No abstract

The introduction of an electronic alerting PSS did not lead to a reduction in mortality when adjusted for severity of illness defined by physiological variables. Predictive performance was not enhanced by the addition of biochemical variables and co-morbidities.

mechanisms. Although we basically agree, we argue that the underlying mechanism(s) motivating the use of vasopressor(s) must be kept in mind. Increasing BP by a pressor combination increasing the vascular tone via different mechanisms might be correct. This approach will work well if hypotension results mainly from the loss of vascular tone. In this case, the proposed approach fits well with the physiological acute cardiovascular response. Sympathetic stimulation, vasopressin release, and angiotensin level increase interact synergistically to increase the vascular tone. However, the decrease in BP in critically ill patients results from more complex interactive mechanisms (eg, heart failure, hypovolemia, abnormal ventriculo-arterial coupling), for which the pure vascular tone control might be insufficient or dangerous. We do not share the "no sense of a norepinephrine association with epinephrine." Epinephrine is the emergency hormone, which links vascular tone, heart function, and metabolic effects to "escape" the life-threatening situation. Its combination with norepinephrine can be then logical for some patients.The second concept ("catecholamine vasopressor support-sparing strategies") proposes the use of "adjunctive" therapies to reduce pressor support. Although theoretically appealing, such adjunctive therapies are not easy to use in practice.The last concept ("microcirculatory protection") is the oldest but the most recently investigated in critical care. Until now, it seemed obvious that the microcirculation changes might be corrected by therapeutic actions focused on macrocirculation, suggesting that microcirculation is passively impaired. This is very different when microcirculation is impaired by a combination of abnormal systemic circulation associated with pure inflammatory mechanisms at the microcirculation level (activated adhering white cells with microthrombosis). This situation frequently occurs in critically ill patients and could be improved by a combination of cardiovascular hemodynamic supports with modulation of the inflammation-induced interaction between endothelial cells and circulating immune cells.