Exercise-induced rise in arterial potassium in patients with chronic heart failure

In patients with chronic heart failure (CHF), exercise is frequently associated with skeletal muscle fatigue and breathlessness due to heightened ventilatory response. The exercise-induced rise in potassium, which is released from the exercising skeletal muscle, has been implicated in ventilatory control during exercise. The aim of the present study was to determine whether the exercise-induced rise in arterial potassium is altered in patients with CHF and to examine the relationship between increased exercise ventilation and exercise-induced hyperkalemia in patients with CHF.

We evaluated 88 patients with CHF (25 patients were in class I, 35 in class II, and 28 in class III according to the New York Heart Association functional classification) and 14 normal subjects. Subjects performed symptom-limited ergometer exercise while expired gas, arterial blood gas, and arterial potassium were analyzed. The increases in ventilation (deltaV(E)), effective alveolar ventilation (deltaVA), and carbon dioxide output (deltaV(CO2)) from rest to peak exercise decreased as the severity of CHF advanced. The ratio of deltaV(E) to deltaV(CO2) was significantly elevated in class III patients, although there was no difference in the ratio of deltaVA to deltaV(CO2) among the four groups. Rest and exercise arterial P(CO2) did not differ among the four groups and was controlled within the normal range. The increase in arterial potassium (deltaK+) from rest to peak exercise was markedly reduced as the severity of CHF advanced: (mean +/- SD) 1.70+/-0.32 mmol/L in normal subjects; 1.46+/-0.27 mmol/L in class I patients; 1.15+/-0.24 mmol/L in class II patients; and 0.78+/-0.24 mmol/L in class III patients. The ratios of deltaVA or deltaV(CO2) to deltaK+ were not different among the four groups. The ratio of deltaV(E) to deltaK+, however, was significantly greater in patients in class III than in normal subjects or patients in class I or II.

The deltaK+ from rest to peak exercise was markedly reduced as the severity of CHF advanced. The increased exercise ventilation due to increased physiologic dead space in severe CHF was not accompanied by the corresponding augmentation of exercise-induced hyperkalemia. Exercise-induced hyperkalemia does not contribute to the increased ventilatory drive to keep normal arterial P(CO2) during exercise in the presence of increased physiologic dead space in severe CHF.