Overview and Management of Potassium Disturbances
Definition
HYPOKALEMIA

K < 3.5 mmol/L
Clinical Manifestations



Neuromuscular: weakness,
paralysis, rhabdomyolysis
(K < 2-2.5)
CV: arrhythmia (v-tach, v-fib),
prolonged QT, PVC’s, U waves
Renal: nephrogenic diabetes
insidpidus, increased ammonia
formation, metabolic alkalosis
Causes




HYPERKALEMIA


K >5.5 mmol/L
Pseudohypekalemia:
K may be falsely elevated
w/:
 hemolysis
 WBC>100,00
 platelets> 800,000
 hereditary
spherocytosis



Neuromuscular: weakness,
paralysis
acute changes are most
dangerous and associated w/
arrhythmia
EKG Changes:
K = 6-7: peaked T waves
K = 7-8: widened QRS,
decrease P amplitude
K = 8-9: sine waves
K > 9: AV dissociation, V-tach,
V-fib








Work-Up
GI losses: diarrhea, laxatives, villous
adenoma, VIPoma
o Intestinal secretions have high
amounts of K
Renal losses: diuretics, mineralcorticoid
excess, vomiting, NGT suction, DKA,
osmotic dieresis, RTA I & II,
hypomagenesium, PCN, amphotericin,
foscarnet, salt wasting nephropathy
o gastric losses  metabolic
alkalosis  increase distal K
secretion
Transcellular shift: alkalemia, insulin
excess, B adrenergic stimulation
(albuterol), high cell proliferation (after
epgoen, GM-CSF, AML)
Other: dialysis, plasmapheresis, sweat
loss, decrease intake from extreme
malnutrition

assess symptoms, BP,
acid-base status, and EKG

24 urine K:
UK > 30 mmol/day 
renal loses
UK <25 mmol/day 
extrarenal losses
Increase Intake: diet ie renal failure
pt, overshooting replacement
Transcellular Shift: academia, insulin
deficiency, hyperosmolality (glucose,
contrast), increase cell destruction,
blood transfusion, beta-blockade,
digoxin OD, vigorous exercise,
succinylcholine
Decrease Renal Excretion:
renal failure
hyporeninemic hypoaldosteronism: DM
nephropathy, NSAIDs, CSA
hypoaldosteronism: adrenal
insufficiency, CAH, ACEI/ARB,
heparin, spironolactone
decreased aldosterone action:
amiloride, triamterene, trimethoprim,
pentamidine, tacrolimus
hyperkalemic type I RTA: decreases
effective circulatory volume


Transtubular K Gradient:
TTKG =
(Urine K) (Plasma Osm)/ (Urine
Osm) (Plasma K)
TTKG > 4 =
renal/endocrine defect
TTKG < 2 = extrarenal
causes

Assess symptoms, diet,
TPMN, med list, BP, acid
base status, EKG
Calculate transtubular K+
gradient
- TTKG > 10 =
extrarenal causes
- TTKG <7 = renal or
endocrine causes
Treatment

mEq KCL needed =
(desired K-measured K)/sCr X 100

Oral Repletion: preferred
method, up to 40 mEq/hr
more  GI upset,
diarrhea, esophagitis

IV Repletion: for symptomatic
pt and EKG changes

Peripheral line: max 10
mEq/hr

Central line: max 20 mEq/hr
(use only for arrhythmias, pt
on cardiac monitor, frequent K
check)

May give PO and IV K+
simultaneously

Replete Mg or patient will be
refractory to K replacement
K = 5.5-6.5, no EKG changes
 d/c offending drugs, diet
 kayexalate: cationic
exchange resin, 15-45
grams po q4-6h prn, avoid
in SBO or ileus
 loop diuretics
K>6.5 + EKG changes or K>8
 CaCl or Ca Gluconate 1 gm
over 2-5 min prn on cardiac
monitor
 Insulin 10 units IVP + D50 1
amp, decrease K up to 1
mmol/L, works in 15-30 min
 NaHCO3 1 amp over 5 min
q30 min, less effective if no
acidosis or in ESRD, works
30-60 min
 Albuterol nebs 10-20 mg,
works 60-90 min
 kayexalate, diuretics
 dialysis