Effects of intravenous solutions on acid-base equilibrium: from crystalloids to colloids and blood components

Intravenous fluid administration is a medical intervention performed worldwide on a daily basis. Nevertheless, only a few physicians are aware of the characteristics of intravenous fluids and their possible effects on plasma acid-base equilibrium. According to Stewart’s theory, pH is independently regulated by three variables: partial pressure of carbon dioxide, strong ion difference (SID), and total amount of weak acids (ATOT). When fluids are infused, plasma SID and ATOT tend toward the SID and ATOT of the administered fluid. Depending on their composition, fluids can therefore lower, increase, or leave pH unchanged. As a general rule, crystalloids having a SID greater than plasma bicarbonate concentration (HCO3–) cause an increase in plasma pH (alkalosis), those having a SID lower than HCO3– cause a decrease in plasma pH (acidosis), while crystalloids with a SID equal to HCO3– leave pH unchanged, regardless of the extent of the dilution. Colloids and blood components are composed of a crystalloid solution as solvent, and the abovementioned rules partially hold true also for these fluids. The scenario is however complicated by the possible presence of weak anions (albumin, phosphates and gelatins) and their effect on plasma pH. The present manuscript summarises the characteristics of crystalloids, colloids, buffer solutions and blood components and reviews their effect on acid-base equilibrium. Understanding the composition of intravenous fluids, along with the application of simple physicochemical rules best described by Stewart’s approach, are pivotal steps to fully elucidate and predict alterations of plasma acid-base equilibrium induced by fluid therapy.Intravenous fluid administration is a medical intervention performed worldwide on a daily basis. Nevertheless, only a few physicians are aware of the characteristics of intravenous fluids and their possible effects on plasma acid-base equilibrium. According to Stewart’s theory, pH is independently regulated by three variables: partial pressure of carbon dioxide, strong ion difference (SID), and total amount of weak acids (ATOT). When fluids are infused, plasma SID and ATOT tend toward the SID and ATOT of the administered fluid. Depending on their composition, fluids can therefore lower, increase, or leave pH unchanged. As a general rule, crystalloids having a SID greater than plasma bicarbonate concentration (HCO3–) cause an increase in plasma pH (alkalosis), those having a SID lower than HCO3– cause a decrease in plasma pH (acidosis), while crystalloids with a SID equal to HCO3– leave pH unchanged, regardless of the extent of the dilution. Colloids and blood components are composed of a crystalloid solution as solvent, and the abovementioned rules partially hold true also for these fluids. The scenario is however complicated by the possible presence of weak anions (albumin, phosphates and gelatins) and their effect on plasma pH. The present manuscript summarises the characteristics of crystalloids, colloids, buffer solutions and blood components and reviews their effect on acid-base equilibrium. Understanding the composition of intravenous fluids, along with the application of simple physicochemical rules best described by Stewart’s approach, are pivotal steps to fully elucidate and predict alterations of plasma acid-base equilibrium induced by fluid therapy

Veno‐venous extracorporeal blood phototherapy increases the rate of carbon monoxide (CO) elimination in CO‐poisoned pigs

Background and objectives: Carbon monoxide (CO) inhalation is the leading causeof poisonrelated deaths in the United States. CO binds to hemoglobin (Hb),displaces oxygen, and reduces oxygen delivery to tissues. The optimal treatmentfor CO poisoning in patients with normal lung function is the administration ofhyperbaric oxygen (HBO). However, hyperbaric chambers are only available inmedical centers with specialized equipment, resulting in delayed therapy. Visiblelight dissociates CO from Hb with minimal effect on oxygen binding. In a pre-vious study, we combined a membrane oxygenator with phototherapy at 623 nmto produce a “mini” photoECMO (extracorporeal membrane oxygenation) de-vice, which improved CO elimination and survival in CO-poisoned rats. Theobjective of this study was to develop a larger photoECMO device (“maxi”photo-ECMO) and to test its ability to remove CO from a porcine model of CO poisoning. Study design/materials and methods: The “maxi” photoECMO device and thephoto-ECMO system (six maxi photo-ECMO devices assembled in parallel), were tested in an in vitro circuit of CO poisoning. To assess the ability of the photo-ECMO device and the photoECMO system to remove CO from CO-poisonedblood in vitro, the half-life of COHb (COHb-t1/2), as well as the percent COHbreduction in a single blood pass through the device, were assessed. In the in vivostudies, we assessed the COHb-t1/2in a CO-poisoned pig under three conditions:(1) While the pig breathed 100% oxygen through the endotracheal tube; (2) whilethe pig was connected to the photo-ECMO system with no light exposure; and (3)while the pig was connected to the photo-ECMO system, which was exposed to red light. Results: The photo-ECMO device was able to fully oxygenate the blood after asingle pass through the device. Compared to ventilation with 100% oxygen alone,illumination with red light together with 100% oxygen was twice as efcient inremoving CO from blood. Changes in gas flow rates did not alter CO eliminationin one pass through the device. Increases in irradiance up to 214 mW/cm2wereassociated with an increased rate of CO elimination. The photo-ECMO devicewas effective over a range of blood flow rates and with higher blood flow rates,more CO was eliminated. A photo-ECMO system composed of six photo-ECMOdevices removed CO faster from CO-poisoned blood than a single photo-ECMOdevice. In a CO-poisoned pig, the photo-ECMO system increased the rate of CO elimination without significantly increasing the animal's body temperature orcausing hemodynamic instability. Conclusion: In this study, we developed a photo-ECMO system and demonstrated its ability to remove CO from CO-poisoned 45-kg pigs. Technical modificaitons of the photo-ECMO system, including the development of a compact, portable device, will permit treatment of patients with CO poisoning at the scene of their poisoning, during transit to a local emergency room, and in hospitals that lack HBO facilities

Leigh Syndrome Mouse Model Can Be Rescued by Interventions that Normalize Brain Hyperoxia, but Not HIF Activation

Leigh syndrome is a devastating mitochondrial disease for which there are no proven therapies. We previously showed that breathing chronic, continuous hypoxia can prevent and even reverse neurological disease in the Ndufs4 knockout (KO) mouse model of complex I (CI) deficiency and Leigh syndrome. Here, we show that genetic activation of the hypoxia-inducible factor transcriptional program via any of four different strategies is insufficient to rescue disease. Rather, we observe an age-dependent decline in whole-body oxygen consumption. These mice exhibit brain tissue hyperoxia, which is normalized by hypoxic breathing. Alternative experimental strategies to reduce oxygen delivery, including breathing carbon monoxide (600 ppm in air) or severe anemia, can reverse neurological disease. Therefore, unused oxygen is the most likely culprit in the pathology of this disease. While pharmacologic activation of the hypoxia response is unlikely to alleviate disease in vivo, interventions that safely normalize brain tissue hyperoxia may hold therapeutic potential.status: publishe