ABSTRACT
Details about the acid-base changes in hemodialysis are scarce in the literature but are potentially relevant to adequate management of patients. We addressed the acid-base kinetics during hemodialysis and throughout the interdialytic period in a cross-sectional study of adults undergoing conventional hemodialysis. Samples for blood gas analysis were obtained from the arterial limb of the arteriovenous fistula before the first session of the week (HD1), immediately at the end of HD1, and on sequential collections at 15, 30, 45, 60, and 120 min post-HD1. Additional blood samples were collected after ∼20 h following the end of the first dialysis and immediately prior to the initiation of the second dialysis of the week. Thirty adult patients were analyzed (55±15 years, 50% men, 23% diabetic; dialysis vintage 69±53 months). Mean serum bicarbonate levels increased at the end of HD1 (22.3±2.7 mEq/L vs 17.5±2.3 mEq/L, P<0.001) and remained stable until 20 h after the end of the session. The mean values of pCO2 before HD1 were below reference and at 60 and 120 min post-HD1 were significantly lower than at the start (31.3±2.7 mmHg and 30.9±3.7 mmHg vs 34.3±4.1 mmHg, P=0.041 and P=0.010, respectively). The only point of collection in which mean values of pCO2 were above 35 mmHg was 20 h post-dialysis. Serum bicarbonate levels remained stable for at least 20 h after the dialysis sessions, a finding that may have therapeutic implications. During dialysis, the respiratory response for correction of metabolic acidosis (i.e., pCO2 elevation) was impaired.
Subject(s)
Humans , Male , Female , Middle Aged , Acid-Base Equilibrium/physiology , Acid-Base Imbalance/blood , Renal Dialysis , Kidney Failure, Chronic/metabolism , Time Factors , Acid-Base Imbalance/metabolism , Blood Gas Analysis , Cross-Sectional Studies , Kidney Failure, Chronic/blood , Kidney Failure, Chronic/therapyABSTRACT
Metabolic acidosis has profound effects on vascular tone. This study investigated the in vivo effects of acute metabolic acidosis (AMA) and chronic metabolic acidosis (CMA) on hemodynamic parameters and endothelial function. CMA was induced by ad libitum intake of 1% NH4Cl for 7 days, and AMA was induced by a 3-h infusion of 6 M NH4Cl (1 mL/kg, diluted 1:10). Phenylephrine (Phe) and acetylcholine (Ach) dose-response curves were performed by venous infusion with simultaneous venous and arterial blood pressure monitoring. Plasma nitrite/nitrate (NOx) was measured by chemiluminescence. The CMA group had a blood pH of 7.15±0.03, which was associated with reduced bicarbonate (13.8±0.98 mmol/L) and no change in the partial pressure of arterial carbon dioxide (PaCO2). The AMA group had a pH of 7.20±0.01, which was associated with decreases in bicarbonate (10.8±0.54 mmol/L) and PaCO2 (47.8±2.54 to 23.2±0.74 mmHg) and accompanied by hyperventilation. Phe or ACh infusion did not affect arterial or venous blood pressure in the CMA group. However, the ACh infusion decreased the arterial blood pressure (ΔBP: -28.0±2.35 mm Hg [AMA] to -4.5±2.89 mmHg [control]) in the AMA group. Plasma NOx was normal after CMA but increased after AMA (25.3±0.88 to 31.3±0.54 μM). These results indicate that AMA, but not CMA, potentiated the Ach-induced decrease in blood pressure and led to an increase in plasma NOx, reinforcing the effect of pH imbalance on vascular tone and blood pressure control.
Subject(s)
Animals , Male , Rabbits , Acetylcholine/administration & dosage , Acidosis/physiopathology , Blood Pressure/drug effects , Endothelium, Vascular/physiopathology , Hypotension/chemically induced , Acute Disease , Acid-Base Imbalance/metabolism , Acidosis/chemically induced , Acidosis/metabolism , Blood Pressure Determination , Bicarbonates/blood , Blood Pressure/physiology , Chronic Disease , Carbon Dioxide/analysis , Endothelium, Vascular/metabolism , Hemodynamics/physiology , Hyperventilation/metabolism , Luminescence , Nitrates/blood , Nitric Oxide/metabolism , Nitrites/bloodSubject(s)
Humans , Acid-Base Equilibrium , Acid-Base Imbalance/metabolism , Carbonic Acid , Hydrochloric Acid , Bicarbonates , Alkalies/adverse effects , Acidosis , Alkalosis , BuffersABSTRACT
Os rins e pulmöes, em conjunto com bem elaborado sistema de ácidos e bases fracas, conhecidas como tampöes, säo os responsáveis pela manutençäo do estado ácido-básico do sangue, mantendo o pH do líquido extracelular sob estreito controle. Em algumas situaçöes clínicas tais como cetoacideose diabética, choque prolongado, insuficiência respiratória e renal, perdas gastro-intestinais, politransfusäo, operaçöes prolongadas e parada cárdio-respiratória pode haver quebra destes mecanismos, instalando-se os diversos quadros de alteraçöes ácido-básicas. O objetivo deste trabalho é revisar conceitos clássicos do equilíbrio ácido-básico e suas principais alteraçöes, especificamente relacionadas ao pós-operatório de cirurgia cardíaca. Também seräo abordadas aquelas situaçöes no pré-operatório que certamente acentuaräo os desvios do equilíbrio ácido-básico que ocorrem após o ato cirúrgico