Decompensation and cellular injury

If hypotension is not corrected promptly, the limited capability of the compensatory circulatory responses to support tissue oxygenation will be overwhelmed and an O 2 deficit may occur. Cellular ischemia induces alterations in cell function which may further exacerbate the circulatory response to the primary disease process. For example, a cellular O2 deficit in prolonged hypotension is accompanied by anaerobic glycolysis and increased lactate production. Excess plasma lactate increases microvascular permeability, thereby promoting intravascular fluid loss. With ischemia, cellular ATP production is also depressed and the membrane's sodium pump fails, thereby further promoting intravascular fluid loss (in this case to the intracellular compartment) ( Wax.m§n.,1996). Fluid shift away from the intravascular space reduces venous return and ventricular preload, thus worsening hypovolemia. As acidosis also depresses myocardial contractility, protracted hypotension leading to tissue ischemia is accompanied by further attenuation of stroke volume (myocardial depressant agents may also be released from ischemic tissues, e.g. the splanchnic circulation). This sequence is particularly deleterious in cardiogenic hypotension where stroke volume may be critically diminished already. Therefore the consequences of the metabolic processes induced by tissue ischemia are a further fall in blood pressure and O 2 delivery, and more tissue ischemia. The course of the primary disease process may then be modified by the consequences of the tissue ischemia—the concept of a vicious cycle which, if not prevented by rapid restoration of tissue oxygenation, hastens multiple organ failure and death.

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