intracellular potassium is maintained at?
140 mEq/L
transcellular distribution of K+ is largely determined by the _______
Na/K ATPase
acidemia can result in potassium ____ due to ____ exchange
efflux from the cell; H+/K+ exchange (usually with HCl retention rather than organic acid)
what happens to ingested K+?
some is distributed into cells with help in insulin; most of it is excreted into urine due to aldosterone (6-8 hours)
high levels of insulin have what effect on K+?
increased cellular uptake of potassium and decreased serum potassium
activation of beta-adrenergic receptors has what effect on K+?
uptake into cells
how to non-selective beta-blockers affect potassium levels?
cause hyperkalemia (beta agonists cause hypokalemia)
digitalis toxicity and hyperglycemia cause ____kalemia
hyper-kalemia (the first inhibits Na/K ATPase, in the second K+ follows water out of cells)
how does DKA affect potassium levels?
patients have hyperkalemia initially (from decreased insulin + hyperglycemia) but an overall low level of potassium and ultimate hypokalemia once insulin corrects the hyperglycemia (due to osmotic diuresis)
key site of potassium excretion regulation
cortical collecting duct
name three mechanisms for increased excretion of potassium in the CCD
increased flow; increased tubular lumen negativity; aldosterone (through increased Na reabsorption and increased potassium channels on principle cells)
clinical signs of hyperkalemia
ascending muscle weakness, ECG changes, cardiac arrhythmias, paralysis when severe
ECG signs of hyperkalemia
peaked T waves with a shortened QT interval initially, followed by increased PR interval and QRS duration, eventually V fib
potential causes of pseudohyperkalemia
thrombocytosis, leukocytosis
healthy adults should be able to secrete up to ___mEq potassium without developing hyperkalemia
280 (normal = 70)
causes of impaired excretion of potassium
defect in RAAS, decreased GFR, defect in the CCD, drugs that cause any of these three things
causes of redistributive hyperkalemia
tissue injury, insulin deficiency, metabolic acidosis, hyperosmolarity, drugs (digoxin, octreotide, beta blockers, somatostatin), oleandar toxicity
causes of hypoaldosteronism in setting of high renin
adrenal insufficiency, enzyme defects, meds (ACE inhibitors, ARBs, heparin, ketoconazole)
causes of hypoaldosteronism in setting of low renin
diabetes mellitus, HIV, meds (NSAIDs, Cox-2 inh, calcineurin inh)
causes of collecting duct defects
meds (amiloride, triamterene, spirinolactone, eplerenone, trimethoprim, pentamidine), tubulointerstitial dz, urinary tract obstruction, defective mineralocorticoid receptor, Gordon syndrome
tx of symptomatic hyperkalemia (or with ECG changes)
IV calcium-chloride or calcium-gluconate (antagonize depolarization) every 5 minutes (unless digoxin toxicity) and insulin, sodium bicarb, and/or nebulized albuterol all temporarily correct hyperkalemia by pulling K+ into cells
tx of hyperkalemia in pt with kidney failure
hemodialysis, loop diuretics to decrease total K+, (sodium bicarb won’t help)
differential for hypokalemia
redistribution, kidney or GI losses, or decreased intake
clinical signs of hypokalemia
abnormal skeletal and cardiac muscle function, including arrhythmias, ECG changes, muscle cramps and weakness, ileus, glucose intolerance
