About: Base excess is a research topic. Over the lifetime, 1411 publications have been published within this topic receiving 31299 citations. The topic is also known as: base deficit & BE.
TL;DR: Two commonly used diagnostic approaches are compared, one relying on plasma bicarbonate concentration and "anion gap," the other on "base excess," with a third method based on physicochemical principles, for their value in detecting complex metabolic acid-base disturbances.
Abstract: We compare two commonly used diagnostic approaches, one relying on plasma bicarbonate concentration and “anion gap,” the other on “base excess,” with a third method based on physicochemical principles, for their value in detecting complex metabolic acid‐base disturbances. We analyzed arterial blood samples from 152 patients and nine normal subjects for pH, P CO 2 , and concentrations of plasma electrolytes and proteins. Ninety-six percent of the patients had serum albumin concentration < 3 SD below the mean of the control subjects. In about one-sixth of the patients, base excess and plasma bicarbonate were normal. In a great majority of these apparently normal samples, the third method detected simultaneous presence of acidifying and alkalinizing disturbances, many of them grave. The almost ubiquitous hypoalbuminemia confounded the interpretation of acid‐base data when the customary approaches were applied. Base excess missed serious acid‐base abnormalities in about one-sixth of the patients; this method fails when the plasma concentrations of the nonbicarbonate buffers (mainly albumin) are abnormal. Anion gap detected a hidden “gap acidosis” in only 31% of those samples with normal plasma bicarbonate in which such acidosis was diagnosed by the third method; when adjusted for hypoalbuminemia, it reliably detected the hidden abnormal anions. The proposed third method identifies and quantifies individual components of complex acid‐base abnormalities and provides insights in their pathogenesis.
TL;DR: The use of balanced crystalloid and colloid solutions in elderly surgical patients prevented the development of hyperchloremic metabolic acidosis and resulted in improved gastric mucosal perfusion when compared with saline-based solutions.
Abstract: The IV administration of sodium chloride solutions may produce a metabolic acidosis and gastrointestinal dysfunction. We designed this trial to determine whether, in elderly surgical patients, crystalloid and colloid solutions with a more physiologically balanced electrolyte formulation, such as Hartmann's solution and Hextend (R), can provide a superior metabolic environment and improved indices of organ perfusion when compared with saline-based fluids. Forty-seven elderly patients undergoing major surgery were randomly allocated to one of two study groups. Patients in the Balanced Fluid group received an intraoperative fluid regimen that consisted of Hartmann's solution and 6% hetastarch in balanced electrolyte and glucose injection (Hextend). Patients in the Saline group were given 0.9% sodium chloride solution and 6% hetastarch in 0.9% sodium chloride solution (Hespan (R)). Biochemical indices and acid-base balance were determined. Gastric tonometry was used as a reflection of splanchnic perfusion. Postoperative chloride levels demonstrated a larger increase in the Saline group than the Balanced Fluid group (9.8 vs 3.3 mmol/L, P = 0.0001). Postoperative standard base excess showed a larger decline in the Saline group than the Balanced Fluid group (-5.5 vs -0.9 mmol/L, P = 0.0001). Two-thirds of patients in the Saline group, but none in the Balanced Fluid group, developed postoperative hyperchloremic metabolic acidosis (P = 0.0001). Gastric tonometry indicated a larger increase in the CO, gap during surgery in the Saline group compared with the Balanced Fluid group (1.7 vs 0.9 kPa, P = 0.0394). In this study, the use of balanced crystalloid and colloid solutions in elderly surgical patients prevented the development of hyperchloremic metabolic acidosis and resulted in improved gastric mucosal perfusion when compared with saline-based solutions.
TL;DR: In this paper, a randomized, randomized, blinded, crossover study was conducted to determine whether correction of acidemia using bicarbonate improves hemodynamics in patients who have lactic acidosis.
Abstract: Study objective To determine whether correction of acidemia using bicarbonate improves hemodynamics in patients who have lactic acidosis. Design Prospective, randomized, blinded, crossover study. Each patient sequentially received sodium bicarbonate and equimolar sodium chloride. The order of the infusions was randomized. Setting Intensive care unit of a tertiary care hospital. Patients Fourteen patients who had metabolic acidosis (bicarbonate less than 17 mmol/L and base excess less than -10) and increased arterial lactate (mean, 7.8 mmol/L). All had pulmonary artery catheters and 13 were receiving catecholamines. Measurements and main results Sodium bicarbonate (2 mmol/kg body weight over 15 minutes) increased arterial pH (7.22 to 7.36, P less than 0.001), serum bicarbonate (12 to 18 mmol/L, P less than 0.001), and partial pressure of CO2 in arterial blood (PaCO2) (35 to 40 mm Hg, P less than 0.001) and decreased plasma ionized calcium (0.95 to 0.87 mmol/L, P less than 0.001). Sodium bicarbonate and sodium chloride both transiently increased pulmonary capillary wedge pressure (15 to 17 mm Hg, and 14 to 17 mm Hg, P less than 0.001) and cardiac output (18% and 16%, P less than 0.01). The mean arterial pressure was unchanged. Hemodynamic responses to sodium bicarbonate and sodium chloride were the same. These data have more than 90% power of detecting a 0.5 L/min (7%) change in mean cardiac output after administration of sodium bicarbonate compared with that after sodium chloride. Even the 7 most acidemic patients (mean pH, 7.13; range, 6.90 to 7.20) had no significant hemodynamic changes after either infusion. Conclusions Correction of acidemia using sodium bicarbonate does not improve hemodynamics in critically ill patients who have metabolic acidosis and increased blood lactate or the cardiovascular response to infused catecholamines in these patients. Sodium bicarbonate decreases plasma ionized calcium and increases PaCO2.
TL;DR: The nomogram is especially useful for calculation of base excess after direct measurement of pH, pCO2 and hemoglobin concentration and the standard bicarbonate can also be calculated from the nomogram.
Abstract: The blood acid-base status comprises the pH, pCO2 and base excess values.The alignment nomogram includes scales for these values together with scales for bicarbonate and total-CO2 of plasma.The nomogram is especially useful for calculation of base excess after direct measurement of pH, pCO2 and hemoglobin concentration. The nomogram is also useful for calculation of both pCO2 and base excess after direct measurement of pH, total-CO2 of plasma and hemoglobin concentration.The standard bicarbonate can also be calculated from the nomogram.
TL;DR: In critically ill patients in which a measurement of lactate level was ordered, lactate and SIG were strong independent predictors of mortality when they were the major source of metabolic acidosis.
Abstract: Acid–base abnormalities are common in the intensive care unit (ICU). Differences in outcome exist between respiratory and metabolic acidosis in similar pH ranges. Some forms of metabolic acidosis (for example, lactate) seem to have worse outcomes than others (for example, chloride). The relative incidence of each type of disorder is unknown. We therefore designed this study to determine the nature and clinical significance of metabolic acidosis in critically ill patients. An observational, cohort study of critically ill patients was performed in a tertiary care hospital. Critically ill patients were selected on the clinical suspicion of the presence of lactic acidosis. The inpatient mortality of the entire group was 14%, with a length of stay in hospital of 12 days and a length of stay in the ICU of 5.8 days. We reviewed records of 9,799 patients admitted to the ICUs at our institution between 1 January 2001 and 30 June 2002. We selected a cohort in which clinicians caring for patients ordered a measurement of arterial lactate level. We excluded patients in which any necessary variable required to characterize an acid–base disorder was absent. A total of 851 patients (9% of ICU admissions) met our criteria. Of these, 548 patients (64%) had a metabolic acidosis (standard base excess < -2 mEq/l) and these patients had a 45% mortality, compared with 25% for those with no metabolic acidosis (p < 0.001). We then subclassified metabolic acidosis cases on the basis of the predominant anion present (lactate, chloride, or all other anions). The mortality rate was highest for lactic acidosis (56%); for strong ion gap (SIG) acidosis it was 39% and for hyperchloremic acidosis 29% (p < 0.001). A stepwise logistic regression model identified serum lactate, SIG, phosphate, and age as independent predictors of mortality. In critically ill patients in which a measurement of lactate level was ordered, lactate and SIG were strong independent predictors of mortality when they were the major source of metabolic acidosis. Overall, patients with metabolic acidosis were nearly twice as likely to die as patients without metabolic acidosis.