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POTASSIUM
- Major intracellular cation
- Concentration of 20x greater inside than outside
- Only 2% of K+ circulates in the plasma

FUNCTIONS:
1. Regulation of neuromuscular excitability
2. Contraction of the heart
3. ICF volume
4. H+ concentration

- Elevated plasma K+ levels decreases the RMP (Resting Membrane Potential) of

the cell
o decreases the net difference between the cell’s RMP and threshold
(Action) potential
- A lower than normal difference increases cell excitability  muscle weakness
- Severe hyperkalemia
o Lack of muscle excitability (higher RMP than threshold potential) 
paralysis or fatal cardiac arrhythmias
- Hypokalemia
o Decreases cell excitability by increasing the RMP  arrhythmia or
paralysis
- Extreme Hypokalemia or Hyperkalemia
o Heart cease to contract
- K+ concentration also affect H+ concentration in the blood
o Hypokalemia (low K+ in blood)
o K+ loss  Na+ and H+ moves into the cell  thereby decreasing the H+
in the ECF  leading to  alkalosis

REGULATION:
1. Kidneys
a. Important in the regulation of the K+ levels
2. Proximal tubules reabsorbs nearly all K+  under the influence of aldosterone 
additional K+ is secreted into the urine in exchange of Na+ (distal tubules and collecting
ducts)  distal nephn is the principal determinant of urinary K+ excretion.
3. If renal failure occurs  accumulation of K+ in blood is probable
4. Excess plasma K+  K+ uptake by the cell from the ECF (in response to the increase in
K+)  upon removal of the K+ from the cell, the K+ is eventually secreted by the kidneys

3 FACTORS THAT INFLUENCES THE DISTRIBUTION OF K+ BETWEEN CESS OF THE ECF

1. K+ loss frequently occurs whenever the Na, K, ATPase pump is inhibited by conditions
such as hypoxia, hypomagnesemia or digoxin overdose
2. Insulin promotes acute entry of K+ into the skeletal muscle and liver by increasing Na, K,
and ATPase acitivity
3. Cathecholamines, such as epinephrine, promote cellular entry of K+, whereas propanolol,
impairs cellular entry of K+.

- Exercise
o K+ is released in cells during exercise

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o Forearm exercise during venipuncture can cause falsely elevated results.

- Hyperosmolality
o Uncontrolled DM  water diffuses from the cells, carrying K+ with water
 leads to gradual depletion of K+ (if kidney is normal)
- Cellular breakdown
o Releases K+ into the ECF

HYPOKALEMIA

I. Causes of Hypokalemia
a. GI loss or urinary loss of K
i. GI LOSS
1. Vomiting
2. Diarrhea
3. Gastric suction
4. Intestinal tumor
5. Malabsorption
6. Cancer therapy
7. Large doses of laxatives
ii. URINARY LOSS
1. Diuretics
2. Nephritis
3. Renal tubular acidosis
a. Tubular excretion of H+ decreases  K+ excretion
increases
4. Hyperaldosteronism
a. Aldosterone promotes Na retention thus K+ loss 
together with metabolic alkalosis
5. Cushing’s Syndrome
6. Hypomagnesemia
a. Promotes urinary loss of K+
b. Also diminishes Na, K, ATPase and enhances the
secretion of aldosterone
7. Acute leukemia
a. Acute myelogenous leukemia
b. Induces renal loss of K+
b. Increased cellular uptake of K+
i. Cellular shift
1. Alkalosis/alkalemiaar u
a. Promotes intracellular loss of H+
b. Minimizes elevation of intracellular pH
c. Plasma K+ decreases by about 0.4 mmol/L per 0.1
unit rise in pH
2. Insulin overdose
a. Promotes entry of K+ into skeletal muscle and liver
cells

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II. Signs and Symptoms

a. K+ decreases below 3 mmol/L
b. Weakness
c. Fatigues
d. Constipation
e. Muscle weakness or paralysis  can interfere breathing
f. Increased risk of arrhythmia
i. Can cause sudden death to patients

III. Treatment
a. Oral KCl replacement of K over several days
b. IV replacement
c. Chronic Mild Hypokalemia
a. Increase food intake rich in K+
i. Dried fruits, nuts, bran cereals, bananas and orange juice

HYPERKALEMIA

- Patients with hyperkalemia usually has an underlying diseases

I. Causes of Hyperkalemia
a. Decreased Renal Excretion
a. Acute or chronic renal failure
b. Hypoaldosteronism
c. Addison’s disease
d. Diuretics
b. Cellular Shift
a. Acidosis
b. Muscle Injury
c. Chemotherapy
d. Leukemia
e. Hemolysis
c. Increased intake
a. Oral or IV potassium replacement therapy
d. Artifactual
a. Sample hemolysis
b. Thrombocytosis
c. Prolonged tourniquet use or excessive fist quenching

II. Signs and Symptoms

a. Muscle weakness
b. Tingling
c. Numbness
d. Mental confusion

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i. Altering neuromuscular conduction

e. Disturbs cardiac conduction
i. Cardiac arrhythmias
ii. Cardiac arrest
f. More than 10 mmol/L
i. Fatal cardiac arrest

III. Treatment
a. Ca2+ may be given to reduce the threshold potential of myocardial cells
b. Ca2+ provides immediate short-lived protection
c. Sodium bicarbonate, glucose or insulin
i. To promote cellular shift of K+ back into the cells
d. Diuretics
i. Quick removal of K+ from the blood (if renal function is inadequate)
ii. If not, sodium polysterene sulfonate enemas (binds to K+ secreted
in the colon)
e. HemoDialysis

DETERMINATION

Specimen
a. Possible artifacts
a. Coagulation process
i. Serum K+ is 0.1-0.7 mmol/L higher than plasma levels
ii. Use HEPARINIZED TUBES
b. Thrombocytosis
i. Elevated K+ levels
c. Hemolyzed samples must be avoided
Methods
a. ISE method of choice
b. Valinomycin  membrane used (to selectively bind the K) causing impedance
change that can correlate to K+ concentration
c. KCl is the inner electrolye solution

REFERENCE VALUE
- Serum 3.5 – 5.1 mmol/L
- Plasma M 3.5 – 4.5 mmol/L
F 3.4 – 4.4 mmol/L
- Urine (24 h) 25-125 mmol/day

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