Tidal volume, lung hyperinflation and arterial oxygenation during general anaesthesia.

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 (HI) of the lungs. The FIO2 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.

Large tidal volume ventilation improves pulmonary gas exchange during lower abdominal surgery in Trendelenburg's position.

Impaired pulmonary gas exchange is a common complication of general anaesthesia. Periodic hyperinflation of the lungs and large tidal volume ventilation were the first preventive measures to be widely embraced, but their effectiveness in clinical practice has never been clearly established by controlled clinical studies. To assess their effects in high-risk patients we studied 24 adults having lower abdominal gynaecological surgery in the Trendelenburg (head down) position. Pulmonary oxygen exchange was determined during four steady-states: awake control (AC), after 30 min of conventional tidal volume (CVT, 7.5 ml.kg-1) or high tidal volume (HVT, 12.7 ml.kg-1) ventilation, introduced in random order, and five minutes after manual hyperinflations (HI) of the lungs. The patients' lungs were ventilated with air/O2 by an Ohmeda volume-controlled ventilator via a circle system. The FIO2 was controlled at 0.5, and FETCO2 was controlled by adding dead space during HVT. Arterial blood gas analysis was used to calculate the oxygen tension-based indices of gas exchange. There was significant deterioration of (A-a)DO2 at 30 min in Group A, whose lungs were first ventilated with CVT (81.6 +/- 7.2 to 166.8 +/- 13.7 mmHg, P less than 0.001); but not in Group B, whose lungs were first ventilated with HVT (77.0 +/- 9.9 to 104.4 +/- 16.8 mmHg). When Group A and B data were pooled there was no difference between randomized CVT and HVT, but improvement occurred after HI. In this model of compromised O2 exchange large inflation volumes (HVT and HI) were of considerable clinical benefit, HVT prevented and HI reversed the gas exchange disorder.

Tussive effect of a fentanyl bolus.

The aim of this study was to investigate the incidence of pre-induction coughing, after an iv bolus of fentanyl. The study sample was 250 ASA physical status I-II patients, scheduled for various elective surgical procedures. The first 100 were randomly allocated to receive 1.5 micrograms.kg-1 fentanyl via a peripheral venous cannula (Group 1), or an equivalent volume of saline (Group 2). Twenty-eight per cent of patients who received fentanyl, but none given saline, coughed within one minute (P less than 0.0001). The second 150 patients were then randomly assigned to three equal pretreatment groups. Group 3 received 0.01 mg.kg-1 atropine iv one minute before fentanyl. Groups 4 and 5 received 0.2 mg.kg-1 morphine im, and 7.5 mg midazolam po, respectively, one hour before fentanyl. Thirty per cent of patients in Group 3, 6% in Group 4, and 40% in Group 5, had a cough response to fentanyl. Fentanyl, when given through a peripheral cannula, provoked cough in a considerable proportion of patients. This was not altered by premedication with atropine or midazolam, but was reduced after morphine (P less than 0.01). Coughing upon induction of anaesthesia is undesirable in some patients, and stimulation of cough by fentanyl in unpremedicated patients may be of clinical importance.