Pathogenesis of Hemodialysis-Associated Hypotension

Primary Pathophysiologic Mechanisms

Hemodialysis-associated hypotension results from two fundamental mechanisms: insufficient intravascular volume to support the ultrafiltration rate and inadequate cardiovascular compensatory responses to volume removal, as noted by the Kidney International guidelines 1, 2
The American Journal of Kidney Diseases recommends that ultrafiltration rates should be carefully managed to avoid excessive fluid removal, as rates as low as 6 mL/h/kg can be associated with higher mortality risk 1, 2

The American Journal of Kidney Diseases suggests that acetate-containing dialysate can contribute to hypotension by decreasing total vascular resistance, increasing venous pooling, and increasing myocardial oxygen consumption 4, 5
The optimal dialysate temperature is between 34-35°C, as higher temperatures can promote peripheral vasodilation and reduce sympathetic tone, whereas lower temperatures can increase peripheral vasoconstriction through enhanced sympathetic activity 4, 5

The American Journal of Kidney Diseases notes that chronic kidney disease patients exhibit impaired neurohormonal responses to intravascular volume loss, including blunted activation of the renin-angiotensin-aldosterone system and sympathetic nervous system 3

The American Journal of Kidney Diseases recommends that antihypertensive medications should be carefully managed before dialysis sessions, as they can exacerbate hypotension by preventing compensatory vasoconstriction and cardiac responses 4, 5

The American Journal of Kidney Diseases suggests that food intake immediately before or during hemodialysis can cause splanchnic vasodilation and decreased peripheral vascular resistance, redirecting blood flow away from the peripheral circulation 4, 5
Anemia can reduce oxygen-carrying capacity and impair cardiovascular compensation, though correction to hemoglobin 11 g/dL can reduce hypotension incidence 4, 5

The Kidney International guidelines note that recurrent intradialytic hypotension can create a cascade of end-organ ischemia affecting the heart, brain, liver, gut, and kidneys, contributing to increased morbidity and mortality 1, 2
Protracted hypotension during hemodialysis may exaggerate urea rebound, compromising dialysis adequacy, as reported by the American Journal of Kidney Diseases 5

The American Journal of Kidney Diseases recommends that dry weight should be carefully set to avoid chronic hypovolemia, as a dry weight set too low can trigger compensatory mechanisms including increased thirst and paradoxically higher interdialytic weight gains 5