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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.”
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
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.”2
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.
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
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.
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.
The drug we use most often in EMS can cause harm if we give it without good reason
Jul 1, 2012
https://www.ems1.com
Updated October 24, 2016
EMS providers began giving oxygen not because it had medically or scientifically demonstrated benefits for patients, but because they could. Yet, inarguably, hypoxia is bad.
John Scott Haldane, who formulated much of our understanding of gas physiology, said in 1917, “Hypoxia not only stops the motor, it wrecks the engine.”
Patients begin to suffer impaired mental function at oxygen saturations below 64 percent. People typically lose consciousness at saturations less than 56 percent, giving airplane passengers no more than 60 seconds to breathe supplemental oxygen when an airplane flying at 30,000 feet suddenly depressurizes [1-3].
More recent studies suggest that hyperoxia, or too much oxygen, can be equally dangerous. Hence the drug EMS providers administer most often may not be as safe as originally thought.
Studies on benefits and dangers of oxygen therapy are not new; intensive care practitioners have long recognized the adverse effects of using high concentration oxygen [4]
The Amercian Heart Association Guidelines for Emergency Cardiac Care and CPR in 2000 and 2005 recommended against supplemental oxygen for patients with saturations above 90 percent. The 2010 ECC Guidelines called for supplemental oxygen only when saturations are less than 94 percent [5]. Though the AHA continues to recommend high-flow oxygen administration when CPR is in progress.
Research on patient outcomes after hyperoxia What is new are prehospital research studies comparing outcomes of patients treated without oxygen or with oxygen titrated to saturations versus patients routinely given high flow oxygen. These data are frightening; they invariably show impressive patient harm from even short periods of hyperoxia.
We’ve known since 1999 that oxygen worsened survival in patients with minor to moderate strokes and made no difference for patients with severe stroke [6]. In fact, the American Heart Association recommended in 1994 against supplemental oxygen for non-hypoxemic stroke patients.
The dangers from giving oxygen to neonates have also been long appreciated [7]. The most compelling outcome studies of neonates published in 2004 and repeated in 2007 showed a significant increase in mortality of depressed newborns resuscitated with oxygen (13 percent) versus room air (8 percent) [9]. This led to the current neonatal resuscitation recommendations for use of room air positive pressure ventilation.
In 2002, a study of 5,549 trauma patients in Texas showed prehospital supplemental oxygen administration nearly doubled mortality [9]. A Tasmanian study of prehospital difficulty breathing patients published in 2010 compared patients treated with oxygen titrated to saturations of 88 to 92 percent to patients treated with non-rebreather oxygen masks.
It showed a reduction in deaths during subsequent hospitalization of 78 percent in COPD patients and 58 percent in all patients [10]. New studies are showing a troubling pattern of worse outcomes associated with hyperoxia post cardiac arrest [11].
Why would oxygen worsen patient outcomes? One mechanism may be absorption atelectasis. Gas laws mandate that increases in the concentration of one gas will displace or lower the concentration of others. Room air normally contains 21 percent oxygen, 78 percent nitrogen, and less than 1 percent carbon dioxide and other gases.
Nitrogen, the most abundant room air gas, is responsible for secretion of surfactant, the chemical that prevents collapse of the alveoli at end expiration. Premature infants often are not developed sufficiently to produce surfactant and require endotracheal administration of animal surfactant.
“Washout” of nitrogen in adult lungs occurs when high concentration oxygen is administered. Lower concentrations of nitrogen can lead to decreased surfactant production with subsequent atelectasis and collapse of alveoli, significantly impeding oxygen exchange.
Oxygen is also a free radical, meaning that it is a highly reactive species owing to its two unpaired electrons. From a physics perspective, free radicals have potential to do harm in the body.
The sun, chemicals in the atmosphere, radiation, drugs, viruses and bacteria, dietary fats, and stress all produce free radicals. Cells in the body endure thousands of hits from free radicals daily.
Normally, the body fends off free radical attacks using antioxidants. With aging and in cases of trauma, stroke, heart attack or other tissue injury, the balance of free radicals to antioxidants shifts.
Cell damage occurs when free radicals outnumber antioxidants, a condition called oxidative stress. Many disease processes including arthritis, cancer, diabetes, Alzheimer’s and Parkinson’s result from oxidative stress.
The concept of free radical damage suggests the old EMS notion that, “high flow oxygen won’t hurt anyone in the initial period of resuscitation” may be dead wrong.
Tissue damage is directly proportionate to the quantity of free radicals present at the site of injury. Supplemental oxygen administration during the initial moments of a stroke, myocardial infarct (MI) or major trauma may well increase tissue injury by flooding the injury site with free radicals.
Finally, consider this: five minutes of supplemental oxygen by non-rebreather decreases coronary blood flow by 30 percent, increases coronary resistance by 40 percent due to coronary artery constriction, and blunts the effect of vasodilator medications like nitroglycerine [12]. These effects were demonstrated dramatically in cath lab studies [13] published in 2005.
Now you know why the ECC Guidelines recommend against supplemental oxygen for chest pain patients without hypoxia. Supplemental oxygen reduces coronary blood flow and renders the vasodilators ALS providers use to treat chest pain ineffective.
Where do we go from here? Knowing that both hypoxia and hyperoxia are bad, EMS providers must stop giving oxygen routinely. Oxygen saturations should be measured on every patient.
Protocols need to be aligned to reflect the current ACLS and BLS ECC guidelines: administer oxygen to keep saturations between 94 and 96 percent. No patient needs oxygen saturations above 97 percent and in truth, there is little to no evidence suggesting any clinical benefit of oxygen saturations above 90 percent in any patient.
Modifications in prehospital equipment will be inherent in controlling oxygen doses administered to patients. In all likelihood, the venturi mask will make a comeback, allowing EMS providers to deliver varied concentrations of oxygen as needed to keep oxygen saturations between 94 and 96 percent.
Few patients will require non-rebreather masks which are prone to deliver too much oxygen (hyperoxia). CPAP (Continuous Positive Airway Pressure) devices will also need redesign as most conventional EMS CPAP delivers 100 percent oxygen. A study conducted by Bledsoe, et al in Las Vegas found that prehospital CPAP using low oxygen levels (28 to 30 percent) was highly effective and safe [14].
Bottom line: the drug we use most often can cause harm if we give it without good reason. In the absence of low saturations, oxygen will not help patients with shortness of breath and it may actually hurt them. The same holds true for neonates and virtually any patient with ongoing tissue injury from stroke, MI or trauma. Indeed, oxygen can be bad.
References:
Akero A, Christensen CC, Edvardsen A, et al. Hypoxaemia in chronic obstructive pulmonary disease patients during a commercial flight. Eur Respir J 2005;25:725–30.
Cottrell JJ, Lebovitz BL, Fennell RG, et al. Inflight arterial saturation: continuous monitoring by pulse oximetry. Aviat Space Environ Med 1995;66:126–30.
Hoffman CE, Clark RT, Brown EB. Blood oxygen saturations and duration of consciousness in anoxia at high altitudes. Am J Physiol 1946;145:685–92.
Alteiemer WA, Sinclair SE. Hyperoxia in the intensive care unit: why more is not always better. Curr Opin Crit Care 2007;13:73-78.
O'Connor RE, Brady W, Brooks SC, Diercks D, Egan J, Ghaemmaghami C, Menon V, O'Neil BJ, Travers AH and Yannopoulos D. 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science Part 10: Acute Coronary Syndromes. Circulation 2010; 122: S787-S817.
Ronning OM, Guldvog B. Should Stroke Victims Routinely Receive Supplemental Oxygen? A Quasi-Randomized Controlled Trial. Stroke 1999;30:2033-2037.
Rabi Y, Rabi D, Yee W: Room air resuscitation of the depressed newborn: a systematic review and meta-analysis. Resuscitation 2007;72:353-363.
Davis PG, Tan A, O’Donnell CP, et al: Resuscitation of newborn infants with 100% oxygen or air: a systematic review and meta-analysis. Lancet 2004;364:1329-1333.
Stockinger ZT, McSwain NE. Prehospital Supplemental Oxygen in Trauma Patients: Its Efficacy and Implications for Military Medical Care. Mil Med. 2004;169:609-612.
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: randomised controlled trial. BMJ 2010;341:c5462.
Kilgannon JH, Jones AE, Parillo JE, at al. Emergency Medicine Shock Research Network (EMShockNet) Investigators. Relationship between supranormal oxygen tension and outcome after resuscitation from cardiac arrest. Circulation 2011;14:2717-2722.
Harten JM, Anderson KJ, Kinsella J, et al. Normobaric hyperoxia reduces cardiac index in patients after coronary artery bypass surgery. J Cardiothorac Vasc Anesth 2005;19:173–5.
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-H1062.
Bledsoe BE, Anderson E, Hodnick R, Johnson S, Dievendorf E. Low-Fractional Oxygen Concentration Continuous Positive Airway Pressure Is Effective In The Prehospital Setting. Prehosp Emerg Care 2012;16:217-221.
About the author
Mike McEvoy, PhD, NRP, RN, CCRN is the EMS Coordinator for Saratoga County, New York and a paramedic supervisor with Clifton Park & Halfmoon Ambulance. He is a nurse clinician in cardiothoracic surgical intensive care at Albany Medical Center where he also Chairs the Resuscitation Committee and teaches critical care medicine. He is a lead author of the “Critical Care Transport” textbook and Informed® Emergency & Critical Care guides published by Jones & Bartlett Learning. Mike is a frequent contributor to EMS1.com and a popular speaker at EMS, Fire, and medical conferences worldwide.Contact Mike at mike.mcevoy@ems1.com.
posted by Dr. Ramon Reyes, MD ∞𓃗#DrRamonReyesMD ∞𓃗 @DrRamonReyesMD
Gracias a todos el Canal somos mas de 1000 participantes en WhatsApp. Recordar este es un canal y sirve de enlace para entrar a los tres grupos; TACMED, TRAUMA y Científico. ahí es que se puede interactuar y publicar. Si le molestan las notificaciones, solo tiene que silenciarlas y así se beneficia de la informacion y la puede revisar cuando usted así lo disponga sin el molestoso sonido de dichas actualizaciones, Gracias a todos Dr. Ramon Reyes, MD Enlace al
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