Prostacyclin in Septic Shock: Conclusion

However, there is increasing evidence that discrete tissue hypoxia may exist on the regional level despite supranormal D02 lack of O2 supply dependency, and normal lactate values For example we can estimate gastrointestinal tissue oxygenation by gastric mucosal tonometry. A recent short report has shown PGI2 to increase D02 and gastric mucosal pH without an increase in whole body V02
We believe that our protocol for hemodynamic stabilization with sufficient volume,inotropic, and vasopressor support to achieve “supranormal” O2 delivery and adequate perfusion pressure pressures provides a reasonable basis on which to test an agent such as PGI2. We recognize that there is no single protocol for resuscitation in septic shock and that these are trade-offs when potentially competing drugs are administered. For instance, we cannot rule out that the norepinephrine given to maintain arterial pressures may have counterbalanced to some degree the vasodilating effects of PGI2. However, in severe septic shock, alpha-agonists vasoconstrictors such as norepinephrine or high doses of dopamine, are necessary to achieve adequate organ perfusion pressures. other Norepinephrine has been shown to be effective in septic shock not only to improve kidney function but also to increase D02 and V02 Even with the norepinephrine given in the present study, systemic vascular resistance remained only about half normal, suggesting that these patients were not overly vasoconstricted.
The PGI2 dosage chosen here was twice that reported previously, including the study in which D02 and V02 improved in nonhyperdynamic patients. Although it is possible that titration of PGI2 in each patient to even higher doses would have had a greater effect on V02, we believe that the dosage was an appropriate experimental choice, particularly in light of the known potential side effects of PGI2 ’ We did observe an increase in intrapulmonary shunt and a decrease in arterial P02 and MAP. In one study that used greater dosages of prostacyclin, V02 was increased only in the two nonsurvivors.
In summary, short-term fixed-dose PGI2 infusion did not reveal a “covert” hypoxia in these patients with septic shock in whom a substantial O2 debt may have been prevented by conventional support. The PGI2 produced a further increase in D02 without a matching increase in V02, and O2 extraction was not increased. A small increase in V02 when calculated by the indirect Fick equation suggests some dependence of mathematical coupling of D02 and V02 data.

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