Practical Evaluation of Acid-Base Balance

1957 ◽  
Vol 3 (5) ◽  
pp. 631-637
Author(s):  
Herbert P Jacobi ◽  
Anthony J Barak ◽  
Meyer Beber

Abstract The Co2 combining power bears a variable relationship to the in vivo plasma bicarbonate concentration, depending upon the type and severity of acid-base distortion. In respiratory alkalosis and metabolic acidosis the Co2 combining power will usually be greater than the in vivo plasma bicarbonate concentration; whereas, in respiratory acidosis and metabolic alkalosis the Co2 combining power will usually be less. Co2 content, on the other hand, will always parallel the in vivo plasma bicarbonate concentration quite closely, being only slightly greater. These facts, together with other considerations which are discussed, recommend the abandonment of the determination of CO2 combining power.

1977 ◽  
Vol 232 (1) ◽  
pp. R10-R17 ◽  
Author(s):  
R. G. DeLaney ◽  
S. Lahiri ◽  
R. Hamilton ◽  
P. Fishman

Upon entering into aestivation, Protopterus aethiopicus develops a respiratory acidosis. A slow compensatory increase in plasma bicarbonate suffices only to partially restore arterial pH toward normal. The cessation of water intake from the start of aestivation results in hemoconcentration and marked oliguria. The concentrations of most plasma constituents continue to increase progressively, and the electrolyte ratios change. The increase in urea concentration is disproportionately high for the degree of dehydration and constitutes an increasing fraction of total plasma osmolality. Acid-base and electrolyte balance do not reach a new equilibrium within 1 yr in the cocoon.


1996 ◽  
Vol 16 (1_suppl) ◽  
pp. 126-129 ◽  
Author(s):  
Mariano Feriani ◽  
Claudio Ronco ◽  
Giuseppe La Greca

Our objective is to investigate transperitoneal buffer fluxes with solution containing lactate and bicarbonate, and to compare the final effect on body base balance of the two solutions. One hundred and four exchanges, using different dwell times, were performed in 52 stable continuous ambulatory peritoneal dialysis (CAPD) patients. Dialysate effluent lactate and bicarbonate and volumes were measured. Net dialytic base gain was calculated. Patients’ acid-base status and plasma lactate were determined. In lactate-buffered CAPD solution, lactate concentration in dialysate effluent inversely correlated with length of dwell time, but did not correlate with plasma lactate concentration and net ultrafiltration. Bicarbonate concentration in dialysate effluent correlated with plasma bicarbonate and dwell time but not with ultrafiltration. The arithmetic sum of the lactate gain and bicarbonate loss yielded the net dialytic base gain. Ultrafiltration was the most important factor affecting net dialytic base gain. A previous study demonstrated that in patients using a bicarbonate-buffered solution the net bicarbonate gain is a function of dwell time, ultrafiltration, and plasma bicarbonate. By combining the predicted data of the dialytic base gain with the calculated metabolic acid production, an approximate body base balance could be obtained with both lactate and bicarbonate-buffered CAPD solutions. The body base balance in CAPD patients is self-regulated by the feedback between plasma bicarbonate concentration and dialytic base gain. The level of plasma bicarbonate is determined by the dialytic base gain and the metabolic acid production. This can explain the large interpatient variability in acid-base correction. Bicarbonate-buffered CAPD solution is equal to lactate solution in correcting acid-base disorders of CAPD patients.


1964 ◽  
Vol 206 (4) ◽  
pp. 875-882 ◽  
Author(s):  
David P. Simpson

Citrate excretion has been studied in dogs under various conditions of acid-base balance in order to determine which factors are responsible for the increased citrate clearance present in metabolic alkalosis. A close relationship, significantly modified by systemic pH, was found between plasma bicarbonate concentration and citrate clearance. In the presence of an alkaline plasma pH, there was a linear relationship between changes in plasma bicarbonate concentration and changes in citrate clearance. Other experiments also demonstrated the influence of plasma bicarbonate concentration on citrate clearance at alkaline pH. Under acidotic conditions citrate clearances were low and changes in plasma bicarbonate concentration had little effect on citrate excretion. A change in plasma pH from an acidotic to an alkalotic state, with a constant plasma bicarbonate concentration, produced an increase in citrate clearance. Thus the coexistence in metabolic alkalosis of high plasma bicarbonate concentration and high plasma pH results in a markedly increased citrate clearance.


1985 ◽  
Vol 248 (6) ◽  
pp. F796-F803 ◽  
Author(s):  
A. M. Kaufman ◽  
C. Brod-Miller ◽  
T. Kahn

Studies were performed to assess the role of changes in the excretion of citrate, a metabolic precursor of bicarbonate, in acid-base balance in diuretic-induced metabolic alkalosis. Rats on a low-chloride diet with sodium sulfate added were studied during a base-line period, 3 days of furosemide administration, and 4 days post-furosemide. During the period of furosemide administration, net acid excretion and plasma bicarbonate concentration increased. In the post-furosemide period, net acid excretion remained higher than base line but plasma bicarbonate concentration did not increase further. Citrate excretion was significantly higher in the post-furosemide period than in base line. Studies substituting sodium neutral phosphate or sodium bicarbonate for dietary sodium sulfate demonstrated greater increases in net acid excretion post-furosemide and, again, no increase in plasma bicarbonate concentration during this period. Citrate excretion was greater than in the sulfate group. The increment in citrate excretion was proportional to the base “load,” defined with respect to changes in net acid excretion and/or dietary bicarbonate. Thus, in these studies alterations of base excretion in the form of citrate play an important role in acid-base balance during diuretic-induced metabolic alkalosis.


1997 ◽  
Vol 273 (5) ◽  
pp. F698-F705
Author(s):  
R. Unwin ◽  
R. Stidwell ◽  
S. Taylor ◽  
G. Capasso

We have studied the effects of acute respiratory alkalosis (ARALK, hyperventilation) and acidosis (ARA, 8% CO2), chronic respiratory acidosis (CRA; 10% CO2 for 7–10 days), and subsequent recovery from CRA breathing air on loop of Henle (LOH) net bicarbonate flux ([Formula: see text]) by in vivo tubule microperfusion in anesthetized rats. In ARALK blood, pH increased to 7.6, and blood bicarbonate concentration ([[Formula: see text]]) decreased from 29 to 22 mM. Fractional urinary bicarbonate excretion ([Formula: see text]) increased threefold, but LOH[Formula: see text]was unchanged. In ARA, blood pH fell to 7.2, and blood [[Formula: see text]] rose from 28 to 34 mM; [Formula: see text] was reduced to <0.1%, but LOH[Formula: see text]was unaltered. In CRA, blood pH fell to 7.2, and blood [[Formula: see text]] increased to >50 mM, whereas[Formula: see text]decreased to <0.1%.[Formula: see text]was reduced by ∼30%. Bicarbonaturia occurred when CRA rats breathed air, yet LOH[Formula: see text]increased (by 30%) to normal. These results suggest that LOH[Formula: see text]is affected by the blood-to-tubule lumen [[Formula: see text]] gradient and[Formula: see text] backflux. When the usual perfusing solution at 20 nl/min was made[Formula: see text] free, mean[Formula: see text]was −34.5 ± 4.4 pmol/min compared with 210 ± 28.1 pmol/min plus [Formula: see text]. When a low-NaCl perfusate (to minimize net fluid absorption) containing mannitol and acetazolamide (2 × 10−4 M, to abolish H+-dependent[Formula: see text]) was used,[Formula: see text]was −112.8 ± 5.6 pmol/min. Comparable values for[Formula: see text]at 10 nl/min were −35.9 ± 5.8 and −72.5 ± 8.8 pmol/min, respectively. These data indicate significant backflux of[Formula: see text] along the LOH, which depends on the blood-to-lumen [[Formula: see text]] gradient; in addition to any underlying changes in active acid-base transport mechanisms, [Formula: see text]permeability and backflux are important determinants of LOH[Formula: see text]in vivo.


1988 ◽  
Vol 255 (1) ◽  
pp. F182-F187 ◽  
Author(s):  
A. M. Kaufman ◽  
T. Kahn

Studies were performed to evaluate whether alterations in the excretion of citrate, a metabolic precursor of bicarbonate, play a quantitatively important role in acid-base balance during bicarbonate feeding in the rat. Potassium depletion (K-DEPL), chloride depletion (Cl-DEPL), or potassium plus chloride depletion (KCl-DEPL) was produced by eliminating potassium, chloride, or potassium chloride from the diet. After 3 days of depletion, sodium bicarbonate (4,000 mueq/24 h) was added to the diet for 7 days. In all groups plasma bicarbonate concentration increased minimally during bicarbonate administration and was similar to normal controls receiving bicarbonate. In K-DEPL, citrate excretion was less than normal but bicarbonate excretion was greater than normal. In Cl-DEPL, bicarbonate excretion was less than normal but citrate excretion was greater than normal. In KCl-DEPL, bicarbonate and citrate excretion were similar to normal. Sodium bicarbonate was also administered to K-DEPL and KCl-DEPL rats in which plasma bicarbonate concentration averaged 32.9 meq/1. The reciprocal relationship between citrate and bicarbonate excretion was not altered by the profound metabolic alkalosis. Again, plasma bicarbonate concentration changed little with sodium bicarbonate administration. These studies suggest that the ability to excrete a base load remains intact despite potassium or chloride depletion or metabolic alkalosis. Complementary alterations of citrate and bicarbonate excretion play an important role in acid-base balance under these conditions.


1982 ◽  
Vol 242 (5) ◽  
pp. G486-G492 ◽  
Author(s):  
G. M. Feldman ◽  
A. N. Charney

The effects of acute respiratory alkalosis and acidosis on intestinal electrolyte transport were studied in adult Sprague-Dawley rats. During in situ intestinal perfusion, anesthetized animals were ventilated with 0, 3, or 8% CO2, creating states of alkalosis (pH 7.64 +/- 0.01), normocapnia (pH 7.45 +/- 0.01), or acidosis (pH 7.26 +/- 0.01), respectively. The plasma bicarbonate concentration decreased 2.0 mM during alkalosis and increased 2.1 mM during acidosis. The jejunum did not respond to the acid-base disturbances. In both the ileum and colon, alkalosis decreased the net absorption of water (-16%), sodium (-23%), and chloride (-42%) and the net secretion of bicarbonate (-33%), whereas acidosis had the opposite effect, i.e., the net absorption of water (41%), sodium (39%), and chloride (32%) increased as did net bicarbonate secretion (33%) (ileal values given). Changes in sodium chloride movement could be correlated with changes in systemic pH and CO2 tension (PCO2), and bicarbonate secretion paralleled changes in the plasma bicarbonate concentration. The acid-base disorders had no effect on ileal and colonic net potassium secretion and transmural potential difference. These studies suggest that systemic pH and/or PCO2 regulate sodium chloride absorption, and the plasma bicarbonate concentration regulates bicarbonate secretion.


1981 ◽  
Vol 51 (2) ◽  
pp. 369-375 ◽  
Author(s):  
S. W. Bledsoe ◽  
D. Y. Eng ◽  
T. F. Hornbein

To test the passive transport hypothesis of cerebrospinal fluid (CSF) [H+] regulation, we altered the relationship between plasma [H+] and the electrical potential difference between CSF and blood (PD) by elevating plasma [K+] during 6-h systemic acid-base disturbances. In five groups of pentobarbital-anesthetized dogs, we increased plasma [K+] from 3.5 to an average of 7.8 meq/l. Hyperkalemia produced an increase in the PD of 6.3 mV by 6 h with normal plasma acid-base status (pHa 7.4), of 8.3 mV with isocapnic metabolic acidosis (pHa 7.2), of 5.3 mV with isocapnic metabolic alkalosis (pHa 7.6), of 9.2 mV with isobicarbonate respiratory acidosis (PaCO2 61 Torr) and of 5.7 mV with isobicarbonate respiratory alkalosis (PaCO2 25 Torr). The change in CSF [H+] at 6 h in each group was the same as that observed in normokalemic animals (Am. J. Physiol. 228: 1134-1154, 1975). This result is not consistent with the passive transport hypothesis. The CSF-blood PD is therefore not an important determinant of CSF [H+] CSF [H+] homeostasis must result from some form of active transport control.


1981 ◽  
Vol 50 (4) ◽  
pp. 819-823 ◽  
Author(s):  
H. Tazawa ◽  
J. Piiper ◽  
A. Ar ◽  
H. Rahn

On day 16 of the chick embryo, a catheter was implanted in the allantoic vein carrying arterialized blood, and a syringe was attached to the blunt end of the shell connecting to the air cell. This technique allowed for repetitive sampling and analysis of air cell gas and arterialized blood when these eggs were exposed to a He-O2 or SF6-O2 atmosphere. Exposure to He-O2 reduced the arterial CO2 tension(PaCO2) from 36 to 17 Torr and increased pH by 0.17 units; exposure to SF6-O2 increased PaCO2 from 37 to 62 Torr and reduced the pH by 0.14 units. These responses were brought about by changes in the gas conductance of the shell, resulting in a diffusive hypocapnia and respiratory alkalosis in He-O2 and a diffusive hypercapnia and respiratory acidosis in SF6-O2. During a 4-h exposure to these foreign gases the observed pH changes were smaller than predicted because of marked shifts of HCO3- into the blood (SF6-O2) or out of the blood (He-O2).


1993 ◽  
Vol 178 (1) ◽  
pp. 71-88 ◽  
Author(s):  
R. G. Boutilier ◽  
R. A. Ferguson ◽  
R. P. Henry ◽  
B. L. Tufts

We measured intracellular acid-base balance and indicators of carbohydrate and high-energy phosphate metabolism as lampreys recovered from exhaustive exercise. A combined respiratory and metabolic acidosis was observed in the locomotory muscle following ‘burst’ exercise. Muscle pH decreased from approximately 7.2 to 6.7, whereas intracellular PCO2 rose from approximately 0.6 to 1.6 kPa. Unlike the situation in similarly stressed teleost fish such as rainbow trout, the respiratory acidosis in muscle persisted for several hours. This apparent CO2 retention in lamprey muscle may be the result of a restricted ability of the circulatory system to transport CO2 due to reduced erythrocyte anion exchange, or it could represent a restricted ability of the muscle itself to clear the intracellular pool of CO2 due to reduced carbonic anhydrase activity. Maximal lactate dehydrogenase activity of lamprey muscle exhibited a marked dependence on pH, increasing in activity by 30 % as pH decreased from 7.2 to 6.7 (reflecting the ‘resting’ to ‘post- exercise’ pH change observed in vivo). Following exhaustive exercise, the acid-base balance of the muscle is influenced by both proton- consuming (e.g. AMP deamination, glycogen replenishment) and proton-producing (e.g. rephosphorylation of creatine) metabolic processes. The net effect is that, although intracellular pH is maximally depressed, energy stores such as phosphocreatine and glycogen are partially restored within 1 h of exhaustive exercise, placing the animal in good stead for further locomotory work.


Sign in / Sign up

Export Citation Format

Share Document