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Choosing the Best Blood Pressure Target for Vasopressor Therapy
JAMA ( IF 51.273 ) Pub Date : 2020-02-12 , DOI: 10.1001/jama.2019.22526
John C. Marshall

Medical research drives innovation and improves outcomes. In cardiology, advances in diagnosis, prevention, and treatment reduced the 30-day mortality from acute myocardial infarction from 20% to 12.4% between 1995 and 2014.1 Similarly, for women diagnosed with breast cancer, 5-year survival has increased from 74% to 88.5% over the past 4 decades2 in parallel with advances in diagnosis and targeted therapy, including chemotherapeutic regimens such as cyclophosphamide, methotrexate, and fluorouracil (CMF), trastuzumab, and aromatase inhibitors.3 However, patient outcomes also improve in the absence of specific technological advances. For example, it is estimated that between 1990 and 2017, the global number of deaths from sepsis declined from 15.7 million (95% uncertainty interval [UI], 14.7-16.7 million) to 11.0 million (95% UI, 10.0-12.1 million).4 This improvement has not occurred because of new drugs and new procedures but rather from improved approaches to resuscitation and physiologic support and from understanding the effects of often subtle variability in management strategies that translate into better patient outcomes. A recurring theme of these insights is that although physiologic support is good, restraint in providing that support is often better, for example, controlling blood glucose levels but not too rigidly using insulin5; administering transfusions but accepting a lower hemoglobin threshold at which to make the decision to transfuse6; or providing ventilator support but limiting distention of the lungs.7 Underlying this theme is an emerging recognition that in acute critical illness, what is normal is not necessarily optimal and that interventions bring both benefits and harms. In this issue of JAMA, Lamontagne and colleagues8 report the results of the 65 trial, an evaluation of blood pressure targets to guide vasopressor therapy. The emergency hemodynamic management of septic shock includes administration of fluids to restore a relative intravascular volume deficit, and the use of vasopressor agents such as norepinephrine to increase blood pressure when fluid alone is insufficient to do so. Increased blood pressure is thought to result in augmented tissue perfusion, although the optimal threshold is unknown. Previous guidelines of the Surviving Sepsis Campaign had recommended that a mean arterial pressure (MAP) threshold of 65 mm Hg should be targeted,9 based on observational data that tissue perfusion is maintained at a MAP as low as 65 mm Hg.10 Implicit in that recommendation is an assumption that harm is only a consequence of a MAP that is too low, and not one that is too high. Prior studies have suggested that a higher blood pressure may be harmful11,12 and that targeting a MAP of 65 mm Hg results in MAP levels of 75 mm Hg or higher because infusions are increased when the pressure is lower than the target but not necessarily reduced when it is higher than the target blood pressure level.12 Moreover, the physiologic objective is not pressure but flow, and for a given pressure, flow is increased when resistance is reduced, as it is in septic shock.
更新日期:2020-02-12

 

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