Mechanisms of hypoxemia and hypocapnia in pulmonary embolism (PE) are incompletely understood. We studied 10 patients at diagnosis (D) and five 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 ventilation scans, and angiography. At D, two-thirds of the pulmonary circulation was obstructed, patients were hypoxemic (PaO2 = 63.0 +/- 11.7 mm Hg) and hypocapnic (PaCO2 = 30.0 +/- 4.1 mm Hg), mixed venous oxygen pressure (PvO2) was reduced (30.9 +/- 3.9 mm Hg), minute ventilation (VE) markedly increased (14.1 +/- 5.1 L/min), and cardiac output measured by applying the Fick principle to arteriovenous oxygen content difference (QT) slightly low (4.7 +/- 1.7 L/min). Hypoxemia was mainly explained by VA/Q inequality, reduced PvO2 also contributed. Hypocapnia was the result of hyperventilation. VA/Q inequality was characterized by shift of VA and Q distribution mean to regions with higher VA/Q ratio through 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 space occurred in occasional patients but were generally insignificant. Regional ventilation and perfusion maps indicated that in the unperfused lung segments, ventilation was reduced. Furthermore, they disclosed overperfused lung segments. At T, hypoxemia and hypocapnia improved considerably. However, temporal imbalances in recovery between regional ventilation and perfusion occurred with the former normalizing sooner. However, perfusion recovered sooner than ventilation in some regions.

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The past and present clinical history of 13 patients with hemodynamic and angiographic diagnosis of chronic thromboembolic pulmonary hypertension (CTPH) was reviewed in order to investigate the reasons for failure of resolution of acute pulmonary embolism (PE) and findings useful for diagnosis of CTPH. All patients had chest radiograph, ECG, arterial blood gas analysis and pulmonary perfusion scintigraphy performed. Clinical assessment demonstrated that no patient had diagnosis and treatment of the several retrospectively identified episodes of PE (from 1 to 8); the lack of diagnosis was due to underestimation of symptoms and signs such as dyspnea (85%), pleuritic chest pain (31%) or phlebitis (46%) that were present months or years earlier. Alternative diagnoses erroneously made were dyspnea of unknown origin (5 cases), left heart failure (4 instances) and pneumonia (2 cases). Once CTPH has developed, chronic dyspnea (92%) and substernal chest pain (100%) are almost always present: chest radiograph and ECG show signs of chronic hypertension such as enlargement of hila (100%), right heart sections (77%), azygos vein (46%) and P pulmonale (67%), T inversion on right precordial leads (75%), S-T segment depression (75%), respectively. Perfusion scintigraphy shows severe perfusion impairment (55.7% of the total vascular bed) paralleled by severe hypoxia (standard PaO₂ = 49 ± 14.1 mm Hg). In conclusion, patients with PE who develop CTPH are not diagnosed and thus untreated because clinical symptoms and signs of acute PE have not been recognized. If CTPH develops, clinical assessment (including simple and noninvasive techniques such as chest radiograph, ECG and blood gas analysis) may show a quite characteristic pattern useful for diagnosis.