O2 therapy is either ‘controlled’ or ‘uncontrolled’.
• Uncontrolled and highest levels thought to be important, e.g.:
• Shock, sepsis, major trauma
• Cardiac arrest and during resuscitation
• CO or cyanide poisoning
• Uncontrolled and SaO2 values between 94 and 98% are thought best. Use when extra O2 is required to raise the SaO2 and where there are no concerns that high PaO2 values will depress ventilatory drive to the point that PaCO2 will rise and pH fall dangerously, e.g.
• Acute heart failure
• Controlled Use when extra O2 is required, but ventilation critically depends on hypoxic drive (BTS recommends 88–92%), e.g.:
• Exacerbations of COPD (particularly when there has been a chronically raised PaCO2, as evidenced by a significant base excess)
• Exacerbations of CF
• Exacerbations of ventilatory failure due to obesity hypoventilation syndrome
• Exacerbations of chronic ventilatory failure due to scoliosis, neuromuscular disease, and any other cause of ‘pump’ failure.
With stable type II ventilatory failure, ventilation still seems to be dominantly driven by PaCO2/pH, but, in exacerbations (when PaO2 usually falls), peripheral chemoreceptor drive from low PaO2 becomes dominant. Thus, O2 therapy must not raise PaO2 above 8kPa (≈ 92% SaO2), as this will ‘turn off’ ventilatory drive, allowing hypoventilation, hypercapnia, acidosis, and potentially death. There is some evidence that high alveolar PO2 also ‘turns off’ hypoxic pulmonary vasoconstriction. This allows an increase in pulmonary blood flow to poorly ventilated areas and reduces CO2 excretion (accounts for ~20% of the PaCO2 rise following excessive FiO2 in COPD exacerbations).
There is increasing evidence that indiscriminate use of O2 in some medical emergencies may actually be harmful and should only be used if the patient is hypoxaemic (<94% and then to achieve no higher than 98%), e.g.:
• Ischaemic heart disease, including MI
• Post-cardiac arrest, once stable
• Sickle cell crisis
• Obstetric emergencies
• Most poisonings (other than CO or cyanide)
• Metabolic or renal acidosis with SOB.
High O2 levels can be toxic through release of free radicals, and this may be the mechanism of damage in some of the above situations. Following lung injury, particularly from paraquat and bleomycin, high O2 concentrations are clearly damaging to the lung; thus, a degree of controlled hypoxia may be preferable.
Delivering uncontrolled O2
This can be done in many ways, essentially by blowing O2 over the face, whilst limiting inhalation of surrounding air, or exhaled CO2.
• Standard O2 face masks (sometimes called high-flow masks). Set the O2 regulator to at least 4L/min, much more if very breathless (to prevent dilution by air drawn into mask by high inspiratory flows via exit holes). Can deliver about 50–60% O2
• Nasal cannulae/prongs/catheters are uncontrolled and deliver unpredictable levels of O2 (depending on flow rate, minute ventilation, and oral vs nasal breathing). Titrate using an O2 saturation monitor
• Non-rebreathe reservoir masks can deliver FiO2 values over 60% by means of a soft plastic bag between the end of the tubing and mask, plus one-way valves between the bag and mask and on the mask exit ports. This mechanism ensures that most of the inspired air is pure O2. The ability of the reservoir to empty on inspiration briefly allows higher inspiratory flows than the actual O2 regulator setting, and the bag valve prevents inhalation of very much exhaled CO2; the mask exit valves close, preventing air inhalation. The usual problem is kinking of the junction between the mask and bag when the head tilts forward, reducing the effectiveness of the reservoir
• Very high FiO2 requires a tight seal and is generally delivered with CPAP masks (using pressures of about 5–7cmH2O). This ensures no air is entrained through blow-off vents or leaks, as well as improving V/Q matching by recruiting collapsed alveoli.
Delivering controlled O2 therapy
This requires the ability to reliably control the FiO2 in order to keep the patient’s SaO2 ≤92% (some prefer ≤90%), but high enough to prevent anaerobic metabolism. This lower acceptable level is debatable: 88% is generous; 85% is likely to be adequate, and 80% may be acceptable if cardiac output is adequate and patient’s usual levels are around this figure.
• FiO2 is controlled through Venturi masks—O2 is directed through a narrow nozzle and exits at speed, lowering the air pressure at this point. This draws in surrounding air, diluting the O2
• A proper Venturi mask mixes O2 and air in the same proportion, regardless of the O2 flow
• The minimum flow setting of the regulator, written on the nozzle, ensures adequate overall flow to prevent diluting air being drawn through the exit holes during inhalation, e.g. a 28% ventimask has a 1:10 entrainment ratio—1L/min O2 entrains 10L/min air (total flow 11L/min); 2L/min O2 entrains 20L/min (total flow 22L/min), etc.
• Nasal cannulae are definitely not controlled O2 therapy and are, in fact, the opposite. If nasal cannulae do deliver too high an FiO2 and ventilation decreases as a consequence, the proportion of the minute ventilation containing the fixed flow nasal O2 will rise, increasing the FiO2 and hence PaO2 still further—a vicious cycle
• Controlled O2 via low flows is also needed sometimes with NIV but rarely requires >1L/min to be entrained; again it should be titrated using the SaO2
• When the patient on NIV is still required to trigger inspiration, again added O2 should be kept to a minimum so as not do depress ventilatory drive
• When adding too much O2, it is easy to be lulled into a false sense of security by an SaO2 value >92%, while the PaCO2 gradually rises undetected.
O2 alert card
should be given to all patients with a previous episode of hypercapnic respiratory failure (see Fig. 58.1). This alerts ambulance crews and medical staff to the potential risk of hypercapnia with high-flow O2 and documents usual resting baseline SaO2. However, some ambulance staff protocols are sufficiently rigid that they may not be allowed to override them. In some areas, letters from the patient’s consultant and head of the ambulance service must be with the patient.
BTS guideline for emergency O2 use in adult patients. Thorax 2008;63(suppl V):1–68.Find this resource:
O’Driscoll R. Emergency O2 use. BMJ 2012;345:39–43 (much more readable than the BTS guidelines).Find this resource:
Home O2 therapy was originally prescribed under three clear headings: (1) long-term (LTOT, treatment of chronic hypoxia in COPD, requiring >15h/day, with the evidence base from two randomized trials), (2) short-burst O2 (SBOT, to cover periods of SOB such as after exercise), and (3) ambulatory to allow activity with less dyspnoea. The distinctions became blurred, and short-term use of O2 for transient SOB was shown in most cases to be of little more value than a fan; the value of LTOT beyond COPD has been extended into other causes of hypoxia (without very much evidence of benefit), and ambulatory O2 is now more available with increasing usage.
The BTS Standards of Care Subcommittee have recently produced useful advice on O2 services (see Further information p. [link]).
Background and indications
Two landmark trials of LTOT in the 1980s—the British MRC Working Party trial and the American Nocturnal O2 Therapy Trial (NOTT) established the value of LTOT. The MRC trial compared COPD patients receiving O2 for 15h/day with controls receiving no O2. The NOTT trial compared continuous daily O2 (average 17.7h/day) with overnight O2 (average 12h). The patients in the MRC trial were on average hypercapnic (mean PaCO2 7.3kPa), whereas those in the NOTT trial were on average normocapnic (mean PaCO2 5.7kPa). The main outcome in both trials was improved survival in those patients receiving O2 for at least 15h/day, though this improved survival was not seen in the MRC trial until after a year of O2 therapy.
The NOTT trial showed a reduced exercise PAP after 6 months of continuous or nocturnal O2 therapy. The 8y survival was related to the fall in mean PAP during the first 6 months of continuous O2 use.
The MRC trial failed to show a fall in mean PAP with LTOT, but the mean annual increase in PAP (3mmHg) in patients in the control arm was not seen in the O2 treated group.
The reason for the improved survival with LTOT is not clear and is unlikely to relate to the small changes in pulmonary haemodynamics seen.
COPD is the disease for which LTOT is most commonly prescribed and the disease in which the original studies were completed. Subsequent O2 studies have shown improved exercise endurance in COPD patients breathing supplemental O2, with improved walking distance and ability to perform daily activities. FEV1 is the strongest predictor of survival in COPD; LTOT does not influence the decline in FEV1.
Additional benefits of LTOT include:
• Reduction of 2° polycythaemia
• Improved sleep quality by reducing hypoxia-associated brain arousals
• Reduced cardiac arrthymias, and potentially reducing the risk of nocturnal sudden death
• Reduced sympathetic outflow, leading to improved renal function, with increased salt and water excretion, and reduced peripheral oedema.
LTOT is the provision of O2 therapy to patients with a chronically low PaO2 (≤7.3kPa, or ≤55mmHg, or SaO2 ≤/≈88%) for ≥15h a day (to include the night, when usually most hypoxic), with the aim of achieving an awake PaO2 >8kPa, or >60mmHg, or SaO2 >/≈91%. PaCO2 levels can be normal or raised.
The indications to which LTOT now covers are:
• Severe chronic asthma
• Pulmonary vascular disease
• Pulmonary malignancy
• Chronic heart failure.
LTOT can also be prescribed if the PaO2 is between 7.3 and 8kPa, if associated with 2° polycythaemia or PHT. PaO2 values above 8kPa should not lead to a prescription for LTOT.
In addition, it can be prescribed for nocturnal hypoventilation, usually in conjunction with NIV or CPAP, e.g. in:
• Neuromuscular or other restrictive disorders
• OSA treated with CPAP therapy but with continuing hypoxia.
This is entirely non-evidence-based (with no guidance on thresholds, etc.) and should only happen following assessment in a specialist unit and following optimization of the NIV or CPAP.
There are exceptional uses such as nocturnal O2 for the Cheynes–Stokes of heart failure (despite adequate awake levels) which can improve sleep quality.
Finally, it is accepted that, in certain terminal diseases, hypoxia-induced dyspnoea can be usefully relieved with LTOT.
Assessment for LTOT
• Should occur when patients are stable and >5 weeks have passed since any exacerbation of their condition
• Fully optimized treatment
• Two sets of arterial gases are taken at least 3 weeks apart to ensure that the patient remains sufficiently hypoxic to merit LTOT
• Blood gases are also taken after 30min on supplemental O2 to ensure the target PaO2 has been reached.
Given the day-to-day fluctuation in blood gases and the relatively arbitrary nature of the cut-offs for qualifying for LTOT, it is very likely that oximetry would be equally precise (or imprecise) as arterial PaO2. However, this is not currently recommended.
Arterial gases, rather than oximetry, may still be preferable when CO2 retention is a possibility, but this can occur overnight follwing LTOT and not be evident during a 30min test. Thus, patients need to be warned about the symptoms of CO2 retention and told to reduce or stop the supplemental O2 if they occur.
Provision of supplemental O2 during exercise and activities of daily living. This may be on its own or in addition to LTOT. The conditions provoking exercise hypoxia are of course similar to the conditions mentioned previously.
The requirement for O2 in these circumstances depends on the degree of activity the patient is likely to achieve. If already on LTOT, then it is likely that ambulatory O2 will be needed when away from home, should there be significant dyspnoea without it. Such patients are often housebound and would only require it for only short periods.
The patient must understand that they need to use the O2 during the exercise/activity, not for recovery afterwards.
Greater use should require actual proof that there is significant exercise hypoxia and dyspnoea and that O2 relieves these.
A 2-month assessment is usually required to determine the likely number of hours of use. A reasonable initial prescription might be for 1–2h/day. Ideally, usage should be regularly reviewed and withdrawn if of no benefit or not being used.
There are now many different options available for supplying portable O2, e.g. conserver devices (delivering pulsed O2 during inspiration only), self-fill cylinders, transportable or portable concentrators, lightweight cylinders, and liquid O2 systems.
Short-burst O2 is now rarely justifed. It may be required for transient situations, such as during exacerbations, but usually either the patient is sufficiently hypoxic to require LTOT or they are not. If it is considered, then proof of efficacy should be sought, particularly given its expense.
• Home O2 should not be supplied to patients who still smoke, due to added fire risk and probable reduced efficacy due to ↑ COHb
• LTOT is provided by an O2 concentrator, set between 0.5 and 8L/min. Some concentrators can deliver 8L/min. Concentrators contain a molecular sieve of zeolite, which traps gas molecules, depending on size and polarity. Can produce up to 96% O2, depending on flow (the argon is also concentrated to 4%)
• Patients may have a higher flow rate for use during activities
• Patients can use nasal prongs or a fixed concentration mask (uncontrolled or controlled O2, e.g. 24% and 28%), depending on physiological requirements and their preference. A back-up cylinder should be prescribed in case of power cuts
• O2 humidification (cold) is possible but rarely necessary or effective. Tube lengths of <1.5m recommended
• LTOT should be used for ≥15h/day in patients with COPD, although survival improves when used for longer; therefore, use should not be restricted to 15h/day
• Patient education in the use of LTOT and machine maintenance is important. Specialist respiratory nurses should be involved with this
• If using SBOT at >3 O2 cylinders/week, an O2 concentrator is more economical.
How to organize home O2
• The UK-wide integrated O2 service (2005) ensured provision of all modalities of domiciliary O2 from one contractor in each area
• The prescriber completes and signs a Home Oxygen Order Form (HOOF), providing the supplier with the patient’s details, an exact prescription of the O2 required, including modality, and details of numbers of each piece of equipment needed (e.g. numbers of O2 cylinders)—the supplier may be able to help advise on this (see Box 58.1)
• The HOOF is used for the prescription of all forms of O2; must include details of the O2 flow rate, % O2, and delivery device/mask required
• HOOF part A can be used by non-specialists (e.g. GPs, out-of-hours services, palliative care) to temporarily prescribe static O2 concentrators or static cylinder, pending specialist assessment
• HOOF part B is completed by specialist respiratory services after formal clinical assessment and provides access to the full range of O2 services
• The O2 supplier will invoice the local commissioning group; it is vital that the above information is completed, otherwise the HOOF will be returned unfilled
• A Home Oxygen Consent Form (HOCF) must be signed by the patient, consenting for the disclosure of relevant medical information, address, telephone number to the O2 supplier and fire brigade
• The HOOF is faxed to the O2 supplier, with copies to the local commissioners, GP, and clinical lead for home O2 services
• The South West (Air Liquide) is currently using a single HOOF.
is needed to ensure:
• Compliance; withdraw if not using despite support and explanation. Home visit within 4 weeks by specialist nurse recommended
• Confirm the ongoing requirement for LTOT. Some patients improve and no longer need LTOT. ABG tensions at 3 months and then yearly monitoring (may be performed by specialist nurses)
• Cancellation with the O2 company as soon as a patients dies
• Inform O2 company of any changes in flow rates/%O2
• Inform O2 company of any changes in patient address, etc.
The BTS standards of care subcommittee, home O2 services sub-committee report. http://www.brit-thoracic.org.uk/Portals/0/Clinical%20Information/Home%20Oxygen%20Service/clinical%20adultoxygenjan06.pdf.
Full BTS guidelines in preparation for 2014.
Patient information. http://www.nhs.uk/conditions/home-oxygen/pages/introduction.aspx.