IMPAIRED VENTILATORY EFFICIENCY IN CHRONIC HEART-FAILURE - POSSIBLE ROLE OF PULMONARY VASOCONSTRICTION

Citation
I. Reindl et al., IMPAIRED VENTILATORY EFFICIENCY IN CHRONIC HEART-FAILURE - POSSIBLE ROLE OF PULMONARY VASOCONSTRICTION, The American heart journal, 136(5), 1998, pp. 778-785
Citations number
34
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
00028703
Volume
136
Issue
5
Year of publication
1998
Pages
778 - 785
Database
ISI
SICI code
0002-8703(1998)136:5<778:IVEICH>2.0.ZU;2-E
Abstract
Background Patients with chronic heart failure show impairment of vent ilatory efficiency, defined as the relation between ventilation and ca rbon dioxide output. It is caused by ventilation of excess physiologic dead space. We hypothesized a role of active vasoconstriction in the increase of physiologic dead space, presumed to lead to alveolar hypop erfusion. Methods and Results in 57 patients with chronic heart failur e (New York Heart Association classification Il through IV, election f raction 25.6% +/- 10.4%) and 7 control subjects, gas exchange at rest and on exercise was compared with hemodynamic measurements and, in a s ubgroup of 15 patients, with endothelin-l, epinephrine, and norepineph rine levels in the pulmonary and systemic circulation. Ventilatory eff iciency at rest ((V) over dot E/(V) over dot CO2 ratio) correlated wit h ventilatory efficiency on exercise ((V) over dot E vs (V) over dot C O2 slope). impairment of ventilatory efficiency correlated strongly ne gative with exercise tolerance (maximal oxygen uptake: r = -0.67) and cardiac output (r = -0.66) and positive with pulmonary hypertension (m ean pulmonary artery pressure: r = 0.69, pulmonary vascular resistance : r = 0.60). None of the vasoconstrictors correlated with reduction of ventilatory efficiency in the subgroup studied. Conclusions Impairmen t of ventilatory efficiency in chronic heart failure is correlated wit h resting pulmonary artery pressures and associated with the impairmen t of exercise capacity. An imbalance of pulmonary vascular tone probab ly leads to both pulmonary hypertension and alveolar hypoperfusion.