I suppose the best place to start is just what got you interested in doing this trial? I know there was Andromeda Shock 1 when you moved on to Andromeda Shock 2, but what was the original driver for looking at this topic?

That's an element that's not much paid attention to because the Andromeda studies are from a line of studies we started in the Netherlands.

The first study we did in this context was the lactate study, where we tried to answer if you use lactate or standard care to guide your resuscitation of patients in shock, will you have an effect on outcome? In the lactate study, we used a personalized treatment schedule where we tried to optimize every aspect of oxygen demand and oxygen delivery.

For instance, we put patients on the ventilator who were spending a lot of energy on breathing, even though their oxygenation was adequate.

We optimized hemoglobin, saturation, cardiac output.

When we had the idea that there was a microcirculatory derangement, we gave nitroglycerin to optimize microcirculatory perfusion.

These were all covers.

Why did you go with dibutamine, an inodilator rather than an inopressor? Or a different inodilator, like a millinone or something like that?