Hypotension and shock, although capable of inducing tissue ischemia and organ failure directly, may also be antecedents of a generalized inflammatory state which complicates reperfusion during therapy. During the early phases of tissue ischemia (before irreversible ischemic cell injury), cell 'priming' occurs. This phenomenon is manifest only when the tissue is reperfused with restoration of blood pressure ( Fig 2). Cell priming by hypoxia leads to the release of second messengers (i.e.
intracellular calcium, cyclic adenosine monophosphate, and reactive O 2 species) during the restoration of blood flow which, in turn, activate the inflammatory cascade. During reperfusion, leukocytes become entrapped in the previously ischemic microcirculation and release O 2 radicals and other inflammatory mediators locally and into the systemic circulation. Paradoxically, therefore, reperfusion following treatment of hypotension may also result in widespread tissue injury, the systemic inflammatory response syndrome, and multiple organ failure ( Wa,x,,m,,a,n,,,,,1,,99,§).
Fig. 2 Mechanisms of cellular and organ injury induced by hypotension and shock. Hypotension and/or hypoxia lead to cellular priming. Resuscitation may be followed by extensive mediator release into the vascular system and subsequent reperfusion injury and inflammation, resulting in further cellular damage and organ injury.
Pathways of hypotension for different disease processes
Although the final pathway of multiple organ failure complicating hypotension (or its treatment) is generally uniform regardless of the cause of the hypotension, the hemodynamic profile characterizing hypotension may vary depending on the disease processes ( Fig 3).
Fig. 3 Pathway and hemodynamic profile of different disease processes commonly leading to hypotension and multiple organ failure. Arrows indicate regular findings; arrows in parentheses represent facultative findings. CO, cardiac output; SVR, systemic vascular resistance.
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