• Y Z Kadiri, J C Kay, K Kovacs, and W H Noble.
• Can Anaesth Soc J. 1980 May 1;27(3):216-22.

AbstractTo 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), PaO2 fell from 10 to 7.7 kPa (76.6 to 58.4 torr) as shunt fraction (Qs/Qt) rose from 19 to 31 per cent. Mean pulmonary artery pressure (ppa), paCO2 and VD/VT remained constant. Starch emboli (63--74 micron) were taken injected. PPA increased significantly and PaO2 dropped further to 5 kPa (37.8 torr) as Qs/Qt rose to 57 per cent. VD/VT increased and PaCO2 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, PaO2, Qs/QT, PaCO2 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 monogenized 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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