A mathematical model of blood-interstitial acid-base balance: application to dilution acidosis and acid-base status

2011 ◽  
Vol 110 (4) ◽  
pp. 988-1002 ◽  
Author(s):  
Matthew B. Wolf ◽  
Edward C. DeLand

We developed mathematical models that predict equilibrium distribution of water and electrolytes (proteins and simple ions), metabolites, and other species between plasma and erythrocyte fluids (blood) and interstitial fluid. The models use physicochemical principles of electroneutrality in a fluid compartment and osmotic equilibrium between compartments and transmembrane Donnan relationships for mobile species. Across the erythrocyte membrane, the significant mobile species Cl−is assumed to reach electrochemical equilibrium, whereas Na+and K+distributions are away from equilibrium because of the Na+/K+pump, but movement from this steady state is restricted because of their effective short-term impermeability. Across the capillary membrane separating plasma and interstitial fluid, Na+, K+, Ca2+, Mg2+, Cl−, and H+are mobile and establish Donnan equilibrium distribution ratios. In each compartment, attainment of equilibrium by carbonates, phosphates, proteins, and metabolites is determined by their reactions with H+. These relationships produce the recognized exchange of Cl−and bicarbonate across the erythrocyte membrane. The blood submodel was validated by its close predictions of in vitro experimental data, blood pH, pH-dependent ratio of H+, Cl−, and HCO3−concentrations in erythrocytes to that in plasma, and blood hematocrit. The blood-interstitial model was validated against available in vivo laboratory data from humans with respiratory acid-base disorders. Model predictions were used to gain understanding of the important acid-base disorder caused by addition of saline solutions. Blood model results were used as a basis for estimating errors in base excess predictions in blood by the traditional approach of Siggaard-Andersen (acid-base status) and more recent approaches by others using measured blood pH and Pco2values. Blood-interstitial model predictions were also used as a basis for assessing prediction errors of extracellular acid-base status values, such as by the standard base excess approach. Hence, these new models can give considerable insight into the physicochemical mechanisms producing acid-base disorders and aid in their diagnoses.

1987 ◽  
Vol 67 (2) ◽  
pp. 427-436 ◽  
Author(s):  
A. L. SCHAEFER ◽  
H. DOORNENBAL ◽  
A. K. W. TONG ◽  
A. C. MURRAY ◽  
A. P. SATHER

In an effort to elucidate physiological factors involved in the development of pale-soft-exudative pork, blood acid base status was assessed in swine from two genetic lines of pigs and their F1 cross. The lines consisted of: (1) pigs that reacted positively (skeletal muscle rigidity) to the respiratory administration of halothane (halothane positive (H+)) based on Pietrain × Lacombe breed crosses, (2) Purebred Lacombe pigs that did not react positively to halothane anesthesia (Lac) and (3) pigs which were the progeny of crossbreeding (C) between halothane positive and negative animals. In addition, time off feed prior to slaughter (0, 24 or 48 h) was imposed as a stressor in order to test response differences among the three lines. The venous blood PCO2, total CO2, bicarbonate ion levels, standard bicarbonate and base excess levels were found to be higher in the H + pigs compared to either Lac or C pigs. All pig lines displayed higher blood pH, total CO2, bicarbonate ion, standard bicarbonate and base excess yet lower PO2 at 24 h off feed compared to 0 h off feed. These data suggest that H+ pigs have a greater tendency toward hypercapnia and a blood base excess than either Lac or C pigs. In addition, the incidence of hypercapnia and blood base excess for H +, Lac and C pigs was greatest at 24 h off feed. Key words: Acid-base stability, pig genotypes, fasting


2018 ◽  
Vol 2018 ◽  
pp. 1-5 ◽  
Author(s):  
Javier Enrique Cely ◽  
Oscar G. Rocha ◽  
María J. Vargas ◽  
Rafael M. Sanabria ◽  
Leyder Corzo ◽  
...  

Background. Acid-base disorders have been previously described in patients with chronic hemodialysis, with metabolic acidosis being the most important of them; however, little is known about the potential changes in acid-base status of patients on dialysis living at high altitudes. Methods. Cross-sectional study including 93 patients receiving chronic hemodialysis on alternate days and living in Bogotá, Colombia, at an elevation of 2,640 meters (8,661 feet) over sea level (m.o.s.l.). Measurements of pH, PaCO2, HCO3, PO2, and base excess were made on blood samples taken from the arteriovenous fistula (AVF) during the pre- and postdialysis periods in the midweek hemodialysis session. Normal values for the altitude of Bogotá were taken into consideration for the interpretation of the arterial blood gases. Results. 43% (n= 40) of patients showed predialysis normal acid-base status. The most common acid-base disorder in predialysis period was metabolic alkalosis with chronic hydrogen ion deficiency in 19,3% (n=18). Only 9,7% (n=9) had predialysis metabolic acidosis. When comparing pre- and postdialysis blood gas analysis, higher postdialysis levels of pH (7,41 versus 7,50, p<0,01), bicarbonate (21,7mmol/L versus 25,4mmol/L, p<0,01), and base excess (-2,8 versus 2,4, p<0,01) were reported, with lower levels of partial pressure of carbon dioxide (34,9 mmHg versus 32,5 mmHg, p<0,01). Conclusion. At an elevation of 2,640 m.o.s.l., a large percentage of patients are in normal acid-base status prior to the dialysis session (“predialysis period”). Metabolic alkalosis is more common than metabolic acidosis in the predialysis period when compared to previous studies. Paradoxically, despite postdialysis metabolic alkalosis, PaCO2 levels are lower than those found in the predialysis period.


1982 ◽  
Vol 53 (6) ◽  
pp. 1551-1555 ◽  
Author(s):  
D. G. Davies ◽  
W. F. Nolan

Cerebral interstitial fluid (ISF) pH of ventral medulla or thalamus, cisternal cerebrospinal fluid (CSF) pH, and arterial blood pH, PCO2, and [HCO-3] were measured in chloralose-urethan-anesthetized, gallamine-paralyzed New Zealand White rabbits during 30-min episodes of either HCl or NaHCO3 intravenous infusions. ISF pH was measured continuously with glass microelectrodes (1- to 2-microns tip diameter). Cisternal CSF pH was measured continuously with an indwelling pH probe (1-mm tip diameter). Both ventral medullary and thalamic ISF [H+] changed significantly, whereas arterial PCO2 remained constant. CSF [H+] did not change. We conclude from these data that 1) changes in blood acid-base conditions are rapidly reflected in cerebral ISF and 2) transient differences in [H+] and [HCO-3] can exist between cerebral ISF and CSF.


2010 ◽  
Vol 299 (1) ◽  
pp. G255-G264 ◽  
Author(s):  
Elise S. Demitrack ◽  
Manoocher Soleimani ◽  
Marshall H. Montrose

Gastric surface pH (pHo) transiently increases in response to focal epithelial damage. The sources of that increase, either from paracellular leakage of interstitial fluid or transcellular acid/base fluxes, have not been determined. Using in vivo microscopy approaches we measured pHowith Cl-NERF, tissue permeability with intravenous fluorescent-dextrans to label interstitial fluid (paracellular leakage), and gastric epithelial intracellular pH (pHi) with SNARF-5F (cellular acid/base fluxes). In response to two-photon photodamage, we found that cell-impermeant dyes entered damaged cells from luminal or tissue compartments, suggesting a possible slow transcellular, but not paracellular, route for increased permeability after damage. Regarding cytosolic acid/base status, we found that damaged cells acidified (6.63 ± 0.03) after photodamage, compared with healthy surface cells both near (7.12 ± 0.06) and far (7.07 ± 0.04) from damage ( P < 0.05). This damaged cell acidification was further attenuated with 20 μM intravenous EIPA (6.34 ± 0.05, P < 0.05) but unchanged by addition of 0.5 mM luminal H2DIDS (6.64 ± 0.08, P > 0.05). Raising luminal pH did not realkalinize damaged cells, suggesting that the mechanism of acidification is not attributable to leakiness to luminal protons. Inhibition of apical HCO3−secretion with 0.5 mM luminal H2DIDS or genetic deletion of the solute-like carrier 26A9 (SLC26A9) Cl−/HCO3−exchanger blocked the pHoincrease normally observed in control animals but did not compromise repair of damaged tissue. Addition of exogenous PGE2significantly increased pHoin wild-type, but not SLC26A9 knockout, animals, suggesting that prostaglandin-stimulated HCO3−secretion is fully mediated by SLC26A9. We conclude that cellular HCO3−secretion, likely through SLC26A9, is the dominant mechanism whereby surface pH transiently increases in response to photodamage.


2007 ◽  
Vol 47 (1) ◽  
pp. 35
Author(s):  
Hari Kushartono ◽  
Antonius H. Pudjiadi ◽  
Susetyo Harry Purwanto ◽  
Imral Chair ◽  
Darlan Darwis ◽  
...  

Background Base excess is a single variable used to quantifymetabolic component of acid base status. Several researches havecombined the traditional base excess method with the Stewartmethod for acid base physiology called as Fencl-Stewart method.Objective The purpose of the study was to compare two differentmethods in identifying hyperlactacemia in pediatric patients withcritical illness.Methods The study was performed on 43 patients admitted tothe pediatric intensive care unit of Cipto MangunkusumoHospital, Jakarta. Sodium, potassium, chloride, albumin, lactateand arterial blood gases were measured. All samples were takenfrom artery of all patients. Lactate level of >2 mEq/L was definedas abnormal. Standard base excess (SBE) was calculated fromthe standard bicarbonate derived from Henderson-Hasselbalchequation and reported on the blood gas analyzer. Base excessunmeasured anions (BE UA ) was calculated using the Fencl-Stewartmethod simplified by Story (2003). Correlation between lactatelevels in traditional and Fencl-Stewart methods were measuredby Pearson’s correlation coefficient .Results Elevated lactate levels were found in 24 (55.8%) patients.Lactate levels was more strongly correlated with BE UA (r = - 0.742,P<0.01) than with SBE (r = - 0.516, P<0.01).Conclusion Fencl-Stewart method is better than traditionalmethod in identifying patients with elevated lactate levels, so theFencl-Stewart method is suggested to use in clinical practice.


1988 ◽  
Vol 136 (1) ◽  
pp. 351-361
Author(s):  
LEONA MATTSOFF ◽  
MIKKO NIKINMAA

We studied the effects of acute external acidification on the acid-base status and plasma and red cell ion concentrations of lampreys. Mortality was observed within 24 h at pH5 and especially at pH4. The main reason for the high sensitivity of lampreys to acid water appears to be the large drop in blood pH: 0.6 and 0.8 units after 24 h at pH5 and pH4, respectively. The drop of plasma pH is much larger than in teleost fishes exposed to similar pH values. The difference in the plasma pH response between lampreys and teleosts probably results from the low buffering capacity of lamprey blood, since red cells cannot participate in buffering extracellular acid loads. Acidification also caused a decrease in both Na+ and C− concentrations and an elevation in K+ concentration of plasma. The drop in plasma Na+ concentration occurred faster than the drop in plasma Cl− concentration which, in turn, coincided with the decrease in total CO2 concentration of the blood.


2019 ◽  
Vol 41 (4) ◽  
pp. 481-491 ◽  
Author(s):  
Lenina Ludimila Sampaio de Almeida ◽  
Luís Henrique Bezerra Cavalanti Sette ◽  
Fernando Luiz Affonso Fonseca ◽  
Leila Silveira Vieira da Silva Bezerra ◽  
Francisco Hélio Oliveira Júnior ◽  
...  

Abstract Introduction: It is unclear whether residual renal function (RRF) in dialysis patients can attenuate the metabolic impact of the long 68-hour interdialytic interval, in which water, acid, and electrolyte accumulation occurs. Objective: to evaluate serum electrolyte levels, water balance, and acid-base status in dialytic patients with and without RRF over the long interdialytic interval (LII). Methodology: this was a single-center, cross-sectional, and analytical study that compared patients with and without RRF, defined by diuresis above 200 mL in 24 hours. Patients were weighed and serum samples were collected for biochemical and gasometric analysis at the beginning and at the end of the LII. Results: 27 and 24 patients with and without RRF were evaluated, respectively. Patients without RRF had a higher increase in serum potassium during the LII (2.67 x 1.14 mEq/L, p < 0.001), reaching higher values at the end of the study (6.8 x 5.72 mEq/L, p < 0.001) and lower pH value at the beginning of the interval (7.40 x 7.43, p = 0.018). More patients with serum bicarbonate < 18 mEq/L (50 x 14.8%, p = 0.007) and mixed acid-base disorder (57.7 x 29.2%, p = 0.042), as well as greater interdialytic weight gain (14.67 x 8.87 mL/kg/h, p < 0.001) and lower natremia (137 x 139 mEq/L, p = 0.02) at the end of the interval. Calcemia and phosphatemia were not different between the groups. Conclusion: Patients with RRF had better control of serum potassium, sodium, acid-base status, and volemia throughout the LII.


1994 ◽  
Vol 14 (1) ◽  
pp. 61-65 ◽  
Author(s):  
Jacques J. Sennesael ◽  
Godelieve C. De Smedt ◽  
Patricia Van der Niepen ◽  
Dierik L. Verbeelen

Objective To assess the possible effects of peritonitis on peritoneal and systemic acid-base status. Design pH, pCO2, lactate, and total leukocyte and differential count were simultaneously determined in the overnight dwell peritoneal dialysis effluent (PDE) and arterial blood in noninfected patients (controls) and on days 1, 3, and 5 from the onset of peritonitis. Setting University multidisciplinary dialysis program. Patients Prospective analysis of 63 peritonitis episodes occurring in 30 adult CAPD patients in a single center. Results In controls, mean (±SD) acid-base parameters were pH 7.41 ±0.05, pCO2 43.5±2.6 mm Hg, lactate 2.5±1.5 mmol/L in the PDE, and pH 7.43±0.04, PaCO2 36.8±3.8 mm Hg, lactate 1.4±0.7 mmol/L in the blood. In sterile (n=6), gram-positive (n=34), and Staphylococcus aureus (n=9) peritonitis PDE pH's on day 1 were, respectively, 7. 29±0.07, 7. 32±0.07, and 7.30±0.08 (p<0.05 vs control). In gram -negative peritonitis (n=14) PDE pH was 7.21 ±0.08 (p<0.05 vs all other groups). A two-to-threefold increase in PDE lactate was observed in all peritonitis groups, but a rise in pCO2 was only seen in gram -negative peritonitis. Acid-base profile of PDE had returned to control values by day 3 in sterile, gram -positive and Staphylococcus aureus peritonitis and by day 5 in gramnegative peritonitis. Despite a slight increase in plasma lactate on the first day of peritonitis, arterial blood pH was not affected by peritonitis. Conclusion PDE pH is decreased in continuous ambulatory peritoneal dialysis (CAPD) peritonitis, even in the absence of bacterial growth. In gram-negative peritonitis, PDE acidosis is more pronounced and prolonged, and pCO2 is markedly increased. Arterial blood pH is not affected by peritonitis.


2007 ◽  
Vol 292 (3) ◽  
pp. G899-G904 ◽  
Author(s):  
Markus Sjöblom ◽  
Olof Nylander

When running in vivo experiments, it is imperative to keep arterial blood pressure and acid-base parameters within the normal physiological range. The aim of this investigation was to explore the consequences of anesthesia-induced acidosis on basal and PGE2-stimulated duodenal bicarbonate secretion. Mice (strain C57bl/6J) were kept anesthetized by a spontaneous inhalation of isoflurane. Mean arterial blood pressure (MAP), arterial acid-base balance, and duodenal mucosal bicarbonate secretion (DMBS) were studied. Two intra-arterial fluid support strategies were used: a standard Ringer solution and an isotonic Na2CO3 solution. Duodenal single perfusion was used, and DMBS was assessed by back titration of the effluent. PGE2 was used to stimulate DMBS. In Ringer solution-infused mice, isoflurane-induced acidosis became worse with time. The blood pH was 7.15–7.21 and the base excess was about −8 mM at the end of experiments. The continuous infusion of Na2CO3 solution completely compensated for the acidosis. The blood pH was 7.36–7.37 and base excess was about 1 mM at the end of the experiment. Basal and PGE2-stimulated DMBS were markedly greater in animals treated with Na2CO3 solution than in those treated with Ringer solution. MAP was slightly higher after Na2CO3 solution infusion than after Ringer solution infusion. We concluded that isoflurane-induced acidosis markedly depresses basal and PGE2-stimulated DMBS as well as the responsiveness to PGE2, effects prevented by a continuous infusion of Na2CO3. When performing in vivo experiments in isoflurane-anesthetized mice, it is recommended to supplement with a Na2CO3 infusion to maintain a normal acid-base balance.


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