Electrolytes – Part 1 – Potassium (K+) Blood

Sample

1. This is done on the serum of the patient.
   1. Separate serum as soon as possible.
2. Plasma can be used but it gives slightly lower values.
3. The random sample may be taken.
4. Serum or plasma is stable for one week at room temperature or at 1°C to 4 °C.

Precautions

1. Avoid hemolysis that may increase the value.
2. Avoid prolonged tourniquet or repeated clenching of the fist during venipuncture, which will increase the potassium value.
3. Increased value of platelets or white blood cell counts will lead to increase value. 
4. EDTA should not be used because it contains K⁺.
5. Serum or plasma should be separated within 3 hours to prevent leakage of the K⁺ from the blood cells.

Indications

1. Potassium is part of electrolytes estimation.
2. Potassium is advised in all serious patients.
3. Potassium is advised in patients with the treatment of diuretics or heart medication.

Pathophysiology

1. Potassium is the main electrolyte of intracellular fluid.
2. About 2 to 3 grams of the potassium is ingested in the food and excreted in the form of salts.
3. Potassium salts are rapidly absorbed by the intestine.
   1. There is very little effect on the plasma level.
   2. After the body needs potassium is excreted through the kidneys.

4. Daily intake of the potassium is 40 to 150 meq/day and the average is 1.5 meq/Kg body weight.
5. The intracellular Potassium is 150 meq/L and in the blood is just approximately 4 meq/L.

6. This ratio of intracellular and extracellular Potassium is very important to maintain membrane electrical potential.
7. Potassium is the primary buffer system in the cells.
8. The main concentration of the potassium is within the cell, almost 90%.
9. The very small amount is present in the blood and bone.
10. When the cells are damaged then Potassium is released into the blood and may give increased value.
11. Excretion of Potassium:
    1. 80 to 90% of Potassium is excreted by the glomeruli in the urine.

1. 2. Lesser amount 10 to 20 % excreted in the sweat and stool.
   3. Potassium’s role in the body is very important.

The site of K loss	K loss
Urine	40 to 120 meq/L
Stool	5 to 10 meq/L
Sweat	0 to 20 meq/L

12. Kidneys do not conserve potassium, so in the case of decreased intake, there may be a deficiency of potassium.
13. A normal adult needs 80 to 200 meq /day of potassium in the diet.
14. Potassium plays an important role in:
    1. Nerve conduction.
    2. Muscular function.
    3. Osmotic pressure.
    4. Protein synthesis.
    5. Acid-base balance.

15. Cardiac out, contraction of the heart muscle, and the rate is controlled by Potassium along with Calcium, and magnesium.
16. Potassium deficiency on ECG shows the presence of U wave.
17. Potassium role in acid-base balance:
    1. H⁺ ions are substituted for Potassium and Sodium in the renal tubules.
    2. Potassium is more important than sodium.
    3. Potassium bicarbonate (K⁺HCO₃^–)  is an only intracellular inorganic buffer.
    4. In Potassium deficiency, in other words, there is a decrease in HCO₃^–, so pH will be relatively acidic.
    5. Now the respiratory center is stimulated by low pH and lowering of pCO₂ through hyperventilation.
18. Potassium concentration depends upon:
    1. Hormonal effect where aldosterone and to some extent glucocorticoids increase Renal Potassium loss.
    2. Absorption of Sodium,  When Sodium is reabsorbed then Potassium is lost.
19. acid-base balance In this case:
20. Alkalosis:   lower the serum Potassium by shifting the K into cells.

21. Acidosis:  Increases the K ⁺  by releasing the K from the cell. This is a reverse phenomenon.
    1. Release from the cells is greater than excretion from the kidneys. This occurs in the acidosis and anoxia.

22. Hyperkalemia is due to increased potassium released into the blood or due to the kidney which cannot excrete the potassium or due to low urine output.

23.  Hypokalemia is due to potassium loss in vomiting, diarrhea, GIt fistula, and diuretics. Aldosterone increase leads to a decrease in potassium.

Signs and Symptoms

1. Potassium level < 2.5 meq/L 
   1. There will be tachycardia.
   2. There is increased muscular irritability.
      1. There are specific cardiac conduction defects.
      2. There is a stoppage of the heart in the systole.
   3. There is a flattened T – wave.
   4. The end result will be cardiac arrest.
2. Potassium level <3.0 meq/L
   1. There are marked neuromuscular symptoms.
3. Hyperkalemia
   1. There is mental confusion.
   2. There is a weakness.
   3. There is a tingling sensation.
   4. Flaccid paralysis of limbs.
   5. There is a weakness of respiratory muscles.
   6. There is bradycardia.
   7. There are prolonged PR and QRS intervals.
   8. There is a peaked T- wave.
4. Critical values are:
   1. Potassium level >7.0 meq/L
      1. There is peripheral vascular collapse.
      2. Inhibit muscle irritability.
      3. Ultimately cardiac arrest and stoppage of a heartbeat.
   2. The potassium level of 10.0 meq/L is fatal for the life of the patient.

NORMAL Potassium (serum)

Source 1

Age	meq/L
Premature cord blood	5.0 to 10.2
Premature 48 hours	3.6 to 6.0
Newborn cord	5.6 to 12.0
Newborn	3.7 to 5.9
Infant	4.1 to 5.3
Child	3.4 to 4.7
Adult	3.5 to 5.1

• To convert to SI units x 1.0 = mmol/L

Source 2

• Adult =  3.5 to 5.0 meq/L
  Child = 3.4 to 4.7 meq/L
• Infants = 4.1 to 5.3 meq/L.
• Newborn = 3.9 to 5.9 meq/L.
• Urine       =  25 to 125 meq /day.

Hyperkalemia or increased serum Potassium level:

1. Increased dietary uptake.
2. Acute and chronic renal failure.
3. Addison’s disease.
4. Decreased Aldosterone, hypoaldosteronism.
5. Hemolysis.
6. Transfusion of hemolyzed blood.
7. Uncontrolled diabetes mellitus.
8. Metabolic acidosis.
9. In Burns, accidents, surgery, chemotherapy, and DIC.
10. Kidney transplant rejection.
11. Decreased excretion of potassium in the urine:
    1. Renal failure.
    2. Acidosis.
    3. Adrenocortical insufficiency.               
12. Changes in ECG. There are the following changes:
    1. T -wave is elevated.
    2. P -wave is flattened.
    3. cardiac arrest may occur without warning any other changes.
    4. Nearly all cases of acidosis are associated with hyperkalemia.

                                                                                                                              

Hypokalemia or decreased Potassium level:

1. 1. Decreased dietary intake.
   2. Dehydration.
   3. Acidosis.
   4. An increased gastrointestinal loss like diarrhea and vomiting.
   5. Excessive sweating.
   6. Starvation and malnutrition.
   7. Cystic fibrosis.
   8. Severe burns.
   9. Respiratory alkalosis.
   10. Renal tubular acidosis.
   11. Respiratory alkalosis.
   12. Diuretics.
   13. Hyperaldosteronism.
   14. Cushing syndrome.
   15. Trauma due to surgery or burns.   
   16. Gastrointestinal losses like vomiting, nasogastric tube, diarrhea, and villous adenoma.
   17. Renal losses like diuretics, antibiotics (ampicillin-B and carbenicillin), hypomagnesemia, renal tubular acidosis, mineralocorticoid excess, congenital adrenal hyperplasia, and Cushing’s syndrome.
   18. There may be transcellular shifts like alkalosis and correction of diabetic ketoacidosis.
   19. Changes in ECG. There are the following changes:
       1. T – waves are depressed.
       2. P – wave has peaked.
       3. ST – depression.
       4. U- wave is prominent.

Pseudohyperkalemia is characterized by:

1. Raised potassium and there are no clinical changes in the patient as cardiac excitability.
2. This can be confirmed by the ECG.
3. In these patients, no treatment is needed and in fact, this may be harmful.
4. In such cases, the potassium may be released in the following conditions:
   1. In vitro hemolysis.
   2. In vitro clot formation.
   3. Thrombocytosis.
   4. Leukocytosis.
   5. Due to tourniquet use.

• Note: Please see more details in Electrolytes.

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