Aims: To evaluate the effects of mild hyperoxia on sympathetic activity during quiet breathing in patients with chronic heart failure (CHF) and, hence, to investigate whether tonic activation of excitatory chemoreceptor afferents contributes to the elevated sympathetic activity in these patients. Sympathetic activation in patients with CHF may result in part from increased chemoreflex sensitivity. Previous studies using microneurography did not demonstrate deactivation of the chemoreceptors while the patients were breathing 100% O2. However, 100% O2 may decrease cardiac output, thereby offsetting the effects on the chemoreflexes.
Setting: University hospital.
Patients and interventions: Ten patients with moderate-to-severe CHF (mean [±SD] age, 53.9 ± 9.2 years; mean ejection fraction, 21.3 ± 4.7%) were assigned to breathing 20 min of O2 as well as room air (3 L/min) applied by nasal prongs. Muscle sympathetic nerve activity (MSNA) was evaluated by microneurography of the peroneal nerve.
Results: The application of O2 resulted in an increase of arterial O2 saturation but no significant change in MSNA during resting ventilation. Although voluntary apneas were no longer with O2 (25.3 ± 5.8 vs 32.6 ± 8.6 s, respectively; p = 0.014), MSNA during the last 10 s of voluntary apnea was lower while breathing O2 (63.5 ± 15.0 vs 59.9 ± 13.9 bursts per minute, respectively; p = 0.02).
Conclusions: The increased MSNA in the patients studied could not be reduced by mild hyperoxia, suggesting that the tonic activation of chemoreflex afferents is unlikely to contribute to the elevated sympathetic activity. That nasal O2 reduces MSNA during apnea may explain the beneficial effects of nocturnal O2 therapy in CHF patients with Cheyne-Stokes respiration.