Components of aircraft life support systems interact with each other and the user.

The life support system in a tactical aircraft provides necessary supplemental oxygen to the aircrew. However, interactions among its various components may generate unexpected breathing loads. We focus here on the interactions between a regulator and breathing mask commonly used together in the U.S. Navy, the CRU-103 regulator and MBU 23/P mask, and some effects of the interactions on the user. The data reported were collected during a larger research effort examining potential physiological and cognitive effects of low regulator inlet pressures. Seventeen participants completed a series of tasks under mild exercise while breathing 40% O2 (balance N2) from an MBU-23/P mask supplied by a CRU-103 regulator with supply pressures 10, 6, 4, and 2 psig (CRU-103 specifications are for inlet pressures from 5 to 120 psig). Variables measured included flow to the mask and pressures at the regulator supply, in the hose to the mask, and in the mask. In addition to restricting inspiratory flow, low inlet pressure to the CRU-103 caused a counterintuitive overshoot in gas delivery pressure at end-inspiration, a mean increase of 1.5 cm H2O between the 10- and 2 psig conditions. The added pressure to the exhalation valve increased the expiratory threshold, the pressure to start expiratory flow, by approximately 2 cm H2O, increasing the effort needed to exhale.

Transcutaneous and End-Tidal CO2 Measurements in Hypoxia and Hyperoxia.

BACKGROUND: Transcutaneous measurement of carbon dioxide (CO2) has been proposed for physiological monitoring of tactical jet aircrew because in some clinical settings it mirrors arterial CO2 partial pressure (Paco2). End-tidal monitoring in laboratory settings is known to give high-fidelity estimates of Paco2.METHODS: The correspondence between end-tidal (PETco2) and transcutaneous Pco2 (tcPco2) was examined in healthy volunteers under laboratory conditions of hyperoxia and hypoxia. Rest and exercise, skin heating and cooling, hyperventilation, and induced CO2 retention were employed.RESULTS: Neither measure followed all known changes in Paco2 and tcPco2 changed when the skin temperature near the probe changed. Bland-Altman analysis showed significant nonzero slopes under most conditions. Regression analysis indicated that oxygen partial pressure (Po2) in tissue measured as transcutaneous Po2 (tcPo2) is an important explanatory variable for tcPco2 in addition to PETco2, and that local skin temperature also has an effect. Additionally, absorption atelectasis from breathing 100% O2 may cause PETco2 to deviate from Paco2.DISCUSSION: Even as a trend indicator for Paco2, tcPco2 is not useful under conditions that resemble those in the highly dynamic tactical jet aircraft environment. PETco2 is also not a good indicator of CO2 status in pilots who breathe nearly 100% O2.Shykoff BE, Lee LR, Gallo M, Griswold CA. Transcutaneous and end-tidal CO2 measurements in hypoxia and hyperoxia. Aerosp Med Hum Perform. 2021; 92(11):864-872.

Risks from Breathing Elevated Oxygen.

INTRODUCTION: Effects of breathing gas with elevated oxygen partial pressure (Po2) and/or elevated inspired oxygen fraction (FIo2) at sea level or higher is discussed. High FIo2 is associated with absorption problems in the lungs, middle ear, and paranasal sinuses, particularly if FIo2 > 80% and small airways, Eustachian tubes, or sinus passages are blocked. Absorption becomes faster as cabin altitude increases. Pulmonary oxygen toxicity and direct oxidative injuries, related to elevated Po2, are improbable in flight; no pulmonary oxygen toxicity has been found when Po2 < 55 kPa [418 Torr; 100% O2 higher than 15,000 ft (4570 m)]. Symptoms with Po2 of 75 kPa [520 Torr; 100% O2 at 10,000 ft (3050 m)] were reported after 24 h and the earliest signs at Po2 of 100 kPa (760 Torr, 100% O2 at sea level) occurred after 6 h. However, treatment for decompression sickness entails a risk of pulmonary oxygen toxicity. Elevated Po2 also constricts blood vessels, changes blood pressure control, and reduces the response to low blood sugar. With healthy lungs, gas transport and oxygen delivery are not improved by increasing Po2. Near zero humidity of the breathing gas in which oxygen is delivered may predispose susceptible individuals to bronchoconstriction.Shykoff BE, Lee RL. Risks from breathing elevated oxygen. Aerosp Med Hum Perform. 2019; 90(12):1041-1049.

Pulmonary effects of repeated six-hour normoxic and hyperoxic dives.

This study examines differential effects of immersion, elevated oxygen partial pressure, and exercise on pulmonary function after series of five daily six-hour dives at 130 kPa (1.3 ATA), with 18 hours between dives. Five cohorts of 10 to 14 divers participated. The exposure phases were resting while breathing O2 or air in the water ("wetO2", "wetAir") or O2 in the hyperbaric chamber ("dryO2"), and exercise in the water while breathing O2 or air ("wetO2X", "wetAirX"). Respiratory symptoms were recorded during and after each dive, and pulmonary function (forced flow-volume) was measured twice at baseline before diving, after each dive both immediately and on the following morning, and three days post diving ("Day+3"). The incidences of symptoms and of flow volume changes from baseline greater than normal limits ("ΔFV") were assessed, as were mean ΔFV. The parameters examined were forced vital capacity (FVC), forced expired volume in 1 second (FEV1), and forced expired flow from 25% to 75% volume expired (FEF25-75). The phases ranked from greatest to least fraction of diver-days with symptoms were wetO2X (56%) > dryO2 (42%) > wetO2 (13%) > [wetAir (2%) or wetAirX (1%)] (p<0.05). FEV1 and FEF25-75 were depressed in the morning following wetO2 and wetO2X and on Day+3 after and wetO2X, but increased immediately following each wetAirX dive. O2 exposures caused symptoms and ΔFV suggestive of pulmonary oxygen toxicity,exacerbated by exercise. Indices of small airway function showed late (17-hour) post-O2 exposure deficits, but, particularly with exercise, improvement was evident early after exposure with or without O2. FEF25-75 and FEV1 remained depressed on Day+3 after wetO2 and wetO2X.

Effects of prolonged and repeated immersions on heart rate variability and complexity in military divers.

BACKGROUND: The influence of prolonged and repeated water immersions on heart rate variability (HRV) and complexity was examined in 10 U.S. Navy divers who completed six-hour resting dives on five consecutive days. Pre-dive and during-dive measures were recorded daily. METHODS: Dependent variables of interest were average heart rate (HR), time-domain measures of HRV [root mean square of successive differences of the normal RR (NN) interval (RMSSD), standard deviation of the NN interval (SDNN)], frequency-domain measures of HRV [low-frequency power spectral density (psd) (LFpsd), low-frequency normalized (LFnu), high-frequency psd (HFpsd), high-frequency normalized (HFnu), low-frequency/ high-frequency ratio (LF/HF)], and non-linear dynamics of HRV [approximate entropy (ApEn)]. A repeated-measures ANOVA was performed to examine pre-dive measure differences among baseline measures. Hierarchical linear modeling (HLM) was performed to test the effects of prolonged and repeated water immersion on the dependent variables. RESULTS: Pre-dive HR (P=0.005) and RMSSD (P⟨0.001) varied significantly with dive day while changes in SDNN approached significance (P=0.055). HLM indicated that HR decreased during daily dives (P=0.001), but increased across dive days (P=0.011); RMSSD increased during daily dives (P=0.018) but decreased across dive days (P⟨0.001); SDNN increased during daily dives (P⟨0.001); LF measures increased across dive days (LFpsd P⟨0.001; LFnu P⟨0.001), while HF measures decreased across dive days (HFpsd P⟨0.001; HFnu P⟨0.001); LF/HF increased across dive days (P⟨0.001); ApEn decreased during daily dives (P⟨0.02) and across dive days (P⟨0.001). CONCLUSIONS: These data suggest that the cumulative effect of repeated dives across five days results in decreased vagal tone and a less responsive cardiovascular system.

Breathing 100% oxygen during water immersion improves postimmersion cardiovascular responses to orthostatic stress.

Physiological compensation to postural stress is weakened after long-duration water immersion (WI), thus predisposing individuals to orthostatic intolerance. This study was conducted to compare hemodynamic responses to postural stress following exposure to WI alone (Air WI), hyperbaric oxygen alone in a hyperbaric chamber (O2 HC), and WI combined with hyperbaric oxygen (O2 WI), all at a depth of 1.35 ATA, and to determine whether hyperbaric oxygen is protective of orthostatic tolerance. Thirty-two healthy men underwent up to 15 min of 70° head-up tilt (HUT) testing before and after a single 6-h resting exposure to Air WI (N = 10), O2 HC (N = 12), or O2 WI (N = 10). Heart rate (HR), blood pressure (BP), cardiac output (Q), stroke volume (SV), forearm blood flow (FBF), and systemic and forearm vascular resistance (SVR and FVR) were measured. Although all subjects completed HUT before Air WI, three subjects reached presyncope after Air WI exposure at 10.4, 9.4, and 6.9 min. HUT time did not change after O2 WI or O2 HC exposures. Compared to preexposure responses, HR increased (+10 and +17%) and systolic BP (-13 and -8%), and SV (-16 and -23%) decreased during HUT after Air WI and O2 WI, respectively. In contrast, HR and SV did not change, and systolic (+5%) and diastolic BP (+10%) increased after O2 HC Q decreased (-13 and -7%) and SVR increased (+12 and +20%) after O2 WI and O2 HC, respectively, whereas SVR decreased (-9%) after Air WI Opposite patterns were evident following Air WI and O2 HC for FBF (-26 and +52%) and FVR (+28 and -30%). Therefore, breathing hyperbaric oxygen during WI may enhance post-WI cardiovascular compensatory responses to orthostatic stress.

Thermoneutral water immersion and hyperbaric oxygen do not alter cortisol regulation.

Research documenting changes in cortisol concentration following hyperbaric exposures has been contradictory, possibly due to the inclusion of many confounding factors. Therefore, the aim of this study was to document short- and long-term cortisol responses following repeated water immersions arid/or exposure to raised partial pressure of oxygen under controlled conditions. Thirty-two Navy divers (31 ± 7 [19-44] years; mean ± SD) were exposed to one of three resting thermoneutral experimental conditions at a pressure of 1.35 atmospheres absolute (atm abs) for six hours on five consecutive days: (1) breathing air while immersed (air; n = 10); (2) breathing 100% oxygen in a hyperbaric chamber (dry; n = 12); or (3) breathing 100% oxygen while immersed (oxygen; n = 10). Divers were at rest for all conditions. Serum cortisol concentrations were measured one hour before and after each dive. The change in cortisol (ug/dL) after diving was similar for air (3.63 ± 5.56), dry (4.91 ± 3.68) and oxygen (3.50 ± 3.48) phases (p > 0.05). There were no differences in preor post-dive cortisol concentrations across dive days for any of the experimental conditions. This study provides evidence that repeated long-duration, thermoneutral immersions and/or hyperbaric oxygen exposures at 1.35 atm abs, under ideal conditions per se do not abnormally alter cortisol concentrations. Observed changes are likely the result of the natural circadian rhythm of cortisol.

Residual oxygen time model for oxygen partial pressure near 130 kPa (1.3 atm).

A two-part residual oxygen time model predicts the probability of detectible pulmonary oxygen toxicity P(P[O2tox]) after dives with oxygen partial pressure (PO2) approximately 130 kPa, and provides a tool to plan dive series with selected risk of P[O2tox]. Data suggest that pulmonary oxygen injury at this PO2 is additive between dives. Recovery begins after a delay and continues during any following dive. A logistic relation expresses P(P[O2tox]) as a function of dive duration (T(dur)) [hours]: P(P[O2tox]) = 100/[1+exp (3.586-0.49 x T(dur))] This expression maps T(dur) to P(P[O2tox]) or, in the linear mid-portion of the curve, P(P[O2tox]) usefully to T(dur). For multiple dives or during recovery, it maps to an equivalent dive duration, T(eq). T(eq) was found after second dives of duration T(dur 2). Residual time from the first dive t(r) = T(eq) - T(dur2). With known t(r), t and T(dur) a recovery model was fitted. t(r) = T(dur) x exp [-k x((t-5)/T(dur)2], where t = t - 5 hours, k = 0.149 for resting, and 0.047 for exercising divers, and t represents time after surfacing. The fits were assessed for 1,352 man-dives. Standard deviations of the residuals were 8.5% and 18.3% probability for resting or exercise dives, respectively.

Cumulative effects of repeated exposure to pO2 = 200 kPa (2 atm).

Even asymptomatic exposures to elevated oxygen partial pressure (pO2) can influence subsequent exposures. Dry chamber dives of three hours' duration at pO2 of 200 kPa were conducted to examine cumulative effects. Experiments were single (n = 27), or paired exposures with surface intervals (SIs) 15 to 17 hours (n = 30), six hours (n = 33), or three hours (n = 36). Flow-volume loops, diffusing capacity, and symptoms were recorded before and after exposures. Immediately after surfacing from second exposures, some significant (p < 0.05) mean changes from baseline in pulmonary function indices occurred for all SIs and persisted for two days for three-hour SIs and for one day for 15-hour SIs. Incidences of symptoms were 15% immediately after one exposure and 28%, 38% and 31% immediately after a second exposure following 15-, six- , or three-hour SIs, respectively. Incidences of changes in pulmonary function indices (deltaPF) were 5%, 11%, 12% and 14% for single exposures or two with 15-, six-, or three-hour SIs, respectively. Two days following the second exposure, resolution of symptoms was incomplete after six- or 15-hour SIs, as was resolution of deltaPF after 15-hour SIs. The incidences indicate non-linear superposition of effects of a first and second exposure, and are not readily explained by delayed-onset injury.

Cardiovascular and autonomic responses to physiological stressors before and after six hours of water immersion.

The physiological responses to water immersion (WI) are known; however, the responses to stress following WI are poorly characterized. Ten healthy men were exposed to three physiological stressors before and after a 6-h resting WI (32-33°C): 1) a 2-min cold pressor test, 2) a static handgrip test to fatigue at 40% of maximum strength followed by postexercise muscle ischemia in the exercising forearm, and 3) a 15-min 70° head-up-tilt (HUT) test. Heart rate (HR), systolic and diastolic blood pressure (SBP and DBP), cardiac output (Q), limb blood flow (BF), stroke volume (SV), systemic and calf or forearm vascular resistance (SVR and CVR or FVR), baroreflex sensitivity (BRS), and HR variability (HRV) frequency-domain variables [low-frequency (LF), high-frequency (HF), and normalized (n)] were measured. Cold pressor test showed lower HR, SBP, SV, Q, calf BF, LFnHRV, and LF/HFHRV and higher CVR and HFnHRV after than before WI (P < 0.05). Handgrip test showed no effect of WI on maximum strength and endurance and lower HR, SBP, SV, Q, and calf BF and higher SVR and CVR after than before WI (P < 0.05). During postexercise muscle ischemia, HFnHRV increased from baseline after WI only, and LFnHRV was lower after than before WI (P < 0.05). HUT test showed lower SBP, DBP, SV, forearm BF, and BRS and higher HR, FVR, LF/HFHRV, and LFnHRV after than before WI (P < 0.05). The changes suggest differential activation/depression during cold pressor and handgrip (reduced sympathetic/elevated parasympathetic) and HUT (elevated sympathetic/reduced parasympathetic) following 6 h of WI.

Exercise carbon dioxide (CO2) retention with inhaled CO2 and breathing resistance.

Combined effects on respiratory minute ventilation (VE)--and thus, on end-tidal carbon dioxide partial pressure (P(ET)CO2)--of breathing resistance and elevated inspired carbon dioxide (CO2) had not been determined during heavy exercise. In this Institutional Review Board-approved, dry, sea-level study, 12 subjects in each of three phases exercised to exhaustion at 85% peak oxygen uptake while V(E) and P(ET)CO2 were measured. Participants inhaled 0%, 1%, 2% or 3% CO2 in air, or 0% or 2% CO2 in oxygen, with or without breathing resistance, mimicking the U.S. Navy's MK 16 rebreather underwater breathing apparatus (UBA). Compared to air baseline (0% inspired CO2 in air without resistance): (1) Oxygen decreased baseline V(E) (p < 0.01); (2) Inspired CO2 increased V(E) and P(ET)CO2 (p < 0.01); (3) Resistance decreased V(E) (p < 0.01); (4) Inspired CO2 with resistance elevated P(ET)CO2 (p < 0.01). In air, V(E) did not change from that with resistance alone. In oxygen, V(E) returned to oxygen baseline. End-exercise P(ET)CO2 exceeded 60 Torr (8.0 kPa) in three tests. Subjects identified hypercapnia poorly. Results support dual optimization of arterial carbon dioxide partial pressure and respiratory effort. Because elevated CO2 may not increase V(E) if breathing resistance and VE are high, rebreather UBA safety requires very low inspired CO2.

Physiologically acceptable resistance of an air purifying respirator.

Physiologically acceptable limits of inspiratory impediment for air purifying respirators (APRs) were sought.Measurements on 30 subjects included pressure in, and flow through, an APR, and respiratory and cardiovascular variables. Exercise with and without APR included ladder climbing, load lift and transfer, incremental running and endurance running, with endurance at 85% peak oxygen uptake. Resistance that did not alter minute ventilation (VE) was judged acceptable long-term. Acceptable short-term impediments were deduced from end exercise conditions. Proposed long-term limits are inspiratory work of breathing per tidal volume (WOBi/VT) ≤ 0.9 kPa and peak inspiratory pressure (P (i) peak) ≤1.2 kPa. Proposed short-term limits are: for VE ≤110 L min(-1), WOBi/VT ≤1.3 kPa and P (i) peak ≤ 1.8 kPa; and for VE >130 L min(-1), WOBi/VT ≤1.6 kPa. A design relation among VE, pressure­flow coefficients of an APR, and WOBi/VT is proposed. STATEMENT OF RELEVANCE: This work generalises results from one APR by considering the altered physiological parameters related to factors inhibiting exercise. Simple expressions are proposed to connect bench-test parameters to the relation between ventilation and work of breathing. Population-based recommendations recognise that those who need more air flow can also generate higher pressures.

Validity and reliability of diastolic pulse contour analysis (windkessel model) in humans.

The present study assessed (1) the impact of the measurement site (lower versus upper extremity) on the corresponding compliance variables and (2) the overall reliability of diastolic pulse contour (Windkessel-derived) analysis in normal and hypertensive subjects. Arterial tonograms were recorded in the supine position from the radial and posterior tibial arteries in 20 normotensive (116+/-12/68+/-8 mm Hg) and 27 essential hypertensive subjects (160+/-16/94+/-14 mm Hg). Ensemble-averaged data for each subject were fitted to a first-order lumped-parameter model (basic Windkessel) to compute whole-body arterial compliance (C(A)) and to a third-order lumped-parameter model (modified Windkessel) to compute proximal compliance (C(1)) and distal compliance (C(2)). Despite high-fidelity waveforms in each subject, the first-order Windkessel model did not yield interpretable (positive) values for C(A) in 50% of normotensives and 41% of hypertensives, whereas the third-order model failed to yield interpretable C(1) or C(2) results in 15% of normotensives and 41% of hypertensives. No between-site correlations were found for the first-order time constant, 2 of the 3 third-order model curve-fitting constants, or C(A), C(1), or C(2) (P>0.50). Mean values for all 3 compliance variables were higher for the leg than the arm (P<0.05 each). We conclude that differences in Windkessel-derived compliance values in the arm and leg invalidate whole-body model assumptions and suggest a strong influence of regional circulatory properties. The validity and utility of Windkessel-derived variables is further diminished by the absence of between-site correlations and the common occurrence of uninterpretable values in hypertensive subjects.