Mikael Gennser

Immersion deaths and deterioration in swimming performance in cold water

BACKGROUND General hypothermia (deep body temperature <35 degrees C) has been implicated in immersion-related deaths, but many deaths occur too quickly for it to be involved. We investigated changes in swimming capability in cold water to find out whether such changes could lead to swim failure and drowning. METHODS Ten volunteers undertook three self-paced breaststroke swims in a variable-speed swimming flume, in water at 25 degrees C, 18 degrees C, and 10 degrees C, for a maximum of 90 min. During each swim, we measured oxygen consumption, rectal temperature, swim speed and angle, and stroke rate and length. Swim failure was defined as being unable to keep feet off the bottom of the flume. FINDINGS All ten swimmers completed 90 min swims at 25 degrees C, eight completed swims at 18 degrees C, and five at 10 degrees C. In 10 degrees C water, one swimmer reached swim failure after 61 min and four were withdrawn before 90 min with rectal temperatures of 35 degrees C when they were close to swim failure. Swimming efficiency and length of stroke decreased more and rate of stroke and swim angle increased more in 10 degrees C water than in warmer water. These variables seemed to characterise impending swim failure. INTERPRETATION Impaired performance and initial cardiorespiratory responses to immersion probably represent the major dangers to immersion victims. Consequently, treatment should be aimed at symptoms resulting from near-drowning rather than severe hypothermia.

Pulmonary edema and hemoptysis after breath-hold diving at residual volume

To simulate pressure effects and experience thoracic compression while breath-hold diving in a relatively safe environment, competitive breath-hold divers exhale to residual volume before diving in a swimming pool, thus compressing the chest even at depth of only 3-6 m. The study was undertaken to investigate whether such diving could cause pulmonary edema and hemoptysis. Eleven volunteer breath-hold divers who regularly dive on full exhalation performed repeated dives to 6 m during a 20-min period. The subjects were studied with dynamic spirometry, video-fibernasolaryngoscopy, and single-breath diffusion capacity of carbon monoxide (Dl(CO)). The duration of dives with empty lungs ranged from 30 to 120 s. Postdiving forced vital capacity (FVC) was reduced from mean (SD) 6.57 +/- 0.88 to 6.23 +/- 1.02 liters (P < 0.05), and forced expiratory volume during the first second (FEV(1.0)) was reduced from 5.09 +/- 0.64 to 4.59 +/- 0.72 liters (P < 0.001) (n = 11). FEV(1.0)/FVC was 0.78 +/- 0.05 prediving and 0.74 +/- 0.05 postdiving (P < 0.001) (n = 11). All subjects reported a (reversible) change in their voice after diving, irritation, and slight congestion in the larynx. Fresh blood that originated from somewhere below the vocal cords was found by laryngoscopy in two subjects. Dl(CO)/alveolar ventilation (Va) was 1.56 +/- 0.17 mmol.kPa(-1).min(-1).l(-1) before diving. After diving, the Dl(CO)/Va increased to 1.72 +/- 0.24 (P = 0.001), but 20 min later it was indistinguishable from the predive value: 1.57 +/- 0.20 (n = 11). Breath-hold diving with empty lungs to shallow depths can induce hemoptysis in healthy subjects. Edema was possibly present in the lower airways, as suggested by reduced dynamic spirometry.

Motion sickness potentiates core cooling during immersion in humans.

1 The present study tested the hypothesis that motion sickness affects thermoregulatory responses to cooling in humans. 2 Ten healthy male volunteers underwent three separate head‐out immersions in 28 °C water after different preparatory procedures. In the ‘control’ procedure immersion was preceded by a rest period. In the ‘motion sickness’ procedure immersion was preceded by provocation of motion sickness in a human centrifuge. This comprised rapid and repeated alterations of the gravitational (G‐) stress in the head‐to‐foot direction, plus a standardized regimen of head movements at increased G‐stress. In the ‘G‐control’ procedure, the subjects were exposed to similar G‐stress, but without the motion sickness provocation. 3 During immersion mean skin temperature, rectal temperature, the difference in temperature between the forearm and 3rd digit of the right hand (ΔTforearm‐fingertip), oxygen uptake and heart rate were recorded. Subjects provided ratings of temperature perception, thermal comfort and level of motion sickness discomfort at regular intervals. 4 No differences were observed in any of the variables between control and G‐control procedures. In the motion sickness procedure, the ΔTforearm‐fingertip response was significantly attenuated, indicating a blunted vasoconstrictor response, and rectal temperature decreased at a faster rate. No other differences were observed. 5 Motion sickness attenuates the vasoconstrictor response to skin and core cooling, thereby enhancing heat loss and the magnitude of the fall in deep body temperature. Motion sickness may predispose individuals to hypothermia, and have significant implications for survival time in maritime accidents.

Venous gas emboli and exhaled nitric oxide with simulated and actual extravehicular activity

The decompression experienced due to the change in pressure from a space vehicle (1013hPa) to that in a suit for extravehicular activity (EVA) (386hPa) was simulated using a hypobaric chamber. Previous ground-based research has indicated around a 50% occurrence of both venous gas emboli (VGE) and symptoms of decompression illness (DCI) after similar decompressions. In contrast, no DCI symptoms have been reported from past or current space activities. Twenty subjects were studied using Doppler ultrasound to detect any VGE during decompression to 386hPa, where they remained for up to 6h. Subjects were supine to simulate weightlessness. A large number of VGE were found in one subject at rest, who had a recent arm fracture; a small number of VGE were found in another subject during provocation with calf contractions. No changes in exhaled nitric oxide were found that can be related to either simulated EVA or actual EVA (studied in a parallel study on four cosmonauts). We conclude that weightlessness appears to be protective against DCI and that exhaled NO is not likely to be useful to monitor VGE.

Pre-dive exercise and post-dive evolution of venous gas emboli.

BACKGROUND Recent studies have indicated that exercise before diving significantly reduces the number of circulating bubbles and the risk of decompression sickness. However, the most effective time delay between exercise and dive is not clear; the present aim was to resolve this. METHODS In a hyperbaric chamber, 10 men were compressed to 18 m for 100 min, then decompressed as per Royal Navy Table 11. Each subject performed three dives: a control dive and two after exercise performed either 24 h or 2 h before diving. Exercise consisted of 40 min submaximal work on a cycle ergometer. Venous gas emboli (VGE) were evaluated using precordial Doppler ultrasound immediately on surfacing, with measurements made at 5-min intervals for 30 min, and at 15-min intervals for at least 2.5 h total using the Kisman Masurel (KM) scale. RESULTS Exercise either 24 or 2 h prior to a dive did not reduce the median number of circulating VGE (median maximum KM grade: control, 2+; for both exercise dives, 3). Bubbles disappeared from the circulation faster after the control dive than the exercise dives. Time to median KM Doppler scores of zero were: control:120 min; 2-h group: 225 min; 24-h group: 165 min. CONCLUSION Cycling exercise prior to diving did not reduce the number of circulating VGE in comparison to control, in contrast to recent studies. A number of factors may be responsible for these findings, including type of exercise performed, wet diving experience, and disparity in Doppler measurement techniques.

Magnetic Resonance Imaging and Neuropathology Findings in the Goat Nervous System following Hyperbaric Exposures

Divers may be at risk of long-term CNS damage from non-symptomatic hyperbaric exposure. We investigated the effect of severe, controlled hyperbaric exposure on a group of healthy goats with similar histories. Thirty goats were exposed to various dive profiles over a period of 5 years, with 17 experiencing decompression sickness (DCS). Brains were scanned using magnetic resonance (MR) imaging techniques. The animals were then culled and grossly examined, with the brain and spinal cord sent for neuropathological examination. No significant correlation was found between age, years diving, DCS or exposure to pressure with MR-detectable lesions in the brain, or with neuropathological lesions in the brain or spinal cord. However, spinal scarring was noted in 3 animals that had suffered from spinal DCS.

Effects of hyperbaric pressure and temperature on atria from ectotherm animals (Rana pipiens and Anguilla anguilla)

1. Spontaneously beating atria from frogs (R. pipiens) and eels (A. anguilla) were compressed hydraulically to 10 MPa. Effects on beating frequency and twitch tension were studied. 2. At low temperatures (8-10 degrees C) compression to 10 MPa caused a slowing of the beat frequency. No effects were noted at higher temperatures (16-24 degrees C). Twitch tension was decreased by pressure at low temperatures and increased at high temperatures. 3. Differences were noted between preparations from cold and warm acclimatized frogs, and from silver and yellow eels, respectively. 4. The effect of temperature acclimatization on pressure and temperature sensitivity is discussed in relation to data on cardiac phospholipid fatty acid composition.

Superior vestibular dysfunction in severe decompression sickness suggests an embolic mechanism

BACKGROUND Both nitrogen bubble embolism and the difficulty of inner ear tissues to wash out nitrogen have been discussed as possible reasons for the selective vulnerability of the inner ear to decompression illness. This case report suggests that nitrogen bubble embolism plays a crucial role in the pathogenesis of inner ear lesions in decompression accidents. CASE REPORT The current patient, a 48-yr-old male dive master, suffered a severe decompression illness with vertigo as the only residual symptom. At the 1-mo follow-up, neuro-otological evaluation revealed a selective lesion of the superior vestibular division of the left labyrinth with normal functioning inferior vestibular division. At vestibular testing, there was no caloric response from the affected left ear, and the head impulse tests for the lateral and anterior semicircular canal were also impaired. Tests of vestibular evoked myogenic potentials (VEMP) showed divergent results. Ocular VEMP in response to left ear stimulation were absent, whereas the cervical VEMP were completely symmetrical and normal. Thus, the lesion profile implies a partial vestibular loss selectively affecting the superior vestibular division of the inner ear. DISCUSSION The most likely explanation for such a selective injury seems to be bubble microembolism coupled with both the specific anatomy of this terminally supplied subunit, and with the slow nitrogen wash-out of the vestibular organ.

Indices of Increased Decompression Stress Following Long-Term Bed Rest

Human extravehicular activity (EVA) is essential to space exploration and involves risk of decompression sickness (DCS). On Earth, the effect of microgravity on physiological systems is simulated in an experimental model where subjects are confined to a 6° head-down bed rest (HDBR). This model was used to investigate various resting and exercise regimen on the formation of venous gas emboli (VGE), an indicator of decompression stress, post-hyperbaric exposure. Eight healthy male subjects participating in a bed rest regimen also took part in this study, which incorporated five different hyperbaric exposure (HE) interventions made before, during and after the HDBR. Interventions i–iv were all made with the subjects lying in 6° HD position. They included (C1) resting control, (C2) knee-bend exercise immediately prior to HE, (T1) HE during the fifth week of the 35-day HDBR period, (C3) supine cycling exercise during the HE. In intervention (C4), subjects remained upright and ambulatory. The HE protocol followed the Royal Navy Table 11 with 100 min spent at 18 m (280 kPa), with decompression stops at 6 m for 5 min, and at 3 m for 15 min. Post-HE, regular precordial Doppler audio measurements were made to evaluate any VGE produced post-dive. VGE were graded according to the Kisman Masurel scale. The number of bubbles produced was low in comparison to previous studies using this profile [Kisman integrated severity score (KISS) ranging from 0–1], and may be because subjects were young, and lay supine during both the HE and the 2 h measurement period post-HE for interventions i–iv. However, the HE during the end of HDBR produced significantly higher maximum bubble grades and KISS score than the supine control conditions (p < 0.01). In contrast to the protective effect of pre-dive exercise on bubble production, a prolonged period of bed rest prior to a HE appears to promote the formation of post-decompression VGE. This is in contrast to the absence of DCS observed during EVA. Whether this is due to a difference between hypo- and hyperbaric decompression stress, or that the HDBR model is a not a good model for decompression sensitivity during microgravity conditions will have to be elucidated in future studies.

Measuring Uptake and Elimination of Nitrogen in Humans at Different Ambient Pressures

BACKGROUND To measure nitrogen (N2) wash-out and uptake requires elaborate set-ups, especially when doing the measurements at increased or decreased ambient pressure. Here we present a transportable device for quantifying N2 turnover in humans which can be used at different ambient pressures. METHODS A modified close-circuit electronic rebreather was used to assess N2 turnover. Changes in N2 volume within the rebreathing circuit, reflecting N2 uptake or washout, were derived from the continuously monitored total system volume and the calculated volumes of oxygen and water vapor. The calculation of continuous N2 volume curves was performed off-line using dedicated computer software. RESULTS Four subjects participated in the proof-of-concept tests. At steady state, the drift in calculated N2 volume in the rebreathing circuit over a 1-h duration was minimal. Three of the subjects participated in additional N2 steady-state measurements where 1019 mL (BTPD) of N2 was injected into the rebreathing circuit over 20 min and the measured volume increase was 1006 ± 32 mL. Lastly, N2 elimination was assessed during decompression to 0.5 atm and while breathing hyperoxic gas. N2 uptake was measured during compression to 1.8 atm. The elimination and uptake curves were deemed to be realistic. DISCUSSION A method for assessing N2 turnover in humans has been developed and a first evaluation has been performed. It is easy to work with operationally and can be used at different ambient pressures. More research is needed in order to further validate it as a method for assessing N2 turnover in humans.Sundblad P, Frånberg O, Siebenmann C, Gennser M. Measuring uptake and elimination of nitrogen in humans at different ambient pressures. Aerosp Med Hum Perform. 2016; 87(12):1045-1050.