Fluid and electrolyte balance 100 mlkgday for the first 10 kg of the patients weight, 50 mlkgday for the

next 10 kg, 20 mlkgday for each remaining kilogram. A 70-kg patient requires the following: 10 kg 100 mlkg (1 L) + 10 kg 50 mlkg (500 ml) + 50 kg 20 mlkg (1 L) = 2,500 mlday of free water. A 23-kg child would need 10 kg 100 ml/kg (1 L) + 10 kg 50 ml/kg (500 ml) + 3 kg 20 mlkg (60 ml) = 1,560 mlday of free water.

Every 1 degree raise in temperature can lead to 12% increase of I v fluids per body weight
Most intravenous fluids contain small amount of dextrose (5%, or 50 gL), providing limited calories (4 kcalg dextrose = 200 kcalL), preventing protein catabolism Dextrose also added to some solutions (e.g., D5 1/2 NS making them isosmotic, to avoid RBC lysis on infusion

Normal requirements are 11.5 mEqkgday for sodium, 0.50.75 mEqkgday for potassium, 11.5 mEqkgday for chloride. Replace deficit of fluid and electrolytes with half in first 8 hours and remaining half in the next 16 hours
Replacement of pre-existing loss usually accomplished over 24 hours, with one-half of replacement given over first 8 hours, and remainder over next 16 hours

In old patients rapid fluid infusion can predispose to congestive heart failure In children rapid infusion is more tolerable

SODIUM

Signs and symptoms of hypo- and hypernatremia usually do not occur unless the changes are severe or occur rapidly. Na deficit = (140 mEqL measured Na) x(body weight 0.6) Hyponatremia
Normal serum sodium levels are between 135 and 145 mEq/L. Hyponatremia is defined as a serum level of less than 135 mEq/L and is considered severe when the serum level is below 125 mEq/L. pneumonia Symptoms : nausea and vomiting, headache, confusion, lethargy, fatigue, appetite loss, restlessness and irritability, muscle weakness, spasms, or cramps, seizures, and decreased consciousness or coma.
[1]

Causes : excess water retention in body : congestive heart failure , SIADH, or overhydration , liver failure, renal failure, or

Neurological symptoms often show for extremely low levels of sodium. When sodium levels in blood become too low, excess water enters cells and causes the cells to swell. Swelling in the brain is especially dangerous because the brain is confined by the skull and is unable to expand. Neurological symptoms most often are due to very low serum sodium levels (usually <115 mEq/L), resulting in intracerebral osmotic fluid shifts and brain edema. This neurological symptom complex can lead to tentorial herniation with subsequent brain stem compression and respiratory arrest, resulting in death in the most severe cases. The severity of neurological symptoms correlates with the rapidity and severity of the drop in serum sodium. A gradual drop, even to very low levels, may be tolerated well if it occurs over several days or weeks, because of neuronal adaptation. The presence of underlying neurological disease, like a seizure disorder, or non-neurological metabolic abnormalities, also affects the severity of neurologic symptoms.

Hypervolemic hyponatremia - both sodium & water content increase, but the water gain is greater

cirrhosis congestive heart failure nephrotic syndrome massive edema of any cause

Euvolemic hyponatremia - total body water increases, but the body's sodium content stays the same

states of severe pain or nausea in the setting of trauma or other damage to the brain SIADH (and its many causes) Hypothyroidism Glucocorticoid excess

Hypovolemic hyponatremia - water & sodium are both lost from body, but the sodium loss is greater

any cause of hypovolemia such as prolonged vomiting, decreased oral intake, severe diarrhea diuretic use (due to the diuretic causing a volume depleted state and thence ADH release, and not a direct result of diuretic-induced urine sodium loss)

Miscellaneous causes of hyponatremia that are not included under the above classification scheme include:

factitious hyponatremia (due to massive increases in blood triglyceride levels, extreme elevation of immunoglobulins as may occur in multiple myeloma, and extreme hyperglycemia) hypothyroidism and adrenal insufficiency (both thyroid hormone and cortisol are required to excrete free water) beer potomania and other malnourished states where poor dietary protein intake leads to inadequate urine solute formation thereby impeding the kidney's ability to excrete free water primary polydipsia (where the amount of urine solute required to excrete huge quantities of ingested water exceeds the body's ability to produce it; this typically occurs when 12 or more litres of water are ingested per day)

Hyponatremia must be corrected slowly in order to lessen the chance of the development of CENTRAL PONTINE MYELINOLYSIS (CPM), a severe neurological disease. In fact, overly rapid correction of hyponatremia is the most common cause of that potentially devastating disorder. During treatment of hyponatremia, the serum sodium should not be allowed to rise by more than 8 mmol/l over 24 hours (i.e. 0.33 mmol/l/h rate of rise). In practice, too rapid correction of hyponatremia and thence CPM is most likely to occur during the treatment of hypovolemic hyponatremia. In particular, once the hypovolemic state has been corrected, the signal for ADH release disappears. At that point, there will be an abrupt water diuresis (since there is no longer any ADH acting to retain the water). A rapid and profound rise in serum sodium can then occur. Should the rate of rise of serum sodium exceed 0.33 mmol/l/h over several hours, vasopressin may be administered to prevent ongoing rapid water diuresis.
[4] [3]

Because sodium distributes throughout total body water, the quantity (body weight 0.6) is used. Sodium should be replaced when hyponatremia is profound (<120 mEqL) or when the loss occurs rapidly and the patient becomes symptomatic. No more than one-half the calculated deficit should be replaced within the first 24 hours. Amyelenosis may result from excessively enthusiastic replacement. Normal saline is used, although hypertonic saline (3% NaCl) may be required in rare circumstances. Hypernatremia results from the loss of free water in excess of sodium. It causes weakness, restlessness, and delirium. The skin becomes dry and the mucous membranes are sticky. Salivation and tear production are decreased,

and an increase in body temperature may also occur. Free water, usually in the form of D 5W, is required and should be administered slowly to prevent a sudden decrease in osmolarity.

HYPERNATREMIA
Hypernatremia or hypernatraemia (see American and British English spelling differences) is an electrolyte disturbance that is defined by an elevatedsodium level in the blood. Hypernatremia is generally not caused by an excess of sodium, but rather by a relative deficit of free water in the body. For this reason, hypernatremia is often synonymous with the less precise term, dehydration. Ordinarily, even a small rise in the serum sodium concentration above the normal range results in a strong sensation of thirst, an increase in free water intake, and correction of the abnormality. Therefore, hypernatremia most often occurs in people such as infants, those with impaired mental status, or the elderly, who may have an intact thirst mechanism but are unable to ask for or obtain water.\ Common causes of hypernatremia include:
[1]

Hypovolemic

Inadequate intake of water, typically in elderly or otherwise disabled patients who are unable to take in water as their thirst dictates. This is the most common cause of hypernatremia.

Excessive losses of water from the urinary tract, which may be caused by glycosuria, or other osmotic diuretics. Water losses associated with extreme sweating. Severe watery diarrhea

Euvolemic Excessive excretion of water from the kidneys caused by diabetes insipidus, which involves either inadequate production of the hormone, vasopressin, from the pituitary gland or impaired responsiveness of the kidneys to vasopressin. Hypervolemic

Intake of a hypertonic fluid (a fluid with a higher concentration of solutes than the remainder of the body). This is relatively uncommon, though it can occur after a vigorous resuscitation where a patient receives a large volume of a concentrated sodium bicarbonate solution. Ingesting seawater also causes hypernatremia because seawater is hypertonic.

Mineralcorticoid excess due to a disease state such as Conn's syndrome or Cushing's disease

Symptoms
Clinical manifestations of hypernatremia can be subtle, consisting of lethargy, weakness, irritability, neuromuscular excitability, and edema. With more severe elevations of the sodium level, seizuresand coma may occur. TREATMENT The cornerstone of treatment is administration of free water to correct the relative water deficit. Water can be replaced orally or intravenously. Water alone cannot be administered as intravenously (because of osmolarity issue) rather can be given with addition to dextrose or saline infusion solutions. However, overly rapid correction of hypernatremia is potentially very dangerous. The body (in particular the brain) adapts to the higher sodium concentration. Rapidly lowering the sodium concentration with free water, once this adaptation has occurred, causes water to flow into brain cells and causes them to swell. This can lead to cerebral edema, potentially resulting in seizures, permanent brain damage, or death. Therefore, significant hypernatremia should be treated carefully by aphysician or other medical professional with experience in treatment of electrolyte imbalances.
[3]

HYPOKALEMIA

Hypokalemia (American English) or hypokalaemia (British English), also hypopotassemia or hypopotassaemia (ICD-9), refers to the condition in which the concentration of potassium (K+) in the blood is low. The prefix hypo- means "under" (contrast with hyper-, meaning "over"); kal- refers to kalium, the Neo-Latin for potassium, and -emia means "condition of the blood."

Normal serum potassium is 3.5 to 5.5 mEq/L; however, in persons with this condition, plasma potassium is 0.5 mEq/L lower. [1] Normal plasma potassium levels are between 3.5 to 5.0 mEq/L;[2] at least 95% of the body's potassium is found inside cells, with the remainder in the blood. This concentration gradient is maintained principally by the Na+/K+ pump.

Signs and symptoms

Mild hypokalemia is often without symptoms, although it may cause a small elevation of blood pressure,[3] and can occasionally provoke cardiac arrhythmias. Moderate hypokalemia, with serum potassium concentrations of 2.5-3 mEq/L (Nl: 3.5-5.0 mEq/L), may cause muscular weakness, myalgia, and muscle cramps (owing to disturbed function of the skeletal muscles), and constipation (from disturbed function of smooth muscles). With more severe hypokalemia, flaccid paralysis and hyporeflexia may result. There are reports of rhabdomyolysis occurring with profound hypokalemia with serum potassium levels less than 2 mEq/L. Respiratory depression from severe impairment of skeletal muscle function is found in many patients. Some electrocardiographic (ECG) findings associated with hypokalemia include flattened or inverted T waves, a U wave, ST depression and a wide PR interval. Due to prolonged repolarization of ventricular Purkinje fibers, a prominent U wave occurs, that is frequently superimposed upon the T wave and therefore produces the appearance of a prolonged QT interval.[4] [edit]Causes Hypokalemia can result from one or more of the following medical conditions: [edit]Inadequate

potassium intake

Perhaps the most obvious cause is insufficient consumption of potassium (that is, a low-potassium diet) or starvation. However, without excessive potassium loss from the body, this is a rare cause of hypokalemia.

[edit]Gastrointestinal/integument

loss

A more common cause is excessive loss of potassium, often associated with heavy fluid losses that "flush" potassium out of the body. Typically, this is a consequence of diarrhoea, excessiveperspiration, or losses associated with surgical procedures. Vomiting can also cause hypokalemia, although not much potassium is lost from the vomitus. Rather, there are heavy urinary losses of K+ in the setting of post-emetic bicarbonaturia that force urinary potassium excretion (see Alkalosis below). Other GI causes include pancreatic fistulae and the presence of adenoma.

[edit]Urinary

loss

Certain medications can cause excess potassium loss in the urine. Diuretics, including thiazide diuretics (e.g. hydrochlorothiazide) and loop diuretics (e.g. furosemide) are a common cause of hypokalemia. Other medications such as the antifungal, amphotericin B, or the cancer drug, cisplatin, can also cause long-term hypokalemia. A special case of potassium loss occurs with 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, -hydroxybutyrate. 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. Alkalosis can cause transient hypokalemia by two mechanisms. First, the alkalosis causes a shift of potassium from the plasma and interstitial fluids into cells; perhaps mediated by stimulation ofNa+-H+ exchange and a subsequent activation of Na+/K+ATPase activity.[5] Second, an acute rise of plasma HCO3- concentration (caused by vomiting, for example) will exceed the capacity of the renal proximal tubule to reabsorb this anion, and potassium will be excreted as an obligate cation partner to the bicarbonate.[6] Metabolic alkalosis is often present in states of volume depletion, so potassium is also lost via aldosterone-mediated mechanisms. 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, e.g., Conn's syndrome (primary hyperaldosteronism). Cushing's syndrome can also lead to hypokalemia due to excess cortisol binding the Na+/K+ pump and acting like aldosterone. Hypertension and hypokalemia can also be seen with a deficiency of the 11-beta-hydroxysteroid dehydrogenase type 2 enzyme which allows cortisols to stimulate aldosterone receptors. This deficiencyknown as apparent mineralocorticoid excess syndromecan 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. 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. As opposed to disease states of primary excesses of aldosterone, blood pressure is either normal or low in Bartter's or Gitelman's.

[edit]Distribution

away from ECF

In addition to alkalosis, other factors can cause transient shifting of potassium into cells, presumably by stimulation of the Na-KATPase.[5] These hormones and medications include insulin,epinephrine, and other beta agonists (e.g. salbutamol or salmeterol), and xanthines (e.g. Theophylline).[7] 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 the normal changes in potassium produced by catechols and/or insulin and/or thyroid hormone, which lead to movement of potassium from the extracellular fluid into the muscle cells.

[edit]Other/ungrouped

There have been a handful of published reports describing individuals with severe hypokalemia related to chronic extreme consumption (4-10 L/day) of colas.[8] The hypokalemia is thought to be from the combination of the diuretic effect of caffeine[9] and copious fluid intake, although it may also be related to diarrhea caused by heavy fructose ingestion.[10][11] A physiological response toHypercapnia, blood potassium (as well as calcium) helps offset Acidosis, which is consistent with chronic, extreme consumption of carbonated beverages.

[edit]Pseudohypokalemia

Pseudohypokalemia is a decrease in the amount of potassium that occurs due to excessive uptake of potassium by metabolically active cells after blood has been drawn. It is a laboratory artifact that may occur when blood samples remain in warm conditions for several hours before processing.[12]

[edit]Pathophysiology Potassium is essential for many body functions, including muscle and nerve activity. The electrochemical gradient of potassium between the 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. Increased potassium levels in the extracellular space will cause hyperpolarization of the resting membrane potential. This hyperpolarization is caused by the effect of the altered potassium gradient on resting membrane potential as defined by the Goldman equation. As a result, a greater than normal stimulus is required for depolarization of the membrane in order to initiate an action potential. In the heart, hypokalemia causes myocytes to become hyperexcitable (or hypo-polarized). Lower membrane potentials in the atrium may cause arrhythmias because of more complete recovery from sodium-channel inactivation, making the triggering of an action potential more likely. In addition, the reduced extracellular potassium (paradoxically) inhibits the activity of the IKr potassium current[13]and delays ventricular repolarization. This delayed repolarization may promote reentrant arrhythmias. [edit]Treatment The most important treatment in severe hypokalemia is addressing the cause, such as improving the diet, treating diarrhea or stopping an offending medication. Patients without a significant source of potassium loss and who show no symptoms of hypokalemia may not require treatment. Mild hypokalemia (>3.0 mEq/L) may be treated with oral potassium chloride supplements (Klor-Con, Sando-K, Slow-K). As this is often part of a poor nutritional intake, potassium-containing foods may be recommended, such as leafy green vegetables, tomatoes, citrus fruits, oranges or bananas.[14] Both dietary and pharmaceutical supplements are used for people taking diuretic medications (seeCauses, above). Severe hypokalemia (<3.0 mEq/L) may require intravenous (IV) supplementation. Typically, a saline solution is used, with 20-40 mEq KCl per liter over 34 hours. Giving IV potassium at faster rates (20-25 mEq/hr) may predispose to ventricular tachycardias and requires intensive monitoring. A generally safe rate is 10 mEq/hr. Even in severe hypokalemia, oral supplementation is preferred given its safety profile. Sustained release formulations should be avoided in acute settings. Difficult or resistant cases of hypokalemia may be amenable to a potassium-sparing diuretic, such as amiloride, triamterene, or spironolactone or eplerenone. Concomittant hypomagnesiumemia will inhibit potassium replacement as magnesium is a cofactor for potassium uptake.[15] When replacing potassium intravenously, infusion via a 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. [16]

Hyperkalemia

Hyperkalemia (hyperkalaemia in British English, hyper- high; kalium, potassium; -emia, "in the blood") refers to the condition in which the concentration of the electrolyte potassium (K+) in the blood is elevated. Extreme hyperkalemia is a medical emergency due to the risk of potentially fatal abnormal heart rhythms (arrhythmia). Normal serum potassium levels are between 3.5 and 5.0 mEq/L;[1] at least 95% of the body's potassium is found inside cells, with the remainder in the blood. This concentration gradient is maintained principally by the Na+/K+ pump.

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 testsfor 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 focus 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 ofAddison's disease, itself a medical emergency. [edit]Causes [edit]Ineffective

elimination

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 Some forms of congenital adrenal hyperplasia Type IV renal tubular acidosis (resistance of renal tubules to aldosterone)

Gordon's syndrome (pseudohypoaldosteronism type II) (familial hypertension with hyperkalemia), a rare genetic disorder caused by defective modulators of salt transporters, including the thiazide-sensitive Na-Cl cotransporter.

[edit]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 agent succinylcholine

[edit]Excessive

intake

Excess intake 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 intake would be seen only with large infusions of KCl or oral doses of several hundred milliequivalents of KCl. [2]

[edit]Lethal

injection

In the United States of America, hyperkalemia is intentionally brought about in an execution by lethal injection. A lethal dose of potassium chloride is the third and last of the three drugs administered, and the one that actually causes death.

[edit]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.[3] 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);[4] 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/mm), leukocytes (> 70 000/mm), or erythrocytes (hematocrit > 55%). People with "leakier" cell membranes have been found, whose blood must be separated immediately to avoid pseudohyperkalemia.[5] [edit]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 thekidney. The renal elimination of potassium is passive (through the glomeruli), and reabsorption 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 voltagegated 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 needed 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. High levels of adrenaline and noradrenaline have a protective effect on the cardiac electrophysiology because they bind to beta 2 adrenergic receptors which when activated, decrease potasssium concentration extracellularly.[6] 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. [edit]Diagnosis 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 transtubular 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. [edit]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 ECGcomplex 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.[7][8] 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.[9][10] [edit]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 transiently lower K+ levels. Choice depends on the degree and cause of the hyperkalemia, and other aspects of the patient's condition.

[edit]Myocardial

excitability

Calcium (Calcium chloride or calcium gluconate) increases threshold potential through a mechanism that is still unclear, thus restoring normal gradient between threshold potential and resting membrane potential, which is elevated abnormally in hyperkalemia. One ampule of Calcium chloride has approximately 3 times more calcium than calcium gluconate. Onset of action is <5 min and lasts about 30-60 min. Doses should be titrated with constant monitoring of ECG changes during administration and the dose should be repeated if ECG changes do not normalize within 3 to 5 min. [edit]Lowering

K+ temporarily

Several medical treatments shift potassium ions from the bloodstream into the cellular compartment, thereby reducing the risk of complications. The effect of these measures tends to be short-lived, but may temporize the problem until potassium can be removed from the body.[11]

Insulin (e.g. intravenous injection of 10-15 units 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.[12] Its effects last a few hours, so it sometimes needs to be repeated while other measures are taken to suppress potassium levels more permanently. Bicarbonate therapy (e.g. 1 ampule (50mEq) infused over 5 minutes) is effective in shifting potassium into the cell. [12] 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 2-selective catecholamine that is administered by nebulizer (e.g. 1020 mg). This drug also lowers blood levels of K+ by promoting its movement into cells.[12]

[edit]Increasing

elimination

Severe cases require hemodialysis or hemofiltration, which are the most rapid methods of removing potassium from the body.[12] These are typically used if the underlying cause cannot be corrected swiftly while temporizing measures are instituted or there is no response to these measures. Sodium polystyrene sulfonate with sorbitol (Kayexalate) either orally or rectally is widely used with the goal to lower potassium over several hours.[12] Removal of potassium is assumed to requiredefecation. However, careful clinical trials to demonstrate the effectiveness of Kayexalate are lacking, and there are small risks of necrosis of the colon.[13] Furosemide may also be used to promote excretion of potassium in the urine.[12] [edit]Long-term

prevention

Preventing recurrence of hyperkalemia typically involves reduction of dietary potassium, removal of an offending medication, and/or the addition of oral bicarbonate or a diuretic (such as furosemide orhydrochlorothiazide). Sodium polystyrene sulfonate and sorbital (Kayexalate) is occasionally used on an ongoing basis to maintain lower serum levels of potassium. Concerns regarding its use are noted in the previous section.i