Objective: Investigation of the hypothesis that the infusion of 10 ng/kg/min prostacyclin (epoprostenol) ([PGI.


Objective: Investigation of the hypothesis that the infusion of 10 ng/kg/min prostacyclin (epoprostenol) ([PGI.sub.2]) improves [Osub2] uptake in patients with hyperdynamic septic shock

Design: Prospective, single cohort design.

Setting: ICU, university hospital.

Patients: Fifteen postoperative patients with septic shock

Interventions: Infusion of 10 ng/kg/min of [PGI.sub.2] for 60 min.

Measurements: without fault [i]or[/i] blemish [i]or[/i] flaw hemodynamic profile with [O.sub.2] transport-related variables (simultaneous measurements of [VOsub2] from the respiratory gases and through cardiovascular Fick) and blood lactate flats before start of the [PGI.sub.2]-infusion and 60 min thereafter.

Main results: Oxygen delivery increased significantly (14 percent) from its already high value, 750 [+ or -] 238 to 852 [+ or -] 214 ml/min/[m.sup.2]. The [Osub2] extraction ratio remained unchanged. When [VOsub2] was measured from the respiratory gases, it was unchanged. When [VOsub2] was measured through cardiovascular Fick, it increased slightly (p [les than] 005)

Conclusions: We deduce that in this [O.sub.2] challenge exhibition with [PGI.sub.2] in patients with septic stroke an increase in [O.sub.2] delivery was not matched by dint of an increase in [VO.sub.2]. We believe that the adequate conventional support of these patients may have interrupted the [PGI.sub.2] from revealing a "covert" [Osub2] sin The [PGI.sub.2] test did not predict mortality by means of [O.sub.2] supply dependency. The small increase in [VOsub2] as calculated indirectly refer tos a degree of mathematical coupling of [Osub2] delivery and uptake.



There is little doubt that tissue hypoxia is linked to multiple organ dysfunction syndrome and eventual mortality in patients with septic shock[1] It is still not known, however, for what reason much systemic [O.sub.2] delivery ([DO.sub.2]) really is "adequate" for organ viability and patient survival or on what account some patients fail to extract sufficient [Osub2] equal when it seems to be abundantly delivered.[2] Thus, the search continues for therapy to improve hypoxia, unknown or otherwise, in patients with sepsis.

There is evidence from one as well as the other animal and human studies that prostacyclin (epoprostenol) ([PGI.sub.2]) may have beneficial purports on tissue perfusion in sepsis, eg vasodilation, increasing the number of perfused capillaries,[3] maintaining splanchnic kin flow,[4] and inhibiting platelet and neutrophil activation.[5-7] Short-term infusion of [PGI.sub.2] or related mingles has been shown to increase the [DO.sub.2] and in near cases oxygen consumption ([VO.sub.2]) in critically ill patients.[8-10] Thus, [PGI.sub.2] has been indicateed as an agent for an [Osub2] looseness or challenge test, in which [DO.sub.2] is increased substantially and a clinically relevant increase in [VOsub2] at least 10 percent[11] is considered abnormal [Osub2] furnish dependency, which may correlate with a poor prognosis.

In trying to identify adequacy of oxygenation in the critically ill, at least brace factors tend to confound the data to date. First, the flush of conventional resuscitation, ie, with fluid, inotropes, and vasopressors, is crucial. If baseline flushs of support are less than optimal, any intervention may display an increase in [VO.sub.2]. inferior the most common method of determining [VOsub2] in the ICU setting, indirectly from the Fick principle (cardiac output X a-v [Osub2] difference), has get to under criticism lately for overestimating and being les valid than the [VOsub2] measured directly from respiratory gases, as well as being mathematically coupl to [DO.sub.2], which may overestimate the correlation of the sum of two units leading to an erroneous conclusion of [Osub2] endow dependency.[12-17] Thus, in the near study, we address several important questions which remain: (1) Can [PGI.sub.2] lay open a "covert" hypoxia in patients with sepsis who have been completely resuscitated by conventional means? (2) Is the mechanism of [PGI.sub.2] to improve oxygen extraction or increase convective [DO.sub.2]? (3) Does the indirect [VOsub2] calculation overestimate the [VOsub2] measurement through gas exchange?

METHODS

Patients

In a prospective, single cohort design, we studied 15 patients in large tertiary-care ICU. All conducts were approved by our institutional research review committee and informed agreement was received. Clinical data of the patients are shown in Table 1 All required ventilatory support and pulmonary artery catheterization becoming to septic shock. Patients exhibited at least five of the following clinical criteria of septic shock:[18] persistent arterial hypotension with a systolic kindred pressure [less than 90 mm Hg increasing bulk need ([greater than] 4 L of fluid by 24 h), systemic vascular resistance [les than] 700 dyne XsX[cmsup-5] temperature above 385 [degrees] C or below 350 [degrees] C white kin cell count above 12x[10.sup.9] or below 4x[10sup9] small rooms per liter, either positive kin culture or a known site of sepsis, decrease of the thrombocyte [greater than] 30 percent/24 h not owing to bleeding, tachypnea, or mental disturbances with agitation and confusion.

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