◄     HYPOCAPNIA (CO₂ deficit): PHYSIOLOGICAL CHANGES ►

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● Less O₂ is released by haemoglobin (Bohr Effect), as a result of less CO₂ and increased alkalinity (pH) in red blood cells.

● Less nitric oxide is released by haemoglobin, 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.

● hyponatraemia (sodium deficiency) result from exchange of sodium ions in interstitial fluid for hydrogen ions in cells.

● hypokalaemia (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 restoured 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 restoured to the blood.

● Elevated platelet level, aggregation, and “adhering” propensity, as a result of nitric oxide retention by

 haemoglobin, means increased greater likelihood of blood clotting (thrombosis).

● Respiratory inhibition, evidenced in by breath holding and sleep apnoea, 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.

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