NITRIC-OXIDE INHALATION REDUCES PULMONARY TIDAL VOLUME DURING EXERCISE IN SEVERE CHRONIC HEART-FAILURE

Multiple mechanisms have been proposed to explain the hyperventilation and the limited exercise capacity in congestive heart failure (CHF) i ncluding increased intrapulmonary pressures, total pulmonary resistanc e, and airway abnormalities. We investigated the hypothesis that inhal ation of nitric oxide could influence the maximum exercise capacity an d excessive ventilatory response to exercise in CHF. Fifteen patients in CHF (mean age 48 +/- 12 years) underwent a control and a nitric oxi de inhalation progressive treadmill exercise test with 30 ppm. We dete rmined the maximum oxygen consumptiom (peak VO2), CO2 production (VCO2 ), minute pulmonary ventilation (VE), respiratory rate, tidal volume ( VT), ventilatory equivalent for oxygen (VE/VO2), ventilatory equivalen t for carbon dioxide (VE/VCO2), estimated physiologic dead space/tidal volume ratio (VD/VT), VE/VCO2 slope, heart rate, systemic arterial pr essure, VE/exercise time slope, and VT/exercise time slope during ever y incremental exercise. Mean maximum exercise values of heart rate, sy stolic systemic arterial pressure, diastolic systemic arterial pressur e, VD/VT, respiratory rate, peak VO2, VO2/heart rate, VE/CO2, and maxi mum exercise time were unchanged by inhalation of nitric oxide. There was a strong trend toward reduction of VE/VO2 from 53 +/- 15 to 47 +/- 12 (p = 0.051) and in maximum VE from 58 +/- 21 to 48 +/- 17 L x min( -1) (p = 0.059). Maximum VT decreased from 1639 +/- 556 to 1406 +/- 47 9 ml (p = 0.04). The VE/VCO2 slope was reduced from 43 +/- 12 to 35 +/ - 8 (p = 0.018). Two patients had signs of pulmonary congestion during peak exercise or the recovery period with inhalation of nitric oxide. The VE/exercise time slope and VT/exercise time slope during incremen tal exercise were reduced by inhalation of nitric oxide, demonstrating a statistically significant minor increase in VE and VT. Inhalation o f nitric oxide attenuated the excessive increase in VT response to exe rcise in CHF. The L-arginine-nitric oxide pathway may be involved in m echanisms contributing to hyperventilation during exercise in CHF.