Segmental Intracellular, Interstitial, and Intravascular Volume Changes during Simulated Hemorrhage and Resuscitation: A Case Study.

This paper describes a new combined impedance plethysmographic (IPG) and electrical bioimpedance spectroscopic (BIS) instrument and software that will allow noninvasive real-time measurement of segmental blood flow, intracellular, interstitial, and intravascular volume changes during various fluid management procedures. The impedance device can be operated either as a fixed frequency IPG for the quantification of segmental blood flow and hemodynamics or as a multi-frequency BIS for the recording of intracellular and extracellular resistances at 40 discrete input frequencies. The extracellular volume is then deconvoluted to obtain its intravascular and interstitial component volumes as functions of elapsed time. The purpose of this paper is to describe this instrumentation and to demonstrate the information that can be obtained by using it to monitor segmental compartment volume responses of a pig model during simulated hemorrhage and resuscitation. Such information may prove valuable in the diagnosis and management of rapid changes in the body fluid balance and various clinical treatments.

Iso-risk air no decompression limits after scoring marginal decompression sickness cases as non-events.

Decompression sickness (DCS) in humans is associated with reductions in ambient pressure that occur during diving, aviation, or certain manned spaceflight operations. Its signs and symptoms can include, but are not limited to, joint pain, radiating abdominal pain, paresthesia, dyspnea, general malaise, cognitive dysfunction, cardiopulmonary dysfunction, and death. Probabilistic models of DCS allow the probability of DCS incidence and time of occurrence during or after a given hyperbaric or hypobaric exposure to be predicted based on how the gas contents or gas bubble volumes vary in hypothetical tissue compartments during the exposure. These models are calibrated using data containing the pressure and respired gas histories of actual exposures, some of which resulted in DCS, some of which did not, and others in which the diagnosis of DCS was not clear. The latter are referred to as marginal DCS cases. In earlier works, a marginal DCS event was typically weighted as 0.1, with a full DCS event being weighted as 1.0, and a non-event being weighted as 0.0. Recent work has shown that marginal DCS events should be weighted as 0.0 when calibrating gas content models. We confirm this indication in the present work by showing that such models have improved performance when calibrated to data with marginal DCS events coded as non-events. Further, we investigate the ramifications of derating marginal events on model-prescribed air diving no-stop limits.

Bioimpedance monitoring of cellular hydration during hemodialysis therapy.

Introduction The aim of this paper is to describe and demonstrate how a new bioimpedance analytical procedure can be used to monitor cellular hydration of End Stage Renal Disease (ESRD) patients during hemodialysis (HD). Methods A tetra-polar bioimpedance spectroscope (BIS), (UFI Inc., Morro Bay, CA), was used to measure the tissue resistance and reactance of the calf of 17 ESRD patients at 40 discrete frequencies once a minute during dialysis treatment. These measurements were then used to derive intracellular, interstitial, and intravascular compartment volume changes during dialysis. Findings The mean (± SD) extracellular resistance increased during dialysis from 92.4 ± 3.5 to 117.7 ± 5.8 Ohms. While the mean intracellular resistance decreased from 413.5 ± 11.7 to 348.5 ± 8.2 Ohms. It was calculated from these data that the mean intravascular volume fell 9.5%; interstitial volume fell 33.4%; and intracellular volume gained 20.3%. Discussion These results suggest that an extensive fluid shift into the cells may take place during HD. The present research may contribute to a better understanding of how factors that influence fluid redistribution may affect an ESRD patient during dialysis. In light of this finding, it is concluded that the rate of vascular refill is jointly determined with the rate of "cellular refill" and the transfer of fluid from the intertitial compartment into the intravascular space.

On diver thermal status and susceptibility to decompression sickness.

In a recent Letter to the Editor, Clarke, et al, indicated that divers who deliberately chill themselves on a dive to reduce risk of decompression sickness (DCS) may be misinterpreting our 2007 Navy Experimental Diving Unit (NEDU) report. Indeed, we did not advocate that divers should risk hypothermia on bottom to reduce risk of DCS, nor do we dispute the authors' overall admonition to avoid diving cold unnecessarily. However, Clarke, et al, imply more generally that results of our study are not applicable to recreational or technical divers because the dives we tested were atypical of dives undertaken by such divers. We wish to clarify that our study does have implications for recreational and technical divers, implications that should not be ignored. The dives we tested were not intended to be typical of dives undertaken in any actual operational context. Instead, we chose to expose divers to temperatures at the extremes of their thermal tolerance in order to ensure that effects of diver thermal status on DCS susceptibility would be found if such effects existed. Our initial test dive profile provided appreciable time both on bottom and during decompression to allow any differential thermal effects during these two dive phases to manifest, while affording a baseline risk of DCS that could be altered by thermal effects without exposing subjects to inordinately high risks of DCS. Our results strongly indicate that the optimal diver thermal conditions for mitigation of DCS risk or minimization of decompression time entail remaining cool during gas uptake phases of a dive and warm during off-gassing phases. While the dose-response characteristics of our observed thermal effects are almost certainly non-linear in both exposure temperature and duration, it is only reasonable to presume that the effects vary monotonically with these factors. We have no reason to presume that such responses and effects under less extreme conditions would be in directions opposite to those found under the conditions we tested. Similarly, responses to thermal exposures even more extreme than we tested might not be larger than the responses we observed, but it would be unwise to ignore the trends in our results under some unfounded presumption that the effects reverse with changes in thermal conditions beyond those tested. Finally, thermal effects on bottom and during decompression in dives to depths other than the 120 feet of sea water (fsw) or 150 fsw depths of the dives we tested are unlikely to be qualitatively different from those observed in our tested dives. The original question has therefore been answered: chill on bottom decreases DCS susceptibility while chill during decompression increases DCS susceptibility. Under conditions encountered by recreational or technical divers, the only open issue is arguably magnitudes of effects, not directions. Neither does lack of technology to control thermal status during a dive render our study results inapplicable. It only renders the diver unable to actively optimize his or her thermal exposure to minimize DCS risk or decompression obligation. Effects of diver thermal status on bottom hold regardless of whether the dive has a decompression long enough for a thermal effect to manifest in the decompression phase of the dive. We pointed out that US Navy decompression tables have historically been developed and validated with test dives in which divers were cold and working during bottom phases and cold and resting during decompression phases. Thus, our results indicate that it is not prudent for very warm divers to challenge the US Navy no-stop limits. However, becoming deliberately chilled on bottom only to remain cold during any ensuing decompression stops is similarly ill-advised. We agree with Clarke et al. that relative conservatism of some dive computer algorithms or alternative decompression tables, or the depth and time roundups necessary to determine table-based prescriptions, work in the diver's favour, but note that diving any profile to a shorter bottom time is a ready means to reduce the risk of DCS - i.e., enhance safety - without compromising comfort. Any active diver heating is best limited while on bottom to a minimal level required to safely complete on-bottom tasks, and dialled up only during decompression. Diver warming during decompression should not be so aggressive as to risk heat stress, and care should be taken to ensure that divers remain hydrated.

Monitoring intracellular, interstitial, and intravascular volume changes during fluid management procedures.

The bioimpedance spectroscopic (BIS) analytical algorithm described in this report allows for the non-invasive measurement of intravascular, interstitial, and intracellular volume changes during various fluid management procedures. The purpose of this study was to test clinical use feasibility and to demonstrate the validity of the BIS algorithm in computing compartmental volume shifts in human subjects undergoing fluid management treatment. Validation was performed using volume changes recorded from 20 end stage renal disease patients. The validation procedure involved mathematically deriving post hoc hematocrit profiles from the BIS data-generated fluid redistribution time profiles. These derived hematocrit profiles were then compared to serial hematocrit values measured simultaneously by a CritLine(®) monitor during 60 routine hemodialysis sessions. Regression and Bland-Altman analyses confirm that the BIS algorithm can be used to reliably derive the continuous and real-time rates of change of the compartmental fluid volumes. Regression results yielded a R (2) > 0.99 between the two measures of hematocrit at different times during dialysis. The slopes of the regression equations at the different times were nearly identical, demonstrating an almost one-to-one correspondence between the BIS and CritLine(®) hematocrits. Bland-Altman analysis show that the BIS algorithm can be used interchangeably with the CritLine(®) monitor for the measurement of hematocrit. The present study demonstrates for the first time that BIS can provide real-time continuous measurements of compartmental intravascular, interstitial and intracellular fluid volume changes during fluid management procedures when used in conjunction with this new algorithm.

Risk of decompression sickness during exposure to high cabin altitude after diving.

BACKGROUND: Postdive altitude exposure increases the risk of decompression sickness (DCS). Certain training and operational situations may require U.S. Special Operations Forces (SOF) personnel to conduct high altitude parachute operations after diving. Problematically, the minimum safe preflight surface intervals (PFSI) between diving and high altitude flying are not known. METHODS: There were 102 healthy, male volunteers (34 +/- 10 [mean +/- SD] yr of age, 84.5 +/- 13.8 kg weight, 26.2 +/- 4.2 kg x m(-2) BMI) who completed simulated 60 fsw (feet of seawater)/60 min air dives preceding simulated 3-h flights at 25,000 ft to study DCS risk as a function of PFSI. Subjects were dry and at rest throughout. Oxygen was breathed for 30 min before and during flight in accordance with SOF protocols. Subjects were monitored for clinical signs of DCS and for venous gas emboli (VGE) using precordial Doppler ultrasound. DCS incidence was compared with Chi-squared; VGE onset time and time to maximum grade with one-way ANOVA (significance at p < 0.05). RESULTS: Three cases of DCS occurred in 155 subject-exposures: 1/35 and 0/24 in 2 and 3 h flight-only controls, respectively; 0/23, 1/37, and 1/36 for 24, 18, and 12 h dive-PFSI-flight profiles, respectively. DCS risk did not differ between profiles (chi2 [4] = 1.33; crit = 9.49). VGE were observed in 19% of flights. Neither VGE onset time nor time to max grade differed between profiles (82 +/- 38 min [p = 0.88] and 100 +/- 40 min [p = 0.68], respectively). CONCLUSION: Increased DCS risk was not detected as a result of dry, resting 60 fsw/60 min air dives conducted 24-12 h before a resting, 3-h oxygen-breathing 25,000 ft flight (following 30 min oxygen prebreathe). The current SOF-prescribed minimum PFSI of 24 h may be unnecessarily conservative.

Mathematical model of diffusion-limited evolution of multiple gas bubbles in tissue.

Models of gas bubble dynamics employed in probabilistic analyses of decompression sickness incidence in man must be theoretically consistent and simple, if they are to yield useful results without requiring excessive computations. They are generally formulated in terms of ordinary differential equations that describe diffusion-limited gas exchange between a gas bubble and the extravascular tissue surrounding it. In our previous model (Ann. Biomed. Eng. 30: 232-246, 2002), we showed that with appropriate representation of sink pressures to account for gas loss or gain due to heterogeneous blood perfusion in the unstirred diffusion region around the bubble, diffusion-limited bubble growth in a tissue of finite volume can be simulated without postulating a boundary layer across which gas flux is discontinuous. However, interactions between two or more bubbles caused by competition for available gas cannot be considered in this model, because the diffusion region has a fixed volume with zero gas flux at its outer boundary. The present work extends the previous model to accommodate interactions among multiple bubbles by allowing the diffusion region volume of each bubble to vary during bubble evolution. For given decompression and tissue volume, bubble growth is sustained only if the bubble number density is below a certain maximum.

Mathematical model of diffusion-limited gas bubble dynamics in unstirred tissue with finite volume.

Models of gas bubble dynamics for studying decompression sickness have been developed by considering the bubble to be immersed in an extravascular tissue with diffusion-limited gas exchange between the bubble and the surrounding unstirred tissue. In previous versions of this two-region model, the tissue volume must be theoretically infinite, which renders the model inapplicable to analysis of bubble growth in a finite-sized tissue. We herein present a new two-region model that is applicable to problems involving finite tissue volumes. By introducing radial deviations to gas tension in the diffusion region surrounding the bubble, the concentration gradient can be zero at a finite distance from the bubble, thus limiting the tissue volume that participates in bubble-tissue gas exchange. It is shown that these deviations account for the effects of heterogeneous perfusion on gas bubble dynamics, and are required for the tissue volume to be finite. The bubble growth results from a difference between the bubble gas pressure and an average gas tension in the surrounding diffusion region that explicitly depends on gas uptake and release by the bubble. For any given decompression, the diffusion region volume must stay above a certain minimum in order to sustain bubble growth.