Sepsis is characterized by a complex combination of cardiovascular derangements, including vasodilatation, hypovolemia, myocardial depression, and altered microvascular flow.[11,12] Vasopressors are used to improve tissue perfusion pressure, while avoiding excessive vasoconstriction in sepsis and septic shock.[13,14] NE is a commonly used vasopressor agent in septic shock. Its strong alpha-adrenergic properties make it a very effective vasopressor agent, and is considered the first vasopressor of choice.[15,16] It is also a key vasoactive agent recommended for restoring MAP in the treatment of septic shock, and it not only performs as a vasopressor but also affects pre-load and tissue perfusion.[17,18] Increasing the dosage of NE significantly augments cardiac output by 11% to 17%, suggesting that NE might recruit blood from the large venous unstressed volume as a method of “endogenous fluid challenge.”
Studies show that increasing the dosage of NE is associated with increases in cardiac output, oxygen delivery, and SvO2. During sepsis, which is characterized by relative cardiac depression, the increase in cardiac output could be explained by the beta-1 adrenergic action of NE.[21,22] Although some studies do not show improved outcome when a higher blood pressure is achieved, other studies show that a lower mean blood pressure of is associated with a higher incidence of renal failure.[4,23] However, it is unclear if vasoconstriction is deleterious for microcirculation. In addition, our results expand previous knowledge by addressing the variation in the usual blood pressure target in individuals.
MAP is a surrogate for systolic and diastolic blood pressures and systemic vascular resistance. An adequate MAP is typically essential to restore effective perfusion pressure and organ perfusion in septic shock patients. On the contrary, CVP is surrogate for volume status and right ventricular function. Thus, we selected these two parameters together as a guide to further set the reference standard for patients.
Our research differs from previous studies in that we did not focus on the specific hemodynamic targets of septic shock resuscitation, such as CVP, ScvO2, and MAP. The purpose of our research was how to make the next recovery decision based on the values of the hemodynamic parameters. As specific target parameter values cannot help us to make the correct treatment choice, some studies obtain the MAP target values only through adjusting the NE dosage. The Surviving Sepsis Campaign guidelines do not provide clinicians with clear recommendations on MAP, CVP targets, parameter-specific numerical reference values to guide recovery, and improve prognosis.
Although we sampled a relatively large cohort, but it was a single center retrospective design, and all patients followed similar basic treatment based on local protocol concerning antibiotics, steroids, and mechanical ventilation. Based on the guidelines, we chose lactate removal as an indication of improvement in tissue perfusion, as a sepsis is associated with difference in microcirculation. However, we need to perform prospective studies to monitor changes in microcirculation to confirm our conclusions.
This study was supported by a grant from the National Natural Science Foundation of China (No. 81501639)
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