Oxygen Therapy Reperfuse, but Remain Poorly Ventilated Tension (Pao2) and Sao2 Are 10–13 Kpa and 94–98%, Respectively

CME: CLINICAL PRACTICE AND ITS BASIS effect (decreased CO2 buffering by oxyhaemoglobin) all contribute to hyper- Respiratory medicine capnia, but the greatest effect is likely to relate to worsened ventilation-perfusion mismatch. Deoxygenated pulmonary Edited by Craig Davidson MD FRCP, arterial blood is diverted away from areas Consultant in Respiratory and Intensive Care Medicine, of diseased lung because alveolar hypoxia St Thomas’ Hospital, London due to poor ventilation causes vasoconstriction and thus decreased local perfusion (ie hypoxic pulmonary vasoconstriction). If high-flow oxygen is The normal ranges of arterial oxygen applied, these alveoli re-oxygenate and Oxygen therapy reperfuse, but remain poorly ventilated tension (PaO2) and SaO2 are 10–13 kPa and 94–98%, respectively. It is apparent and fail to clear CO2. In reasonably that DO cannot be significantly healthy lungs, regional failure to clear Luke S Howard MA DPhil MRCP, Consultant 2 CO can be compensated by an overall Chest Physician, Department of Respiratory enhanced by increasing PaO2 above 16 2 Medicine, Hammersmith Hospital, Imperial kPa, where haemoglobin is 100% satu- increase in ventilation, but impaired res- College Healthcare NHS Trust rated and the amount of oxygen dis- piratory mechanics prohibit this in solved in the plasma is small. This COPD. Other adverse effects of hyperoxia Clin Med 2009;9:156–9 manoeuvre will maximise CaO2 but may relate to effects on the cardiovascular not always optimise DO2. system and the production of reactive Oxygen delivery (DO ) is arguably the oxygen species (discussed in detail else- 2 Oxygen ‘toxicity’ most critical requirement for the mainte- where5). Table 1 summarises some of the nance of normal organ function and can There are many reasons why maximising concepts, with selected references. be illustrated by Equation 1: SaO2 may firstly not optimise DO2 and Hyperbaric oxygen therapy for stroke and secondly may impact adversely on other intracoronary hyperoxaemic reperfusion DO = CaO × cardiac output 2 2 aspects of a patient’s physiology. The for myocardial infarction (MI) are cur- where CaO2 is total oxygen content, best-known example of this occurs rently being explored. It is possible that made up largely of oxygen bound to during acute exacerbations of chronic the significant rise in oxygen tension in haemoglobin and, to a much smaller obstructive pulmonary disease (COPD). infarcted tissue may outweigh the physio- degree, oxygen dissolved in plasma. DO2 Here PaO2 above 10 kPa is associated logical changes and oxidative stress, but therefore depends not only on the degree with respiratory acidosis and worse out- these data are awaited. Studies of supra- 3,4 of oxygenation of the blood but also on comes. Decreased hypoxic drive, physiological DO2 in critical illness have cardiovascular function and haemo- absorption atelectasis and the Haldane so far failed to show benefit.10 globin concentration. Despite its impor- tance, it is not the most tightly regulated physiological parameter for metabolism and gas exchange. This is well illustrated Table 1. The adverse effects of hyperoxia achieved with normobaric oxygen. by a study of repeated venesection Organ/System Effect of hyperoxia resulting in isovolaemic anaemia (5 g/dl) in healthy humans.1 While cardiac Pulmonary • Absorption atelectasis output rose, it was insufficient to main- • Release of hypoxic pulmonary vasoconstriction, leading to worsened ventilation/perfusion matching tain DO2 but because of the steep slope of the oxyhaemoglobin dissociation • Decreased ventilation Pulmonary capillary leak – oxygen toxicity curve at the tissue level, the fall in DO2 • was offset by increased oxygen extrac- Cardiovascular • Coronary vasoconstriction tion, indicated by a reduction in mixed • Increased systemic vascular resistance (increasing cardiac work) venous oxygen (SvO2). Decreased cardiac output (decreasing O delivery) • 2 SvO2 is therefore a much better indi- Reperfusion injury post-myocardial infarction6 cator of oxygen delivery than arterial sat- • • Worsened outcomes post-neonatal resuscitation7 uration (SaO2), and is one of the targets Neurological Neuronal injury post-cardiac arrest in adults8 in resuscitation in sepsis. SaO2 is readily • measurable and helpful in resuscitation, • Increased mortality following minor/moderate stroke9 although attention should be paid to Haematological Decreased CO buffering by haemoglobin (Haldane effect) • 2 integrated physiological function.2 156 Clinical Medicine Vol 9 No 2 April 2009 © Royal College of Physicians, 2009. All rights reserved. CME Respiratory medicine Emergency oxygen use in adults Even when saturations are being 2 Oxygen only when needed to achieve monitored, it may be appropriate normal oxygen saturations, given the Guidelines as other contributors to DO2 absence of proven benefit of aiming Recent guidelines for emergency oxygen (Equation 1) may not yet be known. higher and of concerns over the in adults have been developed under the Furthermore, it can provide a physiological and potentially toxic auspices of the British Thoracic Society margin of safety in the event of effects of hyperoxia. (BTS) in association with 21 UK soci- worsening gas exchange. However, The latter is the position taken by the 5 eties. In determining emergency oxygen this margin of safety may also mask committee. Notably, in the areas reviewed policy, the committee felt two diametri- deterioration11 since saturations will in Table 1, guidelines from other societies cally opposed philosophical positions fall only when the alveolar-arterial recommend administering oxygen to could be assumed due to the paucity of gradient is large or the patients with stroke12 and MI13,14 only in evidence: PaO2/fractional concentration of the event of hypoxaemia. 1 Plentiful oxygen. Maximising SaO2 oxygen in inspired gas (FiO2) ratio Consequently, the guidelines (Fig 1) with high-concentration oxygen falls below 100. Other clinical recognise the necessity for HCO in crit- (HCO) is advisable in many features may flag deterioration, but ical illness, but in other situations recom- situations, particularly in critical patients who need increasing oxygen mend that oxygen is given only if illness when monitoring is to maintain saturations may trigger saturations fall below the normal range unavailable (eg at the roadside). warning systems earlier. (94–98%).5 Aligned with the Surviving Sepsis Campaign,15 the guidelines emphasise that maximised SaO2 is not synonymous with optimised DO2 and that vascular filling, haematocrit and Is the patient cardiac output also need appropriate critically ill*? adjustment. Exception is made, however, for patients at risk of hypercapnic respiratory Yes – treat with No reservoir or bag-valve mask Key Points Optimisation of oxygen delivery Is the patient at risk of requires more than oxygen therapy hypercapnic respiratory and attention should be paid to failure? vascular filling, haematocrit and cardiac output High-concentration oxygen may cause worse outcomes through physiological effects and reactive No – is SpO 2 Yes – aim for SpO 88–92% oxygen species <85%? 2 or level on alert card Emergency oxygen should be pending ABG prescribed to a target saturation (88–92% in those at risk of No – aim for hypercapnic respiratory failure, 94–98% in those not at risk), SpO2 94–98% except in critical illness Start with 24% or 28% Venturi mask Oxygen therapy at home should be assessed, prescribed and followed Start with nasal cannulae up by a specialised oxygen service, (2–6 l/min) or usually led by a respiratory face mask physician in secondary care (5–10 l/min) In active patients, ambulatory oxygen *Critical illness is defined as cardiopulmonary arrest, shock, major trauma and head injury, near- should be prescribed to maintain drowning, anaphylaxis, major pulmonary haemorrhage, carbon monoxide poisoning, status saturations above 90% epilepticus and other life-threatening emergencies. KEY WORDS: chronic obstructive Fig 1. Initial algorithm for inhospital prescription of oxygen. ABG = arterial blood pulmonary disease, hypercapnia, 5 gas; SpO2 = peripheral oxygen saturation. hypoxaemia, oxygen, saturation Clinical Medicine Vol 9 No 2 April 2009 157 © Royal College of Physicians, 2009. All rights reserved. CME Respiratory medicine failure, typically patients with COPD, but HCO, alveolar CO2 (PACO2) will rise. trend to worse outcomes in the former also with neuromuscular and chest wall When PIO2 is reduced to baseline, alve- group. It is beyond the scope of this disorders. The recommended SaO2 is olar PO2 (PAO2) will therefore be lower article to enumerate all the reasons why 88–92%, based on observations that PaO2 than previously (until the CO2 body this trial cannot be used to justify HCO of 7.3–10 kPa is associated with the stores are blown off). Consequently, in COPD exacerbations. One compelling 3 lowest incidence of acidosis. Patients arterial PaO2 will be lower than prior to factor, though, is that in neither group known to be at risk of hypercapnic respi- HCO. It can be considered conceptually was PaO2 allowed to rise significantly. It ratory failure should be given an alert as CO2 occupying more ‘space’ in the was therefore a trial comparing two levels card with a prespecified saturation target alveolus. Thus, if an at-risk patient has of controlled oxygen. Furthermore, with range, usually 88–92%, although for been given HCO, oxygen should be with- regard to the effect of the degree of some this may be lower. Arterial

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