The physiologic response to injury and shock is a complex process that originates from cytokine and catecholamine release due to tissue hypoperfusion and direct tissue injury. Shock is defined as circulatory failure with impaired end-organ perfusion. The shock state is characterized by impaired aerobic metabolism at the cellular level (oxygen delivery, consumption, and/or utilization), which leads to tissue hypoxia, cell death, and eventually organ system dysfunction, organ failure, and death. There are various etiologies that can lead to the physiologic state of shock, but there are four general categories: hypovolemic, distributive, cardiogenic, and obstructive. Traumatic shock can be multifactorial, but the most common etiology is hemorrhage, a subset of hypovolemic shock, thus traumatic shock is hemorrhagic until proven otherwise. As the saying goes, the first, second, and third causes of shock in a trauma patients is hemorrhage. The lethal triad in trauma is a feedback loop of coagulopathy, acidosis, and hypothermia. Trauma-induced coagulopathy (TIC), part of the lethal triad, is a unique pathophysiologic entity seen during traumatic hemorrhagic shock and is a major contributor to morbidity and mortality. Shock in the traumatically injured patient should be identified and intervened on rapidly during the primary survey to prevent progression to irreversible shock and death. Though hemorrhagic shock is certainly the most common, trauma patients may experience any and every type of shock during their hospitalization, particularly with an ever increasing and ever more medically complex population of elderly trauma patients.