PLASMA POTASSIUM RESPONSE TO ACUTE RESPIRATORY ALKALOSIS

Acute respiratory alkalosis (hyperventilation) occurs in clinical sett ings associated with electrolyte-induced complications such as cardiac arrhythmias (such as myocardial infarction, sepsis, hypoxemia, cocain e abuse). To evaluate the direction, magnitude and mechanisms of plasm a potassium changes, acute respiratory alkalosis was induced by volunt ary hyperventilation for 20 (18 and 36 liter/min) and 35 minutes (18 l iter/min). The plasma potassium response to acute respiratory alkalosi s was compared to time control, isocapnic and isobicarbonatemic (hypoc apnic) hyperventilation as well as beta- and alpha-adrenergic receptor blockade by timolol and phentolamine. Hypocapnic hypobicarbonatemic h yperventilation (standard acute respiratory alkalosis) at 18 or 36 lit er/min (Delta PCO2 - 16 and -22.5 mm Hg, respectively) resulted in sig nificant increases in plasma potassium (ca + 0.3 mmol/liter) and catec holamine concentrations. During recovery (post-hyperventilation), a ve ntilation-rate-dependent hy pokalemic overshoot was observed. Alpha-ad renoreceptor blockade obliterated, and beta-adrenoreceptor blockade en hanced the hyperkalemic response. The hyperkalemic response was preven ted under isocapnic and isobicarbonatemic hypocapnic hyperventilation. During these conditions, plasma catecholamine concentrations did not change. In conclusion, acute respiratory alkalosis results in a clinic ally significant increase in plasma potassium. The hyperkalemic respon se is mediated by enhanced alpha-adrenergic activity and counterregula ted partly by beta-adrenergic stimulation. The increased catecholamine concentrations are accounted for by the decrease in plasma bicarbonat e.