Earlier studies have shown that time and flow indices derived from tidal expiratory flow patterns can be used to distinguish the severity of airway obstruction. This study was designed to address two aspects of tidal expiratory flow patterns: 1) how do expiratory flow patterns differ between subjects with normal and obstructed airways; and 2) can a sensitive index of airway obstruction be derived from these pattern differences? Tidal expiratory flow patterns from 66 adult subjects with varying degrees of airway obstructive disease with a forced expiratory volume in one second (FEV1) of 20-121% predicted were examined. In each subject, the expired flow pattern from each consecutive breath was scaled and then averaged together to create a single expired pattern. A detailed examination of the scaled flow patterns in 12 subjects (six with normal airways and six with airway obstruction) showed that the shape of the post-peak expiratory flow portion was different in the subjects with airway obstruction. A slope index, S, was derived from the scaled patterns and found to be sensitive to the severity of airway obstruction, correlating with FEV1 (% pred) with r2=0.74 (p<0.05, n=57). The S index also correlated (r2=0.36, p<0.05, n=47) with the functional residual capacity (FRC) (% pred) which was >100% in subjects with severe airway obstruction and lung overinflation. In subjects with normal airways, three further airflow patterns could be distinguished, which were different from the patterns seen in subjects with the severest airway obstruction. Scaled flow patterns from tidal expiration collected from uncoached subjects, can be used to derive an index of airway obstruction.

1. Progressive exercise and circulatory studies are reporteG on a selecteL group of patients with hypoxaemia and secondary polycythaemia before and after therapeutic decrease of packed cell volume.2. A significant increase in exercise tolerance was demonstrated in a group of seven patients who claimed subjective benefit from the treatment.3. No important circulatory changes were detected at rest after treatment. 4. During steady exercise mean pulmonary artery pressure at any given cardiac output was lower after treatment suggesting a fall in pulmonary vascular resistance. 5. During steady exercise oxygen consumption was increased in five of six patients subjectively improved by the treatment but no consistent changes in arterial lactate concentration or lactate/pyruvate ratio were observed.

Background -A study was performed to determine the elastic equilibrium volume (Vr) of the respiratory system in patients with chronic obstructive pulmonary disease (COPD). Methods -Voluntary relaxed expiration from total lung capacity (TLC) was studied in three groups of subjects: seven patients with severe chronic airways obstruction (COPD), 10 normal subjects, and 15 subjects with restrictive disease. Results -In the normal subjects and the patients with restrictive disease voluntary relaxed expiration from TLC stopped close to end tidal volume (FRC) and the volume expired in this manoeuvre was less than that expired in a slow vital capacity manoeuvre (SVC). In the patients with COPD the voluntary relaxed expiration continued beyond the end tidal volume (FRC) and the volume expired was not different from the SVC. Oesophageal (pleural) pressures and surface diaphragmatic EMG recordings in the patients with COPD supported the premise that relaxation was achieved. Conclusions -In patients with COPD, end tidal volume (FRC) is higher than the elastic equilibrium volume, Vr, of the respiratory system. This is in contrast to patients with restrictive disease and normal subjects in whom end tidal volume (FRC) is close to Vr. This study shows that, in patients with severe chronic obstructive pulmonary disease, V, is at least as small as residual volume (RV).

The cardiorespiratory effects of three different patterns of mechanical ventilation were compared in sixteen anaesthetized goats. Intermittent positive pressure ventilation (IPPV), with an inspiratory: expiratory (I:E) time ratio of 1:3, was compared with an inspiratory hold pattern (IPPVH), with an I:E ratio of 3:1, and with continuous positive pressure ventilation (CPPV) adjusted to produce the same mean airway pressure. In eight animals with normal lungs, IPPVH reduced VD/VT and PaCO2, but produced no changes in oxygenation. CPPV did not significantly alter the efficiency of gas exchange. In a further eight animals, with oleic acid-induced lung damage, both IPPVH and CPPV produced a decrease in both VD/VT and PaCO2. Qs/Qt was significantly reduced by both CPPV and IPPVH, but the effect was more marked with CPPV, and the PaO2 was significantly increased only by CPPV. The increased effectiveness of CPPV in increasing PaO2 in this model may have been due to the greater increase in end-expiratory lung volume produced by this pattern of ventilation.

The first pass uptake, metabolism and recovery of bupivacaine were examined in an intact rabbit lung model using a multiple indicator technique with rapid sequential sampling. The rabbits were allocated to an acidotic group (pH 7.0-7.1) (n = 8) and a control group (n = 10) with normal pH. Bupivacaine recovery rates were not significantly different: median 93.2% (range 48.9-116.5%) and 94.5% (54.9-123.1%) in control and acidotic groups, respectively. Median peak percentage fractional concentrations of bupivacaine were greater in the acidotic group: 6.22% (2.5-7.65%) vs 4.1% (2.5-6.7%) (P less than 0.05). Median maximum instantaneous pulmonary percentage extraction was less in the acidotic animals than in animals with normal pH: 81.2% (47.1-91.9%) vs 91.0% (82.6-94.5%) (P less than 0.01). Median normalized mean percentage transit time was less in the acidotic group (245.3% (163.4-465.3%)) than in the control group (423.9% (313.9-740.4%)) (P less than 0.01). There was no evidence for bupivacaine metabolism by the lung. The results suggest that acidosis reduced bupivacaine lung uptake and increased its rate of passage through the lung, but did not influence overall drug recovery rates. This has clinical implications for bupivacaine related cardiac and cerebral toxicity.