Hypovolemic and hemorrhagic. The most common cause of shock in the injured patient is hypovolemia from hemorrhage. This etiology is assumed and treated until proven otherwise for all trauma patients in shock.

Traumatic shock is a separate entity in injured patients, but includes elements of other forms of shock. Traumatic shock evolves from acute blood loss/hypovolemia and release of pro-inflammatory mediators as a result of direct tissue injury that decreases peripheral vasomotor tone. Acute blood loss itself, irrespective of volume, can also promote pro-inflammatory effects. The combination of these insults results in global hypoperfusion, whereas each component in isolation may not.

Cardiogenic shock results from inadequate pumping function of the heart. Contractility is impaired and cardiac output falls with resultant hypoperfusion. In the injured patient, cardiogenic shock often is due to direct injury to the heart, most often blunt cardiac injury. Secondarily, intrinsic heart disease becomes more common among trauma patients and may lead to impaired heart pump action associated with the stress of injury on pre-existing cardiac disease.

Vasogenic shock occurs when vascular resistance is lowered sufficiently to reduce perfusion pressure in peripheral tissue beds. Underlying etiologies include anaphylaxis, adrenal crisis, sepsis, and neurogenic shock, with the latter two forms seen most commonly in trauma patients.

Obstructive shock occurs when preload to the heart is impeded as a result of obstructed venous filling or direct compression of the heart. In trauma, this occurs in the setting of cardiac tamponade or tension pneumothorax, both of which require prompt diagnosis and treatment during the primary survey.

Afferent signaling. The central nervous system integrates several afferent signals in the setting of hypoperfusion and impaired oxygen delivery. Baroreceptors in the carotid bodies and aortic arch, volume receptors in the atria, and chemorecptors for oxygen tension, CO₂, and PO₂, all sense changes that signal hypoperfusion and act through the hypothalamic–pituitary–adrenal (HPA) axis and autonomic nervous system (ANS) to initiate compensatory mechanisms.

Cardiovascular. The cardiovascular system has three major responses to hypoperfusion, mediated through neuroendocrine pathways. Activation of the ANS results
in an increased heart rate (HR) and contractility through beta-1 receptors, both augmenting cardiac output. Loss of sympathetic input in the setting of neurogenic shock blocks this increase in HR and is classic – albeit not common – for neurogenic shock. Intrinsic pump dysfunction in cardiogenic shock will not be overcome by the increased sympathetic activation. Alpha-1 receptor activation by the ANS and adrenergic hormones result in vascular smooth muscle contraction and increased vascular resistance. The degree of vasomotor tone increase is dependent on the regional tissue bed, with selective shunting of blood from less vital organs (i.e., skin, gut, kidney) to maintain perfusion to the brain and heart during the immediate threat of hypoperfusion. Recent evidence points to decreased HR variability as a poor prognostic indicator in patients with shock, as these highly integrated compensatory relationships become uncoupled and decompensation occurs.

Neuroendocrine. Epinephrine and norepinephrine are released from adrenal medulla to produce vasomotor effects. The renin–angiotensin–aldosterone system is activated in addition to the release of antidiuretic hormone to promote water reabsorption in the kidney and further modulation of regional vascular beds. Cortisol and glucagon release contribute to a catabolic state to increase available energy substrates for cells.

Immunologic and inflammatory. Although a profound inflammatory and immune response is typified in the setting of septic shock, all forms of shock promote a pro-inflammatory state as local tissue injury can become systemic. Important mediators of this reaction include cytokines, complement, oxygen radicals, eicosanoids, and nitric oxide. Important cytokines that have early effects on the systemic pro-inflammatory response include TNF-alpha, IL-1, IL-2, and IL-6. Many of the eicosanoids have strong vasoactive properties. Nitric oxide is recognized as having an increasingly important role in hypoperfusion modulation.

Cellular effects. As oxygen delivery to the cell declines, oxidative phosphorylation and ATP production slow down and the cell shunts substrates into anaerobic metabolism, producing lactate. As the ATP supply is depleted, a variety of energy-dependent cellular functions begin to fail including enzyme synthesis, DNA repair and expression, and signal transduction. Further, the membrane Na⁺/K⁺ ATPase becomes unable to maintain the cell membrane electrochemical gradient with resultant influx of sodium followed by water, causing cell swelling and lysis. Accumulation of metabolism byproducts and radical species are directly toxic to cells. Local and systemic acidosis ensues leading to alteration in enzyme activity and intracellular calcium signaling. Alterations in the local microcirculation are influenced by many metabolic byproducts and can aggravate oxygen debt in the tissue as well as promote further pro-inflammatory damage as a result of neutrophil trapping and activation.