1173

49 mm Hg, 6.52 kPa, Usually hypoxia ’s severe, but the degree of hypercapnia ’/aries widely between patients. In simple terms; hypoxia arises

mainly from venti13tion/perf1.u:ion mismatching, exacerbated by retained ?e’"retions m previously useful lung; hypercapnia. indicating alveolar hypoventilation, is due to impaired .-e7,piratory irive, with acute or chronic insensitivity of the respiratory centre to C02. No patient breathing atmospheric air will sustain a PgC.o-, above 90 mm Hg (11.97 kPa) for long, not only because CO., narcosis reduces his capably to (:0ngh and to breathe, but also because the alveolar-air equation dictates that his Pao2will have come dose to the fatal limit of around 20 mm Hg (2 66 k?a), Proper treatment of an acute exacerbation ?an be rewarding, while poor management can be disastrous. Neglect of simple aspects such as keeping the patient awake to cough, can lead to rapid deterioration. Too high an inspired oxygen with insumcient monitoring can precipitate spiralling hypercapnia, narcosis, and the need for artificial ventilation. In 1965 CAMPBELL clearly laid the guidelines on which modern treatment of acute-on-chronic respiratory failure is based. His advice on controlled oxygen is widely accepted, yet there remain 1_iic:s who opt for a high percentage of inspired oxygen during the initial phase of management. In considering controlled oxygen treatment, it is useful to bear in mind the clinical effects of different degrees of hypoxia. Roughly speaking, a Pao2 of less than 20 mm Hg (2.66 kPa) is fatal; when Pa02 drops below 40 mm Hg (3-32 kPa) there is probably some tissue damage, although the rightward shift of the oxygen dissociation curve caused by coexisting acidosis provides some protection; lesser degrees of hypoxia have important effects on respiration, bone-marrow, and circulation, but these are essentially adaptive, long-term changes. The sharply elbowed curve relating hypoxia to clinical effect has been compared to a climber’s gentle descent towards an abyss, or, in more mundane terms, to a car about to run out of petrol. There are few signs of impending catastrophe in either case. In treatment, one priority must be to raise P a02 to a safe level; but, as in the mountaineering and motoring analogies, the increase need only be a small one to maintain life. 1n praçtical terms, an initial increase in inspired oxygen fraction of a few percent, by 24% ’Ventimask’, is sufficient. This is unlikely to precipitate spiralling hypercapnia, provided that the patient is kept awake and that he expectorates retained secretions. If he makes satisfactory clinical progress during the first critical hour or two, it is usually safe to increase the inspired oxygen fraction to 28% by ven