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This Article Full Text Full Text (PDF) All Versions of this Article: 107/3/755    most recent 00245.2009v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Tsang, J. Y. C. Articles by Swenson, E. R. PubMed PubMed Citation Articles by Tsang, J. Y. C. Articles by Swenson, E. R.

Regional CO₂ tension quantitatively mediates homeostatic redistribution of ventilation following acute pulmonary thromboembolism in pigs

¹James Hogg iCAPTURE Research Laboratory, Division of Critical Care Medicine, Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada; and ²Department of Medicine, University of Washington, and ³Medical Service, Veterans Affairs Puget Sound Health Care System, Seattle, Washington

Submitted 6 March 2009 ; accepted in final form 10 July 2009

Previous studies reported that regional CO₂ tension might affect regional ventilation () following acute pulmonary thromboembolism (APTE). We investigated the pathophysiology and magnitude of these changes. Eight anesthetized and ventilated piglets received autologous clots at time = 0 min until mean pulmonary artery pressure was 2.5 times baseline. The distribution of and perfusion () at four different times (–5, 30, 60, 120 min) was mapped by fluorescent microspheres. Regional and were examined postmortem by sectioning the air-dried lung into 900–1,000 samples of 2 cm³ each. After the redistribution of regional by APTE, but in the scenario assuming that no shift had yet occurred, CO₂ tension in different lung regions at 30 min post-APTE (P_XCO₂) was estimated from the / data and divided into four distinct clusters: i.e., P_XCO₂ < 10 Torr; 10 < P_XCO₂ < 25 Torr; 25 < P_XCO₂ < 50 Torr; P_XCO₂ > 50 Torr. Our data showed that the clusters in higher / regions (with a P_XCO₂ < 25 Torr) received 35% less when measured within 30 min of APTE, whereas, in contrast, the lower / regions showed no statistically significant increases in their . However, after 30 min, there was minimal further redistribution of . We conclude that there are significant compensatory shifts out of regions of low CO₂ tension soon following APTE, and that these variations in regional CO₂ tension, which initiate CO₂-dependent changes in airway resistance and lung parenchymal compliance, can lead to improved gas exchange.

carbon dioxide; cluster analysis; distribution of ventilation; fluorescent microspheres; gas exchange