Terlipressin in patients with septic shock: friend or foe?

Excerpt

Sir: Dr. Morelli et al. investigated the effects of terlipressin on systemic and regional hemodynamics in patients with catecholamine-dependent hyperdynamic septic shock [1]. The conclusion that the terlipressin-linked decrease in cardiac index (CI) represents a positive response during severe septic shock is not entirely correct and should be reconsidered. Notably, the increase in systemic and pulmonary vascular resistance index following terlipressin infusion accounted at the expense of a marked depression in both systemic blood flow and tissue oxygen delivery index (DO₂I). The fact that the oxygen consumption index (VO₂I) also fell raises the very interesting question whether terlipressin reduced the metabolic demand or contributed to a pathologic oxygen supply dependency. The latter condition may occur when DO₂ decreases below threshold levels and oxygen extraction rate (O₂-ER) fails to increase in proportion to the reduced DO₂. As a consequence VO₂ falls, despite an increased oxygen demand. In this regard, Vincent demonstrated that assessing the ratio between the product of CI and O₂-ER before and after the intervention is a valid methodology to determine a pathologic oxygen supply dependency, while avoiding a mathematical coupling between DO₂ and VO₂ [2]. Since CI and O₂-ER are physiologically inversely interrelated, a shift to values below or above 1 indicates a mismatch between DO₂ and VO₂. A ratio of less than 0.65 and greater than 1.35 indicates the presence of a pathologic oxygen supply dependency [2, 3]. To unmask whether insufficient oxygen supply may have been a concern in the patients studied by Morelli et al. [1], we assessed the relationship between CI and O₂-ER as follows: Notably, terlipressin infusion led to a sustained oxygen supply dependency from hour 4 to 10 post treatment [3] (Table 1). The fact that lactate levels did not increase over time needs to be tempered with the realization that lactate is an insensitive marker of tissue hypoxia during sepsis, especially since an increase may just be the result of a hypermetabolism [4]. …