Impaired pulmonary oxygen (O2) exchange is common during general anaesthesia but there is no clinical unanimity as to methods of prevention or treatment. We studied 14 patients at risk for pulmonary dysfunction because of increased age, obesity, cigarette smoking, or chronic lung disease. Pulmonary O2 exchange was measured during four conditions of ventilation: awake spontaneous, conventional tidal volume (CVT, 7 ml.kg-1) or high tidal volume (HVT, 12 ml.kg-1) controlled ventilation, and five min after manual hyperinflation (H1) of the lungs. The F1O2 was controlled at 0.5, and FETCO2 was kept constant by adding dead space during HVT. Eight patients were ventilated with N2O/O2 and six with air/O2. Arterial blood gases were used to calculate the (A-a)DO2. In seven patients (A-a)DO2 worsened after induction of anaesthesia, while in seven there was no change or an improvement. Manual HI significantly reduced (A-a)DO2, but changing tidal volume (VT) had no effect. Using a multivariate model to predict O2 exchange, obesity and type of surgery were significantly associated with worsening, while level of VT and inspiratory gas (N2O or N2) were not significant predictors. Thus patient and surgical factors were more important determinants of pulmonary gas exchange during anaesthesia than were tidal volume or inspiratory gas. Manual HI is a simple and effective manoeuvre to improve gas exchange.

A double-blind study was undertaken to investigate the effect of prewarmed local anaesthetic solution on the latency of onset of caudal blocks. Forty-four (ASA I-II) patients were allocated into two equal groups. In Group A, the local anaesthetic solutions were injected at room temperature (25°C), while in Group B, they were injected at 3rc. All the caudal blocks were performed using 20 ml of lignocaine 1.5% with adrenaline 1:200,000. The speed of onset of perianal analgesia was found to be significantly faster (39%) with the prewarmed local anaesthetic solution (P < 0.05). No adverse effects were observed.

There was significant deterioration of (A-a)D02 at 30 rain in Group A, whose lungs were first ventilated with P < 0.001); but not in Group B,