(Just a little extract from my vet Physiology assignment. Still needs a lot of editing so there are probably some errors)
To understand the act of cardiac glycosides on the heart you need to understand how the myocardial muscle contracts and relaxes. An action potential initiates contraction by opening voltage gated calcium channels on the outer membrane 14. Calcium rushes into the cell releasing the sarcoplasmic reticulum calcium stores. The calcium is key in binding to protein called troponin in the muscle fibre structure to initiate contraction 14.
It is then in the relaxation of the muscle that the cardiac glycoside disrupts the normal physiological process. During normal relaxation calcium would dissociate from triponin and be taken back up into the SR and the rest would be moved out with a Na+/Ca2+ exchange transporter protein in the cell membrane 14. To keep the sodium levels down in the cell to allow this pump to work it interacts with the Na+/K+ ATPase pump which takes the excess sodium out in exchange for potassium into the cell 14.
When the cardiac glycoside binds extracellularly to the Na+/K+ pump it inhibits the pump 3,4,7. Due to this pump’s key role in the Na+ balance the inhibition also effects the Na+/Ca2+ pump causing a build up of extra Ca2+ in the cell 3. This means the next time the heart contracts there will be more Ca2+ in the cells and this will cause call depolarisation and stronger heart contraction contraction. This is why cardiac glycoside poising initially slows the heart rate but increases the hearts contraction forces 3,7.