Potassium intravenous

USP XXII specifies that sodium iodide contains 99—101.5% Nal, calculated on an anhydrous basis (4). It is used iaterchangeably with potassium iodide as a therapeutic agent, except where sodium ion is contraindicated (see Potassium compounds). Intravenous sodium iodide formulations have been used for a variety of diseases, from thyroid deficiency to neuralgia (see Thyroid and antithyroid preparations). However, these solutions are no longer listed ia the XFXUII (4), iadicatiag that their therapeutic value has not been satisfactorily demonstrated. 

Melarsonyl potassium (Mel W, Trimelarsen) [13355-00-5] is a thioarsenite closely related to melarsoprol, and it also has been used for the treatment of trypanosomiasis (172). However, it appears to be more toxic and less effective than melarsoprol. The only advantage of melarsonyl potassium is that it is water-soluble and can be adrninistered intramuscularly or subcutaneously. This property is useful when the intravenous route caimot be employed. 

Curative treatment involves counteracting the paralytic effect of the Ba " ion on the muscle by intravenous infusion of a potassium salt. 

Serum potassium concentration Is Increased by the concurrent administration of Intravenous potassium penicillin 6. The penicillin preparation contains 1.7 mmol of potassium per million units. Thus, a patient receiving 10 million units of the antibiotic receives 17 mmol (m q.) of potassium. 

Intravenous formulations contain either sodium 4 mEq/mL or potassium 4.4 mEq/mL with 3 mmol/mL phosphate ° Symptomatic and severe hypophosphatemia (<1 mg/dL)... 

Patients with acute hyperkalemia usually require other therapies to manage hyperkalemia until dialysis can be initiated. Patients who present with cardiac abnormalities caused by hyperkalemia should receive calcium gluconate or chloride (1 g intravenously) to reverse the cardiac effects. Temporary measures can be employed to shift extracellular potassium into the intracellular compartment to stabilize cellular membrane effects of excessive serum potassium levels. Such measures include the use of regular insulin (5 to 10 units intravenously) and dextrose (5% to 50% intravenously), or nebulized albuterol (10 to 20 mg). Sodium bicarbonate should not be used to shift extracellular potassium intracellularly in patients with CKD unless severe metabolic acidosis (pH less than 7.2) is present. These measures will decrease serum potassium levels within 30 to 60 minutes after treatment, but potassium must still be removed from the body. Shifting potassium to the intracellular compartment, however, decreases potassium removal by dialysis. Often, multiple dialysis sessions are required to remove potassium that is redistributed from the intracellular space back into the serum. 

Intravenous potassium infusions running at rates of greater than 10 mEq/hour require cardiac monitoring. 

It is important that injectable solutions that are to be given intravenously are isotonic, or nearly so. Because of osmotic pressure changes and the resultant exchange of ionic species across red blood cell membranes, nonisotonic solutions, particularly if given in quantities larger than 100 mL, can cause hemolysis or cre-nation of red blood cells (owing to hypotonic or hypertonic solutions, respectively). Dextrose, sodium chloride, or potassium chloride is commonly used to achieve isotonicity in a parenteral formula. 

IVPB, intravenous piggyback K, potassium Na, sodium P04, phosphate. Monitor serum K closely. 

A physician order for an intravenous infusion for a patient weighing 110 lb calls for a 0.25 mEq of potassium chloride per kilogram of bodyweight to be added to 500 mL of D5W. How many milliliters of a sterile solution containing 50 mEq of potassium chloride per 10 mL should be used in preparing the infusion ... 

A liter of a 0.5% intravenous infusion of potassium chloride is to be administered over a period of four hours. How many milliequivalents of potassium are represented in the infusion ... 

Bright JE, Marrs TC. 1988. Pharmacokinetics of intravenous potassium cyanide. Hum Toxicol 7 183-186. 

A patient is prescribed 1 L dextrose 5% with potassium chloride over 6 hours. Treatment is started at 8.00 am. At noon the patient is changed to 1 L normal saline over 12 hours. The patient s total intravenous fluid intake in the period 8.00 am to midnight is ... 

The barium ion is a physical antagonist of potassium, and it appears that the symptoms of barium poisoning are attributable to Ba -induced hypokalemia. The effect is probably due to a transfer of potassium from extracellular to intracellular compartments rather than to urinary or gastrointestinal losses. Signs and symptoms are relieved by intravenous infusion ofKh ... 

ITP idiopathic thrombocytopenic purpura IV intravenous IVP intravenous push JRA juvenile rheumatoid arthritis K/K potassium KVO ke vein open L/d liters per day LA long acting LDL low-density hpoprotein LFT liver function test LH leuteinizing hormone LHRH luteinizing hormone releasing hormone... 

Some simple but powerful solutions have come from this industrial model of quality assurance. For example, just the removal of concentrated potassium chloride solutions from hospital wards can prevent a toxic dose of potassium from being accidentally injected intravenously. Making the color of the tubing different may prevent epidural lines and IV lines being interchanged so that medication intended to go into a vein does not go into the epidural space,or vice versa. 

Diazoxide is a potassium channel opener with a rapid antihypertensive action after intravenous administration. Diazoxide causes hyperglycaemia which may underlie side-effects such as nausea and vomiting, cardiac dysrhythmia and ketosis. Diazoxide was used occasionally in the management of hypertensive emergencies, but it is now largely abandoned for this indication. Diazoxide is an alternative for glucagons in patients with hypogycaemia. 

L A. Nephrotoxicity is the most common and most serious toxicity associated with amphotericin B administration. This is manifested by azotemia (elevated serum blood urea nitrogen and creatinine), and by renal tubular acidosis, which results in the wasting of potassium and magnesium in the urine (leading to hypokalemia and hypomagnesemia, requiring oral or intravenous replacement therapy). Normochromic normocytic anemia is also seen with long-term amphotericin B administration. Elevation of hver enzymes is not associated with the use of amphotericin B. 

Hypercalcemia can be a medical emergency. Because loop diuretics reduce Ca2+ reabsorption significantly, they can be quite effective in promoting Ca2+ diuresis. However, loop diuretics alone can cause marked volume contraction. If this occurs, loop diuretics are ineffective (and potentially counterproductive) because Ca2+ reabsorption in the proximal tubule would be enhanced. Thus, saline must be administered simultaneously with loop diuretics if an effective Ca2+ diuresis is to be maintained. The usual approach is to infuse normal saline and furosemide (80-120 mg) intravenously. Once the diuresis begins, the rate of saline infusion can be matched with the urine flow rate to avoid volume depletion. Potassium chloride may be added to the saline infusion as needed. 

The fundamental treatment for DKA includes aggressive intravenous hydration and insulin therapy and maintenance of potassium and other electrolyte levels. Fluid and insulin therapy is based on the patient s individual needs and requires frequent reevaluation and modification. Close attention has to be given to hydration and renal status, the sodium and potassium levels, and the rate of correction of plasma glucose and plasma osmolality. Fluid therapy generally begins with normal saline. Regular human insulin should be used for intravenous therapy with a usual starting dose of about 0.1 IU/kg/h. 

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