Metabolic alkalosis

Metabolic alkalosis is the least well known of the acid-base disturbances. It can be divided into two groups: saline responsive and saline unresponsive. Saline responsive metabolic alkalosis is the most common and occurs with volume contraction, for example diuretic use or volume depletion. Urinary chloride is low in the saline responsive type. Vomiting or nasogastric suction leads to loss of hydrochloric acid, but the decline in glomerular filtration rate that accompanies this perpetuates the metabolic alkalosis. The kidneys try to reabsorb chloride (hence the urine levels are low), but there is less of it from loss of hydrochloric acid, so the only available anion to be reabsorbed is bicarbonate. Metabolic alkalosis is often associated with hypokalaemia, owing to secondary hyperaldosteronism from volume depletion.

Another cause of saline responsive metabolic alkalosis is when hypercapnia is quickly corrected. Post-hypercapnia alkalosis occurs because hypercapnia directly affects the proximal tubules and decreases sodium chloride reabsorption

Table 3.3 Changes in pH, PaCO2, base excess and standard bicarbonate in different acid-base disturbances.

Acid-base disturbance

pH

PaCO2

Base excess

Standard bicarbonate

Respiratory acidosis

Low

High

Normal

Normal

Metabolic acidosis

Low

Normal

Low

Low

Respiratory alkalosis

High

Low

Normal

Normal

Metabolic alkalosis

High

Normal

High

High

leading to volume depletion. If chronic hypercapnia is corrected rapidly with mechanical ventilation, metabolic alkalosis ensues because there is already a high bicarbonate and the kidney needs time to excrete it. The pH change causes hypokalaemia, which can lead to cardiac arrhythmias.

Saline unresponsive metabolic alkalosis occurs due to renal problems:

• with high blood pressure - excess mineralocorticoid (exogenous or endogenous)

• with normal blood pressure - severe low potassium, high calcium

• exogenous alkali with low glomerular filtration rate

A summary of the changes in pH, PaCO2, and base excess in different acid-base disturbances is shown in Table 3.3.

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