Splanchnic perfusion may be compromised during hemodialysis because of hypovolemia, inflammatory response, and blood flow redistribution. The aim of this study was to assess the response of splanchnic blood flow and oxygen transport to hemodialysis.
A prospective clinical study.
A mixed medical-surgical intensive care unit in a university hospital.
Nine patients with acute renal failure.
A 4-hr period of hemodialysis.
Measurements and Main Results
Systemic (via a pulmonary artery catheter), hepatosplanchnic, and femoral (via dye dilution) blood flow and gastric mucosal Pco2 were measured before, during, and 2 hrs after hemodialysis. During hemodialysis, despite unchanged arterial blood pressure, cardiac output and stroke volume decreased from 3.0 ± 1.0 L/m2/min (mean ± sd) to 2.3 ± 0.7 L/m2/min (p = .02), and from 38 ± 16 mL/m2/min to 28 ± 12 mL/m2/min (p = .01), respectively. Splanchnic but not femoral blood flow decreased from 0.9 ± 0.3 L/m2/min to 0.7 ± 0.2 L/m2/min (p = .02). The blood flows returned to baseline values after dialysis without need for therapeutic interventions. Gastric mucosal-arterial Pco2 gradients were high before dialysis (35 ± 23 torr [4.6 ± 3.1 kPa]) and did not change. Renin but not atrial natriuretic peptide concentration increased during hemodialysis from 13 ± 13 μg/L to 35 ± 40 μg/L and decreased afterward to baseline values (13 ± 13 μg/L;p = .01). Whereas interleukin 6 tended to decrease, tumor necrosis factor α increased during hemodialysis from 74 ± 24 pg/mL to 86 ± 31 pg/mL and continued to increase after hemodialysis to 108 ± 66 pg/mL (p = .022).
Hemodialysis and fluid removal in normotensive patients with acute renal failure may result in a reduction of systemic and splanchnic blood flow that is undetectable using traditional clinical signs. In contrast to what is observed in hypovolemia, the changes in regional blood flow are rapidly reversible after hemodialysis.