We acti

We inhibitor Oligomycin A therefore hypothesize that identification of a critical MAP level lower than 70 mmHg could further decrease vasopressor exposure, the frequency of disease-related events and mortality in septic shock patients. This hypothesis should be tested in future prospective studies.The present data, which were collected from patients treated in 124 intensive care units worldwide, are in accordance with results of previous single-center studies. Two prospective studies evaluating the effects of different MAP levels on tissue perfusion and renal function in septic shock observed that increasing MAP from 65 to 85 mmHg did not improve systemic oxygen metabolism, skin microcirculatory blood flow, splanchnic perfusion nor renal function [3,4].

Similar to our results, relevant increases of norepinephrine were required to increase MAP from 65 to 85 mmHg in both studies. Two retrospective studies applying similar statistical models observed that the critical MAP for 30 or 28-day mortality in septic shock and sepsis was 65 [5] and 60 mmHg [20], respectively.Neither age nor pre-existent arterial hypertension relevantly influenced the association between MAP and 28-day mortality or the occurrence of disease-related events including renal failure. However, considering the wide CIs of the influence of pre-existent hypertension on the association between MAP and mortality, it is possible that the present analysis yielded false-negative results.

Based on current physiologic and pathophysiologic understanding [1], it would be expected that in elderly and/or chronic hypertensive patients organ autoregulation curves, particularly renal, are shifted to the right and higher MAP levels needed to preserve organ function and ensure survival. Preliminary results in another sepsis population similarly suggest that neither age nor chronic arterial hypertension has a clinically relevant impact on the association between MAP and mortality [20].Metabolic Entinostat acidosis related to catecholamine therapy has been typically observed during epinephrine infusion and may originate from epinephrine-related acceleration of metabolism and/or induction of tissue hypoperfusion [21,22]. In earlier studies, catecholamines have repeatedly been associated with disease-related events on cardiac function ranging from ischemia to myocardial stunning and apoptosis [12]. Tachycardia is a particularly common and well-known side effect of catecholamine therapy [12]. The significant association between heart rate during the shock period and 28-day mortality in this patient population confirms the results of an earlier prospective observational study in 48 septic shock patients [15].

Leave a Reply

Your email address will not be published. Required fields are marked *

*

You may use these HTML tags and attributes: <a href="" title=""> <abbr title=""> <acronym title=""> <b> <blockquote cite=""> <cite> <code> <del datetime=""> <em> <i> <q cite=""> <strike> <strong>