Metabolic Alkalosis

Metabolic Alkalosis

David Ray Velez, MD

Table of Contents

Definition
Causes
Physiologic Changes
Compensation
Chloride-Responsiveness
Treatment

Definition

Definition: An Acid-Base Disorder with Alkalosis (Increased pH) Due to a Metabolic Process (Increased Bicarbonate or Decreased Hydrogen)

Arterial Blood Gas (ABG) Analysis

Causes

Upper Gastrointestinal (GI) Hydrogen Loss

  • Vomiting
  • High Nasogastric Tube Output

Renal Hydrogen Loss

  • Furosemide (Lasix)
  • Bartter Syndrome
  • Gitelman Syndrome
  • Conn Syndrome (Primary Mineralocorticoid Excess)

Other Causes

  • Iatrogenic Administration of Sodium Bicarbonate
  • Hypokalemia

Contraction Alkalosis

  • Pathophysiology:
    • Loss of Fluid (High in Sodium and Chloride) without a Proportional Loss of Bicarbonate
    • Also Possibly Effected by RAAS Activation Increasing Bicarbonate Reabsorption
  • Causes:
    • Furosemide (Lasix)
    • Emesis
    • Cystic Fibrosis
    • Congenital Chloride Diarrhea

Physiologic Changes of Alkalosis

Pulmonary Changes

  • Inhibition of Respiratory Drive and Decreased Respiratory Rate
  • Left-Shift of the Oxygen-Hemoglobin Dissociation Curve (Increased Affinity)

Cardiovascular Changes

  • Increased Risk of Arrhythmia
  • Increased Systemic Vascular Resistance (SVR) and Arterial Vasoconstriction

Hematologic Changes

  • Minimal Effects on Coagulation

Renal Changes

  • Increased Bicarbonate Secretion

Electrolyte Changes

  • Hypokalemia
  • Hypocalcemia

Neurologic Changes

  • Cerebral Vasoconstriction and Decreased Intracranial Pressure (ICP)
  • Decreased Cerebral Blood Flow
  • Lightheadedness and Confusion

Hypokalemic Hypochloremic Metabolic Alkalosis

  • Causes: High Upper GI Fluid Losses (Recurrent Emesis of High NG Output)
  • Hypokalemia: From Potassium Excretion in the Urine
    • Hypovolemia Causes a Secondary Hyperaldosteronism
    • Increased Aldosterone Causes Sodium Retention and Potassium Excretion in Urine (Hypernatremia is Also Seen)
  • Hypochloremia: From Direct Loss of HCl in Upper GI Fluid
  • Metabolic Alkalosis: From Hydrogen Loss in Urine (“Paradoxic Aciduria”)
    • Low Potassium Causes Renal Tubules to Retain Sodium and Exchange Hydrogen Instead
    • Would Normally Exchange Potassium for Sodium if Potassium Were Not Deficient
    • Emesis Also Causes Some Loss of HCl (Less Significant than Urine Losses)

Compensation

Metabolic Alkalosis is Compensated by Pulmonary Changes with Decreased Ventilation (Increased CO2)

Expected CO2 = (0.7 x HCO3) + 20 mmHg ± 5

Chloride-Responsiveness

Definition: An Additional Test to Determine the Cause of Metabolic Alkalosis

  • Responsiveness Based on Urine Chloride (UrCl)

Chloride Responsive (UrCl < 10-15)

  • Indicates that Alkalosis is Caused by a Loss of Hydrogen Atoms
  • Causes:
    • Vomiting
    • High NG Output
    • Furosemide
  • Responds Well to Normal Saline Fluid Resuscitation (Replace Volume and Chloride)

Chloride Resistant (UrCl > 20-25)

  • Indicates that Alkalosis is Caused by an Increased Bicarbonate
  • Causes:
    • Hyperaldosteronism
    • Conn Syndrome
    • Bartter Syndrome
    • Hypokalemia
  • Resistant to Normal Saline Fluid Resuscitation

Treatment

Primarily Managed by Treatment of the Underlying Cause

Specific Treatments

  • Fluid Resuscitation with Normal Saline
  • Replace Potassium (Or Add KCl to Fluid) if Hypokalemic
  • Consider Acetazolamide (Diamox) if Additional Diuresis is Required – Carbonic Anhydrase Inhibitor Increases Bicarbonate Excretion in the Urine