Potassium supplements are used as a source of potassium cation for treatment or prevention of potassium depletion in patients in whom dietary measures are inadequate. Conditions which may indicate or result in potassium deficiency include vomiting, diarrhea, drainage of GI fluids, hyperadrenalism, malnutrition, debilitation, prolonged negative nitrogen balance, prolonged parenteral alimentation without addition of potassium, dialysis, metabolic alkalosis, metabolic or diabetic acidosis, GI tract abnormalities which result in poor absorption, certain renal diseases, and familial periodic paralysis characterized by hypokalemia. Potassium should be included in long-term electrolyte replacement regimens and has been recommended for routine prophylactic administration following surgery after adequate urine flow has been established. Administration of certain drugs including thiazide diuretics, carbonic anhydrase inhibitors, furosemide, ethacrynic acid, some corticosteroids, corticotropin, aminosalicylic acid, and amphotericin B may sometimes result in potassium depletion which may warrant potassium replacement therapy. Ingestion of potassium-rich foods and/or use of potassium-containing salt substitutes may prevent potassium depletion in patients receiving potassium-depleting drugs; however, judicious prophylactic administration of potassium may be advisable in selected patients during prolonged diuretic or corticosteroid therapy, especially if they are digitalized.
Potassium chloride is usually the salt of choice in the treatment of potassium depletion, since the chloride ion is required to correct hypochloremia which frequently accompanies potassium deficiency. In addition, hypochloremia may develop if the citrate, bicarbonate, gluconate, or another alkalinizing salt of potassium is administered, particularly in conjunction with chloride-restricted diets. In the rare instances in which metabolic acidosis exists concurrently with potassium depletion (e.g., renal tubular acidosis), alkalinizing salts of potassium are preferred.
Inadequate dietary intake of potassium may play an important role in the development of hypertension, and high dietary intake of potassium (e.g., with supplementation) may protect against the development of high blood pressure and improve blood pressure control in patients with hypertension. As a result, most experts currently recommend that an adequate intake of potassium (about 50-90 mEq daily) be maintained in hypertensive patients as part of lifestyle modifications, particularly in those unable to adequately reduce their sodium intake. Adequate intake of potassium also should be considered as a means of preventing the development of hypertension. Food sources high in potassium such as fruits and vegetables preferably should be used. Alternatively, potassium supplements or salt-substitutes or potassium-sparing diuretics can be used, particularly in patients receiving kaliuretic diuretics. In pooled analysis of data from 33 randomized controlled trials in which potassium supplementation was the only difference between intervention and control groups, such supplementation was associated with a reduction in mean systolic blood pressure of 3.11 mm Hg and a reduction in mean diastolic blood pressure of 1.97 mm Hg. The effects of potassium supplementation appeared to be particularly evident in patients exposed to high sodium intake.
Acute Myocardial Infarction
Prevention of Ventricular Fibrillation
Potassium supplementation, combined with magnesium supplementation if necessary, has been used in patients with an acute myocardial infarction to reduce the risk of ventricular arrhythmias. Although the benefits of this strategy in preventing ventricular fibrillation following a myocardial infarction have not been confirmed by randomized clinical trial data, maintaining serum potassium and magnesium concentrations at levels exceeding 4 and 2 mEq/L, respectively, is considered sound clinical practice. In addition, clinical experience as well as observational data from coronary care unit populations indicate that hypokalemia is a risk factor for the development of ventricular fibrillation.
Glucose-Insulin-Potassium Metabolic Modulation
Potassium chloride has been used IV early in the course of suspected acute myocardial infarction in combination with IV insulin injection (regular insulin) and dextrose (
d-glucose) (referred to as glucose-insulin-potassium or GIK therapy) for metabolic modulation and potential beneficial effects on morbidity and mortality. Initial experience (from the pre-thrombolytic reperfusion era) with such early post-myocardial infarction metabolic modulation therapy showed substantial potential reductions in mortality associated with acute myocardial infarction. Pooled analysis of these early studies (randomized, placebo-controlled) showed a potential mortality reduction benefit of 28% (overall for 9 studies) to 48% (in a subset of 4 studies employing high-dose GIK), depending on the dosage and timing of therapy initiation relative to symptom onset. More recently, evidence of an even greater potential benefit was reported when early GIK therapy was combined with reperfusion (thrombolysis or primary percutaneous transluminal coronary angioplasty [PTCA]). Additional study is needed to elucidate further the role of GIK therapy in the management of acute myocardial infarction.
In the recent study of metabolic modulation, 407 patients admitted within 24 hours of symptom onset of suspected myocardial infarction, regardless of age or ECG findings, were randomly assigned to high-dose GIK (IV infusion of 25% dextrose injection, insulin [human or nonhuman] 50 units/L, and potassium chloride 80 mEq/L at a rate of 1.5 mL/kg per hour for 24 hours), low-dose GIK (IV infusion of 10% dextrose injection, insulin [human or nonhuman] 20 units/L, and potassium chloride 40 mEq/L at a rate of 1 mL/kg per hour for 24 hours), or usual care as a control. GIK therapy was initiated on average within 10.1-11.4 hours of symptom onset. Because of the limited number of patients studied, analysis of results compared the combination of both GIK regimens (overall GIK-treated group) versus usual care as a control. In this study, a reduction in the composite end point of death, nonfatal severe heart failure (greater than Killip class 2), and nonfatal ventricular fibrillation was observed for the overall GIK-treated group as well as for the 252 (61.9%) patients who also underwent reperfusion. The latter group also showed a reduction in mortality rate (relative risk of 0.34; i.e., a 66% reduction), and a strong relationship was observed between the time of symptom onset and the beneficial effect of the infusion. A reduction in mortality rate also was shown for patients treated within 12 hours after symptom onset (relative risk of 0.43; i.e., a 57% reduction), both for the overall GIK-treated group and for those who also underwent reperfusion. Among patients in whom a 24-hour course of GIK infusion therapy was completed, mortality was reduced in both the overall GIK-treated (relative risk of 0.44; i.e., a 56% reduction) and in those who also underwent reperfusion (relative risk of 0.21; i.e., a 79% reduction). At 1-year follow-up, Kaplan-Meier curves showed attenuation of the treatment effect in both the overall GIK-treated group and those who also were reperfused, with a nonsignificant mortality reduction of 19 and 33%, respectively. Despite this attenuation of effect, a consistent, statistically significant mortality reduction was still present at 1 year for patients who received high-dose GIK combined with reperfusion (relative risk of 0.37; i.e., a 63% reduction). GIK therapy was well tolerated, with the principal differences between the GIK-treated and control groups being phlebitis (83% of patients received GIK via a peripheral IV line) and higher serum potassium concentration with GIK.
Because results of this recent study showed that metabolic modulation with dextrose, insulin, and potassium (i.e., GIK therapy) is a feasible strategy in the early hours after an acute myocardial infarction, the American College of Cardiology (ACC), American Heart Association (AHA), and others encourage performance of a larger clinical trial to further elucidate the magnitude of potential benefit and role of such therapy in the management of myocardial infarction. However, the existing results have strong implications for incorporating this fairly simple, inexpensive, and well-tolerated therapy in the care of acute myocardial infarction patients worldwide.
Potassium salts may be used cautiously to abolish arrhythmias of cardiac glycoside toxicity precipitated by a loss of potassium. It has been reported that elevation of plasma potassium concentrations by 0.5-1.5 mEq/L or to the upper limits of normal may be useful in the management of tachyarrhythmias following cardiac surgery. This regimen should not be used in patients with atrioventricular block, however, since potassium may further impair nodal conduction.
Limited data suggest that potassium may be useful in the treatment of thallium poisoning; however, such treatment is limited by the amount of thallium that can be released into the blood without worsening cerebral symptoms.