This document discusses potassium management and provides key details about hypokalemia and hyperkalemia. It covers: - Causes of hypokalemia including redistribution, extrarenal loss, and renal loss. Redistribution can be caused by alkalosis, medications, or increased sympathetic tone. Extrarenal losses include diarrhea, laxative abuse, and sweating. Renal losses are associated with metabolic acidosis or alkalosis. - Treatment of hypokalemia focuses on replacing deficits orally or intravenously, while also treating underlying causes. - Causes of hyperkalemia include increased intake, pseudohyperkalemia, transcellular shifts during conditions like tumor l

1. Potassium Management
Marica A. Lazo, MD

2. Potassium Pearls
O Potassium is the major intracellular cation.
O A healthy adult has roughly 50 mEq/Kg of K+ in
his/her body.
O 70 Kg man = 70x50 = 3500 mEq in body
O Only 2% is found outside the cells and of this only
0.4% of your K+ is found in the plasma.
O Thus serum K+ measurements have limitations at
reflecting TOTAL body K+ stores.
O A 1 mEq/L drop in K+ reflects between 200-400 mEq
total body K+ deficit
O Example: a K+ of 2.5 means that someone is
roughly 300 mEq in the negative. This would
require 7 boluses of 40 mEQ of K+ to make up for
this!

3. Hypokalemia
O Clinical consequences of hypokalemia
usually goes unnoticed.
O Common findings include weakness,
fatigue, constipation, ileus, and respiratory
muscle dysfunction.
O Symptoms seldom occur unless plasma
K+ is less than 3.0 mmol/L.

4. ECG changes
O ST depressions with prominent U waves
and prolonged repolarization

5. ECG changes

6. Hypokalemia - Causes
O Spurious - i.e. K+ is falsely low
O Diminished intake
O Redistribution – i.e. movement into cells
O Extrarenal loss – usually associated with
preservation of renal K+
O Renal loss – often associated with acid-
base disturbances.

7. Spurious Hypokalemia
O Marked leukocytosis and blood tube that
has been sitting at room temp too long
gives time for K+ to enter the white blood
cells and thus falsely lower K+ value.
O Insulin given just prior to blood draw
allows a small amount (about 0.3 mEq) to
shift into cells in the blood tube.

8. Redistribution Hypokalemia
O Transcellular shift
O Alkalosis (response H+ out K+ in) – a key
point is that alkalosis disorders are usually
involved in depletion of total body K+ in
addition to redistribution.
O Increased B adrenergic effect – increases
Na/K ATPase activity. Think of both
medications or increased sympathetic
tone like MI, head trauma, DTs, and
theophylline toxicity.

9. Redistribution Hypokalemia
O Other causes of hypokalemia due to cell
entry include risperidone, quetiapine, and
cesium, hypothermia, barium intoxication,
chloroquine intoxication.

10. Extrarenal K+ Loss
Urine K+ < 20 mEq/24 hours or spot urine K+ of < 30
O Diarrhea – causes loss of HCO3 and K+
thus you get metabolic acidosis +
hypokalemia.
O Chronic Laxative Abuse
O Sweat – 9 mEq/L of K+ in sweat.
O Fasting/inadequate diet – usually no more
than total body deficit of 300 mEq.
O Villous adenoma at rectosigmoid

11. Renal K+ Loss
Urine K+ >20 mEq/24 hours or spot urine K+ of > 30
O Renal hypokalemia with metabolic
acidosis
O RTA type I (distal) and type II (proximal)
O DKA
O Carbonic anhydrase inhibitor therapy
O ureterosigmoidostomy

12. Renal K+ Loss
Urine K+ >20 mEq/24 hours or spot urine K+ of > 30
O Renal hypokalemia with metabolic
alkalosis:
O Almost always occurs with hypokalemia
because virtually every cause of metabolic
alkalosis also causes hypokalemia.
O The excess HCO3 acts as a poorly
reabsorbable anion and carries more Na+
to the collecting tubules leading to
increased Na-K exchange and urinary K
loss.

13. Renal K+ Loss
Urine K+ >20 mEq/24 hours or spot urine K+ of > 30
O Renal hypokalemia with no acid-base
disorder:
O Recovery from ARF, postobstructive
diuresis, and osmotic diuresis, PCNs all
increase Na delivery to collecting tubules
resulting in increased K excretion.
O Low magnesium- think of with resistant
cases. Hypomagnesemia is present in up
to 40% of patients with hypokalemia

15. Renal Vs Extra renal loss
 Urinary K+: > 20 mEq/L – Renal loss
 Urinary K + : < 20 mEq/L – Extrarenal loss
 TTKG : Transtubular Potassium Gradient
( Urine K+ / Plasma K+ )
( Urine Osm / Plasma Osm )
 TTKG : Renal loss : > 4
Extra renal loss : < 4

16. Treatment
O Therapeutic goals
O Prevent life-threatening complications
(arrhythmias, respiratory failure, hepatic
encephalopathy)
O Correct the K+ deficit
O Minimize ongoing losses
O Treat the underlying cause

17. Treatment
O K+ deficit
O (4 – Actual K+) x 300
2
O (4 – 2.5) x 300 = 225 meqs
2
O Estimation of K+ deficit
O 3.0 meq/L= total body K+ deficit of 200-400
meq/70kg
O 2.5 meq/L = 500 meq/70kg
O 2.0 meq/L = 700 meq/70kg

18. Treatment
O Oral therapy
O Generally safer
O Degree of K+ depletion does not correlate
well with the plasma K+
O KCl is usually the preparation of choice
O Kalium durule: 1 durule = 10 meqs KCl
O KCl syrup: 1meq/mL
O Ie. Kalium durule 750mg TID PO x 2-3days
or KCl syrup 15-30cc TID

19. Treatment
O IV therapy
O For severe hypokalemia or those who are
unable to take anything by mouth
O Maximum rate at which potassium is infused
into peripheral veins is usually 10 meq/hr
O Central – 20 meq/hr
O Rate of infusion should not exceed 20
meq/hour unless paralysis or malignant
ventricular arrhythmias are present
O Ie. 40 meqs KCl in 230cc PNSS x 5meq/hr
(32cc/hr) OR 20 meqs KCl in 100cc PNSS x
1hr

20. Hyperkalemia
O Remember that total body K+ is roughly
50 mEq/kg and only a small fraction if
found outside the cells.
O Contrary to struggling to try to replace a
low K+ with mEq after mEq and watching
it slowly climb into the normal range; only
a small shift of intracellular K+ to the
extracellular space or a small amount of
K+ given to a person with a bad kidney
can cause quick problems.
O To get a serum K+ rise by 1 meq/L you
only need to give 100-200 meq of extra
K+.

21. Hyperkalemia
O The most serious effect of hyperkalemia is
cardiac toxicity
O Hyperkalemia partially depolarizes the cell
membrane, which impairs membrane
excitability and is manifest as weakness
that may progress to flaccid paralysis and
hypoventilation if the respiratory muscles
are involved

22. Hyperkalemia - Causes
O Increased K+ intake
O Rarely the sole cause
O Iatrogenic hyperkalemia may result from
overzealous parenteral K+ replacement or
in patients with renal insufficiency
O Pseudohyperkalemia
O Artificially elevated plasma K+ due to K+
movement out of the cells immediately
before or following venipuncture

23. Hyperkalemia - Causes
O Transcellular shift
O Tumor lysis syndrome and rhabdomyolysis
lead to K+ release from cells
O Metabolic acidosis can be associated with
mild hyperkalemia resulting from
intracellular buffering of H+
O Insulin deficiency and hypertonicity
promote K+ shift from the ICF to the ECF

24. HYPERKALEMIA
PSEUDOHYPERK K RETENTION REDISTRIBUTION
GFR < 20 ml/min GFR > 20 ml/min
Hemolysis Renal failure Acidosis
Thrombocytosis Insulin deficiency/DKA
Leukocytosis Beta blockers
Mononucleosis Aldosterone Tubular hyperK Periodic paralysis
deficiency Acquired Digitalis intoxication
Addison’s disease SLE Succinylcholine
RTA Type 4 Obstr. Uro. Exercise
Drugs Amyloidosis Tissue damage
Heparin AIDS
NSAIDs TID
ACE inhibitors Drugs
Cyclosporine Trimethoprim
K sparers

25. EKG Changes
Note the ―tented‖ or ―pinched‖ shape to
Twaves

26. Acute Treatment
O Calcium Gluconate 10 ml of 10% solution
(1gram) IV slowly over 5-10 min.
O Decreases membrane excitability
O Temporarily (1 hour) antagonizes cardiac
effects of hyperkalemia while more
definitive therapy is begun.
O Warning: may induce Digitalis toxicity!
O May precipitate if given with NaHCO3.
O May repeat after 5 min. if ECG does not
improve.

27. Acute Treatment
O Glucose/Insulin – 100 ml of 25% glucose
solution with 10 units of Regular insulin.
Infuse over 15-30 minutes.
O Insulin stimulates cellular uptake of K+ by
activating Na+K+ATPase ( decreasing plasma
K+ )
O Temporarily translocates K+ into cells.
O Effect occurs w/in 30-60 min and lasts about 1
hr.
O May induce hyperglycemia, thus if already
hyperglycemic just use insulin.

28. Acute Treatment
O Beta 2 agonists (Albuterol) - 10-20 mg
over 15 minutes via nebulizer.
O Promotes cellular uptake of K+
O Onset 30 minutes.
O Lowers plasma K+ by 0.5-1.5 mmol/L and
the effect lasts for 2-4 hours
O Potentially dangerous in patients with
coronary artery disease!

29. Acute Treatment
O Lasix – 40 to 80 mg IV.
O Especially helpful in aldosterone deficiency
states and renal failure.
O NaHCO3 – 1 standard amp (50mEq) IV
over 5-10 min.
O Can shift K+ into the cells.
O Mostly used with acidemic states.
O Will precipitate with Calcium!!!! Thus don’t
give while using calcium gluconate.

30. Acute Treatment
O Kayexalate (Sodium Polystyrene
Sulfonate) – 15 g ORALLY 1 to 4 times
daily as a slurry in water or syrup.
O Onset 1-2 hours with duration of 4-6 hours.
O Effect—In the intestine (mostly the large
intestine), Na ions are released and are
replaced by K+ and other cations before
the resin is passed from the body.
O Each gram may remove 1 mEq K+ in
exchange for 1-2 mEq Na+ thus may
cause ECF volume overload.

31. TREATMENT OF HYPERKALEMIA
MEDICATION MECHANISM OF DOSAGE PEAK EFFECT
ACTION
Calcium Antagonism of 10-30 ml of 10% 5 minutes
gluconate membrane solution IV over
actions 10 minutes
Insulin and Increased K entry 10 units insulin 30-60 min.
glucose to cells plus 50 ml D20
Sodium Increased K entry 50 meq IV over 5 30-60 min.
bicarbonate to cells minutes
Albuterol Increased K entry 10-20 mg IV or 30-60 min.
to cells nebulized