Abstract

JORGE, Miguel A.  and  IRRAZABAL, Célica L.. Pathophysiology of shock: New perspectives. Medicina (B. Aires) [online]. 2011, vol.71, n.5, pp.469-476. ISSN 0025-7680.

Metabolic activity can be down-regulated throughout the reduction of mitochondrial population. Lowering O₂ demand in cardiogenic, hemorrhagic and septic shock is here examined through clinical observations and trials. A decrease in the availability of O₂ will be followed by reductions in mitochondrial population and, therefore, in a decrease in O₂ demand. This response may lessen or prevent the acquisition of an O₂ debt; until now, cornerstone in the pathophysiology of shock. The cost of this adaptation is less energy production, and the resulting energy deficit has been linked to multiple organ failure (MOF), a complication of acute inflammatory processes and shock. MOF is better tolerated than anaerobic metabolism and is potentially reversible if the triggering causes are reversed and the energy level is re-established through mitochondrial biogenesis.Decoupling of mitochondrial oxidative phosphorylation occurs in both experimental models and in clinical septic shock. In critical patients this phenomenon may be detected by an inordinate increase in VO₂ in response to a therapeutically increased DO₂. This hipermetabolic stage can be mistakenly interpreted as the repayment phase of an O₂ debt.

Keywords : Oxygen consumption; Shock; Energy metabolism; Mitochondrial disease; Critical illness.

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