| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
* From the Departments of Anesthesiology and
Intensive Care Unit,
Gunma University School of Medicine, Maebashi, Japan and the Department of Anesthesia, Ashikaga Red Cross Hospital, Ashikaga, Japan
Address correspondence to: Koh-ichi Nishikawa MD PhD, Molecular Neuropharmacology Lab., Department of Anesthesiology, A-1050, Weill Medical College of Cornell University, 1300 York Ave., New York, NY 10021, USA. Phone: 212-746-1150; Fax: 212-746-4879; E-mail: nishikaw{at}news.sb.gunma-u.ac.jp
 |
Abstract |
|---|
 TOP Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Methods: Fifteen patients scheduled for elective orthopedic surgery were enrolled in this study. Anesthesia was maintained with the continuous infusion of propofol and with nitrogen (N2) and oxygen (O2) (6 L•min–1, FIO2, 0.33). In all patients, the lungs were ventilated with a Servo 900C ventilator equipped with a gas mixer for O2, N2O, and N2. After obtaining baseline data, N2 was replaced with N2O maintaining FIO2 constant at 0.33. The changes in fractional concentration of O2, N2O, and N2 were continuously measured using mass spectrometer in a breath-by-breath basis. PaO2 and hemodynamic data were obtained at 1, 5, 10, 30 and 60 min after the start of N2O inhalation.
Results: Five minutes after N2O inhalation, FETO2 increased from 0.27 ± 0.01 to 0.31 ± 0.02 (P < 0.01) and PaO2 increased from 172.0 ± 22.5 mmHg to 201.0 ± 10.3 mmHg (P < 0.01). These effects produced by N2O were observed for 30 min.
Conclusions: These results confirm the concept of second gas effect of N2O on oxygen uptake in humans and provide evidence that the PaO2 increase correlated with the increase in FETO2 after N2O inhalation.
|
Introduction |
|---|
|
TOPAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
In previous papers, the end-tidal and inspired gas samples were intermittently collected for concentration analysis. Thus, the ratio of alveolar (end-tidal) concentration (FA) to the inspired concentration (FI) was used to present data. In this study, we used the respiratory gas mass spectrometer (RGMS) that allowed us to measure continuously fractional concentrations of both inspiratory and expiratory gases in patients under general anesthesia on a breath-by-breath basis. This study was undertaken to test the concept that the second gas effect of N2O on oxygen exists in humans and to clarify the relationship between alveolar oxygen concentration and PaO2 after N2O inhalation using RGMS.
|
Methods |
|---|
|
TOPAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
), scheduled for minor orthopedic surgery of the lower extremities were enrolled in this study. Patients with clinically important pulmonary, cardiovascular, hepatic, renal, or neurological diseases were excluded. Also excluded were patients who were taking medications known to influence anesthetic requirements.
|
Respiratory gas concentrations were continuously measured using the respiratory gas mass spectrometry (AMIS 2000SP, Innovision A/S, Odense, Denmark) sampling gases from the slip-joint port of the endotracheal tube. Respiratory gas was sampled through a 0.2-mm-ID Teflon tube at a rate of 15 ml•min–1 and respiratory data were saved on a PC personal computer. The response time of this respiratory analyzer is 60 msec. This system allowed us to measure the respiratory gas concentration on a breath-by-breath basis. Proper calibration of the mass spectrometer was verified using calibration gases dictated by the manufacturer's instructions. After baseline data were obtained, inspiratory N2 was replaced with N2O by switching the gas mixer dial quickly from air/oxygen mode to N2O/oxygen. FIO2 was kept constant at 0.33 throughout the study period. The PaO2 was measured at 1, 5, 10, 30, and 60 min using blood gas analyzer ABL 520 (Radiometer, Copenhagen, Denmark) and hemodynamic variables including heart rate and systemic blood pressure were recorded simultaneously.
Statistical analysis
All variables were presented as mean ± SD. Data were analyzed by one-way analysis of variance (ANOVA) for repeated measures and Fisher's least significant difference technique. Differences were considered significant at P < 0.05.
|
Results |
|---|
|
TOPAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
shows hemodynamic blood gas analysis data before and after N2O inhalation. There were no differences in heart rate or systemic blood pressure during the study. A small dose of fentanyl was administered to eight patients and ephedrine was used in three. Figure 1A shows a sample trace of respiratory gas fractional concentrations measured by RGMS on a breath-by-breath basis. Figure 1B shows a magnified trace of FIO2 and EETO2 in the same recording. After N2O inhalation, FETO2 increased to maximal level within five minutes and then gradually decreased. Figure 2 shows the changes of FIO2 and FETO2 measured by RGMS system before and after N2O inhalation. Five minutes after the N2O inhalation, FETO2 increased from 0.27 ± 0.01 to 0.31 ± 0.02 (n =15, P < 0.01). The PaO2 significantly increased from 172.0 ± 22.5 mmHg to 201.0 ± 10.3 mmHg and correlated with the increase in FETO2 at five minutes (n = 15, P < 0.01, Figure 3). The effects produced by N2O inhalation on FETO2 and PaO2 were observed for at least 30 min.
|
|
|
|
|
Discussion |
|---|
|
TOPAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Although recent publications have questioned the concept of the second gas effect in clinical practice,9,10 our results confirm and support the classical explanation of this concept. As for oxygen, Rackow et al.11 predicted alveolar hyper-oxygenation during the induction of anesthesia, and Bojrab et al.12 reported the increase in PaO2 during N2O inhalation. Our findings were consistent with these reports that first showed the increase in PaO2 after the start of N2O inhalation. Our results are also consistent with a recent study that demonstrated the existence of the second gas effect in humans using the new inhalation anesthetic, desflurane, in combination with N2O.13 Desflurane has a blood/gas coefficient indistinguishable from that of N2O. Thus, the rate of rise of the alveolar concentration should be the same for both desflurane and N2O during their administration, regardless of the inspired concentrations. However, the administration of N2O 65% increased the FA/FI ratio for both N2O and concurrently administrated desflurane relative to the administration of N2O 5%, suggesting that the second gas effect results from the uptake of substantial volumes of N2O.
Recently, Sun et al.9 reported that the second gas effect was not a valid concept. Although there are some experimental design differences between our study and theirs, our results do not support their suggestion. They administered N2O 80% rather than 67% and showed that a high concentration of N2O did not facilitate the rise of FA/FI during five minutes measurements. We do not know how the administration of N2O 80% affects cardiac output, however, N2O stimulates the central sympathetic nervous system as well as influencing pulmonary chemoreceptors. Cardiac output may also affect PaO2.14 We selected orthopedic patients in whom surgical stimulation was expected to be minimal and surgical stimulation was minimized by the additional fentanyl administration. In fact, no changes were observed in heart rate or systemic blood pressure during the study. Thus, we concluded that it was unlikely that changes in cardiac output were responsible for the changes in FETO2 and PaO2, although we were unable to measure changes of cardiac output. We did not use any volatile anesthetic gas in this study. Therefore, FRC wash-in was eliminated. Finally, we tried to keep FIO2 constant at 0.33 throughout the study because a change in FIO2 affects both FETO2 and PaO2. The FIO2 showed a small change immediately after N2O inhalation due to the delay in adjusting oxygen fraction at 0.33 in several patients: however, it could be stabilized at 0.33 in a few minutes. Thus, we considered that changes in FIO2 were not responsible for the changes in FETO2 and PaO2.
The changes in both FETO2 (alveolar oxygen concentration) and PaO2 after N2O inhalation have not been demonstrated previously. We determined the relationship between FETO2 and PaO2, and clearly showed that the PaO2 increase correlated with the increase in FETO2. As shown in Figure 2
, FETO2 one minute after N2O inhalation was not different from baseline because of large variability. Sixty minutes after N2O, the FETO2 value was still higher than that of baseline, whereas PaO2 had returned to control. We do not know if there are clinical implications for this difference or whether the difference arises from statistical problems.
In conclusion, our results confirm the concept of the second gas effect of N2O on oxygen uptake in humans under general anesthesia in a breath-by-breath basis and that provide evidence that PaO2 increase correlated with the increase in alveolar oxygen concentration after N2O inhalation.
|
Acknowledgments |
|---|
Accepted for publication February 11, 2000.
|
References |
|---|
|
TOPAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
2 Epstein RM, Rackow H, Salanitre E, Wolf GL. Influence of the concentration effect on the uptake of anesthetic mixtures: the second gas effect. Anesthesiology 1964; 25: 364–71.[Medline]
3 Tunstall ME, Hawksworth GM. Halothane uptake and nitrous oxide concentration. Arterial halothane levels during Caesarean section. Anaesthesia 1981; 36: 177–82.[Medline]
4
Watanabe S, Asakura N, Taguchi N. Supramaximal second gas effect: more rapid rise of alveolar halothane concentration during ipsilateral lung N2O administration compared to bilateral administration. Anesth Analg 1993; 76: 76–9.
5 Poon CS, Wiberg DM, Ward SA. Dynamics of gaseous uptake in the lungs: the concentration and second gas effects. IEEE Trans Biomed Eng 1981; 28: 823–31.[Medline]
6 Kitahata LM, Taub A, Conte AJ. The effect of nitrous oxide on alveolar carbon dioxide tension: a second-gas effect. Anesthesiology 1971; 35: 607–11.[Medline]
7
Korman B, Mapleson WW. Concentration and second gas effects: can the accepted explanation be improved? Br J Anaesth 1997; 78: 618–25.
8
Mapleson WW, Korman B. Concentration and second-gas effects in the water analogue. Br J Anaesth 1998; 81: 837–43.
9
Sun X-G, Su F, Shi Y-Q, Lee C. The "second gas effect" is not a valid concept. Anesth Analg 1999; 88: 188–92.
10
Lin CY, Wang JS. Supramaximal second gas effect: a nonexistent phenomenon. Anesth Analg 1993; 77: 870–2.
11
Rackow H, Salanitre E, Frumin MJ. Dilution of alveolar gases during nitrous oxide excretion in man. J Appl Physiol 1961; 16: 723–8.
12 Bojrab L, Stoelting RK. Extent and duration of the nitrous oxide second-gas effect on oxygen. Anesthesiology 1974; 40: 201–3.[Medline]
13
Taheri S, Eger EI II. A demonstration of the concentration and second gas effects in humans anesthetized with nitrous oxide and desflurane. Anesth Analg 1999; 89: 774–80.
14 Philbin DM, Sullivan SF, Bowman FO Jr, Malm JR, Papper EM. Postoperative hypoxemia: contribution of the cardiac output. Anesthesiology 1970; 32: 136–42.[Medline]
This article has been cited by other articles:
 |
|
 |
|
  J. F. A. Hendrickx, R. Carette, H. J. M. Lemmens, and A. M. De Wolf Large volume N2O uptake alone does not explain the second gas effect of N2O on sevoflurane during constant inspired ventilation Br. J. Anaesth., March 1, 2006; 96(3): 391 - 395. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Peyton, R. M. Carette, J. F. A. Hendrickx, A. M. De Wolf, W. Hess, J. Kannmacher, and J. Kruse Contamination of anaesthetic gases with nitric oxide and its influence on oxygenation Br. J. Anaesth., May 1, 2005; 94(5): 687 - 688. [Full Text] [PDF]
|
|
|
|
 |
|
 L. J. Goldman Anesthetic Uptake of Sevoflurane and Nitrous Oxide During an Inhaled Induction in Children Anesth. Analg., February 1, 2003; 96(2): 400 - 406. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C.-Y. Lin and K. Nishikawa Second gas effect of N2O Can J Anesth, September 1, 2001; 48(8): 828 - 829. [Full Text]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
