Early Human Pathophysiological Responses to Exertional Hypobaric Decompression Stress.

INTRODUCTION: Consistent blood biomarkers of hypobaric (altitude) decompression stress remain elusive. Recent laboratory investigation of decompression sickness risk at 25,000 ft (7620 m) enabled evaluation of early pathophysiological responses to exertional decompression stress.METHODS: In this study, 15 healthy men, aged 20-50 yr, undertook 2 consecutive (same-day) ascents to 25,000 ft (7620 m) for 60 and 90 min, breathing 100% oxygen, each following 1 h of prior denitrogenation. Venous blood was sampled at baseline (T0), immediately after the second ascent (T8), and next morning (T24). Analyses encompassed whole blood hematology, endothelial microparticles, and soluble markers of cytokine response, endothelial function, inflammation, coagulopathy, oxidative stress, and brain insult, plus cortisol and creatine kinase.RESULTS: Acute hematological effects on neutrophils (mean 72% increase), eosinophils (40% decrease), monocytes (37% increase), and platelets (7% increase) normalized by T24. Consistent elevation (mean five-fold) of the cytokine interleukin-6 (IL-6) at T8 was proinflammatory and associated with venous gas emboli (microbubble) load. Levels of C-reactive protein and complement peptide C5a were persistently elevated at T24, the former by 100% over baseline. Additionally, glial fibrillary acidic protein, a sensitive marker of traumatic brain injury, increased by a mean 10% at T24.CONCLUSIONS: This complex composite environmental stress, comprising the triad of hyperoxia, decompression, and moderate exertion at altitude, provoked pathophysiological changes consistent with an IL-6 cytokine-mediated inflammatory response. Multiple persistent biomarker disturbances at T24 imply incomplete recovery the day after exposure. The elevation of glial fibrillary acidic protein similarly implies incomplete resolution following recent neurological insult.Connolly DM, Madden LA, Edwards VC, D'Oyly TJ, Harridge SDR, Smith TG, Lee VM. Early human pathophysiological responses to exertional hypobaric decompression stress. Aerosp Med Hum Perform. 2023; 94(10):738-749.

Decompression Sickness Risk in Parachutist Dispatchers Exposed Repeatedly to High Altitude.

INTRODUCTION: Occurrences of severe decompression sickness (DCS) in military parachutist dispatchers at 25,000 ft (7620 m) prompted revision of exposure guidelines for high altitude parachuting. This study investigated residual risks to dispatchers and explored the potential for safely conducting repeat exposures in a single duty period.METHODS: In this study, 15 healthy men, ages 20-50 yr, undertook 2 profiles of repeated hypobaric chamber decompression conducting activities representative of dispatcher duties. Phase 1 comprised two ascents to 25,000 ft (7620 m) for 60 and then 90 min. Phase 2 included three ascents first to 25,000 ft for 60 min, followed by two ascents to 22,000 ft (6706 m) for 90 min. Denitrogenation was undertaken at 15,000 ft (4572 m) with successive ascents separated by 1-h air breaks at ground level.RESULTS: At 25,000 ft (7620 m), five cases of limb (knee) pain DCS developed, the earliest at 29 min. Additionally, multiple minor knee "niggles" occurred with activity but disappeared when seated at rest. No DCS and few niggles occurred at 22,000 ft (6706 m). Early, heavy, and sustained bubble loads were common at 25,000 ft, particularly in older subjects, but lighter and later loads followed repeat exposure, especially at 22,000 ft.DISCUSSION: Parachutist dispatchers are at high risk of DCS at 25,000 ft (7620 m) commensurate with their heavy level of exertion. However, the potential exists for repeated safe ascents to 22,000 ft (6706 m), in the same duty period, if turn-around times breathing air at ground level are brief. Older dispatchers (>40 yr) with functional right-to-left (intracardiac or pulmonary) vascular shunts will be at risk of arterialization of microbubbles.Connolly DM, D'Oyly TJ, Harridge SDR, Smith TG, Lee VM. Decompression sickness risk in parachutist dispatchers exposed repeatedly to high altitude. Aerosp Med Hum Perform. 2023; 94(9):666-677.

Lung volumes, pulmonary ventilation, and hypoxia following rapid decompression to 60,000 ft (18,288 m).

INTRODUCTION: Rapid decompressions (RD) to 60,000 ft (18,288 m) were undertaken by six subjects to provide evidence of satisfactory performance of a contemporary, partial pressure assembly life support system for the purposes of flight clearance. METHODS: A total of 12 3-s RDs were conducted with subjects breathing 56% oxygen (balance nitrogen) at the base (simulated cabin) altitude of 22,500 ft (6858 m), switching to 100% oxygen under 72 mmHg (9.6 kPa) of positive pressure at the final (simulated aircraft) altitude. Respiratory pressures, flows, and gas compositions were monitored continuously throughout. RESULTS: All RDs were completed safely, but one subject experienced significant hypoxia during the minute at final altitude, associated with severe hemoglobin desaturation to a low of 53%. Accurate data on subjects' lung volumes were obtained and individual responses post-RD were reviewed in relation to patterns of pulmonary ventilation. The occurrence of severe hypoxia is explained by hypoventilation in conjunction with unusually large lung volumes (total lung capacity 10.18 L). CONCLUSIONS: Subjects' lung volumes and patterns of pulmonary ventilation are critical, but idiosyncratic, determinants of alveolar oxygenation and severity of hypoxia following RD to 60,000 ft (18,288 m). At such extreme altitudes even vaporization of water condensate in the oxygen mask may compromise oxygen delivery. An altitude ceiling of 60,000 ft (18,288 m) is the likely threshold for reliable protection using partial pressure assemblies and aircrew should be instructed to take two deep 'clearing' breaths immediately following RD at such extreme pressure breathing altitudes.

Decompression sickness risk at 6553 m breathing two gas mixtures.

INTRODUCTION: The risk of severe decompression sickness (DCS) increases rapidly above 6248 m (20,500 ft) and is greater when breathing higher proportions of inert gas. Contemporary aircrew may be exposed to higher cabin altitudes while breathing molecular sieve oxygen concentrator (MSOC) product gas containing variable concentrations of oxygen, nitrogen, and argon. This study assessed the risk of DCS at 6553 m (21,500 ft) breathing two simulated MSOC product gas mixtures. METHODS: In a hypobaric chamber, 10 subjects each undertook 2 4-h exposures at 6553 m breathing either 75% O2:21% N2:4% Ar or 56% 02:42% N2:2% Ar. Subjects undertook regular activities simulating in-flight movements of fast jet aircrew. Venous gas emboli (VGE) "bubble" load was graded every 15 min using 2D and Doppler echocardiography by experienced operators blinded to breathing gas composition. RESULTS: DCS occurred in five exposures (25%), the earliest after less than 90 min at altitude. All were minor, single-site, uncomplicated limb bends that resolved with recompression. VGE occurred in 85% of exposures with some early-onset, heavy loads. Survival (Probit) analysis indicated that breathing 56% oxygen significantly decreased VGE latency relative to breathing 75% oxygen (relative potency 3.05). CONCLUSIONS: From 20 experimental exposures, the risk of DCS at 6553 m is estimated at 5% by 90 min and 20% at 3 h. Exploiting the negative predictive value of VGE latency as a surrogate measure of protection from DCS, at high cabin altitudes better MSOC performance (higher product gas oxygen concentrations) will protect more aircrew for longer.