After preoxygenation/hyperventilation, all patients had an Spo2 of 100%. After 60 s of apnea, all patients were still 100% saturated. By 90 s of apnea, one patient in Group P and two in Group H had an Spo2 of <99%. At the time of intubation, one patient in Group P and two in Group H had an Spo2 of <98%. The time to tracheal intubation was similar in both groups (Group H, 115 ± 9 s versus P, 117 ± 11 s). No adverse event was noted during the study period.
This study is the first to investigate the effects of voluntary hyperventilation versus preoxygenation with normal ventilation on Paco2 during rapid-sequence induction. We assumed that Paco2 would start to increase as soon as respiration stopped and that a brief period of voluntary hyperventilation, caused by decreasing the initial Paco2, would result in a decreased Paco2 after intubation (1–3). This conception is based on studies that examined the rate of increase of Paco2 in humans under stable anesthesia (7,8). Our study clearly establishes that this is not the case during rapid-sequence induction of anesthesia.
In a series of five healthy adults scheduled for various surgeries, Eger and Severinghaus (7) observed that Paco2 increased by 13.4 mm Hg during the first minute of apnea and by 3.0 mm Hg/min thereafter. After one hour of hyperventilation, the rate of increase of Paco2 in the first minute of apnea was significantly smaller than before hyperventilation (9.6 vs 13.4 mm Hg, P < 0.05).
Gentz et al. (8) studied the rate of increase of Paco2 during apneic oxygenation after shorter periods of hypocapnia. Nineteen patients (32–75 yr old, ASA status I–III) scheduled for elective surgery under general endotracheal anesthesia were studied. Once anesthetized and mechanically ventilated, and before each apneic period, patients’ Paco2 was held constant for approximately 10 minutes between 35 and 40 mm Hg (normocapnic group) or 25 and 30 mm Hg (hypocapnic group). Contrary to the results of Eger and Severinghaus (7), patients in the hypocapnic group had a larger rate of increase of Paco2 than the Normocapnic group in the first minute of apnea (9.4 vs 7.6 mm Hg, P < 0.009). The authors hypothesized that this finding was caused in part by widening of the arteriovenous gradient of Pco2 with a subsequent shift of CO2 stores.
Williams et al. (4) showed that hyperventilation could blunt the increase of ICP induced by apnea in anesthetized dogs. The authors studied the effect of two minutes of apnea on ICP, compliance, and cerebral blood volume in 19 adult dogs during normocapnia (Paco2 from 35 to 40 mm Hg), hypocapnia (Paco2 from 24 to 28 mm Hg), and hypercapnia (Paco2 from 50 to 58 mm Hg). Their results suggest that hyperventilated dogs have a smaller ICP increase (68%) during apnea than normoventilated dogs (204%). However, this study had several methodologic limitations. Surprisingly, dogs in the hypocapnia group had a preapnea ICP significantly higher than the normocapnia group (P < 0.05). After two minutes of apnea, although ICP increased more in the normocapnia group than the hypocapnia group (204% vs 68%), both groups attained similar ICP. Finally, dogs were hyperventilated for an undetermined period of time (but for at least 30 minutes), making results difficult to compare with those of previous studies.
The measurement of the rate of increase of Paco2 was not a primary objective of this study. However, Table 2 clearly shows that we obtained an increase of approximately 10.5 mm Hg in Group H in the two-minute period between the post-O2 and postintubation ABG. The increase was three times slower in Group P, with only 3.5 mm Hg during the same two-minute period. This is at least in part in agreement with the results obtained by Gentz et al. (8), with short periods of hyperventilation.
Paco2 is determined by a balance between CO2 metabolic production, elimination, and physiologic stores within the body. CO2 elimination is dependent on alveolar ventilation, cardiac output, and Hb level. During apneic oxygenation, oxygen is drawn in by mass movement and replaces the oxygen that crosses the alveolar/capillary membrane, but no significant amount of CO2 is eliminated. Cardiac output varies during anesthesia induction. Thiopental, by decreasing peripheral resistances, decreases afterload, resulting in a brief increase in cardiac output. An acute change in Hb level, which is the primary buffer for respiratory gases in the body, could have an effect on subsequent CO2 loading. In our study, all patients received the same induction regimen; they were apneic and had similar Hb levels during the study period. Consequently, after the preoxygenation/hyperventilation period, CO2 elimination should have been minimal in both groups.
CO2 physiologic stores are very large, estimated at approximately 120 L, and they have been theoretically described in terms of a multicompartment model (9) : a rapid compartment represented by blood, brain, kidneys, and other well perfused tissues, a medium compartment representing skeletal muscles and other tissues with moderate blood flow, and a slow compartment including bone and fat. Each compartment has its own time constant, and the long time constants of the medium and slow compartment buffer change in the rapid compartment. By using this model, we can assume that long periods of hyperventilation would permit equilibration of the different compartments and result in a new Paco2 steady state. After such hyperventilation, the Paco2 would then return to normal at a slower pace during apnea, explaining the results obtained by Eger and Severinghaus (7). Shorter periods of hyperventilation, however, would decrease only the CO2 stores in the rapid compartment, resulting in a shift of CO2 from the medium and slow compartments during an apneic period. This would bring an additional source of CO2 to the central compartment and explain the greater increase of Paco2 observed in this study and that by Gentz et al. (8), when patients were hyperventilated for brief periods of time as compared with normoventilated patients.
The last determinant of Paco2 is CO2 metabolic production. Previous studies (7,8) have been performed on anesthetized patients with stable metabolic rates. In our study, however, the metabolic rate was certainly not constant. Patients in Group H were asked to voluntarily hyperventilate for two minutes before anesthesia induction. This maneuver requires a significant effort, possibly resulting in increased CO2 production. Although anesthesia induction with thiopental lowers metabolic rate, patients who hyperventilated still had a greater CO2 charge to eliminate, which, combined with a widening of the arteriovenous CO2 gradient, resulted in a more important Paco2 increase. In fact, after only 60 seconds of apnea, patients who hyperventilated already increased their Paco2 to the level of Group P. When compared with that of similar groups in previous studies (7,8), the increase of Paco2 in Group P (3.3 mm Hg over two minutes) was smaller and clinically nonsignificant. This may be attributed to the metabolic sparing effect of thiopental and the resulting decrease in CO2 production.
We chose to voluntarily hyperventilate patients for two minutes because it was previously determined that one minute of hyperventilation could significantly decrease Paco2(10), and more than two minutes would be very strenuous for patients. Two minutes of hyperventilation was in fact sufficient for patients in Group H to decrease their baseline Paco2 by an average of 10.1 mm Hg.
In summary, after only 60 seconds of apnea, Paco2 in hyperventilated patients had increased to levels similar to those after preoxygenation with normal ventilation. Because ICP variations induced by changes in Paco2 are rapid (11), occurring in a matter of seconds after changes in Paco2, the anticipated ICP changes would then parallel the Paco2 values. Therefore, no benefit could be expected from this maneuver. Furthermore, the increase in patient effort and the anxiety potentially associated with it are not justified by its effectiveness and may in fact result in an increased ICP (2). We conclude that voluntary hyperventilation in patients with increased ICP before rapid-sequence induction should no longer be advocated as a means of blunting an increase in Paco2 and its possible repercussion on ICP.
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© 2001 International Anesthesia Research Society
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