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Research Article Free access | 10.1172/JCI112556

Increased left ventricular stiffness impairs filling in dogs with pulmonary emphysema in respiratory failure.

A Gomez and S Mink

Find articles by Gomez, A. in: PubMed | Google Scholar

Find articles by Mink, S. in: PubMed | Google Scholar

Published July 1, 1986 - More info

Published in Volume 78, Issue 1 on July 1, 1986
J Clin Invest. 1986;78(1):228–240. https://doi.org/10.1172/JCI112556.
© 1986 The American Society for Clinical Investigation
Published July 1, 1986 - Version history
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Abstract

In a chronic canine model of pulmonary emphysema, we studied the interaction between left ventricular (LV) mechanics and pulmonary disease during severe hypoxemia. The hypoxemia was similar to that which may occur during a severe exacerbation of chronic obstructive lung disease. In six dogs with papain-induced emphysema and in seven dogs without emphysema, LV mechanics were examined when a hypoxic gas mixture was inspired to reduce PO2 to about 35 mmHg (hypoxic study) and during nonhypoxic conditions (room air study). In both groups, LV diastolic compliance was reduced during the hypoxic study by a similar amount. This finding could not be explained in terms of ventricular interdependence. Our analysis suggested that hypoxia decreased diastolic compliance (i.e., increased LV diastolic stiffness) by impairing LV relaxation. The primary effect of hypoxia was to decrease the extent to which LV relaxation occurred for a given end-diastolic pressure, while the rate of LV relaxation was decreased just slightly. This study indicates that severe hypoxemia because of respiratory failure may impair myocardial relaxation leading to a decrease in LV filling.

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