The inflammatory process characterizing sepsis includes release of various mediators, most of which induce peripheral vasodilation and lead to increased microvascular permeability. Ventricular function is initially unaffected, and upregulation of cardiac output (which is necessary to maintain blood pressure in the presence of the vasodilatation typical of sepsis) is often sufficient to maintain perfusing pressures. Hypotension characterizing severe sepsis may occur when intravascular fluid volume is profoundly depressed (because of excessive venodilatation or microvascular fluid losses), myocardial depressant substances limit the ability to augment cardiac output, and/or the patient has underlying heart disease.

Sepsis is also characterized by microcirculatory injury, including depressed capillary perfusion and capillary dropout, both of which occur even without severe hypotension. With abnormalities in interorgan distributions of systemic flow, these microcirculatory abnormalities could explain the inability to extract O 2 maximally in sepsis. A primary cellular defect may also exist whereby tissues are limited in their ability to utilize available O 2—the concept of histiotoxic anoxia. However, this concept remains controversial and very difficult to investigate with existing tools. Any hypotension further exacerbates microcirculatory flow abnormalities and may cause the 'sludge' phenomenon, indicating severe microvascular plugging ( Hinsh.a.w..,199.§.).

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