1 Department of Anesthesia, University Health Network, University of Toronto, Toronto, Canada, M5G 2C4 2 Present address: Department of Anesthesiology and Resuscitology, Nagoya City University Medical School, Nagoya, 467-8601, Japan
*Corresponding author. E-mail joe.fisher @utoronto.ca
Accepted for publication: July 18, 2003
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Abstract |
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Methods. Fourteen patients were studied after approximately 1 h of anaesthesia with isoflurane. Control patients were allowed to recover in the routine way. Isocapnic hyperpnoea patients received 23 times their intraoperative ventilation using a system to maintain end tidal PCO2 at 4550 mm Hg. We measured time to removal of the airway and rate of change of bispectral index (BIS) during recovery.
Results. With isocapnic hyperpnoea, the time to removal of the airway was markedly less (median and interquartile range values of 3.6 (2.73.7) vs 12.1 (6.817.2) min, P<0.001); mean (SD) BIS slopes during recovery were 11.8 (4.4) vs 4.3 (2.7) min1 (P<0.01) for isocapnic hyperpnoea and control groups, respectively. Isocapnic hyperpnoea was easily applied in the operating room.
Conclusions. Isocapnic hyperpnoea at the end of surgery results in shorter and less variable time to removal of the airway after anaesthesia with isoflurane and nitrous oxide.
Br J Anaesth 2003; 91: 78792
Keywords: anaesthesia, recovery; anaesthetic techniques, extubation; pharmacokinetics; ventilation
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Introduction |
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Sasano and colleagues5 demonstrated in dogs that isocapnic hyperpnoea speeded recovery from isoflurane-maintained anaesthesia. These results may not be applicable clinically if V·E cannot be increased mechanically in patients whose airways are controlled with laryngeal masks or tracheal tubes as they recover from anaesthesia. Recovery in humans and dogs may differ because of differences in proportion of muscle and fat, distribution of blood flow to the brain, and sensitivity of the brain to anaesthetics.6 Post-surgical pain, which was absent in the dogs, may also affect arousal.7
In this study, we compared emergence from anaesthesia with isoflurane-nitrous oxide in patients who were allowed to recover under assisted spontaneous ventilation (control group) with those who were treated with isocapnic hyperpnoea after surgery. We measured time to removal of the airway and the rate of change of bispectral index (BIS) during recovery.
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Methods |
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To begin the recovery period, isoflurane and nitrous oxide were turned off (time=0). In the control group, patients continued to breathe via the circle anaesthetic circuit. Oxygen flow was set greater than 10 litre min1, and the anaesthetist was instructed to assist ventilation as clinically indicated to prevent hypoxia, treat excess hypercarbia, and provide for the elimination of volatile anaesthetics. In the isocapnic hyperpnoea group, the anaesthetic circuit was disconnected from the patients airway. The patients lungs were then manually ventilated with the isocapnic hyperpnoea apparatus to maintain end-tidal PCO2 (PE'CO2) at 4550 mm Hg independent of V·E and without re-breathing. The target ventilation was 15 litre min1 measured using the ventilation monitor (Datex AS/3, Helsinki, Finland). The airway was removed (and timing stopped) when patients responded to the command to open their eyes. We monitored vital signs, tidal gas, and vapour concentrations, exhaled minute volume (Datex AS/3, Helsinki, Finland), and the BIS (Aspect Medical Systems, Newton, MA, USA). Data from the AS/3 were digitized at 60 Hz using a DI-720 analogue-to-digital converter (Dataq, Akron, OH, USA) and recorded continuously. Times from turning off the vaporizer to removal of the airway were recorded.
Isocapnic hyperpnoea apparatus
The isocapnic hyperpnoea apparatus (Fig. 1) was configured for the operating room as a modified self-inflating bag (Pulmanex, SensorMedics, Yorba Linda, CA, USA) supplied by gases from a compact manifold (SensorMedics) on a stand beside the anaesthetic machine. The manifold was supplied with pure carbon dioxide from an E-size cylinder; oxygen was supplied via a T-piece to the manifold from the anaesthetic machine supply. The manifold had a flowmeter that supplied the self-inflating bag with the basal oxygen flow calculated to be equal to that alveolar ventilation resulting in PCO2 of 50 mm Hg. The manifold also contained a gas blender that blended the pure carbon dioxide and oxygen to provide a mixture of carbon dioxide 6%:oxygen 94% (reserve gas) and a demand regulator that supplied the reserve gas to the low-pressure relief valve of the self-inflating bag. With this system, when V·E is equal to or less than the basal oxygen flow, the resuscitation bag functions normally, providing oxygen 100%. When however, V·E is increased above the oxygen flow, the balance of the inspired gas consists of reserve gas drawn through the low-pressure relief valve. The volume of fresh gas entering the alveoli determines the alveolar PCO2 (PACO2) and allows the elimination of the volatile anaesthetic. The reserve gas does not affect the PACO2 (because its PCO2 is approximately equal to that in the alveoli), but does increase the gas flow allowing washout of the volatile anaesthetic.
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Power analysis
We assumed that the average time to emergence in the control group would be about 10 min with an SD of 5 min. Assuming an alpha of 0.05 and a probability of accepting the null hypothesis of 0.8, power analysis predicted a sample size of 13 to identify a reduction of the recovery time by 50%.
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Results |
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Discussion |
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The experimental protocol required following a practice that may conflict with usual practice. Opioid administration (type and dose) was restricted in the later part of anaesthetic maintenance; the concentrations of nitrous oxide and isoflurane adjusted accordingly, and maintained without tapering, until the end of surgery. Nevertheless, the protocol provided comparable conditions to test the two strategies for recovery from anaesthesia. Patients were randomized only at the end of surgery so anaesthetists were unable to bias their anaesthetic technique towards either group. In addition, BIS provided an objective measure of recovery.
How much isocapnic hyperpnoea will speed recovery from anaesthesia in practice will depend on the details of the anaesthetic (e.g. agent used, depth and duration of anaesthesia, changes in agent concentration towards the end of surgery, use of adjuvant drugs such as opioids and benzodiazepines, type of airway management), surgery, and patient characteristics (e.g., age, sex, body size, sensitivity to various anaesthetics). Nevertheless, for any given operation and anaesthetic that uses an anaesthetic vapour, there will be a range of recovery times, which could be reduced by increasing the rate of vapour elimination. Isocapnic hyperpnoea may allow this.
To reduce recovery from anaesthesia, much effort and expense has been devoted to developing anaesthetics with low blood solubility, (). In contrast, we have taken the approach of increasing anaesthetic clearance by increasing V·E. The rationale for hyperpnoea to speed emergence from anaesthesia follows from the relation between the factors determining the clearance of volatile anaesthetic agent from the blood passing through the lung as expressed by:
where is the solubility of the vapour in blood, Q· is cardiac output, and V·E is alveolar ventilation.1
Figure 4 illustrates that with only an approximately 3.5-fold increase in V·E, the clearance of isoflurane (=1.38)8 becomes equal to that of desflurane (
=0.42).8 Times to removal of the airway in our control subjects were within those reported previously for isoflurane but those in our subjects treated with isocapnic hyperpnoea were within the 410 min range expected for desflurane and sevoflurane (see tables VI and VII in Patel and Goa8).
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Sasano and colleagues5 recently introduced a new method of non re-breathing isocapnic hyperpnoea, which avoids the risk of hypercarbia. Manual hyperventilation is applied using a separate circuit consisting of a modified standard self-inflating bag (Fig. 1). Patients can be monitored routinely with pulse oximeter and capnograph. The isocapnic hyperpnoea circuit provides oxygen at low V·E and, when V·E is increased, adds carbon dioxide in the form of carbon dioxide 6% in oxygen, in direct proportion to the increase in V·E in order to maintain isocapnia.13 The separate circuit, in contrast to using carbogen (carbon dioxide 5%, oxygen 95%), maintains isocapnia independent of V·E without increasing the rate of consumption of the carbon dioxide absorbent.
The isocapnic hyperpnoea circuit has an additional fail-safe feature. Even with only mild hyperpnoea (10 litre min1) and with a complete failure of oxygen flow (oxygen flow=0), in a 70 kg male, the PaCO2 would equilibrate between 70 and 80 mm Hg, which is unlikely to be dangerous in most well-oxygenated patients. Moreover, hyperpnoea with reserve gas alone will still result in the patient waking within the same time as with the oxygen flow and therefore the PE'CO2 might not have time to reach that equilibrium value.
Increased V·E affects the rate of elimination of isoflurane from the lungs.2 As the equilibration of isoflurane in the blood with the tissues is very rapid,14 the removal of isoflurane from the blood via the lungs will be followed closely by removal from the vessel rich group (VRG). The clearance of anaesthetic from the various parts of the VRG will also depend on their respective blood flows. Conventional hyperventilation and reduction of PaCO2 at the end of surgery reduces blood flow to the brain, and may delay the clearance of anaesthetic from the brain relative to other tissues of the VRG. This would offset the effect of more rapid elimination from the blood on time to recovery. For an equivalent minute ventilation, maintaining normocapnia and higher brain blood flow should allow more rapid equilibration of partial pressures of anaesthetic between brain and arterial blood. However, further investigation is required to ascertain whether isocapnic hyperpnoea shortens or improves the quality of emergence compared with hyperventilation.
A further consideration is the effect of hyperpnoea on cardiovascular stability. Henderson and Haggard9 increased V·E to 3070 litre min1 in their ether-anaesthetized patients and noted a decrease in arterial pressure of only 515 mm Hg. Deliberate hyperpnoea does not decrease stroke volume or arterial pressure in animals15 16 or humans.17 We observed no cardiovascular effects of increased V·E with isocapnic hyperpnoea to, at most, 20 litre min1. However, the isocapnic hyperpnoea was applied during recovery when arterial pressure and heart rate naturally increase and this may have obscured any such effects.
Isocapnic hyperpnoea may also speed up the elimination from the blood, via the lung, of other volatile agents such as carbon monoxide18 19 and be useful as a research tool in studying the pharmacokinetics of such agents, or in other instances in which it is necessary to keep the patients PCO2 constant.
Conclusion
Isocapnic hyperpnoea was successfully applied in the operating room and, for our anaesthetic protocol, resulted in faster, less variable emergence time.
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References |
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