Elsevier

American Heart Journal

Volume 134, Issue 4, October 1997, Pages 737-744
American Heart Journal

Nitric oxide inhalation reduces pulmonary tidal volume during exercise in severe chronic heart failure,☆☆,

https://doi.org/10.1016/S0002-8703(97)70058-9Get rights and content

Abstract

Multiple mechanisms have been proposed to explain the hyperventilation and the limited exercise capacity in congestive heart failure (CHF) including increased intrapulmonary pressures, total pulmonary resistance, and airway abnormalities. We investigated the hypothesis that inhalation of nitric oxide could influence the maximum exercise capacity and excessive ventilatory response to exercise in CHF. Fifteen patients in CHF (mean age 48 ± 12 years) underwent a control and a nitric oxide inhalation progressive treadmill exercise test with 30 ppm. We determined the maximum oxygen consumptiom (peak VO 2 ), CO 2 production (VCO 2 ), minute pulmonary ventilation (VE), respiratory rate, tidal volume (VT), ventilatory equivalent for oxygen (VE/VO 2 ), ventilatory equivalent for carbon dioxide (VE/VCO 2 ), estimated physiologic dead space/tidal volume ratio (VD/VT), VE/VCO 2 slope, heart rate, systemic arterial pressure, VE/exercise time slope, and VT/exercise time slope during every incremental exercise. Mean maximum exercise values of heart rate, systolic systemic arterial pressure, diastolic systemic arterial pressure, VD/VT, respiratory rate, peak VO 2 , VO 2 /heart rate, VE/CO 2 , and maximum exercise time were unchanged by inhalation of nitric oxide. There was a strong trend toward reduction of VE/VO 2 from 53 ± 15 to 47 ± 12 ( p = 0.051) and in maximum VE from 58 ± 21 to 48 ± 17 L × min -1 ( p = 0.059). Maximum VT decreased from 1639 ± 556 to 1406 ± 479 ml ( p = 0.04). The VE/VCO 2 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 incremental exercise were reduced by inhalation of nitric oxide, demonstrating a statistically significant minor increase in VE and VT. Inhalation of nitric oxide attenuated the excessive increase in VT response to exercise in CHF. The l -arginine-nitric oxide pathway may be involved in mechanisms contributing to hyperventilation during exercise in CHF. (Am Heart J 1997;134:737-44.)

Section snippets

Subjects

Fifteen patients (12 men and three women) with a mean age of 48 ± 12 years who had severe left ventricular dysfunction and chronic heart failure for >6 months were enrolled in this study. The mean left ventricular ejection fraction measured by radionuclide scintigraphy was 19% ± 5% and mean right ventricular ejection fraction was 20% ± 7%. Three patients were in New York Heart Association functional class II, 11 in functional class III, and one in functional class IV, despite full treatment

Rest

Mean resting values of heart rate, systolic systemic arterial pressure, diastolic systemic arterial pressure, estimated VD/VT, respiratory rate, VT, oxygen uptake, and VE/VO 2 were unchanged by nitric oxide inhalation (Table I). In contrast, there was a trend toward an increase in minute ventilation and oxygen uptake and a reduction in VE/VCO 2 with nitric oxide inhalation.

Peak exercise

From rest to maximum exercise in both control and nitric oxide inhalation conditions, an increase was observed in heart

Discussion

The attenuated increase in VT and pulmonary ventilation associated with a reduction in the VE/VCO 2 slope during nitric oxide inhalation testing suggests a non-CO 2 signal for control of VT, dependent on, mediated by, or influenced by nitric oxide inhalation in heart failure during exercise. It is believed that a non-CO 2 signal for ventilation is enhanced in heart failure based on a steeper VE/CO 2 slope dependent on the severity of heart failure with a correlation with peak VO 2 . 12

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