Knowledge of oxygen therapy
Knowledge of oxygen therapy
Knowledge of oxygen therapy. Oxygen is the foundation of life. There are currently many ICU interventions to improve oxygen delivery and ensure oxygen metabolism in end organs. Here, we mainly discuss the way of oxygen delivery to the lungs, oxygen delivery equipment (non-tracheal intubation patients), and side effects of oxygen. Long-term oxygen therapy is beyond the scope of discussion.
Simply put, the amount of oxygen transferred from the lungs to the bloodstream can be increased in the following ways:
- Increase inhaled oxygen concentration (FiO2)
- Increase mean airway pressure
- Increasing the average airway pressure of the lungs can be achieved in the following ways:
- Increase tidal volume (but high tidal volume may be harmful)
- Extend the ratio
- Add or increase positive end expiratory pressure (PEEP)
In view of the benefits of PEEP, increasing PEEP is currently the best way to increase airway pressure, but there is still some controversy. Inhaled oxygen concentration can be adjusted by changing the oxygen supply of the machine.
Theoretical knowledge of the physiological principles of oxygen delivery, the influence of oxygen delivery equipment and pathological conditions on oxygen delivery is the basis for the study of oxygen delivery.
2. Physiology and Pathology
At the cellular level, mitochondrial aerobic metabolism requires oxygen to produce ATP. Before reaching the mitochondria, oxygen needs to cross several barriers and there are several procedures. The partial pressure of oxygen produced by the dry atmosphere at sea level is 159mmHg. After passing through the alveolar, arterial blood, vascular circulation and interstitium, the partial pressure of oxygen in the mitochondria is 4-22mmHg. This change in oxygen partial pressure is called the oxygen cascade. Increasing the inspired oxygen concentration is to avoid tissue hypoxia, which is just one of many interventions.
Hypoxia is harmful at the level of tissues and organs. Brain tissue is the least tolerant of hypoxia. When the acute hypoxia makes the arterial oxygen saturation below 80%, even among healthy people, consciousness disturbance and anxiety will occur. At the tissue level, insufficient oxygen delivery can cause ATP to be formed through anaerobic glycolysis. This metabolic process can produce lactic acid and cause metabolic acidosis.
Tissue hypoxia can be divided into the following four types:
1. Hypotonic hypoxia: The oxygen dissolved in the blood decreases. Low inhaled oxygen concentration (such as high altitude), respiratory failure and V/Q imbalance can cause hypotonic hypoxia.
2. Blood hypoxia: reduced hemoglobin and decreased oxygen carrying capacity. CO poisoning can also cause lower hemoglobin to transport oxygen to the tissues, causing blood hypoxia;
3. Circulating hypoxia: normal oxygen content, insufficient circulating blood volume. This can be local such as peripheral vascular disease (embolism) or systemic (low cardiac output syndrome)
4. Organizational hypoxia: oxygen delivery is normal, but oxygen utilization is impaired. Organelles and mitochondria cannot use oxygen. Cyanide poisoning is a classic example of tissue hypoxia.
3. Oxygen delivery equipment
Like many drugs, the oxygen supply should be titrated continuously. Long-term supply of more oxygen is also harmful. For most people, it is recommended to use a series of methods to maintain the oxygen saturation at 94-98%, and the entire process should be continuously titrated. Some special people need special goals.
Under normal breathing conditions, the inhaled oxygen flow rate can reach 60L/min, but in respiratory distress, it can reach 100L/min.
The amount of oxygen entering the trachea depends on two aspects: 1. The patient’s peak inhaled oxygen flow rate; 2. The oxygen flow rate that the oxygen supply device can provide; if the oxygen flow rate provided by the device is lower than the patient’s peak inspiratory oxygen flow rate, then Air will enter the airway, dilute the oxygen, and reduce the inhaled oxygen concentration. The use of a high-flow mask, the addition of a reservoir and the use of a closed mask (CPAP mask) can increase the inhaled oxygen concentration.
3.1 Nasal cannula
The oxygen concentration of the nasal cannula depends on the oxygen flow rate setting and the patient’s own inspiratory flow rate. Generally speaking, every increase of 1 L/min of oxygen flow can increase the inspired oxygen concentration by 4%. Inhalation of 6 L/min of oxygen through a nasal cannula can reach the maximum inhaled oxygen concentration, usually between 40-50%. Patients generally can tolerate nasal cannula oxygen inhalers and are willing to continue using them. If the oxygen flow rate exceeds 4–5 L/can cause dryness, pain, and discomfort in the nasal cavity, it should be avoided. [Editor’s note: The oxygen flow rate of the nasal cannula should be set between 1-5 and should not continue to increase. Even if it continues to increase, it will not increase the inhaled oxygen concentration, but it will cause patient intolerance.
3.2 Ordinary mask
Ordinary masks have side holes that allow air to enter, and the inhaled oxygen concentration will vary with the patient’s breathing. The oxygen flow rate between 5 and 10L/min can provide 40% to 60% of the inspired oxygen concentration. It is not recommended to reduce the inhaled oxygen flow rate of ordinary masks to 5 L/min or below, because the flow rate is too low to squeeze out the exhaled CO2 out of the mask, causing full use of the gas.
3.3 Venturi inner cover
The venturi cover can provide 24% to 50% oxygen, and the inhaled oxygen concentration can be very accurate. The venturi inner cover mixes air and oxygen in a certain proportion to achieve a continuous and stable inhaled oxygen concentration. An increase in oxygen flow will involve more air and increase the amount of gas reaching the mask. In this case, the inhaled oxygen concentration can remain unchanged. Increased minute ventilation or hyperventilation syndrome can reduce the concentration of oxygen reaching the airway. When you need to precisely control the oxygen concentration and low-concentration oxygen inhalation, such as COPD patients, you can use a venturi mask.
3.4 Non-repetitive inhalation mask
The non-repetitive inhalation mask is equipped with a storage bag that can be filled when oxygen is supplied. When the patient inhales, it can provide a high concentration of oxygen. The one-way valve on the mask can prevent the exhaled carbon dioxide from entering the mask. An oxygen flow rate of 10 to 15L/min can provide an oxygen concentration of 60 to 90%.
3.5 Air section mask
As its name suggests, the tracheal mask is used to inhale oxygen for patients who have spontaneous breathing after tracheotomy. They bypass the upper airway and therefore need to be humidified, especially for long-term use. The oxygen flow rate is usually adjusted based on the target oxygen saturation.
3.6 Non-invasive mask
CPAP masks can improve oxygen delivery in two ways: 1. Increase the pressure of the airway; 2. Increase the concentration of inhaled oxygen. It is necessary to use a well-sealed mask for CPAP non-invasive ventilation, and a constant airway pressure and inhaled oxygen concentration can be given during the oxygen supply process. During exhalation, the airway pressure does not return to the baseline level. This situation is similar to PEEP in invasive ventilation and positive expiratory pressure (EPAP) in noninvasive ventilation.
This can increase the functional residual capacity and help open the alveoli for gas exchange. Other advantages of CPAP include: reducing the work of breathing, reducing the dynamic obstruction of the upper airway; reducing preload and afterload; reducing pulmonary vascular resistance. CPAP can be used to treat sleep apnea syndrome and acute heart failure. If the patient has hypercapnia, CPAP is more suitable. It should be noted that some patients cannot tolerate tightly covered masks; long-term use can cause excessive pressure on the bridge of the nose and skin damage.
4. Oxygen therapy for specific patients
4.1 COPD patients
Patients such as COPD are prone to hypercapnia (which should also include chronic neuromuscular diseases and obstructive hypopnea syndrome). If the oxygen supply is large, the partial pressure of CO2 can increase. In the past, it was believed that elevated oxygen partial pressure would reduce the stimulation of hypoxia on the central nervous system, causing insufficient oxygen drive, leading to increased carbon dioxide partial pressure. However, recent studies have shown that V/Q imbalance plays a greater role in the increase in carbon dioxide partial pressure.
When oxygen is supplied, the pulmonary arteries originally contracted due to hypoxia will dilate, causing uneven blood flow distribution, increasing alveolar dead space, breaking the original compensatory ventilation-blood flow mechanism, causing V/Q imbalance, thereby increasing carbon dioxide content Pressure. The Helton effect theory pointed out that an increase in the partial pressure of carbon dioxide will reduce the ability of hemoglobin to combine with oxygen. At the same time, if a high concentration of oxygen is given to patients with COPD, the central nervous system will lack hypoxic stimulation and cause a reduction in driving pressure. Causes of elevated carbon dioxide. But their role may not be as important as previously thought. The work of breathing in patients with acute exacerbation of COPD has significantly increased. It is necessary to recognize that increased arterial carbon dioxide partial pressure is a manifestation of respiratory fatigue, which indicates that cardiac arrest is about to occur.
For patients with acute episodes of COPD, if it is not particularly severe, it is currently recommended to use a venturi mask to supply 24% inhaled oxygen concentration to adjust the oxygen flow rate to 4L/min. It is recommended to ensure that the patient’s oxygen partial pressure is between 88-92% through continuous clinical observation, blood gas analysis, and oxygen saturation monitor. Out-of-hospital studies have found that the use of oxygen supply methods that control the oxygen concentration can improve the prognosis of COPD patients. [Editor’s note: For COPD patients, try to reduce the inhaled oxygen concentration]
COPD patients with severe disease or about to undergo a cardiac arrest need to supply higher oxygen to ensure oxygen saturation, especially in the initial treatment stage. For these patients, invasive or non-invasive ventilation can be used. Once the situation is stable, an oxygen titration should be performed, setting the saturation target at 88-92%. It should be noted that restoring oxygen supply is more important than improving the partial pressure of carbon dioxide. Persistent hypoxia can be fatal.
4.2 Oxygen therapy for patients with acute coronary syndrome
It is generally believed that oxygen therapy is the first-line treatment option for patients with acute coronary syndrome. Oxygen therapy has a certain effect in patients with myocardial ischemia. However, recent studies have confirmed that oxygen therapy is not beneficial and can cause potential harm. Conventional oxygen therapy can increase the area of myocardial infarction, which may be because oxygen therapy can cause coronary artery constriction. Oxygen therapy is controversial in the treatment of ACS, and more research is needed in the future to confirm the role of oxygen therapy. Currently, patients with ACS should not receive oxygen therapy unless there is hypoxia.
4.3 Oxygen therapy for patients with acute stroke
It is also controversial whether to take oxygen therapy for patients with acute stroke. Studies have found that oxygen therapy can worsen the prognosis of such patients.
4.4 Oxygen therapy for shock patients
For a long time, oxygen therapy has been advocated to treat shock. Some studies have found that maintaining 100% oxygen saturation for patients with hemorrhagic shock can help maintain blood pressure and improve survival. This may be because oxygen inhalation can reduce the work of breathing in shock patients (increased work of breathing can cause diaphragm fatigue). Animal experiments confirmed that apnea is a form of death in shock patients.
4.5 Oxygen therapy for patients with cardiac arrest
For newborns, hyperoxemia is harmful. The current study also found that for patients resuscitated from cardiac arrest, hyperoxemia can make the prognosis worse. This may be because oxygen therapy increases the production of free radicals.
5. The harm of oxygen
Oxygen therapy is not without risks. Potential hazards include physiological hazards and physical hazards such as fire. Excess oxygen supply is associated with side effects of many organs.
5.1 Central Nervous System
Exposure to hyperbaric oxygen at 2 atmospheres can cause grand epilepsy. This is known as the Robert effect and was first described in the 19th century. This side reaction limits the application of hyperbaric oxygen chambers. The cause of hyperbaric oxygen-induced epilepsy is unknown. Other central system symptoms include dizziness, vomiting, headache, confusion, tinnitus, paresthesias, and facial twitching.
Exposure of newborns to high concentrations of oxygen can cause abnormal retinal development (ROP), especially for premature infants with anaesthesia, which lasts until 44 weeks. Neonatal oxygen therapy therefore needs to be strictly controlled, and the saturation should not exceed 95%. The mechanism of ROP is unknown, which may be related to hyperoxia-induced vasoconstriction and abnormal vascular proliferation. More seriously, it may cause retinal detachment and blindness.
Hyperoxemia can cause lung damage, which limits the wide range of oxygen therapy. Prolonged inhalation of 100% oxygen can affect the entire airway.
Alveoli lacks nitrogen and oxygen is absorbed, which can cause alveoli to collapse and cause atelectasis; acute bronchitis is the earliest manifestation of oxygen poisoning, which usually occurs after 4-22 hours of inhalation of pure oxygen. Diffuse alveolar injury followed, after the inspired oxygen concentration exceeded 60% for more than 48 hours.
Prolonged hyperoxia will cause ARDS-like changes, endothelial cells will be damaged, and the interstitium will be edema. The long-term effects of oxygen poisoning are similar to those of ARDS pulmonary fibrosis, which can cause gas exchange disorders. A retrospective study found that if the surviving ARDS patients inhale more than 60% of the oxygen concentration for more than 24 hours, it will cause lung diffusion dysfunction.
The mechanism of oxygen poisoning may be related to oxygen free radicals. Excessive oxygen free radicals cause insufficient detoxification of the body. Free radicals can affect cell outcomes at various levels. Cell membranes, mitochondria and other organelles will continue to be damaged by excessive oxygen. Animal experiments have confirmed that the use of antidote or superoxide dismutase can improve related tolerance.
In order to avoid injury, clinicians should be very cautious to avoid inhaled oxygen concentration exceeding 50%; increasing PEEP and changing ventilation strategies are ways to reduce inhaled oxygen concentration.
5.4 Drug-induced oxygen-related lung injury
Some chemotherapy drugs, such as bleomycin, can aggravate oxygen-related damage to the lungs. At present, the mechanism of this damage is not clear, and it may be related to inflammation and gene expression. Even after chemotherapy is over, bleomycin can cause oxygen-related damage to the lungs. There are currently no randomized controlled trials to confirm this situation. At present, for such patients, there is no safety threshold for oxygen concentration. It is generally recommended that the oxygen concentration be as low as possible, and the saturation should be set between 88-92%. Other drugs have similar effects, but the evidence is insufficient, such as amiodarone, which is currently known to cause pulmonary toxicity, but the mechanism is different.
6. Permissive hypoxia
Whether traditional oxygen therapy is suitable for critically ill patients is currently controversial. Some authors recommend personalized treatment for different patients, and for some patients, hypoxia may be appropriate. This is the permissive hypoxemia strategy. This concept is mainly to avoid the harm caused by hyperoxia, especially the high air pressure and high inhaled oxygen concentration. At present, the exact value of oxygen partial pressure for critically ill patients is still controversial, and further research is needed in the future.
Acute hypoxemia is dangerous, urgent treatment is necessary, and there should be no delay due to the side effects of oxygen therapy. Oxygen therapy equipment can determine whether their use is reasonable. The oxygen saturation should be titrated during treatment. For most patients, saturation between 94% and 98% is appropriate. For patients with hypercapnia, the saturation can be lower. After the patient’s condition is stable, it is very important to limit the inhaled oxygen concentration to avoid oxygen-related damage to the lungs.
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