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Carbon dioxide (CO₂) retention, or hypercapnia, is a known risk of diving that can cause mental and physical impairments leading to life-threatening accidents. Often, such accidents occur due to elevated inspired carbon dioxide. For instance, in cases of CO₂ elimination system failures during rebreather dives, elevated inspired partial pressure of carbon dioxide (PCO₂) can rapidly lead to dangerous levels of hypercapnia. Elevations in PaCO₂ (arterial pressure of PCO₂) can also occur in divers without a change in inspired PCO₂. In such cases, hypercapnia occurs due to alveolar hypoventilation. Several factors of the dive environment contribute to this effect through changes in minute ventilation and dead space. Predominantly, minute ventilation is reduced in diving due to changes in respiratory load and associated changes in respiratory control. Minute ventilation is further reduced by hyperoxic attenuation of chemosensitivity. Physiologic dead space is also increased due to elevated breathing gas density and to hyperoxia. The Haldane effect, a reduction in CO₂ solubility in blood due to hyperoxia, may contribute indirectly to hypercapnia through an increase in mixed venous PCO₂. In some individuals, low ventilatory response to hypercapnia may also contribute to carbon dioxide retention. This review outlines what is currently known about hypercapnia in diving, including its measurement, cause, mental and physical effects, and areas for future study., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

Hyperoxia during diving has been suggested to exacerbate hypercapnic narcosis and promote unconsciousness. We tested this hypothesis in male volunteers (12 at rest, 10 at 75 W cycle ergometer exercise) breathing each of four gases in a hyperbaric chamber. Inspired Po2 (PiO2 ) was 0.21 and 1.3 atmospheres (atm) without or with an individual subject's maximum tolerable inspired CO2 (PiO2 = 0.055-0.085 atm). Measurements included end-tidal CO2 partial pressure (PetCO2 ), rating of perceived discomfort (RPD), expired minute ventilation (V̇e), and cognitive function assessed by auditory n-back test. The most prominent finding was, irrespective of PetCO2 , that minute ventilation was 8-9 l/min greater for rest or exercise with a PiO2 of 1.3 atm compared with 0.21 atm (P < 0.0001). For hyperoxic gases, PetCO2 was consistently less than for normoxic gases (P < 0.01). For hyperoxic hypercapnic gases, n-back scores were higher than for normoxic gases (P < 0.01), and RPD was lower for exercise but not rest (P < 0.02). Subjects completed 66 hyperoxic hypercapnic trials without incident, but five stopped prematurely because of serious symptoms (tunnel vision, vision loss, dizziness, panic, exhaustion, or near syncope) during 69 normoxic hypercapnic trials (P = 0.0582). Serious symptoms during hypercapnic trials occurred only during normoxia. We conclude serious symptoms with hyperoxic hypercapnia were absent because of decreased PetCO2 consequent to increased ventilation., (Copyright © 2014 the American Physiological Society.)

To test the hypothesis that the fractal character of breathing and heart rate are independent, inter-breath intervals (IBI) and R-R intervals (RRI) were measured during rest and two levels of exercise at 1 and 2.8 ATA in a hyperbaric chamber in 18 male and female subjects (ages 19-74 years). Both RRI and IBI showed fractal properties. Fractal dimensions (D) for IBI were (mean +/- S.D.) 1.33 +/- 0.11, 1.29 +/- 0.12, 1.19 +/- 0.16 (rest, light and heavy exercise at 1ATA); 1.33 +/- 0.13, 1.25 +/- 0.13, 1.18 +/- 0.14 (same conditions at 2.8 ATA). Corresponding D for RRI were 1.19 +/- 0.11, 1.05 +/- 0.07 and 1.02 +/- 0.05 (1ATA); 1.20 +/- 0.10, 1.03 +/- 0.04 and 1.01 +/- 0.02 (2.8 ATA). The fractal dimension of each variable decreased with exercise and was unaffected by hyperbaric exposure. These two systems were not cross-correlated under any of the six conditions. During rest and light and moderate exercise at 1 and 2.8 ATA the results are consistent with heart rate variability and breathing rate variability being mutually independent of one another.