Intradialytic hypotension and splanchnic shifting: Integrating an overlooked mechanism with the detection of ischemia-related signals during hemodialysis.

Abstract

In the most simple analysis, a patient's hematocrit during hemodialysis will rise when the rate of ultrafiltration exceeds the rate at which the fluid is mobilized from extravascular spaces; the greater the rise in hematocrit, the lower blood volume is and the more likely intradialytic hypotension (IDH) is to occur. A secondary mechanism of IDH may be due to sudden shift of blood volume away from the heart under conditions of borderline cardiac filling. A substantial portion of blood volume resides in the splanchnic venous system. During the early part of dialysis, a centripetal shift of red cells from this anatomical region to the central circulation has been documented to occur. The magnitude of this shift is unpredictable, and it may depend on the level of splanchnic vasoconstriction predialysis. The amount of splanchnic shift may also be reduced in patients with autonomic dysfunction. Once this central shift in blood volume has occurred, it can be reversed during further ultrafiltration due to ischemia-induced release of vasodilatory molecules that cause dilation of upstream splanchnic arterioles; this causes increased transmission of arterial pressure to the splanchnic veins, acutely increasing their capacity. The increased splanchnic venous capacity may cause a sudden shift of blood away from the central circulation to fill these veins under conditions where cardiac filling has already been reduced. The result can be severe IDH due to insufficient cardiac filling and cardiac output. One fruitful preventive approach might be to continuously monitor the blood or dialysate for the sudden appearance of such ischemia-related molecules or other signals which may herald not only dialysis hypotension but tissue stunning, warning that the fluid removal rate should be immediately reduced.