FIGURE 10.2 Sequence of cardiovascular derangements in shock states Alterations in cardiac preload, afterload, and contractility decrease effective cardiac output, leading to several neurohumoral responses that attempt to restore organ perfusion As the shock state progresses, these compensatory mechanisms fail to maintain effective cardiac output and clinical deterioration from compensated to uncompensated shock becomes evident The inability of cells to efficiently utilize oxygen to produce energy in the form of ATP has been termed “cytopathic hypoxia” and is largely attributable to mitochondrial bioenergetic dysfunction The inability of mitochondria to use oxygen to sustain ATP production results in an energy deficit that can impair cellular metabolism and, ultimately, organ function Mitochondrial dysfunction has been postulated to explain the increasingly recognized paradox of progressive organ injury following shock (particularly in sepsis and after trauma) despite minimal cell death even after restoration of tissue oxygen delivery TYPES OF SHOCK