Hypotension in the setting of trauma is often arbitrarily defined as a systolic blood pressure below 90 mm Hg. The sensitivity and specificity of this cut-off point as an indicator of severe hemorrhage is poor. Elderly patients, who normally have a higher baseline blood pressure, may be in shock long before the systolic blood pressure falls to 90 mm Hg. On the other end, pediatric patients and many adults have normal perfusion 90 mm Hg or lower. Some suggest that a threshold of 110 mm Hg be used in trauma patients, since this is a more sensitive mortality predictor though it will be non-specific.

Similar to blood pressure, heart rate is an inaccurate indicator of severe bleeding. Often, the heart rate will increase in the absence of bleeding, because of other adrenergic inputs, such as anxiety, fear, or pain. More dangerously, heart rate may remain normal – or even decrease – in the face of major blood loss; beta blockers, high spinal cord injury, or simply advanced age are the most common reasons. Failure to mount a tachycardic response after bleeding in trauma patients is an ominous sign. For the stated reasons, the clinical assessment of hypovolemia cannot rely upon any single factor, but is rather made on the basis of multiple signs and symptoms. The measurement of metabolic markers, notably elevated serum lactate (over 3.0) and arterial blood gas analysis (looking for base deficit) can help the clinician detect occult hypovolemia or shock.

If hypovolemia is caused by unchecked bleeding, the physician must balance the need for aggressive versus limited fluid resuscitation. New thought suggests delayed resuscitation, also known as “permissive” hypotension, in the context of uncontrolled hemorrhage The suggested mechanism for worse outcomes with early, aggressive resuscitation is that increased blood pressure and dilution of clotting factors disrupts clots and augments bleeding and mortality. Of note, most of the supporting data is derived from models of vascular injury, which does not
comprehensively address the pathophysiology of blunt trauma. Also, hypotensive episodes have a detrimental effect in traumatic brain injury, making the optimal endpoint of blood pressure in this setting less clear; the exact blood pressure targets are unknown during the early pre-resuscitation phase.

In non-trauma bleeding patients, who may have multiple co-morbidities, be older, and tolerate poorly an ongoing metabolic deficit with delayed resuscitation. Overall, it seems that this relatively new concept is applicable in selected cases, most commonly the patient with penetrating torso injury or ruptured abdominal aortic aneurysm. At the other end of the spectrum lies the patient who is in septic shock, with relative hypovolemia resulting from the increase in the intravascular space from vasodilatation compounded by loss of fluid through capillary leak. The urgent need for resuscitation is often overlooked in these patients, allowing prolonged periods of cellular hypoperfusion. The approach to shock and early therapies, including physiologic targets, is discussed in detail elsewhere (see the chapter Sepsis and Septic Shock). The Society of Critical Care Medicine has created guidelines to aid with care as part of the Surviving Sepsis Campaign. Adherence to these guidelines can decrease morbidity and mortality. Fluid resuscitation plays an important role among septic patients but also early provision of appropriate antibiotics is essential; delay in such therapy is associated with a time-dependent increase in mortality.

Hypertonic saline permits resuscitation with smaller volumes and has been suggested to have anti-inflammatory effects. Despite this, prospective studies have failed to show a difference in mortality between hypertonic and isotonic fluid resuscitation.

At this point, isotonic crystalloids remain the mainstay of sepsis-related fluid resuscitation. Large volume saline infusions can create metabolic acidosis and while similarly large Ringer’s lactate can create a mild alkalosis.