COPD & Emphysema Support Group
COPD is a progressive disease characterized by airflow obstruction or limitation. Emphysema is characterized by loss of elasticity of the lung tissue, destruction of structures supporting the alveoli and of capillaries feeding the alveoli. Both have symptoms that include shortness of breath, among other respiratory troubles. If you are a COPD or Emphysema sufferer, join...
Oxygen Therapy in COPD: What Do We Know?
M. Bradley Drummond, M.D. and Robert A. Wise, M.D.
Division of Pulmonary and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland
There are known knowns; there are things we know we know. We also know there are known unknowns, that is to say we know there are some things we do not know. But there are also unknown unknownsthe ones we don't know we don't know.Donald Rumsfeld
Facts are stupid things.Ronald Reagan
It's what a fellow thinks he knows that hurts him.Kin Hubbard
While the death rates for other chronic diseases decline in the United States, the death rate for chronic obstructive pulmonary disease (COPD) continues to increase (1, 2). It is time to reassess what is and is not known about oxygen therapy for COPD. Long-term oxygen therapy improves survival in some populations with COPD (3, 4). The Nocturnal Oxygen Treatment Trial (NOTT) and Report of the Medical Research Council (MRC) evaluated long-term oxygen therapy in patients with COPD with severe hypoxemia. Both studies demonstrated a survival benefit with supplemental oxygen, but only in those who were instructed to use it 1524 h per day. Current guidelines and Medicare reimbursement policies are derived from these two relatively small studies (290 patients) (5, 6). Guidelines and reimbursement policies for patients with exercise desaturation were promulgated with even less evidence. Medicare charges for oxygen were $2.2 billion in 2002, with annual inflation of 1213% per year (7, and unpublished CMS data). The economic impact of oxygen use in populations with COPD necessitates further studies.
In this issue of the Journal (pp. 343349), Nonoyama and colleagues evaluate the effect of oxygen therapy in patients with COPD experiencing desaturation with exertion, but not at rest (8). Data are lacking regarding benefit of oxygen therapy in this setting (9). A novel design was used to approach this clinical question. N-of-1 randomized controlled trials were implemented to study the effects of oxygen on individual participants. In this design, participants serve as their own controls, crossing over between two masked treatments several times. The strength of the design is its ability to observe individual responses to an intervention and thus account for variable responses of individuals, mitigating the need for larger trials that aim to define responses on a population basis (10). Such trials can be used to personalize treatments for patients while we are awaiting the fulfillment of promises of pharmacogenetics to predict individual responses to treatment. However, this trial design does have limitations. It assumes that the treatment effect is of rapid onset and offset, without carry-over effects between treatment periods. These assumptions are likely true for some oxygen effects, but not others. For example, the effect of oxygen on increasing peak exercise capacity in patients with COPD is of rapid onset and offset. However, if oxygen treatment in such patients is accompanied by increased aerobic exercise, there may be training effects that take weeks or months to occur and weeks or months to dissipate (11). Moreover, several issues prevent the broad clinical implementation of this design: the need for consent and institutional oversight, a research infrastructure to conduct such trials for clinical purposes, and potentially negative attitudes by patients and physicians in a therapeutic relationship.
This study presents several key findings regarding the short- and long-term effects of oxygen therapy. It confirms the previously described increase in exercise capacity seen acutely with oxygen therapy in patients with COPD with mild hypoxemia (12, 13). It has been unclear if this observation translates into a more persistent increase in clinical endurance outside of the laboratory. To address this, the authors measured home five-minute walk testing and dyspnea scores. Throughout the intervention periods, which included two-week periods of either oxygen or placebo in a random sequence repeated three times, a minimal improvement was seen in distance walked with oxygen (427 versus 412 steps, P = 0.04). While the modified Borg dyspnea scale did decrease (less dyspnea) with oxygen from 3.2 to 2.8 (P = 0.04), the difference was small. Other dyspnea indices did not improve with oxygen therapy. The authors conclude that only a small proportion of patients with mild resting hypoxemia and exercise desaturation receive an important benefit from home oxygen. Implicit in this conclusion is the assumption that patients were in fact mobile and active during the study period. After all, an intervention designed to improve dyspnea will have no effect if the patient is not involved in activities that induce dyspnea. The authors acknowledge the impact of activity level on benefit of oxygen therapy. In this study, the total time per day participants used the portable cylinder was 0.7 0.6 hours in the oxygen group and 0.6 0.6 hours with placebo cylinders. Essentially, patients used portable oxygen approximately 40 minutes per day, raising question as to their level of dyspnea-inducing activities and confirming the findings of Pitta and colleagues that patients with COPD acclimate to an inactive lifestyle (14). This observation highlights a key distinction in clinical descriptors of COPD: functional capacity (what a patient is able to do) versus functional status (what a patient actually does). This study shows that oxygen therapy with exertion in those with exercise desaturation increases functional capacity but not functional status.
The findings by Nonoyama and colleagues challenge those of us who prescribe oxygen to explore the intricacies of real-world activity levels of our patients and how oxygen may benefit those individuals. It also challenges us to learn what supplemental oxygen therapy can accomplish when coupled with an exercise training program designed to potentiate oxygen's effects. Continued efforts with innovative approaches, such as those used by Nonoyama, will allow the treatment of COPD to move away from the limited data of the past into a future where COPD no longer damages and shortens the lives of so many.
M. Bradley Drummond, M.D. and Robert A. Wise, M.D.
Division of Pulmonary and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland
There are known knowns; there are things we know we know. We also know there are known unknowns, that is to say we know there are some things we do not know. But there are also unknown unknownsthe ones we don't know we don't know.Donald Rumsfeld
Facts are stupid things.Ronald Reagan
It's what a fellow thinks he knows that hurts him.Kin Hubbard
While the death rates for other chronic diseases decline in the United States, the death rate for chronic obstructive pulmonary disease (COPD) continues to increase (1, 2). It is time to reassess what is and is not known about oxygen therapy for COPD. Long-term oxygen therapy improves survival in some populations with COPD (3, 4). The Nocturnal Oxygen Treatment Trial (NOTT) and Report of the Medical Research Council (MRC) evaluated long-term oxygen therapy in patients with COPD with severe hypoxemia. Both studies demonstrated a survival benefit with supplemental oxygen, but only in those who were instructed to use it 1524 h per day. Current guidelines and Medicare reimbursement policies are derived from these two relatively small studies (290 patients) (5, 6). Guidelines and reimbursement policies for patients with exercise desaturation were promulgated with even less evidence. Medicare charges for oxygen were $2.2 billion in 2002, with annual inflation of 1213% per year (7, and unpublished CMS data). The economic impact of oxygen use in populations with COPD necessitates further studies.
In this issue of the Journal (pp. 343349), Nonoyama and colleagues evaluate the effect of oxygen therapy in patients with COPD experiencing desaturation with exertion, but not at rest (8). Data are lacking regarding benefit of oxygen therapy in this setting (9). A novel design was used to approach this clinical question. N-of-1 randomized controlled trials were implemented to study the effects of oxygen on individual participants. In this design, participants serve as their own controls, crossing over between two masked treatments several times. The strength of the design is its ability to observe individual responses to an intervention and thus account for variable responses of individuals, mitigating the need for larger trials that aim to define responses on a population basis (10). Such trials can be used to personalize treatments for patients while we are awaiting the fulfillment of promises of pharmacogenetics to predict individual responses to treatment. However, this trial design does have limitations. It assumes that the treatment effect is of rapid onset and offset, without carry-over effects between treatment periods. These assumptions are likely true for some oxygen effects, but not others. For example, the effect of oxygen on increasing peak exercise capacity in patients with COPD is of rapid onset and offset. However, if oxygen treatment in such patients is accompanied by increased aerobic exercise, there may be training effects that take weeks or months to occur and weeks or months to dissipate (11). Moreover, several issues prevent the broad clinical implementation of this design: the need for consent and institutional oversight, a research infrastructure to conduct such trials for clinical purposes, and potentially negative attitudes by patients and physicians in a therapeutic relationship.
This study presents several key findings regarding the short- and long-term effects of oxygen therapy. It confirms the previously described increase in exercise capacity seen acutely with oxygen therapy in patients with COPD with mild hypoxemia (12, 13). It has been unclear if this observation translates into a more persistent increase in clinical endurance outside of the laboratory. To address this, the authors measured home five-minute walk testing and dyspnea scores. Throughout the intervention periods, which included two-week periods of either oxygen or placebo in a random sequence repeated three times, a minimal improvement was seen in distance walked with oxygen (427 versus 412 steps, P = 0.04). While the modified Borg dyspnea scale did decrease (less dyspnea) with oxygen from 3.2 to 2.8 (P = 0.04), the difference was small. Other dyspnea indices did not improve with oxygen therapy. The authors conclude that only a small proportion of patients with mild resting hypoxemia and exercise desaturation receive an important benefit from home oxygen. Implicit in this conclusion is the assumption that patients were in fact mobile and active during the study period. After all, an intervention designed to improve dyspnea will have no effect if the patient is not involved in activities that induce dyspnea. The authors acknowledge the impact of activity level on benefit of oxygen therapy. In this study, the total time per day participants used the portable cylinder was 0.7 0.6 hours in the oxygen group and 0.6 0.6 hours with placebo cylinders. Essentially, patients used portable oxygen approximately 40 minutes per day, raising question as to their level of dyspnea-inducing activities and confirming the findings of Pitta and colleagues that patients with COPD acclimate to an inactive lifestyle (14). This observation highlights a key distinction in clinical descriptors of COPD: functional capacity (what a patient is able to do) versus functional status (what a patient actually does). This study shows that oxygen therapy with exertion in those with exercise desaturation increases functional capacity but not functional status.
The findings by Nonoyama and colleagues challenge those of us who prescribe oxygen to explore the intricacies of real-world activity levels of our patients and how oxygen may benefit those individuals. It also challenges us to learn what supplemental oxygen therapy can accomplish when coupled with an exercise training program designed to potentiate oxygen's effects. Continued efforts with innovative approaches, such as those used by Nonoyama, will allow the treatment of COPD to move away from the limited data of the past into a future where COPD no longer damages and shortens the lives of so many.
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My 6mo twin DD's are EBF and just started rice cereal on the first. Everything has been going fine except this morning one of them had a diaper rash (lots of redness around her anus). I read this as one of the signs of an allergy. BUT I did just buy a different brand diaper yesterday (which they have used randomly before w/no issues). Do you think its the cereal or the diaper? Im ready to start...
I think it is general knowledge pulse ox saturations are not the only tool used to determine the need for oxygen. These can affected by other things, for instance, by whether a person is smoking - it results in a higher reading, thus making it not a true picture of what is really happening This is why ABG tests, x-rays, spirometery and PFT's, etc are done to get an accurate picture of its need.
Low oxygen levels for prolonged periods of time can, in fact, affect your heart and other organs, which is why generally when people are prescribed oxygen for 24/7, it should be used as prescribed.
Then too, sometimes oxygen is indicated should a person be recovering from pneumonia or an severe excerbation, etc. and is discontinued when the person's lungs have healed sufficiently.
Pulmonary rehab is great and can and does improve endurance and strengthen muscles making breathing easier and improving flow of blood carrying oxygen, but it cannot repair irreversible damage. Additionally, it can also indicate when a person might need supplemental oxygen as often in the case of those with COPD, a person's level may drop to an unacceptable level when doing more strenuous tasks or simply walking.
Just as people are different with different opinions, so are doctors, so it's probably best to listen to your own doctor and if you are not getting the proper tests needed to insist on them to determine whether or not supplemental oxygen is needed. It could also be there are doctors who have patients, seen by someone not well versed in COPD, found more than half their patients should have been on oxygen but aren't as they were under diagnosed.
Some only require oxygen while sleeping, others only when exercising - some only 2 hours a day, others 16 hours a day and yet others 24.7.
My point is unless a patient is monitored when their oxygen sats drop they may not know there is a problem until other health problems start to occur and in some unfortunate cases organ failure and death.
For those interested, here is an interesting web page on Low Oxygen Levels:
http://www.heartfailuresolutions.com/oxygen/low-oxygen-levels-how-low-is-too-low-and-should-you-worry#
Doctors are prone to disagree on occasion but as patients the best we can do is follow the advice of our own personal medical advisers.
Breathe good
O2 use is a funny thing. Its so dependent on so many variables at this time- age, stage, reserves, compliance, exercise/mobility and affect of other health care problems.
My Dr.s like your Jona- in his opinion, my reserves and recovery are still strong enough that he fears placing me on )2 24/7 would not be as positive overall at this time. Since I've searched so long and hard to find a care team I trust, I'll ride with his opinion. MAkes it easy because this one really talks to me and gives me clear medically based reasons and research to help me and my "team" make the best decision for my care.
Finally!!!!!!
Hugs, Lisa
Blessings Pam