title: Hemorrhagic shock.
abstract: A great deal has been learned about the pathophysiologic condition of hemorrhagic shock. The response of the hormonal and inflammatory mediator systems in patients in hemorrhagic shock appears to represent a distinct set of responses different from those of other forms of shock. The classic neuroendocrine response to hemorrhage attempts to maintain perfusion to the heart and brain, often at the expense of other organ systems. This intense vasoconstriction occurs via central mechanisms. The response of the peripheral microcirculation is driven by local tissue hypoperfusion that results in vasodilation in the ischemic tissue bed. Activation of the systemic inflammatory response by hemorrhage and tissue injury is an important component of the pathophysiologic condition of hemorrhagic shock. Activators of this systemic inflammatory response include ischemia/reperfusion injury and neutrophil activation. Capillary "no-flow" with prolonged ischemia and "no-reflow" with reperfusion may initiate neutrophil activation in patients in hemorrhagic shock. The mechanisms that lead to decompensated and irreversible hemorrhagic shock include (1) "arteriolar hyposensitivity" as manifested by progressive arteriolar vasodilation and decreased responsiveness of the microcirculation to alpha-agonists, and (2) cellular injury and activation of both proinflammatory and counterinflammatory mechanisms. These changes represent a failure of the microcirculation. Redistribution of cardiac output and persistent gut ischemia after adequate resuscitation may also contribute to the development of irreversible hemorrhagic shock. Treatment of hemorrhagic shock includes rapid operative resuscitation to limit activation of the mediator systems and abort the microcirculatory changes that result from hemorrhagic shock. Volume resuscitation and control of hemorrhage, should occur simultaneously. The end point in volume resuscitation of hemorrhagic shock must be maintenance of organ system and cellular function. Whether we use adequate urine output, correction of lactic acidemia, optimization of oxygen delivery, or oxygen consumption as our specific goal, the general objective is to provide adequate crystalloid solution and packed red blood cells to achieve and maintain normal organ and cellular perfusion and function.
authors.affiliation: Section of Trauma/Surgical Critical Care, University of Pittsburgh Medical Center, Pennsylvania, USA.
authors.forename: A B
authors.initials: AB
authors.lastname: Peitzman
authors.forename: T R
authors.initials: TR
authors.lastname: Billiar
authors.forename: B G
authors.initials: BG
authors.lastname: Harbrecht
authors.forename: E
authors.initials: E
authors.lastname: Kelly
authors.forename: A O
authors.initials: AO
authors.lastname: Udekwu
authors.forename: R L
authors.initials: RL
authors.lastname: Simmons
mesh_terms: D000311:Adrenal Glands / Q000503:physiopathology; D000818:Animals; D002490:Central Nervous System / Q000503:physiopathology; D005110:Extracellular Space; D006321:Heart / Q000503:physiopathology; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D007422:Intestines / Q000503:physiopathology; D007668:Kidney / Q000503:physiopathology; D008099:Liver / Q000503:physiopathology; D008168:Lung / Q000503:physiopathology; D008833:Microcirculation / Q000502:physiology; D009490:Neurosecretory Systems / Q000503:physiopathology; D009504:Neutrophils / Q000502:physiology; D009569:Nitric Oxide / Q000502:physiology; D012771:Shock, Hemorrhagic / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy
chemical_list: D018836:Inflammation Mediators; D009569:Nitric Oxide