Plasma potassium response to acute respiratory alkalosis

Abstract

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 (delta 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 alpha-adrenergic activity and counterregulated partly by beta-adrenergic stimulation. The increased catecholamine concentrations are accounted for by the decrease in plasma bicarbonate.

Voluntary activation of the sympathetic nervous system and attenuation of the innate immune response in humans

“…Furthermore, the effect of the length of the training and the length of propensity for altered responses after training has yet to be determined. However, the effects on epinephrine are likely a consequence of both the hyperventilation phase and hypoxia due to breath retention, as both have been demonstrated to increase epinephrine levels (18,(21)(22)(23)(24). The hyperventilation-induced increase in epinephrine was shown to be dependent on decreased levels of bicarbonate, as hyperventilation combined with bicarbonate infusion (resulting in hypocapnia and alkalosis, but normal bicarbonate levels) nullified epinephrine increase (24).…”

“…However, the effects on epinephrine are likely a consequence of both the hyperventilation phase and hypoxia due to breath retention, as both have been demonstrated to increase epinephrine levels (18,(21)(22)(23)(24). The hyperventilation-induced increase in epinephrine was shown to be dependent on decreased levels of bicarbonate, as hyperventilation combined with bicarbonate infusion (resulting in hypocapnia and alkalosis, but normal bicarbonate levels) nullified epinephrine increase (24). In 2 3 4 5 6 7 8 -1 0 1 2 3 4 5 6 7 8 time (hours post-LPS) concordance, in the present study, bicarbonate levels were significantly lower in the trained subjects during practicing of the breathing techniques compared with control subjects.…”

Secondary Responses to Altered Acid-Base Status

“…This secondary hypobicarbonatemic response is completed within 5 to 10 minutes and remains stable for several hours. Hypocapnia of 20 to 120 minutes' duration resulting from either voluntary hyperventilation in normal individuals or controlled hyperventilation in anesthetized patients undergoing minor surgical procedures yielded a mean 11,12 Sustained hypocapnia causes an additional decrease in plasma [HCO 3 Ϫ ] owing to suppression of renal acidification. A new steady state emerges within 2 to 3 days.…”

An association between transient hypokalemia and severe acute oxaliplatin-related toxicity predominantly in women

“…Acute respiratory alkalosis (hyperventilation) has been reported to result in a clinically signifi cant increase in plasma potassium levels with a resultant post-hyperventilation ventilation-rate dependent hypokalemic overshoot on recovery. However, in our study patients, levels of serum bicarbonate remained similar both before and after chemotherapy suggesting that ventilation-related alkalosis was unlikely [7]. Calcium and magnesium infusions were not used in our patients and it is unclear if they would have had any protective effects.…”