HYPOCAPNIA (CO2
deficit): PHYSIOLOGICAL CHANGES
● Less oxygen 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 oxygen, sugar, and nutrients.
● Vasoconstriction is a direct effect
of lowered PCO2 in the blood plasma, which means reduced oxygen and
glucose supply.
● Extracellular
alkalosis results in
electrolyte deficits and imbalances in plasma, cerebrospinal, lymph, and interstitial
fluids.
● Hyponatremia
(sodium deficiency) is the result of exchange of sodium ions in
interstitial fluid for hydrogen ions in cells.
● Hypokalemia (potassium deficit) is the result of 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 tissues
cells.
● Intracellular
(lactic) acidosis
(lower pH inside of cells), as a result of anaerobic glycolysis,
is the consequence of decreasing oxygen supply (vasoconstriction
and Bohr Effect) while simultaneously increasing its demand (higher metabolism).
● Muscular
calcium-magnesium imbalance
is the result of 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 direct consequence of chronic
hypocapnia, where, because of inadequate CO2, exchange activity of
sodium ions for hydrogen ions in the kidneys is reduced, and thus 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 be the result of 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.
Copyrighted by
Behavioral Physiology Institute,