Epoprostenol (Veletri or Flolan) is an inhaled or intravenous prostanoid vasodilator which is most often used as a therapeutic option for pulmonary arterial hypertension (pHTN). When given intravenously, it dilates both the systemic and pulmonary arterial vasculature to decrease both systemic and pulmonary vascular resistances to augment cardiac output; however, systemic vasodilation can lead to hypotension that decreases coronary perfusion pressure which outweighs the pulmonary benefits of epoprostenol. Of note, this medication is also a potent inhibitor of platelet aggregation.
As an intensivist and cardiac anesthesiologist, I routinely initiate INHALED epoprostenol therapy for patients with issues ranging from V/Q mismatch to significant right heart strain likely due to high pulmonary artery (PA) pressures coming off cardiopulmonary bypass. Pulmonary artery branches that supply hypoxemic, poorly ventilated alveoli undergo constriction as part of hypoxic pulmonary vasoconstriction (HPV) – a physiologic compensation to minimize V/Q mismatch by shunting blood to well ventilated alveolar segments.
By administering inhaled epoprostenol, the medication is only carried down to alveoli that are ventilated AND perfused. The uptake of this medication by the perfusing pulmonary artery segments allows the drug to exert its effects on this vascular bed with minimal systemic side effects.
So what’s the difference between Veletri and Flolan? They’re both different formulations of the same active drug; however, the key difference is that Veletri contains arginine-mannitol (compared to glycine-mannitol in Flolan) making it more stable at room temperature.
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