Near-infrared spectroscopy during lower body negative pressure

Early diagnosis of blood loss is a high priority for treatment of circulatory
shock since hemorrhage is a leading cause of death in civilian and military
trauma. Unfortunately, compensatory mechanisms that buffer against changes in
regulated variables, such as blood pressure and arterial oxygen saturation,
make standard physiologic measurements poor indicators for early assessment of
shock. Standard examinations of mental status, pulse character, and pulse rate
provide late information about the severity of blood loss. Subsequently, the
appearance of hypotension and other signs and symptoms of shock does not mark
the beginning of circulatory compromise but rather represents the beginning of
decompensation when it may be too late to introduce effective life-saving
interventions.

The objective of this study is the investigate whether near-infrared
spectroscopy in combination with a vascular occlusion test is able to detect
the early changes in muscular oxygenation in a model of controlled hypovolemia
induced by lower body negative pressure.

With the use of a neoprene skirt, designed to form an airtight seal between the
subject and the chamber, the application of negative pressure to the lower body
(below the iliac crest) results in a redistribution of blood away from the
upper body (head and heart) to the lower extremities and abdomen. This model,
therefore, provides conditions of controlled, experimentally induced
hypovolemic hypotension, offering a unique method for investigating new
monitoring devices, such as the multi-depth InSpectra (see below for
description). Although absolute equivalence between the magnitudes of negative
pressure applied and actual blood loss cannot be determined at this time,
review of available human and animal data has revealed ranges of effective
blood loss (or fluid displacement) caused by LBNP. Considering the magnitude of
induced central hypovolemia, Soller et al. have previously proposed that 10*20
mm Hg negative pressure produces hemodynamic responses equivalent to those
resulting from blood loss of 400*550 mL, 20*40 mm Hg LBNP induces hemodynamic
responses equivalent to blood loss of 550*1000 mL, and >40 mm Hg LBNP induces
responses equivalent to blood loss of >1000 mL.
Each subject will be reported to the laboratory for a progressive LBNP protocol
that is designed to test his or her tolerance to experimentally induced
hypotensive hypovolemia. The subject will first be instrumented with
noninvasive devices for hemodynamic and tissue oxygenation measurements
(described below).
The LBNP protocol consists of a 5-min baseline period followed by 5 min of
chamber decompression to -20 (5 min), -40 (15 min, including a 3-min vascular
occlusion test), and -60 mm Hg (5 min) until either the onset of cardiovascular
collapse or the completion of 5 min at -60 mm Hg. Cardiovascular collapse is
defined by one or a combination of the following criteria: a) a precipitous
fall in systolic blood pressure (SBP) >15 mm Hg and/or a sudden bradycardia; b)
progressive diminution of SBP <70 mm Hg; or c) voluntary subject termination
due to discomfort from presyncopal symptoms, such as sweating, nausea,
dizziness, or gray-out. At the onset of cardiovascular collapse, the chamber
vacuum will be released to ambient pressure to rapidly restore blood flow and
blood pressure. To ensure subject safety, an Advanced Cardiac Life Support
provider or physician will be present in the laboratory during all LBNP tests.

During the gradual application of lower body negative pressure lightheadedness
could ensue. The volunteer participants will have direct access to a push
button system that can terminate the lower body negative pressure and thus stop
the experiment immediately. NIRS and the VOT are both noninvasive, painless and
entirely safe techniques. During the experiments a trained physician will be
present at all times to ensure the safety of each participant.