The latter may be caused by dehydration from vomiting or diarrhea, by severe environmental fluid losses, or by rapid and substantial loss of blood. Shock can be produced by decreases in cardiac output (cardiogenic), by sepsis (distributive), or by decreases in intravascular volume (hypovolemic). Life-threatening decreases in blood pressure often are associated with a state of shock – a condition in which tissue perfusion is not capable of sustaining aerobic metabolism. Instead, therapy should be aimed at restoring intravascular volume and adequate hemodynamic parameters. Moreover, hemoglobin concentration should not be the only therapeutic guide in actively bleeding patients. However, maintaining a higher hemoglobin level of 10 g/dl is a reasonable goal in actively bleeding patients, the elderly, or individuals who are at risk for myocardial infarction. A hemoglobin level of 7–8 g/dl appears to be an appropriate threshold for transfusion in critically ill patients with no evidence of tissue hypoxia. The optimal method of resuscitation has not been clearly established. On the other hand, the use of intravenous fluids, crystalloids or colloids, and blood products can be life saving in those patients who are in severe hemorrhagic shock. It now appears that patients with moderate hypotension from bleeding may benefit by delaying massive fluid resuscitation until they reach a definitive care facility. Resuscitation may well depend on the estimated severity of hemorrhage. The primary goals are to stop the bleeding and to restore circulating blood volume. This review addresses the pathophysiology and treatment of hemorrhagic shock – a condition produced by rapid and significant loss of intravascular volume, which may lead sequentially to hemodynamic instability, decreases in oxygen delivery, decreased tissue perfusion, cellular hypoxia, organ damage, and death.
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