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Sildenafil augments the effect of inhaled nitric oxide for postoperative pulmonary hypertensive crises.

Pulmonary hypertension remains a major complication after surgical correction of congenital heart disease. Inhaled nitric oxide (NO) has been shown to reduce, but not eliminate, potentially life-threatening episodic pulmonary hypertensive crises.1 NO increases intracellular cyclic guanosine monophosphate (cGMP), resulting in smooth muscle vasodilation. Phosphodiesterase type 5 (PDE5) is responsible for cGMP breakdown in lung tissue. We hypothesized that sildenafil (Viagra; Pfizer Laboratories, New York, NY), a selective and potent inhibitor of PDE5, may augment pulmonary vasodilation with NO and reduce the risk of pulmonary hypertensive crises in an at-risk postoperative patient.