Relationship between blood pH and potassium and phosphorus during acute metabolic acidosis

Oster, James R.; Pérez, Guido O.; Vaamonde, Carlos A.

doi:10.1152/ajprenal.1978.235.4.f345

Cited by 35 publications

(33 citation statements)

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“…It was found that the presence of d ‐lactataemia in acidemic calves resulted in significantly lower odds for hyperkalemia but significantly higher odds for the presence of hypokalemia 8. This is in line with the results of experimental studies which reported that a hyperkalemic state can be induced by infusions with inorganic acids such as HCl or ammonium chloride but not if organic acids such as lactic acid, acetic acid or ß‐hydroxybutyrate are infused 24, 25, 26. This disparate effect on K + homeostasis was related to intracellular moving of organic anions which is believed to result in a higher degree of intracellular acidosis and Na + loading and consequently a higher Na + /K + ‐ATPase activity resulting in a net cellular uptake of potassium ions 27.…”

Section: Discussionsupporting

confidence: 78%

Risk Factors for the Development of Hypokalemia in Neonatal Diarrheic Calves

Trefz

Lorch

Zitzl

et al. 2015

Veterinary Internal Medicne

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BackgroundNeonatal diarrheic calves have a clear negative potassium balance because of intestinal losses and decreased milk intake but in the presence of acidemia, they usually show normokalemic or hyperkalemic plasma concentrations.ObjectivesTo assess whether marked hypokalemia occurs in response to the correction of acidemia and dehydration and to identify factors that are associated with this condition.AnimalsEighty‐three calves with a clinical diagnosis of neonatal diarrhea.MethodsProspective cohort study. Calves were treated according to a clinical protocol using an oral electrolyte solution and commercially available packages of 8.4% sodium bicarbonate, 0.9% saline and 40% dextrose infusion solutions.ResultsThe proportion of hypokalemic calves after 24 hours of treatment (19.3%) was twice as great as it was on admission to the hospital. Plasma K+ after 24 hours of treatment was not significantly correlated to venous blood pH values at the same time but positively correlated to venous blood pH values on admission (r = 0.51, P < .001). Base excess on admission (Odds ratio [OR] = 0.81, 95% confidence interval [CI] = 0.70–0.94), duration of diarrhea (OR = 1.37, 95% CI = 1.05–1.80), milk intake during hospitalization (OR = 0.54, 95% CI = 0.37–0.79) and plasma sodium concentrations after 24 hours (OR = 1.12, 95% CI = 1.01–1.25) were identified to be independently associated (P < .05) with a hypokalemic state after 24 hours of treatment.Conclusions and Clinical ImportanceFindings of this study suggest that marked depletion of body potassium stores is evident in diarrheic calves that suffered from marked metabolic acidosis, have a low milk intake and a long history of diarrhea.

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Section: Discussionsupporting

confidence: 78%

Risk Factors for the Development of Hypokalemia in Neonatal Diarrheic Calves

Trefz

Lorch

Zitzl

et al. 2015

Veterinary Internal Medicne

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“…Fluxes of potassium among the fluid compartments were previously thought to be solely determined by changes in acidity. Other factors, however, have been identified as modulators of the plasma potassium response (5); prominent among them is the nature of the anion escorting the protons responsible for acidemia (6)(7)(8)(9). In sharp contrast with mineral acid acidosis that consistently leads to hyperkalemia, acute organic acid acidosis is not associated with a significant increase in plasma potassium (10).…”

Section: Introductionmentioning

confidence: 99%

Role of the endocrine pancreas in the kalemic response to acute metabolic acidosis in conscious dogs.

Adrogué¹,

Chap²,

Ishida³

et al. 1985

J. Clin. Invest.

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Metabolic acidosis due to organic acids infusion fails to elicit hyperkalemia. Although plasma potassium levels may rise, the increase is smaller than in mineral acid acidosis. The mechanisms responsible for the different effects of organic acid acidosis and mineral acid acidosis remain undefined, although dissimilar hormonal responses by the pancreas may explain the phenomena. To test this hypothesis, beta-hydroxybutyric acid (7 meq/kg) or hydrochloric acid (3 meq/kg) was infused over 30 min into conscious dogs (n = 12) with chronically implanted catheters in the portal, hepatic, and systemic circulation, and flow probes were placed around the portal vein and hepatic artery. Acid infusion studies in two groups of anesthetized dogs were also done to assess the urinary excretion of potassium (n = 14), and to evaluate the effects of acute suppression of renal electrolyte excretion on plasma potassium and on the release/uptake of potassium in peripheral tissues of the hindleg (n = 17). Ketoacid infusion caused hypokalemia and a significant increase in portal vein plasma insulin, from the basal level of 27±4 uU/ml to a maximum of 84±22 ,U, ml at 10 min, without changes in glucagon levels. By contrast, mineral acid acidosis of similar severity resulted in hyperkalemia and did not increase portal insulin levels but enhanced portal glucagon concentration from control values of 132±25 pg/ml to 251±39 pg/ml at 40 min. A significant decrease in plasma glucose levels due to suppression of hepatic release was observed during ketoacid infusion, while no changes were observed with mineral acid infusion. Plasma flows in the portal vein and hepatic artery remained unchanged from control values in both acid infusion studies. Differences in renal potassium excretion were ruled out as determinants of the disparate kalemic responses to organic acid infusion compared with HCO acidosis. Evaluation of the arteriovenous potassium difference across the hindleg during ketoacid infusion demonstrates that peripheral uptake of potassium is unlikely to be responsible for the observed hypokalemia. Although the tissue responsible for the different kalemic responses could not be defined with certainty, the data are compatible with an hepatic role in response to alterations in the portal vein insulin and/or glucagon levels in both acid infusion studies. We propose that cellular uptake of potassium is enhanced by hyperinsulinemia Correspondence and reprint requests should be addressed to Dr.

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“…However, it is even difficult to interpret the studies in dogs with clarity. Either severe hyperkalemia (1,28) or an unchanged plasma [K ϩ ] (29) were reported during post-IV HCl equilibration periods using arterial plasma samples.…”

Section: Discussionmentioning

confidence: 99%

Acute Metabolic Acidosis

Wiederseiner

Muser²,

Lutz

et al. 2004

Journal of the American Society of Nephrology

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Abstract. Despite the high incidence of acute metabolic acidosis, there are no reliable human data to enable physicians to accurately diagnose this disorder. In addition, there is uncertainty about the direction and magnitude of plasma potassium changes in acute metabolic acidosis. The systemic and renal acid-base, electrolyte, and endocrine response to acute acid loads (imposed by three timed NH 4 Cl infusions into the duodenum, 0.9 mmol of NH 4 Cl per kg of body weight over 30 min each) was characterized in six healthy male subjects in whom a metabolic steady-state had been established. Arterialized blood CO 2 tension decreased by 0.85 mmHg per mmol/L decrease in plasma bicarbonate concentration and blood hydrogen ion concentration increased by 0.45 nmol/L per mmol/L decrease in plasma bicarbonate concentration. Plasma potassium did not change significantly (ϩ0.02 Ϯ 0.02 mmol/L per mmol decrease in plasma bicarbonate concentration). Plasma insulin increased and plasma glucagon levels decreased in acute metabolic acidosis, while catecholamines and aldosterone were not affected significantly. These data provide the first diagnostic criteria for the diagnosis of acute metabolic acidosis in humans. The finding of a hyperinsulinemic response in acute metabolic acidosis suggests that an insulin response counterregulates any acidemia-induced cellular potassium efflux, resulting in stable plasma potassium concentrations.

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Relationship between blood pH and potassium and phosphorus during acute metabolic acidosis

Cited by 35 publications

References 0 publications

Risk Factors for the Development of Hypokalemia in Neonatal Diarrheic Calves

Risk Factors for the Development of Hypokalemia in Neonatal Diarrheic Calves

Role of the endocrine pancreas in the kalemic response to acute metabolic acidosis in conscious dogs.

Acute Metabolic Acidosis

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