How can hemodialysis-associated hypotension be explained and controlled - particular in diabetic and arteriosclerotic patients?

Patients with diabetic and/or artheriosclerotic vascular disease are often unable to tolerate volume removal during HD and develop dialysis-associated symptoms such as cerebral symptoms, cramps and hypotension. They may have a disturbed baroreceptor-mediated response of the sympathetic nervous syste m due to sclerosis of the arcus aortae. Also the peripheral vascular resist ance responds inadequately to the volume removal resulting in a sudden decr ease in cardiac output and diminished oxygen delivery to the tissue with de crease in PaO2. The same patients are able to produce an adequate vasoconst rictor response and maintain cardiovascular stability during comparable vol ume removal in presence of well-balanced correction of acid-base status wit h maintaining normal PaCO2 of 40 mm Hg during HD. In high-risk patients (n = 20) we studied arterial acidbase status before/after 4 hours HD with a st andard bicarbonate dialysate (stBic HD) of 32 mMol/l (group A). We found a correction of metabolic acidosis in a low normal range. Therefore, we addit ionally administered continuosly 120 ml NaHCO3- of 8.3% solution over the v enous line during 4 hours stBic HD (group B). Comparison of acid-base statu s was done between both groups before and after HD: group A/B before HD: pH 7.35 +/- 0.08/7.37 +/- 0.05 n.s.; PaCO2 (mmHg) 31.95 +/- 3.43/37.0 +/- 4.1 , p < 0.01; BE -7.0 +/- 4.23/-4.0 +/- 2.38, n.s.; HCO3-(mMol/l) 17.7 +/- 3. 5/20.7 +/- 2.0, p < 0.05; after HD: pH 7,47 +/- 0.06/7.46 +/- 0.03, n.s.;Pa CO2 32.0 +/- 3.43/40.0 +/- 2.5, p < 0.01; BE 0.08 +/- 2.5/4.3 +/- 0.9, p < 0.01; HCO3 23.6 +/- 2.32/28.3 +/- 0.72, p < 0.01; Delta BW (kg) 3.9 +/- 1.9 /3.9 +/- 1.5, n.s. Conclusion: Only well-balanced correction of acid-base d isorder in HD-treated patients guaranties a stable normal PaCO2. This facil itates a symptom-free HD in high-risk patients, even when diminished vascul ar elasticity impairs an adequate baroreceptor-mediated hemodynamic respons e to volume removal. A stable PaCO2 at 40 mmHg is imperative to induce sudd en vasoconstriction by chemoreceptors during weak PaO2 decrease due to dimi nishing cardiac output during volume removal in patients who are not able t o react adequately by baroreceptor response. A lowering PaO2 during volume removal could be answered with the early sudden ventilatory response by che moreceptors only in presence of normal PaCO2. A normal cerebral blood flow depends on a normal PaCO2, too, resulting in symptom-free HD.