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Treatment
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A deficit of approximately 4 5 mEq/kg exists for each 1 mEq/L decrement in serum potassium concentration below a level of 4 mEq/L The safest way to treat mild to moderate deficiency is with oral potassium, and all potassium formulations are easily absorbed Dietary potassium is almost entirely coupled to phosphate rather than chloride and is therefore not effective in correcting potassium loss associated with chloride depletion, such as from diuretics or vomiting In the setting of abnormal renal function and mild to moderate diuretic dosage, 20 mEq/d of oral potassium is generally sufficient to prevent hypokalemia, but 40 100 mEq/d over a period of days to weeks is needed to treat hypokalemia and fully replete potassium stores Intravenous potassium replacement is indicated for patients with severe hypokalemia and for those who cannot take oral supplementation For severe deficiency, potassium may be given through a peripheral intravenous line in a concentration that should not exceed 40 mEq/L at rates of up to 40 mEq/L/h Continuous ECG monitoring is indicated, and the serum potassium level should be checked every 3 6 hours For the initial administration, avoid glucose-containing fluid to prevent further shifts of potassium into the cells
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Fluid & Electrolyte Disorders
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Table 21 6 Causes of hyperkalemia
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Spurious Leakage from erythrocytes when separation of serum from clot is delayed (plasma K+ normal) Marked thrombocytosis or leukocytosis with release of K+ (plasma K+ normal) Repeated fist clenching during phlebotomy, with release of K+ from forearm muscles Specimen drawn from arm with K+ infusion Decreased excretion Renal failure, acute and chronic Renal secretory defects (may or may not have frank renal failure): renal transplant, interstitial nephritis, systemic lupus erythematosus, sickle cell disease, amyloidosis, obstructive uropathy Hyporeninemic hypoaldosteronism (often in diabetic patients with mild to moderate nephropathy) or selective hypoaldosteronism (some patients with AIDS) Heparin (regardless of molecular size; suppresses aldosterone secretion) Drugs that inhibit potassium excretion (spironolactone, eplerenone, triamterene, ACE inhibitors, angiotensin II receptor blockers, trimethoprim, NSAIDs, cyclosporine, tacrolimus) Shift of K+ from within the cell Massive release of intracellular K+ in burns, rhabdomyolysis, hemolysis, severe infection, internal bleeding, vigorous exercise Metabolic acidosis (in the case of organic acid accumulation eg, lactic acidosis a shift of K+ does not occur since organic acid can easily move across the cell membrane) Hypertonicity (solvent drag) Insulin deficiency (metabolic acidosis may not be apparent) Hyperkalemic periodic paralysis Drugs: succinylcholine, arginine, digitalis toxicity, -adrenergic antagonists -Adrenergic stimulation Excessive intake of K+ ACE, angiotensin-converting enzyme; NSAIDs, nonsteroidal anti-inflammatory drugs
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opening properties (K-channel syndrome), such as cyclosporine, isoflurane, or nicorandil (not yet availble in the United States) Hyperkalemia is commonly seen in HIV-infected patients and has been attributed to impaired renal excretion of potassium due to the use of pentamidine or trimethoprimsulfamethoxazole or to hyporeninemic hypoaldosteronism
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Clinical Findings
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An elevated K+ concentration interferes with normal neuromuscular function to produce muscle weakness and, rarely, flaccid paralysis; abdominal distention and diarrhea may occur Electrocardiography is not a sensitive method for detecting hyperkalemia, since nearly half of patients with a serum potassium level greater than 65 mEq/L will not manifest ECG changes ECG changes in hyperkalemia include peaked T waves of increased amplitude, widening of the QRS, and biphasic QRS T complexes Inhibition of atrial depolarization despite normal conduction through usual pathways may occur This sinoventricular rhythm resembles a junctional mechanism and occurs because of greater sensitivity of atrial myocytes to hyperkalemia than is the case for ventricular muscle cells The heart rate may be slow; ventricular fibrillation and cardiac arrest are terminal events
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Prevention
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To prevent hyperkalemia, patients with congestive heart failure and creatinine clearances < 30 60 mL/min who are treated with ACE inhibitors or potassium-sparing diuretics should have close monitoring of their serum potassium (eg, obtaining a serum potassium level within 1 week of initiation of the drug and then within 1 week of any dose increase)
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