"Hyperkalemia" (My Synopsis of AFP)

Hyperkalemia
JOYCE C. HOLLANDER-RODRIGUEZ, M.D., and JAMES F. CALVERT, JR., M.D.,Oregon Health & Science University, Portland, Oregon
Am Fam Physician. 2006 Jan 15;73(2):283-290.
http://www.aafp.org/afp/2006/0115/p283.pdf

         Once potassium is ingested, it goes to the pancreas and causes release of insulin. The insulin drives the potassium from the extracellular space into the cells. The increase of potassium also causes the release of renin, which stimulates the conversion of angiotensin I into angiotensin II. The ATII causes secretion of aldosterone, which causes renal excretion of potassium and retention of sodium.
     When evaluating a patient for hyperkalemia, the first step is to rule out the artificial causes, such are hemolysis in the test tube (pseudohyperkalemia), traumatic venipuncture, lab error, and repeatedly making a fist during the blood draw. The three true causes of hyperkalemia are;
1. medication side effects
2. altered distribution of potassium between the cells and the extracellular space
3. impaired renal excretion
     Medication induced hyperkalemia is commonly seen in patients who take ACEI with spironolactone. NSAIDs will decrease renin, which will decrease potassium excretion.  Adrenal insufficiency will cause hyperkalemia, hyponatremia, and muscular weakness. Impaired renal excretion is caused by renal failure, renal hypoperfusion, and hypoaldosteronism. Congential causes include pseudohypoaldosteronism, which is aldosterone resistance of the kidney. Hyporeninemic hypoaldosteronism is associated with RTA IV. It can be treated with fludrocortisone.
     Symptoms of hyperkalemia include muscular weakness, flaccid paralysis, ileus, and ECG changes (peaked T waves, loss of P wave, widened QRS). Lab tests include serum electrolytes, spot urine, transtubular potassium gradient, and fractional excretion of potassium. Patients may also present with decreased renal function and metabolic acidosis.
     ECG changes, acidosis, or a potassium level of 6.0 mEq is typically the cutoff point for emergent potassium reduction. If the ECG is abnormal and the potassium is elevated, then calcium gluconate can be given. Calcium gluconate will protect the myocardium against the potassium, but does not lower it. Insulin or a beta-2 agonist can be used to drive the extracellular potassium into the cell, but the total body potassium is not lowered. Kayexalate will bind the potassium in the colon and excrete it, thus lowering the potassium. Sorbitol can be given with it to reduce constipation. Furosemide can be added to reduce volume overload from the increased sodium (it was exchanged for the potassium in the colon). Potassium can be excreted renally by using loop diuretics as well, as long as the renal function is intact.