Randomized comparison of three methods of induction of anaesthesia with sevoflurane{dagger}

C. L. Knaggs1 and G. B. Drummond2,*

1 Clinical Neurosciences and 2 Department of Anaesthesia, Critical Care, and Pain Medicine, Royal Infirmary, Edinburgh EH16 4SA, UK

* Corresponding author: Department of Anaesthesia, Critical Care, and Pain Medicine, Royal Infirmary, 51 Little France Crescent, Edinburgh EH16 4SA, UK. E-mail: g.b.drummond{at}ed.ac.uk

Accepted for publication March 15, 2005.


    Abstract
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 Footnotes
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
Background. Rebreathing will occur if a low gas flow and a Mapleson D circuit are used to induce anaesthesia with a volatile anaesthetic agent. This has the advantage that it allows ventilation to be sustained when consciousness is lost, and specific manoeuvres such as breath-holding or vital capacity breaths are not needed to facilitate induction of anaesthesia. However, if the fresh gas flow were too small, this would slow induction by limiting the rate of delivery of the anaesthetic agent. To assess the impact of fresh gas flow and rebreathing, we compared induction using sevoflurane 8% given by three different methods.

Methods. We randomly allocated 65 patients to receive induction of anaesthesia from either a Mapleson A breathing system with a fresh gas flow of 9 litre min–1 (group A9), a Mapleson D system with a fresh flow of 6 litre min–1 (group D6) or a Mapleson D system with a fresh flow of 3 litre min–1 (group D3). We measured times for induction, end-tidal sevoflurane and end-tidal carbon dioxide.

Results. The median (quartiles) induction times were 58 (45, 72), 50 (42, 65) and 64 (52, 92) s in the groups A9, D6 and D3 respectively. Induction of anaesthesia took longer (P<0.01) and was more variable in group D3. In this group, end-tidal sevoflurane concentration at the time of induction of anaesthesia was lower (P<0.05). In group A9, end-tidal carbon dioxide was less (P<0.05).

Conclusions. In adult patients allowed to breathe normally, prompt and consistent inhalation induction of anaesthesia with sevoflurane is obtained when fresh gas flow is limited to 6 litre min–1 from a Mapleson D circuit, but smaller flows are impractical.

Keywords: anaesthesia, induction, inhalation ; breathing system, Mapleson ; carbon dioxide, rebreathing


    Introduction
 Top
 Footnotes
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
Induction of anaesthesia by inhalation of sevoflurane is popular for day surgery because this agent is easy to breathe and acts rapidly. However, loss of consciousness is often associated with transient reduction or cessation of breathing, interfering with the process of anaesthetic uptake and prolonging induction.1 To overcome this problem, several methods for inhalation induction have been suggested, all of which work, at least in part, by allowing carbon dioxide accumulation, which will sustain breathing. These are usually based on voluntary manoeuvres such as breath holding.2 3 A disadvantage of such methods is that some patients may find them difficult to understand and carry out.

Addition of carbon dioxide to the inhaled gas facilitates induction of anaesthesia,4 but this is rarely feasible and has inherent dangers. We found that by using a breathing circuit with a reduced fresh gas flow rate, inhalation induction was possible without requiring patients to make voluntary manoeuvres, such as vital capacity breaths or breath holds. The reduced fresh gas flow rate allowed rebreathing, carbon dioxide values increased slightly, and breathing was better maintained.1

However, there are likely to be limitations to this in that too small a fresh gas flow rate will reduce the rate of delivery of anaesthetic to the patient, limit anaesthetic uptake and slow anaesthetic induction. To clarify a practical limit, we compared induction of anaesthesia using three methods: (i) non-rebreathing; (ii) mild rebreathing; and (iii) moderate rebreathing. We compared the time taken to induce anaesthesia and also the respired anaesthetic and carbon dioxide values. We used loss of arm tone to indicate onset of anaesthesia as this is a reliable and clinically useful measure of induction of anaesthesia.5 6


    Methods
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
We obtained approval for the study from our local Research Ethics Committee. Each patient gave written informed consent. We recruited women, ASA I or II, about to have minor gynaecological surgery, and noted their age, height and weight. We did not recruit patients who were taking opioid analgesics, sedatives or antidepressants. No premedication was used. ECG, pulse oximetry and non-invasive arterial pressure were monitored in all patients and an i.v. cannula was placed after infiltration with 1% lidocaine.

We prepared opaque envelopes, blocked in groups of 15, containing equal allocations to the three groups. The envelope was opened just before induction of anaesthesia. We used coaxial disposable circuits (Intersurgical), and oxygen as the carrier gas. The allocations were: a Mapleson A circuit and a gas flow of 9 litre min–1 (group A9), which would effectively eliminate rebreathing; a coaxial Mapleson D(Bain circuit) supplied with a fresh gas flow of 6 litre min–1, which induces mild rebreathing (group D6); and a Mapleson D system supplied with a fresh gas flow of 3 litre min–1 (group D3), which causes moderate rebreathing. We used the Mapleson A circuit as, in pilot studies with a fresh gas flow of 9 litre min–1, we found that rebreathing could occur with the coaxial Mapleson D circuit. Gas was sampled at the mask connection and analysed for carbon dioxide and sevoflurane (Datex S/5 type F-CMI; Instrumentarium, Helsinki, Finland).

The patients lay supine on a trolley with the head supported on a single pillow. After baseline measurements of pulse, arterial pressure and oxygen saturation, the patient was asked to hold one arm straight out, at about 45° to the horizontal, and to maintain that position for as long as possible. The oxygen flow was started and the mask was applied to the patient's face to obtain a gas-tight seal. When the gas analyser indicated a good trace for carbon dioxide, the sevoflurane vaporizer was set to 0.5%, and increased after every two breaths, in the sequence 1, 2, 4 and 8%. The time from when the vaporizer was set to 8% to the time when the arm became horizontal was taken as the time for induction of anaesthesia.

In the first 37 patients, recordings were made of gas composition and flow using an infrared analyser (Datex Cardiocap II, type CG-IGS; Datex, Helsinki, Finland). This monitor provides analogue waveform signals for gases, which are not available from the Datex S/5. Signals from the monitor were recorded through an analogue-to-digital (AD) converter (Micro 1401, CED 2501; Cambridge Electronic Design, Cambridge, UK) and a desktop computer (PC type, running Windows 2000, using Spike software, type 2.03, supplied by CED). Each breathing system was connected to the patient mask by two bacterial filters. The first, next to the mask, allowed separation of the patient from the circuit. The other was used as a pneumotachograph. We measured the pressure across this filter with a transducer (Furness FC044; Furness Controls Limited, Bexhill, UK) and recorded the signal via the AD converter.

The time courses of end-tidal values for sevoflurane and carbon dioxide were taken from the records and fitted to a second-order polynomial using a statistical software package (Prism, version 4.00 for Windows; GraphPad Software, San Diego, CA, USA). To compare these values between the groups, we used values obtained from the time the vaporizer was set to 8% and 40 s later, when data from all the patients were used. After this time, data from fewer patients were available because some patients had become anaesthetized and data were no longer collected. Statistical comparisons between the groups were made with the Kruskal–Wallis test, followed if necessary by Dunn's test. Data are presented as median (quartile values) unless otherwise stated.


    Results
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 Abstract
 Introduction
 Methods
 Results
 Discussion
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We asked 101 patients to participate in the study. Of these, 72 agreed, but we were only able to study 67 for various operational reasons. In the first 37, we recorded carbon dioxide and sevoflurane concentrations and obtained satisfactory records in 35. The groups were well matched for age, height, and weight (Table 1). No clinical difficulties occurred during induction of anaesthesia. Pulse oximeter values remained above 95% throughout the procedure in all patients.


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Table 1 Characteristics of the patients studied. The patients in the kinetic study were a subset of the induction study patients

 
The induction times for the groups A9, D6 and D3 were 58 (45, 72), 50 (42, 65) and 64 (52, 92) s respectively (P<0.01). The induction time for group D3 was not only significantly greater, but the scatter of induction times was greater (Fig. 1).



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Fig 1 Individual induction times for the three groups of patients. The horizontal line indicates the median value. P<0.05 for differences between the groups.

 
The patterns of change in end-tidal carbon dioxide and sevoflurane are shown in Figure 2. There was a highly significant difference between the fitted polynomial curves for both variables (P<0.001). End-tidal carbon dioxide started and remained significantly lower in group A9 (P<0.05), and the end-tidal sevoflurane values were consistently lower in group D3 (P<0.05). At the time of loss of consciousness, the end-tidal sevoflurane concentration was also lower in these patients. At the time of induction of anaesthesia, the values of end-tidal sevoflurane were 4.1 (3.5,4.5), 3.5 (3.3,4.2) and 2.8 (2.4,3.1)% for the groups A9, D6 and D3 respectively (P<0.05).



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Fig 2 End-tidal values for sevoflurane (upper row) and carbon dioxide (lower row) for individual subjects in the three groups of patients. The heavy line indicates the best fit curve for the first 40 s, when data for all the patients were included.

 

    Discussion
 Top
 Footnotes
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
We set out to assess the limit of fresh gas flow that could be used practically for induction of anaesthesia without requiring specialized respiratory manoeuvres. As we had suspected, a fresh gas flow of 3 litre min–1 reduced the rate of increase of sevoflurane concentration and increased the time to induce anaesthesia. Thus, for most patients, a fresh gas flow rate of 6 litre min–1 will provide prompt and reliable induction of anaesthesia with no need for maximal expiration, inspiration or breath-holding. The only instruction needed is to warn the patient to take a breath in before breathing from the mask, to avoid the reservoir bag collapsing at the first inspiration. It is also necessary to obtain a good mask fit to prevent air entrainment which will reduce rebreathing. This can be checked easily from the capnograph tracing, which should display carbon dioxide during inspiration. The Mapleson A system, supplied with 9 litre min–1 of gas, will function much like a circle system when the same flow is set.

Comparisons of the many different studies of this topic are difficult. Many have used premedication,7 8 nitrous oxide9 10 and different inhaled agents,11 all of which are possible sources of variation. Nitrous oxide appears to contribute little to the efficacy of inhalation induction.12 Some workers found it difficult to distinguish between different agents13 but other comparisons have been unequivocal.11 In addition, the methods of assessing time to induction are disparate. In particular, volunteer studies give more consistent and better results, because the subjects may be more cooperative and more able to perform the manoeuvres correctly than patients, who may be anxious, inattentive and unfamiliar with the process. For example, in this study, many patients when asked to breathe normally would breathe very slowly when the mask was applied. Consequently, the time over which the fresh gas concentration was increased differed between patients. To limit the effect of this variation, which would conceal the differences between treatments, we chose to measure the time taken to induce anaesthesia from the time when the fresh gas concentration was set at 8%, which was eight breaths from the start of the induction. Before 8% sevoflurane was present in the inspired gas, the end-tidal concentration remained very small. By using steps of doubling the concentration we could increase the concentration rapidly and without any evidence of airway irritation. This was necessary as our patients had no premedication, and in our pilot study some patients coughed or held their breath if given 8% to breathe immediately.

As an end-point for anaesthetic induction we used descent of the arm. This is a simple, consistent and reliable index, which represents deeper anaesthesia than other indexes, such as the cessation of finger tapping, the lash reflex or dropping a weight.5 We asked the patients to breathe normally, and achieved times for induction of anaesthesia that were similar to those obtained in volunteers after vital capacity manoeuvres, using nitrous oxide 67% and sevoflurane 4.5%.14 We believe that this is the result of using the effects of partial rebreathing offered by the Mapleson D circuit, and is a practical method for routine clinical use.

Since the Mapleson A system allows selective inspiration of fresh gas, end-tidal carbon dioxide in this group will be controlled solely by the patient's intrinsic respiratory drive. In contrast, in those groups breathing from the Mapleson D circuit, there is a degree of rebreathing and the level of carbon dioxide in the circuit gases is regulated by several factors. The most important is the rate of elimination of carbon dioxide from the breathing system, which is regulated by the fresh gas flow, since this washes carbon dioxide out of the spill valve. The difference between the carbon dioxide in the breathing system and the alveolar gas will depend upon alveolar ventilation and also on the pattern of breathing. The generally low values of end-tidal carbon dioxide indicate the drive to breathe from wakefulness and probable anxiety in patients before surgery. In such patients, loss of consciousness leads to loss of ventilatory drive.15 16 Adding carbon dioxide to the inspired gas has been used to accelerate induction of anaesthesia with isoflurane, but modern anaesthetic machines do not provide this option, which is intrinsically unsafe.4 Using the patient's own carbon dioxide is simple and effective. After induction, transfer to a circle system with a carbon dioxide absorber and flow rates of less than 1 litre min–1 are appropriate, usually after transfer from the anaesthetic room to the operating theatre.

In theory, it would be logical to adjust the fresh gas flow according to the carbon dioxide production of the patient, which can be predicted from body weight.17 In this way the degree of hypercapnia may be regulated. However, our patients had relatively uniform physical characteristics. In patients with different characteristics, such as children and wasted or muscular patients, the appropriate gas flows could be altered to meet their predicted carbon dioxide production or anaesthetic requirement. We suggest that this would be in the order of 100 ml kg–1. Since anaesthetic uptake is likely to be related to the same physical characteristics as carbon dioxide production (muscle mass and cardiac output), this gas flow may well also deliver the appropriate quantity of anaesthetic vapour.

In a previous smaller study, we could not distinguish between the time to induction of anaesthesia using 3 and 6 litre min–1, and found that the rate of induction with the Magill circuit was slower5 because more patients became apnoeic when rebreathing did not occur. In theory, a lower rate of delivery of anaesthetic vapour to the patient would delay the increase in alveolar, arterial and brain concentration and slow induction. This concern was substantiated by the present study, and the mechanism demonstrated: the rate of increase in end-tidal concentration was slower and the time to induction of anaesthesia was significantly longer in group D3. It is of interest that the end-tidal concentration, measured at the end-point of loss of arm tone, was lowest in the patients in whom the induction was slower, showing a smaller difference between arterial and brain concentrations when the alveolar concentration increased less rapidly.

In summary, we have shown that rapid and consistent inhalation induction of anaesthesia can be obtained in unpremedicated patients, without using specific breathing strategies, if a Mapleson D circuit is used with a fresh gas flow of 6 litre min–1.


    Acknowledgments
 
Funded in part by the University of Edinburgh (Neuroscience teaching) and partly by Lothian Health Board Endowment fund 70780.


    Footnotes
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 Footnotes
 Abstract
 Introduction
 Methods
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 Discussion
 References
 
{dagger} Presented in part at the Anaesthetic Research Society meeting held in Cardiff, UK, July 2002, and published in abstract form in Br J Anaesth 2002; 89: 673P. Back


    References
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 Footnotes
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
1 Guracha Boru K, Drummond GB. Comparison of breathing methods for inhalation induction of anaesthesia. Br J Anaesth 1999; 83: 650–3[Abstract/Free Full Text]

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3 Ruffle JM, Snider MT. Comparison of rapid and conventional inhalation inductions of halothane oxygen anaesthesia in healthy men and women. Anesthesiology 1987; 67: 584–7[ISI][Medline]

4 Coleman SA, McCrory JW, Vallis CJ, Boys RJ. Inhalation induction of anaesthesia with isoflurane: effect of added carbon dioxide. Br J Anaesth 1991; 67: 257–61[Abstract]

5 Strickland TL, Drummond GB. Comparison of pattern of breathing with other measures of induction of anaesthesia, using propofol, methohexital, and sevoflurane. Br J Anaesth 2001; 86: 639–44[Abstract/Free Full Text]

6 Thompson S, Drummond GB. Loss of volition and pain response during induction of anaesthesia with propofol or sevoflurane. Br J Anaesth 2001; 87: 283–6[Abstract/Free Full Text]

7 Loper K, Reitan J, Bennett H, Benthuysen J, Snook L. Comparison of halothane and isoflurane for rapid anaesthetic induction. Anesth Analg 1987; 66: 766–8[Abstract]

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9 Wilton NCT, Thomas VL. Single breath induction of anaesthesia, using a vital capacity breath of halothane, nitrous oxide and oxygen. Anaesthesia 1986; 41: 472–6[ISI][Medline]

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12 O'Shea H, Moultrie S, Drummond GB. Influence of nitrous oxide on induction of anaesthesia with sevoflurane. Br J Anaesth 2001; 87: 286–8[Abstract/Free Full Text]

13 Bacher A, Burton AW, Uchida T, Zornow MH. Sevoflurane or halothane anesthesia: can we tell the difference? Anesth Analg 1997; 85: 1203–6[Abstract]

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17 Bain JA, Spoerel WE. Flow requirements for a modified Mapleson-D system during controlled ventilation. Can Anaesth Soc J 1973; 20: 629–36[ISI][Medline]





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