What is contraction alkalosis and what are its characteristic lab values?

Contraction Alkalosis: Definition and Laboratory Values

Contraction alkalosis is a metabolic alkalosis characterized by decreased extracellular fluid volume leading to increased bicarbonate concentration, elevated blood pH, hypochloremia, and often hypokalemia. 1

Pathophysiology

Contraction alkalosis occurs through the following mechanisms:

• Volume contraction: Reduction in extracellular fluid volume without proportional loss of bicarbonate
• Concentration effect: As fluid volume decreases, bicarbonate becomes more concentrated
• Renal mechanisms: Volume depletion activates renin-angiotensin-aldosterone system, which:
  • Enhances sodium reabsorption
  • Increases hydrogen and potassium excretion
  • Promotes bicarbonate retention

Characteristic Laboratory Values

The diagnostic laboratory findings in contraction alkalosis include:

Parameter	Typical Finding
Arterial pH	Elevated (>7.45)
Serum bicarbonate	Elevated (>26 mEq/L)
Serum chloride	Decreased (<98 mmol/L)
Serum potassium	Often decreased (<3.5 mEq/L)
Urinary chloride	Variable: <20 mEq/L in volume depletion; elevated in diuretic-induced cases
Blood urea nitrogen (BUN)	Often elevated due to prerenal azotemia
Serum creatinine	May be elevated due to reduced renal perfusion

Clinical Scenarios and Variations

Contraction alkalosis commonly occurs in:

1. Diuretic therapy (especially loop and thiazide diuretics)

   • Laboratory profile: Hypokalemia, hypochloremia, elevated urinary chloride

2. Vomiting or nasogastric suction

   • Laboratory profile: Hypokalemia, hypochloremia, low urinary chloride

3. Bartter syndrome

   • Laboratory profile: Hypokalemia, hypochloremic metabolic alkalosis, normotensive hyperreninemic hyperaldosteronism 2

4. Post-hypercapnic states

   • Laboratory profile: Elevated bicarbonate with normalized CO₂

Maintaining Factors

Several factors help maintain contraction alkalosis:

• Volume depletion: Reduces glomerular filtration rate
• Hypochloremia: Limits bicarbonate excretion
• Hypokalemia: Enhances proximal bicarbonate reabsorption
• Aldosterone excess: Promotes hydrogen ion secretion

Clinical Significance

Severe metabolic alkalosis (pH ≥7.55) is associated with:

• Increased mortality in critically ill patients
• Neurological symptoms (confusion, seizures)
• Cardiac arrhythmias
• Respiratory depression
• Electrolyte imbalances

Diagnostic Approach

When evaluating suspected contraction alkalosis:

1. Measure arterial blood gases to confirm alkalemia
2. Check serum electrolytes (sodium, potassium, chloride, bicarbonate)
3. Assess volume status (postural vital signs, skin turgor, mucous membranes)
4. Measure urinary chloride to differentiate causes:
   • Low urinary chloride (<20 mEq/L): Volume contraction
   • High urinary chloride (>20 mEq/L): Diuretic use or Bartter syndrome

Treatment Principles

Treatment should address both the alkalosis and its underlying cause:

1. Volume repletion: Isotonic saline (0.9% NaCl) is first-line therapy to correct volume depletion and chloride deficit 1
2. Potassium chloride supplementation: To correct hypokalemia, targeting 4.0-5.0 mEq/L 1
3. Address underlying cause: Discontinue offending diuretics, treat vomiting, etc.
4. Severe cases: May require mineral acids (ammonium chloride or dilute hydrochloric acid) 3

Pitfalls to Avoid

• Using potassium-sparing diuretics without close monitoring
• Administering non-chloride potassium salts when hypochloremia is present
• Correcting potassium too rapidly (maximum rate: 20 mEq/hour via peripheral vein) 1
• Failing to monitor serum electrolytes within 24 hours of initiating therapy

By understanding the pathophysiology and laboratory profile of contraction alkalosis, clinicians can effectively diagnose and manage this common acid-base disturbance.