Clinical Management of Electrolyte and Acid-Base Disorders

Posted on Dec 9, 2025 in Medicine

Electrolyte Imbalances: Sodium and Potassium

Sodium (Na⁺)

Sodium is the primary cation in the Extracellular Fluid (ECF).

  • Regulates osmotic forces.
  • Transported through cells by the sodium-potassium pump.
  • Secreted into mucus and other bodily secretions.

1. Hyponatremia (Plasma Na⁺ < 135 mEq/L)

A hypotonic alteration, meaning the ECF is diluted.

Causes of Hyponatremia
  • Losses from increased sweating, vomiting, or diarrhea.
  • Certain diuretic drugs combined with a low salt diet.
  • Hormonal imbalances (decreased aldosterone, increased ADH).
  • Increased water intake.
Effects of Hyponatremia
  • Low sodium leads to hypotonic alteration (dilution).
  • Decreased osmotic pressure in ECF, leading to increased hydrostatic pressure and increased Intracellular Fluid (ICF).
  • Manifestations include cerebral edema: confusion, headache, and seizures.

2. Hypernatremia (Plasma Na⁺ > 145 mEq/L)

A hypertonic alteration, meaning the ECF is concentrated.

Causes of Hypernatremia
  • Insufficient Antidiuretic Hormone (ADH), such as in Diabetes Insipidus.
  • Watery diarrhea.
  • Prolonged periods of rapid respiration.
  • Ingesting large amounts of sodium without adequate water balance.
Effects of Hypernatremia
  • Weakness.
  • Dry, rough mucous membranes.
  • Increased thirst.

Potassium (K⁺)

Potassium is the primary cation in the Intracellular Fluid (ICF).

  • Insulin moves potassium from the blood into cells.
  • Secreted primarily via urine.
  • Level is significantly influenced by acid-base balance.

1. Hypokalemia (Plasma K⁺ < 3.5 mEq/L)

Causes of Hypokalemia
  • Losses from excessive diarrhea.
  • Certain diuretic drugs or insulin administration.
  • Excessive aldosterone.
  • Decreased dietary intake.
Effects of Hypokalemia
  • Muscles become unresponsive to stimuli, potentially leading to paralysis.

2. Hyperkalemia (Plasma K⁺ > 5 mEq/L)

Causes of Hyperkalemia
  • Renal failure.
  • “Potassium-sparing” diuretics.
  • Leakage of intracellular potassium into extracellular fluids (e.g., trauma).
  • Displacement of potassium from cells by severe acidosis.
Effects of Potassium Imbalance (Cardiac)
  • Cardiac dysrhythmias are common. Hyperkalemia may progress to cardiac arrest.
  • Hyperkalemia causes prolonged depolarization and impairs repolarization, decreasing excitability, which can lead to cardiac arrest.
Severe Hyperkalemia EKG Findings
  • Wide QRS complex.
  • Longer PR interval.
  • Tall, narrow T wave.

Electrolyte Imbalances: Calcium and Magnesium

Calcium (Ca²⁺)

Calcium is an important extracellular cation.

  • Balance is controlled by Parathyroid Hormone (PTH), which raises Ca²⁺, and calcitonin, which lowers Ca²⁺.
  • Vitamin D promotes calcium reabsorption from the intestine (calcitriol is activated in the kidneys).

Forms of Calcium in Plasma

  1. Protein bound: Bound to albumin (40%).
  2. Complexed: Chelated with citrate, phosphate, or sulfate (10%).
  3. Ionized (Free): (50%). This is the only type detected by PTH.

Hypocalcemia (Plasma Ca²⁺ < 4.3 mEq/L)

Causes of Hypocalcemia
  • Hypoparathyroidism (low PTH leads to decreased Ca reabsorption).
  • Deficient serum albumin.
  • Renal failure (abnormal calcium loss from the kidney).
Effects of Hypocalcemia
  • Increased excitability of nerve membranes.
  • Spontaneous stimulation of skeletal muscle (tetany).

Hypercalcemia (Plasma Ca²⁺ > 5.3 mEq/L)

Causes of Hypercalcemia
  • Uncontrolled release of calcium ions from bones (e.g., neoplasms).
  • Hyperparathyroidism (excessive PTH).
  • Increased calcium and Vitamin D intake.
Effects of Hypercalcemia
  • Depressed neuromuscular activity.
  • Decreased neural excitability (manifesting as lethargy and stupor).

Magnesium (Mg²⁺)

Magnesium is primarily an intracellular ion.

Hypomagnesemia (< 1.8 mg/dL)

  • Often occurs with alcoholism.
  • Neuromuscular effects: Increased reflexes, convulsions.
  • Cardiovascular effects: Hypertension, cardiac dysrhythmias.

Hypermagnesemia (> 3.0 mg/dL)

  • Often occurs with renal failure.
  • Depresses neuromuscular function (decreased reflexes and muscle weakness).

Hormonal Regulation of Fluid and Electrolytes

  1. Antidiuretic Hormone (ADH): Decreases water excretion (released during dehydration). Promotes reabsorption of water from kidney tubules.
  2. Aldosterone: Released during decreased blood sodium. Promotes reabsorption of sodium (from urine back to blood) and increases potassium excretion in urine.
  3. Atrial Natriuretic Peptide (ANP): Released during increased blood sodium. Increases sodium excretion, increases water excretion (via osmosis), and decreases blood volume and blood pressure (BP).

pH Balance and Acid-Base Disorders

The body regulates pH primarily through the respiratory system and the kidneys.

  • The respiratory system alters carbonic acid levels (via CO₂) to change pH rapidly.
  • The kidneys modify the excretion rate of acids and the absorption of bicarbonate ions (HCO₃⁻) to regulate pH. This is the most significant, but slowest, mechanism.

Definitions of pH Imbalances

  • Acidosis: Blood pH is below 7.35.
  • Alkalosis: Blood pH is above 7.45.

Types of Primary Acid-Base Disorders

  1. Respiratory Acidosis: Excessive retention of CO₂ leading to excess H₂CO₃ (decreased pH).
  2. Metabolic Acidosis: Arterial blood H⁺ increases, and HCO₃⁻ falls (decreased pH).
  3. Respiratory Alkalosis: Excessive loss of CO₂ (e.g., hyperventilation) (increased pH).
  4. Metabolic Alkalosis: Arterial blood H⁺ falls, and HCO₃⁻ rises (increased pH).

Interpreting Arterial Blood Gases (ABGs)

  1. Blood pH: Indicates overall state (low pH = acidosis, high pH = alkalosis).
  2. PaCO₂: Indicates respiratory component (low CO₂ = respiratory alkalosis, high CO₂ = respiratory acidosis).
  3. HCO₃⁻: Indicates metabolic component (low HCO₃⁻ = metabolic acidosis, high HCO₃⁻ = metabolic alkalosis).

Specific Acid-Base Disorders and Compensation

1. Respiratory Acidosis

Breathing is depressed, CO₂ increases, and pH decreases.

  • Compensation: Kidneys conserve HCO₃⁻ and eliminate H⁺.
  • Causes:
    • Acute: Pneumonia, airway obstruction, chest injuries, or drugs that depress respiration.
    • Chronic: Common with Chronic Obstructive Pulmonary Disease (COPD).

2. Metabolic Acidosis

Noncarbonic acids increase, or there is an increased loss of HCO₃⁻ buffer. H⁺ increases, HCO₃⁻ decreases, and pH decreases.

  • Compensation: Hyperventilation increases pH; kidneys conserve bicarbonate and eliminate H⁺.
  • Causes:
    • Diarrhea: Loss of HCO₃⁻ from the intestines.
    • Renal disease or failure: Decreased acid excretion.
    • Diabetic Ketoacidosis (DKA): Increased formation of acidic ketones.

3. Respiratory Alkalosis

Caused by hyperventilation (decreased CO₂ and increased pH).

  • Compensation: Kidneys conserve H⁺ and eliminate HCO₃⁻.
  • Causes: Anxiety, high fever, head injuries, or brain stem tumors.

4. Metabolic Alkalosis

Caused by an increase in serum HCO₃⁻, decreased hydrochloric acid from the stomach (e.g., vomiting), or increased ingestion of antacids.

  • Compensation: Breathing is depressed to retain CO₂; kidneys conserve H⁺ and eliminate bicarbonate.

Manifestations and Management of Alkalosis

Alkalosis involves increased irritability of the nervous system and is often associated with hypokalemia.

Management involves addressing the underlying cause and supporting compensatory mechanisms:

  • Compensatory hypoventilation (retaining CO₂, decreasing pH).
  • Kidneys secrete urine with a high pH (retaining H⁺, eliminating HCO₃⁻).