HYPOCAPNIA (CO2 deficit): PHYSIOLOGICAL CHANGES
- Less O2 is released by hemoglobin (Bohr Effect), as a result of less CO2 and increased alkalinity (pH) in red blood cells.
- Less nitric oxide is released by hemoglobin, resulting in vasoconstriction and reduced supply of O2 and glucose.
- Vasoconstriction is a direct effect of lowered PCO2 in the blood plasma, which means reduced O2 and glucose supply.
- Extracellular alkalosis results in electrolyte imbalances in plasma, cerebrospinal, lymph, and interstitial fluids.
- Hyponatremia (sodium deficiency) result from exchange of sodium ions in interstitial fluid for hydrogen ions in cells.
- Hypokalemia (potassium deficit) results from exchange of potassium ions in interstitial fluid for hydrogen ions in cells.
- Increased cellular excitability and metabolism is the result of excessive sodium and potassium ions in cells.
- Intracellular (lactic) acidosis (lower pH inside of cells), as a result of anaerobic glycolysis, is the consequence of decreasing oxygen supply (vasoconstriction & Bohr Effect) while simultaneously increasing its demand (higher metabolism).
- Muscular calcium-magnesium imbalance results from alkalosis and the exchange of hydrogen ions for calcium ions.
- Smooth muscle constriction is a direct effect of lowered PCO2, leading to vascular, gut, and bronchial constriction.
- Bicarbonate deficit reduces extracellular acid buffering capacity as a result of chronic hypocapnia where, because of inadequate CO2, bicarbonate ions in the kidneys are excreted instead of restored to the blood.
- Sodium depletion is a consequence of chronic hypocapnia, where, because of inadequate CO2, exchange activity of sodium ions for hydrogen ions in the kidneys is reduced, and sodium ions are excreted instead of restored to the blood.
- Elevated platelet level, aggregation, and “adhering” propensity, as a result of nitric oxide retention by hemoglobin, means increased greater likelihood of blood clotting (thrombosis).
- Respiratory inhibition, evidenced in by breath holding and sleep apnea, may result from brainstem inhibitory reflexes.
- Antioxidant depletion may result from excitotoxin production (e.g., glutamate) during chronic hypocapnia.
- Systemic inflammation may be a direct consequence of chronic hypocapnia.
Click here for more details: acid-base balance, kidney physiology, and electrolyte balance. What are the effects of these physiological changes? Click here to learn more: symptoms and deficits and acute effects.