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| {{Infobox_Disease | | | __NOTOC__ |
| Name = Hyperkalemia |
| | {| class="infobox" style="float:right;" |
| Image = K-TableImage.png |
| | |- |
| Caption = [[potassium]] |
| | | [[File:Siren.gif|30px|link=Hyperkalemia resident survival guide]]|| <br> || <br> |
| DiseasesDB = 6242 |
| | | [[Hyperkalemia resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']] |
| ICD10 = {{ICD10|E|87|5|e|70}} |
| | |} |
| ICD9 = {{ICD9|276.7}} |
| | {| class="infobox" style="float:right;" |
| ICDO = |
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| OMIM = |
| | | [[File:Critical_pathways_.gif|88px|link=Hyperkalemia critical pathways]]|| <br> || <br> |
| MedlinePlus = |
| | |} |
| MeshID = D006947 |
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| }} | | {{Patient}} |
| {{Hyperkalemia}} | | {{Hyperkalemia}} |
| {{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh@perfuse.org] | | {{CMG}}; {{AE}} [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh13579@gmail.com]; [[Jogeet Singh Sekhon]] |
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| ==Overview==
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| '''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 [[arrhythmia]]s.
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| ==[[Hyperkalemia history and symptoms | History and Symptoms ]]== | | ==[[Hyperkalemia overview|Overview]]== |
| Symptoms are fairly nonspecific, and generally include [[malaise]], [[palpitations]] and [[muscle weakness]]; mild breathlessness may indicate [[metabolic acidosis]], one of the settings in which hyperkalemia may occur. Often, however, the problem is detected during screening [[blood test]]s for a medical disorder, or it only comes to medical attention after complications have developed, such as [[cardiac arrhythmia]] or [[Cardiac arrest|sudden death]].
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| During the medical history taking, a doctor will dwell on [[Nephrology|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 diseases|autoimmune disorders]], may be signs of [[Addison's disease]], itself a medical emergency.
| | ==[[Hyperkalemia historical perspective|Historical Perspective]]== |
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| ==Diagnosis== | | ==[[Hyperkalemia classification|Classification]]== |
| 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. 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.
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| In many cases, [[medical ultrasonography|renal ultrasound]] will be performed, since hyperkalemia is highly suggestive of renal failure.
| | ==[[Hyperkalemia pathophysiology|Pathophysiology]]== |
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| Also, [[electrocardiography]] (EKG/ECG) may be performed to determine if there is a significant risk of cardiac [[arrhythmias]] (see [[#ECG/EKG Findings|ECG/EKG Findings]], below).
| | ==[[Hyperkalemia causes|Causes]]== |
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| ==Differential diagnosis== | | ==[[Hyperkalemia differential diagnosis|Differentiating Hyperkalemia from other Diseases]]== |
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| Causes include:
| | ==[[Hyperkalemia epidemiology and demographics|Epidemiology and Demographics]]== |
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| === Ineffective elimination from the body=== | | ==[[Hyperkalemia risk factors|Risk Factors]]== |
| * [[Renal insufficiency]]
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| * [[Medication]] that interferes with urinary excretion:
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| ** [[ACE inhibitor]]s and [[angiotensin II receptor antagonist|angiotensin receptor blockers]]
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| ** Potassium-sparing [[diuretic]]s (e.g. [[amiloride]] and [[spironolactone]])
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| ** [[Non-steroidal anti-inflammatory drugs|NSAIDs]] such as [[ibuprofen]], [[naproxen]], or [[Celebrex|celecoxib]]
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| ** The [[Immunosuppressive drug#Drugs acting on immunophilins|calcineurin inhibitor]] immunosuppressants [[ciclosporin]] and [[Prograf|tacrolimus]]
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| ** The antibiotic [[trimethoprim]]
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| ** The antiparasitic drug [[pentamidine]]
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| * [[Mineralocorticoid]] deficiency or resistance, such as:
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| ** [[Addison's disease]]
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| ** [[Hypoaldosteronism|Aldosterone deficiency]], including reduced levels due to the blood thinner, [[heparin]]
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| ** Some forms of [[congenital adrenal hyperplasia]]
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| ** Type IV [[renal tubular acidosis]] (resistance of renal tubules to aldosterone)
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| * Gordon's syndrome (“familial hypertension with hyperkalemia”), a rare genetic disorder caused by defective modulators of salt transporters, including the [[thiazide-sensitive Na-Cl cotransporter]].
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| === Excessive release from cells=== | | ==[[Hyperkalemia screening|Screening]]== |
| * [[Rhabdomyolysis]], [[burn (injury)|burns]] or any cause of rapid tissue [[necrosis]], including [[tumor lysis syndrome]]
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| * Massive [[blood transfusion]] or massive [[hemolysis]]
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| * Shifts/transport out of cells caused by [[acidosis]], low [[insulin]] levels, [[beta-blocker]] therapy, [[digoxin]] overdose, or the paralyzing anesthetic [[succinylcholine]]
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| === Excessive intake=== | | ==[[Hyperkalemia natural history, complications, and prognosis|Natural history, Complications and Prognosis]]== |
| * [[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 massive doses of oral KCl supplements.
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| ===Lethal injection=== | | ==Diagnosis== |
| Hyperkalemia is intentionally brought about in an execution by lethal injection, [[potassium chloride]] being the third and last of the three drugs generally administered to cause death, after [[sodium thiopental]] has rendered the subject unconscious, then [[pancuronium bromide]] has been added to cause respiratory collapse.
| | [[Hyperkalemia diagnostic study of choice|Diagnostic study of choice]] | [[Hyperkalemia history and symptoms|History and Symptoms]] | [[Hyperkalemia physical examination|Physical Examination]] | [[Hyperkalemia laboratory findings|Laboratory Findings]] | [[Hyperkalemia electrocardiogram|Electrocardiogram]] | [[Hyperkalemia x ray|X-Ray Findings]] | [[Hyperkalemia echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[Hyperkalemia CT scan|CT-Scan Findings]] | [[Hyperkalemia MRI|MRI Findings]] | [[Hyperkalemia other imaging findings|Other Imaging Findings]] | [[Hyperkalemia other diagnostic studies|Other Diagnostic Studies]] |
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| ===Pseudohyperkalemia===
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| 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 doctors.<ref>Sevastos N et al. (2006) Pseudohyperkalemia in serum: the phenomenon and its clinical magnitude. J Lab Clin Med, 147(3):139-44; PMID 16503244.</ref> Pseudohyperkalemia is typically caused by [[hemolysis]] during [[venipuncture]] (by either excessive vacuum of the blood draw or by a syringe needle that is of too fine a gauge); excessive tournequet time or fist clenching during phlebotomy (which presumably leads to efflux of potassium from the muscle cells into the bloodstream).<ref>Don BR et al. (1990) Pseudohyperkalemia caused by fist clenching during phlebotomy. N Engl J Med, 322(18):1290-2; PMID 2325722.</ref>; or by a delay in the processing of the blood specimen. It can also occur in specimens from patients with abnormally high numbers of [[platelet]]s (>1,000,000/mm³), [[leukocyte]]s (> 100 000/mm³), or [[erythrocyte]]s (hematocrit > 55%). People with "leakier" [[cell membrane]]s have been found, whose blood must be separated immediately to avoid pseudohyperkalemia.<ref>Iolascon A et al. (1999) Familial pseudohyperkalemia maps to the same locus as dehydrated hereditary stomatocytosis. Blood, 93(9):3120-3; PMID 10216110.</ref>
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| ==Complete Differential Diagnosis of Hyperkalemia==
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| === Decreased Renal Potassium Excretion ===
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| * [[Acute Renal Failure]]
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| * [[Addison's Disease]]
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| * Bilateral adrenalectomy
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| * [[Chronic Renal Failure]]
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| * [[Congestive Heart Failure]]
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| * Drugs
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| * Gordon's Syndrome
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| * Graft-versus-host disease of the kidney
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| * Hyporeninemic hypoaldosteronism
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| * Postuterojejunostomy
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| * Primary defect in potassium transport
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| * Renal tubular acidosis
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| * Specific enzyme defect
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| * Tubular unresponsivness
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| === Increased Potassium Cellular Release ===
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| * [[Burns]]
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| * [[Chemotherapy]]
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| * [[Crush Syndrome]]
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| * Depolarizing muscle paralysis
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| * [[Diabetic ketoacidosis]]
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| * [[Drugs]]
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| * Heavy exercise
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| * [[Hyperkalemic periodic paralysis]]
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| * Hyperosmolar states
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| * Hypoinsulinemia
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| * Insulin Deficiency
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| * Intravascular [[hemolysis]]
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| * [[Mannitol]] hyperosmolality
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| * [[Metabolic Acidosis]]
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| * Radiocontrast hyperosmolality
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| * [[Respiratory Acidosis]]
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| * [[Rhabdomyolysis]]
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| * Tourniquet Syndrome
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| * [[Trauma]]
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| * [[Tumor Lysis Syndrome]]
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| === Pseudohyperkalemia ===
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| * Delayed centrifugation hemolysis
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| * Extravascular hemolysis
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| * [[Leukocytosis]]
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| * Rapid aspiration hemolysis
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| * Stagnation hemolysis
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| * [[Thrombocytosis]]
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| === Excess Potassium Intake ===
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| * Dietary excess
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| * IV potassium replacement
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| * KCl
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| * Oral potassium intake
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| * Potassium-containing drugs
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| * Transfusion
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| ==Pathophysiology==
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| 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 potential]]s in [[nerve cell]]s. Its main dietary sources are vegetables (tomato and potato), fruits (orange and banana) and meat. Elimination is through the [[gastrointestinal tract]] and the [[kidney]].
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| 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]].
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| 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. | |
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| Increased extracellular potassium levels result in [[depolarization]] of the membrane potentials of cells. This depolarization opens some [[sodium channel|voltage-gated sodium channel]]s, but not enough to generate an action potential. After a short while, the open sodium channels inactivate and become [[refractory period|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]].
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| 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.
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| === Laboratory Evaluation ===
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| ====Initial====
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| * Calcium
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| * Phosphate
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| * Magnesium
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| * Blood urea nitrogen (BUN)/creatinine
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| ====Extensive Evaluation====
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| * Cortisol
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| * Renin
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| * Aldosterone levels
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| * Transtubular potassium gradient (by assessing potassium+ secretion)
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| ===Electrocardiographic Findings===
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| [[Electrocardiography]] (ECG) is generally done early to identify any influences on the heart, as hyperkalemia may cause fatal [[arrhythmias]]. With moderate hyperkalemia, there is reduction of the size of the P wave and development of tent-shaped T waves. Further hyperkalemia will lead to widening of the [[QRS complex]], that ultimately may become [[sinusoidal]] in 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 [[#Pathophysiology|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.
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| Spcific findings include the following:
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| ====Tall, narrow, and peaked [[T waves]]====
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| * Earliest sign of hyperkalemia
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| * Occurs with K > 5.5 meq/li
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| * Differential diagnosis of this EKG change includes the T wave changes of [[bradycardia]] or [[stroke]]. Prominent [[U wave]]s and [[QTc]] prolongation are more consistent with [[stroke]] than hyperkalemia.
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| ====Intraventricular conduction defect====
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| #* Observed when K > 6.5 meq/li
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| #* There is a modest correlation of the [[QRS]] duration with serum K
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| #* As the K rises, the [[QRS]] complexes may resemble sine waves
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| #* Generally the widening is diffuse and usually there is no resemblance of the morphology to that of either [[LBBB]] or [[RBBB]]
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| ====Decrease of the amplitude of the P wave or an absent P wave====
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| * Decreased [[P wave]] amplitude occurs when the K is > 7.0 meq/li
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| * [[P wave]]s may be absent when the K is > 8.8 meq/li
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| * The impulses are still being generated in the [[SA node]] and are conducted to the ventricles through specialized atrial fibers without depolarizing the atrial muscle
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| * Moderate or sever hyperkalemia can cause [[sinus arrest]] <ref name="pmid16792034">{{cite journal |author=Bonvini RF, Hendiri T, Anwar A |title=Sinus arrest and moderate hyperkalemia |journal=[[Annales De Cardiologie Et D'angéiologie]] |volume=55 |issue=3 |pages=161–3 |year=2006 |month=June |pmid=16792034 |doi= |url= |issn=}}</ref>
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| ====ST segment changes simulating current of injury====
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| * Have been labeled the dialyzable current of injury
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| ====Cardiac arrhythmias: bradyarrhythmias, tachyarrhythmias, atrioventricular conduction defects====
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| * Occurs with severe hyperkalemia, not mild to moderate hyperkalemia
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| <gallery>
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| Image:Hyperkalemia.jpg|Tall, symmetric, narrow based T waves in a hyperkalemic patient.
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| Image:Ecg hyperkaliemie.jpg|A patient's EKG with hyperkalemia.
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| Image:Ecg hyperkaliemie2.jpg|Same patient's EKG during treatment.
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| </gallery>
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| ==Treatment== | | ==Treatment== |
| 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.
| | [[Hyperkalemia medical therapy|Medical Therapy]] | [[Hyperkalemia surgery|Surgery]] | [[Hyperkalemia primary prevention|Primary Prevention]] | [[Hyperkalemia secondary prevention|Secondary Prevention]] | [[Hyperkalemia cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Hyperkalemia future or investigational therapies|Future or Investigational Therapies]] |
| * [[Calcium]] supplementation (calcium gluconate 10% (10ml), preferably through a [[central venous catheter]] as the calcium may cause [[phlebitis]]) does not lower potassium but decreases [[myocardium|myocardial]] excitability, protecting against life threatening [[arrhythmias]].
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| * [[Insulin]] (e.g. intravenous injection of 10-15u of (short acting) insulin (e.g. Actrapid) {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]].
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| * [[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<sup>+</sup> for Na<sup>+</sup>, thus leading to stimulation of the [[sodium-potassium ATPase]].
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| * [[Salbutamol]] (albuterol, Ventolin<sup>®</sup>) is a β<sub>2</sub>-selective catacholamine that is administered by nebuliser (e.g. 10-20 mg). This drug promotes movement of K into cells, lowering the blood levels.
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| * [[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 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.
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| * Refractory or severe cases may need [[dialysis]] to remove the potassium from the circulation.
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| * 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<sup>®</sup>) or [[hydrochlorothiazide]]).
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| ==See also== | | ==Case Studies== |
| * [[Hypokalemia]]
| | [[Hyperkalemia case study one|Case #1]] |
| * [[Renal failure]]
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| ==References==
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| <references />
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| [[de:Hyperkaliämie]]
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| [[ja:高カリウム血症]]
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