This CE activity is approved by EMS World Magazine, an organization accredited by the Continuing Education Coordinating Board for Emergency Medical Services (CECBEMS), for 1.5 CEUs. There are two ways to take the CE test that accompanies this article and receive 1.5 hours of CE credit accredited by CECBEMS: 1. Click here to download a PDF of the test. The PDF has instructions for completing the test. 2. Or go to www.rapidce.com to take the test and immediately receive your CE credit. Questions? E-mail editor@EMSWorld.com.
- Review oxygen absorption and consumption physiology
- Introduce complications including oxygen toxicity, absorbative atelectasis and carbon dioxide narcosis
- Explain unique situations of oxygen toxicity in hyperbaric medicine and neonatology
- Identify techniques to prevent complications
Oxygen is an essential tool in prehospital care and the most commonly administered drug in the out-of-hospital setting. Prehospital providers administer oxygen to correct hypoxemia and hypoxia, and also as an adjunctive treatment in pain management. When administered, oxygen can decrease both the work of breathing and myocardial workload. However, like all drugs, oxygen has side effects. Used incorrectly, oxygen can cause serious harm.
Adequate oxygen delivery and absorption is essential for proper function at the cellular, tissue and organ levels. The body tolerates inadequate oxygen availability for a short period; however, when demand exceeds oxygen availability for greater than a few minutes, hypoxia will develop, leading to cellular and organ dysfunction, including eventual cellular death.
When a breath is taken or artificial ventilation is delivered, air passes through the mouth and the trachea entering the respiratory system. The tracheobronchial tree first divides at the carina; there are a total of 23 divisions in each branch before finally reaching the alveoli. Air that does not pass though all 23 divisions does not participate in gas exchange and constitutes the “dead space.” Gas exchange occurs when air reaches the alveoli; oxygen diffuses into the bloodstream while carbon dioxide diffuses from the bloodstream into the alveoli. Recall from the EMS classroom that both oxygen (~21%) and carbon dioxide (\< 1%) make up only a small percentage of the air we breathe. By far, nitrogen makes up the majority of the air at nearly 79%. This nitrogen is actually quite important to oxygen absorption, for nitrogen is not as easily absorbed by the body and is the primary gas that creates the pressure inside the alveoli which allows it to stay inflated. Alveoli experiencing atelectasis are not inflated and do not participate in oxygen or carbon dioxide exchange. Pulmonary surfactant, excreted by alveolar cells, coats the alveoli, making it easier to remain open.
It is possible to measure the amount of oxygen absorbed by the body. The majority of the body’s oxygen is attached to hemoglobin as oxyhemoglobin and is measured via arterial oxygen saturation (SaO2). Pulse oximetry (SpO2) is very similar but cannot distinguish between oxygen and carbon monoxide attached to hemoglobin. In prehospital care, in the absence of suspected carbon monoxide cases, SpO2 and SaO2 should be essentially the same. Normally less than 5% of oxygen available in the bloodstream is not attached to hemoglobin; rather it is dissolved in the plasma. This dissolved oxygen is measured as the pressure of arterial oxygen, called PaO2, and is measured in millimeters of mercury (mm Hg). A normal PaO2 is 80–100 mm Hg but can decrease to as little as 60 mm Hg without significant clinical symptoms. Under normal conditions, a PaO2 of 60 mm Hg is associated with a SpO2 of 90%. When supplemental oxygen is administered, more and more oxygen is dissolved into the bloodstream increasing the PaO2. There is no maximum PaO2 value when supplemental oxygen is applied.