|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 James Hogg Pulmonary Research Laboratory, University of British Columbia, Vancouver, B.C., Canada
2 Department of Medicine, University of Washington, Seattle, WA, USA
3 Department of Physiology and Biophysics, University of Washington, Seattle, WA, USA; Department of Medicine, University of Washington, Seattle, WA, USA
* To whom correspondence should be addressed. E-mail: jtsang{at}interchange.ubc.ca.
We studied the spatial distribution of the abnormal VA/Q units in a porcine model of acute pulmonary thromboembolism (APTE), using the fluorescent microsphere (FMS) technique. Four piglets (~22 Kg) were anaesthetized and ventilated with room air in the prone position. Each received about 20 grams pre-formed blood clots at time = 0 minutes via a large bore central venous catheter, until the mean pulmonary artery pressure reached 2.5 times baseline. The distributions of regional ventilation (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 µm FMS for labelling ventilation and intravenous injection of 15 µm FMS for labelling perfusion. Our results showed that at time = 30 minutes 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 minutes, there were modest recoveries in the hemodynamics and gas exchange towards baseline. Redistribution pattern was mostly seen in regional Q while VA remained relatively unchanged. We concluded that the hypoxemia seen after APTE could be explained by the mechanical diversion of blood flow 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 ventilation, accounted for most of the resultant hypoxemia.
This article has been cited by other articles:
![]() |
H. T. Robertson and M. P. Hlastala Microsphere maps of regional blood flow and regional ventilation J Appl Physiol, March 1, 2007; 102(3): 1265 - 1272. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |