Mitochondria produce metabolic energy, serve as biosensors for oxidative stress, and eventually become effector organelles for cell death through apoptosis. The extent to which these manifold mitochondrial functions are altered by previously unrecognized actions of anesthetic agents seems to explain and link a wide variety of perioperative phenomena that are currently of interest to anesthesiologists from both a clinical and a scientific perspective. In addition, many surgical patients may be at increased perioperative risk because of inherited or acquired mitochondrial dysfunction leading to increased oxidative stress. This review summarizes the essential aspects of the bioenergetic process, presents current knowledge regarding the effects of anesthetics on mitochondrial function and the extent to which mitochondrial state determines anesthetic requirement and potential anesthetic toxicity, and considers some of the many implications that our knowledge of mitochondrial dysfunction poses for anesthetic management and perioperative medicine.

MITOCHONDRIA not only generate and modulate bioenergy but also serve as the final effectors for the termination of cell viability as organisms approach the end of their lifespan. Therefore, the implications of these processes with regard to understanding evolution, disease, aging, and death are profound. Particularly relevant to anesthesiologists is the role of mitochondria in determining the response of the nervous system to anesthetic agents, in initiating mechanisms of cell injury or protection after ischemic, hypoxic, or toxic injuries, and their ability to precipitate critical illness in individuals with inherited or acquired mitochondrial disorders. These aspects of mitochondrial biology and pathophysiology will be briefly summarized in this clinically oriented review.