Mechanisms for hemodynamic instability related to renal replacement therapy: a narrative review

Abstract

Hemodynamic instability related to renal replacement therapy (HIRRT) is a frequent complication of all renal replacement therapy (RRT) modalities commonly used in the intensive care unit. HIRRT is associated with increased mortality and may impair kidney recovery. Our current understanding of the physiologic basis for HIRRT comes primarily from studies of end-stage kidney disease patients on maintenance hemodialysis in whom HIRRT is referred to as 'intradialytic hypotension'. Nonetheless, there are many studies that provide additional insights into the underlying mechanisms for HIRRT specifically in critically ill patients. In particular, recent evidence challenges the notion that HIRRT is almost entirely related to excessive ultrafiltration. Although excessive ultrafiltration is a key mechanism, multiple other RRT-related mechanisms may precipitate HIRRT and this could have implications for how HIRRT should be managed (e.g., the appropriate response might not always be to reduce ultrafiltration, particularly in the context of significant fluid overload). This review briefly summarizes the incidence and adverse effects of HIRRT and reviews what is currently known regarding the mechanisms underpinning it. This includes consideration of the evidence that exists for various RRT-related interventions to prevent or limit HIRRT. An enhanced understanding of the mechanisms that underlie HIRRT, beyond just excessive ultrafiltration, may lead to more effective RRT-related interventions to mitigate its occurrence and consequences.

Keywords: Acute kidney injury; Blood pressure; Dialysis; Hemodynamic instability; Hypotension; Intradialytic hypotension; Renal replacement therapy.

Fig. 1

Summary of underlying mechanisms that contribute to HIRRT. Mechanisms include: (1) hypovolemia, (2) systolic/diastolic dysfunction, and (3) decreased vascular tone from distributive shock. They can be due to patient- or RRT-related factors or both. There is often an overlap of these mechanisms. HIRRT is associated with increased mortality. HIRRT (i.e., recurrent hypotension) may impair renal recovery, a phenomenon that may be exacerbated by impaired kidney blood flow autoregulation in AKI

Fig. 2

Contributors to hypovolemia and HIRRT in critically ill patients with AKI requiring RRT. Both RRT-related and patient-related factors can contribute to hypovolemia and the development of HIRRT in the context of inadequate physiologic compensation

Fig. 3

Contributors to cardiac dysfunction and HIRRT in critically ill patients with AKI requiring RRT. Both RRT and patient-related factors are implicated, in the presence of inadequate physiologic compensation. RRT induces transient episodes of reduced myocardial perfusion, leading to myocardial stunning, which is seen as regional wall motion abnormalities (RWMAs). UF and osmolar shifts can induce hypovolemia which can precipitate a Bezold–Jarisch reflex. Patient factors include underlying cardiac disease, critical illness and associated treatment (mechanical ventilation, fluid and vasopressors) and complications of critical illness such as bowel ischemia which itself can be exacerbated by HIRRT (not shown)

Fig. 4

Contributors to decreased vascular tone that lead to HIRRT in critically ill patients with AKI requiring RRT (+) and some treatment strategies (−). Question mark represents an unproven, theoretical effect on vascular tone. RRT-related and patient-related factors are represented on the top and bottom of the figure, respectively