the ejected amount is lowered due to chaotic activation of the ventricle which prevents normal, synchronised contraction. Different parts of the myocardium contract at different times, greatly diminishing the contraction efficiency (the heart is basically just shaking).
Increased heart rate (leading to a shortened action potential duration) is associated with lower ejection fraction (http://www.sciencedirect.com/science/article/pii/0002914979903953); even though the contractility per unit time is increased via beta-adrenergic stimulation that usually drives the increased heart rate; CaMKII also plays role via ICaL and SERCA modulation.
The relationship between action potential duration and contractility, if heart rate is not to be taken into account, would probably require further assumptions/knowledge. Contractility is more about calcium transient amplitude than action potential duration itself.
The stroke volume (amount of blood ejected per beat) is clearly affected. For instance, with atrial fibrillation the SV gets reduced by about 30%. Depending on the arrhythmia, this can be worse and, of course, with VF (ventricular fibrillation) it drops to about zero. We are very resilient, though, and can live with the ejection fraction (actual SV/ 'ideal' SV) as low as about 30%.
i have another question, how this reduction is distributed, is reglary by pulse when the heart rate the SV reduces or irigulary and stay aleatory by puls and constante by a limited time.