Hyperkalemia
 |
Resident Survival Guide |
For patient information, click here
|
Hyperkalemia Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Hyperkalemia On the Web |
|
American Roentgen Ray Society Images of Hyperkalemia |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [2]; Raviteja Guddeti, M.B.B.S. [3]
Synonyms and keywords: Hyperkalaemia.
Overview
Hyperkalemia (AE) or Hyperkalaemia (BE) is an elevated blood level (above 5.0 mmol/L) of the electrolyte potassium. The prefix hyper- means high (contrast with hypo-, meaning low). The middle kal refers to kalium, which is Latin for potassium. The end portion of the word, -emia, means "in the blood". Extreme degrees of hyperkalemia are considered a medical emergency due to the risk of potentially fatal arrhythmias
Pathophysiology
Potassium is the most abundant intracellular cation. It is critically important for many physiologic processes, including maintenance of cellular membrane potential, homeostasis of cell volume, and transmission of action potentials in nerve cells. Its main dietary sources are vegetables (tomato and potato), fruits (orange and banana) and meat. Elimination is through the gastrointestinal tract and the kidney.
The renal elimination of potassium is passive (through the glomeruli), and resorption is active in the proximal tubule and the ascending limb of the loop of Henle. There is active excretion of potassium in the distal tubule and the collecting duct; both are controlled by aldosterone.
Hyperkalemia develops when there is excessive production (oral intake, tissue breakdown) or ineffective elimination of potassium. Ineffective elimination can be hormonal (inaldosterone deficiency) or due to causes in the renal parenchyma that impair excretion.
Increased extracellular potassium levels result in depolarization of the membrane potentials of cells. This depolarization opens some voltage-gated sodium channels, but not enough to generate an action potential. After a short while, the open sodium channels inactivate and become refractory, increasing the threshold to generate an action potential. This leads to the impairment of neuromuscular, cardiac, and gastrointestinal organ systems. Of most concern is the impairment of cardiac conduction which can result in ventricular fibrillation or asystole.
Patients with the rare hereditary condition of hyperkalemic periodic paralysis appear to have a heightened sensitivity of muscular symptoms that are associated with transient elevation of potassium levels. Episodes of muscle weakness and spasms can be precipitated by exercise or fasting in these subjects.==[[Hyperkalemia ==Causes==
|
Resident Survival Guide |
|
Hyperkalemia Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Hyperkalemia On the Web |
|
American Roentgen Ray Society Images of Hyperkalemia |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [4]; Associate Editor(s)-In-Chief: Priyamvada Singh, M.B.B.S. [5]; Raviteja Guddeti, M.B.B.S. [6]
Causes
Common Causes
- ACE inhibitors
- Acidosis
- Addisonian crisis
- Beta blockers
- Blood transfusion and complications
- Cirrhosis
- Diabetic nephropathy
- Increased ingestion of high potassium foods
- Malnutrition
- Renal tubular acidosis
- Renal failure
Causes by Organ System
- ↑ Sevastos N et al. (2006) Pseudohyperkalemia in serum: the phenomenon and its clinical magnitude. J Lab Clin Med, 147(3):139-44; PMID 16503244.
- ↑ Don BR et al. (1990) Pseudohyperkalemia caused by fist clenching during phlebotomy. N Engl J Med, 322(18):1290-2; PMID 2325722.
- ↑ Iolascon A et al. (1999) Familial pseudohyperkalemia maps to the same locus as dehydrated hereditary stomatocytosis. Blood, 93(9):3120-3; PMID 10216110.