Prostacyclin in Septic Shock

Prostacyclin in Septic ShockThere is little doubt that tissue hypoxia is linked to multiple organ dysfunction syndrome and eventual mortality in patients with septic shock. It is still not known, however, how much systemic O2 delivery (D02) really is “adequate” for organ viability and patient survival or why some patients fail to extract sufficient O2 even when it seems to be abundantly delivered. Thus, the search continues for therapy to improve hypoxia, occult or otherwise, in patients with sepsis.
There is evidence from both animal and human studies that prostacyclin (epoprostenol) (PGI2) may have beneficial effects on tissue perfusion in sepsis, eg, vasodilation, increasing the number of perfused capillaries, maintaining splanchnic blood flow, and inhibiting platelet and neutrophil activation.’ Shortterm infusion of PGI2 or related compounds has been shown to increase the D02 and in some cases oxygen consumption (V02) in critically ill patients.’ Thus, PGI2 has been suggested as an agent for an O2 flux or challenge test, in which D02 is increased substantially and a clinically relevant increase in V02, at least 10 percent, is considered abnormal O2 supply dependency, which may correlate with a poor prognosis.
In trying to identify adequacy of oxygenation in the critically ill, at least two factors tend to confound the data to date review order antibiotics online. First, the level of conventional resuscitation, ie, with fluid, inotropes, and vasopressors, is crucial. If baseline levels of support are less than optimal, any intervention may show an increase in V02. Second, the most common method of determining V02 in the ICU setting, indirectly from the Fick principle (cardiac output X a-v O2 difference), has come under criticism lately for overestimating and being less valid than the V02 measured directly by respiratory gases, as well as being mathematically coupled to D02, which may overestimate the correlation of the two, leading to an erroneous conclusion of O2 supply dependency. Thus, in the present study, we address several important questions which remain: (1) Can PGI2 uncover a “covert” hypoxia in patients with sepsis who have been fully resuscitated by conventional means? (2) Is the mechanism of PGI2 to improve oxygen extraction or increase convective D02? (3) Does the indirect V02 calculation overestimate the V02 measurement by gas exchange?

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