2012 preoxygenation and prevention of desaturation during intubation

AIRWAY/REVIEW ARTICLE
Preoxygenation and Prevention of Desaturation During
Emergency Airway Management
Scott D. Weingart, MD, Richard M. Levitan, MD
From the Division of Emergency Critical Care, Department of Emergency Medicine, Mount Sinai School of Medicine, New York, NY (Weingart); and
the Department of Emergency Medicine, Thomas Jefferson University Hospital, Philadelphia, PA (Levitan).
Patients requiring emergency airway management are at great risk of hypoxemic hypoxia because of primary lung
pathology, high metabolic demands, anemia, insufficient respiratory drive, and inability to protect their airway
against aspiration. Tracheal intubation is often required before the complete information needed to assess the
risk of periprocedural hypoxia is acquired, such as an arterial blood gas level, hemoglobin value, or even a chest
radiograph. This article reviews preoxygenation and peri-intubation oxygenation techniques to minimize the risk of
critical hypoxia and introduces a risk-stratification approach to emergency tracheal intubation. Techniques
reviewed include positioning, preoxygenation and denitrogenation, positive end expiratory pressure devices, and
passive apneic oxygenation. [Ann Emerg Med. 2011;xx:xxx.]
0196-0644/$-see front matter
Copyright © 2011 by the American College of Emergency Physicians.
doi:10.1016/j.annemergmed.2011.10.002
INTRODUCTION
Maintaining hemoglobin saturation during airway
management is critical to patient safety. Desaturation to below
70% puts patients at risk for dysrhythmia, hemodynamic
decompensation, hypoxic brain injury, and death.1,2
The
challenge for emergency physicians is to secure a tracheal tube
rapidly without critical hypoxia or aspiration. In patients
without pulmonary pathology, adequate hemoglobin, or low
metabolic demands and an initial pulse oximetry reading of
100% on room air, there is a low risk of desaturation after
adequate preoxygenation. Conversely, in a septic patient with
multilobar pneumonia who is already hypoxemic (oxygen
saturation Յ90%) despite 100% oxygen at high flow, there is
an immediate risk of critical tissue hypoxia during tracheal
intubation.
This article reviews preoxygenation and peri-intubation
oxygenation techniques to minimize the risk of hypoxemia
during emergency tracheal intubation of adult patients. It
introduces a risk-stratification approach based on initial pulse
oximetry level in response to oxygen administration and
provides recommendations about specific techniques based on
periprocedural risk. Techniques reviewed include positioning,
preoxygenation and denitrogenation, use of positive pressure
devices to increase mean airway pressure, and passive apneic
oxygenation during tracheal intubation efforts.
WHAT IS THE RATIONALE FOR PROVIDING
PREOXYGENATION BEFORE TRACHEAL
INTUBATION?
Preoxygenation allows a safety buffer during periods of
hypoventilation and apnea. It extends the duration of safe
apnea, defined as the time until a patient reaches a saturation
level of 88% to 90%, to allow for placement of a definitive
airway. When patients desaturate below this level, their status is
on the steep portion of the oxyhemoglobin dissociation curve
and can decrease to critical levels of oxygen saturation (Ͻ70%)
within moments (Figure 1).3
The standard anesthesia induction of elective operative
patients is performed by administering a sedative, providing
manual ventilations, administering a muscle relaxant, and then
continuing manual ventilations until placement of a definitive
airway. Preoxygenation is not mandatory in these patients
because ventilation is continued throughout the induction
period and because they have normal physiology and low
metabolic needs.
For operative patients with high aspiration risk caused by
bowel pathology, body habitus, or critical illness,
anesthesiologists developed rapid sequence induction. As
originally conceived, this technique is the simultaneous
administration of the sedative and paralytic with no ventilation
while waiting for the paralytic to take effect, unless needed to
prevent hypoxemia. This induction method has been adapted to
the emergency department (ED), where all patients requiring
airway management are assumed to be at risk for aspiration; our
default technique is a rapid sequence tracheal intubation.
In a patient breathing room air before rapid sequence
tracheal intubation (PaO2 Ϸ90 to 100 mm Hg), desaturation
will occur in the 45 to 60 seconds between sedative/paralytic
administration and airway placement. In the 1950s,
anesthesiologists realized that the safest way to perform rapid
sequence tracheal intubation would be by filling the patient’s
alveoli with a high fraction of inspired oxygen (FiO2) before the
Volume xx, . x : Month  Annals of Emergency Medicine 1

procedure.4
Studies by Heller and Watson5
and Heller et al6
show markedly increased time to desaturation if the patients
received preoxygenation with 100% oxygen rather than room
air before tracheal intubation.5,6
For preoxygenation in the ED, we have 3 goals: (1) to bring
the patient’s saturation as close to 100% as possible; (2) to
denitrogenate the residual capacity of the lungs (maximizing
oxygen storage in the lungs); and (3) to denitrogenate and
maximally oxygenate the bloodstream.7
The first 2 goals are
imperative; denitrogenating and oxygenating the blood adds
little to the duration of safe apnea8
because oxygen is poorly
soluble in blood, and the bloodstream is a comparatively small
oxygen reservoir compared with the lungs (5% versus 95%).
Recommendation: Preoxygenation extends the duration of
safe apnea and is recommended for every ED tracheal
intubation.
WHAT IS THE BEST SOURCE OF HIGH FIO2 FOR
PREOXYGENATION?
The duration of safe apnea times in most of the
preoxygenation literature is predicated on anesthesia circuits
that are capable of delivering 90% to 100% FiO2 when used
with a well-fitting mask. However, the usual source of oxygen
during ED preoxygenation is a facemask with an oxygen
reservoir. This device is erroneously referred to as the
nonrebreather mask despite an absence of 1-way valves covering
all of its ports. True nonrebreather masks set at 15 L/minute for
patients with normal ventilatory patterns are capable of
delivering near 90% FiO2,9
but these devices are rarely available
in EDs. Standardly available nonrebreather masks at flow rates
of 15 L/minute deliver only 60% to 70% FiO2, do not provide
complete denitrogenation, and accordingly do not maximize the
duration of safe apnea.9
Standardly available nonrebreather masks can deliver FiO2
greater than or equal to 90% by increasing the flow rate to 30 to
60 L/minute.10
Such flow rates may be achievable on most flow
regulators in EDs by continuing to open the valve, though there
will be no calibrated markings beyond 15 L/minute.
Some ED providers use the self-inflating bag-valve-mask
device to provide preoxygenation. Bag-valve-mask devices
lacking 1-way inhalation and exhalation ports will deliver only
close to room air FiO2 when not actively assisting
ventilations.11,12
Even with ideal 1-way valves, the devices will
deliver oxygen only in 2 circumstances: the patient generates
enough inspiratory force to open the valve or the practitioner
squeezes the bag. In both circumstances, to obtain any FiO2
above that of room air, a tight seal must be achieved with the
mask, which usually requires a 2-handed technique.13
A bag-
valve-mask device hovering above the patient’s face provides
only ambient FiO2.
Recommendation: Standard reservoir facemasks with the
flow rate of oxygen set as high as possible are the recommended
source of high FiO2 for preoxygenation in the ED.
FOR WHAT PERIOD OF TIME SHOULD THE
PATIENT RECEIVE PREOXYGENATION?
Ideally, patients should continue to receive preoxygenation
until they denitrogenate the functional residual capacity of their
lungs sufficiently to achieve greater than 90% end-tidal oxygen
level.14
Although the mass spectrometers in many EDs allow the
measurement of end-tidal oxygen levels, in practice this is rarely
performed. Instead, expediency often demands an empiric
timing of preoxygenation.
Three minutes’ worth of tidal-volume breathing (the
patient’s normal respiratory pattern) with a high FiO2 source is
an acceptable duration of preoxygenation for most patients.15,16
This tidal-volume breathing approach can be augmented by
asking the patient to exhale fully before the 3-minute
period.17,18
Cooperative patients can be asked to take 8 vital-capacity
breaths (maximal exhalation followed by maximal
inhalation).16,19,20
This method generally can reduce the
preoxygenation time to approximately 60 seconds.16
Unfortunately, many ill ED patients cannot take vital-capacity
breaths.
The above times are predicated on a source of FiO2 greater
than or equal to 90% and a tightly fitting mask that prevents
entrainment of room air.21
Recommendation: Patients with an adequate respiratory
drive should receive preoxygenation for 3 minutes or take 8
breaths, with maximal inhalation and exhalation.
CAN INCREASING MEAN AIRWAY PRESSURE
AUGMENT PREOXYGENATION?
Mean airway pressure may be increased during
preoxygenation through the use of techniques such as
Figure 1. Oxyhemoglobin dissociation curve demonstrates
the SpO2 from various levels of PaO2. Risk categories are
overlaid on the curve. Patients near an SpO2 of 90% are at
risk for precipitous desaturation, as demonstrated by the
shape of the curve.
Preoxygenation and Prevention of Desaturation During Emergency Airway Management Weingart & Levitan
2 Annals of Emergency Medicine Volume xx, . x : Month 

noninvasive positive-pressure ventilation. If patients have not
achieved a saturation greater than 93% to 95% before tracheal
intubation, they have a higher likelihood of desaturation during
their apneic and tracheal intubation periods.2,16,18,22,23
If
patients do not achieve this saturation level after 3 minutes of
tidal-volume breathing with a high FiO2 source, it is likely that
they are exhibiting shunt physiology; any further augmentation
of FiO2 will be unhelpful.24
Shunt physiology refers to alveoli
that are perfused but not ventilated because of conditions such
as pulmonary edema or pneumonia, in which the alveoli are
filled with fluid or collapsed. The net effect is a physiologic
right-to-left shunt; blood coming from the pulmonary arteries is
returned to the pulmonary veins without oxygenation. In the
short term, shunt physiology can be partially overcome by
augmenting mean airway pressure, thereby improving the
effectiveness of preoxygenation and extending the safe apnea
time.
Evidence for the use of increased mean airway pressure as a
preoxygenation technique can be found in Table 1. In a study
particularly relevant to the ED, Baillard et al23
examined
hypoxemic critically ill patients requiring tracheal intubation in
the ICU. At the end of the preoxygenation period, the
noninvasive positive-pressure ventilation group had a 98%
mean SpO2, whereas the standard group had one of 93%. In the
noninvasive positive-pressure ventilation group, 6 of 26 patients
were unable to improve their hypoxemic saturations with high
FiO2 until they received positive pressure. During the tracheal
intubation procedure, the standard group’s levels decreased to
saturations of 81% compared with 93% in the noninvasive
positive-pressure ventilation group. Twelve of the control group
and 2 of the noninvasive positive-pressure ventilation group had
saturation levels below 80%.
No negative cardiovascular effects27,31
or appreciable gastric
distention was observed in noninvasive positive pressure
preoxygenation studies.25
The latter result was likely due to the
low pressures used in these studies; gastric distention and
resulting aspiration is unlikely at pressures below 25 cm
H2O.32-35
The data on the absence of any cardiovascular side
Table 1. Evidence for increased mean airway pressure as a preoxygenation technique.
Study Patients Intervention Comparator Outcome
Delay et al25
RCT of 28 obese,
operative patients
Noninvasive ventilation Spontaneous ventilation
at zero pressure
The patients in the noninvasive
positive-pressure ventilation
group achieved faster and
more complete
denitrogenation than the
standard group, as
measured by an exhaled
oxygen level Ͼ90%.
Futier et al26
RCT of 66 obese,
operative patients
Two treatment groups: noninvasive
ventilation or noninvasive
ventilation with post–tracheal
intubation recruitment maneuver
Spontaneous ventilation
at zero pressure
At the end of preoxygenation,
PaO2 was higher in the NPPV
and NPPVϩRM groups
compared with the spont
vent group and remained
higher after TI and the onset
of mechanical ventilation
Cressey et al27
RCT of 20 morbidly
obese women
undergoing
bariatric surgery
CPAP preoxygenation Spontaneous ventilation
at zero pressure
Showed a 40-s increase in
time to desaturation through
the use of noninvasive
positive pressure.
Nonsignificant primary
outcome.
Gander et al28
RCT of 30 morbidly
obese operative
patients
at zero pressure
The time until reaching a
saturation of 90% after
apnea was extended by a
minute in the CPAP group
Herriger et al29
RCT of 40 ASA I–II
operative patients
at zero pressure
Application of positive airway
pressure during induction of
anesthesia in adults
prolongs the nonhypoxic
apnea duration by Ͼ2 min
Antonelli et al30
RCT of 26 hypoxemic
ICU patients
requiring
bronchoscopy
Noninvasive ventilation Spontaneous ventilation
at zero pressure
The PaO2/FiO2 ratio improved
in the noninvasive positive-
pressure ventilation group
and worsened in the high-
FiO2-alone group
RCT, Randomized controlled trial; NPPV, noninvasive positive-pressure ventilation; RM, recruitment maneuver; CPAP, continuous positive airway pressure; ASA, Ameri-
can Society of Anesthesiologists; TI, tracheal intubation.
Weingart & Levitan Preoxygenation and Prevention of Desaturation During Emergency Airway Management

effects may not be applicable to volume-depleted critically ill
patients.36
The benefits of noninvasive positive-pressure ventilation for
preoxygenation in the ED should primarily be observed in
patients who cannot achieve acceptable saturations with high
FiO2 alone.31
If tracheal intubation is attempted with
saturations below 90%, these patients can critically desaturate in
seconds.37
Positive pressure may be applied with standalone
disposable continuous positive airway pressure (CPAP) masks38
;
with CPAP masks connected to noninvasive machines or
standard ventilators; or by using a positive end-expiratory
pressure (PEEP) valve on a standard bag mask (Figure 2). Even
in departments without immediate CPAP systems, single-use
PEEP valves are inexpensive and require minimal modification
of practice.
In critically ill patients with very high degrees of shunting,
apneic oxygenation (discussed below) alone is unlikely to be
helpful.39
If patients require CPAP during their preoxygenation
period, it may benefit them to have the device left on until the
moment of tracheal intubation. Whatever predisposed them to
experience shunting will recur during the apneic period if they
remain at zero airway pressure.40
PEEP also prevents absorption
atelectasis caused by breathing high FiO2 gas level, increasing
the efficacy of apneic oxygenation.41
Recommendation: CPAP masks, noninvasive positive-
pressure ventilation, or PEEP valves on a bag-valve-mask device
should be considered for preoxygenation and ventilation during
the onset phase of muscle relaxation in patients who cannot
achieve saturations greater than 93% to 95% with high FiO2.
IN WHAT POSITION SHOULD THE PATIENT
RECEIVE PREOXYGENATION?
Supine positioning is not ideal to achieve optimal
preoxygenation. When one is placed flat, it is more difficult to
take full breaths and more of the posterior lung becomes prone
to atelectatic collapse,3
which reduces the reservoir of oxygen
contained within the lungs and therefore reduces safe apnea
time.
Lane et al42
performed a randomized controlled trial of
patients preoxygenated in a 20-degree head-up position
versus a control group that was left supine. After 3 minutes
of preoxygenation, the patients received sedation and muscle
relaxation and were then allowed to decrease their saturation
from 100% to 95%. The head-up group took 386 seconds to
reach this saturation versus 283 seconds in the control
group.42
Recently, Ramkumar et al43
confirmed these results,
with the 20-degree head-up group taking 452 seconds to
desaturate versus 364 seconds for the supine group.
Altermatt et al44
examined specifically preoxygenation in
obese patients (body mass index Ͼ35). This randomized
controlled trial compared safe apnea times in intubated
patients who received preoxygenation in a sitting position
compared with those preoxygenated while lying flat. After
rapid sequence induction of anesthesia, the trachea was
intubated and the patient was left apneic and disconnected
from the anesthesia circuit until SpO2 level decreased from
100% to 90%. Using the time taken for desaturation to 90%
as the outcome, the patients preoxygenated in a sitting
position took 214 seconds to desaturate versus 162 seconds
for patients preoxygenated while lying flat.44
Dixon et al45
showed similar benefits in a third randomized controlled trial
in patients with body mass index greater than 40 who were
placed in the 25-degree head-up position.
Reverse Trendelenburg position (head of stretcher 30 degrees
higher than the foot) also improves preoxygenation and may be
useful in patients who cannot bend at the waist or shoulders, ie,
those immobilized for possible spinal injury.46
An additional benefit of head elevation is better laryngeal
exposure during direct laryngoscopy.47
Recommendation: Patients should receive preoxygenation in
a head-elevated position whenever possible. For patients
immobilized for possible spinal injury, reverse Trendelenburg
position can be used.
HOW LONG WILL IT TAKE FOR THE PATIENT
TO DESATURATE AFTER PREOXYGENATION?
Although breathing at a high FiO2 level will slightly
increase the bloodstream stores of oxygen, the primary
benefit of preoxygenation is the creation of a reservoir of
oxygen in the alveoli. When a patient is breathing room air,
Figure 2. A disposable PEEP valve. This inexpensive item
is a strain gauge capable of PEEP settings from 5 to 20
cm H2O. When placed on the exhalation port of a bag-
valve-mask device (inset), it allows the device to provide
PEEP/CPAP when the patient is spontaneously breathing
and during assisted ventilations. If combined with a nasal
cannula set to 15 L/minute, it will provide CPAP even
without ventilations. The generation of positive pressure is
predicated on a tight mask seal.

450 mL of oxygen is present in the lungs; this amount
increases to 3,000 mL when a patient breathes 100% oxygen
for a sufficient time to replace the alveolar nitrogen. A
patient breathing room air will have a total oxygen reservoir
in the lungs and bloodstream of approximately 1.0 to 1.5 L,
whereas an optimally preoxygenated patient will have 3.5 to
4.0 L.3
Oxygen consumption during apnea is approximately
250 mL/minute (3 mL/kg per minute); in healthy patients,
the duration of safe apnea on room air is approximately 1
minute compared with approximately 8 minutes when
breathing at a high FiO2 level.3
Benumof et al48
used physiologic modeling to calculate
the time to desaturation less than 90% after the
administration of succinylcholine for various patient groups
after apnea. The times were 8 minutes, 5 minutes, and 2.7
minutes for healthy adults, moderately ill adults, and obese
adults, respectively.
The desaturation curves of Benumof et al48
have been
extensively reproduced in the emergency medicine literature,
but the extended times in these models are predicated on
factors that are very different from those present in many
emergency tracheal intubations. The curves assume complete
denitrogenation and alveolar concentrations of oxygen at
80%. The model by Benumof et al48
assumes preoxygenation
with a device capable of generating approximately 90% FiO2
and optimal time for preoxygenation. It also ignores pulse
oximeter lag time. In sick patients, especially those with poor
cardiac output, the readings on a finger-probe pulse oximeter
may lag behind the actual central arterial circulation by 30 to
60 seconds.49
The times depicted by the desaturation curves
are not applicable to critically ill ED patients or those with
poor cardiac output.50-52
The effect of shunting, increased metabolic demand, anemia,
volume depletion, and decreased cardiac output are synergistic
in dramatically reducing oxygen storage in the lungs and
shortening safe apnea in critically ill patients. As calculated by
Farmery and Roe,51
desaturation to 85% may be as short as 23
seconds in critically ill patients versus 502 seconds in a healthy
adult.51
Mort52
studied ICU patients with blood gas measurements
before and after preoxygenation, using bag-valve-mask
ventilation. Average PaO2 was only 67 mm Hg at baseline and
increased to a mean of only 104 mm Hg after 4 minutes of bag-
valve-mask ventilation. In less than 20% of patients did
preoxygenation increase the PaO2 by 50 mm Hg. The author’s
conclusion was that preoxygenation is only marginally effective
in critically ill patients. It is important for clinicians to
appreciate that PaO2 values in this range are on the steep section
of the pulse oximetry curve (Figure 1).
Recommendation: Given the unique variables involved in
each ED tracheal intubation, it is impossible to predict the
exact duration of safe apnea in a patient. Patients with high
saturation levels on room air or after oxygen administration
are at lower risk and may maintain adequate oxygen
saturation as long as 8 minutes. Critically ill patients and
those with values just above the steep edge of the
desaturation curve are at high risk of hypoxemia with
prolonged tracheal intubation efforts and may desaturate
immediately.
CAN APNEIC OXYGENATION EXTEND THE
DURATION OF SAFE APNEA?
Alveoli will continue to take up oxygen even without
diaphragmatic movements or lung expansion. In an apneic
patient, approximately 250 mL/minute of oxygen will move
from the alveoli into the bloodstream. Conversely, only 8 to 20
mL/minute of carbon dioxide moves into the alveoli during
apnea, with the remainder being buffered in the bloodstream.53
The difference in oxygen and carbon dioxide movement across
the alveolar membrane is due to the significant differences in gas
solubility in the blood, as well as the affinity of hemoglobin for
oxygen. This causes the net pressure in the alveoli to become
slightly subatmospheric, generating a mass flow of gas from
pharynx to alveoli. This phenomenon, called apneic
oxygenation, permits maintenance of oxygenation without
spontaneous or administered ventilations. Under optimal
circumstances, a PaO2 can be maintained at greater than 100
mm Hg for up to 100 minutes without a single breath, although
the lack of ventilation will eventually cause marked hypercapnia
and significant acidosis.54
Apneic oxygenation is not a new concept; it has been
described in the medical literature for more than a century, with
names such as apneic diffusion oxygenation, diffusion
respiration, and mass flow ventilation.55,56
A summary of
human evidence for apneic oxygenation is available as a
supplement to this article (Table E1, available online at http://
www.annemergmed.com).
Neurocritical care physicians and neurologists are familiar
with the use of apneic oxygenation to prevent desaturation
while performing brain death examinations.63-65
Apneic
oxygenation has also been used to continue oxygenation during
bronchoscopies and otolaryngeal procedures.66-68
Two studies merit specific mention because they extend the
technique to situations applicable to emergency tracheal
intubation. In a randomized controlled trial of anesthesia
patients, Taha et al69
demonstrated no desaturation during the
course of 6 minutes in patients receiving 5 L/minute of oxygen
through a nasal catheter. Conversely, the control group
desaturated to the study cutoff of 95% in an average of 3.65
minutes. Ramachandran et al70
performed a randomized
controlled trial of obese patients requiring tracheal intubation
for elective surgery. The apneic oxygenation group received 5
L/minute of oxygen through nasal cannulas during their apneic
period. The apneic oxygenation group had significant
prolongation of the time spent with a SpO2 greater than or
equal to 95% (5.29 versus 3.49 minutes), a significant increase
in patients with SpO2 greater than or equal to 95% at the 6-
minute mark (8 patients versus 1 patient), and significantly
higher minimum SpO2 (94.3% versus 87.7%).

Apneic oxygenation as described above will allow continued
oxygenation but will have no significant effect on carbon
dioxide levels. Although extracorporeal carbon dioxide removal,
high oscillatory flow, or acid buffers can allow apneic
ventilation, as well as oxygenation, these therapies are outside
the scope of current ED practice.
To provide apneic oxygenation during ED tracheal
intubations, the nasal cannula is the device of choice. Nasal
cannulas provide limited FiO2 to a spontaneously breathing
patient,71
but the decreased oxygen demands of the apneic state
will allow this device to fill the pharynx with a high level of
FiO2 gas.70
By increasing the flow rate to 15 L/minute, near
100% FiO2 can be obtained. Although providing high flow
rates with a conventional, nonhumidified nasal cannula can be
uncomfortable because of its desiccating effect on the
nasopharynx, after the patient has been sedated it should cause
no deleterious effects for the short interval of airway
management. Tailor-made high-flow nasal cannulas are also
available that will humidify the oxygen, allowing flow rates up
to 40 L/minute.72
The patients’ mouths being open did not negatively affect
the FiO2 provided.73
If any potential obstruction caused by
redundant nasal tissue is discovered, nasal trumpets will allow a
direct conduit from the nasal cannula to the oropharynx.
Although facemasks and nonrebreather masks can provide
high FiO2 levels to spontaneously breathing patients (depending
on flow rates), they provide minimal oxygen to apneic
patients,74
likely because of the 2 exhalation valves venting the
fresh gas flow. Bag-valve-mask devices provide no oxygen to
apneic patients unless manual ventilations are delivered. Even
with manual ventilations, a continuous flow of high-level FiO2
will not be available with this device.
Conventional ventilators or noninvasive ventilation machines
do not supply a continuous flow of gas when placed on
conventional or noninvasive settings. The minimal negative
inspiratory pressures generated during apneic oxygenation are
insufficient to trigger gas delivery with these machines.
Although the high-flow CPAP setups found in many ICUs can
provide both positive pressure and high FiO2 levels for apneic
oxygenation, they are not commonly available in EDs.
An additional benefit to the use of nasal cannula devices is
that they can be left on during the tracheal intubation attempts.
This has been described with an acronym, NO DESAT (nasal
oxygen during efforts securing a tube)75
; it allows the continued
benefits of apneic oxygenation while tracheal intubation
techniques are performed. The nasal cannula can be placed
under a facemask (or bag-valve-mask device) during
preoxygenation, and then it remains on, administering oxygen
through the nose throughout oral tracheal intubation with
direct or video laryngoscopy.
Recommendation: Apneic oxygenation can extend the
duration of safe apnea when used after the administration of
sedatives and muscle relaxants. A nasal cannula set at 15
L/minute is the most readily available and effective means of
providing apneic oxygenation during ED tracheal intubations.
WHEN AND HOW SHOULD WE PROVIDE
MANUAL VENTILATIONS DURING THE APNEIC
PERIOD?
Practitioners should not initiate laryngoscopy before full
muscle relaxation to maximize laryngeal exposure and to avoid
triggering the patient’s gag reflex and active vomiting just before
apnea. Ventilation provides 2 potential benefits during the onset
phase of muscle relaxation: ventilation and increased
oxygenation through alveolar distention and reduction in
shunting.
The first benefit is minimal in most clinical scenarios. On
average, PaCO2 increases 8 to 16 mm Hg in the first minute of
apnea and then approximately 3 mm Hg/minute
subsequently.53
It is rare that this degree of PaCO2 increase and
pH decrease will be clinically significant. An exception is a
profound metabolic acidosis, such as severe salicylate toxicity, in
which patients compensate for the acidosis through hyperpnea
and tachypnea. Aggressive ventilation is needed for such patients
because cardiovascular collapse with cessation of self-ventilation
has been reported.76
A second exception is in situations of
increased intracranial pressure, in which the carbon dioxide
increase can lead to cerebral vasodilation.
The second benefit, increased oxygenation, is crucial;
patients starting with a pulse oximetry reading of less than or
equal to 90% will not tolerate apnea for 60 seconds. Ventilation
during the onset phase of muscle relaxation can create alveolar
distention and lengthen the duration of safe apnea during
tracheal intubation efforts, assuming it is conducted carefully.
Bag-valve-mask device inspiratory pressures greater than 25 cm
H2O can overwhelm the esophageal sphincter and put the
patient at risk for regurgitation and aspiration.34,35
When
providers are inexperienced or under stress, this pressure is easily
exceeded.77
If ventilations during apnea are required, it may be
preferable to use an automated device such as a handheld or
conventional ventilator with built-in inspiratory pressure limits
and PEEP.78,79
If a bag-valve-mask device is used during the onset of
muscular relaxation, a PEEP valve will provide sustained
alveolar distention. Ventilations should be delivered slowly
(during 1 to 2 seconds), involve a low volume (6 to 7 mL/kg),
and be administered at as low a rate as tolerable for the clinical
circumstances (6 to 8 breaths/min).80
Although not clinically
proven, there may be a benefit to head elevation in reducing the
risk of passive regurgitation in such patients, in addition to the
significant physiologic benefits of oxygenation in a head-
elevated position.
A significant risk of positive-pressure ventilation in the
critically ill patient involves decreased venous return and
hypotension. This is especially significant in low flow states
from any cause (hypotension), volume depletion, acute
respiratory distress syndrome, and obstructive airway disease
(with attendant risks of intrinsic PEEP). Overventilation in such

patients may precipitate hemodynamic collapse, and clinicians
must be mindful of rate, volume, and speed of ventilation in
these situations. Relative hypoventilation and resultant
permissive hypercapnia may be required to avoid hemodynamic
collapse.81
Recommendation: The risk/benefit of active ventilation
during the onset phase of muscle relaxants must be carefully
assessed in each patient. In patients at low risk for desaturation
(Ͼ95% saturation), manual ventilation is not necessary. In
patients at higher risk (91% to 95% saturation), a risk-benefit
assessment should include an estimation of desaturation risk and
the presence of pulmonary pathology. In hypoxemic patients,
low-pressure, low-volume, low-rate ventilations will be required.
WHAT POSITIONING AND MANEUVERS
SHOULD THE PATIENT RECEIVE DURING THE
APNEIC PERIOD?
Apneic oxygenation requires a patent airway for oxygen to
reach the hypopharynx and be entrained into the trachea; once
the patient is sedated and paralyzed, it is imperative to keep the
posterior pharyngeal structures and tongue from occluding the
passage of gas. Head elevation, chin lift, and jaw thrust will
accomplish this in most patients; a jaw thrust alone should be
used if there is risk for cervical spine injury. In some patients, a
nasal trumpet or oral airway may also be required. Patients with
sleep apnea or obesity often need a combination of jaw
distraction, lifting of submandibular soft tissue, and nasal or
oral airways.
Positioning the patient with their external auditory meatus
on the same horizontal plane as their sternal notch maximizes
upper airway dimensions and facilitates direct laryngoscopy.82,83
Head elevation relative to the thorax also permits optimal jaw
distraction, and conversely atlanto-occipital extension pivots the
base of tongue and epiglottis against the posterior pharynx and
promotes obstruction. In all but the thinnest patients, a head-
elevated position requires lifting of the head of the bed
somewhat, plus padding under the head and upper shoulders.
The face plane of the patient should be parallel to the ceiling.
For the superobese, this positioning requires a very large ramp.
In cervical spine precautions, elevating the head relative to the
neck is not possible, but as previously noted the foot of the
stretcher should be tilted downward to improve pulmonary
function.
Cricoid pressure, considered an essential aspect of rapid
sequence tracheal intubation when it was first conceived, has
come under increasing scrutiny within anesthesia and
emergency medicine.84,85
Theoretically, the application of firm
pressure to the cricoid cartilage compresses the esophagus while
keeping the trachea patent, but in practice this is not always the
case.86
Computed tomography and magnetic resonance imaging
scanning have shown that cricoid pressure causes lateral
displacement of the esophagus in more than 90% of patients
and laryngeal/tracheal compression in 80%.87,88
Numerous
ventilation studies have found that cricoid pressure hinders bag-
valve-mask device ventilation, increases peak inspiratory
pressure, and reduces tidal volumes.34,84,89-94
For the same
reasons that the airway obstruction induced by cricoid pressure
may preclude effective manual ventilation, it may limit the
effectiveness of apneic oxygenation as well.
Recommendation: Patients should be positioned to
maximize upper airway patency before and during the apneic
period, using ear-to–sternal notch positioning. Nasal airways
may be needed to create a patent upper airway. Once the apneic
period begins, the posterior pharyngeal structures should be
kept from collapsing backwards by using a jaw thrust. Cricoid
pressure may negatively affect apneic oxygenation, but studies
examining this question in the setting of modern emergency
airway management do not exist to our knowledge.
DOES THE CHOICE OF PARALYTIC AGENT
AFFECT PREOXYGENATION?
The choice of paralytic agent may influence the time to
desaturation during airway management. In a study of operative
patients, the time to desaturation to 95% was 242 seconds in
patients receiving succinylcholine versus 378 seconds in a group
given rocuronium.95
Similarly, in obese patients undergoing
surgery, the succinylcholine group desaturated to 92% in 283
seconds versus 329 seconds in the rocuronium group.96
When
used at a dose of greater than or equal to 1.2 mg/kg,
rocuronium provides intubating conditions identical to those of
succinylcholine.97
It is hypothesized that the fasciculations induced by
succinylcholine may cause increased oxygen use. Pretreatment
medications to prevent fasciculations minimize the difference in
desaturation times.95
Recommendation: In patients at high risk of desaturation,
rocuronium may provide a longer duration of safe apnea than
succinylcholine.
RISK STRATIFICATION AND CONCLUSIONS
Patients requiring emergency airway management can be
risk stratified into 3 groups, according to pulse oximetry after
initial application of high-flow oxygen. The recommended
techniques to use for patients in each group are shown in
Table 2, and a logistic flow of preoxygenation steps is shown
in Figure 3.
Head-elevated positioning is simple and easy to apply in all
patients; in the patient immobilized for cervical spine injury, it
is beneficial to tilt the foot of the bed downward.
Patients at lowest risk (saturations of 96% to 100%) should
be properly positioned and receive preoxygenation; active
ventilation is not needed. Passive apneic oxygenation during
tracheal intubation efforts may not be necessary in these low-
risk patients, but it will extend safe apnea in the event of
repeated tracheal intubation attempts.
Patients in the 91% to 95% saturation group after receiving
high FiO2 levels are at high risk of critical desaturation during

emergency tracheal intubation. Positioning, preoxygenation,
and passive oxygenation should be used. For these patients,
consideration should be given to using PEEP during
preoxygenation and while awaiting muscle relaxation, but the
risks and benefits of these techniques must be assessed case by
case.
For patients initially hypoxemic with high FiO2 levels
(saturation of 90% or less), aggressive efforts must be made to
Figure 3. Logistic flow of preoxygenation and prevention of desaturation.
Table 2. Risk categorization of patients during preoxygenation.*
Risk Category, Based
on Pulse Oximetry
While Receiving High-
Flow Oxygen
Preoxygenation Period
(3 Minutes)
Onset of Muscle Relaxation
(Ϸ60 Seconds)
Apneic Period During Tracheal
Intubation (Variable
Duration, Depending on
Airway Difficulty; Ideally
<30 Seconds)
Low risk, SpO2
96%–100%
Nonrebreather mask with
maximal oxygen flow rate
Nonrebreather mask and nasal
oxygen at 15 L/min
Nasal oxygen at 15 L/min
High risk, SpO2
91%–95%
Nonrebreather mask or CPAP or
bag-valve-mask device with
PEEP
Nonrebreather mask, CPAP, or bag-
valve-mask device with PEEP and
nasal oxygen at 15 L/min
Hypoxemic, SpO2
90% or less
CPAP or bag-valve-mask device
with PEEP
CPAP or bag-valve-mask device with
PEEP and nasal oxygen at 15 L/
min
*Risk categories are based on patient’s initial response to high-flow oxygen through a tightly fitting nonrebreather mask. Patients who are already hypoxemic
exhibit shunt physiology and are prone to rapid desaturation during the peri-intubation. Patients with saturations of 91% to 95% have values close to the preci-
pice of the steep portion of the oxyhemoglobin dissociation curve and should be considered high risk. Patients with saturations greater than or equal to 96%
are at low risk for peri-intubation desaturation. Patients in all risk categories should receive preoxygenation in a head-elevated position (or reverse-Trendelen-
burg if there is a risk of spine injury).

maximize saturation before tracheal intubation. These patients
will require PEEP during preoxygenation, ventilation during the
onset of phase of muscle relaxants, and passive oxygenation
during tracheal intubation.
Videos of the techniques described in this article can be
found at http://emcrit.org/preoxygenation.
Supervising editors: Gregory W. Hendey, MD; Donald M. Yealy,
MD
Funding and support: By Annals policy, all authors are required
to disclose any and all commercial, financial, and other
relationships in any way related to the subject of this article
as per ICMJE conflict of interest guidelines (see
www.icmje.org). The authors have stated that no such
relationships exist.
Publication dates: Received for publication June 25, 2011.
Revisions received July 20, 2011; September 4, 2011; and
September 28, 2011. Accepted for publication October 4,
2011.
Address for correspondence: Richard M. Levitan, MD, E-mail
airwaycam@gmail.com.
REFERENCES
1. Mort TC. The incidence and risk factors for cardiac arrest during
emergency tracheal intubation: a justification for incorporating the
ASA guidelines in the remote location. J Clin Anesth. 2004;16:
508-516.
2. Davis DP, Hwang JQ, Dunford JV. Rate of decline in oxygen
saturation at various pulse oximetry values with prehospital rapid
sequence intubation. Prehosp Emerg Care. 2008;12:46-51.
3. Lumb AB. Nunn’s Applied Respiratory Physiology. 7th ed. Oxford:
Churchill Livingstone; 2010:568.
4. Morton HJ, Wylie WD. Anaesthetic deaths due to regurgitation or
vomiting. Anaesthesia. 1951;6:190-201.
5. Heller ML, Watson TR Jr. Polarographic study of arterial
oxygenation during apnea in man. N Engl J Med. 1961;264:326-
330.
6. Heller ML, Watson TR Jr, Imredy DS. Apneic oxygenation in man:
polarographic arterial oxygen tension study. Anesthesiology.
1964;25:25-30.
7. Campbell IT, Beatty PC. Monitoring preoxygenation. Br J Anaesth.
1994;72:3-4.
8. Baraka A, Ramez Salem M. Preoxygenation. In: Hagberg CA, ed.
Benumof’s Airway Management: Principles and Practice. 2nd ed.
Philadelphia, PA: Mosby; 2007:303-318.
9. Vender JS, Szokol JW. Oxygen delivery systems, inhalation
therapy, and respiratory therapy. In: Hagberg CA, ed. Benumof’s
Airway Management: Principles and Practice. 2nd ed.
Philadelphia, PA: Mosby; 2007:321-345.
10. Earl JW. Delivery of high FiO2. Available at: http://
www.rcjournal.com/abstracts/2003/?idϭOF-03-257. Accessed
April 11, 2011.
11. Nimmagadda U, Salem MR, Joseph NJ, et al. Efficacy of
preoxygenation with tidal volume breathing. Comparison of
breathing systems. Anesthesiology. 2000;93:693-698.
12. Mills PJ, Baptiste J, Preston J, et al. Manual resuscitators and
spontaneous ventilation—an evaluation. Crit Care Med. 1991;19:
1425-1431.
13. Joffe AM, Hetzel S, Liew EC. Anesthesiology. 2010;113:873-879.
14. Bhatia PK, Bhandari SC, Tulsiani KL, et al. End-tidal oxygraphy
and safe duration of apnoea in young adults and elderly patients.
Anaesthesia. 1997;52:175-178.
15. Hamilton WK, Eastwood DW. A study of denitrogenation with
some inhalation anesthetic systems. Anesthesiology. 1955;16:
861-867.
16. Baraka AS, Taha SK, Aouad MT, et al. Preoxygenation:
comparison of maximal breathing and tidal volume breathing
techniques. Anesthesiology. 1999;91:612-616.
17. Baraka AS, Taha SK, El-Khatib MF, et al. Oxygenation using tidal
volume breathing after maximal exhalation. Anesth Analg. 2003;
97:1533-1535.
18. Baraka A, Haroun-Bizri S, Khoury S, et al. Single vital capacity
breath for preoxygenation. Can J Anaesth. 2000;47:1144-1146.
19. Pandit JJ, Duncan T, Robbins PA. Total oxygen uptake with two
maximal breathing techniques and the tidal volume breathing
technique: a physiologic study of preoxygenation. Anesthesiology.
2003;99:841-846.
20. Rapaport S, Joannes-Boyau O, Bazin R, et al. [Comparison of
eight deep breaths and tidal volume breathing preoxygenation
techniques in morbid obese patients]. Ann Fr Anesth Reanim.
2004;23:1155-1159.
21. Benumof JL. Preoxygenation: best method for both efficacy and
efficiency. Anesthesiology. 1999;91:603-605.
22. El-Khatib MF, Kanazi G, Baraka AS. Noninvasive bilevel positive
airway pressure for preoxygenation of the critically ill morbidly
obese patient. Can J Anaesth. 2007;54:744-747.
23. Baillard C, Fosse JP, Sebbane M, et al. Noninvasive ventilation
improves preoxygenation before intubation of hypoxic patients.
Am J Respir Crit Care Med. 2006;174:171-177.
24. Nunn JF. Applied Respiratory Physiology. 4th ed. Oxford, England:
Butterworth-Heinemann; 1995:156–197.
25. Delay JM, Sebbane M, Jung B, et al. The effectiveness of
noninvasive positive pressure ventilation to enhance
preoxygenation in morbidly obese patients: a randomized
controlled study. Anesth Analg. 2008;107:1707-1713.
26. Futier E, Constantin JM, Pelosi P, et al. Noninvasive ventilation
and alveolar recruitment maneuver improve respiratory function
during and after intubation of morbidly obese patients: a
randomized controlled study. Anesthesiology. 2011;114:1354-
1363.
27. Cressey DM, Berthoud MC, Reilly CS. Effectiveness of continuous
positive airway pressure to enhance pre-oxygenation in morbidly
obese women. Anaesthesia. 2001;56:680-684.
28. Gander S, Frascarolo P, Suter M, et al. Positive end-expiratory
pressure during induction of general anesthesia increases
duration of nonhypoxic apnea in morbidly obese patients. Anesth
Analg. 2005;100:580-584.
29. Herriger A, Frascarolo P, Spahn DR, et al. The effect of positive
airway pressure during pre-oxygenation and induction of
anaesthesia upon duration of non-hypoxic apnoea. Anaesthesia.
2004;59:243-247.
30. Antonelli M, Conti G, Rocco M, et al. Noninvasive positive-
pressure ventilation versus conventional oxygen supplementation
in hypoxemic patients undergoing diagnostic bronchoscopy.
Chest. 2002;121:1149-1154.
31. Jaber S, Jung B, Corne P, et al. An intervention to decrease
complications related to endotracheal intubation in the intensive
care unit: a prospective, multiple-center study. Intensive Care
Med. 2010;36:248-255.
32. Vyas H, Milner AD, Hopkin IE. Face mask resuscitation: does it
lead to gastric distension? Arch Dis Child. 1983;58:373-375.
33. Ho-Tai LM, Devitt JH, Noel AG, et al. Gas leak and gastric
insufflation during controlled ventilation: face mask versus
laryngeal mask airway. Can J Anaesth. 1998;45:206-211.

34. Lawes EG, Campbell I, Mercer D. Inflation pressure, gastric
insufflation and rapid sequence induction. Br J Anaesth. 1987;
59:315-318.
35. Ruben H, Knudsen EJ, Carugati G. Gastric inflation in relation to
airway pressure. Acta Anaesthesiol Scand. 1961;5:107-114.
36. Jellinek H, Krafft P, Fitzgerald RD, et al. Right atrial pressure
predicts hemodynamic response to apneic positive airway
pressure. Crit Care Med. 2000;28:672-678.
37. Tanoubi I, Drolet P, Donati F. Optimizing preoxygenation in adults.
Can J Anaesth. 2009;56:449-466.
38. Leman P, Greene S, Whelan K, et al. Simple lightweight
disposable continuous positive airways pressure mask to
effectively treat acute pulmonary oedema: randomized controlled
trial. Emerg Med Australas. 2005;17:224-230.
39. Engstrom J, Hedenstierna G, Larsson A. Pharyngeal oxygen
administration increases the time to serious desaturation at
intubation in acute lung injury: an experimental study. Crit Care.
2010;14:R93.
40. Neumann P, Berglund JE, Fernandez Mondejar E, et al. Dynamics
of lung collapse and recruitment during prolonged breathing in
porcine lung injury. J Appl Physiol. 1998;85:1533-1543.
41. Rothen HU, Sporre B, Engberg G, et al. Prevention of atelectasis
during general anaesthesia. Lancet. 1995;345:1387-1391.
42. Lane S, Saunders D, Schofield A, et al. A prospective,
randomised controlled trial comparing the efficacy of pre-
oxygenation in the 20 degrees head-up vs supine position.
Anaesthesia. 2005;60:1064-1067.
43. Ramkumar V, Umesh G, Philip FA. Preoxygenation with 20° head-
up tilt provides longer duration of non-hypoxic apnea than
conventional preoxygenation in non-obese healthy adults. J
Anesth. 2011;25:189-194.
44. Altermatt FR, Munoz HR, Delfino AE, et al. Pre-oxygenation in the
obese patient: effects of position on tolerance to apnoea. Br J
Anaesth. 2005;95:706-709.
45. Dixon BJ, Dixon JB, Carden JR, et al. Preoxygenation is more
effective in the 25 degrees head-up position than in the supine
position in severely obese patients: a randomized controlled
study. Anesthesiology. 2005;102:1110-1115; discussion 1115A.
46. Boyce JR, Ness T, Castroman P, et al. A preliminary study of the
optimal anesthesia positioning for the morbidly obese patient.
Obes Surg. 2003;13:4-9.
47. Lee BJ, Kang JM, Kim DO. Laryngeal exposure during
laryngoscopy is better in the 25 degrees back-up position than in
the supine position. Br J Anaesth. 2007;99:581-586.
48. Benumof JL, Dagg R, Benumof R. Critical hemoglobin
desaturation will occur before return to an unparalyzed state
following 1 mg/kg intravenous succinylcholine. Anesthesiology.
1997;87:979-982.
49. Ding ZN, Shibata K, Yamamoto K, et al. Decreased circulation
time in the upper limb reduces the lag time of the finger pulse
oximeter response. Can J Anaesth. 1992;39:87-89.
50. Drummond GB, Park GR. Arterial oxygen saturation before
intubation of the trachea. An assessment of oxygenation
techniques. Br J Anaesth. 1984;56:987-993.
51. Farmery AD, Roe PG. A model to describe the rate of
oxyhaemoglobin desaturation during apnoea. Br J Anaesth. 1996;
76:284-291.
52. Mort TC. Preoxygenation in critically ill patients requiring
emergency tracheal intubation. Crit Care Med. 2005;33:2672-
2675.
53. Eger EI, Severinghaus JW. The rate of rise of PaCO2 in the apneic
anesthetized patient. Anesthesiology. 1961;22:419-425.
54. Nielsen ND, Kjaergaard B, Koefoed-Nielsen J, et al. Apneic
oxygenation combined with extracorporeal arteriovenous carbon
dioxide removal provides sufficient gas exchange in experimental
lung injury. ASAIO J. 2008;54:401-405.
55. Hirsch H. Uber kunstliche Atmung durch Ventilation der Trachea
[dissertation]. Giessen; 1905.
56. Volhard F. Uber kunstliche Atmung durch Ventilation der Trachea
und eine einfache Vorrichtung zur hytmischen kunstlichen
Atmung. Munch med NVochensch. 1908:209-211.
57. Comroe JH Jr, Dripps RD. Artificial respiration. JAMA. 1946;130:
381-383.
58. Enghoff H, Holmdahl MH, Risholm L. Oxygen uptake in human
lungs without spontaneous or artificial pulmonary ventilation. Acta
Chir Scand. 1952;103:293-301.
59. Holmdahl MH. Pulmonary uptake of oxygen, acid-base
metabolism, and circulation during prolonged apnoea. Acta Chir
Scand Suppl. 1956;212:1-128.
60. Frumin MJ, Epstein RM, Cohen G. Apneic oxygenation in man.
Anesthesiology. 1959;20:789-798.
61. Babinski MF, Sierra OG, Smith RB, et al. Clinical application of
continuous flow apneic ventilation. Acta Anaesthesiol Scand.
1985;29:750-752.
62. Teller LE, Alexander CM, Frumin MJ, et al. Pharyngeal insufflation
of oxygen prevents arterial desaturation during apnea.
Anesthesiology. 1988;69:980-982.
63. al Jumah M, McLean DR, al Rajeh S, et al. Bulk diffusion apnea
test in the diagnosis of brain death. Crit Care Med. 1992;20:
1564-1567.
64. Marks SJ, Zisfein J. Apneic oxygenation in apnea tests for brain
death. A controlled trial. Arch Neurol. 1990;47:1066-1068.
65. Perel A, Berger M, Cotev S. The use of continuous flow of oxygen
and PEEP during apnea in the diagnosis of brain death. Intensive
Care Med. 1983;9:25-27.
66. Barth L. [Therapeutic use of diffusion breathing in bronchoscopy].
Anaesthesist. 1954;3:227-229.
67. Payne JP. Apnoeic oxygenation in anaesthetised man. Acta
Anaesthesiol Scand. 1962;6:129-142.
68. Lee SC. Improvement of gas exchange by apneic oxygenation with
nasal prong during fiberoptic intubation in fully relaxed patients. J
Korean Med Sci. 1998;13:582-586.
69. Taha SK, Siddik-Sayyid SM, El-Khatib MF, et al. Nasopharyngeal
oxygen insufflation following pre-oxygenation using the four deep
breath technique. Anaesthesia. 2006;61:427-430.
70. Ramachandran SK, Cosnowski A, Shanks A, et al. Apneic
oxygenation during prolonged laryngoscopy in obese patients: a
randomized, controlled trial of nasal oxygen administration. J Clin
Anesth. 2010;22:164-168.
71. Kory RC, Bergmann JC, Sweet RD, et al. Comparative evaluation
of oxygen therapy techniques. JAMA. 1962;179:767-772.
72. Waugh JB, Granger WM. An evaluation of 2 new devices for nasal
high-flow gas therapy. Respir Care. 2004;49:902-906.
73. Wettstein RB, Shelledy DC, Peters JI. Delivered oxygen
concentrations using low-flow and high-flow nasal cannulas.
Respir Care. 2005;50:604-609.
74. Tiep B, Barnett M. High flow nasal vs high flow mask oxygen
delivery: tracheal gas concentrations through a head extension
airway model. In: Respiratory Care 2002 Open Forum 2002;
October 5-8, 2002; Tampa, FL.
75. Levitan RM. NO DESAT! Nasal oxygen during efforts securing a
tube. Emergency Physicians Monthly. December 9, 2010.
Available at: http://www.epmonthly.com/features/current-
features/no-desat-/. Accessed October 22, 2011.
76. Stolbach AI, Hoffman RS, Nelson LS. Mechanical ventilation was
associated with acidemia in a case series of salicylate-poisoned
patients. Acad Emerg Med. 2008;15:866-869.

77. Aufderheide TP, Lurie KG. Death by hyperventilation: a common
and life-threatening problem during cardiopulmonary resuscitation.
Crit Care Med. 2004;32:S345-351.
78. von Goedecke A, Voelckel WG, Wenzel V, et al. Mechanical
versus manual ventilation via a face mask during the induction of
anesthesia: a prospective, randomized, crossover study. Anesth
Analg. 2004;98:260-263.
79. von Goedecke A, Wenzel V, Hormann C, et al. Effects of face
mask ventilation in apneic patients with a resuscitation
ventilator in comparison with a bag-valve-mask. J Emerg Med.
2006;30:63-67.
80. von Goedecke A, Wagner-Berger HG, Stadlbauer KH, et al. Effects
of decreasing peak flow rate on stomach inflation during bag-
valve-mask ventilation. Resuscitation. 2004;63:131-136.
81. Oddo M, Feihl F, Schaller MD, et al. Management of mechanical
ventilation in acute severe asthma: practical aspects. Intensive
Care Med. 2006;32:501-510.
82. Collins JS, Lemmens HJ, Brodsky JB, et al. Laryngoscopy and
morbid obesity: a comparison of the “sniff” and “ramped”
positions. Obes Surg. 2004;14:1171-1175.
83. Levitan RM, Mechem CC, Ochroch EA, et al. Head-elevated
laryngoscopy position: improving laryngeal exposure during
laryngoscopy by increasing head elevation. Ann Emerg Med.
2003;41:322-330.
84. Ellis DY, Harris T, Zideman D. Cricoid pressure in emergency
department rapid sequence tracheal intubations: a risk-benefit
analysis. Ann Emerg Med. 2007;50:653-665.
85. Brimacombe JR, Berry AM. Cricoid pressure. Can J Anaesth.
1997;44:414-425.
86. Petito SP, Russell WJ. The prevention of gastric inflation—a
neglected benefit of cricoid pressure. Anaesth Intensive Care.
1988;16:139-143.
87. Smith KJ, Dobranowski J, Yip G, et al. Cricoid pressure displaces
the esophagus: an observational study using magnetic resonance
imaging. Anesthesiology. 2003;99:60-64.
88. Smith KJ, Ladak S, Choi PT, et al. The cricoid cartilage and the
esophagus are not aligned in close to half of adult patients. Can
J Anaesth. 2002;49:503-507.
89. Allman KG. The effect of cricoid pressure application on airway
patency. J Clin Anesth. 1995;7:197-199.
90. Hartsilver EL, Vanner RG. Airway obstruction with cricoid
pressure. Anaesthesia. 2000;55:208-211.
91. Hocking G, Roberts FL, Thew ME. Airway obstruction with cricoid
pressure and lateral tilt. Anaesthesia. 2001;56:825-828.
92. Saghaei M, Masoodifar M. The pressor response and airway
effects of cricoid pressure during induction of general anesthesia.
Anesth Analg. 2001;93:787-790.
93. Mac GPJH, Ball DR. The effect of cricoid pressure on the cricoid
cartilage and vocal cords: an endoscopic study in anaesthetised
patients. Anaesthesia. 2000;55:263-268.
94. Palmer JH, Yentis SM. Cricoid pressure application to awake
volunteers: discomfort cannot be used to indicate appropriate
force. Can J Anaesth. 2005;52:114-115.
95. Taha SK, El-Khatib MF, Baraka AS, et al. Effect of
suxamethonium vs rocuronium on onset of oxygen desaturation
during apnoea following rapid sequence induction. Anaesthesia.
2010;65:358-361.
96. Tang L, Li S, Huang S, et al. Desaturation following rapid
sequence induction using succinylcholine versus rocuronium in
overweight patients. Acta Anaesthesiol Scand. 2011;55:203-208.
97. Perry JJ, Lee JS, Sillberg VA, et al. Rocuronium versus
succinylcholine for rapid sequence induction intubation. Cochrane
Database Syst Rev. 2008;(2):CD002788.

Table E1. Evidence for apneic oxygenation to extend the duration of safe apnea.
Study Patients Intervention Comparator Outcome
Comroe et al57
Obs trial of 2 patients
with neurologic
injuries
Endotracheal insufflation
of 6–11 L/min of
oxygen
None Observation of long duration till
SaO2 Ͻ90% in numerous
separate experiments
Enghoff et al58
Obs study of 7
operative patients
Tubing placed down ET
tube connected to 100%
FiO2
None No decrease in ABG PaO2 for 5–7
min
Holmdahl59
Documentation of
separate Obs
studies
Endotracheal insufflation
of 100% FiO2
None Extended time until desaturation
in separate studies
Frumin et al60
Obs study of 8
operative patients
Intubated, administered
100% FiO2 and left
apneic
None No desaturation for between 18
and 55 min. Patients had
marked hypercapnia and
commensurate decreased pH.
Babinski et al61
Obs study of 5
operative patients
Two endobronchial
catheters placed
None 30 min of apnea without
significant desaturation
Teller et al62
RCT, blinded,
crossover trial of 12
pts
Nasopharyngeal catheters
attached to 100% FiO2
at 3 L/min
Nasopharyngeal catheters
attached to room air
Outcome was a sat of Յ92% or
10 min. None of the patients in
the insufflation arm
desaturated below 98% during
the 10 min.
Taha et al69
RCT of 30 pts Nasal catheters attached
to 5L/min of 100% FiO2
Room air No desaturation during the course
of the 6-min predetermined
stopping point in patients
receiving apneic oxygenation.
The control group desaturated
to the study cutoff of 95% in an
average of 3.65 min.
Ramachandran et al70
RCT of 30 obese,
operative patients
Nasal cannula attached to
5 L/min 100% FiO2
Room air The apneic oxygenation group had
significant prolongation of SpO2
Ն95% time (5.29 versus 3.49
min), a significant increase in
patients with SpO2 Ն95% at
the 6-min mark (8 patients
versus 1 patient), and
significantly higher minimum
SpO2 (94.3% versus 87.7%).
Obs, Observational trial.
11.e1 Annals of Emergency Medicine Volume xx, . x : Month 

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