Anesthetics for Induction of Anesthesia (also see Chapter 10 )

Any intravenously administered anesthetic given to a trauma patient in hemorrhagic shock may potentiate profound hypotension and even cardiac arrest as a result of inhibition of circulating catecholamines. Although propofol and thiopental are the mainstays of intravenous induction in the OR, their use in trauma patients is especially problematic because both drugs are vasodilators and both have a negative inotropic effect. Etomidate is a frequently espoused alternative; published reports suggest that it is associated with more cardiovascular stability than other intravenous hypnotic drugs in the trauma population.^{[21] [22] [23]}

Ketamine continues to be popular for induction in trauma patients because it causes a release of catecholamines, primarily by direct action on the CNS.^[24] However, it is also a direct myocardial depressant.^{[25] [26]} In normal patients, the effect of catecholamine release masks the cardiac depression and results in hypertension and tachycardia. In hemodynamically stressed patients, on the other hand, cardiac depression may be unmasked and lead to cardiovascular collapse.^[27]

Hypovolemic patients will become hypotensive with the administration of any induction anesthetic because of interruption of compensatory sympathetic outflow. Previously healthy young patients can lose up to 40% of their blood volume before experiencing a decrease in arterial BP, which can lead to potentially catastrophic circulatory collapse with anesthetic induction, regardless of the agent chosen. The dose of anesthetic must be decreased in the face of hemorrhage, down to none at all in patients with life-threatening hypovolemia. Rapid-sequence intubation may proceed with muscle relaxants alone, although onset time may be prolonged in a patient with circulatory impairment. Subsequent patient recall of intubation and emergency procedures is highly variable and affected by the presence of coexisting TBI, intoxication, and the depth of hemorrhagic shock. Decreased cerebral perfusion appears to inhibit memory formation but cannot be reliably associated with any particular BP or chemical marker. Administration of 0.2 mg of scopolamine (a tertiary ammonium vagolytic) has been advocated to inhibit memory formation in the absence of anesthetic drugs in this situation, but it may interfere with subsequent neurologic examination because of its long half-life. Small doses of midazolam will reduce the incidence of patient awareness, but can also contribute to hypotension. Although recall of ED and OR events is not unusual in this circumstance, anesthesia provider liability appears to be limited; a recent analysis of intraoperative awareness lawsuits in the ASA Closed Claims Database revealed no claims related to surgery in trauma patients. ^[28]