PubMed Health⌕ Search

Biomedical subjects

B K Kambestad

Publications and source records attributed to B K Kambestad.

10 recordsLinked to original sources

Persistent small-airways dysfunction after exposure to hyperoxia.

To assess the contribution of hyperoxia to reduced pulmonary function after a deep saturation dive, a shallow saturation dive to a pressure of 0.25 MPa with the same profile of hyperoxic exposure as in a deep saturation dive to 3.7 MPa was conducted. The PO2 was 40 kPa, with periods of 75 kPa for 2 h every 2nd day during the first 14 days, 50 kPa the next 12 days, and a gradual fall to 21 kPa over the last 2 days in decompression. Seven submariners and one professional diver aged 22-27 yr participated. Pulmonary function, including static and dynamic lung volumes and flows and transfer factor for carbon monoxide (TLCO), were measured twice before, immediately after, 1 mo after, and 1 and 3 yr after the dive. As reported previously, there was a significant reduction in TLCO and in maximal expiratory flow rates at low lung volumes immediately after the dive. At the follow-up examinations 1 and 3 yr after, there was no recovery of the maximal expiratory flow rates. Forced midexpiratory flow rate was still reduced by 8.7 +/- 5.6% (P < 0.05) and 9.3 +/- 7.1% (P < 0.01), respectively. Forced expired volume in 1 s and forced vital capacity were not significantly reduced. There was a complete recovery of the TLCO. The findings are consistent with the studies indicating development of airway obstruction in divers, and the findings indicate that exposure to hyperoxia contributes to this effect.

Adult↗

Mechanisms of reduced pulmonary function after a saturation dive.

Deep saturation diving has been shown to have prolonged effects on pulmonary function. We wanted to assess the relative contribution of various factors that could contribute to these effects. Pulmonary function was, therefore, measured before and after 17 different saturation diving operations to depths of 5-450 m of sea water, corresponding to absolute pressures of 0.15-4.6 MPa. Four to fifteen divers participated in each operation. The measurements included static and dynamic lung volumes and flows, transfer factor of the lungs for carbon monoxide (TLCO), and closing volume. The dives were characterized by the cumulative hyperoxic and hyperbaric exposures, and the load of venous gas microemboli encountered during decompression was measured in 41 divers in three dives to 0.25, 1.2 and 3.7 MPa. TLCO was reduced by 8.3 +/- 7.0% mean +/- SD after the dives, this correlated with cumulative hyperoxic exposure and load of venous gas microembolism, independently of each other. Closing volume was increased and forced mid-expiratory flow rate reduced, in correlation with cumulative hyperoxic exposure. An increase in total lung capacity correlated with cumulative hyperbaric exposure. We conclude that hyperoxia, hyperbaria, and venous gas microembolism all contribute to the changes in pulmonary function after a single saturation dive, and all may explain some of the long-term effects of diving on pulmonary function.

Adult↗

Calculation of radiation induced complication probabilities for brain, liver and kidney, and the use of a reliability model to estimate critical volume fractions.

Radiation induced normal tissue complication probability is calculated for three different organs: brain, liver and kidney. The model applied is a reliability model where the volume effect of the tissue is described by the structural parameter, k, which reflects the architecture of the functional subunits (p) and the irradiated volume fraction (n). For partial, homogeneous irradiation of the brain, a k-value close to unity was found, and the respective values for liver and kidney were 0.92 and 0.77. An extension of the reliability model to account for individual inactivation probability of the subunits allows calculation of complication probability for inhomogeneous dose distributions. For the brain, intercomparison of a three-field and a two-field technique demonstrated a small reduction in complication probability for the former at low total doses. At high total doses a minimum complication probability was achieved applying a three-field technique, being three times less than that associated with the two-field technique.

Brain↗

Pulmonary function one and four years after a deep saturation dive.

The pulmonary function of 24 Norwegian divers who had participated in a deep saturation dive to pressures of 3.1-4.6 MPa was reevaluated one and four years later. Twenty-eight divers performing ordinary saturation diving to pressures of 0.8-1.6 MPa and followed over a three-year period served as referents. A significant reduction in forced expiratory volume in 1 s (FEV1.0) of 210 (SD 84) ml (P < 0.001) occurred the first year after the dive. Thereafter the annual reduction in FEV1.0 was 28 (SD 62) ml.year-1; this value did not differ from the 35 (SD 80) ml.year-1 of the referents. The forced midexpiratory flow rate and forced expiratory flow rates at low lung volumes were also significantly reduced one year after the deep dive, and the closing volume was increased. No significant changes occurred in forced vital capacity. The results agree with those of cross-sectional studies on divers' lung function and indicate the development of airflow limitation in relation to diving exposure.

Adult↗

Electroencephalography, evoked potentials and MRI brain scans in saturation divers. An epidemiological study.

One hundred and fifty-six air and saturation divers, mean age 33.6 (range 21-49) years, were examined. The control group consisted of 100 offshore workers and policemen with the health requirements to have a diving certificate, mean age 34.0 (range 22-48) years. The examination protocol included electroencephalography (EEG), visual evoked potentials (VEPs), brain-stem auditory evoked potentials (BAEPs) and magnetic resonance imaging (MRI) of the brain and brain-stem. Abnormal EEGs, with focal slow waves mostly in the temporal regions and sharp potentials, were found in 18% of the divers and in 5% of the controls (P = 0.003). Abnormal EEGs correlated significantly with the exposure to saturation diving (P = 0.0006) and the prevalence of decompression sickness (P = 0.0102). Alcohol consumption was negatively correlated with abnormal EEGs (P = 0.0006). Mean I-III BAEP latency was increased (P = 0.047) in the diver group. P100 VEP latency decreased with age (21-49 years). High signal intensity changes obtained by MRI were found in 33% of the divers and in 43% of the controls (P = 0.14). It is concluded that the nervous system of saturation divers is influenced by their occupation and that EEG is a useful method in the health examination of divers.

Adult↗

Neurological long term consequences of deep diving.

Forty commercial saturation divers, mean age 34.9 (range 24-49) years, were examined one to seven years after their last deep dive (190-500 metres of seawater). Four had by then lost their divers' licence because of neurological problems. Twenty seven (68%) had been selected by neurological examination and electroencephalography before the deep dives. The control group consisted of 100 men, mean age 34.0 (range 22-48) years. The divers reported significantly more symptoms from the nervous system. Concentration difficulties and paraesthesia in feet and hands were common. They had more abnormal neurological findings by neurological examination compatible with dysfunction in the lumbar spinal cord or roots. They also had a larger proportion of abnormal electroencephalograms than the controls. The neurological symptoms and findings were highly significantly correlated with exposure to deep diving (depth included), but even more significantly correlated to air and saturation diving and prevalence of decompression sickness. Visual evoked potentials, brainstem auditory evoked potentials, and magnetic resonance imaging of the brain did not show more abnormal findings in the divers. Four (10%) divers had had episodes of cerebral dysfunction during or after the dives; two had had seizures, one had had transitory cerebral ischaemia and one had had transitory global amnesia. It is concluded that deep diving may have a long term effect on the nervous system of the divers.

Adult↗

Visual evoked and brain stem auditory evoked potentials in divers.

Visual evoked potentials (VEP) were examined in 14 divers during dives to 360 metres of seawater (msw). All latencies increased significantly with depth. VEP and brain stem auditory evoked potentials (BAEP) were similarly examined in 18 divers before and after these dives. N75 was significantly increased after compared to before the dive, while there was no significant difference in the P100 and N145 latencies. BAEP I-V latency was significantly decreased after the dives. VEP and BAEP were examined in 156 divers and 99 controls. There was no significant difference in VEP. BAEP I-III interpeak latency was significantly increased for the divers, but with no significant changes in I-V and III-V latencies. VEP and BAEP were examined in 26 divers after treatment for neurological decompression sickness. There was no significant difference compared to the control group. The conclusions are that VEP and BAEP change transitorily with influence of hyperbaric pressure, but do not measure major permanent disturbances in the divers' visual and auditory pathways.

Adult↗

Characteristics of the response to exercise in professional saturation divers.

Exercise testing with measurements of expired minute ventilation (VE), oxygen uptake (VO2), and carbon dioxide elimination (VCO2) was done in 63 professional saturation divers, in the screening programs for selection of divers, to 10 different experimental and operational saturation dives. Their experience as divers averaged 9.8 yr (range 1-20), and they averaged 276 days (range 5-900) in saturation. The maximal pressure they had ever been exposed to averaged 2.01 MPa (range 0.8-5.1). The divers were compared with a control group of 47 offshore workers and policemen matched for age, height, and smoking habits and with reference values for the general healthy population. There were no significant differences in peak work load achieved, VO2peak and VCO2peak. VE at VO2peak and the corresponding ventilatory equivalents for oxygen uptake (VE(peak)/VO2peak) and carbon dioxide elimination (VE(peak)/VCO2peak) were significantly higher in divers (P less than 0.05), but VE, VE/VO2 and VE/VCO2 were not different at lower work loads. VE(peak)/VCO2peak correlated positively with years of diving experience when corrected for age (P less than 0.01). Divers had higher tidal volumes and lower breathing frequencies at ventilations lower than 40% of VE(peak), but maximal tidal volumes were not different. Tidal volume at a VE of 30 liter.min(-1) correlated negatively with FEV1 (P less than 0.05). The results are in agreement with the transient changes in pulmonary function and exercise tolerance demonstrated after a single saturation dive, and indicate that these changes may not be completely reversible.

Adult↗

Influence of occupational diving upon the nervous system: an epidemiological study.

Neurological signs and symptoms were recorded from 156 air and saturation divers and 100 controls. Fifty one (33%) of the divers had had symptoms from the central nervous system during decompression. Also, 22 (14%) had been unconscious while diving. In total 79 (51%) had had decompression sickness (DCS). Twelve (8%) of the divers and no controls had had specific neurological symptoms (vision disturbances, vertigo, reduced skin sensitivity) in non-diving situations, and six (4%) of the divers (no controls) had had episodes of cerebral dysfunction (seizures, transient cerebral ischaemia, transient amnesia). The divers had significantly more general symptoms from the nervous system and more abnormal neurological findings than the controls. The most prominent symptoms were difficulties in concentration and problems with long and short term memory. The most prominent abnormal findings in the divers were compatible with dysfunction in the distal spinal cord or nerve roots, and polyneuropathy. The general neurological symptoms and findings were independently significantly correlated with diving exposure, prevalence of DCS, and age.

Adult↗

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.

Adult↗