Metabolic Alkalosis

Question 1

What is the general pathophysiology behind metabolic alkalosis and compensation

Answer 1

Accumulation of extracellular bicarbonate resulting in an increased pH. Respiratory compensation by hypoventilation causing CO2 retention

Question 2

What are GI and Renal causes that generate metabolic alkalosis?

Answer 2

GI: Vomiting, gastric suction
Renal: High rate of Na delivery, High mineral corticoid levels, K depletion, higher rates of renal ammoniagenesis

Question 3

What are causes of maintaining metabolic alkalosis?

Answer 3

Most common: Volume depletion
Relative volume depletion: CHF
Hypokalemia

Question 4

What are the pulmonary, hematologic, Neurologic, electrolyte, and Lactic alkalosis manifestations of metabolic alkalosis

Answer 4

Pulm: suppress ventilation. CO2 retention and hypoxemia
Heme: BOHR effect, impaired O2 delivery to tissues
Neuro: vasoconstriction of the cerebral circulation, confusion, obtunded, decreased Cai+ (paresthesias, tetany, seizures)
Electrolyte: Hypokalemia, hypomagnesemia (Cardiac arrhythmia)
Lactic alkalosis: Compensatory hypoventilation is overridden by hypoxia drive resulting in normal PCO2 with elevated blood lactic acid levels

Question 5

Treatment plan for metabolic alkalosis including tx for volume depletion, hypochloermia, hypokalemia, gastric losses, hyperkalemia, primary mineralcorticoid excess, impaired renal function, and hydrochloric acid infusion

Answer 5

Volume depletion: Isotonic fluid
Hypochloremia: KCL supplement
Hypokalemia: KCL
Gastric losses: stop suctioning, administer H2 blocker or PPI if unable to stop
Hyperkalemia: Diamox (Acetazolamide)
Primary mineral corticoid excess: Aldactone
Impaired Renal function: HD
Hydrochloric acid infusion: only if pH>7.55, 100mls/h over 12 hours, central line and frequent chemistries