Plasma potassium response to acute respiratory alkalosis

Plasma potassium response to acute respiratory alkalosis

Plasma potassium response to acute respiratory alkalosis. Acute respiratory alkalosis (hyperventilation) occurs in clinical settings associated with electrolyte-induced complications such as cardiac arrhythmias (such as myocardial infarction, sepsis, hypoxemia, cocaine abuse). To evaluate the direct...

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Bibliographic Details
Published in:Kidney international Vol. 47; no. 1; pp. 217 - 224
Main Authors: Krapf, Reto, Caduff, Pia, Wagdi, Philippe, Stäubli, Max, Hulter, Henry N.
Format: Journal Article Conference Proceeding
Language:English
Published: New York, NY Elsevier Inc 01-01-1995
Nature Publishing
Subjects:
Acute Disease
Adult
Alkalosis, Respiratory - blood
Alkalosis, Respiratory - complications
Biological and medical sciences
Epinephrine - blood
Humans
Hyperkalemia - etiology
Hyperkalemia - metabolism
Male
Medical sciences
Metabolic diseases
Miscellaneous
Norepinephrine - blood
Other metabolic disorders
Phentolamine - pharmacology
Potassium - blood
Receptors, Adrenergic, alpha - metabolism
Receptors, Adrenergic, beta - metabolism
Timolol - pharmacology
Water-Electrolyte Balance
Human
Hormone
Venous blood
Pathophysiology
Acute
Hydroelectrolytic balance
Carbon dioxide
Acid base balance disorder
Catecholamine
Sympathetic nervous system
Inorganic element
Blood plasma
Partial pressure
Respiratory alkalosis
Hyperventilation
Potassium
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Summary:Plasma potassium response to acute respiratory alkalosis. Acute respiratory alkalosis (hyperventilation) occurs in clinical settings associated with electrolyte-induced complications such as cardiac arrhythmias (such as myocardial infarction, sepsis, hypoxemia, cocaine abuse). To evaluate the direction, magnitude and mechanisms of plasma potassium changes, acute respiratory alkalosis was induced by voluntary hyperventilation for 20 (18 and 36 liter/min) and 35 minutes (18 liter/min). The plasma potassium response to acute respiratory alkalosis was compared to time control, isocapnic and isobicarbonatemic (hypocapnic) hyperventilation as well as beta- and alpha-adrenergic receptor blockade by timolol and phentolamine. Hypocapnic hypobicarbonatemic hyperventilation (standard acute respiratory alkalosis) at 18 or 36 liter/min (Δ PCO2 – 16 and -22.5 mm Hg, respectively) resulted in significant increases in plasma potassium (ca + 0.3 mmol/liter) and catecholamine concentrations. During recovery (post-hyperventilation), a ventilation-rate-dependent hypokalemic overshoot was observed. Alpha-adrenoreceptor blockade obliterated, and beta-adrenoreceptor blockade enhanced the hyperkalemic response. The hyperkalemic response was prevented under isocapnic and isobicarbonatemic hypocapnic hyperventilation. During these conditions, plasma catecholamine concentrations did not change. In conclusion, acute respiratory alkalosis results in a clinically significant increase in plasma potassium. The hyperkalemic response is mediated by enhanced alphaadrenergic activity and counterregulated partly by beta-adrenergic stimulation. The increased catecholamine concentrations are accounted for by the decrease in plasma bicarbonate.
Bibliography:ObjectType-Article-2
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ISSN:0085-2538
1523-1755
DOI:10.1038/ki.1995.26