Pathophysiology of dialysis hypotension: An update

Dialysis hypotension occurs because a large volume of blood water and solut es are removed over a short period of time, overwhelming normal compensator y mechanisms, including plasma refilling and reduction of venous capacity, due to reduction of pressure transmission to veins. In some patients, seemi ngly paradoxical and inappropriate reduction of sympathetic tone may occur, causing reduction of arteriolar resistance, increased transmission of pres sure to veins, and corresponding increase in venous capacity. Increased seq uestration of blood in veins under conditions of hypovolemia reduces cardia c filling, cardiac output, and, ultimately, blood pressure. Adenosine relea se due to tissue ischemia may participate in reducing norepinephrine releas e locally, and activation of the Bezold-Jarisch reflex, perhaps in patients with certain but as yet undefined cardiac pathology, may be responsible fo r sudden dialysis hypotension. Patients with diastolic dysfunction may be m ore sensitive to the effects of reduced cardiac filling. The ultimate solut ion 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 b ut ultimately increases thirst and interdialytic weight gain, with a possib le adverse effect on hypertension. Blood volume monitoring with ultrafiltra tion or dialysis solution sodium feedback loops are promising new strategie s. Maintaining tissue oxygenation via an adequate blood hemoglobin level se ems to be important. Use of adenosine antagonists remains experimental. Giv en the importance of sympathetic withdrawal, the use of pharmacologic sympa thetic agonists is theoretically an attractive therapeutic strategy. (C) 20 01 by the National Kidney Foundation, Inc.