this link, falsely leads you to think its anticoagulation. We use it for it's prostiglandin vasodilator effects, esp. refractory pulmonary HTN in our pre and esp. post heart transplant patients. Even more esp. those who were borderline both lung and heart transplant, where we elected just a heart due to instability and lack of lung donor. We also use it, rare, on our hearts. Due to the vasodilation at the arterioles, we have decreased venous congestion, increased venous return which in theory equals higher RV filling, more filling to the coronary sinus, decreased afterload, decreased wedge pressures.
The pure pulmonary Htn use can decrease RV filling pressures and allows a "normal" RA/RV pressure, giving time for O2/C02 exchange, with less barrotrauma to the pulmonary vasculature, all with the anticoagulation princpals due to not irritating, yet facilitating the clotting casscade.
All this assuming your RA/RV pressures are not through the roof, independent of your wedge. you drop them with this drug and there goes your starling's law, you need to have the volume, especially with an independent dilated RA/RV to give you high enough filling pressures. Vasodilating the arterioles at this point is detromental, when this presents a different problem, not fixed by flolan.. fixed by fluid like in you fresh RV infarcts
luckily, for efficacy of the drug, pure right sided heart failure is RARE, wich makes this a wonder drug, if used in a select population
this drugs use though, is a bugger for nursing