Electrolytes – Part 1 – Potassium (K+) Blood

Sample
- This is done on the serum of the patient.
- Separate serum as soon as possible.
- Plasma can be used but it gives slightly lower values.
- The random sample may be taken.
- Serum or plasma is stable for one week at room temperature or at 1°C to 4 °C.
Precautions
- Avoid hemolysis that may increase the value.
- Avoid prolonged tourniquet or repeated clenching of the fist during venipuncture, which will increase the potassium value.
- Increased value of platelets or white blood cell counts will lead to increase value.
- EDTA should not be used because it contains K+.
- Serum or plasma should be separated within 3 hours to prevent leakage of the K+ from the blood cells.
Indications
- Potassium is part of electrolytes estimation.
- Potassium is advised in all serious patients.
- Potassium is advised in patients with the treatment of diuretics or heart medication.
Pathophysiology
- Potassium is the main electrolyte of intracellular fluid.
- About 2 to 3 grams of the potassium is ingested in the food and excreted in the form of salts.
- Potassium salts are rapidly absorbed by the intestine.
- There is very little effect on the plasma level.
- After the body needs potassium is excreted through the kidneys.
- Daily intake of the potassium is 40 to 150 meq/day and the average is 1.5 meq/Kg body weight.
- The intracellular Potassium is 150 meq/L and in the blood is just approximately 4 meq/L.
- This ratio of intracellular and extracellular Potassium is very important to maintain membrane electrical potential.
- Potassium is the primary buffer system in the cells.
- The main concentration of the potassium is within the cell, almost 90%.
- The very small amount is present in the blood and bone.
- When the cells are damaged then Potassium is released into the blood and may give increased value.
- Excretion of Potassium:
- 80 to 90% of Potassium is excreted by the glomeruli in the urine.
-
- Lesser amount 10 to 20 % excreted in the sweat and stool.
- 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 |
- Kidneys do not conserve potassium, so in the case of decreased intake, there may be a deficiency of potassium.
- A normal adult needs 80 to 200 meq /day of potassium in the diet.
- Potassium plays an important role in:
- Nerve conduction.
- Muscular function.
- Osmotic pressure.
- Protein synthesis.
- Acid-base balance.
- Cardiac out, contraction of the heart muscle, and the rate is controlled by Potassium along with Calcium, and magnesium.
- Potassium deficiency on ECG shows the presence of U wave.
- Potassium role in acid-base balance:
- H+ ions are substituted for Potassium and Sodium in the renal tubules.
- Potassium is more important than sodium.
- Potassium bicarbonate (K+HCO3–) is an only intracellular inorganic buffer.
- In Potassium deficiency, in other words, there is a decrease in HCO3–, so pH will be relatively acidic.
- Now the respiratory center is stimulated by low pH and lowering of pCO2 through hyperventilation.
- Potassium concentration depends upon:
- Hormonal effect where aldosterone and to some extent glucocorticoids increase Renal Potassium loss.
- Absorption of Sodium, When Sodium is reabsorbed then Potassium is lost.
- acid-base balance In this case:
- Alkalosis: lower the serum Potassium by shifting the K into cells.
- Acidosis: Increases the K + by releasing the K from the cell. This is a reverse phenomenon.
- Release from the cells is greater than excretion from the kidneys. This occurs in the acidosis and anoxia.
- 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.
- Hypokalemia is due to potassium loss in vomiting, diarrhea, GIt fistula, and diuretics. Aldosterone increase leads to a decrease in potassium.
Signs and Symptoms
- Potassium level < 2.5 meq/L
- There will be tachycardia.
- There is increased muscular irritability.
- There are specific cardiac conduction defects.
- There is a stoppage of the heart in the systole.
- There is a flattened T – wave.
- The end result will be cardiac arrest.
- Potassium level <3.0 meq/L
- There are marked neuromuscular symptoms.
- Hyperkalemia
- There is mental confusion.
- There is a weakness.
- There is a tingling sensation.
- Flaccid paralysis of limbs.
- There is a weakness of respiratory muscles.
- There is bradycardia.
- There are prolonged PR and QRS intervals.
- There is a peaked T- wave.
- Critical values are:
- Potassium level >7.0 meq/L
- There is peripheral vascular collapse.
- Inhibit muscle irritability.
- Ultimately cardiac arrest and stoppage of a heartbeat.
- The potassium level of 10.0 meq/L is fatal for the life of the patient.
- Potassium level >7.0 meq/L
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:
- Increased dietary uptake.
- Acute and chronic renal failure.
- Addison’s disease.
- Decreased Aldosterone, hypoaldosteronism.
- Hemolysis.
- Transfusion of hemolyzed blood.
- Uncontrolled diabetes mellitus.
- Metabolic acidosis.
- In Burns, accidents, surgery, chemotherapy, and DIC.
- Kidney transplant rejection.
- Decreased excretion of potassium in the urine:
- Renal failure.
- Acidosis.
- Adrenocortical insufficiency.
- Changes in ECG. There are the following changes:
- T -wave is elevated.
- P -wave is flattened.
- cardiac arrest may occur without warning any other changes.
- Nearly all cases of acidosis are associated with hyperkalemia.
Hypokalemia or decreased Potassium level:
-
- Decreased dietary intake.
- Dehydration.
- Acidosis.
- An increased gastrointestinal loss like diarrhea and vomiting.
- Excessive sweating.
- Starvation and malnutrition.
- Cystic fibrosis.
- Severe burns.
- Respiratory alkalosis.
- Renal tubular acidosis.
- Respiratory alkalosis.
- Diuretics.
- Hyperaldosteronism.
- Cushing syndrome.
- Trauma due to surgery or burns.
- Gastrointestinal losses like vomiting, nasogastric tube, diarrhea, and villous adenoma.
- Renal losses like diuretics, antibiotics (ampicillin-B and carbenicillin), hypomagnesemia, renal tubular acidosis, mineralocorticoid excess, congenital adrenal hyperplasia, and Cushing’s syndrome.
- There may be transcellular shifts like alkalosis and correction of diabetic ketoacidosis.
- Changes in ECG. There are the following changes:
- T – waves are depressed.
- P – wave has peaked.
- ST – depression.
- U- wave is prominent.
Pseudohyperkalemia is characterized by:
- Raised potassium and there are no clinical changes in the patient as cardiac excitability.
- This can be confirmed by the ECG.
- In these patients, no treatment is needed and in fact, this may be harmful.
- In such cases, the potassium may be released in the following conditions:
- In vitro hemolysis.
- In vitro clot formation.
- Thrombocytosis.
- Leukocytosis.
- Due to tourniquet use.
- Note: Please see more details in Electrolytes.