Contraction Alkalosis
Definition
Contraction alkalosis refers to:
Metabolic alkalosis that results from reduction in extracellular fluid volume, which concentrates serum bicarbonate and enhances renal bicarbonate reabsorption.
Pathophysiology
1️⃣ Basic Mechanism
Contraction alkalosis occurs due to two simultaneous mechanisms:
A. Hemoconcentration of Bicarbonate
- Loss of Na⁺ + water from extracellular space
- Total body bicarbonate remains initially unchanged
- Because ECF volume shrinks → HCO₃⁻ concentration rises
👉 Example
If bicarbonate = 24 mmol/L in 14 L ECF
Loss of 4 L fluid → same bicarbonate now distributed in 10 L
→ Concentration rises
B. Enhanced Renal Bicarbonate Retention
This is the more important sustaining mechanism
Volume contraction activates:
- Renin–angiotensin–aldosterone system (RAAS)
- Increased proximal tubular sodium reabsorption
- Increased hydrogen ion secretion
- Increased bicarbonate reabsorption
2️⃣ Renal Physiology Behind Contraction Alkalosis
✔ Proximal Tubule
Volume depletion → Angiotensin II activation → stimulates:
- Na⁺/H⁺ exchanger (NHE3)
- Increased hydrogen secretion into tubular lumen
- Increased bicarbonate reabsorption into blood
✔ Distal Nephron
Aldosterone causes:
- Increased Na⁺ reabsorption
- Increased:
- H⁺ secretion
- K⁺ secretion
👉 Leads to:
- Alkalosis maintenance
- Hypokalemia (frequently associated)
✔ Chloride Depletion
Most contraction alkalosis is also:
👉 Chloride responsive alkalosis
Because:
- Low chloride reduces ability of kidney to excrete bicarbonate
- Bicarbonate secretion in collecting duct requires chloride exchange
Common Clinical Causes
1️⃣ Diuretic Therapy (Most Common ICU Cause)
Especially:
- Furosemide
- Bumetanide
- Hydrochlorothiazide
Mechanism:
- NaCl + water loss
- Volume contraction
- RAAS activation
- Potassium loss → worsens alkalosis
2️⃣ Gastrointestinal Chloride Loss
✔ Vomiting
✔ Nasogastric suction
Loss of:
- HCl
- Sodium
- Chloride
- Water
Result:
- Volume contraction
- Chloride depletion
- Bicarbonate retention
3️⃣ Post-Hypercapnic State
After rapid correction of chronic respiratory acidosis:
- Kidneys have retained bicarbonate
- CO₂ suddenly falls
- Leads to metabolic alkalosis
4️⃣ Mineralocorticoid Excess States
- Primary hyperaldosteronism
- Cushing syndrome
Mechanism:
- Increased hydrogen and potassium secretion
Laboratory Findings
ABG
- ↑ pH
- ↑ HCO₃⁻
- Compensatory ↑ PaCO₂
Electrolytes
Typical triad:
✔ Hypokalemia
✔ Hypochloremia
✔ Volume depletion
Urine Chloride
|
Urine Chloride |
Interpretation |
|
<10–20 mEq/L |
Chloride responsive alkalosis |
|
>20 mEq/L |
Chloride resistant alkalosis |
👉 Contraction alkalosis usually = low urine chloride
Why Volume Contraction Maintains Alkalosis (Conceptual Summary)
Volume depletion causes:
- Angiotensin II → proximal bicarbonate reabsorption
- Aldosterone → distal hydrogen secretion
- Chloride depletion → impaired bicarbonate excretion
- Hypokalemia → intracellular H⁺ shift
All promote persistent alkalosis.
Management
Step 1 – Identify Type of Metabolic Alkalosis
👉 Check urine chloride
Step 2 – Treat Underlying Cause
✔ Chloride Responsive (Most Contraction Alkalosis)
Treatment:
- Isotonic saline
- Potassium replacement
- Stop diuretics if possible
Mechanism:
- Restores volume
- Restores chloride
- Allows kidney to excrete bicarbonate
✔ Severe or Refractory Cases
Consider:
- Acetazolamide
- Carbonic anhydrase inhibitor
- Promotes bicarbonate excretion
- Useful in ventilated ICU patients
✔ Life-Threatening Alkalosis (pH > 7.55)
Rare but may require:
- Hydrochloric acid infusion (ICU setting)
- Dialysis (renal failure patients)

