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potassium cl er 10 meq capsule

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Potassium Depletion

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.

Other Uses

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.

Dosage and Administration


The acetate, bicarbonate, chloride, citrate, and gluconate salts of potassium are administered orally. Potassium chloride, potassium acetate, and potassium phosphate may be administered by slow IV infusion. Rarely, potassium-containing injections are given by hypodermoclysis, in which case potassium concentrations should not exceed 10 mEq/L in order to avoid local pain. Whenever possible, potassium supplements should be given orally since the relatively slow absorption from the GI tract prevents sudden, large increases in plasma potassium concentrations. Oral potassium supplements should preferably be administered as liquid with or after meals with a full glass of water or fruit juice to minimize the possibility of GI irritation and a saline cathartic effect. Enteric-coated (no longer commercially available in the US) and wax matrix tablets must be swallowed and not allowed to dissolve in the mouth. Other commercially available oral dosage forms of potassium should be dissolved and/or diluted and administered according to the instructions of the manufacturer.

Potassium for injection concentrates must be diluted with a compatible IV solution prior to administration. Diluted solutions of potassium acetate, potassium chloride, and potassium phosphate for injection concentrates must be administered slowly. Potassium injections should generally be administered only in patients with adequate urine flow. In dehydrated patients, 1 liter of potassium-free fluid should be administered prior to initiating potassium therapy. Generally, potassium concentrations in IV fluids should not exceed 40 mEq/L and the rate of administration should not exceed 20 mEq/hour. However, higher potassium concentrations (e.g., 60-80 mEq/L) administered more rapidly occasionally may be needed initially in cases of severe hypokalemia and associated cardiac arrhythmias or for the management of diabetic ketoacidosis or the diuretic phase of acute renal failure. Local vascular intolerance may limit the ability to administer such concentrated solutions. In such cases, use of a large vein with a relatively high blood flow (e.g., femoral vein) or splitting and administering the dose in less concentrated solutions via 2 veins simultaneously can be considered. Administration of such concentrated potassium solutions via a subclavian, jugular, or right atrial catheter should be avoided since local potassium concentrations achieved in the heart may be high and potentially cardiotoxic. The ECG should be monitored closely when the rate of IV potassium administration exceeds 20 mEq/hour. Peaking of the T wave or other ECG changes associated with hyperkalemia (see Cautions: Hyperkalemia) indicate that the rate of potassium infusion is excessive and should be reduced.

Viaflex Plus containers of potassium chloride injections should be checked for minute leaks by firmly squeezing the bag. The injection should be discarded if the container seal is not intact or leaks are found or if the solution is cloudy or contains a precipitate. The injection in plastic containers should not be used in series connections with other plastic containers, since such use could result in air embolism from residual air being drawn from the primary container before administration of fluid from the secondary container is complete.

Oral administration of potassium supplements or ingestion of potassium-rich foods should replace IV potassium therapy as soon as possible.


Dosage of potassium supplements is usually expressed as mEq of potassium and depends on the requirements of the individual patient. The normal adult daily requirement and the usual dietary intake of potassium is 40-80 mEq; infants may require 2-3 mEq/kg or 40 mEq/m daily. Potassium replacement requirements can be estimated only by initial clinical condition and response, ECG monitoring, and/or plasma potassium determinations. Prophylactic administration of potassium supplements may be necessary in some patients in order to maintain plasma potassium concentration above 3.0 mEq/L. The average oral dosage of potassium supplements for the prevention of hypokalemia is about 20 mEq daily, and the usual oral dosage of potassium for the treatment of potassium depletion is 40-100 mEq or more daily. However, it is important to remember that dosage must be individualized for each patient. Forty mEq of potassium is provided by approximately:

3.9 g of potassium acetate
4.0 g of potassium bicarbonate
3.0 g of potassium chloride
4.3 g of potassium citrate
9.4 g of potassium gluconate
5.4 g of monobasic potassium phosphate
3.5 g of dibasic potassium phosphate

Oral potassium supplements are usually administered in 2-4 doses daily. To avoid serious hyperkalemia, replacement of potassium deficits must be undertaken gradually usually over a 3- to 7-day period depending on the severity of the deficit. Potassium dosage for adults should usually not exceed 150 mEq daily, and the dosage for young children should not exceed 3 mEq/kg daily. Close monitoring of the ECG and plasma potassium concentrations is essential during IV administration of potassium.

Acute Myocardial Infarction

Potassium chloride supplementation is used in patients with acute myocardial infarction to maintain serum potassium concentrations at greater than 4 mEq/L; serum magnesium concentrations should be maintained at greater than 2 mEq/L. 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 these levels is considered sound clinical practice.

Although additional study is needed to more fully elucidate the role of early (within 24 hours of symptom onset) metabolic modulation of suspected myocardial infarction (referred to as glucose-insulin-potassium or GIK therapy), potassium chloride has been infused IV at a concentration of 40 or 80 mEq/L in combination with 10 or 25% dextrose injection, respectively, and regular insulin 20 or 50 units/L, respectively. The low-dose solution (40 mEq potassium, 10% dextrose, and 20 units insulin [regular]) was infused at a rate of 1 mL/kg per hour for 24 hours and the high-dose solution (80 mEq potassium, 25% dextrose, and 50 units insulin [regular]) was infused at a rate of 1.5 mL/kg per hour for 24 hours. Although both regimens appear to be beneficial, current evidence suggests that the high-dose regimen may be more effective and therefore preferred.(See Acute Myocardial Infarction: Glucose-Insulin-Potassium Metabolic Modulation, in Uses.)


GI and Other Local Effects

Adverse effects of potassium salts may include nausea, vomiting, diarrhea, flatulence, and abdominal pain or discomfort. Small bowel ulcerations have been reported following administration of enteric-coated potassium chloride tablets (no longer commercially available in the US). Ulcerations have been accompanied by stenosis, hemorrhage, obstruction, and perforation; surgery is frequently required and deaths have been reported. A few cases of small bowel ulceration, stricture, and perforation have been associated with wax matrix formulations of potassium chloride. Esophageal ulceration and stricture have occurred in patients with esophageal compression associated with an enlarged left atrium, and mouth ulceration occurred when a patient sucked rather than swallowed the wax matrix tablets. Following release of the drug from wax matrix tablets, the expended wax matrix is not absorbed systemically and may be detected in feces. Numerous wax matrices accumulated in a patient with partial obstruction of the lower bowel causing an impaction. To date, the incidence of GI lesions (ulceration, stricture, and perforation) with wax matrix tablets appears to be much lower than with enteric-coated (no longer commercially available in the US) tablets (less than 1 per 100,000 patient-years vs 40-50 per 100,000 patient-years). Extended-release tablets containing coated potassium chloride crystals are also formulated to minimize the likelihood of the drug causing GI lesions, but the frequency of GI lesions with these tablets currently is not known. Like enteric-coated tablets (no longer commercially available in the US), the wax matrix tablets and extended-release tablets containing coated crystals of the drug should be administered with caution and should be discontinued immediately if abdominal pain, distention, severe vomiting, or GI bleeding occurs. (See Cautions: Precautions and Contraindications.) Some authorities question the use of any potassium tablet, since use of dilute liquid preparations of potassium minimizes the risk of GI complications.

Pain at the site of injection and phlebitis may occur during IV administration of solutions containing 30 mEq or more potassium per liter.


Hyperkalemia is the most common and serious hazard of potassium therapy. Since an exact measurement of potassium deficiency is not usually possible, potassium supplements should be administered slowly and with caution. The presence of adequate renal function must be confirmed, and frequent observations of the clinical status of the patient and periodic ECGs and/or determinations of plasma potassium concentrations should be made. ECG changes are probably the most important indicator of potassium toxicity and include tall, peaked T waves, depression of the ST segment, disappearance of the P wave, prolongation of the QT interval, and widening and slurring of the QRS complex. Clinical signs and symptoms of potassium overdosage include paresthesia of the extremities, listlessness, mental confusion, weakness or heaviness of the legs, flaccid paralysis, cold skin, gray pallor, peripheral vascular collapse with fall in blood pressure, cardiac arrhythmias, and heart block. Extremely high plasma potassium concentrations (8-11 mEq/L) may cause death from cardiac depression, arrhythmias, or arrest. It has been suggested that hyperkalemia may decrease the excitability of the myocardium to electrical stimulation resulting in the possibility that the myocardium may not respond to implanted pacemakers.

Except in the presence of severe renal impairment, hyperkalemia is not likely to result from oral administration or from slow IV administration of dilute solutions of potassium. Nonetheless, hyperkalemia can occur from therapeutic doses of potassium salts and, when detected, must be treated immediately since lethal plasma potassium concentrations can be reached within a few hours. Hyperkalemia may result from rapid IV administration of potassium solutions. Hyperkalemia has occurred following addition of concentrated potassium chloride solutions to infusions from a hanging flexible plastic container, apparently as a result of pooling of the concentrated potassium solution at the base of the container and infusion of undiluted solution. Squeezing the container did not facilitate mixing but tended to pump the concentrated solution into the infusion chamber. Mixing of the solutions can be achieved if the plastic container is inverted during the addition of potassium solutions and subsequently agitated and/or kneaded.

Treatment of hyperkalemia depends on its severity and various regimens have been recommended. It must be kept in mind that rapid lowering of plasma potassium concentrations in digitalized patients can cause cardiac glycoside toxicity. Administration of potassium-rich foods and drugs and potassium-sparing diuretics must be discontinued. In patients with severe hyperkalemia, measures which facilitate shift of potassium into cells, such as administration of sodium bicarbonate, a calcium salt, and/or dextrose with or without insulin, have been recommended. In patients with plasma potassium concentrations greater than 6.5 mEq/L, IV infusion of 40-160 mEq of sodium bicarbonate over a 5-minute period has been recommended. This dose may be repeated after 10-15 minutes if ECG abnormalities persist. Dextrose therapy usually consists of IV infusion of 300-500 mL of 10-25% dextrose injection containing 5-10 units of insulin per 20 grams of dextrose over a 1-hour period. Some clinicians report that dextrose is less reliable and does not produce effects as rapidly as does sodium bicarbonate. In addition, studies indicate that the addition of insulin to an infusion solution results in adsorption of insulin to the glass and tubing. For this reason, it has been recommended that insulin be given as a separate injection. Patients whose ECGs show absent P waves or a broad QRS complex and who are not receiving cardiac glycosides should immediately be given 0.5-1 g (5-10 mL of a 10% solution) of calcium gluconate or another calcium salt IV over a 2-minute period (with continuous ECG monitoring) to antagonize the cardiotoxic effects of potassium. If ECG abnormalities persist, repeated doses of the calcium salt may be given, allowing 1-2 minutes between doses. When hyperkalemia is associated with water loss, administration of potassium-free fluids may be useful to decrease plasma potassium concentrations.

When the ECG approaches normal, efforts should be directed toward removal of excess potassium from the body. Some adsorption and/or exchange of potassium may be accomplished by administration of sodium polystyrene sulfonate orally or as a retention enema. Hemodialysis or peritoneal dialysis will reduce plasma potassium concentrations and may be required in patients with renal insufficiency. Administration of large doses of sodium chloride has been recommended to increase urinary excretion of potassium in patients with functional kidneys. Other drugs which have been used in an effort to reduce plasma potassium concentrations include testosterone to promote anabolism, and desoxycorticosterone acetate in patients with adrenal insufficiency who have adequate renal function.

Precautions and Contraindications

Potassium supplements should be administered with caution in patients with cardiac disease. These drugs may intensify symptoms of myotonia congenita. Potassium supplements should not be administered to patients receiving potassium-sparing drugs such as amiloride, spironolactone, and triamterene. Potassium should generally not be given in the immediate postoperative period until urine flow is established. In patients with renal impairment, its use must be carefully controlled by frequent determinations of plasma potassium concentrations.

Because intestinal and gastric ulceration and bleeding have occurred with extended-release potassium chloride preparations, these dosage forms of the drug should be reserved for patients who cannot tolerate or refuse to take liquid or effervescent potassium preparations or for those in whom there is a problem of compliance with these latter dosage forms. If abdominal pain, distension, severe vomiting, or GI bleeding occurs in patients receiving an extended-release preparation, the drug should be discontinued immediately and the possibility of intestinal obstruction or perforation considered. Because Micro-K LS contains docusate sodium as a dispersing agent, minor changes in consistency of feces may commonly occur; these changes are generally well tolerated. However, rarely, patients may experience diarrhea and cramping or abdominal pain. Patients with severe or chronic diarrhea or who are dehydrated generally should not receive supplemental potassium therapy using Micro-K LS.

Some preparations of potassium contain the dye tartrazine (FD&C yellow No. 5), which may cause allergic reactions including bronchial asthma in susceptible individuals. Although the incidence of tartrazine sensitivity is low, it frequently occurs in patients who are sensitive to aspirin.

Potassium supplements are contraindicated in patients with severe renal impairment with oliguria, anuria, or azotemia; untreated chronic adrenocortical insufficiency (Addison's disease); the hyperkalemic form of familial periodic paralysis or other hyperkalemias; acute dehydration; heat cramps; or extensive tissue breakdown such as severe burns. Wax matrix formulations of potassium chloride should not be administered to patients with esophageal compression caused by an enlarged left atrium; a liquid preparation of potassium should be used in these patients. Solid oral dosage forms of potassium supplements are contraindicated in patients in whom there is a structural, pathological (e.g., diabetic gastroparesis), and/or pharmacologic (e.g., induced by anticholinergic agents) cause for arrest or delay in passage of the dosage form through the GI tract; an oral liquid preparation of potassium should be used in these patients.



Potassium salts are well absorbed from the GI tract. Enteric-coated potassium chloride tablets (no longer commercially available in the US) pass through the stomach releasing the drug in the small intestine and may produce dangerously high, localized concentrations of potassium chloride. Ingestion of sugar-coated tablets containing potassium chloride imbedded in a wax matrix (e.g., Kaon-Cl, Slow-K) produces a slow release of the drug. The wax matrix and potassium chloride crystals are blended so that the salt can be slowly leached from the tablet by GI fluids, and thus the potassium chloride is gradually released over a large segment of the intestine. Compared to liquid preparations, absorption of potassium from a single dose in these wax matrix formulations is somewhat delayed, probably because of the time required for dissolution of the drug. However, when potassium chloride is administered chronically, the bioavailability of potassium from the wax matrix preparations appears to be similar to that of liquid preparations of the drug. Dangerously high, localized concentrations of potassium chloride are not likely to occur with this dosage form unless blockage of passage of the tablet through the GI tract occurs. Similarly, extended-release granules for suspension and tablets containing coated potassium chloride crystals produce a slow release of the drug and minimize the likelihood of high, localized concentrations in the GI tract.


Potassium first enters the extracellular fluid and is then actively transported into the cells where its concentration is up to 40 times that outside the cell. Dextrose, insulin, and oxygen facilitate movement of potassium into cells. In healthy adults, plasma potassium concentrations generally range from 3.5-5 mEq/L. Plasma concentrations up to 7.7 mEq/L may be normal in neonates. Plasma potassium concentrations, however, are not necessarily accurate indications of cellular potassium concentrations; cellular deficits can occur without decreases in plasma potassium concentrations and hypokalemia may occur without substantial depletion of cellular potassium. Changes in extracellular fluid pH produce reciprocal effects on plasma potassium concentrations. A change of 0.1 unit in plasma pH has been reported to produce an inverse change of 0.6 mEq/L in plasma potassium concentration. Potassium concentrations in gastric and intestinal secretions are higher than plasma concentrations, and diarrheal fluid may contain up to 60 mEq/L.


Potassium is excreted mainly by the kidneys. The cation is filtered by the glomeruli, reabsorbed in the proximal tubule, and secreted in the distal tubule, the site of sodium-potassium exchange. Tubular secretion of potassium is also influenced by chloride ion concentration, hydrogen ion exchange, acid-base equilibrium, and adrenal hormones. Healthy patients on potassium-free diets usually excrete 40-50 mEq of potassium daily. Surgery and/or tissue injury result in increased urinary excretion of potassium which may continue for several days. Postoperative patients or patients under stress of disease with normal kidneys may excrete up to 80-90 mEq of potassium daily, even though they are not receiving any potassium. Small amounts of potassium may be excreted via the skin and intestinal tract, but most of the potassium excreted into the intestine is later reabsorbed.

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