Hypokalemia

Potassium is a major intracellular cation, and its intracellular-to-extracellular ratio determines the transmembrane potential. The sodium delivery and distal tubular flow rate, mineralocorticoids, anion excretion, systemic pH and dietary factors influence the body's potassium balance.

Both Hyperkalemia and hypokalemia are commonly seen in the elderly. Hyperkalemia usually occurs with renal failure. Pseudo-hyperkalemia occurs where there is haemolysis.

1.0Hypokalemia Definition

• Hypokalemia is a medical condition characterized by an abnormally low potassium level in the blood. Potassium is a vital electrolyte that helps regulate various bodily functions, including muscle contractions, nerve signals, and fluid balance.
• Serum K+ less than 3.5 meq/L is labeled as hypokalemia.

2.0Causes of Hypokalemia

• Gastrointestinal Losses: Excessive vomiting, diarrhea, or use of laxatives can lead to significant potassium loss.
• Diuretics: Certain diuretics, particularly loop diuretics and thiazide diuretics can cause potassium loss through increased urine output.
• Kidney Disorders: Conditions affecting kidney function, such as hyperaldosteronism or renal tubular acidosis, can result in potassium loss.
• Hormonal Imbalances: Disorders such as Cushing's syndrome or primary hyperaldosteronism can lead to hypokalemia.
• Inadequate Intake: A diet low in potassium can contribute to hypokalemia, though this is less common in well-nourished individuals.
• Medications: Certain medications, including antibiotics and corticosteroids, can impact potassium levels.

3.0Symptoms of Hypokalemia

• Symptoms may vary from mild to severe and can include:
• ECG changes due to hypokalemia
• Cardiac arrhythmia
• Severely impaired neuromuscular function
• Diaphragmatic weakness and respiratory failure
• Patients on digoxin or antiarrhythmic therapy  
• Organic heart disease
• Diabetic ketoacidosis
• Hyperosmolar Nonketotic state
• Serum potassium of less than 3.0 meq/L
• Inability to receive or tolerate oral potassium.

4.0Phenomena  of Hypokalemia

Cardiac manifestations:

• ECG Changes in Hypokalemia 
• T wave flattening/inversion
• Appearance of U wave
• Depressed ST segment
• Atrial and ventricular ectopics
• Predisposition to digitalis intoxication
• Sinus bradycardia
• Paroxysmal atrial or junctional tachycardia
• Atrioventricular block
• Ventricular tachycardia (torsade de pointes)
• Ventricular fibrillation

Neuromuscular Weakness:

• Gastrointestinal: constipation, ileus
• Striated muscle: weakness, paralysis, hyporeflexia.

Renal manifestations:

• Decrease in GFR and RBF
• Concentration defect
• Increased renal NH3 production
• Metabolic alkalosis

5.0Management of Hypokalemia

• A fall in serum potassium from 1 meq/L implies a loss of approximately 100-200 meq potassium from the body. 
• Oral replacement is desirable for slow correction. 
• Intravenous replacement is indicated when potassium depletion is severe and produces symptoms and signs requiring rapid correction or when the patient is unable to tolerate oral medications. 
• For intravenous therapy by the peripheral route in a nonurgent setting, 20-40 meq/L of KCl is added to each litre of saline over 4-6 h. 
• Potassium concentration should not exceed 60 meq/L when given by the peripheral route, as it can lead to local pain and sclerosis. By the central route, 20 meq KCl in 100 mL normal or half-strength normal saline can be given at the rate of 5-20 meq/hr through a syringe pump (preferably femoral vein). 
• In life-threatening arrhythmias, potassium can be administered rapidly (up to 40 meq/hour for a few hours) with ECG monitoring in the ICU. During (K+) replacement, serum K+ should be monitored repeatedly. Once serum potassium has been raised to a safer limit (generally above 3 meq/L), the rest of the replacement may be done slowly by the oral route. 
• This could be achieved by adding a potassium-rich diet, potassium salt, or potassium chloride suspension. Treatment usually starts with 10-20 meq of potassium chloride given two to four times per day (20-80 meq/day). Associated hypomagnesemia, if present, should be corrected.  

6.0Hypokalemia Correction

Correcting hypokalemia involves restoring potassium levels to their normal range. The approach depends on the severity of the hypokalemia and the underlying cause. Here’s a general guide to calculating the amount of potassium needed for correction:

Hypokalemia Correction Formula

1. Determine the Potassium Deficit: To estimate the total potassium deficit, you can use the following formula: Potassium Deficit (mEq)=Body Weight (kg)×Desired Change in Serum Potassium
2. The correction factor typically used is 0.2 L/kg, which represents the estimated extracellular fluid volume where potassium is distributed.

Example Calculation:

Body weight: 70 kg

Desired change in serum potassium: 4.0 mEq/L (assuming the target is 4.0 mEq/L from a lower level, e.g., 3.0 mEq/L)

Correction factor: 0.2 L/kg

3. Potassium Deficit=70 kg × 4.0 mEq/L−3.0 mEq/L)×0.2 L/kg
4. Potassium Deficit = 70 × 1.0×0.2=14 mEq

This means the patient needs approximately 14 mEq of potassium to correct the deficit.

Determine the Rate of Replacement

The rate of potassium replacement should be carefully monitored to avoid complications such as hyperkalemia or cardiac arrhythmias.

Generally:

• Oral Potassium: For mild hypokalemia, oral potassium supplements are preferred and can be given at a dose of 20-40 mEq every 2-4 hours.
• Intravenous Potassium: For more severe cases, potassium is administered intravenously. The maximum recommended infusion rate is typically 10-20 mEq/hour to prevent complications. Always use an infusion pump for accuracy and monitor the patient’s ECG and serum potassium levels closely.

7.0Hypokalemic periodic paralysis

Hypokalemic periodic paralysis (hypoPP) is a rare genetic disorder that causes episodes of severe muscle weakness. The disorder is caused by mutations in skeletal muscle ion channels, mainly those that affect calcium or sodium. It's characterized by low blood potassium levels (hypokalemia) and a sudden onset of flaccid paralysis that can last for several hours. 

Episodes are usually triggered by strenuous exercise, a high-carbohydrate diet, or other factors, such as: 

• Cold 
• Stress, excitement, or fear 
• Salt intake 
• Prolonged immobility 
• Use of glucocorticoids or alcohol 
• Anesthetic procedures 
• Viral illness 
• Certain medications 
• Rest after exercise 
• Sleep 
• Temperature extremes 
• The first attack can occur between the ages of two and 30, and episodes can last from one to 72 hours, with an average of nearly 24 hours. Although people with hypoPP usually regain their muscle strength between attacks, some may develop persistent muscle weakness later in life. 
• To prevent recurrence, patients are usually advised to avoid carbohydrate-rich meals and vigorous exercise. Other treatments include: Vigilant preoperative evaluation, Perioperative monitoring, Aggressive treatment of hypokalemia when it occurs, Administration of nonselective β-blockers, and Acetazolamide (250 to 750 mg/day).