Nature of Acid-Base Disturbance in Salicylate Intoxication

JAMA ◽  
1963 ◽  
Vol 183 (12) ◽  
pp. 183
Keyword(s):  
Acid Base ◽  
Salicylate Intoxication ◽  
Acid Base Disturbance ◽  
Base Disturbance

THE RENAL RESPONSE TO ADMINISTRATION OF ACETAZOLAMIDE (DIAMOX®) DURING SALICYLATE INTOXICATION

PEDIATRICS ◽  
1959 ◽  
Vol 23 (6) ◽  
pp. 1103-1114
Author(s):  
Robert Schwartz ◽  
Francis X. Fellers ◽  
John Knapp ◽  
Sumner Yaffe
Keyword(s):  
Organic Acids ◽  
Neurologic Complications ◽  
Acid Base ◽  
Alkaline Urine ◽  
Acid Urine ◽  
Therapeutic Value ◽  
Before And After ◽  
Salicylate Intoxication ◽  
Acid Base Disturbance ◽  
Base Disturbance

Advanced salicylate intoxication in young children may produce severe acidosis due not only to the production and accumulation of organic acids in tissues, but also to the diminished content of buffer cation which is secondary to the loss of buffer cation during the excretion of organic acids. The excretion of an intensely acid urine all but prevents the excretion of free salicylate and thereby perpetuates the toxic effects of this ion. Despite severe deficit of buffer cation, the kidney responds to administration of a carbonic anhydrase inhibitor with excretion of alkaline urine. The magnitude of the loss of buffer cation is unpredictable both before and after enzyme inhibition. However, the systemic acidosis may be controlled by infusion of solutions of sodium bicarbonate, but frequent determinations of pH and content of carbon dioxide in the serum are mandatory. While the alterations in acid-base disturbance may be controlled during administration of acetazolamide, the occurrence of neurologic complications late in the course must be accepted as a serious additional hazard which may preclude the successful therapeutic value of this agent.

Metabolic Alkalosis Secondary to Baking Soda Treatment of a Diaper Rash

PEDIATRICS ◽  
1981 ◽  
Vol 67 (6) ◽  
pp. 820-822
Author(s):  
Jose Gonzalez ◽  
Ronald J. Hogg
Keyword(s):  
Case Report ◽  
Side Effects ◽  
Sodium Bicarbonate ◽  
Complete Resolution ◽  
Metabolic Alkalosis ◽  
Acid Base ◽  
Prior Application ◽  
Acid Base Disturbance ◽  
Base Disturbance

A 4-month-old infant was seen with hypokalemic metabolic alkalosis that was associated with prior application of liberal amounts of sodium bicarbonate (baking soda) to a diaper rash. After exclusion of other etiologies of the infant's acid-base disturbance, a complete resolution occurred following discontinuation of the baking soda applications. This case report provides a reminder of the significant side effects that may result from the excessive use of a seemingly harmless household substance.

Branchial ion uptake in arctic grayling: resting values and effects of acid-base disturbance

1976 ◽  
Vol 64 (3) ◽  
pp. 711-725
Author(s):  
J. N. Cameron
Keyword(s):  
Ion Exchange ◽  
Hypercapnic Acidosis ◽  
Compensation Mechanism ◽  
Acid Base ◽  
Arctic Grayling ◽  
Unidirectional Flux ◽  
Acid Base Disturbance ◽  
Base Disturbance ◽  
Na Uptake

1. Techniques for the measurement of unidirectional flux rates in fish which require no anaesthesia or surgery are described. 2. Resting values for Cl- uptake at 10 and 17 degrees C were 8–03 +/− 1–11 and 13–52 +/− 0–95 mu-equiv. 200 g-1 h-1 (+/− S.E.), respectively; and for Na+ the rates were 15–49 +/− 0–40 and 26–30 +/− 0–36, respectively. 3. Hypercapnic acidosis caused an increase in Na+ uptake, presumably through Na+/H+ (or NH+4) exchange. It is suggested that this is a compensation mechanism leading to the increase in blood buffering observed in response to hypercapnia. 4. Alkalosis was observed following acute temperature increase and was accompanied by an increase in the rate of Cl-/HCO-3 exchange and also by an increase in Na+/H+ exchange. 5. The role of these branchial ion exchange mechanisms in overall acidbase regulation is discussed.

The effects of enforced activity on ventilation, circulation and blood acid-base balance in the semi-terrestrial anuran, Bufo marinus

1980 ◽  
Vol 84 (1) ◽  
pp. 273-287
Author(s):  
D. G. McDonald ◽  
R. G. Boutilier ◽  
D. P. Toews
Keyword(s):  
Time Course ◽  
Ventilation Rate ◽  
Strenuous Exercise ◽  
Acid Base Balance ◽  
Acid Base ◽  
Arterial Blood ◽  
Base Balance ◽  
Lactate Levels ◽  
Acid Base Disturbance ◽  
Base Disturbance

Strenuous exercise results in a marked blood acid-base disturbance which is accompanied by large increases in ventilation rate, heart rate and mean arterial blood pressure. Recovery to normal resting values follows an exponential time course with a half-time of approximately 2 h for all parameters except Pa, CO2 and ventilation rate. The latter return to normal by 30 min following the exercise period. Analysis reveals that there is initially a large discrepancy between the quantity of metabolic acids buffered in the blood and the blood lactate levels. The significance of this finding is discussed. Significant changes in the concentrations of chloride, bicarbonate and lactate, in both plasma and erythrocytes, accompany the blood acid-base disturbance. Chloride and bicarbonate appear to be passively distributed between the two compartments according to a Gibbs-Donnan equilibrium whereas lactate only slowly permeates the erythrocyte.

An Analysis of Acid-Base Disturbances in the Haemolymph Following Strenuous Activity in the Dungeness Crab, Cancer Magister

1979 ◽  
Vol 79 (1) ◽  
pp. 47-58
Author(s):  
D. G. McDONALD ◽  
B. R. McMAHON ◽  
C. M. WOOD
Keyword(s):  
Lactate Concentration ◽  
Dungeness Crab ◽  
Acid Base ◽  
Cancer Magister ◽  
Rapid Release ◽  
Strenuous Activity ◽  
Lactate Levels ◽  
Acid Base Disturbance ◽  
Base Disturbance

Enforced activity causes a marked depression of haemofymph pH in Cancer magister. Both lactate concentration and PCOCO2 of the haemolymph are elevated immediately following exercise but resting PCOCO2 is restored within 30 min whereas resting lactate levels are not restored for at least 8 h. The haemolymph acid-base disturbance is caused largely by elevated haemolymph lactate levels but a Davenport analysis based on measurements of pH and total CO2 reveals a marked discrepancy between the amount of metabolic acid buffered by the haemolymph and the lactate anion concentration. This appears due to a more rapid release of lactate from the tissues than H+ ions produced with lactate.

scholarly journals A paraneoplastic potassium and acid-base disturbance

2019 ◽  
Vol 86 (3) ◽  
pp. 187-197
Author(s):  
Samuel P. Wiles ◽  
Matthew Kiczek ◽  
Gregory W. Rutecki
Keyword(s):  
Acid Base ◽  
Acid Base Disturbance ◽  
Base Disturbance

scholarly journals Rapid blood acid-base regulation by European sea bass (Dicentrarchus labrax) in response to sudden exposure to high environmental CO2

2022 ◽  
Author(s):  
Daniel W. Montgomery ◽  
Garfield T. Kwan ◽  
William G. Davison ◽  
Jennifer Finlay ◽  
Alex Berry ◽  
...  
Keyword(s):  
Dicentrarchus Labrax ◽  
Sea Bass ◽  
Apical Surface ◽  
Acid Excretion ◽  
Acid Base ◽  
European Sea Bass ◽  
Exposure Levels ◽  
Tissue Acidosis ◽  
Acid Base Disturbance ◽  
Base Disturbance

Fish in coastal ecosystems can be exposed to acute variations in CO2 of between 0.2-1 kPa CO2 (2,000 - 10,000 µatm). Coping with this environmental challenge will depend on the ability to rapidly compensate the internal acid-base disturbance caused by sudden exposure to high environmental CO2 (blood and tissue acidosis); however, studies about the speed of acid-base regulatory responses in marine fish are scarce. We observed that upon sudden exposure to ∼1 kPa CO2, European sea bass (Dicentrarchus labrax) completely regulate erythrocyte intracellular pH within ∼40 minutes, thus restoring haemoglobin-O2 affinity to pre-exposure levels. Moreover, blood pH returned to normal levels within ∼2 hours, which is one of the fastest acid-base recoveries documented in any fish. This was achieved via a large upregulation of net acid excretion and accumulation of HCO3− in blood, which increased from ∼4 to ∼22 mM. While the abundance and intracellular localisation of gill Na+/K+-ATPase (NKA) and Na+/H+ exchanger 3 (NHE3) remained unchanged, the apical surface area of acid-excreting gill ionocytes doubled. This constitutes a novel mechanism for rapidly increasing acid excretion during sudden blood acidosis. Rapid acid-base regulation was completely prevented when the same high CO2 exposure occurred in seawater with experimentally reduced HCO3− and pH, likely because reduced environmental pH inhibited gill H+ excretion via NHE3. The rapid and robust acid-base regulatory responses identified will enable European sea bass to maintain physiological performance during large and sudden CO2 fluctuations that naturally occur in coastal environments.

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