It is well recognized that the procedure of hemodialysis is associated with significant changes in blood pressure and systemic hemodynamics; 20–30% of treatments are complicated by intradialytic hypotension (IDH). There are now an increasing number of studies using electrocardiographic, isotopic and echocardiographic techniques that show that subclinical myocardial ischemia occurs during dialysis. This concept is supported by some studies showing that dialysis can induce acute rises in troponins and creatinine kinase MB, although this has not been found by all authors. Some of this controversy may at least in part be due to the collection of blood samples immediately postdialysis, which is likely to be too early to reliably detect dialysis-induced elevations of cardiac enzymes. Cardiovascular death is the biggest single cause of mortality in dialysis patients and of this sudden death comprises the largest proportion. As such, there is a large body of evidence examining whether dialysis is pro-arrhythmogenic. It is clear that dialysis can increase QTc interval and QT dispersion and is capable of inducing arrhythmias on Holter monitoring, likely due to the interaction of multiple factors, some of which prime for the development of arrhythmias (particularly the presence of preexisting cardiac disease), and some of which act as triggers. However, the link between these electrocardiographic alterations and sudden death is relatively poorly studied. This review summarizes the available literature regarding the acute cardiac effects of dialysis in relation to the above, and discusses how these acute changes may contribute to the genesis of uremic cardiomyopathy and longer term cardiac outcomes.