How much oxygen copd

The patients with the highest blood oxygen tensions had the worst acidosis, supporting the premise that excessive oxygen can lead to respiratory acidosis in this setting. In a more recent study, Joosten and colleagues demonstrated that an oxygen tension above These patients will be issued an "oxygen alert card" Figure 1 with individualized instructions for oxygen therapy during future exacerbations. The card should be carried by the patients at all times and made available to health care providers to help guide oxygen therapy.

However, a Venturi mask uses a special valve that entrains air using the Venturi principle Figure 2. This delivers a fixed dose of oxygen even if the flow rate is increased and thus helps to ensure that the patient receives a constant and safe dose of oxygen. Managing oxygen appropriately in the setting of a COPD exacerbation can be challenging.

Obviously, for the hypoxic patient, oxygen can be life-saving. But clinicians must be aware of the challenges and risks of oxygen therapy in patients with severe COPD and take advantage of published guidelines to help ensure the safest and most appropriate care.

Domiciliary oxygen for chronic obstructive pulmonary disease. Cochrane Database Syst Rev. Stoller JK. Acute exacerbations of chronic obstructive pulmonary disease.

N Engl J Med. Evaluation of five oxygen delivery devices in spontaneously breathing subjects by oxygraphy. Emergency oxygen therapy for the COPD patient. Emerg Med J. One year period prevalence study of respiratory acidosis in acute exacerbations of COPD: implications for the provision of non-invasive ventilation and oxygen administration. Boyle M, Wong J. Prescribing oxygen therapy. British Thoracic Society.

Guideline for emergency oxygen use in adult patients. Downs JB. Has oxygen administration delayed appropriate respiratory care? Fallacies regarding oxygen therapy. Respir Care. The effects of oxygen therapy in patients presenting to an emergency department with exacerbation of chronic obstructive pulmonary disease. Med J Aust. Severinghaus JW. Simple, accurate equations for human blood O2 dissociation computations. J Appl Physiol. To sign up for updates or to access your subscriber preferences, please enter your email address below.

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Put a minus sign just before words you don't want. They calculated how much of the observed change Pa CO2 could be due to the Haldane effect based on the observed change in Hb O2 saturation in their patients. The pulmonary vasculature can dilate and constrict to alter blood flow and match ventilation to perfusion figure 2 , and the primary driver of vascular dilation and increased perfusion is alveolar O2.

Administering supplemental O2 screws up this careful balance. Diseased sections of lung see increased PaO2 and steal perfusion away from better functioning areas. This results in shunting, dead space ventilation, and eventually hypercarbia. Robinson et al. The role of hypoventilation and ventilation-perfusion redistribution in oxygen-induced hypercapnia during acute exacerbations of chronic obstructive pulmonary disease.

Population: 22 hospitalized patients with a diagnosis of acute COPD exacerbation. Methods: Inert gas was infused into each patient using a peripheral venous catheter.

Results: Ventilation perfusion heterogeneity i. Minute ventilation decreased significantly in the retainers but not the non-retainers. Finally, dead space ventilation increased significantly in the retainer group, but was unchanged in the non-retainer group. Robinson et al came to the exact opposite conclusion that Aubier et al did 20 years earlier in their landmark study.

They concluded that hypoventilation theory 1, which I just called a myth was the cause of oxygen induced hypercapnia in COPD patients. Controversy: Other authors have drawn different conclusions from the Robinson et al study.

For example, Abdo and Heunks [4] suggest that hypercarbia in the retainer group was likely due to the increase in dead space ventilation which was unchanged in the non-retainers. I hope this has been an enjoyable tour through pulmonary physiology. Both large studies that looked at this theory found that supplemental O2 does lead to hypoventilation.

Aubier et al. The chemistry is sound, and the effect likely causes some hypercarbia, but we have minimal direct evidence for it. It also cannot account for all of the hypercarbia that has been observed in the above studies. Aubrier et al. Great post, thanks for stratisfying the different theories. The answer is probably: it depends. But I was hoping yall could speak to that a little. This will require specialized equipment to provide high-flow, low F IO 2 to patients at risk.

Another recommendation is that pre-hospital providers operate up-draft nebulizers for bronchodilator delivery with room air if pressurized metered-dose inhalers are unavailable. During aerosol therapy, oxygen can be provided via nasal cannula. An example of such a card is shown in Figure 2. Proposed example of an oxygen alert card that can be provided to patients with chronic respiratory disease at risk for hypercarbia.

This includes patients with COPD as well as those with neuromuscular disease and obesity hypoventilation syndrome. Changing care paradigms for COPD patients in pre-hospital and emergency room settings will require a full-scale educational initiative.

To date, these ideas have not had widespread support. The fear of hypoxemia, rightfully so, has overshadowed the known consequences of hyperoxia in COPD. Training ambulance crews in the physiology behind carbon dioxide retention and the use of oxygen delivery devices is paramount.

COPD is a progressive, irreversible disease that is primarily managed by symptom control. At the end stages of life, COPD subjects suffer from debilitating dyspnea and fear of suffocation. Dyspnea is profound in the last days of life, and oxygen for relief of symptoms is commonly prescribed, often at the request of families.

The common-sense approach that oxygen can relieve dyspnea is not based in fact. A randomized controlled trial of oxygen versus air in subjects at the end of life failed to show any advantage of oxygen. Interestingly, dyspnea was improved by continuous-flow oxygen, but not with pulse-dose oxygen delivery. These findings suggest that perhaps the impact of nasal oxygen flow at the end of life is secondary to washing out the upper-airway dead space versus increasing oxygenation.

If this is true, high-flow nasal oxygen or air may be useful in alleviating dyspnea in palliative care. At the end of a week study period, subjects receiving HFNC had improved health-related quality of life scores and a reduction in hypercapnia compared with traditional oxygen therapy.

In these subjects, arterial carbon dioxide was reduced by an average of 4 mm Hg. However, there were no changes in arterial oxygenation, dyspnea, spirometry, lung volumes or 6-min walk distance. HFNC disrupts our normal classification of oxygen therapy appliances. The addition of heat and humidity and a wider bore heated cirucit allows the cannula to transition to a high flow device. High flow at low inspired oxygen concentrations, preventing hyperoxia is safe with the added benefit of washing out the deadspace and providing a low level of end expiratory pressure.

Patients who qualify for LTOT have a number of options for home oxygen delivery. An extensive review of these devices was published by McCoy in Medicare provides a page document that details the requirements for reimbursable home oxygen therapy. On one hand these rules are explicit and complex Table 3.

From a clinical standpoint, however, the orders fail to address issues related to maintenance of adequate oxygen saturation at all levels of activity. Concerns regarding oxygen prescription appear to be universal, as publications from the United States, the United Kingdom, Spain, and Australia have all addressed this issue in the last 20 years.

Complicating this problem is that home oxygen therapy reimbursement focuses on the equipment, not the care provided by a respiratory therapist familiar with the nuances of device performance. The recent Medicare change to a competitive bidding process for home oxygen therapy appears to put further cost pressures on suppliers and limits options for patients. A successful home oxygen therapy program begins with a clear and cogent prescription for oxygen therapy that is goal-oriented.

The current system tends to default to the supplier which device to choose, despite unknown efficacy. A prescription that is explicit with respect to desired S pO 2 , with and without activity, should be the standard. Whether this is possible under the changing reimbursement system remains to be seen. Based on reimbursement, logistics, and performance, there are a number of options for home oxygen delivery. In many cases, this includes a device for in home use, a portable device for mobility, and a backup system.

Table 4 lists the advantages and disadvantages of home oxygen delivery devices. Oxygen cylinders represent the original source of oxygen supply. Cylinders can provide continuous flow or be fitted with demand regulators to prolong duration of operation and efficacy.

However, the short duration of operation, weight, handling, and logistics of replacing cylinders render this the least favorable option for home therapy. Small cylinders continue to be used for ambulation or as back-up systems in some situations. Liquid oxygen systems provide a number of advantages compared with other devices. Liquid oxygen is more easily stored, transported, and transfilled than gaseous oxygen.

Stationary liquid systems can be used to fill portable devices to enhance patient mobility. Liquid systems are also capable of high flows and are the best option for subjects with greater oxygen requirements.

At present, the logistics and costs of liquid systems have limited its adoption in home care. Portable liquid systems extend the time patients can be away from home but cannot be used for air travel. Oxygen concentrators are the most common device used for home oxygen therapy. When discussing oxygen concentrators, purity is essentially the F IO 2 of the gas delivered to the patient. Concentrators are also capable of pulse-dose delivery to maximize efficacy and minimize power use.

Current stationary concentrators weigh between 30 and 35 pounds and run more efficiently than previous devices. This includes lower power consumption, quieter operation, and reduced costs of ownership. Certain portable concentrators allow filling of small cylinders to allow the patient to travel away from home. These devices have greater costs, and there are a number of logistics issues that must be overcome.

Patient acceptance of this responsibility is important for successful use. Portable oxygen concentrators POCs provide patients prolonged mobility outside the home through the use of batteries and operation from automobile power and other sources.

Most POCs are also safe for air travel. POCs can provide continuous flow or pulse dose also known as short-burst or intermittent flow. Depending primarily on size, POCs can provide a continuous flow of 0. A common clinical conundrum with POC is the use of the pulse-dose mode. Most devices are labeled with dimensionless settings of 1—3 or 1—6.

This labeling is confusing for caregivers and patients alike. Again, the complicating factor is the patient's choice of a small, attractive, unobtrusive device that in all likelihood will not relieve hypoxemia during activity. The dose of oxygen during a h period is important to achieve the therapeutic objective.

The POC may fail in this goal if not chosen properly. A number of investigations have highlighted this problem. For example, a device with a maximum oxygen-generating capacity of 0. In these 2 examples, the maximum setting 1—6 for each device provides drastically different oxygen delivery to the patient.

This issue is further complicated when respiratory frequency exceeds the oxygen-generating capacity of the POC. In this case, the operation of the POC must adopt one of 3 methods: 1 deliver a constant pulse volume at a reduced oxygen purity; 2 deliver a reduced pulse volume at a constant oxygen purity; 3 Deliver a constant pulse volume, responding only to every 2—3 breaths. These are clinically relevant differences that may result in drastically different oxygen saturations in active subjects. Choice of a POC should be a joint decision that includes patient desires for simplicity, cost, and weight along with testing to assure adequate patient oxygenation during use.

Jacobs et al 87 have recently described patient perceptions related to home oxygen therapy. They analyzed almost 2, responses.

A third of subjects reported feeling very or somewhat unprepared to operate their equipment. Half of respondents reported oxygen problems, most frequently reporting equipment malfunction, lack of physically manageable portable systems, and lack of portable systems with high flows. Importantly, subjects living in Competitive Bidding Program areas reported oxygen problems more often than those who did not.

Those subjects reporting problems with their oxygen systems also experienced increased health-care resource utilization. I agree with previous discussions suggesting that POC should be labeled with the pulse volume at each setting to make the capabilities more transparent to patients and caregivers.

Several investigators have explored the use of closed-loop oxygen flow to overcome problems associated with varying patient demand during activity and changes in patient condition. A least one system is FDA-cleared. Lellouche and colleagues 91 — 94 have generated much of this work, using a system known as FreeO 2. They demonstrated efficacy and greater duration of time in desired saturation ranges compared with traditional oxygen therapy during exercise, during COPD exacerbations, and in emergency care.

Figure 3 demonstrates duration of time at S pO 2 target between FreeO 2 and conventional oxygen therapy during exercise walking. Percentage of time spent within the predefined S pO 2 ranges during the 3 tested conditions compressed air, constant low-flow oxygen [O 2 ], and FreeO 2 , during the endurance shuttle walk test A and during the min recovery period B.

These closed-loop systems are deceptively simple, and safety concerns related to excess oxygen delivery, monitoring respiratory frequency, and alerts to caregivers are important components.

In fact, the use of an alert, letting caregivers know when oxygen requirements have increased, could be an underappreciated advantage of closed-loop oxygen flow. The use of noninvasive ventilation NIV in chronic respiratory disease combined with oxygen therapy at home has recently been reported. Median oxygen flow was 1. After 12 months, 64 subjects completed the month trial. The median time to readmission or death was 4. The adjusted hazard ratio was 0. The month risk of readmission or death was This demonstrated an absolute risk reduction of Oxygen therapy is a mainstay of treatment in COPD patients with resting hypoxemia.

Other uses of LTOT for moderate hypoxemia, exercise-induced hypoxemia, nocturnal oxygen desaturation, and palliative care do not have strong evidence-based support. Despite these findings, oxygen is often delivered in these scenarios. Oxygen therapy during an exacerbation of COPD is potentially life-saving, but excessive oxygen is often delivered, to the detriment of survival.

Current use of oxygen in pre-hospital and emergency care needs to match the knowledge regarding excess oxygen delivery from half a century ago. Closed-loop oxygen delivery might play a role in this arena. Devices for home oxygen delivery continue to face cost pressures, and reimbursement for professional respiratory care services is limited.

A better appreciation of POC performance by caregivers and patients may lead to improved efficacy. A number of these issues have remained unchanged since the last R espiratory C are Journal Conference on oxygen therapy Table 5.

I was really intrigued by an earlier comment you made about the coronary vasoconstrictor effect, and I'd be interested in your opinion. Of course, I think we know that O 2 is a vasodilator in pulmonary hypoxic conditions. Is that a situation where it's reasonable to supplement O 2? The data on O 2 therapy and asthma are virtually nonexistent.

If you have asthma and you need O 2 , that is a real poor predictor of how well you're doing. Conventional wisdom suggests that if you're going to give an updraft nebulizer for their asthma, that you should power it with O 2.

There is a study 1 looking at the impact of oxygenation in subjects with asthma showing the same rise in P CO 2 and fall in pH, almost what you see in COPD. It's not as severe, but again that's changing ventilation perfusion, because you're filling the alveoli that have low ventilation with O 2 and allowing them to collapse. Neil [MacIntyre], I'm going to turn the tables and ask you a question that you would probably ask me if our roles were reversed. Yes, thank you.

Sam [Giordano], maybe you can respond — Sam has been at the center of this vortex. Perhaps you can at least explain what the uproar has been. I'll be glad to. I'm speaking in my role as chair of the United States COPD Coalition, which is a patient advocacy group consisting of state coalitions. There indeed is a lot of concern in the patient community. They're afraid that CMS [Centers for Medicare and Medicaid Services] will use the results of this study to raise the threshold requirement for reimbursement of supplemental oxygen.

The Coalition invited Bob to provide a briefing at one of our member webinars on the study a few months ago. He did a wonderful job of putting the results in perspective and offering reassurance to patients and providers.

I think that the salient takeaway from the study — and it seems like patients seem to get it — is what you told me on the telephone several months ago, Bob.

The results do not mean they will not get O 2 if they get some symptom relief. But, and again as Bob pointed out, there are certain patients who may be on O 2 who fall into the moderately hypoxemic category who don't want to be on supplemental oxygen, and derive no symptom relief. This study indicates that there isn't a medical reason for them to continue.

I'll chime in and generally agree with everyone here. There are data, and Rich reviewed them, on the hypoxemic subject with exercise who gets on O 2. Not in all studies, but in general, increase their 6-min walk test distance, and they get functional benefit from it. I think that's real. There are other studies that show that it will reduce pulmonary artery pressure, and that seems to be real. What the current studies show is that those physiologic changes don't necessarily spill over into mortality or exacerbation benefits.

Nevertheless, these intermediate values of increased exercise tolerance, reduced symptoms, and the like are legit, and from every indication I get, CMS is not interested in going after those indications. I think the chances of the rules changing, at least in the foreseeable future, are pretty low. Exactly on point. We spoke with CMS regarding this concern.

They were involved in discussions we had with the Coalition and the community. They were emphatic that they're not going to change reimbursement policy based on one study.

I would like to transition to CMS reimbursement policy for O 2 , which is something Rich threw out to the group during his presentation. For the first time in over 30 years, I think CMS is aware of the mistake we made by trying to commoditize O 2.

There are far too many technical nuances associated with supplemental oxygen systems to make this approach work for patients. Because it's treated like a commodity, you can buy a case of Depends with bidding but you can't really bid on O 2 and still offer a full range of delivery systems without the potential for underserving patient needs. Rich showed us several pictures of O 2 concentrators, and the long and the short of it is if a concentrator is not continuous-flow-capable, its output cannot be equated to L flow.

On the other hand if the device is capable of continuous flow, weight and battery life are factors. This variance in performance is confusing to patients and physicians alike.

The Internet offers so many benefits, but in this case, perhaps not. It seems patients get online and contact manufacturers directly. They are told by some sales people that their device will meet their needs but then discover the opposite in some cases. I am beginning to think that CMS does understand, now, that it may be time to change the way we prescribe O 2. I started as an inhalation therapist a couple of years before Medicare was passed and implemented.

I was just on the tail of O 2 tents and iron lungs. So, I remember the oxygen prescription was to maintain a target O 2 concentration inside of a tent. At the time, we never anticipated having all of these different delivery devices with a wide variety of technical capabilities. The biggest common denominator, with regard to the O 2 prescription should be targeting a pulse oximeter saturation range.

Better yet, have a respiratory therapist or a nurse who has delved into this technology, as several have, or a physical therapist or others to provide advice regarding the right piece of equipment for each patient. We're not even getting the proper order. They know about changing the form; we hope they will do that.

I'm amazed that we're still debating controlled O 2. And here we are 60 years later still debating what was demonstrated very clearly then. Dr Newhouse is the chief medical officer for InspiRx. NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail.

We do not capture any email address. Skip to main content. Research Article Conference Proceedings. Richard D Branson. He is also Editor in Chief of R C. View this table: View inline View popup Download powerpoint.