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In recording observations made while caring for a trauma victim in the late nineteenth century, Warren78 characterized what we now term shock as a momentary pause in the act of death. Great strides have been made in our understanding of shock since that description. The current concept of shock is a series of sesllae of tissue perfusion that is inadequate to maintain normal metabolic and nutritional functions.53 Blalock's work,9 which established an etiologic classification of shock, was the major contribution to the field of shock research before 1945. Although his original classification has been expanded and modified (Table 1), this paradigm persists as a valuable starting point for understanding the fundamental concepts of shock. Many of the primary descriptive features of the shock states remain clinical in nature—a series of bedside patient observations, vital signs, urine output, and so forth. This certainly makes sense in view of the fact that the pioneers of clinical shock research had little in the way of more invasive monitoring systems and were reliant on developing their insights based on little more than physical examination. From this perspective, it stands to reason that the success or failure of a given therapeutic measure developed to resuscitate a patient from shock has historically been based on whether it induced a “normalization” of overtly abnormal clinical variables. One need look no further than the World Wars to confirm the clinical success of transfusion and fluid resuscitation in soldiers who would have otherwise succumbed to hemorrhagic shock before surgical control of their bleeding sites. Despite continued improvements in resuscitative prehospital care, transfusion and fluid therapy, and surgical approaches, resuscitation directed at normalization of bedside tests in patients presenting with shock from any cause fails. Death or significant morbidity occurs because of secondary organ failure in 12% to 18% of patients initially presenting with severe shock.76 Meanwhile, basic laboratory research efforts have confirmed a 20% mortality rate, over the long term, in animals successfully resuscitated using fluid volumes based on direct measurements of intravascular and extravascular fluid deficits.64 Other studies have provided key insights as to the pathophysiology of shock states, yielding concepts such as tissue acidosis, “irreversible” shock, and tissue oxygen debt—none of which can be quantified using traditional clinical observations.67 In addition, tremendous advances in invasive and noninvasive monitoring systems design allow clinicians to recruit far more sensitive and specific organ and cellular data to assist in treating established shock.72 Given the clear record of successful treatment of most patients in shock using nothing more than clinically evident outcomes, however, whether one need progress beyond the use of bedside tests to resuscitate patients in shock, whatever the cause, remains controversial. Because any adjunctive assessment or intervention chosen to supplement bedside testing and conventional management must lead to improved outcomes and be usable and efficient in the hectic environment of the care of shock patients, each should be evaluated and chosen carefully.
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Dabrowski et al. (2000) studied this question.
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