Vasoplegic Syndrome After Cardiovascular Surgery: A Review of
Pathophysiology and Outcome Oriented Therapeutic Management
Abstract
Vasoplegic syndrome (VPS) is defined as systemic hypotension due to
profound vasodilatation and loss of systemic vascular resistance (SVR),
despite normal or increased cardiac index (CI). It occurs in 9- 44% of
cardiac surgery patients after cardiopulmonary bypass (CPB) and is
associated with significant morbidity and mortality. The pathogenesis of
VPS is multifactorial involving the activation of contact, coagulation,
and complement systems and the activation of leukocytes. platelets and
endothelial cells resulting in an imbalance in the regulation of the
vascular tone; inducible nitric oxide synthase [iNOS] triggered by
inflammatory cytokines during CPB produces nitric oxide (NO), which
increases vascular levels of cyclic guanosine monophosphate (cGMP),
resulting in vasodilation. leading to postcardiac surgery VPS. Standard
treatment options for severe refractory VPS are extremely limited and
include vasopressor support. latest Surviving Sepsis Campaign guidelines
also consider that the best therapeutic management of vascular hypo-
responsiveness to vasopressors could be a combination of multiple
vasopressors, including norepinephrine (NE) and early prescription of
vasopressin. This review will address the various definitions, risk
factors, pathophysiology, potential cardiac candidates, and potential
therapeutic interventions for VPS following cardiac surgery focussed on
the outcome. This review did not require any ethical approval or consent
from the patients.