SummaryAlphaxalone-alphadolone (Althesin), diluted and administered as a controlled infusion, was used as a sedative for 30 patients in an intensive therapy unit. This technique allowed rapid and accurate control of the level of sedation. It had three particularly useful applications: it provided "light sleep," allowed rapid variation in the level of sedation, and enabled repeated assessment of the central nervous system. Sedation was satisfactory for 86% of the total time, and no serious complications were attributed to the use of the drug. Furthermore, though alphaxalone-alphadolone was given for periods up to 20 days there was no evidence of tachyphylaxis or delay in recovery time.

Oesophageal (oes) and central venous pressure (CVP) were compared as indices of transpulmonary pressure change (deltap). The mean increase of deltaPoes over deltapCVP was 2.8 cm H2O. The size and variability of the increase were similar to the expected difference between oesophageal and pleural pressure fluctuations occurring in the supine patient. Central venous pressure may be more accurate and reliable than oesophageal pressure for estimations of transpulmonary pressure change in the supine position.

The cardiorespiratory effects of etomidate were measured in two groups of six patients with aortic or mitral valve disease. The induction of anaesthesia with etomidate 0.3 mg kg-1 was followed by a second dose 10 min later. After the first dose, a 19% decrease in systemic arterial pressure was associated with a decrease in systemic vascular resistance and left ventricular heart work. Cardiac index, pulmonary artery pressure and wedge pressure all decreased slightly. Central venous pressure and heart rate did not change. A slight increase in respiratory frequency failed to prevent an increase in PACO2. Changes after the second dose were similar. The two groups of patients did not differ significantly in their response to etomidate. No patient complained of pain during injection, nor did myoclonic movements occur.

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Two cases of lactic acidosis are described in which the time sequence of events made it certain that phenformin was the precipitating cause. In one patient the condition arose because of self administration of an overdose; in the other, phenformin had been administered to a patient on maintenance dialysis. After recovery, and in the absence of phenformin therapy the second patient was able to clear an intravenous lactate load at a rate similar to that observed in other patients on Chronic dialysis.-A review of the literature re-emphasizes the possible danger of phenformin in the presence of diminished renal or hepatic function, which should be shown to be normal before starting the drug and assessed periodically during therapy.