• John Y C Tsang, Wayne J E Lamm, Ian R Starr, and Michael P Hlastala.
• James Hogg iCAPTURE Research Laboratory, 1081 Burrard St., Vancouver, BC, Canada V6Z 1Y6. jtsang@interchange.ubc.ca
• J. Appl. Physiol. 2005 May 1; 98 (5): 1862-8.

AbstractWe studied the spatial distribution of the abnormal ventilation-perfusion (Va/Q) units in a porcine model of acute pulmonary thromboembolism (APTE), using the fluorescent microsphere (FMS) technique. Four piglets ( approximately 22 kg) were anesthetized and ventilated with room air in the prone position. Each received approximately 20 g of preformed blood clots at time t = 0 min via a large-bore central venous catheter, until the mean pulmonary arterial pressure reached 2.5 times baseline. The distributions of regional Va and blood flow (Q) at five time points (t = -30, -5, 30, 60, 120 min) were mapped by FMS of 10 distinct colors, i.e., aerosolization of 1-mum FMS for labeling Va and intravenous injection of 15-mum FMS for labeling Q. Our results showed that, at t = 30 min following APTE, mean Va/Q (Va/Q = 2.48 +/- 1.12) and Va/Q heterogeneity (log SD Va/Q = 1.76 +/- 0.23) were significantly increased. There were also significant increases in physiological dead space (11.2 +/- 12.7% at 60 min), but the shunt fraction (Va/Q = 0) remained minimal. Cluster analyses showed that the low Va/Q units were mainly seen in the least embolized regions, whereas the high Va/Q units and dead space were found in the peripheral subpleural regions distal to the clots. At 60 and 120 min, there were modest recoveries in the hemodynamics and gas exchange toward baseline. Redistribution pattern was mostly seen in regional Q, whereas Va remained relatively unchanged. We concluded that the hypoxemia seen after APTE could be explained by the mechanical diversion of Q to the less embolized regions because of the vascular obstruction by clots elsewhere. These low Va/Q units created by high flow, rather than low Va, accounted for most of the resultant hypoxemia.

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