COMPARISON OF THE PULMONARY DYSFUNCTION CAUSED BY CARDIOGENIC AND NONCARDIOGENIC PULMONARY-EDEMA

Citation
Gr. Bernard et al., COMPARISON OF THE PULMONARY DYSFUNCTION CAUSED BY CARDIOGENIC AND NONCARDIOGENIC PULMONARY-EDEMA, Chest, 108(3), 1995, pp. 798-803
Citations number
20
Categorie Soggetti
Respiratory System
Journal title
ChestACNP
ISSN journal
00123692
Volume
108
Issue
3
Year of publication
1995
Pages
798 - 803
Database
ISI
SICI code
0012-3692(1995)108:3<798:COTPDC>2.0.ZU;2-O
Abstract
We designed a series of experiments to compare the pulmonary dysfuncti on observed in models of cardiogenic and noncardiogenic pulmonary edem a in chronically instrumented awake sheep. Cardiogenic pulmonary edema was induced by inflating the balloon of a Foley catheter surgically p ositioned in the mitral valve orifice causing increased left atrial pr essure (up arrow PLA). Noncardiogenic pulmonary edema was induced by i ntravenous infusion of Perilla ketone (PK). Calculated microvascular p ressure remained constant during PK infusion but increased from 9.4+/- 0.7 to 42.8+/-2.4 cm H2O during up arrow PLA. Comparable increases in lung lymph flow (QL) were observed in the two protocols (five to seven times baseline). Pulmonary edema as quantified by chest radiograph sc ores increased from 0 (normal) to 2.9+/-0.5 and 3.6+/-0.1 in the PK an d up arrow PLA groups, respectively. Room air alveolar to arterial oxy gen pressure difference (P[A-a]O-2) increased from 24+/-3 to 46+/-7 mm Hg in the PK group and from 23+/-4 to 56+/-6 mm Hg in the up arrow PL A group. Dynamic compliance of the lungs (Cdyn) expressed as the perce ntage of the baseline value decreased to 53 +/- 7 and 50 +/- 7% in the PK and up arrow PLA groups, respectively. Resistance to airflow acros s the lungs (RL) increased from 2.5+/-0.6 to 3.3+/-0.8 cm H2O . L(-1). sec(-1) in the PK group and from 1.4+/-0.3 to 4.2+/-1.1 in the up arr ow PLA group. Significant correlations were observed between changes i n the severity of pulmonary edema observed on chest radiographs, Cdyn, Delta P(A-a)O-2, and QL in both the up arrow PLA groups. We conclude that similar degrees of pulmonary edema, regardless of the mechanism, are associated with similar changes in QL, Cdyn, and Delta P(A-a)O-2. Hydrostatic pulmonary edema appeared to cause greater changes in RL th an that resulting from increased microvascular permeability.