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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