These interventions are essential to the management of severely increased potassium levels accompanied by life-threatening ECG changes. This may be accomplished through the use of cation exchange resins, loop diuretics, or dialysis. The second approach is to increase potassium elimination from the body. 9 – 11 This is only a temporary measure, however, and is best suited for the management of acute hyperkalemia. 1 The first approach is to shift intracellular potassium using a combination of intravenous (IV) insulin plus glucose (to offset hypoglycemia), albuterol, or sodium bicarbonate. 1 For individuals with moderate (6 to 7 mEq/L) or severe (greater than 7 mEq/L) hyperkalemia, two general approaches can be used to lower serum potassium levels. 1, 8 Asymptomatic patients with mild hyperkalemia (defined as a serum potassium level of 5 to 6 mEq/L) usually do not require specific treatment. In general, the treatment of hyperkalemia is governed by the patient’s clinical presentation, by how rapidly the disorder developed, by the severity of the potassium abnormality, and by the presence of ECG changes. For patients who are chronically at risk for hyperkalemia, the main treatment goal is to control serum potassium levels. The goals of treatment in patients with acute hyperkalemia are to reverse adverse cardiac effects, shift potassium into the cells, remove potassium from the body, ameliorate the patient’s signs and symptoms, and normalize serum potassium levels while avoiding overcorrection. In addition, a complete urine analysis should be performed and an ECG should be obtained. 7 The diagnosis of hyperkalemia requires a complete clinical history, a review of the patient’s medication profile, a physical examination, and the determination of serum potassium levels. Hyperkalemia is most commonly associated with renal insufficiency, heart failure, and the use of medications, including those that affect the renin–angiotensin–aldosterone system (RAAS), potassium-sparing diuretics, and nonsteroidal anti-inflammatory drugs (NSAIDs). Signs and symptoms of the disorder include muscle twitching, cramping, weakness, paralysis, paresthesia (face, hands, and feet), electrocardiogram (ECG) changes (e.g., peaked T-waves, a prolonged PR-interval, the loss of P waves, a widened QRS complex, and a shortened QT-interval), and arrhythmias (e.g., bradyarrhythmias, ventricular fibrillation, and asystole). 4 The clinical manifestations of hyperkalemia are associated with alterations in neuromuscular and cardiac function. 3 It is a fairly common electrolyte disorder, affecting approximately 10% of hospitalized patients, and has the potential to cause life-threatening cardiac arrhythmias. Hyperkalemia results from extracellular shifts of potassium, excessive ingestion of potassium, and/or impaired elimination of potassium by the kidneys. Hyperkalemia is defined as a serum potassium level exceeding 5 mEq/L the disorder may be fatal when the potassium level is greater than 6.5 mEq/L. 1, 2 Physiologic serum potassium levels range from 3.5 to 5.0 mEq/L. Potassium, the second most-abundant cation in the body, performs several important physiological functions, including cellular metabolism, glycogen and protein synthesis, and maintenance of the electrical action potential across cell membranes, especially in the myocardium.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |