The Relationship between Arterial Pco2 and Hydrogen Ion Concentration in Chronic Metabolic Acidosis and Alkalosis

1974 ◽  
Vol 46 (1) ◽  
pp. 113-123 ◽  
Author(s):  
J. M. Bone ◽  
J. Cowie ◽  
Anne T. Lambie ◽  
J. S. Robson

1. An analysis was made of the relationship which exists between arterial [H+], Pco2 and [HCO3−] in twenty-five patients with stable metabolic acidosis and alkalosis and in three normal subjects. 2. Contrary to previous reports, the relationship between Pco2 and [H+] was nonlinear and could best be described in terms of a rectangular hyperbola (Pco2 = 962/([H+]-12). 3. The relationship between Pco2 and [HCO3−] was curvilinear and best described by the quadratic function 23.8 (Pco2)2−12Pco2[HCO3−] −962 [HCO3−] = 0. 4. The small acute changes in [H+],−[HCO3−] and Pco2 produced by infusion of the weak organic acid 5,5−dimethyl 2,4−oxazolidinedione (DMO) could be predicted from the curvilinear regression.

1984 ◽  
Vol 56 (4) ◽  
pp. 1039-1044 ◽  
Author(s):  
S. M. Menitove ◽  
D. M. Rapoport ◽  
H. Epstein ◽  
B. Sorkin ◽  
R. M. Goldring

The relationship between the resting response to CO2 rebreathing and the ventilatory response to CO2 production during exercise was examined in 20 healthy untrained male subjects and in six patients with obesity hypoventilation syndrome. Patients were chosen because of a severely reduced response to CO2 rebreathing. There was no correlation between the CO2 rebreathing response and the exercise ventilatory response in the normal subjects, the patients, or in the group considered as a whole. This lack of correlation could not be accounted for by differences in ventilatory and occlusion pressure responses nor by reporting responses as a function of a change in hydrogen ion concentration. The independence of the CO2 rebreathing response and the exercise ventilatory response suggests the CO2 rebreathing response does not measure the relevant parameters of ventilatory control during exercise.


1983 ◽  
Vol 61 (2) ◽  
pp. 166-173 ◽  
Author(s):  
M. Bercovici ◽  
C. B. Chen ◽  
M. B. Goldstein ◽  
B. J. Steinbaugh ◽  
M. L. Halperin

There is a linear relationship between the [Formula: see text] and blood hydrogen ion concentration in normal dogs, but for theoretical reasons to be discussed, we questioned whether this relationship would apply in animals with metabolic acidosis or alkalosis. To study this in more detail, animals were divided into three groups: normal, metabolically acidotic, and metabolically alkalotic. Following anesthesia and bilateral ureteral ligation, dogs were intubated and ventilated to produce acute steady-state [Formula: see text] values corresponding to the range observed during disease states. Changes in the volume and electrolyte composition of the gastrointestinal fluid and urine as well as the concentration and distribution of lactate were evaluated in all experiments. We observed the previously described linear relationship between the [Formula: see text] and blood hydrogen ion concentration in normal dogs, but the slope of the regression line differed significantly from those of dogs with metabolic acidosis and metabolic alkalosis. On the other hand, there was a consistent relationship between the ratio of the [Formula: see text] values, but not the absolute [Formula: see text], and the change in the plasma bicarbonate concentration over a wide range of [Formula: see text] values in all groups of dogs. The chemical basis for these observations will be discussed.


1976 ◽  
Vol 51 (3) ◽  
pp. 2P-3P
Author(s):  
W. S. J. Ruddell ◽  
L. M. Blendis ◽  
C. L. Walters

1982 ◽  
Vol 243 (4) ◽  
pp. E265-E271
Author(s):  
G. S. Reddy ◽  
G. Jones ◽  
S. W. Kooh ◽  
D. Fraser

Chronic metabolic acidosis had been shown to influence the renal metabolism of 25-hydroxyvitamin D3. Using the isolated perfused rat kidney model, we evaluated the rates of synthesis of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] in vitamin D-depleted [D(-)] and 24,25-dihydroxyvitamin D3 [24,25(OH)2D3] in vitamin D-replete [D(+)] rats. Metabolic acidosis was induced in both groups of rats by feeding aqueous ammonium chloride for 9 days. Kidneys isolated from D(-) acidotic rats (mean pH, 7.11) exhibited a decreased rate of 1,25(OH)2D3 synthesis (0.79 +/- 0.17 pmol produce . h-1 . g kidney-1) when compared with that (1.27 +/- 0.09) of D(-) nonacidotic (mean pH, 7.33) rats. There was a significant negative linear correlation between the rate of synthesis of 1,25(OH)2D3 and the hydrogen ion concentration of the animal (r = 0.79, P less than 0.005). The rate of synthesis of 24,25(OH)2D3 by the kidneys from D(+) acidotic (mean pH, 7.06) and nonacidotic (mean pH, 7.39) rats did not differ (0.81 +/- 0.21 vs. 0.60 +/- 0.12 pmol product . h-1 . g kidney-1). It is concluded that chronic acidosis suppressed 1-hydroxylase activity, but does not suppress 24-hydroxylase activity.


2020 ◽  
pp. 2182-2198
Author(s):  
Julian Seifter

The normal pH of human extracellular fluid is maintained within the range of 7.35 to 7.45. The four main types of acid–base disorders can be defined by the relationship between the three variables, pH, Pco2, and HCO3 –. Respiratory disturbances begin with an increase or decrease in pulmonary carbon dioxide clearance which—through a shift in the equilibrium between CO2, H2O, and HCO3 –—favours a decreased hydrogen ion concentration (respiratory alkalosis) or an increased hydrogen ion concentration (respiratory acidosis) respectively. Metabolic acidosis may result when hydrogen ions are added with a nonbicarbonate anion, A−, in the form of HA, in which case bicarbonate is consumed, or when bicarbonate is removed as the sodium or potassium salt, increasing hydrogen ion concentration. Metabolic alkalosis is caused by removal of hydrogen ions or addition of bicarbonate. Laboratory tests usually performed in pursuit of diagnosis, aside from arterial blood gas analysis, include a basic metabolic profile with electrolytes (sodium, potassium, chloride, bicarbonate), blood urea nitrogen, and creatinine. Calculation of the serum anion gap, which is determined by subtracting the sum of chloride and bicarbonate from the serum sodium concentration, is useful. The normal value is 10 to 12 mEq/litre. An elevated value is diagnostic of metabolic acidosis, helpful in the differential diagnosis of the specific metabolic acidosis, and useful in determining the presence of a mixed metabolic disturbance. Acid–base disorders can be associated with (1) transport processes across epithelial cells lining transcellular spaces in the kidney, gastrointestinal tract, and skin; (2) transport of acid anions from intracellular to extracellular spaces—anion gap acidosis; and (3) intake.


Blood ◽  
1972 ◽  
Vol 40 (5) ◽  
pp. 740-746 ◽  
Author(s):  
Jane F. Desforges ◽  
Philip Slawsky

Abstract With the use of 14C-DMO (14C-5, 5-dimethyl-2,3-oxazolidinedione), a weak organic acid, we measured the intraerythrocytic hydrogen ion concentration in 16 acidotic and alkalotic patients. Whole blood pH, red cell 2,3-diphosphoglycerate, hemoglobin, oxyhemoglobin, plasma pCO2, and plasma bicarbonate were measured simultaneously on heparinized arterial blood. The results show: (1) hydrogen ion concentration in the red cell varies directly with that of whole blood, (2) red cell concentration of 2,3-diphosphoglycerate varies inversely with the whole blood hydrogen ion concentration, and (3) red cell 2,3-diphosphoglycerate concentration also varies inversely with the intracellular hydrogen ion concentration. There were no significant relationships between the arterial total hemoglobin or oxyhemoglobin and intracellular or whole blood pH, nor was there any relationship between plasma pCO2 or plasma bicarbonate and intracellular or whole blood pH. We concluded that in a number of clinical conditions in which the hydrogen ion concentration is altered, the cellular pH parallels that of the whole blood and that the 2,3-diphosphoglycerate concentration varies with the hydrogen ion concentration.


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