As the primary natural pacemaker, the cardiomyocytes of the sinoatrial node (SAN) initiate each individual heartbeat through cyclic spontaneous depolarisation. Recently, it has been shown that patients suffering from kidney problems and therefore undergoing haemodialysis (HD) suffer from a decreasing heart rate, which can lead to sudden cardiac death. The resulting changes in electrolyte concentrations, particularly a reduction in extracellular calcium, can be the cause of a decreasing heart rate, which can lead to severe bradycardia and cardiac arrest. In addition, increased sympathetic tone has been observed in these patients.

It is therefore hypothesised that altered electrolyte levels, particularly reduced extracellular calcium levels, which impair SAN pacemaker function, are usually compensated to some extent by increased sympathetic tone. A sudden loss of sympathetic tone results in the low basal SAN beat rate resulting from hypocalcaemic conditions being exposed, causing extreme bradycardia. The combination of these two mechanisms may help to explain the high prevalence of SCD in CKD patients.