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Clinical Investigations: CARDIOLOGY |

Exercise-Induced Rise in Arterial Potassium in Patients With Chronic Heart Failure*: Relation to Excessive Exercise Ventilation

Yasuhiko Tanabe, MD; Masahiro Ito, MD; Yukio Hosaka, MD; Eiichi Ito, MD; Kaoru Suzuki, MD; Minoru Takahashi, MD
Author and Funding Information

*From the Department of Internal Medicine (Drs. Tanabe, M. Ito, Hosaka, E. Ito, and Suzuki), Niigata Prefectural Shibata Hospital, Niigata, Japan; and the First Department of Internal Medicine (Dr. Takahashi), Niigata University School of Medicine, Niigata, Japan.

Correspondence to: Yasuhiko Tanabe, MD, Niigata Prefectural Shibata Hospital, Ohtemachi 4–5-48, Shibata City, Niigata, 957-8588 Japan



Chest. 1999;116(1):88-96. doi:10.1378/chest.116.1.88
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Objectives: 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.

Methods and results: 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 (ΔV̇e), effective alveolar ventilation (ΔV̇a), and carbon dioxide output (ΔV̇co2) from rest to peak exercise decreased as the severity of CHF advanced. The ratio ofΔ V̇e to ΔV̇co2 was significantly elevated in class III patients, although there was no difference in the ratio of ΔV̇a toΔ V̇co2 among the four groups. Rest and exercise arterial Pco2 did not differ among the four groups and was controlled within the normal range. The increase in arterial potassium (ΔK+) 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 ofΔ V̇a or ΔV̇co2 toΔ K+ were not different among the four groups. The ratio of ΔV̇e to ΔK+, however, was significantly greater in patients in class III than in normal subjects or patients in class I or II.

Conclusions: TheΔ K+ 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 Pco2 during exercise in the presence of increased physiologic dead space in severe CHF.

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