Oxygen consumption in sepsis and septic shock.

摘要: This review article examines the pathophysiology of septic shock, with special attention to concept supply-dependent consumption and implications this has for therapy. Patients shock require higher levels oxygen delivery (DO2) maintain aerobic metabolism. When DO2 is inadequate, peripheral tissues switch anaerobic metabolism decreases. The lactic acidosis that occurs a reasonable clinical marker supply dependency inadequate tissue perfusion. Maximizing an important part hemodynamic resuscitation patients shock. To achieve goal, intravascular volume must be restored myocardial depression associated sepsis treated optimize cardiac output. normalization arterial lactate concentration goal resuscitative efforts.