COPD/Hypoxic Drive Question

[jrm818]

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.

 

[yowzer]

There are no problems with giving high flow O2 to anyone, assuming they need it. Even if they'd be fine with a cannula or none at all, it won't hurt until they get the bill.

Hypoxic drive is a myth. See http://home.pacbell.net/whitnack/The_Death_of_the_Hypoxic_Drive_Theory.htm and many other google hits.

 

[Guardian]

Off the top of my head, this is the way I learned it...when you breath, you take in O2 and blow off CO2. When you have COPD, the air is trapped in the lungs and you get an abnormally high amount of CO2 and an abnormally low amount of O2. This is because you're not blowing off and taking in as much as you were before COPD. Normally, a decrease in CO2 tells your body to breath. But if you have chronically high PaCO2, then you body relies more on the chronically low PaO2 to tell you when to breath. When you give high flow O2, the body loses both mechanisms that tell it to breath. Current literature says this is not the case in emergency settings.

yowzer's google article is above me but if you can understand it, then you're way beyond me.

 

[Guardian]

jrm818, what kind of emt student are you, ALS or BLS? Why the heck are you trying to learn more than what's in the book anyway? You should be coming on here bragging about the latest toy on your belt or lightbar on your car. Don't be coming on here talking about all this medical crap.



Interesting though, it does seem that after you would give a copd pt o2 and it caused apnea, that eventually the O2 level would drop causing stimulation to breath again, I hope someone can clear this up for us.

 

[jrm818]

Yowzer: Thanks for that link - I acutally read the first 5 google hits above that....and a whole bunch of other places they sent me...but I got frusturated and decided to do some acutal school work before reading the one you sent. I gave it a quick once over and it looks like pretty much what I was looking for...but I'll have to read it in depth tomorrow and figure out what all those big words mean...

jrm818, what kind of emt student are you, ALS or BLS? Why the heck are you trying to learn more than what's in the book anyway? You should be coming on here bragging about the latest toy on your belt or lightbar on your car. Don't be coming on here talking about all this medical crap.



Interesting though, it does seem that after you would give a copd pt o2 and it caused apnea, that eventually the O2 level would drop causing stimulation to breath again, I hope someone can clear this up for us.

I'm a BLS student. I acutally put my lightbar on my belt....and unfortunatly that took up all the room I had left....those three radios and the satelite phone take up so much darn space...I'm still holding out for the rotating light on my hat though.... .....at any rate.... since I can't obsess about cool toys anymore I got terribly depressed and decided to do something crazy and learn a thing or two about fixing people that aren't working right....

thanks for the input, though....and yea...hopefully someone can make this make sense to me (If Yowzer's article doesn't once I read it while acutally awake)

 

[Ridryder911]

Now for those whom that think oxygen does no harm, please read from this EMT...
http://www.waterinstitute-wise.ca/pathophysiology-of-emphysema.php

R/r 911

 

[VentMedic]

Good article but most of the material is more than 25 years old. During the past 25 years much more research has been done with understanding hypoxic drive.

You can also visit your local trach/vent farm for more information about hesitating on giving oxygen to pts that "might" be a CO2 retainer. "He's now a vegetable but we didn't knock out his hypoxic drive".
The actual number of people who are retainers in the COPD category is very small. The actual number of that group that may be sensitive to short term O2 use is even smaller.

You have the heart and brain to consider into the equation.

You can always remove oxygen, you can't replace brain cells or heart muslce.

If they do go sombulent, it could be because they haven't slept for days struggling to breathe before they called EMS. They believe help has arrived. These pts will probably get tubed anyway for a couple of days just to take the load off the rest of their body systems. Some have so many intubations in their hx they could practicularly tube themselves. Some will even ask to be vented for a day or so. If you're BLS you can surely assist their respirations enough to make it to the hospital.

Do you actually think home oxygen pts keep their O2 at 2L? They will max out their concentrators at 5 or 6 whenever they feel the need. In the hospital we are constantly reminding them to at least keep the flow meter turned down when we do rounds or let us re-evaluate them for more O2.

On Shunt studies done regularly at outpatient clinics, COPD pts breathe 100% O2 via Douglas bag or demand valve with nose clips for 30 minutes. Most feel refreshed afterward, not sleepy.

There are lectures given all over the country to re-educate health care professionals about the hypoxic drive.

We also have had a who new group of COPD pts to study over the last 30 years in the form of premature babies with BPD. You may have a 6 y/o that maintains a CO2 of 60 for normal.

More current readings:
(as mentioned in a previous post)
http://home.pacbell.net/whitnack/The_Death_of_the_Hypoxic_Drive_Theory.htm

1. The Control of Breathing in Clinical Practice, Caruana-Montaldo, et al, Chest 117/1 Jan., 2000, pages 205-225
2. Debunking Myths of Chronic Obstructive Pulmonary Disease (Editorial) Hoyt, Crit Care Med 1997 Vol. 25, Number 9, pgs. 1450-51
3. Respiratory Failure, Campbell and Arnott, et al, Lancet 1960, ii 12, 1-7
4. The J. Burns Amberson Lecture---The Management of Acute Respiratory Failure in Chronic Bronchitis and Emphyzema by E.J.M. Campbell, Am Rev Resp Dis 1967, Oct. 96(4):626-639
5. (Hypothesis) Hypercapnea During Oxygen Therapy in Acute Exacerbation of Chronic Respiratory Failure, Rudolf, et al Lancet Sept. 3, 1977, pages 483-486
6. Effects of the Administration of O2 on Ventilation and Blood Gases in Patients with Chronic Obstructive Pulmonary Disease During Acute Respiratory Failure, Aubier, et al, Am. Rev. Resp. Dis. Vol. 122 pages 747-754 1980
7. (Editorial) Hypercapnea during oxygen therapy in airways obstruction: a reappraisal. Stradling, Thorax 1986 41:897-902
8. Correspondence (Aubier and Stradling regarding study cited in # 6 above, Am Rev Resp Dis. Oct. 16th, 1986

9. Central Respiratory Drive in Acute Respiratory Failure of Patients with Chronic Obstructive Pulmonary Disease, Aubier, et al, Am Rev Resp Dis Volume 122, pages 191-199, 1980

10. Hyperoxic-induced Hypercapnea in Stable Chronic Obstructive Pulmonary Disease, Sassoon, et al, Am Rev. Resp. Dis. 1987 135gs. 907-911
11. Inter-individual Variability of the Response to Oxygen Administration in Hypercapneic Patients, Gasparini, et al, Eur J of Resp Dis., 1986; 69(suppl 146) 427-443
12. Oxygen-induced Hypercarbia in Obstructive Pulmonary Disease, Dunn, et al, Am Rev Resp Dis 1991, 144:526-530
13. Causes of Hypercapnia with Oxygen Therapy in Patients with Chronic Obstructive Pulmonary Disease by Hanson, et al, Crit. Care Med 1996 Vol. 24 pgs. 23-28

14. Influence of Inspired oxygen concentration on deadspace, respiratory drive, and PaCO2 in intubated patients with chronic obstructive pulmonary disease, Crossley, et al, Crit Care Med 1997 Vol. 25, Number 9, pages 1522-1526
15. O2-induced changes in Ventilation and Ventilatory Drive in COPD. ****, et all, Am J Resp Crit Care Med vol 115, pages 609-614, 1997
16. The Role of Hypoventilation and Ventilation-Perfusion Redistribution in Oxygen-induced Hypercapnea during Acute Excacerbation of Chronic Obstructive Pulmonary Disease, Robinson, et al, Am. J. Resp. Crit. Care Med Vol. 161, pgs. 1524-1529 2000
17. Carbon dioxide responsiveness in COPD patients with and without chronic hypercapnia Scano, et al, Eur. Resp. J. 1995 8:78-85
18. May 98 issue of Clinical Pulmonary Medicine is an article titled Acute Respiratory Failure in Chronic Obstructive Pulmonary
Disease” by Schiavi
19.Supplemental Perioperative Oxygen to Reduce the Incidence of Surgical-Wound Infection, Robert Greif et al, The New England Journal of Medicine -- January 20, 2000 -- Vol. 342, No. 3

20.Tissue oxygenation, anemia, and perfusion in relation to wound healing in surgical patients by Jonsson K, et al, Ann Surg 1991 Nov;214(5):605-13

21. Oxygen and wound healing by LaVan FB; Hunt TK, Clin Plast Surg 1990 Jul;17(3):463-72

22.Oxygen Supplementation and Cardiac-Autonomic Modulation in COPD* Matthew N. Bartels, MD, MPH; John M. Gonzalez, BS; Woojin Kim, BS and Ronald E. De Meersman, PhD Chest. 2000;118:691-696

23.The Relationsip between Chronic Hypoxemia and Activation of the Tumor Necrosis Factor-x system in Patients with Chronic Obstructive Pulmonary Disease, by Noriaki, et al, Am Jr. Resp Crit Care Med Volume 161 Number 4 April 2000, 1179-1184

24.Elevated O2 cost of ventilation contributes to tissue wasting in COPD. Mannix ET; Manfredi F; Farber MO, Chest 1999 Mar;115(3):708-13

25.November 97 issue of Clinical Pulmonary Medicine, MacNee and Skwarski article titled “The Pathogenesis of Peripheral Edema in Chronic Obstructive Pulmonary Disease”

26.Oxygen Pressue Field Theory for Perfusionists, Nov. 1999, by Gary Grist BS, RN, CCP, Chief Perfusionist The Childrens Mercy Hospital, Kansas City, MO

27.Long term domiciliary oxygen therapy in chronic hypoxic cor pulmonale complicating chronic bronchitis and emphysema, Report of the Medical Research Council Working Party, Lancet 1981; 1(8222):681-686

28.Incidence of Nocturnal Desaturation While Breathing Oxygen in COPD Patients Undergoing Long-term Oxygen Therapy by Robert Plywaczewski, MD, et al, Chest. 2000;117:679-683.)

29. Uncontrolled Oxygen Administration and Respiratory Failure in Acute Asthma, Chien, et al, Chest 117/3/March 2000 pgs. ;728-733

 

[Ridryder911]

welcome to the forum Ventmedic.. (just was trying to get them to think outside the box a little..)



R/r 911

 

[Airwaygoddess]

Hi Ventmedic!! Welcome to the tribe, great post, this is a big concern with EMTS and students alike. A breath of fresh air!! ^_^

 

[VentMedic]

AirwayGoddess, Thank you for the welcome.
And thank you R/r 911 for more thought,

Oxygen...A subject dear to me. Your reference did have some present some good points for thought. I keep in touch with Jeff Whitnack ("Death of the Hypoxic Drive Theory") who keeps me well referenced on the subject.

There will be a short lecture on hypoxic drive at San Francisco General Hospital...I believe in April. There will be some serious work presented also in SF May 18-23 at the American Thoracic Society Conference. Serious academic types that enjoy indepth insight on the cardiopulmonary system should check it out if in the SF Bay area.

A little humor from one of my pulmonologists:
A really depressed COPD pt over heard some nurses and medics talking about the hypoxic drive and how 100% O2 could cause a COPDer to become sombulent and apneic. Before leaving the hospital, the COPD pt found a NRBM. He took it home and one night when he was really depressed he hooked it up to one of his two H tanks he had as backup in case of power failure. He went through one tank and nothing. He was half way through the second tank, when he pulled the mask just slightly off his face and thought..."this hypoxic drive stuff ain't working out like they said, or maybe I was meant to live a little longer." With the mask still near his face he lit a cigarette while thinking about....

And to all a good night.

 

[jrm818]

Thanks for all the responses.

Ok from what I can gather primarily from the Whitnack paper, the Schiavi paper he references, and a couple of others is this:

The “transition to hypoxic drive” never really occurs – but administration of high concentrations of O2 to COPD patients can result in hypercapnia and a decrease in respiratory drive. This retention of CO2 occurs only in some patients, and generally occurs only in association with “acute exacerbations rather than [as] a constant characteristic of individual patients.” (Robinson et. al, citation #16 in the Whitman article)

Current understanding generally holds that these observations of somnolence and apnea with the administration of O2 to COPD patients is a result of some combination of the following(it seems a bit disputed which is the primary cause of increasing PCO2, or if they perhaps simply build upon one another):

1. The Haldane affect whereby CO2 which was bound to hemoglobin is driven into blood plasma by increased uptake of O2 by hemoglobin

And

2. V/Q mismatch caused by the lack of hypoxia induced vasoconstriction in “bad” alveoli (the presence of which characterizes COPD) – “bad” alveoli being alveoli which are relatively ineffective at blood/gas exchange and severely hindered in their ability to expel CO2. This leads to an increase in deadspace in the lungs as there are now areas of the lung which are well-perfused but poorly ventilated due to the under-performing aveoli. The result is a decrease in both uptake of O2 despite the increased atmospheric partial pressure of that gas, as well as a decrease in the expulsion of CO2 from circulation.

Bronchodialition may also occur, further exacerbating the increase in deadspace.


But: Robinson et. al, cited in Whitnack, also suggest that the effect of “2” is fairly small, that the primary distinguishing characteristic of CO2 “retainers” is a decrease in ventilation following administration of O2, and that the observed increase in deadspace may be a result rather than a cause of hypercapnia.

In other words - there seems to be no set consensus as to why hypercapnia is observed, and little agreement as to whether depressed ventilation even is observed following O2 administratoin.

Is that right? Am I way off base? Did I miss something crucial?


Ventmedic:

I read in a few places what you suggest – that the number of retainers is quite low. The Robinson study seemed to suggest that they comprised a rather larger segment of the COPD population (granted the sample size was very small – 22 patients). Do you have any sense as to why this would be the case?

And a new question to everyone:

There does seem to be a consensus that too high a concentration of O2 can be harmful to COPD patients. While it seems like to an extent that this may be unavoidable – as correcting hypoxia is clearly the primary concern, and resulting hypercarbia or V/Q mismatch are most readily corrected by positive pressure ventilation, there also seems to be a suggestion that any such complications can be avoided by more judicious application of O2 – sufficient to prevent hypoxia but not necessarily the “highest concentration available” as my book (and apparently the national standard curriculum) recommends. Specifically Schiavi recommends that FiO2 be increased slowly until hypoxia is overcome. While this recommendation is made in reference to intensive care procedures rather than emergent care procedures, it seems to me like perhaps a more reasonable approach to O2 administration in EMS could be provided – i.e. the administering lowest concentration of O2 sufficient to overcome hypoxia. Thoughts?

 

[yowzer]

A little humor from one of my pulmonologists:
A really depressed COPD pt over heard some nurses and medics talking about the hypoxic drive and how 100% O2 could cause a COPDer to become sombulent and apneic. Before leaving the hospital, the COPD pt found a NRBM. He took it home and one night when he was really depressed he hooked it up to one of his two H tanks he had as backup in case of power failure. He went through one tank and nothing. He was half way through the second tank, when he pulled the mask just slightly off his face and thought..."this hypoxic drive stuff ain't working out like they said, or maybe I was meant to live a little longer." With the mask still near his face he lit a cigarette while thinking about....

Bada bing, bada BOOM!

 

[VentMedic]

jrm818 ,

The study you sited for more retainers to be a relatively lg part of the COPD population....the 22 pts were probably hand selected carefully out of a specific group of individuals that would have a high probability of being retainers to prove fit into their study. COPD a broad term and covers a wide range. If you select mostly emphysema...maybe more retainers. When I'm doing ABGs all day, I may have 2 out of 20 "COPD" pts that are actually retainers. And, I'm doing ABGs so we can see how much we can wean a pt off high flow. This may take my entire shift and 2 more to accomplish getting the pt safely to "2L". I have to be patient and wait for all the other therapies to do their magic.

You definitely did your homework.

Now for a practical sense;
In PreHospital, you have what the pt is telling you and what he/she looks like. You may have a pulse oximeter.

The pulse ox is my least favorite tool in the emergency situation. You will look at the number and it can skew your analysis of any presentation or comment from the patient. Factors you do not know, the actual amount of Hb (unless you have the newer model p. ox), the COHb (I do not titrate home O2 on smokers unless I have a COOX value), the MetHb (nitrates and some chemo pt). If you see 100%..."you can't be short of breath".

The "stereotypical COPD CO2 retainer" which reseachers love so much may also have polycythemia - increased RBC - Hb. This gives them more O2 carrying capacity so they can function at a SpO2 of 88% quite well. Just like a world class athlete training in the mountains of Colorado. A person who is compromised on Hb...will not function well at 88%. This has to be taken into consideration in home care perscriptions.

Thus; back to the point:
1) what are your O2 protocols and what is you medical director's view
2) what is the patient saying
3) what does the pt look like

COPD pts often have many complex medical issues besides the lungs. Unfortunately, certain trigger words like COPD can distract a person from doing a good assessment of all systems.

As for as protocols, even in the ER we have to follow the orders of the "doc of the night" unless we call our Medical Director or C.C. doc to over-ride. Some things we can automatically trump. If the pt is not going to be seriously harmed until we can get him out of the ER, we just wait.

TIDBIT: Pulmonary emboli is most often missed in COPD CO2 retainer pts most often in the ER. Somebody will glance at the blood gas and think that is normal. However, if the pH is very alkalotic the pt may actually be hyperventilating even if his CO2 is 60. A simple formula can tell by the HCO3 how much CO2 the pt is compensated for. The pt may live at 80 or 90.

Again, excellent research...

 

[Airwaygoddess]

I know that is the truth but that is soooooo bad!! ^_^

 

[Airwaygoddess]

Hate it when the O2 tanks go BOOM!

 

[jeepmedic]

good Thread. The main thing I look at when treating a Pt. with Shortness of Breath is How they feel and how they react. That is if they are awake of course.

 

[jrm818]

thanks a lot for all the input - especially the practical info - all very helpful.

 

[fm_emt]

I nominate this for "Most Informative Thread Of The Year."

 

[Airwaygoddess]

I nominate this for "Most Informative Thread Of The Year."

HERE! HERE!

 

[Jon]

Best. Post. Ever.