Conclusions
Vasoplegia is a common feature of all advanced shock states, with norepinephrine remaining the cornerstone of vasoplegia-induced hypotension. However, given our improved understanding of vasoplegia, management is likely to evolve from a standardized therapy with norepinephrine alone to a multimodal strategy with two or more vasopressors. Based on new pathophysiological data, numerous potential drugs are currently being investigated. Nevertheless, these new potential treatments or therapeutic strategies should be evaluated not only for their ability to increase arterial pressure but also for their capacity to improve survival or decrease major morbidity as well as for their effectiveness/cost ratio.
Abbreviations
ACTH: Adrenocorticotropic hormone; AT1: Angiotensin type 1; AVP: Arginine vasopressin; cGMP: Cyclic guanosine monophosphate; CIRCI: Critical illnessrelated corticosteroid insufficiency; COX2: Cyclooxygenase 2; GPCR: G protein-coupled receptor; GRK: GPCR kinase; IL: Interleukin; iNOS: Inducible nitric oxide synthase; MAP: Mean arterial blood pressure; MB: Methylene blue; NO: Nitric oxide; SOFA: Sequential Organ Failure Assessment; SSC: Surviving Sepsis Campaign; TNF: Tumor necrosis factor; V1: Vasopressin type 1; VSMC: Vascular smooth muscle cell
Acknowledgements
We thank Pierre Pothier for editing the manuscript.
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Crit Care. 2018;22(52) © 2018 BioMed Central, Ltd.
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