Prehospital Oxygen Therapy

Objectives
At the end of this lesson, the student should be able to:

1. Discuss the role of oxygen in respiratory pathophysiology.

2. Identify the components of various oxygen delivery systems.
3. Describe indications for prehospital oxygen therapy.
4. Recognize potential complications related to supplemental oxygen administration.

Case Study
"Is everyone clear?" was my question to my partner and the fire department first responders as I charged the
defibrillator. We were attempting to resuscitate a 17-year-old male who had collapsed during football practice. The
patient was in persistent ventricular fibrillation (VF) and had not responded to the first 200 joule biphasic defibrillation.
There was no evidence of trauma and the coach reported that there were not any past medical problems, medications,
or allergies listed on the patient's information sheet. The shock was delivered and the patient's whole body jerked
violently. The firefighters immediately resumed chest compressions, my partner administered another 1 mg dose of
epinephrine as well as a 300 mg dose of amiodarone through an IV in the patients left antecubital vein, and I
intubated the patient. After the endotracheal tube was placed I verified its position with auscultation as well as
continuous waveform end tidal CO2 monitoring. Using a bag valve mask (BVM), I ventilated the patient with 100
percent oxygen. I was nervous and the scene was one of the most challenging of my career. In my haste I squeezed
the BVM rapidly. Fortunately, my partner reminded me that current evidence-based recommendations from the
American Heart Association state that intubated patients should only receive 10 breaths per minute or one breath
every six seconds.1 I focused and bagged the patient at the appropriate rate.

After two minutes of CPR the patient remained in VF and he was defibrillated again. The other players and the coaches
watched nervously as we worked.After the shock was delivered the patient's ETCO2 level suddenly rose from 25mmHg
to 96mmHg. CPR was continued until the end of the two minute cycle. When compressions were paused for rhythm
analysis a narrow complex tachycardia at a rate of 132 beats per minute was present and the patient had a bounding
carotid pulse. The patient remained unresponsive and apneic but his heart rate was stable and he had a blood
pressure of 104/80 mmHg, without any vasopressors. A 12 lead EKG was captured and there was no evidence of ST
elevation myocardial infarction (STEMI). The patient's blood glucose was found to be 110 mg/dL. While the patient was
packaged for transport, a normal saline bolus was administered and I continued to ventilate the patient. Now calmer, I
bagged the patient slowly. I monitored the patient's ETCO2 and pulse oximetry. The rate of ventilationswas titrated to
maintain an ETCO2 between 25 and 40 mmHg and an SPO2 of at least 94percent.

The patient was placed in the ambulance and transport to the closest appropriate facility was initiated. While enroute
to the hospital the patient maintained adequate perfusion. The patient was in a normal sinus rhythm at a rate of 90
beats per minute. His blood pressure was 112/90 mmHg. Approximately 20 minutes after the return of spontaneous
circulation (ROSC) the patient began to exhibit spontaneous respirations, movement of the extremities, as well as
gagging. It seemed to me that extubation would be dangerous so I contacted online medical direction. The physician
approved an order to administer 150 mg (2mg/kg) of Ketelar (ketamine) as well as 5mg of IV Versed (midazolam).
The medication was administered and the patient stopped struggling. His vital signs remained stable throughout the
remaining 10 minutes of transport. Upon arrival at the hospital the patient's parents were waiting at the ER entrance
along with hospital staff. The patient was transferred to a bed and care was transferred to the staff.

Introduction
Oxygen is a naturally occurring atmospheric gas and is an essential element for sustained life. At sea level the air
contains 21 percent oxygen and humans require it to survive. During normal breathing air is inspired through the
nose and mouth, travels through trachea, bronchus, and bronchioles. The oxygen and other gases in the air are
absorbed into the bloodstream in the alveoli and carbon dioxide is released. The process of respiration is a delicate
balance that is controlled by neurological and chemical systems. If there is any disruption in this complex process the
body will be unable to maintain homeostasis. There are a variety of pathologies and injuries that disrupt the body's
ability to maintain adequate oxygen levels. Without rapid intervention patients suffering respiratory disease or injury
will quickly become hypoxic (oxygen deprived) and may suffer permanent injury or death. The administration of
supplemental oxygen,also known as oxygen therapy, has been used to help mitigate these deadly illnesses and injuries
and has been a mainstay of prehospital medical care since its inception. In the past it was assumed that any sick or

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 injured patient would benefit from high-flow oxygen. Providers were taught to put patients on oxygen because it might
be beneficial and it would not harm them. Evidence-based research has shown that this is not necessarily the
case.2,3,4 Today's providers must give the right volume of oxygen to the right patients in the same way that any other
drug is administered. Judicious oxygen administration is a change in dogma that can be especially difficult for
experienced providers to accept. This course is intended to help teach EMTs and paramedics give the right amount of
oxygen to the right patients by describing the role of oxygen in respiratory pathophysiology, identifying the
components of various oxygen delivery systems, describing the indications for prehospital oxygen therapy, and finally
recognizing potential complications related to supplemental oxygen administration.

Discuss the Role of Oxygen in Respiratory Pathophysiology

In the lungs the bronchus divides into bronchi that subsequently subdivide into smaller and smaller bronchioles. The
tiny bronchioles are smooth muscle tubes that terminate in clusters of alveoli. The alveoli are like miniscule balloons or
bunches of grapes that have membranes that are a single cell thick. Each lung contains approximately 33 million
alveoli and each alveolus is around 0.33 mm in diameter.5 It is at the alveoli where gas exchange occurs.
Oxygen-poor blood from the right ventricle of the heart flows into the lungs and carbon dioxide diffuses out across the
alveoli's cell membrane. Oxygen then diffuses into the blood where it binds to hemoglobin and then flows through the
pulmonary veins back to the left heart. After the blood moves through the left atrium and left ventricle it is then
pumped into systemic circulation. The clusters of alveoli are bathed in a proteinaceous substance known as
surfactant.6 Surfactant helps to keep the alveoli inflated by reducing surface tension across the cell membranes. If
there is decreased surfactant the alveoli can collapse leading to a condition known as atelectasis. Any obstruction,
edema, or disruption of the alveoli or airways will impede gas exchange and ventilation.

The oxygenated hemoglobin flows through the arterial circulation to the capillary beds where the oxygen then diffuses
across the cell membranes. The individual cells use the oxygen along with nutrients from the digestive system to
create adenosine triphosphate (ATP) which is chemical energy. The creation of ATP using oxygen is known as aerobic
metabolism and the only waste products that are created are carbon dioxide and water. When the cellular environment
becomes oxygen depleted anaerobic metabolism occurs. Anaerobic metabolism is much less efficient and produces
toxic by-products like lactic acid. Aerobic metabolism produces 15 times more ATP than anaerobic metabolism.7 There
are no cells in the body that can survive with only anaerobic metabolism for long periods of time. The highly
specialized cells in the brain and heart are unable to function at all in oxygen depleted environments and will begin to
die within a matter of minutes if nothing changes.8

Respiration is the mechanical process of breathing which facilitates the movement of air into the body. There are a
number of muscles involved in this process and they include the diaphragm, the internal intercostal muscles, the
external intercostal muscles, the abdominal muscles, and the pectoral muscles. The phrenic nerve innervates the
diaphragm and the intercostal nerves innervate the rest of the muscles of the chest wall.9 The diaphragm is the
primary muscle of breathing.10 People are able to control their respiratory effort but you do not stop breathing when
you are asleep. The diaphragm is dome-shaped and is attached posteriorly to the lumber vertebrae and anteriorly to
the costal arch. It forms a physical barrier between the chest and the abdomen. The only structures that pass through
it are the aorta, vena cava, and the esophagus. During inspiration the diaphragm contracts, pulling distally, and along
with the contraction of other muscles of the chest wall increases the thoracic space which creates negative pressure
and brings air into the lungs. During exhalation the diaphragm relaxes proximally, decreasing the thoracic space,
which allows for positive pressure and the outflow of air. Normal exhalation is a passive process but during forceful
exhalation like coughing the posterior intercostal muscles contract which pulls the ribs and sternum downward further
compressing the thoracic spaces.

During normal breathing there is a large volume of air that is moved in and out the lungs. A healthy adult male has a
total lung capacity of approximately six liters. Healthy adult women tend to have about one-third less total lung
capacity because of smaller lung size.11 While at rest every breath is about 500mL and this is known as tidal volume.
The amount of air that moves in and out of the lungs during maximum breathing efforts is known as vital capacity.
Inspiratory reserve volume is the deepest breath that a person can take after a normal breath. The expiratory reserve
volume is the amount of air that can be forcefully exhaled after a normal breath. Unless there is an injury or illness the
lungs remain inflated all of the time and the air that supports this is known as the residual volume. The feeling of pain
and breathlessness after having the "wind knocked out" is related to a decrease in the residual volume of air.12
Throughout the respiratory system there are many areas like the trachea and bronchioles where there are no alveoli
and consequently no gas exchange occurs in these areas. Areas within the respiratory system where there is no gas
exchange are known as dead spaces. When providing assisted ventilations to an adult patient with a bag valve mask
approximately one liter of air is delivered with each squeeze of the bag. Dead spaces are the reason that twice the
normal tidal volume is delivered. When evaluating a patient's respiratory status, it is important to recognize that it is a
function of both his or her respiratory rate and his or her tidal volume. This calculation is known as minute volume.
(minutevolume= respiratory rate x tidal volume) It is understood that providers are not going to do this calculation in
the field but it remains important to consider both the rate and the quality of the patient's respirations.

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 When a healthy adult is breathing normally he or she will exhibit a regular pattern of inhalation and exhalation. Each
breath will have adequate tidal volume. There should be audible breath sounds on both sides of the chest that
correlate with the rise and fall of the chest. There will be some abdominal movement and the whole process should
appear silent and effortless.13 The normal respiratory rate for adults is 12 to 20 breaths per minute. The normal
respiratory rate for children is 15 to 30 breaths per minute. Infants breathe between 25 and 50 times per minute.14

The passive or effortless process of breathing is governed by both neurological systems as well as chemical feedback
loops. In the brain the medulla oblongata, found on the lower half of the brain stem controls autonomic functions like
breathing. It is believed that it initiates the ventilation cycle in response to elevated carbon dioxide levels in
circulation.15 Within the medulla oblongata there are two areas that control breathing. They are the dorsal respiratory
group (DRG) and the ventral respiratory group (VRG). The DRG is the primary pacemaker for the respiratory control
system. By sending repetitive signals through the phrenic nerve to the diaphragm it controls the basic pattern of
normal respirations. The VRG sends signals that help facilitate forced inspiration and expiration. The DRG is regulated
by the pons which is another area in the brainstem. Within the pons the pneumotaxic center works to shut the DRG
down as needed which leads to shorter, faster respirations. The apneustic center also located within the pons
stimulates the DRG which results in longer, deeper respirations.16 The pneumotaxic center and the apneustic center
are used by the body to increase respirations during periods of high stress. These systems all have an impact on lung
volume. The Hering-Breuer reflex prevents the medulla oblongata and the pons from causing overexpansion injuries in
the lungs. There are unique stretch receptors in the chest wall that are activated by this reflex when the lungs are too
full or too empty which then stop or start inspiration and expiration as needed.

The respiratory centers of the brain are influenced by chemical processes within the body. These chemical feedback
loops help to maintain blood concentration of oxygen and carbon dioxide, as well as an acid base balance within a
narrow margin. In the simplest sense respiration is stimulated by an increase in arterial CO2 levels. As the CO2 levels
increase in the arterial blood stream the pH levels in the respiratory center drops. The decrease in pH activates the
medulla oblongata as well as the pons and the increased respiration occurs. When arterial CO2 levels decrease, the pH
levels in the respiratory center increase which causes decreased respirations. When a person hyperventilates and then
passes out for a brief period it is the result of this system. There is a pathologically activated secondary system that
helps control breathing called hypoxic drive. Hypoxic drive causes increased respirations when arterial oxygen levels
decrease. The hypoxic drive is controlled by areas in the aorta, carotid arteries, and brain that can function as oxygen
sensors. People who suffer from severe chronic obstructive pulmonary disease (COPD) retain high levels of CO2 even
when they are not suffering from acute exacerbation of their disease. Consequently, the hypoxic drive becomes the
primary source of respiratory stimulation. It was noted in a very old study that some COPD patients who received high
levels of supplemental oxygen over long periods of time experienced respiratory depression. It was believed that the
hypoxic drive caused this. Consequently, some EMS providers believed that high-flow oxygen could be harmful to
some COPD patients. There is no evidence that oxygen delivered by EMS to COPD patients while on the scene or
enroute to the emergency department causes decreased respirations.17 If the patient is hypoxic or is experiencing
respiratory distress do not hesitate.Provide him or her with the appropriate amount of oxygen.

When there are changes to the body's acid base balance both the respiratory system and the renal system work in
conjunction to return the body to its balanced state of homeostasis. When there is excess acid in the body (hydrogen
ions) the bicarbonate buffer system is activated and carbon dioxide and water are formed. The excess carbon dioxide
can then be eliminated through exhalation. When an alkalotic state occurs (decreased acid) decreased respiration
increases CO2 levels and the system works in reverse. When a decrease in the pH of arterial blood occurs due to
elevation of CO2 , due to respiratory depression, it is known as respiratory acidosis. Conversely when there is an
increase in the pH of arterial blood, related to excessive exhalation, it is known as respiratory alkalosis. If there are
changes in arterial pH due to primarily metabolic problems, it is known as metabolic acidosis and metabolic alkalosis
respectively.

The physiological processes that ensure that the body's cells receive adequate oxygen are complex and involve a
multitude of different anatomical systems. When delivering supplemental oxygen to ill or injured patients providers
must use the tools at their disposal to try and ensure that adequate amounts of oxygen reach its destination. This is
accomplished by using the appropriate delivery device based upon the patient's clinical presentation.

Identify the Components of Various Oxygen Delivery Systems

Medical grade oxygen (100 percent oxygen) is stored in steel or aluminum cylinders. There are a variety of sizes and
they are typically painted green but they can also be silver, chrome, or a combination of the three colors. Prehospital
oxygen cylinders are given a letter designation based upon their volume. D cylinders are small, relatively light, and are
easily carried to patients. They contain only 350 liters of oxygen. On the other end of the spectrum, M cylinders are
very large and heavy. M cylinders contain 3,000 liters of oxygen and are typically fixed in a bracket in the ambulance.
Generally, a full cylinder will have 2,000 psi of oxygen and it is recommended that when a cylinder drops below 500psi

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 it is replaced with a full one.18 The reason for this is two-fold. First, it will help prevent providers from running out of
oxygen while treating a patient. The second is that it allows the safe residual pressure of 200 psi to remain in the
cylinder at all times. If a cylinder is drained completely, moisture can get in leading to corrosion and damage.

Oxygen cylinders contain compressed gas and must be treated with a modicum of care. They should be regularly
inspected for signs of wear such as rusting, dents, or any other abnormal change in shape. The cylinders must also be
hydrostatically tested every 10 years. This is a process where the tank is taken apart, cleaned, and tested under
pressure to make sure it maintains its structural integrity. The cylinder's test date should be stamped in the metal near
the top including the month and year. Many EMS agencies contract with private distributors who exchange empty
oxygen cylinder and replace them with full ones. Typically, any testing and maintenance of the cylinders will be
handled by the distributor. However, some providers are expected to use cascade or concentrator systems to fill their
own cylinders. If you are expected to do this, ensure that you follow all safety procedures. In general, when handling
oxygen cylinders take precautions not to bang or damage them, especially the stem and the valve at the top.
Furthermore, it must be remembered that 100 percent oxygen supports rapid combustion and should never be used
near any open flame or cigarette. Caution should also be used in areas where there is the possibility of electrical
sparking or arcing. When storing or transporting oxygen the cylinder should be stored in bracket or strapped down.
This is especially important when using a portable oxygen tank in the back of a moving ambulance. The cylinder must
be secured so that it cannot break free in the event of a collision. An unsecured oxygen cylinder can become a deadly
missile during an accident.

The delivery of oxygen is measured in liters per minute. The duration of flow from any given cylinder is based upon the
liters per minute that are flowing as well as the size of the cylinder. This can be calculated using the following formula

([tank pressure-200psi (the safe residual volume)]x the cylinder constant)/ flow rate in liters per minute

The cylinder constant accounts for the volume of the various different sized cylinders.

Cylinder constants19

D cylinder= 0.16

E cylinder= 0.28

M cylinder= 1.56

Example: You place a patient in your ambulance on high-flow oxygen (15L/min via non-rebreather mask). The oxygen
is supplied from a M cylinder that has 2000psi. How long will the oxygen in the cylinder last?

[(2000psi-200psi)x1.56)/ 15L per min= 187.2 minutes of oxygen

What if you have a portable E cylinder with same pressure of 2000psi?

[(2000psi-200psi)x0.16]/15L per min= 19.2 minutes of oxygen

The take home message is that the size of the cylinder has a significant impact on the volume of gas that it can hold.
An E tank and an M tank may have the same PSI but the volume of gas that each holds at that pressure is vastly
different. When a patient is placed on supplemental oxygen providers must consider the amount of gas that is
available versus the time that it will take to transport the patient to the receiving facility.

People who suffer from chronic respiratory diseases will frequently use supplemental oxygen in their homes. This
oxygen is stored in a variety of ways including cylinders and concentrators. Oxygen concentrators are electrically
powered and pull in ambient air and concentrate the oxygen in order to deliver it to the patient. The benefit of these
systems is that they do not have cylinders that have to be replaced. Typically, however, they are only able to deliver
relatively low flow rates (2-6L/min). They also depend on electrical power to function which can be problematic in the
event of a power outage. Hospitals and other facilities that use large volumes of medical oxygen will often store it in
the liquid form. This allows them to maintain a supply in a very condensed state. Liquid oxygen is volatile and the
storage tanks are usually permanently fixed in an upright position.

When the valve at the top of an oxygen cylinder is opened the gas comes out at the pressure that is in the cylinder
(2000psi if it is full). Therapy regulators are attached to the cylinder in order to decrease the pressure to 50psi and
allow for the flow rate to be adjusted by the providers. The majority of regulators used in EMS can be adjusted from
1L/min to 25L/min. There are two types of regulators that are used in the field. They the Bourdon-gauge flow-meter
and the pressure compensated flow-meter. Bourdon-gauge flow-meters are typically found on portable cylinders and
the pressure display is not affected by gravity, meaning that it can placed in any position. Pressure compensated
flow-meters use a float ball in a tapered tube and must be in the upright position to function. They are usually found
mounted on the walls inside ambulances. Regardless of the specific type of regulator that is used providers must

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 ensure that it is designed to be used with medical oxygen and that it has been properly maintained. Petroleum based
lubricants must never be used with oxygen regulators because they can further increase the risk of fire and/or
explosion.

There are a variety of devices for delivering supplemental oxygen to patients. When preparing to do this, providers
must ensure that the patient's airway is open, protected, and his or her respirations are adequate. If the patient's
airway is obstructed or he or she is not breathing adequately it will not matter how much oxygen is delivered because
it will not make it to the patient's circulation. The adjuncts that are used to open and secure airways are beyond the
scope of this discussion. The rest of this discussion will focus on oxygen delivery systems for patients who have open
and protected airways.

The nasal cannula is used, primarily, to deliver-low flow oxygen to patients with minor to moderate respiratory
distress. This device has small prongs that are placed in the patient's nares and oxygen flows through them. Nasal
cannulas can deliver 24 percent to 44 percent oxygen at flow rates from 1-6L/min.20 In most cases the nasal cannula is
well-tolerated even among people who suffer from claustrophobia. Nasal cannulas are used frequently in the
prehospital setting and the possible complications are minor and infrequent. When patients are on oxygen via a nasal
cannula for an extended period of time they may experience drying or soreness in the mucous membranes of their
nares. This can be mitigated by placing an oxygen humidifier in the system. These are simple devices where the
oxygen from the regulator flows through a container of sterile water prior to being delivered to the patient. There is
some recent data suggesting that nasal cannulas can be used effectively with high-flow oxygen to help pre-oxygenate
apneic patients prior to intubation.21,22 When this technique is employed the patient is placed on 15L/min via nasal
cannula for at least one minute while assisted ventilation also continues prior to the intubation attempt. It appears
that doing this increases the amount of oxygen in the dead spaces and allows providers to pass an endotracheal tube
without making the patient hypoxic.

The non-rebreather mask with an oxygen reservoir bag has been the ubiquitous oxygen delivery device in EMS for
years. This system employs a soft plastic oxygen mask and an oxygen reservoir bag separated by a one-way valve.
The bag fills with oxygen and allows the patient to breathe it in. The exhaled air leaves the mask through small holes
in the sides of the mask that are covered with flapper valves. When 15L/min is delivered through a non-rebreather
mask the patient is able to breath between 90 percent and 100 percent oxygen.23 These masks should be used with
patients who are suffering from significant respiratory distress. Some patients may experience anxiety and
claustrophobia when placed on a non-rebreather mask. If the patient is experiencing significant dyspnea but he or she
is unable to tolerate a mask, then providers must work to coach him or her and can try and deliver the oxygen with
blow-by technique.

While not as common in EMS, some services use partial non-rebreather masks, simple masks, and tracheostomy
masks. Partial non-rebreather masks have an oxygen reservoir bag but no one-way valve. This allows expired air to
enter the bag and decreases the amount of oxygen that the patient receives. Simple masks do not have an oxygen
reservoir bag. Both partial non-rebreather masks and simple masks deliver between 35 percent and 60 percent oxygen
with the flow rate between six and 10L/min. Increasing the flow to over 10L/min does not increase the oxygen
concentration that is delivered to the patient.24 Tracheostomy masks are used for patients who breathe through a
tracheostomy. Trach patients do not inspire air through their nose or mouth so traditional masks and cannulas will not
benefit them. Tracheostomy masks are the appropriate size and shape to fit over a tracheostomy and they have a
strap that can be secured around the patient's neck. Take note, if a tracheostomy mask is not available a
non-rebreather mask can be placed sideways over a tracheostomy and it will deliver oxygen to the patient.

There are some patients who are prescribed a specific concentration of oxygen by their physician. Venturi masks are
often used in this capacity. These devices have venturi valves attached to a soft plastic mask that draw ambient air in
as the oxygen flows through. There are various valves that can, deliver 24percent, 28percent, 35percent, or
40percentoxygen respectively.25 Venturi masks are often found in the hospital and long-term care settings for patients
with advanced respiratory disease. There is little to no application for them in the acute care setting.

When a patient is experiencing bronchospasm or another obstructive process he or she often needs to inhale
medication along with oxygen in order to relieve the dyspnea. Nebulizers are used to facilitate this. Doses of
medication like albuterol, Atrovent, or epinephrine are placed in a reservoir that is attached to a mask or a mouth
piece. When oxygen flows through the system the medication is turned into an aerosol mist and is then inhaled into
the lungs where it works directly on the tissue to reduce inflammation.

Continuous positive airway pressure (CPAP) masks provide significant support to patients experiencing severe
respiratory distress. They have become commonplace in prehospital care and aggressive use of CPAP is associated in a
significant reduction in patients progressing from respiratory distress to respiratory failure. Patients who suffer from
advanced COPD and congestive heart failure (CHF) have very high rates of mortality and morbidity associated with
being intubated and placed on ventilators. EMS CPAP reduces the need for intubation among these patients
significantly.26 CPAP increases pressure within the lungs, helps to re-inflate collapsed alveoli, pushes oxygen across

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 the alveolar membrane, and forces interstitial fluid back into the pulmonary circulation.27 Patients who are placed on
CPAP in conjunction with beta agonists (albuterol) for COPD and nitrates for CHF will often experience dramatic relief
in relatively short periods of time. Most CPAP circuits require oxygen flow of between 15 and 25L/min so they will use
gas very quickly and that must be considered when determining the appropriate facility to triage patients to. Providers
should have a low threshold for placing patients experiencing severe respiratory distress on CPAP. The incidence of
complications is low and the benefits are significant. Keep in mind, however, CPAP is NOT a replacement for assisted
ventilations. The primary contraindications for CPAP are respiratory arrest or ineffective ventilations, altered mentation
to the point that the patient is unable to protect his or her airway, hypotension, pneumothorax or other chest trauma,
active GI bleeding or vomiting, and inability to tolerate the mask.28 The complications caused by CPAP can include
barotrauma, hypotension, drying of mucous membranes, and skin irritation/ breakdown around the mask. If
complications do occur the mask can be removed, and in most cases, the issues will resolve on their own.

When a patient is in respiratory arrest or has ineffective respirations a bag valve mask (BVM) is used. Adult BVMs have
an oxygen reservoir that holds one liter of 100 percent oxygen and when it is squeezed, that volume is delivered
through a mask. The mask can also be removed and the BVM can be connected to an endotracheal tube. There are
also pediatric, infant, and neonatal-sized BVMs available. A BVM can be used by a single rescuer or two rescuers.
When a single rescuer uses a BVM he or she should use one hand to clamp the mask tightly around the patient's nose
and mouth. A good seal between the mask and the patient's mouth is imperative to deliver effective ventilations. The
rescuer can then use his or her other hand to compress the bag. When two rescuers are available, one rescuer uses
both hands to hold the mask against the patient's face and maintains the seal and the other rescuer compresses the
bag. The two rescuer technique allows for more effective ventilation than the single rescuer technique. When
ventilating a patient with a BVM it is recommended that the patient is given 10 breaths per minute or one breath every
six seconds. In the moment this rate seems exceedingly slow however excessive ventilation can lead to complications
that will be described later in the module.

Describe Indications for Prehospital Oxygen Therapy

Respiratory distress occurs when there is any disruption in the normal processes of breathing. In the prehospital
environment any patient who complains of difficulty breathing should receive supplemental oxygen. The goal is to
titrate the therapy to relieve his or her distress and maintain an oxygen saturation of at least 96 percent without
hyperoxygenation.

The assessment of the patient's breathing status begins as soon as you approach him or her. The patient's position is
the first thing to be evaluated and can be a good indication of the effort associated with his or her respirations. A
patient who is awake, sitting up in a normal position, and who appears to be relaxed is probably experiencing minor
distress at the worst. Conversely, a patient who is unconscious and prone on the ground will likely have a
compromised airway and poor respirations. A patient who is found in the tripod position is exhibiting signs of
respiratory distress. The tripod position is when the patient is sitting upright, leaning forward on outstretched arms,
with his or her head up, andhis or her chin forward. In this position the patient is trying to catch his or her breath by
increasing intrathoracic pressure naturally. If the patient is found in bed or sleeping in a recliner the elevation of the
head should be noted. Many congestive heart failure patients experience orthopnea where they become dyspneic when
in the supine position. Their symptoms may be progressive over a number of days where they have to prop
themselves up more and more to maintain adequate breathing.

Upon arrival at the patient's side his or her skin signs should be evaluated and can also be a barometer of the efficacy
of their ventilation. Normal skin signs include skin that is warm and dry with normal color and turgor. Patients who are
hypoxic will quickly start to become pale, diaphoretic, and to develop cyanosis which is a bluish coloring to the skin.
Cyanosis first presents in the lips and nail beds but can spread to the face, chest, abdomen, and extremities as the
hypoxia worsens. Patients who suffer from advanced COPD and have chronic hypoxemia often develop erythrocytosis
(elevated red blood cell count) as the body tries to compensate for low oxygen levels. These patients may appear red
and flushed even when they are severely hypoxic. The vernacular term "pink puffers" was coined to describe these
patients who also tend to breathe with pursed lips. Pursed lip breathing is another way that the body reacts to
dyspnea. When a person breathes through pursed lips it increases positive end expiratory pressure (PEEP) and can
help to increase intrathoracic pressure, alveolar inflation, and oxygen absorption. The term "blue bloaters" describes
people who are experiencing CHF exacerbation. They will appear cyanotic from hypoxia and swollen from fluid
retention.

People who are experiencing dyspnea will often exhibit increased work of breathing. This is the use of accessory
muscles, intercostal retractions, nasal flaring, and increased respiratory rate. Some patients may present with
increased work of breathing but a normal SPO2 reading. These patients are experiencing respiratory distress and
should be treated accordingly. The patient is managing to compensate for whatever process is causing his or her
difficulty breathing, but without intervention he or she will become tired and then when he or she cannot maintain the
increased work of breathing he or she will quickly become severely hypoxic. Other signs of inadequate breathing

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 include respirations that are too slow or too fast, shallow breathing, and abnormal respiratory patterns, as well as
asymmetric chest wall movement. There are a variety of pathologies and injuries that result in abnormal respiratory
patterns. Cheyne-Stokes respiration is characterized by breathing that gradually increases in rate and depth, then
decreases to apnea, and then repeats itself. Apneustic respirations are prolonged gasping inhalation followed by little
to no exhalation. Cheyne-Stokes and apneustic respirations are caused by injury to respiratory centers in the brain
stem.29 Kussmaul's respirationsare deep and rapid and areseen in patients who are suffering from diabetic
ketoacidosis. Biot's respiration (ataxic respiration) is irregular in rate, depth, and quality with periods of apnea and is
the result of increased intracranial pressure. Agonal respiration is slow, shallow, irregular, and occasionally gasping
sounds that result from cerebral anoxia. Patients who have recently suffered cardiac arrest but still have neurologic
activity may present with agonal respiration.30 Asymmetric chest wall movementoccurs when one side of the chest
does not rise and fall with inhalation and exhalation. This may bethe result of lung collapse that is typically caused by
trauma to the chest.

Lung sound should be auscultated on all patients, especially those who are experiencing respiratory distress.
Auscultation should occurbilaterally in the apexes and bases on both the anterior and posterior sides of the chest.
Adventitious sound such as wheezing, rales, and rhonchi should be noted. Listening to lung sounds proficiently takes
practice and finesse as well as a quality stethoscope. Differentiating between the dyspnea that is caused by COPD,
CHF, and pneumonia is one of the most difficult things that EMS providers are asked to do. We do not have blood work
or radiographs to help so our clinical decision-making has to be based upon lung sounds as well as the other signs and
symptoms. Wheezing is caused by swelling to the lower airways caused by bronchospasm. Pulmonary edema causes
rales which sounds like bubbles blown in a glass of milk. Rhonchi are the result of viscous mucous consolidation as well
as inflammation that is most frequently associated with bronchiolitis, pneumonia, aspiration, or chronic bronchitis.31
The absence of lung sounds can also be a significant finding. Diminished lung sounds can be related to severe
obstruction, edema, consolidation, pleural effusion, or pneumothorax. In order to adequately evaluate lung
sounds,providers need to work in a relatively quiet environment and have the patient breathe as deeply as possible
without talking.

Arterial oxygen saturation is determined by pulse oximetry and is a measurement of the percentage of hemoglobin
that is saturated with oxygen. It is an important part of the prehospital patient assessment and can provide valuable
information to providers. A normal SPO2 reading is anything that is greater than 95%. Any patient who is hypoxic,
meaning his or her SPO2 is less than 95 percent, should receive supplemental oxygen. There are a number of factors
that can lead to inaccurate SPO2 findings including carbon monoxide poisoning, hypovolemia, poor peripheral
circulation, abnormal hemoglobin conditions, and hypothermia. The patient's SPO2 must always be evaluated within
the context of his or her overall presentation. As was previously mentioned some patients may be able to maintain a
normal SPO2 when they are working extremely hard to breathe. Conversely, if a patient has a pulse oximetry reading
of 70 percent and he or she is awake, talking, breathing normally, and has normal skin signs then you should consider
the possibility of an erroneous reading.

Patients who are experiencing any of the previously described signs and symptoms of respiratory distress should be
given supplemental oxygen. The goal of current best practices is to get them the appropriate volume with the
appropriate delivery device. We can no longer put every patient on a non-rebreather mask and assume that high-flow
oxygen will be beneficial regardless of the actual problem. If a patient presents with minor or moderate distress a
stepwise approach where you start with a nasal cannula and work up as needed may be appropriate. Patients who are
experiencing severe dyspnea should receive immediate and aggressive treatment with high-flow oxygen and/or CPAP.
However, if the patient improves de-escalation can be considered. Make sure that you always follow local protocols
and do not hesitate to contact online medical command if you are unsure of what to do.

Recognize Potential Complications while Using Prehospital Oxygen

Therapy
Medical oxygen is a drug that is administered to patients who are experiencing respiratory distress. Even though
oxygen is a naturally occurring atmospheric gas when it is administered to patients there is the possibility for
complications as well as adverse effects. The incidence of complications in the prehospital environment is low and the
intent of this discussion is not to deter providers from giving dyspneic patients supplemental oxygen. The goal is to
help providers understand the effect of the drug that they are administering within a whole body framework and to
encourage targeted therapy based upon the patient's clinical needs. If you think the patient needs oxygen do not
hesitate to give it to him or her.

When oxygen is administered it passes through the nares and oropharynx. Unless the gas is humidified it has a
moisture content of zero and will dry out the sensitive mucous membranes in these areas. Over long periods of time
this can lead to pain, discomfort, and occasional epistaxis. The plastic from the various devices that rest against the
patient's skin can also cause irritation and eventual tissue breakdown.32 If the patient is going to be in your care for

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 an extended period of time it is advisable to try and mitigate these problems. Humidification systems can be easily
added to most if not all oxygen delivery devices and gauze can be used to pad the areas where plastic rests against
the patient's skin.

Hyperoxiaoccurs when tissues and organs are exposed to higher than normal partial pressures of oxygen. Dalton's law
states that in a mixture of non-reacting gases the total pressure of the mixture is equal to the sum of the partial
pressures of the gases in the mixture. Air at sea level contains 21 percent oxygen, 78 percent nitrogen, and two
percent other gases. When patients breathe with supplemental oxygen, that balance changes drastically. One hundred
percent oxygen has significantly increased pressure and displaces all the other gases in the mixture. That shift can
lead to hyperoxia. Recent research shows that hyperoxia can cause harm in a variety of ways.33

Absorption atelectasisoccurs when individual alveoli become deflated due to decreased surfactant availability and it can
lead to complete lung collapse. When patients are exposed to high partial pressure of oxygen it significantly reduces
the amount of nitrogen available and nitrogen washout can occur. Under normal conditions the nitrogen in inspired air
is responsible for the production of surfactant. When patients are on high-flow oxygen for even a short period of time
nitrogen levels drop and surfactant production can decrease.

A free radical is a molecule that has at least one free electron in its outermost valence. The free electron leads to
increased reactivity with other molecules. Oxygen is a free radical and has two free electrons making it a highly
reactive. The healthy body balances this with antioxidants which can bind the reactive oxygen molecules before they
cause damage. When patients suffer from major illness or injury the balance shifts and free radicals outnumber the
antioxidants. When this happens oxidative stress can occur. Oxidative stress is when there are insufficient
antioxidants to neutralize the free radicals and the reactive molecules interact with the DNA, proteins, and lipids within
the body's cells in an effort to stabilize. This interaction destabilizes the cell components and has been linked to
neurodegenerative diseases like Parkinson's and Alzheimer's, gene mutations, certain cancers, chronic fatigue
syndrome, fragile X syndrome, heart and blood vessel disorders, atherosclerosis, heart failure, heart attack, and
inflammatory diseases.34 In general oxidative stress is a reason to avoid high-flow oxygen among patients who do not
absolutely need it.

Supplemental oxygen can also have a negative impact on patients who are suffering from specific disease processes
such as acute coronary syndrome (ACS), COPD, post-cardiac arrest, and trauma. High-flow oxygen has been linked to
increased mortality and morbidity among ACS patients because 100 percent oxygen via NRB reduces coronary artery
flow by 30 percent after five minutes and it also reduces the effects of vasodilators like nitroglycerine.35,36 In 2010,
after reviewing all evidence, the American Heart Association changed its recommendations and stated,"There is
insufficient evidence to support routine use of high-flow oxygen in the treatment of uncomplicated MI, and it may
increase mortality."37,38 While previous theories that prehospital administration of supplemental oxygen to COPD
patientscould cause respiratory depression have been shown to be unfounded there is evidence that titrated therapy is
better in the long term. One study found that titrated oxygen administration compared to high-flow oxygen reduced
mortality by 58 percent for COPD patients.39 Early studies of CPAP with low FiO2(28-32%) have shown it to be highly
effective while avoiding hyperoxia.40 Post-cardiac arrestpatients are especially sensitive to the oxidative stress caused
by free radicals. When treating patients who have achieved the return of spontaneous circulation, providers must avoid
excessive ventilation. The AHA recommends administering 10-12breaths per minute and the titration of therapy to
maintainan ETCO2 between 25-40mmHg as well as an SPO2 of at least 94 percent. The authors of a 2004 study from
Tulane University observed 5,090 trauma patients who did not require artificial ventilation.They found that there was
no improvement among patients who received supplemental oxygen and some experienced worse outcomes. They
concluded that there is no benefit to administering supplemental oxygen to trauma patients who are not experiencing
dyspnea.41,42

Case Conclusion
The patient remained stable in the emergency department and was admitted to the ICU a few hours later. The staff
there ensured that he did not become febrile and kept him sedated for 36 hours. After that he was extubated and
found to be neurologically intact. The cardiologists determined that the patient suffered a sudden cardiac arrest that
was caused by a previously undiagnosed electrical aberrancy within the patient's heart. The patient had an automatic
internal cardiac defibrillator placed one week after the cardiac arrest. He was discharged two days after that. A few
months later my partner and I as well as the other providers that cared for the patient had the opportunity to meet
with him and his family. It was very emotional for everyone there and it was a great reminder of why I do this job.

Conclusion
Patients who are experiencing respiratory distress should receive supplemental oxygen. Providers must evaluate the
patient and base their oxygen administration on the clinical findings. There is no reason to place patients who are not
experiencing difficulty breathing on oxygen. It is good practice to treat supplemental oxygen like any other medication

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 and to follow the seven rights of drug administration. They are: the right drug, the right dose, the right time, the right
route, the right patient, the right reason, and the right documentation. If providers do this then they will help to
ensure that their patients receive the appropriate prehospital oxygen therapy.

Author Simon Taxel, Peer Reviewers Travis Baker, Rebecca Brazeal, George Petit MD, et al. Copyright CE Solutions. All
Rights Reserved.

References

1. Website: Highlights of the 2015 American Heart Association Guidelines Ypdate for CPR and ECC. AHA Website.
Available at:https://eccguidelines.heart.org/wp-content/uploads/2015/10/2015-AHA-Guidelines-Highlights-
English.pdf. Accessed July 10, 2016.
2. 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.
3. Website: Collopy, Kevin T. Kivlehan, Sean M. Snyder, Scott R. Oxygen Toxicity. EMS world Website. Available at:
http://www.emsworld.com/article/10523286/oxygen-toxicity. Accessed July 10, 2016.
4. Journal Article: 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.
5. Book Chapter: Anatomy and physiology. In:Ed. Pollack, Andrew N. MD FAAOS. Nancy Caroline's Emergency Care
in The Streets. Seventh Edition. Jones and Bartlett Learning. Burlington Ma. 2013: 183-332
6. Ibid
7. Ibid
8. Ibid
9. Ibid
10. Ibid
11. Ibid
12. Ibid
13. Ibid
14. Ibid
15. Ibid
16. Ibid
17. Website: Limmer, Daniel D. Mistovich, Joseph J. Krost, William S. Beyond the Basics: COPD. EMS World website.
Available at: http://www.emsworld.com/article/10321673/beyond-the-basics-copd. Accessed July 16, 2016.
18. Book Chapter: Airway Management. In:Ed. Pollack, Andrew N. MD FAAOS. Nancy Caroline's Emergency Care in
The Streets. Seventh Edition. Jones and Bartlett Learning. Burlington Ma. 2013: 750-845
19. Ibid
20. Ibid
21. Journal article: Patel A, Nouraei SA. Transnasal Humidified Rapid-Insufflation Ventilatory Exchange (THRIVE): a
physiological method of increasing apnoea time in patients with difficult airways. Anaesthesia. 2015
Mar;70(3):323-9.
22. Journal article: Miguel-Montanes R, Hajage D, Messika J, Bertrand F, Gaudry S, Rafat C, Labbé V, Dufour N,
Jean-Baptiste S, Bedet A, Dreyfuss D, Ricard JD. Use of high-flow nasal cannula oxygen therapy to prevent
desaturation during tracheal intubation of intensive care patients with mild-to-moderate hypoxemia. Crit Care
Med. 2015 Mar;43(3):574-83
23. Book Chapter: Airway Management. In:Ed. Pollack, Andrew N. MD FAAOS. Nancy Caroline's Emergency Care in
The Streets. Seventh Edition. Jones and Bartlett Learning. Burlington Ma. 2013: 750-845
24. Ibid
25. Ibid
26. Ibid
27. Ibid
28. Ibid
29. Ibid
30. Ibid
31. Ibid
32. Website: Collopy, Kevin T. Kivlehan, Sean M. Snyder, Scott R. Oxygen Toxicity. EMS world Website. Available at:
http://www.emsworld.com/article/10523286/oxygen-toxicity. Accessed July 10, 2016.
33. Website: McCevoy, Mike. Can Oxygen Hurt Our Patients? EMS1.com. Available at: http://www.ems1.com
/columnists/mike-mcevoy/articles/1308955-Can-oxygen-hurt-our-patients/. Accessed: July 9, 2016.
34. Website: Manadal, Anaya MD. What is oxidative stress? News Medical. Life sciences and medical website.
Available at: http://www.news-medical.net/health/What-is-Oxidative-Stress.aspx. Accessed July 20, 2016.
35. Website: Gandy, William E. Grayson, Steven. More Oxygen Can't Hurt…Can it? EMS world website. Available at:
http://www.emsworld.com/article/10915304/the-dangers-of-giving-too-much-oxygen. Accessed July 10, 2016.
36. Journal Article: McNulty PH, et al. Effects of supplemental oxygen administration on coronary blood flow in

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 patients undergoing cardiac catheterization. Am J Physiol Heart CircPhysiol, 2005; 288: H1057–62.
37. Website: Gandy, William E. Grayson, Steven. More Oxygen Can't Hurt…Can it? EMS world website. Available at:
http://www.emsworld.com/article/10915304/the-dangers-of-giving-too-much-oxygen. Accessed July 10, 2016.
38. Journal Article: 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.
39. Journal article: 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.
40. Journal Article: Bledsoe BE, et al. Low-fractional oxygen concentration continuous positive airway pressure is
effective in the prehospital setting. PrehospEmerg Care, 2012 Apr–Jun; 16(2): 217–21.
41. Journal Article: 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.
42. Website: Gandy, William E. Grayson, Steven. More Oxygen Can't Hurt…Can it? EMS world website. Available at:
http://www.emsworld.com/article/10915304/the-dangers-of-giving-too-much-oxygen. Accessed July 10, 2016.

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