Effects of opiates in chronic bronchitis.

It has been standard teaching for many years that opiates should not in any circumstances be given to dyspnoeic patients with chronic bronchitis, but the evidence on which this view is based is derived almost solely from clinical impressions. Although morphine and its derivatives have been shown to diminish the ventilatory response to carbon dioxide in normal human volunteers (Loeschcke, Sweel, Kough, and Lambertsen, 1953), there have been virtually no scientifically controlled observations on the effect of opiates in patients with ventilatory failure complicating chronic bronchitis and emphysema. Attempts have been made in such patients to study retrospectively the effect of opiates on respiration by observing the changes which occur in minute volume and in the carbon dioxide tension, oxygen saturation, and pH of arterial blood during recovery from injections of morphine. In one such study on five patients with severe emphysema (Wilson, Hoseth, and Dempsey, 1954) these measurements were made 'during narcosis' after the injection of 15 mg. morphine, and 'on recovery'. Since the morphine had been administered (on incorrect indications) before the patients were admitted to hospital in ventilatory failure, and no precise time relationships are given, it cannot be assumed that the severe hypercapnia, hypoxaemia, and respiratory acidosis which were found on analysis of arterial blood samples taken 'during narcosis' were solely due to the central action of morphine on respiration, since they may have been partly or even mainly due to secondary effects such as bronchial obstruction by secretions. The authors based their conclusion that morphine caused central depression of respiration on the observation that the figures for arterial carbon dioxide tension, pH, and oxygen saturation and for respiratory minute volume improved significantly 'on recovery from sedation'. This conclusion seems to be inadmissible because the time interval between the withdrawal of the two arterial samples was not stated, and because precise details of the treatment the patients had received during this period were not given. Even a few effective coughs could, by clearing the airways, have produced a marked reduction in the degree of hypercapnia and hypoxaemia, and the administration of respiratory stimulants, which, according to the text, some patients may have received, would totally invalidate the results of the investigation. Our interest in the subject was aroused by the difficulty we experienced in relieving intense dyspnoea in patients with chronic bronchitis and emphysema who had reached the terminal stages of chronic ventilatory failure. In one particular patient, whose respiratory distress was such that he repeatedly expressed a desire to die, we considered it would be justifiable to give an opiate as a last resort, and we observed the effect of the drug on the arterial blood gas status. The arterial oxygen saturation (Sao2), estimated on each occasion while the patient was breathing oxygen from a Venturi mask at the 25% gauge setting, had for several weeks fluctuated between 75% and 85%', and the arterial carbon dioxide tension (Paco2) had varied between 90 mm. Hg and 100 mm. Hg, but the arterial pH had remained within the normal range. It was decided to give him in the first instance a very small dose of opiate (papaveretum, 10 mg. subcutaneously), and to increase the dose only if this did not produce any alarming change in his clinical state or in his arterial blood gas status. The patient claimed that after the injection he was able to breathe more comfortably, and his respiratory efforts seemed less laboured. This effect was augmented when he was given 20 mg. papaveretum on two subsequent occasions, but he became relaxed and slightly drowsy with the higher dose. Samples of arterial blood were withdrawn immediately before each injection and again 90 minutes later. The figures obtained for Paco2,