Why the study?
Vasoplegia following cardiopulmonary bypass can lead to catecholamine resistance and heightened mortality, requiring potential therapeutic interventions beyond standard vasopressors.
This narrative review highlights the pathophysiology of vasoplegia after cardiopulmonary bypass and discusses emerging targeted therapies, including angiotensin II and nitric oxide scavengers.
Should not yet change post-CPB vasoplegia management; leaves open the need for RCTs on angiotensin II and NO scavengers.
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.
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Barnes et al. (2020) studied this question.
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