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.

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.

scholarly journals Blood total carbon dioxide content and bicarbonate can be used together to predict blood pH correctly in venous blood samples

Renal Failure ◽  
2013 ◽  
Vol 36 (1) ◽  
pp. 145-146
Author(s):  
Fatih Bulucu ◽  
Mustafa Çakar ◽  
Ömer Kurt ◽  
Fatih Yeşildal ◽  
Hakan Şarlak
Keyword(s):  
Carbon Dioxide ◽  
Venous Blood ◽  
Total Carbon ◽  
Carbon Dioxide Content ◽  
Blood Samples ◽  
Blood Ph

scholarly journals Selected Arterial Blood Gasometry Parameters as Indicators of Blood Transfusion Effectiveness in Foals with Haemolytic Disease

2014 ◽  
Vol 58 (3) ◽  
pp. 467-471
Author(s):  
Artur Stopyra ◽  
Anna Snarska
Keyword(s):  
Carbon Dioxide ◽  
Blood Transfusion ◽  
Partial Pressure ◽  
Carbon Dioxide Tension ◽  
Haematological Parameters ◽  
Haemolytic Disease ◽  
Transfusion Therapy ◽  
Arterial Blood ◽  
Blood Ph ◽  
Ph Increase

Abstract The aim of the study was to determine the suitability of basic haematological, biochemical, and gasometric tests in checking the effectiveness of transfusion therapy in foals during isoerythrolysis. The number of red blood cells, haemoglobin, haematocrit, and partial pressure of carbon dioxide, oxygen, and blood pH was determined immediately before and several times after blood transfusion. The concentration of serum free bilirubin was also measured to confirm haemolysis. Fluids (0.9% NaCl, multielectrolytic fluid, 5% glucose) and antibiotics (penicillin, amikacin) were provided to the foals. The lowest values of haematological parameters were observed before transfusion. This was accompanied by decreased partial pressure of oxygen, low pH, and increased arterial carbon dioxide tension. Transfusion of whole blood led to a gradual normalisation of the haematological parameters, also accompanied by the normalisation of gasometric indicators (decrease in pCO2 and pO2 and pH increase). Monitoring of selected haematological and gasometric parameters allows to evaluate the efficacy of blood transfusion during treatment of haemolytic disease of foals.

STUDIES OF RESPIRATORY INSUFFICIENCY IN NEWBORN INFANTS

PEDIATRICS ◽  
1957 ◽  
Vol 19 (3) ◽  
pp. 387-398
Author(s):  
Herbert C. Miller ◽  
Franklin C. Behrle ◽  
Ned W. Smull ◽  
Richard D. Blim
Keyword(s):  
Carbon Dioxide ◽  
Oxygen Saturation ◽  
Respiratory Insufficiency ◽  
Newborn Infants ◽  
Respiratory Acidosis ◽  
Carbon Dioxide Tension ◽  
Carbon Dioxide Content ◽  
Severe Hypoxemia ◽  
Acid Base ◽  
Marked Tendency

Serial determinations of pH, carbon dioxide tension, carbon dioxide content and oxygen saturation of the blood were made on newborn infants and correlated with the trends of their respiratory rates. Some infants whose respiratory rates were normal from birth and some whose rates were initially high but subsequently returned to normal levels exhibited mild uncompensated respiratory acidosis for 3 or 4 hours after birth. Thereafter, acid-base balances were normal. All infants whose respiratory rates followed either of the above two trends oxygenated their blood 91% or better within a few minutes of birth. There was a marked tendency for infants whose respiratory rates increased significantly on the first day or two after birth to have a moderate to severe uncompensated respiratory acidosis which was worse at birth and sometimes persisted for several days, usually with improvement. Some of the infants whose respiratory rates increased significantly after birth had moderate to severe hypoxemia, which also was worse at birth and tended to improve with increasing age. The hypothesis was advanced that one of the basic difficulties in neonatal respiratory insufficiency was a reduction of resting tidal volume; the latter was universally associated with a significant increase in respiratory rates during the first day or two after birth and sometimes with an uncompensated respiratory acidosis and occasionally with hypoxemia.

CERTAIN ASPECTS OF THE RENAL REGULATION OF BODY COMPOSITION

PEDIATRICS ◽  
1954 ◽  
Vol 14 (6) ◽  
pp. 567-572
Author(s):  
ROBERT E. COOKE
Keyword(s):  
Carbon Dioxide ◽  
Extracellular Space ◽  
Carbonic Acid ◽  
Plasma Concentrations ◽  
Extracellular Volume ◽  
Extracellular Fluid ◽  
Carbon Dioxide Tension ◽  
Plasma Sodium ◽  
Renal Tubules ◽  
Bicarbonate Concentration

THE pH of extracellular fluid is determined by the ratio of the plasma concentrations of bicarbonate ion to carbonic acid, as given in the classical Henderson-Hasselbach equation. [See Equation in Source Pdf] The denominator the carbonic acid concentration, [H2CO3], is proportional to the carbon dioxide tension of the blood. The carbon dioxide tension (pCO2) is primarily dependent upon respiratory function, since metabolism (hence carbon dioxide production) is relatively constant. The numerator of the equation—the bicarbonate concentration of extracellular fluid—is determined by the difference between nonvolatile cations and anions. Since there are almost limitless quantities of bicarbonate available to the organism from cell metabolism, [See Equation in Source Pdf] bicarbonate concentration must change whenever nonvolatile cation (largely sodium) is altered in relation to nonvolatile anion (largely chloride). Thus in most states extracellular bicarbonate concentration is dependent upon the ratio of sodium to chloride in extracellular fluid. The quantity of water filtered at the glomeruli and reabsorbed by the renal tubules each day is approximately 15 times the extracellular volume. The quantity of sodium chloride filtered and reabsorbed daily is approximately 15 times that contained in the extracellular space and 150 times that usually ingested and excreted each day. Therefore, the ratio of plasma sodium to chloride in any steady state is determined by the composition of the renal tubular reabsorbate, as Cushny pointed over 30 years ago. In a sense the kidney perfuses the extracellular space with large quantities of tubular reabsorbate. Tubular reasorbate—the net quantity of materials reabsorbed by the tubules. This term is analogous to glomerular filtrate—the quantity of materials filtered by the glomeruli.

Sign in / Sign up

Export Citation Format

Share Document