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Review
. 2018 Aug 7;13(8):1297-1303.
doi: 10.2215/CJN.12141017. Epub 2018 Feb 26.

Mechanisms, Clinical Implications, and Treatment of Intradialytic Hypotension

Affiliations
Review

Mechanisms, Clinical Implications, and Treatment of Intradialytic Hypotension

Patrick B Reeves et al. Clin J Am Soc Nephrol. .

Abstract

Individuals with ESKD requiring maintenance hemodialysis face a unique hemodynamic challenge, typically on a thrice-weekly basis. In an effort to achieve some degree of euvolemia, ultrafiltration goals often involve removal of the equivalent of an entire plasma volume. Maintenance of adequate end-organ perfusion in this setting is dependent on the institution of a variety of complex compensatory mechanisms. Unfortunately, secondary to a myriad of patient- and dialysis-related factors, this compensation often falls short and results in intradialytic hypotension. Physicians and patients have developed a greater appreciation for the breadth of adverse outcomes associated with intradialytic hypotension, including higher cardiovascular and all-cause mortality. In this review, we summarize the evidence for adverse outcomes associated with intradialytic hypotension, explore the underlying pathophysiology, and use this as a basis to introduce potential strategies for its prevention and treatment.

Keywords: Chronic; Fluid Therapy; Goals; Hemodialysis; Hemodynamics; Humans; Kidney Failure; Physicians; Plasma Volume; blood pressure; end-stage renal disease; hypotension; renal dialysis; ultrafiltration.

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Figures

Figure 1.
Figure 1.
Schematic demonstrating normal and inadequate compensatory mechanisms to maintain BP in response to hemodialysis with ultrafiltration (blue background denotes venous circulation; red background denotes arterial circulation). Top: Normal compensatory responses involve activation of the sympathetic nervous system, renin-angiotensin-aldosterone system (RAAS) and possibly increased vasopressin release, in addition to adequate plasma refill. Together these facilitate maintenance of BP via increased venous return and cardiac preload, increased cardiac output, and arteriolar vasoconstriction. Bottom: When any aspect of the normal compensatory response is impaired, the maintenance of adequate perfusion pressure may be compromised, leading to intradialytic hypotension. UF, ultrafiltration.

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