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Review
. 2020 Jun 25:8:2050312120935466.
doi: 10.1177/2050312120935466. eCollection 2020.

Vasoplegia after cardiopulmonary bypass: A narrative review of pathophysiology and emerging targeted therapies

Affiliations
Review

Vasoplegia after cardiopulmonary bypass: A narrative review of pathophysiology and emerging targeted therapies

Theresa J Barnes et al. SAGE Open Med. .

Abstract

Cardiovascular disease remains the leading cause of death in the United States, and cardiopulmonary bypass is a cornerstone in the surgical management of many related disease states. Pathophysiologic changes associated both with extracorporeal circulation and shock can beget a syndrome of low systemic vascular resistance paired with relatively preserved cardiac output, termed vasoplegia. While increased vasopressor requirements accompany vasoplegia, related pathophysiologic mechanisms may also lead to true catecholamine resistance, which is associated with further heightened mortality. The introduction of a second non-catecholamine vasopressor, angiotensin II, and non-specific nitric oxide scavengers offers potential means by which to manage this challenging phenomenon. This narrative review addresses both the definition, risk factors, and pathophysiology of vasoplegia and potential therapeutic interventions.

Keywords: Vasoplegia; cardiopulmonary bypass; hydroxocobalamin; methylene blue; surgical shock; vasoconstrictor agents.

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Conflict of interest statement

Declaration of conflicting interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Figures

Figure 1.
Figure 1.
Biochemical pathways and therapies for vasoplegia. Red lines denote inhibition; green arrows denote stimulation. iNOS: inducible nitric oxide synthase; NO: nitric oxide; cGMP: cyclic guanosine monophosphate; KATP: potassium-adenosine triphosphate; H2S: hydrogen sulfide.

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