The Consequences of Cardiac Autonomic Dysfunction in Multiple Organ Dysfunction Syndrome

Abstract

The development of multiple organ dysfunction syndrome (MODS) is characterized by activation of innate immunity, resulting in an inappropriate release of inflammatory mediators leading to cellular damage in parenchymal organs and to inflammatory, metabolic, and neuroendocrine disturbances [1]. There is increasing evidence that autonomic dysfunction may contribute substantially to the development of MODS since continuous communication between all vital organs through autonomic nervous system signals is a fundamental feature in healthy humans [2, 3]. An ‘uncoupling’ of these neurally mediated organ interactions in MODS and sepsis may potentially alter neural reflexes and thus cause a disruption of appropriate interorgan communication, thereby advancing single organ dysfunction into MODS. There may also be a diminished reactivity of the organ to reflex stimuli. Taking into consideration the interference of the mediators and toxins with cardiac cellular signal transduction, blunted or dysfunctional cellular responses possibly contribute to decreased reflex responses of the target organ, leading to an impairment in the autonomic balance of the heart.