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Hyperkalemia
Classification and external resources

potassium
ICD-10 E87.5
ICD-9 276.7
DiseasesDB 6242
MedlinePlus 001179
eMedicine emerg/261
MeSH D006947

Hyperkalemia (hyper- high; kalium, potassium; -emia, "in the blood") is an elevated blood level of the electrolyte potassium. Extreme hyperkalemia is a medical emergency due to the risk of potentially fatal abnormal heart rhythms (arrhythmia).

Contents

Signs and symptoms

Symptoms are fairly nonspecific and generally include malaise, palpitations and muscle weakness; mild hyperventilation may indicate a compensatory response to metabolic acidosis, which is one of the possible causes of hyperkalemia. Often, however, the problem is detected during screening blood tests for a medical disorder, or it only comes to medical attention after complications have developed, such as cardiac arrhythmia or sudden death.

During the medical history taking, a physician will dwell on kidney disease and medication use (see below), as these are the main causes. The combination of abdominal pain, hypoglycemia and hyperpigmentation, often in the context of a history of other autoimmune disorders, may be signs of Addison's disease, itself a medical emergency.

Diagnosis

In order to gather enough information for diagnosis, the measurement of potassium needs to be repeated, as the elevation can be due to hemolysis in the first sample. The normal serum level of potassium is 3.5 to 5 mEq/L. Generally, blood tests for renal function (creatinine, blood urea nitrogen), glucose and occasionally creatine kinase and cortisol will be performed. Calculating the trans-tubular potassium gradient can sometimes help in distinguishing the cause of the hyperkalemia. Exercise induced hyperkalemia is known as Sperry Syndrome and is prevalent with cross country and marathon runners. Dr Ashley Sperry first diagnosed this condition during the 1993 Iditarod race in Anchorage, Alaska when participants experienced symptoms similar to heart attacks after consuming Inuit beverages with large amounts of potassium and then physically exerting themselves.

In many cases, renal ultrasound will be performed, since hyperkalemia is highly suggestive of renal failure.

Also, electrocardiography (EKG/ECG) may be performed to determine if there is a significant risk of cardiac arrhythmias (see ECG/EKG Findings, below).

Differential diagnosis

Causes include:

Ineffective elimination from the body

Excessive release from cells

Excessive intake

  • Intoxication with salt-substitute, potassium-containing dietary supplements, or potassium chloride (KCl) infusion. Note that for a person with normal kidney function and nothing interfering with normal elimination (see above), hyperkalemia by potassium intoxication would be seen only with large infusions of KCl or oral doses of several hundred milliequivalents of KCl.[1]

Lethal injection

Hyperkalemia is intentionally brought about in an execution by lethal injection, with potassium chloride being the third and last of the three drugs administered to cause death.

Pseudohyperkalemia

Pseudohyperkalemia is a rise in the amount of potassium that occurs due to excessive leakage of potassium from cells, during or after blood is drawn. It is a laboratory artifact rather than a biological abnormality and can be misleading to caregivers.[2] Pseudohyperkalemia is typically caused by hemolysis during venipuncture (by either excessive vacuum of the blood draw or by a collection needle that is of too fine a gauge); excessive tourniquet time or fist clenching during phlebotomy (which presumably leads to efflux of potassium from the muscle cells into the bloodstream);[3] or by a delay in the processing of the blood specimen. It can also occur in specimens from patients with abnormally high numbers of platelets (>500,000/mm³), leukocytes (> 70 000/mm³), or erythrocytes (hematocrit > 55%). People with "leakier" cell membranes have been found, whose blood must be separated immediately to avoid pseudohyperkalemia.[4]

Pathophysiology

Potassium is the most abundant intracellular cation. It is critically important for many physiological 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 (in aldosterone 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.

During extreme exercise, potassium is released from active muscle and the serum potassium rises to a point that would be dangerous at rest. For unclear reasons, it appears as if the high levels of adrenaline and noradrenaline have a protective effect on the cardiac electrophysiology.[5]

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.

ECG findings

With mild to moderate hyperkalemia, there is reduction of the size of the P wave and development of peaked T waves. Severe hyperkalemia results in a widening of the QRS complex, and the EKG complex can evolve to a sinusoidal shape. There appears to be a direct effect of elevated potassium on some of the potassium channels that increases their activity and speeds membrane repolarization. Also, (as noted above), hyperkalemia causes an overall membrane depolarization that inactivates many sodium channels. The faster repolarization of the cardiac action potential causes the tenting of the T waves, and the inactivation of sodium channels causes a sluggish conduction of the electrical wave around the heart, which leads to smaller P waves and widening of the QRS complex.

The serum K+ concentration at which electrocardiographic changes develop is somewhat variable.[6][7] Although the factors influencing the effect of serum potassium levels on cardiac electrophysiology are not entirely understood, the concentrations of other electrolytes, as well as levels of catecholamines, play a major role.[8][9]

Treatment

Acute: When arrhythmias occur, or when potassium levels exceed 6.5 mmol/l, emergency lowering of potassium levels is mandated. Several agents are used to lower K levels. Choice depends on the degree and cause of the hyperkalemia, and other aspects of the patient's condition.

  • Calcium supplementation (calcium gluconate 10% (10ml), preferably through a central venous catheter as the calcium may cause phlebitis) does not lower potassium but decreases myocardial excitability, protecting against life threatening arrhythmias.
  • Insulin (e.g. intravenous injection of 10-15u of regular insulin {along with 50ml of 50% dextrose to prevent hypoglycemia}) will lead to a shift of potassium ions into cells, secondary to increased activity of the sodium-potassium ATPase.
  • Bicarbonate therapy (e.g. 1 ampule (45mEq) infused over 5 minutes) is effective in cases of metabolic acidosis. The bicarbonate ion will stimulate an exchange of cellular H+ for Na+, thus leading to stimulation of the sodium-potassium ATPase.
  • Salbutamol (albuterol, Ventolin) is a β2-selective catecholamine that is administered by nebulizer (e.g. 10–20 mg). This drug promotes movement of K into cells, lowering the blood levels.
  • Refractory or severe cases may need dialysis to remove the potassium from the circulation.

Prevention:

  • Preventing recurrence of hyperkalemia typically involves reduction of dietary potassium, removal of an offending medication, and/or the addition of a diuretic (such as furosemide (Lasix) or hydrochlorothiazide).
  • Polystyrene sulfonate (Calcium Resonium, Kayexalate) is a binding resin that binds K within the intestine and removes it from the body by defecation. Calcium Resonium (15g three times a day in water) can be given by mouth. Kayexelate (30g) can be given by mouth or as an enema. In both cases, the resin absorbs K within the intestine and carries it out of the body by defecation. This medication may cause diarrhea.

See also

References

  1. ^ Su M, Stork C, Ravuri S, et al. (2001). "Sustained-release potassium chloride overdose". J. Toxicol. Clin. Toxicol. 39 (6): 641–8. doi:10.1081/CLT-100108499. PMID 11762675. 
  2. ^ Sevastos, N; Theodossiades, G; Efstathiou, S; Papatheodoridis, GV; Manesis, E; Archimandritis, AJ (March 2006). "Pseudohyperkalemia in serum: the phenomenon and its clinical magnitude". J. Lab. Clin. Med. 147 (3): 139–144. doi:10.1016/j.lab.2005.11.008. PMID 16503244. 
  3. ^ Don, BR; Sebastian, A; Cheitlin, M; Christiansen, M; Schambelan, M (May 1990). "Pseudohyperkalemia caused by fist clenching during phlebotomy". N. Engl. J. Med. 322 (18): 1290–1292. PMID 2325722. 
  4. ^ Iolascon, A; Stewart, GW; Ajetunmobi, JF; et al. (May 1999). "Familial pseudohyperkalemia maps to the same locus as dehydrated hereditary stomatocytosis (hereditary xerocytosis)". Blood 93 (9): 3120–3123. PMID 10216110. http://www.bloodjournal.org/cgi/pmidlookup?view=long&pmid=10216110. 
  5. ^ Lindinger, MI (April 1995). "Potassium regulation during exercise and recovery in humans: implications for skeletal and cardiac muscle". J. Mol. Cell. Cardiol. 27 (4): 1011–1022. doi:10.1016/0022-2828(95)90070-5. PMID 7563098. http://linkinghub.elsevier.com/retrieve/pii/0022-2828(95)90070-5. 
  6. ^ Wrenn KD, Slovis CM, Slovis BS. The ability of physicians to predict hyperkalemia from the ECG. Ann Emerg Med 20: 1229-1232, 1991. PMID 1952310
  7. ^ Aslam S, Friedman EA, Ifudu O. Electrocardiography is unreliable in detecting potentially lethal hyperkalaemia in haemodialysis patients. Nephrol Dial Transplant 17: 1639-1642, 2002. PMID 12198216
  8. ^ Surawicz B. Electrolytes and the Electrocardiogram. Am J Cardiol 12: 656-662, 1963. PMID 5338052
  9. ^ Leitch SP, Patterson DJ. Interactive effects of K+, acidosis, and catecholamines on isolated rabbit heart: implications for exercise. J Appl Physiol 77: 1164-1171, 1994. PMID 7836118

External links

USDA National Nutrient Database for Standard Reference, Release 20]

Simple English

Hyperkalemia is a medical term to indicate that the level of potassium in the blood is too high. Depending on the level of potassium in the blood, this can be a medical emergency. A level that is too high can lead to abnormal hearth rhythms.

Many medications can cause hyperkalemia, and it is much more likely to occur in people kidney problems.

Although hyperkalemia often doesn't cause symptoms, doctors worry about hyperkalemia because it can cause a sudden change of heart rhythm in people who had not been having any symptoms. These abnormal heart rhythms can be deadly.

In the cases where death penalty is carried out using lethal injection, a hyperkalemia may be provoked atificially. Some of the mixtures used in the injections contain potassium chloride which will raise the level of potassium in the blood considerably.








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