Potassium Serum

Potassium is the major intracellular cation, with a 20 fold greater concentration in the cells than in the extracellular fluid. Only 2% of total body potassium circulates in the plasma. The sodium potassium ATPase pump is largely responsible for maintaining this important ratio. The kidneys are also important in regulating potassium balance. Proximal tubules reabsorb nearly all of the filtered potassium. Under the influence of aldosterone, additional potassium is secreted by the distal tubules and collecting ducts in exchange for sodium. Maintaining normal potassium levels is important for regulation of neuromuscular excitability, cardiac contractility and rhythm, extracellular volume, and acid base balance.

Hypokalemia is defined as a plasma potassium concentration less than 3 meq/L. The primary mechanisms are excessive GI or urinary loss of potassium, increased cellular uptake, or inadequate dietary intake. GI loss results from vomiting, diarrhea, gastric suction, or intestinal fistula discharge. Diuretics, such as thiazides and furosemide, promote potassium secretion in the distal tubules. Kidney disorders, such as renal tubular acidosis, cause excessive urinary loss of potassium. Hyperaldosteronism leads to excessive urinary secretion of potassium and metabolic acidosis. Hypomagnesemia causes hypokalemia by promoting both urinary and fecal loss of potassium. Magnesium deficiency diminishes sodium potassium ATPase activity and enhances aldosterone secretion. Alkalemia and insulin are the two major causes of increased cellular uptake of potassium. Alkalemia promotes intracellular loss of hydrogen ion. To preserve electroneutrality, both potassium and sodium enter cells. Plasma potassium decreases by 0.4 meq/L for every 0.1 unit rise in pH. Insulin promotes the entry of potassium into muscle and hepatocytes. Reduced dietary intake of potassium is a rare cause of hypokalemia, but may be an important factor in patients taking diuretics.

Hyperkalemia occurs frequently in hospitalized patients with a reported incidence of 1 to 10%. A recent article investigated the causes of 242 episodes of hyperkalemia in 206 inpatients at the University of Pittsburgh Medical Center between February 15 and June 30, 1996 (Arch Intern Med 1998; 158: 917-24). Hyperkalemia was defined as a critical plasma potassium level of 6 meq/L or more. The incidence of hyperkalemia in this study was 2.3%. Approximately 2 hyperkalemic episodes occurred per day during the study period. Most of the elevated potassium levels fell between 6.0 and 7.1 meq/L, but a few values were as high as 9.0 meq/L. Further investigation revealed that most cases of hyperkalemia were multifactorial in origin.



% of Cases

Renal failure




Potassium supplements/ TPN




Cyclosporine/ Tacrolimus


Beta Blockers




ACE inhibitors






K sparing diuretics










Penicillin G


RBC transfusion




Renal failure was present in more than two thirds of the patients. Hyperglycemia was the second most common contributor to hyperkalemia. Medications contributed to the development of hyperkalemia in 63% of cases. The drugs most often implicated are listed in the table. Heparin causes hyperkalemia by suppressing aldosterone.

Another recent study revealed that 194 of 1818 (11%) medical outpatients using angiotensin converting enzyme (ACE) inhibitors developed hyperkalemia, which was defined as a potassium level above 5.1 meq/L (Arch Intern Med 1998; 158:26-32). The majority of patients had potassium levels between 5.1 and 5.5 meq/L, but one fifth of the patients had higher levels. Independent risk factors for developing hyperkalemia included a serum creatinine level above 1.5 mg/dL, BUN greater than 18 mg/dL, congestive heart failure, and the use of long acting ACE inhibitors. Patients over the age of 70 with a BUN of 25 mg/dL or higher were more likely to develop severe hyperkalemia (potassium > 6.0 meq/L).

Hyperkalemia can cause muscle weakness by decreasing the ratio of intra to extracellular potassium, which alters neuromuscular conduction. Muscle weakness does not usually develop until plasma potassium reaches 8 meq/L. Hyperkalemia disturbs cardiac conduction, which can cause arrhythmias. Plasma potassium levels between 6 and 7 meq/L may alter the ECG, while levels greater than 10 meq/L may precipitate cardiac arrest.

Factitious causes of hyperkalemia include:

  • In vitro hemolysis
  • Traumatic phlebotomy
  • Too small bore of needle
  • Butterfly needle w/ excessive syringe pressure
  • Vacutainer tubes placed directly on large bore catheter
  • Collection with syringe and injection into Vacutainer tubes
  • Elevated platelet count

0.15 mEq/L increase for every 100,000 cells/uL increase

  • Elevated leukocyte count
  • Contamination with IV fluids
  • Contamination with anticoagulant (K3EDTA concentration exceeds 15 mEq/L)
  • Aged specimens

More accelerated at 4oC than at 25oC

Serum sitting on clot

Respun serum separator tube

Plasma is the preferred specimen for patients with platelet counts greater than 600,000/uL. Erroneously high potassium results are also produced by centrifugation of SST tubes in fixed angle centrifuges. Under these conditions, the separation gel does not form a complete barrier and potassium leaks out of red blood cells into the plasma during specimen storage.

Reference range is 3.6 to 5.0 mEq/L (Vitros analyzer). Levels <3.0 and >6.0 mEq/L are considered critical values. Serum potassium levels run slightly higher (0.4 mEq/L) than plasma levels, even in patients with normal platelet counts.

Specimen requirement is one SST tube of blood. Hemolysis should be avoided because it will cause false elevation of potassium.

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