Relation of oxygen transport patterns to the pathophysiology and therapy of shock states.

Descriptions of the sequence of hemodynamic and oxygen transport events have characterized the various types of shock syndromes and have shown that reduced VO2 is the earliest pathophysiologic event; it precedes the initial hypotensive crisis. Reduced or inadequate VO2, produced by low flow, by maldistribution of flow, and by increased metabolic demand is the primary pathogenic event that produces the shock state as well as the regulatory mechanism that stimulates compensatory reactions including increases in heart rate, myocardial contractility, cardiac output and minute ventilation. Sequential hemodynamic and oxygen transport patterns are related to the degree of the shock state and its outcome; the patterns of survivors and nonsurvivors can be predicted from these patterns by multivariate analyses. A branch chain decision tree for fluid resuscitation of critically ill postoperative patients was developed from decision rules based on objective, physiologic, heuristic data of survivors. Criteria were defined for initiating and stopping fluids, inotropic agents, vasodilators and vasopressors; colloids were found empirically to be more effective than crystalloids in reaching the optimal hemodynamic and oxygen transport goals. The use of a branch chain decision tree helps to achieve expeditiously therapeutic goals by providing a coherent organized patient management plan. In prospective studies, therapy that supports compensatory increases in CI and DO2 produces the survivor pattern and was demonstrated to improve survival rates. This confirms the validity of an organized physiologic approach in contrast to the traditional approach whose objectives are to search for physiologic and biochemical abnormalities and then to restore them to normal if and when they are discovered. This approach emphasizes aggressive fluid management in tacit acknowledgement that unrecognizes hypovolemia, delay in treatment of hypovolemia or inadequate volume therapy all lead to low VO2 which is the primary precipitating event in most patients with postoperative, hemorrhagic, traumatic and septic shock. The essence of this plan is to maintain prophylactically the patient in an optimal hemodynamic state that does not allow him to develop tissue hypoxia from blood volume, hemodynamic and oxygen transport deficits. However, episodes of reduced CI, DO2 and VO2 often occur intraoperatively with little or no hypotension or with hypotension which is treated by administration of ephedrine or other vasopressors.