptors which normally detect the ph of the blood and adjust respiration accordingly
and
2. An increase in the activity of the liver to remove carbonic acid from the blood and increase the buffering of the blood (leading to a stable ph even in the presence of CO2 levels which would raise PH in a normal patient). Assuming that's correct, that part makes sense to me.
What I dont' understand is why such a patient would degrade when placed on high-flow O2. The explination I've heard is that as the P02 of the blood increases, the body of the COPD patient decides that the current respiraiton rate is more than sufficent, and retards respiration. That makes sense too. But supposedly such a patient will become hypoxic, and eventually go into respiratory arrest. That makes no sense to me :unsure: - it seems that such a patient would be fully able to respond to a decrease in oxygen in the blood and increase respirations again until adequate oxygenation is restored.
What I suspect is going on is that these patients do not become hypoxic at all, but rather have sufficient oxygenation and suffer from an accumulation of CO2 as a result of the decreased respiratory rate - perhaps an increase sufficient to overcome the increased buffering of the blood by the liver, and cause acidosis....or something like that.
I've done a bit of digging tonight, and have been unable to find anything that explains this to my satisfaction, my book is useless for anything beyond painfully basic information, and it'll be a few days before I can ask my instructor - so I was hoping maybe someone here could provide some clarity. Thanks a lot for any insight.
Let me preface this by saying that I konw you're supposed to give high flow O2 if indicaed, regardles of COPD status, and just be ready for any problems - that isn't the source of my confusion....but I got curious about exactly what is going on with COPD patients who have transitioned to a hypoxic respiratory drive.
From what I gather the transition to hypoxic drive from CO2 controled respiration occurs because of some combination of at least two things. Namely
1. The down-regulation or degredaditon of chemoreceptors which normally detect the ph of the blood and adjust respiration accordingly
and
2. An increase in the activity of the liver to remove carbonic acid from the blood and increase the buffering of the blood (leading to a stable ph even in the presence of CO2 levels which would raise PH in a normal patient). Assuming that's correct, that part makes sense to me.
What I dont' understand is why such a patient would degrade when placed on high-flow O2. The explination I've heard is that as the P02 of the blood increases, the body of the COPD patient decides that the current respiraiton rate is more than sufficent, and retards respiration. That makes sense too. But supposedly such a patient will become hypoxic, and eventually go into respiratory arrest. That makes no sense to me :unsure: - it seems that such a patient would be fully able to respond to a decrease in oxygen in the blood and increase respirations again until adequate oxygenation is restored.
What I suspect is going on is that these patients do not become hypoxic at all, but rather have sufficient oxygenation and suffer from an accumulation of CO2 as a result of the decreased respiratory rate - perhaps an increase sufficient to overcome the increased buffering of the blood by the liver, and cause acidosis....or something like that.
I've done a bit of digging tonight, and have been unable to find anything that explains this to my satisfaction, my book is useless for anything beyond painfully basic information, and it'll be a few days before I can ask my instructor - so I was hoping maybe someone here could provide some clarity. Thanks a lot for any insight.