Changes in plasma potassium concentration during acute acid-base disturbances

doi:10.1016/0002-9343(81)90182-0

The American Journal of Medicine

Volume 71, Issue 3, September 1981, Pages 456-467

https://doi.org/10.1016/0002-9343(81)90182-0 Get rights and content

Abstract

It has been widely held that the changes in plasma potassium concentration observed during acute acid-base disorders are solely determined by the associated changes in blood acidity. However, a critical examination of the literature uncovers wide differences among the four cardinal acid-base disorders with respect to the associated changes in plasma potassium concentration. In fact, the data suggest that a host of factors other than the attendant changes in plasma hydrogen ion concentration may well modulate the intercompartmental distribution of body potassium during acid-base disorders. In this study we review the qualitative, quantitative and mechanistic aspects of the plasma potassium response to acute alterations in blood acidity.

References (109)

C Van Ypersele de Strihou
Potassium homeostasis in renal failure
Kidney Int
(1977)
PM Beigelman
Potassium in severe diabetic ketoacidosis
Am J Med
(1973)
D.S. Fraley et al.
Correction of hyperkalemia by bicarbonate despite constant blood pH
Kidney Int
(1977)
D.R. Held et al.
Effect of acute respiratory acidosis on arterial plasma osmolality
Respir Physiol
(1971)
D.S. Fraley et al.
Isohydric regulation of plasma potassium by bicarbonate in the rat
Kidney Int
(1976)
F.J. Gennari et al.
Role of the kidney in potassium homeostasis. Lessons from acid-base disturbances
Kidney Int
(1975)
R Nielsen
Effect of low pH and high CO₂ tension of the cell volume of rabbit renal cortex slices
Biochem Biophys Acta
(1972)
S Adler et al.
Potassium and intracellular pH
Kidney Int
(1977)
T Bakker-Grunwald
Effect of anions on potassium self-exchange in ascitis tumor cells
Biochem Biophys Acta
(1978)
J.P. Knochel
Role of glucoregulatory hormones in potassium homeostasis
Kidney Int
(1977)

GC Viberti

Glucose-induced hyperkalemia: a hazard for diabetics

Lancet

(1978)

B Goott et al.

The relationship of the sympathoadrenal system to potassium flux and cardiac irritability induced by alterations in blood pH

J Thorac Cardiovasc Surg

(1960)

ME Morris et al.

Blood pH/plasma catecholamine relationships: Respiratory acidosis

Br J Anaesthesiol

(1962)

J.C. Mithoefer et al.

Myocardial potassium exchange during respiratory acidosis: the interaction of carbon dioxide and sympatho-adrenal discharge

Respir Physiol

(1968)

G.G. Nahas et al.

Increased rate of catecholamine synthesis during respiratory acidosis

Respir Physiol

(1968)

E Carlsson et al.

β-adrenoceptor blockers, plasma potassium, and exercise

Lancet

(1978)

RH Sterns et al.

Disposition of intravenous potassium in anuric man: A kinetic analysis

Kidney Int

(1979)

B.G. Walker et al.

Inhibition of insulin by acidosis

Lancet

(1963)

G Giebisch et al.

The extrarenal response to acute acid-base disturbances of respiratory origin

J Clin Invest

(1955)

RC Swan et al.

Neutralization of infused acid by nephrectomized dogs

J Clin Invest

(1955)

RC Swan et al.

Distribution of sodium bicarbonate infused into nephrectomized dogs

J Clin Invest

(1955)

D.H. Simmons et al.

Acid-base alterations and plasma potassium concentration

Am J Physiol

(1959)

O Siggaard Andersen

Acute experimental acid-base disturbances in dogs

Scand J Clin Lab Invest

(1962)

F.Q. Nuttall

Serum electrolytes and their relation to acid-base balance

Arch Intern Med

(1965)

G.B. Spurr et al.

Intra- and extracellular K⁺ concentrations of cardiac and skeletal muscle during acute respiratory acid-base alterations

Am J Med Sci

(1966)

JM Burnell et al.

The effect in humans of extracellular pH change on the relationship between serum potassium concentration and intracellular potassium

J Clin Invest

(1956)

B.H. Scribner et al.

Interpretation of the serum potassium concentration

Metabolism

(1956)

P Gabow

Disorders of potassium metabolism

BM Brenner et al.

Potassium homeostasis

W.B. Schwartz et al.

The internal distribution of hydrogen ions with varying degrees of metabolic acidosis

J Clin Invest

(1957)

R.B. Tobin

Varying role of extracellular electrolytes in metabolic acidosis and alkalosis

Am J Physiol

(1958)

P.A. Poole-Wilson et al.

Intracellular pH and K⁺ of cardiac and skeletal muscle in acidosis and alkalosis

Am J Physiol

(1975)

J.R. Oster et al.

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

Am J Physiol

(1978)

J.R. Oster et al.

Plasma potassium response to acute metabolic acidosis induced by mineral and nonmineral acids

Mineral Electrolyte Metab

(1980)

W.B. Abrams et al.

The effect of acidosis and alkalosis on the plasma potassium concentration and the electrocardiogram of normal and potassium depleted dogs

Am J Med Sci

(1951)

R.E. Keating et al.

The movement of potassium during experimental acidosis and alkalosis in the nephrectomized dog

Surg Gynecol Obstet

(1953)

C.E. Orringer et al.

Natural history of lactic acidosis after grand-mal seizures: a model for the study of an anion-gap acidosis not associated with hyperkalemia

N Engl J Med

(1977)

M Fulop

Serum potassium in lactic acidosis and ketoacidosis

N Engl J Med

(1979)

D.A. Nardone et al.

Mechanisms in hypokalemia: clinical correlation

Medicine (Baltimore)

(1978)

RM Epstein et al.

Circulatory changes following rapid correction of severe hypercapnic acidosis by 2-amino-2-hydroxymethyl-1,3-propanediol

Ann NY Acad Sci

(1961)

T.E. Bennett et al.

The hypoglycemic activity of 2-amino-2-hydroxymethyl-1,3-propanediol

Ann NY Acad Sci

(1961)

A-H Samiy et al.

The use of 2-amino-2-hydroxymethyl-1,3-propanediol in the management of renal acidosis

Ann NY Acad Sci

(1961)

E.B. Brown et al.

Intracellular hydrogen ion changes and potassium movement

Am J Physiol

(1963)

J.R. Elkinton et al.

Effects in man of acute experimental respiratory alkalosis and acidosis on ionic transfers in the total body fluids

J Clin Invest

(1955)

W.O. Fenn et al.

Effects of carbon dioxide inhalation on potassium liberation from the liver

Am J Physiol

(1956)

G.B. Spurr et al.

Cardiac and skeletal muscle electrolytes in acute respiratory alkalemia and acidemia

J Appl Physiol

(1960)

J.J. Cohen et al.

The nature of the carbon dioxide titration curve in the normal dog

J Clin Invest

(1964)

NC Brackett et al.

Carbon dioxide titration curve of normal man

N Engl J Med

(1965)

K.H. Kilburn

Movements of potassium during acute respiratory acidosis and recovery

J Appl Physiol

(1965)

U Finsterer et al.

Effects of acute hypercapnia and hypocapnia on plasma and red cell potassium, blood lactate and base excess in man during anesthesia

Acta Anaesthesiol Scand

(1978)

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^☆: This study was supported in part by Grant HL-00759 from the National Heart, Lung and Blood Institute and Grant AM-07078 from the National Institute of Arthritis, Metabolism and Digestive Disease.

¹: From the Departments of Medicine, Baylor College of Medicine and Tufts University School of Medicine, and the Renal Services, The Methodist Hospital, Houston, Texas.

²: From the New England Medical Center, Boston, Massachusetts.

View full text

ReviewChanges in plasma potassium concentration during acute acid-base disturbances☆

Abstract

Kidney Int

Am J Med

Kidney Int

Respir Physiol

Kidney Int

Kidney Int

Biochem Biophys Acta

Kidney Int

Biochem Biophys Acta

Kidney Int

Lancet

J Thorac Cardiovasc Surg

Br J Anaesthesiol

Respir Physiol

Respir Physiol

Lancet

Kidney Int

Lancet

The extrarenal response to acute acid-base disturbances of respiratory origin

J Clin Invest

Neutralization of infused acid by nephrectomized dogs

J Clin Invest

Distribution of sodium bicarbonate infused into nephrectomized dogs

J Clin Invest

Acid-base alterations and plasma potassium concentration

Am J Physiol

Acute experimental acid-base disturbances in dogs

Scand J Clin Lab Invest

Serum electrolytes and their relation to acid-base balance

Arch Intern Med

Intra- and extracellular K+ concentrations of cardiac and skeletal muscle during acute respiratory acid-base alterations

Am J Med Sci

The effect in humans of extracellular pH change on the relationship between serum potassium concentration and intracellular potassium

J Clin Invest

Interpretation of the serum potassium concentration

Metabolism

Disorders of potassium metabolism

Potassium homeostasis

The internal distribution of hydrogen ions with varying degrees of metabolic acidosis

J Clin Invest

Varying role of extracellular electrolytes in metabolic acidosis and alkalosis

Am J Physiol

Intracellular pH and K+ of cardiac and skeletal muscle in acidosis and alkalosis

Am J Physiol

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

Am J Physiol

Plasma potassium response to acute metabolic acidosis induced by mineral and nonmineral acids

Mineral Electrolyte Metab

The effect of acidosis and alkalosis on the plasma potassium concentration and the electrocardiogram of normal and potassium depleted dogs

Am J Med Sci

The movement of potassium during experimental acidosis and alkalosis in the nephrectomized dog

Surg Gynecol Obstet

Natural history of lactic acidosis after grand-mal seizures: a model for the study of an anion-gap acidosis not associated with hyperkalemia

N Engl J Med

Serum potassium in lactic acidosis and ketoacidosis

N Engl J Med

Mechanisms in hypokalemia: clinical correlation

Medicine (Baltimore)

Circulatory changes following rapid correction of severe hypercapnic acidosis by 2-amino-2-hydroxymethyl-1,3-propanediol

Ann NY Acad Sci

The hypoglycemic activity of 2-amino-2-hydroxymethyl-1,3-propanediol

Ann NY Acad Sci

The use of 2-amino-2-hydroxymethyl-1,3-propanediol in the management of renal acidosis

Ann NY Acad Sci

Intracellular hydrogen ion changes and potassium movement

Am J Physiol

Effects in man of acute experimental respiratory alkalosis and acidosis on ionic transfers in the total body fluids

J Clin Invest

Effects of carbon dioxide inhalation on potassium liberation from the liver

Am J Physiol

Cardiac and skeletal muscle electrolytes in acute respiratory alkalemia and acidemia

J Appl Physiol

The nature of the carbon dioxide titration curve in the normal dog

J Clin Invest

Carbon dioxide titration curve of normal man

N Engl J Med

Movements of potassium during acute respiratory acidosis and recovery

J Appl Physiol

Review
Changes in plasma potassium concentration during acute acid-base disturbances☆

Intra- and extracellular K⁺ concentrations of cardiac and skeletal muscle during acute respiratory acid-base alterations

Intracellular pH and K⁺ of cardiac and skeletal muscle in acidosis and alkalosis