are usually smaller to reduce hyperinflation of the excessively compliant native lung and compression of the less compliant transplanted lung.

After SLT for PPH, a PEEP of 5 to 10 cm H20 is used for at least 36 hours, as it is believed that this minimizes the development of edema in the allograft. These patients are typically mechanically ventilated for 48-72 hours and are kept heavily sedated and often paralyzed in an effort to decrease the occurrence of pulmonary hypertensive crisis. They are also maintained with the native lung in a dependent position to promote inflation and drainage of the transplanted lung.

Prolonged periods of post-operative ventilatory requirement may occasionally be seen in lung transplant recipients. There are many potential reasons for inability to tolerate extubation but important processes to consider include: ischemia-reperfusion injury, early graft dysfunction, gas trapping, and phrenic nerve injury. Ischemia-reperfusion injury is an area of intense investigation and appears to be related to anoxic injury to the lung sustained during the period of preservation.

Gas trapping can occur in a native emphysematous lung following SLT and can be recognized radiographically as hyperinflation of the native lung and simultaneous compression of the allograft. When recognized this can be treated by positioning the patient with the allograft side up, bronchodilator therapy, and occasionally a double lumen endotracheal tube to allow to independent lung ventilation.

Clinically detectable diaphragmatic paralysis due to phrenic nerve injury is a rare complication of lung transplantation but should be considered in patients who require prolonged mechanical ventilation. Long term effects of phrenic nerve injury are uncommon. In patients requiring prolonged ventilatory support, early tracheostomy improves patient comfort, facilitates mobilization, allows oral nutrition and expedites liberation from the ventilator.

Ischemia-Reperfusion-Induced Lung Injury

Ischemia-reperfusion-induced lung injury remains a significant cause of early morbidity and mortality after lung transplantation. The syndrome typically occurs within the first 72 hours after transplantation and is characterized by nonspecific alveolar damage, lung edema, and hypoxemia. Neutrophil-mediated oxidant injury to the lung sustained at reperfusion appears to play a role. The clinical spectrum can range from mild hypoxemia associated with few infiltrates on chest x-ray to a picture similar to severe acute respiratory distress syndrome requiring mechanical ventilation, moderate levels of PEEP and FI02, pharmaco-logic therapy and occasionally nitric oxide or extracorporeal membrane oxygen-ation.31,32 In addition, this syndrome can also be associated with an increased risk of acute rejection that may lead to graft dysfunction in the long term.21

Hemodynamic and Fluid Management

The lung allograft is extremely sensitive to volume. Therefore, minimizing fluid administration and careful use of diuretics are crucial in these patients. Most patients are maintained on low dose dopamine infusion (1-3 ^g/kg/min) for the

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