This review demonstrates mechanisms and management of hemodynamic instability during renal replacement therapy, suggesting improved monitoring methods.
Hemodynamic instability associated with renal replacement therapy (HIRRT) is a frequent and life-threatening event, with a potential adverse impact on the technique’s performance to preserve homeostasis, acid-base balance, and control fluid balance, and is associated with worse patient outcomes. HIRRT has a complex and multifactorial pathogenesis, in relation to RRT’s impact on both cardiac output and peripheral vasomotor tone. Among these, fluid removal by net ultrafiltration is a potent modifier of effective blood volume and may reduce cardiac output in preload-dependent patients (i.e., patients in whom an excessive decrease in preload will potentially lead to a decrease in cardiac output). Recent data support that advanced hemodynamic monitoring, associating continuous cardiac output monitoring with frequent preload-dependence assessment and perfusion indices, may help refine bedside physiological reasoning in the face of HIRRT, to limit inadequate fluid removal cessation when reduced preload has been ruled out. Advances in both the physiological understanding of HIRRT mechanisms and the application of integrative strategies aiming to prevent HIRRT are described in the review, with a specific emphasis on the RRT settings most capable of impacting the incidence of this complication.
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Bitker et al. (2026) studied this question.
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