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 makes it possible to achieve a partial pressure of oxygen (pO2) of up to 760 mmHg.
- Hyperbaric oxygenation. The procedure is performed in specialized hyperbaric chambers under increased pressure. The main advantage of the method is the ability to provide absolutely any required level of oxygen tension in arterial blood (paO2).
Upon reaching the optimal therapy regimen, normalization of vital activity is observed in the body. In the respiratory system, an adequate volume of alveolar ventilation is restored, which occurs primarily due to a decrease in respiratory rate. The cardiovascular system responds by optimizing cardiac output against the background of bradycardia. In addition, there is a decrease in circulating blood volume (CBV), which is associated with the physiological redistribution of blood.
Mechanism of pathogenic action
The result of oxygen exposure directly depends on the appropriateness of therapy. If the oxygen supply is excessive or clinically unjustified, oxygen poisoning develops instead of hypoxia elimination. It is based on the toxic effect of excess oxygen, which is realized through three key mechanisms:
- Generation of excess reactive oxygen species (ROS). Free radicals cause direct damage to cell membranes, structural proteins, enzymes, and nucleic acids.
- Activation of LPO. Excessive and uncontrolled intensification of free-radical lipid peroxidation occurs, as well as peroxidation of other organic compounds.
- Suppression of cellular respiration. Excess oxygen has a direct and indirect inhibitory effect on respiratory enzymes, which paradoxically leads to an aggravation of energy deficiency in cells.
Clinical forms of oxygen poisoning
The toxic effect of hyperoxygenation can manifest as three pathological conditions. They may occur separately, develop sequentially, or present in combination.
1. Hypoventilatory condition (respiratory tract damage) The external respiration system suffers first, as it is in direct contact with the gas. The degree of damage is strictly tied to the partial pressure of O2. When inhaling a mixture containing 95% oxygen, the damage dynamics are as follows:
- After 4–22 hours: inflammation and damage to the respiratory mucosa develop.
- More than 24 hours: profound damage to the 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 condition This form develops only under increased barometric pressure (in a hyperbaric chamber). At normal atmospheric pressure, breathing pure oxygen does not cause convulsions. The pathology manifests within a timeframe ranging from several minutes to several hours. The pathogenesis is based on damage to neurons of the brain and spinal cord, leading to excessive excitation of nerve centers and motor neurons, culminating in convulsions.
3. General toxic condition Occurs during prolonged breathing of pure oxygen. Various target organs take the toxic blow:
- Eyes: damage to the retina and lens occurs.
- Blood: destruction of red blood cells (hemolysis) develops.
- Internal organs: the myocardium, kidneys, and endocrine glands are affected.
The outcome of the general toxic condition is the development of severe multiple organ dysfunction syndrome.
Principles of treatment
The only way to eliminate the state of oxygen poisoning is the immediate correction of the breathing mixture. The patient must be switched to breathing air with a normal (physiological) oxygen content to interrupt the cascade of toxic reactions.
Briefly: answers to topical questions
Which antioxidant defense systems are depleted in the event of an excess of reactive oxygen species?
In case of an excess of free radicals and the development of oxidative stress, sources directly point to the depletion of the antioxidant defense — the glutathione peroxidase system.
Cellular antioxidant defense factors include:
- Superoxide dismutase — an enzymatic factor.
- Catalase — an enzymatic factor.
- Glutathione peroxidase — an enzymatic factor.
- Tocopherols — a non-enzymatic factor.
- Glutathione-containing substances — non-enzymatic factors.
The three forms of oxygen poisoning are easy to remember using the "LMB" rule (Lungs, Brain, Everything else): hypoventilatory (lungs affected), convulsive (brain affected in the hyperbaric chamber), and general toxic (multiple organ dysfunction).
Class and exam questions
Why does circulating blood volume decrease during hyperoxygenation?
This occurs due to the physiological redistribution of blood in the body, which accompanies the optimization of cardiac output and the decrease in heart rate.
Can breathing pure oxygen through a mask cause convulsions?
No, at normal barometric pressure, pure oxygen does not cause convulsions. The convulsive condition develops exclusively under increased pressure, for example, during hyperbaric oxygenation sessions.
How quickly are the lungs damaged when inhaling 95% oxygen?
Damage and inflammation of the respiratory mucosa begin as early as 4–22 hours. If inhalation continues for more than a day, pulmonary edema, atelectasis, and acute respiratory distress syndrome (ARDS) develop.
What else to study on this topic
- Mechanisms of reactive oxygen species (ROS) generation in hyperoxia
- Biochemistry of free-radical lipid peroxidation (LPO)
- Pathogenesis of acute respiratory distress syndrome (ARDS)
- Mechanisms of air-blood barrier damage
- Multiple organ dysfunction syndrome as an outcome of the general toxic condition
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