In a recent survey, we found that it is common practice at the end of an anesthetic case to increase fresh gas flow to rapidly remove anesthetic from the breathing circuit. Seventy-eight percent of the anesthesiologists surveyed also used hyperventilation to rapidly remove anesthetic from the lungs (survey of 60 anesthesiologists at ASA 2005 meeting). Hyperventilation may not have been universally adapted because it decreases Paco2, depresses respiratory drive, and may slow the return of spontaneous breathing.
To prevent the decrease in Paco2 during hyperventilation, some anesthesia machines were equipped with a tank containing 100% CO2. During hyperventilation, the flow of CO2 was adjusted to maintain normal or slightly increased Paco2. In 1989, 60% of the anesthesiologists in the United Kingdom routinely administered CO2 to their patients (1). The practice is very seldom used in the United States today because of the risk of inadvertent hypercapnia (2).
We have found that adding deadspace to the patient’s airway is a simpler and safer method of controlling Paco2 during hyperventilation. Added deadspace is routinely used for the noninvasive measurement of cardiac output (NICO, Respironics Inc., Murrysville, PA) and to stimulate respiratory drive in intensive care unit patients (3). In animals, we measured a 60% reduction in emergence time when deadspace was used to maintain hypercapnia during hyperventilation (4). In the current patient study, we measure emergence times with mild hypercapnia and hyperventilation.
Figure 1 shows the device we assembled to enable hypercapnic hyperventilation. It adds deadspace to the patient’s airway as the patient breathes through a 22 mm ID corrugated collapsible breathing hose. The device and the hose have a combined deadspace volume of 882 mLs when fully extended. The patient breathes in through 18 g of medical grade activated charcoal in a 0.95-cm thick canister that is 7.5 cm in diameter. The charcoal adsorbs the volatile anesthetic from the deadspace by trapping it in micropores located on the surface of the charcoal granules. The charcoal granules are retained in a polycarbonate filter housing between layers of filter cloth.
After IRB approval, we obtained written informed consent from 20 ASA I or II patients scheduled to receive elective surgery. All patients underwent anterior cruciate ligament repair surgery. Table 1 shows patient characteristics and duration of surgery. A coin was tossed at the beginning of the study and subsequently after every six patients were studied to decide whether the patient would receive the device. The subsequent five patients that qualified for the study were alternately assigned to one of the two groups (with and without the device). Each patient was premedicated with 1–2 mg of midazolam IV and was given a femoral nerve block before surgery. Anesthesia was induced with 150 μg of remifentanil, 2.0 mg/kg of propofol, and 1.0 mg/kg of succinylcholine. We maintained anesthesia with 1.2% isoflurane (1 MAC) for the duration of the procedure. Nitrous oxide was not used. A continuous infusion of remifentanil was titrated to meet the patient’s needs beyond 1 MAC of the inhaled anesthetic.
We set the respiratory rate at 8 breaths/min and the tidal volume was adjusted to keep the end-tidal CO2 (ETco2) concentration at 33 mmHg (Narkomed II, North American Dräger, Telford, PA). A gas analyzer (Datex AS/3, Datex-Ohmeda, Helsinki, Finland) measured the inspired and ETco2 and anesthetic concentrations continuously. We recorded the sedation level continuously using a bispectral index monitor (BIS, Aspect Medical Systems, Newton, MA). The anesthesiologist was blinded to the BIS reading.
When the surgeon applied the first adhesive wound closure strip, we turned off the vaporizer and increased the fresh gas flow to 10 L/ min. In patients in whom the device was used, we inserted the device in the airway with the rebreathing hose fully distended to 665 mL. We increased the respiratory rate to 16 breaths/min and increased the tidal volume as needed to double the minute ventilation. We adjusted the length of the rebreathing hose to prevent the ETco2 concentration from increasing higher than 55 mmHg. In the patients in whom the device was not used, we left the tidal volume unchanged. Tracheal extubation occurred after a positive response to command to open eyes and command to open mouth.
We recorded the time from when the vaporizer was turned off until the patients opened their eyes in response to command, until the patients opened their mouths in response to command, until the normalized BIS increased to 0.95, and until tracheal extubation. The BIS data were normalized using the equation:
where preemergence BIS is the average of all BIS recording over the min before turning off the vaporizer and maximum BIS is the highest BIS number recorded after the vaporizer was turned off.
Analysis was performed using SigmaStat version 2.03 (SPSS Inc). The two groups were compared using a two tailed Student’s t-test and the results were expressed as means ± sd. P values <0.05 were judged to be significant.
Figure 2 shows the time to open eyes, time to open mouth, time to normalized BIS to increase to 0.95, and time to tracheal extubation, with and without hypercapnic hyperventilation. All time differences were statistically significant (P < 0.001). Figure 3 shows the normalized BIS recordings during emergence for both groups. Tables 1 and 2 give the minute ventilation, ETco2 and the total dose of midazolam and propofol for the two groups. When the device was not used, increasing the fresh gas flow to 10 L/min at the start of emergence caused the minute volume to increase, even though the ventilator settings were not changed. When the device was used, the minute volume more than doubled because we increased the respiratory rate, the tidal volume, and the fresh gas flow. When the device was used, the inspired anesthetic concentration decreased below 0.1 vol% after the first breath and remained below 0.1 vol% until tracheal extubation. Hypercapnic hyperventilation was tolerated in patients without coughing or gagging.
The time from turning off the vaporizer to tracheal extubation was shortened by an average of 59% with an increase in the minute ventilation and the addition of airway deadspace. Adding deadspace caused the ETco2 to increase to 51.9 ± 5.7 mm Hg (mean ± sd). The time to tracheal extubation was 17.7 ± 4.7 min without the device and 7.2 ± 2.1 min with the device, for an average time difference of 10.5 min. When it is important to provide rapid emergence for patient assessment or for rapid patient turnover, the device should be considered, especially after surgical procedures where it is important to maintain a high concentration of the volatile anesthetic right up to the end of the procedure (i.e., to reduce the risk of patient movement, intraoperative awareness, or muscle rigidity). The device might also prove useful should a surgery end abruptly and without warning.
Other methods have been used to induce hypercapnia during hyperventilation. Vesely et al. (5) and Sasano et al. (6) added CO2 to the patient’s inspired gas during hyperventilation. Rebreathing seems to be a simpler method because it does not require a CO2 source and a controller. A CO2 absorber bypass valve found on some anesthesia machines can be used to produce hypercapnia during hyperventilation. However, the anesthetic gas is rebreathed along with the CO2 and emergence time may not be shortened unless a charcoal absorber is added (7).
Hyperventilation has been studied by Vesely et al. (5). They maintained the patient’s ETco2 at 47 mmHg and measured emergence times after isoflurane anesthesia with and without hyperventilation. They found that the time to tracheal extubation was 3.6 min in patients who were hyperventilated and 12.1 min in patients who were not hyperventilated. Sasano et al. (8) measured emergence times in dogs after isoflurane and nitrous oxide anesthesia and found that hyperventilation decreased the time to tracheal extubation from 17.5 to 6.6 min. Clearly, hyperventilation shortens emergence time when Paco2 is controlled.
Higher Paco2 during hyperventilation results in a shorter emergence time (9). Gopalakrishnan, and Sakata (10) found that hypercapnic pigs (ET co2 = 55 mm Hg) woke up 2.6 ± 0.9 min after desflurane anesthesia, whereas hypocapnic pigs (23 mm Hg) woke up after 5.8 ± 2.4 min., when all animals were hyperventilated (10). Because of its low solubility, emergence after desflurane is minimally affected by hyperventilation, but significantly shortened by hypercapnia and the resulting increase in cerebral bloodflow. In response to hypercapnia, cerebral arterial smooth muscle dilates, and cerebral bloodflow increases 6% per mm Hg change in Paco2 (11,12). The increase in bloodflow results in a more rapid clearance of volatile anesthetic from cerebral tissue, especially when combined with hyperventilation to decrease the arterial concentrations of the volatile anesthetic and increase the cerebral capillary/tissue gradient (9). Because hypercapnia increases bloodflow and hyperventilation increases the diffusion gradient, both are important in rapidly removing volatile anesthetic from the brain (13).
A third factor is our use of charcoal to eliminate rebreathing of anesthetic gases in the study group. In the control group, the fresh gas flow rate was increased to 10 L/min to reduce the amount of rebreathing, but it did not eliminate rebreathing. In a future study, we recommend using charcoal in both groups, so hypercapnia and hyperventilation can be studied independent of rebreathing.
Our study has several limitations. The observer who recorded the time when the patients opened their eyes and mouths was not blinded as to the presence or absence of the device. Also, the decision as to when to perform tracheal extubation was based on the anesthesiologist’s clinical judgment and the anesthesiologist was not blinded to the device. Fortunately, the anesthesiologist was blinded to the BIS readings and the time for the BIS ratio to increase to 0.95 paralleled the times to open eyes and mouths and time to tracheal extubation, which are less subjective measures of emergence (Fig. 2).
We used an older generation anesthesia machine in which the ventilator was not compensated for changes in fresh gas flow. When we increased the fresh gas flow to 10 L/min, the delivered minute ventilation increased from 7 to 12 L/min and the patients in whom the device was not used became slightly hypocapnic (ETco2 = 28 ± 2 mm Hg) at the time of tracheal extubation (Table 2). It would have been better to keep the control patients normocapnic so as not to bias the results in favor of the device.
Future studies are needed to define guidelines regarding the optimal amount of hyperventilation and hypercapnia for providing the safest and most rapid emergence. The amount of each will likely be dependent on the inhaled anesthetic used, the depth and duration of the anesthetic, and the patient’s physiologic state (13). Hyperventilation with large tidal volumes can produce barotrauma and lung injury and may decrease stroke volume or arterial blood pressure in critically ill patients (14,15). Hyperventilation with rapid respiratory rates (and short expiratory times) may result in air trapping and alveolar over-distension in patients with restrictive airway disease. Increasing the respiratory rate also shortens the inspiratory time, and the tidal volume decreases if the inspiratory flow rate is not changed. Should the tidal volume become smaller than the rebreathing deadspace, hypoxia could result from inadequate oxygen supply. Hypercapnia is associated with an increased risk of cardiac arrhythmias and is contraindicated in patients who have pulmonary hypertension and in neurosurgical patients in whom the increased cerebral bloodflow may cause excessively high intracranial pressure. Paco2 levels are sometimes kept at 65 mm Hg in ICU patients where benefits include higher tissue oxygen pressures (16,17). Future studies are needed to measure emergence times and other outcomes, including postoperative cognitive function, at CO2 levels above 55 mm Hg (18). Arterial blood gases should be analyzed in future studies to measure the alveolar to arterial CO2 gradient during hyperventilation. Future studies are needed in the pediatric population, in patients who are breathing spontaneously, and in patients receiving pressure support ventilation.
We found that emergence time after isoflurane anesthesia was shortened by approximately 59% when hyperventilation was used to rapidly flush the anesthetic from the lungs and hypercapnia was induced using airway deadspace. When it is important to provide rapid emergence after surgical procedures, hypercapnic hyperventilation should be considered in those cases where it is important to maintain a high concentration of the volatile anesthetic right up to the end of the procedure. Hypercapnic hyperventilation may be useful to shorten emergence time when surgery ends abruptly and without warning.
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