Classification and General Etiology
The sole primary cause of exogenous hypoxia is a drop in the partial pressure of oxygen in the inspired gas mixture ($P_iO_2$). Depending on the ambient atmospheric pressure during this process, two fundamentally different forms of the pathology are distinguished:
- Normobaric (pressure is normal).
- Hypobaric (pressure is reduced).
Normobaric Exogenous Hypoxia
Occurs when total atmospheric pressure ($P_{atm}$) remains normal, but oxygen in the air is displaced by other gases (such as carbon dioxide, methane, or nitrogen).
Typical Settings:
- Confinement in tight, sealed, or poorly ventilated spaces (mines, submarines, wells).
- Failure of air regeneration systems.
- Medical errors during mechanical ventilation or gas administration.
Pathogenesis: During prolonged confinement, an individual continuously consumes $O_2$ and produces $CO_2$. This results in arterial hypoxemia, inevitably combined with hypercapnia (excess carbon dioxide). The body attempts to compensate for the oxygen shortage via hyperventilation, but in a sealed environment, this only worsens the situation: the remaining oxygen is consumed much faster. Progressive hypercapnia leads to a drop in pH, establishing respiratory acidosis.
Hypobaric Exogenous Hypoxia
Develops due to a general reduction in atmospheric pressure, which automatically entails a drop in $P_iO_2$. This occurs during high-altitude ascent or in a controlled hypobaric chamber.
Main Forms:
- Mountain sickness — occurs during active (hiking) ascent. In addition to oxygen deprivation and low barometric pressure, individuals face severe physical exertion, cold, and intense solar radiation.
- Altitude sickness — develops during passive ascent (in unpressurized aircraft, chairlifts). The main difference from mountain sickness is the absence of a significant muscular fatigue component.
- Decompression sickness.
Pathogenesis: Exposure to a rarefied atmosphere causes arterial hypoxemia, which triggers compensatory pulmonary hyperventilation. However, because there is no excess $CO_2$ externally, rapid breathing leads to the massive washout of blood carbon dioxide. This results in hypocapnia followed by respiratory alkalosis (an elevated pH).
Blood Gas Alterations
Both forms share common features: decreased partial pressure of oxygen in arterial ($p_aO_2$) and venous ($p_vO_2$) blood, saturation ($S_aO_2$, $S_vO_2$), and oxygen content ($CaO_2$, $C_vO_2$). Meanwhile, the oxygen capacity of the blood and the arteriovenous oxygen difference ($C_{a-v}O_2$) remain within normal limits.
The main differences lie in carbon dioxide parameters and acid-base balance:
| Parameter | Normobaric | Hypobaric |
|---|---|---|
| Atmospheric Pressure ($P_{atm}$) | Normal | Decreased |
| $CO_2$ Tension ($p_aCO_2$) | Increased (hypercapnia) | Decreased (hypocapnia) |
| pH | Decreased (acidosis) | Increased (alkalosis) |