Clinical Dilemmas in Dialysis: Managing the Hypotensive Patient
Pathophysiology of dialysis hypotension: An update,☆☆

https://doi.org/10.1053/ajkd.2001.28090Get rights and content

Abstract

Dialysis hypotension occurs because a large volume of blood water and solutes are removed over a short period of time, overwhelming normal compensatory mechanisms, including plasma refilling and reduction of venous capacity, due to reduction of pressure transmission to veins. In some patients, seemingly paradoxical and inappropriate reduction of sympathetic tone may occur, causing reduction of arteriolar resistance, increased transmission of pressure to veins, and corresponding increase in venous capacity. Increased sequestration of blood in veins under conditions of hypovolemia reduces cardiac filling, cardiac output, and, ultimately, blood pressure. Adenosine release due to tissue ischemia may participate in reducing norepinephrine release locally, and activation of the Bezold-Jarisch reflex, perhaps in patients with certain but as yet undefined cardiac pathology, may be responsible for sudden dialysis hypotension. Patients with diastolic dysfunction may be more sensitive to the effects of reduced cardiac filling. The ultimate solution is reducing the ultrafiltration rate by use of longer dialysis sessions, more frequent dialysis, or reduction in salt intake. Increasing dialysis solution sodium chloride levels helps maintain blood volume and refilling but ultimately increases thirst and interdialytic weight gain, with a possible adverse effect on hypertension. Blood volume monitoring with ultrafiltration or dialysis solution sodium feedback loops are promising new strategies. Maintaining tissue oxygenation via an adequate blood hemoglobin level seems to be important. Use of adenosine antagonists remains experimental. Given the importance of sympathetic withdrawal, the use of pharmacologic sympathetic agonists is theoretically an attractive therapeutic strategy. © 2001 by the National Kidney Foundation, Inc.

Section snippets

Incidence and effect on outcomes

Dialysis hypotension occurs in up to 20% of dialysis sessions. Whereas it seems that frequent intradialytic hypotension would lead to increased morbidity and mortality, this has not been well documented. A low predialysis blood pressure (BP) is a marker of increased mortality,1 but this may be due to the fact that low predialysis BP is a marker of pre-existing cardiac disease in the end-stage renal disease (ESRD) population. Similarly, patients with frequent hypotensive episodes during dialysis

Basic concepts

The pathophysiology of dialysis hypotension was reviewed in 1991.6 The basic concepts have not changed, and the reader is referred to that publication for detailed references. Several important points can be re-emphasized. The blood volume in a typical dialysis patient is approximately 4.5 L, with a corresponding plasma volume of approximately 3 L.7 In patients undergoing thrice-weekly dialysis schedules and gaining 1.5 kg/d, the therapeutic requirement is to remove 3 L of fluid per dialysis

Cardiac compensatory mechanisms

Changes in cardiac rate in response to hypovolemia are often impaired in dialysis patients. Whereas cardiac rate changes may be important in increasing cardiac output from baseline (eg, during physical activity), they appear to be less important in maintaining cardiac output under conditions of decreased filling. For example, studies in dogs receiving propranolol during hemorrhage indicate that this cardiac rate change is of minimal importance in maintaining cardiac output during hypovolemia.8

Plasma refilling

The primacy of plasma refilling is indicated by the fact that, if one does not remove fluid during dialysis, intradialytic hypotension is rare, indeed. This clarifies the fact that the ultimate cause of hypotension is reduced cardiac filling. The initial compensatory mechanism is refilling of the plasma water space from surrounding tissue spaces. As a result of refilling, even though 1 entire plasma volume is removed during dialysis, the blood volume typically decreases only by 5% to 20%.11

The

Venous capacity: Interaction with arterial tone

Detailed hemodynamic analysis of IHEs suggests 2 important things. (1) There is no sudden decrease in plasma volume just before a hypotensive episode. (2) IHEs seem to be due to a decrease in cardiac output engendered by reduced cardiac filling.23, 24 How can this be explained?

Most of the 3 L or so of plasma volume resides in the veins, and several organ perfusion systems, notably skin and splanchnic, contain veins that can markedly alter their capacity.25 A slight loss in venous tone in either

References (39)

  • AW Yu et al.

    Splanchnic erythrocyte content decreases during hemodialysis: A new compensatory mechanism for hypovolemia

    Kidney Int

    (1997)
  • M Nishimura et al.

    Enhanced production of nitric oxide may be involved in acute hypotension during maintenance hemodialysis

    Am J Kidney Dis

    (1998)
  • G Ligtenberg

    Regulation of blood pressure in chronic renal failure: Determinants of hypertension and dialysis-related hypotension

    Neth J Med

    (1999)
  • SP Kelleher et al.

    Sympathetic nervous system in the loss of autoregulation in acute renal failure

    Am J Physiol

    (1984)
  • Adequacy of dialysis and nutrition in continuous peritoneal dialysis: Association with clinical outcomes

    J Am Soc Nephrol

    (1996)
  • JK Leypoldt et al.

    Determination of circulating blood volume by continuously monitoring hematocrit during hemodialysis

    J Am Soc Nephrol

    (1995)
  • E Ritz et al.

    Dialysis hypotension—Is it related to diastolic left ventricular malfunction?

    Nephrol Dial Transplant

    (1987)
  • HP Krepel et al.

    Variability of relative blood volume during haemodialysis

    Nephrol Dial Transplant

    (2000)
  • JC Van Stone et al.

    The effect of dialysate sodium concentration on body fluid distribution during hemodialysis

    Trans Am Soc Artif Intern Organs

    (1980)
  • Cited by (285)

    View all citing articles on Scopus

    Address reprint requests to John T. Daugirdas, MD, Professor of Medicine, University of Illinois at Chicago, VA Chicago Hospital—West Side, 820 South Damen Ave, Chicago, IL 60612. E-mail: [email protected]

    ☆☆

    0272-6386/01/3804-0402$35.00/0

    View full text