Potassium Metabolism

With age, total body potassium decreases. This decrease reflects the decrease in lean body muscle mass, which contains about 75% of intracellular potassium. Although aldosterone secretion decreases with age, the kidney's ability to regulate potassium excretion under normal dietary conditions is unaffected. Because most of the total body stores of potassium are within cells, measurement of serum potassium is often inadequate for estimating total body potassium.

Hypokalemia

A decrease in serum potassium concentration < 3.5 mEq/L; total body potassium may be normal or decreased.

Hypokalemia is common in the elderly. Common causes include decreased intake of potassium during acute illness, nausea and vomiting, and treatment with thiazide or loop diuretics. About 20% of patients receiving thiazide diuretics develop hypokalemia, which is dose-dependent but usually mild. Other causes are listed in Table 57-3.

Symptoms, Signs, and Diagnosis

Mild hypokalemia rarely produces symptoms. Common symptoms of more severe hypokalemia are fatigue, confusion, and muscle weakness and cramps from impaired skeletal muscle function. Severe hypokalemia (< 2.5 mEq/L) can result in frank paralysis, as occurs with periodic paralysis. Smooth muscle function of the GI tract can also be affected, leading to adynamic ileus. Cardiac function can be affected, resulting in atrial and ventricular ectopic beats, atrial and ventricular tachycardia, ventricular fibrillation, and sudden death, particularly in patients with preexisting heart disease or those taking digitalis preparations. The ECG often shows ST-segment depression, T-wave flattening, and a prominent U wave. With severe hypokalemia, atrioventricular conduction disturbances can develop.

Measuring urinary potassium excretion may help establish if urinary loss is abnormal. Urinary excretion of > 20 mEq/L suggests an excessive loss in a patient with hypokalemia.

Treatment

Treatment consists of correcting the underlying cause (if possible), correcting total body deficits, and restoring normal serum potassium concentrations.

When urgent treatment is not required, potassium chloride 10 to 20 mEq po q 4 to 8 h should be given until the serum potassium concentration is normal. If hypokalemia is caused by a thiazide diuretic, supplemental potassium or a potassium-sparing diuretic such as triamterene, amiloride, or spironolactone may maintain normal blood potassium concentrations once the deficit has been corrected.

When urgent treatment is needed (ie, when the patient has severe symptoms or an arrhythmia), potassium chloride should be given IV. The potassium concentration in the IV fluid usually should not exceed 40 mEq/L, and the administration rate should not exceed 10 to 20 mEq/h with a total dose of 200 mEq/24 h. As long as 10 mEq/h is given each hour, a large deficit can almost always be overcome. Because ongoing additional losses are common, the serum concentration should be measured often (usually every 6 hours). Repeated doses of 10 mEq/h are often needed. If no central venous access is available, the potassium concentration cannot exceed 10 mEq/100 mL of fluid without a high risk of phlebitis and early loss of that access site. If central venous access is available, the potassium concentration can be about 40 mEq/L without risk of central vein scarring, stenosis, or occlusion. Again, the patient should be closely monitored, especially for cardiac function. With IV dosing of substantial amounts of potassium to the elderly, the volume of the IV fluid and the sodium tonicity of that fluid can cause problems.

Hyperkalemia

An increase in serum potassium concentration > 5 mEq/L; total body potassium can be high but is more often normal or even low; however, distribution between intracellular and extracellular compartments is abnormal.

Hyperkalemia may be mild (5.0 to 5.5 mEq/L), moderate (5.5 to 6.0 mEq/L), or severe (> 6.0 mEq/L).

Etiology

Hyperkalemia can be caused by a number of disorders or drugs (see Table 57-4). A relatively small shift of potassium from the intracellular to the extracellular compartment can result in marked hyperkalemia in patients with metabolic acidosis, especially diabetic ketoacidosis.

Only in patients with renal disease or impaired tubular function does excessive intake lead to hyperkalemia. Patients with acute oliguric renal failure are at especially high risk. Cellular uptake is stimulated by insulin, aldosterone, epinephrine (through -receptor stimulation), and alkalosis and can modulate the impact of high oral potassium intake on serum levels. Chronic renal disease with hyperkalemia may result from diseases with primary tubular injury (eg, obstructive uropathy) or from chronic analgesic abuse. Primary or secondary adrenal insufficiency must also be considered. Active GI bleeding, especially in a patient with a reduced glomerular filtration rate, can also lead to hyperkalemia.

An elevated serum potassium concentration may result from pseudohyperkalemia caused by hemolysis or from the release of potassium from platelets during sample storage.

Symptoms, Signs, and Diagnosis

Hyperkalemia may be asymptomatic until cardiac toxicity develops. Initial ECG changes are a shortened QT interval and tall, narrow T waves. At higher potassium concentrations (usually >= 5.5 mEq/L), hyperkalemia can cause nodal and ventricular arrhythmias along with widened QRS complexes and prolonged PR intervals. Ultimately, ventricular fibrillation or asystole can develop. Nonspecific neuromuscular symptoms, including vague weakness and paresthesias, may occur. With severe hyperkalemia, dramatic symptoms (eg, severe weakness, flaccid paralysis) may occur.

Treatment

Severe or rising hyperkalemia may constitute a medical emergency. Atrioventricular block or changes in the QRS complex or P wave on the ECG should be treated with calcium chloride IV using the rule of 10's: 10 mL of 10% calcium chloride every 10 minutes as needed. A glucose-insulin-bicarbonate solution can also be used to shift potassium into cells. If these measures are ineffective, hemodialysis should be initiated promptly.

Moderate hyperkalemia without significant ECG changes should be treated with sodium polystyrene sulfonate 15 to 30 g po dissolved in a 50% oral solution of sorbitol (30 to 60 mL). Sodium polystyrene sulfonate can also be given as a retention enema of 60 g in 120 mL of 50% sorbitol at 4- to 6-hour intervals. Furosemide 40 to 160 mg IV may be used. IV 0.9% sodium chloride is often essential to ensure the maximum renal capacity for excreting potassium. Potassium levels should be checked every 2 to 4 hours.

Mild hyperkalemia may be treated by restricting potassium intake to 40 to 60 mEq/day. Drugs and foods that may contribute to hyperkalemia should be discontinued. Furosemide 40 to 80 mg po bid to qid or fludrocortisone acetate 0.05 to 0.2 mg/day po may be useful in patients with chronic renal disease or hypoaldosteronism.