The Introduction of Oxygen Therapy
Table of Contents
Introduction
Oxygen therapy, commonly abbreviated as OT, includes normobaric oxygen therapy and hyperbaric oxygen therapy. Normobaric oxygen therapy is a method of treating diseases by inhaling pure oxygen or high-concentration oxygen at atmospheric pressure. The primary purpose of normobaric oxygen therapy is to correct general systemic hypoxia by increasing the partial pressure of oxygen in arterial blood (PaO₂) and arterial oxygen saturation (SaO₂), thereby restoring normal tissue oxygenation. Normobaric oxygen therapy is effective primarily for hypoxic hypoxia. In contrast, the main purpose of hyperbaric oxygen therapy is not only to correct specific forms of hypoxia (such as carbon monoxide poisoning, cerebral edema, cerebral infarction, and sudden deafness) but also to play a crucial role in the treatment of many other non-hypoxic conditions and numerous medical emergencies (such as air embolism, decompression sickness, anaerobic bacterial infections, and pulmonary edema).
1. Physiological and Pathophysiological Basis of Oxygen Therapy
Oxygen is an essential substance for sustaining life; in healthy individuals, oxygen supply primarily comes from the air. Air is a mixture of gases, with oxygen accounting for 20.93% of its composition. At standard atmospheric pressure (101.3 kPa), the partial pressure of oxygen in air is 21.2 kPa. After air is inhaled into the respiratory tract, it is warmed and humidified, producing saturated water vapor at body temperature. The partial pressure of this saturated water vapor is 6.0 kPa; therefore, the partial pressure of oxygen in the inspired air is 19.9 kPa. The inspired air mixes with residual air in the alveoli, diluting the oxygen concentration and reducing the partial pressure of oxygen in the alveolar gas to 14.0 kPa. Alveolar gas undergoes diffusion exchange with blood in the pulmonary capillaries within the alveoli. Once equilibrium is reached, due to the influence of age and individual differences, PaO₂ ranges from 10.7 to 13.3 kPa (80–100 mmHg); a value below 10.7 kPa (80 mmHg) is considered hypoxemia; If PaO₂ < 8.0 kPa (60 mmHg) and SaO₂ is significantly reduced, resulting in a substantial decrease in blood oxygen content, this constitutes respiratory failure.
At rest, to maintain normal oxidative metabolism in a healthy person, 5.6 mL of oxygen must be supplied to tissues for every 100 mL of blood flowing through them. The body consumes approximately 250 mL of oxygen per minute; hypoxia can disrupt the body’s physiological functions. The oxygen requirements for metabolism vary among different tissue cells. Although adult brain tissue accounts for only 2% of body weight, it consumes 20% of the body’s total oxygen (50% in infants); therefore, brain cells are most sensitive to hypoxia. The brain can survive for only 8 minutes in an oxygen-deprived state; severe hypoxia can cause brain cell necrosis, leading to impaired consciousness and irreversible central nervous system sequelae. Cardiac muscle is also highly sensitive to hypoxia, which can cause severe arrhythmias and even cardiac arrest. Therefore, prompt oxygen therapy to correct hypoxia is a critical measure for maintaining normal oxidative metabolism and function in the body’s tissues and organs. It buys time for critically ill patients and creates the conditions necessary for implementing comprehensive resuscitation measures.
2. Types of Oxygen Therapy
Oxygen therapy is divided into normobaric oxygen therapy and hyperbaric oxygen therapy. Normobaric oxygen therapy is further classified into three types: low-concentration, medium-concentration, and high-concentration oxygen therapy.
2.1 Normal-Pressure Oxygen Therapy
(1) Normal-pressure low-concentration oxygen therapy: This refers to the administration of 24%–35% oxygen at normal atmospheric pressure. It is primarily used for hypoxic patients with abnormal respiratory regulation accompanied by CO₂ retention, such as those with chronic obstructive pulmonary disease (COPD).
① Principle: These patients have severe CO₂ retention, and their respiratory centers are insensitive to CO₂ stimulation; respiratory maintenance depends on hypoxic stimulation. High-concentration oxygen administration eliminates the driving effect of hypoxic respiration, whereas low-concentration oxygen therapy can both alleviate the damage caused by hypoxia to the body and prevent respiratory depression resulting from the loss of the hypoxic respiratory drive.
The relationship curve between PaO₂ and SaO₂ is S-shaped. In healthy individuals, an increase in inspired oxygen concentration of just 2% can raise PaO₂ by 2.0 kPa (15 mmHg); even a slight increase in PaO₂ results in a significant rise in SaO₂. For example, if a patient’s PaO₂ is 4.0 kPa (30 mmHg), low-concentration oxygen therapy—increasing the inspired oxygen concentration from 21% to 25%—can raise PaO₂ from 4.0 kPa (30 mmHg) to 6.0 kPa (45 mmHg) and SaO₂ from 57% to 80%, thereby removing the patient from the risk of hypoxia. In patients with moderate-to-severe hypoxia accompanied by CO₂ retention, increasing the inspired oxygen concentration by 7% (from 21% to 28%) will not cause PaCO₂ to rise by more than 2.7 kPa (20 mmHg).
② Specific Method: Begin with an oxygen concentration of 24%, and monitor to ensure the rise in PaCO₂ does not exceed 0.7–2.0 kPa (5–10 mmHg). If the patient can be aroused and cough, the oxygen concentration may be increased to 28%; If the PaCO₂ increase does not exceed 2.7 kPa (20 mmHg) and the patient’s condition is stable, this indicates that the oxygen concentration is appropriate. After 1–2 days of oxygen therapy, if the PaCO₂ is <6.7 kPa (50 mmHg), the oxygen concentration may be increased to 35% to raise PaO₂ above the physiological threshold of 9.3 kPa (70 mmHg).
(2) Normal-pressure moderate-concentration oxygen therapy: Treatment with oxygen at an inhalation concentration of 40%–60%. The oxygen concentration can be adjusted according to clinical needs to alleviate hypoxemia; this is suitable for patients with hypoxia but without CO₂ retention.
(3) Normal-pressure high-concentration oxygen therapy: This refers to oxygen administration at concentrations exceeding 60%. It is indicated for severe hypoxia—such as that resulting from an abnormal ventilation-perfusion ratio, right-to-left shunting, acute respiratory and circulatory arrest, or carbon monoxide poisoning—in patients with no (or mild) CO₂ retention.
2.2 Hyperbaric Oxygen Therapy
Hyperbaric oxygen therapy differs from normobaric oxygen therapy not merely in terms of quantity, but in that it produces a qualitative change based on quantitative differences. Normobaric oxygen therapy is effective only for treating hypoxemia, whereas hyperbaric oxygen therapy not only provides effective treatment for hypoxemia but also has other benefits. A comparison of the effects of hyperbaric oxygen therapy and normobaric oxygen therapy is shown in Table 1-5-0-1:
Table 1-5-0-1: Comparison of Hyperbaric Oxygen Therapy and Ambient-Pressure Oxygen Therapy
3. Assessment of Hypoxia and Indications for Ambient-Pressure Oxygen Therapy
3.1 Hypoxia Assessment Tests
Since acute, short-term hypoxia can increase the body’s tolerance to hypoxia, oxygen therapy is not required in such cases. However, more severe, persistent hypoxia necessitates oxygen therapy; for this reason, the concept of indications for ambient-pressure oxygen therapy has been proposed. The following experimental data can serve as a reference for determining when oxygen therapy is needed.
(1) A PO₂ of at least 0.7–2.0 kPa (5–10 mmHg) is required to maintain oxygen metabolism and high-energy metabolism within cellular mitochondria; therefore, PaO₂ must reach at least 3.3 kPa (25 mmHg).
(2) When hemoglobin levels and cardiac output are normal, the minimum PaO₂ the human body can tolerate is 3.3 kPa (25 mmHg); below this value, brain cells die due to an inability to absorb oxygen. It is generally accepted that a drop in PaO₂ to 2.7 kPa (20 mmHg) is immediately life-threatening.
(3) PaO₂ < 4.0 kPa (30 mmHg) or SaO₂ < 50% is the critical threshold for life-threatening conditions, with the potential to result in death.
(4) When PaO₂ > 4.0 kPa (30 mmHg), most tissues can still maintain adequate function.
(5) PaO₂ > 6.7 kPa (50 mmHg) or SaO₂ > 75% is the minimum safe threshold. In cases of hypoxia, it is ideal to correct PaO₂ to 8.0–8.7 kPa (60–65 mmHg) through oxygen therapy.
3.2 Assessment of Hypoxia and Indications for Ambient-Pressure Oxygen Therapy
See Table 1-5-0-2 for the assessment of hypoxia severity and indications for oxygen therapy.
Table 1-5-0-2: Assessment of Hypoxia Severity and Indications for Oxygen Therapy
4. Indications for Normal-Pressure Oxygen Therapy
4.1 Hypoventilation
Oxygen therapy is indicated for hypoventilation caused by any reason that results in hypoxia (or accompanied by CO₂ retention); however, oxygen administration is not a substitute for treatment of the underlying cause. For patients with respiratory center depression, respiratory stimulants should be administered in addition to oxygen, and assisted ventilation should be used when necessary to increase ventilation; In cases of obstructive hypoventilation, airway obstruction must first be eliminated—for example, by relieving bronchospasm, clearing sputum, or removing foreign bodies—otherwise oxygen therapy will be ineffective. Tracheal intubation or tracheostomy may be performed if necessary.
4.2 Ventilation-to-Perfusion (VA/Q) Ratio Imbalance
In healthy individuals, the VA/Q ratio is 0.8. A VA/Q imbalance may result from normal blood perfusion but insufficient pulmonary ventilation (VA/Q < 0.8), or from normal ventilation but insufficient or interrupted blood perfusion (e.g., pulmonary infarction; VA/Q > 0.8). Both conditions can lead to insufficient hemoglobin oxygenation (functional shunting) and result in hypoxemia. Increasing the oxygen concentration in the inspired air raises the oxygen concentration in the alveolar gas, which can correct VA/Q imbalance caused by inadequate ventilation and enhance oxygen diffusion. High-concentration oxygen therapy is more effective; however, in patients with marked CO₂ retention and abnormal respiratory regulation, high-concentration oxygen therapy may cause respiratory depression, which not only fails to improve hypoxia but may also exacerbate CO₂ retention.
4.3 Diffusion Impairment
For oxygen to diffuse from the alveoli into the blood, it must pass through the alveolar-capillary membrane, which includes the alveolar epithelium, basement membrane, interstitium, and alveolar capillary endothelium. Thickening of the alveolar membrane, pulmonary edema, thickening of the capillary walls, or a reduction in the gas diffusion area can all impair diffusion function, leading to hypoxia. Any pulmonary disease in which thickening of the alveolar-capillary membrane causes hypoxemia is collectively referred to as “alveolar-capillary obstruction syndrome.” This is commonly seen in pulmonary interstitial fibrosis and pulmonary edema; in such patients, inhalation of pure oxygen can yield good results. Because CO₂ has a high diffusion capacity, diffusion impairment is typically characterized primarily by hypoxia, with no significant CO₂ retention.
4.4 Right-to-Left Shunt
This type of hypoxia occurs when a portion of venous blood bypasses pulmonary oxygenation and enters the left heart or arterial system directly. It is seen in congenital heart disease, arteriovenous fistulas (anatomical shunts), or atelectasis (functional shunts). Inhaling pure oxygen or undergoing hyperbaric oxygen therapy increases the blood’s dissolved oxygen content, thereby improving this type of hypoxia.
4.5 Patients with Acute Heart Failure and Shock
Patients in this category have poor tolerance to hypoxia; even a PaO₂ level of 6.7 kPa (50 mmHg) can be life-threatening, and a PaO₂ level of 8.0 kPa (60 mmHg) may still trigger arrhythmias and a decrease in cardiac output. Therefore, for these patients, oxygen therapy should be administered as soon as PaO₂ drops to 9.3 kPa (70 mmHg).
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5. Methods of Oxygen Administration
5.1 Oxygen Administration via Nasal Cannula or Nasal Pliers
This method involves inserting a soft cannula through the nasal cavity to the level of the soft palate, or placing plastic nasal prongs in one nasal vestibule to administer oxygen. This method is simple, practical, and comfortable, and is the most commonly used in clinical practice. The oxygen flow rate generally does not exceed 6 L/min, and the oxygen concentration is kept below 50%. The disadvantage of this method is that the oxygen concentration is unstable and easily affected by tidal volume and respiratory rate. For example, if the tidal volume is large and the respiratory rate is slow, the inhaled oxygen concentration is high; conversely, it is low. Mouth breathing can also cause the oxygen concentration to drop. In addition, excessive flow rates during oxygen administration via a nasal cannula or nasal prongs can irritate the nasal mucosa, which patients often find intolerable; To reduce the impact of the airflow, multiple small holes can be drilled in the sidewall of the distal end of the cannula to disperse the airflow. The nasal prong method is more effective than the nasal cannula method at reducing airflow irritation to the mucosa. The formula for calculating the inspired oxygen concentration for nasal cannula (or nasal prong) oxygen therapy is:
Inspired oxygen concentration (%) = 21 + 4 × oxygen flow rate (L/min)
5.2 Oxygen Administration via Mask or Hood
A mask refers to the administration of oxygen through a rubber mouth-and-nose mask. It provides a fixed oxygen concentration and is more comfortable than oxygen delivery via a tube, but it has a large dead space and results in higher oxygen consumption. The following are common types of masks:
(1) Simple mask: Oxygen is introduced through one side, and exhaled air escapes from around the edges of the mask. To eliminate rebreathing caused by the mask’s dead space, the flow rate should not be less than 4 L/min; if an oxygen concentration of 40%–50% is required, the oxygen flow rate must be 12–15 L/min.
(2) Venturi mask: This is a mask capable of controlling oxygen concentration. It works by using a high-velocity oxygen jet to create negative pressure, which draws in air to dilute the oxygen. By adjusting the air inlet, the oxygen concentration can be controlled within a range of 24%–40% (e.g., 24%, 28%, 35%, 40%) without being affected by changes in respiratory rate or tidal volume.
(3) CO₂-mixed mask: This consists of two parts—the mask and a breathing bag. There is no one-way valve between the mask and the oxygen bag; exhaled CO₂ mixes with the incoming oxygen. The oxygen concentration is lower, while the CO₂ concentration is higher (some believe this promotes vasodilation, but it is difficult to achieve the ideal oxygen concentration, and the side effects of high CO₂ concentrations cannot be ignored). It is rarely used in clinical practice.
(4) One-way valve mask: Equipped with an expandable oxygen bag, this mask stores 100% oxygen inside the bag during exhalation. During inhalation, oxygen from the bag is drawn in through a one-way valve, ensuring that the patient inhales pure oxygen. This type of mask is used in hyperbaric oxygen chambers where air is pressurized.
Currently, hyperbaric oxygen chambers also feature gel-padded hoods that offer greater comfort than masks. For children and tracheostomy patients, these hoods improve patient compliance, ensure oxygen concentration, and enhance treatment efficacy.
5.3 Oxygen Tent
Oxygen tents allow for the control of temperature, humidity, and oxygen concentration, and can filter and disinfect the air; however, due to their complex equipment, high cost, and difficult maintenance, they are rarely used in clinical practice. They are suitable for providing oxygen to newborns or patients with extensive burns.
5.4 Ventilator-Delivered Oxygen
Oxygen is delivered via positive pressure from a ventilator, connected through an endotracheal tube, tracheostomy, or a non-invasive oral-nasal mask. This method is commonly used for resuscitation in patients with severe respiratory failure or respiratory arrest. It not only corrects hypoxia but also removes retained CO₂. Because mechanical ventilation is used, the oxygen concentration can be adjusted as needed based on the patient’s condition (21%–100%), thereby increasing PaO₂ while maintaining PaCO₂ at normal levels (<65 mmHg).
5.5 Extracorporeal Membrane Oxygenation (ECMO)
ECMO is a method of respiratory and circulatory support that has emerged in recent years. ECMO provides patients with continuous extracorporeal respiration and circulation. Its basic principle involves drawing blood from a vein, fully oxygenating it and removing CO₂ through a membrane lung outside the body, and then returning the oxygenated blood to the systemic circulation. ECMO is particularly suitable for conditions involving severe circulatory and respiratory dysfunction. Its drawbacks include high cost and the fact that it is not yet widely available in some hospitals (especially at the primary care level).
5.6 Other Civilian and Commercial Oxygen Therapies
In addition to the oxygen administration methods and types of oxygen therapy commonly used in medical procedures described above, there are other forms of oxygen therapy in daily life. For example: ① Low-pressure chambers can simulate the low atmospheric pressure and hypoxic conditions found at high altitudes; they are primarily used in aerospace research, but also have some applications in sports training and high-altitude acclimatization; ② Portable hyperbaric chambers can generate less pressure than medical hyperbaric chambers (gauge pressure of 0.04 MPa or less), but they are easy to transport and are primarily used for outdoor rescue operations and civilian treatment; ③ Home oxygen therapy is primarily used by patients with chronic conditions prone to hypoxia (such as chronic obstructive pulmonary disease and cor pulmonale) to alleviate hypoxic symptoms during stable phases of their illness. Home oxygen generation is the main source for commercial oxygen therapy, while oxygen bars provide pure oxygen for recreational and wellness purposes.
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6. Precautions for Oxygen Therapy
Oxygen therapy can easily cause certain side effects and complications; special care should be taken during its administration.
6.1 Warming and Humidification
(1) Warming: When ambient temperatures are low, the inhaled gas should be warmed (to 37°C) to reduce irritation to the respiratory tract.
(2) Humidification: Oxygen is a dry gas; direct inhalation can cause the respiratory tract mucosa to dry out, make secretions viscous, and impair ciliary movement. Therefore, oxygen should be humidified using a humidifier bottle; for patients with a tracheostomy or endotracheal tube, fluids should be dripped periodically to humidify the airway.
6.2 Close Monitoring
(1) Closely monitor the effectiveness of oxygen therapy: Observe whether hypoxia has improved. If the patient’s condition improves after oxygen administration—with improved mental status, increased respiratory amplitude, decreased respiratory rate, alleviated dyspnea, and a heart rate reduction of 10 beats per minute or more—this indicates that oxygen therapy is effective; Conversely, if, after oxygen administration, respiratory amplitude decreases, the patient becomes confused, experiences increased salivation, or the coma worsens, this indicates a deterioration of the condition and inappropriate oxygen therapy. It is best to perform an arterial blood gas analysis immediately and check whether the oxygen flow is insufficient (e.g., due to blockages in the oxygen delivery system or impaired ventilation) or excessive (respiratory depression caused by too high a concentration), and take appropriate measures.
(2) Closely monitor blood pressure and peripheral circulation in the extremities.
6.3 Fire Safety Precautions
them securely and protect them from shock and oil to prevent explosions.
6.4 Prevention of Oxygen Toxicity
Adverse reactions to normobaric oxygen therapy are directly proportional to oxygen concentration and duration of oxygen administration, while toxic reactions to hyperbaric oxygen therapy are directly proportional to oxygen partial pressure and duration. To prevent oxygen toxicity, oxygen concentration, pressure, and duration of oxygen administration must be controlled. The oxygen concentration limits and pressure limits are as follows.
(1) For normobaric oxygen therapy, inhaling 40% oxygen is generally considered safe; inhalation of pure oxygen should not exceed 8 hours.
(2) The pressure limits for hyperbaric oxygen therapy are: 3 ATA < 1 hour, 2.5 ATA < 1.5 hours, and 2.0 ATA < 2 hours.
7. Indications and Methods for Discontinuing Oxygen Therapy
7.1 Indications for Discontinuing Oxygen Therapy
After oxygen therapy, the patient’s condition has stabilized; hypoxia and CO₂ retention have improved; the heart rate has slowed compared to before; and breathing has become more stable. After breathing room air for 30 minutes, PaO₂ > 60 mmHg and PaCO₂ < 50 mmHg.
7.2 Methods for Discontinuing Oxygen Therapy
Use a gradual tapering approach: if the patient’s condition remains stable while the oxygen flow rate is reduced, continue to gradually decrease the flow rate until oxygen therapy is completely discontinued.
8. Side Effects of Oxygen Therapy and Their Management
Common side effects and complications during oxygen therapy are as follows:
8.1 Oxygen Toxicity
(1) Causes and Characteristics: Prolonged administration of oxygen at atmospheric pressure can lead to pulmonary and ocular oxygen toxicity. Hyperbaric oxygen therapy at excessively high pressures and/or for prolonged durations may also result in cerebral oxygen toxicity.
(2) Prevention and Management: The primary measure to prevent oxygen toxicity during atmospheric-pressure oxygen therapy is to control the duration of oxygen administration. If oxygen toxicity occurs, oxygen therapy should be discontinued and symptomatic treatment administered.
8.2 Atelectasis
(1) Causes and Characteristics: If a patient’s bronchi are completely obstructed while breathing normal air, the nitrogen in the alveoli is virtually insoluble in the blood. Even as oxygen from the alveoli gradually enters the alveolar capillaries, a certain amount of gas remains in the alveoli, making alveolar collapse unlikely; However, if a patient inhales oxygen at a concentration greater than 80%, and the bronchi are completely obstructed, the primary gas in the alveoli is oxygen. Due to the persistent partial pressure gradient of oxygen between the alveoli and the venous end of the alveolar capillaries, oxygen continuously diffuses from the alveoli into the capillaries, causing the previously expanded alveoli to gradually atrophy and collapse, leading to atelectasis. Based on a similar principle, alveoli in areas with a low ventilation-to-perfusion ratio are also prone to collapse when high-concentration oxygen is inhaled, leading to atelectasis.
(2) Preventive Measures: Control the concentration and duration of oxygen administration; instruct patients to cough up sputum frequently, perform deep breathing exercises, and change their lying position regularly to prevent the obstruction and accumulation of secretions.
8.3 Airway Dryness
(1) Causes and Characteristics: During endotracheal intubation with oxygen therapy, the body loses the humidifying effect of the upper respiratory tract on inhaled gas. If unhumidified, high-concentration oxygen is inhaled continuously for more than 48 hours, the bronchial mucosa may be damaged by direct irritation from the dry gas, resulting in reduced secretions that become viscous and crusty, making them difficult to cough up.
(2) Preventive Measures: Use a humidifier or administer nebulized inhalation therapy.
8.4 Respiratory Depression
(1) Causes and Characteristics: In patients with hypoxia accompanied by severe CO₂ retention (such as those with COPD or obesity-hypoventilation syndrome), respiratory effort is primarily maintained by hypoxic stimulation of peripheral chemoreceptors. When oxygen therapy is administered without restricting the oxygen flow rate, the high concentration of inhaled oxygen eliminates the respiratory drive caused by hypoxia, which can lead to more severe CO₂ retention and respiratory depression.
(2) Prevention and Management: Patients with chronic hypoxia accompanied by CO₂ retention should avoid inhaling high-concentration oxygen. If respiratory depression occurs, the oxygen concentration should be immediately reduced, respiratory stimulants should be administered, and mechanical ventilation should be used to assist breathing if necessary.
8.5 Retinopathy of Prematurity
(1) Causes and Characteristics: Clinical observations have shown that premature infants with respiratory distress syndrome who receive high-flow oxygen therapy may develop posterior lens fibrosis, which can lead to retinal detachment and blindness.
(2) Preventive Measures: Care must be taken to control the partial pressure of oxygen when administering oxygen therapy to premature infants.
