Hyperaldosteronism stands as a common mediator in metabolic
alkalosis as it lead to enhanced K+ and H+ excretion, with sodium and
bicarbonate retention (hypokalaemic alkalosis). Diuretic therapy,
secondary aldosteronism in cirrhotics and severe vomiting are the common
causes of metabolic alkalosis.
Clinical features:
1- Manifestations of the cause
2- Manifestations of neuromuscular irritability owing to the decreased
ionized calcium.
Treatment:
1- Of the cause
2- Support respiratory and renal compensatory mechanisms.
3- If there is renal failure with severe metabolic alkalosis, dialysis may be
provided.Respiratory Alkalosis
Excessive pulmonary wash of Co 2 will result in alkalosis owing to
directing the reaction (H 2 O + Co 2 ́ H 2 CO 3 ́ H+ HCo 3 - )^ to the left with
consequent reduction in H+.
The renal defence mechanism will include the increase in HCo 3 -
secretion and retention of H+. This mechanism is relatively slow. It needs
24 hours to be established.
For each 10 mmHg increase in PCo 2 , there is a 2.5 mmol/L
decrease in plasma HCo 3.