Assessment of the interaction of hyperbaric N2, CO2, and O2 on psychomotor performance in divers.

Diving narcosis results from the complex interaction of gases, activities, and environmental conditions. We hypothesized that these interactions could be separated into their component parts. Where previous studies have tested single cognitive tasks sequentially, we varied inspired partial pressures of CO2, N2, and O2 in immersed, exercising subjects while assessing multitasking performance with the Multi-Attribute Task Battery II (MATB-II) flight simulator. Cognitive performance was tested under 20 conditions of gas partial pressure and exercise in 42 male subjects meeting U.S. Navy age and fitness profiles. Inspired nitrogen (N2) and oxygen (O2) partial pressures were 0, 4.5, and 5.6 ATA and 0.21, 1.0, and 1.22 ATA, respectively, at rest and during 100-W immersed exercise with and without 0.075-ATA CO2 Linear regression modeled the association of gas partial pressure with task performance while controlling for exercise, hypercapnic ventilatory response, dive training, video game frequency, and age. Subjects served as their own controls. Impairment of memory, attention, and planning, but not motor tasks, was associated with N2 partial pressures >4.5 ATA. Sea level O2 at 0.925 ATA partially rescued motor and memory reaction time impaired by 0.075-ATA CO2; however, at hyperbaric pressures an unexpectedly strong interaction between CO2, N2, and exercise caused incapacitating narcosis with amnesia, which was augmented by O2 Perception of narcosis was not correlated with actual scores. The relative contributions of factors associated with diving narcosis will be useful to predict the effects of gas mixtures and exercise conditions on the cognitive performance of divers. The O2 effects are consistent with O2 narcosis or enhanced O2 toxicity.

Predictors of increased PaCO2 during immersed prone exercise at 4.7 ATA.

During diving, arterial Pco(2) (Pa(CO(2))) levels can increase and contribute to psychomotor impairment and unconsciousness. This study was designed to investigate the effects of the hypercapnic ventilatory response (HCVR), exercise, inspired Po(2), and externally applied transrespiratory pressure (P(tr)) on Pa(CO(2)) during immersed prone exercise in subjects breathing oxygen-nitrogen mixes at 4.7 ATA. Twenty-five subjects were studied at rest and during 6 min of exercise while dry and submersed at 1 ATA and during exercise submersed at 4.7 ATA. At 4.7 ATA, subsets of the 25 subjects (9-10 for each condition) exercised as P(tr) was varied between +10, 0, and -10 cmH(2)O; breathing gas Po(2) was 0.7, 1.0, and 1.3 ATA; and inspiratory and expiratory breathing resistances were varied using 14.9-, 11.6-, and 10.2-mm-diameter-aperture disks. During exercise, Pa(CO(2)) (Torr) increased from 31.5 +/- 4.1 (mean +/- SD for all subjects) dry to 34.2 +/- 4.8 (P = 0.02) submersed, to 46.1 +/- 5.9 (P < 0.001) at 4.7 ATA during air breathing and to 49.9 +/- 5.4 (P < 0.001 vs. 1 ATA) during breathing with high external resistance. There was no significant effect of inspired Po(2) or P(tr) on Pa(CO(2)) or minute ventilation (Ve). Ve (l/min) decreased from 89.2 +/- 22.9 dry to 76.3 +/- 20.5 (P = 0.02) submersed, to 61.6 +/- 13.9 (P < 0.001) at 4.7 ATA during air breathing and to 49.2 +/- 7.3 (P < 0.001) during breathing with resistance. We conclude that the major contributors to increased Pa(CO(2)) during exercise at 4.7 ATA are increased depth and external respiratory resistance. HCVR and maximal O(2) consumption were also weakly predictive. The effects of P(tr), inspired Po(2), and O(2) consumption during short-term exercise were not significant.

Pulmonary gas exchange in diving.

Diving-related pulmonary effects are due mostly to increased gas density, immersion-related increase in pulmonary blood volume, and (usually) a higher inspired Po(2). Higher gas density produces an increase in airways resistance and work of breathing, and a reduced maximum breathing capacity. An additional mechanical load is due to immersion, which can impose a static transrespiratory pressure load as well as a decrease in pulmonary compliance. The combination of resistive and elastic loads is largely responsible for the reduction in ventilation during underwater exercise. Additionally, there is a density-related increase in dead space/tidal volume ratio (Vd/Vt), possibly due to impairment of intrapulmonary gas phase diffusion and distribution of ventilation. The net result of relative hypoventilation and increased Vd/Vt is hypercapnia. The effect of high inspired Po(2) and inert gas narcosis on respiratory drive appear to be minimal. Exchange of oxygen by the lung is not impaired, at least up to a gas density of 25 g/l. There are few effects of pressure per se, other than a reduction in the P50 of hemoglobin, probably due to either a conformational change or an effect of inert gas binding.

Effects of age and exercise on physiological dead space during simulated dives at 2.8 ATA.

Physiological dead space (Vds), end-tidal CO(2) (Pet(CO(2))), and arterial CO(2) (Pa(CO(2))) were measured at 1 and 2.8 ATA in a dry hyperbaric chamber in 10 older (58-74 yr) and 10 younger (19-39 yr) air-breathing subjects during rest and two levels of upright exercise on a cycle ergometer. At pressure, Vd (liters btps) increased from 0.34 +/- 0.09 (mean +/- SD of all subjects for normally distributed data, median +/- interquartile range otherwise) to 0.40 +/- 0.09 (P = 0.0060) at rest, 0.35 +/- 0.13 to 0.45 +/- 0.11 (P = 0.0003) during light exercise, and 0.38 +/- 0.17 to 0.45 +/- 0.13 (P = 0.0497) during heavier exercise. During these conditions, Pa(CO(2)) (Torr) increased from 33.8 +/- 4.2 to 35.7 +/- 4.4 (P = 0.0059), 35.3 +/- 3.2 to 39.4 +/- 3.1 (P < 0.0001), and 29.6 +/- 5.6 to 37.4 +/- 6.5 (P < 0.0001), respectively. During exercise, Pet(CO(2)) overestimated Pa(CO(2)), although the absolute difference was less at pressure. Capnography poorly estimated Pa(CO(2)) during exercise at 1 and 2.8 ATA because of wide variability. Older subjects had higher Vd at 1 ATA but similar changes in Vd, Pa(CO(2)), and Pet(CO(2)) at pressure. These results are consistent with an effect of increased gas density.

Treatment of decompression illness and latrogenic gas embolism.

The mainstay of treatment of gas bubble disease is therapeutic recompression while the patient is breathing oxygen. The patient should be recompressed as soon as possible; however, patients should be considered for recompression even after several days' delay. Treatments should be repeated if possible until symptoms have either resolved or stabilized. Appropriate hydration is essential. The use of HBO is generally safe, relatively nontoxic, and is possible even in neonates. Pharmacologic agents (e.g., anticoagulants, lidocaine, antiplatelet agents, corticosteroids, inhibitors of calcium flux) may be useful adjuncts to recompression therapy but they require further study. For patients who respond poorly to recompression therapy, the next advance in the treatment of DCI-induced neural injury is likely to be due to the development of agents that reduce the effects of reperfusion injury and delayed cell death.

Brain computerized tomography after hyperbaric oxygen therapy for carbon monoxide poisoning.

The role of brain computerized tomography (CT) imaging in predicting clinical outcome was investigated in patients receiving hyperbaric oxygen therapy for serious carbon monoxide (CO) poisoning. From a series of 48 consecutive patients suffering loss of consciousness from CO exposures, the records of 40 selected patients were evaluated to determine how their CT findings correlated with clinical outcome. A neuroradiologist blinded to patient outcome confirmed the radiographic findings. CT abnormalities consisted of globus pallidus hypodensities (nine patients), subcortical white matter hypodensities (four), cerebral cortical lesions (one), cerebral edema (one), hippocampal lesions (one), and complete loss of gray-white differentiation (one). Of the patients with globus pallidus lesions, 44% manifested incomplete recovery, whereas white matter lesions reflected a 74% incidence of morbidity. Age, duration of CO exposure, and interval between CO exposure and treatment did not significantly relate to clinical outcome. The blood carboxyhemoglobin levels correlated with clinical prognosis (P < 0.05) and, importantly, CT results significantly predicted clinical outcome (P < 0.05). A normal scan correlated highly with a complete recovery, whereas an abnormal scan predicted incomplete recovery or death, despite prior HBO therapy. The current study establishes prognostic validity for brain CT imaging for evaluating clinical outcome after HBO therapy for CO poisoning.

Treatment of cervical necrotizing fasciitis with hyperbaric oxygen therapy.

Hyperbaric oxygen therapy has significantly improved the management of necrotizing fasciitis of the extremities and trunk. Its role in cervical necrotizing fasciitis has not been fully evaluated. Historically, necrotizing fasciitis has been associated with considerable morbidity and mortality. This report discusses our experience with cervical necrotizing fasciitis in six patients treated from 1986 to 1993 who received hyperbaric oxygen therapy. All patients survived. In all cases infection was of probable odontogenic origin. Most patients in whom necrotizing fasciitis develops have identifiable risk factors; however, two patients in this series were previously healthy, and there was no relationship between hospital course and identified risk factors. Clinical presentation and microbiology are reviewed together with the rationale for hyperbaric oxygen therapy as an adjunct to broad-spectrum antibiotics and aggressive early surgical debridement.

Cerebral oxygen availability by NIR spectroscopy during transient hypoxia in humans.

The effects of mild hypoxia on brain oxyhemoglobin, cytochrome a,a3 redox status, and cerebral blood volume were studied using near-infrared spectroscopy in eight healthy volunteers. Incremental hypoxia reaching 70% arterial O2 saturation was produced in normocapnia [end-tidal PCO2 (PETCO2) 36.9 +/- 2.6 to 34.9 +/- 3.4 Torr] or hypocapnia (PETCO2 32.8 +/- 0.6 to 23.7 +/- 0.6 Torr) by an 8-min rebreathing technique and regulation of inspired CO2. Normocapnic hypoxia was characterized by progressive reductions in arterial PO2 (PaO2, 89.1 +/- 3.5 to 34.1 +/- 0.1 Torr) with stable PETCO2, arterial PCO2 (PaCO2), and arterial pH and resulted in increases in heart rate (35%) systolic blood pressure (14%), and minute ventilation (5-fold). Hypocapnic hypoxia resulted in progressively decreasing PaO2 (100.2 +/- 3.6 to 28.9 +/- 0.1 Torr), with progressive reduction in PaCO2 (39.0 +/- 1.6 to 27.3 +/- 1.9 Torr), and an increase in arterial pH (7.41 +/- 0.02 to 7.53 +/- 0.03), heart rate (61%), and ventilation (3-fold). In the brain, hypoxia resulted in a steady decline of cerebral oxyhemoglobin content and a decrease in oxidized cytochrome a,a3. Significantly greater loss of oxidized cytochrome a,a3 occurred for a given decrease in oxyhemoglobin during hypocapnic hypoxia relative to normocapnic hypoxia. Total blood volume response during hypoxia also was significantly attenuated by hypocapnia, because the increase in volume was only half that of normocapnic subjects. We conclude that cytochrome a,a3 oxidation level in vivo decreases at mild levels of hypoxia. PaCO is an important determinant of brain oxygenation, because it modulates ventilatory, cardiovascular, and cerebral O2 delivery responses to hypoxia.

Pulmonary gas exchange in humans exercising at sea level and simulated altitude.

In a previous study of normal subjects exercising at sea level and simulated altitude, ventilation-perfusion (VA/Q) inequality and alveolar-end-capillary O2 diffusion limitation (DIFF) were found to increase on exercise at altitude, but at sea level the changes did not reach statistical significance. This paper reports additional measurements of VA/Q inequality and DIFF (at sea level and altitude) and also of pulmonary arterial pressure. This was to examine the hypothesis that VA/Q inequality is related to increased pulmonary arterial pressure. In a hypobaric chamber, eight normal subjects were exposed to barometric pressures of 752, 523, and 429 Torr (sea level, 10,000 ft, and 15,000 ft) in random order. At each altitude, inert and respiratory gas exchange and hemodynamic variables were studied at rest and during several levels of steady-state bicycle exercise. Multiple inert gas data from the previous and current studies were combined (after demonstrating no statistical difference between them) and showed increasing VA/Q inequality with sea level exercise (P = 0.02). Breathing 100% O2 did not reverse this increase. When O2 consumption exceeded about 2.7 1/min, evidence for DIFF at sea level was present (P = 0.01). VA/Q inequality and DIFF increased with exercise at altitude as found previously and was reversed by 100% O2 breathing. Indexes of VA/Q dispersion correlated well with mean pulmonary arterial pressure and also with minute ventilation. This study confirms the development of both VA/Q mismatch and DIFF in normal subjects during heavy exercise at sea level. However, the mechanism of increased VA/Q mismatch on exercise remains unclear due to the correlation with both ventilatory and circulatory variables and will require further study.

Physiological responses to exercise at 47 and 66 ATA.

Five male volunteers served as subjects for exercise studies during three dives to pressures of 47 and 66 ATA while breathing gases containing 0.5 ATA PO2 and varying amounts of N2 and He. The inspired gas density ranged from 1.1 g/l (BTPS) at the surface to 17.1 g/l at the highest pressure. Dyspnea at rest and during exercise was evident in all divers and was predominantly inspiratory in nature. Despite the dyspnea, divers were able to perform work requiring an O2 consumption larger than 2 l/min STPD at each depth. Compared with surface measurements, moderate work at depth was associated with alveolar hypoventilation, arterial hypercapnia, very large physiological dead space, and higher levels of arterial lactate and signs of simultaneous respiratory and metabolic acidosis. The increase of ventilation that accompanies the onset of acidemia at the surface was not present at depth. Acidemia at depth was more severe, and its onset occurred at lesser work rates than at 1 ATA. No large differences could be ascertained when a variety of responses obtained with inspired gas having a density of 7.9 g/l at 47 ATA were compared with those obtained with an inspired gas density of 17.1 g/l at 66 ATA. It appears that the major impact of the environment on the physiological responses to work was almost fully manifested at a pressure of 47 ATA with a He-O2 gas mixture. It is cautioned that maximum work tolerance may be an insufficient assessment of the physiological condition of a diver exposed to these high pressures.