Types of Alkalosis
Alkalosis is classified into two primary types based on the underlying mechanism: respiratory alkalosis and metabolic alkalosis. 1
Respiratory Alkalosis
Respiratory alkalosis occurs when excessive ventilation leads to decreased arterial CO2 levels (hypocapnia), resulting in elevated blood pH above 7.45. 2
Mechanism
- Hyperventilation causes excessive elimination of CO2, reducing carbonic acid formation and increasing pH 2
- The condition affects virtually every organ system in the body and produces multiple metabolic abnormalities 2
Key Metabolic Effects
- Changes in potassium, phosphate, and calcium handling 2
- Development of mild lactic acidosis 2
- Altered renal handling of electrolytes 2
Common Etiologies
- Pulmonary disorders: Direct lung pathology causing increased ventilation 2
- Extrapulmonary disorders: Conditions outside the lungs triggering hyperventilation 2
- Hyperventilation syndrome: A common cause in emergency settings, diagnosed by exclusion 1, 2
- Psychogenic disorders: Anxiety, panic disorders, and stress-related hyperventilation 1
Clinical Manifestations
- Cardiac effects including tachycardia, ventricular and atrial arrhythmias, and chest pain (both ischemic and nonischemic) 2
- Pulmonary vasodilation 2
- Gastrointestinal changes in perfusion, motility, and electrolyte handling 2
- Abnormal breathing patterns with abrupt onset of rapid, shallow breathing during exercise 1
- Decreased PetCO2 and PaCO2 levels 1
Diagnostic Features During Exercise Testing
- Impressive hyperventilation with abnormal increases in Ve, Ve/VCO2, and respiratory frequency 1
- Respiratory alkalosis evident by decreased PetCO2 and PaCO2 1
- Chronic respiratory alkalosis may show a downregulated PaCO2 set point at rest 1
Metabolic Alkalosis
Metabolic alkalosis is characterized by primary elevation of serum bicarbonate and arterial pH above 7.45, with compensatory increase in PaCO2 due to adaptive hypoventilation. 1, 3
Mechanism of Generation
- Gain of bicarbonate: Through oral or parenteral HCO3- administration, or via lactate, acetate, or citrate administration 4, 3
- Loss of acid: Either via gastrointestinal tract (vomiting) or kidney (diuretics) 4, 3
Factors Maintaining Metabolic Alkalosis
- Decreased glomerular filtration rate 5, 4
- Volume contraction 5, 4, 3
- Hypokalemia 5, 4, 3
- Hypochloremia 5, 4, 3
- Aldosterone excess 5, 4, 3
- Elevated arterial CO2 3
Major Clinical States
- Diuretic-induced: Most common in congestive heart failure patients, caused by chloruretic diuretics activating the renin-angiotensin system 6, 4
- Vomiting: Loss of gastric acid 4, 3
- Mineralocorticoid excess: Including primary hyperaldosteronism 4, 3
- Bartter syndrome: Genetic tubulopathy causing salt wasting, hypokalemia, and metabolic alkalosis with polyhydramnios in severe cases 1, 4, 3
- Gitelman syndrome: Similar genetic tubulopathy with later presentation 4, 3
- Licorice ingestion: Mineralocorticoid-like effects 4, 3
- Excess calcium-alkali ingestion 3
Clinical Significance
- Severe metabolic alkalosis (arterial pH ≥7.55) in critically ill patients is associated with significantly increased mortality 3
- Effects include central nervous system changes, myocardial dysfunction, skeletal muscle abnormalities, and hepatic effects 5, 4
Diagnostic Approach
- Urinary chloride excretion: Fractional chloride excretion usually >0.5% in conditions like Bartter syndrome helps distinguish renal from extrarenal salt losses 1, 7
- Paradoxical aciduria: May occur in hypokalemic metabolic alkalosis despite systemic alkalosis, due to enhanced hydrogen ion secretion in the distal tubule 7
- Serum electrolytes showing hypokalemia (typically <3.5 mmol/L), hypochloremia, and elevated bicarbonate 7, 6
Treatment Principles
- Eliminate generation and maintenance factors 6, 4
- Chloride and potassium repletion: Essential for correction 6, 4
- Acetazolamide: Enhances renal bicarbonate excretion 6, 4
- Hydrochloric acid: For direct titration of base excess in severe cases 6, 4
- Low-bicarbonate dialysis: When accompanied by kidney failure 6, 4
- Address underlying cause: Discontinue diuretics, treat vomiting, manage heart failure appropriately 6, 3
Important Caveats
- Potassium-sparing diuretics should be used cautiously in salt-wasting disorders like Bartter syndrome, as they may worsen volume depletion despite improving hypokalemia 7
- In congestive heart failure, aldosterone antagonists should be integral to the diuretic regimen 6
- Correction of volume depletion and electrolyte abnormalities (especially potassium and chloride) is essential rather than attempting to correct aciduria directly in paradoxical aciduria 7