Lower body negative pressure as a model to study progression to acute hemorrhagic shock in humans.
Hemorrhage is a leading cause of death in both civilian and battlefield trauma. Survival rates increase when victims requiring immediate intervention are correctly identified in a mass-casualty situation, but methods of prioritizing casualties based on current triage algorithms are severely limited. Development of effective procedures to predict the magnitude of hemorrhage and the likelihood for progression to hemorrhagic shock must necessarily be based on carefully controlled human experimentation, but controlled study of severe hemorrhage in humans is not possible. It may be possible to simulate hemorrhage, as many of the physiological compensations to acute hemorrhage can be mimicked in the laboratory by applying negative pressure to the lower extremities. Lower body negative pressure (LBNP) sequesters blood from the thorax into dependent regions of the pelvis and legs, effectively decreasing central blood volume in a similar fashion as acute hemorrhage. In this review, we compare physiological responses to hemorrhage and LBNP with particular emphasis on cardiovascular compensations that both share in common. Through evaluation of animal and human data, we present evidence that supports the hypothesis that LBNP, and resulting volume sequestration, is an effective technique to study physiological responses and mechanisms associated with acute hemorrhage in humans. Such experiments could lead to clinical algorithms that identify bleeding victims who will likely progress to hemorrhagic shock and require lifesaving intervention(s).
Cooke
William H
WH
US Army Institute of Surgical Research, Fort Sam Houston, TX 78234-6315, USA. William.Cooke@amedd.army.mil
Ryan
Kathy L
KL
Convertino
Victor A
VA
D000208:Acute Disease; D000818:Animals; D018450:Disease Progression; D006339:Heart Rate; D006470:Hemorrhage / Q000097:blood / Q000150:complications* / Q000503:physiopathology*; D006801:Humans; D008150:Lower Body Negative Pressure; D018377:Neurotransmitter Agents / Q000097:blood; D012771:Shock, Hemorrhagic / Q000209:etiology* / Q000503:physiopathology
D018377:Neurotransmitter Agents