Aurora Health Care
EMS Continuing Education
3rd Quarter 2014 Packet
There remains confusion among healthcare providers about oxygen administration. For many years EMS
providers were taught to provide high levels of oxygen on almost any patient they encountered. While
this had potentially negative effects, those effects were presumed to be insignificant in the pre-hospital
setting. We know this is not the case and felt it appropriate to discuss this topic. The following two
articles are reprinted from EMS World. References for both articles are attached for additional review.
More Oxygen Can’t HurtCan It?
By William E. "Gene" Gandy, JD, LP and Steven "Kelly" Grayson, NREMT-P, CCEMT-P
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-thannormal 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.”
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 delayedsequence 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.
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
evidence, while limited, which 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 lowflow. 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, et al. 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.
Oxygen Toxicity
by Kevin T. Collopy, BA, FP-C, CCEMT-P, NREMT-P, WEMT, Sean M. Kivlehan, MD, MPH,
NREMT-P, Scott R. Snyder, BS, NREMT-P
Oxygen is an essential tool in pre-hospital 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.
Oxygen Absorption
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 pre-hospital 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.
Oxygen Consumption
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.
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.
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 one that is less than 7.35.
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.
The most common complications are a consequence of the delivery systems. Plastic systems, oxygen
masks and nasal cannulas are used, and all of these devices are skin irritants which can cause
significant skin irritation and breakdown when used long term. Patients who are on long-term
oxygen systems often try to prevent skin irritation by padding their delivery systems, such as by
padding their nasal cannula behind the ears with nasal tissues. Other common areas of skin
breakdown are across the bridge of the nose and beneath the nares.
Typically oxygen systems deliver oxygen that has nearly zero moisture content. When this oxygen
passes through the mucous membranes in the mouth and nose, it is humidified by pulling moisture
from the mucous membranes so it is humid by the time it reaches the alveoli. While this protects the
alveoli and bronchioles, the nasal and oral mucous membranes quickly dry out. Dry mucous
membranes lose their ability to humidify the air we breathe and also become uncomfortable.
Applying oxygen via a humidifier can help prevent this from occurring.
Oxygen Toxicity
Recall from earlier in this article that under high oxygen environments, cells metabolize oxygen more
quickly. This is because there is an increased pressure from the dissolved oxygen, the PaO2, forcing
oxygen into the cell, thereby increasing oxygen consumption and the production of the toxic oxygen
molecule byproduct O2-. Since production of the enzyme to eliminate O2- is fixed, the toxic molecules
build up over time.4 After roughly 24 hours of this oxygen-rich environment, enough toxic molecules
accumulate to clinically see evidence of cellular damage.1
An oxygen-rich environment is determined by looking at how much oxygen a patient receives.
Delivering less than 60% oxygen to otherwise healthy lungs is generally considered a low oxygen
delivery rate and typically is not associated with the development of clinical oxygen toxicity.
However, diseased or injured lungs have been shown to develop symptoms of oxygen toxicity when
receiving 50% oxygen or more.4
An early result of oxygen toxicity is capillary leakage, which leads to edema throughout the body,
particularly pulmonary edema. Pulmonary edema generally appears first and when untreated can
lead to acute lung injury and acute respiratory distress syndrome (ARDS).1 Central nervous system
symptoms include altered mental status, respiratory depression and seizures. When awake, some
patients also experience visual and auditory disturbances.
Oxygen toxicity has been well documented since the early 1900s and still today remains clinically
significant for patients on ventilator support, premature infants and patients receiving hyperbaric
oxygen treatment.4 A detailed discussion of ventilator management is beyond the scope of this
article. However, EMS is seeing a rise in patients being managed with hyperbaric oxygen and
newborns are regularly born outside of the hospital setting.
Toxicity in Hyperbaric Medicine
Hyperbaric oxygen therapy is an important tool in modern medicine for management in a variety of
situations including diving emergencies, wound management and carbon monoxide toxicity.
Regardless of what hyperbaric medicine is being used to manage, its goal is to increase oxygen
availability to organ tissues by increasing oxygen dissolved in the plasma through an increase in the
atmospheric pressure. To illustrate this, administering 100% oxygen at sea level, or 1 atmospheric
pressure, can produce a maximum PaO2 of 510 mm Hg. By increasing the environment to 3
atmospheric pressures, PaO2 can be increased to 1,530 mm Hg.4 This increase speeds healing by
allowing tissues to have increased oxygen available for metabolism. Specifically in diving-related
emergencies, hyperbaric medicine compresses nitrogen bubbles that may have formed in the
patient’s body tissues to allow the body to more easily eliminate nitrogen that may cause pain (i.e.,
the bends) and emboli.
While hyperbaric oxygen has true benefits, there are legitimate dangers to its utilization as well. As
stated above, hyperbaric oxygen increases oxygen available at the tissue level. Also recall from earlier
that the more oxygen available, the faster the cell will metabolize oxygen, and over time this can lead
to an accumulation of free oxygen radicals. At normal atmospheric pressures (1 atmosphere) this
takes 12 to 16 hours of constant 100% oxygen exposure; this timeframe is reduced to 3 to 6 hours at 2
atmospheres.4 This is significant because the same valuable treatments can become dangerous; thus
the utilization of hyperbaric oxygen must be closely monitored and controlled.
Neonatal Oxygen Administration
A host of changes occur during and shortly after the birth of a neonate. The neonate’s fetal
hemoglobin has a higher affinity for oxygen than adult hemoglobin, which allows them to tolerate
lower measured oxygen levels better.4 In reality, measured blood gasses are quite different for the
neonate than in the adult and the normal blood gasses are summarized in Table I. The most
significant numbers for EMS providers to note are that the neonate’s normal SaO2 and PO2 are much
lower than normal adult values. Healthy neonates tolerate these low values well and transition to
adult values within about a week.4
Administering supplemental oxygen to neonatal patients has been common, particularly during
resuscitation. However, supplemental oxygen can bring the neonate’s oxygen levels well beyond their
established normal levels; one of the side effects of this is vascular constriction. This vascular
constriction can cause a temporary loss of blood flow in the neonatal retina, leading to long-term
vision problems. This occurs in addition to traditional oxygen toxicity, which is also a risk for the
neonate because they are not capable of managing increased PO2 levels as well as an adult.4
In response to this risk, and based on fairly recently published data that showed neonates
resuscitated with room air had a higher survivability than those resuscitated with 100% oxygen, the
American Heart Association changed their recommendations in regards to oxygen administration
during neonatal resuscitation. Immediate 100% oxygen is no longer recommended. Instead, they
suggest initiating resuscitation with room air, and only administer oxygen if the neonate’s heart rate
stays 60 after 90 seconds of resuscitation. Once it’s administered, continue administering oxygen
until the heart rate normalizes.5
Absorbative Atelectasis
Not all alveoli are used on a minute-to-minute basis. For example, when resting and sleeping fairly
shallow breaths are taken and only a fraction of the body’s alveoli participate in gas exchange. When
exercising more oxygen is needed so deeper breaths are taken to increase the volume of air inhaled,
and thus more alveoli participate in gas exchange.
As mentioned earlier, nitrogen helps create pressure inside the lungs to keep alveoli propped open
because nitrogen does not easily pass though the alveolar membranes. Inactive alveoli, which are
those not being ventilated with the average resting breath, contract and have a reduced air volume.
However, some nitrogen still remains in these alveoli to keep them open and ready for use.
When supplemental oxygen is administered, less nitrogen is inhaled. At 50% oxygen, there is still
roughly 50% nitrogen in inhaled air. However, once greater than 50% oxygen is delivered, oxygen
replaces nitrogen as the primary gas in the lungs. The term for this is nitrogen washout, because the
oxygen literally pushes out the nitrogen over time. Complete nitrogen washout takes 15 minutes
when breathing 100% oxygen.
With the nitrogen washed out, the gas helping keep alveoli inflated is eliminated and alveoli begin to
collapse. Absorbative atelectasis, also called denitrogenation absorption atelectasis, is the collapse of
the alveoli due to the loss of the partial pressure of nitrogen within the lungs.4 Thus at higher oxygen
levels fewer alveoli are available to participate in gas exchange.
Absorbative atelectasis has clinically significant applications for prehospital providers. It is difficult
to identify when absorbative atelectasis has occurred since the only sign is a decreased inspiratory
volume. However, there are clues that it may be taking place. Patients who are breathing
spontaneously may complain of increased shortness of breath or anxiety when oxygen levels are
increased. Another clue may be that an increased ventilator rate is needed when delivering 100%
oxygen compared to when using lower oxygen levels. While these subtle changes are unlikely to be
noticed during short transports, providers whose systems include longer transport times (greater
than 30 minutes), and those who participate in interfacility transports, may observe these changes,
indicating a need to decrease oxygen delivery rates.
Carbon Dioxide Narcosis/Oxygen-Induced Hypercapnia
Chemoreceptors are discussed in both EMT and paramedic classes. Peripheral chemoreceptors,
located in the carotid arteries and the aortic arch, are sensitive to oxygen changes and trigger breaths
when PaO2 drops below 60 mm Hg. Central chemoreceptors have primary control over breathing and
are located in the medulla of the brain and bathed in cerebral spinal fluid. When the CO2 levels rise,
hydrogen ion levels rise, causing a pH decrease, and the brain’s respiratory center is triggered to
“blow off” carbon dioxide via respiration. In patients with chronically high CO2 levels and low PaO2
levels, such as patients with advanced COPD, the central chemoreceptors can become desensitized
because their pH is persistently low due to excessive hydrogen ions in their cerebral spinal fluid.
When this occurs, their respirations are triggered, in theory, by peripheral chemoreceptors sensing
hypoxia.2
Patients who have chronic ventilatory failure, defined as a chronically increased PaCO2 exceeding 50
mm Hg and decreased PaO2 below 55 mm Hg, need oxygen when their oxygen levels fall below the
patient’s established baseline.4 They also need titrated oxygen when they present in respiratory
distress. A recent synopsis of research on patients experiencing an exacerbation of COPD found that
45 minutes of prehospital-administered high-flow oxygen (8 liters per minute) increased patient
mortality. The research found decreased mortality when SpO2 was maintained between 88%–92%
using titrated oxygen via nasal cannula alone instead of high-flow oxygen and led to
recommendations of avoiding high-flow oxygen during prehospital care of patients with advanced
COPD.6,7
On occasion, a relatively rare condition known as oxygen-induced hypercapnia can develop in these
patients, which results from oxygen administration. When oxygen is administered for an extended
period (hours to days) the patient’s already high carbon dioxide levels rise even further, which leads
to lethargy and slow and shallow breathing. Without intervention, respiratory arrest develops.
Although the exact mechanism for oxygen-induced hypercapnia is not clearly known, it is thought to
be a combination of the suppression of the theoretical hypoxic drive as well as an oxygen-induced
pulmonary perfusion mismatch.2 Other texts suggest that when oxygen is applied to the
asymptomatic patient with a history of an advanced COPD, their lungs are exposed to an increased
oxygen saturation. The body quickly recognizes that it can maintain the same PaO2 without having to
work as hard, and over time the body adjusts to the alveolar oxygen levels to maintain their arterial
oxygen levels as their baseline. The net result of this can be a decreased respiratory rate.4
The well documented and clinically important piece of this condition is that oxygen-induced
hypercapnia most commonly occurs in otherwise asymptomatic, relaxed and unstimulated patients,
such as a patient who is sleeping. It does not occur in patients with acute respiratory distress, who
often are experiencing a catecholamine release stimulating increased respiratory and circulatory
rates.2
Clinical symptoms of oxygen-induced hypercapnia include a rising CO2 level, which can be measured
with a side-stream CO2 device, altered mental status including confusion, complaints of headaches,
and a somnolent appearance.1
Prevention of Complications
Preventing complications from oxygen administration is fairly straightforward. To start, whenever
possible, pad the straps and tubing of oxygen delivery systems, particularly on patients who receive
oxygen long term. Also, consider increasing the use of humidified oxygen to prevent drying out
mucous membranes. Oxygen humidifiers are inexpensive and greatly increase patient comfort. Also,
elevating a patient’s head and chest at least 30 degrees promotes lung expansion and helps prevent
aspiration.
Never withhold oxygen from patients who are in respiratory distress or hypoxic. Oxygen is truly a
lifesaving drug. During major resuscitations, such as cardiac arrest and major traumas, 100% oxygen
is indicated. However, for most all other patients, consider limiting oxygen to maintain SpO2 in the
90%–95% range; this also keeps the PaO2 above 60 mm Hg.1 Research has consistently shown that
oxygen’s maximum benefit is obtained when delivered in the 22%–50% range4, and its benefit is
limited after 6 hours of administration.3
Neonatal patient management requires special consideration. Whenever possible, utilize room air
when initiating resuscitation. Only administer oxygen when the neonate remains bradycardic after
90 seconds of resuscitation efforts.5
Summary
The administration of oxygen is safe and effective for patients who are in respiratory distress or who
are hypoxic. Never feel that oxygen needs to be withheld. However, keep in mind that there are real
consequences to the long term utilization of high-flow oxygen. To help prevent potential
complications from oxygen administration, reach for the nasal cannula before the non-rebreather
mask, and apply just enough oxygen to maintain normal saturations.
References
1. Morton PG, et al, eds., Critical Care Nursing, a Holistic Approach, 8th edition.
Philadelphia, PA: Lippincott, Williams & Wilkins, 2005.
2. Des Jardins T, Burton GG. Clinical Manifestations and Assessment of Respiratory
Disease, 5th edition. St. Louis, MO: Elsevier, 2006.
3. O’Connor RE, et al. Acute Coronary Syndromes: 2010 American Heart Association
Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.
Circulation 122: S787–817, 2010.
4. Shapiro BA, et al. Clinical Application of Blood Gases, 5th Edition. St. Louis, MO:
Elsevier, 1994.
5. Kattwinkel J, et al, Neonatal Resuscitation: 2010 American Heart Association
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