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

Previous studies reported that regional CO(2) tension might affect regional ventilation (V) 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 V and perfusion (Q) at four different times (-5, 30, 60, 120 min) was mapped by fluorescent microspheres. Regional V and Q were examined postmortem by sectioning the air-dried lung into 900-1,000 samples of approximately 2 cm(3) each. After the redistribution of regional Q by APTE, but in the scenario assuming that no V shift had yet occurred, CO(2) tension in different lung regions at 30 min post-APTE (P(X)CO(2)) was estimated from the V/Q data and divided into four distinct clusters: i.e., P(X)CO(2) < 10 Torr; 10 < P(X)CO(2) < 25 Torr; 25 < P(X)CO(2) < 50 Torr; P(X)CO(2) > 50 Torr. Our data showed that the clusters in higher V/Q regions (with a P(X)CO(2) < 25 Torr) received approximately 35% less V when measured within 30 min of APTE, whereas, in contrast, the lower V/Q regions showed no statistically significant increases in their V. However, after 30 min, there was minimal further redistribution of V. We conclude that there are significant compensatory V shifts out of regions of low CO(2) tension soon following APTE, and that these variations in regional CO(2) tension, which initiate CO(2)-dependent changes in airway resistance and lung parenchymal compliance, can lead to improved gas exchange.