Reductions in serum potassium influence myocardial cell excitability by increasing membrane potential, diastolic depolarization, duration of refractory period and action potential, and decreasing conduction velocity. Disturbances in electrolyte balance typically involve alterations in two or more cations whose effects can be additive or antagonist. Serum magnesium and calcium have been demonstrated to influence the electrophysiologic effects of potassium imbalances. The arrhythmogenic potential of hypokalemia is thought to result from electrical inhomogeneity, alterations in conduction, changes in automaticity and disturbances in sodium pump kinetics. Potassium balance is maintained by two separate, yet interrelated, systems: distribution and the balance between intake and excretion. Cell wall integrity, osmolality, hormones and acid-base balance influence the relative concentrations of potassium between the intracellular and extracellular compartments. Renal excretion is the major route of elimination and is affected by acid-base balance, potassium and sodium intake, urinary flow rates and mineralocorticoid states. Serum potassium is not an accurate reflection of total body potassium stores. Acute hypokalemia differs from chronic, for the former results in a change in only the serum potassium concentration, whereas the latter is accompanied by a reduction in both the total body stores and serum levels. The importance of intracellular and extracellular concentrations lies in their determination of the resting membrane potential and, therefore, membrane excitability. Although experimental studies have demonstrated an association between ventricular ectopy and hypokalemia, the clinical studies to date have reported conflicting results. The arrhythmogenic role of hypokalemia has been examined in ambulatory hypertensive patients with acute myocardial infarctions and those with magnesium deficiencies, the results of which have been difficult to interpret because of differences in study design, durations, and characteristics of study population. During general anesthesia, both experimental and clinical studies have failed to demonstrate an increase in the incidence of ventricular ectopy in hypokalemic patients. The common practice of acute repletion therapy or cancellation is not warranted based on the studies to date. Repletion therapy is neither inexpensive nor benign. In one study of 4921 hospitalized patients, the frequency of dangerous complications of oral and/or intravenous potassium therapy was approximately 1 in 175. Certain patients are susceptible to hyperkalemia, so commonly prescribed medication can promote elevations in serum potassium including indomethacin, amiloride, beta-adrenergic blocking agents, and angiotensin-converting enzyme inhibitors. Evaluation of hypokalemia should include identification of the etiology precipitating the electrolyte imbalance. Examinations should include the duration and severity of the depletion, history of past and present illness, current medications, and the presence of concurrent electrolyte disturbances.(ABSTRACT TRUNCATED AT 400 WORDS)