After intravenous administration of epinephrine, serum potassium level shows a typically biphasic course. The initial rise is followed by a persistent fall to a lower level than the starting-concentration. The initially observed hyperkalemia is supposed to be caused by a potassium release from hepatocytes, mediated by an alpha 1-adrenoreceptor stimulation. The subsequent hypokalemia seems to be caused by the beta 2-mimetic component of epinephrine effecting the uptake of this ion into striated muscle cells. There are numerous clinical reports of marked hypokalemia as a consequence of beta 2-mimetic therapy. The additive effect of elevated endogenous catecholamines with the therapeutically applied epinephrine during cardiopulmonary resuscitation may be the cause of the elevated potassium levels often observed under these conditions. On the other hand, low serum potassium levels were measured in patients after successful resuscitation, as well as in patients with multiple trauma and with severe head injury. Moreover, hypokalemia seems to be a frequent event in the acute phase of myocardial infarction. A catecholamine-induced potassium shift into the cell is considered to be the cause of this decrease. The question whether in the case of myocardial infarction the hypokalemia is in itself arrhythmogenic as yet is not resolved. Because of the present knowledge about the influence of catecholamines on potassium metabolism it seems advisable to monitor potassium levels regularly during the above situations.