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Canadian Journal of Anesthesia, Vol 27, 216-222, Copyright © 1980 by Canadian Anesthesiologists' Society

Pulmonary Embolism Distribution to Ventilated and Unventilated Lungs in the Dog: A Cause of Hypoxaemia

YAHAYA Z. KADIRI 1, J. COLIN KAY 1, KALMAN KOVACS 2, and WILLIAM H. NOBLE 1

1 Department of Anaesthesia, The University of Toronto and St. Michael's Hospital, Toronto, Ontario
2 Department of Pathology, The University of Toronto and St. Michael's Hospital, Toronto, Ontario

To examine a possible mechanism which could cause arterial hypoxaemia following pulmonary embolism, we collapsed and did not ventilate one lung in each of eleven dogs, to produce hypoxic pulmonary vasoconstriction. In five dogs (Starch Group), PaOO2 fell from 10 to 7.7 kPa (76.2 to 58.4 torr) as shunt fraction (Qs/Qt) rose from 19 to 31 percent. Mean pulmonary artery pressure (PPA), PaCOCO2 and VD/VT remained constant. Starch emboli (63-74 µ) were then injected. PPA increased significantly and PaOO2 dropped further to 5 kPa (37.8 torr) as Qs/Qt rose to 57 per cent. VD/VT increased and Pacoco2 remained constant. Microscopic examination of the lungs showed that three times as many emboli went to the ventilated lung compared to the unventilated lung. Six dogs (Blood Clot Group) received 51Cr labelled autologous blood clot. Changes after emboli in PPA, PaOO2, Qs/Qt, PaCOCO2 and VD/VT were similar to the results in the Starch group. 125I serum albumin was then injected and the dogs were sacrificed. The lungs were homogenized separately and the 51Cr and 125I counted. The 51Cr counts indicated 66 per cent of the blood clot emboli went to the ventilated lung. Following embolization, the 125I counts suggested a shift in perfusion to the unventilated lung. We conclude from these results that emboli are preferentially distributed to ventilated lung. After embolization PPA increases. At least in this pulmonary embolism model the increased PPA may overcome hypoxic pulmonary vasoconstriction, redistribute blood to non-ventilated lung and create arterial hypoxaemia






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Copyright © 1980 by the Canadian Anesthesiologists' Society.