Objectives: To describe different paradigms that define the stress response, and to postulate how stress is implicated in the pathophysiology of critical illness.
Design: Articles were identified through a search of PubMed and Google Scholar.
Results: The stress response represents a bundle of adaptive behavioral, physiological, and cellular responses. Although generally beneficial, an important adverse consequence of excessive stress is organ dysfunction. Many interventions currently applied to the critically ill patient are additive and may contribute to organ dysfunction, renewed deterioration, and impaired or delayed recovery. Resilience (ρ) summarizes the interaction among predisposition factors, injury (or stressors), and the body's allostatic responses. Resilience changes over the course of critical illness but is potentially measurable and may be used to identify at-risk patients and to tailor therapy.
Conclusion: Critical illness may represent a stress-related decompensation syndrome mediated by neural, endocrine, bioenergetic, and immune systems. As patients pass through the separate phases of critical illness, consideration should be given to different therapeutic end points. This may be particularly pertinent during the established organ dysfunction phase where targeting of normal values may have deleterious consequences. Improved strategies could thus emerge from an increased knowledge and monitoring of the stress response, and what constitutes an optimal adaptive state as it evolves in the course of critical illness.