Use of Oxygen Therapy in COPD

oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

See also the separate records Chronic Obstructive Pulmonary Disease (COPD), Diagnosing COPD, Management of Stable COPD and Acute Exacerbations of COPD.

  • The respiratory drive is normally largely initiated by PaCO2 but in chronic obstructive pulmonary disease (COPD) hypoxia can be a strong driving force and so if the hypoxia is corrected then the respiratory drive will be reduced. There will also be a loss of physiological hypoxic vasoconstriction which is partly protecting the patient from the effects of areas of gross alveolar hypoventilation.[1]
  • Therefore, oxygen therapy in COPD must be used with care in the acute setting but it can have distinct benefits in the long-term. Chronic hypoxaemia causes slowly progressive pulmonary hypertension with the development of right ventricular hypertrophy and possible cor pulmonale with secondary polycythaemia. Secondary polycythaemia increases blood viscosity and hence resistance to flow. There is also sludging and a tendency to thrombosis.
  • A Cochrane review of randomised controlled trials (RCTs) of long-term oxygen therapy for COPD had the main outcome measure of survival on home oxygen therapy.[2] The conclusions from the 5 trials were:
    • Long-term oxygen therapy (LTOT) improved survival in COPD patients with severe hypoxaemia but few comorbidities.
    • LTOT did not improve survival in patients with moderate hypoxaemia or in those with mild-to-moderate hypoxaemia and arterial desaturation at night.
    • Those with desaturation at night were probably getting benefit from nocturnal oxygen and did not need it for a full 15 hours a day.
    • LTOT reduces mortality from secondary vascular complications but does not affect the progression of the airways disease.
  • Clinical Knowledge Summaries recommend that, if the patient will not stop smoking, oxygen therapy should be withheld.[3] There is a real risk of fire and burns to the face and any benefit relating to polycythaemia is counteracted by smoking.
  • For most COPD patients, you should be aiming for an SaO2 of 88-92%,[4] (compared with 94-98% for most acutely ill patients NOT at risk of hypercapnic respiratory failure). Mark the target saturation clearly on the drug chart.
  • The aim of (controlled) oxygen therapy is to raise the PaO2 without worsening the acidosis. Therefore give oxygen at no more than 28% (via venturi mask, 4l/min) or no more than 2 L/minute (via nasal prongs) in patients with a history of COPD until arterial blood gases (ABGs) have been checked.[5] Treat patients aged over 50 with possible COPD in the same way (eg long-term smokers with a history of chronic breathlessness) and get ABGs urgently.
    It is particularly important to check ABGs promptly if the patient has been brought in as emergency by an ambulance: ambulance crews have to give high flow oxygen if a patient is hypoxic, regardless of previous history.
  • Measure ABGs within 60 minutes of starting supplemental oxygen or changing its concentration. If PaO2 improves with an associated drop in PaCO2 and the pH is relatively unaffected (pH >7.26) then the concentration of the supplemental oxygen may be increased to maintain PaO2 >7.5 kPa.
  • Oxygen therapy will have to be complemented with bronchodilators (eg salbutamol 5 mg or terbutaline 10 mg, made up to 5 mL with normal saline) and high-dose oral steroids (eg prednisolone 30 mg daily).[1] In the presence of purulent sputum, antibiotics will also be required (see your local hospital policy for choice of antibiotic).
  • If acidosis develops (falling pH) with a rising PaCO2, other therapeutic interventions need to be discussed with the acute medical team; the intensive treatment unit (ITU) may need to be involved and decisions regarding ceiling of care have to take place at this point. Noninvasive positive pressure ventilation (NIPPV), intermittent positive pressure ventilation (IPPV) and doxapram are all options.
  • Check ABGs on air before discharge in those who presented with a low pO2 and/or hypercapnia to guide later formal assessment for LTOT.
  • 4 to 6 weeks' follow-up should include consideration of LTOT assessment - not before, as the patient needs to be clinically stable.[6]

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Once this is started, LTOT is likely to be lifelong. It is usually given over a minimum of 15 hours a day, including overnight when arterial hypoxaemia worsens during sleep (some advocate 18 or even 24 hours a day).

  • Assess the need for oxygen therapy in people with any of the following:
  • Consider assessment for people with severe airflow obstruction (FEV1 30-49% predicted).
  • Assess by measuring ABGs on two occasions at least 3 weeks apart in people with confirmed stable COPD who are receiving optimum medical management. Obtaining ABGs in the community can be difficult and may require a visit to the local hospital or involvement of the Specialist Respiratory Nurse.
  • Offer LTOT to people with PaO2 less than 7.3 kPa when stable, or greater than 7.3 and less than 8 kPa when stable and with secondary polycythaemia, peripheral oedema, nocturnal hypoxaemia or pulmonary hypertension.
  • Be aware that inappropriate oxygen therapy in people with COPD may cause respiratory depression.
  • All healthcare settings should have a pulse oximeter to ensure all people needing LTOT are identified and to review people receiving LTOT at least once a year.
  • People receiving LTOT should breathe supplemental oxygen for at least 15 hours a day. If they smoke, warn them about the risk of fire and explosion.
  • Use oxygen concentrators to provide the fixed supply for LTOT at home.
  • Refer people who are hypercapnic or acidotic on LTOT to a specialist centre for consideration of long-term noninvasive ventilation (NIV).
  • NIV should be used as the treatment of choice for persistent hypercapnic ventilatory failure during exacerbations not responding to medical therapy.
  • Offer ambulatory oxygen to people already on LTOT who want to use oxygen outside the home, following assessment by a specialist.
  • Consider it in motivated individuals who have exercise desaturation and PaO2 less than or equal to 7.3 kPa and whose exercise capacity and/or breathlessness improve with oxygen.
  • The benefits of ambulatory therapy include:
    • It can improve exercise tolerance and breathlessness but there is no evidence of benefit from oxygen before or after exercise in most patients with chronic obstructive pulmonary disease (COPD).[8]
    • It may allow increased daily oxygen use and/or better compliance.

The British Thoracic Society (BTS) Working Party which developed the guidance for clinicians on assessment of patients for oxygen allocated categories for prescription of ambulatory oxygen:[9]

  • Grade 1 oxygen requirements (LTOT low activity). These patients are mainly housebound or do not leave the home without assistance and will need only an occasional portable cylinder. The oxygen flow rate will be the same as the patient uses for LTOT, as they will be sedentary. The average time of use will be approximately 1 hour per day but may vary.
  • Grade 2 oxygen requirements (LTOT active group). This includes patients receiving LTOT who are mobile and need to leave the home on a regular basis. They will require referral to specialist care for full assessment for ambulatory oxygen. This will involve the determination of the oxygen flow rate required to abolish desaturations below 90% during exercise. At present there is no reliable tool to predict which patients will be compliant users of ambulatory oxygen and so the working group suggests that patients are first provided with ambulatory oxygen sufficient for 2 hours' use daily and then asked to monitor their daily usage. All patients should be seen after 2 months when their true requirement can be determined and the oxygen order adjusted if necessary.
  • Grade 3 requirements (non-LTOT patients who are exercise desaturators). They will require referral to specialist care for more detailed assessment as to whether they meet the criteria for ambulatory oxygen.
  • Short-burst oxygen therapy refers to the intermittent use of supplemental oxygen at home for 10-20 minutes at a time to relieve dyspnoea. It is usually provided from cylinders. It is often prescribed for patients who do not meet the criteria for LTOT but who remain breathless after minimal exertion despite other therapy.
  • Consider short-burst oxygen therapy (from cylinders) only for episodes of severe breathlessness not relieved by other treatments and continue only if breathlessness improves.[7]

Prescription

See separate related article Prescribing Oxygen for full details but some aspects are repeated here.

  • Patients need to be assessed first by a specialist team before a GP can make the prescription.
  • The supply of home oxygen has been transferred from community pharmacies to regional oxygen supply companies in England and Wales.[9][10] These companies are responsible for supplying cylinders, concentrators and liquid oxygen as part of an integrated service.
  • Oxygen should be ordered directly from one of four regional supply companies via the Home Oxygen Order Form (HOOF)[11] which has replaced prescribing of oxygen on FP10 prescriptions.
  • Form completion notes are on the back - ensure you specify all the details (notably, the oxygen concentration).
  • Regular orders should take three days; emergency ones should be delivered in four hours.[10]
  • These arrangements do not apply to Scotland and Northern Ireland.

Maximising benefit

  • As a general rule, it is more economical to use an oxygen concentrator rather than cylinders if oxygen is required for more than 8 hours per day or if prescriptions exceed 21 cylinders per month. Use nasal prongs at 2-4 L/minute (depending on ABGs).
  • There is no benefit from LTOT for less than 15 hours a day.
  • Smokers should stop smoking or benefit is unlikely. There is a very significant risk of burns and fire.
  • Get optimum benefit from other forms of therapy, including inhalers.

Monitoring[6]

  • The patient's ABGs need to be monitored. Simply measuring SaO2 is not enough, as assessment of hypercapnia and its response to oxygen therapy is required.
  • ABGs can be radial, femoral or from the earlobe. Collect a sample when the patient has been breathing air for at least 30 minutes after having received any prior supplemental oxygen.
  • Once therapy has started, measure ABGs with oxygen therapy (for at least 30 minutes on therapy, using the same equipment as at home if possible), to assess response and ensure pO2 is >8.0 kPa without unacceptable hypercapnia.
  • Subsequently, measure ABGs when the patient is clinically stable and on optimal therapy on two occasions at least three weeks apart.
  • All patients should be visited at home within 4 weeks of prescription by a specialist nurse, physiotherapist or technician (depending on local arrangements), experienced in the provision of domiciliary oxygen therapy. The aim is to provide education and support and to measure the SaO2 with oximetry both on air and with therapy. This should be 92% or above with therapy.
  • It is important to maintain 6-monthly follow-up with reassessment for early recognition of problems. The BTS recommends domiciliary assessment by a respiratory health worker.

Travel

Travel by land or sea presents few problems:

  • Reduced pO2 in airline cabins will increase hypoxia in those patients with hypoxia at sea level. The BTS suggests that flying is relatively contra-indicated in those with hypercapnia or gross hypoxia breathing air (pO2 <6.7 kPa).
  • Most major airlines can provide supplemental inflight oxygen and assistance with embarkation if arranged in advance.
  • It is usually possible to arrange temporary provision of LTOT from a local chemist during a holiday but many patients can manage well without LTOT for several days.

Further reading & references

  1. Moulton and Yates; Lecture Notes in Emergency Medicine; Blackwell Publishing (2006)
  2. Crockett AJ, Cranston JM, Moss JR, et al; A review of long-term oxygen therapy for chronic obstructive pulmonary disease. Respir Med. 2001 Jun;95(6):437-43.
  3. Chronic obstructive pulmonary disease, Clinical Knowledge Summaries (November 2010)
  4. Emergency Oxygen Use in Adult Patients, British Thoracic Society, October 2008
  5. Denniston AK, O'Brien C, Stableforth D; The use of oxygen in acute exacerbations of chronic obstructive pulmonary disease: a prospective audit of pre-hospital and hospital emergency management. Clin Med. 2002 Sep-Oct;2(5):449-51.
  6. Working Group on Home Oxygen Services, British Thoracic Society (January 2006); Clinical Component for the home oxygen service in England and Wales
  7. Chronic obstructive pulmonary disease; NICE Clinical Guideline (June 2010)
  8. Nandi K, Smith AA, Crawford A, et al; Oxygen supplementation before or after submaximal exercise in patients with chronic obstructive pulmonary disease.; Thorax. 2003 Aug;58(8):670-3.
  9. Wedzicha JA, Calverley PMA; All change for home oxygen services in England and Wales; Thorax 2006;61:7-9 [full text]
  10. Home Oxygen Service: Briefing Note, Dept of Health; Advice for contractors, including names of regional suppliers
  11. EMIS HOOF Wizard

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Olivia Scott
Current Version:
Document ID:
2908 (v25)
Last Checked:
21/01/2011
Next Review:
20/01/2016