ghazal Serum K level lt35 meq l It can be divided into disorder of internal balance shifting between intracellular and extracellular External balance decrease K intake and increased output ID: 928023
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Slide1
hypokalemia
Dr
bandar
ghazal
Slide2Serum K level <3.5
meq
/l
It can be divided into disorder of :
internal balance ( shifting between intracellular and extracellular ) .
External balance (decrease K intake and increased output ) .
Slide3K level 3 – 3.5
meq
/l usually asymptomatic , because the ratio of intracellular to extracellular K is the main determinant of the membrane potential of electrically active tissue .
Weakness .
Paralysis .
Decrease GI motility , nausea , ileus .
Cardiac arrhythmia .
Rhabdomyolysis
in
sever hypokalemia .
Slide4On ECG :
ST depression
Decrease T wave amplitude
Increase U wave amplitude
V.
Tach
, V. fib .
Slide5Slide6Slide7Slide8Approach
Cause of hypokalemia usually can determined by HISTORY
and lab evaluation
Rarely hypokalemia is spurious :
As it may occur with leukemia or high leukocyte , when delayed sample process allow large number of leukocyte to take up K .
Slide9Internal balance
:
Usually Total body K is ok , problem in distribution .
Insulin B2 agonist
Shift K to intracellular
Soluble barium intake
Block k exit from cells
Can produce sever hypokalemia with level below 2
meq
/ l
Increased cell production after repletion with B12 ,
folate
can cause hypokalemia .
Slide10Hypokalemic periodic paralysis :
Autosomal dominant disorder
Acquired disease occur with hyperthyroid PT
Present with attacks sever muscle weakness and paralysis .
Slide11External balance
:most common
Total body K deficit
Either due to :
decrease intake :
Only Severely compromised k diet can lead to hypokalemia , as the kidney can cease K excretion .
Or
increased excretion :
The major determinants of renal K excretion is distal tubular flow and aldosterone .
Gold standard to distinguish between renal and extrarenal loss is 24 hour urine collection for K
Alternative spot urine K – creatinine ratio a value <13
meq
/g identify extrarenal losses ( GI , lack intake , shift )
Slide12GI loss such as diarrhea and laxative abuse
Frequently metabolic acidosis is present
Renal loss :
Medications such as diuretic
Aldosterone excess (HTN , metabolic alkalosis )
Hypomagnesemia
Tubular defects (
liddle
,
bartter
,
gitelman
syndrome
Renal tubular acidosis )
Slide13Slide14Liddle
syndrome :
Rare genetic (autosomal dominant )cause of HTN hypokalemia metabolic alkalosis
NA retention
Caused by mutation in Na channel in principle cells of the late distal tubule and collecting duct
Renin and aldosterone level are decreased
Treated by
amiloride
Triamterene
Slide15MANAGEMENT
For each 1
meq
/ L decrease in k plasma level the total body k deficit can be up to 200
meq
.
IV K 20
meq
/h via peripheral line ( Maximum )
IV k 40
meq
/ h via central line , with close monitoring
Oral supplement for mild hypokalemia (3 - 3.5 ) with k chloride , k bicarbonate
Concurrent
hypomagnesemia
should be treated to prevent ongoing K loss
K sparing diuretics : in case of K wasting