It is difficult to summarise when so much that has been said is tentative but it is probably fair to state that:
1) The cardiotonic effect is not primarily on the action potential mechanism or on the contractile mechanism but is on "excitation-contraction coupling."
2) The sensitivity to cardiac glycosides of the sodium and potassium transport mnechanism in the muscle membrane is sufficient for sodium and potassium transport to be affected by cardiac glycoskies in therapeutic concentrations.
3) it is doubtful whether therapeutic doses of cardiac glycosides cause appreciable lowering of the internal potassium concentration. A gain in sodiumn may occur.
4) A positive inotropic action is probably associated with increased uptake of calcium.
5) It is possible that the cardiotonic action of the cardiac glycosides is caused by interference with the removal or inactivation of the calcium that enters the muscle at each contraction. Such interference might be a primary effect of the cardiac glycoside or it might be secondary to a rise in the intracellular sodium concentration.