Reperfusion injury in single-lung transplant recipients with pulmonary hypertension and emphysema

The early postoperative course of single-lung transplant recipients depends on the recipient's underlying lung pathophysiology and the degree of ischemic-reperfusion injury. We examined the effect of pulmonary hemodynamics and preoperative diagnosis on early allograft function and the effects of pulmonary hemodynamics, allograft blood flow, and chest radiographs on length of mechanical ventilation and intensive care unit length of stay.

We retrospectively collected data on 30 single-lung transplant recipients, 15 each with pretransplantation pulmonary hypertension and emphysema. Blood flow to the allografts was quantitated by perfusion scans obtained on the first postoperative day. Chest radiographs were graded for reperfusion injury. Pulmonary and hemodynamic data, gas exchange parameters, duration of mechanical ventilation, and intensive care unit stay were recorded.

Patients with pulmonary hypertension had a prolonged intensive care unit stay compared with emphysema patients, but pulmonary artery pressures were not quantitatively related to duration of ventilation during the intensive care unit stay. There was no difference in the severity of allograft infiltrate between the emphysema and pulmonary hypertensive patients. The day 1 chest radiograph score was highly predictive of an intensive care unit stay of > or = 7 days, although the threshold score of those with pulmonary hypertension was significantly lower than in emphysema patients. Allograft blood flow and pulmonary hypertension were not contributors to early graft dysfunction. Allograft perfusion decreased with increasing radiographically demonstrated infiltrate in those with emphysema but not in those with pulmonary hypertension.

Elevated allograft blood flow and pressures do not exacerbate radiographically confirmed reperfusion injury. Reperfusion injury is the major cause of early respiratory morbidity after single-lung transplantation. Allograft perfusion in emphysema patients decreases in response to reperfusion injury, but pulmonary hypertension patients remain almost entirely dependent on allograft function, even with severe chest radiograph scores. This may be an important mechanism by which single-lung transplant recipients with emphysema, unlike those with pulmonary hypertension, are able to mitigate the degree of respiratory impairment associated with reperfusion injury.