Each of these fluid volumes, the plasma, the interstitial, and the intracellular, is in equilibrium; however, disturbances such as acute blood loss result in fluid shifts in attempt to maintain effective circulating volume [10]. Compensatory mechanisms, such as vasoconstriction and increased heart rate, are the physiologic responses to blood loss in order to maintain cardiac output. Catecholamine release immediately stimulates increase in the peripheral vascular resistance leading to increased diastolic pressure and reduced pulse pressure while simultaneously increasing heart rate. Histamine, bradykinin, β-endorphins, prostanoids, and cytokines directly impact vascular permeability and increase vasoconstriction. Intravascular fluid is preferentially shunted to the heart, brain, and kidneys and away from the viscera and muscle. At the cellular level, inadequate oxygen due to poor tissue perfusion changes energy production to anaerobic metabolism which initially leads to metabolic acidosis and end-organ damage. End-organ damage causes a systemic inflammatory response syndrome (SIRS) increasing vascular permeability, which causes fluid leak and increased hypotension. Hypoperfusion also leads to increased thrombomodulin which complexes with thrombin leading to protein C activation. Decreased available thrombin means less fibrinogen cleavage and platelet activation. This is one mechanism that leads to trauma-induced coagulopathy (TIC) worsening the effects of hemorrhage.

Compensatory vasoconstriction of afferent arterioles results in decreased capillary hydrostatic forces; less fluid is lost from the intravascular space into the interstitium. Increases in plasma oncotic pressure secondary to reduced renal filtration increase the amount of water that diffuses from the interstitium to the intravascular space. Activation of the renin-angiotensin-aldosterone axis increases sodium retention, which facilitates renal fluid retention. Angiotensin also increases systemic vascular tone, which contributes to the reduced capillary hydrostatic forces. Decreased pressure in the atria and increased plasma oncotic pressure stimulate the release of antidiuretic hormone (ADH) from the posterior pituitary. ADH acts to increase renal distal tubule permeability to water through the production and placement of aquaporins in the luminal membrane and, as such, provides a delayed response to volume loss.

Hemorrhagic shock is classified based on the volume of blood lost from the circulation and the resulting disturbances in hemodynamics observed. It is important to remember that hemorrhage may be more than what is easily appreciated as blood lost into the environment. Blood loss into potential spaces such as the hemithorax, abdomen, and retroperitoneum can approach life-threatening levels without appreciable external loss (Table 10.1). Knowing the location of hemorrhage is vital. A thorough physical exam as well as chest and pelvic film aid in the identification of the source of bleeding. Focused assessment with sonography for trauma (FAST) can also localize the bleeding in order to expedite appropriate treatment.

The treatment of hemorrhage is ultimately by control of the active bleeding, but volume replacement is usually necessary as well. Patients that are at risk of shock must be identified to guide presurgical treatment. Clinicians must be aware of patient injury pattern, age, time of transport, and previous fluid therapy to help with patient outcomes. The degree of IV replacement is dictated by the patient response to fluids.

Current standard of care is prehospital IV fluid administration in the trauma patient. The previous treatment of all trauma patients was 2 l IV crystalloid as the initial resuscitation. However this has been modified for improved patient outcome. The type and volume of fluid are based on patient blood loss and degree of shock. Patients can be rapid responders, transient responders, or nonresponders after initial fluid bolus. Rapid responders are those that have immediate return of vital signs to normal with the administration of crystalloid. The need for blood transfusion is low, and after initial bolus, the need for further crystalloid is low. Often one liter is sufficient in these patients. Transient responders are those patients with moderate and ongoing blood loss (type II–III shock). They will initially regain normal vital signs but will deteriorate after fluid is stopped. The need for immediate blood in these patients is moderate to high, and these patients will likely need operative intervention immediately. Nonresponders are those patients that have lost greater than 40 % of the blood volume. The vital signs do not respond to initial fluid bolus. Patients need immediate blood products to maintain adequate blood pressure in order to get to the operation room (OR) for definitive-operative repair. In order to appropriately administer fluids, clinicians must be familiar with the types of fluid available.