Directly after tracheal intubation, the amount of atelectasis significantly increased in the control group (4.1% ± 2.0%; P = 0.005) but remained unchanged in the PEEP group (0.4% ± 0.7%; P = 0.0002 compared with control) (Fig. 2 and 3).
Blood gas analysis showed no differences before the anesthesia induction (Table 2). After the anesthesia induction and intubation, while mechanical ventilation was performed with 100% oxygen, Pao2 was significantly higher and Paco2 significantly lower in the PEEP group (Table 2).
The major finding of the present study is that, despite the use of 100% oxygen, application of PEEP throughout the induction period effectively prevents atelectasis formation and improves oxygenation.
Another technique for the prevention of atelectasis has been previously investigated (10). This method, consisting of an administration of only 30% oxygen, was also effective in preventing atelectasis formation during the anesthesia induction. However, this technique has not been introduced in clinical practice because of concerns of an increased risk of hypoxia during anesthesia induction. Indeed, the aim of breathing O2 is to increase the margin of safety before apnea; however, the use of only 30% of oxygen may actually decrease this margin of safety. Another study shows that the administration of 80% oxygen avoids atelectasis formation, but the apnea time until hypoxemia develops is still shorter than when the administration is performed with 100% oxygen (411 seconds versus 303 seconds) (12). Conversely, preventing atelectasis formation with the application of PEEP despite the use of 100% oxygen is more likely to maintain this margin of safety; it might even increase this margin by an increase in functional residual capacity and thus in the intrapulmonary oxygen store, as shown by the higher Pao2 seen in the PEEP group (Table 2).
Atelectasis has been evaluated by CT scanning, as previously described (7). To avoid excessive radiation exposure, we chose to scan only one segment, located 1 cm above the diaphragm. This level may not be representative of the whole lung, but it seemed to be a compromise between the most affected bases of the lungs and the less affected apical regions (4).
We have not exactly measured the time taken for intubation and the delay between the end of mechanical ventilation and second CT scan. Nevertheless, no patient had a difficult intubation, and only one attempt was required in all cases. Therefore, the time between the end of mechanical ventilation and the second CT scan might not have exceeded two minutes in any case.
Impact of atelectasis on gas exchange was directly evaluated by blood gas analysis. Previous studies have shown that anesthesia induced an increase in pulmonary shunt (measured by the inert gas technique) and that the magnitude of this shunt correlated with the amount of atelectasis (3,5). Moreover, these studies have also shown a good correlation between oxygenation (Pao2) and the amount of atelectasis. Hypoxemia may occur during the induction of general anesthesia because of difficulties in airway management. Therefore, before the induction of general anesthesia, all patients are administered 100% of oxygen to increase the margin of safety (the time before hypoxemia may develop). We have shown that with the application of PEEP during the induction period, this margin is preserved while atelectasis is prevented. Moreover, PEEP increases lung volume and therefore the oxygen store, and oxygenation is improved. Therefore, the margin of safety may also be increased.
A potential risk of mechanical ventilation by mask with PEEP is exposing a sedated, paralyzed patient to stomach insufflations and, as a result, increasing the risk of regurgitation and bronchoaspiration. This risk exists with an insufflation pressure more than 20 mm Hg, which can be obtained with manual ventilation (13,14). Alarm limits of the ventilator can be set to 20 mm Hg, and it is also possible to ventilate a patient in the pressure-controlled mode, which will prevent the use of higher pressure via the face mask.
In this study, BMI differed significantly between both groups (Table 1). Control patients had a slightly larger BMI than PEEP patients but still <27 kg/m2. In one study, a weak correlation has been shown between obesity and atelectatic surface (R2 = 0.12; P < 0.05) when 38 patients, including morbidly obese patients, were studied (15). But we have shown that for patients with a BMI <27 kg/m2, there was no correlation between BMI and atelectatic surface (16). Therefore, the small difference between the BMI of the two groups (24 versus 22 kg/m2) is unlikely to be the main cause of the difference in the atelectasis and oxygenation seen after the anesthesia induction.
There was also a significant difference regarding Paco2 after the induction between both groups. The ventilation was standardized (10 mL/kg at 10 breaths/min); therefore, the mode of ventilation could not have been the cause of this difference. This difference may have been caused by the fact that PEEP helped to maintain airways open and may therefore have increased the alveolar minute ventilation. Application of PEEP may have deleterious effects on dead space, i.e., PEEP can induce overdistension of already expanded alveoli with reduction of perfusion and therefore increase alveolar dead space. In healthy lungs, this effect is not seen until PEEP levels exceed 10–15 cm H2O (17). Nevertheless, if this phenomenon had occurred in our study, the Pao2 should have increased in the PEEP group and not decreased; therefore, application of PEEP had probably no effect on dead space in our study.
Application of CPAP (6 cm H2O) for 5 min in conscious patients followed by 5 min of mechanical ventilation with PEEP (6 cm H2O) in sedated patients is safe, simple, and well accepted by patients. This technique prevents atelectasis formation during an anesthesia induction. Furthermore, it improves oxygenation and probably increases the margin of safety before intubation. On the contrary, when the induction of general anesthesia is performed without PEEP or CPAP, mild atelectasis will develop within minutes. Increasing the margin of safety may reduce the incidence of hypoxemia episodes during general anesthesia.
Indeed, mild to moderate hypoxemia, defined as an arterial saturation of between 85% and 90%, occurs in approximately half of all patients undergoing elective surgery, and the hypoxemia can last from a few seconds to up to 30 minutes (2). More alarming is the fact that approximately 20% of the patients may suffer from severe hypoxemia, i.e., the oxygen saturation is less than 81% for up to 5 min during anesthesia (2). Thirty-three percent of hypoxemic events occur during anesthesia induction, one-third during surgery and the last third during awakening and in the postanesthesia care unit (18). Moreover, it has been shown that elderly surgical patients who have had a perioperative pulmonary complication have increased mortality, particularly in the first three months after surgery (19). For these reasons, all attempts should be made to prevent perioperative hypoxemia and particularly during the induction period.
In conclusion, this technique should be considered for all anesthesia induction, at least in patients at risk of difficult airway management.
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© 2003 International Anesthesia Research Society
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