Medicine – Metabolic Alkalosis

Metabolic alkalosis is a primary increase in serum bicarbonate that raises blood pH. It usually occurs because of loss of hydrogen ions, gain of alkali, or renal retention of bicarbonate.

The typical blood-gas pattern is:

↑ pH + ↑ HCO₃⁻.

The lungs compensate by reducing ventilation, causing a secondary:

↑ PaCO₂.

1. Vomiting

The original notes correctly include:

Vomiting.

Vomiting causes loss of gastric hydrochloric acid.

This removes:

Hydrogen ions

and

Chloride.

The result is:

Metabolic alkalosis.

2. Why Vomiting Causes Alkalosis

The basic sequence is:

Vomiting → loss of HCl → loss of H⁺ → relative increase in HCO₃⁻ → metabolic alkalosis.

Volume depletion also activates the:

Renin–angiotensin–aldosterone system.

This promotes renal sodium reabsorption in exchange for:

Potassium and hydrogen ion secretion.

Therefore the alkalosis may become persistent.

3. Chloride Depletion

Vomiting also causes:

Chloride depletion.

Without enough chloride, the kidney has difficulty excreting bicarbonate efficiently.

Therefore vomiting commonly produces:

Chloride-responsive metabolic alkalosis.

This is why treatment often includes:

Isotonic saline plus potassium replacement when appropriate.

4. Hypokalaemia

The original notes include:

Hypokalaemia.

Hypokalaemia and metabolic alkalosis are closely linked.

Low extracellular potassium causes potassium to move out of cells while hydrogen ions move:

Into cells.

This reduces extracellular hydrogen ion concentration and contributes to:

Alkalosis.

5. Renal Effects of Hypokalaemia

Hypokalaemia also stimulates the kidney to:

Increase hydrogen ion secretion

and

Increase bicarbonate reabsorption.

Therefore hypokalaemia can both:

Cause and maintain metabolic alkalosis.

6. The Potassium–Alkalosis Cycle

Metabolic alkalosis itself can worsen potassium loss.

Therefore a vicious cycle may occur:

Hypokalaemia → increased H⁺ secretion → alkalosis → further renal K⁺ loss → worse hypokalaemia.

This is why potassium replacement is often important in treatment.

7. Burns

The original notes include:

Burns.

Burns are not one of the most classic direct causes of metabolic alkalosis.

However, metabolic alkalosis may occur in burn patients because of:

Volume depletion.

Chloride loss.

Diuretic treatment.

Gastric losses.

So burns are better thought of as an indirect clinical setting rather than a primary mechanism.

8. Ingestion of Alkali

The original notes correctly include:

Ingestion of alkali.

Excess bicarbonate or other absorbable alkali can increase serum bicarbonate.

Examples include excessive intake of:

Sodium bicarbonate.

Calcium carbonate-containing antacids.

This can produce:

Metabolic alkalosis.

9. Milk-Alkali Syndrome

A classic example is:

Milk-alkali syndrome, now often called calcium-alkali syndrome.

This occurs with excessive intake of:

Calcium plus absorbable alkali.

It may cause:

Hypercalcaemia.

Metabolic alkalosis.

Kidney injury.

10. Hyperaldosteronism

The original notes correctly include:

Hyperaldosteronism.

Aldosterone acts in the distal nephron to increase:

Sodium reabsorption

while increasing secretion of:

Potassium

and

Hydrogen ions.

Therefore excess aldosterone can cause:

Hypokalaemic metabolic alkalosis.

11. Primary Hyperaldosteronism

Primary hyperaldosteronism may result from:

Adrenal adenoma.

Bilateral adrenal hyperplasia.

The typical biochemical pattern is:

Hypertension.

Hypokalaemia, sometimes absent.

Metabolic alkalosis.

Suppressed renin.

12. Secondary Hyperaldosteronism

Secondary increases in aldosterone can also contribute to metabolic alkalosis.

Examples include:

Renal artery stenosis.

Severe volume depletion.

Heart failure in selected settings.

Here renin is usually:

Elevated, unlike primary hyperaldosteronism.

13. Diuretics – Important Additional Cause

An important cause not listed in the original notes is:

Loop and thiazide diuretics.

These cause sodium and chloride loss, leading to:

Volume contraction.

This activates RAAS and increases distal sodium delivery.

The result is increased:

K⁺ secretion

and

H⁺ secretion.

Therefore:

DIURETICS → HYPOKALAEMIC METABOLIC ALKALOSIS.

14. Contraction Alkalosis

Loss of sodium chloride and water can reduce extracellular fluid volume.

If bicarbonate is retained in a smaller extracellular volume, serum bicarbonate concentration rises.

This is often called:

Contraction alkalosis.

It commonly occurs with:

Vomiting.

Nasogastric suction.

Diuretic use.

15. Nasogastric Suction

Nasogastric suction removes gastric hydrochloric acid.

Therefore it acts similarly to vomiting:

Loss of HCl → metabolic alkalosis.

This is a classic hospital-associated cause.

16. Mineralocorticoid Excess

Besides primary hyperaldosteronism, other states of mineralocorticoid excess can cause:

Hypertension + hypokalaemia + metabolic alkalosis.

Examples include:

Cushing syndrome with mineralocorticoid effects.

Apparent mineralocorticoid excess.

Liquorice excess.

Liddle syndrome, although aldosterone is low in Liddle syndrome.

17. Renal Tubular Causes

Inherited renal salt-wasting disorders can also produce metabolic alkalosis.

Important examples include:

Bartter syndrome.

Gitelman syndrome.

Both typically produce:

Hypokalaemic metabolic alkalosis

because of chronic renal sodium and chloride loss with secondary RAAS activation.

18. Bartter Syndrome

Bartter syndrome resembles chronic loop-diuretic action.

It causes:

Renal salt wasting.

Secondary hyperaldosteronism.

Hypokalaemia.

Metabolic alkalosis.

Blood pressure is usually:

Normal or low, not hypertensive.

19. Gitelman Syndrome

Gitelman syndrome resembles chronic thiazide action.

Typical findings include:

Hypokalaemic metabolic alkalosis.

Hypomagnesaemia.

Low urinary calcium.

Again, blood pressure is usually:

Normal or low.

20. Post-Hypercapnic Metabolic Alkalosis

Patients with chronic respiratory acidosis, such as chronic hypercapnic COPD, retain bicarbonate as renal compensation.

If the PaCO₂ is then corrected rapidly, the previously retained bicarbonate may persist temporarily.

This produces:

Post-hypercapnic metabolic alkalosis.

21. Respiratory Compensation

The respiratory system compensates for metabolic alkalosis by:

Hypoventilation.

This raises PaCO₂ and helps lower the pH toward normal.

However, compensation is limited because excessive hypoventilation would cause:

Hypoxaemia.

22. Typical Blood-Gas Pattern

In a simple metabolic alkalosis:

pH is increased.

HCO₃⁻ is increased.

PaCO₂ is secondarily increased.

If PaCO₂ is not appropriately elevated, consider an additional respiratory disorder.

23. Symptoms

Symptoms depend on the severity and associated electrolyte disturbances.

Possible features include:

Weakness.

Muscle cramps.

Paraesthesia.

Tetany.

Palpitations.

Confusion.

Arrhythmias.

Many symptoms are related to accompanying:

Hypokalaemia

or

Reduced ionised calcium.

24. Urine Chloride – Important Diagnostic Tool

Metabolic alkalosis can be usefully divided according to:

Urine chloride.

This helps distinguish causes that are likely to respond to saline from those that are not.

25. Low Urine Chloride

A low urine chloride generally suggests:

Chloride-responsive metabolic alkalosis.

Typical causes include:

Vomiting.

Nasogastric suction.

Remote diuretic use.

Volume depletion.

These often improve with:

Sodium chloride and potassium replacement.

26. High Urine Chloride

A high urine chloride suggests:

Chloride-resistant metabolic alkalosis

or ongoing renal chloride loss.

Causes include:

Current diuretic use.

Hyperaldosteronism.

Bartter syndrome.

Gitelman syndrome.

27. Vomiting – Note Form

Vomiting:

Loss of gastric HCl.

↓

Loss of H⁺ and Cl⁻.

↓

Volume contraction + RAAS activation.

↓

↑ HCO₃⁻ retention.

↓

Metabolic alkalosis.

28. Hypokalaemia – Note Form

Low K⁺:

H⁺ shifts into cells.

↓

Renal H⁺ secretion increases.

↓

Bicarbonate reabsorption increases.

↓

Metabolic alkalosis.

29. Alkali Ingestion – Note Form

Excess bicarbonate/absorbable alkali:

↓

↑ HCO₃⁻ load.

↓

If renal excretion cannot compensate:

↓

Metabolic alkalosis.

30. Hyperaldosteronism – Note Form

Excess aldosterone:

↑ Na⁺ reabsorption.

↓

↑ K⁺ secretion.

↓

↑ H⁺ secretion.

↓

Hypokalaemia + metabolic alkalosis.

31. Diuretics – Note Form

Loop or thiazide diuretics:

NaCl loss.

↓

Volume contraction.

↓

RAAS activation.

↓

↑ distal Na⁺ reabsorption in exchange for K⁺ and H⁺.

↓

Hypokalaemic metabolic alkalosis.

32. Important Corrections and Clarifications

The strongest classic causes from the original list are:

VOMITING.

HYPOKALAEMIA.

ALKALI INGESTION.

HYPERALDOSTERONISM.

Burns are not usually listed as a primary direct mechanism. If metabolic alkalosis occurs in a patient with burns, think about associated:

Volume depletion, chloride loss, gastric losses, or diuretic therapy.

An important omitted cause is:

LOOP AND THIAZIDE DIURETICS.

These are among the most common causes of metabolic alkalosis in clinical practice.

Key Clinical Pattern

Remember:

METABOLIC ALKALOSIS = ↑ pH + ↑ HCO₃⁻.

Major mechanisms are:

LOSS OF H⁺ → vomiting or gastric suction.

LOSS OF NaCl/VOLUME → diuretics and contraction alkalosis.

EXCESS MINERALOCORTICOID → hyperaldosteronism.

EXCESS ALKALI → bicarbonate or calcium-alkali syndrome.

HYPOKALAEMIA → maintains and worsens alkalosis.

A useful final distinction is:

LOW URINE CHLORIDE → think vomiting/volume depletion.

HIGH URINE CHLORIDE → think diuretics, hyperaldosteronism, Bartter or Gitelman syndrome.