Digoxin increases intracellular calcium and thus increases contractility. It also increases parasympathetic activity, which slows down the rate by a mechanism that I'm not immediately aware of. Think of it this way though... Anecdotally, if you increase contractility, you increase cardiac output and thus you increase perfusion. If you increase perfusion, there are various mechanisms (RAAS, baroreceptors, etc.) that will decrease sympathetic activity and lower HR. Katyq82 is correct that they are 2 different systems. However, they are heavily interconnected. You just need to understand the mechanisms by which they communicate. If you want to really understand how cardiac conduction works, read Dale Dubins Rapid Interpretation of EKGs. It's an easy read and does a GREAT job of breaking it all down.