Hemodynamic response to lower body negative pressure in hemodialysis patients

Background Hypovolemia is thought to have an important role in the pathogenesis of dialysis-related hypotension. Methods: We studied the effect of hypovolemia simulated by lower body negative pressure (LBNP) in 11 hypotension-prone (HP) and 11 hypotension-resistant (HR) hemodialysis patients. LBNP was applied stepwise from 0 to -20 to -40 mm Hg. Systolic arterial pressure, heart rate, and central venous pressure (CVP) were recorded continuously after cannulation of the right jugular vein. Stroke volume index was measured at each step echocardiographically. At the end of each level of LBNP, blood samples were obtained to measure norepinephrine (NE), epinephrine (E), and atrial natriuretic peptide (ANP) levels. Results: At baseline, UP (12 +/- 5 and 16 7 mm Hg), heart rate (72 +/- 9 and 70 +/- 13 beats/min), cardiac index (2.3 +/- 0.6 and 2.5 +/- 0.9 L/min), NE (median, 341 pg/mL [range, 198 to 789 pg/mL] and 365 pg/mL [range, 177 to 675 pg/mL] or 2.02 nmol/L [range, 1.17 to 4.66 nmol/L] and 2.16 nmol/L [range, 1.05 to 4.00 nmol/L]), E (median, 46 pg/mL [range, 18 to 339 pg/mL] and 58 pg/mL [range, 21 to 122 pg/mL] or 251 pmol/L [range, 98 to 1,951 pmol/L] and 317 pmol/L [range, 115 to 666 pmol/L]) were similar, whereas systolic arterial pressure (141 +/- 26 versus 164 +/- 22 mm Hg) and ANP (median, 441 pg/mL [range, 152 to 1,330 pg/mL] versus 804 pg/mL [range, 517 to 3,560 pg/mL] ng/L) were lower (P < 0.05) in HP patients. In response to LBNP (-40 mm Hg), CVP decreased by 6.5 +/- 4.0 mm Hg in the HP group and 4.9 +/- 4.9 mm Hg in the HR group. In HP patients, this decrease was associated with a greater decrease in SI (37% +/- 16% versus 27% +/- 16%) and systolic arterial pressure (19% +/- 21% versus 4% +/- 14%) than in HR patients. Plasma ANP levels did not change, whereas increases in NE and E levels were similar in HP and HR patients. Conclusion: Patients who frequently experience episodes of hypotension during dialysis also are prone to develop hypotension during LBNP, which results from reduced myocardial contractile reserve and/or inadequate sympathetic tone. (C) 2003 by the National Kidney Foundation, Inc.