Use of Oxygen Therapy in COPD

See also our records on:
Chronic Obstructive Pulmonary Disease (COPD)
Diagnosing COPD
Management of Stable COPD
Acute Exacerbations of COPD

Description

The British Thoracic Society defines COPD as a "chronic, slowly progressive disorder characterised by airflow obstruction (reduced FEV₁ and FEV₁/VC ratio) that does not change markedly over several months." This definition is shared by the NICE guidelines on COPD from February 2004.¹ Airflow obstruction is defined as a reduced FEV₁ and a reduced FEV₁/FVC ratio such that FEV₁ is less than 80% of that predicted and FEV₁/FVC is less than 0.7.

Pink puffers and blue bloaters

In normal people the respiratory drive is largely initiated by PaCO₂ but in COPD hypoxia can be a strong driving force and so if this is corrected the respiratory drive will be reduced. Patients with COPD have traditionally been divided into pink puffers and blue bloaters based on their physiological response to abnormal blood gases.² The former work hard to maintain a normal pO₂ which is why they puff away. They tend to have a barrel-shaped, hyperinflated chest and breath through pursed lips. The latter are blue because of hypoxia and polycythaemia. They are often obese and have water retention. This is why they are bloated. The blue bloaters are dependent upon hypoxia for their respiratory drive and to give oxygen and deprive them of this will lead to signficant hypercapnia and acid base imbalance. Although this concept is widely taught and acknowledged academically, in clinical practice patients tend not to be clearly in one or the other of these two categories.

Cost of COPD to the NHS

COPD is a major cause of morbidity, with high usage of resources in Primary and Secondary Care. It costs the NHS about £500 million a year and 95% is caused by smoking.³ The cost per patient in the UK is probably in excess of £1,600 per annum.⁴

The potential dangers of giving oxygen in COPD have long been known but the potential benefits were not appreciated until the 1980s.^5,6 As described above, hypoxia can be a strong driving force in these patients (particularly among the blue bloaters); administering oxygen will reduce this drive in these patients. Additionally, there will be a loss of physiological hypoxic vasoconstriction which is partly protecting the patient from the effects of areas of gross alveolar hypoventilation.² Hence 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. The last increases blood viscosity and hence resistance to flow. There is also sludging and a tendency to thrombosis.

When oxygen is used in patients who are not thought to have COPD, especially those with terminal cancer, such caution is not required.⁷ If a general practitioner thinks that a patient with COPD may benefit from oxygen, that patient should first be assessed by a respiratory physician or a specialist respiratory team.

Clinical Knowledge Summaries recommend that if the patient will not stop smoking, that oxygen therapy should be withheld.⁸ There is a real risk of fire and burns to the face and any benefit relating to polycythaemia is counteracted by smoking.

The acute episode

• For most patients, you should be aiming for an SaO₂ of 85-92%.²
• The aim of (controlled) oxygen therapy is to raise the PaO₂ without worsening the acidosis. Therefore, do not prescribe oxygen at >28% (via venturi mask) or 2 L/min (via nasal prongs) in patients over 50 with a history of COPD until arterial blood gases (ABGs) have been checked.⁹
  

  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 (e.g. salbutamol 5mg or terbutaline 10mg, made up to 5mL with normal saline) and high dose oral steroids (e.g. prednisolone 30mg daily).² In the presence of purulent sputum, antibiotics will also be required (see your local hospital policy for choice of antibiotic).
• Admission to be hospital should be considered in those patients who:^2,10
  • Have chest x ray changes
  • Have SaO₂<90%, pH<7.35 or PaO₂<7kPa
  • Are acutely confused
  • Are already on long term oxygen therapy (LTOT)
  • Are in poor or deteriorating health ± have significant co-morbidity
  • Had a rapid onset of the exacerbation
  • Have worsening peripheral oedema
  • Have developed new signs (e.g. cyanosis)
  • Are not coping at home
  • Show poor activity levels
• If acidosis develops (falling pH) with a rising PaCO₂, other therapeutic interventions need to be discussed with the acute medical team; ITU may need to be involved and decisions regarding ceiling of care have to take place at this point. NIPPV, 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.³

Long term oxygen therapy (LTOT) is where there is provision of continual use oxygen therapy in the home for patients with chronic hypoxaemia (PaO₂ at/below 7.3kPa/55mmHg) with an oxygen flow rate sufficient to raise the waking O₂ tension to above 8kPa (60mmHg).³ Once this is started, it is likely to be lifelong. It is usually given over a minimum of 15 hours a day, including over night when arterial hypoxaemia worsens during sleep (some advocate 18 or even 24 hours a day).

Indications

In the following section, levels of evidence are given and the reader is referred to the article on different levels of evidence or to the NICE explanation of its grading of evidence.

NICE states that the following are indications for considering LTOT:

• Patients with a PaO₂ of less than 7.3kPa when stable or PaO₂ of 7.3 to 8.0kPa when stable but an additional risk feature such as secondary polycythaemia (with a haematocrit > 55%), nocturnal hypoxaemia (consider this where there is a history of morning headaches), peripheral oedema or pulmonary hypertension.¹⁰ This is given as level of evidence A.
• Oxygen should be used for at least 15 hours a day as there is no benefit for shorter durations.¹¹ Evidence level A.

The British Thoracic Society specifically states that LTOT should not be prescribed in those chronically hypoxaemic patients with a PaO₂>8kPa.³ If the patient has borderline ABGs but other factors suggesting they would benefit, reassess in 3 months. NICE suggests assessment of the need for oxygen therapy in patients with the following (evidence level D):

• Severe airflow obstruction with FEV₁ of less than 30% of predicted.
• Associated cyanosis, polycythaemia or peripheral oedema.
• Elevated jugular venous pressure.
• Oxygen saturation less than 92% when breathing air.
• Consider assessment for moderate airflow obstruction (FEV₁ 30 to 49% of predicted). Evidence level D.
• Ambulatory oxygen therapy may be of benefit in those who wish to continue therapy outside the home - see below. Evidence level D.
• Short bursts of oxygen therapy for episodes of breathlessness should only be used if all other methods fail - see below. Evidence level C.

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.¹¹ The conclusions from the 5 trials were:

• Long-term oxygen therapy improved survival in COPD patients with severe hypoxaemia but few co-morbidities.
• Long-term oxygen therapy 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.

Prescription

See 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.^12,13 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)¹⁴ 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.¹²
• 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/min (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 also the very significant risk of burns and fire.
• Get optimum benefit from other forms of medication including inhalers.

Monitoring³

• 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 ear lobe. Collect a sample with 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) who are 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 contraindicated in those with hypercapnia or gross hypoxia breathing air (pO₂ <6.7 kPa).
• Most major airlines can provide supplemental in-flight 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.

Ambulatory oxygen therapy

The BTS Working Party which developed the guidance for clinicians on assessment of patients for oxygen allocated categories for prescription of ambulatory oxygen:¹³

• 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 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.

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 COPD.¹⁵
• It may allow increased daily oxygen use and/or better compliance.

There is not a great deal of evidence for benefit (NICE level D). Appropriate assessment of patients is essential so that the right patients are treated with home oxygen for the right period of time and with appropriate flow rates to obtain optimal benefits and reduce the chance of adverse effects.¹³ Refer to specialists.

Following specialist assessment, the team can authorise the equipment so that the GP does not have to issue a prescription. GPs can continue to prescribe oxygen for symptomatic relief in palliative care or where a patient needs short burst of oxygen. If a patient requires long term or ambulatory oxygen, the GP can refer patients to the specialist team to assess and prescribe for particular needs.

A portable cylinder, size DD provides 2 L/min oxygen for just under 4 hours and at 4 L/min for just under 2 hours. NICE notes that many of the devices in use are not currently available on prescription.¹

This 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.Traditional indications have included:³

• Pre-oxygenation before exercise
• Breathlessness post exercise
• Control of breathlessness at rest
• Use after an acute exacerbation of COPD whilst awaiting LTOT

However NICE notes that short-burst oxygen therapy is one of the most expensive therapies used in the NHS yet its evidence base is poor.¹ It may simply be an expensive placebo that cools the face rather than correcting hypoxia.

The NICE recommendation is that short-burst oxygen therapy should only be considered for episodes of severe breathlessness in patients with COPD not relieved by other treatments. It should only continue to be prescribed if an improvement in breathlessness following therapy has been documented.