The delivery of oxygen to tissue mitochondria depends on several factors including: inspired oxygen concentration (FiO2); alveolar ventilation; ventilation-perfusion distribution within the lung; haemoglobin and concentrations of agents such as carbon monoxide which may bind to haemoglobin; influences on the oxygen-haemoglobin dissociation curve; cardiac output; and distribution of capillary blood flow within the tissues.
Oxygen therapy improves hypoxaemia by increasing alveolar PO2 in poorly ventilated lung units. However, in conditions where desaturated blood is completely bypassing aerated lung (e.g. a right to left cardiac shunt, or a completely consolidated lobe), increasing FiO2 has little or no effect on arterial PO2. Indeed, when a shunt is present, careful measurement of arterial PO2 when breathing 100% oxygen allows calculation of the percentage of the cardiac output flowing through the shunt.
Normally, high-flow oxygen (35-60%) is appropriate treatment in respiratory failure (e.g. severe asthma, pulmonary oedema or pneumonia) because respiratory drive is high. A small percentage of patients with severe chronic COPD and type II respiratory failure develop abnormal tolerance of raised CO2 and may become dependent on hypoxic drive to breathe. In these patients only, lower concentrations of oxygen (24-28%) may be needed to avoid precipitating worsening respiratory depression (see below).
Toxic effects of oxygen
100% oxygen is both irritant and toxic if inhaled for more than a few hours. Premature infants develop retrolental fibroplasia and blindness if exposed to excessive concentrations. In adults, pulmonary oxygen toxicity (manifested by pulmonary oedema and free radical damage leading ultimately to fibrosis) would not be expected to occur unless the patient had been treated with inappropriately high concentrations of oxygen for more than 24 hours.
Administration of oxygen
Oxygen should always be prescribed in writing with clearly specified flow rates or concentrations.
•High concentrations, such as 40-60% oxygen via a high-flow mask, are particularly useful in acute type I respiratory failure such as commonly occurs in pneumonia, asthma or pulmonary oedema. When high-flow masks are used for prolonged periods, the oxygen should be humidified by passing it over warm water.
•Low concentrations. Venturi masks (24% or 28%), are the most accurate method of delivering controlled oxygen therapy in type II respiratory failure. However, once patients are stable, if a low concentration of oxygen is required continuously for more than a few hours, 1-2 litres per minute delivered via nasal cannulae allows patients to eat and to undergo physiotherapy etc. while continuing to receive oxygen. It is important to realise that the actual percentage of oxygen received from nasal cannulae will vary widely depending on minute ventilation, nasal blockage and any tendency to mouth-breathe. Humidification is not necessary with low-flow masks or nasal cannulae, as a high proportion of atmospheric air is mixed with oxygen.
Monitoring of response to therapy
In patients with acute respiratory failure, close monitoring is essential and arterial blood gases taken on presentation should be repeated within 20 minutes to establish that treatment has achieved acceptable PaO2 levels. If hypoxia persists despite appropriate oxygen therapy, progressive hypercapnia (PaCO2 > 6.6 kPa (50 mmHg)) with acute respiratory acidosis develops or the patient becomes exhausted, an early decision should be made about whether it is appropriate to support ventilation temporarily by means of non-invasive ventilation or formal intubation and mechanical ventilation. Very ill patients may require immediate ventilatory support on presentation.
CHRONIC AND 'ACUTE ON CHRONIC' TYPE II RESPIRATORY FAILURE
The most common cause of chronic type II respiratory failure is COPD. Here CO2 retention may occur on a chronic basis, the acidaemia being corrected by renal retention of bicarbonate, which results in the plasma pH remaining within the normal range. This 'compensated' pattern, which is also seen in some patients with chronic neuromuscular disease or kyphoscoliosis, is maintained until there is a further pulmonary insult, such as an exacerbation of COPD which precipitates an episode of 'acute on chronic' respiratory failure.
ASSESSMENT AND MANAGEMENT OF 'ACUTE ON CHRONIC' TYPE II RESPIRATORY FAILURE
N.B. Patient may not appear distressed despite being critically ill
· Conscious level (response to commands, ability to cough)
· CO2 retention (warm periphery, bounding pulses, flapping tremor)
· Airways obstruction (wheeze, prolonged expiration, hyperinflation, intercostal indrawing, pursed lips)
· Cor pulmonale (peripheral oedema, raised JVP, hepatomegaly, ascites)
· Background functional status and quality of life
· Signs of precipitating cause
· Maintenance of airway
· Treatment of specific precipitating cause
· Frequent physiotherapy ± pharyngeal suction
· Nebulised bronchodilators
· Controlled oxygen therapy
o Start with 24% controlled-flow mask
o Aim for a PaO2 > 7 kPa (52 mmHg) (a PaO2 < 5 (37 mmHg) is dangerous)
· If PaCO2 continues to rise or patient cannot achieve a safe PaO2 without severe hypercapnia and acidaemia, respiratory stimulants (e.g. doxapram) or mechanical ventilatory support may be required
The further acute increase in PaCO2 results in acidaemia and worsening hypercapnia, and may lead to drowsiness and eventually to coma. The principal aim of treatment in acute on chronic type II respiratory failure is to achieve a safe PaO2 (> 7.0 kPa (52 mmHg)) without increasing PaCO2 and acidosis, while identifying and treating the precipitating condition. These patients usually have severe pre-existing lung disease, and only a small insult may be required to tip the balance towards severe respiratory failure. Moreover, in contrast to acute severe asthma, a patient with 'acute on chronic' type II respiratory failure due to COPD may not feel overtly distressed despite being critically ill with severe hypoxaemia, hypercapnia and acidaemia.