Sierra Acai Company
Sierra Acai Company
Open 7 Days a Week
MonaVie Independent Distributor
Distributor Training
Shop Online
Enroll Now
Buy Wholesale and maintain an Active status for 2 months and we will refund your $39 Distributor Fee
Friends
Buy Wholesale and maintain an Active status for 2 months and we will refund your $39 Distributor Fee
07-SEPTEMBER-2008 03:17:44 - Hyperkalemia Hyperkalemia Classification and external resources potassium ICD-10 E87.5 ICD-9 276.7 DiseasesDB 6242 MedlinePlus 001179 eMedicine emerg/261 MeSH D006947 Hyperkalemia AE or Hyperkalaemia BE is an elevated blood level of the electrolyte potassium. The prefix hyper- means high contrast with hypo-, meaning low. The middle kal refers to kalium, which is neo-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. Contents 1 Signs and symptoms 2 Diagnosis 3 Differential diagnosis 3.1 Ineffective elimination from the body 3.2 Excessive release from cells 3.3 Excessive intake 3.4 Lethal injection 3.5 Pseudohyperkalemia 4 Pathophysiology 5 ECG findings 6 Treatment 7 See also 8 External links 9 References Signs and symptoms Symptoms are fairly nonspecific, and generally include malaise, palpitations and muscle weakness; mild hyperventilation may indicate metabolic acidosis, 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. 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 Renal insufficiency Medication that interferes with urinary excretion: ACE inhibitors and angiotensin receptor blockers Potassium-sparing diuretics e.g. amiloride and spironolactone NSAIDs such as ibuprofen, naproxen, or celecoxib The calcineurin inhibitor immunosuppressants ciclosporin and tacrolimus The antibiotic trimethoprim The antiparasitic drug pentamidine Mineralocorticoid deficiency or resistance, such as: Addison's disease Aldosterone deficiency, including reduced levels due to the blood thinner, heparin Some forms of congenital adrenal hyperplasia Type IV renal tubular acidosis resistance of renal tubules to aldosterone 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. Excessive release from cells Rhabdomyolysis, burns or any cause of rapid tissue necrosis, including tumor lysis syndrome Massive blood transfusion or massive hemolysis Shifts/transport out of cells caused by acidosis, low insulin levels, beta-blocker therapy, digoxin overdose, or the paralyzing anesthetic succinylcholine 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 massive doses of oral KCl supplements. Lethal injection 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. 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.1 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 tournequet time or fist clenching during phlebotomy which presumably leads to efflux of potassium from the muscle cells into the bloodstream;2 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 1,000,000/mm³, leukocytes 100 000/mm³, or erythrocytes hematocrit 55%. People with leakier cell membranes have been found, whose blood must be separated immediately to avoid pseudohyperkalemia.3 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 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.4 Patients with the rare herary 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. 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. 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. 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. Refractory or severe cases may need dialysis to remove the potassium from the circulation. 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. See also Hypokalemia Renal failure External links Content of Selected Foods per Common Measure, sorted by nutrient content Potassium USDA National Nutrient Database for Standard Reference, Release 20 List of foods rich in potassium National Kidney Foundation site on potassium content of foods References ^ 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. ^ 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. ^ Iolascon, A; Stewart, GW; Ajetunmobi, JF; et al May 1999. Familial pseudohyperkalemia maps to the same locus as dehydrated herary stomatocytosis herary xerocytosis. Blood 93 9: 3120-3123. PMID 10216110. ^ 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. PMID 7563098. Schaefer, TJ; Wolford, RW August 2005. Disorders of potassium. Emerg. Med. Clin. North Am. 23 3: 723-747. doi:10.1016/j.emc.2005.03.016. PMID 15982543. Kasper, Dennis L.; Harrison, Tinsley Randolph; Braunwald, Eugene; Fauci, Anthony S.; Hauser, Stephen L; Longo, Dan L.; Jameson, J. N. St C. 2005. Harrison's Principles of Internal Medicine, 16th Ed., New York: McGraw-Hill, 258-261. ISBN 0-07-140235-7. Rose; Post, Theodore 2001. Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed., New York: McGraw-Hill, 888-930. ISBN 0-07-134682-1. v d e Water-electrolyte imbalance and acid-base imbalance E86-E87, 276 Volume status Dehydration/Hypervolemia - Hypovolemia Electrolyte Na+ Hypernatremia/Hyponatremia K+ Hyperkalemia/Hypokalemia Cl- Hyperchloremia/Hypochloremia Acid-base Acidosis: Metabolic - Respiratory - Lactic - Ketosis Alkalosis: Metabolic, Respiratory Mixed disorder of acid-base balance Retrieved from http://en..org/wiki/Hyperkalemia Categories: Metabolic disorders | Electrolyte disturbances | Endocrinology | Medical emergencies | Nephrology | Potassium Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages العربية Bosanski Deutsch Eesti Español Français Italiano 日本語 Polski Português Tiếng Việt This page was last modified on 24 August 2008, at 21:42
39 Reasons to Drink Acai Juice Every Day
What is MonaVie - Watch the 8-minute video
Discovering MonaVie Video
The Power of You Video
Effects of MonaVie Active on Antioxidant Capacity in Humans
Log into your Wholesale MonaVie Account
So many of us do not eat a balanced diet, get enough sleep, have too much stress, or are impacted with toxins and pollutants. Drinking 2 ounces of MonaVie twice a day will help your body detoxify as well as build your immune system. Its the smartest thing you can do for yourself, so start today. Buying MonaVie through our company guarantees you support 7 days a week and, if you would like to share MonaVie with your family and friends we will guide you from start to finish.
1. Click on Enroll Now (30 - 55% off retail price)
2. Pay $39 for your Wholesale ID number.
3. NO minimum order required.
4. MonaVie is delivered to your door in 3 to 5 days.