Returning to normal pH after acidosis, similar to reperfusion after ischemia, is prone to arrhythmias. The type and mechanisms of these arrhythmias have never been explored and were the aim of the present work. Langendorff perfused rat/mice hearts and rat isolated myocytes were subjected to respiratory acidosis and then returned to normal pH. Monophasic action potentials and left ventricular developed pressure were recorded. Removal of acidosis provoked ectopic beats that were blunted by 1 µM of the CaMKII inhibitor KN-93, 1 µM thapsigargin, to inhibit SR Ca²⁺ uptake, and 30 nM ryanodine or 45 µM dantrolene, to inhibit SR Ca²⁺ release and were not observed in a transgenic mouse model with inhibition of CaMKII targeted to the SR. Acidosis increased the phosphorylation of Thr¹⁷ site of phospholamban (PT-PLN) and SR Ca²⁺ load. Both effects were precluded by KN-93. The return to normal pH was associated with an increase in SR Ca²⁺leak, when compared with control or with acidosis at the same SR Ca²⁺ content. Ca²⁺ leak occurred without changes in the phosphorylation of ryanodine receptors (RyR2) and was blunted by KN-93. Experiments in planar lipid bilayers confirmed the reversible inhibitory effect of acidosis on RyR2. Ectopic activity was triggered by membrane depolarizations (DADs), primarily occurring in epicardium and were prevented by KN-93. The results reveal that arrhythmias after acidosis are dependent on CaMKII activation and are associated to an increase in SR Ca²⁺ load, which appears to be mainly due to the increase in PT-PLN.