Gas Exchange in Chronic Thromboembolism after Pulmonary Thromboendarterectomy
Chronic large vessel thromboembolic pulmonary hypertension is characterized by widespread obstruction of the main, lobar, and segmental pulmonary arteries that develops when thromboemboli fail to resolve and are incorporated into the arterial wall. Pulmonary thromboendarterectomy is the treatment of choice for this disorder because it greatly reduces pulmonary vascular resistance, improves cardiac output, and restores exercise tolerance. It also relieves hypoxemia, which is uniformly present by the time functional impairment is significant. buy diabetes drugs
Hypoxemia in this disorder is the consequence of moderate ventilation-perfusion inequality and a limited cardiac output which depresses mixed venous Po2. The broadening of the Va/Q distribution is most likely due to the mechanical effects of complete and partial central vascular obstruction, which redistributes perfusion to the remaining nonobstructed pulmonary capillary bed. Thromboendarterectomy, by removing central obstructions, should restore normal Va/Q relationships. However, vessels in the nonobstructed segments of the lung suffer the effects of chronic pulmonary hypertension, including medial and intimal hypertrophy and obliteration, and this is likely to contribute to additional Va/Q inequality. Consequently, thromboendarterectomy may leave significant residual Va/Q inequality behind, and the improvement in hypoxemia may then simply reflect the relief of right ventricular compromise and increased cardiac output. The objective of this study was to determine how much improvement in Va/Q relationships is achieved by thromboendarterectomy, and to assess the relative importance of an improved cardiac output to the resolution of hypoxemia following surgery.