Introduction
Background
Hyperkalemia is a potentially life-threatening illness that can be difficult to diagnose because of a paucity of distinctive signs and symptoms. The physician must be quick to consider hyperkalemia in patients who are at risk for this disease process. Because hyperkalemia can lead to sudden death from cardiac arrhythmias, any suggestion of hyperkalemia requires an immediate ECG to ascertain whether electrocardiographic signs of electrolyte imbalance are present.
Pathophysiology
Potassium is a major ion of the body. Nearly 98% of potassium is intracellular, with the concentration gradient maintained by the sodium- and potassium-activated adenosine triphosphatase (Na+/K+ –ATPase) pump. The ratio of intracellular to extracellular potassium is important in determining the cellular membrane potential. Small changes in the extracellular potassium level can have profound effects on the function of the cardiovascular and neuromuscular systems. The normal potassium level is 3.5-5.0 mEq/L, and total body potassium stores are approximately 50 mEq/kg (3500 mEq in a 70-kg person).
Minute-to-minute levels of potassium are controlled by intracellular to extracellular exchange, mostly by the sodium-potassium pump that is controlled by insulin and beta2 receptors. A balance of GI intake and renal potassium excretion achieves long-term potassium balance.
Hyperkalemia is defined as a potassium level greater than 5.5 mEq/L.1 Ranges are as follows:
- 5.5-6.0 mEq/L - Mild
- 6.1-7.0 mEq/L - Moderate
- 7.0 mEq/L and greater - Severe
Hyperkalemia results from the following:
- Decreased or impaired potassium excretion - As observed with acute or chronic renal failure2 (most common), potassium-sparing diuretics, urinary obstruction, sickle cell disease, Addison disease, and systemic lupus erythematosus (SLE)
- Additions of potassium into extracellular space - As observed with potassium supplements (eg, PO/IV potassium, salt substitutes), rhabdomyolysis, and hemolysis (eg, blood transfusions, burns, tumor lysis)
- Transmembrane shifts (ie, shifting potassium from the intracellular to extracellular space) - As observed with acidosis and medication effects (eg, acute digitalis toxicity, beta-blockers, succinylcholine)
- Factitious or pseudohyperkalemia - As observed with improper blood collection (eg, ischemic blood draw from venipuncture technique), laboratory error, leukocytosis, and thrombocytosis
Frequency
United States
Hyperkalemia is diagnosed in up to 8% of hospitalized patients.
Mortality/Morbidity
- The primary cause of morbidity and death is potassium's effect on cardiac function.3
- The mortality rate can be as high as 67% if severe hyperkalemia is not treated rapidly.4
Sex
The male-to-female ratio is 1:1.
Clinical
History
- Hyperkalemia can be difficult to diagnose clinically because complaints may be vague. The history is most valuable in identifying conditions that may predispose to hyperkalemia.
- Hyperkalemia frequently is discovered as an incidental laboratory finding.
- Cardiac and neurologic symptoms predominate.
- Patients may be asymptomatic or report the following:
- Generalized fatigue
- Weakness
- Paresthesias
- Paralysis
- Palpitations
- Hyperkalemia is suggested in any patient with a predisposition toward elevated potassium level. Potential potassium level elevation is observed in the following:
- Acute or chronic renal failure, especially in patients who are on dialysis
- Trauma, including crush injuries (rhabdomyolysis), or burns
- Ingestion of foods high in potassium (eg, bananas, oranges, high-protein diets, tomatoes, salt substitutes). This alone is not likely to cause clinically significant hyperkalemia in most people; it is often a contributing factor to an acute potassium elevation.
- Medications - Potassium supplements, potassium-sparing diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), beta-blockers, digoxin, succinylcholine, and digitalis glycoside
- Medication combinations (ie, spironolactone, ACE inhibitors)5
- Redistribution - Metabolic acidosis (diabetic ketoacidosis [DKA]), catabolic states
Physical
- Evaluation of vital signs is essential to determine hemodynamic stability and presence of cardiac arrhythmias related to the hyperkalemia.1
- Cardiac examination may reveal extrasystoles, pauses, or bradycardia.
- Neurologic examination may reveal diminished deep tendon reflexes or decreased motor strength.
- In rare cases, muscular paralysis and hypoventilation may be observed.
- Search for the stigmata of renal failure, such as edema, skin changes, and dialysis sites.
- Look for signs of trauma that could put the patient at risk for rhabdomyolysis.
Causes
- Pseudohyperkalemia
- Hemolysis (in laboratory tube) most common
- Thrombocytosis
- Leukocytosis
- Venipuncture technique (ie, ischemic blood draw from prolonged tourniquet application)
- Redistribution
- Acidosis
- Insulin deficiency
- Beta-blocker drugs
- Acute digoxin intoxication or overdose
- Succinylcholine
- Arginine hydrochloride
- Hyperkalemic familial periodic paralysis
- Excessive endogenous potassium load
- Hemolysis
- Rhabdomyolysis
- Internal hemorrhage
- Excessive exogenous potassium load
- Parenteral administration
- Excess in diet
- Potassium supplements
- Salt substitutes
- Diminished potassium excretion
- Decreased glomerular filtration rate (eg, acute or end-stage chronic renal failure)
- Decreased mineral corticoid activity
- Defect in tubular secretion (eg, renal tubular acidosis II and IV)
- Drugs (eg, NSAIDs, cyclosporine, potassium-sparing diuretics)
- Laboratory error6
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References
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Further Reading
Keywords
hyperkalemia, high potassium level, electrolyte imbalance, sodium-potassium pump, potassium level greater than 5.5 mEq/L, acute renal failure, chronic renal failure, potassium-sparing diuretics, urinary obstruction, sickle cell disease, Addison disease, systemic lupus erythematosus, SLE, rhabdomyolysis, hemolysis, acidosis, acute digitalis toxicity, beta-blockers toxicity, succinylcholine toxicity, pseudohyperkalemia
