Importance of venous return, venous resistance, and mean circulatory pressure in the physiology and management of shock.

906 Physiology and Management of Shock (Bressak, Raffin) PHYSIoLoGIC BACKGROUND A reasonable, unifying definition of shock at the cellular level is inadequate oxygen consumption by the cell for its metabolic needs. The negative consequence is the accumulation of an oxygen debt with eventual cellular dysfunction and death. Inadequate oxygen consumption (shock) can result from the following: (1) inadequate oxygen content of the blood; (2) inadequate circulation of the blood (cardiac output); (3) failure to deliver the circulated blood to the cell (microperfusion); and (4) failure of the cell to utilize the delivered oxygen (cellular dysfunction). In our discussion, we shall focus on inadequate circulation (cardiac output) as the limiting factor in oxygen consumption (shock). Traditionally, cardiac function has been viewed as the sole determinant of cardiac output. This function has been divided into preload, inotropy, afterload, and heart rate; cardiac output can be maximized by increasing preload and inotropy, decreasing afterload, and optimizing heart rate. 1.2 Guyton et aP emphasized that the regulation of cardiac output is determined by the interaction between the vasculature and the heart. In steady state, the heart cannot eject more blood than it receives from the vasculature and the vasculature cannot return more blood than it receives from the heart. Cardiac output must equal venous return. The physiology ofthese separate systems can best be understood graphically. A family of Starling curves shows the regulation ofcardiac output by the heart (Fig 1); maximal cardiac output requires adequate preload (indirectly measured as atrial pressure) and inotropy