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| {{Infobox_Disease | | | __NOTOC__ |
| Name = Hypokalemia |
| | {| class="infobox" style="float:right;" |
| Image = K-TableImage.png |
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| Caption = [[Potassium]] |
| | | <figure-inline><figure-inline>[[File:Siren.gif|link=Hypokalemia resident survival guide|41x41px]]</figure-inline></figure-inline>|| <br> || <br> |
| DiseasesDB = 6445 |
| | | [[Hypokalemia resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']] |
| ICD10 = {{ICD10|E|87|6|e|70}} |
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| ICD9 = {{ICD9|276.8}} |
| | {{Hypokalemia}} |
| ICDO = |
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| OMIM = |
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| MedlinePlus = 000479 |
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| MeshID = D007008 |
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| }} | |
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| {{SI}}
| | '''For patient information on this page, click [[Hypokalemia (patient information)|here]]''' |
| {{CMG}}'''; Associate Editor-In-Chief:''' {{CZ}}; '''Assistant Editor(s)-In-Chief:''' [[User:Jack Khouri|Jack Khouri]]
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| ==Overview==
| | {{CMG}}'''; Associate Editor-In-Chief:''' {{CZ}}; {{AIDA}} [[User:Aditya Govindavarjhulla|Aditya Govindavarjhulla, M.B.B.S.]] [mailto:agovi@wikidoc.org] ; '''Assistant Editor(s)-In-Chief:''' [[User:Jack Khouri|Jack Khouri]] |
| '''Hypokalemia''' is a potentially fatal condition in which the body fails to retain sufficient [[potassium]] to maintain health. It is defined as a serum potassium level below 3.5 mEq/L. The condition is also known as '''potassium deficiency'''. The prefix ''hypo-'' means low (contrast with ''hyper-'', meaning high). The middle ''kal'' refers to ''kalium'', which is Neo-Latin for potassium. The end portion of the word, ''-emia'', means "in the blood" (note, however, that hypokalemia is usually indicative of a ''systemic'' potassium deficit). | |
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| == Potassium Homeostasis and the role of the kidney ==
| | {{SK}} Hypokalaemia; potassium levels low (plasma or serum); potassium - low; low blood potassium; potassium depletion |
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| Normally, total potassium excretion in stool is low and most ingested K is absorbed. The kidney is the main regulator of Potassium balance through excretion (the kidney excretes 90-95% of dietary potassium). At the glomerulus, potassium is freely filtered and then largely reabsorbed in the proximal tubule and thick ascending loop of Henle (>60 % of filtered potassium). The cortical collecting duct receives 10–15% of filtered potassium and constitutes the kidney’s major site of potassium excretion. Potassium excretion at the cortical collecting duct depends on the amount of Sodium delivered there and the activity of aldosterone. The absorption of sodium by the principal cells of the cortical collecting ducts is mediated by the apical epithelial sodium channels (ENaC); when the amount of sodium delivered to the cortical collecting duct is very high, the absorption of sodium increases without concomitant absorption of the accompanying anions (eg, bicarbonates and chloride ions) which are not easy to absorb. This physiologic process causes the formation of a negative charge within the cortical collecting duct lumen causing potassium and proton secretion. Aldosterone increases sodium absorption at the cortical collecting duct by means of enhancing the activity of Na-K-ATPase pumps, and augmenting the number of the ENaC channels.
| | ==[[Hypokalemia overview|Overview]]== |
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| ==Pathophysiology== | | ==[[Hypokalemia historical perspective|Historical Perspective]]== |
| === The physiologic role of potassium ===
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| Potassium is essential for many body functions, especially excitable cells such as [[muscle]] and [[nerve]] cells. Diet, mostly meats and fruits, is the major source of potassium for the body. Potassium is the principal [[intracellular]] [[cation]], with a concentration of about 145 mEq/L, as compared with a normal value of 3.5 - 5.0 mEq/L in [[extracellular]] fluid, including blood. More than 98% of the body's potassium is intracellular; measuring it from a blood sample is relatively insensitive, with small fluctuations in the blood corresponding to very large changes in the total bodily reservoir of potassium.
| | ==[[Hypokalemia pathophysiology|Pathophysiology]]== |
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| === The cellular effect of Hypokalemia === | | ==[[Hypokalemia causes|Causes]]== |
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| The electrochemical gradient of potassium between intracellular and extracellular space is essential for nerve function; in particular, potassium is needed to repolarize the [[cell membrane]] to a resting state after an [[action potential]] has passed. Decreased potassium levels in the extracellular space will cause hyperpolarization of the resting membrane potential ie, it becomes more negative. This [[hyperpolarization (biology)|hyperpolarization]] is caused by the effect of the altered potassium gradient on [[resting membrane potential]] as defined by the [[Goldman equation]]. As a result, the cell becomes less sensitive to excitation and a greater than normal stimulus is required for depolarization of the membrane in order to initiate an action potential. Clinically, this membrane hyperpolarization results in muscle flaccid paralysis, rhabdomyolysis (in severe hypokalemia) and paralytic ileus. At the Renal level, hypokalemia can cause metabolic alkalosis due to potassium/proton exchange across the cells and nephrogenic diabetes insipidus.
| | ==[[Hypokalemia differential diagnosis|Differentiating Hypokalemia from other Diseases]]== |
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| | ==[[Hypokalemia epidemiology and demographics|Epidemiology and Demographics]]== |
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| ==Causes== | | ==[[Hypokalemia risk factors|Risk Factors]]== |
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| Hypokalemia can be the consequence of decreased ingestion (rare), increased losses (GI or renal) or transcellular shift from the extracellular to the intracellular compartment (insulin). | | ==[[Hypokalemia natural history|Natural History, Complications and Prognosis]]== |
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| * Perhaps the most obvious cause is insufficient [[eating|consumption]] of potassium (that is, a low-potassium diet). However, without excessive potassium loss from the body, this is a rare cause of hypokalemia. Alcoholism, anorexia nervosa, dental problems and dysphagia can all impair food intake and cause hypokalemia. In the hospital setting, hypokalemia can present in patients on total parenteral nutrition.
| | ==[[Hypokalemia Diagnosis|Diagnosis]]== |
| | [[Hypokalemia laboratory findings#Diagnostic Algorithm|Diagnostic Algorithm]] | [[Hypokalemia history and symptoms | History and Symptoms]] | [[Hypokalemia physical examination|Physical Examination]] | [[Hypokalemia laboratory findings | Laboratory Findings]] | [[Hypokalemia electrocardiogram | Electrocardiogram]] | [[Hypokalemia other diagnostic studies|Other Diagnostic Studies]] |
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| | ==[[Hypokalemia treatment|Treatment]]== |
| * Excessive loss of potassium, often associated with excess [[water]] loss, which "flushes" potassium out of the body. Typically, this is a consequence of [[vomiting]], [[diarrhea]], or excessive [[perspiration]].
| | [[Hypokalemia medical therapy| Medical Therapy]] | [[Hypokalemia primary prevention|Primary Prevention]] | [[Hypokalemia secondary prevention|Secondary Prevention]] | [[Hypokalemia cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Hypokalemia future or investigational therapies|Future or Investigational Therapies]] |
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| * Certain [[medication]]s can accelerate the removal of potassium from the body; including [[thiazide diuretic]]s, such as [[hydrochlorothiazide]]; [[loop diuretic]]s, such as [[furosemide]]; as well as various [[laxative]]s. The antifungal [[amphotericin B]] has also been associated with hypokalemia.
| | ==Case Studies== |
| | [[Hypokalemia case study one|Case #1]] |
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| * A special case of potassium loss occurs with [[DKA|diabetic ketoacidosis]]. In addition to urinary losses from [[polyuria]] and volume contraction, there is also obligate loss of potassium from kidney tubules as a [[cationic]] partner to the negatively charged [[ketone]], β-hydroxybutyrate.
| | ==Related Chapters== |
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| * [[Hypomagnesemia]] can cause hypokalemia. [[Magnesium]] is required for adequate processing of potassium. This may become evident when hypokalemia persists despite potassium supplementation. Other electrolyte abnormalities may also be present.
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| * Disease states that lead to abnormally high [[aldosterone]] levels can cause hypertension and excessive urinary losses of potassium. These include [[renal artery stenosis]] and tumors (generally non-malignant) of the [[adrenal]] glands. Hypertension and hypokalemia can also be seen with a deficiency of the 11β-hydroxylase enzyme which allows cortisol to stimulate aldosterone receptors. This deficiency can either be congenital or caused by consumption of [[glycyrrhizin]], which is contained in extract of licorice, sometimes found in [[Herbal supplements]], candies and chewing tobacco.
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| * Rare [[hereditary]] defects of renal salt transporters, such as [[Bartter syndrome]] or [[Gitelman syndrome]] can cause hypokalemia, in a manner similar to that of diuretics.
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| * Rare [[hereditary]] defects of muscular ion channels and transporters that cause [[hypokalemic periodic paralysis]] can precipitate occasional attacks of severe hypokalemia and muscle weakness. These defects cause a heightened sensitivity to [[catechols]] and/or [[insulin]] and/or [[thyroid hormone]] that lead to sudden influx of potassium from the extracellular fluid into the muscle cells.
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| * Transcellular potassium shift to the intracellular space by beta-agonist drugs or insulin can cause hypokalemia.
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| ==Pathophysiology of Hypokalemic Heart Arrythmias== | |
| Potassium is essential to the normal muscular function, in both voluntary (i.e skeletal muscle, e.g. the arms and hands) and involuntary muscle (i.e. smooth muscle in the intestines or cardiac muscle in the heart). Severe abnormalities in potassium levels can seriously disrupt [[heart|cardiac function]], even to the point of causing [[cardiac arrest]] and [[death]]. As explained above, hypokalemia makes the resting potential of potassium [E(K)] more negative. In certain conditions, this will make cells less excitable. However, in the heart, it causes myocytes to become hyperexcitable. This is due to two independent effects that may lead to aberrant cardiac conduction and subsequent arrhythmia:
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| #There are more inactivated sodium (Na) channels available to fire, and
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| #The overall potassium permeability of the ventricle is reduced (perhaps by the loss of a direct effect of extracellular potassium on some of the potassium channels), which can delay ventricular repolarization.
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| == Differential Diagnosis<ref>Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:89</ref><ref>Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:202-203</ref> ==
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| * Acute hyperventilation
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| * [[Pancreatitis|Acute pancreatitis]]
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| * [[Adrenogenital Syndrome]]
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| * Alcoholism with reduced intestinal absorption of potassium
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| * Alkalosis
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| * Anabolic states or conditions of rapid cell multiplication
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| * [[Anorexia Nervosa]]
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| * Barium or toluene ingestion
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| * [[Bartter's Syndrome]]
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| * [[Bilateral Adrenal Hyperplasia]]
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| * [[Bulimia]]
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| * Carbenoxolon
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| * Chewing tobacco
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| * Chloroquine overdose
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| * Chronic glomerulonephritis
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| * [[Inflammatory Bowel Disease|Chronic inflammatory bowel disease]]
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| * Chronic laxative abuse
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| * Clay ingestion
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| * [[Cushing's Syndrome]]
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| * [[Diabetes Insipidus]]
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| * Diabetes with glucosuria
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| * [[Diabetic Ketoacidosis]]
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| * [[Ddx:Diarrhea|Diarrhea]]
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| * Digibind therapy
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| * Drugs
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| * Excessive sweating
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| * "Fad" diets
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| * [[Gastroenteritis]]
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| * Gastrointestinal (GI) fistula
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| * Geophagia
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| * Heart failure
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| * Heriditary pseudohyperaldosteronism
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| * Hyperaldosteronism
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| * Hypokalemic periodic paralysis
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| * Hypomagnesemia
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| * [[Ddx:Hypothermia|Hypothermia]]
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| * Hypovolemia
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| * [[Ileus]]
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| * [[Leukemia]]
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| * Licorice excess
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| * [[Liddle's Syndrome]]
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| * Malabsorption syndrome
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| * [[Hypertension|Malignant hypertension]]
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| * Metabolic acidosis
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| * Mineralacorticoid excess
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| * Nasogastric suction
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| * Polyuric phase after acute renal failure
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| * Postoperative
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| * Pseudohypokalemia
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| * [[Pyloric Stenosis]]
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| * [[Renal Artery Stenosis]]
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| * [[Renal Tubular Acidosis]]
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| * Renin-secreting tumor
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| * Starvation
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| * Steroid therapy
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| * Stress
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| * Total parenteral nutrition
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| * Ureterosigmoidostomy
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| * Villous adenoma of the rectum
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| * [[Ddx:Nausea and Vomiting|Vomiting]]
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| ==Diagnosis==
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| === History and Symptoms ===
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| * [[Ddx:Fatigue|Fatigue]]
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| * Weakness
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| * [[Ddx:Nausea and Vomiting|Vomiting]]
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| * [[Ddx:Constipation|Constipation]]
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| * Muscle cramps
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| * Respiratory muscle weakness
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| ==== Heart ====
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| * Hypertension
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| * Life-threatening arhythmias
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| * Heart block
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| * Potentiation of digoxin
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| ==== Other ====
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| * Rhabdomyolysis
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| * Dehydration
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| * Ileus
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| * Hepatic encephalopathy
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| * [[Ddx:Hyperglycemia|Hyperglycemia]]
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| * Nephrogenic diabetes insipidus
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| ===Signs and symptoms===
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| There may be no symptoms at all, but severe hypokalemia may cause:
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| *[[Muscle weakness]] and [[myalgia]]
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| *Increased risk of [[hyponatremia]] with resultant [[mental confusion|confusion]] and [[seizure]]s
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| *Disturbed heart rhythm (ranging from [[Cardiac ectopy|ectopy]] to [[arrhythmias]])
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| *Serious [[arrhythmia]]s
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| == Laboratory Findings ==
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| * Complete blood count (CBC)
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| * Blood urea nitrogen (BUN)/creatinine
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| * Calcium
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| * Magnesium
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| * Glucose
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| * Arterial blood gases
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| * Renin levels
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| * Urinary sodium
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| * Urine potassium
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| * Transtubular potassium gradient
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| ===Electrocardiographic Findings===
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| # ST segment depression, decreased T wave amplitude, prominent U waves
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| #* seen in 78% of patients with a K < 2.7 meq
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| #* seen in 35% of patients with a K > 2.7 and < 3.0
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| #* seen in 10% of patients with a K > 3.0 and < 3.5
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| #* U waves are also prominent in bradycardia and LVH
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| # Prolongation of the QRS duration
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| #* uncommon except in severe hyperkalemia
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| # Increase in the amplitude and duration of the P-wave
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| # Cardiac arrhythmias and AV block
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| # Contrary to popular belief there is not prolongation of the QTc, this is artifactually prolonged due to the U wave. In some cases there is fusion of the T and the U wave making interpretation impossible.
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| <div align="center">
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| <gallery heights="175" widths="175">
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| Image:Hypokalemia.jpg|Long QT interval, ST segment depression, low T waves amplitude and TU wave fusion in a hypokalemic patient.
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| Image:KJcasu18-3.jpg|Consecutive ECGs of a patient with hypokalemia. ECG1
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| </gallery>
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| </div>
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| <div align="center">
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| <gallery heights="117" widths="117">
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| Image:KJcasu18-2.jpg|Consecutive ECGs of a patient with hypokalemia. ECG2
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| Image:KJcasu18-1.jpg|Consecutive ECGs of a patient with hypokalemia. After correction of potassium levels.
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| Image:V10.ht14.jpg|Hypokalemia with LVH. Image courtesy of Dr Jose Ganseman
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| </gallery>
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| </div>
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| ==Treatment==
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| The most important step in severe hypokalemia is removing the cause, such as treating [[diarrhea]] or stopping offending medication.
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| Mild hypokalemia (>3.0 mEq/L) may be treated with oral potassium chloride supplements (Sando-K®, Slow-K®). As this is often part of a poor nutritional intake, potassium-containing foods may be recommended, such as tomatoes, orange oranges or bananas. Both dietary and pharmaceutical supplements are used for people taking diuretic medications (see '''Causes''', above).
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| Severe hypokalemia (<3.0 mEq/L) may require [[intravenous]] supplementation. Typically, [[saline (medicine)|saline]] is used, with 20-40 mEq KCl per liter over 3-4 hours. Giving intravenous potassium at faster rates may predispose to [[ventricular tachycardia]]s and requires intensive monitoring.
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| Difficult or resistant cases of hypokalemia may be amenable to [[amiloride]], a potassium-sparing diuretic, or [[spironolactone]].
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| When replacing potassium intravenously, infusion via central line is encouraged to avoid the frequent occurrence of a burning sensation at the site of a peripheral iv, or the rare occurrence of damage to the vein. When peripheral infusions are necessary, the burning can be reduced by diluting the potassium in larger amounts of IV fluid, or mixing 3 ml of 1% lidocaine to each 10 meq of kcl per 50 ml of IV fluid. The practice of adding lidocaine, however, raises the likelihood of serious medical errors [http://www.ismp.org/newsletters/acutecare/articles/20040212_2.asp].
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| ==See also==
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| * [[Hypomagnesemia]] | | * [[Hypomagnesemia]] |
| * [[Hyperkalemia]] | | * [[Hyperkalemia]] |
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| ==References==
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| {{Reflist}}
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| [[Category:Electrophysiology]] | | [[Category:Electrophysiology]] |
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| [[Category:Intensive care medicine]] | | [[Category:Intensive care medicine]] |
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| [[de:Hypokaliämie]]
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| [[fr:Hypokaliémie]]
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| [[it:Ipokaliemia]]
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| [[pl:Hipokaliemia]]
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| [[pt:Hipocaliémia]]
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| [[ru:Гипокалиемия]]
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| [[sv:Hypokalemi]]
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| [[vi:Hạ kali máu]]
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| [[Category:Inborn errors of metabolism]]
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| {{WikiDoc Help Menu}} | | {{WikiDoc Help Menu}} |
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