Due to limited remote triage monitoring capabilities, combat medics cannot currently distinguish bleeding soldiers from those engaged in combat unless they have physical access to them. The purpose of this study was to test the hypothesis that low-level physiological signals can be used to develop a machine-learning algorithm for tracking changes in central blood volume that will subsequently distinguish central hypovolemia from physical activity. Twenty-four subjects underwent central hypovolemia via lower body negative pressure (LBNP), and a supine-cycle exercise protocol. Exercise workloads were determined by matching heart rate responses from each LBNP level. Heart rate and stroke volume (SV) were measured via Finometer. ECG, heat flux, skin temperature, galvanic skin response, and two-axis acceleration were obtained from an armband (SenseWear Pro2) and used to develop a machine-learning algorithm to predict changes in SV as an index of central blood volume under both conditions. The algorithm SV was retrospectively compared against Finometer SV. A model was developed to determine whether unknown data points could be correctly classified into these two conditions using leave-one-out cross-validation. Algorithm vs. Finometer SV values were strongly correlated for LBNP in individual subjects (mean r = 0.92; range 0.75-0.98), but only moderately correlated for exercise (mean r = 0.50; range -0.23-0.87). From the first level of LBNP/exercise, the machine-learning algorithm was able to distinguish between LBNP and exercise with high accuracy, sensitivity, and specificity (all ≥90%). In conclusion, a machine-learning algorithm developed from low-level physiological signals could reliably distinguish central hypovolemia from exercise, indicating that this device could provide battlefield remote triage capabilities.

The purpose of this study was to test the hypotheses that digital infrared thermographic imaging (DITI) during simulated uncontrolled hemorrhage will reveal 1) respiratory rate and 2) changes of skin temperature that track reductions of stroke volume. In 45 healthy volunteers (25 men and 20 women), we recorded the ECG, finger photoplethysmographic arterial pressure, respiratory rate (pneumobelt and DITI of the nose), cardiac output (inert rebreathing), and skin temperature of the forehead during lower body negative pressure (LBNP) at three continuous decompression rates; slow (-3 mmHg/min), medium (-6 mmHg/min), and fast (-12 mmHg/min) to an ending pressure of -60 mmHg. Respiratory rates calculated from the pneumobelt (14.7 ± 0.9 breaths/min) and DITI (14.9 ± 1.2 breaths/min) were not different (P = 0.21). LBNP induced an average stroke volume reduction of 1.3 ml/mmHg regardless of decompression speed. Maximal reductions of stroke volume and forehead temperature were -100 ± 12 ml and -0.32 ± 0.12°C (slow), -86 ± 12 ml and -0.74 ± 0.27°C (medium), and -78 ± 5 ml and -0.17 ± 0.02°C (fast). Changes of forehead temperature as a function of changes of stroke volume were best described by a quadratic fit to the data (slow R(2) = 0.95; medium R(2) = 0.89; and fast R(2) = 0.99).Our results suggest that a thermographic camera may prove useful for the remote assessment of traumatically injured patients. Life sign detection may be determined by verifying respiratory rate. Determining the magnitude and rate of hemorrhage may also be possible based on future algorithms derived from associations between skin temperature and stroke volume.

No relationships reported)Skeletal muscle blood flow remains elevated after exercise and this sustained postexercise vasodilation is mediated by histamine H1-and H2-receptor activation. Previous research has suggested this elevation in blood flow is in excess of local O2 demand; however, the effect of blood flow on tissue oxygenation in the previously active muscle has not been examined. PURPOSE:To determine the effect of reducing blood flow via histamine-receptor blockade on tissue oxygenation following exercise. METHODS:Thirteen healthy recreationally active subjects (5 females, 8 males, ages 18-25) performed 60 min of whole body aerobic exercise on a cycle ergometer on two separate days. On one day, subjects were given 540 mg fexofenadine and 300 mg ranitidine at 1 hr preexercise to block H1 and H2 receptors (blockade day). On the other day, subjects did not receive any drug (control day). Order of days was randomized. Measurements of leg blood flow (Doppler ultrasound of the femoral artery), whole body VO2 (dilution hood), and tissue oxygen index (near-infrared spectroscopy of the vastus lateralis muscle) were taken for 20 min preexercise and 60 min postexercise on both days. Femoral vascular conductance was calculated using femoral artery blood flow and mean arterial pressure. RESULTS:Femoral vascular conductance increased 50.1±9.0% from preexercise to postexercise on the control day, but only 27.5±8.2% on the blockade day (both p<0.05 vs. pre, p=0.08 across days). Tissue oxygen index was similar preexercise and postexercise on both the control and blockade days (+1.5±0.8 vs. +1.3±1.%, p=0.3 vs. pre, p=0.9 across days). VO2 was also unchanged postexercise (p=0.9 vs. pre).CONCLUSION: Consistent with our prior studies, much of the sustained postexercise vasodilation is dependent on activation of H1-and H2-receptors. However, in contrast to our expectation, the observation of unchanged postexercise tissue oxygen index values suggests that local perfusion may not exceed local O2 demand. Interestingly, manipulation of blood flow by histamine blockade had no clear impact on tissue oxygen index, suggestive of an independence of O2 delivery within skeletal muscle tissue from femoral artery blood flow.Arterial pressures oscillate with the frequency of respiration, and these oscillations are translated directly to the cerebrovasculature. For this reason, intrinsic cerebrovascular control is assessed at the low frequency (LF; .07-.2 Hz). When humans breathe spontaneously, it is possible that breathing frequency encroaches on these non-respiratory rhythms, thereby confounding the interpretation of intrinsic cerebrovascular control. PURPOSE:To test the hypothesis that controlled breathing (CB) decreases, and spontaneous breathing (SB) increases the reliance of cerebral blood velocity on arterial pressure within the LF range in both the supine and upright postures. METHODS:We recorded ECG, finger arterial pressure (Finometer), transcranial Doppler ultrasound of the middle cerebral artery, and end-tidal CO2 in 20 healthy m...