Na+-K+ ATPase In The Membranes Of The Heart Muscle

Firstly lets explain some basic things that are nessesary for this question:
The direction of the passive transport (thought membrane proteins) of molecules and ions is affected by two things:
1) The concentration of the solute in and out of the cell: The molecules and ions tend to move from higher concentrations to lower concentrations.
2) (only for charged solutes/ ions) The membrane potential: The cytoplasmic side of the plasma membrane is usually at a negative potential relative to the outside. So, positively charged ions are pulled in the cell.
-So, the net force driving a charged solute across the mambrane is a combosite of the above two forces. (This net driving force is called electrochemical gradient.)

The Na+/K+ ATPase uses energy (ATP) to actively transport the Na+ and K+ to the opposite side of their electrochemical gradient. (Na+ out of the cell and K+ in the cell.) That keeps the concentration of Na+ out of the cell much higher than it is in the cell. And because Na+ is also positively charged, the electrochemical gradient of Na+ is very high. (see Essential Cell Biology chapter 12: Carrier proteins and their functions)

Na+/Ca2+ exchanger uses the energy that is stored in the electrochemical gradient of sodium (Na+) by allowing Na+ to flow down its gradient across the plasma membrane in exchange for the countertransport of calcium ions (Ca2+). http://en.wikipedia.org/wiki/Sodium-calcium_exchanger

Now, ouabain and digitalis are drugs that inhibits the Na+/K+ ATPase http://en.wikipedia.org/wiki/Ouabain. That results to a decrease to the electrochemical gradient of sodium (Na+), and so the function of Na+/Ca2+ exchanger is also decreased. Ultimately, the Ca2+ ions stay in the cell longer, which results to a more forceful (and longer) contraction. (To see how does Ca++ affects the contraction, see Essential Cell Biology Chapter 17: "Muscle contraction is triggered by a sudden rise in Ca 2+")