Acute saline infusion reduces alveolar-capillary membrane conductance and increases airflow obstruction in patients with left ventricular dysfunction

Citation
S. Puri et al., Acute saline infusion reduces alveolar-capillary membrane conductance and increases airflow obstruction in patients with left ventricular dysfunction, CIRCULATION, 99(9), 1999, pp. 1190-1196
Citations number
43
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CIRCULATION
ISSN journal
00097322 → ACNP
Volume
99
Issue
9
Year of publication
1999
Pages
1190 - 1196
Database
ISI
SICI code
0009-7322(19990309)99:9<1190:ASIRAM>2.0.ZU;2-E
Abstract
Background-Impaired alveolar-capillary membrane conductance is the major ca use for the reduction in pulmonary diffusing capacity for carbon monoxide ( DLCO) in heart failure. Whether this reduction is fixed, reflecting pulmona ry microvascular damage, or is variable is unknown. The aim of this study w as to assess whether DLCO and its subdivisions, alveolar-capillary membrane conductance (DM) and pulmonary capillary blood volume (Vc), were sensitive to changes in intravascular volume. In addition, we examined the effects o f volume loading on airflow rates. Methods and Results-Ten patients with left ventricular dysfunction (LVD) an d 8 healthy volunteers were studied, DM and Vc were determined by the Rough ton and Forster method. The forced expiratory volume in 1 second (FEV1), vi tal capacity, and peak expiratory flow rates (PEFR) were also recorded. In patients with LVD, infusion of 10 mL . kg(-1) body wt of 0.9% saline acutel y reduced DM (12.0+/-3.3 versus 10.4+/-3.5 mmol . min(-1) . kPa(-1), P<0.00 5), FEV1 (2.3+/-0.3 versus 2.1+/-0.4 L, P<0.0005), and PEFR (446+/-55 versu s 414+/-56 L . min(-1), P<0.005), All pulmonary function tests had returned to baseline values 24 hours later. In normal subjects, saline infusion had no measurable effect on lung function. Conclusions-Acute intravascular volume expansion impairs alveolar-capillary membrane function and increases airflow obstruction in patients with LVD b ut not in normal subjects. Thus, the abnormalities of pulmonary diffusion i n heart failure, which were believed to be fixed, also have a variable comp onent that could be amenable to therapeutic intervention.