A supplement to JEMS sponsored by Physio-Control, Inc.

elsevier March 2009

Trend Setters
How continuous cardiac,
CO & EtCO2 monitoring are
reshaping prehospital care
 trend setters

TABLE OF
CONTENTS
4 introduction Exciting changes in patient
monitoring I By A.J. Heightman, MPA, EMT-P

5 Where There’s CO, There’s Not Always Fire

How Pulse CO-Oximetry serves as an important
assessment & triage tool I By Bryan E. Bledsoe, DO,
FACEP, & Mike McEvoy, PhD, RN, EMT-P

9 What Is Methemoglobinemia? What this

level means in your patients & why you should
monitor it I By Bryan E. Bledsoe, DO, FACEP, & Mike McEvoy,
PhD, RN, EMT-P

14 Universal Capnography A vital asset that

improves patient care on almost any call
I By Patricia A. Brandt, RN, BSN, MHR

18 getting the trend Maximizing the potential of

the prehospital 12-lead ECG I By Tim Phalen

Disclosure of Author Relationships: Contributing authors have been asked to disclose any relation-
ships they may have with commercial supporters of this supplement or with companies that may have
relevance to the content of the supplement. Such disclosure at the end of each article is intended to
provide readers with sufficient information to evaluate whether any material in the supplement has been
influenced by the writer’s relationship(s) or financial interests with said companies.

LIFEPAK 15 is a registered trademark of Physio-Control, Inc. Masimo, the Radical logo, Rainbow, SET,
SpCO, SpMet, Pulse CO-Oximeter and Pulse CO-Oximetry are trademarks or registered trademarks of
Masimo Corp.

Vice President/Publisher Jeff Berend

Editorial Director A.J. Heightman, MPA, EMT-P
Managing Editor Lisa Bell, EMT-B
Advertising Director Judi Leidiger
Cover Photo Courtesy Physio-Control, Inc.
Trend Setters is a supplement sponsored by Physio-Control, Inc., with support from Masimo and Oridion, and published by Elsevier Public Safety,
525 B Street, Ste. 1900, San Diego, CA 92101-4495; 800/266-5367 (Fed ID # 13-1958712). Copyright 2009 Elsevier Inc. No material may be
reproduced or uploaded on computer network services without the expressed permission of the publisher. Subscription information: To subscribe
to an Elsevier publication, visit www.jems.com. Advertising information: Rates are available on request. Contact Elsevier Public Safety, Advertising
Department, 525 B Street, Ste. 1900, San Diego, CA 92101-4495; 800/266-536.

The
Conscience
of EMS
JOURNAL OF EMERGENCY MEDICAL SERVICES

march 2009 Trend Setters 3

 introduction
Exciting changes in
patient monitoring
T
This editorial supplement discusses important enhance-
ments in prehospital monitoring being presented by
Physio-Control’s new monitor/defibrillator—the LIFEPAK
15. These monitor enhancements illustrate how new
technology will enable you to do your job easier, recognize
dangerous trends occurring in your patient’s condition, bet-
ter document those trends (and the care you rendered), and
present that documentation and trending data to receiving
emergency department staff.
Physio-Control’s LIFEPAK 15 monitor/defibrillator
(510(k) pending) offers Masimo’s breakthrough Rainbow
SET Pulse CO-Oximetry technology as an option to allow
crews to non-invasively and continuously monitor carboxy-
hemoglobin, methemoglobin and oxygen levels in the blood.
Through use of a revolutionary sensor that employs 7+
wavelengths of light to collect and analyze an extraordinarily
rich stream of physiological data, crews can now accurately
measure carbon monoxide and methemoglobin levels in the
blood in addition to oxygen saturation and pulse rates.
To illustrate the importance of this new technology, this
supplement explains the basics of carbon monoxide and
methemoglobin and monitoring for both. Being able to
monitor oxygen and carbon monoxide concentrations in a
patient’s blood eliminates the risk of misdiagnosing unsus-
pected CO poisoning as flu or fatigue, and will enable crews
to detect and treat potentially life-threatening conditions.
Dr. Bledsoe’s article describes the utility of the met­
hemoglobin detection. Similar to CO, the symptoms of
methemoglobinemia can be misdiagnosed but have dire
consequences. This new technology uses the same finger
probe used in pulse oximetry and will enable crews to non-
invasively detect carbon monoxide and methemoglobin lev-
els in a patient’s blood and better understand their patient’s
medical status in the field and render treatments sooner.
As with most changes introduced in EMS, particu-
larly the introduction of new technology, there are often
questions and some degree of skepticism, with naysayers
asking, “Why do we need it now when we’ve done just fine
without it in the past?”
The reality is that in the short 40-year history of modern
EMS, we’ve experienced numerous changes in the educa-
tion of our personnel and the refinement of the equipment
deployed in the field. Let’s look back at our evolution.
In the 1970s, EMS crews were using bouncing-ball
ECG scopes, three-lead cable/electrode sets, defibrillation
paddles and monophasic energy to render care to patients.
And, for a while, the only way to externally pace a patient’s
heart was to hook up a separate pacing device that then
had to be linked into our monitor/defibrillators.
4 Trend Setters Journal of Emergency Medical Services (JEMS)
By A.J. Heightman, MPA, EMT-P
Battery life was also a major issue, with non-replaceable
batteries that weighed almost as much as the inner work-
ings of the monitor/defibrillators.
In the late ’70s, pulse oximetry arrived as an important
assessment tool for our crews. But it also added another
device that had to be carried into, and accounted for, at
each emergency scene.
Hospitals had monitor/defibrillators that could assess
multiple patient parameters and 12-lead ECGs, but they
were too large to take out in the field. But in the ’80s and
’90s, technological advances and better engineering enabled
us to reduce the weight of our monitor/defibrillators and
integrate more capabilities into compact cases.
Having internal pacing capabilities and replaceable,
rechargeable batteries were major advancements for
prehospital systems, but that was only the beginning. Soon,
longer-lasting batteries and biphasic defibrillation were
added and we thought we had really taken our monitoring
and defibrillation capabilities to the highest level.
Then, because it was difficult to hear blood pressures us-
ing stethoscopes in moving ambulances (still is), engineers
designed electronic BP capabilities into prehospital moni-
tors. And integral pulse oximetry was introduced in cardiac
monitors, with EMS systems quickly adopting it as a useful
feature that could be immediately available to crews, assist
them in determining the severity of patient illnesses and
reduce the amount of equipment that needed to be carried.
However, when 12-lead ECG capabilities were offered,
many EMS agencies were ambivalent, scoffing at the extra
training (and wires/electrodes) it required. But cardiologists
and EMS medical directors soon convinced progressive
ALS systems that if they truly wanted to assess and provide
the earliest treatment, they should use 12-lead ECGs.
Thus, we have embraced the prehospital monitoring
enhancements that have been presented to us over the past
40 years and need to understand the impact that cardiac
trending and the measurement of methemoglobin, carboxy-
hemoglobin and oxyhemoglobin in the blood will have
on the assessment and care of our patients. Being able to
monitor multiple vital signs and patient parameters, and
generate comprehensive reports that show your care and
patient trending, truly brings critical care technology to the
field. These changes will be good for you and your patients.
A.J. Heightman, MPA, EMT-P, is the editor-in-chief of JEMS and the editorial
director of Elsevier Public Safety. He has served as director of operations
for Cetronia Ambulance in Allentown, Pa., and as executive director of the
Eastern Pennsylvania Emergency Medical Services Council. Contact him at
a.j.heightman@elsevier.com.
 By Bryan E. Bledsoe, DO, FACEP, & Mike McEvoy, PhD, RN, EMT-P

transported while those without

Where There’s CO,

elevated levels remained at the
scene—averting a significant mul-
tiple casualty incident and excess use

There’s Not
of EMS and hospital resources.

Always Fire
How Pulse CO-Oximetry serves as an important
assessment & triage tool
Introduction
CO poisoning remains the most com-
mon cause of poisoning in industrial-
ized countries.1 CO is an odorless,
tasteless and colorless gas that results
from the incomplete combustion of
carbon-containing substances, such
as wood and petroleum products.
The incidence of CO poisoning tends

O
to peak following disasters and cold
On March 5, 2008, paramedics from Wake County EMS in Raleigh, N.C., re- weather and is related to the use of
sponded to a 10-year-old child with a headache. The family called EMS from their heaters and gasoline-powered devices,
vehicle because they couldn’t locate a hospital. On arrival at the vehicle, paramed- such as portable generators.2
ics Junith Peterson and Beth Staley found and assessed the child. They learned Hemoglobin, the chemical in the
the family had eaten together at a local restaurant earlier in the evening and then blood responsible for transport-
went to sleep shortly after that. Around 10 p.m., several family members had ing oxygen, is highly susceptible to
awakened with headaches, including the child. the effects of CO. Hemoglobin will
The paramedics quickly formulated a differential diagnosis that included preferentially bind CO over oxygen
food poisoning and carbon monoxide (CO) poisoning. A Pulse CO-Oximeter until the molecule contains nothing
was applied to each family member, and all were found to have elevated car- but CO (see Figure 1). In addition,
boxyhemoglobin (SpCO) levels. Additional ambulances were summoned, and CO will actually displace the oxy-
the family was transported to the hospital. gen already bound to hemoglobin.
During assessment, the paramedics had also learned the family was staying The resultant combination of CO
in a local hotel. The Raleigh Fire Department was notified, and an engine was and hemoglobin is a compound
sent to the hotel. Dangerously high environmental CO levels were detected called carboxyhemoglobin (COHb),
within the hotel, and 50 people were safely evacuated. Three hotel guests had which cannot transport oxygen to
elevated SpCO levels and were transported to the hospital. Through the use body tissues. This binding is fairly
of Pulse CO-Oximetry, only those patients with elevated SpCO levels were irreversible.
The body rids itself of CO
through both the breakdown
Figure 1: Oxygen vs. CO of carboxyhemoglobin and
the slow off-loading of CO
from the heme portions of
Carbon Monoxide
the hemoglobin molecule.
When CO is released from
the hemoglobin, it’s removed
Oxygen from the body through the
respiratory system. The
illustration courtesy robyn dickson/cielo azul publications

removal of CO from car-

boxyhemoglobin takes four
to six hours in room air
conditions. The CO removal
rate can be decreased to ap-
proximately 80 minutes with
the administration of 100%
oxygen. Hyperbaric oxygen
(HBO) therapy, and possibly

march 2009 Trend Setters 5

continuous positive airway pressure
(CPAP), can speed CO elimination
even more.
Recently, it has been shown that
CO also affects other iron-containing
proteins, such as myoglobin, neuro-
globin and cytochrome oxidase. In
fact, much of the adverse effects seen
in CO poisoning are more related
to CO binding to non-hemoglobin
iron-containing proteins rather than
hemoglobin itself.3 We’ve always
known that the signs and symp-
toms of CO poisoning are strikingly
similar to cyanide poisoning. Now,
we know this is due to the fact that
both CO and cyanide bind to the
enzyme cytochrome oxidase and in-
hibit the normal processing of oxy-
gen and the subsequent formation
of energy within the cells. With the
advent of Pulse CO-Oximetry, pre-
hospital personnel can now rule in
or rule out CO exposure in patients
who have had possible exposure to
products of combustion.4
Signs & Symptoms
of CO Poisoning
The signs and symptoms of CO expo-
sure can be extremely vague, making
prehospital diagnosis difficult (see
Table 1, p. 7). In addition, because
the pathophysiological effects of CO
poisoning are extremely complex,
there’s often no identifiable relation-
ship between carboxyhemoglobin
levels and the signs and symptoms
found.5 Thus, diagnosis and detec-
tion of CO poisoning requires the
use of technology. Although common
environmental (four-gas) detectors
used by fire departments can detect
CO in the surrounding environment,
they cannot determine specific levels
in a given patient. Patient CO levels
can be detected only through exhaled
carbon monoxide gas monitoring or
through Pulse CO-Oximetry.
Pulse CO-Oximetry
Pulse CO-Oximetry is a monitor-
ing technology that uses multiple
wavelengths of light to measure levels
of carboxyhemoglobin in the blood.
Light waves are emitted from light-
6 Trend Setters Journal of Emergency Medical Services (JEMS)
emitting diodes (LEDs), pass through a finger vascular bed and are detected by
photoreceptors on the other side (see Figure 2). The amount of light received by
these photoreceptors is fed into a processor, which then determines the percent-
age of carboxyhemoglobin present. Because Pulse CO-Oximetry is an indirect
measure of carboxyhemoglobin levels, it reports these levels as SpCO, which cor-
responds to actual carboxyhemoglobin levels in the patient.6 Therefore, you’re
able to get a continuous reading and can monitor the effects of treatment.
Generally speaking, when a patient with CO poisoning receives 100% oxy-
gen in the prehospital setting, you’ll see a steady decline in SpCO levels. With
Physio-Control’s LIFEPAK 15, historical patient trending data is recorded
for up to eight hours and available to print out as a summary for emergency
department (ED) and documentation purposes.
Indications for Pulse CO-Oximetry
With the advent of any new technology, it’s important to define the role
of the technology in the prehospital and emergency setting. The detection
and monitoring of SpCO levels have several applications and advantages
for prehospital professionals. These include detection and diagnosis of CO
poisoning, differential diagnosis of CO and cyanide poisoning, monitoring
and rehabilitation of firefighters and other emergency personnel, historical
PHOTO Dennis Merritt
As more is learned about the effects of CO, there’s a growing body of scientific evidence that shows that both
acute and chronic CO exposure can lead to such problems as early cardiovascular death.
trending of CO levels during prehospital care, and epidemiological monitor-
ing and detection.
Detection & diagnosis of CO poisoning: In the past, the diagnosis of CO
poisoning in the prehospital setting has been virtually impossible. Thus, many
patients have been transported who did not have CO poisoning. Likewise, some
High-concentration oxygen should be provided early in cases of
suspected cyanide poisoning because CO is often also present.
patients with CO poisoning may not have been transported. It’s clear from the
medical literature that the earlier CO poisoning is diagnosed and treated, the
better the ultimate outcome for the patient. Thus, obtaining a fairly definitive
diagnosis in the prehospital setting is of paramount importance.
It’s important to point out that exclusion of CO poisoning in the pre-
hospital setting can be almost as important as detection. CO emergencies
 often involve numerous both acute and chronic
people and can severely Table 1: Signs & Symptoms of CO Poisoning CO exposure can lead to
tax prehospital and hos- Malaise Confabulation Visual disturbances such problems as early
pital resources. Thus, the Flu-like symptoms Agitation Syncope cardiovascular death and
ability to exclude CO Fatigue Nausea Seizures even neurological diseases.
poisoning as a diagnosis Dyspnea on exertion Vomiting Fecal incontinence Because of this risk, the
can help to avoid un- Chest pain Diarrhea Urinary incontinence National Fire Protection
necessary transport and Palpitations Abdominal pain Memory disturbances Association (NFPA) has
the associated expenses Lethargy Headache Gait disturbances published a standard
to the EMS system and Confusion Drowsiness Bizarre neurologic symptoms (NFPA 1584) that calls
the patients. Depression Dizziness Coma for medical monitoring
Calls involving CO Impulsiveness Weakness Death of firefighters on the fire
detector alarm activa- Hallucination Confusion ground and in certain
tions are a common training situations. NFPA
fire service response. 1584 recommends both
Traditionally, firefighters have utilized atmospheric monitors to assess for en- the use of pulse oximetry and CO
vironmental CO poisoning, often missing toxic levels of CO when a structure detection.8 This can be accomplished
was ventilated prior to their arrival. With the availability of technology to with Pulse CO-Oximetry (as a stand-
screen people for CO poisoning, firefighters are now able to accurately and alone device) or through the patient
safely determine whether CO detector alarms are indicative of real danger to monitoring capabilities of a cardiac
building occupants. monitor, such as the LIFEPAK 15
Differential diagnosis of CO & cyanide poisoning: Now that a safe antidote (with the CO and pulse oximetry
(hydroxocobalamin) is available for cyanide poisoning, it’s important to try to modules). With the guidance of medi-
determine whether a patient may be suffering from cyanide poisoning.7 In the cal directors, fire departments must
past, this was extremely difficult in both the prehospital and hospital settings. develop policies and procedures for
When confronted by a poisoned patient, especially one who came from an CO monitoring and subsequent treat-
environment where they were exposed to products of combustion, prehospi- ment if elevated CO levels are found.
tal personnel should attempt to distinguish the etiology. As discussed earlier, Historical trending of CO levels
the effects of CO poisoning and cyanide poisoning are extremely similar. For during prehospital care: High-
example, in a patient who presents with chest pain, altered mental status, dys- concentration oxygen therapy signifi-
rhythmias or shock, it’s often unclear whether the cause is cyanide or a large cantly increases the rate of carboxy-
dose of CO. Thus, the determination of a SpCO can help direct the best course hemoglobin elimination. Thus, it’s
of treatment. If the patient has a relatively high SpCO, then CO is more likely not uncommon for an EMS crew to
the cause (although this does not necessarily exclude concomitant cyanide detect an elevated SpCO in a patient,
poisoning). Likewise, if the patient has a relatively low SpCO but has signifi- provide high-concentration oxygen
cant signs and symptoms, cyanide may be more likely and hydroxocobalamin therapy during assessment and trans-
administration should be considered. In addition, high-concentration oxygen port, and subsequently deliver the
should also be provided, because both toxins are often present. patient to the ED with near normal
Firefighter monitoring & rehabilitation: It has always been thought that SpCO readings.
CO exposure is an occupational risk for firefighters. As more is learned about The ability to provide historical
the effects of CO, there’s a growing body of scientific evidence that shows that trending data (and patient docu-
mentation) will demonstrate to the
Figure 2 ED staff the degree of CO exposure
and the response to treatment. It’s
important to point out that this
goes beyond documentation issues.
Early high-concentration oxygen
administration can prevent many of
the serious effects (both short-term
and long-term) of CO poisoning.
On the other hand, there’s growing
IMAGE COURTESY MASIMO CORP.

evidence that indicates late admin-

istration of oxygen can induce the
formation of dangerous chemicals
called “oxygen free-radicals.” These
Light waves are processed to determine the percentage of carboxyhemoglobin present in the blood. harmful chemicals are thought to

march 2009 Trend Setters 7

be associated with many of the del-
eterious, and sometimes permanent,
effects of CO poisoning.
Epidemiological monitoring &
detection: As an example of how
important CO monitoring capa-
bilities are, we’ll look at a 2008
case involving firefighters in Walker
County, Ga., who were called to a
local brake factory after an employee
went home sick. On closer evalua-
tion, several workers exhibited signs
and symptoms of CO exposure. The
fire agency’s four-gas meter showed
markedly elevated levels of CO in the
factory. However, the source of the CO
was unclear.
The firefighters measured the
SpCO levels of the affected workers.
They then obtained a floor plan (pre-
plan) for the building and marked
where each worker had been and
the SpCO level found in that worker.
Through this method, they deter-
mined that workers in a certain area
of the building had a higher SpCO
than those in other areas. Once the
firefighters were able to localize
the area with high CO levels, they
investigated and determined that a
recently installed furnace was the CO
source. In addition, through Pulse
CO-Oximetry, they were able to
triage exposed patients and send
those with low SpCO levels home
while routing those with elevated
levels to the hospital for treatment.
This process and use of field tech-
nology allowed for a more appropriate
use of resources and reduced un-
necessary hospital costs and worker’s
compensation costs for the employer.
Thus, the informed use of Pulse CO-
Oximetry can, in certain situations,
be used to identify the source of a CO
exposure when the results of environ-
mental monitoring devices are unclear.
Summary
New and evolving technologies are
revolutionizing the practice of pre-
hospital care. The ability to monitor
beat-to-beat changes in a patient’s
condition allows EMTs and para-
medics to provide rapid and de-
finitive treatment. As we learn more
8 Trend Setters Journal of Emergency Medical Services (JEMS)
PHOTO COURTESY PHYSIO-CONTROL, INC.
Because high-concentration oxygen therapy helps the body eliminate carboxyhemoglobin, it’s not uncommon to
deliver a CO-exposed patient to the ED with near normal SpCO readings.
about the deleterious effects of CO, it is becoming increasingly clear that early
diagnosis and treatment makes a difference. This concept not only applies to
EMS patients, but also has significant applications in monitoring and main-
taining the health and safety of emergency personnel in dangerous fire and
industrial situations.
Bryan Bledsoe, DO, FACEP, is a board-certified emergency physician and clinical professor of emergency
medicine at the University of Nevada School of Medicine and the University Medical Center of Southern
Nevada. He’s a frequent contributor to JEMS and regular speaker at EMS conferences worldwide. Contact
him at bbledsoe@earthlink.net.
Mike McEvoy, PhD, RN, EMT-P, is the EMS coordinator for Saratoga County. N.Y., as well as a criti-
cal care nurse and an instructor in critical care medicine at Albany Medical College. He’s active in
firefighter health and safety research and a regular speaker at fire and EMS conferences. Contact him at
mcevoymike@aol.com.
Disclosure: Dr. Bledsoe serves as a consultant and speaker for Masimo and has reported receiving
honoraria from Masimo. Dr. McEvoy serves as a consultant and speaker for Masimo and has reported receiv-
ing honoraria from Masimo and Physio-Control, Inc.
REFERENCES
1. Kao LW, Nañagas KA: “Carbon monoxide poisoning.” Emergency Medicine Clinics of North America.
89:1161–1194, 2005.
2. Hampson NB, Stock AL: “Storm-related carbon monoxide poisoning: Lessons learned from recent
epidemics.” Undersea and Hyperbaric Medicine. 33:257–263, 2006.
3. Iheagwara KN, Thom SR, Deutschman CS, et al: “Myocardial cytochrome oxidase activity is decreased
following carbon monoxide exposure.” Biochimica et Biophysica Acta. 1772:1112–1116, 2007.
4. Alarie Y: “Toxicity of fire smoke.” Critical Reviews in Toxicology. 32:259–289, 2002.
5. Chee KJ, Nilson D, Partridge R, et al: “Finding needles in a haystack: Case series of carbon monoxide
poisoning detected using new technology in the emergency department.” Toxicology Review.
46:461–469, 2008.
6. Barker SJ, Curry J, Redford D, et al: “Measurement of carboxyhemoglobin and methemoglobin by pulse
oximetry: A human volunteer study.” Anesthesiology. 105:892–897, 2006.
7. Shepherd G, Velez LT: “Role of hydroxocobalamin in acute cyanide poisoning.” Annals of Pharmaco-
therapy. 42:661–669, 2008.
8. National Fire Protection Association: “NFPA 1584: Standard on the Rehabilitation Process for Members
During Emergency Operations and Training Exercises (2008 Edition).” NFPA: Quincy, Mass., 2008.
 By Bryan E. Bledsoe, DO, FACEP, & Mike McEvoy, PhD, RN, EMT-P

per kilogram. Following administra-

What Is
tion, the patient significantly im-
proves over the next 30 minutes. Her
cyanosis clears, and other signs and

Methemoglobin?
symptoms of methemoglobinemia
abate. She is monitored for 12 hours
and discharged home.

Introduction
What this level means in your patients & Hemoglobin, an iron-containing
why you should monitor it protein that transports oxygen, is
essential for life. It’s produced and
contained within the red blood cells

A
(erythrocytes), which constantly
An ambulance is dispatched to a local oral surgery clinic for a patient with circulate throughout the circulatory
difficulty breathing. The paramedic crew arrives promptly and is brought system, delivering oxygen to all body
back to a surgical room. The patient is a middle-aged female in respira- tissues. The typical lifespan of a red
tory distress and exhibiting marked cyanosis. The paramedics question blood cell is approximately 120 days.
the dentist and the dental assistant about the procedure. The patient was Hemoglobin is made up of four
being prepped to have a dental implant placed and some mucosal lesions protein chains—normally two alpha
removed with a laser. She had not yet been sedated, but the staff had (α) and two beta (β) chains. Each of
washed her mouth with 30 mL of a 20% benzocaine solution for mucosal the four chains contains an iron-
anesthesia. In addition, the dentist had also administered a mandibular based structure called a “heme.” The
nerve block with 2% lidocaine. heme structure is where oxygen binds
The patient was asymptomatic at the start of the procedures and later to hemoglobin. Thus, each molecule
began to complain of palpitations and shortness of breath. The dentist’s of hemoglobin can bind four mol-
office staff placed the patient on a pulse oximeter,
which showed an oxygen saturation (SpO2) of 89%
and a pulse rate of 140 beats per minute. On arrival,
the EMS crew found she was receiving oxygen at 2 L
per minute via a nasal cannula.
The crew examines the patient and finds marked
cyanosis, anxiousness and some chest discomfort.
They replace the nasal cannula with a non-rebreather
mask and increase the delivered oxygen concentration
to near 100%.
Despite these actions, the patient’s cyanosis persists,
as do her other signs and symptoms. ECG leads are
placed, and patient monitoring probes are applied.
The carbon monoxide screen (SpCO) is moderately
high at 14%. However, the methemoglobin level
(SpMet) is detected at 43%. The patient is questioned
about prior problems with local anesthetics and
denies any history of problems or reactions. She is a
non-smoker, has a carbon monoxide (CO) detector in
her home, and reports no recent activities that might
be associated with CO exposure.
The crew moves the patient to the ambulance and
notifies the local emergency department (ED) of the
high SpMet level. An IV line is placed, and she’s rap-
PHOTO KEVIN LINK

idly transported to the hospital. There, she’s promptly

evaluated by ED staff, who confirm the likely diagnosis
of methemoglobinemia. A 1% solution of methylene Increased levels of methemoglobin reduce the blood’s ability to transport oxygen,
blue is administered intravenously at a dose of 1 mg leading to hypoxia.

march 2009 Trend Setters 9

ecules of oxygen (O2). When oxygen
is bound to hemoglobin, the resultant or deficiency in the enzyme systems that convert (reduce) methemoglobin
molecule is called “oxyhemoglobin.”
When oxygen is not bound, the mol-
ecule is called “deoxyhemoglobin.”
Because heme is a metal (iron), it
contains an electrical charge. When
oxygen is not bound to the iron
molecule, the iron molecule is in the
ferrous (Fe2+) charge state. When oxy- others (see Table 1). These are typically oxidizing agents and will induce a
gen binds to the iron, a process called change in the charge state of the iron, thus forming methemoglobin.2
“oxidation” changes the charge to the
ferric (Fe3+) charge state. Iron in the
ferric state cannot bind oxy-
gen until it’s reduced back to
the ferrous state. This reaction
process is necessary to under-
stand in order to understand
methemoglobin (MetHb).
Methemoglobin is a form
of hemoglobin in which the
iron molecules are in the ferric
(Fe3+) state. Thus, methemoglo-
bin can neither bind nor trans-
port oxygen. Methemoglobin
has a bluish-brown color.
Normally, there are enzyme
systems (e.g., methemoglobin
reductase) that can restore
methemoglobin to the ferrous
(Fe2+) state, forming deoxy-
hemoglobin, so it can again
transport oxygen. Typically,
less than 2% of the hemoglobin
in the body is in the form of
methemoglobin and cannot
bind or transport oxygen.
However, several conditions
and drugs can cause abnormal
elevations of methemoglobin.1
Pathophysiology
Normally, methemoglo-
bin forms and disappears
without significantly af-
fecting the body. However,
because methemoglobin cannot
transport oxygen, hypoxemia will
steadily develop as methemoglobin
levels rise—a phenomenon called
“methemoglobinemia.” Two factors
can lead to elevated methemoglo-
bin levels. The first is the presence
of drugs that oxidize the iron on
hemoglobin (changing it from
a ferrous to a ferric state). This
10 Trend Setters Journal of Emergency Medical Services (JEMS)
causes an increase in methemoglobin production. The other is a problem
back to deoxyhemoglobin. This deficiency subsequently decreases the rate
of methemoglobin elimination. Typically, methemoglobinemia is the result
of both of these factors.
Methemoglobin results most frequently from toxic exposure. Several drugs
and toxins induce methemoglobin production, including drugs used for local
anesthesia (e.g., benzocaine, lidocaine), drugs used to treat cyanide poisoning
(e.g., amyl nitrite and sodium nitrite), certain antibiotics, nitroglycerin and
Some people are born with deficiencies in the enzyme systems that reduce
methemoglobin to deoxyhemoglobin. Typically, these people are identified at
birth because of persistent cyanosis.
Table 1: Agents Implicated in However, not all infants who develop
methemoglobinemia have enzyme
Acquired Methemoglobinemia deficiencies. In infants, methemoglobin-
Amyl nitrite (cyanide antidote) emia can result from systemic acidosis
Aniline derivatives (dyes) related to an infection, diarrhea or de-
Benzocaine (local anesthetic) hydration. Infants may also be suscepti-
Bismuth subnitrite (antiseptic) ble to oxidizing toxins. This appears to
Butyl nitrite (antianginal, recreational drug be more common in rural areas where
“poppers”) well water may contain a high level of
Chloroquine (anti-malarial) nitrates, usually from fertilizer runoff
Dapsone (anti-tubercular agent) and seepage into an aquifer.
Lidocaine (local anesthetic)
Menthol (local anesthetic) Signs & Symptoms
Naphthalene (mothball agent) As methemoglobin levels increase,
Phenytoin (anticonvulsant) the amount of normal hemoglobin
Nitric oxide (vasodilator) available for oxygen transport falls.
Nitroglycerin (antianginal) Eventually, signs and symptoms of
Nitrophenol (hydrocarbon, irritant) hypoxia will develop. Thus, the signs
Nitrates (antianginals) and symptoms of methemoglobin-
Nitrites (antianginals) emia depend on the percentage of
Paraquat (herbicide) methemoglobin (SpMet) present.
Phenacetin (older analgesic) Methemoglobinemia results in a
Phenols (aromatic hydrocarbons) functional anemia. This means that
Propellants (for room deodorizers) although total hemoglobin stores are
Pyridium (urinary tract anesthetic) normal, the amount of hemo­globin
Quinones (oxidizing agents) available to transport oxygen is
Silver nitrate (cauterizing agent) decreased (see Table 2, p. 12). Body
Smoke inhalation systems that are highly dependent
Sodium nitroprusside (antihypertensive) on oxygen, such as the nervous and
Sulfonamides (antibiotics) cardiovascular systems, are usually
the first and most profoundly affected
as methemo­globinemia develops.
The signs and symptoms of methemoglobinemia are quite similar to the
signs and symptoms of CO poisoning. The similarity in patient presentation
is due to the fact that both conditions decrease the oxygen-carrying capacity
of the blood by increases in abnormal hemoglobin types. When methemoglo-
binemia and carbon monoxide poisoning occur concomitantly, the signs and
symptoms of hypoxemia increase markedly.
Non-Invasive Technology
Methemoglobin levels can be measured through a multi-function Pulse
CO-Oximetry finger probe, if the methemoglobin module is installed in your
 monitor (see Figures 1 and 2). Pulse CO-Oximeters use multiple wavelengths istered if SpMet levels are measured.
of light to measure and distinguish the various types of hemoglobin present (de- The nitrites can cause dangerous
oxyhemoglobin, oxyhemoglobin, carboxyhemoglobin and methemoglobin). The elevations in selected individuals,
Pulse CO-Oximeter processes the data and reports oxygen saturation (SpO2), particularly children and women, and
carboxy­hemoglobin percentage (SpCO) and methemoglobin percentage (SpMet). can now be monitored (see Figure 3).
These findings allow personnel to exclude methemoglobinemia as a diagnosis. If Thus, prehospital methemoglobin
methemoglobinemia is present, it will allow for ongoing measurement. monitoring is valuable in cases involv-
Additionally, as seen in the case example, the presence of methemoglo- ing persistent cyanosis, nitric oxide
binemia falsely elevates reported Pulse CO-Oximeter SpCO values. The and nitrate therapy, administration of
LIFEPAK 15 can record SpMet trends for intervals up to eight hours. There- a cyanide antidote kit, elevated SpCO
fore, these data can be printed out in a prehospital patient summary to show readings and risk of inflammation.
ED staff any trends and changes in the patient’s condition that occurred in Persistent cyanosis: Most cyanotic
the field setting. This capability is especially valuable when the prehospital patients will respond favorably to
treatment improves or eradicates a patient’s methemoglobinemia. supplemental oxygen administration.
However, in those that do not, elevated
Patients to Monitor methemoglobin levels should be
Although methemoglobinemia is relatively uncommon, prehospital personnel considered a cause, because elevated
will be increasingly likely to encounter it. First, the development of freestand- methemoglobin levels can be treated
ing surgical centers has resulted in more patients receiving local and general with a relatively safe antidote.

Figure 1: LIFEPAK 15 Monitor/Defibrillator* Trend Summary of SpMet

COURTESY PHYSIO-CONTROL, INC.

*Pending 510(k) Clearance

Figure 2: LIFEPAK 15 Monitor/Defibrillator Tracing of SpMet

*
COURTESY PHYSIO-CONTROL, INC.

*Pending 510(k) Clearance

anesthesia outside of the traditional hospital setting. Second, because of Most cases of methemoglobine-
hospital specialization, critically ill or injured patients are often transported mia encountered in the prehospital
between facilities, and some of these patients are receiving medications (e.g., setting will be due to the effects
sodium nitroprusside, nitric oxide, nitroglycerin) that can induce methemo- of drugs and toxins. Elevated
globinemia.3 Methemoglobin monitoring of these patients provides an added methemoglobin levels have been
margin of safety during critical care transport. detected following the administra-
Third, the use of older cyanide antidotes (amyl nitrite and sodium nitrite), tion of benzocaine, lidocaine and
which purposely induce methemoglobin formation, can be more safely admin- other local anesthetics. In one study,

march 2009 Trend Setters 11

signs and symptoms of hemoglobin to
typically developed Table 2: Signs & Symptoms of Methemoglobinemia methemoglobin
within 20 minutes. (changes the heme
SpMet Signs and Symptoms
SpMet concentra- groups from the
1–3% Normal, asymptomatic
tions ranged from ferrous [Fe2+] to the
3–15% Slight grayish-blue discoloration
19–75%. Deaths ferric [Fe3+] state).
15–20% Cyanotic, but asymptomatic
were reported.4 Cyanide then pref-
25–50% Headache, dyspnea, confusion, weakness, chest pain
Other drugs, such erentially binds to
50–70% Altered mental status, delirium
as certain antibiot- methemoglobin in-
>70% Fatal
ics, can also induce stead of cytochrome
methemoglobinemia. oxidase, thus freeing
Nitric oxide & nitrate therapy: up cytochrome oxidase for energy production by the cells. The third
Nitric oxide (NO) therapy is often step in the cyanide antidote kit, sodium thiosulfate, converts cyano­
used to treat newborns with hy- methemoglobin to normal hemoglobin and thiocyanate. Thiocyanate is
poxic respiratory failure (HRF). subsequently excreted.
NO is administered as a gas and However, because methemoglobin cannot transport oxygen, the oxygen-
causes pulmonary vasodilation carrying capacity of the blood falls as methemoglobin levels rise. This is
through smooth muscle relaxation. especially important in patients who are small (e.g., children and women) or
This serves to increase the partial have pre-existing disease. In addition, concomitant poisoning with carbon
pressure of oxygen in arterial blood monoxide will further decrease the oxygen carrying capacity of the blood as
(PaO2). Some centers are starting to carboxyhemoglobin levels (SpCO) rise. Because of these factors, it’s prudent to
use NO in adults with adult respira- measure both SpMet and SpCO levels when administering the nitrite compo-
tory distress syndrome (ARDS). NO nents of the cyanide kit. Of note, the cyanide antidote hydroxocobalamin does
induces the oxidation of hemoglobin not induce methemoglobinemia.6
to methemoglobin. Thus, it’s impor- Elevated SpCO readings: A phenomenon seen with Pulse CO-Oximetry
tant to monitor methemoglobin lev- technology is a tendency to report falsely elevated CO readings in the presence
els during NO therapy—especially of significant methemoglobinemia. SpCO readings are not considered reliable
in neonates in whom levels of fetal when SpMet levels exceed 5%. A valuable benefit of Pulse CO-Oximetry then
hemoglobin (HgF) are elevated. Ide- is that low SpMet readings can be used to confirm the accuracy of significant-
ally, SpMet levels should be kept at ly elevated SpCO measurements.
less than 5%.5 Risk of inflammation: The free-radical compound nitric oxide (NO) is
Several other drugs used in the produced when hemoglobin is converted to methemoglobin. Methemoglobin
critical care setting can induce releases free heme and iron, which activate the cells that line blood vessels
methemoglobin formation. The (endothelial cells). These cells release NO, causing an inflammatory response.
most commonly encountered of This inflammatory response, initiated by NO and other free radicals, is a cas-
these are sodium nitroprusside and cade of events called “oxidative stress.” Oxidative stress has been linked to the
nitroglycerin. Sodium nitroprus- development of numerous conditions, including atherosclerosis, heart disease,
side is used to lower blood pressure. Alzheimer’s disease, Parkinson’s disease and other chronic conditions. Measure-
Nitroglycerin is used for angina ment of SpMet levels, especially over time, may help identify those at increased
and is a vasodilator and subse- risk of oxidative stress and the subsequent problems associated with it.
quently decreases cardiac work.
When administered at doses often Treatment
encountered in the critical care Patients found to have elevated methemoglobin levels but who are as-
setting, both of these drugs can ymptomatic should be treated conservatively with supplemental oxygen
lead to methemoglobin formation. and monitoring. However, patients with elevated SpMet levels (generally >
As methemoglobin levels rise, the 20–30%) who are symptomatic may benefit from antidotal treatment. The
amount of hemoglobin available for antidote for methemoglobinemia is the dye methylene blue. Methylene blue
oxygen transport falls. This can be reduces methemoglobin to deoxyhemoglobin. Thereafter, the dye is recycled.
problematic in patients with severe The typical dose of methylene blue is 1–2 mg per kilogram body weight in-
cardiac or respiratory disease and fused intravenously over three to five minutes. It’s supplied in a 1% solution
who are otherwise highly dependent (10 mg/mL).
on adequate oxygen delivery. The decision to administer methylene blue in the prehospital setting is
Cyanide antidote: The first two one of local medical directors and should consider patient acuity mix and
components of the cyanide anti- transport times. It’s important to point out that methylene blue is a dye
dote kit (amyl nitrite and sodium and following administration, pulse oximeters and laboratory instruments
nitrite) induce the conversion will register erroneous readings for a short period of time (usually less than

12 Trend Setters Journal of Emergency Medical Services (JEMS)

 Figure 3: Methemoglobinemia Diagnosis Strategy
cyanotic patient

newborn child or adult

respiratory disease YES improves with improves with YES respiratory disease
heart disease oxygen oxygen heart disease

NO

cyanotic heart disease oxygen

severe repiratory LOW saturation NO
disease sp02

HIGH

other diagnosis LOW methemoglobin methemoglobin LOW other diagnosis

monitor monitor

HIGH HIGH

oxidant drug exposure oxidant drug exposure

enzyme deficiency severe YES methylene blue methylene blue YES well water nitrates
acidosis response response severe acidosis

NO NO

other diagnosis other diagnosis

20 minutes). Using a Pulse CO-Oximeter can help avoid drawing repeated REFERENCES
blood samples by providing continuous monitoring of SpO2 and SpMet 1. Wright RO, Lewander WJ, Woolf AD: “Methemo-
levels once the effects of the dye subside. globinemia: Etiology, pharmacology, and clinical
management.” Annals of Emergency Medicine.
Summary 34:646–656, 1993.
Methemoglobinemia, although uncommon, is a concern for EMS providers— 2. Umbreit J: “Methemoglobin—It’s not just
especially during critical care transport. The ability to measure and monitor blue: A concise review.” American Journal of
SpMet levels in the prehospital setting allows for more definitive care, an Hematology. 82:134–144, 2007.
improved safety margin for the patient, and better documentation for the 3. Alapat PM, Zimmerman JL: “Toxicology in the
providers and medical staff. As with all monitoring technologies, it’s wise Critical Care Unit.” Chest. 133:1006–1013,
to consider these findings with the overall patient condition and physical 2008.
exam findings. 4. Abu Laban RB, Zed J, Purssell RA, et al: “Severe
methemoglobinemia from topical anesthetic
Bryan Bledsoe, DO, FACEP, is a board-certified emergency physician and clinical professor of emergency spray: Case report, discussion and qualita-
medicine at the University of Nevada School of Medicine and the University Medical Center of Southern tive systematic review.” Canadian Journal of
Nevada. He’s a frequent contributor to JEMS and regular speaker at EMS conferences worldwide. Contact Emergency Medicine. 3:51–56, 2001.
him at bbledsoe@earthlink.net. 5. Ware LE: “Inhaled nitric oxide in infants and
Mike McEvoy, PhD, RN, EMT-P, is the EMS coordinator for Saratoga County. N.Y., as well as a critical care nurse children.” Critical Care Nursing Clinics of North
and an instructor in critical care medicine at Albany Medical College. He’s active in firefighter health and safety America. 14:1–6, 2002.
research and a regular speaker at fire and EMS conferences. Contact him at mcevoymike@aol.com. 6. Geller RJ, Barthold C, Sairs JA, et al: “Pediatric
Disclosure: Dr. Bledsoe serves as a consultant and speaker for Masimo has reported receiving cyanide poisoning: Causes, manifestations,
honoraria from Masimo. Dr. McEvoy serves as a consultant and speaker for Masimo has reported receiving management, and unmet needs.” Pediatrics.
honoraria from Masimo and Physio-Control, Inc. 118:2146–2158, 2006.

march 2009 Trend Setters 13

 By Patricia A. Brandt, RN, BSN, MHR

As your partner tries to get ad-

Universal
ditional medical history from the
mother, you approach the teen,
who’s leaning forward in the classic

Capnography
tripod position, gasping for breath
and clutching her inhaler. When you
ask how many times she has used
the inhaler, she manages to force out
a single word —“lots.”
A vital asset that can improve While you offer reassuring words,
patient care on almost any call you simultaneously attach the leads
to the monitor, place the pulse oxi-
metry probe on her finger and begin

Y
oxygen administration.You also
You’re on a 24, and as the end of your shift approaches, you marvel at how apply a nasal filterline, which you
quiet it has been. Then, you mentally kick yourself for eliciting the “quiet attach to the capnography outlet of
jinx,” because moments later, you’re dispatched to a severe difficulty breath- your monitor.
ing call. On arrival, you’re met by the patient’s mother, who frantically tells The monitor shows sinus
you her 15-year-old daughter can’t breathe. The mother, nearly hysterical, tachycardia at a rate of 140 and
says the girl has recently been evaluated by the doctor for asthma. an oxygen saturation reading of
98%, which at one time would have
been a reassuring sign. However,
your newly acquired knowledge of
capnography, along with the very
sharp shark-fin waveform on the
monitor’s capnography display and
an end-tidal CO2 (EtCO2) reading
of 70, give you reason to think oth-
erwise. Your partner has already set
up an updraft treatment, and you
begin to administer the broncho-
dilator immediately. After several
minutes, although your patient’s
respiratory rate has decreased,
the ominous shark-fin waveform
and elevated EtCO2 reading—now
78—remain.
You recognize the decreased respi-
ratory rate is not a sign of improve-
ment from the updraft but instead a
warning that your patient is becom-
ing extremely tired from trying to
maintain adequate oxygenation.
Although your protocols allow for
a second updraft, you know you’re
running out of time and choose to
contact medical control to obtain
PHOTO courtesy PHYSIO-CONTROL, INC.

orders for the administration of

magnesium sulfate IV. Upon receiv-
ing the required order, you admin-
ister it, and the patient’s breathing
eases within minutes.You’re also
Because it provides real-time assessment of respiratory, circulatory and metabolic status, capnography is an
relieved to see the more normal
incredibly important assessment tool in a multitude of emergency conditions. box-like capnography waveform and

14 Trend Setters Journal of Emergency Medical Services (JEMS)

 in the cardiac arrest patient to help
to determine the effectiveness of
Figure 1: Normal Capnography Waveform CPR compressions, recognize the
return of spontaneous circulation
and assist with decisions regarding
End-Tidal the termination of resuscitation.3
D In addition to being an essen-
C tial assessment tool in intubated
patients, capnography has been
B shown to be an extremely valuable
A
technology to use in non-intubated
patients. It provides EtCO2 readings
and exhibits the related waveform.
A–B: Respiratory baseline C–D: Expiratory plateau The configuration of this waveform
B–C: Expiratory upslope D: End-tidal value can be used in the intubated and
non-intubated patient to assess the
adequacy of ventilation, status of
metabolic activity and effective-
ness of circulation. The normal
Figure 2: Hyperventilation capnogram will consist of box-like
waveforms directly related to the dif-
ferent phases of the respiratory cycle
RR EtCO2 (see Figure 1).
Patients who are hyperventilating
Normal will have a capnogram with a faster
rate but lower amplitude of wave-
forms, resulting from the decreased
45 CO2 in each breath (see Figure 2).
Patients who are hypoventilating
0 will have a lower rate but a higher
amplitude of waveforms, resulting
Hyperventilation from the increased amount of CO2
45 being released with each breath (see
Figure 3).
The final basic capnographic
waveform results from the physi-
0 ological effects of bronchospasm.
Bronchospasm causes a slower and
more erratic emptying of CO2 from
an EtCO2 reading of 45, which confirm a significant resolution of the severe the alveoli, which results in a slower
bronchospasm. rise in the expiratory upstroke.
Instead of the normal box-like wave-
Powerful Capabilities form, the presence of bronchospasm
Capnography is the monitoring of CO2 concentration in respiratory gases. results in the characteristic shark-fin
Because capnography provides a real-time assessment of respiratory, circula- shape of the bronchospastic wave-
tory and metabolic status, it can be an incredibly important and powerful form (see Figure 4).
assessment tool for determining patient status, appropriate treatment and
treatment effectiveness for a multitude of emergency conditions.1 The vast Respiratory Emergencies
majority of patients with emergent conditions will benefit from capnography. Patients with asthma and chronic
Initially, capnography was primarily used by anesthesiologists to monitor obstructive pulmonary disease
the respiratory status of mechanically ventilated patients in the operating (COPD), as in the opening case
room. But eventually, for this same purpose, it was adopted in the field. study, can be monitored for the pres-
Using capnography to ensure successful intubation has become the gold ence and severity of bronchospasm
standard and is mandated in many EMS systems. The detection of CO2 on and the choice and effectiveness of
expiration is a completely objective confirmation of tracheal intubation.2 treatment. Patients who are sedated
Also, because capnography directly correlates with cardiac output, it’s useful or receiving pain management can

march 2009 Trend Setters 15

be monitored for hypoventilation, Figure 3: Hypoventilation
and capnography can assist in deci-
sions regarding continued adminis-
tration of sedatives or pain control.4 RR EtCO2
Decisions regarding the need for
intubation or assisted ventilation
Normal
for the overdose patient can also be
guided by capnography. 45
Patients who are hyperventilat-
ing and exhibiting anxiety can be 0
particularly difficult diagnostic
categories. Capnography can provide
Hypoventilation
assistance in determining a working 45
diagnosis, because hyperventilation
with normal or high EtCO2 levels is
0
much more likely to reflect pathol-
ogy, whereas hyperventilation with
low EtCO2 levels is more likely to
reflect anxiety. The capnography
waveforms can even be used as a
biofeedback technique when coach-
Figure 4: Bronchospasm
ing the anxious patient to decrease
their respiratory rate. Normal
45
Metabolic Emergencies
Capnography can also be useful in 0
evaluating diabetic ketoacidosis
and helping to differentiate diabetic
ketoacidosis and hyperglycemic hy- Bronchospasm
perosmolar non-ketotic coma. It can 45
also aid in determining treatment
for sympathomimetic overdoses, 0
including the administration of ben-
zodiazepines (which can be guided
by increases in EtCO2).
The severity of hypothermia and
hyperthermia can be determined by Capnography should be carefully monitored in the patient with acute
capnography and clinical decision myocardial infarction to evaluate the impact on cardiac output. It can be
making can be adjusted. Even the especially useful in the patient who may need pressor support or fluid chal-
severity of metabolic acidosis associ- lenges in order to assess the effectiveness and need for increased or contin-
ated with gastroenteritis, especially ued administration. Patients with inferior wall myocardial infarction with
in children, can be determined with right ventricular involvement may obtain enhanced benefit from this moni-
the use of capnography. toring, because they may often require large amounts of infused fluids to
maintain adequate blood pressure. In this case, capnography would reflect
Circulatory Emergencies changes in cardiac output even prior to blood pressure improvement.
The presence of bronchospasm in
the congestive heart failure (CHF) Future Uses
patient can be assessed with cap- Research into expanded uses of capnography is ongoing and may reveal
nography. It can be especially use- even more evidence-based uses. The EMS community has recognized the
ful in the patient with co-existent exciting potential for capnography to be used as a primary assessment
CHF and COPD. If bronchospasm tool in many emergency situations, such as detection of pulmonary emboli,
isn’t present, the unnecessary sepsis, thyrotoxicosis and malignant hyperthermia.5 Other areas that appear
administration of bronchodila- promising include the use of capnography to regulate CO2 levels for patients
tors can be avoided, and their with head injury and stroke.
potentially harmful cardiac effects Capnography is also being studied as a way to continually assess the re-
prevented. spiratory status during seizures and in patients who have undergone neuro-

16 Trend Setters Journal of Emergency Medical Services (JEMS)

muscular blockade. Its use has even been suggested in the triage of patients
involved in a bioterrorism event. Its practical uses are almost limitless.
Another Case
Let’s take a look at another scenario, this one involving a trauma patient.
As you arrive on scene at a single vehicle crash, you note an SUV had
apparently lost control on the wet road and impacted a light pole with
moderate force. The driver appears somewhat dazed but responsive and
still restrained by his lap and shoulder belt.
His initial vital signs are a BP of 120/70, HR of 72 and RR of 16.Your
head to toe assessment reveals the telltale red seatbelt marks across his chest
and abdomen. There are no other obvious signs of injury.
As you maintain C-spine immobilization, you contemplate the transport
destination.You’re about two miles from a community hospital and about
12 miles from the Level 1 trauma center. The patient doesn’t meet any of
the criteria to mandate transport to the trauma center, so as you begin to
attach the monitor leads and apply oxygen via nasal cannula per your EMS
protocols, you suggest transporting to the closer hospital.
As the capnography from the nasal filterline initializes, you note a normal
capnography waveform with a low EtCO2 reading of 30 mmHg. This imme-
diately concerns you because the patient’s respiratory rate continues to be at
an apparently normal rate of 16.
As you start en route, you note that the EtCO2 has dropped to 28.You
recheck the BP and note a systolic blood pressure of 110, but due to the fur-
ther decrease in EtCO2, you divert to the Level 1 trauma center because you
know that blood loss and the resulting decrease in cardiac output transports
less CO2 to the alveoli and causes an almost immediate drop in EtCO2.
On arrival, the patient is immediately triaged to the trauma room where
an abdominal tap confirms intra-abdominal bleeding. The patient is emer-
gently transferred to the OR. Once again capnography has helped you
identify a significant vital sign variance and provide the highest level of care
to your patient.
In Conclusion
Hopefully this article has increased your interest in the use of capnography
in not only the intubated but also the non-intubated patient. Watch for a
Orange County Fire Rescue Department
The Prototype Agency for Universal Capnography
Orange County (Fla.) Fire Rescue Department (OCFRD), with 1,200
firefighter/EMS personnel, is the 25th largest fire department in the
nation. It was also one of the first departments to embrace universal
capnography, having used it for intubated and non-intubated patients
since 2002.
“Orange County Fire Rescue EMTs and paramedics rely on
capnography as one of their most important assessment tools,” states
EMS Battalion Chief Jose P. Gainza Jr. “They know that the real-time,
objective information that they get from capnography regarding the
patient’s respiratory, circulatory and metabolic status can have a big
impact on their treatment decisions and ultimately impact the patient
outcome in a very positive way.” That’s why the Fire Chief Carl Plaugher
and their medical director, Dr. George Ralls, a former firefighter/para-
medic himself, are so committed to its use.
march 2009 Trend Setters 17
complete capnography learning
program to be sponsored by Physio-
Control, Inc. in the near future.
Pat Brandt has worked in EMS for more than 25
years as an EMS transport nurse, an emergency
department nurse, a paramedic educator and as
an EMS quality manager. Recently retired from
Orange County (Fla.) Fire Rescue Department,
she now leads her own medical education and
consulting business in Dunlap, Tenn. Contact her
at brandtp@bledsoe.net.
Disclosure: The author has reported receiving
honoraria and/or research support, either directly
or indirectly, from Physio-Control, Inc.
REFERENCES
1. Eipe N, Tarshis J: “A system of classification for
the clinical uses of capnography.” Canadian
Journal of Anesthesia. www.cja-jca.org/cgi/
content/full/54/suppl_1/44578
2. American Heart Association: Currents, Winter
Edition 2005–2006.
3. Levine RL, Wayne MA, Miller CC: “End-tidal
carbon dioxide and outcome of out-of-hospital
cardiac arrest.” The New England Journal of
Medicine. 337(5):301–306, 1997.
4. Krauss B, Hess D: “Capnography for procedural
sedation and analgesia in the emergency
department.” Annals of Emergency Medicine.
50(2):172–181, 2007.
5. Blonshine S: “Expanding the knowledge base:
New applications of capnography.” AARC Times.
February 1999. 51–53.
Capnography is mandatory per protocol for all intubated and
artificially ventilated patients and all patients who are chemically
or physically restrained. It’s also a component of almost every other
treatment protocol, including all patients with respiratory distress,
chest pain, decreased level of consciousness and trauma, and any
patient receiving sedation or pain management. OCFRD facilitates this
with the use of 167 capnography-equipped LIFEPAK 12 monitors.
Every rescue and fire apparatus in the department carries a
LIFEPAK 12 with capnography capabilities to ensure that those assess-
ment tools are available to every patient in an expedient manner. In
addition, all oxygen nasal cannulas have been replaced with Oridion
combination filterlines that deliver oxygen and provide capnography
through the same cannula. Universal capnography is literally a way of
life at OCFRD.
 By Tim Phalen

classic chest pain to obtain an ECG.

More than a
So the original question remains,
“Who should get a 12-lead?”
One approach to consider is

Trend
shown in Figure 1. This approach is
offered not as a protocol recommen-
dation, but rather as a starting point
for discussion and critical thinking.
In reviewing Figure 1, it’s obvious
Maximizing the potential of the that all cardiac chest pain patients
prehospital 12-lead ECG should have a 12-lead. However, not
all anginal equivalents and atypi-
cal pain presentations necessarily

M
require a 12-lead.
Most EMS providers are aware of the increased attention hospitals are giv- When faced with an anginal equiv-
ing the prehospital 12-lead ECG. Although they’ve been around for years, alent or atypical pain presentation, it’s
recent research, recommendations and reimbursement structures have led to worthwhile to recall the three groups
the increased use and valuation of 12-lead ECGs within the hospital. With of patients most likely to present in
this renewed interest, it’s appropriate to examine strategies to maximize the a non-classic manner: the elderly,
benefits of prehospital 12-lead ECGs. females and diabetics. Therefore, you
In terms of improving ST-elevation myocardial infarction (STEMI) care, should seriously consider obtain-
two goals are primary: First, increase the number of identified STEMI pa- ing a 12-lead when you encounter a
tients and, second, reduce the time to treatment. The answers to the follow- non-classic presentation in an elderly
ing questions will shed light on strategies to improve EMS contribution to female or diabetic patient.
STEMI care. Although the questions may appear overly simplistic, they may As a final double-check before
yield some surprising answers. deciding against a 12-lead, use your
own clinical instinct. If you have
Who Gets a 12-Lead? a gut feeling this patient might be
EMS agencies have chest pain protocols. However, according to one study of experiencing AMI, run a 12-lead.
more than 434,877 patients with a discharge diagnosis of acute myocardial No harm will result from obtaining
infarction (AMI), 33% had no chest pain.1 By implication, if EMS uses chest it. Similarly, it may be fruitful to ask
pain exclusively to “suspect AMI” and run a 12-lead, then one-third of AMIs about obvious cardiac risk factors.
could be missed. When using this or a similar
To maximize the likelihood of catching STEMI on the 12-lead, it’s approach, the number of 12-leads
necessary to go beyond chest pain as the only patient complaint that would obtained will certainly increase, but
prompt a 12-lead ECG. So what other complaints should raise suspicion of hopefully so will the number of iden-
possible AMI? Table 1 lists some “pain equivalents,” or anginal equivalents, tified STEMIs. Remember, finding
associated with AMI and STEMI. STEMI is like panning for gold:You
Beyond the anginal equivalents, many AMI patients have pain that
may not immediately seem cardiac in nature. Chest pain that’s inter-
mittent, sharp, low intensity or not sub-sternal may be attributed to a Anginal Equivalents
Table 1:
variety of other conditions. However, although costracondritis, pleurisy Associated with AMI & STEMI
and other conditions may indeed produce these types of complaints, they
don’t preclude AMI. Aside from “non-cardiac sounding” chest pain, many Respiratory distress
AMI patients complain of pain to the abdomen, jaw, shoulder, teeth and Sense that something is “wrong”
elbow. All of these can be categorized as “atypical pain” presentations. “Weakness”
Certainly, not all atypical pain is from AMI; in fact, only a minor- “Fatigue”
ity of these complaints are due to myocardial infarction. When these “Dizziness”
complaints are encountered, however, we must seriously consider the “Malaise”
possibility of AMI. “Syncope or near syncope”
With the extensive list of anginal equivalents (pain-free but not com- Alterations in blood sugar
plaint-free) and atypical pain presentations (some pain present but not Alterations in level of consciousness
“classic” cardiac pain), it may seem that everyone should be getting a 12- (particularly in the elderly)
lead ECG. Obviously, not everyone needs a 12-lead, but we can’t wait for

18 Trend Setters Journal of Emergency Medical Services (JEMS)

Figure 1: Who should get a 12-lead? For example, a patient may have
an isolated posterior wall infarc-
tion. In that case, the 12-lead
~ 50%

~ 15%

~ 35%
Classic Chest Pain Atypical pain Anginal equivalents ECG may show some depression
in the range of V1 to V3 or even
V4 but would not demonstrate ST
elevation. If additional leads were
Female? obtained from the patient’s back,
Elderly? ST elevation might be found.
Diabetic?
NO Figure 3 shows an example
YES
of when an initial 12-lead did
not show ST-segment elevation.
However, the paramedic on the call
Cardiac Risk factors?
YES Clinical Instinct? suspected AMI clinically and noted
the ST depression in the range of
V1–V4. This prompted the acquisi-
Obtain a 12-lead ECG tion of V4r (of the right ventricle)
and V8–V9 (of the posterior wall).
Because the additional leads were
obtained, this STEMI was identified
don’t expect to find a gold nugget in every pan, but when you do find one and directed for reperfusion.
it’s worth all the effort. Likewise, it can be expected that most 12-leads will
not identify STEMI; however, when STEMI is identified, and time to treat- How Often Do Changes
ment is shortened, mortality and morbidity will decrease. Occur & Why?
A clear answer is still emerging, but
When Do You Obtain the 12-Lead? departments have reported a range
Getting early and (preferably) sequential ECGs can help improve the rate of 7–34% of prehospital 12-lead
of STEMI recognition. Examine the 12-lead ECGs in Figure 2. Both trac- ECGs capturing dynamic changes in
ings were obtained at the scene of a suspected AMI. ST elevation is obvious STEMI. Although not necessarily
in the first ECG, but it
disappeared only 12 Figure 2: If at First It’s Normal ... Keep Your Eye On It
minutes later when the
second ECG was taken.
Obviously, if efforts had
been limited to a single
ECG in the field, STEMI
recognition may have
been delayed.

How Many Leads?

Although the 12-lead
ECG is currently the
best, most available,
most economical, most
informative screening
tool for STEMI, it’s not
perfect. The 12-lead ECG
has two “blind spots.”
COURTESY MARIN COUNTY (CALIF.) FIRE DEPARTMENT

The 12-lead ECG doesn’t

directly “see” the right
ventricle or the posterior
wall of the left ventricle.
Additional leads can be
used to allow health-care
providers to screen for
STEMI in those areas. The first ECG was non-diagnostic, but the second ECG—taken only 12 minutes later—identified a STEMI with elevation in V1–V4.

march 2009 Trend Setters 19

representative of all Figure 3: More Leads Is Sometimes Better
response-area demograph-
ics, the findings of one
community are summa-
rized on Figure 4. In this
case, 34% of the STEMI
patients had either ST
elevation that was gone
in later ECGs or had ST
elevation present only in
later ECGs.
Dynamic ischemic
changes on an ECG can
result from many potential
causes. It may be impos-
sible to tell exactly which
is responsible in any given
situation, but here are a

COURTESY PERSON COUNTY EMS

few possibilities.
Infarct is dynamic
in nature: An ongo-
ing interplay of fac-
The first ECG is an initial 12-lead that did not show ST-segment elevation. However, because the paramedic suspected AMI clinically
tors contributes to and noted the ST depression in the range of V1–V4, additional leads were obtained (V4r and V8–V9), and this STEMI was identified
ECG changes. Among and directed for reperfusion.
them are variations in
myocardial oxygen demand and transient changes can
chemical factors in the clotting make a difference.
process, which can induce coronary Better recognition
artery vasoconstriction. For these of STEMI: The ECG
and other reasons, ST changes can changes associated
occur simply as part of the infarct with AMI and STEMI
process. can be dynamic. Serial
EMS treatment: Oxygen has been (consecutive) ECGs can
shown to reduce or eliminate ST increase the likeli-
change.2 In addition, nitroglycerin hood of catching those
can dilate the target coronary artery changes. Researchers
and also reduce or eliminate ST have determined that,
elevation.3 when compared with
Vasospastic angina: Prinzmetal’s the initial 12-lead ECG
angina results from coronary artery at emergency depart-
vasospasm. During episodes of ment (ED) presentation,
vasospasm, the ST segment typically ST monitoring improves
PHOTO courtesy physio-control, inc.

elevates. Nitroglycerin often relieves the sensitivity and

the vasospasm and the ST eleva-
tion along with it. Trending can help
capture this (see sidebar, p. 22).
Do ECG Changes
Matter?
Transient changes on the ECG are
more than just interesting little
quirks of electrocardiography. In
some cases, they can completely
alter the diagnosis and resulting
treatment, and there are several
specific ways that the presence of
specificity in recogniz-
ing acute coronary
syndrome (ACS) and
AMI. In the case of
Dynamic ECG changes are one criterion used to identify high-risk AMI, one study has
unstable angina patients. shown that diagnostic
sensitivity improved
from 55.4% in the initial ECG to 68.1% with serial ECGs.4,5
Improved identification of reperfusion candidates: Not all infarct
patients improve with immediate reperfusion. STEMI is the primary indi-
cation that a patient would benefit from either fibrinolytics or percutane-
ous intervention (PCI), such as angioplasty and stenting. Serial ECGs help
better identify not only MI, but also the subset of infarct patients who are

20 Trend Setters Journal of Emergency Medical Services (JEMS)

candidates for immediate reperfusion.
The 2004 ECC Guidelines make serial ECGs a Class I recommenda- Patients with
Table 2:
tion in the ED: “If the clinical ECG is not diagnostic of STEMI but the Treatment Time of
patient remains symptomatic and there is a high clinical suspicion for
STEMI, serial ECGs at five- to 10-minute intervals or continuous 12- 90 Minutes or Less
lead ST-segment monitoring should be performed to detect the potential
development of ST elevation.”3 Patients with no 12-lead ECG 37.5%
LBBB & other confounding patterns: Left bundle branch block Patients with 12-lead presented
at arrival 51.0%
(LBBB) frequently causes ST elevation when no infarct exists and, Patients with STEMI Alert
in that sense, is an imitator of infarct. However, AMI can also pro- from field 85.7%
duce a new onset LBBB, and in that setting immediate reperfusion
is indicated.
Unfortunately, it can be difficult to determine if the presence of LBBB To date, little work has been
on the ECG of a suspected AMI patient is pre-existing or is a new onset. done to determine the number of
If the LBBB is infarct-induced, it has a high mortality rate—up to 60%. patients whose diagnosis or treat-
Therefore, the patients who may need reperfusion the most are the least ment decision could be made from
likely to receive it. However, dynamic changes on serial ECGs shed light information exclusively present on
on the situation. A hallmark of infarct is change over time. If a patient has the prehospital ECG. However, one
had an LBBB for the past 15 years, it’s not likely to change much during recent study looked at how often
the next 15 minutes. But when changes occur in a short period of time, the prehospital 12-lead contained
suspect AMI. information that would identify
When AMI is suspected clinically, LBBB is present on the 12-lead and high-risk unstable angina patients. It
changes are observed in serial ECGs, then new onset LBBB is presumed found that 22% of patients with ACS
to be infarct-induced. Such patients are potential candidates for immedi- (not necessarily AMI or STEMI) had
ate reperfusion. evidence of ischemia that was not
Better identification of high-risk unstable angina: AMI and STEMI are present on arrival at the hospital.6
two points on the continuum of ACS. Another point on that continuum is This is an important finding.
unstable angina. In this condition, the coronary artery is often blocked by
a blood clot but shows no evidence of tissue death. Hence, it can’t be called How Do You Communicate
infarction. Treatment of unstable angina varies depending on certain find- Your ECG Findings?
ings. High-risk unstable angina patients, although not eligible for immediate Once specific ECG findings sug-
reperfusion, may receive an urgent catheterization. Dynamic ECG changes gest STEMI has been identified,
are one criterion used to identify high-risk unstable angina patients. minutes matter. It’s imperative to
communicate that the patient is a
potential candidate for immediate
Figure 4: Prehospital Serial ECGs & Final Diagnoses reperfusion. Some possible commu-
nication strategies include present-
ing the 12-lead at arrival or using
12-lead obtained
on 9,087 the radio to alert the receiving
EMS patients facility of your ECG findings and
transmitting the ECG.
Several studies have looked
at various strategies. One recent
8,796 patients = 331 patients =
No ECG evidence ECG evidence example of the importance of early
of STEMI of STEMI notification demonstrated the results
shown in Table 2.
When deciding which commu-
102 (31%) = STEMI nication strategy works best for a
detected to No STEMI particular community, several fac-
8 (3%) = No STEMI to STEMI tors, such as terrain, cellular cover-
Source: Rowley J, McGinnis-Hainsworth D, Megargel R, age and budget, must be taken into
et al: “Value of Serial Prehospital ECGs in the Diagnosis of consideration. Bear in mind, recent
ST-Elevation Myocardial infarction (STEMI).” Paper Presenta- 91(27%) = Both ECGs normal
tion. Annual Meeting of the National Association of EMS
technological improvements make
Physicians, Registry Resort, Naples, Fla., 2008. 130 (39%) = STEMI 12-lead transmission much more
detected on both ECGs reliable and practical than even a
few years ago.

march 2009 Trend Setters 21

 ST-SEGMENT Trending Capabilities
Because of the dynamic nature of acute coronary syndromes, when
STEMI is suspected but the initial ECG is non-diagnostic, EDs are
generally required to either manually obtain a 12-lead ECG every five
to 10 minutes or use an ST-segment monitor to trend the ST segment
(a Class I recommendation).
At least one prehospital monitor offers a feature known as “ST
segment trending,” which emulates the function of an ST-segment
monitor. In units with ST trending, once the “12-lead” button is
pressed, the device not only samples and prints a 12-lead ECG
but will then automatically re-sample a 12-lead every 30 seconds
thereafter. This re-sampling is done internally, and the 12-lead is not
printed out or displayed on the screen.
The monitor analyzes the re-sampled ECGs and identifies changes
of at least 1 mm in the ST segment, whether upward or downward.
Such a change in one sample may be due to an ischemic event or
may simply be the result of patient movement or artifact. Therefore,
the ST-segment trending algorithm requires the change to persist for
five samples, or about two and a half minutes, before meeting the
threshold for an alert.
If the ST segment change meets that threshold, a new 12-lead is
printed, alerting the care provider and documenting the event. The
ECGs in Figure 1 captured the STEMI by use of this feature.

Practical Considerations
EMS has a logistical advantage
when it comes to performing serial
ECGs. In the ED, patients outnum-
ber the staff, but in the field an
entire team focuses on one cardiac
patient. In the ED, patients aren’t
typically assigned their own 12-
lead machine, but in the field, that’s
precisely the case.
In the ED, repeat ECGs are often
done at 30-minute intervals; EMS
can easily get a repeat ECG with
every set of vitals, or if ST trending
is available, automatically obtain
a 12-lead every 30 seconds (see
sidebar, p. 22).
With practice, 12-leads can be
obtained on scene with little or no
increase in scene time. In many
situations, it’s possible to work the
12-lead into the call early on, even
before nitroglycerin would be
administered. When this is fea-
sible, it provides an opportunity
to establish a baseline ECG before
medications are administered. As
mentioned above, this process is
worthwhile but should be done
without delaying treatment.
Conclusion
When it comes to recognizing
STEMI, EMS is in a privileged
position. Who better to obtain early
ECGs, serial ECGs as often as every
30 seconds and even get additional
leads when indicated? No one.
Although dynamic changes won’t
occur in every patient, or even every shift, routine acquisition of early and
serial 12-lead ECGs increases the likelihood of recognizing STEMI, thus
shortening the time to lifesaving treatment.
Increasing our level of suspicion as to who should get a 12-lead, striving
to obtain the first 12-lead as early as possible and prioritizing the impor-
tance of serial ECGs are three important steps to improve STEMI care.
Considering that EMS is in the unique position to obtain early and repeat
ECGs, the logical question to ask ourselves is, “Are we seizing this valuable
opportunity?”
Finding STEMI is like panning for gold: You don’t expect to find a gold
nugget in every pan, but when you do find one it’s worth all the effort.
Tim Phalen has presented 12-lead education to more than 35,000 participants. He is the co-author of
the textbook The 12-lead ECG in Acute Coronary Syndromes and developer of online 12-lead and STEMI
educational programs. He can be reached through his Web site at ECGSolutions.com.
Disclosure: Tim Phalen serves as a consultant to Physio-Control, Inc. He has also provided education
sponsored by Physio-Control, Inc.
REFERENCES
1. Canto JG, Shlipak MG, Rogers WJ, et al: “Prevalence, clinical characteristics and mortality without
chest pain among patients with myocardial infarction presenting.” JAMA. 283(24):3223–3229, 2000.
2. Harvey RA, Fuller FP: “The dynamic nature of ST segment and T-wave changes during acute MI.”
Prehospital and Disaster Medicine. 12(4):313–317, 1997.
3. Antman EM, Anbe DT, Armstrong PW, et al: “ACC/AHA guidelines for the management of patients with
ST-elevation myocardial infarction.” Circulation. 110(9):e82–292, 2004.
4. Fesmire FM, Percy RF, Bardoner JB et al: “Usefulness of automated serial 12-lead ECG monitoring
during the initial emergency department evaluation of patients with chest pain.” Annals of Emergency
Medicine. 31(1):3–11, 1998.
5. Jernberg T, Lindhal B, Wallentin L: “ST-segment monitoring with continuous 12-lead ECG improves
early risk stratification in patients with chest pain and ECG nondiagnostic of acute myocardial infarc-
tion.” Journal of the American College of Cardiology. 34(5):1413–1419, 1999.
6. Drew BJ, Dempsey ED, Joo TH, et al: “Pre-hospital synthesized 12-lead ECG ischemia monitoring with
trans-telephonic transmission in acute coronary syndromes: Pilot study results of the ST SMART trial.”
Journal of Electrocardiology. 37(suppl.):214–221, 2004.

22 Trend Setters Journal of Emergency Medical Services (JEMS)

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