Beyond Mean Arterial Pressure During Cardiopulmonary Bypass: Endothelial Reactivity, Oxygen Delivery, and Organ-Specific Perfusion.
TL;DR
Collectively, these investigations demonstrate that CPB-associated factors such as non-pulsatile flow and the kinetics of CPB initiation, early hypotension, hemodilution, hypothermia, systemic inflammation, oxidative stress, and anesthetic-induced vasodilation impair endothelial-mediated vascular responsiveness.
Abstract
Background: Management of mean arterial pressure (MAP) during cardiopulmonary bypass (CPB) is traditionally guided by fixed pressure targets. Accordingly, literature-defined “safe” MAP thresholds during CPB range widely, from approximately 50 to 80 mmHg, reflecting marked heterogeneity in clinical practice and physiological assumptions. These thresholds implicitly rely on preserved vascular autoregulation. Materials and Methods: A narrative literature review was conducted using PubMed, MEDLINE, and Embase databases to identify experimental and clinical studies published in English addressing MAP management during CPB and its interaction with endothelial function, oxygen delivery (DO₂), oxygen exposure, arterial carbon dioxide tension (PaCO₂), and neurological or renal outcomes. Search terms included cardiopulmonary bypass, mean arterial pressure, autoregulation, endothelial dysfunction, oxygen delivery, hyperoxia, PaCO₂, cerebral vasoreactivity, and acute kidney injury. Randomized controlled trials, observational studies, physiological investigations, and mechanistic reports were included. Reference lists were manually screened to identify additional relevant studies. The evidence was synthesized to construct a pathophysiological framework focused on dynamic autoregulatory impairment during CPB. Results: Eighteen studies were included in the qualitative synthesis. Collectively, these investigations demonstrate that CPB-associated factors such as non-pulsatile flow and the kinetics of CPB initiation, early hypotension, hemodilution, hypothermia, systemic inflammation, oxidative stress, and anesthetic-induced vasodilation impair endothelial-mediated vascular responsiveness. This impairment reduces vasodilatory reserve and results in a progressive upward shift of the lower limit of autoregulation during CPB. Conclusions: The evidence synthesized in this review indicates that endothelial dysfunction acquired during CPB reduces vasodilatory capacity and dynamically elevates the minimum autoregulatory pressure. This mechanism provides a physiological explanation for the wide range of “safe” MAP thresholds reported in the literature and challenges the adequacy of fixed pressure targets. Individualized perfusion strategies integrating MAP with DO₂, oxygen exposure, PaCO₂ control, and endothelial reactivity are required to optimize cerebral and renal protection during CPB.