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Atelectasis and its prevention during anaesthesia

1998; Lippincott Williams & Wilkins; Volume: 15; Issue: 4 Linguagem: Inglês

10.1097/00003643-199807000-00002

1365-2346

Göran Hedenstierna,

Cardiovascular and Diving-Related Complications

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. The magnitude of shunt correlates well with the size of the atelectasis [13]. It has also been demonstrated by single photon emission computed tomography (SPECT) that the shunt is located in dependent lung regions, corresponding to the location of atelectasis [14]. An interesting finding is that neither the atelectasis nor the shunt increase with the age of the patient [15]. This may appear surprising because gas exchange impairment worsens as the patient gets older [16]. However, perfusion of poorly ventilated lung regions ('low V˙A/Q˙) increases with age [15]. The cause of low V˙A/Q˙; has not been fully established. However, airway closure increases with age and may be a major contributor to impaired ventilation [17]. Moreover, closure of airways above FRC, i.e. during an ordinary breath, seems to be more common during anaesthesia than in the awake patient [18], although this finding remains controversial. Prevention of atelectasis during anaesthesia Atelectasis may be prevented or reversed in different ways. Some of these procedures have already been touched on in the paragraph on mechanisms of atelectasis. The procedures that will be discussed are: (1) PEEP; (2) maintenance or restoration of respiratory muscle tone; (3) recruitment manoeuvres; and (4) minimization of pulmonary gas resorption. PEEP The application of a PEEP of 10 cmH2O has been tested in several studies and will consistently reopen collapsed lung tissue [2, 13]. However, some atelectasis persists in most patients. Further increases in the PEEP level may have reopened this tissue. However, PEEP appears not to be the ideal procedure. Firstly, shunt is not reduced and the arterial oxygenation not, on average, improved. This was demonstrated already in 1974 by Hewlett et al. who warned against the 'indiscriminate use of PEEP in routine anaesthesia' [19]. The persistance of the shunt may be explained by the redistribution of blood flow towards the most dependent parts of the lung when intrathoracic pressure is increased, so that any remaining atelectasis at the bottom of the lung receives a larger share of the pulmonary blood flow with, rather than without, PEEP [20]. The increased intrathoracic pressure will also impede venous return and reduce cardiac output. This results in a lower venous oxygen tension for a given oxygen uptake which augments the desaturating effect of shunted blood and perfusion of poorly ventilated regions on arterial oxygenation [21]. Secondly, the lung re-collapses rapidly after discontinuation of PEEP. Within 1 min after cessation of PEEP the collapse is as large as it was before the application of PEEP [6]. Maintenance of muscle tone The use of an anaesthetic that allows maintenance of respiratory muscle tone will prevent atelectasis formation. Ketamine does not impair muscle tone and does not cause atelectasis. However, if muscle relaxation is required, atelectasis will appear as with other anaesthetics [8]. Another approach is to restore respiratory muscle function, at least in part, by a diaphragm pacing. This method has been tested by applying phrenic nerve stimulation. This reduced the atelectatic area [6]. However, the effect was small and it can be argued that the technique is too complicated to become routine during anaesthesia and surgery. Recruitment manoeuvres The use of a sigh manoeuvre or a double tidal volume, has been advocated to reopen any collapsed lung tissue [22]. However, the atelectasis is not affected by an ordinary tidal volume, nor by a deep sigh with an airway pressure up to +20 cmH2O [23]. Not until an airway pressure of 30 cmH2O was reached did the atelectasis decrease to approximately half the initial value. For a complete reopening of all collapsed lung tissue an inflation pressure of 40 cmH2O was required with the breath being held for 15 s [23]. Such a large inflation pressure and subsequent expiration with pressures falling to −20 cm H2O, resulted in a vital capacity measurement comparable with that measured during spontaneous breathing with the patient awake. Although approved for lung function studies in anaesthetized subjects [24], it may be argued that such a manoeuvre can be risky and cause barotrauma [25]. Another procedure was therefore tested with repeated inflations of the lung to an airway pressure of +30 cmH2O. However, this caused only marginal further opening of lung tissue after the first manoeuvre [23]. A full vital capacity manoeuvre with an inflation to +40 cmH2O therefore seems necessary to completely re-open the lung. Minimizing gas resorption Ventilation of the lungs with pure oxygen after a vital capacity manoeuvre that had reopened previously collapsed lung tissue, resulted in a rapid reappearance of the atelectasis [9]. If, on the other hand, ventilation was made with 40% O2 in nitrogen atelectasis reappeared slowly and 40 min after the vital capacity manoeuvre only 20% of the initial atelectasis had reappeared. Thus, ventilation during anaesthesia should be with a moderate inspired oxygen fraction (e.g. 0.3-0.4) and be increased only if arterial oxygenation is compromised. Moreover, avoidance of the pre-oxygenation procedure during induction of anaesthesia more and less eliminated the atelectasis formation during anaesthesia [10]. If the pre-oxygenation period was prolonged from a standard 2-3 min to 4-5 min the volume of atelectasis increased further [26]. Thus, avoidance of the pre-oxygenation or at least lowering of the inspired oxygen fraction during the induction phase will reduce or avoid the formation of atelectasis during the subsequent anaesthesia. It is obvious that lowering the inspired oxygen fraction may increase the risk of hypoxaemia in a difficult and prolonged intubation. However, the present findings call for a reevaluation of the present standard procedures for inducing anaesthesia. In summary, atelectasis is produced in most patients during anaesthesia and is a major cause of impaired oxygenation. Causative mechanisms seem to be loss of respiratory muscle tone and gas resorption. Avoidance of high inspired oxygen fractions during induction and maintenance of anaesthesia, and intermittent 'vital capacity' manoeuvres prevent or reduce the atelectasis formation. G. Hedenstierna Department of Clinical Physiology, University Hospital, Uppsala, Sweden