Hyperkalemia is a condition caused by an abnormally high concentration of potassium in the blood. Potassium is a key element in contraction of muscles (including the heart) and for the functioning of many complicated proteins (enzymes). Potassium is found primarily in the skeletal muscle and bone, and participates with sodium to contribute to the normal flow between the body fluids and the cells of the body (homeostasis). The concentration of potassium in the body is regulated by the kidneys, and balance is maintained through excretion in urine. When the kidneys are functioning normally, the amount of potassium in the diet is usually sufficient for use by the body and the excess is excreted. Chemical and hormonal influences also help regulate the internal potassium balance. When hyperkalemia occurs, there is an imbalance resulting from a dysfunction of these normal processes.
Normally, 98% of the potassium in the body is found in the cells of various tissues, while only about 2% is circulating in the blood. When hyperkalemia occurs, it may come about because of an increase in total body potassium or as a result of increased release of potassium from the cells to the blood.
Abnormally high levels of potassium in the blood or urine suggest the presence of another underlying medical condition. Because potassium helps to regulate muscle activity, including the activity of heart (cardiac) muscle, hyperkalemia needs to be taken seriously.
Some individuals with hyperkalemia may not have symptoms (asymptomatic). Occasionally, symptoms may include nausea, irregular heartbeat and/or slow and weak pulse. The latter two of these signs indicate a potential emergency. Blood potassium may be high and the pulse may be weak.
Because hyperkalemia affects the heart, examination by electrocardiography (ECG) is essential. An ECG may pick up abnormalities of the heartbeat including several potentially life-threatening conditions, such as slower-than-normal rhythms (bradycardia), partial-to-complete heart blocks, and an uncontrolled rapid heart beat (fibrillation). A type of paralysis in which muscle tone is lacking in the extremities (flaccid paralysis) may be present. Individuals with hyperkalemia may experience a loss of deep tendon reflexes, and difficulties in speaking (phonation) and breathing.
Hyperkalemia is a symptom of some other underlying medical condition. Diseases and disorders that reduce the kidney’s ability to excrete potassium are often the causes of the excess potassium. Such disorders include inflammatory disease of the kidneys (acute tubular nephrosis); acute or chronic kidney failure, excessive acid production (metabolic or diabetic acidosis), or a deficiency of the hormone aldosterone (Addison’s disease). Other causes may include multiple transfusions of stored blood, internal acid-base disturbances, sickle-cell anemia, excess sugar in the blood (hyperglycemia), and excessive dietary intake of potassium. The use of drugs that act in opposition to the hormone aldosterone (aldosterone antagonists), muscle relaxant succinylcholine, extensive burns, crushing injuries that cause bleeding into surrounding soft tissue (e.g., fatty tissue) or conditions causing bleeding in the gastrointestinal tract may also cause hyperkalemia.
Males are more prone to hyperkalemia than are women. It is also more likely to occur among the very aged and the very young than among those at mid-life. Individuals with kidney malfunction associated with diabetes (diabetic nephropathy or interstitial renal disease), an abnormally low level of the enzyme renin (hyporeninemia), or abnormally low levels of the hormone aldosterone (hypoaldosteronism), may increase the risk for hyperkalemia.
Indications of hyperkalemia include a slow pulse in combination with high levels of potassium in the blood and particular patterns of ECG changes.
Treatment of acute hyperkalemia may require intravenous calcium as a temporary measure . Since such treatment lasts for only about an hour, other measures are required. Depending upon the cause of hyperkalemia, glucose and insulin may be administered intravenously. Diuretics or sodium polystyrene may be administered to increase the body's excretion of potassium. Dialysis may also be required but only after more conservative treatments have failed.
Periodic paralysis may be treated with the drug albuterol. Calcium gluconate may be administered to reverse certain heart abnormalities. If no ECG abnormalities are present, the drug sorbitrol may be prescribed. Other treatment is symptomatic and supportive.
Information on current clinical trials is posted on the Internet at www.clinicaltrials.gov. All studies receiving U.S. government funding, and some supported by private industry, are posted on this government web site.
For information about clinical trials being conducted at the NIH Clinical Center in Bethesda, MD, contact the NIH Patient Recruitment Office:
Tollfree: (800) 411-1222
TTY: (866) 411-1010
For information about clinical trials sponsored by private sources, contact:
Beers MH, Berkow R, eds. The Merck Manual, 17th ed. Whitehouse Station, NJ: Merck Research Laboratories; 1999:138-39.
Singer GG, Brenner BM. Fluid and Electrolyte Disturbances. In: Fauci AS, Braunwald E, Isselbacher KJ, et al., eds. Harrison’s Principles of Internal Medicine. 14th ed. McGraw-Hill Companies. New York, NY; 1998:274-76.
Berkow R, ed. The Merck Manual-Home Edition. Whitehouse Station, NJ: Merck Research Laboratories; 1997:670-71.
Kokko JP. Disturbances in Potassium Balance. In: Bennett JC, Plum F. Eds. Cecil Textbook of Medicine. 20th ed. W.B. Saunders Co., Philadelphia, PA; 1996:541-43.
Littmann L, Monroe MH, Kerns WP2nd, et al. Brugada syndrome and “Brugada sign” Clinical spectrum with a guide for the clinician. Am Heat J. 2003;145:768-78.
Sidorov VY, Woods MC, Wikswo JP. Effects of elevated extracellular potassium on the stimulation mechanism ofdiastolic cardiac tissue. Biophys J. 2003;84:3470-79.
Juurlink DN, Mamdani M, Kopp A, et al. Drug-drug interactions among elderly patients hospitalized for drug toxicity. JAMA. 2003;289:1652-58.
Kovacic V, Roguljic L, Kovacic V. Metabolic acidosis of chronically hemodialysed patients. Am J Nephraol. 2003;23:158-64.
Su M, Chu J, Howland MA, et al. Amiodarone attenuates fluoride-induced hyperkalemia in vitro. Acad Emerg Med. 2003;10:105-09.
Muensterer OJ. Hyperkalemic paralysis. Age Ageing. 2003;32:114-15.
Caliskan Y, Kalayoglu-Besisik S, Sargin D, et al. Cyclosporine-associated hyperkalemia: report of four allogenic blood stem-cell transplant cases. Transplantation. 2003;75:1069-72.
Imbriano LJ, Durham JH, Maesaka JK. Treating interdialytic hyperkalemia with fludrocortisone. Semin Dial. 2003;16:5-7.
Mildenberger E, Versmold HT. Pathogenesis and therapy on non-oliguric hyperkalemia of the premature infant. Eur J Pediatr. 2002;161:415-22.
Gennari FJ, Segal AS. Hyperkalemia: An adaptive response on chronic renal insufficiency. Kidney Int. 2002;62:1-9.
Somers MP, Brady WJ, Perron AD, et al. The prominent T wave: electrocardiographic differential diagnosis. Am J Emerg Med. 2002;20:243-51.
Baz EM, Kanazi GE, Mahfouz RA, et al. An unusual case of hyperkalaemic-induced cardiac arrest in a paediatric patient during transfusion of a “fresh” 6-day-old blood unit. Transfus Med. 2002;12:383-86.
Kim HJ, Han SW. Therapeutic approach to hyperkalemia. Nephron. 2002;92 Suppl 1:33-40.
Helfrich E, de Vries TW, van Roon EN. Salbutamol for hyperkaelemia in children. Acta Paediatr. 2001;90:1213-16.
FROM THE INTERNET
Lederer E, Erbeck K. Hyperkalemia. eMedicine. Last Updated: April 16, 2003. 26pp.
Koren A. Hyperkalemia. In: Medical Encyclopedia. MedlinePlus. Update date 1/19/2002. 4pp.
Garth D. Hyperkalemia. eMedicine. Last Updated: July 25, 2001. 14pp.
Go Ask Alice! Columbia University’s Health Question & Answer Internet Service. High Potassium (Hyperkalemia). Feb 26, 1999. 2pp.