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 the normal 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.
Causes
There are a number of possible causes of potassium imbalance.
Hypokalemia
Because many foods contain potassium, hypokalemia rarely results from a dietary deficiency. Instead, potassium loss results from:
❑ excessive GI or urinary losses, such as vomiting, gastric suction, diarrhea, dehydration, anorexia, or prologed laxative use
❑ 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 ingestion of licorice, and severe serum magnesium deficiency.
Hyperkalemia
Generally, 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 renal failure; or from 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.
Signs and symptoms
See Clinical features of potassium imbalance.
Diagnosis
❑ Hypokalemia: serum potassium levels less than 3.5 mEq/L.
❑ Hyperkalemia: serum potassium levels greater than 5 mEq/L.
Additional tests may be necessary to determine the underlying cause of the imbalance.
Treatment
Potassium imbalances are treated as follows:
Hypokalemia
Replacement therapy with potassium chloride (I.V. or by mouth) is the primary treatment for hypokalemia. 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.
Hyperkalemia
For the management of 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 a cardiac glycoside.
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 the cells. Infusions should be followed by dextrose 5% in water because an infusion of 10% to 15% glucose will stimulate the secretion of endogenous insulin.
Sodium polystyrene sulfonate (Kayexalate) with 70% sorbitol produces an exchange of sodium ions for potassium ions in the intestine. Hemo-dialysis or peritoneal dialysis also help remove excess potassium.
Special considerations
For hypokalemia:
❑ Check serum potassium and other electrolyte levels in patients who are likely to develop a potassium imbalance and in those requiring potassium replacement; they risk overcorrection to hyperkalemia.
❑ Carefully assess intake and output.
CLINICAL TIP: Remember that the kidneys excrete 80% to 90% of ingested potassium. Never give supplementary potassium to a patient whose urine output is less than 600 ml/day. Also, measure GI loss from suctioning or vomiting.
❑ Administer slow-release potassium or dilute oral potassium supplements in 4 oz (118.3 ml) or more of water or other fluid to reduce gastric and small-bowel irritation.
❑ Determine the patient’s chloride level. As appropriate, give a potassium chloride supplement if the level is low and potassium gluconate if it’s normal.
❑ Give I.V. potassium only after it’s diluted in solution; potassium is irritating to vascular, subcutaneous, and fatty tissues and may cause phlebitis or tissue necrosis if it infiltrates.
❑ Infuse potassium slowly (no more than 20 mEq/L/hour) to prevent hyperkalemia. Never administer it by I.V. push or bolus; it may cause cardiac arrest.
❑ Carefully monitor patients receiving a cardiac glycoside because hypokalemia will enhance its action and may produce signs and symptoms 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, dark green leafy vegetables, milk, dried fruits, apricots, and peanuts.
❑ Monitor cardiac rhythm, and be alert for irregularities.
For hyperkalemia:
❑ As for 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). Watch for signs and symptoms of hypokalemia with prolonged use and of hypoglycemia (muscle weakness, syncope, hunger, and diaphoresis) with repeated insulin and glucose treatment.
❑ Watch for signs of hyperkalemia in predisposed patients, especially those with decreased urine output or those receiving oral or I.V. potassium supplements.
CLINICAL TIP: Administer up 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.
❑ Before giving a blood transfusion, check to see how long ago the blood was donated; older blood cell hemolysis releases potassium. Infuse only fresh blood for patients with average to high serum potassium levels.
❑ Watch for cardiac arrhythmias.
Pictures
Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 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: Handbook of Diseases, Copyright © 2008 Williams & Wilkins.
More About Causes of Hyperkalemia
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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