No abstract

Deadspace was measured in nine healthy subjects in the supine position, premedicated but awake and breathing spontaneously at a rate of 12 b.p.m. and subsequently under anaesthesia with artificial ventilation with frequencies of 12 and 24 b.p.m. The minute volume was kept at a relatively constant value. The physiological deadspace was calculated using the Bohr equation and the division into anatomical and alveolar deadspace was made with the aid of capnography. Physiological deadspace was increased by anaesthesia and IPPV, mainly as a consequence of increased rebreathing in the apparatus deadspace. There was no significant change in the anatomical deadspace. Thus, the expected reduction in deadspace brought about by endotracheal intubation was nullified by an increase in the anatomical deadspace distal to the carina. The VDanat/VT ratio remained constant on changing the respiratory frequency. A significant alveolar deadspace was measured during spontaneous breathing. This was unchanged by the induction of anaesthesia and the institution of artifical ventilation. On changing the frequency, the VDalv/VT ratio remained constant. It is concluded that both the anatomical and the alveolar deadspaces increasing with increasing tidal volume, but are unaffected by the breathing rate.

Pulmonary gas distribution, functional residual capacity (FRC), closing capacity (CC), arterial oxygen tension (PaO2) and alveolar-arterial oxygen tension gradient (PAO2-PAO2) were measured in seven subjects before and after the induction of extradural analgesia for routine surgery. It was found that pulmonary gas distribution was within normal limits throughout the study, although there were two patients in whom airway closure occurred consistently within the tidal volume. In both cases this was associated with a low PaO2. CC and FRC were substantially unchanged by the induction of extradural analgesia. Changes in (PAO2-PaO2) and PaO2 were usually not large, and are apparently related to factors other than changes in lung geometry.

Nine healthy volunteers were investigated, both while awake and breathing spontaneously, and while anaesthetized with IPPV, in all cases at rates of both 12 and 24 b.p.m. Gas flow and volume were measured with a pneumotachography. The transpulmonary pressure (the pressure difference between the trachea or the buccal cavity and the oesophagus) was also recorded. The distribution of gas was analysed by means of nitrogen washout curves, which also permitted the determination of functional residual capacity (FRC). Lung compliance during IPPV was approximately half that during spontaneous breathing. During IPPV the compliance was dependent on the frequency of ventilation, being lower with the greater frequency. Pulmonary resistance was approximately twice as great with artificial ventilation, but no significant relationship to frequency was demonstrated. Gas distribution was within normal limits and in this respect there was no difference between low and high rates of spontaneous breathing. With IPPV at the higher rate, gas distribution was significantly less even, but still within normal limits. Dfferences in FRC under the different conditions during the experiments were not significant, but the values obtained were lower with artificial ventilation. Neither the reduction in dynamic lung compliance induced by anaesthesia and artificial ventilation, nor its dependence on the frequency of such ventilation, can be explained with certainty by changes in gas distribution.

The measurement of systolic time intervals (STI) has been widely used as a non-invasive method of assessing the inotropic state of the heart, and normal values are available for healthy individuals breathing spontaneously. The present study was performed in order to evaluate how intermittent positive pressure ventilation (IPPV) affects STI. Ten subjects were investigated before and during halothane anaesthesia for routine surgery. Oesophageal pressure, respiratory minute volume and frequency, arterial blood-gas tensions, cardiac output and heart rate were also measured simultaneously. As expected, the institution of IPPV was associated with a reduction in cardiac output and an increase in oesophageal pressure. Paco2 was reduced. These changes were associated with a considerable lengthening of electro-mechanical systole. This was due to a lengthened pre-ejection period (PEP), whereas the left ventricular ejection time (LVET) was slightly shortened. These changes were even more marked during artifical hyperventilation. The changes in STI are attributed mainly to the reduction of venous return to the heart, subsidiary factors being intrathoracic pressure, myocardial inotropy and vascular resistance.