Respiratory correlates of muscle sympathetic nerve activity in heart failure

1. Sympathetic activation in congestive heart failure indicates a poor prognosis. Haemodynamic correlates of increased sympathetic nerve traffic to muscle (MSNA) and to the heart have been well characterized, but these account for only 50 to 60% of the variance in sym pathetic activity between patients. 2. In healthy subjects, breathing pattern modulates MSNA and positive airway pressure consistently increases MSNA. However, in patients with heart failure, the influence of spontaneous breathing pattern and of short-term application of nasal continuous positive airway pressure on MSNA have not been described. 3. Spontaneous breathing frequency, tidal volume, end-expiratory lung volume, Pco(2) and MSNA were recorded, along with blood pressure, heart rate and stroke volume in 14 men with congestive heart failure of idiopathic or ischaemic origin (left ventricular ejection fraction < 35%). Measurements were made during baseline rest, followed by 45 min of either nasal continuous positive airway pressure applied at 10 cmH(2)O (n = 9), or spontaneous breathing, in the absence of nasal continuous positive airway pressure (time control; n = 6). 4. At baseline, there was a significant positive correlation between MSNA burst frequency and breathing frequency (r = 0.758, P = 0.001), and an inverse correlation between MSNA burst incidence and tidal volume (r = -0.705, P = 0.005). These relationships were independent of left ventricular election fraction, stroke volume or cardiac output. 5. Nasal continuous positive airway pressure increased end-expiratory lung volume, but had no effect on breathing frequency, tidal volume or MSNA. In patients with congestive heart failure, there is a significant independent and previously unrecognized correlation between spontaneous breathing pattern and MSNA; patients with rapid shallow breathing exhibit the highest degree of sym pathetic activation. In distinct contrast to healthy subjects, the short-term application of nasal continuous positive airway pressure at 10 cmH(2)O does not increase MSNA in congestive heart failure.