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Summary The anatomical basis of gas exchange impairment in the anaesthetised horse was studied by computerised tomography (CT; three Shetland ponies) and morphological analysis (one pony and three horses). By means of CT, densities were seen in dependent lung regions early during anaesthesia, both with spontaneous breathing and with mechanical ventilation. The densities remained for some time where they had initially been created when the animal was turned from dorsal to sternal recumbency. Deep insufflation of the lungs reduced the dense area. Gas exchange was impaired roughly in proportion to the dense area. On histological analysis, the densities were atelectatic and congested with blood. Gravimetry showed no more extravascular water per unit lung tissue in the atelectatic than in the ‘normal’ regions, and the blood content was increased only slightly. It is concluded that the horse develops atelectasis in dependent lung regions early during anaesthesia in dorsal recumbency, and that atelectasis is the most likely explanation for the large shunt and impaired arterial oxygenation regularly seen during anaesthesia.

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Regional ventilation and perfusion were studied in 10 anesthetized paralyzed supine patients by single-photon emission computerized tomography. Atelectasis was estimated from two transaxial computerized tomography scans. The ventilation-perfusion (V/Q) distribution was also evaluated by multiple inert gas elimination. While the patients were awake, inert gas V/Q ration was normal, and shunt did not exceed 1% in any patient. Computerized tomography showed no atelectasis. During anesthesia, shunt ranged from 0.4 to 12.2. Nine patients displayed atelectasis (0.6-7.2% of the intrathoracic area), and shunt correlated with the atelectasis (r = 0.91, P < 0.001). Shunt was located in dependent lung regions corresponding to the atelectatic area. There was considerable V/Q mismatch, with ventilation mainly of ventral lung regions and perfusion of dorsal regions. Little perfusion was seen in the most ventral parts (zone 1) of caudal (diaphragmatic) lung regions. In summary, shunt during anesthesia is due to atelectasis in dependent lung regions. The V/Q distributions differ from those shown earlier in awake subjects.

Pulmonary gas exchange and the development of atelectasis were studied in eight essentially lung-healthy patients, awake and during halothane anaesthesia with mechanical ventilation. Gas exchange was evaluated by a multiple inert-gas elimination technique and conventional blood-gas analysis, and atelectasis was studied by computerized tomography (CT). Ventilation and lung perfusion were well matched in the majority of the patients when awake. In two patients there was low perfusion of poorly ventilated regions (low VA/Q). One patient had a shunt corresponding to 4% of cardiac output. None of the patients showed signs of atelectasis on the CT scans. After 15 min of anaesthesia, shunt had appeared in all patients, ranging from 1% in two patients (unchanged from the awake state) to 17%. The major VA/Q mode was widened and ventilation of poorly perfused regions (high VA/Q) was noted in seven patients. Densities in dependent lung regions (interpreted as atelectasis) were seen on the CT scans in six patients. The extent of atelectasis was significantly correlated both to the magnitude of shunt (r = 0.93, P less than 0.01) and to the impairment of arterial oxygenation (r = 0.99, P less than 0.001). The findings indicate that atelectasis in dependent lung regions during halothane anaesthesia creates shunting of blood flow and that atelectasis is the major or sole cause of impaired gas exchange in the lung-healthy, anaesthetized subject.