Answer: c Neurogenic shock results from interruption of sympathetic vasomotor input and develops after spinal cord injury, spinal anesthesia, and severe head injury. Under normal conditions, baseline sympathetic activity establishes a degree of arteriolar and venous constriction. Ablation of this tone results in decreased systemic vascular resistance and a dramatic increase in venous capacity, causing hypotension due to relative hypovolemia. Arteriolar dilatation not only lowers the systemic vascular resistance but also allows previously unopened vascular beds to be perfused, greatly expanding venous capacity. Removal of sympathetic inputs to innervated portions of the venous system allows further venodilatation. Restoration of an effective, albeit expanded, intravascular volume may require extremely large volumes of resuscitation fluid to restore normal cardiac filling pressures. This will restore cardiac output and reverse hypotension. However, pharmacologic intervention with vasoactive drugs may be necessary and is preferable to excessive volume resuscitation. Post-shock sequelae are infrequent. Although there is significant hypotension with neurogenic shock, there is usually little if any hypoperfusion. Thus, activation of inflammatory cascade and subsequent organ injury rarely occur. A major pitfall in the management of neurogenic shock arises when there is coexistent hemorrhage or ongoing volume loss that is not appreciated. This is not an unusual situation because cervical spine trauma causing paraplegia or severe head injury is frequently associated with multiple injuries. Thus, in trauma the initial response to neurogenic shock is large volume resuscitation regardless of the presumed etiology. If hemodynamic instability persists after initial trauma resuscitation, one must assume that the cause is not neurogenic and search for occult blood loss or cardiogenic causes of shock