Types and Physiological Effects of Oxygen Therapy
To eliminate hypoxia in medical practice, two main modes of hyperoxygenation are used:
- Normobaric oxygenation. The patient breathes 100% oxygen at normal atmospheric pressure. This method achieves a partial pressure of oxygen ($pO_2$) of up to 760 mmHg.
- Hyperbaric oxygenation. The procedure is performed in specialized hyperbaric chambers under increased pressure. The main advantage of this method is the ability to provide virtually any required level of arterial oxygen tension ($paO_2$).
When the optimal therapy regimen is achieved, normalization of vital functions is observed. In the respiratory system, an adequate volume of alveolar ventilation is restored, primarily through a decrease in respiratory rate. The cardiovascular system responds by optimizing cardiac output against the background of bradycardia. In addition, a decrease in circulating blood volume (CBV) is noted due to physiological blood redistribution.
Mechanism of Pathogenic Action
The outcome of oxygen exposure directly depends on the appropriateness of therapy. If oxygen delivery is excessive or clinically unjustified, oxygen toxicity develops instead of correcting hypoxia. This is based on the toxic effects of excess oxygen, which operate through three key mechanisms:
- Excess Reactive Oxygen Species (ROS) Generation. Free radicals cause direct damage to cell membranes, structural proteins, enzymes, and nucleic acids.
- Activation of Lipid Peroxidation. An uncontrolled intensification of free radical lipid peroxidation and other organic compounds occurs.
- Inhibition of Tissue Respiration. Excess oxygen exerts a direct and indirect inhibitory effect on respiratory enzymes, paradoxically leading to worsening cellular energy deficits.
Clinical Forms of Oxygen Toxicity
The toxic effects of hyperoxygenation can manifest as three pathological conditions. They may occur independently, develop sequentially, or present in combination.
1. Hypoventilatory State (Respiratory System Damage) The respiratory system suffers first because it is in direct contact with the gas. The degree of damage is strictly tied to the partial pressure of $O_2$. When inhaling a mixture containing 95% oxygen, the damage progression is as follows:
- After 4–22 hours: inflammation and damage to the airway mucosa develop.
- More than 24 hours: profound damage to lung tissue occurs. The permeability of the air-blood barrier decreases, atelectasis and pulmonary edema develop. The final stage is the development of acute respiratory distress syndrome (ARDS).
2. Convulsive State This form develops only under increased barometric pressure (in a hyperbaric chamber). At normal atmospheric pressure, breathing pure oxygen does not cause seizures. The pathology manifests within minutes to hours. The pathogenesis is based on damage to neurons in the brain and spinal cord, leading to excessive excitation of neural centers and motor neurons, culminating in seizures.
3. General Toxic State Occurs with prolonged breathing of pure oxygen. Various target organs bear the toxic brunt:
- Eyes: damage to the retina and lens.
- Blood: destruction of erythrocytes (hemolysis) develops.
- Internal organs: the myocardium, kidneys, and endocrine glands are affected.
The culmination of the general toxic state is the development of severe multiple organ dysfunction syndrome (MODS).
Principles of Treatment
The only way to reverse oxygen toxicity is the immediate correction of the breathing gas mixture. The patient must be switched to breathing air with a normal (physiological) oxygen content to interrupt the cascade of toxic reactions.