The Ventilatory Response in Diabetic Ketoacidosis

1974 ◽  
Vol 46 (4) ◽  
pp. 539-549 ◽  
Author(s):  
M. Fulop ◽  
N. Dreyer ◽  
H. Tannenbaum
Keyword(s):  
Metabolic Acidosis ◽  
Diabetic Ketoacidosis ◽  
Ventilatory Response ◽  
Hydrogen Ion ◽  
Inverse Relation ◽  
Bicarbonate Concentration ◽  
Plasma Bicarbonate ◽  
Arterial Blood ◽  
Blood Ph ◽  
Ion Activity

1. Previous studies of the ventilatory response to metabolic acidosis have usually considered only patients with arterial blood pH above 7·10. To define the response during more severe acidaemia, arterial CO2 tension and pH were measured in fifty-three episodes of diabetic ketoacidosis, including twenty-four with pH below 7·10, and ten with pH below 7·00. 2. The relation between arterial CO2 tension, and both blood pH and plasma bicarbonate concentration, in these cases with generally severe metabolic acidaemia (mean pH 7·12 ± SD 0·13), was very similar to the relations between those variables found by others in patients with less severe acidaemia, such as that due to renal failure. 3. As arterial blood hydrogen ion activity increased, arterial CO2 tension decreased inversely, reflecting well-sustained hyperventilation, even during profound acidaemia. 4. The inverse relation between arterial CO2 tension and hydrogen ion activity suggests that during metabolic acidosis, alveolar ventilation increases in direct proportion to the increased blood hydrogen ion activity.

The Ventilatory Response in Severe Metabolic Acidosis

1976 ◽  
Vol 50 (5) ◽  
pp. 367-373 ◽  
Author(s):  
M. Fulop
Keyword(s):  
Metabolic Acidosis ◽  
Ventilatory Response ◽  
Acute Hypoxia ◽  
Carbon Dioxide Tension ◽  
Pulmonary Insufficiency ◽  
Plasma Lactate ◽  
Severe Metabolic Acidosis ◽  
Arterial Blood ◽  
Blood Ph ◽  
Insufficient Time

1. The ventilatory response to severe metabolic acidosis was studied by measuring arterial blood carbon dioxide tension and pH in sixty-seven patients with blood pH < 7·10, none of whom had hypercapnia, pulmonary oedema, or chronic pulmonary insufficiency. The results were compared with those previously found in patients with uncomplicated diabetic ketoacidosis. 2. By that comparison, fifty-two of the sixty-seven patients with blood pH < 7·10 were judged to have ‘appropriate hypocapnia’, and fifteen had ‘submaximal hypocapnia’. Thirteen of the latter fifteen had circulatory failure and/or acute hypoxia, and seven of nine in whom it was measured had plasma lactate >9 mmol/l. 3. Hyperventilation was therefore usually well sustained in these patients with severe metabolic acidosis, except in most of those with acute tissue hypoxia. The latter may have had insufficient time to achieve maximum hyperventilation in response to their acidosis, or perhaps their submaximal hypercapnia presaged imminent failure of the hyperventilatory response.

Ventilatory response to chronic metabolic acidosis and alkalosis in the dog

1984 ◽  
Vol 56 (6) ◽  
pp. 1640-1646 ◽  
Author(s):  
N. E. Madias ◽  
W. H. Bossert ◽  
H. J. Adrogue
Keyword(s):  
Metabolic Acidosis ◽  
Metabolic Alkalosis ◽  
Ventilatory Response ◽  
Wide Spectrum ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Arterial Pco2 ◽  
Plasma Bicarbonate ◽  
Oral Sodium ◽  
Chronic Change

Systematic data are not available with regard to the anticipated appropriate responses of arterial PCO2 to primary alterations in plasma bicarbonate concentration. In the present study, we attempted to rigorously characterize the ventilatory response to chronic metabolic acid-base disturbances of graded severity in the dog. Animals with metabolic acidosis produced by prolonged HCl feeding and metabolic alkalosis of three different modes of generation, i.e., diuretics (ethacrynic acid or chlorothiazide), gastric drainage, and administration of deoxycorticosterone acetate (alone or in conjunction with oral sodium bicarbonate), were examined. The results indicate the existence of a significant and highly predictable ventilatory response to chronic metabolic acid-base disturbances. Moreover, the magnitude of the ventilatory response appears to be uniform throughout a wide spectrum of chronic metabolic acid-base disorders extending from severe metabolic acidosis to severe metabolic alkalosis; on average, arterial PCO2 is expected to change by 0.74 Torr for a 1-meq/l chronic change in plasma bicarbonate concentration of metabolic origin. Furthermore, the data suggest that the ventilatory response to chronic metabolic alkalosis is independent of the particular mode of generation.

scholarly journals Red Cell 2,3-Diphosphoglycerate and Intracellular Arterial pH in Acidosis and Alkalosis

Blood ◽  
1972 ◽  
Vol 40 (5) ◽  
pp. 740-746 ◽  
Author(s):  
Jane F. Desforges ◽  
Philip Slawsky
Keyword(s):  
Whole Blood ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Red Cell ◽  
Hydrogen Ion Concentration ◽  
Plasma Bicarbonate ◽  
Weak Organic Acid ◽  
Arterial Blood ◽  
Blood Ph ◽  
Clinical Conditions

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.

Skeletal carbon dioxide stores during metabolic acidosis

1984 ◽  
Vol 247 (2) ◽  
pp. F326-F330 ◽  
Author(s):  
J. A. Bettice
Keyword(s):  
Carbon Dioxide ◽  
Metabolic Acidosis ◽  
Diabetic Ketoacidosis ◽  
Carbon Dioxide Tension ◽  
Carbon Dioxide Content ◽  
Chemical Induction ◽  
Bicarbonate Concentration ◽  
Blood Ph ◽  
Exchangeable Fraction

These experiments were performed to examine the buffering functions of skeletal carbon dioxide during metabolic acidosis. Acidosis of several days duration was produced in rats either by inclusion of acidogenic substances in the diet or by chemical induction of diabetic ketoacidosis. Titrimetric methods were used to measure the carbon dioxide content of bone, which was divided into readily exchangeable and slowly exchangeable pools according to a model described in the text. Acid feeding resulted in a mild acidemia (blood pH greater than 7.25), whereas profound metabolic acidemia occurred during diabetic ketoacidosis (blood pH less than 7.00). Total bone carbon dioxide was reduced during both forms of metabolic acidosis. This reduction in skeletal carbon dioxide occurred within the first 24 h after the onset of metabolic acidosis, was associated with a decline in the readily exchangeable fraction of skeletal carbon dioxide, and was directly proportional to the declines in extracellular bicarbonate concentration and plasma carbon dioxide tension.

ERRATA

PEDIATRICS ◽  
1980 ◽  
Vol 65 (5) ◽  
pp. 1006-1006
Keyword(s):  
Metabolic Acidosis ◽  
Diagnostic Approach ◽  
Acid Base ◽  
Arterial Blood ◽  
Blood Ph ◽  
P 351 ◽  
Normal Acid

In the article "A Diagnostic Approach to Metabolic Acidosis in Children" by Kappy and Morrow (Pediatrics 65:351-356, 1980) on p 351 under "Normal Acid-Base Physiology" the normal arterial blood pH is maintained at 7.40 (H+ = 39.8 nEq/liter not mEq/liter.

Origin of Glycosylated Hemoglobin Al in Chronic Renal Failure

1983 ◽  
Vol 6 (2) ◽  
pp. 77-82 ◽  
Author(s):  
S. De Marchi ◽  
E. Cecchin ◽  
C. Camurri ◽  
P. Quaia ◽  
A. Raimondi ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Blood Urea Nitrogen ◽  
Serum Ferritin ◽  
Serum Iron ◽  
Urea Nitrogen ◽  
Plasma Bicarbonate ◽  
Arterial Blood ◽  
Blood Ph

In chronic renal failure both HbAI and HbAlc levels have been reported to be elevated. In order to investigate the causes of such increase we measured HbAI (cation-exchange chromatography), blood urea nitrogen, arterial blood pH, plasma bicarbonate, phosphatemia, serum iron and serum ferritin before dialysis in 60 uremic patients receiving long term hemodialysis. The increased levels of HbAI do not correlate with glucose intolerance, phosphatemia, blood urea nitrogen, time averaged concentration of urea, serum iron and serum ferritin. On the contrary the presence of a highly significant correlation between HbAI and arterial blood pH (p < 0.001) and between HbAI and plasma bicarbonate (p < 0.001) seems to emphasize a major role for acidosis in increasing the HbAI levels in uremic patients on long term hemodialysis.

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.

Alveolar hypercapnia augments pulmonary C-fiber responses to chemical stimulants: role of hydrogen ion

2002 ◽  
Vol 93 (1) ◽  
pp. 181-188 ◽  
Author(s):  
Qihai Gu ◽  
Lu-Yuan Lee
Keyword(s):  
Hydrogen Ion ◽  
Right Atrial ◽  
Mechanical Stimuli ◽  
Hydrogen Ions ◽  
Lung Inflation ◽  
C Fibers ◽  
Arterial Blood ◽  
Blood Ph ◽  
C Fiber

To determine whether the excitabilities of pulmonary C fibers to chemical and mechanical stimuli are altered by CO2-induced acidosis, single-unit pulmonary C-fiber activity was recorded in anesthetized, open-chest rats. Transient alveolar hypercapnia (HPC) was induced by administering CO2-enriched gas mixture (15% CO2, balance air) via the respirator inlet for 30 s, which rapidly lowered the arterial blood pH from a baseline of 7.40 ± 0.01 to 7.17 ± 0.02. Alveolar HPC markedly increased the responses of these C-fiber afferents to several chemical stimulants. For example, the C-fiber response to right atrial injection of the same dose of capsaicin (0.25–1.0 μg/kg) was significantly increased from 3.07 ± 0.70 impulses/s at control to 8.48 ± 1.52 impulses/s during HPC ( n = 27; P < 0.05), and this enhanced response returned to control within ∼10 min after termination of HPC. Similarly, alveolar HPC also induced significant increases in the C-fiber responses to right atrial injections of phenylbiguanide (4–8 μg/kg) and adenosine (0.2 mg/kg). In contrast, HPC did not change the response of pulmonary C fibers to lung inflation. Furthermore, the peak response of these C fibers to capsaicin during HPC was greatly attenuated when the HPC-induced acidosis was buffered by infusion of bicarbonate (1.36–1.82 mmol · kg−1 · min−1 for 35 s). In conclusion, alveolar HPC augments the responses of these afferents to various chemical stimulants, and this potentiating effect of CO2 is mediated through the action of hydrogen ions on the C-fiber sensory terminals.

Use of Tris Buffers for Quality Control of Blood pH

1974 ◽  
Vol 20 (10) ◽  
pp. 1337-1340 ◽  
Author(s):  
Jack H Ladenson ◽  
Carl H Smith ◽  
David N Dietzler ◽  
J E Davis
Keyword(s):  
Quality Control ◽  
Control Program ◽  
Hydrogen Ion ◽  
National Bureau ◽  
Quality Control Program ◽  
Blood Ph ◽  
Relative Standard ◽  
Ion Activity ◽  
Primary Standards ◽  
Routine Quality Control

Abstract Tris(hydroxymethyl)aminomethane buffers have been established as sensitive and convenient indicators of the reliability of blood pH analysis. These buffers were compatible for routine use with blood-pH equipment from major manufacturers, except for two instruments. A seven-month study demonstrated the necessity of a routine quality-control program, as well as the need for systematic cleaning and maintenance of pH equipment. Tris(hydroxymethyl)aminomethane buffers were found not to be suitable as primary standards because we could not obtain the stated values with commercial pH equipment that had been standardized with phosphate buffers from the National Bureau of Standards. The relative standard deviation for measurement of hydrogen ion activity, 4.1% , indicates a need for improvement in the design and operation of equipment for the measurement of blood pH.

Relative effects of systemic pH, PCO2, and bicarbonate concentration on ileal ion transport

1983 ◽  
Vol 245 (2) ◽  
pp. G230-G235 ◽  
Author(s):  
A. N. Charney ◽  
L. P. Haskell
Keyword(s):  
Exchange Process ◽  
Respiratory Acidosis ◽  
Electrolyte Transport ◽  
Sodium Absorption ◽  
Sprague Dawley ◽  
Bicarbonate Concentration ◽  
In Situ Perfusion ◽  
Plasma Bicarbonate ◽  
Blood Ph ◽  
Before And After

To determine the relative effects of systemic pH, CO2 tension (PCO2), and bicarbonate concentration on ileal electrolyte transport, states of acute metabolic acidosis and alkalosis were created in Sprague-Dawley rats by gavage feeding (NH4)2SO4 and NaHCO3, respectively. During in situ perfusion of the ileum in anesthetized animals, electrolyte transport was measured before and after respiratory compensation of the systemic pH. Acute respiratory acidosis and alkalosis also were studied by ventilating animals with 0, 3, or 8% CO2. When animals in all groups were considered, net sodium absorption correlated very well with blood pH (r = -0.97). Net bicarbonate secretion correlated with the plasma bicarbonate concentration (r = 0.91) independently of blood pH and PCO2. Net chloride absorption correlated with blood PCO2 (r = 0.92) and was altered when systemic pH and bicarbonate concentration changed in opposite directions. Alterations in luminal pH and PCO2 did not affect electrolyte transport. These results suggest that systemic pH affects a sodium chloride absorptive process and that the plasma bicarbonate concentration affects a chloride absorptive-bicarbonate secretory exchange process in the rat ileum.

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