Fluid, Electrolyte & Acid–Base Balance
Body water compartments, water and sodium balance, electrolytes, buffers and acid–base disorders
By the end of this unit you can…
- ✓Describe body water content and the fluid compartments, and compare their electrolyte composition
- ✓Explain how water intake and output are regulated, including thirst and ADH
- ✓Describe the regulation of sodium, potassium, calcium and the roles of aldosterone, ANP and the RAAS
- ✓Explain how chemical buffers, the respiratory system and the kidneys regulate pH
- ✓Classify and interpret respiratory and metabolic acidosis and alkalosis, including compensation
Key terms
Practice →1Body fluids & compartments
Water makes up about 50–60% of body mass in adults — more in infants (~73%, little fat, low bone mass), less in females and the elderly, because adipose tissue is low in water (~20%) while skeletal muscle is ~75% water.
| Compartment | Share of body water | Includes |
|---|---|---|
| Intracellular fluid (ICF) | ~2/3 (≈25 L) | Fluid inside all cells |
| Extracellular fluid (ECF) | ~1/3 (≈15 L) | Interstitial fluid (~80% of ECF) and plasma (~20%), plus lymph, CSF, synovial fluid, humors of the eye, serous fluids, GI secretions |
Electrolytes dissociate into ions and have the greatest osmotic power. ECF's main cation is Na⁺ and main anion Cl⁻; ICF's main cation is K⁺ and main anion HPO₄²⁻ (phosphate). Plasma has more protein than interstitial fluid. Because the plasma membrane is permeable to water, water moves by osmosis between compartments until osmolalities match — sodium largely determines ECF volume (“water follows salt”).
2Water balance
| Water intake (~2500 mL/day) | Water output (~2500 mL/day) |
|---|---|
| Beverages ~60% | Urine ~60% |
| Foods ~30% | Insensible loss through skin and lungs ~28% |
| Metabolic water (cellular respiration) ~10% | Sweat ~8%; feces ~4% |
Thirst is controlled by the hypothalamic thirst center. Osmoreceptors detect a rise in plasma osmolality (as little as 2–3%); a large drop in blood volume or pressure, angiotensin II and a dry mouth also stimulate thirst. Drinking moistens the mouth and stretches the stomach, which inhibits thirst quickly — before the water is even absorbed — to prevent overdrinking.
ADH (antidiuretic hormone) from the posterior pituitary is released when osmoreceptors detect ↑ osmolality (or with large drops in BP/volume). ADH inserts aquaporins in the collecting ducts → water is reabsorbed → urine becomes concentrated and plasma osmolality falls. Low osmolality → less ADH → dilute urine.
| Disorder | What happens |
|---|---|
| Dehydration | Water output > intake (hemorrhage, burns, vomiting, diarrhea, sweating, diuretics) → thirst, dry skin, ↓ urine output, ↑ osmolality; can cause confusion and hypovolemic shock |
| Hypotonic hydration (water intoxication) | Too much water → ECF diluted (hyponatremia) → water moves into cells → swelling; cerebral edema can cause seizures, coma |
| Edema | Accumulation of fluid in the interstitial space (↑ capillary hydrostatic pressure, ↓ plasma proteins, blocked lymphatics, ↑ capillary permeability) |
3Electrolyte balance
Sodium is the most abundant ECF cation and the main determinant of ECF osmolality and volume. Its regulation is linked to blood pressure and volume.
- Aldosterone
- From the adrenal cortex; ↑ Na⁺ reabsorption (and water follows, if ADH present) and ↑ K⁺ secretion in the DCT and collecting ducts. Triggered mainly by angiotensin II and directly by ↑ plasma K⁺.
- Renin–angiotensin–aldosterone system (RAAS)
- ↓ BP/volume → granular cells release renin → angiotensinogen → angiotensin I → (ACE, lungs) angiotensin II → vasoconstriction, aldosterone, ADH, thirst.
- Atrial natriuretic peptide (ANP)
- Released by the atria when stretched (↑ BP/volume); inhibits Na⁺ reabsorption, renin, aldosterone and ADH → natriuresis and diuresis → BP falls.
- Others
- Estrogen enhances NaCl reabsorption (premenstrual water retention); progesterone and glucocorticoids have smaller effects.
- 1Baroreceptors and the kidney's granular cells detect ↓ BP.
- 2Renin converts angiotensinogen (liver) → angiotensin I; ACE converts it to angiotensin II.
- 3Angiotensin II: vasoconstriction, aldosterone (Na⁺ and water retention), ADH release and thirst.
- 4Blood volume and pressure rise → negative feedback reduces renin.
| Ion | Main role | Regulated by | Imbalance |
|---|---|---|---|
| K⁺ | Resting membrane potential (especially heart) | Aldosterone (secretion), plasma K⁺ itself; insulin and epinephrine shift K⁺ into cells | Hyper- and hypokalemia both disturb cardiac rhythm — can cause cardiac arrest |
| Ca²⁺ | Bone, clotting, muscle contraction, nerve function | PTH (↑ blood Ca²⁺), calcitriol, calcitonin | Hypocalcemia → ↑ neuromuscular excitability, tetany; hypercalcemia → weakness, arrhythmia |
| Cl⁻ | Major ECF anion; follows Na⁺ | Indirectly via Na⁺; acid–base (exchanged for HCO₃⁻) | — |
| HPO₄²⁻ | Bone, ATP, buffer | PTH ↓ its reabsorption | — |
4Acid–base balance
Normal arterial blood pH is 7.35–7.45 (venous and interstitial fluid ~7.35; ICF ~7.0). pH < 7.35 is acidosis; pH > 7.45 is alkalosis. Most H⁺ comes from metabolism: CO₂ (→ carbonic acid), phosphorus-containing proteins, lactic acid from anaerobic respiration, and ketone bodies from fat breakdown.
Three lines of defense, from fastest to most powerful:
| System | Speed | How |
|---|---|---|
| Chemical buffers | Seconds — first line | Bind or release H⁺ immediately; can't remove acid from the body |
| Respiratory system | Minutes | Changes ventilation to expel or retain CO₂ (volatile acid) |
| Kidneys | Hours to days — most powerful | Excrete H⁺ (nonvolatile/fixed acids), reabsorb or generate HCO₃⁻ |
- Bicarbonate buffer system
- Main ECF buffer: H₂CO₃ ⇌ H⁺ + HCO₃⁻. A strong acid is converted to weak carbonic acid by bicarbonate; a strong base is neutralized by carbonic acid.
- Phosphate buffer system
- Works mainly in urine and ICF: H₂PO₄⁻ ⇌ H⁺ + HPO₄²⁻.
- Protein buffer system
- Most plentiful and powerful buffer — in ICF and plasma. Amino acids' carboxyl and amine groups release or bind H⁺; hemoglobin buffers H⁺ in RBCs.
CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻. ↑ CO₂ → ↑ H⁺ → ↓ pH. Chemoreceptors detect rising CO₂/H⁺ → breathing deepens and speeds up → more CO₂ blown off → pH rises. Hypoventilation does the opposite.
Only the kidneys can rid the body of fixed (metabolic) acids and regulate blood HCO₃⁻. Tubule cells secrete H⁺ (buffered in the urine by phosphate and ammonia → ammonium (NH₄⁺)), reabsorb filtered HCO₃⁻ and generate new HCO₃⁻. In alkalosis, type B intercalated cells secrete HCO₃⁻.
5Acid–base imbalances
Normal arterial values: pH 7.35–7.45, PCO₂ 35–45 mmHg, HCO₃⁻ 22–26 mEq/L. PCO₂ reflects the respiratory component; HCO₃⁻ reflects the metabolic component.
| Disorder | Primary change | Common causes | Compensation |
|---|---|---|---|
| Respiratory acidosis | ↑ PCO₂ (> 45) | Hypoventilation: COPD, pneumonia, drug overdose (opioids), airway obstruction — the most common imbalance | Kidneys ↑ HCO₃⁻ reabsorption and H⁺ secretion |
| Respiratory alkalosis | ↓ PCO₂ (< 35) | Hyperventilation: anxiety, pain, high altitude, fever | Kidneys ↓ HCO₃⁻ (excrete it), retain H⁺ |
| Metabolic acidosis | ↓ HCO₃⁻ (< 22) | Diabetic ketoacidosis, lactic acidosis, severe diarrhea (loss of bicarbonate), kidney failure, alcohol/aspirin overdose | Rapid, deep breathing (Kussmaul) blows off CO₂ |
| Metabolic alkalosis | ↑ HCO₃⁻ (> 26) | Vomiting (loss of stomach HCl), excess antacids, some diuretics | Slow, shallow breathing retains CO₂ |
- 1Look at pH: < 7.35 acidosis, > 7.45 alkalosis.
- 2Look at PCO₂: if it moves in the direction that explains the pH (high in acidosis, low in alkalosis), the problem is respiratory.
- 3Look at HCO₃⁻: if it explains the pH (low in acidosis, high in alkalosis), the problem is metabolic.
- 4If the other value is moving in the opposite (corrective) direction, compensation is occurring; if pH is back in range, it is fully compensated.