Potassium hyperkalemia

Other Potassium and Sodium Disorders. Potassium and/or sodium deficiency can lead to muscle weakness and sodium deficiency to nausea. Hyperkalemia resulting in cardiac arrest is possible from 18 g/d of potassium combined with inadequate kidney function. Faulty utilisation of K" and/or Na" can lead to Addison s or Cushing s disease. 

Potassium-sparing by diuretic agents, particularly spironolactone, enhances the effectiveness of other diuretics because the secondary hyperaldosteronism is blocked. This class of diuretics decreases magnesium excretion, eg, amiloride can decrease renal excretion of potassium up to 80%. The most important and dangerous adverse effect of all potassium-sparing diuretics is hyperkalemia, which can be potentially fatal the incidence is about 0.5% (50). Therefore, blood potassium concentrations should be monitored carehiUy. 

Hyperkalemia is an excess of potassium in the blood. Clinical symptoms are muscle weakness and cardiac arrhythmias. It is caused by, e.g., hyperaldosteronism and angiotensin-converting enzyme (ACE) inhibitors. 

ACE inhibitors do not completely block aldosterone synthesis. Since this steroid hormone is a potent inducer of fibrosis in the heart, specific antagonists, such as spironolactone and eplerenone, have recently been very successfully used in clinical trials in addition to ACE inhibitors to treat congestive heart failure [5]. Formerly, these drugs have only been applied as potassium-saving diuretics in oedematous diseases, hypertension, and hypokalemia as well as in primary hyperaldosteronism. Possible side effects of aldosterone antagonists include hyperkalemia and, in case of spironolactone, which is less specific for the mineralocorticoid receptor than eplerenone, also antiandrogenic and progestational actions. 

The hypotensive effects of most antihypertensive dru are increased when administered with diuretics and other antihypertensives. Many dnigp can interact with the antihypertensive drugs and decrease their effectiveness (eg, antidepressants, monoamine oxidase inhibitors, antihistamines, and sympathomimetic bronchodilators). When the ACE inhibitors are administered with the NSAIDs, their antihypertensive effect may be decreased. Absorption of the ACE inhibitors may be decreased when administered with the antacids. Administration of potassium-sparing diuretics or potassium supplements concurrently with the ACE inhibitors may cause hyperkalemia. When the angiotensin II receptor agonists are administered with... 

Hyperkalemia (increase in potassium in the blood), a serious event, may be seen with the administration of potassium-sparing diuretics. Hyperkalemia is most likely to occur in patients with an inadequate fluid intake and urine output, those with diabetes or renal disease tiie elderly, and those who are severely ill. In patients taking spironolactone, gynecomastia (breast enlargement in tiie male) may occur. This reaction appears to be related to both dosage and duration of therapy. The gynecomastia is usually reversible when therapy is discontinued, but in rare instances, some breast enlargement may remain. 

POTASSIUM-SPARING DIURETICS. Ratients taking the potassium-sparing diuretics are at risk for hyperkalemia Serum potassium levels are monitored frequently, particularly during initial treatment. 

Older adults are particularly prone to fluid volume deficit and electrolyte imbalances (see Display 46-1) while taking a diuretic. The older adult is carefully monitored for hypokalemia (when taking the loop or thiazide diuretic and hyperkalemia (with the potassium-sparing diuretics... 

The nurse must closely observe patients receiving a potassium-sparing diuretic for signs of hyperkalemia (see Display 46-1), a serious and potentially fatal electrolyte imbalance The patient is closely monitored for hypokalemia during loop or thiazide diuretic therapy. A supplemental potassium supplement may be prescribed to prevent hypokalemia. The primary health care provider may also encourage the patient to include... 

Nausea, vomiting, diarrhea, abdominal pain, and phlebitis have been seen with oral and IV administration of potassium. Adverse reactions related to hypo- or hyperkalemia are listed in Display 58-2. 

Potassium is contraindicated in patients who are at risk for experiencing hyperkalemia, such as those with renal failure, oliguria, or azotemia (file presence of nitrogen-containing compounds in the blood), anuria, severe hemolytic reactions, untreated Addison s disease (see Chap. 50), acute dehydration, heat cramps, and any form of hyperkalemia Potassium is used cautiously in patients with renal impairment or adrenal insufficiency, heart disease, metabolic acidosis, or prolonged or severe diarrhea. Concurrent use of potassium with... 

Potassium is abundant in animal and plant cells (Birch and Pradgeham 1994). Hypokalemia (deficiency) and hyperkalemia (accumulation of K[I]) may both occur. As the normal range of K[I] in plasma is small, and the consequences of hyperkalemia fatal, the method of determination must be precise and accurate to detect lower and higher than normal levels (hypokalemia and hyperkalemia, respectively). The preferred method of determination is PISE. 

Treatment depends on degree of hyperkalemia and presence/severity of signs and symptoms (sometimes irrespective of actual serum potassium level). Mild 5.5-6 mEq/L—furosemide and sodium polystyrene sulfonate. Moderate 6.1-7 mEq/L—insulin, glucose, sodium bicarbonate,... 

The major risk related to aldosterone antagonists is hyperkalemia. Therefore, the decision for use of these agents should balance the benefit of decreasing death and hospitalization from HF and the potential risks of life-threatening hyperkalemia. Before and within one week of initiating therapy, two parameters must be assessed serum potassium and creatinine clearance (or serum creatinine). Aldosterone antagonists should not be initiated in patients with potassium concentrations greater than... 

Aldosterone antagonists Hypotension, hyperkalemia, increased serum creatinine BP and HR every shift during oral administration during hospitalization, then once every 6 months baseline SCr and serum potassium concentration SCr and potassium at 48 hours, at 7 days, then monthly for 3 months, then every 3 months thereafter following hospital discharge... 

Assess possible correctable etiologies, including myocardial ischemia, serum potassium concentration (for hyperkalemia), and thyroid function tests (for hypothyroidism). 

Potassium balance is also primarily regulated by the kidney via the distal tubular cells. Reduction in nephron mass decreases tubular secretion of potassium, leading to hyperkalemia. Hyperkalemia is estimated to affect more than 50% of patients with stage 5 CKD.28... 

As nephron mass decreases, both the distal tubular secretion and GI excretion are increased because of aldosterone stimulation. Functioning nephrons increase FEK up to 100% and GI excretion increases as much as 30% to 70% in CKD,30 as a result of aldosterone secretion in response to increased potassium levels.30 This maintains serum potassium concentrations within the normal range through stages 1 to 4 CKD. Hyperkalemia begins to develop when GFR falls below 20% of normal, when nephron mass and renal potassium secretion is so low that the capacity of the GI tract to excrete potassium has been exceeded.30... 

Medications can increase the risk of hyperkalemia in patients with CKD, including angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers, used for the treatment of proteinuria and hypertension. Potassium-sparing diuretics, used for the treatment of edema and chronic heart failure, can also exacerbate the development of hyperkalemia, and should be used with caution in patients with stage 3 CKD or higher. 

Patients with CKD should avoid abrupt increases in dietary intake of potassium because the kidney is unable to increase potassium excretion with an acute potassium load, particularly in latter stages of the disease. Hyperkalemia resulting... 

Hyperkalemia is generally asymptomatic in patients with CKD until serum potassium levels are greater than 5.5 mEq/L (5.5 mmol/L), when cardiac abnormalities present. 

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. 

Solutions that contain sodium citrate/citric acid (Shohl s solution and Bicitra) provide 1 mEq/L (1 mmol/L) each of sodium and bicarbonate. Polycitra is a sodium/potassium citrate solution that provides 2 mEq/L (2 mmol/L) of bicarbonate, but contains 1 mEq/L (1 mmol/L) each of sodium and potassium, which can promote hyperkalemia in patients with severe CKD. The citrate portion of these preparations is metabolized in the liver to bicarbonate, while the citric acid portion is metabolized to C02 and water, increasing tolerability compared to sodium bicarbonate. Sodium retention is also decreased with these preparations. However, these products are liquid preparations, which may not be palatable to some patients. Citrate can also promote aluminum toxicity by augmenting aluminum absorption in the GI tract. 

The body s normal daily potassium requirement is 0.5 to 1 mEq/kg (0.5 to 1 mmol/kg) or 40 to 80 mEq (40 to 80 mmol) to maintain a serum potassium concentration of 3.5 to 5 mEq/L (3.5 to 5 mmol/L). Potassium is the most abundant cation in the ICF, balancing the sodium contained in the ECF and maintaining electroneutrality of bodily fluids. Because the majority of potassium is intracellular, serum potassium concentration is not a good measure of total body potassium however, clinical manifestations of potassium disorders correlate well with serum potassium. The acid-base balance of the body affects serum potassium concentrations. Hyperkalemia is routinely seen in... 

---