Pulmonary arterial hypertension (PAH) is a progressive, debilitating, and frequently terminal disease of the pulmonary vasculature.1 Over the past 20 years, the introduction of medications including calcium channel blockers (CCBs), phosphodiesterase-5 inhibitors (PDE5i), endothelin receptor antagonists (ERA), and prostacyclin therapies have significantly improved the treatment and prognosis of PAH.2 Despite these advancements, however, many patients continue to suffer unacceptably high morbidity and mortality.3 In light of this fact, it is notable that a subset (∼5%–10%) of patients with idiopathic pulmonary arterial hypertension (IPAH) can respond to oral CCBs and have a significantly improved prognosis.4 The initiation of CCBs in patients with PAH, however, must be done with caution; unresponsive patients can experience dangerous and even fatal hemodynamic compromise.5 In order to identify those patients in whom CCBs will be safe and potentially effective, it is essential that an acute vasodilator challenge be performed with a short-acting vasoactive agent such as adenosine, epoprostenol, or inhaled nitric oxide (iNO), iNO being the most common agent.6-9 During this challenge, the patient’s hemodynamic responses are carefully monitored with the aid of right heart catheterization (RHC). Under current recommendations, a patient is considered an acute vasodilator responder and appropriate for CCBs if the mean pulmonary arterial pressure (mPAP) falls by ≥10 mmHg to an absolute value <40 mmHg without a degradation in cardiac output (CO).3 Although the use of RHC with an acute vasodilator challenge is an accepted part of the evaluation in patients with PAH, little has been published with regard to its standardization and protocolization.10 For instance, most investigations have focused on patients categorized into World Health Organization (WHO) group I disease with IPAH. However, recent publications suggest that patients with pulmonary hypertension (PH) diagnoses other than IPAH may benefit from acute vasodilator testing and the use of CCBs.11,12 Other details regarding the protocolization of acute vasodilator challenge, such as the optimal length of time to adequately observe a patient for an acute vasodilatory response, are likewise unknown or unclear in the literature. In the timed response to inhaled nitric oxide study, we examined, in patients with diverse PH diagnoses, the effect of iNO administered for acute vasoreactivity testing at 5 and 10 minutes. We performed a single-center, retrospective analysis of patients with suspected PH prospectively enrolled in a quality control initiative entailing RHC with acute vasodilator challenge and hemodynamic measurements recorded at 5 and 10 minutes. Our goal is to better define the length of time necessary for vasoreactivity testing in patients with PH.