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Pathophysiology of Hemorrhagic Shock
The pathophysiology of hemorrhagic shock involves a decrease in systemic oxygen delivery to a level less than what is required to maintain cellular function.
For the polytrauma patient, brain injury is the most common cause of early death followed by acute blood loss as the second most common cause of early death . In the U.S., 150,000 people die each year due to injury and many of these deaths occur in relatively younger individuals, which causes an aggregate loss of productive life of over 3.3 million years . This results in an annual cost to society of USD 2.34 billion in today’s dollars from lost wages and medical costs. In prospective studies that examine resuscitation after trauma the median time to hemorrhagic death is 2.0 to 2.6 h . Hemorrhage is the most common cause of shock in the injured, and a substantial number of trauma patients will arrive at hospital with profound physiologic disturbances due to acute circulatory failure. Dr. Samuel D Gross, regarded as one of the most innovative and influential surgeons of the 19th century described shock simply as, “… a rude unhinging of the machinery of life”. Indeed, this remarkable characterization of hemorrhagic shock remains as informative today as certainly it was over 175 years ago .
The polytrauma victim with significant hemorrhage suffers a life-threatening acute reduction in oxygen delivery (DO 2) to tissue. DO 2 depends on both an adequate circulating blood volume representing sufficient oxygen carrying capacity, and effective cardiovascular function to maintain the circulation of blood to capillary beds in the periphery.
Furthermore, between 25% to 35% of hemorrhaging patients will develop a biochemically evident coagulopathy (trauma-induced coagulopathy; TIC) before arrival to the emergency department, which can manifest clinically as either hypercoagulable or hypocoagulable states, or both. In the polytrauma patient the presence of TIC is associated with higher transfusion requirements, increased I.C.U. and hospital length of stay (LOS), prolonged requirement for mechanical ventilation, an increase in the incidence of multiorgan dysfunction, and, most concerning of all, a threefold to fourfold higher rate of mortality . TIC has deleterious effects independent of injury severity, level of shock, degree of acidosis or depth of hypothermia .
2. Pathophysiology of Hemorrhagic Sock
Oxygen Delivery/Utilization Imbalance
This entry is adapted from 10.3390/jcm10204793
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