Gas Exchange in Chronic Thromboembolism after Pulmonary Thromboendarterectomy: Discussion (Part 2)
Although thromboendarterectomy reduces Va/Q maldistribution over the long term, the mechanism of improvement may be more complicated than the simple relief of central vascular obstruction which then restores segmental Va/Q balance. Over 140 patients with chronic thromboembolic pulmonary hypertension have undergone thromboendarterectomy at the University of California, San Diego and it is our current impression that in most cases, postoperative improvement in right ventricular function and hemodynamics is prompt, but gas exchange improves more gradually over a period of weeks to months. This may be because relief of mechanical obstruction leaves behind Va/Q abnormalities in vessels impaired by the effects of pulmonary hypertension which then remodel slowly thereafter, or because thromboendarterectomy injures operated vessels and adversely affects the postoperative perfusion distribution. flovent inhaler
Perfusion scans obtained two weeks after surgery, a time when the resting hemodynamics are normal and gas exchange is poor, reveal decreased perfusion of lung segments which were not obstructed preopera-tively, and increased perfusion of operated segments, suggesting a steal of perfusion from high resistance nonobstructed segments to low resistance newly reperfused segments, which worsens overall Va/Q relationships and leads to hypoxemia in spite of improved cardiac output. Because the small vessels distal to central obstructions also surprisingly share in the vascular changes of pulmonary hypertension, including medial and intimal hypertrophy and obliteration, thromboendarterectomy may lead to reperfusion of vessels initially too impaired for satisfactory gas exchange creating shunt, or to inadequate perfusion of ventilated areas with the development of high Va/Q regions. In such a situation, surgery could provide a hemodynamic benefit without a gas exchange benefit.