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Furosemide, sold under the brand name Lasix among others, is a loop diuretic medication used to treat edema due to heart failure, liver scarring, or kidney disease. [4] Furosemide may also be used for the treatment of high blood pressure. [4] It can be taken intravenously or orally. [4]
Hypokalemia is a low level of potassium (K +) in the blood serum. [1] Mild low potassium does not typically cause symptoms. [3] Symptoms may include feeling tired, leg cramps, weakness, and constipation. [1] Low potassium also increases the risk of an abnormal heart rhythm, which is often too slow and can cause cardiac arrest. [1] [3]
Potassium-sparing diuretics or antikaliuretics [1] refer to drugs that cause diuresis without causing potassium loss in the urine. [2] They are typically used as an adjunct in management of hypertension, cirrhosis, and congestive heart failure. [3] The steroidal aldosterone antagonists can also be used for treatment of primary hyperaldosteronism.
Excretion is the most common cause of hypokalemia and can be caused by diuretic use, metabolic acidosis, diabetic ketoacidosis, hyperaldosteronism, and renal tubular acidosis. [3] Potassium can also be lost through vomiting and diarrhea. [14]
The biological half-life of furosemide is limited by absorption from the gastrointestinal tract into the bloodstream. The apparent half-life of its excretion is higher than the apparent half-life of absorption via the oral route. Therefore, furosemide taken intravenously is twice as potent as an equivalent dose taken orally. [6]
If overcorrection does occur, a 5% dextrose in water infusion may be given to temporarily lower sodium levels. [2] total of 8 mmol per liter during the first day with the use of furosemide and replacing sodium and potassium losses with 0.9% saline.
Hypoaldosteronism may result in high blood potassium and is the cause of 'type 4 renal tubular acidosis', sometimes referred to as hyperkalemic RTA or tubular hyperkalemia. However, the acidosis, if present, is often mild. It can also cause urinary sodium wasting, leading to volume depletion and hypotension. [citation needed]
In addition, factors such as rapid infusion, concurrent use of more than one drug known to prolong QT interval, diuretic treatment, electrolyte derangements (hypokalemia, hypomagnesemia, or hypocalcemia), advanced age, bradyarrhythmias, and female sex have all been shown to be risk factors for developing drug-induced QT prolongation. [2]