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JAMA. 1970;213(6):1028.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Lack of understanding of the pathophysiologic abnormalities associated with pulmonary embolism has made the clinical diagnosis difficult to establish. Many diseases often have both clinical and laboratory abnormalities found in pulmonary embolism, common among which are left ventricular failure or chronic obstructive pulmonary disease alone, or both coexisting.

Using xenon Xe 133 methods, Bass and coworkers¹ have shown that the hypoperfusion secondary to vascular obstruction by pulmonary embolism was unaccompanied by regional hypoventilation; this disparity resulted in increase in dead space ventilation and high ventilation/perfusion VA/Q ratio. Using the same xenon Xe 133 methods in patients with chronic obstructive pulmonary disease, Anthonisen and associates² have demonstrated that the regional hypoventilation within diseased airways was accompanied by regional hypoperfusion; however, there was a greater decrease in regional ventilation than in regional perfusion, and the resultant increased dead space ventilation was associated with a low V_A/Q ratio. Applying . . . [Full Text PDF of this Article]

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