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Anesth Analg 2004;98:257-259 © 2004 International Anesthesia Research Society
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Abstract |
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Breathing 100% oxygen at the end of general anesthesia has been shown to worsen postoperative pulmonary gas exchange when an endotracheal tube is used. Counter measures, such as high positive end-expiratory pressure or the vital-capacity maneuver, may limit this effect. Such strategies, however, may be impracticable, or even contraindicated, when the laryngeal mask airway (LMA) is used. Because of the vast differences in design between the LMA and endotracheal tube, we examined postanesthetic blood gas tensions in patients after emergence from anesthesia breathing oxygen via LMA. Sixty-four ASA physical status I–II patients undergoing general anesthesia for 60 min with LMA were randomly assigned to receive either 100% or 30% oxygen during emergence from anesthesia and removal of LMA. Postoperative blood gas measurements were taken at 30 and 60 min after removal of the LMA. At either measurement, patients treated with 100% oxygen essentially had the same arterial partial pressure of oxygen (60-min measurement: 83 ± 8 versus 85 ± 7 mm Hg [mean ± SD], P = 0.14) as those treated with 30% oxygen. We conclude that breathing 100% oxygen at the end of general anesthesia does not worsen postoperative pulmonary gas exchange when an LMA is used.
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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High inspiratory fractions of oxygen (FIO2), during either induction of or emergence from anesthesia, results in atelectasis (1,2), intrapulmonary right-to-left shunt (2,3), depression of lung function (4,5), and depressed arterial oxygenation in several studies performed using endotracheal tubes (ETTs) (6,7). The laryngeal mask airway (LMA) is an increasingly used alternative to the ETT, and in comparison their physical properties are considerably different. Given the large diameter and the comparably short tubular section of the LMA, it remains uncertain whether emergence on oxygen has the same results on lung function as compared with the ETT. This study examined whether high FIO2 during emergence from anesthesia using the LMA results in different arterial partial pressures of oxygen after emergence.
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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Sixty-four adults (ASA physical status I–II, aged 18–65 yr) scheduled for elective peripheral musculoskeletal surgery with an estimated duration of 30–60 min were studied. Ethical committee approval and written informed consent were obtained. Exclusion criteria were a known or predicted difficult airway, smoking history, mouth opening <2.5 cm, a body mass index >30 kg/m2, or risk of aspiration (fasted <6 h).
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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Distribution of all datasets was found to be gaussian (Table 1). Demographic data were comparable. For no variable recorded were differences found between patients treated with 30% oxygen and those treated with 100% oxygen.
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Discussion |
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This study evaluates the effect of pure oxygen or 30% oxygen-in-nitrogen breathing during emergence from anesthesia on postanesthetic pulmonary gas exchange. To isolate the gas mixture effect from other influences, LMA and total IV anesthesia were used. Comparing postanesthetic blood gases of patients ventilated with either 100% or 30% oxygen in nitrogen did not show any differences. Our results contrast with those of several laboratory and clinical studies performed with ETTs and muscle relaxation (1,6,7).
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 study was supported by institutional funding of the Department of Anesthesiology and Critical Care Medicine, Klinikum am Steinenberg, Reutlingen, Germany.
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References |
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- Magnusson L, Zemgulis V, Wicky S, et al. Atelectasis is a major cause of hypoxemia and shunt after cardiopulmonary bypass: an experimental study. Anesthesiology 1997; 87: 1153–63.[Web of Science][Medline]
- Tokics L, Hedenstierna G, Strandberg A, et al. Lung collapse and gas exchange during general anesthesia: effects of spontaneous breathing, muscle paralysis, and positive end-expiratory pressure. Anesthesiology 1987; 66: 157–67.[Web of Science][Medline]
- Tenling A, Hachenberg T, Tyden H, et al. Atelectasis and gas exchange after cardiac surgery. Anesthesiology 1998; 89: 371–8.[Web of Science][Medline]
- Loeckinger A, Kleinsasser A, Keller C, et al. Administration of oxygen before tracheal extubation worsens gas exchange after general anesthesia in a pig model. Anesth Analg 2002; 95: 1772–6.
[Abstract/Free Full Text] - Rothen HU, Sporre B, Englberg G, et al. Airway closure, atelectasis and gas exchange during general anaesthesia. Br J Anaesth 1998; 81: 681–6.
[Abstract/Free Full Text] - Hedenstierna G. Airway closure, atelectasis and gas exchange during anaesthesia. Minerva Anestesiol 2002; 68: 332–6.[Medline]
- Benoit Z, Wicky S, Fischer JF, et al. The effect of increased FIO2 before tracheal extubation on postoperative atelectasis. Anesth Analg 2002; 95: 1777–81.
[Abstract/Free Full Text] - Rothen HU, Sporre B, Englberg G, et al. Prevention of atelectasis during general anaesthesia. Lancet 1995; 345: 1387–91.[Web of Science][Medline]
- Lindahl SG, Mure M. Dosing oxygen: a tricky matter or a piece of cake? Anesth Analg 2002; 95: 1472–3.
[Free Full Text] - Hedenstierna G, Rothen HU. Atelectasis formation during anesthesia: causes and measures to prevent it. J Clin Monit Comput 2000; 16: 329–35.[Web of Science][Medline]
- Tschernko EM, Bambazek A, Wisser W, et al. Intrapulmonary shunt after cardiopulmonary bypass: the use of vital capacity maneuvers versus off-pump coronary artery bypass grafting. J Thorac Cardiovasc Surg 2002; 124: 732–8.
[Abstract/Free Full Text] - Brimacombe J. The advantages of the LMA over the tracheal tube or facemask: a meta-analysis. Can J Anaesth 1995; 42: 1017–23.[Web of Science][Medline]
- West JB. Ventilation-perfusion inequality and overall gas exchange in computer models of the lung. Respir Physiol 1969; 7: 88–110.[Web of Science][Medline]
- Berry A, Brimacombe J, Keller C, Verghese C. Pulmonary airway resistance with the ETT versus laryngeal mask airway in paralyzed anesthetized adult patients. Anesthesiology 1999; 90: 395–7.[Web of Science][Medline]
- Hedenstierna G, Tokics L, Lundquist H, et al. Phrenic nerve stimulation during halothane anesthesia: effects of atelectasis. Anesthesiology 1994; 80: 751–60.[Web of Science][Medline]
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