Hypokalemia &

Hyperkalemia
Koay Khang Siean
Pharmacist

Pre-test
Which of the following medications
will cause hyperkalemia?
a.
b.
c.
d.
e.
f.

Frusemide
Spironolactone
Valsartan
Enalapril
Hydrochlorothiazide
All of the above

Normal plasma concentration: 3.5-5

mmol/L

1 mmol K= 1 mEq K (EqUS)

98% Intracellular, 2% Extracellular
Balance between IC and EC is
maintained by
a. Hormones: Aldosterone,
Cathecolamine (epinephrine)
b. Insulin
c. Acid-base balance
Renal (main) and Gastrointestinal
excretion

Aldosterone
H2O & Na reabsorption
Potassium lost

Hypokalemia
Definition:

mmol/L

Serum concentration < 3.5

Causes
Mechanism

Clinical scenario

Causes

Increased K+
shift to IC

Increased pH
Insulin/ carbohydrate load
2-receptor agonist
Hypothermia

Metabolic alkalosis
ISS/Insulin infusion
Salbutamol

Increased GI
losses

Vomiting
Diarrhea
Interstinal fistula
Enteral tube drainage
Chronic laxative use

Increased
urinary losses

Mineralcorticoid excess
Diuretic use

Aldosterone
Loop & thiazide
diuretic

Bartter syndrome, which presents as normotension, hypokalemia,

hypochloremic metabolic alkalosis, and renal potassium wastage, is
characterized by impaired renal sodium and chloride reabsorption.

Hypokalemia 2 Hypomagnesemia
>50%

of cases of clinically significant hypokalemia

Effect: reducing the intracellular potassium
concentration and promoting renal potassium
wasting.
Mechanism :Mg impairs the function of the
sodium-potassium ATPase pump, thereby promoting
potassium wasting.
When concomitant hypokalemia and
hypomagnesemia exist, the magnesium deficiency
should be corrected first; other wise, full repletion of
the potassium deficit is difficult to achieve.

Drug induced hypokalemia

Treatment of hypokalemia
Reduction

of potassium losses
Replenishment of potassium stores
Evaluation for potential toxicities
Determination of the cause to prevent future
episodes, if possible

every
200-400
1 mmol/L mmol
=
deficit in
K store
For serum K < 3 mmol/L

Electrolyte Condition
Dose1
s
Potassium, Asymptomatic,
40-100mmol/day divided in 2-5
PO
mild hypokalemia doses
Limit 20-25 mmol/dose
Mild-Moderate
May up to 120-240 mmol/day in 3-4
hypokalemia
divided doses
Limit 40-60 mmol/dose
Prevention of
20-40 mmol/day in 1-2 divided doses
hypokalemia
Potassium, Serum K 2.5-3.5
Max infusion rate: 10
IV
mmol/L
mmol/hour
Max conc: 40 mmol/L

Max 24hour dose: 200

mmol
Serum K
Max infusion rate: 40
<2.5mmol/L
mmol/hour

Max 24hour dose: 400

mmol
Central line only,
continuous ECG

Quiz
time

1 tablet of SLOW-K contains how

many moles of K?

Tipssssss: Back to form4 chemistry class~~~

Given molecular weight of K = 39; Cl = 35.5

Mole = gram / molecular weight

= 600mg/ (39+35.5)
= 8 mmol

SLOWK

mmol
/tab

If 1 tab of SLOW-K 600mg = 8 mmol

how many mEq of K in 1 ml of IV KCl ?

1amp KCl= 1g/10ml KCl=1000mg/10ml

Mole = gram / molecular weight
= 1000mg/ (39+35.5)
= 13.4 mmol/amp
= 1.34 mmol/ml
= 1.34 mEq in 1 ml

Closer look to
what we have

SLOW-K tablet
Slow

released tablet
1 tablet contain 600mg KCL (8 mmol K)
Associated with GI erosion
Counseling point
1.
2.
3.

Take with meals and full glass of water

or other liquid
Do not crush/ chew the tablet
Sit up-right

KCl 1g/10ml Injection

1

amp contains 1g KCl (13.4 mmol K)

Whenever possible, IV KCl should be
prepare in saline solution. Dextrosecontaining solution will _____________
and worsen the existing hypoK
Rate?
Dilution?
Line?

Line

Max Dilution

Max Rate

Peripheral vein

10 mmol in 100ml

10 mmol/hour

Central vein

20-40mmol in 100ml

40 mmol/hour

Common practice:
1g KCl in 1 pint NS over 1 hours, administer through
peripheral vein.
Dilution: 13.4 mmol/500ml = 0.03 mmol/ml
Rate: 13.4 mmol/1= 13.4 mmol/hour
1g KCl in 100ml NS over 1 hours, administer through
peripheral vein.
Dilution: 13.4 mmol/100ml = 0.134 mmol/ml
Rate: 13.4 mmol/1= 13.4 mmol/hour

Non-pharmacotherapy

Hyperkalemia
Definition: Serum potassium > 5 mmol/L
Severity

Serum level

Mild

5.1-5.9 mmol/L

Moderate

6-7 mmol/L

Severe

>7 mmol/L

System

Symptoms

ECG changes

CVS

Ventricular fibrillation, asystole

Neuromuscular

Muscle weakness, flaccid paralysis, deep tendon

reflex depressed or absent

threshold
potential

HypoNa
HypoCal
HypoMg

susceptibility to the cardiac

effects of hyperkalemia

Causes
Mechanism

Clinical scenario

Increased intake

CKD

K+ shift ICEC

Acidosis
Insulin deficiency
-adrenergic blockade
Digoxin overdose
Rewarming after hypothermia (after cardiac
surgery)
Succinylcholine

Reduced urinary
excretion

Kidney dysfunction
Intravascular volume depletion
Hypoaldosteronism
Drug induced

Pseudohyperkalemia: hemolysis/ thrombocytosis/ leucocytosis, release of IC K

into serum

Drug induced hyperkalemia

There are 5 key steps in the

treatment of hyperkalemia

Never walk away without

completing all of these steps

Drug therapy in hyperkalemia

Regime

Dose

Potassium
lowering effect

Comment

Calcium gluconate

10 ml over 2-10
min.
2nd dose after 5min.

Onset: 1-3min
Duration: 30-60min

IV Insulin +
Dextrose

IV 10 U Insulin +
50ml D50 over 530min

0.6-1 mmol

Onset: 15-30min
Duration: 2 hours

IV Salbutamol

0.5mg over 15min

1 mmol

Onset: 30-60 min

Duration: 2 hours

Neb Salbutamol

10-20mg

10mg 0.52-0.88
mmol
20mg 0.66-0.98
mmol

Onset: 30min
Duration: 2 hours

IV Insulin + IV
Salbutamol

1.5 mmol

Peak: 60min

IV Insulin + Neb
Salbutamol

1.2 mmol

Peak: 60min

Sodium bicarbonate

50ml over 5min

Insufficient evidence

Onset:~30min

Calcium polystyrene
sulfonate

15-30g q4-6hours

1g resin 2mmol
K

Onset: slow

Dialysis

1.2-1.5 mmol

Calcium gluconate
Dose: IV calcium gluconate 10% 10-20ml over 1 to
3 minutes.
Mechanism: Calcium counteracts the depolarizing
effect of hyperkalemia by increasing the threshold
potential, thus making it less negative and moving
it away from the resting potential.
When the hyperkalemia presents with a digitalis
overdose, calcium should be used cautiously
because it can worsen the cardiotoxic effects of
digoxin

Comparing two calcium salts

Calcium
chloride
1g
=elemental Ca 273mg
=Ca 13.6 mEq
=Ca 6.8 mmol
(3x > Cal glc)

Risk of extravasation
*tissue necrosis
Central line preferred

Calcium
gluconate
1g
=elemental Ca 93mg
=Ca 4.65 mEq
=Ca 2.33 mmol

Can be administered
peripherally

After Calcium
Shift K into cell
Insulin

+ glucose
Neb -agonist
IV -agonist
Insulin + glucose+ agonist

Insulin + Glucose
Dose: IVP regular insulin 10 U + 25g glucose
Mechanism: Insulin activity of Na-K-ATPase
activity
Glucose prevent hypoglycemia
> 13.9 mmol, insulin alone can be used.

Quiz
time
25g of glucose= ? amp
Dextrose 50

Dextrose 50 = 50%
= 50g dextose /100ml
25g dextrose= 50ml dextrose
= 5 vials (1 vial =10ml)

-agonists
Dual-mechanism
1. Stimulate Na-K-ATPase pump to
promote cellular uptake.
2. Stimulate pancreatic -receptor to
increase insulin secretion

Drug

Dose

Salbutamol IV 0.5mg over 15min

(Albuterol) Neb 10-20mg over 10min (4-5x >dose for
bronchospasm)
Terbutaline SC 0.7 mcg/kg
Remark:
1. Inhaled route variable bioavailability
2. Cardiac side effect: tachycardia (cardiac ischemic ??)
3. 40% of patient may be resistant to salbutamol
4. Patient may be no response if already receiving nonselective 2
blocker
Conclusion: Should not be used alone
Paul N. Lanken. Intensive Care Unit Manual 2013. Elsevier Health Sciences

Sodium bicarbonate
Use in patient with concomitant metabolic acidosis
Mechanism: Raise extracellular pH
Dose: IVB/ IVI 50-100mmol over 5min

Less effective in
1. hyperK not related to metabolic acidosis
2. ESRD
Complication:
3. Volume overload
4. Metabolic alkalosis

Calcium polystyrene sulphonate

Mechanism: Exchange Ca for K GI excretion
Dose:
Oral:
15g TDS-QID ,3-4ml per gram of resin.
Or 15-30g/day in 2-3 dvd, each dose in 30-50ml H2O
More effective, longer transit time
Rectal:
30g resin in 150ml of water or 10% dextrose.
Givas a daily retention enema (at least 9 hours)
Preferred in GI problem.

Concern
Slow effect

1.

Onset 2 hours
Maximum effect not seen at 6 hours
Rectal route more effective but lesser magnitude

GI necrosis

2.

Especially in sorbitol
Risk higher when used as retention enema in patient
who had recent GI surgery and bowel dysfunction
Constipationadd laxative

Conclusion:
1. Stop kalimate when K <5 mmol/L
2. Slow onset, rare but serious side effect
make it a poor choice in acute
hyperkalemia.

Diuretics
Acetazolamide,

Loop diuretics, thiazide

diuretics
+ NaHCo3 mitigate water retention
Should be used in volume expended
patient
Avoid volume depletion reduced
distal nephron flow reduced K
excretion

Dialysis
Hemodialysis-

most effective, remove K

more than peritoneal dialysis
Immediate hypokalemic effect, last
during the dialysis
Glc-free dialysate remove 30% more K
than 200mg/L dialysate

A real story in Malaysia

The killing fruit in renal patients

Thank you