Nasal oxygen and muscle sympathetic nerve activity in heart failure

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% O(2). However, 100% O(2) may decrease cardiac output, thereby offsetting the effects on the chemoreflexes.

University hospital.

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 O(2) 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.

The application of O(2) resulted in an increase of arterial O(2) saturation but no significant change in MSNA during resting ventilation. Although voluntary apneas were no longer with O(2) (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 O(2) (63.5 +/- 15.0 vs 59.9 +/- 13.9 bursts per minute, respectively; p = 0.02).

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 O(2) reduces MSNA during apnea may explain the beneficial effects of nocturnal O(2) therapy in CHF patients with Cheyne-Stokes respiration.