Main points of oxygen therapy for acute myocardial infarction

Last month, Taiwanese actor Gao Yixiang caused widespread concern due to sudden cardiac death. Similarly, acute myocardial infarction should also attract our attention. This magazine specially invited Meng Qingyi, the chief physician of the emergency department of the First Medical Center of Beijing General Hospital to popularize acute myocardium Knowledge about infarction.

Acute myocardial infarction (AMI) is caused by a severe reduction or interruption of coronary blood supply on the basis of coronary artery disease, resulting in severe and persistent acute ischemia in the corresponding myocardium. Hypoxemia is often complicated, and oxygen inhalation is one of the basic measures for the treatment of acute myocardial infarction.

First, the concept of hypoxia
In addition to eliminating the causes of hypoxia, all types of hypoxia treatment can give patients oxygen. However, the effects of oxygen therapy vary depending on the type of hypoxia. Oxygen therapy works best for hypotonic hypoxia. Because the patient’s PaO2 (arterial blood oxygen pressure) and SaO2 (arterial blood oxygen saturation) were significantly lower than normal. Inhaling oxygen can increase the alveolar oxygen partial pressure, increase PaO2 and SaO2, increase blood oxygen content, and thus increase oxygen supply to the tissue. However, hypotonic hypoxia caused by the flow of venous blood into the arteries, because the shunted blood is directly incorporated into the arterial blood without the alveoli, so the effect of inhaling oxygen on improving its hypoxia is small.

PaO2 and SaO2 are normal in patients with blood hypoxia, circulating hypoxia, and tissue hypoxia. Because the hemoglobin that can bind oxygen has reached about 95% saturation, although oxygen absorption can significantly increase PaO2, the increase in SaO2 is very limited. However, oxygen inhalation can increase dissolved oxygen in the plasma. Generally, when inhaling air at sea level, the dissolved oxygen in 100ml of blood is only 0.31ml; when inhaling pure oxygen, it can reach 1.7ml; when inhaling 3 atmospheres of pure oxygen, the dissolved oxygen can increase to 6ml. The normal tissue uptake of oxygen from 100ml of blood is about 5ml. It can be seen that inhaling high-concentration oxygen or hyperbaric oxygen to increase the amount of dissolved oxygen in the plasma can improve the oxygen supply of the tissue.

In the case of tissue hypoxia, oxygen supply is generally unobstructed, but the ability of the tissue to use oxygen is reduced; increasing the partial pressure gradient of oxygen between plasma and tissue through oxygen therapy to promote the diffusion of oxygen may also have a certain therapeutic effect. Carbon monoxide poisoning inhales pure oxygen, which increases the oxygen partial pressure of blood, and oxygen competes with CO to combine with hemoglobin, thereby accelerating the dissociation of HbCO and promoting the discharge of CO, so the oxygen treatment effect is better.

Second, the method of oxygen supply
During cardiopulmonary resuscitation, artificial respiration is performed immediately. The first aid person blows air into the lungs of the patient with an oxygen concentration of 16% to 17%. Ideally, the partial pressure of oxygen in the alveoli can reach 80mmHg. During cardiac arrest or cardiopulmonary resuscitation, low cardiac output, peripheral oxygen release disorders, and large dynamic and quiescent blood oxygen differences all contribute to tissue hypoxia. Other factors include intrapulmonary shunts and respiratory diseases caused by abnormal ventilation. Hypoxia in tissues leads to anaerobic metabolism and metabolic acidosis. Chemical and electrolyte treatments can affect acid-base imbalances.

Based on the above reasons, it is recommended to inhale 100% pure oxygen when BLS (Basic Life Support) and ACLS (Advanced Cardiovascular Life Support). High oxygen partial pressure can increase the solubility of oxygen in arterial blood, and then increase the oxygen transport in the body ( Cardiac blood output x blood oxygen concentration), inhalation of 100% pure oxygen for a short period of time is beneficial and harmless, and only long-term inhalation of high concentration of oxygen will produce oxygen poisoning.

In patients with acute coronary syndrome, the first 2 to 3 hours of oxygen inhalation through the nasal catheter is 4L / min. For continuous or repeated myocardial ischemia, or complicated myocardial infarction with congestive heart failure, arrhythmia, oxygen inhalation for 3 to 6 hours Until the patient’s hypoxemia is corrected and clinically stable.

As a basic operation, oxygen inhalation is widely used in clinical practice. The methods of oxygen inhalation include nasal catheter method, nasal congestion method, mask method, double-lumen nasal catheter method, and oxygen account method. Which method is currently used in China depends on the local customs and the situation of patients.

Third, the side effects of oxygen supply
Although oxygen is necessary for life activities, oxygen above 0.5 atmospheres has a toxic effect on any cell and can cause oxygen intoxication. The mechanism of cell damage during oxygen poisoning is generally considered to be related to the toxic effect of reactive oxygen species. The occurrence of oxygen poisoning depends on the oxygen partial pressure and not the oxygen concentration.

The relationship between the oxygen partial pressure (PiO 2) and the oxygen concentration (FiO 2) of the inhaled air is as follows: PiO2 = (PB-6.27) × FiO2, where PB is the pressure of the inhaled gas (kPa). 6.27 (kPa, 47mmHg) is the water vapor pressure.

When divers work in seawater at a depth of 50m (PB is about 608kPa or 4560mmHg), although the oxygen concentration of the inhaled gas is normal (FiO2 = 0.21), the partial pressure of oxygen (FiO2) is as high as 126.4kPa (948mmHg), which can cause oxygen poisoning On the contrary, astronauts work in a 1/3 atmosphere environment, even if they inhale pure oxygen (FiO 2 = 1), PiO 2 is only 27.5kPa (206mmHg), which is not prone to oxygen poisoning. When the oxygen partial pressure of the inhaled air is too high, the oxygen partial pressure of the alveolar gas and arterial blood increases with the increase of the partial pressure of oxygen between the blood and the tissue cells, and the diffusion of oxygen accelerates. Oxygen and poisoning.

Special Note:
There are two types of human oxygen poisoning, lung and brain. During hyperbaric oxygen therapy, patients with neurological symptoms should be distinguished from “cerebral oxygen poisoning” and “hypoxic encephalopathy” caused by hypoxia.

(A) Pulmonary oxygen poisoning.

Occurred after inhaling about one atmosphere of oxygen for 8 hours, post-sternal pain, cough, dyspnea, decreased vital capacity, and PaO2 decreased. The lungs were inflammatory, with inflammatory cell infiltration, congestion, edema, bleeding, and atelectasis. If oxygen poisoning occurs in patients undergoing oxygen therapy, PaO2 will decrease when oxygen is absorbed, which will increase the anoxia, which will make it difficult to reconcile the treatment. Therefore, oxygen concentration and time should be controlled during oxygen therapy to prevent the occurrence of oxygen poisoning.

(B) Cerebral oxygen poisoning.

Inhaling 2 to 3 atmospheres of oxygen can cause cerebral oxygen poisoning in a short period of time (several minutes of oxygen inhalation at 6 atmospheres; tens of minutes of oxygen inhalation at 4 atmospheres). Patients mainly suffer from vision, hearing impairment, and nausea , Convulsions, syncope and other neurological symptoms, severe cases can coma and die.

(3) During hyperbaric oxygen therapy, patients with neurological symptoms should distinguish between “cerebral oxygen poisoning” and “hypoxic encephalopathy” caused by hypoxia.

The former patient was unconscious after convulsions, and the patient was awake during the convulsions; the latter was unconscious and then convulsed. Oxygen poisoning should be controlled, but oxygen therapy should be strengthened for hypoxic encephalopathy.