Pathology - Metabolic Alkalosis

Pathology - Metabolic Alkalosis 
Etiology 
Saline-responsive metabolic alkalosis is induced by a decrease in extracellular volume resulting from vomiting, diuretic usage, or posthypercapnia alkalosis.

Saline-resistant metabolic alkalosis is typically caused by an excess of mineralocorticoids (such as in Conn syndrome, renovascular disease, or Cushing disease), use of alkalis with reduced glomerular filtration rate (e.g., antacids), or severe hypokalemia.

Pathology 
Main issue: Elevated levels of HCO3.
Compensatory response: Hypoventilation leads to an increase in Pco2 to elevate bicarbonate concentration.

Symptoms and Signs 
Metabolic alkalosis is typically linked with hypokalemia, which exacerbates the condition by enhancing bicarbonate absorption in the proximal tubule and hydrogen ion release in the distal tubule.
May manifest with symptoms of dehydration such as sunken eyes, reduced skin elasticity, tiredness, low blood pressure, and muscle weakness due to low potassium levels. It can also lead to reduced blood flow to the brain and irregular heartbeats.

Laboratory results: Elevated pH, elevated Pco2, elevated HCO3, low potassium levels.

Therapy 
Saline-responsive: Replenishment of fluids and electrolytes.
Treat the root cause of excess mineralocorticoid and replenish potassium to address saline resistance.
Remuneration: An rise of 1 mEq/L in HCO3 results in a 0.7 mm Hg increase in pCO2.