Disorders of sodium and chloride balance
 |
This article seems to not fulfill most of the items on our Editorial Process checklist. As such, it's going to be deleted soon. To the author of this article: if you still work on this article, make sure to replace this template with the Under construction template. However, be aware that if you don't make any changes to the article after that soon enough, the article will still be deleted. To find out what you need to do to improve this article, read Help:Editorial process. Feel free to ask for help on Forum:Support. To see how articles on WikiLectures should look like, check out articles in Category:Finished articles. For more information, contact the user who inserted this template, you can find them in the Page History (under the "Actions" button). Last user who modified this page: ShadyMedic |
Introduction[edit | edit source]
Sodium (Na⁺) and chloride (Cl⁻) are the main extracellular electrolytes responsible for maintaining osmolarity, extracellular volume, nerve conduction, and acid–base balance. Their concentrations are tightly regulated by renal, hormonal, and neural mechanisms. Disorders of sodium and chloride balance are common and can lead to significant neurological, cardiovascular, and metabolic complications.
Definition[edit | edit source]
Sodium balance disorders reflect disturbances in water homeostasis or total body sodium content.
Chloride balance disorders often accompany sodium abnormalities but also relate to acid–base disturbances.
Sodium determines osmolarity, while chloride contributes to electroneutrality and acid–base regulation.
Types of Disorders[edit | edit source]
1. Hyponatremia (Low Sodium)[edit | edit source]
Hyponatremia is defined as serum Na⁺ < 135 mmol/L.
Causes[edit | edit source]
- Excess water retention
- SIADH (syndrome of inappropriate ADH secretion)
- Heart failure, cirrhosis, nephrotic syndrome
- Kidney failure
- Loss of sodium
- Vomiting, diarrhea
- Diuretics (especially thiazides)
- Addison’s disease (low aldosterone)
- Dilutional hyponatremia
- Excessive water intake
- Postoperative ADH secretion
Clinical features[edit | edit source]
- Headache, nausea
- Confusion, irritability
- Seizures in severe cases
- Risk of cerebral edema
Purpose of compensation[edit | edit source]
- Suppress ADH
- Increase free-water excretion
- Restore normal osmolarity
2. Hypernatremia (High Sodium)[edit | edit source]
Hypernatremia = serum Na⁺ > 145 mmol/L.
Usually due to water deficit rather than sodium excess.
Causes[edit | edit source]
- Water loss
- Fever, sweating
- Diarrhea
- Diabetes insipidus (central or nephrogenic)
- Reduced intake
- Elderly, infants, impaired thirst mechanism
- Sodium gain (less common)
- Hypertonic IV fluids
- Excess sodium ingestion
Clinical features[edit | edit source]
- Strong thirst
- Neurological symptoms due to cell shrinkage
- Irritability → lethargy → seizures
- Risk of intracranial hemorrhage in severe cases
Body response[edit | edit source]
- ADH ↑
- Thirst ↑
- Kidneys concentrate urine
3. Hypochloremia (Low Chloride)[edit | edit source]
Hypochloremia often occurs together with hyponatremia, metabolic alkalosis, or fluid loss.
Causes[edit | edit source]
- Vomiting → loss of gastric HCl
- Diuretics
- Cystic fibrosis
- SIADH
- Chronic respiratory acidosis compensation
Clinical features[edit | edit source]
- Weakness, fatigue
- Tetany (due to alkalosis)
- Dehydration symptoms
Associated pathophysiology[edit | edit source]
- Metabolic alkalosis can develop due to loss of chloride ions
- Impaired renal ability to reabsorb sodium without accompanying chloride
4. Hyperchloremia (High Chloride)[edit | edit source]
Usually associated with metabolic acidosis or excess chloride intake.
Causes[edit | edit source]
- Infusion of normal saline (0.9% NaCl)
- Renal tubular acidosis (Type I and II)
- Severe dehydration
- Chronic kidney disease
- Excessive dietary salt intake
Clinical features[edit | edit source]
- Fatigue
- Rapid breathing (respiratory compensation for acidosis)
- Decreased bicarbonate (hyperchloremic acidosis)
Underlying mechanism[edit | edit source]
- Excess chloride reduces bicarbonate concentration
- Leads to non–anion gap metabolic acidosis
Pathophysiological Aspects[edit | edit source]
1. Neurological Effects[edit | edit source]
Because sodium determines plasma osmolarity, abnormalities lead to:
- Brain swelling in hyponatremia
- Brain shrinkage in hypernatremia
Both conditions can cause:
- Confusion
- Seizures
- Coma (severe cases)
2. Cardiovascular Effects[edit | edit source]
- Sodium retention → increased intravascular volume → hypertension, edema
- Sodium loss → hypotension, tachycardia
3. Renal and Hormonal Regulation[edit | edit source]
Hormones involved:
| Hormone | Effect on Na⁺ and Cl⁻ |
|---|---|
| Aldosterone | Na⁺ reabsorption ↑, Cl⁻ follows |
| ADH | Water reabsorption ↑ (affects Na⁺ concentration) |
| Natriuretic peptides (ANP/BNP) | Increase Na⁺ excretion |
| Angiotensin II | Stimulates Na⁺ reabsorption, thirst |
Disturbances in these systems contribute to sodium and chloride disorders.
4. Acid–Base Balance and Chloride[edit | edit source]
Chloride shifts strongly influence acid–base status:
- Hypochloremia → metabolic alkalosis
- Hyperchloremia → metabolic acidosis (normal anion gap)
This relationship is a key diagnostic clue.
Conclusion[edit | edit source]
Sodium and chloride play essential roles in maintaining osmolarity, acid–base balance, and extracellular fluid volume. Disorders of these electrolytes can cause significant neurological, cardiovascular, and renal complications. Understanding the mechanisms behind hypo- and hypernatremia, as well as hypo- and hyperchloremia, is important for recognizing pathophysiological changes and guiding appropriate evaluation.
References[edit | edit source]
- Guyton & Hall. Textbook of Medical Physiology.
- Boron & Boulpaep. Medical Physiology.
- Rose BD. Clinical physiology of acid–base and electrolyte disorders.
- Hall JE. Sodium, chloride, and extracellular fluid balance.
