Development of academic anaesthesia in the UK up to the end of 1998.
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Biomedical subjects
Publications and source records attributed to J F Nunn.
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Planetary atmospheres depend fundamentally upon their geochemical inventory, temperature and the ability of their gravitational field to retain gases. In the case of Earth and other inner planets, early outgassing released mainly carbon dioxide and water vapour. The secondary veneer of comets and meteorites added further volatiles. Photodissociation caused secondary changes, including the production of traces of oxygen from water. Earth's gravity cannot retain light gases, including hydrogen. but retains oxygen. Water vapour generally does not pass the cold trap at the stratopause. In the archaean, early evolution of life, probably in hydrothermal vents, and the subsequent development of photosynthesis in surface waters, produced oxygen, at 3500 Ma or even earlier, becoming a significant component of the atmosphere from about 2000 Ma. Thereafter banded iron formations became rare, and iron was deposited in oxidized red beds. Atmospheric levels of carbon dioxide and oxygen have varied during the Phanerozoic: major changes may have caused extinctions. particularly the Permian/Triassic. The declining greenhouse effect due to the long-term decrease in carbon dioxide has largely offset increasing solar luminosity, and changes in carbon dioxide levels relate strongly to cycles of glaciation.
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During routine anesthesia, normal arterial oxygenation cannot be ensured by observation of the patient or by any practicable measurement technique. It is therefore essential to have an understanding of the factors which influence the arterial PO2. The factors influencing the alveolar PO2 are simple and the actual level may be predicted with considerable accuracy. However, the arterial PO2 cannot easily be predicted because of the large and variable alveolar-arterial PO2 differences which occur during anaesthesia. Measurement of alveolar-arterial PO2 difference during anaesthesia requires the calculation of the ideal alveolar PO2 by an equation which allows for the fact that inert gas is seldom in equilibrium under these circumstances. Analytical techniques must be selected for their freedom from interference by anaesthetic gases. Alveolar-arterial PO2 differences encountered in routine surgical patients correspond to a calculated venous admixture within the range 5-25 per cent of total pulmonary blood flow. Somewhat higher values are encountered when the alveolar PO2 falls below 120 mm.Hg. It is not possible to foresee those patients who develop extensive venous admixture. It is probable that the principal component of the venous admixture is blood flow through atelectatic lung, although its recognition by radiography is difficult. It is often possible to reduce the alveolar-arterial PO2 difference by hyperinflation of the lung.
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Arterial PO2 (PaO2) has been related to inspired oxygen concentration (FIO2 range 0.21-0.60) in 20 patients, breathing spontaneously, while recovering from a range of conditions treated in an intensive therapy unit. There was a highly significant linear trend (P < 0.001) for the mean venous admixture ("virtual shunt"), calculated from the iso-shunt diagram (model A), to increase from 0.11 to 0.19 as FIO2 decreased from 0.60 to 0.21. As this appeared to be caused by relative ventilation/perfusion (V/Q) mismatch, we prepared a second model (model B) with a variable two-compartment relative V/Q mismatch in addition to a shunt. Regression of the degree of mismatch on the shunt gave good agreement between predicted and observed PaO2 values (mean bias -0.17 kPa, pooled within patient SD 1.22). Model B is now proposed to extend the applicability of the iso-shunt diagram for FIO2 values less than 0.35. Published postoperative PaO2 data from other workers showed good agreement with our final model (mean bias 0.10 kPa, pooled SD 0.41). The new diagram may therefore have wide applicability in the field of anaesthesia and intensive care.
We have measured the partial pressure of isoflurane simultaneously in inspired gas (PIiso), end-expired gas (PE'iso), mixed-expired gas (PEiso), arterial (Paiso) and mixed venous blood (Pviso) in six patients (aged 57-79 yr) anaesthetized with nitrous oxide, oxygen and isoflurane before surgery and after PE'iso had been stable for at least 15 min. We related these changes to the various indices of pulmonary maldistribution to determine if they were sufficient to explain reported differences between PE'iso and Paiso. Alveolar deadspace dilution of end-expired gas was calculated for carbon dioxide and this dilution factor used to calculate the "ideal" alveolar Piso (PAiso) from the observed inspired and end-expired concentrations. Shunt fraction was measured for oxygen and then used to calculate the partial pressure of isoflurane in the pulmonary end-capillary blood (Pc'iso) from the partial pressure in arterial and mixed venous blood. Mean (SE) values were: PIiso 0.69 (0.05) kPa; PE'iso 0.52 (0.04) kPa; PAiso 0.50 (0.04) kPa; Pc'iso 0.38 (0.04) kPa; Paiso 0.35 (0.03) kPa and Pviso 0.22 (0.02) kPa; Paiso: PE'iso 0.66 (0.02) kPa. The mean "ideal" alveolar to pulmonary end-capillary Piso difference was 0.12 (0.01) kPa and highly significant (P < 0.001). Paiso was substantially less than PE'iso but, for isoflurane, the difference was reasonably constant (range 0.14-0.22 kPa). The difference was attributable in part to the effects of shunt and deadspace, but also a failure of equilibration of isoflurane between the alveolar gas and pulmonary end-capillary blood. It is likely to be different for other anaesthetics. We conclude that, while PE'iso may adequately reflect Paiso for isoflurane, it cannot be assumed that the relation between end-expiratory gas and arterial partial pressures is the same for all anaesthetics.
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The accuracy of 21 anaesthetists in estimating tidal volumes from reservoir bag movements was assessed using a model lung apparatus. The breathing system configuration (Mapleson A or D), the grade of anaesthetist, and the years of anaesthetic experience had no effect on accuracy. Greater precision of tidal volume estimation was observed with larger tidal volumes and lower fresh gas flows. The mean systematic error of 18 of the 21 anaesthetists was greater than zero, indicating a general tendency to overestimate tidal volume. This study therefore strengthens the view that clinical observations should be supplemented with information from continuous monitoring devices.
Disagreements exist between previous studies of the contribution of the rib cage (RC) and abdomen-diaphragm (AD) components to CO2-stimulated ventilation. These studies used dissimilar techniques of CO2 stimulation and varying methods of data processing and presentation, thus precluding direct comparisons. We have therefore studied two methods of CO2 stimulation in 12 subjects, using a Read's rebreathing method and a modified steady-state technique. Respiratory inductive plethysmography was used to assess the RC and AD contributions to ventilation. Mean slopes for the ventilatory response to CO2 were the same for both methods (mean 2.56 L.min-1.mmHg-1), and the intercepts were significantly different (43.7 mmHg for rebreathing and 38.0 for modified steady state: P less than 0.001). There was a small, but significant, increase in the percentage RC contribution to ventilation during hypercapnia of 0.97%/mmHg PCO2 for rebreathing and 0.62 for steady state (P less than 0.01 and P less than 0.05, respectively), and these values were not significantly different from each other. Using our data in comparison with other studies, we have been able to show that differences in processing and presentation of data have given rise to wide variations in conclusions.
Conventional lateral radiography was used in 18 elderly male patients to investigate the changes induced by general anaesthesia in the upper airway. The effect of tongue traction under anaesthesia was studied similarly in another 11 patients. Following induction of anaesthesia, there were highly significant approximations to the posterior pharyngeal wall of the soft palate (median change 1.3 mm, 95% confidence interval (Cl) 0.3-2.6 mm; P = 0.006), tongue base (mean change 6.5 mm, 95% Cl 5.3-7.7 mm; P less than 0.001) and epiglottis (mean change 3.8 mm, 95% Cl 3.1-4.5 mm; P less than 0.001). Apparent radiographic occlusion of the airway occurred most consistently at the level of the soft palate (17 of 18 patients), sometimes at the level of the epiglottis (four patients), but the tongue base did not touch the posterior pharyngeal wall in any patient. Traction on the tongue failed to clear the nasopharyngeal obstruction. Attempted inspiration under anaesthesia caused major secondary collapse of the pharynx, with multiple sites of obstruction, similar to that found in obstructive sleep apnoea.
Of three possible early biochemical changes which were investigated in rats after hyperoxia, one was shown to be a useful marker of damage in this species. Mitochondrial oxygen uptake measured in lung homogenates has already been reported to be impaired after 24 h. With a purified mitochondrial fraction, we found significant impairment after only 3 h exposure to 100% oxygen. To our knowledge, this is the earliest significant change reported in this species. The antioxidants N-acetyl cysteine, dimethyl sulphoxide and allopurinol were found to ameliorate the injury. This suggests a possible link with the pulmonary damage and survival of rats in hyperoxia, which may be modulated also by antioxidant therapy.
Soft tissue lateral neck radiography was used in 22 male patients older than 60 yr, to determine the cause of pharyngeal airway obstruction during anaesthesia, before and after insertion of a Guedel airway. In six of the patients, the airway was radiologically and clinically clear with the head in the neutral position. Nine patients showed obstruction of the airway by a "shelf" of tongue, but seven were cleared clinically by dorsiflexion at the atlanto-occipital joint, and the remaining two by the Esmarch-Heiberg manoeuvre. In four of the 22 patients, the Guedel airway was lodged in the vallecula in the neutral position. This was cleared clinically by dorsiflexion at the atlanto-occipital joint in all these patients. In three patients the Guedel airway was obstructed by the epiglottis, but this was cleared by dorsiflexion at the atlanto-occipital joint in two; in the third patient, the Guedel airway slipped into the vallecula after dorsiflexion at the atlanto-occipital joint and remained there despite the Esmarch-Heiberg manoeuvre. There was only one instance in 66 trials of a clinically obstructed airway without an apparent radiological cause. However, there were 10 instances in 66 trials of a clinically clear airway with an apparent radiological cause for obstruction.