Answer: d Hypovolemic shock is readily diagnosed when there is an obvious source of volume loss and overt signs of hemodynamic instability and increased adrenergic output are present. After acute hemorrhage, hemoglobin and hematocrit values do not change until compensatory fluid shifts have occurred or exogenous fluid is administered. These values decrease once transcapillary refill, osmotic-induced shifts, or non-RBC volume resuscitation expands the blood volume. It is imperative that the distinction be made between hypovolemic and cardiogenic forms of shock, because appropriate therapy differs dramatically. Restoration of perfusion in hypovolemic shock requires reexpansion of circulating blood volume in conjunction with necessary interventions to control ongoing volume loss. Continued hemodynamic instability after fluid resuscitation implies that shock has not been reversed or that there is ongoing blood or volume loss. In severe, prolonged hypovolemia, ventricular contractile function may itself become depressed and require inotropic support to maintain ventricular performance, but in general, pharmacologic interventions directed toward increased contractility in situations of inadequate preload are ineffective, further complicate metabolic derangements, and are not indicated until adequate volume replacement has been completed. Complications are less frequent after treatment of hemorrhagic shock than in situations of septic or traumatic shock. In the later circumstances, the massive activation of inflammatory mediator response systems and consequences of their disseminated, indiscriminate cellular injury can be quite profound