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Biomedical subjects

E Thorsen

Publications and source records attributed to E Thorsen.

34 records · Page 2Linked to original sources
PubMed1995

Effects of venous gas microemboli on pulmonary gas transfer function.

Dynamic lung volumes and flows, slope of phase III of the single breath oxygen test (delta-N2), closing volume (CV), and transfer factor for carbon monoxide (TICO) were measured before and 1 h after an air dive in a hyperbaric chamber to a pressure of 0.49 MPa for 40 min. Six divers had a bottom time of 20 min and a rate of decompression of 50 kPa x min-1, and six divers had a bottom time of 24 min and a rate of decompression of 100 kPa x min-1. Decompression stops were 5 min at 0.16 MPa and 10 min at 0.13 MPa for both groups. As control exposure they were breathing O2 at atmospheric pressure for 40 min. The dive and control exposure were done on different days within 1 wk, in random order. Doppler ultrasound monitoring for venous gas microemboli (VGM) was done during the first hour after the dive. VGM were detectable in all six divers with the fast decompression rate and in one subject with the slow rate (P < 0.01). In the subjects having VGM there was a significant reduction in TICO of -5.9 +/- 4.4% compared with -0.5 +/- 3.4% after the control exposure (P = 0.034). In the five subjects without detectable VGM, the changes in TICO were -2.8 +/- 3.7% and 0.2 +/- 3.8%, respectively. There were no significant changes in dynamic lung volumes and flows, CV, or delta-N2. A reduction in TICO may reflect effects of VGM after dives in which the effect of O2 exposure is negligible.

Adult↗
PubMed1994

Bronchial response to breathing dry gas at 3.7 MPa ambient pressure.

In diving, pulmonary mechanical function is limited by the increased density of the gas breathed. Breathing cold and dry gas may cause an additional increase in airways resistance. We have measured forced vital capacity, forced expired volume in 1 s (FEV1) and forced midexpiratory flow rate (FEF25%-75%) before and after breathing dry or humid gas at 29-32 degrees C during a standardized exercise intensity on a cycle ergometer at an ambient pressure of 3.7 MPa. The atmosphere was a helium and oxygen mixture with a density of 6.8 kg.m-3. Six professional saturation divers aged 26-37 years participated in the study. There were no significant differences in convective respiratory heat loss between the exposures. The mean evaporative heat loss was 67 W (range 59-89) breathing dry gas and 37 W (range 32-43) breathing humid gas, corresponding to water losses of 1.7 g.min-1 (range 1.5-2.2) and 0.9 g.min-1 (range 0.8-1.1), respectively. There was a significant reduction in FEV1 of 4.6 (SD 3.6)% (P < 0.05), and in FEF25%-75% of 5.8 (SD 4.7)% (P < 0.05) after breathing dry gas. There were no changes after breathing humid gas. By warming and humidifying the gas breathed in deep saturation diving bronchoconstriction may be prevented.

Adult↗
PubMed1994

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↗
PubMed1993

Contribution of hyperoxia to reduced pulmonary function after deep saturation dives.

Pulmonary function was measured before and after a 28-day saturation dive to a pressure of 0.25 MPa in eight subjects. PO2 was 40 kPa, with periods of 75 kPa for 2 h every 2nd day during the first 14 days, 50 kPa for the next 12 days, and a gradual fall to 21 kPa over the last 2 days in decompression. A 28-day saturation dive with six subjects to a pressure of 0.15 MPa and a PO2 of 21 kPa was used as control. The measurements included static and dynamic lung volumes and flows, transfer factor for carbon monoxide (TLCO), and a cycle ergometer exercise test. There was a significant reduction in TLCO of 9.8 +/- 6.0% (P < 0.001) after the dive when values were corrected for hemoglobin concentration changes. Effective alveolar volume was unchanged. There was a reduction in forced midexpiratory flow rate of 9.8 +/- 7.0% (P < 0.01), but forced vital capacity and forced expired volume in 1 s were unchanged. Peak oxygen uptake was reduced by 10.1 +/- 5.3% (P < 0.001). There were no significant changes in any of the lung function variables after the control dive. Exposure to raised PO2 contributes significantly to the changes in pulmonary function that have been reported after deep saturation dives to pressures of 3.1-4.6 MPa with a similar profile of oxygen exposure. TLCO is apparently a more sensitive index than vital capacity for oxygen toxicity.

Adult↗
PubMed1993

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↗
PubMed1992

Respiratory effects of warm and dry air at increased ambient pressure.

We have measured in 7 divers forced vital capacity (FVC), forced expired volume in 1 s (FEV1), and forced midexpiratory flow rate (FEF25-75%) before and after exposure to dry or humid breathing gas of 35.3 degrees-36.8 degrees C (air) when diving to pressures of 117-600 kPa. The response was compared with the subjects' reactivity to pharmacologic bronchoprovocation with methacholine. Baseline FEV1 and FEF25-75% decreased in accordance with increasing gas density. Relative to baseline, there was a significant reduction after the dives in FEV1 of 4.0 +/- 6.1% (P less than 0.05) and in FEF25-75% of 8.6 +/- 9.7% (P less than 0.01) with exposure to dry breathing gas. By analysis of variance the reduction in the lung function variables below baseline were related to the breathing gas characteristic (dry/humid) (P less than 0.01), bronchial hyperreactivity (P less than 0.02), and ambient pressure (P less than 0.02) independently of each other. There was no significant change in FVC after the exposures. Humid breathing gas was considered more comfortable than dry breathing gas, and the upper comfort limit for breathing gas temperature was higher with humid breathing gas. Convective respiratory heat loss was negligible in these experiments, indicating that dry gas itself had a significant bronchoconstrictive effect. Bronchial hyperreactivity may cause increased risk of development of bronchial obstruction and air trapping during diving.

Adult↗
PubMed1991

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↗
PubMed1990

Pulmonary mechanical function and diffusion capacity after deep saturation dives.

To assess the effects of deep saturation dives on pulmonary function, static and dynamic lung volumes, transfer factor for carbon monoxide (T1CO), delta-N2, and closing volume (CV) were measured before and after eight saturation dives to pressures of 3.1-4.6 MPa. The atmospheres were helium-oxygen mixtures with partial pressures of oxygen of 40-60 kPa. The durations of the dives were 14-30 days. Mean rate of decompression was 10.5-13.5 kPa/hour. A total of 43 divers were examined, six of whom took part in two dives, the others in one only. Dynamic lung volumes did not change significantly but total lung capacity (TLC) increased significantly by 4.3% and residual volume (RV) by 14.8% (p less than 0.05). CV was increased by 16.7% (p less than 0.01). The T1CO was reduced from 13.0 +/- 1.6 to 11.8 +/- 1.7 mmol/min/kPa (p less than 0.01) when corrected to a haemoglobin concentration of 146 g/l. Effective alveolar volume was unchanged. The increase in TLC and decrease in T1CO were correlated (r = -0.574, p less than 0.02). A control examination of 38 of the divers four to six weeks after the dives showed a partial normalisation of the changes. The increase in TLC, RV, and CV, and the decrease in T1CO, could be explained by a loss of pulmonary elastic tissue caused by inflammatory reactions induced by oxygen toxicity or venous gas emboli.

Adult↗
PubMed1990

Divers' lung function: small airways disease?

Pulmonary function was measured in 152 professional saturation divers and in a matched control group of 106 subjects. Static lung volumes, dynamic lung volumes and flows, transfer factor for carbon monoxide (T1CO), transfer volume per unit alveolar volume (KCO), delta-N2, and closing volume (CV) were measured and compared with reference values from recent Scandinavian studies, British submariners, and the European Community for Coal and Steel (ECCS) recommended reference values. Diving exposure was assessed as years of diving experience, total number of days in saturation and depth, and as the product of days in saturation and mean depth. Divers had significantly lower values for forced expired volume in one second (FEV1), FEV1/forced vital capacity (FVC) ratio, FEF25-75%, FEF75-85%, FEF50%, FEF75%, T1CO, and KCO compared with the controls and a significantly higher CV. There was a positive correlation between diving exposure and CV, whereas the other variables had negative correlations with diving exposure. Values for the control group were not different from the predictive values of Scandinavian reference studies or British submariners, although the ECCS standard predicted significantly lower values for the lung function variables both in divers and the control group. The pattern of the differences in lung function variables between the divers and controls is consistent with small airways dysfunction and with the transient changes in lung function found immediately after a single saturation dive. The association between reduced pulmonary function and previous diving exposure further indicates the presence of cumulative long term effects of diving on pulmonary function.

Adult↗
PubMed1990

Exercise tolerance and pulmonary gas exchange after deep saturation dives.

Pulmonary function and exercise tolerance were measured before and after three saturation dives to a pressure of 3.7 MPa. The atmospheres were heliox with partial pressures of oxygen of 40 kPa during the bottom phase and 50 kPa during the compression and decompression phase. The bottom times were 3, 10, and 13 days. Decompression time was 13 days. Precordial Doppler monitoring was done daily during the decompression, and an estimate of the total bubble load on the pulmonary circulation was calculated as the accumulated sum of bubble scores recorded for each diver. Nine of the 18 divers had chest symptoms with retrosternal discomfort or nonproductive cough after the dive. There were no changes in dynamic lung volumes. Transfer factor for carbon monoxide was significantly reduced from 12.3 +/- 1.2 to 10.9 +/- 1.3 mmol.kPa-1.min-1 (P less than 0.01), and maximum oxygen uptake was reduced from 3.98 +/- 0.36 to 3.42 +/- 0.37 l/min STPD (P less than 0.01) after the dives. Resting heart rate was increased from 64 +/- 6 to 75 +/- 8 min-1 (P less than 0.01). The ventilatory requirements in relation to oxygen uptake and carbon dioxide elimination were significantly increased (P less than 0.01) after the dives. The physiological dead space fraction of tidal volume was significantly higher and showed an increase with larger tidal volumes (P less than 0.05). Anaerobic threshold estimated from gas exchange data decreased from an oxygen uptake of 2.30 +/- 0.25 to 1.95 +/- 0.28 l/min STPD (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Improved cardiac performance by salbutamol, a selective beta 2-agonist, in chronic cor pulmonale.

The effects of salbutamol, a relative specific beta 2-agonist, on hemodynamics and arterial blood oxygenation, were studied in 12 patients with chronic cor pulmonale. The studies were done during heart catheterization at rest (n = 12) and during arm bicycle exercise (n = 7) before and during salbutamol infusion of 0.2 microgram/kg/min. At rest, salbutamol significantly increased cardiac index on average by 31%, stroke volume index by 11%, and heart rate by 12 beats/min. Mean pulmonary artery pressure was not changed by salbutamol, whereas a small reduction in mean arterial pressure was observed. The vascular resistance was reduced by 15% in pulmonary and 24% in systemic circulation. Similar hemodynamic changes by salbutamol were observed during exercise. Arterial oxygen tension and saturation were not changed by salbutamol, but a significant rise in mixed venous oxygen saturation and oxygen delivery were observed both at rest and during exercise. Thus, salbutamol infusion improves the cardiac performance in patients with chronic cor pulmonale through a chronotropic effect combined with vasodilation in both the systemic and pulmonary circulation and thereby increased stroke volume. No deleterious effects on arterial blood oxygenation by salbutamol infusion were observed.

Aged↗
PubMedDate not supplied

Electroencephalography and magnetic resonance imaging in neurological decompression sickness.

The purpose of this study was to evaluate the use of electroencephalography (EEG) and magnetic resonance imaging (MRI) in the clinical evaluation of acute decompression sickness (DCS) in the central nervous system (CNS). Twenty-one patients treated because of acute DCS in the CNS during 1999-2001 were included, 15 patients with clinical cerebral DCS and five with clinical spinal cord DCS. Seven patients had abnormalities in their EEG, five with cerebral DCS and two with spinal cord DCS. MRI showed high intensity lesions in the spinal cord in four patients with clinical spinal cord DCS and in one with clinical cerebral DCS. Cerebral lesions were not identified by MRI in any patient. In conclusion, EEG showed unspecific abnormalities in only one third of the cases. Conventional MRI with a 1.5 T scanner may be of help in the diagnosis of DCS in the spinal cord, but not in the brain. EEG and MRI have low sensitivity in the diagnosis of acute DCS in the CNS. Recompression treatment of DCS should still be guided by clinical neurological examination and assessment of symptoms.

Adolescent↗
PubMedDate not supplied

Post-exercise reduction in diffusing capacity of the lung after moderate intensity running and swimming.

A reduction in transfer factor of the lung for carbon monoxide (Tl(co)) is a consistent finding after saturation dives and is reported after some open sea air dives. Several diving associated factors may contribute to this reduction in Tl(co) including hyperoxia, venous gas microembolism, increased breathing resistance and immersion. Exercise, which inevitably is associated with open sea diving, may itself cause a reduction in Tl(co) up to at least 12 hours post-exercise. Six trained swimmers and six trained runners who had never dived performed 30 min moderate intensity swimming and running on different days and in random order at approximately 75% of their maximal heart rate. Lung function including a flow-volume loop and Tl(co) was measured 30 min before and 60-90 min after exercise. There were no significant changes in dynamic lung volumes or maximal expiratory flow rates, but there was a reduction in Tl(co) of 4.5 (SD = 4.8) and 4.7 (SD = 4.6) % after swimming and running respectively (p < 0.01). There was no difference in this response between runners and swimmers, and the response was not associated with lung size. Even moderate exercise preceding measurements of Tl(co) should generally be accounted for, and this effect may contribute significantly to lung function changes immediately after open sea dives.

Adult↗