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| The dangers of too much O2 |
More Oxygen Can’t Hurt…Can It?
What have we learned about oxygen? The dangers of too much O2
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 Os. We’re due for a chest pain call.” “Watch your mouth,” said Larry, grinning as he tossed her the last of the Twinkies he’d saved. “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, seventh edition, from my EMT class back in 2000.”
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.
As Adriane checked out the D cylinders and M tank, she said offhandedly, “Better be sure we have plenty of Os. We’re due for a chest pain call.” “Watch your mouth,” said Larry, grinning as he tossed her the last of the Twinkies he’d saved. “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, seventh edition, from my EMT class back in 2000.”
The Problem
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.
Trauma Patients
Over the last 20 years we’ve been in the habit of giving high-flow oxygen to just about everybody. Every trauma patient gets oxygen at 15 lpm by non-rebreather mask, regardless of their blood oxygen saturation. What many do not realize is that this was taught not because it was beneficial, but because it was considered an acceptable risk when time limitations necessitated deletion of much of the medical theory during the 1994 revision of the EMT-Basic curriculum. Everyone was taught to deliver high-flow oxygen by non-rebreather without understanding why it was beneficial…or potentially harmful. There is no medical evidence to support this practice unless the patient is hypoxic or in shock.
In 2004, Tulane MDs Zsolt Stockinger and Norman McSwain monitored
5,090 trauma patients not requiring assisted ventilation to see whether
supplemental oxygen improved their outcomes. The results showed those
who received oxygen did no better or worse than those who did not. The
authors concluded supplemental oxygen does not improve survival in
traumatized patients who are not in respiratory distress.1
In fact, it is true that 100% oxygen given by non-rebreather reduces coronary artery flow by 30% after 5 minutes. It also reduces the effects of vasodilators such as nitroglycerin.3
This is not exactly a result we’d desire while treating a patient with coronary artery disease. For this reason, the American Heart Association’s emergency cardiac care guidelines have, since 2010, recommended as follows: There is insufficient evidence to support [oxygen’s] routine use in uncomplicated ACS. If the patient is dyspneic, hypoxemic or has obvious signs of heart failure, providers should titrate therapy, based on monitoring of oxyhemoglobin saturation, to ≥94% (Class I, LOE C).4
In a Cochrane review of the literature, researchers in New Zealand led by Meme Wijesinghe found that, although evidence is limited, it suggests that routine use of high-flow oxygen in uncomplicated MI may result in a greater infarct size and possibly increase the risk of mortality.5 These authors concluded it is well-established that arterial oxygen tension is a major determinant of coronary artery blood flow and that high-flow oxygen therapy can cause a reduction in cardiac output and stroke volume. They concluded there is insufficient evidence to support the routine use of high-flow oxygen in the treatment of uncomplicated MI, and that it may increase mortality.
Chest Pain Patients
It has been our traditional practice to give high concentrations of oxygen to patients with chest pain and MI, for reasons no better than “this is how we’ve always done it.” As Israeli physician Chaim Lotan said at a conference in 2011, “We have been brainwashed into using oxygen” even though recent data suggests it has harmful effects that are mediated primarily by coronary artery vasoconstriction. “Before I started looking into the data,” Lotan said, “I didn’t understand how much damage we were causing by giving oxygen.”2In fact, it is true that 100% oxygen given by non-rebreather reduces coronary artery flow by 30% after 5 minutes. It also reduces the effects of vasodilators such as nitroglycerin.3
This is not exactly a result we’d desire while treating a patient with coronary artery disease. For this reason, the American Heart Association’s emergency cardiac care guidelines have, since 2010, recommended as follows: There is insufficient evidence to support [oxygen’s] routine use in uncomplicated ACS. If the patient is dyspneic, hypoxemic or has obvious signs of heart failure, providers should titrate therapy, based on monitoring of oxyhemoglobin saturation, to ≥94% (Class I, LOE C).4
In a Cochrane review of the literature, researchers in New Zealand led by Meme Wijesinghe found that, although evidence is limited, it suggests that routine use of high-flow oxygen in uncomplicated MI may result in a greater infarct size and possibly increase the risk of mortality.5 These authors concluded it is well-established that arterial oxygen tension is a major determinant of coronary artery blood flow and that high-flow oxygen therapy can cause a reduction in cardiac output and stroke volume. They concluded there is insufficient evidence to support the routine use of high-flow oxygen in the treatment of uncomplicated MI, and that it may increase mortality.
Stroke Patients
Stroke patients should be managed similarly. Administer supplemental oxygen to stroke patients who are hypoxemic or when oxygen saturations are not obtainable; the goal is to maintain a saturation of 94% or greater.COPD Patients
The role of oxygen in chronic obstructive pulmonary disease (COPD)
patients has been debated for decades. Issues such as a theoretical
“hypoxic drive” in patients with COPD and chronic hypercarbia have led
to controversies over how much oxygen to give them. While hypoxia must
be corrected quickly when it exists, the definition of hypoxia in terms
of oxygen saturation has been unclear. For example, a normal person
without a respiratory condition breathing room air will usually have a
saturation varying from 97%–99%, depending on tidal volume and other
normal respiratory variances. It is almost impossible to achieve 100%
saturation by breathing room air. We know a saturation of 90% correlates
to approximately 60 mmHg pressure, and that is the normal threshold of
respiratory distress. However, COPD patients may be accustomed to less
saturation, and they typically do well at 88%–92%.
In a study of 405 patients in Australia published in 2010, Dr.
Michael Austin and colleagues compared the outcomes of COPD patients who
were given standard high-flow oxygen treatment with those given
titrated oxygen treatment by paramedics. Titrated oxygen treatment
reduced mortality compared with high-flow oxygen by 58% for all
patients.6
In a 2012 study of prehospital noninvasive
ventilation in patients with pulmonary edema and/or COPD, asthma and
pneumonia, a team led by Dr. Bryan Bledsoe found that use of CPAP with a
low oxygen percentage (FiO2) of 28%–32% was highly effective
in treatment of respiratory emergencies by medics. Since most CPAP
setups deliver 100% oxygen, it may be worthwhile for services to explore
the value of using setups with a lower oxygen percentage.7
Now we know that while ischemia is responsible for most cases of cardiac arrest, managing reperfusion of ischemic cardiac cells is more complicated than we thought. Because of the role of ROS (free radicals), we now understand that a flood of oxygen into previously ischemic cardiac cells is harmful.
The latest post-cardiac arrest care guidelines from AHA recommend the following: Avoid excessive ventilation. Start at 10–12 breaths/min and titrate to target PetCO2 of 35–40 mmHg. When feasible, titrate FiO2 to minimum necessary to achieve SpO2 equal to or greater than 94%.8
In the early days of EMS, venturi masks were popular and routinely used for COPD and cardiac patients. Following the 1994 revision of the EMT National Standard Curriculum, these were largely abandoned because it was felt high concentrations of oxygen were an acceptable risk, given the curriculum’s time limitations. We may see a return of venturi masks to EMS as we become more aware of the need to limit oxygen percentages in our therapy.
In the past 20 years, the debate in oxygen therapy has largely been confined to high-flow versus low-flow. Given the current research and assessment tools available to us, it would seem the debate should shift to low-flow versus no supplemental oxygen at all. We have the means to titrate oxygen therapy to patients’ needs, and those needs most often can be met by low-flow oxygen.
By no means do we suggest that patients who need oxygen be denied it. Hypoxia must be corrected immediately. But you can have too much of a good thing.
Post-Cardiac Resuscitation Patients
Finally, the role of oxygen after cardiac resuscitation must be mentioned. At one time we attempted to push as much oxygen as possible into cardiac arrest patients on the theory that myocardial oxygen supplies were quickly dwindling, and that if we wanted to save people, we had to replenish the missing oxygen. During arrest, and if we were fortunate enough to get a return of spontaneous circulation, we bagged patients as fast and hard as we could, thinking we were restoring oxygen to ischemic cardiac and brain cells.Now we know that while ischemia is responsible for most cases of cardiac arrest, managing reperfusion of ischemic cardiac cells is more complicated than we thought. Because of the role of ROS (free radicals), we now understand that a flood of oxygen into previously ischemic cardiac cells is harmful.
The latest post-cardiac arrest care guidelines from AHA recommend the following: Avoid excessive ventilation. Start at 10–12 breaths/min and titrate to target PetCO2 of 35–40 mmHg. When feasible, titrate FiO2 to minimum necessary to achieve SpO2 equal to or greater than 94%.8
Conclusion
In Adriane’s copy of Emergency Care and Transportation, pulse oximetry was not even mentioned because it was not routinely available on ambulances then. Now that we routinely monitor SpO2 for most patients and know what we do about the dangers of hyperoxygenation, it makes sense to give only as much oxygen as the patient requires.In the early days of EMS, venturi masks were popular and routinely used for COPD and cardiac patients. Following the 1994 revision of the EMT National Standard Curriculum, these were largely abandoned because it was felt high concentrations of oxygen were an acceptable risk, given the curriculum’s time limitations. We may see a return of venturi masks to EMS as we become more aware of the need to limit oxygen percentages in our therapy.
In the past 20 years, the debate in oxygen therapy has largely been confined to high-flow versus low-flow. Given the current research and assessment tools available to us, it would seem the debate should shift to low-flow versus no supplemental oxygen at all. We have the means to titrate oxygen therapy to patients’ needs, and those needs most often can be met by low-flow oxygen.
By no means do we suggest that patients who need oxygen be denied it. Hypoxia must be corrected immediately. But you can have too much of a good thing.
References
1. Stockinger ZT, McSwain NE Jr. Prehospital supplemental oxygen in trauma patients: its efficacy and implications for military medical care. Mil Med, 2004 Aug; 169(8): 609–12.
2. Hughes S. Oxygen for MI: More harm than good? TheHeart.org, www.theheart.org/article/1270299.do.
3. McNulty PH, et al. Effects of supplemental oxygen administration on coronary blood flow in patients undergoing cardiac catheterization. Am J Physiol Heart Circ Physiol, 2005; 288: H1057–62.
4. Circulation, 2010; 122: S787–817.
5. Wijesinghe M, Perrin K, Ranchord A, Simmonds M, Weatherall M, Beasley R. Routine use of oxygen in the treatment of myocardial infarction: systematic review. Heart, 2009; 95: 198–202.
6. Austin MA, Wills KE, Blizzard L, Walters EH, Wood-Baker R. Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomized controlled trial. BMJ, 2010 Oct 18; 341: c5462.
7. Bledsoe BE, Anderson E, Hodnick R, Johnson L, Johnson S, Devendorf E. Low-fractional oxygen concentration continuous positive airway pressure is effective in the prehospital setting. Prehosp Emerg Care, 2012 Apr–Jun; 16(2): 217–21.
8. Circulation, 2010; 122: S768–86.
William E. “Gene” Gandy, JD, LP, has been a paramedic and EMS
educator for more than 30 years. He has implemented a two-year associate
degree paramedic program for a community college, served as both a
volunteer and paid paramedic, and practiced in both rural and urban
settings and in the offshore oil industry. He has testified in court as
an expert witness in a number of cases involving EMS providers and
lectures on medical/legal aspects of EMS. He lives in Tucson, AZ.
Steven “Kelly” Grayson, NREMT-P, CCEMT-P, is a critical care
paramedic for Acadian Ambulance in Louisiana. He has spent the past 14
years as a field paramedic, critical care transport paramedic, field
supervisor and educator. He is a former president of the Louisiana EMS
Instructor Society and board member of the Louisiana Association of
Nationally Registered EMTs. He is a frequent EMS conference speaker and
author of the book En Route: A Paramedic’s Stories of Life, Death, and Everything In Between, and the popular blog A Day in the Life of an Ambulance Driver.
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