PMID: 9699094

Issn Print: 0265-0215

Publication Date: 1998/07/01


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Atelectasis and its prevention during anaesthesia

G. Hedenstierna

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Ten to 15 years ago atelectasis was demonstrated in anaesthetized patients, neonates as well as adults [1, 2]. The atelectasis can be demonstrated by computed X-ray tomography but is invisible on conventional chest X-ray. It is located in the most dependent parts of both lungs and appears in almost 90% of all patients who are anaesthetized [3]. It develops whether the anaesthesia is intravenous (i.v.) or inhalational and whether the patient is breathing spontaneously or is paralysed and ventilated mechanically [4]. The atelectasis is greatest near the diaphragm in the supine patient and decreases in size towards the apex [5]. The atelectasis covers ≈5% of the transverse pulmonary area near the diaphragm, with a large variation from zero to 10-15%. In the average patient, the atelectasis may not look too impressive. However, it should be remembered that the collapsed area comprises four times more lung tissue than the aerated regions. Thus, in the average patient the atelectasis comprises about 15-20% of the lung tissue close to the diaphragm and about 10% of the total lung tissue [5]. In the extreme cases almost half the lung can be collapsed during anaesthesia, before any surgery has taken place!
The atelectasis appears soon after induction of anaesthesia, and can be seen as soon as it has been possible to make a CT scan [2]. Moreover, positive end-expiratory pressure (PEEP), can reopen collapsed lung tissue but as soon as the PEEP is discontinued the atelectasis reappears within 1 min [6]. The rapid formation of atelectasis after induction of anaesthesia and discontinuation of PEEP may suggest that a major cause of atelectasis is compression of lung tissue rather than slow absorption of gas in occluded airways [7]. In humans anaesthetized with ketamine, which allows the maintenance of respiratory muscle tone, no atelectasis developed until the patient was paralysed and mechanically ventilated [8]. Tensing the diaphragm by phrenic nerve stimulation reduced the atelectasis in anaesthetized patients [6]. These findings all fit with the concept of compression or gravity dependent atelectasis.
However, two recent observations have made the explanation of atelectasis formation during anaesthesia more complex. First, collapsed lung tissue can be re-expanded by a vital capacity manoeuvre (see also below), but if the lungs are ventilated with pure oxygen they rapidly re-collapse, within 5 min after the vital capacity manoeuvre [9]. If, on the other hand, the lungs are ventilated with 40% O2 in nitrogen after the re-expansion, the lungs remain open with no or only little atelectasis formation for half an hour or longer. Second, if anaesthesia is induced without 'preoxygenation' and ventilation is given with 30% O2 in nitrogen, no or little atelectasis is formed [10]. These observations underscore the importance of the inspired oxygen fraction which suggests that the rate of absorption of gas from the alveoli may play an important role in the formation of atelectasis. However, breathing oxygen alone for more than half an hour does not promote atelectasis [2]. However, if the oxygen breathing is done at a reduced lung volume atelectasis may ensue, a suggestion supported by the reduction in compliance and oxygenation in healthy volunteers during chest strapping [11]. Ketamine anaesthesia did not promote atelectasis, despite induction during oxygen breathing, as referred to above [8]. Ketamine has been shown not to reduce functional residual capacity (FRC) [12]. Thus, for atelectasis to occur during anaesthesia, there must be both a reduced respiratory muscle tone with reduced FRC and ventilation with high fractions of oxygen, at least for a period of time. Atelectasis is thus a result of both compression of lung tissue and gas resorption.
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