MECHANISMS OF HYPOXEMIA AND HYPOCAPNIA IN PULMONARY-EMBOLISM

Mechanisms of hypoxemia and hypocapnia in pulmonary embolism (PE) are incompletely understood. We studied 10 patients at diagnosis (D) and f ive of these again after 10 to 14 d of heparin treatment (T). Patients had right heart catheterization, assessment of ventilation-perfusion ratio (VA/Q) distribution by inert gas, radioisotopic perfusion and ve ntilation scans, and angiography. At D, two-thirds of the pulmonary ci rculation was obstructed, patients were hypoxemic (Pa-o2 = 63.0 +/- 11 .7 mm Hg) and hypocapnic (Pac(o2) = 30.0 +/- 4.1 mm Hg), mixed venous oxygen pressure (Pv(o2)) was reduced (30.9 +/- 3.9 mm Hg), minute vent ilation (VE) markedly increased (14.1 +/- 5.1 L/min), and cardiac outp ut measured by applying the Fick principle to arteriovenous oxygen con tent difference (QT slightly low (4.7 +/- 1.7 L/min). Hypoxemia was ma inly explained by VA/Q inequality, reduced Pv(o2) also contributed. Hy pocapnia was the result of hyperventilation. VA/Q inequality was chara cterized by shift of VA and Q distribution mean to regions with higher VA/Q ratio though a fraction of blood flow (19.0 +/- 24.3% of cardiac output) went to lung units with low VA/Q ratio. Log SDQ and log SDVA were increased. Shunt, diffusion limitation, or true alveolar dead spa ce occurred in occasional patients but were generally insignificant. R egional ventilation and perfusion maps indicated that in the unperfuse d lung segments, ventilation was reduced. Furthermore, they disclosed overperfused lung segments. MT, hyperemia and hypocapnia improved cons iderably. However, temporal imbalances in recovery between regional ve ntilation and perfusion occurred with the former normalizing sooner. H owever, perfusion recovered sooner than ventilation in some regions.