Circulatory mechanisms of shock and their mediators.

Abstract

Traditional concepts of shock therapy have been based on conventional monitoring. However, the availability of invasive monitoring systems has provided the means to describe the patterns of oxygen transport in various acute life-threatening illnesses. Surgical trauma provides a useful model for investigation of other shock syndromes, because measurements may be made in the preoperative control period, during the hemodynamic crisis intraoperatively, and sequentially throughout the postoperative period for survivors and nonsurvivors. This provides a time-related pattern of physiologic events that may form the basis for the physiologic evaluation of mechanisms operative in survivors and nonsurvivors. Physiologic alterations which are compensatory may be identified from the survivor pattern and differentiated from decompensations associated with the lethal course. The DO2 pattern reflects circulatory functional changes which may limit body metabolism as reflected by VO2. The body compensates for tissue hypoxia and increased metabolic needs by increased flow and DO2 in sepsis and trauma, and by increased oxygen extraction in hemorrhagic and cardiogenic shock where flow is limited. The interactions of survivors' hemodynamic and oxygen transport patterns define compensatory responses which primarily are increased cardiac output, DO2, and VO2. Inadequate compensations and decompensations of shock are clearly manifest by the nonsurvivor pattern. Therapeutic goals may be defined by the values of the survivor patterns; reduced mortality and morbidity result when these goals are vigorously applied prospectively (17-19).