At one time it was thought that suppression of hypoxic drive was the cause of CO2 retention. Changes in CO2 is one of the main controls of ventilation in normal people. In patients with a chronically high CO2 the chemoreceptors in the brain become blunted and the patient depends on hypoxaemia to stimulate ventilation, something that normally occurs only at altitude or during illness. If these patients are given too much oxygen, their "hypoxic drive" is abolished, breathing will slow, and PaCO2 will rise as a result, causing CO2 narcosis and eventually apnoea. Although this is the traditional explanation for CO2 retention, some studies have shown that minute volume and respiratory rate are unchanged in such patients and alternative explanations are as follows:
• There is release of hypoxic vasoconstriction with oxygen therapy, with a change in ventilation-perfusion in the lung and an increase in dead space ventilation. Hypoxic vasoconstriction is an important physiological mechanism in normal people, designed to improve the match between perfusion and ventilation by diverting blood away from poorly ventilated areas. Patients with COPD have a poor chemical drive for breathing and compensatory hyperventilation does not occur.
• There is a reduced ventilatory drive in some patients with COPD, both in response to hypercapnia and hypoxaemia. The reasons for this are not really known, but genetic factors play a part (the "normal" family members of hypercapnic COPD patients often demonstrate blunted hypercapnic and hypoxaemic responses). Acquired loss of drive as an adaptation to increased work of breathing is also implicated. In "CO2 retainers" a different pattern of ventilation has been observed, with lower tidal volumes but an increased respiratory rate. This could be a compensatory mechanism designed to reduce the work of breathing.
• The Haldane effect may also play a part. When haemoglobin is saturated with oxygen, the amount of carbon dioxide it can carry is reduced. Most CO2 is carried in solution and when the affinity of haemoglobin for H+ ions is reduced, the number of H+ ions in solution increases as a result. Patients with COPD do not compensate.
Patients with severe mechanical impairment of lung function are susceptible to CO2 retention as described above. This includes some, but by no means all, patients with COPD. Various studies show that when CO2 retention exists, it occurs when the FEV1 is <10 litre. It may be that these patients are particularly prone to CO2 retention during an acute exacerbation of their illness. Other patients are also vulnerable to CO2 retention for example those with obstructive sleep apnoea. Such patients require controlled oxygen therapy using a Venturi mask to get the PaO2 to around 8 0 kPa (60 mmHg).
One in five patients with COPD admitted to hospital has a respiratory acidosis. The more severe the respiratory acidosis, the greater the mortality. Some of this acidosis is caused by uncontrolled oxygen therapy. A recent study looked at oxygen administration in 101 consecutive admissions via the Emergency Department in patients with COPD. The British Thoracic Society recommends that patients with COPD should receive 28% oxygen via a Venturi mask until the results of arterial blood gases are known. In this study 56% patients received more than 28% oxygen and the median time from ambulance to arterial blood gas analysis was 1 hour. Inhospital mortality was 14% for patients who received more than 28% oxygen and 2% for those who received 28% oxygen or less. Many patients identified their condition as asthma to the ambulance crew. This study was heavily criticised by subsequent letters which illustrate the ongoing debate on the cause of CO2 retention and the correct use of oxygen therapy in acute exacerbations of COPD.
It is important to note that depriving a critically ill patient from oxygen can be harmful. Experts in critical care point out that hypoxaemia can be fatal. In certain circumstances it may be necessary to administer higher concentrations of oxygen to patients with COPD if they are acutely and severely hypoxaemic, pending ventilation.
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