(Circulation. 1997;96:2221-2227.)
© 1997 American Heart Association, Inc.
Articles |
Lung Function and Exercise Gas Exchange in Chronic Heart Failure
From Harbor–UCLA Medical Center, UCLA School of Medicine (K.W., Y.-Y. Z., L.L.), Torrance, Calif; Herzzentrum Ludwigshafen (A.G.), Department of Cardiology and Pneumonology, Ludwigshafen, Germany; Ospedale Cardiologico G.M. Lancisi (R.B.), Ancona, Italy; 2nd Department of Internal Medicine, Tokyo Medical and Dental University (A.K.), Tokyo, Japan; and Istituto di Cardiologia dell'Universita degli Studi (P.G.A.), Centro di Studio per le Richerche Cardiovascolari del Consiglio Nazionale delle Richerche, Fondazione Monzino, IRCCS, Milan, Italy.
Correspondence to Karlman Wasserman, MD, PhD, Harbor–UCLA Medical Center, Box 405, 1000 W Carson St, Torrance, CA 90509.
Background The ventilatory response to exercise in patients with chronic heart failure (HF) is greater than normal for a given metabolic rate. The objective of the present study was to determine the mechanism(s) for the high ventilatory output in patients with chronic HF.
Methods and Results Centers in Germany, Italy, Japan, and
the United States participated in this study. Each center contributed
studies on patients and normal subjects of similar age and sex. One
hundred thirty patients with chronic HF and 52 healthy subjects
participated. Spirometric and breath-by-breath gas exchange
measurements were made during rest and increasing cycle exercise.
Arterial blood was sampled for measurement of pH,
PaCO2, PaO2, and
lactate during exercise in 85 patients. Resting forced expiratory
volume in 1 second (FEV1) and vital capacity (VC) were
proportionately reduced at all levels of impairment. Patients with more
severe HF had greater tachypnea and a smaller tidal volume
(VT) at a given exercise expired volume per unit time
(
E). This was associated with an expiratory flow
pattern characteristic of lung restriction. E and
CO2 as a function of
O2 were increased during exercise in HF
patients. The increases were greater the lower the peak
O2 per kilogram of body weight. The
ratio of VD (physiological dead space)
to VT and the difference between arterial and
end tidal PCO2 at peak
O2 also increased inversely with peak
O2/kg. In contrast, the difference
between alveolar and arterial PO2
and PaCO2 were both normal, on average, at peak
O2 regardless of the level of
impairment. The more severe the exercise limitation, the higher the
lactate and the lower the HCO3- at a given
O2, although pH was tightly
regulated.
Conclusions The increase in E in chronic
HF patients is caused by an increase in VD/VT
due to high ventilation/perfusion mismatching, an increase in
CO2 relative to
O2 resulting from
HCO3- buffering of lactic acid, and a decrease
in PaCO2 due to tight regulation of
arterial pH. With regard to the excessive
E in HF patients, the increases in
VD/VT and CO2
relative to O2 are more important as the
patient becomes more exercise limited. Regional hypoperfusion but not
hypoventilation typifies lung gas exchange in HF. This and other
mechanisms might account for the restrictive changes leading to
exercise tachypnea in HF patients.
Key Words: ventilation • perfusion • oxygen • metabolism • hypertension, pulmonary
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