Perioperative pulmonary arterial hypertension (PAH) is a common complication of chest surgery with cardiopulmonary bypass (CPB) and its etiology is multifactorial. Patients undergoing this surgery often have underlying conditions, such as left ventral dysfunction or valvular diseases, that predispose them to perioperative PAH [1]. The mechanisms contributing to PAH in cardiac surgery include left ventricular systolic or diastolic dysfunction, and mitral or valvular diseases, both pre- and postoperatively. Additional factors such as systemic inflammatory response, pulmonary reperfusion syndrome, and the need for blood transfusions can exacerbate PAH. Moreover, extracorporeal circulation during CPB can trigger pulmonary damage through cytokine release, complement activation, and ischemia-reperfusion injury. Protamine administration, often used at the end of CPB, can lead to severe pulmonary vasoconstriction by disrupting the balance between vasoconstrictors and vasodilators. Hypoxia, hypercarbia, pulmonary embolism, and mitral prosthesis-patient mismatch also contribute to the development of PAH [1]. When PAH occurs, it can lead to increased right ventricular afterload, potentially resulting in right ventricular dysfunction, which is a critical complication during cardiac surgery [2]. Importantly, PAH is a significant prognostic factor in cardiac surgery, as it is associated with increased morbidity and mortality [[3], [4], [5], [6]]. In general, lowering pulmonary artery pressure (PAP) and improving right ventricular function are considered essential for a safe weaning from CPB. There are no international guidelines regarding the preferred use of inhaled or intravenous vasodilators, making their use in managing perioperative PAH during chest surgeries with CPB a subject of debate [[7], [8], [9]]. During chest surgery with CPB, intravenous vasodilators have been used to manage perioperative PAH; however, this can cause systemic arterial hypotension due to systemic vascular dilation [[10], [11], [12]]. To avoid the resultant hypotension, vigilant monitoring is required, along with volume loading and the use of vasoconstrictors such as norepinephrine. Alternatively, the use of inhaled vasodilators has been suggested to avoid systemic hypotension. Inhaled vasodilators have been suggested to prevent systemic hypotension. These agents induce the direct vasodilation of the pulmonary vasculature, thereby promoting selective pulmonary effects. Inhaled nitric oxide is an established agent and recent studies have suggested that inhaled prostacyclin analogs can improve pulmonary hemodynamics in patients undergoing cardiac surgery; however, their clinical impact remains uncertain [[13], [14], [15]].