HPNS effects among 18 divers during compression to 360 msw on heliox

Heliox compression deeper than 16 ATA can lead to EEG changes associated with confusion and somnolence. In man the symptoms termed the high pressure neurologic syndrome (HPNS) can also include increased tremor, memory problems, dizziness, nausea, and vomiting. In a series of 3 dives at NUTEC, a compression profile developed for operational use down to 360 msw was evaluated. In each dive 6 different divers were compressed to 360 msw on heliox. Neuropsychologic and neurophysiologic testing were performed repeatedly. The HPNS testing revealed only mild effects of the compression. Only 3 divers had impairments of more than 2 SD in peripheral motor function compared to their predive average. Memory was impaired periodically in 2 divers. The same was found for perceptual speed and reasoning. Fifty percent of the divers had an increase of more than 2 SD in postural tremor, but that had minimal effect on their motor performance. Six of the 18 divers had an EEG power spectrum with both alpha band inhibition and theta increase. While the performance impairment was most marked around 240 msw, the EEG changes occurred mainly deeper than 300 msw. In only 1 of the 18 divers marked EEG changes, marked tremor increase, and marked cognitive performance impairment were observed at the same time. Although mild HPNS was observed, the divers were little impaired during the compression to 360 msw. The results confirm that using a compression profile with rates decreasing progressively with increasing depth, and with several intermediate stops, provides fit divers at depth. By using standard batteries of HPNS testing we were able to obtain evidence for the acceptability of this compression profile.     

Central nervous system reactions during heliox and trimix dives to 51 ATA, DEEP EX 81

Two groups of divers were compressed to 500 msw with heliox (n = 3) and trimix (n = 3). They were followed with repeated neuropsychological and neurological tests during compression, at stable intermediate depths, and at 500 msw. For the heliox group there was a marked increase in tremor and EEG slow waves and reduction in handgrip strength. For the trimix group the tremor increase did not occur, but the EEG changes were the same as in the heliox group. On motor tests only the trimix group showed impaired finger dexterity and manual dexterity. The same occurred for fine visuomotor coordination, but both groups had increased intentional tremor. On cognitive tests the same difference occurred. The trimix group was markedly impaired in reasoning and long-term memory, while only a mild impairment was found in the heliox group. Dizziness and other symptoms of high pressure nervous syndrome (HPNS) occurred in both groups. Conclusion: There were marked HPNS effects during compression for both groups. Only tremor was inhibited by the nitrogen. In addition, the trimix group was impaired because of nitrogen narcosis. These data indicated that 10% nitrogen did not inhibit HPNS effects during compression to 500 msw, but the considerable differences between subjects shows that susceptibility to compression must be an important area for future research.     

EEG and evoked potential changes during gas- and liquid-breathing dives to 1000 msw

To test the hypothesis that compression in helium gas and compression without gas (hydrostatic compression) both produce the same neurological symptoms of high pressure nervous syndrome (HPNS), groups of 4 to 5 dogs were exposed to one of the following: (a) a 2-h surface control breathing He-O2 gas; (b) compression to 700-1000 msw breathing He-O2 gas; (c) a 2-h liquid-breathing control [ventilation with warmed (38 degrees C), oxygenated fluorocarbon liquid, FC-80]; and (d) "near hydrostatic" compression to 700-1000 msw while being ventilated with liquid from a sealed reservoir. Power spectra obtained from scalp-recorded EEG signals revealed a significant compression-related shift of power from the normally dominant 5-8 Hz band to the 8-11 Hz band. This effect was greatest at 600 msw and occurred equally in both dive groups. At very high pressures (greater than 900 msw) power in this 6-10 Hz range became reduced whereas 16-22 Hz activity increased as the EEG flattened. Somatosensory evoked potentials (SEPs) were elicited by subdermal electrical stimulation in the foreleg (n = 120). The latency of P1 (approximately 31 ms) did not change in any group; transmission time to cortex was unaltered by time or pressure. However, the "late-wave" P4 (approximately 250 ms) was slowed by 32-35 ms at 1000 msw in both groups (P less than 0.003 in He-O2). Since these main symptoms were provoked equally in both He-O2 and FC-80 dive groups, helium pressure did not play a significant role in the etiology of HPNS in this animal model. It is concluded that the HPNS is primarily a result of excessive pressure per se or rate of change of pressure per se.     

Effects of a H2-He-O2 mixture on the HPNS up to 450 msw

A H2-He-O2 mixture with 54 to 56% hydrogen was studied with 6 subjects (professional divers) during 2 dives to 450 m. The 38-h compression was the same as that used with other types of breathing mixtures (He-O2 and He-N2-O2). The results obtained during compression and during the stay at 450 m in H2-He-O2 show that the EEG changes (increase of theta activities in the anterior regions of the skull, decrease of alpha activities) are similar to those found with other respiratory mixtures. On the other hand, the other symptoms of high pressure neurologic syndrome (HPNS) were clearly improved for the same depths. Thus, neurologic symptoms (tremor, dysmetria, myoclonia, drowsiness) are nonexistent, and the performances during psychometric tests remain similar to those of the surface. Hydrogen, with its narcotic potency, suppresses some symptoms of HPNS and seems to open new perspectives for deep diving.     

Topographic electroencephalographic studies in a hyperbaric environment--specific reference to high pressure nervous syndrome

Hyperbaric chamber dives at various equivalent depths below sea level, i.e. 7, 14, 19 and 31 atmosphere absolute (ATA) with helium-oxygen or helium-nitrogen-oxygen have been performed at the Japan Marine Science and Technology Center. A two-dimensional (topographic) display of the scalp EEG was used during simulated underwater experiments to determine; 1) Whether there are any characteristic EEG patterns in high pressure nervous syndrome (HPNS), 2) the relationship between the EEG changes and the compression rate, and 3) the relationship between the EEG changes and the characteristic signs and symptoms of HPNS. A two-way analysis of variance and a distribution analysis technique revealed that the topographic brain patterns depended on the diving depth and indicated the most affected brain areas during compression and decompression. Significant correlations between the diving depth and the EEG potentials were observed at different brain locations. Alpha waves showed a diffuse cortical distribution. Theta wave activity was more localized in the frontal midline region. These waves developed paroxysmally in relatively brief bursts supplanting or intermixing with normal background EEG rhythms. In our subjects, frontal midline theta activity was associated mostly with some of the characteristic features of HPNS, such as a transient episode of laughter or euphoria at depths greater than 21 ATA. An intimate correlation between frontal midline theta wave and laughter was observed. Frontal midline theta waves may be related to emotional activities induced by helium under high pressure. There were significant individual variations in susceptibility and subjective signs and symptoms. The EEG is of great value in studying man's physiological reactions in an undersea environment and also very important in selecting divers who are relatively more tolerant of a severe hyperbaric environment.     

Evaluation of noise within the MK 12 SSDS helmet and its effect on divers' hearing

The noise inside the U.S. Navy MK 12 SSDS helmet was measured and its effect on the hearing of divers assessed. Seven male divers completed 20 dives while breathing air at simulated depths ranging from 1.8 to 30.5 msw with dive durations ranging from 40 to 120 min. Microphones recorded sound pressure levels inside the helmet while the diver was in the water and exercising. Average corrected sound intensity levels in the helmet ranged from 90.5 dB(A) at 1.8 msw to 97.3 dB(A) at 30.5 msw. Diver hearing threshold level shifts were recorded as a function of helmet noise exposure; moderate threshold shifts were observed at depths of 9.1 msw or deeper after 120-min dives. The hearing of all divers completing dives up to 120 min returned to predive levels within 24 h after noise exposure. However, dive durations in excess of 120 min at 9.1 and 20.1 msw resulted in substantial auditory shifts in 1 diver, which required 2-3 d to recover to predive levels. These results suggest that the impact of helmet noise on diver hearing should be included in planning operations using the MK 12 SSDS.     

Extremely deep recreational dives: the risk for carbon dioxide (CO(2)) retention and high pressure neurological syndrome (HPNS)

Clear differences between professional and recreational deep diving are disappearing, at least when taking into account the types of breathing mixtures (oxygen, nitrox, heliox, and trimix) and range of dive parameters (depth and time). Training of recreational deep divers is conducted at depths of 120-150 metres and some divers dive to 180-200 metres using the same diving techniques. Extremely deep recreational divers go to depths of more than 200 metres, at which depths the physical and chemical properties of breathing gases create some physiological restrictions already known from professional deep diving. One risk is carbon dioxide retention due to limitation of lung ventilation caused by the high density of breathing gas mixture at great depths. This effect can be amplified by the introduction of the additional work of breathing if there is significant external resistance caused by a breathing device. The other risk for deep divers is High Pressure Neurological Syndrome (HPNS) caused by a direct compression effect, presumably on the lipid component of cell membranes of the central nervous system. In deep professional diving, divers use a mixture of helium and oxygen to decrease gas density, and nitrogen is used only in some cases for decreasing the signs and symptoms of HPNS. The same approach with decreasing the nitrogen content in the breathing mixture can also be observed nowadays in deep recreational diving. Moreover, in extremely deep professional diving, hydrogen has been used successfully both for decreasing the density of the breathing gas mixture and amelioration of HPNS signs and symptoms. It is fair to assume that the use of hydrogen will be soon "re-invented" by extremely deep recreational divers. So the scope of modern diving medicine for recreational divers should be expanded also to cover these problems, which previously were assigned exclusively to professional and military divers.     

Decompression from a deep nitrogen/oxygen saturation dive--a case report

Ten divers participated in a 4.5 d nitrogen/oxygen saturation dive to 165 fsw. There were daily 2 h excursions to 61 msw (200 fsw). The divers breathed air during the excursions and 0.51 bar (0.5 atm) oxygen in nitrogen at 50.3 msw (165 fsw). The final decompression began 6 h after the last excursion. The oxygen partial pressure was 0.51 bar (0.5 atm) from 50.3 to 13.7 msw (165 to 45 fsw), and air was used from 13.7 msw (45 fsw) to the surface. By 6.1 msw (20 fsw), four divers had developed decompression sickness. A fifth diver developed decompression sickness during a commercial air flight 68 h after surfacing. Comparison of ascent rates for this dive and for air or nitrogen/oxygen saturation dives reported in the literature suggests that deeper dives require slower rates of ascent. Dives shallower than 30.5 msw (100 fsw) had a mean ascent rate of 1 msw/h (3.2 fsw/h) and 14 decompression incidents in 107 man-exposures. Dives deeper than 30.5 msw (100 fsw) had a mean rate of 0.76 msw/h (2.5 fsw/h) and 14 incidents in 45 man-exposures.     

Cognitive and emotional changes during a simulated 686-m deep dive

Three experienced divers were subjected simultaneously to world record hyperbaric pressures using an oxygen-helium-10% nitrogen breathing mixture. The simulated depth reached by these divers was 686 m (2250 ft). Cognitive and emotional state measures were obtained predive, during compression, decompression, and postdive. Although the divers showed no overt signs of nitrogen narcosis or HPNS, declines in memory, adaptive, and spatial functions were seen at 670 m. These performance deficits were reversed when the divers returned to surface pressures. The observed declines in performance are discussed in light of their implications for future dives.     

Electronystagmography and saturation deep diving at 4.6 MPa

In the course of the ENTEX V and VIII saturation deep diving experiments at 4.6 MPa for 12 d, electronystagmography monitoring was performed on divers before, during, and after the stay in the diving chamber. In a vestibular sense, these dives were well-tolerated subjectively, clinically, and infraclinically by the divers. However, a decrease in the nystagmus induced by caloric stimulation was seen in 4 out of 8 divers during the confinement period at 0.2 MPa and in 6 out of 8 divers upon reaching 4.6 MPa, followed by variable responses dependent on the subject, with total recovery on reaching the surface. These results are explained on one hand in terms of the thermal conductivity of helium, and on the other in terms of a rough form of HPNS.     

Hyperbaric liver dysfunction in saturation divers

Earlier demonstration of elevated blood thyroid hormones and transaminase activities during controlled chamber dives to 540 and 660 msw [at AMTE(PL), Gosport, England; 1980 and 1981] led to the suspicion that high compression may interfere with liver function. Further studies, here described, of blood thyroid hormone level changes during the course of subsequent dives indicate that thyroxine and reverse triiodothyronine elevations are to be expected during any period of sustained compression, to depths as shallow as 61 msw. Moreover, blood levels of thyroxine-binding globulin (TBG), measured in the 540 and 660 msw dives, were also shown to rise, probably accounting for the hormone changes. This elevation is not confined to TBG, being demonstrable in at least six other glycoproteins (sex hormone-binding globulin, transferrin, ceruloplasmin, haptoglobin, alpha 1 acid glycoprotein, and alpha 2 macroglobulin). Since all these proteins share identical or very similar metabolic fates within the liver, these findings lend further weight to our hyperbaric liver dysfunction theory. How such disturbances may come about is discussed, together with its possible implications apropos high pressure nervous syndrome and divers' well-being and capabilities while at depth.     

Nerve conduction velocity in man during deep diving to 360 msw

The function of the sensory and motor median nerves was examined in 6 divers during a simulated dive to 360 meters of seawater (msw), with a mixture of helium and oxygen (heliox) as breathing gas. Divers were examined in the compression chamber before the dive, at 360, 300, 240, 130, 50, and 5 msw, and with skin temperatures ranging from 29.2 degrees to 35.2 degrees C. Examinations were performed with superficial stimulating and recording electrodes. Fast sensory nerve conduction decreased with increase in hyperbaric pressure and with decrease in skin temperature. There was no significant correlation between slow sensory conduction and hyperbaric pressure. Distal motor latency increased with increase in hyperbaric pressure and with decrease in skin temperature. The effect of pressure was independent of temperature. No significant functional changes were detected in the main nerve trunk proximal to the wrist or in the F-wave responses.     

High altitude dives from 7000 to 14,200 feet in the Himalayas

Indian Navy divers carried out no-decompression dives at altitudes of 7000 to 14,200 ft (2134-4328 m) in the Nilgiris and Himalayas from May to July 1988. Seventy-eight dives on air and 22 dives on oxygen were carried out at various altitudes. The final dives were at Lake Pangong Tso (4328 m) in Ladakh, Himalayas, to a maximum of 140 feet of sea water (fsw) [42.6 meters of sea water (msw)] equivalent ocean depth in minimum water temperature of 2 degrees C. Oxygen diving at 14,200 ft (4328 m) was not successful. Aspects considered were altitude adaptation, diminished air pressure diving, hypothermia, and remote area survival. Depths at altitude were converted to depths at sea level and were applied to the Royal Navy air tables. Altitude-related manifestations, hypoxia, hypothermia, suspected oxygen toxicity, and equipment failure were observed. It is concluded that stress is due to effects of altitude and cold on man and equipment, as well as changes in diving procedures when diving at high altitudes. Equivalent air depths when applied to Royal Navy tables could be considered a safe method for diving at altitudes.     

An investigation of cardiovascular reflexes during a trimix saturation dive to 450 msw (GUSI 17).

The study examines the hypothesis that the carotid sinus heart rate baroreflex responses are changed in human subjects on exposure to 450 msw. Baroreceptor reflex changes in heart rate (expressed as ms/mmHg applied pressure) were evoked by application of negative or positive pressure to a cuff surrounding the neck. At 450 msw using trimix, the mean resting heart rate of divers slowed significantly from 64 +/- 1.3 beats/min at surface to 55 +/- 1.4 beats/min at 450 msw, respiratory rate decreased from 15 +/- 1.4 at surface to 11 +/- 2 at 450 msw, and sinus arrhythmia increased. There was no change in arterial blood pressure. Baroreceptor reflex sensitivity to an increased carotid sinus transmural pressure was reduced from 5.6 +/- 2.9 (mean +/- SEM) at surface to 2.4 +/- 0.8 ms.mmHg-1 at 450 msw; sensitivity to decreased carotid sinus transmural pressure increased from 2.2 +/- 0.4 ms.mmHg-1 at surface to 5.1 +/- 0.2 ms.mmHg-1 at 450 msw. A progressive shortening of cardiac interval during breath hold in expiration was also noted. When this shortening of interval was incorporated into the analysis of baroreceptor reflex sensitivity, no significant change in sensitivity was observed but the overall baroreflex stimulus-response relationship shifted downward.     

CNS reactions at 51 ATA on trimix and heliox and during decompression

Two groups of divers (Group A and B) were compressed to 500 msw with trimix (n = 3) and heliox (n = 3). After 4 d at saturation depth Group A had a gas change to heliox. Both groups were followed with repeated neuropsychological and neurological tests during compression, at stable intermediate depths and at saturation depth. There were marked high pressure nervous syndrome effects during compression for both groups. Only tremor was inhibited by the nitrogen. In addition Group A was impaired due to nitrogen narcosis. During trimix and heliox saturation there was only some recovery in the EEG. Group B had a sustained high tremor during the saturation. On visuomotor and cognitive functions Group B performed up to predive level on the 3rd d at saturation while Group A was heavily impaired during the whole trimix saturation period. Although dizziness and tremor were the main symptoms in Group B, Group A reported concentration trouble, euphoria, and upset stomach during the saturation phase. Minor changes occurred in the EEG during the gas change. There was, however, a marked increase in postural tremor and recovery on cognitive tests relating to the elimination of the nitrogen. Up to the completion of the gas change no severe symptoms were reported. Six hours after the gas change, severe symptoms occurred with visual and auditory hallucinations and myoclonic jerks as the dominant characteristics. Some symptoms lasted for 12 h. During decompression there was a steady normalization in both groups.     

Central nervous system oxygen toxicity in closed circuit scuba divers II

Central nervous system oxygen toxicity is currently the limiting factor in underwater swimming/diving operations using closed-circuit oxygen equipment. A dive series was conducted at the Navy Experimental Diving Unit in Panama City, FL, to determine whether these limits can be safely extended and also to evaluate the feasibility of making excursions to increased depth after a previous transit at a shallower depth for various lengths of time. A total of 465 man-dives were conducted on 14 different experimental profiles. In all, 33 episodes of oxygen toxicity were encountered, including 2 convulsions. Symptoms were classified as probable, definite, or convulsion. Findings were as follows: symptom classification is a useful tool in evaluating symptoms of oxygen toxicity; safe exposure limits should generally be adjusted only as a result of definite symptoms or convulsions; the following single-depth dive limits are proposed: 20 fsw (6.1 msw)--240 min, 25 fsw (7.6 msw)--240 min, 30 fsw (9.1 msw)--80 min, 35 fsw (10.7 msw)--25 min, 40 fsw (12.2 msw)--15 min, 50 fsw (15.2 msw)--10 min; a pre-exposure of up to 4 h at 20 fsw causes only a slight increase in the probability of an oxygen toxicity symptom on subsequent downward excursions; a pre-exposure depth of 25 fsw will have a more adverse effect on subsequent excursions than will 20 fsw; a return to 20 fsw for periods of 95-110 min seems to provide an adequate recovery period from an earlier excursion and enables a second excursion to be taken without additional hazard; nausea was the most commonly noted symptom of oxygen toxicity, followed by muscle twitching and dizziness; dives on which oxygen toxicity episodes were noted had a more rapid rate of core temperature cooling than dives without toxicity episodes; several divers who had passed the U.S. Navy Oxygen Tolerance Test were observed to be reproducibly more susceptible to oxygen toxicity than the other experimental divers.     

Intentional tremor on a helium-oxygen chamber dive to 49.5 ATA

Tremor is a well-recognized manifestation of the high pressure nervous syndrome (HPNS). As such, its measurement and analysis during deep hyperbaric exposures can be an important index of central nervous system integrity. During the U.S. Navy's experimental chamber dive to a depth equivalent to 1600 fsw (49.5 ATA), objective measures of intentional tremor were obtained at several depths. Six subjects were pressurized in 6 days to 49.5 ATA. After spending 7 days at this pressure, they were decompressed in 19 days to the surface. Measures of intentional tremor were obtained predive and at pressure levels of 13.1, 31.3, 49.5, 40.4, and 31.3 ATA using the Naval Medical Research Institute Mark 3 Mod 1 tremor device. Each subject's microtremor was measured while he produced a force of 50 grams and 500 grams against a finger force transducer. Unlike previous studies of HPNS tremor, special attention was given to amplitude rather than frequency analysis. All subjects displayed a marked increase in tremor that interfered with fine motor performance at depths greater than 1000 fsw. A statistically significant increase in signal frequency was also observed.     

U.S. Navy saturation diving and diver neuropsychologic status

The neuropsychologic status of 25 male U.S. Navy saturation divers was assessed before and after saturation dives conducted at the Navy Experimental Diving Unit. Between 1982 and 1986, 5 dives to simulated depths of 198 to 335 msw were accomplished. Eighteen divers completed 1 dive, and 7 divers completed 2 saturation dives during this period. Dive durations ranged from 26 to 31 d, with helium-oxygen used as the breathing medium. On each dive the men engaged in strenuous, meaningful, in-water work on the bottom. Comparison of neuropsychologic assessment battery results pre- and postdives did not reveal permanent changes in neuropsychologic status. Transient alterations in affect, visual focusing, and physical activity level presented upon surfacing but resolved within 10 d.     

Analysis of neurologic symptoms in deep diving: implications for selection of divers

Eighteen professional divers (age range 24-33 yr, mean 28.3) participated in one simulated dive to 360 meters of seawater (msw) in a helium-oxygen (heliox) atmosphere with equal compression and decompression profiles. All divers were given an extensive neurologic examination before diving. Clinical neurologic symptoms observed during the dives were equilibrium disorder, sleep disturbances, fatigue, nausea, loose stools, stomach pain, tremor, mental disturbances, reduced appetite, and headache. Symptoms were scored individually by each diver. The symptoms were analyzed statistically by factor analysis, which grouped them into four factors. These symptoms are presumably related to functional disturbances in the brain stem and the cerebellum. Factor 3 symptoms (tremor, mental disturbances, reduced appetite) correlated significantly to a history of predive decompression sickness (P = 0.006) and to cerebral concussion (P = 0.023). Three divers were periodically unable to work at bottom due to equilibrium disorder, diarrhea, or nausea. One diver with mild polyneuropathy and slight cerebral atrophy as seen by computerized tomography and another diver with abnormal electroencephalography were periodically unable to work due to equilibrium disorder and nausea, respectively. We advocate that divers with signs of central or peripheral nervous system dysfunction should not be selected for deep diving.