This Article Abstract Full Text (PDF) CME: Take the course for this article: Induced Hypercarbia During Emergence from Inhalation Anesthesia Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Gopalakrishnan, N. A. Articles by Westenskow, D. R. Search for Related Content PubMed PubMed Citation Articles by Gopalakrishnan, N. A. Articles by Westenskow, D. R. Related Collections Anesthetic Techniques Ventilation Pharmacology

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ANESTHETIC PHARMACOLOGY

Hypercapnia Shortens Emergence Time from Inhaled Anesthesia in Pigs

From the Department of Anesthesiology, University of Utah, Salt Lake City, Utah.

Address correspondence to Nishant A. Gopalakrishnan, BS, University of Utah, Department of Anesthesiology, 30 N. 1900 East, 3C444 SOM, Salt Lake City, UT 84132. Address e-mail to nishant{at}abl.med.utah.edu.

	Abstract

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BACKGROUND: Anesthetic clearance from the lungs and the circle rebreathing system can be maximized using hyperventilation and high fresh gas flows. However, the concomitant clearance of CO₂ decreases PAco₂, thereby decreasing cerebral blood flow and slowing the clearance of anesthetic from the brain. This study shows that in addition to hyperventilation, hypercapnia (CO₂ infusion or rebreathing) is a significant factor in decreasing emergence time from inhaled anesthesia.

METHODS: We anesthetized seven pigs with 2 MAC_PIG of isoflurane and four with 2 MAC_PIG of sevoflurane. After 2 h, anesthesia was discontinued, and the animals were hyperventilated. The time to movement of multiple limbs was measured under hypocapnic (end-tidal CO₂ = 22 mm Hg) and hypercapnic (end-tidal CO₂ = 55 mm Hg) conditions.

RESULTS: The time between turning off the vaporizer and to movement of multiple limbs was faster with hypercapnia during hyperventilation. Emergence time from isoflurane and sevoflurane anesthesia was shortened by an average of 65% with rebreathing or with the use of a CO₂ controller (P < 0.05).

CONCLUSIONS: Hypercapnia, along with hyperventilation, may be used clinically to decrease emergence time from inhaled anesthesia. These time savings might reduce drug costs. In addition, higher PAco₂ during emergence may enhance respiratory drive and airway protection after tracheal extubation.

	Introduction

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Rapid removal of anesthetic vapor during emergence allows for a rapid recovery from anesthesia. In addition, rapid return of consciousness is desirable to allow patients to quickly leave the operating suite. Rapid removal of an anesthetic is also desirable in clinical procedures that require the patient to be awakened during the surgery (1).

Recovery time after inhaled anesthesia depends on alveolar ventilation, solubility of the drug in blood and tissue, cerebral blood flow, and duration of anesthesia duration (2,3). However, when hyperventilation is used during emergence to quickly decrease the alveolar and arterial concentration of the anesthetic, the rate of CO₂ removal from the lungs exceeds its rate of production and hypocapnia ensues. Hypocapnia decreases cerebral blood flow, which, in turn, decreases the rate of clearance of anesthetic from the brain. Vesely et al. (4) maintained normocapnia during hyperventilation and showed the role of increased minute ventilation in decreasing emergence time. We maintained hypercapnia during hyperventilation to show the role of increased PAco₂ in decreasing emergence time.

Normocapnia or hypercapnia can be maintained during hyperventilation by introducing CO₂ into the inspired gas mixture. A survey of anesthesiologists in the United Kingdom in 1989 showed that 60% of them infused CO₂ during emergence. They were, however, concerned with the risks of hypoxia and inadvertent hypercapnia, and 80% of them thought that limiting the flow of CO₂ to <1 L/min would improve safety (5–7). Perhaps a safer approach would be to add dead-space to the breathing circuit to induce hypercapnia (8). Rebreathing of CO₂ recovers the CO₂ that would otherwise be eliminated during hyperventilation. However, rebreathing of anesthetic gas might delay emergence unless an anesthetic adsorbent (activated charcoal) is placed between the patient and the added dead-space.

Our study measured the decrease in emergence time in pigs after isoflurane and sevoflurane anesthesia when hypercapnia was maintained during hyperventilation using rebreathing of CO₂ or feedback-controlled infusion of CO₂.

	METHODS

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We tested two methods of increasing PAco₂ during hyperventilation. Figure 1 shows a block diagram of the feedback controller we implemented and tuned to actively induce and maintain hypercapnia during hyperventilation. The feedback controller introduced CO₂ into the breathing circuit at the optimum rate, dependent on the tidal volume and respiratory rate setting, and provided an ideal control condition against which to compare rebreathing which has a much slower rate of increase in end-tidal CO₂ (Etco₂).

View larger version (11K): [in this window] [in a new window]   Figure 1. Block diagram of feedback controller.

The controller consists of a CO₂SMO Plus monitor (Novametrix Medical Systems, Inc., USA) to measure Etco₂, inspired tidal volumes and respiratory rate. The computer ran a proportional-integral (PI) control algorithm which compares the measured Etco₂ from the previous breath to the desired target Etco₂ and determines the amount of CO₂ to be added to the inspired gas in the subsequent breath. The PI controller uses the equation

where CO(t) and CO(t – 1) are the controller output for the current and previous breath, Etco₂(t) and Etco₂(t – 1) are the Etco₂ for the current and previous breath, Setco₂ is the target Etco₂, K_p and K_i are the proportional and integral constants, and T is the sampling period. A timer circuit is used to regulate the amount of CO₂ added to the inspired gas depending on the value sent to it by the PI controller. The inlet pressure to the valve is maintained at 20 psi. The integral and proportional constants were tuned as functions of minute volume and respiratory rate using a mechanical test lung (TTL Test Lung, MI Instruments, MI) connected to an anesthesia ventilator (Modulus CD, Ohmeda, Madison, WI).

The constants K_p and K_i are functions of respiratory rate and tidal volume, so that the controller has the same response time, regardless of the patient's minute ventilation. The controller was tuned to produce a stable response and achieve its target level within 30 s. CO₂ was introduced into the inspired gas mixture during the start of inspiration to prevent artifacts in the capnogram that would have been seen if the patient had exhaled spontaneously during the inspiratory period. When a spontaneous exhalation occurred earlier than expected, the CO₂ waveform was segmented into six sections to calculate Etco₂ accurately. The section with the minimum standard deviation of CO₂ after the dead-space gas had been exhaled was used to calculate Etco₂.

In addition to testing an infusion system, we also used the rebreathing device shown in Figure 2 to passively increase PAco₂ during hyperventilation. The device consists of a rebreathing hose, a canister filled with anesthetic adsorbent and two valves to maintain unidirectional flow of gas through the adsorbent. The rebreathing hose is a 22-mm ID corrugated breathing hose having 150 mL of dead-space when collapsed and 665 mL when fully extended. The canister holds 18 g of medical grade activated charcoal to adsorb anesthetic from the inspired gas as it is rebreathed.

View larger version (6K): [in this window] [in a new window]   Figure 2. Rebreathing device with rebreathing hose, agent adsorber, and one-way valves.

After Institutional Animal Care and Use Committee approval, we studied 11 pigs of either sex weighing 34–44 kg. We induced anesthesia with Telazol (tiletamine hydrochloride, zolazepam hydrochloride) (10 mg/kg). The animal's trachea was intubated without the use of muscle relaxants. Anesthesia was maintained in seven pigs with 2 MAC_PIG of isoflurane (3.1%). In four pigs, anesthesia was maintained with 2 MAC_PIG of sevoflurane (3.94%). The volatile anesthetic concentration was monitored continuously using an anesthetic gas analyzer (CapnoMAC Ultima, Datex-Ohmeda, Helsinki, Finland). We placed electrocardiogram leads, pulse oximetry probe, invasive arterial blood pressure sensor with arterial line, and a rectal temperature probe on each animal to monitor vital signs. The sedation level was monitored using Bispectral Index (BIS, Aspect Medical Systems, Newtton, MA). The mean arterial blood pressure was maintained above a minimum limit of 50 mm Hg by titrating the infusion of lactated Ringer's solution. The respiratory rate was set at 10 breaths/min. The tidal volume was adjusted to maintain Etco₂ at 33 mm Hg with a circle absorber rebreathing circuit (Modulus CD, Ohmeda, Madison, WI). Etco₂, inspired and expired drug concentrations, and BIS were recorded electronically using a personal computer running custom software written in Borland C++ Builder (Inprise Corporation, USA).

Emergence time was measured after 2 h of anesthesia. Emergence began when the vaporizer was turned off. The fresh gas flow was increased to 10 L/min and the respiratory rate was set to 20 breaths/min, resulting in an approximate doubling of minute ventilation during emergence. Once awake, each animal was reanesthetized and emerged from anesthesia three times under the following conditions. The order of emergence was randomly selected.

• Etco₂ increased slowly from 33 to 55 mm Hg by CO₂ rebreathing.
  
• Etco₂ increased rapidly from 33 to 55 mm Hg by the CO₂ controller.
  
• Etco₂ decreased to hypocapnic level (approximately 22 mm Hg) during hyperventilation without adding CO₂.
  

We recorded the time from when the vaporizer was turned off until the return of spontaneous breathing and movement of two or more limbs. Spontaneous breathing during mechanical ventilation was determined by irregular movement of the chest wall and artifacts in the capnogram. Once there was movement of multiple limbs, the animals were reanesthetized by turning on the vaporizer to 2 MAC_PIG and increasing fresh gas flow to 10 L/min. Once the BIS level, arterial blood pressure, and heart rate returned to the values recorded before turning off the vaporizer, anesthesia was maintained for an additional 30 min before the next emergence.

The BIS data recorded electronically during each emergence were normalized using the following equation:

where preemergence BIS is the average BIS 2 min before turning off the vaporizer and maximum BIS is the maximum BIS value observed during emergence and subsequent induction. The time for the normalized BIS to reach 0.95 from the time the vaporizer was turned off was calculated for each emergence.

Analysis was performed using SigmaStat version 2.03 (SPSS, Chicago, IL). The effect of the anesthetic and method of emergence on the time to movement of multiple limbs, time to spontaneous breathing and time for the normalized BIS to increase to 0.95 were compared using two-way repeated measures ANOVA. Post hoc Bonferroni tests were performed when the interaction effects were found to be significant.

	RESULTS

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Table 1 lists the time between when the vaporizer was turned off and return of spontaneous breathing. Figure 3 shows the normalized BIS during emergence from isoflurane and sevoflurane. Figure 4A and B show the average time to movement of multiple limbs and the average time for the normalized BIS to increase to 0.95 during emergence. The time to movement of multiple limbs, time to spontaneous breathing and time to normalized BIS to increase to 0.95 were significantly shorter when hypercapnia was maintained during emergence from isoflurane and sevoflurane (P < 0.05).

View larger version (37K): [in this window] [in a new window]   Figure 3. Normalized BIS during emergence from 2 MACPIG of isoflurane and sevoflurane anesthesia for the three emergence scenarios.

View larger version (26K): [in this window] [in a new window]   Figure 4. Average time between turning off the vaporizer and movement of multiple limbs (A) and rise of normalized BIS to 0.95 during emergence (B) after 2 MACPIG of isoflurane and 2 MACPIG of sevoflurane anesthesia (mean + sd).

Emergence times were not statistically different when rebreathing was used from those obtained when the CO₂ controller was used. After isoflurane anesthesia, the feedback controller increased the Etco₂ from 33 mm Hg to the target of 55 mm Hg in 30.68 ± 6 s (0%–95%) (Fig. 5). In steady-state, the average Etco₂ was 55.06 ± 0.63 mm Hg (mean ± sd).

View larger version (25K): [in this window] [in a new window]   Figure 5. Step response of the controller for a step change in the CO2 controller's set point and a doubling of minute ventilation.

	DISCUSSION

Top Abstract Introduction METHODS RESULTS DISCUSSION REFERENCES

 
The time to emergence from isoflurane and sevoflurane anesthesia was 66% ± 6% faster when hypercapnia was induced by partial CO₂ rebreathing and 63% ± 4% faster when induced by feedback control of the inspired CO₂. If similar results are found in patients, anesthesiologists might be inclined to use the simpler rebreathing device. Use of the device might reduce drug costs by allowing the use of more soluble, less expensive anesthetics. Higher PAco₂ during emergence may help to enhance respiratory drive after tracheal extubation. The possibility of intraoperative awareness towards the end of the case could be decreased since the anesthetic would not have to be titrated down to achieve the desired emergence time.

Our results show that hypercapnia is a significant factor in reducing emergence time during hyperventilation. After 2 h of isoflurane or sevoflurane anesthesia, the time to movement of multiple limbs decreased by an average of 64% when hypercapnia was added to hyperventilation. Hypercapnia increases cerebral blood flow by 6.0% ± 2.6% per mm Hg increase in PAco₂, and thus accelerates the rate of clearance of anesthetic from the brain (9). Increasing PAco₂ during emergence might have shortened emergence time by mechanisms other than increasing cerebral blood flow and thus clearance rate. Increasing PAco₂ might increase sympathetic response and respiratory response of the animal attempting to breathe spontaneously during mechanical ventilation (10,11).

Hypercapnia reduced the standard deviation between emergence times by 72% when the rebreathing device was used. Predictability of emergence time is important when anticipating and planning for the end of a clinical procedure. Emergence times are similar for rebreathing and for an optimally tuned CO₂ controller. Partial CO₂ rebreathing is potentially the simpler and safer technique to produce hypercapnia during hyperventilation because it avoids the safety issues associated with a tank of 100% CO₂. Clinicians may well be inclined to use the rebreathing device rather than the controller because of its low cost. The volume of the expandable/compressible rebreathing tube can be adjusted to achieve the optimum dead space to tidal volume ratio. Although we do not yet have enough experience to identify the optimum ratio, a one-to-one ratio appears to provide enough non-rebreathing to rapidly washout nitrous oxide as well as provide adequate uptake of fresh oxygen. The corrugated tube used in the rebreathing tube promotes enough mixing between the fresh gas and the rebreathed gas to provide fresh oxygen uptake and nitrous oxide washout when the tidal volume is equal to the dead-space volume.

An anesthetic adsorbent is needed to remove anesthetic from the rebreathed gas. With rebreathing, adsorption efficiency of medical grade activated charcoal is nearly 100% for all volatile anesthetics. Advocates of closed circuit anesthesia techniques were first to use charcoal in their closed circle absorber breathing circuits to rapidly decrease the inspired anesthetic concentration during emergence (12,13). The efficiency of charcoal decreases because of adsorption of water vapor by the charcoal granules with subsequent reduction in the surface area (14). We placed one-way valves in the device to ensure that moist gas exhaled by the patient bypasses the activated charcoal while inspired gas flows through it.

Hyperventilation in combination with normal to high PAco₂ shortens emergence time from volatile anesthetics. Vesely et al. (4) compared emergence times from isoflurane-nitrous oxide anesthesia, with and without hyperventilation, when Etco₂ was kept at 46.8 mm Hg. Their study found a 70% decrease in emergence time (8.5 min) between the experimental and the control groups, with minute ventilations of 17 and 5.9 L/min. The study of Vesely et al. clearly shows the importance of hyperventilation in decreasing emergence time. Hyperventilation with even larger minute volume could shorten emergence time further, but might also cause barotrauma, decrease stroke volume in critically ill patients, and induce release of mediator, such as cytokines, into the circulation (15–17).

A study in 1923 (18) found that hypercapnia and hyperventilation shortened emergence time from 74–15 min after ether anesthesia. OH Medical, Inc. and Dräger both manufactured anesthesia machines that were equipped with a tank of CO₂ that was used to maintain hypercapnia during hyperventilation. CO₂ canister bypass valves were provided so that CO₂ was not absorbed by the soda lime absorber (19). CO₂ canister bypass is of limited use in shortening emergence time because the high fresh gas flows needed to clear the anesthetic from the breathing circuit also clears the rebreathed CO₂ from the breathing circuit. Sasano et al. (20) used the combination of a standard resuscitation bag, a demand-based regulator and a gas cylinder containing 94% oxygen and 6% CO₂ to maintain isocapnia during hyperventilation. However, CO₂ is rarely used today because of the inherent risks of over-infusion leading to extreme hypercapnia (5,6). An alternative would be to use computer-based feedback to control the Etco₂ by infusion of CO₂ where a computer could monitor the process for safety.

Besides speeding emergence, mild hypercapnia has the following potential benefits. It may provide better tissue oxygenation, attenuate lung injury (21,22), promote an early return of spontaneous respiration (23), and improved postsurgery cognition (24). It should be noted that Etco₂ is routinely increased to 65 mm Hg without adverse effects in the sedated patient in the intensive care unit and in patients undergoing laparoscopic procedures with CO₂ insufflation. Hypercapnia is clearly contraindicated in patients at risk from increased intracranial pressure (25) or pulmonary hypertension.

During hypercapnia, pigs that received isoflurane emerged faster than pigs that received sevoflurane (Fig. 4). Sevoflurane has a lower blood/gas partition coefficient and a faster recovery profile (26), but it requires a larger increase in ventilation to enhance clearance to the same extent as isoflurane. Additionally, sevoflurane produces a smaller change in cerebrovascular resistance in response to a change in PAco₂ when compared to isoflurane (27). Hypercapnia with hyperventilation may have caused a larger percent increase in cerebral blood flow with isoflurane leading to a faster emergence. The observed differences could also have been due to interanimal variability, which becomes more significant with a smaller sample size.

This study has several limitations. The observer who measured the time when the animal moved multiple limbs and time to return of spontaneous breathing was not blinded to the presence or absence of the rebreathing device or the feedback controller. However, BIS data were not subject to observer bias and the BIS monitor gave differences in emergence time similar to those observed by the investigators. The difference in the time taken for the normalized BIS to increase to 0.95 was statistically significant and followed a trend similar to that of the time to movement of multiple limbs (Fig. 4). Because the study found large time differences in emergence time with and without the devices, and since statistically significant differences were observed in the BIS increase times, we believe PAco₂ makes a difference in emergence time.

Anesthesia was maintained at 2 MAC for only 30 min between the first and second emergence and the second and third emergence, which could have affected emergence time. Emergence from anesthesia is dependent on the duration of anesthesia and tissue depots of anesthetic. These stores may not be equal at the end of each 30 min period. The order of emergence for each animal was randomized to minimize the effects of a prior emergence and longer anesthesia duration. But our sample size may have been too small to avoid cross-over effects.

Hypercapnia in conjunction with hyperventilation was found to decrease emergence time from inhaled anesthetics. Both rebreathing and CO₂ infusion shortened emergence after volatile anesthesia. The rebreathing device described in this study provides a simple means of enabling hypercapnic hyperventilation in a clinical setting. Further studies are required to determine the optimal level of hypercapnia and hyperventilation for the most rapid and safest emergence.

	Footnotes

 
Accepted for publication November 21, 2006.

Supported by National Institutes of Health, National Institute of General Medical Sciences grant GM072661; Department of Anesthesiology, University of Utah; Society for Technology in Anesthesia Research Grant; and Axon Medical, Inc., Salt Lake City, UT.

Potential Conflict of Interest: Authors Joseph Orr, Dwayne Westenskow, and Derek Sakata have a potential conflict of interest. Joseph Orr and Dwayne Westenskow receive salary and hold an equity position in Axon Medical, Inc., the company that funded part of the research. Joseph Orr, Dwayne Westenskow, and Derek Sakata are in a position to receive royalties from the sale of the rebreathing adsorber device.

Reprints will not be available from the authors.

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This Article Abstract Full Text (PDF) CME: Take the course for this article: Induced Hypercarbia During Emergence from Inhalation Anesthesia Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Gopalakrishnan, N. A. Articles by Westenskow, D. R. Search for Related Content PubMed PubMed Citation Articles by Gopalakrishnan, N. A. Articles by Westenskow, D. R. Related Collections Anesthetic Techniques Ventilation Pharmacology