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Critical Care  1999 

Agitation in the ICU: part one Anatomical and physiologic basis for the agitated state

DOI: 10.1186/cc348

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Abstract:

Prior to the technological revolution in critical care medicine, agitation was a relatively minor issue. Little could be done for critically ill patients but make them as comfortable as possible and observe them for treatable decompensations. Modern ICUs now have the potential to return critically ill patients to productivity using technological advances in monitoring and closely titrated care, effectively pinning the patient firmly to the bed with tubes and appliances. As a result of our high-tech hemodynamic monitoring and support devices, we have conferred upon the already hemodynamically unstable patient new kinds of stress we never had to deal with before, and simplistic, symptomatic 'shotgun' sedation no longer applies.The temporal lobes and the Hesh gyrus receive auditory information, modulate memory and language skills and relay information to the cortex where cognitive judgments are made and motor responses are integrated [1]. The thalamus and basal ganglia act as relay stations between lower centers and the cortex [2]. The brainstem enables endurance and survival capabilities, modulating heart rate, respiratory function and autonomic actions [3]. The pineal gland is thought to modulate sleep-wake cycles [4]. The hippocampal area including the mammillary bodies modulates spatial memory formation, declarative memory, working memory, memory indexing/storage, relating expectancy to reality, and internal inhibition. Memory is recorded in several parts of the brain at same time as 'memory molecules' for storage. These molecules are modulated by limbic system, especially the mammillary bodies. Bilateral hippocampal resection results in short-term anterograde amnesia [5]. The hippocampus has receptors for neurosteroids, both mineralocorticoid and glucocorticoid. The mineralocorticoid receptors (high affinity) are agonized by alderosterone, and antagonized by spironolactone. The glucocorticoid receptors (low affinity) are agonized by dexamethasone. There are no kno

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