It was 0635. Larry and Adriane always got to the station early to check out the truck and, if a late call came in, take it so Greg and Chad could get off on time. This was an arrangement the Medic 2 crews shared, and it worked well for them.
As Adriane checked out the D cylinders and M tank, she said offhandedly, “Better be sure we have plenty of O2. We’re due for a chest pain call.” “Watch your mouth,” said Larry, grinning. “You know what happens when you say things like that.”
Twenty minutes later they were at the home of Doris, one of their regular patients, a 64-year-old type 2 diabetic who was, in fact, experiencing chest pain she described as 5 on a scale of 0–10.
While Larry attached the 12-lead, Adriane noted the pulse oximeter read 97% on room air, so she put Doris on a non-rebreather mask and turned the oxygen on at 15 liters per minute. “You can’t have enough of this good stuff,” she said. “Let’s get that sat up to 100% for those heart cells.”
After giving an aspirin, starting an IV and giving a squirt of nitroglycerin, they transported Doris to the nearby Level III hospital, where she went immediately to the cath lab, got a stent in her right coronary artery, went to the CCU and eventually returned home three days later, feeling great.
“Good job, folks,” Dr. Chutney said at the chart review the next week, “but here’s something I need to pass along to you: We don’t do 15 liters per minute by non-rebreather for routine chest pain patients anymore.”
“Why?” said Adriane. “In my book it says not to worry about problems from too much oxygen, that they only develop after several days of more than 50% inspired oxygen delivered at higher-than-normal pressures.”
“What book are you reading from, Adriane?” asked Dr. Chutney.
“From my Orange Book,” said Adriane, “Emergency Care and Transportation of the Sick and Injured, 7th edition, from my EMT class back in 2000.”
In 2000 that was what we were taught about oxygen therapy for patients with chest pain. But times have changed. We now know that while some oxygen may be good, more is not necessarily better.
We have always known that oxygen is necessary for all animal life, and that lack of oxygen damages tissues. It is beyond argument that patients who are hypoxic must receive supplemental oxygen. What we’ve not always known is that too much oxygen can harm patients in a number of ways.
One is through reactive oxygen species (ROS), often called free radicals. A radical is an atom that has one or more unpaired electrons. Oxygen has two unpaired electrons that make it susceptible to radical formation. When ROS form in cells, damage can occur. Hypoxic cells are greatly susceptible to ROS. These can damage tissues throughout the body, but of particular concern are lung, heart and brain tissues. Not all radicals are bad, and the role of radicals is far beyond the scope of this article, but we know that damage to the plasma membranes, mitochondria and endomembrane systems by ROS is significant.
High oxygen concentrations can also cause atelectasis. Air is about 21% oxygen and 79% nitrogen. The alveoli depend on nitrogen to maintain surfactant production and alveolar patency; when high concentrations of oxygen are administered, oxygen may “wash out” nitrogen and leave the alveoli susceptible to a lack of gas as oxygen diffuses into the blood, causing them to collapse. This “washout” may be desirable temporarily in patients being preoxygenated for rapid- or delayed-sequence intubation, but over time atelectasis may occur and this is not good. Once intubation is accomplished, a natural mixture of gases must be allowed to reconstitute in the lungs to avoid collapse of alveoli and atelectasis. There is little to be gained by achieving an oxygen pressure of greater than 100 mmHg.