A physicochemical model of crystalloid infusion on acid-base status.

The objective of this study is to develop a physicochemical model of the projected change in standard base excess (SBE) consequent to the infused volume of crystalloid solutions in common use. A clinical simulation of modeled acid-base and fluid compartment parameters was conducted in a 70-kg test participant at standard physiologic state: pH =7.40, partial pressure of carbon dioxide (PCO2) = 40 mm Hg, Henderson-Hasselbalch actual bicarbonate ([HCO3]HH) = 24.5 mEq/L, strong ion difference (SID) = 38.9 mEq/L, albumin = 4.40 g/dL, inorganic phosphate = 1.16 mmol/L, citrate total = 0.135 mmol/L, and SBE =0.1 mEq/L. Simulations of multiple, sequential crystalloid infusions up to 10 L were conducted of normal saline (SID = 0), lactated Ringer's (SID = 28), plasmalyte 148 (SID = 50), one-half normal saline þ 75 mEq/L sodium bicarbonate (NaHCO3; SID = 75), 0.15 mol/L NaHCO3 (SID = 150), and a hypothetical crystalloid solution whose SID = 24.5 mEq/L, respectively. Simulations were based on theoretical completion of steady-state equilibrium and PCO2 was fixed at 40 mm Hg to assess nonrespiratory acid-base effects. A crystalloid SID equivalent to standard state actual bicarbonate (24.5 mEq/L) results in a neutral metabolic acid-base status for infusions up to 10 L. The 5 study solutions exhibited curvilinear relationships between SBE and crystalloid infusion volume in liters. Solutions whose SID was greater than 24.5 mEq/L demonstrated a progressive metabolic alkalosis and less, a progressive metabolic acidosis. In a human model system, the effects of crystalloid infusion on SBE are a function of the crystalloid and plasma SID, volume infused, and nonvolatile plasma weak acid changes. A projection of the impact of a unit volume of various isotonic crystalloid solutions on SBE is presented. The model's validation, applications, and limitations are examined.

Reversal of idiopathic pulmonary arterial hypertension and allograft pneumonectomy after single lung transplantation.

Prior to the advent of effective medical therapies, the only treatment option for patients with idiopathic pulmonary arterial hypertension (IPAH) was lung transplantation. We present the case of a woman who underwent single-lung transplantation for the treatment of IPAH > 10 years ago in whom chronic rejection developed. Despite complete obliteration of the allograft, it was noted that her PA pressure levels had almost normalized. Therefore, an allograft pneumonectomy was performed. To our knowledge, this is the first reported case of the regression of pulmonary vascular disease following lung transplantation with subsequent successful removal of the allograft.

Comparative quantitative acid-base analysis in coronary artery bypass, severe sepsis, and diabetic ketoacidosis.

The main objective of this study was to assess the relationship of standard base excess (SBE) to delta strong ion difference effective (DeltaSIDe) in critical illness. Critical illness is characterized by variable plasma nonvolatile weak acid components (DeltaA(-)), and SBE becomes discordant with DeltaSIDe. The author hypothesized that both acid-base models are equivalent when SBE and DeltaSIDe are corrected for DeltaA(-). A retrospective chart review was performed to assess this hypothesis by looking at changes in SBE, DeltaSIDe, and DeltaA(-) in 30 coronary artery bypass graft surgery patients, 30 severe sepsis patients, and 15 diabetic ketoacidosis patients. SBE equals the sum of the DeltaSIDe and DeltaA(-). The SBE quantifies the magnitude of the metabolic acid-base derangement, the DeltaSIDe quantifies the plasma strong cation/anion imbalance, and the DeltaA(-) quantifies the magnitude of the hypoalbuminemic alkalosis. The partitioning of SBE into physicochemical components can facilitate analyses of complex acid-base disorders in critical illness.