Anesth Analg 2000;91:749-751
© 2000 International Anesthesia Research Society
GENERAL ARTICLES
Hyperbaric Nitrogen Prolongs Breath-Holding Time in Humans
Hiroaki Morooka, MD,
Yoshitaka Wakasugi, ME,
Hiroko Shimamoto, MD,
Osamu Shibata, MD, and
Koji Sumikawa, MD
Department of Anesthesiology, Nagasaki University School of Medicine, Nagasaki, Japan
Address correspondence and reprint requests to Hiroaki Morooka, MD, Department of Anesthesiology, Nagasaki University School of Medicine, Nagasaki 852-8501, Japan. Address e-mail to morooka{at}net.nagasaki-u.ac.jp
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Abstract
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Either an increase in PaCO2 or a decrease in PaO2, can affect respiratory stimulation through respiratory centers, thus influencing breath-holding time (BHT). This study was designed to determine whether and how hyperbaric air could influence BHT in comparison with hyperbaric oxygen in humans. We studied 36 healthy volunteers in a multiplace hyperbaric chamber. BHT, pulse oximeter, and transcutaneous carbon dioxide tension were measured at 1 and 2.8 atmosphere absolute (ATA) in two groups. Group A (n = 20) breathed air. Group O (n = 16) breathed oxygen with a face mask (5 L/min). BHTs were 108 ± 28 s at 1.0 ATA and 230 ± 71 s at 2.8 ATA in Group A, and 137 ± 48 s at 1.0 ATA and 180 ± 52 s at 2.8 ATA in Group O. Transcutaneous carbon dioxide tension in Group A (59 ± 2 mm Hg) was higher than that in Group O (54 ± 2 mm Hg) at the end of maximal breath-holding at 2.8 ATA. The prolongation of BHT in hyperbaric air is significantly greater than that in hyperbaric oxygen.
Implications: Breath-holding time is significantly prolonged in hyperbaric air than it is in hyperbaric oxygen. The mechanism involves the anesthetic effect of nitrogen suppressing the suffocating feeling during breath-holding.
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Introduction
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The diving response is known as "diving bradycardia" and prolonged breath-holding time (BHT) (1). Diving bradycardia is induced by apnea and cold water face immersion. PaCO2 and PaO2 and psychological factors could affect BHT (2). Increasing PaCO2 and decreasing PaO2 drive respiratory stimulation through respiratory centers. BHT can be increased by training through unconscious hyperventilation before breath-holding and psychological adaptation (3). However, the effect of high atmospheric pressure on BHT has not yet been investigated. This study was performed to determine whether and how hyperbaric air could influence BHT in comparison with hyperbaric oxygen.
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Methods
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After we obtained institutional human investigation committee approval and written, informed consent, 36 healthy volunteers were studied in the multiplace hyperbaric chamber (PHC-50; TABAI ESPEC, Osaka, Japan). BHT, pulse oximeter (SpO2) (N-200 pulse oximeter; NELLCOR, Hayward, CA) and transcutaneous carbon dioxide tension (TCPCO2) (TCM3; Radiometer, Brønshøj, Denmark) were measured at 1.0 and 2.8 atmosphere absolute (ATA) in two groups. Group A (n = 20) breathed air. Group O (n = 16) breathed oxygen with a face mask (5 L/min). BHT was defined as the time from cessation of respiratory air flow after the standardized prebreath-hold inhalation to the beginning of air flow at the breaking point and measured with a stopwatch by a person closely observing the subject (1). Data were presented as mean ± SD. The differences were analyzed by using Student’s t-test. P value < 0.05 was considered statistically significant.
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Results
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The two study groups were comparable with respect to demographic data (Table 1). BHT in Group A was 108 ± 28 s at 1.0 ATA and 230 ± 71 s at 2.8 ATA. BHT in Group O was 137 ± 48 s at 1.0 ATA and 180 ± 52 s at 2.8 ATA. BHT at 2.8 ATA was significantly longer than BHT at 1.0 ATA in both groups (P < 0.001 in Group A, P < 0.05 in Group O). BHT at 1.0 ATA in Group O was significantly longer than that in Group A (P < 0.05), whereas BHT at 2.8 ATA in Group A was significantly longer than that in Group O (P < 0.05). In Group A, the lowest SpO2 was 88 ± 5% at 1.0 ATA, whereas in Group O, SpO2 showed no change from 100% during breath-holding, and the SpO2 at 2.8 ATA was always 100% in both groups. At 2.8 ATA, TCPCO2 in Group A (59 ± 2 mm Hg) was significantly higher (P < 0.05) than that in Group O (54 ± 2 mm Hg) at the end of maximal breath-holding (Figure 1).
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Figure 1. Breath-holding time (BHT) at 1.0 and 2.8 atmosphere absolute (ATA) in two groups (mean ± SD; number is indicated in parentheses). Group A (n = 20) breathed air. Group O (n = 16) breathed oxygen with a face mask (5 L/min). BHT was defined as the time from cessation of respiratory air flow after the standardized prebreath-hold inhalation to the beginning of air flow at the breaking point and was measured with a stopwatch by a person closely observing the subject. Pulse oximeter values (SpO2) at the end of BHT at 1.0 and 2.8 ATA in two groups (mean SD). Transcutaneous carbon dioxide tension (TCPCO2) at 1.0 and 2.8 ATA in two groups.
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Discussion
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An increase in PaCO2 or a decrease in PaO2 can affect breathing, as can certain kinds of muscular activity in the Mueller and Valsalva maneuvers lengthen BHT (2). Although emotional and psychological factors can also affect BHT, we did not examine these in this experiment. At 1.0 ATA, a decrease in PaO2 might have stimulated breathing in Group A, as shown by a decrease in SpO2 to 88% ± 5%, but there was no hypoxic drive in Group O, because SpO2 was always 100%. Also, an increase in PaCO2 might have stimulated breathing in Group O. The decrease in PaO2 rather than the increase in PaCO2 could have stimulated breathing in Group A at 1.0 ATA. Sasse et al. (4) reported that the PaO2 decreased to approximately 60 mm Hg during the average BHT while breathing room air. According to the oxygen dissociation curve, SpO2 is 89% when PaO2 is 50 mm Hg at pH 7.40 at 37°C. This SpO2 value coincided with that at BHT at 1.0 ATA in Group A. Thus, the hypoxic drive probably worked at 1.0 ATA in Group A. However, there was no hypoxic drive at 2.8 ATA, because SpO2 was always 100% in both groups. Thus, the increase in PaCO2 probably caused stimulation of breathing at 2.8 ATA.
Suppression by hyperbaric air of the ventilatory response to CO2 could be the reason why BHT in Group A was longer than that in Group O at 2.8 ATA. TCPCO2 in Group A was higher than that in Group O at the end of BHT. Inspiratory nitrogen tension was estimated to be approximately 1680 mm Hg at 2.8 ATA in Group A. In humans, nitrogen narcosis, which occurs at approximately 4.0 ATA (5), is characterized by euphoria, impaired cognitive function, neuromuscular incoordination, and ultimately, loss of consciousness. Barthelemy-Requin et al. (6) have suggested that some of the symptoms of nitrogen narcosis may be linked to the decrease in extracellular dopamine levels. The minimum alveolar concentration of nitrogen is a higher pressure than 44.5 ATA in dogs, 35.3 ATA in mice, and 100 ATA in rats (7–9). However, a low concentration of nitrogen, such as 2.8 ATA, has some anesthetic effect in humans. Reducing the ventilatory response to CO2 occurs in assisted breath-hold divers (10). Perhaps some physical effect would occur at <4.0 ATA, and the anesthetic effect of nitrogen would suppress the ventilatory response to CO2 at 2.8 ATA.
Although the reason why BHT at 2.8 ATA was longer than BHT at 1.0 ATA in Group O is unclear, nitrogen might play a role. Winter et al. (11) reported that air could exert an anesthetic effect even at atmospheric pressure. Because inhalation of 5 L/min oxygen via a face mask provides aproximately 65% of inspired oxygen, the concentration of oxygen in a face mask was measured with an oxygen sensor. Inspiratory nitrogen tension at 2.8 ATA (estimated approximately 740 mm Hg) was higher than that at 1.0 ATA (estimated approximately 260 mm Hg) in Group O. Thus, nitrogen may be involved in this mechanism. However, Tarasiuk and Grossman (12) have shown that hyperbaric pressure in itself depresses central respiratory activity in an isolated brainstem-spinal cord rat model. However, it is still unclear whether hyperbaric pressure in itself could influence respiratory activity. Alternatively, a dose-related effect of nitrogen may be related to the respiratory response to CO2. The difference in the effect of face masks (there were no face masks in Group A) may be related to a psychological effect. Further experiments are required to elucidate these points.
In conclusion, high atmospheric pressure of either air or oxygen prolongs BHT. The prolongation by hyperbaric air is significantly longer than that by hyperbaric oxygen. The mechanism involves the anesthetic effect of nitrogen suppressing the suffocating feeling during breath-holding.
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References
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Accepted for publication May 26, 2000.
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Abstract
Introduction
