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*Department of Anesthesiology and Resuscitology, Nagoya City University Medical School, Nagoya, Japan; Department of Anesthesiology, The Toronto General Hospital, Toronto, Canada; and Department of Physiology, Queen’s University, Kingston, Ontario, Canada
Address correspondence and reprint requests to Joseph A. Fisher, Department of Anesthesia, Toronto General Hospital, 585 University Ave., Toronto, ON, Canada M5G 2C4. Address e-mail to joseph.fisher{at}utoronto.ca
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Abstract |
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IMPLICATIONS: A simple modification to a standard resuscitation bag allows one to increase ventilation without decreasing blood carbon dioxide levels. In dogs, we confirmed that this circuit can be used to accelerate the elimination of and recovery from volatile anesthetics.
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Introduction |
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E) to maintain isocapnia, hypercapnia may occur (5).
In 1998, our group described a simple circuit that clamps PETCO2 of a spontaneously breathing subject despite increases in E (isocapnic hyperpnea; IH) by passively increasing inspired PCO2 in proportion to E (6). Using the same underlying principle (see below), we made a simple modification to a standard resuscitation bag and then performed a pilot study in isoflurane-anesthetized dogs to assess the feasibility of using IH to accelerate recovery from anesthesia.
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Methods |
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E equal to or less than the FGF, the apparatus functions as an unmodified resuscitation bag, providing 100% oxygen. However, when E increases above FGF, whether spontaneously or as a result of manually assisted ventilation, the balance of the inspirate consists of reserve gas drawn through the low-pressure relief valve. The concentration of CO2 in the reserve gas provides a minimal gradient for CO2 elimination. Because of the concentration of CO2 in the reserve gas, the gradient for CO2 elimination is minimized, thereby maintaining isocapnia. Therefore, alveolar ventilation (A) and, hence, CO2 elimination, will depend primarily on FGF and be relatively independent of the volume of reserve gas breathed. Because neither the FGF nor the reserve gas contains any anesthetic, they both contribute to the washout of anesthetic gas from the lung. After institutional ethics board approval, we studied four mongrel dogs (25–38 kg) of either sex by using a cross-over protocol, with each dog serving as its own control. Experiments were performed in an animal surgical suite with facilities similar to those in operating rooms in our institution. Anesthesia was induced with methohexital 5 mg/kg IV. The trachea was then intubated and the dogs ventilated for 90 min via a circle anesthetic circuit with oxygen flow set at 4 L/min. Anesthesia was maintained with isoflurane in oxygen. The output of the isoflurane vaporizer was adjusted to give an end-tidal concentration of 2.5% (corresponding to 1.7 minimum alveolar anesthetic concentration [MAC]) (3), and the ventilation was adjusted to maintain PETCO2 at 40 mm Hg. Each dog was anesthetized on two separate occasions separated by at least 2 days. The following variables were monitored: arterial blood pressure (maintained >100 mm Hg when necessary with ephedrine), ventilatory flow, airway CO2 and isoflurane concentrations (Capnomac Ultima; Datex Engstrom, Helsinki, Finland), oxygen saturation, and rectal temperature. We maintained oxygen saturation >98% and temperature within 1°C of the initial value. Airway PCO2, isoflurane concentration, and flow were digitized and recorded.
After 90 min of anesthesia, the animal was disconnected from the anesthetic circuit and recovered with either of two methods, randomized as to order. For the first (control recovery), we used intermittent manual ventilation with a standard resuscitation bag supplied with 100% oxygen (1–4 L/min as necessary to keep PETCO2 <50 mm Hg) until spontaneous ventilation returned. Thereafter, the dog was allowed to breathe spontaneously through the resuscitation bag until it no longer tolerated the endotracheal tube. The PETCO2 was allowed to increase to a maximum of 50 mm Hg, simulating clinical practice. For the second (IH recovery), we applied IH with the apparatus at approximately three times the dog’s E under anesthesia. FGF was set to approximately half the dog’s E while ventilated under anesthesia to allow PETCO2 to increase to a level similar to that during control recovery. If spontaneous ventilatory efforts returned, assisted breaths were synchronized with the dog’s efforts until it would no longer tolerate the endotracheal tube. Expired gas was directed to the scavenger.
Recovery from anesthesia was assessed each minute by sweeping the cornea with gauze and pinching the tail with a spring clamp. The dog was tracheally extubated when it roused and would no longer tolerate the endotracheal tube, as indicated by violent coughing and shaking of its head. As recovery progressed, the dog was continuously encouraged to stand. The times to both extubation and the ability to stand unaided were noted. All times were determined by reviewing a videotape of the emergence from anesthesia.
A paired Student’s t-test was used to compare the times to extubation and times to stand unaided during the two recovery protocols.
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Results |
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The end-tidal isoflurane concentration decreased more rapidly during IH recovery as compared with control recovery (Fig. 2). The mean time to extubation decreased by 62%, from an average of 17.5 to 6.6 min (P = 0.012) (Fig. 3). The mean time from the end of anesthetic administration to standing unaided was reduced 40%, from 31.0 to 18.5 min (P = 0.018); this was caused mainly by the decrease in time to tracheal extubation, because there was no difference in the time from extubation to standing between control and IH recoveries. There were no differences between groups in total ephedrine dose or body temperature at time of arousal. After IH, there was no posthyperventilation apnea.
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Discussion |
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Although the effect of IH on the actual times of clinical recovery would have varied from those in our model had we changed such factors as the anesthetic vapor used, inspired concentration, duration of anesthesia, and the use of adjuvant anesthetics (e.g., benzodiazepines, narcotics, or N2O), the ease of application of the apparatus at the end of anesthesia would have been little affected. This apparatus may therefore be a useful adjuvant during the recovery phase from anesthesia with different volatile anesthetics.
In this pilot study, we used our apparatus to decrease the alveolar concentration of anesthetic without decreasing the PCO2 and observed the dogs’ recoveries. Hyperventilation with currently available anesthetic circuits can result in either maintenance of isocapnia (Mapleson "D") or hypocapnia (circle circuit), but in either case, limitation of FGF results in rebreathing of anesthetic and thus failure to increase anesthetic elimination. The effects of hypocapnia on the time required for recovery from anesthesia may offset those of decreased alveolar anesthetic concentration for two main reasons. First, hypocapnia decreases cerebral blood flow (4), which would decrease the rate of vapor anesthetic washout for a given brain-blood partial pressure gradient. Second, hypocapnia can result in posthyperventilation apnea, during which anesthetic mobilized from tissues is not eliminated via the lungs. Although Stoelting and Eger (2) demonstrated that hyperventilation decreases the alveolar concentration of various vapor anesthetics in dogs, they did not control the dogs’ PCO2 during hyperventilation and did not observe their dogs’ clinical recovery from anesthesia.
The efficacy of this circuit is depicted in Figure 4, in which we compare, in a human, the effect on airway PCO2 at progressively greater E with (Fig. 4A) and without (Fig. 4B) the isocapnia attachment. With the attachment, PCO2 did not increase despite the increasing contribution of the reserve gas (containing CO2) to the subject’s E because the addition of CO2 is proportional to the increase in E. Similarly, if the subject then decreased his ventilation back toward resting, his Pco2 would not increase because the proportion of E made up of reserve gas would also decrease proportionally. This approach to maintaining isocapnia represents a marked departure from previous attempts, in which CO2 was added to all the inhaled gas independent of E. The advantages of IH cannot be duplicated by ventilation with carbogen (or reserve gas) alone because alveolar ventilation (and hence PETCO2) would remain a function of E.
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In summary, we modified a standard resuscitation bag to maintain isocapnia by supplying a gas containing a mixture of oxygen and CO2 to its inspiratory relief valve. This apparatus was successfully used to accelerate recovery from isoflurane anesthesia in dogs. Our experience indicates that this apparatus should be easy to use in the operating room and that a trial of IH in the clinical setting is warranted.
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Acknowledgments |
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The authors thank Dr. David Wilson for kindly allowing the use of his conditioned laboratory animals, the animal facility staff at the Toronto Western Hospital for their assistance, and Drs. David Bevan and Alison Froese for helpful comments.
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