LAUSR

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.