Abstract
Critically ill patients who manifest hemodynamic instability, have cardiovascular homeostatic mechanisms which are failing to compensate for the stresses to which they are exposed. Accordingly, organ perfusion can not be consistently maintained at a level necessary to sustain normal bodily function. At the most basic level, in severe hemorrhagic shock, circulatory homeostatic mechanisms preserve coronary and cerebrovascular blood flow, by maintaining peripheral vasomotor tone and cardiac output at a sufficient enough level to maintain perfusion of maximally dilated coronary and cerebral vessels. This important goal is accomplished by a coordinated autonomic outpouring of sympathetic activity which induces both metabolic, vascular tone and cardiac contractile changes, which collectively sustain heart and brain viability. This maximal stress response, if sustained, induces profound tissue dysfunction of the remainder of the body and is not compatible with life. However, as a transient manoeuvre, it can sustain vital organ function long enough for more definitive manoeuvres to be accomplished, which will be associated with increased visceral organ blood flow.
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Mehta, N.K., Pinsky, M.R. (1998). Pharmacologic support of the hemodynamically unstable patient. In: Critical Care Nephrology. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-5482-6_5
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DOI: https://doi.org/10.1007/978-94-011-5482-6_5
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