Potassium imbalance
Potassium, a cation that’s the dominant cellular electrolyte, facilitates contraction of both skeletal and smooth muscles — including myocardial contraction — and figures prominently in nerve impulse conduction, acid-base balance, enzyme action, and cell membrane function. Because serum potassium level has such a narrow range (3.5 to 5 mEq/L), a slight deviation in either direction can produce profound clinical consequences. Paradoxically, both hypokalemia (potassium deficiency) and hyperkalemia (potassium excess) can lead to muscle weakness and flaccid paralysis, because both create an ionic imbalance in neuromuscular tissue excitability. Both conditions also diminish excitability and conduction rate of the heart muscle, which may lead to cardiac arrest. (See Clinical effects of potassium imbalance.)
Causes
Because many foods contain potassium, hypokalemia seldom results from a dietary deficiency. Instead, potassium loss may result from:
❑ excessive GI losses, such as diarrhea, dehydration, anorexia, or chronic laxative abuse (Vomiting and gastric suction cause dehydration, resulting in hyperaldosteronism [sodium retention and potassium excretion occur.])
❑ trauma (injury, burns, or surgery), in which damaged cells release potassium, which enters serum or extracellular fluid, to be excreted in the urine
❑ chronic renal disease, with tubular potassium wasting
❑ certain drugs, especially potassium-wasting diuretics, steroids, and certain sodium-containing antibiotics (carbenicillin)
❑ acid-base imbalances, which cause potassium shifting into cells without true depletion in alkalosis
❑ prolonged potassium-free I.V. therapy
❑ hyperglycemia, causing osmotic diuresis and glycosuria
❑ Cushing’s syndrome, primary hyperaldosteronism, excessive licorice ingestion, and severe serum magnesium deficiency.
Hyperkalemia results from the kidneys’ inability to excrete excessive amounts of potassium infused I.V. or administered orally; from decreased urine output, renal dysfunction or failure; or the use of potassium-sparing diuretics, such as triamterene, by patients with renal disease. It may also result from any injuries or conditions that release cellular potassium or favor its retention, such as burns, crushing injuries, failing renal function, adrenal gland insufficiency, dehydration, or diabetic acidosis.
Diagnosis
Confirming diagnosis Serum potassium levels less than 3.5 mEq/L confirm hypokalemia; serum levels greater than 5 mEq/L confirm hyperkalemia.
Additional tests may be necessary to determine the imbalance’s underlying cause. Hypokalemia is also associated with hypomagnesemia, so further study of other electrolytes is warranted.
Treatment
For hypokalemia, replacement therapy with potassium chloride (I.V. or orally) is the primary treatment. When diuresis is necessary, spironolactone, a potassium-sparing diuretic, may be administered concurrently with a potassium-wasting diuretic to minimize potassium loss. Hypokalemia can be prevented by giving a maintenance dose of potassium I.V. to patients who may not take anything by mouth and to others predisposed to potassium loss.
For hyperkalemia, rapid infusion of 10% calcium gluconate decreases myocardial irritability and temporarily prevents cardiac arrest but doesn’t correct serum potassium excess; it’s also contraindicated in patients receiving cardiac glycosides. As an emergency measure, sodium bicarbonate I.V. increases pH and causes potassium to shift back into the cells. Insulin and 10% to 50% glucose I.V. also move potassium back into cells. Infusions should be followed by dextrose 5% in water because infusion of 10% to 15% glucose will stimulate endogenous insulin secretion. Sodium polystyrene sulfonate with 70% sorbitol produces exchange of sodium ions for potassium ions in the intestine. Hemodialysis or peritoneal dialysis also aids in removal of excess potassium.
Special considerations
For hypokalemia:
❑ Check serum potassium and other electrolyte levels in patients apt to develop potassium imbalance and in those requiring potassium replacement; they risk overcorrection to hyperkalemia.
❑ Assess intake and output carefully. Remember, the kidneys excrete 80% to 90% of ingested potassium. Never give supplementary potassium to a patient whose urine output is below 600 ml/day. Also, measure GI loss from suctioning or vomiting.
❑ Administer slow-release potassium or dilute oral potassium supplements in 4 oz (118 ml) or more of water or other fluid to reduce gastric and small-bowel irritation. Determine the patient’s chloride level. As ordered, give a potassium chloride supplement if the level is low; potassium gluconate if it’s normal.
❑ Give potassium I.V. only after it’s diluted in solution (usually, 10 mEq/100 ml of fluid); potassium is very irritating to vascular, subcutaneous, and fatty tissues and may cause phlebitis or tissue necrosis if it infiltrates. Infuse slowly (no more than 20 mEq/L/hour through central administration or 10 mEq/hour through peripheral administration) to prevent hyperkalemia.
Alert Never administer by I.V. push or bolus; it may cause cardiac arrest.
❑ Carefully monitor patients receiving cardiac glycosides because hypokalemia enhances the action of these drugs and may produce signs of digoxin toxicity (anorexia, nausea, vomiting, blurred vision, and arrhythmias).
❑ To prevent hypokalemia, instruct patients (especially those predisposed to hypokalemia due to long-term diuretic therapy) to include in their diet foods rich in potassium — oranges, bananas, tomatoes, milk, dried fruits, apricots, peanuts and dark green, leafy vegetables.
❑ Monitor cardiac rhythm and report any irregularities immediately.
For hyperkalemia:
❑ As in hypokalemia, frequently monitor serum potassium and other electrolyte levels, and carefully record intake and output.
❑ Administer sodium polystyrene sulfonate orally or rectally (by retention enema) in patients with significant potassium elevations because of intravascular sodium shifting. Watch for signs of hypokalemia with prolonged use and for clinical effects of hypoglycemia (muscle weakness, syncope, hunger, diaphoresis) with repeated insulin and glucose treatment.
❑ Watch for signs of hyperkalemia in predisposed patients, especially those with poor urine output or those receiving potassium supplements orally or I.V. Administer no more than 10 to 20 mEq/L of potassium chloride per hour; check the I.V. infusion site for signs of phlebitis or infiltration of potassium into tissues. Also, before giving a blood transfusion, check to see how long ago the blood was donated; cell hemolysis in older blood releases potassium. Infuse only fresh blood for patients with average to high serum potassium levels.
❑ Monitor for and report cardiac arrhythmias.
Pictures
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
Other Book Chapters Related to Hyperkalemia
Read excerpts from these other book chapters related to Hyperkalemia:
Medical Books Excerpts
- Hyperkalemia
- "The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter" (2000)
- [ read ]
Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2008 Williams & Wilkins.
More About Causes of Hyperkalemia
» Next page: Hyperkalemia (The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
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