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Department of Anesthesiology and Critical Care Medicine, *Klinikum am Steinenberg, Reutlingen, Germany; and
The Leopold-Franzens University of Innsbruck, Innsbruck, Austria
Address correspondence and reprint requests to Arnulf Benzer, MD, Department of Anesthesiology, Critical Care and Emergency Medicine, The Leopold-Franzens University of Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria. Address e-mail to arnulf.benzer{at}uibk.ac.at
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Abstract |
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IMPLICATIONS: The endotracheal tube and laryngeal mask airway are substantially different artificial airways used to ventilate the lungs of anesthetized patients. Breathing 100% oxygen before removing the endotracheal tube results in lung function defects. This study shows that oxygen breathing before removing the laryngeal mask airway has no effect on pulmonary function.
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Introduction |
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Breathing 100% oxygen may lead to atelectasis (7,8). Atelectasis associated with pulmonary shunt (2) may develop during induction of and emergence from anesthesia when 100% oxygen is practiced (9). Moreover, there is a close association between atelectasis and intrapulmonary shunt (1).
The vital-capacity maneuver, namely to briefly inflate the lungs to an airway pressure of approximately 40 cm H2O, eliminates oxygen-induced atelectasis (10,11). If an LMA is used instead of an ETT, the vital-capacity maneuver may result in gastric insufflation and is thus impractical in this setting. Nevertheless, oxygen breathing before removal of the LMA is a matter of routine at many institutions during emergence from anesthesia.
This study was performed to investigate whether FIO2 during emergence from anesthesia affects postanesthetic arterial oxygenation when an LMA is used.
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Methods |
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Patients were premedicated with oral midazolam 7.5 mg 1 h preoperatively. Anesthesia was induced in the supine position with the patient’s head on a standard pillow 5 cm in height. A standard anesthesia protocol was followed and routine monitoring performed. Patients breathed oxygen for 3 min. Anesthesia was induced with remifentanil 0.3 µg · kg-1 · min-1 and propofol 2.5–3.0 mg/kg given over 30 s and the classic LMA inserted when there was no response to jaw thrust. Additional boluses of propofol 0.5 mg/kg were given as required until an adequate level of anesthesia was achieved for placement. One experienced LMA user (>200 uses) inserted/fixed the LMA (size 4 for women, size 5 for men) according to the manufacturer’s instructions. Once an effective airway was obtained, the intracuff pressure was set and held constant at 60 cm H2O using a digital manometer. The airway was connected to a Julian® ventilator (Draeger Medizintechnik GmbH, Luebeck, Germany). Positive pressure ventilation was started with a constant square wave inspiratory flow profile. Tidal volume was set at 7 mL/kg and the respiratory rate adjusted to maintain the ETCO2 at 40 mm Hg. A positive end-expiratory pressure of 3 cm H2O was applied in all patients. The inspiratory/expiratory time ratio was set at 1:1 and maintained. Anesthesia maintenance was performed in a total IV manner using continuous infusion rates of remifentanil and propofol titrated according to hemodynamic variables. FIO2 during the surgical procedure was 0.3 in all patients. No muscle relaxants were given. The following intraoperative complications were documented: failed LMA use, hypoxia (SpO2 <90%), airway obstruction, gagging/retching/hiccup, and coughing during removal.
At the end of surgery, remifentanil and propofol infusions were discontinued and patients were randomly assigned to receive either an increased FIO2 of 100% or an unchanged FIO2 of 0.3. Patients were not physically disturbed, and the ProSealTM LMA (PLMATM) (The Laryngeal Mask Co. Ltd., Oxon, UK) was removed when the patients were able to open their eyes and mouth to command. Time from discontinuation of drug administration to removal of PLMATM was recorded as emergence time. Patients were then transported to the postanesthesia care unit with pulse oxymetry for monitoring of SpO2 breathing room air; supplemental oxygen was given if SpO2 decreased to <90%. Postoperative analgesics were given to the patients using a standardized nursing protocol. Arterial blood gas samples were drawn on room air from the nondominant radial artery by single puncture 30 and 60 min after removal of the PLMATM. Blood gas measurements were taken with a standard technique. The blood gas machine was accurate to 0.1% (PaO2), and was calibrated before each blood gas measurement. FIO2, ETCO2, heart rate, noninvasive mean arterial blood pressure, and oxyhemoglobin saturation (SpO2) were continuously monitored. Intraoperative and postoperative data were collected by a blinded investigator.
Sample size was selected for a type I error of 0.05 and a power of 0.9 and was based on a pilot study of 6 patients with a measured difference in arterial PaO2 of 10% between the ventilation groups. Distribution of data was determined using Kolmogorov-Smirnov analysis. Statistical analysis was performed with the paired t-test (two tailed). Unless otherwise stated, data are presented as mean ± SD. Significance was taken to be P < 0.05. For all calculations, the SPSS computer software package (SPSS Inc., Chicago, IL) was used.
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Results |
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Discussion |
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Many studies have been performed in patients and laboratory animals to evaluate the effect of oxygen on gas exchange during anesthesia (1–5). This investigation was performed because the results of these studies may not be fully applicable to patients after ventilation using the LMA. The LMA is increasingly used in anesthetic practice and has some advantages over the tracheal tube (12).
Traditionally, postanesthetic hypoxemia is attributed to hypoventilation, ventilation/perfusion (
A/
) inequality, venous admixture, and diffusion limitation. A laboratory investigation using the inert gas elimination technique (4) showed that after oxygen breathing and extubation, A/ was increased (4). In this particular experiment, increases in shunt flow were not observed after oxygen breathing. This is particularly interesting because many studies demonstrated atelectasis and shunt simultaneously (1,5,6,11) during anesthesia. Our experiment showed no differences in postanesthetic blood gases of patients ventilated with either 100% or 30% oxygen in nitrogen via LMA which is in contrast to the results of studies obtained from intubated individuals (1,4–6,11). One may speculate that the vasodilating actions of oxygen produce a wider dispersion of pulmonary blood flow whereas the ETT induces reflex bronchoconstriction and more low A/ units. The latter may persist to some extent even after tube removal.
PaO2 after anesthesia was low in our patients (Table 1), given the average age of approximately 30 years, but was still within the normal range. Using a simplified alveolar gas equation:
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where PaO2 is the alveolar partial pressure of oxygen and Pb the barometric pressure, we found PaO2 to be approximately 90 mm Hg. Hence, the alveolar-arterial oxygen pressure difference was <8 mm Hg, indicating low A/ inequality and/or intrapulmonary shunt (13). This in turn is compatible with a low degree of atelectasis.
Significant differences in resistance to gas flow were found when comparing the LMA and ETT (14). In this study, not only was the LMA’s device resistance less than the resistance of the ETT, but also subglottic airway resistance during breathing with the LMA. The latter suggests that the LMA triggers less reflex bronchoconstriction than does the ETT, thus reducing the risk of atelectasis (14). Put differently, use of the LMA may preserve lung function by preventing atelectasis formation in the presence of increased FIO2.
Another factor in atelectasis occurrence is neuromuscular blockade. Atelectasis during anesthesia is also a matter of respiratory muscle tone, particularly that of the diaphragm. Muscle relaxation often used to facilitate tracheal intubation may contribute to atelectasis. Hedenstierna et al. (15) demonstrated that the volume of atelectasis can be reduced by phrenic nerve stimulation.
We conclude that oxygen breathing during emergence from anesthesia does not disturb postanesthetic gas exchange when an LMA is used. Our results are in contrast to oxygen breathing during emergence using an ETT. Postanesthetic differences in gas exchange between the LMA and ETT are likely attributable to less reflex bronchoconstriction, less pulmonary airway resistance to gas flow, and the absence of neuromuscular blockade.
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Acknowledgments |
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This article has been cited by other articles:
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  K. Goldmann, C. Roettger, and H. Wulf Use of the ProSealTM laryngeal mask airway for pressure-controlled ventilation with and without positive end-expiratory pressure in paediatric patients: a randomized, controlled study Br. J. Anaesth., December 1, 2005; 95(6): 831 - 834. [Abstract] [Full Text] [PDF]
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