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EM Critical Care



Respiratory Monitoring
In The Emergency Department

Robert T. Arntfield, MD, FRCPC

Instructor, Department of
Emergency Medicine, Mount Sinai
School of Medicine, New York, NY

Associate Editor

Lillian L. Emlet, MD, MS, FACEP

Assistant Professor, Department of
Critical Care Medicine, Department
of Emergency Medicine, University
of Pittsburgh Medical Center,
Pittsburgh, PA; Program Director,
EM-CCM Fellowship of the
Multidisciplinary Critical Care
Training Program, Pittsburgh, PA

Scott Weingart, MD, FACEP

Assistant Professor, Department of
Michael A. Gibbs, MD, FACEP
Emergency Medicine, Mount Sinai
School of Medicine, New York, NY; Professor and Chief, Department
of Emergency Medicine, Maine
Director of Emergency Critical Care,
Medical Center, Portland, ME; Tufts
Elmhurst Hospital Center, New
University School of Medicine,
York, NY
Boston, MA

Editorial Board
Benjamin S. Abella, MD, MPhil,
Assistant Professor, Department
of Emergency Medicine and
Department of Medicine / Section
of Pulmonary Allergy and Critical
Care, University of Pennsylvania
School of Medicine, Philadelphia,
PA; Clinical Research Director,
Center for Resuscitation Science,
Philadelphia, PA

Chad M. Meyers, MD

Director of Emergency Critical Care, Department of

Emergency Medicine, Bellevue Hospital, New York, NY;
Assistant Professor of Clinical Emergency Medicine, NYU
School of Medicine, New York, NY

Scott Weingart, MD, FACEP

onitoring the respiratory status of emergency department (ED) patients is a critical step to understanding their
condition and monitoring their response to interventions. Endtidal carbon dioxide (ETCO2) can be determined with colorimetric capnometers or monitored quantitatively in real-time with
continuous capnometry. ETCO2 monitoring is used for verifying
endotracheal tube (ETT) placement, monitoring during procedural sedation, monitoring after traumatic brain injury (TBI),
estimating prognosis of continued cardiopulmonary resuscitation
(CPR), and detecting return of spontaneous circulation (ROSC)
during cardiac arrest. Pulse oximetry, widespread in most EDs,
noninvasively monitors oxygenated hemoglobin. Though it is not
a good indicator of endotracheal intubation, the widespread use
of pulse oximetry in the ED has reduced arterial blood gas (ABG)
sampling and provided a noninvasive method of quickly titrating
down fraction of inspired oxygen (FiO2) in mechanically ventilated patients. In caring for critically ill patients, the emergency
clinician should be familiar with and comfortable using both
pulse oximetry and capnometry, with special attention paid to the
limitations of each method.

In this issue of EMCC, we discuss the use of pulse oximetry and
ETCO2 in the assessment and management of the critically ill patient
in the ED.


Volume 1, Number 1

Robert Green, MD, BSc, DABEM,

Associate Professor, Department
of Anaesthesia: Division of Critical
Care Medicine, Department of
Emergency Medicine, Dalhousie
University, Halifax, Nova Scotia,

Andy Jagoda, MD, FACEP

Professor and Chair, Department
of Emergency Medicine, Mount
Sinai School of Medicine; Medical
Director, Mount Sinai Hospital, New
York, NY

Assistant Professor, Department of Emergency Medicine,

Mount Sinai School of Medicine, New York, NY; Director of
Emergency Critical Care, Elmhurst Hospital Center, New
York, NY
Peer Reviewer

Andy Jagoda, MD, FACEP

Professor and Chair, Department of Emergency Medicine,

Mount Sinai School of Medicine, New York, NY; Medical
Director, Mount Sinai Hospital, New York, NY
CME Objectives
Upon completion of this article, you should be able to:


Understand the use of colorimetric ETCO2 devices and

the situations in which these devices are not accurate.
Understand the use of continuous waveform ETCO2
devices and their role in intubation confirmation, the
assessment of mechanically ventilated patients, and
cardiac arrest.
Understand the use of pulse oximetry to assess
oxygenation in sick patients in the ED.

Portions of this article were excerpted from Critical Care

Monitoring In The Emergency Department, Emergency
Medicine Practice, 2007. The authors have no financial ties,
sponsorships, or competing interests in regards to monitoring
technologies or the manufacturers of specific monitoring
devices described in this article. Prior to beginning this
activity, please see CME Information on page 12.

Julie Mayglothling, MD
Emanuel P. Rivers, MD, MPH, IOM
Assistant Professor, Department of
Vice Chairman and Director
Emergency Medicine, Department
of Research, Department of
of Surgery, Division of Trauma/
Emergency Medicine, Senior
Critical Care, Virginia Commonwealth
Staff Attending, Departments
University, Richmond, VA
of Emergency Medicine and
Surgery (Surgical Critical Care),
Henry Ford Hospital, Detroit, MI;
William A. Knight, IV, MD
Christopher P. Nickson, MBChB,
Clinical Professor, Department of
Assistant Professor of Emergency
Emergency Medicine and Surgery,
Medicine, Assistant Professor of
Supervising Registrar, Department
Wayne State University School of
Neurosurgery, Emergency Medicine
of Emergency Medicine, Sir Charles
Medicine, Detroit, MI
Mid-Level Program Medical Director,
Gairdner Hospital, Perth, Australia
University of Cincinnati College of
Medicine, Cincinnati, OH
Isaac Tawil, MD
Jon Rittenberger, MD, MS
Assistant Professor, Department of
Assistant Professor, Department
Surgery, Department of Emergency
Haney Mallemat, MD
of Emergency Medicine, University
Medicine, University of New
Associate Professor, Department of of Pittsburgh School of Medicine,
Mexico Health Science Center,
Critical Care / Emergency Medicine, Pittsburgh, PA; Attending,
Albuquerque, NM
University of Maryland Medical
Emergency Medicine and PostCenter, Baltimore, MD; Department Cardiac Arrest Services,
of Critical Care, Shock Trauma
UPMC-Presbyterian Hospital,
Research Editor
Center, Baltimore, MD
Pittsburgh, PA
Jennifer L. Galjour, MD, MPH
Department of Emergency Medicine,
Evie Marcolini, MD, FAAEM
Mount Sinai School of Medicine,
Assistant Professor, Department of
New York, NY
Emergency Medicine and Critical
Care, Yale School of Medicine, New
Haven, CT


critical care area receiving active chest compressions.

You glance at the EMS monitor and note a slow narrow complex rhythm; chest compressions are continued,
and his prehospital capnography tubing is connected to
the ED monitor. The characteristic waveform reassures
you of proper ETT placement, and the ETCO2 is 14 mm
Hg. You obtain central access, and a round of ACLS
drugs is administered. At the following rhythm check,
you note ventricular fibrillation; he receives another
shock, and chest compressions continue. You now note an
ETCO2 of 36 mm Hg, a central pulse is appreciated, and
his plethysmographic waveform becomes clearly defined.
Hypothermia is induced, and the patient is admitted to
the cardiac critical care unit.

ABG: Arterial blood gas

CBF: Cerebral blood flow
CO2: Carbon dioxide
COPD: Chronic obstructive pulmonary disease
CPR: Cardiopulmonary resuscitation
ED: Emergency department
ETCO2: End-tidal carbon dioxide
ETT: Endotracheal tube
FiO2: Fraction of inspired oxygen
PaCO2: Partial pressure of carbon dioxide in arterial
PvCO2: Partial pressure of carbon dioxide in venous
SaO2: Arterial oxygen saturation
SpO2: Pulse oximeter oxygen saturation
ROSC: Return of spontaneous circulation
RSI: Rapid sequence intubation
SD: Standard deviation
TBI: Traumatic brain injury
VBG: Venous blood gas


Ventilation (the pulmonary exchange of carbon

dioxide [CO2] and its subsequent expiration) is
typically monitored in the ED by 2 modalities:
colorimetric capnometry or continuous infrared
spectroscopy. Colorimetric capnometers display
a threshold concentration of CO2 qualitatively or
semiquantitatively by color change, providing
the clinician with confirmation of ETT placement.
(See Table 1.) Capnometry by infrared absorbance
spectroscopy, on the other hand, allows continuous
quantitative assessment of CO2 concentrations displayed by numerical value. Many capnometers also
graphically depict the CO2 waveform as a function
over time; this capability (known as capnography)
provides the clinician with additional information regarding the patients ventilatory status. (See
Figure 1.) Volumetric capnography, a modality not
widely available, plots expired CO2 concentration
along with exhaled volume during the respiratory
cycle, providing information regarding alveolar
and anatomic dead space. This may allow for additional applications, including the bedside diagnosis
or exclusion of pulmonary embolism.1,2

Critical Appraisal Of The Literature

Evidence regarding the clinical application of monitoring devices was initiated with a PubMed search
of literature published between 1950 and 2010 using
the keywords capnometry, capnography, end-tidal CO2,
pulse oximetry, and reflectance oximetry. The results
were reviewed, and relevant citations from each
study were searched manually.

A search for practice guidelines and clinical
policies identified the following: The American College of Emergency Physicians 2001 Clinical Policy,
Verification of Endotracheal Tube Placement;
the American Society of Anesthesiologists 2005
Standards of Basic Anesthetic Monitoring; the
American Association for Respiratory Cares 2003
Clinical Practice Guidelines, Capnography/Capnometry During Mechanical Ventilation; and the
2005 International Consensus on Cardiopulmonary
Resuscitation and Emergency Cardiovascular Care
Science with Treatment Recommendations Section
on Advanced Life Support.

Table 1. Semiquantitative Colorimetric


Case 1

An EMS notification of prehospital cardiac arrest is

received by your community ED. Per the paramedic crew,
the patient is a 62-year-old man initially complaining of
chest tightness who became unresponsive and apneic during transport approximately 3 minutes prior to arrival.
The rhythm was noted initially to be ventricular fibrillation; after a single biphasic countershock, his rhythm
became organized, but he remained pulseless. He was
intubated en route and is now being wheeled into your

EMCC 2011

Capnometer Color

CO2 Concentration (%)

Fenem Capnometer Color


CO2 Concentration (mm





2.3 or less








15.2 or more


Greater than

Colorimetric end-tidal CO2 detectors provide continuous semiquantitative measurement of end-tidal CO2 using a pH-sensitive chemical
strip that changes color upon exposure to the gas. The normal range
of CO2 concentrations in hemodynamically stable patients is greater
than 4%.5,6 Volume 1, Number 1

Correlation Of ETCO2 To Arterial CO2

the correlation between partial pressure of carbon

dioxide in arterial blood (PaCO2) and ETCO2 may
be somewhat reliable in stable unintubated ED
patients,8 it is typically considered unreliable in
critically ill patients and may be assumed only with

Despite pitfalls in using the absolute value
of a single ETCO2 reading to gauge PaCO 2, it
seems intuitive that if the PaCO2-ETCO2 gradient is constant, increases or decreases in ETCO2
on the monitor should reflect those occurring
with the PaCO2 in the blood. Disappointingly,
however, stability of the PaCO2-ETCO2 gradient
is only found to occur in 60% to 80% of patients
studied across several anesthesia studies, with
the gradient subject to unpredictable amounts of
widening or narrowing. 4 This phenomenon was
further demonstrated in a study of multitrauma
patients, which found a 27% erroneous prediction
of PaCO2 change by ETCO2.14 One very helpful
observation, however, is that the PaCO2-ETCO2
gradient is almost always positive (ie, PaCO2 is
nearly always higher than ETCO2), and when a
negative gradient exists, it is typically very small.
Therefore, while a low ETCO 2 value may provide
little informat ion regarding a patients ventilatory status, a high ETCO2 value almost always
correlates with an equal or higher PaCO2 value.
This concept may prove particularly beneficial
during the continuous monitoring of patients at
risk for tiring out, such as those patients with
status asthmaticus or decompensated conges-

ETCO2 concentration (the concentration of CO2 at

the end of exhalation) typically underestimates
PaCO2 concentration in healthy individuals by 4 to
5 mm Hg.3 Regrettably, this gap precludes using
ETCO2 as a noninvasive determination of PaCO2.
The discrepancy between ETCO2 and PaCO2, the
so-called PaCO2-ETCO2 gradient, is a critical consideration one that is influenced by 3 primary
The PaCO2-ETCO2 gradient will be increased in
the acute scenario by any disorder that decreases pulmonary blood flow (thereby increasing
alveolar dead space). Such conditions include
pulmonary embolism, cardiogenic shock, cardiac arrest, or hypovolemia.
The fixed amount of functional or anatomic
dead space related to the trachea and other
conducting airways also contributes to the
Lastly, any condition that decreases exhaled
tidal volume, such as obstructive lung disease,
increases the gradient. This is due to inadequate expulsion of CO2 contained inside the
obstructed alveoli. The amount of such wasted
ventilation can be measured using a parameter
known as the dead space/tidal volume ratio
(VD/VT) or dead space fraction.7

Thus, the determinants of the PaCO2-ETCO2
gradient are multifactorial, and the magnitude of
their effect is often unpredictable. Therefore, while

Figure 1. Capnography Interpretation





The expiratory limb of the capnogram is typically divided into 3 (or occasionally 4) phases. Phase I represents the emptying of CO2 free anatomic dead
space. Phase II represents a mixture of gas from the anatomic dead space and CO2 containing alveoli. Phase III represents the emptying of CO2 from
the alveoli. The slope of Phase III is positive in patients with normal pulmonary function and is a reflection of the continuous elimination of CO2 from
the blood into the alveoli, the heterogeneous ventilation-perfusion ratio, and the asynchronous emptying of alveoli. However, the slope of Phase III is
increased by certain pathologic states such as chronic obstructive pulmonary disease and asthma; it can be a valuable tool in assessing the pulmonary status of the critically ill. Occasionally, a terminal upswing (Phase IV) will be present in the pregnant or obese patient. Finally, Phase O represents
inspiration.15 (Used with permission of Chad Meyers, MD.) Volume 1, Number 1

EMCC 2011

tive heart failure. Likewise, in situations in which

targeted PaCO2 levels may be of value (such as in
patients with evidence of increased intracranial pressure and acute brain herniation), a high ETCO2 value
may signal the need for adjustments in the patients
mechanical ventilatory parameters or, at the minimum, the need to check a blood gas.

For healthy patients, the partial pressure of carbon dioxide in venous blood (PvCO2) is commonly
acknowledged to be 5 to 8 mm Hg higher than the
PaCO2, and in a prospective study of 112 hemodynamically stable ED patients with chronic obstructive pulmonary disease (COPD) exacerbations, arterial hypercarbia was ruled out in all cases where
the PvCO2 was found to be below 45 mm Hg.17 The
relationship between PvCO2 and PaCO2 has been
shown to be unreliable, however, in critically ill
patients with shock states or circulatory failure.16 In
these situations, the PvCO2 becomes significantly
elevated as the body buffers the lactic acid being
produced. Thus, while it is acceptable to consider
low or normal PvCO2 measurements reassuring
in patients with respiratory failure, if the PvCO2 is
elevated, especially in the context of hypotension,
then obtaining an ABG and PaCO2 determination is
more appropriate.

severe TBI) who underwent prehospital intubation and compared auscultation to capnometry
with capnography for confirmation of proper ETT
placement. Successful intubation was observed in
73 patients; however, 8 patients were intubated
into the esophagus all of which were detected by
capnometry. Of those, 4 were incorrectly thought to
be in the trachea based upon auscultation.23 Further
emphasizing the importance of accurate determination of ETT placement is Silvestri et als study that
showed a 69% mortality associated with unrecognized misplaced ETTs and 100% mortality if the
patient was apneic upon arrival to the ED.22

Additionally, the use of continuous ETCO2 in
confirming prehospital intubation during cardiac
arrest has also been shown to be more effective than
colorimetric capnometry and auscultation. The presence of ETCO2 greater than 5 mm Hg after 6 breaths
was found to be 100% sensitive and 100% specific for
correct placement of the ETT, while qualitative capnometry was 100% specific but only 80% sensitive
in cardiac arrest. Both methods were 100% sensitive
and 100% specific in non-arrest intubations.24

For emergent, in-hospital intubations, The
American College of Emergency Physicians endorses the nearly perfect accuracy of ETCO2 for ETT
confirmation but does not differentiate between the
utility of qualitative, quantitative, or continuous
ETCO2 detectors for the verification or reconfirmation of ETT placement.25 Continuous ETCO2 monitoring from initial ETT placement, and continuing
through surgery, is considered standard of care by
the American Society of Anesthesiologists to both
confirm initial ETT placement and to ensure rapid
recognition if extubation were to occur.26

ETCO2 Monitoring Applications

Verification Of ETT Placement

Perhaps the most useful application of continuous
ETCO2 monitoring is to allow real-time confirmation of adequate ventilation through capnographic
waveform analysis. Continuous ETCO2 monitoring is a valuable tool for preventing misplacement
of the ETT, either through continuous verification
of placement following intubation or for airway
management during CPR or transport. This is
especially true when one considers the fallibility
of traditional physical examination techniques.
For instance, auscultation over the chest does not
detect up to 15% of esophageal intubations, while
fogging in the ETT is reported in up to 85% of
esophageal intubations.18

From the prehospital point of view, esophageal intubations have been reported to range from
between 2%19 to 6%.20 In a study from the Orlando,
Florida EMS system, Katz and Falk reported that
27 out of 108 (25%) patients who had a prehospital
intubation arrived in the ED with an unrecognized,
misplaced ETT: 18 in the esophagus and 9 above
the vocal cords.21 However, when ambulances and
aeromedical units were equipped with continuous ETCO2 monitors, Silvestri et al reported in a
follow-up study that the incidence of unrecognized
misplaced ETTs was 0%, compared to the 23%
incidence of misplaced ETTs in those units where
continuous ETCO2 monitoring was not available.22
Likewise, Grmec et al studied 81 patients (58 with

EMCC 2011

Monitoring During Procedural Sedation

When performing procedural sedation, reliable
monitoring of the patients ventilatory status is
crucial. While clinical indicators like chest rise or the
plethysmography-derived respiratory rate provided
by electrocardiogram lead placement can be used,
monitoring the capnographic waveform for hypopneic and bradypneic hypoventilatory patterns
provides the clinician with a quick and more accurate indication of acute respiratory events.27 Burton
et al reported that capnographic changes (defined as
a change in ETCO2 level greater than 10 mm Hg or
intrasedation ETCO2 less than 30 mm Hg or greater
than 50 mm Hg) predicted respiratory events by up
to 271 seconds.28 Similar findings were observed
in a study of 132 patients receiving propofol for
conscious sedation in the ED. The results of this
randomized controlled study showed that patients
monitored by capnography had significantly fewer
hypoxic episodes compared to those where the treating physician was blinded to the capnography data.
In both groups, all hypoxic episodes were able to
be predicted by respiratory depression seen on the
4 Volume 1, Number 1

capnograph a median of 60 seconds before the onset

of hypoxia.29

Often, nasal prongs with an additional port
are used to provide continuous CO2 sampling. If
commercial devices are not available, a regular nasal cannula can be suitably modified. (See Figure
2.) It is important to note that the CO2 waveform
will show ventilatory rate and duration but that
the amplitude of the waveform is not a measure
of ventilatory depth. Rather, this vertical height
of the wave portrays the amount of CO2 being
exhaled through the intra-nasal cannula.30 While
ETCO2 monitoring for sedation is considered
standard of care in the United States in operating
suites, its necessity during sedation in the ED is

still controversial. ETCO2 monitoring may be most

contributory in those patients undergoing preoxygenation and/or oxygen administration during
their deep sedation in the ED. In these cases, the
continuation of normal oxygen saturation on the
pulse oximeter readout can fail to indicate hypoventilation or apnea; this makes ETCO2 monitoring a superior real-time monitoring solution to
identify oversedation or apnea in these patients.
When ETCO2 monitoring is not available, it may
be preferable to withhold supplemental oxygen
altogether so that drops in the pulse oximeter
reading can be used more reliably as an indicator of hypoventilation and hypercapnea, as was
shown in a case series of 513 patients.30 If using
pulse oximetry in either situation, knowledge of
the lag effect, as described in the Pulse Oximetry
Lag section (page 7), will be important.

Further reading on the use of ETCO2 for procedural sedation can be found in an excellent review
written by Krauss and colleagues.27

Figure 2. Modified Nasal Cannula For

Noninvasive Monitoring Of End-Tidal CO2

Monitoring After TBI

Hyperventilation with hypocapnia may worsen
outcome in brain-injured patients.18 Therefore,
monitoring of ETCO2 is emerging as a fundamental component of TBI management not only in the
hospital but also in the prehospital arena. After TBI,
there may be a period of prolonged hypoperfusion
with cerebral blood flow (CBF) reduced by as much
as two-thirds of normal. Hyperventilation can further decrease CBF, potentially to the point of cerebral
ischemia or by converting ischemic areas into infarction. Evidence from in-hospital studies indicates that
prophylactic early hyperventilation can seriously
compromise cerebral perfusion and worsen patient
outcome.31 Further, inadvertent hyperventilation
during prehospital transport is associated with increased mortality.18

Several studies have demonstrated the in
cidence of induced hypocapnia during the field
management of TBI patients. In a retrospective
study from San Diego, 59 adult severe TBI patients
who were unable to be intubated without rapid
sequence intubation (RSI) were matched to 177
historical nonintubated controls. The study utilized
ETCO2 monitoring and found an association be
tween hypocapnia and mortality and a statistically
significant association between ventilatory rate and
ETCO2. Both the lowest and final ETCO2 readings
were associated with increased mortality versus
matched controls. ETCO2 monitoring was used in
144 patients to assess whether closer monitoring
would result in a lower rate of inadvertent severe
hyperventilation (defined as an ETCO2 less than
25) after RSI. Patients with ETCO2 monitoring had
a significantly lower incidence of severe hyperventilation. For those patients who were severely

A nasal cannula may be quickly adapted for end-tidal CO2 monitoring

by inserting a 16-gauge angiocatheter into the tubing as shown. After
securing in place with tape, the angiocatheter may be connected
directly to the capnometer. When utilizing a nasal cannula altered by
this method to monitor end-tidal CO2, it cannot be used as an oxygen
source as this will prevent the accurate sampling of exhaled CO2 by
the capnometer. A second nasal cannula or an oxygen mask can be
used to provide supplemental oxygen. (Used with permission of Scott
Weingart, MD.) Volume 1, Number 1

EMCC 2011

day 2 and optimized on antiplatelet drugs, beta-blockers,

and lipid-lowering agents prior to discharge.

hyperventilated, there was a statistically significant

increase in mortality (56% vs 30%).18 However, as
previously discussed, the PaCO2-ETCO2 gradient in
traumatically injured patients is unreliable, specifically in regards to low ETCO2 concentrations. A
recent study by Lee et al examined 77 patients and
showed a poor concordance between ETCO2 and
PaCO2 in multitrauma patients.32 Therefore, the
reliance on ETCO2 as an indicator of hypocapnia
must be further evaluated in the emergency setting
before it is used to guide ventilatory management
of traumatically brain injured patients in the ED.
PaCO2 remains the gold standard.

ETCO2 Key Points

Capnography allows for the continuous verification of ETT placement, which is essential in the
unstable prehospital and ED environment in
which patients are frequently moved; achieving
adequate sedation can be difficult, and accidental
extubation is an ongoing risk.
Continuous capnography by spectroscopy may
be superior to qualitative CO2 detectors in detecting correct ETT placement during cardiac arrest.
An ETCO2 less than 10 mm Hg following 20
minutes of CPR is predictive of death and indicates that continued attempts at resuscitation are
likely futile.
A rapid increase in ETCO2 concentration during
CPR often represents ROSC and can be a useful guide in determining timing of rhythm and
pulse checks.
Continuous noninvasive ETCO2 monitoring
can be useful in the monitoring of patients with
tenuous respiratory status, such as those with
severe reactive airway disease or congestive
heart failure.
While a low ETCO2 concentration is difficult
to interpret, an ETCO2 concentration greater
than 40 mm Hg will almost always indicate
hypercapnia. The degree of hypercapnia may be
underrepresented by the ETCO2.

Prognosis Of Continued CPR

As discussed previously, pulmonary CO2 exchange
is affected by multiple factors at the level of the
alveoli. In contrast to this, at extremely low flow
states, ETCO2 is determined almost entirely by
pulmonary flow secondary to a logarithmic relation
ship between cardiac output and ETCO2 that exists
during cardiac arrest.33 This relationship between
pulmonary flow and ETCO2 during arrest makes
capnometry an important prognostic marker during
CPR in the ED. In multiple studies, an ETCO2 level
during CPR of 10 mm Hg or less 20 minutes after
the initiation of resuscitation in patients with pulseless electrical activity accurately predicted death
in patients suffering prehospital arrest.34-37 These
findings were also supported by a small prospective
trial of both in- and out-of-hospital arrest39 and were
only minimally affected by variations of ventilatory
rate.40 However, the initial ETCO2 had no correlation with outcome or survival,34 and very low initial
ETCO2 (less than 6 mm Hg) has been associated with
survival.40 Accordingly, the 2010 Advanced Cardiac
Life Support guidelines state, Persistently low
ETCO2 values (less than 10 mm Hg) during CPR in
intubated patients suggest that ROSC is unlikely,
and they consider ETCO2 unreliable immediately
after starting CPR.41 One caution is that the prognostic value of ETCO2 has not been established in
supraglottic airways or in those receiving bag valve
mask ventilations.41 Further, the absence of color
change on a colorimetric device is not sufficiently
accurate to allow cessation of resuscitation.41,42

Pulse Oximetry
Case 2

Your asthmatic patient has become so exhausted that she

is barely moving any air. She will not tolerate noninvasive
ventilation, and its obvious that she needs to be intubated. You hand the laryngoscope to a trusted fourth-year
resident. He proceeds to place the tube and states that he
saw it pass through the cords. A few seconds later, the pulse
oximeter reading drops to 40%. You shake your head and
grab the laryngoscope. Your resident points out the yellow
color change of the ETCO2 detector, but you now notice the
pulse oximeter is reading 36%. You place the blade and are
surprised to note that the tube is clearly between the cords.
After another minute, the pulse oximeter is reading 100%.

Detection Of ROSC During Cardiac Arrest

A sudden rise in ETCO2 during CPR may indicate
ROSC. An increase of more than 10 mm Hg from the
patients baseline should prompt a rhythm check
and, if the rhythm is organized, a pulse check.43-49


Pulse oximeters are almost uniformly present in

modern EDs. Noninvasive pulse oximeters differentiate oxyhemoglobin from reduced hemoglobin
utilizing differing absorption compon ents at the
2 wavelengths 660 nm and 940 nm. To distinguish
arterial from venous oxyhemoglobin or deoxyhemoglobin, the pulsatile AC component is then
divided by the nonpulsatile DC component to de-

Case Conclusion

An ECG of the patient after regaining his pulse revealed

ST elevations in the lateral precordial leads. The patient
was taken to the cardiac catheterization lab for revascularization on hospital day 1 He was extubated on hospital

EMCC 2011 Volume 1, Number 1

termine the arterial pulse-added absorbance. This

value corresponds to the pulse oximeter oxygen
saturation (SpO2).50

While typically considered accurate when compared to arterial concentrations of oxygen determined by ABG co-oximetry, there are several limitations and misconceptions regarding the accuracy
of pulse oximetry that should be addressed when
considering its reliability in the monitoring of the
critically ill ED patient.

associated with their own limitations, including

distortion of findings by venous pulsation and the
incidence of skin burn.56)

Because of overlap in the absorbance of light at
660 nm and 940 nm, dyshemoglobinemias result in a
distortion of true oxygen saturation when measured
by traditional pulse oximeters. Based on animal
studies, the presence of methemoglobinemia causes a
significant overestimation of SpO2 by pulse oximetry.
With increasing concentration of methemoglobin,
SpO2 has been found to plateau at approximately
85%.57 Likewise, a carboxyhemoglobinemia level of
70% results in a SpO2 of 90%, while the actual measured SaO2 on the blood gas is 30%.58 In response to
this limitation, a new generation of pulse oximeters
that can noninvasively differentiate oxyhemoglobin,
deoxyhemoglobin, methemoglobin, and carboxyhemoglobin saturation have become available.59

Ambient light has been shown to have no effect
on the accuracy of oximetry readings in hemody
namically stable patients.60 Additionally, when
studied in healthy volunteers, the accuracy of pulse
oximetry was preserved with red fingernail polish but
noted to be decreased in the presence of darker colors
(eg, black, blue, or green)61; however, it is felt to be
clinically insignificant among critically ill, mechanically ventilated patients.62 Dark skin pigmentation
has also been suggested as a source of interference in
the accuracy of pulse oximetry; however, this was not
supported by an investigation of 284 ED patients.63

While motion artifact has presented a significant problem to oximeter design, recent advances
in motion-resistant and read-through motion using
different algorithms have improved accuracy and
rely less on lengthening of signal averaging times,
which may lead to missing significant short-lived
hypoxemic events.64

Pulse Oximetry Limitations And


The reliability of pulse oximetry is reduced in states

of severe hypoxia. While pulse oximeters possess
an accuracy of 2% to 1 standard deviation (SD)
when in the range of 70% to 100% arterial oxygen
saturation (SaO2), their accuracy falls to 3% SD
between 50% and 70% SaO2, and they are generally
not considered accurate when determining oxygen
saturations below 50%.50

The accuracy of pulse oximetry has also been
questioned in the heterogeneous population of the
critically ill as a whole. The incidence of intraopera
tive pulse oximetry data failure (frequently due to
hypotension and/or hypothermia) was found to
be 9% in a review of 9203 anesthesia records.51 In
almost every case, the data failures were due to the
inability of the pulse oximeter to pick up a strong
enough pulse to generate a good waveform; in
this setting, the pulse oximeter readings cannot be
deemed accurate.

However, if an acceptable plethysmographic
waveform can be detected, the reliability of pulse
oximetry has been demonstrated over a wide range of
clinical scenarios. When compared with invasive arterial measurements, the accuracy of pulse oximetry measured by finger probe was not reduced in states of poor
peripheral perfusion (cardiac index less than 2.2) or
low peripheral temperature (less than 28C [82.4F]).52
Additionally, although pulse oximetry was previously
considered inaccurate in the presence of hemoglobin
levels less than 5 g/dL, a small study of patients with
a hematocrit of less than 20% provided evidence that
SpO2 was accurate at hemoglobin concentrations as
low as 2.3 g/dL.53 These results were supported by a
study that showed no significant effect of moderate
anemia or acidemia on the accuracy of SpO2.54

While SpO2 readings may eventually correlate
with ABG determination of blood oxygenation,
there still may be significant delay associated with
the detection of hypoxemia in hypothermic, vasoconstricted, or low-flow states. In a study of healthy
volunteers, a response time of 131 seconds and 215
seconds to hypoxic events was found during induced vasoconstriction or hypothermia, respectively.
This delay was significantly reduced (22 seconds
and 40 seconds) by the use of forehead reflectance
oximetry probes.55 (However, forehead probes are Volume 1, Number 1

Pulse Oximetry Lag

While it is intuitive to think about pulse oximetry as

a real-time monitoring technique, even in healthy
patients what is actually being seen is the patients
past.65,66 The reason for this phenomenon is the time
delay until redistribution of oxygenated blood from
central to peripheral circulation and prolonged signal
averaging times. In patients with good cardiac output, this lag time may be 20 to 30 seconds; in patients
with shock, this time can extend to 90 seconds.67 That
this lag is at least partially caused by peripheral vasoconstriction is demonstrated by a study showing that
a digital block decreases the lag time.68

Pulse Oximetry Applications

The presence of continuous pulse oximeters is

considered necessary during all phases of definitive airway management.69 A study examining the
contribution of pulse oximetry to ED patient care
demonstrated that those monitored by pulse oxim7

EMCC 2011

Case Conclusion

etry were found to have significantly fewer episodes

of hypoxemia during emergency intubation (27%
vs 15%), and hypoxemic episodes were of shorter
duration than nonmonitored patients (1.4 minutes
vs 0.7 minutes).70 Additionally, a systematic review
of perioperative pulse oximetry in more than 20,000
patients showed a reduced incidence of hypoxemia
and increased incidence of both naloxone and oxygen administration in those patients monitored with
oximetry.71 However, the usefulness of pulse oximetry in avoiding hypoxemia during airway management should not be misconstrued to suggest utility
in verifying correct ETT placement. In a series of
preoxygenated patients, SpO2 was unable to detect
esophageal intubation at 30 seconds.72

The availability of pulse oximetry has been
shown to substantially reduce ABG sampling in the
ED without an increase in adverse outcomes.73 Pulse
oximetry can also be used to safely and quickly
titrate down the FiO2 in mechanically ventilated patients from potentially toxic oxygen concentrations.74

After intubation, the patient was given 2 g of IV magnesium and started on a terbutaline drip. She was admitted
to the ICU. After 2 days of mechanical ventilation with
inhaled and systemic corticosteroids, she passed a weaning trial and was extubated.

Pulse Oximetry Key Points

As long as a good waveform is present, pulse

oximetry remains accurate over a wide range of
critical illnesses, including shock, hypothermia,
and significant anemia.
Although pulse oximetry is necessary during
all phases of definitive airway management
in order to reduce the length and frequency of
hypoxic events, it lacks sensitivity in verifying
correct ETT placement.
Pulse oximetry readings may actually be showing desaturations that occurred up to 90 seconds
in the past. This leads to the common clinical
scenario of a large drop in the pulse oximetry

Common Pitfalls In Respiratory Monitoring In The ED

1. Utilizing normal SpO2 as an indicator of correct ETT placement.

While pulse oximetry is a valuable tool in preventing hypoxic events, because of the shape of
the oxyhemoglobin dissociation curve, significant desaturation may occur before changes in
SpO2 are evident.

on supplemental oxygen, even a small amount

of ventilation will maintain oxygenation, but the
CO2 will continue to rise to potentially injurious
levels. While some feel that this can be assessed
by careful visualizations of chest excursions, a
number of poor outcomes in the field of anesthesia led to mandatory use of ETCO2 monitoring during sedation. Very few EDs are as quiet
or calm as the operating room, so to think we
would be more successful than our anesthesia
colleagues at physical examination monitoring
does not seem logical.

2. Relying on ETCO2 as an estimate of PaCO2.

While ETCO2 may reflect PaCO2 in hemodynamically stable healthy volunteers, its relationship is unpredictable and unreliable in patients
who are unstable or who have abnormal pulmonary function. For example, monitoring of the
decompensated COPD patient for hypercapnia
by ETCO2 alone may lead to overconfidence in
clinical status and the overlooking of significant
clinical deterioration (ie, an ETCO2 of 30 mm Hg
may actually reflect a PaCO2 of 95 mm Hg due
to significant pulmonary shunting).

4. Being reassured by a normal SpO2 following

smoke inhalation.

The presence of carboxyhemoglobinemia following smoke inhalation may mask significant
hypoxia due to the limitations of traditional
pulse oximetry caused by the overlap of light
absorbance between oxyhemoglobin and carboxyhemoglobin.

3. Placing the patient on supplemental oxygen

without ventilatory monitoring during procedural sedation.

When on room air, elevations of CO2 and decreases in oxygen pressure will cause the pulse
oximetry values to slowly drift down as the CO2
occupies space in the alveoli and the patient begins to inspire volumes below the critical cut-off
for saturation. However, if the patient is placed

EMCC 2011

5. Relying on monitoring devices over clearly

contradictory clinical judgment.

Since all monitoring devices are sometimes
inaccurate, clinical gestalt still plays a large role
in the evaluation of a critically ill patient. If a patient looks much sicker than a monitoring device
indicates, continued vigilance is often rewarded.
8 Volume 1, Number 1

reading immediately following successful placement of the ETT. While sometimes terrifying, the
drop often reflects the desaturation during the
apneic period prior to ETT placement.

a predictor of the arterial PaCO2 in the emergency department setting. Emerg Med J. 2004;21(5):557-559. (Prospective,
observational; 73 patients)
9. Russell GB, Graybeal JM. The arterial to end-tidal carbon
dioxide difference in neurosurgical patients during craniotomy. Anesth Analg. 1995;81(4):806-810. (Prospective, observational; 35 patients)
10. Curley FJ. In: Irwin RRJ, ed. Routine Monitoring of Critically Ill
Patients, in Intensive Care Medicine. Philadelphia: Lippincott
Williams and Wilkins; 2003:226-246. (Review, text)
11. Kerr ME, Zempsky J, Sereika S, et al. Relationship between
arterial carbon dioxide and end-tidal carbon dioxide in
mechanically ventilated adults with severe head trauma. Crit
Care Med. 1996;24(5):785-790. (Prospective, observational; 35
12. AARC clinical practice guideline. Capnography/capnometry during mechanical ventilation--2003 revision & update.
Respir Care. 2003;48(5):534-539. (Review, practice guidelines)
13. Prause G, Hetz H, Lauda P, et al. A comparison of the endtidal-CO2 documented by capnometry and the arterial PaCO2
in emergency patients. Resuscitation. 1997;35(2):145-148.
(Prospective, observational; 27 subjects)
14. Russell GB, Graybeal JM. Reliability of the arterial to endtidal carbon dioxide gradient in mechanically ventilated patients with multisystem trauma. J Trauma. 1994;36(3):317-322.
(Prospective, observational; 9 patients, 171 measurements)
15. Kodali BS. Physiology of capnography: components of a
time capnogram. 2007;3/07. [cited 4/21/07]; 7th:Available
from: (Review)
16. Adrogu HJ, Rashad MN, Gorin AB, et al. Assessing
acid-base status in circulatory failure. N Engl J Med.
1989;320(20):1312-1316. (Prospective; 105 patients)
17. Kelly AM, Kyle E, McAlpine R. Venous pCO(2) and pH
can be used to screen for significant hypercarbia in emergency patients with acute respiratory disease. J Emerg Med.
2002;22(1):15-19. (Prospective; 112 patients)
18. Davis DP, Dunford JV, Poste JC, et al. The impact of hypoxia
and hyperventilation on outcome after paramedic rapid
sequence intubation of severely head-injured patients. J
Trauma. 2004;57(1):1-8; discussion 8-10. (Retrospective; 426
19. Stewart RD, Paris PM, Pelton GH, et al. Effect of varied
training techniques on field endotracheal intubation success
rates. Ann Emerg Med. 1984;13(11):1032-1036. (Prospective,
observational; 779 patients)
20. Pelucio M, Halligan L, Dhindsa H. Out-of-hospital experience with the syringe esophageal detector device. Acad
Emerg Med. 1997;4(6):563-568. (Prospective, observational;
168 patients)
21. Katz SH, Falk JL. Misplaced endotracheal tubes by paramedics in an urban emergency medical services system. Ann
Emerg Med. 2001;37(1):32-37. (Prospective, observational;
108 patients)
22. Silvestri S, Ralls GA, Krauss B, et al. The effectiveness of
out-of-hospital use of continuous end-tidal carbon dioxide
monitoring on the rate of unrecognized misplaced intubation
within a regional emergency medical services system. Ann
Emerg Med. 2005;45(5):497-503. (Prospective, observational;
153 patients)
23. Grmec S, Mally S. Prehospital determination of tracheal tube
placement in severe head injury. Emerg Med J. 2004;21(4):518520. (Prospective, observational; 81 patients)
24. Grmec S. Comparison of three different methods to confirm
tracheal tube placement in emergency intubation. Intensive
Care Med. 2002;28(6):701-704. (Prospective, observational;
345 patients)
25. American College of Emergency Physicians policy statement: verification of endotracheal tube placement.
2001;10/2001. [cited 2/6/07]; Available from: http://www.

Respiratory monitoring is of primary importance
in emergency medicine. If the patient is not maintaining adequate oxygenation and ventilation, they
will decompensate. ETCO2 and pulse oximetry
allow bedside assessment of these 2 parameters.
When used together in conjunction with clinical
assessment, they allow a noninvasive picture of the
patients status. Proper understanding of what the
readings mean and grasping the pitfalls in interpretation are crucial to deriving maximal benefit from
these technologies. After reading this article, readers
should have a clear understanding of how to use
respiratory monitoring to benefit patients.

Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are
equally robust. The findings of a large, prospective,
randomized, and blinded trial should carry more
weight than a case report.

To help the reader judge the strength of each
reference, pertinent information about the study,
such as the type of study and the number of patients
in the study, are included in bold type following the
reference, where available.

Kline JA, Israel EG, Michelson EA, et al. Diagnostic accuracy of a bedside D-dimer assay and alveolar dead-space
measurement for rapid exclusion of pulmonary embolism: a
multicenter study. JAMA. 2001;285(6):761-768. (Prospective,
observational; 380 patients)
2. Verschuren, F, et al. Volumetric capnography as a screening
test for pulmonary embolism in the emergency department.
Chest. 2004;125(3):841-850. (Prospective, observational; 45
3. Nunn JF, Hill DW. Respiratory dead space and arterial to
end-tidal carbon dioxide tension difference in anesthetized
man. J Appl Physiol. 1960;15:383-389. (Prospective, observational; 12 patients)
4. Wahba RW, Tessler MJ. Misleading end-tidal CO2 tensions.
Can J Anaesth. 1996;43(8):862-866. (Review)
5. Ornato JP, Shipley JB, Racht EM, et al. Multicenter study of
a portable, hand-size, colorimetric end-tidal carbon dioxide
detection device. Ann Emerg Med. 1992;21(5):518-523. (Prospective, observational; 227 patients)
6. Goldberg JS, Rawle PR, Zehnder JL, et al. Colorimetric
end-tidal carbon dioxide monitoring for tracheal intubation.
Anesth Analg. 1990;70(2):191-194. (Prospective, observational; 62 intubations)
7. Yamanaka MK, Sue DY. Comparison of arterial-end-tidal
PaCO2 difference and dead space/tidal volume ratio in
respiratory failure. Chest. 1987;92(5):832-835. (Prospective,
observational; 17 patients)
8. Yosefy C, Hay E, Nasri Y, et al. End tidal carbon dioxide as Volume 1, Number 1

EMCC 2011

(Review, practice guidelines)
26. American Society of Anesthesiologists: Standards for basic
anesthetic monitoring. 2005;10/2005. [cited 2/6/2007];
Available from: (Review, practice guidelines)
27. Krauss B, Hess DR. Capnography for procedural sedation
and analgesia in the emergency department. Ann Emerg Med.
2007;50(2):172-181. (Review)
28. Burton JH, Harrah JD, Germann CA, et al. Does end-tidal
carbon dioxide monitoring detect respiratory events prior
to current sedation monitoring practices? Acad Emerg Med.
2006;13(5):500-504. (Prospective, observational; 59 patients)
29. Deitch K, Miner J, Chudnofsky CR, et al. Does end tidal CO2
monitoring during emergency department procedural sedation and analgesia with propofol decrease the incidence of
hypoxic events? A randomized, controlled trial. Ann Emerg
Med. 2010;55(3):258-264. (Randomized controlled trial; 132
30. Witting MD, Lueck CH. The ability of pulse oximetry to
screen for hypoxemia and hypercapnia in patients breathing
room air. J Emerg Med. 2001;20(4):341-348. (Retrospective;
513 arterial blood gas results)
31. Muizelaar JP, Marmarou A, Ward JD, et al. Adverse effects of
prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurg. 1991;75(5):731739. (Prospective, randomized; 103 patients)
32. Lee SW, Hong YS, Han C, et al. Concordance of end-tidal
carbon dioxide and arterial carbon dioxide in severe traumatic brain injury. J Trauma. 2009;67(3):526-530. (Prospective;
77 patients)
33. Ornato JP, Garnett AR, Glauser FL. Relationship between
cardiac output and the end-tidal carbon dioxide tension. Ann
Emerg Med. 1990;19(10):1104-1106. (Animal model)
34. Levine RL, Wayne MA, Miller CC. End-tidal carbon dioxide
and outcome of out-of-hospital cardiac arrest. N Engl J
Med. 1997;337(5):301-306. (Prospective, observational; 150
35. Wayne MA, Levine RL, Miller CC. Use of end-tidal carbon
dioxide to predict outcome in prehospital cardiac arrest. Ann
Emerg Med. 1995;25(6):762-767. (Prospective, observational;
90 patients)
36. Grmec S, Kupnik D. Does the Mainz Emergency Evaluation Scoring (MEES) in combination with capnometry
(MEESc) help in the prognosis of outcome from cardiopulmonary resuscitation in a prehospital setting? Resuscitation.
2003;58(1):89-96. (Prospective; 246 patients)
37. Grmec S, Klemen P. Does the end-tidal carbon dioxide
(EtCO2) concentration have prognostic value during out-ofhospital cardiac arrest? Eur J Emerg Med. 2001;8(4):263-269.
(Prospective; 139 patients)
38. Kolar M, Krizmaric M, Klemen P, et al. Partial pressure of
end-tidal carbon dioxide successful predicts cardiopulmonary resuscitation in the field: a prospective observational
study. Crit Care. 2008;12(5):R115. (Prospective, observational; 737 cases of out-of-hospital cardiac arrest)
39. Sanders AB, Kern KB, Otto CW, et al. End-tidal carbon
dioxide monitoring during cardiopulmonary resuscitation. A
prognostic indicator for survival. JAMA. 1989;262(10):13471351. (Prospective, observational; 34 patients)
40. Callaham M, Barton C. Prediction of outcome of cardiopul
monary resuscitation from end-tidal carbon dioxide concentration. Crit Care Med. 1990;18(4):358-362. (Prospective,
observational; 55 patients)
41. Neumar RW, Otto CW, Link MS, et al. Part 8: adult advanced
cardiovascular life support: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2010;122(18 Suppl
3):S729-S767. (Guideline)
42. Nakatani K, Yukioka H, Fujimori M, et al. Utility of colori-

EMCC 2011

metric end-tidal carbon dioxide detector for monitoring during prehospital cardiopulmonary resuscitation. Am J Emerg
Med. 1999;17(2):203-206. (Prospective; 121 patients)
43. Bhende MS, Thompson AE. Evaluation of an end-tidal CO2
detector during pediatric cardiopulmonary resuscitation.
Pediatrics. 1995;95(3):395-399. (Prospective, observational; 40
44. Pokorn M, Necas E, Kratochvl J, et al. A sudden increase in
partial pressure end-tidal carbon dioxide (P(ET)CO(2)) at the
moment of return of spontaneous circulation. J Emerg Med.
2010;38(5):614-621. (Prospective; 108 patients)
45. Sehra R, Underwood K, Checchia P. End tidal CO2 is a quantitative measure of cardiac arrest. Pacing Clin Electrophysiol.
2003;26(1 Pt 2):515-517. (Prospective; 31 cardiac arrest/VF
46. Entholzner E, Felber A, Mielke L, et al. Assessment of endtidal CO2 measurement in reanimation. Anasthesiol Intensivmed Notfallmed Schmerzther. 1992;27:473476.
47. Garnett AR, Ornato JP, Gonzalez ER, et al. End-tidal carbon
dioxide monitoring during cardiopulmonary resuscitation.
JAMA. 1987;257(4):512-515. (Prospective; 23 patients)
48. Bhende MS, Karasic DG, Karasic RB. End-tidal carbon
dioxide changes during cardiopulmonary resuscitation after
experimental asphyxial cardiac arrest. Am J Emerg Med.
1996;14(4):349-350. (Prospective; 11 animals)
49. Falk JL, Rackow EC, Weil MH. End-tidal carbon dioxide
concentration during cardiopulmonary resuscitation. N Engl
J Med. 1988;318(10): 607-611. (Prospective; 10 patients)
50. Tremper KK, Barker SJ. Pulse oximetry. Anesthesiology.
1989;70(1):98-108. (Review)
51. Reich DL, Timcenko A, Bodian CA, et al. Predictors of pulse
oximetry data failure. Anesthesiology. 1996;84(4):859-864.
(Retrospective; 9203 patients)
52. Palve H, Vuori A. Accuracy of three pulse oximeters at low
cardiac index and peripheral temperature. Crit Care Med.
1991;19(4):560-562. (Prospective, observational; 33 patients)
53. Jay GD, Hughes L, Renzi FP. Pulse oximetry is accurate in acute anemia from hemorrhage. Ann Emerg Med.
1994;24(1):32-35. (Prospective, observational; 17 patients)
54. Perkins GD, McAuley DF, Giles S, et al. Do changes in pulse
oximeter oxygen saturation predict equivalent changes in
arterial oxygen saturation? Crit Care. 2003;7(4):R67. (Prospective, observational; 41 patients, 1085 measurements)
55. MacLeod DB, Cortinez LI, Keifer JC, et al. The desaturation response time of finger pulse oximeters during mild
hypothermia. Anaesthesia. 2005;60(1):65-71. (Prospective; 10
56. Shelley KH, Tamai D, Jablonka D, et al. The effect of venous
pulsation on the forehead pulse oximeter wave form as a
possible source of error in SpO2 calculation. Anesth Analg.
2005;100(3):743-747. (Prospective, observational; 25 patients)
57. Barker SJ, Tremper KK, Hyatt J. Effects of methemoglobinemia on pulse oximetry and mixed venous oximetry.
Anesthesiology. 1989;70(1):112-117. (Animal model)
58. Barker SJ, Tremper KK. The effect of carbon monoxide inhalation on pulse oximetry and transcutaneous PO2. Anesthesiology. 1987;66(5):677-679. (Animal model)
59. Barker SJ, Curry J, Redford D, et al. Measurement of carboxyhemoglobin and methemoglobin by pulse oximetry: a
human volunteer study. Anesthesiology. 2006;105(5):892-897.
(Prospective, observational; 10 patients)
60. Fluck RR Jr, Schroeder C, Frani G, et al. Does ambient
light affect the accuracy of pulse oximetry? Respir Care.
2003;48(7):677-680. (Prospective, observational; 54 patients)
61. Cot CJ, Goldstein EA, Fuchsman WH, et al. The effect of
nail polish on pulse oximetry. Anesth Analg. 1988;67(7):683686. (Prospective, randomized, single-blind; 14 patients)
62. Hinkelbein J, Genzwuerker HV, Sogl R, et al. Effect of nail
polish on oxygen saturation determined by pulse oximetry

10 Volume 1, Number 1

CME Questions

in critically ill patients. Resuscitation. 2007;72(1):82-91. (Prospective, observational; 50 patients)

63. Adler JN, Hughes LA, Vivilecchia R, et al. Effect of skin
pigmentation on pulse oximetry accuracy in the emergency
department. Acad Emerg Med. 1998;5(10):965-970. (Prospective, observational; 284 patients)
64. Barker SJ. Motion-resistant pulse oximetry: a comparison
of new and old models. Anesth Analg. 2002;95(4):967-972.
(Prospective, observational; 70 patients)
65. Tobias JD. Cerebral oximetry monitoring with near infrared
spectroscopy detects alterations in oxygenation before pulse
oximetry. J Intensive Care Med. 2008;23(6):384-388. (Prospective; 10 patients)
66. Foo JY, Wilson SJ, Dakin C, et al. Variability in time delay
between two models of pulse oximeters for deriving the
photoplethysmographic signals. Physiol Meas. 2005;26(4):531544. (Prospective; 9 healthy adults)
67. Xue FS, Liao X, Tong SY, et al. Effect of epidural block
on the lag time of pulse oximeter response. Anaesthesia.
1996;51(12):1102-1105. (Prospective; 36 patients)
68. Soltani HA, Hashemi SJ, Tavakkol K. Effect of digital block
on SpO2, lag time and height of plethysmographic wave of
pulse oximeter in presence of shock simulation. European
Journal of Anaesthesiology. 2004;21:23.
69. Murphy MF. In: Walls RM, ed. Manual of Emergency Airway
Management. Philadelphia, PA: Lippincott Williams &
Wilkins; 2004:333-335. (Review, text)
70. Mateer JR, Olson DW, Stueven HA, et al. Continuous pulse
oximetry during emergency endotracheal intubation. Ann
Emerg Med. 1993;22(4):675-679. (Prospective, observational;
284 patients)
71. Pedersen T, Moller AM, Pedersen BD. Pulse oximetry for
perioperative monitoring: systematic review of randomized,
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72. Guggenberger H, Lenz G, Federle R. Early detection of
inadvertent oesophageal intubation: pulse oximetry vs.
capnography. Acta Anaesthesiol Scand. 1989;33(2):112-115.
(Retrospective, observational; 21 patients)
73. Kellerman AL, Cofer CA, Joseph S, et al. Impact of portable
pulse oximetry on arterial blood gas test ordering in an urban emergency department. Ann Emerg Med. 1991;20(2):130134. (Prospective, observational; 20,120 patient visits)
74. Rotello LC, Warren J, Jastremski MS, et al. A nurse-directed
protocol using pulse oximetry to wean mechanically
ventilated patients from toxic oxygen concentrations. Chest.
1992;102(6):1833-1835. (Prospective; 13 patients)

Take This Test Online!

Current subscribers receive CME credit absolutely
free by completing the following test. Online testing
is available at
Each issue includes 3 AMA PRA Category 1 CreditsTM
Take This Test Online!
1. The use of colorimetric capnometry has been
shown to be more effective than the use of
continuous ETCO2 in confirming prehospital
intubation during cardiac arrest.

a. True

b. False
2. Continuous waveform ETCO2 monitoring can
be used to:

a. Verify correct ETT placement after RSI and

throughout intubation

b. Predict adverse respiratory events in

procedural sedation

c. Guide rhythm checks and demonstrate

ROSC during CPR

d. All of the above
3. An ETCO2 of less than 10 mm Hg during cardiac arrest:

a. Predicts dismal outcome at any point during

cardiac arrest

b. Indicates that the respiratory therapist

should decrease ventilation frequency

c. Always indicates a poorly positioned ETT

d. Is predictive of a very low likelihood of

ROSC, when measured during CPR, 20

minutes into a code
4. During a cardiac arrest, the patients ETCO2
suddenly changes from 12 to 28 mm Hg. At this
point, you should:

a. Increase your rate of bagging

b. Administer more epinephrine

c. Increase the depth of your compressions

d. Stop compressions and check the patients

5. Monitoring by pulse oximetry has been shown
to result in:

a. Fewer episodes of hypoxemia

b. Longer episodes of hypoxemia

c. Decreased incidence of both naloxone and

oxygen administration

d. None of the above Volume 1, Number 1


EMCC 2011

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professional judgment. It covers a highly technical and
complex subject and should not be used for making
specific medical decisions. The materials contained
herein are not intended to establish policy, procedure,
or standard of care. EM Critical Care and EMCC are
trademarks of EB Practice, LLC. Copyright 2011 EB
Practice, LLC, d.b.a. EB Medicine. All rights reserved.
No part of this publication may be reproduced in any
format without written consent of EB Practice, LLC.
This publication is intended for the use of the individual
subscriber only and may not be copied in whole or
part or redistributed in any way without the publishers
prior written permission including reproduction for
educational purposes or for internal distribution within a
hospital, library, group practice, or other entity. Volume 1, Number 1


EMCC 2011