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To test the hypothesis that components of heart period variability track autonomic function during simulated hemorrhage in humans.Prospective experimental laboratory intervention.Human physiology laboratory.A total of 33 healthy, nonsmoking, volunteer subjects (23 men, ten women).Progressive lower body negative pressure was applied in 5-min stages until the onset of impending cardiovascular collapse.The electrocardiogram, beat-by-beat finger arterial pressure, and muscle sympathetic nerve activity from the peroneal nerve were recorded continuously. Pulse pressure was calculated from the arterial pressure waveform and used as an estimate of relative changes of central blood volume. Heart period variability was assessed in both time and frequency domains. Application of lower body negative pressure caused progressive reductions of R-R interval and pulse pressure and progressive increases of muscle sympathetic nerve activity. Arterial pressures changed minimally and late. R-R interval time domain variability measures and spectral power at the high frequency (0.15-0.4 Hz) decreased progressively with lower body negative pressure (p.001). Both R-R interval high-frequency power and time domain variability measures correlated inversely with muscle sympathetic nerve activity and directly with pulse pressure (all amalgamated R2.88, all por = .001).Components of heart period variability track early compensatory autonomic and hemodynamic responses to progressive reduction in central blood volume. Such analyses, interpreted in conjunction with standard vital signs, may contribute to earlier assessments of the magnitude of blood volume loss during hemorrhage.

To compare the responses of noninvasively measured tissue oxygen saturation (StO2) and calculated muscle oxygen tension (PmO2) to standard hemodynamic variables for early detection of imminent hemodynamic instability during progressive central hypovolemia in humans.Prospective study.Research laboratory.Sixteen healthy human volunteers.Progressive lower body negative pressure (LBNP) to onset of cardiovascular collapse.Noninvasive measurements of blood pressures, heart rate, and stroke volume were obtained during progressive LBNP with simultaneous assessments of StO2, PmO2, and muscle oxygen saturation (SmO2). Forearm SmO2 and PmO2 were determined with a novel near infrared spectroscopic measurement device (UMMS) and compared with thenar StO2 measured by a commercial device (HT). All values were normalized to the duration of LBNP exposure required for cardiovascular collapse in each subject (i.e., LBNP maximum). Stroke volume was significantly decreased at 25% of LBNP maximum, whereas blood pressure was a late indicator of imminent cardiovascular collapse. PmO2 (UMMS) was significantly decreased at 50% of maximum LBNP while SmO2 (UMMS) decreased at 75% of maximum LBNP. Thenar StO2 (HT) showed no statistical change throughout the entire LBNP protocol.Spectroscopic assessment of forearm muscle PO2 and SmO2 provides noninvasive and continuous measures that are early indicators of impending cardiovascular collapse resulting from progressive reductions in central blood volume.

Objective: Increased negative intrathoracic pressure during spontaneous inspiration through an impedance threshold device (ITD) causes elevated arterial blood pressure in humans. This study was performed to determine whether the acute increase in blood pressure induced by breathing through an ITD is associated with increased stroke volume and cardiac output. Design: Randomized, blinded, controlled trial. Setting: Laboratory. Subjects: Ten women and ten men. Interventions: We measured hemodynamic and respiratory responses during two separate ITD conditions: 1) breathing through a face mask with an ITD (impedance of 6 cm H 2 O [0.59 kPa]) and 2) breathing through the same face mask with a sham ITD (control). Stroke volume was measured by thoracic bioimpedance. Measurements and Main Results: Compared with the control condition, ITD produced higher stroke volume (124 + or - 3 vs. 137 + or - 3 mL; p = .013), heart rate (63 + or - 3 vs. 68 3 beats/min; p = .049), cardiac output (7.69 vs. 9.34 L/min; p = .001), and systolic blood pressure (115 + or - 2 to 122 + or - 2 mm Hg [15.33 + or - 0.3 to 16.26 + or - 0.3 kPa]; p = .005) without affecting expired minute ventilation (6.2 + or - 0.4 to 6.5 + or - 0.4 L/min; p = .609). Conclusions: Breathing with an ITD at relatively low impedance increases systolic blood pressure by increasing stroke volume and cardiac output. The ITD may provide short-term protection against cardiovascular collapse induced by orthostatic stress or hemorrhage.

To determine whether heart period variability provides added value in identifying the need for lifesaving interventions (LSI) in individual trauma patients with normal standard vital signs upon early medical assessment.Retrospective database review.Helicopter transport to Level 1 trauma center and first 24 hrs of in-hospital care.Prehospital trauma patients requiring helicopter transport to Level 1 trauma center.Heart period variability was analyzed from electrocardiographic recordings collected from 159 prehospital trauma patients with normal standard vital signs (32 LSI patients, 127 No-LSI patients). Although 13 of the electrocardiogram derived metrics demonstrated simple (i.e., univariate) discrimination between groups, at the multivariate level, only fractal dimension by curve length (FD-L) was uniquely associated with group membership (LSI vs. No-LSI, p = .0004). Whereas the area under the receiver operating characteristics curve for FD-L was 0.70, the overall correct classification rate (true positives and true negatives) of 82% was only 2% higher than the baseline prediction rate of 80% (i.e., no information except for the known proportion of overall No-LSI cases, 127 of 159 patients). Furthermore, 84% of the individual FD-L values for the LSI group were within the range of the No-LSI group.Only FD-L was uniquely able to distinguish patient groups based on mean values when standard vital signs were normal. However, the accuracy of FD-L in distinguishing between patients was only slightly better than the baseline prediction rate. There was also very high overlap of individual heart period variability values between groups, so many LSI patients could be incorrectly classified as not requiring an LSI if a single heart period variability value was used as a triage tool. Based on this analysis, heart period variability seems to have limited value for prediction of LSIs in prehospital trauma patients with normal standard vital signs.

Objective: To test the hypothesis that an impedance threshold device would increase systolic blood pressure, diastolic blood pressure, and mean arterial blood pressure and delay the onset of symptoms and cardiovascular collapse associated with severe central hypovolemia. Design: Prospective, randomized, blinded trial design. Setting: Human physiology laboratory. Patients: Nine healthy nonsmoking normotensive subjects (five males, four females). Interventions: Central hypovolemia and impending cardiovascular collapse were induced in human volunteers by applying progressive lower body negative pressure (under two experimental conditions: a) while breathing with an impedance threshold device set to open at -7cm H2O pressure (active impedance threshold device); and b) breathing through a sham impedance threshold device (control). Measurements and Main Results: Systolic blood pressure (79 5 mm Hg), diastolic blood pressure (57 + or - 3 mm Hg), and mean arterial pressure (65 7 + or - 4 mm Hg) were lower ( p less than .02) when subjects (n 9) breathed through the sham impedance threshold device than when they breathed through the active impedance threshold device at the same time of cardiovascular collapse during sham breathing (102 7 + or - 3, 77 7 + or - 3, 87 + or 3 mm Hg, respectively). Elevated blood pressure was associated with 23% greater lower body negative pressure tolerance using an active impedance threshold device (1639 220 mm Hg-min) compared with a sham impedance threshold device (1328 + or - 144 mm Hg-min) ( p = .02). Conclusions: Use of an impedance threshold device increased systemic blood pressure and delayed the onset of cardiovascular collapse during severe hypovolemic hypotension in spontaneously breathing human volunteers. This device may provide rapid noninvasive hemodynamic support in patients with hypovolemic hypotension once the blood loss has been controlled but before other definitive therapies are available.

Over the last years, tissue microcirculatory and regional perfusion and oxygenation have made an important entry into the functional hemodynamic monitoring of critically ill patients (1). Clinical assessment of these parameters has become possible by the introduction of optical spectroscopic technologies such as near-infrared spectroscopy. This technique is based on the oxygen-dependent optical absorption of blood in the near-infrared spectrum. There are three prime factors which distinguish the currently available devices: 1) the algorithm used to calculate regional/ microcirculatory hemoglobin saturation; 2) the spatial separation of the illumination and detection fiber, which determines the measurement depth; and 3) the location of the probe. In a recent issue of Critical Care Medicine, Soller et al (2) presented a study in volunteers where a decrease in venous return (as a model of hypovolemia) was induced by lower limb negative pressure. In the model, they compared a self-developed near-infrared spectroscopy device, which measures a parameter called muscle oxygen tension, to a commercially available device from Hutchinson Technology (HT), which measures a parameter called tissue oxygen saturation and has been studied clinically (3 5). The authors concluded that their device has superior sensitivity to detect acute hypovolemia when compared with the HT device. However, in their study design, two of the above-mentioned factors were not under experimental control resulting in a faulty conclusion. This may lead to confusion in the field of those using the near-infrared spectroscopy technique and needs to be addressed.