Hyper/Hypo- kalemia Flashcards
2 mechanisms leading to hyperkalemia
redistribution from or into cells
decreased urinary excretion
5 factors driving K into cells, hypokalemia
insulin, B2 stimulation, alkalosis, anabolism, hypoK periodic paralysis
6 factors driving K out of cells, hyperK
insulin deficit, increased tonicity, cell injury, nonselective B blocker, alpha stimulation, mineral acidosis
contrast mineral and organic acidosis w/ cellular K shift
mineral: causes hyperkalemia as H+ are exchanged for K+ to maintain neutrality, Cl- cant enter cell
organic: no hyperkalemia because organic anions can enter cell w/ H+, maintining neutrality w/o k+ exiting
3 factors impairing K+ excretion
- more positive lumen
- low flow and Na delivery to CCD
- low aldo or aldo activity
describe the effects of amiloride on CCD and pH/electrolytes
block ENaC channels:
- lumen more positive
- less K+ excretion (K sparing diuretic)
- higher serum K+
- less H+ secretion
- lower arterial pH
example of a hyperkalemic distal RTA, type IV
risk factors for hyperkalemia
low eGFR
anything that interferes with RAAS- HIV, DM, meds like ACE inhibs, heparin, NSAIDs, ketoconazle
CHF
causes of psueodhyperK, lab errors
hemolysis w/i tube, excess tourniquet, severe leukocytosis/thrombocytosis (plts clump and relaese K+ in tube)
after ruling out a solely cellular redistribution cause of hyperK, what is the next step?
problem of low renal excretion:
- renal failure w/ low GFR
- low urine flow from hypovolemia
- hyperK distal RTA
6 categories of hyperK distal RTA causes
interference w/ RAAS pathway or end target ENaC
- impaired renin- HIV, DM, NSAIDs, tacrolimus
- ACE inhibs
- ARBs
- impaired aldo metabolism- adrenal disease, heparin, ketoconazole
- aldo receptor blockers- spironolactone and eplerinone
- ENaC blockers- amiloride, triamterene, pentamidine (also pseudohypoaldo type I- loss of fn at ENaC)
2 types of hypoaldo found in hyperK distal RTA
low renin- blocking RAAS upstream of renin release (DM, HIV, UTO, NSAIDs)
high renin- problem downstream of renin, up of aldo (ACEi, ARBs, heparin, adrenal insufficiency)
what can make excess K intake a problem
w/o normal kidney fn, healthy kidney can excrete most excess K
salt subs, juice, clay, burnt matches, excess bananas can be problems
describe the EKG changes from hyperK
tall peaked T wave w/ short QT at K=6, gets worse w/ higher K values, eventually lose p wave and have ventricular block then v-fib around K=9
causes by increased membrane potential, eventually this is above the threshold and no regulation against firing potentials
protective therapy w/ EKG changes
IV Ca, brings threshold for depolariztion back above the membrane potential that has been elevated by high K
3 categories of hyperK tx
stabilize Em: IV Ca
increase cellular entry: insulin, B2 agonist (albuterol), bicarb (w/ pH lower than 7.2)
K removal: dialysis, exchange resin (Na polystryrene sulfnonate), maybe loop/thiazide diuretics
DDx of hypokalemia (3)
increased cell entry, low intake or GI loss, renal losses
3 factors enhancing K+ renal excretion
more negative CCD lumen, more flow/Na delivery to CCD, more aldo
how to distinguish b/w GI loss (and prior diuretic use), redistribution and kidney loss (or current diuretic use)
urine K/Cr ratio: K/Crx100
below 13-15= GI loss or redistribution
above 20= renal loss or current diuretics
which diuretics/ syndromes cause hypoK
loop (bartters syndrome): less Na and K reabsorption at NKCC
thiazide (Gitelman): less Na reabsorb at NCC
both cause increase Na delivery and flow rate to CCD (more K secretion) and volume loss which stimulates RAAS, aldo to secrete more K
what should be considered w/ hypoK w/o HTN
assess urinary K excretion w/ K/Cr ratio: distinguish b/w GI and renal losses
if renal, determine acid base status
- acid: RTA, toulene, DKA
- alkali: diuretics, vomiting, NG suction, Bartter/gitelman
- neutral: leukemia, polydipsia, tylenol OD
what should be considered w/ hypoK w/ HTN
measure renin and aldo
high in both: renal HTN, renin tumor, malignant HTN
high aldo low renin: primary aldo
low both: SAME, Liddle, cushings
ALL w/ HTN will have alkalosis (either aldo or aldo effects cause more H+ secretion)
tx of hypoK
hard to estimate K deficit, dont want to overshoot
give KCl 40-60 mEq at a time
