Breathing mechanics and gas exchange were studied in 10 extremely obese subjects (average weight 138 kg) prior to and during anaesthesia with mechanical ventilation. Breathing mechanics were analysed from measurements of transpulmonary pressure (during anaesthesia, trans-chest wall pressure as well) inspiratory gas flow and tidal volume. Gas exchange was studied by analysing inspired and from the Bohr equation, and the division into anatomical and alveolar dead space was arrived at by capnography. The patients were anaesthetised with neuroltpt agents and ventilated with an air-oxygen mixture. Lung compliance during spontaneous breathing was below normal and decreased further during artificial ventilation. Chest wall compliance measured during anaesthesia was within normal limits. Lung resistance was above normal during spontaneous breathing and increased further during mechanical ventilation. Total dead space was normal during spontaneous breathing and increased moderately during artificial ventilation, the increment coming mainly from alveolar dead space. A moderate hypoxaemia was recorded during spontaneous breathing, and the alveolar-arterial oxygen tension difference was slightly elevated. During anaesthesia this difference was markedly greater. It is concluded that the most probable reason for the relative hypoxaemia is right-to-left shunting.
Airway closure (closing capacity, CC), FRC, total efficiency of ventilation (lung clearance index, LCI) and distribution of inspired gas (nitrogen washout declay percentage, NWOD) were determined by nitrogen washout techniques and arterial PO2and PCO2 measured by standard electrodes in 10 extremely obese subjects, prior to an during anaesthesia and artifical ventilation. CC was normal, but because of small FRC, airway closure occurred within a tidal breath in 9 out of 10 subjects during spontaneous breathing, when awake. PO2 was reduced, the hypoxaemia correlating to the magnitude of airway closure. LCI was normal, but NWOD was borderline. During anaesthesia, CC was unaltered by FRC was further reduced, so that in nine subjects sirway closure occurred above FRC and tidal volume together. A marked increase in relative hypoxaemia was recorded. LCI and NWOD rose, indicating less efficient and less even ventilation. It is concluded that airway closure reasonably explains the marked hypoxaemia in obese subjects during anaesthesia, and that it may also be the reason for the uneven distribution of inspired gas.
Ventilation-perfusion (VA/Q) ratios were studied by means of an inert gas elimination technique in healthy subjects with an average age of 51 years in the supine posture (a) when awake, (b) during inhalational anaesthesia, spontaneously breathing, (c) during mechanical ventilation, and (d) when a positive end-expiratory pressure (PEEP) was applied. In the awake subject a bimodal distribution of VA/Q was recovered in most patients, one mode centered around the ratio of 1 and another, smaller mode, within low VA/Q-regions. Any shunt was less than 3% of cardiac output. With anaesthesia and spontaneous breathing, the low VA/Q mode was reduced and the shunt increased to an average of 6.2%. With mechanical ventilation, the major VA/Q mode was widened while the shunt was further increased in 4 of 10 subjects (mean 8.6%). With PEEP, the shunt was reduced and a new mode within high VA/Q-regions appeared. The shunt and low VA/Q-regions appeared. The shunt and low VA/Q-regions may be explained in terms of airway closure while the high VA/Q mode with PEEP may be attributed to the development of a zone I.
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