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Six indexes for diagnosing uneven ventilation by tracer gas washout were studied. The indexes were lung clearance index, mixing ratio, Becklake index, multiple-breath alveolar mixing inefficiency, moment ratio, and pulmonary clearance delay, all of which increase with impaired pulmonary gas mixing. In model lung tests, indexes that compared the actual washout curve with a calculated ideal curve (mixing ratio, multiple-breath alveolar mixing inefficiency, and pulmonary clearance delay) were unaffected by changes in tidal volume and series dead space, whereas the others varied markedly. In both spontaneously breathing and mechanically ventilated patients all indexes showed a significant difference between smokers and nonsmokers (P less than 0.002), but the indexes were somewhat different in their assessment of different ventilatory patterns. However, the mean value for all indexes, with the exception of mixing ratio, was smallest with a fast insufflation followed by an end-inspiratory pause. Any of the indexes may be useful if its limitations are recognized, but mixing ratio, multiple-breath alveolar mixing inefficiency, and pulmonary clearance delay seem preferable, because they are not affected by changes in tidal volume and dead space fraction.

A modification of a computerized tracer gas (SF6) washout method was designed for serial measurements of functional residual capacity (FRC) and ventilation homogeneity in mechanically ventilated very-low-birth-weight infants with tidal volumes down to 4 ml. The method, which can be used regardless of the inspired O2 concentration, gave accurate and reproducible results in a lung model and good agreement compared with He dilution in rabbits. FRC was measured during 2-4 cmH2O of positive end-expiratory pressure (PEEP) in 15 neonates (700-1,950 g), most of them with mild-to-moderate respiratory distress syndrome. FRC increased with body weight and decreased (P less than 0.05) with increasing O2 requirement. Change to zero end-expiratory pressure caused an immediate decrease in FRC by 29% (P less than 0.01) and gave FRC (ml) = -1.4 + 17 x weight (kg) (r = 0.83). Five minutes after PEEP was discontinued (n = 12), FRC had decreased by a further 16% (P less than 0.01). The washout curves indicated a near-normal ventilation homogeneity not related to changes in PEEP. This was interpreted as evidence against the presence of large volumes of trapped alveolar gas.

Thirty hypertensive patients scheduled for cholecystectomy or hernia repair under general anaesthesia with thiopentone-fentanyl-nitrous oxide-pancuronium were divided into two groups of 15. One group received metoprolol tablets 200 mg in a slow release form, once daily for at least 2 weeks including the morning of surgery. In addition, metoprolol 15 mg was injected i.v. shortly before the induction of anaesthesia. The other group received placebo tablets and saline. Two patients in the treatment group and one patient in the placebo group were subsequently excluded, because of complications during treatment. Metoprolol significantly reduced arterial pressure both during undisturbed anaesthesia, during intubation and after extubation. A similar tendency was observed also during surgery, although it was not quite significant (P = 0.055). However, metoprolol had no effect on variations in systemic vascular resistance. Mean pulmonary arterial pressures during anaesthesia and surgery were significantly greater in the control, than in the metoprolol, group. Central venous pressure (CVP) and pulmonary arterial occlusion pressure (PAOP) increased significantly in both groups in response to the surgical stimulus. There was no significant difference between the groups in PAOP and CVP. One patient in the metoprolol group had marked bradycardia (minimum heart rate 26 beat min-1) after neostigmine and atropine; otherwise metoprolol pretreatment was tolerated well.