Despite the multiple causes of the shock state, all causes possess the common abnormality of oxygen supply not meeting tissue metabolic demands. Compensatory mechanisms may mask the severity of hypoxemia and hypoperfusion, since catecholamines and extracellular fluid shifts initially compensate for the physiologic derangements associated with patients in shock. Despite the achievement of normal physiologic parameters after resuscitation, significant metabolic acidosis may continue to be present in the tissues, as evidenced by increased lactate levels and metabolic acidosis. This review discusses the major endpoints of resuscitation in clinical use.
- Oxygen demand
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