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End-tidal carbon dioxide (ETCO2) refers to the partial pressure or concentration value of carbon dioxide in the mixed alveolar gas exhaled at the end of expiration. The normal value is 35-45mmHg. The measurement of ETCO2 and its waveform have special clinical significance in assessing metabolic, pulmonary ventilation, and pulmonary blood flow changes, and is the sixth vital sign in addition to temperature, respiration, pulse, blood pressure, and oxygen saturation. It has important application value in clinical anesthesia, cardiac pulmonary cerebral resuscitation, pre-hospital emergency care, intensive care, and post-anesthesia recovery.
Carbon dioxide (CO2) produced by tissue cell metabolism is transported to the lungs through capillaries and veins and is exhaled out during expiration. The alveolar carbon dioxide partial pressure (ETCO2) is determined by the amount of carbon dioxide produced in the body (VCO2) and the pulmonary ventilation (VA), which is ETCO2=VCO2×0.863/VA, where 0.863 is a constant to convert gas volume to pressure. CO2 has strong diffusion capacity and easily enters the alveolar space from the pulmonary capillaries. The CO2 in the alveoli and arteries is in complete equilibrium, and the exhaled gas should be alveolar gas. Under normal conditions, ETCO2≈PACO2 (alveolar carbon dioxide partial pressure)≈PaCO2 (arterial carbon dioxide partial pressure). ETCO2 measurement can be achieved by infrared method, mass spectrometry method, and colorimetry method. The infrared method commonly used in clinical practice can be divided into two types: sidestream and mainstream, depending on the way the gas is sampled.
The first use of ETCO2: indicating pulmonary embolism
In patients with pulmonary embolism, carbon dioxide exchange with the alveoli decreases due to the obstruction of blood flow returning to the lungs by the emboli, resulting in ETCO2 lower than the normal value. When ETCO2 is less than 28mmHg and accompanied by other signs of pulmonary embolism or risk factors, the possibility of pulmonary embolism should be highly considered. ETCO2 monitoring can reflect cardiac output in severely traumatized patients with normal ventilation, and can be used to predict the prognosis of severe trauma patients. At this time, the low ETCO2 value is not caused by low CO2 levels in the blood, but by reduced blood flow to the lungs. If the clinical doctor normalizes ETCO2 by reducing ventilation, it will cause an increase in CO2 levels in the arterial blood. In a pre-hospital study in London in 2004, the average ETCO2 value of survivors in severely traumatized patients requiring intubation was 31mmHg, and the average TCO2 value of deceased patients was 24mmHa.
The second application of ETCO2: monitoring ventilation
ETCO2 monitoring can be used to assess the ventilation status of critically ill patients, and can detect abnormalities earlier than pulse oximetry. When sedative drugs are overdosed or high-dose anesthetic drugs such as opioid drugs are given by the clinical doctor, ETCO2 can predict respiratory depression, respiratory failure, and suffocation in the patient. A study showed that after administering sedatives such as fentanyl and midazolam, ETCO2 can increase by 7mmHg. When ETCO2 exceeds 50mmHg, respiratory depression is considered present; when it exceeds 70mmHg, respiratory failure is considered present; and when it exceeds 80mmHg, complete suffocation is very likely. By observing ETCO2, clinical doctors can intervene in a timely manner to avoid further deterioration of the patient's condition.
