renal-exam 1-potassium

about 3500 mEq(50-55 mEq/kg), potassium is the primary intracellular cation

120-150 mEq/L

3.5-5 mEq/L

ratio of intra and extra K determinant of resting membrane potential, regulate protein and glycogen syn

decrease: BP, risk of stroke, risk of ventricular arr, inhbiit free radical form, vascular smooth muscle proliferation and arterial thrombosis, strong bones

50 mEq/day, most get 50-150mEq

promotes K into cells, and Na transport out of cells

increase pump activity, increase K into cells

dual mechanism, increase pump activity and stimulate blood glucose, increases insulin

to maintain electroneutrality, metabolic acidosis(increase H in blood, pump increases H into cells and K out of cells, increase in serum K), metabolic alkalosis(decrease H in blood, pump increases H into blood and increases K into cells, decreases serum potassium)

collecting duct, secreted via na-k-atpase pump. reabsorbed via h-k-atpase

activatesin collecting duct, secretion of k into the tubules in exchange for Na

enhances sodium reabsoprtion and increases potassium secretion

increased, potassium secretion increases, and reabsoprtion decreases, seen with polyuria and diuretics

increases 3-4 x's with decreased renal fxn, potassium secreted into sm int and colon in response to aldosterone

3.0-3.5 mEq/L

2.5-3.0 mEq/L

<2.5 mEq/L

every decrease in 0.3mEq/L K, 100 mEq total body K deficit

increased avail of insulin, elevated B2 adrenergic activity, metabolic alk, anabolic states, refeeding syn, treatment of pernicious anemia

MC excess, increased distal sodium delivery, increased flow to the distal nephron

correct both or it will be hard to correct hypokalemia

B2 agonists, theophylline, caffeine, insulin overdose, GM-CSF, diuretics, MCs, high dose GCs, high dose IV PCN abxs, drugs assoc with Mg depletion(AGs, cis, amp B, foscarnet)

muscle weakness, muscle cramps, paresthesia, impairment of respiratory muscle fxn

arr, St segment depression, T wave depression, U-wave elevation

treat underlying cause

Wax matrix capsules-higher incidence of GI ulceratin, microencapsulateed-can be dissolved in H20 or sprinkled on applesauce, effervescent tablets, liquids and powders-tastes bad, Gi irritation, NV, IV-phlebitis can occur

• chloride-use in presence of chloride depletion or metabolic alkalosis
• bicarbonate, citrate, acetate(precursors to bicarbonate, use if metabolic acidosis, gluconate

oral is preferred(less risk of tx-induced hyperkal, no phlebitis), IV-severe hypo <2.5, pts with EKG changes, pts unable to tolerate oral formulation, precautions

needs to be diluted, peripheral more irritation than central(less volume), invert bag and squeeze, can add lidocaine 10-30mg/L, can also burn, central line 100-400 mEq/L, periph 10-100mEq/L

adult: max(no EKG)-10 mEq/hr, (with EKG)-20mEq/hr unless life threatening arr present, then up to 40 mEq/hr

Child: max(no EKG)-0.5 mEq/kg/hr up to a max of 10 mEq/hr, with EKG-1 mEq/kg/hr up to a max of 20 mEq/hr

check serum potassium q 40 mEq of potassium replaced

40-100 mEq/d

20 mEq/day

normal: 3.5-5, 4-4.5 mEq/l in pts with CVD disease

salt substitutes (10 mEq K/gm about 200 mEq/tablespoon or potassium containing food-usually coupled with phos or citrate, less likely to correct hypokalemica assoc with calcium depletion(diuretic induced), hypokal assoc with hypomag-magnesium oxide (mag ox 400 qid) po or magnesium chloride (slow-mag qid)

5.0-6.0 mEq/L

6.1-6.9mEq/L

>7mEq/L

salt substitutes, enteral nutrition, dietary supplements, K repletion, metamucil effervescent

pseduohyperkalemia(hemolysis of RBC), metabolic acidosis, insuin deficiency(diabetic ketoacidosis), tissue catabolism(trauma, tumor lysis syn, rhabdomyolysis)

hypoaldosteronism(addison's, retaining more K), decreased sodium delivery, renal failure

ACE/ARBs(hypoaldosteronism), potassium-sparing diuretics(ami, triam, spirono, eplerenone)(impaired potassium excretion), dig toxicity(decreased Na-k-atpase activity_

muscle weakness (K>7 mEq/L)-more common with hypokalemia

palpitations, peaked T wave (>5.5-6), prolonged PR interval and widening of QRS (6-7), slowed cardiac conduction (7-8), ventricular fibrillation (9-10_ asystole (10-12)

antagonize action on heart with calcium, redistribute K inside cells (insuline and albu) remove excess potassium(diuretics, SPS, hemodialysis)

decrease intake, d/c offending agents, diuretics(furo 20-40 mg po or IV (over 5 min)q 4-6 hr prn

antagonize action on cardiac muscle, redistribute potassium

with ca gluc (or chloride-3 x's more ca bad with extrav) 1 gm over 5-10 min(slow IV push), onset 1-2 min, dur:30 min, may repeat if no effect in 5-10 min(short-term, will only buy time)

insulin 10 units plus or minus glucose 50 gm over 5 minutes, onset 10-20 min, duration 4-6 hours(drives K into cells) or albu 10-20 mg nebulized, onset-30 min, duration-2 hours

1. diuretics 2. SPS-4-6 hours for onseet, use in caution with CHF risk of volume overload, exchanges 1 mEq potassium for 1 mEq/sodium/gm of resin, PO-15-60 gm in 60-240 mL of 20% sorbitol, rectal dose 30-60 gm + 150 ml water, 3. hemodialysis(most effective, but takes awhile to set up)

if decrease aldosterone level-fludrocortisone 0.1 mg PO d to TIW, if increased aldosterone level and increase BP-diuretic, if above efforts fail, low potassium diet plus or minus kayexalate...after measuring aldosterone levels