Oxygen Toxicity

What EMS providers need to know about possible complications from oxygen administration

Oxygen consumption, abbreviated VO2, is the total amount of oxygen used by the body and is determined by oxygen demand, oxygen availability, and the body’s ability to extract oxygen from hemoglobin and plasma. The inability to extract oxygen from hemoglobin occurs in sickle-cell anemia and other similar conditions, but is otherwise beyond the scope of this article. For more information on anemia, review the previous EMS World CE articles.

Unfortunately it is not possible to precisely measure cellular oxygen demand. However it is well understood that oxygen demand increases when the body is stressed, such as during serious injury or illness, following surgery, due to infection and while experiencing pain and/or anxiety. Oxygen demand decreases whenever metabolism slows; this is one reason why patients are cooled following cardiac arrest. More information on the benefits of therapeutic hypothermia will be in a CE article later this year.

Cellular oxygen consumption depends on an adequate oxygen supply. Cells do not function as effectively when oxygen supplies become inadequate because the cells must then shift to anaerobic metabolism. Anaerobic metabolism creates a cellular oxygen debt, which exacerbates tissue dysfunction and hypoxia. Clinically there are several signs and symptoms of oxygen debt, including: anxiety, shortness of breath, tachypnea, tachycardia, hypertension, confusion and cyanosis (late).2

Some progressive EMS systems have begun carrying an iSTAT, which allows paramedics to determine certain lab values. Two of these, lactic acid and pH, can help identify an oxygen debt. In anaerobic metabolism, which occurs when cells are hypoxic, the metabolism byproduct lactic acid rises significantly. The consequence of a rising lactic is a decline in pH, which is why over time anaerobic metabolism leads to the development of a metabolic acidosis. When capable, determine a lactic acid level as well as a pH; lactic acid is considered elevated at levels exceeding 2.2 mm/L, and a pH consistent with acidosis is \

Not surprisingly, cells function poorly in low oxygen environments, and extremely efficiently in oxygen-rich environments. As oxygen availability increases, cellular function increases until they are functioning at full capacity. Essentially, the more oxygen that is available, the better the cell functions. However, there is a point of oxygen administration where additional oxygen does not provide any additional benefit, and over time this supplemental oxygen can become harmful.

The point at which additional oxygen is unnecessary can be estimated in the prehospital setting. To begin, administer supplemental oxygen to restore a normal SpO2, which the American Heart Association currently recommends as at least 94%.3 Once SpO2 is normal, slowly decrease the amount of oxygen being administered and identify the lowest oxygen delivery rate that maintains SpO2 at 94%.1 When a patient can maintain an SpO2 of 94% on room air, supplemental oxygen is generally unnecessary.3

In the hospital setting, cellular oxygen consumption is determined by comparing oxygen content in the arteries and veins. The difference between the two is the amount of oxygen the body takes from the blood for use. These blood draws are referred to as arterial and venous blood gasses respectively.

There is a reason to go through all of this information about what happens to the cells in a hypoxic environment, and how to determine how much oxygen to give to patients. Supplemental oxygen is needed to prevent hypoxia and keep cells functioning properly. However, during normal cellular metabolism oxygen is systematically changed and an O2- molecule is produced as a byproduct, which is oxygen with an extra negatively charged electron. This oxygen molecule is considered a free radical “toxic” molecule because it has the ability to damage cell membranes. Normally the body avoids damage from these toxic oxygen molecules because enzymes within each cell are produced that quickly destroy the “toxic” oxygen molecule.4 However, these enzymes are produced at a fixed rate that does not increase when metabolism (oxygen consumption) increases.

Complications of Oxygen Delivery

Like every other drug, oxygen administration has complications. Common complications include skin irritation and breakdown as well as a drying of the mucous membranes. Less common but more serious complications include oxygen toxicity, absorbative atelectasis and carbon dioxide narcosis.