Influence of chronic metabolic acid-base disorders on the acute CO2 titration curve

1983 ◽  
Vol 55 (4) ◽  
pp. 1187-1195 ◽  
Author(s):  
N. E. Madias ◽  
H. J. Adrogue
Keyword(s):  
Titration Curve ◽  
Respiratory Acidosis ◽  
Whole Body ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Hydrogen Ion Concentration ◽  
Plasma Bicarbonate ◽  
Arterial Blood ◽  
Acid Base Equilibrium ◽  
Body Response

Previous studies from this laboratory have characterized the “whole-body” response to acute hypercapnia in normal dog and humans. A more recent investigation has demonstrated that this response is markedly altered by graded degrees of chronic respiratory acidosis. The present studies were carried out to assess the influence, if any, of chronic metabolic acid-base disturbances on the acute CO2 titration curve in the dog. To this purpose we first produced a broad range of chronic plasma bicarbonate concentration of metabolic nature. Metabolic acidosis (n = 14) was produced by prolonged HCl-feeding and metabolic alkalosis (n = 11) by diuretics and a chloride-free diet. Animals with normal acid-base status (n = 4) were also studied. After the establishment of a chronic steady state of acid-base equilibrium, we then performed an acute CO2 titration of the unanesthetized dogs within a large environmental chamber. Three levels of inspired CO2 fraction (FICO2) were employed ranging from 4 to 15%. The results indicate that chronic metabolic acid-base disturbances exert a dramatic influence on the whole-body response to acute hypercapnia. The acute change in plasma bicarbonate for a given change in partial pressure of CO2 in arterial blood (PaCO2) or plasma pH decreases as a function of the chronic level of plasma bicarbonate concentration. Yet the ability of the organism to defend plasma hydrogen ion concentration is progressively strengthened as the chronic level of plasma bicarbonate increases.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of chronic respiratory acid-base disorders on acute CO2 titration curve

1985 ◽  
Vol 58 (4) ◽  
pp. 1231-1238 ◽  
Author(s):  
H. J. Adrogue ◽  
N. E. Madias
Keyword(s):  
Titration Curve ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Ion Concentration ◽  
Whole Body ◽  
Acid Base ◽  
Hydrogen Ion Concentration ◽  
Plasma Bicarbonate ◽  
Base Disorder ◽  
Acid Base Status

We have recently shown that background presence of chronic metabolic acid-base disorder markedly alters in vivo acute CO2 titration curve. These studies were carried out to assess the influence of chronic respiratory acid-base disorders on response to acute hypercapnia and to explore whether the chronic level of plasma pH is the factor responsible for alterations in the CO2 titration curve. We compared whole-body responses to acute hypercapnia of dogs with preexisting chronic respiratory alkalosis (n = 8) with that of normal animals (n = 4) and animals with chronic respiratory acidosis (n = 13). Chronic respiratory alkalosis and acidosis, as well as the acute CO2 titrations, were produced in unanesthetized dogs within a large environmental chamber. For comparison with our data on chronic metabolic acidosis and alkalosis, plasma bicarbonate levels, which are secondarily altered in chronic respiratory acid-base disorders, were used as an index of chronic acid-base status of the animals. Results indicate that, as with chronic metabolic acid-base disorders, a larger increment in plasma bicarbonate occurs during acute hypercapnia when steady-state plasma bicarbonate is low (respiratory alkalosis) than when it is high (respiratory acidosis). Yet, in further analogy with the metabolic studies, plasma hydrogen ion concentration is better defended at higher plasma bicarbonate levels in accordance with mathematical relationships defined by the Henderson-Hasselbalch equation. Combined results demonstrate that the influence of chronic acid-base status on whole-body response to acute hypercapnia is independent of initial plasma pH.

scholarly journals Acid-base regulation and ion transfers in the carp (Cyprinus carpio): pH compensation during graded long- and short-term environmental hypercapnia, and the effect of bicarbonate infusion

1986 ◽  
Vol 126 (1) ◽  
pp. 41-61 ◽  
Author(s):  
J. B. Claiborne ◽  
N. Heisler
Keyword(s):  
Cyprinus Carpio ◽  
Respiratory Acidosis ◽  
Exposure Period ◽  
Environmental Water ◽  
Ambient Water ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Arterial Blood ◽  
Carp Cyprinus Carpio

To study both temporal and quantitative effects of hypercapnia on the extent of pH compensation in the arterial blood, specimens of carp (Cyprinus carpio) were exposed to a PCO2 of about 7.5 mmHg (1 mmHg = 133.3 Pa) (1% CO2) in the environmental water for several weeks, and a second group of animals was subjected to an environmental PCO2 of about 37 mmHg (5% CO2) for up to 96 h. A third series of experiments was designed to test the possibility that infusion of bicarbonate would increase the extent of plasma pH compensation. Dorsal aortic plasma pH, PCO2 and [HCO3-], as well as net transfer of HCO3- -equivalent ions, NH4+, Cl- and Na+, between fish and ambient water, were monitored throughout the experiments. Exposure to environmental PCO2 of 7.5 mmHg resulted in the expected respiratory acidosis with the associated drop in plasma pH, and subsequent compensatory plasma [HCO3-] increase. The compensatory increase of plasma bicarbonate during long-term hypercapnia continued during 19 days of exposure with plasma bicarbonate finally elevated from 13.0 mmoll-1 during control conditions to 25.9 mmoll-1 in hypercapnia, an increase equivalent to 80% plasma pH compensation. Exposure to 5% hypercapnia elicited much larger acid-base effects, which were compensated to a much lesser extent. Plasma pH recovered to only about 45% of the pH depression expected at constant bicarbonate concentration. At the end of the 96-h exposure period, plasma [HCO3-] was elevated by a factor of 2.5 to about 28.2 mmoll-1. The observed increase in plasma bicarbonate concentration during 5% hypercapnic exposure was attributable to net gain of bicarbonate equivalent ions from (or release of H+-equivalent ions to) the environmental water. Quantitatively, the gain of 15.6 mmol kg-1 was considerably larger than the amount required for compensation of the extracellular space, suggesting that acid-base relevant ions were transferred for compensation of the intracellular body compartments. The uptake of bicarbonate-equivalent ions from the water was accompanied by a net release of Cl-and, to a smaller extent, by a net uptake of Na+, suggesting a 75% contribution of the Cl-/HCO-3 exchange mechanism. Infusion of bicarbonate after 48 h of exposure to 7.5 mmHg PCo2 had only a transient effect on further pH compensation. The infused bicarbonate was lost to the ambient water, and pre-infusion levels of bicarbonate were reattained within 24 h. Repetition of the infusion did not result in a notable improvement of the acid-base status.(ABSTRACT TRUNCATED AT 400 WORDS)

Acid-Base Relationships in the Blood of the Toad, Bufo Marinus: I. The Effects of Environmental CO2

1979 ◽  
Vol 82 (1) ◽  
pp. 331-344 ◽  
Author(s):  
R. G. BOUTILIER ◽  
D. J. RANDALL ◽  
G. SHELTON ◽  
D. P. TOEWS
Keyword(s):  
Respiratory Acidosis ◽  
Initial Response ◽  
Untreated Animal ◽  
Abrupt Increase ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Ph Values ◽  
Arterial Blood ◽  
Toad Bufo ◽  
Ambient Co2

An abrupt increase in ambient CO2, resulted in a marked respiratory acidosis which took place within 30 min. During this time there was a considerable reduction in the PCO2. difference between arterial blood and inspired gas caused by an increase in ventilations. Prolonged CO2 exposure (24 h) showed that there was some compensation for the acidosis in that plasma bicarbonate concentrations increased substantially. At the same time, however, the PCO2 of arterial blood always rose so that the net result was usually only a small increase in pH. Upon return to air, the blood was backtitrated along a buffer line elevated above and parallel to that seen during the initial response to hypercapnia. The fall in arterial blood PCO2, during the early stages of recovery often led to pH values higher than those seen in the untreated animal. After 48 h in air, recovery had gone further with PCO2 pH and [HCO3-] levels approaching but rarely reaching the pre-exposure values.

Practical Evaluation of Acid-Base Balance

1957 ◽  
Vol 3 (5) ◽  
pp. 631-637
Author(s):  
Herbert P Jacobi ◽  
Anthony J Barak ◽  
Meyer Beber
Keyword(s):  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Acid Base Balance ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Practical Evaluation ◽  
Base Balance

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.

Role of endothelin-1 in renal regulation of acid-base equilibrium in acidotic humans

2012 ◽  
Vol 303 (7) ◽  
pp. F991-F999 ◽  
Author(s):  
Alexandra Pallini ◽  
Henry N. Hulter ◽  
Jurgen Muser ◽  
Reto Krapf
Keyword(s):  
Metabolic Acidosis ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Endothelin 1 ◽  
Plasma Bicarbonate ◽  
Human Volunteers ◽  
Acid Base Equilibrium ◽  
Normal Human ◽  
Mineralocorticoid Activity

Endothelin-1 inhibits collecting duct sodium reabsorption and stimulates proximal and distal tubule acidification in experimental animals both directly and indirectly via increased mineralocorticoid activity. Diet-induced acid loads have been shown to increase renal endothelin-1 activity, and it is hypothesized that increased dietary acid-induced endothelin-1 activity may be a causative progression factor in human renal insufficiency and that this might be reversed by provision of dietary alkali. We sought to clarify, in normal human volunteers, the role of endothelin-1 in renal acidification and to determine whether the effect is dependent on dietary sodium chloride. Acid-base equilibrium was studied in seven normal human volunteers with experimentally induced metabolic acidosis [NH4Cl 2.1 mmol·kg body weight (BW)−1·day−1] with and without inhibition of endogenous endothelin-1 activity by the endothelin A/B-receptor antagonist bosentan (125 BID p.o./day) both during dietary NaCl restriction (20 mmol/day) and NaCl repletion (2 mmol NaCl·kg BW−1·day−1). During NaCl restriction, but not in the NaCl replete state, bosentan significantly increased renal net acid excretion in association with stimulation of ammoniagenesis resulting in a significantly increased plasma bicarbonate concentration (19.0 ± 0.8 to 20.1 ± 0.9 mmol/l) despite a decrease in mineralocorticoid activity and an increase in endogenous acid production. In pre-existing human metabolic acidosis, endothelin-1 activity worsens acidosis by decreasing the set-point for renal regulation of plasma bicarbonate concentration, but only when dietary NaCl provision is restricted.

scholarly journals A redefinition of normal acid-base equilibrium in man: Carbon dioxide tension as a key determinant of normal plasma bicarbonate concentration

1979 ◽  
Vol 16 (5) ◽  
pp. 612-618 ◽  
Author(s):  
Nicolaos E. Madias ◽  
Horacio J. Adrogué ◽  
Gary L. Horowitz ◽  
Jordan J. Cohen ◽  
William B. Schwartz
Keyword(s):  
Carbon Dioxide ◽  
Carbon Dioxide Tension ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Base Equilibrium ◽  
Normal Plasma ◽  
Acid Base Equilibrium ◽  
Normal Acid

Respiratory Acidosis and Alkalosis

2017 ◽  
Author(s):  
Horacio J Adrogué ◽  
Nicolaos E Madias
Keyword(s):  
Carbonic Acid ◽  
Clinical Manifestations ◽  
Respiratory Acidosis ◽  
Respiratory Alkalosis ◽  
Body Fluids ◽  
The Body ◽  
Acid Base ◽  
Acid Base Equilibrium ◽  
Therapeutic Principles ◽  
The Impact

Respiratory acid-base disorders are those disturbances in acid-base equilibrium that are expressed by a primary change in CO2 tension (Pco2) and reflect primary changes in the body’s CO2 stores (i.e., carbonic acid). A primary increase in Pco2 (and a primary increase in the body’s CO2 stores) defines respiratory acidosis or primary hypercapnia and is characterized by acidification of the body fluids. By contrast, a primary decrease in Pco2 (and a primary decrease in the body’s CO2 stores) defines respiratory alkalosis or primary hypocapnia and is characterized by alkalinization of the body fluids. Primary changes in Pco2 elicit secondary physiologic changes in plasma [HCO3ˉ] that are directional and proportional to the primary changes and tend to minimize the impact on acidity. This review presents the pathophysiology, secondary physiologic response, causes, clinical manifestations, diagnosis, and therapeutic principles of respiratory acidosis and respiratory alkalosis.  This review contains 4 figures, 3 tables, and 59 references. Key words: Respiratory acidosis, respiratory alkalosis, primary hypercapnia, primary hypocapnia, hypoxemia, pseudorespiratory alkalosis

Acid-base balance and plasma composition in the aestivating lungfish (Protopterus)

1977 ◽  
Vol 232 (1) ◽  
pp. R10-R17 ◽  
Author(s):  
R. G. DeLaney ◽  
S. Lahiri ◽  
R. Hamilton ◽  
P. Fishman
Keyword(s):  
Plasma Osmolality ◽  
Respiratory Acidosis ◽  
Electrolyte Balance ◽  
Plasma Composition ◽  
Total Plasma ◽  
Acid Base Balance ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Arterial Ph ◽  
Base Balance

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.

The effects of enforced activity on ventilation, circulation and blood acid-base balance in the aquatic gill-less urodele, Cryptobranchus alleganiensis; a comparison with the semi-terrestrial anuran, Bufo marinus

1980 ◽  
Vol 84 (1) ◽  
pp. 289-302
Author(s):  
R. G. Boutilier ◽  
D. G. McDonald ◽  
D. P. Toews
Keyword(s):  
Recovery Period ◽  
Respiratory Acidosis ◽  
Bufo Marinus ◽  
Acid Base Balance ◽  
Acid Base ◽  
Post Exercise ◽  
Arterial Blood ◽  
Cryptobranchus Alleganiensis ◽  
Base Balance ◽  
Lower Magnitude

A combined respiratory and metabolic acidosis occurs in the arterial blood immediately following 30 min of strenuous activity in the predominantly skin-breathing urodele, Cryptobranchus alleganiensis, and in the bimodal-breathing anuran, Bufo marinus, at 25 degrees C. In Bufo, the bulk of the post-exercise acidosis is metabolic in origin (principally lactic acid) and recovery is complete within 4-8 h. In the salamander, a lower magnitude, longer duration, metabolic acid component and a more pronounced respiratory acidosis prolong the recovery period for up to 22 h post-exercise. It is suggested that fundamental differences between the dominant sites for gas exchange (pulmonary versus cutaneous), and thus in the control of respiratory acid-base balance, may underline the dissimilar patterns of recovery from exercise in these two species.

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