Thirty postoperative patients were allocated randomly to receive oxygen by Hudson face mask at 4 litre min-1 (group I) or 2 litre min-1 (group II) via nasal cannulae. From 22:00 on the first night after operation, the position of the nasal cannula or face mask was observed for 8 h using video and oxyhaemoglobin saturation (SpO2) recorded simultaneously. In group I the mask remained on and positioned correctly in five patients. In the 10 other patients it was removed a total of 28 times, 17 for nursing tasks, for a median time of 2 min 39 s (range 30 s to 7 h 40 min 40 s). In group II the nasal cannula was removed once in one patient for 16 min 38 s and eight times in another for a total of 1 h 18 min 7 s. Average SpO2 with mask on was 98% (range 96.1-99.9%), with mask off 95% (range 89.8-98.8%) and with cannula 97% (range 90.8-99.3%). We conclude that nasal cannulae are more likely to remain in position than face masks and maintain an adequate saturation in most patients.
Patients may not receive prescribed oxygen because the oxygen face mask becomes displaced. Using video, we have observed the position of the face mask in 20 postoperative patients and recorded the timing and the events associated with mask displacement. Correct placement of the mask was confirmed at the start of the 8-h study period from 22:00 on the first night after operation. The mask remained on continuously and positioned correctly in only one patient. In the other 19 patients, it was removed 64 times (range 1-10 times per patient). The mask was removed 45 times for nursing tasks such as mouth care and temperature measurement and these represented 70% of the total number of times that the mask was not in position. Other reasons for removal were vomiting, retching and removal by the patient. The mask remained off a median time of 6 min 55 s per episode (range 46 s to 7 h 46 min 57 s) and per patient a median of 1 h 6 min 48 s (range 1 min to 7 h 46 min 57 s). Mask removal resulted in an average decrease in oxygen saturation of 4%. Oxygen by mask at 4 litre min-1 maintained an average saturation > or = 95% in most, but not all, of the patients.
SummaryTo examine factors determining the haemodynamic and metabolic responses to treatment of diabetic ketoacidosis with alkali, groups of anaesthetised and ventilated rats with either diabetic ketoacidosis (mean arterial pH 6.86-6.96, mean arterial blood pressure 63-67 mmHg) or hypovolaemic shock due to blood withdrawal (mean pH a 7.25-7.27, mean arterial blood pressure 36-41mmHg) were treated with sodium chloride ('saline'), sodium bicarbonate or 'Carbicarb' (equimolar bicarbonate plus carbonate). In the diabetic ketoacidosis series, treatment with either alkali resulted in deterioration of mean arterial blood pressure and substantial elevation of blood lactate, despite a significant rise in myocardial intracellular pH determined by 31p-magnetic resonance spectroscopy. These effects were accompanied by falling trends in the ratios of myocardial phosphocreatine and ATP to inorganic phosphate. Erythrocyte 2,3-bisphosphoglycerate was virtually absent in animals with diabetic ketoacidosis of this severity and duration. In contrast, in shock due to blood withdrawal, infusion of saline or either alkali was accompanied by a transient elevation of mean arterial blood pressure and no significant change in the already elevated blood lactate; erythrocyte 2,3-bisphosphoglycerate was normal in these animals. The effect of alkalinization in rats with severe diabetic ketoacidosis was consistent with myocardial hypoxia, due to the combination of very low initial erythrocyte 2,3-bisphosphoglycerate, alkali-exacerbated left shift of the haemoglobin-oxygen dissociation curve and artificial ventilation. No evidence was found for any beneficial effect of 'Carbicarb' in either series of animals; 'Carbicarb' and sodium bicarbonate could be deleterious in metabolic acidosis of more than short duration. [Diabetologia (1995) 38: 889-898]
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