Just Breathe

Rapid-Sequence
Intubation

LESSON 24

By Joshua T. McClain, MD; Benjamin J. Lawner, DO, EMT-P;

and Kenneth H. Butler, DO, FACEP
Dr. McClain is an emergency medicine physician at Meritus Health in Hagerstown,
Maryland. Dr. Lawner is an adjunct assistant professor and Dr. Butler is an associate
professor in the Department of Emergency Medicine at the University of Maryland
School of Medicine in Baltimore.

Reviewed by John C. Greenwood, MD

OBJECTIVES
On completion of this lesson, you should be able to: CRITICAL DECISIONS
1. Explain how to properly position and oxygenate patients n How should patients be positioned for RSI?
undergoing RSI.
2. Discuss the ideal pharmacologic agents for n How should patients be oxygenated during RSI?
pretreatment, induction, and paralysis. n Which pretreatment agents should be considered?
3. Describe the evidence surrounding the use of cricoid
pressure. n Is there an ideal induction agent?
4. Demonstrate techniques and strategies for maximizing n What paralytic agents are most effective, and when
the clinician’s view during RSI. should they be used?
FROM THE EM MODEL n Should cricoid pressure be applied during RSI?
19.0 Procedures and Skills Integral to the Practice
n What techniques can be used to maximize the view
of Emergency Medicine
during RSI?
19.1 Airway Techniques
19.1.1 Intubation
The ability to perform rapid-sequence intubation (RSI) is an essential skill for the practice of emergency
medicine. The decision to intubate must often be made at a moment’s notice and with only limited knowledge of the
patient’s history. Unfortunately, failure to intubate a patient on the first attempt more than doubles the risk of adverse
events.1-3 Because these choices can mean the difference between life and death, clinicians must possess an in-depth
understanding of ideal oxygenation conditions, medication strategies, and patient positioning.

December 2019 n Volume 33 Number 12 19

 CASE PRESENTATIONS
■ CASE ONE
A 59-year-old man with a history
of hypertension and atrial fibrillation
arrives via ambulance after being
found with an altered level of
consciousness. He is breathing
spontaneously but has a Glasgow
Coma Scale (GCS) score of 5. The
patient’s wife mentions that he takes
a prescription for warfarin. His
physical examination reveals a blown
left pupil. His vital signs are blood
pressure 186/101, heart rate 66,
respiratory rate 9, rectal temperature
36.9°C (98.4°F), and oxygen
saturation 97% on a nonrebreather
mask.
Suspecting an intracranial bleed
with elevated intracranial pressure,
the emergency physician elevates the
head of the patient’s bed, administers
CRITICAL DECISION
How should patients be
positioned for RSI?
Proper patient positioning during
RSI is essential. A completely flat
position should be avoided. Alignment
of the clivus with the external auditory
meatus, correlating with the ear and the
sternal notch respectively, may produce
superior laryngoscopic and intubating
views.4 In obese patients, a ramped
position is often required to align
the ear and sternal notch; this can be
achieved by placing several blankets or
pillows under the patient’s head, neck,
and upper back (Figure 1).5
Along with ear-to-sternal-notch
positioning, the head of the bed should
be elevated to at least 20 degrees
for preoxygenation and during the
intubation attempt. Patients in a
flat position have increased work of
breathing during the preoxygenation
period and increased rates of
atelectasis.6 When the head of the bed
is elevated 20 degrees, patients appear
to take about 1 minute and 30 seconds
longer to desaturate than when the bed
is flat.7
20 Critical Decisions in Emergency Medicine
hypertonic saline and vitamin K, and
requests fresh frozen plasma from
the blood bank. The clinical team
prepares to intubate the patient in
order to obtain a CT scan.
■ CASE TWO
An obese 44-year-old woman
with a history of COPD presents in
respiratory distress on noninvasive
positive-pressure ventilation (NIPPV).
EMS administered a nebulizer
treatment and steroids en route. A
brief history reveals that the patient
has been intubated twice in the past
for respiratory distress.
She has severely decreased air
entry bilaterally and diffuse, faint
wheezing. Her vital signs are blood
pressure 143/79, heart rate 114,
respiratory rate 22, and oxygen
CRITICAL DECISION
How should patients be
oxygenated during RSI?
During the preoxygenation and apneic
oxygenation periods, oxygen should be
administered via nasal cannula at a rate
of 15 L/min. Apneic oxygenation creates
a diffusion gradient from the pharynx to
the lungs, providing oxygenation even in
the absence of ventilation. In one study of
obese men undergoing general anesthesia,
patients receiving apneic oxygenation
took 1 minute and 40 seconds longer to
desaturate than patients not receiving
apneic oxygenation.8 Although research
has been mixed, the rate of first-pass
success may be higher (and the risk of
hypoxemia may be lower) in emergency
department patients who receive apneic
oxygenation.9,10
In addition to a nasal cannula, low-
risk patients (those with preintubation
oxygen saturation levels of 96%-100%
on a nonrebreather mask) can be
preoxygenated with a nonrebreather
mask. Medium-risk patients (those
with a preintubation oxygen saturation
level of 91%-95% on a nonrebreather
mask) can be preoxygenated with
a nonrebreather mask, a bag valve
saturation 81% on NIPPV. The
clinician prepares to intubate the
patient.
■ CASE THREE
A 73-year-old man presents with
altered mental status. His daughter
states that the patient has become
progressively incoherent over the past
few days. His medical history includes
Alzheimer disease and diabetes mellitus.
His GCS score is 7. The examination
reveals dry mucous membranes.
His vital signs are blood pressure
68/42, heart rate 128, respiratory rate
24, temperature 39.3°C (102.7°F), and
oxygen saturation 94% on room air.
His finger-stick blood glucose level is
185 mg/dL. The physician considers
intubating the patient for airway
protection.
mask (BVM) with a positive end-
expiratory pressure (PEEP) valve, or
continuous positive airway pressure
(CPAP). High-risk patients (those with
a preintubation oxygen saturation of
≤90% on a nonrebreather mask) should
be preoxygenated using a BVM with a
PEEP valve or CPAP.6
If available, high-flow nasal cannula
oxygen therapy can also be used for the
preoxygenation and apneic oxygenation
of medium- and high-risk patients.11
High-flow nasal cannula oxygen
therapy increases patient comfort,
induces a small amount of CPAP, and
creates a higher fraction of inspired
oxygen (FiO2).12
Clinicians should fully understand
how their institution’s oxygen delivery
devices work. When using a BVM, a
tight seal should be achieved. The bag
does not need to be squeezed if the
patient is breathing spontaneously,
can tolerate the tight seal, and is able
to generate enough force to open the
one-way valve. To avoid a problematic
drop in FiO2, this method should only
be used with bags that possess a one-
way exhalation port.13 Hovering the
bag above the patient’s face — another
common mistake — provides no
advantage over room air.6
When it comes to oxygen delivery via
a nonrebreather mask, an ideal mask can
deliver upward of 90% FiO2; however,
many emergency departments are not
equipped with true nonrebreather masks.
The masks found in most acute settings
typically deliver only 60% to 70% FiO2.
Rates higher than this can be achieved
by increasing the flow rate past the
15 L/min mark, which can achieve rates
as high as 30 to 60 L/min.6
The recommended duration for
preoxygenation has generally been
3 minutes of tidal volume breathing,
or 8 maximal breaths.14 When there is a
mask leak, which occurs often with the
use of standard emergency department
nonrebreather masks, 3 minutes of
tidal volume breathing may provide
better oxygenation.15 In such cases, the
addition of a nasal cannula can also
increase the FiO2.
bagging during the apneic period should
be mandatory to prevent hypercapnia
(eg, salicylate overdose, severe metabolic
acidosis, increased intracranial pressure).
Ultimately, the decision to bag or not
to bag during RSI is a balance of risks
(aspiration) and benefits (preventing
desaturation).6,18
CRITICAL DECISION
Which pretreatment agents
should be considered?
Pretreatment involves the
administration of medications to at-risk
FIGURE 1. Ramped Patient Position
A.
patients prior to induction. This may be
necessary for several reasons, including
increased intracranial pressure, a
history of cardiovascular disease, and
shock states.
In the past, lidocaine was routinely
used to blunt the sympathetic response
to laryngoscopy in patients for whom the
concomitant rise in intracranial pressure
would be particularly detrimental.
However, subsequent research has
shown no evidence to support the use of
lidocaine in clinical practice.19
Fentanyl, which appears to blunt

To Bag or Not To Bag?

Another controversy in airway
management is whether or not patients
should be “bagged” after a sedative and
paralytic have been administered. Any
patient who is desaturating should be
bagged. But what about a patient who
is not desaturating? In a 1961 study,
pressures kept below 15 cm H2O did
not cause gastric insufflation.16 Another B.
study published in 2013 randomized
patients undergoing elective surgery into
groups with pressures of 10, 15, 20, and
25 cm H2O after an induction agent was
administered.
The investigators in the 2013 study
listened and looked for gastric insufflation
and observed the antrum size while
bagging. As pressures increased, so did
the levels of insufflation. In the pressure-
of-10 group, there was no increase in the
gastric antrum size; however, this pressure
would be inadequate for long-term
ventilation. In the pressure-of-15 group,
ventilation was optimal, but the antrum
size did increase by a small degree.17
Current recommendations regarding
bagging during the apneic period are
mixed. Based on current evidence,
practitioners should limit pressures to
10 to 15 cm H2O if they are going to bag. A. Flat; no attempt is made to achieve the best airway position.
Excluding a few subgroups for whom B. Ramping improves upper-airway patency and decreases work of breathing.

December 2019 n Volume 33 Number 12 21

 TABLE 1. IV Induction and Neuromuscular-Blocking Agents for RSI
Dose if
Hemodynamically
Agent Standard Dose Compromised Comments
Etomidate 0.2-0.3 mg/kg Full dose may be Rapid onset, short duration. Few hemodynamic effects.
required, but lower Preferred for hypotensive patients with head injuries or
doses are safer. coronary artery disease.
Ketamine 1.0-2.0 mg/kg Lower end of dose Longer duration. Sympathetic stimulation, bronchodilation,
dreams, salivation. Preferred for patients with asthma.
Propofol 2.0-2.5 mg/kg given at Total dose may be Slow injection preferred over rapid bolus administration.
40 mg every 10 seconds as low as 10%. Rapid bolus may result in cardiorespiratory depression.
Titrate dose to response. Maintenance doses by infusion are
preferred: 0.3-3.0 mg/kg/hr for prolonged sedation. Avoid in
patients with hypovolemia.
Fentanyl and Fentanyl 1.0-4.0 mcg/kg Reduce by 50%. Can cause respiratory depression during initial
midazolam for pain; midazolam administration. Excellent for prolonged sedation and pain
5.0-10.0 mg for sedation control, but monitor vital signs often.
Succinylcholine 0.6-1.5 mg/kg Consider increasing Short-acting. Many contraindications and adverse effects.
total dose. Clinical duration 4-6 minutes.
Rocuronium 0.6-1.5 mg/kg Consider increasing Onset time is equal to that of succinylcholine. Clinical
total dose. duration 30-60 minutes.
Vecuronium 0.08-0.10 mg/kg Consider increasing Onset time 2-3 minutes. Clinical duration 25-40 minutes.
total dose.

increases in blood pressure and
heart rate, should be considered for
patients with potential intracranial
hypertension.20 The medication should
also be considered for patients with a
history of ischemic heart disease and for
those at risk of an aortic aneurysm or
dissection.21 Pretreatment with esmolol
at a dose of 1.5 mg/kg can be used if
heart rate elevation is a major peri-
intubation concern.22
Patients in shock present a serious
challenge for emergency physicians.
Patients with preintubation hypotension
have a much greater risk of cardiac
arrest and death than those who are
normotensive.23 If time and clinical
status permit, isotonic fluids, blood
products, and vasopressors should be
provided as clinically indicated, with
a goal of increasing the mean arterial
pressure prior to intubation. It is
important to remember that RSI and
NIPPV can cause dramatic decreases in
blood pressure.
CRITICAL DECISION
Is there an ideal induction
agent?
Because of their favorable
hemodynamic profiles, ketamine and
etomidate have emerged as the induction
agents of choice in many emergency
departments (Table 1).24 There
appears to be no difference between
the two drugs in mortality rate and
hemodynamic effects.25,26
Ketamine causes dissociative
amnesia and provides analgesia through
the NMDA receptor. An induction
dose of 1 to 2 mg/kg has traditionally
been recommended; however,
patients in shock should receive no
more than 1.5 mg/kg (or even less
if the patient may be catecholamine
depleted). Etomidate stimulates the
gamma-aminobutyric acid receptor to
produce a sedative amnestic state.21
The traditional dose is 0.3 mg/kg;
unlike with propofol and ketamine,
which require dose reductions in cases
of shock, the etomidate dose should
remain unchanged or only be increased
minimally.27
Sepsis
Ketamine should usually be the first-
line induction agent for patients with
sepsis. Although several small studies
have found a relationship between
etomidate and adrenal suppression,
subsequent research has questioned
the clinical significance of this
association.28-30
One study showed that a single dose
of etomidate for intubation did not
increase the rate of in-hospital deaths
and other adverse outcomes. However,
another study found that a single
dose of etomidate increased mortality
secondary to adrenal insufficiency in
septic patients. Given the conflicting
literature and the fact that ketamine is a
viable alternative, etomidate should be
avoided in septic patients.31,32
Traumatic Brain Injuries
Historically, ketamine has been
avoided in patients who may have
suffered intracranial injuries based
on studies and case reports published
in the 1970s, which demonstrated an
association between ketamine and
increased intracranial pressure.33 In
recent years, this cause-and-effect
relationship has been challenged.21
Current literature even suggests that
ketamine is appropriate for patients
with traumatic brain injuries because of
its ability to increase cerebral perfusion
pressure and reduce the release of
glutamate, which can be neurotoxic.33
CRITICAL DECISION
What paralytic agents are
most effective, and when
should they be used?
Paralytic agents should be used
during all RSI attempts. In a study that
compared how laryngoscopy performed
with etomidate plus a paralytic versus
etomidate alone, acceptable intubating
conditions were reported in 79% of the

22 Critical Decisions in Emergency Medicine

patients who received the paralytic but
only in 13% of those who did not.34
Airway trauma occurred in 28% of
nonparalyzed patients, aspiration in 15%,
and death in 3%. The researchers did not
observe any of these complications in the
group receiving a paralytic.35
Rocuronium vs Succinylcholine
Because of the undifferentiated
nature of emergency department
cases and the extensive risks and side
effects associated with succinylcholine,
rocuronium should be the emergency
physician’s first-line paralytic.
Rocuronium has few side effects, and
its only absolute contraindication
is in patients with an allergy to
nondepolarizing paralytics.36 At a dose
of 1.2 mg/kg, rocuronium produces
intubating conditions equivalent to
1.5 mg/kg of succinylcholine when both
are compared at 45 seconds.37
The main concern with
succinylcholine is the effect it has on
FIGURE 2. Surface Anatomy of the Hyoid Bone, Thyroid, and Cricoid
Cartilage
Hyoid bone
Thyroid cartilage
Cricoid cartilage
COURTESY OF THE NEW YORK SCHOOL OF REGIONAL ANESTHESIA
serum potassium levels. In healthy
patients who receive the drug, serum
potassium concentrations rise an
average of 0.5 to 1 mEq/L. In patients
with comorbidities or acute medical
conditions, receptor upregulation can
lead to much larger increases. The
risk is greatest in patients with severe
infections, in those with upper- and
lower-motor neuropathies (including
diabetic peripheral neuropathy and
severe peripheral vascular disease),
after exposure to certain toxins and
medications, in patients who require
immobilization, and in those with burns
or trauma.38
In addition to receptor upregulation,
life-threatening hyperkalemia
secondary to succinylcholine-induced
rhabdomyolysis has been documented in
several case reports.39 Other side effects
of the drug include masseter muscle
spasms, malignant hyperthermia, and
increased intracranial pressure.24,40
Another benefit of rocuronium
is that patients who receive it take
longer to desaturate than those who
receive succinylcholine. Patients given
succinylcholine also desaturate to lower
oxygen levels and take longer to achieve
resaturation compared with patients
who receive rocuronium.41,42
A common misconception is that
succinylcholine is safer because of its
short duration of action. However, using
a paralytic in the emergency department
should be an all-or-nothing scenario. As
noted by emergency medicine researcher
Reuben Strayer, “Emergency clinicians
who believe they are protected against a
‘can’t intubate, can’t ventilate’ scenario
by the short duration of succinylcholine
are usually wrong and make dangerous
decisions as a result.”43 Furthermore,
the use of a short-acting drug leaves
physicians where they were in the first
place: needing to intubate the patient.
In the rare circumstance that
the physician would like to reverse
rocuronium paralysis, sugammadex can
be used. Sugammadex was approved by
the FDA in 2015 as a reversal agent for
rocuronium bromide and vecuronium
bromide.44 However, it is important
to be aware that up to 1% of patients
who are given the emergent reversal
dose of 16 mg/kg have hypersensitivity
reactions.45
CRITICAL DECISION
Should cricoid pressure be
applied during RSI?
Major controversy surrounds the use
of cricoid pressure, sometimes called the
Sellick maneuver. The technique was first
described by Scottish physician Alexander
Monro, who used it to revive drowning
victims. The maneuver was popularized
in 1960s when British anesthesiologist
Brian Sellick promoted its efficacy for
controlling gastric regurgitation during
the induction of anesthesia.46 Sellick
hypothesized that, by applying backward
pressure to the cricoid cartilage (Figure
2) against the cervical vertebrae, he
could occlude the upper esophagus. His
original study involved 26 patients, who
experienced no aspiration events when
cricoid pressure was applied; however,
3 of the subjects experienced aspiration
when the pressure was released.47
December 2019 n Volume 33 Number 12 23
 Several more recent studies have
questioned whether the application
of cricoid pressure occludes the
esophagus, which lies lateral to the
airway in an estimated 60% of patients.
When pressure is applied, the trachea
can be displaced laterally instead of
being compressed against the cervical
vertebrae.48,49 Nonetheless, the positioning
of the esophagus may actually be
irrelevant, as the cricoid ring is attached
to the hypopharynx, not the esophagus,
and the two structures move together as
a unit. Cricoid pressure appears to reduce
the diameter of the hypopharynx by an
average of only 35%.50
The application of cricoid pressure
is not without risks, including airway
compression and compromised glottic
views.49,51 The other concern is that
the technique may actually cause the
problems it sets out to prevent. In one
study, when 20 newtons of force were
applied to the cricoid cartilage, the lower
esophageal sphincter pressure decreased
from 24 to 15 mm Hg. A force of
40 newtons caused the pressure to drop
to 13 mm Hg.52 One of the largest studies
on the use of cricoid pressure found the
procedure to be ineffective for preventing
regurgitation or death in patients
undergoing caesarian deliveries.53
Major medical organizations
have also noted the lack of evidence
supporting cricoid pressure. In 2010,
FIGURE 3. Miller and Macintosh Blades
Miller blades
24 Critical Decisions in Emergency Medicine
the American Heart Association
removed the technique from its CPR
and emergency cardiovascular care
guidelines. In addition, the Eastern
Association for the Surgery of Trauma
no longer endorses the maneuver as a
level 1 recommendation.54
CRITICAL DECISION
What techniques can be
used to maximize the view
during RSI?
Blades
Although video laryngoscopy
generally outperforms direct
laryngoscopy, emergency physicians
should master the direct technique
so that it can be used when video
equipment is unavailable or in situations
where video imaging cannot provide
an adequate view.55,56 Inexperienced
clinicians may find more success with
curved Macintosh blades over straight
Miller blades, which may provide poorer
intubating views (Figure 3).57,58 However,
research suggests that Miller blades may
outperform Macintosh models when
using a paraglossal approach.59 Although
Miller blades have traditionally
been preferred for pediatric patients,
Macintosh blades can provide similar
views with comparable success and
failure rates.60,61
Macintosh blades
Other refining factors can be
applied to blade selection when several
options are available. In general, English
Macintosh blades outperform standard
Macintosh models.62 It is important
to select the shortest handle available,
especially when intubating obese
patients; adipose tissue in the chest and
neck can hinder blade insertion when
using a longer handle.63 Finally, the
Macintosh 3 and Macintosh 4 blades
provide different benefits. A Macintosh 4
can be used as a Miller in most patients
with a grade 3 or 4 airway; however,
the device places the clinician at a
mechanical disadvantage during most
intubations because of its longer blade
length.
Tubes
Traditional arcuate stylets are slowly
being phased out in favor of straight-
to-cuff models, which provide greater
maneuverability without the midportion
of the tube obscuring the laryngeal inlet
— a drawback of arcuate devices. The
ideal angle at the cuff is 25 degrees, but
there appears to be a dramatic drop-off
in the ability to intubate with angles
above 35 degrees.64
Epiglottis-Only View
If the laryngoscopic view remains
limited to the epiglottis, several
alternative approaches exist. First, the
clinician should advance the blade
further into the vallecula to ensure
adequate engagement of the hyoepiglottic
ligament. If this fails to fix the problem,
external laryngeal manipulation can
be attempted. In such cases, a modified
approach (in which the physician
attempting the intubation adjusts an
assistant’s hand) appears to perform
better than the classic approach.65 Finally,
using a head-lift position may help bring
the airway into view.66
If the laryngeal view remains
elusive after employing these options,
a difficult-airway algorithm should be
followed (Figure 4). Although these
techniques are beyond the scope of
this article, other options may entail
changing blades, switching to or
from video laryngoscopy, inserting a
supraglottic airway device (SAD), using
a fiberoptic scope, seeking assistance, or
creating a surgical airway.
 FIGURE 4. Management of Unanticipated, Difficult Tracheal Intubation in Adults

PLAN A: Facemask ventilation and tracheal intubation If in difficulty call for help!
• Optimize the patient’s head and neck position.
• Preoxygenate.
• Provide adequate neuromuscular blockade. Succeed
• Attempt direct or video laryngoscopy (max 3+1 attempts). Confirm tracheal intubation with capnography.
• Provide external laryngeal manipulation.
• Use a bougie.
• Remove cricoid pressure.
• Maintain oxygenation and anaesthesia.

Declare failed intubation

PLAN B: Maintaining oxygenation via SAD insertion STOP AND THINK

Options (consider risks and benefits):
• A 2nd-generation device is recommended.
Succeed 1. Wake the patient up.
• Change the device or size (maximum 3 attempts).
• Oxygenate and ventilate. 2. Intubate the trachea via SAD.
3. Proceed without intubating the trachea.
Declare failed supraglottic ventilation 4. Perform a tracheostomy or cricothyroidotomy.

PLAN C: Facemask ventilation

Succeed
• If face-mask ventilation is impossible, administer Wake the patient up.
paralytic agents.
• For the final attempt at face-mask ventilation, use a Postoperative and follow-up care
two-person technique and adjuncts. • Formulate an immediate airway-management plan.
Declare “can’t intubate, can’t oxygenate” scenario • Monitor for complications.
• Complete an airway alert form.
PLAN D: Emergency front of neck access • Explain the process to the patient, both in
person and in writing.
Perform a scalpel cricothyroidotomy.
• Submit a written report to the patient’s primary
Adapted from Difficult Airway Society 2015 guidelines. care physician and the local database.

Passage difficult airway is anticipated, consider Once the tube has been passed, it
If an acceptable view of the vocal going straight to a bougie approach to should be secured, and postintubation
cords has been achieved but the tube increase the likelihood of success.68 sedation and ventilator management
remains difficult to pass, the clinician Clinicians should not assume that should ensue.
bougie “stoppage” or the ability to
can attempt a bougie intubation, try Summary
feel tracheal rings are signs of being
downsizing the tube, or try rotating
in the trachea; these “indications” RSI is a necessary skill in the
the tube counterclockwise so that the practice of emergency medicine. A
can be unreliable.70 Success can be
bevel faces posteriorly.67,68 A bougie can confirmed by visualizing the tube pass thorough understanding of proper
be used in several ways; clinicians are through the vocal cords, using end-tidal patient positioning, ideal oxygenation
encouraged to find the technique that capnography, and noting the presence of conditions, and optimal medication
works best for them, as no approach bilateral lung sounds and the absence of strategies provide the foundation for
has been shown to be superior.69 If a sounds in the stomach upon ventilation. a successful intubation. Practices that
are unsupported by the literature, such
as the application of cricoid pressure,
should be avoided.
Having a firm grasp of the
different tools available during
RSI, and understanding how that
n Placing patients in the ear-to-sternal-notch position provides the best
equipment works, allows emergency
chance for laryngoscopic success.
n All patients should be oxygenated via nasal cannula during the physicians to optimize their intubation
preoxygenation and apneic periods. attempts. Finally, having confidence in
n Ketamine is the preferred induction agent for patients in septic shock, as approaching the epiglottis-only view,
etomidate poses a potential risk of significant adrenal suppression. and having an algorithm at hand in the
n Rocuronium should be the paralytic of choice. Succinylcholine has many event that complications arise, affords
contraindications that can be problematic in the emergent setting, where a
the highest chance of success while
patient’s full history is not always known.
decreasing the risk of adverse outcomes.

December 2019 n Volume 33 Number 12 25

 CASE RESOLUTIONS
■ CASE ONE
To stabilize the man with the
suspected intracranial bleed, the
physician proceeded with RSI. The
head of the bed was kept elevated, and
the patient was placed in a position
where his ears aligned with his
sternal notch. A nasal cannula was
placed under the nonrebreather mask.
Fentanyl was used as a pretreatment
agent to prevent a sympathetic
response to the intubation.
The clinician chose rocuronium
as a paralytic agent in order to
avoid the potential increase in
intracranial pressure associated
with succinylcholine. After the
induction agent and paralytic were
administered, the patient was bagged
for 45 seconds to prevent hypercapnia
while the paralytic took effect. He
was successfully intubated on the first
attempt.
REFERENCES
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importance of first pass success when performing
orotracheal intubation in the emergency department.
Acad Emerg Med. 2013 Jan;20(1):71-78.
2. Mort TC. Emergency tracheal intubation:
complications associated with repeated laryngoscopic
attempts. Anesth Analg. 2004 Aug;99(2):607-613.
3. Hasegawa K, Shigemitsu K, Hagiwara Y, et al; Japanese
Emergency Medicine Research Alliance Investigators.
Association between repeated intubation attempts
and adverse events in emergency departments: an
analysis of a multicenter prospective observational
study. Ann Emerg Med. 2012 Dec;60(6):749-754.
4. Greenland KB, Edwards MJ, Hutton NJ. External
auditory meatus-sternal notch relationship in adults in
the sniffing position: a magnetic resonance imaging
study. Br J Anaesth. 2010 Feb;104(2):268-269.
5. Collins JS, Lemmens HJ, Brodsky JB, Brock-Utne JG,
Levitan RM. Laryngoscopy and morbid obesity: a
comparison of the “sniff” and “ramped” positions.
Obes Surg. 2004 Oct;14(9):1171-1175.
n Assuming that hovering a BVM above a patient’s face increases oxygen
delivery over room air; a tight seal is necessary.
n Applying cricoid pressure to your patient. Studies show that this approach
does not prevent aspiration and can actually worsen views during intubation.
n Failing to have an algorithm for the epiglottis-only view. The blade should first
be inserted further into the vallecula. If this doesn’t work, external laryngeal
manipulation should be attempted, followed by a head lift.
26 Critical Decisions in Emergency Medicine
■ CASE TWO
The obese woman with a COPD
exacerbation underwent RSI. She was
kept on NIPPV for preoxygenation
and was placed in a ramped position
to maximize the view of her
larynx. Etomidate and rocuronium
were chosen as induction and
paralytic agents, respectively. Video
laryngoscopy and a straight-to-cuff
stylet bent at 25 degrees were used to
maximize success.
During the initial attempt, an
epiglottis-only view was encountered.
The physician attempted to insert
the laryngoscope blade further into
the vallecula without success. With
the help of an assistant, external
laryngeal manipulation enabled
visualization of the cords and led to a
successful intubation.
6. Weingart SD, Levitan RM. Preoxygenation and
prevention of desaturation during emergency airway
management. Ann Emerg Med. 2012 Mar;59(3):165-175.
7. Lane S, Saunders D, Schofield A, Padmanabhan
R, Hildreth A, Laws D. A prospective, randomised
controlled trial comparing the efficacy of
preoxygenation in the 20 degrees head-up vs. supine
position. Anaesthesia. 2005 Nov;60(11):1064-1067.
8. Ramachandran SK, Cosnowski A, Shanks A, Turner CR.
Apneic oxygenation during prolonged laryngoscopy
in obese patients: a randomized, controlled trial of
nasal oxygen administration. J Clin Anesth. 2010
May;22(3):164-168.
9. Semler MW, Janz DR, Lentz RJ, et al. Randomized trial
of apneic oxygenation during endotracheal intubation
of the critically ill. Am J Respir Crit Care Med. 2016
Feb;193(3):273-280.
10. Sakles JC, Mosier JM, Patanwala AE, Arcaris B, Dicken
JM. First pass success without hypoxemia is increased
with the use of apneic oxygenation during rapid
sequence intubation in the emergency department.
Acad Emerg Med. 2016 Jun;23(6):703-710.
■ CASE THREE
Suspecting that the elderly man
was suffering from septic shock, the
clinician delayed intubation until the
patient’s hemodynamics could be
maximized. Three large-bore IV lines
were established. Despite being given
a 1-L bolus of normal saline, his blood
pressure failed to improve. He was
started on vasopressors through an IV
line, and he was oxygenated via nasal
cannula and a nonrebreather mask.
In light of the mixed evidence
regarding the use of etomidate in cases
of sepsis, the clinician used ketamine
as an induction agent; rocuronium
was administered to avoid the life-
threatening risk of hyperkalemia
associated with succinylcholine.
The patient was intubated without
difficulty, started on broad-spectrum
antibiotics, and admitted to the ICU.
11. Vourc’h M, Asfar P, Volteau C, et al. High-flow nasal
cannula oxygen during endotracheal intubation in
hypoxemic patients: a randomized controlled clinical
trial. Intensive Care Med. 2015 Sep;41(9):1538-1548.
12. Ward JJ. High-flow oxygen administration by nasal
cannula for adult and perinatal patients. Respir Care.
2013 Jan;58(1):98-122.
13. Nimmagadda U, Salem MR, Joseph NJ, et al. Efficacy
of preoxygenation with tidal volume breathing.
Comparison of breathing systems. Anesthesiology.
2000 Sep;93(3):693-698.
14. Baraka AS, Taha SK, Aouad MT, El-Khatib MF,
Kawkabani NI. Preoxygenation: comparison of maximal
breathing and tidal volume breathing techniques.
Anesthesiology. 1999 Sep;91(3):612-616.
15. Russell T, Ng L, Nathan E, Debenham E.
Supplementation of standard preoxygenation
with nasal prong oxygen or machine oxygen flush
during a simulated leak scenario. Anaesthesia. 2014
Oct;69(10):1133-1137.
16. Ruben H, Knudsen EJ, Carugati G. Gastric inflation
in relation to airway pressure. Acta Anaesthesiol
Scand.1961 Oct;5:107-114.
17. Bouvet L, Albert ML, Augris C, et al. Real-
time detection of gastric insufflation related to
facemask pressure-controlled ventilation using
ultrasonography of the antrum and epigastric
auscultation in nonparalyzed patients: a prospective,
randomized, double-blind study. Anesthesiology. 2014
Feb;120(2):326-334.
18. Brown, JP. Werrett G. Bag-mask ventilation in rapid
sequence induction. Anaesthesia. 2009 Jul;64(7):
784-785.
19. Robinson N, Clancy M. In patients with head injury
undergoing rapid sequence intubation, does
pretreatment with intravenous lignocaine/lidocaine
lead to an improved neurological outcome? A review of
the literature. Emerg Med J. 2001 Nov;18(6):453-457.
20. Harris CE, Murray AM, Anderson JM, Grounds RM,
Morgan M. Effects of thiopentone, etomidate and
propofol on the haemodynamic response to tracheal
intubation. Anaesthesia. 1988 Mar;43:32-36.
21. Stollings JL, Diedrich DA, Oyen LJ, Brown DR.
Rapid-sequence intubation: a review of the process and
considerations when choosing medications.
Ann Pharmacother. 2014 Jan;48(1):62-76.
22. Ugur B, Ogurlu M, Gezer E, Nuri Aydin O, Gürsoy
F. Effects of esmolol, lidocaine and fentanyl on
haemodynamic responses to endotracheal intubation:
a comparative study. Clin Drug Investig. 2007;27(4):
269-277.
23. Kim WY, Kwak MK, Ko BS, et al. Factors associated
with the occurrence of cardiac arrest after emergency
tracheal intubation in the emergency department.
PLoS One. 2014 Nov 17;9(11):e112779.
24. Brown III CA, Walls RW. Airway. In: Marx JA, Hockberger
RS, Walls RM, et al, eds. Rosens’ Emergency Medicine
Concepts and Clinical Practice. 8th ed. Philadelphia PA:
Elsevier Saunders; 2014:03-19.
25. Jabre P, Combes X, Lapostolle F, et al; KETASED
Collaborative Study Group. Etomidate versus ketamine
for rapid sequence intubation in acutely ill patients: a
multicentre randomised controlled trial. Lancet. 2009
Jul 25;374(9686):293-300.
26. Price B, Arthur AO, Brunko M, et al. Hemodynamic
consequences of ketamine vs etomidate for
endotracheal intubation in the air medical setting.
Am J Emerg Med. 2013 Jul;31(7):1124-1132.
27. Shafer SL. Shock values. Anesthesiology. 2004
Sep;101(3):567-568.
28. Hildreth AN, Mejia VA, Maxwell RA, Smith PW, Dart
BW, Barker DE. Adrenal suppression following a single
dose of etomidate for rapid sequence induction:
a prospective randomized study. J Trauma. 2008
Sep;65(3):573-579.
29. Duthie DJ, Frasier R, Nimmo WS. Effect of induction of
anaesthesia with etomidate on corticosteroid synthesis
in man. Br J Anaesth. 1985 Feb;57(2):156-159.
30. Lundy JB, Slane ML, Frizzi JD. Acute adrenal
insufficiency after a single dose of etomidate. J
Intensive Care Med. 2007 Mar-Apr;22(2):111-117.
31. McPhee LC, Badawi O, Fraser GL, et al. Single-dose
etomidate is not associated with increased mortality in
ICU patients with sepsis: analysis of a large electronic
ICU database. Crit Care Med. 2013 Mar;41(3):774-783.
32. Chan CM, Mitchell AL, Shorr AF. Etomidate is
associated with mortality and adrenal insufficiency
in sepsis: a meta-analysis*. Crit Care Med. 2012
Nov;40(11):2945-2953.
33. Filanovsky Y, Miller P, Kao J. Myth: ketamine should not
be used as an induction agent for intubation in patients
with head injury. CJEM. 2010 Mar;12(2):154-157.
34. Bozeman WP, Kleiner DM, Huggett V. A comparison
of rapid-sequence intubation and etomidate-only
intubation in the prehospital air medical setting.
Prehosp Emerg Care. 2006 Jan-Mar;10(1):8-13.
35. Li J, Murphy-Lavoie H, Bugas C, Martinez J, Preston
C. Complications of emergency intubation with
and without paralysis. Am J Emerg Med. 1999
Mar;17(2):141-143.
36. Highlights of prescribing information: Zemuron
(rocuronium bromide). Access data FDA. https://
www.accessdata.fda.gov/drugsatfda_docs/label/
2010/020214s034lbl.pdf. Accessed November 12, 2019.
37. Tran DT, Newton EK, Mount VA, Lee JS, Wells GA,
Perry JJ. Rocuronium versus succinylcholine for rapid
sequence induction intubation. Cochrane Database
Syst Rev. 2015 Oct 29;(10):CD002788.
38. Martyn JA, Richtsfeld M. Succinylcholine-induced
hyperkalemia in acquired pathologic states: etiologic
factors and molecular mechanisms. Anesthesiology.
2006 Jan;104(1):158-169.
39. Gronert GA. Cardiac arrest after succinylcholine:
mortality greater with rhabdomyolysis than receptor
upregulation. Anesthesiology. 2001 Mar;94(3):523-529.
40. Minton MD, Grosslight K, Stirt JA, Bedford RF.
Increases in intracranial pressure from succinylcholine:
prevention by prior nondepolarizing blockade.
Anesthesiology. 1986 Aug;65(2):165-169.
41. 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 Apr;65(4):358-361.
42. Tang L, Li S, Huang S, Ma H, Wang Z. Desaturation
following rapid sequence induction using
succinylcholine vs. rocuronium in overweight patients.
Acta Anaesthesiol Scand. 2011 Feb;55(2):203-208.
43. Strayer RJ. Rocuronium versus succinylcholine:
Cochrane synopsis reconsidered. Ann Emerg Med.
2011 Aug;58(2):217-218.
44. Drug Trial Snapshot: Bridion (sugammadex). https:// 65. Hwang J, Park S, Huh J, et al. Optimal external
www.fda.gov/drugs/drug-approvals-and-databases/ laryngeal manipulation: modified bimanual
drug-trial-snapshot-bridion Updated February 16, 2016. laryngoscopy. Am J Emerg Med. 2013 Jan;31(1):32-36.
Accessed November 12, 2019. 66. Law JA, Broemling N, Cooper RM, et al; Canadian
45. Jahr JS, Miller JE, Hiruma J, Emaus K, You M, Airway Focus Group. The difficult airway with
Meistelman C. Sugammadex: a scientific review recommendations for management—part 1—difficult
including safety and efficacy, update on regulatory tracheal intubation encountered in an unconscious/
issues, and clinical use in Europe. Am J Ther. 2015 induced patient. Can J Anaesth. 2013 Nov;60(11):
Jul-Aug;22(4):288-297. 1089-1118.
46. Bhatia N, Bhagat H, Sen I. Cricoid pressure: where 67. Johnson DM, From AM, Smith RB, From RP, Maktabi
do we stand? J Anaesthesiol Clin Pharmacol. 2014 MA. Endoscopic study of mechanisms of failure of
Jan;30(1):3-6. endotracheal tube advancement into the trachea
during awake fiberoptic orotracheal intubation.
47. Sellick BA. Cricoid pressure to control regurgitation
Anesthesiology. 2005 May;102(5):910-914.
of stomach contents during induction of anaesthesia.
Lancet. 1961 Aug 19;2(7199):404-406. 68. Messa MJ, Kupas DF, Dunham DL. Comparison
of bougie-assisted intubation with traditional
48. Tsung JW, Fenster D, Kessler DO, Novik J. Dynamic
endotracheal intubation in a simulated difficult airway.
anatomic relationship of the esophagus and trachea
Prehosp Emerg Care. 2011 Jan-Mar;15(1):30-33.
on sonography: implications for endotracheal tube
confirmation in children. J Ultrasound Med. 2012 69. Baker JB, Maskell KF, Matlock AG, Walsh RM, Skinner
Sep;31(9):1365-1370. CG. Comparison of preloaded bougie versus standard
bougie technique for endotracheal intubation
49. Smith KJ, Dobranowski J, Yip G, Dauphin A, Choi
in a cadaveric model. West J Emerg Med. 2015
PT. Cricoid pressure displaces the esophagus: an Jul;16(4):588-593.
observational study using magnetic resonance imaging.
70. Shah KH, Kwong BM, Hazan A, Newman DH, Wiener
Anesthesiology. 2003 Jul;99(1):60-64.
D. Success of the gum elastic bougie as a rescue airway
50. Rice MJ, Mancuso AA, Gibbs C, Morey TE, Gravenstein in the emergency department. J Emerg Med. 2011
N, Deittle LA. Cricoid pressure results in compression of Jan;40(1):1-6.
the postcricoid hypopharynx: the esophageal position
is irrelevant. Anesth Analg. 2009 Nov;109(5):1546-1552.
51. Oh J, Lim T, Chee Y, et al. Videographic analysis of
glottic view with increasing cricoid pressure force.
Ann Emerg Med. 2013 Apr;61(4):407-413.
52. Tournadre JP, Chassard D, Berrada KR, Boulétreau P.
Cricoid cartilage pressure decreases lower esophageal
sphincter tone. Anesthesiology. 1997 Jan;86(1):7-9.
53. Fenton PM, Reynolds F. Life-saving or ineffective? An
observational study of the use of cricoid pressure and
maternal outcome in an African setting. Int J Obstet
Anesth. 2009 Apr;18(2):106-110.
54. Trikha A, Vasudevan B. Cricoid pressure: time to
release the pressure! “The Indian Anaesthetists’ Forum
website.”. http://180.149.244.185:9898/iaforum/Article_
Folder/Cricoid-Pressure-Time-to-Release-the-Pressure.
pdf Published February 2015. Accessed November 12,
2019.
55. Mechlin MW, Hurford WE. Emergency tracheal
intubation: techniques and outcomes. Respir Care.
2014 Jun;59(6):881-892.
56. Sakles JC, Mosier J, Chiu S, Cosentino M, Kalin L.
A comparison of the C-MAC video laryngoscope to
the Macintosh direct laryngoscope for intubation in
the emergency department. Ann Emerg Med. 2012
Dec;60(6):739-748.
57. Amornyotin S, Prakanrattana U, Vichitvejpaisal P, Vallisut
T, Kunanont N, Permpholprasert L. Comparison of the
clinical use of Macintosh and Miller laryngoscopes for
orotracheal intubation by second-month nurse students
in anesthesiology. Anesthesiol Res Pract. 2010.
58. Arino JJ, Velasco JM, Gasco C, Lopez-Timoneda F.
Straight blades improve visualization of the larynx
while curved blades increase ease of intubation: a
comparison of the Macintosh, Miller, McCoy, Belscope
and Lee-Fiberview blades. Can J Anaesth. 2003
May;50(5):501-506.
59. Achen B, Terblanche OC, Finucane BT. View of the
larynx obtained using the Miller blade and paraglossal
approach, compared to that with the Macintosh blade.
Anaesth Intensive Care. 2008 Sep;36(5):717-721.
60. Varghese E, Kundu R. Does the Miller blade truly
provide a better laryngoscopic view and intubating
conditions than the Macintosh blade in small children?
Paediatr Anaesth. 2014 Apr 2;24(8):825-829.
61. Passi Y, Sathyamoorthy M, Lerman J, Heard C, Marino
M. Comparison of the laryngoscopy views with the
size 1 Miller and Macintosh laryngoscope blades
lifting the epiglottis or the base of the tongue in
infants and children <2 yr of age. Br J Anaesth. 2014
Nov;113(5):869-874.
62. Asai T, Matsumoto S, Fujise K, Johmura S, Shingu K.
Comparison of two Macintosh laryngoscope blades in
300 patients. Br J Anaesth. 2003 Apr 1;90(4):457-460.
63. Delaney JS, Al-Kashmiri A, Baylis PJ, Aljufaili M, Correa
JA. The effect of laryngoscope handle size on possible
endotracheal intubation success in university football,
ice hockey, and soccer players. Clin J Sport Med. 2012
Jul;22(4):341-348.
64. Levitan RM, Pisaturo JT, Kinkle WC, Butler K, Everett
WW. Stylet bend angles and tracheal tube passage
using a straight-to-cuff shape. Acad Emerg Med. 2006
Dec;13(12):1255-1258.
December 2019 n Volume 33 Number 12 27
 Primetime
Viewing
Video Laryngoscopy

LESSON 6

By Samuel Kim, MD, Calvin A. Brown III, MD

and Alexander Y. Sheng, MD
Dr. Kim is an emergency medicine resident at Boston University Medical Center
in Boston, Massachusetts. Dr. Brown is assistant professor of emergency medicine
at Harvard Medical School, director of faculty affairs at Brigham and Women’s
Hospital Urgent Care, and an attending physician in the Department of Emergency
Medicine at Brigham and Women’s Hospital in Boston, Massachusetts. Dr. Sheng is
the assistant residency program director and an assistant professor in the Depart-
ment of Emergency Medicine, also at Boston University Medical Center.
Reviewed by Frank LoVecchio, DO, MPH, FACEP

OBJECTIVES
On completion of this lesson, you should be
able to:
1. Describe the major limitations of conventional direct
CRITICAL DECISIONS
laryngoscopy.
n What clinical presentations warrant the use of
2. List the advantages of video laryngoscopy for difficult
video laryngoscopy over direct laryngoscopy?
intubations.
3. Describe the major video laryngoscopes available and n When and how should video laryngoscopy
the design differences between each device. be used as a first-line instrument for airway
4. Explain the strengths and weakness of each of the management?
major video laryngoscopes.
n What technical challenges are of greatest
5. Apply video laryngoscopy in a variety of difficult airway
scenarios. concern when using video laryngoscopy?
n Do all VL models have emergency
FROM THE EM MODEL
department applications, and what are the
19.0 Procedures and Skills Integral to the Practice benefits and limitations of each?
of Emergency Medicine
19.4 Diagnostic and Therapeutic Procedures
19.4.4 Head, Ear, Eye, Nose, and Throat

March 2016 n Volume 30 Number 3 13

 CASE PRESENTATIONS
■ CASE ONE
An 84-year-old woman with
severe shortness of breath arrives via
ambulance. She reports sudden-onset
chest pain at rest with progressive
dyspnea. Vital signs are blood pressure
122/56, a heart rate 99, and oxygen
saturation 93% on non-rebreather
facemask. The patient is tachypneic
and in respiratory distress, using
accessory muscles to breathe. Her
jugular vein pulsations are elevated,
and diffuse crackles and a 2/6
systolic murmur are noted at the apex
radiating to the axilla.
The patient has 1+ bilateral lower-
extremity edema. An ECG shows
lateral-wall STEMI, and a portable
chest radiograph shows diffuse
pulmonary edema. Furosemide and
nitroglycerin are administered, and
she is placed on bilevel positive airway
pressure (BI-PAP); however, she
continues to struggle.
The emergency physician suspects
ischemic mitral regurgitation from
papillary muscle rupture. Cardiology
at the bedside recommends
immediately catheterization.
Preparations are made to secure the
airway for impending respiratory
failure prior to percutaneous coronary
intervention.
There is a rapidly growing body of
evidence to support the use of video
laryngoscopy for the management of both
routine and difficult airways. Emergency
physicians, in particular, must understand
the design and clinical applications of
these devices to achieve improved first-
pass success.
All resuscitative efforts ultimately will
fail if the patient cannot be adequately
oxygenated and ventilated. For the
majority of those who are critically ill
or injured, this requires the successful
placement of an endotracheal tube (ETT).
Since it first was introduced in the early
1940s, direct laryngoscopy (DL) has
been a reliable and successful method
for obtaining glottic visualization and
tracheal intubation. While nearly every
14 Critical Decisions in Emergency Medicine
■ CASE TWO
EMS arrives with a 91-year-
old man who has been transferred
from an outside hospital. He was
a restrained passenger in a motor
vehicle that rear-ended a bus at a
high rate of speed. EMS reports that
he had to be extricated and appears
to have an unstable C2 fracture and
weakness in both of his arms.
Upon arrival, the patient is supine
on a stretcher and is wearing a
cervical collar. Vital signs are stable
and he is conversant, in no obvious
distress, and complaining of neck
pain. A secondary survey reveals
tenderness to palpation on the
posterior midline of the man’s neck.
An outside cervical spine CT shows a
displaced pedicle fracture of C2, and
significant soft-tissue swelling from
C2 down to C5.
Shortly thereafter, the patient
suddenly begins having difficulty
speaking and breathing, and
complains of feeling “strangled.”
Within minutes, he appears to be
in respiratory distress. Suspecting
a retropharyngeal hematoma,
the clinician decides to intubate
emergently to secure airway
protection.
other aspect of medicine has undergone
dramatic advances in recent decades,
however, DL largely has remained
unchanged.
Direct visualization, which requires a
straight line of sight from the operator’s
eye to the glottic inlet, can be difficult
or even impossible to acquire in many
emergency department patients. Cervical
spine precautions, reduced mouth
openings, small mandibles, airway
obstruction, blood, vomit, secretions,
and large tongues all contribute to poor
direct visualization.
Some of these challenges can be over-
come with optimal patient positioning,
meticulous DL technique, and external
laryngeal manipulation. However, even
in the hands of a skilled operator, many
■ CASE THREE
A 42-year-old woman with facial
swelling and a history of hereditary
angioedema is brought to the emergency
department of a small community
hospital by EMS. Thirty minutes
before her symptoms began, she ate an
omelet seasoned with a “new” type of
pepper. She immediately experienced
a tingling sensation in her face, which
has progressed to worsening facial,
periorbital, and lingual edema within the
last hour.
On arrival, she is afebrile. Vital signs
are blood pressure 115/74; heart rate 89;
and oxygen saturation 94% on room air,
which improved to 97% with an oxygen
facemask (reservoir at 15 L/min flow).
Edema is apparent in her face, lips, and
the area around her eyes. The patient’s
tongue is swollen, filling the majority of
her oral cavity, and her voice is hoarse;
expiratory wheezing and stridor are noted.
While awaiting fresh frozen plasma
from the blood bank, antihistamines,
steroids, and epinephrine are administered
without effect. C1 esterase-inhibitor
concentrates are not readily available in
this emergency department. Meanwhile,
the patient develops worsening stridor,
voice changes, and decreasing oxygen
saturation on a non-rebreather mask. The
decision is made to intubate.
patients remain difficult — or even im-
possible — to intubate under direct vision.
Many of these patients will require mul-
tiple attempts and prolonged intubation
times, which can put them at risk for dire
traumatic and hypoxic consequences.
Through improved glottic visual­
ization and user-friendly designs, video
laryngoscopy (VL) has transformed
our current understanding of what
constitutes a difficult-to-manage airway,
and has provided a new process for
overcoming these clinical challenges.
Over the past decade, advances in video-
enhanced devices have launched an
“airway management revolution.”
Fundamentally, all video laryngoscopes
possess the same critical design elements
that improve glottic visualization. Each
device features a curved blade structure
with a narrow profile that can curl FIGURE 2. GlideScope AVL Reusable
around the tongue to mirror an oral
airway. Embedded along the curve of
the blade are a microcamera and light
source that enable glottic illumination
and the acquisition of an image that
then is displayed on a video screen. This
configuration allows the provider to “see
around corners” and obviates the need
for a direct line of sight — a critically
important benefit for many emergency
department patients.

CRITICAL DECISION
What clinical presentations
warrant the use of video
laryngoscopy over direct
laryngoscopy?
Difficult airway attributes are
common in emergency department
presentations, and poor glottic
visualization is among the most frequent
reasons why intubation attempts fail.
Even with optimal positioning and
technique, patients with suboptimal
glottic views are good candidates for
video laryngoscopy.
While we know what constitutes a
difficult DL attempt, the factors that
contribute to a problematic VL are still
unclear, as typical predictors of poor
direct visualization (restricted mouth
opening, reduced neck mobility, anterior
airways, etc.) do not necessarily portend
poor video views.1-3
There is a growing body of
literature that supports the superiority
of glottic views with VL in both
operative and emergency department
patients. Research suggests that when
FIGURE 1. GlideScope Ranger
a difficult DL is predicted based on a
pre-intubation bedside assessment, VL
should be used as an immediate backup,
or even employed as the initial method of
intubation.4,5
CRITICAL DECISION
When and how should video
laryngoscopy be used as a
first-line instrument for airway
management?
Although video laryngoscopes have
been successful in “rescuing” poor direct
views, there is little evidence about
whether these devices should be used
for routine intubations, or reserved for
difficult or failed airways.6 While the
focus has been on showing how VL
can “backup” DL, video laryngoscopy
is gaining traction as a viable stand-
alone option that can be employed in
virtually any clinical situation. Recent
registry data suggests that VL is being
used nearly as often as DL for emergency
department intubations.7
Although VL improved visualization,
early experience with GlideScope
laryngoscopy suggested that it might not
improve first-pass intubation success or
time to tube placement.8 These results
may have been confounded by the
intubators’ inexperience. In adept, well-
trained hands, VL is comparable to DL
in this regard.9 In emergency department
populations, GlideScope use actually
appears to improve first-pass success.10,11
Some portable video laryngoscopes,
including the GlideScope Ranger
(Figure 1), were created for prehospital
scenarios; their compact size and
specially designed screens function well
in high-glare environments. Although
real-life field experience is limited, these
tools have been successfully integrated
into both ground and air-transport
prehospital settings.
In the hands of ground personnel, the
GlideScope Ranger shows improved rates
of success, fewer attempts, and a shorter
time to intubation and ventilation
compared to DL.12 Conversely, the
Pentax Airway Scope (AWS) has
demonstrated inferior intubation success
rates when used in daylight environments
because of screen glare.13
CRITICAL DECISION
What technical challenges are
of greatest concern when using
video laryngoscopy?
Most video laryngoscopes are user-
friendly; however, transitioning from
tube placement under direct visualization
to intubation by indirect vision may be
difficult for some operators. Devices
with integrated tube channels, including

March 2016 n Volume 30 Number 3 15


FIGURE 3. Storz C-MAC
the Pentax Airway Scope, initially may
be easier to learn than the Macintosh
blade.14
More practice may be required with
devices that require the ETT to be placed
independently by hand (eg, GlideScope
or McGrath). The curved trajectory of
the ETT as it approaches the laryngeal
inlet can make navigation of the cords
challenging.15
VL offers superior glottic exposure
over DL in nearly every scenario.
However, devices with distal image
acquisition are susceptible to soiling
by airway bleeding and secretions,
which can make it difficult to maintain
adequate visualization. To achieve
indirect visualization of the laryngeal
inlet and vocal cords, the ETT must
follow the same trajectory of the blade as
it approaches the airway.
Since this path follows a steep
arc and not a straight line, it can be
difficult to navigate the vocal cords
with the tube tip; the stylet often must
be retracted to complete the intubation.
This unique extra step can result in a
slightly prolonged time to tracheal tube
placement, although it does not affect
intubation success.13 According to a
recent study, predictors of difficult VL
include patients with poor upper lip
bite tests (Table 1), although the study
only included subjects with grade I or
II Cormack and Lehane (C-L) glottic
views.16
16 Critical Decisions in Emergency Medicine
CRITICAL DECISION a rigid stylet, which should be used to
Do all VL models have
emergency department
applications, and what are the
benefits and limitations of each?
GlideScope Video
Laryngoscope
Anatomy
The GlideScope Video Laryngoscope
(GVL), which has been on the market for
more than a decade, is the prototypical
VL model. The standard GVL system
consists of a curved Macintosh-like
blade; its 80-degree hyperacute anterior
angulation curves around the tongue.
LED lights are positioned along the
underbelly of the blade with a video
camera that utilizes complementary
metal-oxide semiconductor (CMOS)
technology. A light source is placed in
close proximity to a rectangular glass
window, enabling the LEDs to warm the
lens to prevent misting and fogging (a
common problem with such devices).
A single video cable transmits
processed images to a 7-inch LCD
display, which can be placed on a
flat surface or mounted to a mobile
stand and brought to the bedside. The
original GVL blade comes in a variety
of shapes and sizes (GVL-2 through
GVL-5) suitable for virtually any patient
population — from small children to
adults with physical limitations such as
morbid obesity.
Most average-sized adults can be
intubated with a size 3 or 4 blade.
Standard GVL blades are reusable; after
each intubation, they must undergo
cleaning to remove gross debris, as well
as high-level disinfection. The handle,
made of high-grade medical plastic, is
submersible.
Every GlideScope system includes
TABLE 1. Upper Lip Bite Test
Class I: Lower incisors can bite the
upper lip above the vermilion line.
Class II: Lower incisors can bite the
upper lip below the vermilion line.
Class III: Lower incisors cannot bite
the upper lip.
maintain ETT shape during intubation
by allowing the tube to follow the curved
trajectory of the blade without becoming
deformed.
The GlideScope Cobalt AVL (Figure
2) is a disposable, single-use system that
circumvents the cost and downtime
associated with the maintenance and
disinfection of the original model. Both
pediatric and standard-sized wands are
available.
The GlideScope Ranger is a
lightweight, portable version originally
designed for field use. The handle, cable,
and display are built into one self-
contained unit, and its 3.5-inch LCD
screen remains visible despite sun glare.
Devices in the GlideScope family
also include a steel video blade with
geometry similar to that of direct
laryngoscopes. This “direct intubation
trainer” is designed to allow the operator
to maintain skill with conventional DL
mechanics, while benefitting from video
enhancements that facilitate real-time
instructor feedback. The most recent
GlideScope iteration features a thin
titanium profile and disposable high-
grade plastic blades.
Technique
Limited by its shape and design, the
GlideScope does not function and should
not be used as a direct laryngoscope.
Like all such devices, the GlideScope is
a left-handed instrument. After opening
the patient’s mouth, the blade should be
inserted directly in the midline with the
top surface of the blade touching, but
not manipulating, the tongue. While the
patient can be placed in the “sniffing
position,” this is not required.
With an eye on the screen, the
intubator should guide the distal tip
of the blade around the tongue while
watching for key midline structures,
including the uvula and the tip of the
epiglottis. The blade tip should be
maneuvered into the vallecula and then
a gentle backward lift should be used to
expose the laryngeal inlet.
A common mistake is to advance
the blade too far into the hypopharynx,
which results in an “up-close” image
of the vocal cords that appears highly
optimized; in reality, however, the
blade may be too close and incorrectly
positioned in the laryngeal inlet.
Ultimately, the blade competes for
the same space as the approaching ETT,
making tube delivery exceptionally
difficult. The tip of the ETT should be
inserted in the corner of the right side
of the patient’s mouth, with the tube
parallel to the ground. As the tube is
advanced behind or adjacent to the blade
and its distal tip guided toward the tip
of the laryngoscope, the user should
look at the screen while rotating the tube
counterclockwise 90 degrees. (The tip
of the ETT should be held at 12 o’clock,
positioned in front of the laryngeal inlet
curving into the trachea.)
Under real-time video supervision,
the operator should advance the
ETT through the vocal cords while
simultaneously withdrawing the
stylet by about 5 cm to complete the
intubation. Withdrawal, which can be
done by the operator’s thumb or by an
assistant, should follow the arc of the
instrument, eventually curving into the
patient’s chest.
Obtaining an optimal view of the
glottis with the GlideScope is rarely
difficult. However, passage of the ETT
through the glottis while observing
the screen can be challenging for two
reasons. First, some familiarity with the
instrument is required. Second, due to
the hyperangulation of the GlideScope
blade, the tip of the ETT must follow the
same path with an anterior trajectory
that can impinge on the trachea at
a sharp angle and fail to advance.
Withdrawal of the stylet makes the end
FIGURE 4. McGrath Series 5
of the ETT flexible, enabling it to pass
easily into the trachea.
The device is appropriate as a primary
intubation tool, although it traditionally
has been reserved for cases that are
difficult or impossible to complete
under direct vision. The minimal force
required to expose the glottis makes
the GlideScope useful for patients in
C-spine immobilization. Its sharp distal
angulation allows better visualization of
the anterior larynx.
Evidence
Among inexperienced operators, the
device is able to provide a C-L grade I or
II view in nearly every patient in which
its used, with glottic visualization equal
to or better than DL. Although rare,
failures can occur due to the difficulty
of passing the ETT, despite a sufficient
glottic view.17
Success with this device is high (96%
to 98%), even in patients who exhibit
hallmarks of difficult laryngoscopy
(eg, those with morbid obesity, cervical
spine disease, or a cervical collar). The
device performs equally well compared
to flexible bronchoscopes in morbidly
obese patients.29 The GlideScope also
has shown promise as a rescue device,
succeeding in 94% of intubations where
DL failed. Evidence of altered upper-
airway anatomy or head and neck
surgery appear to be the only predictors
of GlideScope difficulty.18 The device’s
only limitation is that the patient’s
mouth opening must be greater than
15 mm to accommodate the passage of
the widest portion of the blade.
In a recent study aimed at identifying
the clinical features associated with
difficult GlideScope laryngoscopy,
patients with high upper lip bite
test scores and short sternothyroid
distances required multiple attempts or
lengthier intubation times. Despite these
complications, a grade I or II view was
obtained in every patient (all of whom
were undergoing general anesthesia).16
In the hands of prehospital providers,
the GlideScope also has been associated
with improved intubation success (97%
compared to 95% with DL), fewer
attempts (1.2 versus 2.3), less time
without ventilation (37 seconds versus
55 seconds), and shorter time to
intubation (21 versus 42 seconds).12
Storz C-MAC
Anatomy
The Storz C-MAC (Figure 3) is
a reincarnation of the older video
Macintosh laryn­goscope (V-MAC).
While the video Macintosh was a hybrid
scope that combined both fiberoptic and
video elements, the C-MAC utilizes a
CMOS chip technology similar to that
used in the GlideScope.
The device’s shape is that of
a traditional direct Macintosh
laryngoscope. A newer hyperangulated
blade (called the “D-blade” or difficult
blade) recently has been designed to help
visualize a more anterior and superior
larynx. A micro camera and light source
are blended into the blade; and a video
cartridge slips into the back of the
handle, attached by a single cord to a
high-resolution digital display that can
sit on a flat surface or mount to a mobile
pole.
The blades intrinsically possess
anti-fog properties (the light source is
contained in the blade itself, warming
the lens), and the monitor system can
record both still images and video clips.
Technique
Since the standard C-MAC
blades feature Macintosh geometry,
the mechanics of laryngoscopy are
more akin to that of DL. Because of
this, the trajectory to the airway is
straighter, which can help facilitate
the manipulation of the ETT tip to
the laryngeal inlet. While it is possible
March 2016 n Volume 30 Number 3 17
 curved video wand (called a “Camera
Stick”) houses the light source with a
single-use disposable hard plastic blade.
The McGrath’s main advantage is its
portability; it weighs only 325 grams,
and requires neither cables nor a separate
n Use a rigid stylet when intubating with the GlideScope; this can help the display unit. However, the device’s small
ETT navigate the sharper anterior angulation of the blade to reach the size can make it vulnerable to theft and
laryngeal inlet.
damage during transport. The video
n If maintaining DL skill is important in your practice, consider using a wand and blade cover are fully adjustable
C-MAC blade, which maintains standard Macintosh geometry and can be to three different lengths.
used when DL mechanics are desired. The newest version of the device
n Consider VL as the initial method for routine and difficult intubations, includes a slightly larger screen and an
and be familiar with the specific devices available in your emergency angled blade designed for both video and
department. direct viewing. However, when used as
n Devices with plastic covers that go over or envelop the video and light a direct laryngoscope, the device may
elements (eg, C-MAC, GlideScope Cobalt, McGrath Series 5) are prone to not provide adequate direct views of the
fogging. Either warm the device or apply a commercial anti-fog solution glottic inlet.24
prior to the intubation attempt.
Technique
Much like the GlideScope, the
“good” glottic views (C-L grade I or II) McGrath is designed to be inserted in
to intubate without one, a malleable
compared to DL. Of the patients with the midline and “hugged” around the
stylet should be used for the majority of
an initial grade IV direct view, a grade tongue, while being rotated backwards
emergency tracheal intubations; rigid
I or II video view was obtained nearly until the glottis can be visualized. The
stylets are unnecessary.19
80% of the time. This data also supports tip of the blade should be positioned in
When using the C-MAC, the operator
the argument that early recourse to the vallecula. A slight upward lift may
can either insert the blade as if using
VL should be considered when glottic be required to expose the glottis. A
a conventional direct laryngoscope,
visualization is suboptimal.20 malleable stylet with a curve that follows
or place the blade in the midline and
Video laryngoscopes also provide the arc of the blade should be used within
advance it using a GlideScope-like
gentler intubation attempts since less the tracheal tube to maintain its shape.
technique. With its anti-fog features,
wider field of view, ease of use, and effort is required to obtain an acceptable Evidence
mobility, the C-MAC has become view. The force exerted on the maxillary
Although not as extensively studied
particularly popular in emergency incisors by the V-MAC is less than that
as the GlideScope, the McGrath has
department settings. associated with a standard Macintosh
performed well in operative reports,
blade (2.1 N versus 15.3 N).21
Evidence obtaining a C-L grade I or II view in
As with the GlideScope, the V-MAC
99% of subjects.25 The model also may
Because the C-MAC is a newer allows trainees to view the procedure on
be a particularly valuable rescue tool
device, it has yet to collect the robust the screen in real time — a benefit that
after DL has failed. In one operative
body of evidence seen with the can improve the intubation process and
study of patients undergoing general
GlideScope; however, early studies are reduce the learning curve.22 Preliminary
anesthesia with unsuccessful DL, the
encouraging. In one dual-center study, experience with the C-MAC shows
McGrath successfully intubated patients
V-MAC laryngoscopy succeeded in it performs on par with other video
producing the best attainable direct 95% of the time (58/61).9 As with other
laryngoscopes in its class. The device
and video view and a higher number of also may provide better first-pass success video laryngoscopes, novice clinicians
(93% versus 84%) in predicted difficult may take longer to intubate when using
airways.23 the instrument than when using DL — a
FIGURE 5. Pentax Airway Scope caveat that reflects the additional skill
McGrath Series 5 required to indirectly navigate the ETT
Anatomy through the vocal cords.26
Compact and lightweight, the The Pentax Airway Scope
McGrath Series 5 video laryngoscope
features a 1.7-inch integrated LCD
(AWS-100)
screen mounted on the end of its handle Anatomy
(Figure 4). The monitor pivots and is The portable, self-contained Pentax
adjustable to maintain optimal viewing Airway Scope includes a video camera,
during different phases of insertion. A 2.4-inch LCD rectangular display,

18 Critical Decisions in Emergency Medicine

disposable blade, and tube holder (Figure
5). While the design is similar to that
of other video laryngoscopes, several
unique features are worth noting. Green
“crosshairs” on the display allow the
operator to properly position the device;
when the ETT is advanced, it is more
likely to traverse the laryngeal opening
into the trachea.
The device’s handle is attached to a
flexible video/light wand that fits inside
a disposable plastic sheath and provides
a 90-degree field of view. The blade,
made from fog- and contamination-
resistant Lexan plastic, incorporates
a tracheal channel that holds the tube
during insertion and facilitates its
passage during intubation. The channel
can accommodate tubes with internal
diameters from 6.0 to 8.5 mm.
Durable and highly water-resistant,
the AWS-S100 model is particularly
useful in outdoor prehospital
environments. However, the lack of a
robust anti-fog mechanism and tendency
CASE RESOLUTIONS
■ CASE ONE
Airway equipment was prepared
at the bedside to intubate the elderly
woman with STEMI, including size-3
Macintosh and Miller blades, and a
GlideScope video laryngoscope and
bougie as backups. The patient was
preoxygenated with BL-PAP with a
starting oxygen saturation of 97%.
Etomidate (10 mg) and succinyl­
choline (100 mg) were administered
intravenously. Fasciculations appeared
30 seconds later with flaccid paralysis
at 50 seconds. The emergency
physician’s first direct look with the
Mac 3 provided a C-L grade III view;
it became apparent that the patient
suffered from advanced degenerative
temporomandibular joint (TMJ), which
limited the opening of her mouth. The
view was not improved, even with use
of the Miller blade and backwards,
upwards, rightwards pressure.
The patient desaturated, but was
successfully bagged and preoxygenated.
A second attempt was made with the
for secretions and blood to contaminate
the device’s optics can compromise
visualization during intubation.
Technique
Much like other video laryngoscopes,
the AWS is advanced in the midline after
the vocal cords have been positioned in
the target site.
Evidence
In 100 elective surgery patients,
the Pentax AWS obtained a grade I
view in all cases, while the Mac blade
achieved this only 65% of the time.
The integrated channel, as opposed
to freehanding, may result in faster
times to intubation compared to the
GlideScope in patents with normal
airway anatomy. 27
The Pentax also shows encouraging
results in patients at risk for cervical
spine injury.28 Even in the hands of novice
operators, intubation with the Pentax
may be faster and more successful than
with DL.14 The screen, which is difficult
GlideScope, which provided a full-
grade I Cormack-Lehane glottic view,
despite the patient’s rigid TMJ.
A 7.5-mm ETT was passed through
the cords under video visualization and
secured, and the patient was taken to
the catheterization lab for definitive
treatment of a ST-segment elevation
myocardial infarction.
■ CASE TWO
The emergency physician anticipated
intubation difficulties in the elderly
car accident victim. Anesthesia was
notified, but could not spare any
personnel. The patient began to
deteriorate.
A topical anesthesia with nebulized
and atomized lidocaine was applied,
and ketamine (0.5 mg/kg) was
administered intravenously. A backup
cricothyroidotomy kit was prepared.
Intubation was attempted with a
C-MAC video laryngoscope. A direct
look failed to visualize any glottis
structures; however, a grade IIa view
was achieved on the video screen. The
to view in bright light, can result in
harder and longer intubation attempts in
outdoor daylight settings.13
King Vision
Anatomy
The King Vision video laryngoscope
is among the newest devices on the
market. Introduced in late 2011, it
incorporates a reusable monitor and
stalk, which fit into a disposable plastic
handle containing both video and light
elements. The tool features a 24-inch
diagonal monitor with a full-color,
OLED anti-glare display that provides a
160-degree viewing angle (Figure 6).
Its handle is ergonomically designed
to reduce the impact on teeth and
prevent the lift of soft tissue. The
device’s disposable blades feature
coated, anti-fog lenses; CMOS chips;
micro cameras; and white LED lights.
Ultra-portable and water resistant, the
device is highly adaptable to prehospital
environments.
patient was intubated successfully with
a 7-0 ETT on first attempt using the
video view.
■ CASE THREE
When preparing equipment to
intubate the 42-year-old woman with
angioedema, the emergency physician
discovered that the fiberoptic broncho-
scope normally available had been sent
for repairs. The clinician adjusted his
plan to attempt an awake look with a
King Vision video laryngoscope, while
simultaneously preparing for an
emergent bedside cricothyroidotomy.
A benzocaine 20% metered spray
with atomizer was used to desensitize
the posterior pharynx. The King
Vision was inserted with the patient
sitting upright. A C-L grade II view
was achieved; and, despite significant
supraglottic swelling, a 7-0 ETT was
successfully placed. The patient was
immediately sedated with propofol.
Fresh frozen plasma arrived minutes
later, and the patient was admitted to
the ICU.
March 2016 n Volume 30 Number 3 19

n Failing to practice the techniques for tube delivery with video
laryngoscopy, which requires different hand-eye coordination, stereotactic
skills, and experience than with DL.
n Advancing a video laryngoscope too deeply. This can result in a
disorienting view of the esophageal opening, which is created when the
camera is directed posterior to the laryngeal inlet.
n Intubating without a stylet or with the wrong stylet.
n Attempting to intubate without maintaining a curve on the tracheal tube;
this mistake will make the procedure challenging or even impossible.
Technique
The King Vision should be introduced
into the patient’s mouth in much the
same way it is with the GlideScope
and Pentax AWS. Once fully inserted,
slight upward force may be required
to optimize the glottic view. If using a
channeled blade, the tube simply can be
pushed forward while the glottic opening
is kept in the middle of the screen.
Alternatively, a preformed stylet and
ETT can be “freehanded” to complete
the intubation.
Innovative, lightweight, compact, and
affordable, the device includes the design
elements that have proved successful
in other VL models. Although formal
studies are lacking, promising research is
underway.
Summary
VL is changing the landscape of
emergency airway management. DL is
a time-tested technique that relies on
an outdated tool. Video laryngoscopes
are highly successful, easy to use,
and improve glottic visualization in
almost every conceivable scenario. The
combination of improved visualization,
high first-pass success and gentler
attempts undoubtedly will translate
into a safer, more reliable intubation
experience for the patient and provider.
In modern medicine, these devices
help facilitate airway management
education, quality assurance, and
research through their ability to record
still images and videos. While they
traditionally have been thought of as
“rescue” tools, there is no evidence that
20 Critical Decisions in Emergency Medicine
we should relegate them to this role.
Trauma, bleeding, and airway
swelling will occur with serial
laryngoscopy attempts. Each device has
its advantages and disadvantages, and
the final choice will depend on practice
setting, departmental budgets, provider
preference, and the ability to reprocess
reusable equipment. However, one thing
is clear — when available, VL is quickly
becoming standard care.
For the same reason we’ve moved
away from ordering oral contrast
dye studies to diagnose appendicitis
or performing diagnostic peritoneal
lavage for unstable trauma patients, we
should begin to migrate away from DL.
Although DL represents “the way we’ve
always done it,” we must now perform
intubation “the way it should be done.”
REFERENCES
1. Walls RM. Identification of the Difficult and
Failed Airway. In: Manual of Emergency Airway
Management, 3rd Ed. LW&W; 2008:81-93.
2. Reed MJ, Dunn MJ, McKeown DW. Can an airway
assessment score predict difficulty at intubation
in the emergency department? Emerg Med J.
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3. Hagiwara Y, Watase H, Okamoto H, et al. Prospective
validation of the modified LEMON criteria to predict
difficult intubation in the ED. Am J Emerg Med.
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4. Kaplan MB, Hagberg CA, Ward DS, et al.
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the larynx during routine intubation. J Clin Anesth.
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5. Sakles JC, Mosier J, Chiu S, et al. A comparison of
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direct laryngoscope for intubation in the emergency
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6. Piepho T, Fortmueller K, Heid FM, et al. Performance
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Anaesthesia. 2011;66(12):1101-1105
7. Brown CA 3rd, Blair AE, Pallin DJ, et al. Techniques,
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8. Platts-Mills TF, Campagne D, Chinnock B, et al. A
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9. Noppens RR, Möbus S, Heid F, et al. Evaluation of
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10. Sakles JC, Mosier JM, Chiu S, Keim SM. Tracheal
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11. Mosier JM, Stolz U, Chiu S, Sakles JC. Difficult
airway management in the emergency department:
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laryngoscopy. J Emerg Med. 2012;42(6):629-634.
12. Wayne MA, McDonnell M. Comparison of traditional
versus video laryngoscopy in out-of-hospital tracheal
intubation. Prehosp Emerg Care. 2010;14(2):278-282.
13. Ueshima H, Asai T. Tracheal intubation in daylight
and in the dark: a randomised comparison of the
Airway Scope, Airtraq, and Macintosh laryngoscope
in a manikin. Anaesthesia. 2010;65(7):684-687.
14. Liu L, Tanigawa K, Kusunoki S, et al. Tracheal
intubation of a difficult airway using Airway Scope,
Airtraq, and Macintosh laryngoscope: a comparative
manikin study of inexperienced personnel. Anesth
Analg. 2010;110(4):1049-1055.
15. Walls RM, Samuels-Kalow M, Perkins A. A new
maneuver for endotracheal tube insertion during
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2010;39(1):86-88.
16. Tremblay MH, Williams S, Robitaille A, Drolet P. Poor
visualization during direct laryngoscopy and high
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17. Cooper RM, Pacey JA, Bishop MJ, McCluskey
SA. Early clinical experience with a new video
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18. Aziz MF, Healy D, Kheterpal S, et al. Routine clinical
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20. Brown CA 3rd, Bair AE, Pallin DJ, et al. Improved
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21. Lee RA, van Zundert AA, Maassen RL, et al. Forces
applied to the maxillary incisors during video-assist-
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22. Kaplan MB, Ward DS, Berci G. A new video
laryngoscope—an aid to intubation and teaching.
J Clin Anesth. 2002;14(8):620-626.
23. Aziz MF, Dillman D, Fu R, Brambrink AM.
Comparative effectiveness of the C-MAC video
laryngoscope versus direct laryngoscopy in
the setting of the predicted difficult airway.
Anesthesiology. 2012;116(3):629-636.
24. Wallace CD, Foulds LT, McLeod GA, et al. A
comparison of the ease of tracheal intubation
using a McGrath MAC® laryngoscope and a
standard Macintosh laryngoscope. Anaesthesia.
2015;70(11):1281-1285.
25. Shippey B, Ray D, McKeown D. Case series: the
McGrath videolaryngoscope—an initial clinical
evaluation. Can J Anaesth. 2007;54(4):307-313.
26. Walker L, Brampton W, Halai M, et al. Randomized
controlled trial of intubation with the McGrath
Series 5 videolaryngoscope by inexperienced
anaesthethists. Br J Anaesth. 2009;103(3):440-445.
27. Teoh WH, Shah MK, Sia AT. Randomised comparison
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intubation in patients with normal airway anatomy.
Anaesthesia. 2009;64(10):1125-1129.
28. Liu EH, Goy RW, Tan BH, Asai T. Tracheal intubation
with videolaryngoscopes in patients with cervical
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 Down the Tube
Postintubation Care
of the Critically Ill

LESSON 12

By Matthew A. Roginski, MD, MPH; Christopher J. Hogan, MD,

FACEP, FCCM; and Michael G. Buscher, DO, FAAEM
Dr. Roginski is the assistant medical director of DHART and an assistant professor
of medicine in the Sections of Emergency and Critical Care Medicine at Dartmouth-
Hitchcock Medical Center in Lebanon, New Hampshire. Dr. Hogan is an associate
professor in the Departments of Emergency Medicine and Surgery at Virginia
Commonwealth University Medical Center in Richmond. Dr. Buscher is an attending
physician in the Departments of Emergency Medicine and Internal Medicine (Critical
Care) at Yale New Haven Health, Bridgeport Hospital in Bridgeport, Connecticut.

Reviewed by George Sternbach, MD, FACEP

OBJECTIVES
On completion of this lesson, you should be able to: CRITICAL DECISIONS
1. Discuss how to choose an initial ventilator setting, and n What factors should be considered when choosing
describe techniques for evaluating complications like a patient’s initial ventilator settings, and how
air trapping and high alveolar pressures.
should potential complications be avoided?
2. Summarize the ideal sedative and analgesic agents for
intubated patients. n What sedatives and analgesic agents are preferred
3. Identify hemodynamically unstable postintubation for intubated patients in the ED?
patients using invasive and noninvasive measures. n What is the best approach for assessing and
4. Recognize and manage deadly postintubation managing hemodynamic instability?
pathologies. n How should metabolic derangements be managed?
5. Identify acute interventions to limit the risk of ventilator-
n What causes of postintubation cardiac arrest
associated pneumonia.
should emergency physicians be prepared to
FROM THE EM MODEL address?
19.0 Procedures and Skills Integral to the Practice n What can be done to decrease the risk of
of Emergency Medicine ventilator-associated pneumonia?
19.1 Airway Techniques
Given the escalating number of high-acuity cases and frequency of prolonged boarding, intubated patients
must often be managed in the emergency department for extended periods. Although most emergency
physicians are highly skilled in emergent airway management, they must also be adept at performing various
mechanical ventilation techniques, following sedation and analgesia regimens, and treating the complex acid base
and hemodynamic derangements that many of these patients exhibit.

June 2020 n Volume 34 Number 6 17

 CASE PRESENTATIONS
■ CASE ONE
A 31-year-old man presents
in respiratory distress; he is blue
and unresponsive. His vital signs
are blood pressure 180/90, heart
rate 125, and oxygen saturation
83% with minimal lung sounds on
examination. His wife frantically
explains that the patient is healthy
at baseline with the exception of
sleep apnea and nasal polyps. He
was diagnosed with an upper-
respiratory infection earlier this
week, but his symptoms have
worsened today.
The patient is intubated but is
difficult to ventilate with a bag-
valve-mask. Once on a ventilator,
his peak pressures reach 78 cm
H 2 0. His arterial blood gas (ABG)
measurement includes a pH of 7.12
and partial pressure of carbon
dioxide (pCO 2) of 81 mm Hg.
CRITICAL DECISION
What factors should be
considered when choosing
a patient’s initial ventilator
settings, and how should
potential complications be
avoided?
Managing the ventilator of a newly
intubated emergency department patient
is an active process, and every decision
has downstream effects on morbidity
and mortality.1,2 The goal of ventilatory
management is to provide support and
avoid causing iatrogenic harm while
the underlying process is being treated.
It can be particularly challenging to
balance adequate ventilatory support
and lung protection when managing
critically ill patients, as no single
ventilator mode can accomplish
oxygenation and ventilation goals. All
ventilator settings require clinicians to
be mindful of tidal volumes, airway
pressures, and respiratory rates to avoid
causing harm.
18 Critical Decisions in Emergency Medicine
■ CASE TWO
A 38-year-old woman arrives
via ambulance after being found
unresponsive by her roommate, who
says the patient has a history of
depression and recently underwent a
breakup. EMS reports that the patient
was unresponsive, tachypneic (40 bpm),
tachycardic (145 bpm), hypotensive
(88/40 mm Hg) and febrile (38.4°C
[101.1°F]) at the scene.
Upon arrival, the patient is
unresponsive and tachypneic, localizing
to painful stimuli. Her oxygen
saturation is 99% on room air, and her
blood glucose level is 130 mg/dL. After
being preoxygenated, she is sedated
and paralyzed with etomidate and
rocuronium, respectively. The patient
is intubated with a 7.5-endotracheal
tube (ETT); her vocal cords are
visualized, and a positive color change
is noted on capnography. As the ETT is
being secured, she begins to seize and
becomes hypoxic.
Volume Control
For patients without evidence of
lung injury, a targeted tidal volume of
6 to 8 mL/kg of predicted body weight
is safe place to start. Recent research
shows that low tidal volume ventilation
reduces the risk of lung injury and acute
respiratory distress syndrome (ARDS) in
patients with normal-appearing lungs.1-3
If evidence of a lung injury is present at
the time of intubation, it is important to
reduce tidal volumes to 6 mL/kg of ideal
body weight. This strategy can improve
outcomes in patients with ARDS.4
Shortly after intubation, it can be helpful
to evaluate the patient’s height with a
tape measure to accurately calculate
their ideal body weight.
Plateau Pressure
Along with targeting low tidal
volumes, it is also important to avoid
overdistending the alveoli and increasing
the transpulmonary pressure gradient.5
The plateau pressure is a commonly
accepted surrogate when monitoring
for overdistention. When evaluating a
■ CASE THREE
A 74-year-old man with oxygen-
dependent emphysema presents from
a local nursing home in respiratory
distress. His caregiver reports that he
has been febrile and more confused
recently with increased sputum
production. When EMS arrived,
he was sitting upright in bed, in a
tripod position and in significant
distress. They promptly placed him on
continuous positive airway pressure
(CPAP), nebulized albuterol, and IV
methylprednisolone.
Upon arrival, the patient is in
respiratory distress and remains
hypoxic on CPAP. His initial vital signs
are blood pressure 100/60, heart rate
110, respiratory rate 40, and oxygen
saturation 84%. After an additional
albuterol nebulizer is administered
through the CPAP, a chest x-ray shows
hyperinflated lungs with bilateral infil­
trates. The decision is made to perform
a rapid-sequence intubation (RSI).
patient without active respiratory effort,
plateau pressure (Figure 1) should be
measured at the end of inspiration.
When flow in the airways approach zero,
the pressure equilibrates throughout
the circuit, and the plateau pressure
represents the pressure in the alveoli.
The aim is to keep plateau pressure
under 30 cm H2O to avoid barotrauma.
The etiology of elevated plateau
pressures is multifactorial; it can result
from a combination of increased volume
and alveolar overdistention, reduced
chest wall compliance, or abdominal
distention that compresses the thoracic
cavity. A general approach is to reduce
the pressure to less than 30 cm H2O.
A first step in reducing this pressure is
to decrease the patient’s tidal volume
and ensure the absence of dynamic
hyperinflation.
Dynamic Hyperinflation
Dynamic hyperinflation, also
known as auto-PEEP or breath
stacking, is a phenomenon in which
the lungs fail to completely empty
before the next ventilator-delivered
breath. This is commonly seen
when patients with obstructive lung
disease (eg, emphysema, asthma) are
intubated. Because these patients
do not completely exhale before the
next delivered breath, lung volumes
progressively increase over multiple
respiratory cycles. As the volume of air
in the lungs rises, so does the pressure;
this dynamic increases the risk of
complications, including pneumothorax
and cardiovascular collapse from
decreased preload.
FIGURE 1. Pressure Waveform of a Mechanical Ventilator on Volume Control
Mode of a Relaxed Patient
Plateau
Pressure
Pressure
While it is commonly taught to
disconnect crashing patients with
obstructive lung disease from the
ventilator to allow complete exhalation,
evidence of hyperinflation can be
detected long before cardiovascular
collapse. This complication can be
checked at the bedside by observing the
flow curve in a relaxed patient (Figure 2)
and assessing the total positive end-
expiratory pressure (PEEP) compared
the set PEEP.
During a normal respiratory cycle,
the flow at the end of exhalation
Total PEEP
is zero. This concept can be easily
demonstrated by being mindful of
the pause after a normal spontaneous
exhalation. The process is shown on
the ventilator when the flow returns to
baseline. If the flow does not return to
zero before the next breath, the patient
may be exhaling when the breath is
being delivered — a problem that can
lead to dynamic hyperinflation.
A similar thought experiment is
to have the patient exhale only half
the total lung volume before taking
another breath, which can become very
uncomfortable after a small number of
respiratory cycles. The total PEEP (ie,
the total pressure in the thorax) can
be measured during an end-expiratory
hold in a relaxed patient. The difference
between the total PEEP and the
PEEP set on a ventilator is “auto-
PEEP,” which reflects the unintended
excess pressure caused by dynamic
hyperinflation. While there is no clear,

Auto-PEEP harmful cutoff, monitoring a trend is

helpful when manipulating respiratory
rates and tidal volumes in patients
with obstructive lung disease. This
Inspiratory Expiratory
Hold Hold condition can be treated by increasing
the absolute exhalation time, a process
The inspiratory hold allows the measurement of plateau pressure. Flow stops during that is best accomplished by reducing
this pause; the alveolar pressure can be measured because pressure equilibrates along the respiratory rate.
the ventilator circuit when there is zero flow. Similarly, an expiratory hold inhibits the
Oxygen Toxicity
ventilator from delivering the next breath and allows the pressure to equilibrate. To
calculate “auto-PEEP” subtract the set PEEP from the total PEEP. The difference is the Hyperoxia has been increasingly
auto PEEP. To acutely measure these variables, the patient must be sedated without recognized as a harmful pathological
exerting spontaneous respiratory effort. entity in the critically ill. The goal
of oxygen management is to obtain
a therapeutic level of oxygenation
FIGURE 2. Square-Flow Waveform of a Mechanical Ventilator with the lowest fraction of inspired
oxygen (FiO2) and lowest PEEP. For a
majority of newly intubated patients, an
Inhalation oxygenation goal above 92% suffices,
(+)

and the clinician should attempt to

Zero Flow titrate the PEEP to reduce the FiO2 to
Flow

under 60%.6

Obstructive Lung Disease

(-)

Exhalation Hypercarbic respiratory failure is

the primary physiologic disturbance in
Complete Continued patients with obstructive lung disease
Exhalation Exhalation who require mechanical ventilation.
An elevated partial pressure of carbon
Positive flow represents ventilator-assisted inhalation, and negative flow represents
dioxide (pCO2) can commonly be
passive exhalation. The exhalation arm approaching zero between breaths indicates
complete exhalation. If the exhalation arm of the flow curve does not approach zero
seen in the ABG measurements of
before the next ventilator-delivered breath (noted by the star), incomplete exhalation is newly intubated patients. While the
indicated, and breath stacking will occur. reflexive response to an elevated pCO2
is to increase the minute ventilation

June 2020 n Volume 34 Number 6 19


TABLE 1. Tips for Managing Obstructive Lung Disease
“Low and A low tidal-volume strategy with a low respiratory rate. Typically,
slow” strategy 6-8 mL/kg of predicted body weight with a respiratory rate of
12-14 breaths/minute.
Tolerate It is important to tolerate hypercarbia because reflexive
hyercarbia hyperventilation may significantly harm patients.
Check for To assess for adequate exhalation time, check the total PEEP with an
air trapping end-expiratory hold, and evaluate the expiratory limb of the flow curve
to ensure that it returns to zero before the patient’s next breath.
by increasing the respiratory rate or
tidal volume, this is counterproductive
and commonly leads to dynamic
hyperinflation.
“Low and slow” is a helpful
approach when determining a patient’s
initial ventilator settings (Table 1).
As previously mentioned, a low
tidal volume (6-8 mL/kg of ideal
body weight) is important for lung
protection, but the degree of dynamic
hyperinflation is ultimately related to
respiratory rate and absolute exhalation
time. The most effective way to achieve
a longer absolute exhalation time is
through a low respiratory rate; 10 to
14 breaths per minute is a safe start.
Decreasing the inspiratory time may
also be beneficial.
An elevation in the patient’s pCO2
level is an expected consequence of the
“low and slow” strategy. While many
clinicians are uncomfortable with
respiratory acidosis, it is a necessary
aspect of ventilator management
in patients with severe obstructive
disease. Patients with pure respiratory
acidosis can tolerate acidemia to a
pH of 7.2.6 Hypercarbia generally
improves as the adjunctive therapies
(eg, steroids, bronchodilators) improve
the underlying disease.
When prescribing permissive
hypercapnia, it is important to
remember that most patients tolerate
respiratory acidosis and acidemia
without much consequence. However,
clinicians must be mindful of the
populations that do not tolerate
permissive hypercapnia, including
pregnant patients and those with
severe left or right ventricular failure,
pulmonary hypertension, intracranial
hemorrhage, elevated ICP, and salicylate
or sodium channel-blocker overdose.6
20 Critical Decisions in Emergency Medicine
Sepsis and ARDS
Patients who develop impaired
oxygen exchange with diffuse bilateral
infiltrates or altered respiratory
mechanics without hydrostatic
pulmonary edema are at high risk for
ARDS.7 In these cases or when there
is a concern for lung injury, special
attention must be paid to the lung
protective ventilation strategy.8 Lung
protection should be prioritized over the
normalization of blood gas.4,5,7
While ARDS is a heterogenous
disease, it is important that the
prevalence of high inflation pressures
and collapsed lung units adjacent to
open lung units increase the risk of
further lung damage.5,9 A low tidal
volume ventilation strategy has been
shown to improve mortality.4 Key steps
in the initial management of a patient
with ARDS are:
1. Provide a low tidal volume (6mL/kg
predicted body weight).
2. Increase PEEP to recruit atelectatic
lung segments and keep them
expanded.
3. Avoid barotrauma by initially
attempting to reduce the plateau
pressure below 30 cm H2O.
4. Avoid oxygen toxicity by decreasing
the FiO2 to under 60%.
5. Tolerate permissive hypercarbia.
Pulmonary Hypertension
The fragile hemodynamic balance
inherent in pulmonary hypertension
makes this pathophysiology difficult to
manage on a ventilator. These patients
are exquisitely sensitive to changes
in preload and afterload.10 After
intubation, the goals are centered around
maintaining a low tidal volume and low
plateau pressures to limit the effects on
vascular preload.
Unlike patients with ARDS or
emphysema, these patients cannot
tolerate permissive hypercarbia
or hypoxia because of pulmonary
vasoconstriction and increased right
ventricular afterload.11 Worsening
afterload may precipitate further failure.
Key concepts for managing pulmonary
hypertension are normocarbia,
normoxia, low tidal volumes, and low
PEEP and plateau pressures.
CRITICAL DECISION
What sedatives and analgesic
agents are preferred for
intubated patients in the
emergency department?
Analgesia and sedation are
critical components in the care of any
intubated patient, but these elements
are often overlooked. It is vital for
every emergency physician to have a
rapidly accessible sedation package at
their disposal. Appropriate analgesia
and sedation can be as important as the
intubation itself — too much, even early
in the course, is predictive of delayed
extubation and increased mortality;
too little can lead to increased energy
expenditure, immunomodulation, and
even post-traumatic stress disorder.12,13
Pain, agitation, and delirium are
closely linked and should be targeted
with specific medications. Although
intubated patients have frequently been
managed with benzodiazepines alone,
recent Society of Critical Care Medicine
(SCCM) guidelines recommend a
“pain-first” approach.14 The old
practice of administering a bolus of
benzodiazepines followed by a paralytic
agent is no longer an acceptable method
of managing intubated patients.
Sedatives should be used once the
patient’s pain has been addressed,
except when the immediate initiation of
deep sedation is indicated, as in cases
of intracranial hypertension, severe
respiratory failure, status epilepticus,
and the prevention of awareness
during chemical paralysis. The latter
is an extremely important point to
remember, especially when using long-
acting paralytics like rocuronium.
There is ample evidence to show
that patients who undergo RSI in the
emergency department frequently
receive inadequate analgesia and
sedation — sometimes none at all —
so it is vital to have these medications
available.15,16
Once the paralytics wear off, the
primary goal should be to optimize
analgesia. Pain is the most common
memory patients have of their critical
illness. Because sedatives can mask
pain, clinicians should ensure adequate
analgesia before initiating a sedation
regimen.12 Common sources of pain
include the ETT itself, manipulation of
post-traumatic injuries, wound care,
invasive procedures, nursing care, in-
line ETT suctioning, and prolonged
immobility.
Opioids are most frequently used
for managing pain in the critically ill.
While the optimal drug and dose for
each individual patient depends on many
factors, fentanyl and remifentanil are
generally regarded as first-line treatments
because of their quick onset, benign
hemodynamic profile, and unlikely
accumulation in those with renal
dysfunction.
If not initiated while the patient
is paralyzed, sedatives should be
administered once pain has been
addressed. The most common sedative
agents, which act via the GABAA
receptor, include propofol, etomidate,
benzodiazepines, and barbiturates. A
newer agent, dexmedetomidine, works
as an agonist of the alpha-2 adrenergic
receptor. Finally, ketamine is a NMDA
receptor antagonist that inhibits the
influx of calcium into the cells.
Propofol
The most commonly used sedative is
propofol, which has powerful anxiolytic
and amnestic properties but no
analgesic effect. Propofol is a complex
drug with three half-lives, ranging
from minutes to days, but its duration
of action is much shorter because it
rapidly crosses the blood-brain barrier
and distributes to the peripheral tissue.
Adverse reactions to the drug include
pain at the injection site, an increased
risk of bacterial infections, and
cardiovascular effects (eg, hypotension).
Propofol can also cause hyperlipidemia
and propofol infusion syndrome, but
these complications are most often
encountered in the ICU setting.
Benzodiazepines
Although benzodiazepines are
inexpensive and readily available, recent
evidence points to a number of untoward
effects, including a longer duration
of mechanical ventilation, longer ICU
and hospital lengths of stay, increased
delirium, and long-term cognitive
dysfunction.14 Furthermore, parenteral
infusions of lorazepam include propylene
glycol, which can lead to metabolic
acidosis and acute kidney injury.39 To
this end, the 2013 SCCM guidelines
recommend sedation strategies using non-
benzodiazepine agents to improve clinical
outcomes.14
Dexmedetomidine
It is important to remember that
analgesics are poor sedatives — and
vice versa — so the ideal “agent” is
either a drug with both properties or,
more likely, a combination of two
medications (eg, propofol and fentanyl).
Dexmedetomidine is a newer, centrally
acting, highly selective, alpha-2 adrenergic
agonist that possesses sedative, anxiolytic,
and analgesic properties. It is currently
approved in the US and Canada for the
short-term sedation (<24 hours) of patients
receiving mechanical ventilation.17
The drug is not associated with
respiratory depression, which is helpful
when liberating patients from mechanical
ventilation; however, it is associated
with bradycardia and hypotension.
Dexmedetomidine is of particular interest
in the critical care community because
studies suggest it may reduce the duration
of mechanical ventilation and incidence of
delirium.18
Ketamine
Ketamine, another agent with both
neuroleptic and analgesic properties,
is a rapidly acting drug that produces
dissociative anesthesia. Patients breathe
spontaneously, and because the drug
activates the sympathetic nervous system,
mean arterial pressure (MAP) and heart
rate often increase. The widespread use
of ketamine is limited by adverse drug
reactions, including hallucinations,
delirium, tachycardia, and increased
myocardial oxygen demand; however,
short-term use in the emergency
department is generally safe and well
tolerated.17
Special Populations
In the same way that certain
conditions warrant a nuanced ventilation
strategy, there are certain patient
populations for which a specific sedative
or analgesic are preferred.
A combination of propofol
and fentanyl is reasonable for
analgosedation in neuro-critically
ill patients. Continuous infusions of
sedatives and opioids are generally
considered protective for the injured
brain in the acute phase.19 Both
agents are rapidly effective and have
a short duration of action when
stopped, allowing easier monitoring of
neurologic function when needed.
Most patients with an injured
or ill brain manifest hypertension,
and propofol decreases intracranial
pressure and the cerebral metabolic
rate of oxygen while preserving
cerebral autoregulation. It should be
noted, however, that propofol can
cause hypotension. Because even one
episode of hypotension can increase
mortality in those with brain injuries, the
medication should be started at a low
dose and carefully titrated while closely
monitoring for complications.
Propofol decreases cerebral electrical
activity and can also be used to achieve
burst suppression in patients with
seizures. Ketamine and dexmedetomidine
can also be considered; however, given
the lack of good evidence to support
their use in this population, this decision
should be made in consultation with a
neurologist or neurosurgeon.
Propofol is also considered the
first-line treatment for patients who are
withdrawing from alcohol and require
intubation. Because most of these
patients have already received a large
quantity of benzodiazepines, the GABA
receptor-agonist properties of propofol
can help treat their severe withdrawal.
These patients also require analgesia
while intubated.
Some smaller studies have examined
dexmedetomidine for the treatment of
alcohol withdrawal syndrome. While
the drug can prevent intubation in
some patients and blunt the tachycardia
and hypertension seen with severe
withdrawal, it is not recommended as
a single agent and does not obviate the
June 2020 n Volume 34 Number 6 21
 need for benzodiazepines.20 As such,
propofol is more commonly used to
manage withdrawal in patients who have
already been intubated.
Initial treatment with fentanyl and
a benzodiazepine is a valid option for
hypotensive medical patients. Fentanyl
does not precipitate histamine release,
and neither agent has significant
hemodynamic effects. Ketamine may also
have a role in this patient population
owing to its positive hemodynamic and
dissociative effects. Once the patient
can be started on vasopressors, it is
acceptable to consider transitioning to a
propofol drip if needed for sedation.
CRITICAL DECISION
What is the best approach
for assessing and managing
hemodynamic instability?
Peri-intubation instability can be
mitigated prior to intubation with some
preparation and forethought, time
permitting. Hypotension is an ominous
finding and should heighten awareness
that complications may occur. Although
an elevated diastolic blood pressure
reflects increased vascular tone that may
be maintaining perfusion pressures, this
may resolve once a patient is induced
and intubated.
Hypovolemia can be addressed
prophylactically in high-risk patients,
including those with sepsis and large,
insensible volume losses caused by fever,
vomiting, or diarrhea. This is especially
true with trauma patients, for whom
blood transfusions should be considered
if tachycardia, a labile blood pressure
(ie, any low reading), tachypnea, or
altered mental status are present before
the decision to intubate is made. An
infusion of crystalloid solution (250 mL-
500 mL) is not detrimental, even for
fluid-overloaded patients.
The choice of induction medications
also impacts postintubation
hemodynamics. If a patient is in cardiac
arrest or is about to arrest, no sedation
or paralytic is needed. In such cases,
the administration of these agents
wastes time and exposes the patient to a
multitude of risks. Classically, etomidate
is the agent of choice because it causes
less hypotension than other agents,
22 Critical Decisions in Emergency Medicine
possibly because it does not trigger
histamine release.21 Ketamine is also an
excellent choice because of its minimal
impact on the cardiovascular system and
rapid onset of action. Lastly, propofol
has been associated with hypotension,
particularly in hypovolemic patients;
however, a half-dose may mitigate this
potential outcome.
After ensuring that there is a secure
airway and adequate ventilation, it
is paramount to assess the patient’s
circulation. Physiologically speaking,
airway, breathing, and circulation are
intertwined, so altering one parameter
may impact the others. For example,
the negative pressure generated by a
spontaneously breathing tachypneic
patient can bolster cardiac output by
augmenting preload. Transitioning
from negative-pressure ventilation
may decrease venous return to the
heart, causing hypotension or arrest.
Intubation independently increases the
risk of death.22
In most cases, the first sign of trouble
is the blood pressure measurement
taken immediately after the ETT
tube is secured. Overall, noninvasive
blood pressure cuffs are accurate in
determining normal MAP, but individual
diastolic and systolic blood pressures can
vary widely when compared to arterial
line measurements.23 Additionally,
different monitors may provide differing
values depending on the manufacturer’s
proprietary algorithm.
Overall, noninvasive blood
pressure measurements are unreliable
in critically ill patients; an arterial
line should be considered early before
patients lose their radial pulses from
worsening decompensation. Leg and
thigh blood pressures correlate with
upper-arm cuff MAPs, but these values
may be unreliable when evaluating a
hypotensive or tachycardic patient.24
Transthoracic Echocardiography
Bedside ultrasound, specifically a
limited transthoracic echocardiogram
(LTTE), can be helpful for assessing
perfusion and intravascular volume.
Ultrasound imaging is a safe,
noninvasive method for measuring
the diameter of the inferior vena cava
(IVC) and the degree of collapse and
fluctuations associated with ventilator-
delivered respirations. This modality can
help evaluate the fluid responsiveness of
apneic patients on controlled mechanical
ventilation.
LTTE is less reliable in patients
who are breathing spontaneously
because the degree of IVC fluctuation
is a function of both respiratory effort
and the pressure applied to assist
ventilation. Without standardized
ventilator settings, this approach
has not been proven to be a reliable
indicator of fluid responsiveness.25 In
the recently paralyzed and intubated
patient, these measures are ideal for
assessing hemodynamic instability in
the postintubation period. An IVC
diameter less than 1.5 cm is suggestive
of low intravascular volumes.26 More
importantly, this measurement can be
reassessed after blood or crystalloid are
provided, allowing the clinician to trend
the patient’s response.
Mitigating Complications
Some patients with heightened
vagal tone can develop bradycardia as
the laryngoscope or GlideScope presses
the back of the pharynx or as the ETT
is advanced. Preintubation atropine
should be considered when intubating
pediatric patients, who are infamous for
manifesting this phenomenon; however,
some research suggests that the drug may
not prevent reflex bradycardia entirely.27
The administration of atropine can help
clinicians quickly determine if vagal
stimulation is the cause of the patient’s
bradycardia and hypotension.
Hypotension, far and away the
most frequent complication in the
postintubation period, is associated
with increased hospital mortality.22 Both
pre- and postintubation hypotension
are also associated with peri-intubation
cardiac arrest. Other factors that have
been associated with postintubation
hypotension are advanced age, the use
of neuromuscular blockers, preexisting
COPD, sepsis, and extremes in body
weight.28
Complications that arise during
intubation (eg, hypoxemia, esophageal
intubation, vomiting/aspiration, arrest,
and suspected sepsis) also predispose
patients to postprocedure hypotension.29
Importantly, a preintubation blood
pressure under 140 mm Hg is a
significant indicator of postintubation
hypotension and its associated
complications; as such, hypotension
before induction is an ominous sign and
should be addressed if time permits.
The usual first-line response
to a decompensating patient in
nonhemorrhagic shock is a 20-mL/kg
fluid bolus given rapidly, but only half to
two-thirds of patients with septic shock
respond to this intervention.25 Although
the utility of early goal-directed therapy
has recently been dispelled in emergency
department patients, hypotension must
be corrected promptly.30
Whenever possible, patients
with trauma or GI bleeding should
receive blood products before
crystalloid solutions are administered.
Postintubation instability can generally
be corrected by allowing time for the
induction agents to wear off while
adding intravascular volume. Patients
may develop tachycardia as they become
more alert after intubation; furthermore,
their underlying pathology (eg, trauma,
hypoxia) may still be in play and can be
accompanied by hypertension. However,
if hypotension or tachycardia persist,
other etiologies should be pursued,
including an occult ischemia/infarct,
poorly controlled infectious source,
ongoing hemorrhage, or septic shock.
Norepinephrine
For most cases of shock,
norepinephrine is a good initial agent to
use once the decision to use vasopressors
has been made. However, in the peri-
intubation period, the drug has been
associated with in-hospital and 90-
day mortality, even after controlling
for the patients’ original illness.31,32
Its mechanism of increased systemic
vascular resistance (alpha-1 agonist),
coupled with its significant effect upon
arterial and venous capacitance vessels,
enhances venous return to the heart.
A patient’s lack of response to
norepinephrine should cause alarm.
For instance, does the patient have a
spinal injury that might require a pure
alpha agonist, such as phenylephrine?
This agent is a favorite pressor of
anesthesiologists and has been used in
the emergency department with good
effect.33 In a proper concentration (40
μg/mL), phenylephrine can also be
given through a peripheral IV for a
short period of time, enabling further
treatment of any instabilities.34
Some research suggests that older
and/or sicker patients may already
have a heightened adrenergic tone
that prevents the expected response
to norepinephrine. In such cases,
agents that do not use an adrenergic-
stimulation pathway may be more
beneficial. Although vasopressin has
been advocated, it does not appear to be
superior to norepinephrine.35
CRITICAL DECISION
How should metabolic
derangements be managed?
Metabolic acidosis arises when
fixed acids in the blood increase. This
can occur when a patient gains a strong
acid (eg, in cases of ketoacidosis or
lactic acidosis) or loses their base (eg,
in cases of diarrhea or renal failure). To

TABLE 2. Common Metabolic Derangements

Initial Blood Blood Gas
Primary Compensatory Gas Results Blood Gas Results After Results After Full
Disburbance Common Causes Mechanism (uncompensated) Partial Compensation Compensation
Respiratory Hypoventilation Increase bicarbonate pH decreased pH decreased but pH normal
acidosis due to: (kidney and red PaCO2 increased closer to normal PaCO2 increased
(ie, primary • Pneumonia blood cells) PaCO2 increased
Bicarbonate normal Bicarbonate increased
increase in PaCO2) • Asthma Compensation slow Bicarbonate increased
• COPD (several days, maybe
• Depression of weeks)
respiratory center
Respiratory Hypoventilation Decrease pH increased pH decreased but pH normal
acidosis due to: bicarbonate (kidney PaCO2 decreased closer to normal PaCO2 decreased
(ie, primary • Pain and red blood cells)
Bicarbonate normal PaCO2 decreased Bicarbonate decreased
decrease in PaCO2) • Anxiety attack Compensation slow Bicarbonate decreased
• Stimulation of (several days, maybe
respiratory center weeks)
Metabolic acidosis • Renal failure Decrease PaCO2 pH decreased pH decreased but pH normal
(ie, primary • Diabetic (ie, increase PaCO2 normal closer to normal PaCO2 decreased
decrease in ketoacidosis respiratory ventilation) PaCO2 increased
Bicarbonate Bicarbonate decreased
bicarbonate) • Circulatory
Compensation rapid decreased Bicarbonate decreased
failure/shock
(minutes/hours)
Metabolic acidosis • Excessive Increase PaCO2 pH increased pH increased but closer Full compensation
(ie, primary bicarbonate (ie, increase PaCO2 normal to normal is rare in metabolic
increase in ingestion respiratory ventilation) PaCO2 decreased alkalosis beause the
Bicarbonate
bicarbonate) • Potassium decreased ventilation
Compensation rapid increased Bicarbonate increased
depletion required would threaten
(minutes/hours)
• Vomiting of blood oxygenation.
gastric acid Full compensation
is prevented by
“hypoxaemic drive.”

June 2020 n Volume 34 Number 6 23

 compensate for these abnormalities, the
body hyperventilates to decrease arterial
PCO2.
If a patient with metabolic acidosis
requires RSI, hyperventilation is
necessary to prevent acidosis from
worsening. The retained CO2 from
apnea or a “normal” respiratory rate
can worsen pH and lead to depressed
myocardial activity, increased
arrhythmias, elevated intracranial
pressure, and possibly death.
As such, a modified RSI approach
should be used when intubating
any patient with metabolic acidosis.
This approach has been termed
“resuscitation-sequence intubation”
with a focus on resuscitation measures
(eg, fluid resuscitation, vasopressors,
optimizing oxygenation) before
intubation, if possible.36 It is also
prudent to consider alternatives to
typical RSI medications, such as
ketamine or dexmedetomidine, which
can facilitate intubation without
altering the patient’s minute ventilation.
Another population at risk of
intubation-associated decline are those
with salicylate overdose. This toxidrome,
which classically causes metabolic
acidosis and respiratory alkalosis, can
be diagnosed clinically by the presence
of tachypnea (Table 2). Decreasing
respiratory alkalosis in these patients
increases the passage of salicylate into
the central nervous system.
Because intubation and mechanical
ventilation can rapidly worsen
outcomes, intubation should be avoided
whenever possible. If the procedure
is necessary for the management of
n Provide analgesia to every intubated patient, and then quickly move to
sedation if agitation persists.
n Be prepared for cardiac arrest or further hypotension and instability when
managing patients who are hypotensive before induction for intubation. A
bolus of crystalloid solution or pressors should be considered.
n Measure the patient’s height to accurately prescribe a lung-protective
ventilation strategy of 6 to 8 mL/kg of predicted body weight.
n Perform an inspiratory hold to evaluate the patient’s plateau pressure and
an expiratory hold to check for auto-PEEP.
24 Critical Decisions in Emergency Medicine
true respiratory failure, a sodium
bicarbonate infusion should be initiated
prior to intubation. It is important
to avoid long-acting sedatives and
paralytic agents and consider pressure-
controlled ventilation to allow increased
tidal-volume breaths.
CRITICAL DECISION
What causes of postintubation
cardiac arrest should
emergency physicians be
prepared to address?
Although cardiac arrest occurs in
2% to 4% of intubated patients, it
occurs twice as frequently in emergent
intubations than in elective ones.22,37,38
Peri-intubation cardiac arrest is
usually a bradycardic or pulseless
electrical activity event. Risk factors
associated with these complications
include increased patient age, a high
BMI, and procedural complications
(eg, multiple intubation attempts,
hypoxia, hypotension); furthermore,
preprocedural hypotension is frequently
present.
Hypotension may represent a
hypovolemic state, underlying cardiac
ischemia, or advanced septic shock,
any of which can overwhelm the
patient’s compensation mechanisms. As
intubation and mechanical ventilation
change the chest physiology from
negative to positive pressure, these
underlying problems can lead to cardiac
arrest or profound hypotension.
Below is a short list of postintubation
cardiac arrest etiologies that must either
be treated or ruled out. In addition, the
usual suspects (eg, underlying cardiac
ischemia/infarct, overwhelming sepsis)
must be carefully considered.
Tension Pneumothorax
Tension pneumothorax is the
most worrisome complication of
intubation. Regardless of how well
chest compressions are done and how
closely the ACLS protocol is followed,
there will be no resolution of arrest until
the tension pneumothorax is treated.
Although this phenomenon can occur for
many reasons, trauma and underlying
illness are the most frequent causes.
Bilateral chest tubes should be placed
first in patients who present in cardiac
arrest with associated recent or distant
trauma.
Bedside ultrasound should also
be used to evaluate for the absence
of lung sliding and the presence of
the lung point sign, findings that are
specific for pneumothorax. However,
it is important to recognize that other
pulmonary etiologies can cause these
findings as well.39,40 Patients with
known COPD or bullous lung disease
and those who appear Marfanoid may
also be candidates for early chest tube
placement in the postintubation period.
Of note, chest x-rays should not delay
placement of a chest tube when a tension
physiology is being considered.
Pericardial Tamponade
While pericardial tamponade is
not caused by intubation, the change
from negative-pressure to positive-
pressure ventilation can often diminish
preload past a point at which cardiac
arrest ensues. Pericardial tamponade is
addressed in ACLS and ATLS protocols,
and an evaluation of the pathology is
best addressed by bedside ultrasound. In
such cases, physical examination findings
and chest radiographs are nonspecific.
Overwhelming Acidosis
Metabolic, respiratory, and
mixed acidosis are other causes of
postintubation cardiac arrest that are
not directly caused by intubation;
however, the brief period in which a
patient cannot offload carbon dioxide
can be enough to overwhelm their
metabolic balance. Typically, these
patients present with metabolic acidosis
(eg, aspirin overdose, ethylene glycol,
diabetic ketoacidosis) for which they
appropriately develop an increased
respiratory drive to offload carbon
dioxide.
Patients with acidosis often present
on the verge of respiratory failure
because their work of breathing is
unsustainable; furthermore, when
they are sedated and paralyzed, they
completely lose this compensation
mechanism. Shortly after induction
and intubation (a period during which
the patient is not breathing and CO2
accumulates) these patients either seize
or arrest.
Acidosis will continue if this risk
is not considered because, per ACLS
protocols, patients in cardiac arrest
are only intermittently ventilated.
Capnography is instrumental for
monitoring such cases. Although an
ABG measurement can ultimately
confirm metabolic derangements, these
test results take a relatively long time in
most institutions.
Esophageal Intubation
Cardiac arrest in the postintubation
period should be attributed to a
misplaced ETT until proven otherwise.
In many cases, these events are preceded
by hypoxia. Again, CO2 capnography
or capnometry will also be abnormal
and should be addressed long before a
chest x-ray is obtained. In such cases,
a second look with traditional or video
laryngoscopy should be part of the
patient’s workup.
CRITICAL DECISION
What can be done to
decrease the risk of ventilator-
associated pneumonia?
Ventilator-associated pneumonia
(VAP), a known complication of
mechanical ventilation, is defined as
pneumonia that did not appear to be
incubating at the time of admission but
develops more than 48 to 72 hours after
endotracheal intubation. The disease
is thought to result from a leakage of
oropharyngeal secretions around the
ETT cuff and into the lungs.41 Ventilator-
associated pneumonias are particularly
important because they increase the
length of mechanical ventilation and
the length of stay, elevate the risk of
morbidity and mortality, and increase
health care costs.
While these cases are often
diagnosed in the ICU, a number
of simple emergency department
interventions can reduce this risk.
First, there is moderate evidence to
recommend ventilating patients without
benzodiazepine sedation. If analgesics
alone can make the patient comfortable,
sedation should be avoided.42
Several studies also suggest that
patients should be positioned with
the head of bed elevated 30 to 45
degrees. While evidence to support this
approach is poor and often conflicting,
it remains a basic practice because of
its simplicity, lack of cost, and potential
benefits. Supine positioning predisposes
patients to the microaspiration of
gastric contents, so most should remain
in a semirecumbent position unless
contraindications (eg, unstable spine
fractures) exist.
Subglottic secretion removal is
also recommended to reduce the risk
of VAP. Commercially available ETTs
with subglottic suction ports allow
continuous or intermittent suction.
While these tubes are more expensive
than traditional ETTs, a 2005 meta-
analysis of nearly 900 patients showed
that subglottic suction reduced the
risk of VAP by 49%.43 However, these
devices do not appear to reduce the
length of mechanical ventilation, ICU
stays, or mortality.
Endotracheal cuff pressure
management is also extremely
important. Although the movement of
secretions from the oropharynx into
the lungs increases the risk of VAP,
an effective cuff seal may reduce the
passage of secretions. The recommended
range for cuff pressure is 20 to 30 cm
H2O. Pressures under 20 cm H2O
are associated with a greater risk of
pneumonia.
Finally, there is moderate
evidence to support oral care with
chlorhexidine solution for all intubated
patients. Success with this approach
is primarily reported in the cardiac
surgery population; data to endorse
its use in a general population is more
equivocal. However, the cost and
safety of chlorhexidine have made
it a ubiquitous treatment. Research
from the Netherlands points to
decreased mortality when selectively
decontaminating the oropharynx with
antibiotics, although this practice
has not been adopted in the US over
concerns regarding antibiotic-resistant
infections.

Summary
n Failing to provide immediate analgesia and sedation following intubation, Emergency departments are receiving
especially when using long-acting paralytic agents. an increasing number of critically ill
n Allowing a suspected acidotic patient to undergo a prolonged period of intubated patients, many of whom
not being ventilated while undergoing intubation. This mistake can lead to require substantial bedside care prior to
seizures or cardiac arrest. ICU admission. Emergency physicians
n Hyperventilating a patient with asthma or emphysema because of hypercarbia. cannot expect their job to end once a
This leads to breath stacking and eventual hemodynamic collapse if not patient’s airway is secure. It is important
recognized early.
to understand the detrimental effects
n Setting the ventilator immediately after intubation and not returning to assess
that accompany improper mechanical
the need for changes. It is important to remember that, once intubated,
critically ill patients have a dynamic physiology and changing ventilatory needs. ventilation and be prepared to prescribe
appropriate ventilator settings.

June 2020 n Volume 34 Number 6 25

 CASE RESOLUTIONS
■ CASE ONE
A postintubation chest x-ray
of the young man in respiratory
distress showed clear lung fields.
An end-expiratory hold maneuver
was performed while the patient
was still paralyzed, which revealed
a total PEEP of 40 cm H 2O with
a set PEEP of 5 cm H 2O. His
ETT was promptly removed from
the ventilator for approximately
20 seconds, enabling complete
exhalation. After the patient was
reattached to the ventilator, the rate
was decreased to 12 breaths/minute.
IV methylprednisolone and inhaled
bronchodilators were initiated.
Because significant patient-
ventilator dyssynchrony and severe
airflow obstruction persisted,
analgesia and sedation were
increased, and the patient was
chemically paralyzed again. The
emergency physician was willing to
tolerate the patient’s hypercarbia to
prioritize adequate ventilation, while
closely monitoring for end-expiratory
flow and auto-PEEP.
The patient was transferred
to the ICU, where his airflow
obstruction and bronchospasm
significantly improved overnight.
Intubated patients also require
the thoughtful administration of
analgesia and sedation, and it is vital
to understand the different agents
that can fulfill this role. Finally, these
patients can manifest significant acid-
base and hemodynamic disturbances,
including peri-intubation cardiac arrest.
Recognizing the most likely causes of
these complications may help prevent
them altogether.
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2. Fuller BM, Mohr NM, Drewry AM, Carpenter CR.
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3. Serpa Neto A, Cardoso SO, Manetta JA, et al.
Association between use of lung-protective ventilation
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26 Critical Decisions in Emergency Medicine
He was extubated to a nasal cannula
with intermittent bronchodilators. The
patient was quickly transferred out
of the ICU and discharged home on
hospital day two.
■ CASE TWO
Even without an ABG measurement,
the astute emergency physician
recognized that the woman with a
presumed overdose was profoundly
acidotic. She was immediately
hyperventilated to blow off any
accumulated CO2 , and a bolus of
crystalloid solution was administered.
The patient quickly stopped seizing, and
her MAP improved slightly.
Early laboratory tests revealed a
pH of 7.0 and high anion-gap acidosis.
The patient continued to breathe over
a ventilator rate of 18 breaths/minute,
so pressure support was added while
taking measures to avoid auto-PEEP.
Further laboratory tests revealed renal
failure and an elevated ethylene glycol
level, consistent with poisoning, and the
patient was transferred to a tertiary care
facility for further management.
■ CASE THREE
The elderly man with emphysema
was determined to be septic and likely
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4. Acute Respiratory Distress Syndrome Network, Brown
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5. Tobin MJ. Principles and Practice of Mechanical
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6. Mosier JM, Hypes C, Joshi R, Whitmore S,
Parthasarathy S, Cairns CB. Ventilator strategies and
rescue therapies for management of acute respiratory
failure in the emergency department. Ann Emerg Med.
2015 Nov; 66(5):529-541.
7. Malhotra A. Low-tidal-volume ventilation in the acute
respiratory distress syndrome. N Engl J Med. 2007
Sep;257(11):1113-1120.
8. ARDS Definition Task Force, Ranieri VM, Rubenfeld GD,
et al. Acute respiratory distress syndrome: the Berlin
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definition. JAMA. 2012 Jun;307(23):2526-2533.
Amato MBD, Meade MO., SlutskyAS, et al. Driving
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10. Wilcox SR, Kabrhel C, Channick RN. Pulmonary
hypertension and right ventricular failure in emergency
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11. Zamanian RT, Haddad F, Doyle RL, Weinacker AB.
Management strategies for patients with pulmonary
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2007 Sep;35(9):2037-2050.
12. Reade MC, Finfer S. Sedation and delirium in the
intensive care unit. N Engl J Med. 2014 Jan;370(5):
444-454.
obtained, the patient was started
on high-flow oxygen, and volume
resuscitation was initiated. Given his
profound hypotension, peripheral
norepinephrine was administered
while volume resuscitation was
continued.
When the patient’s MAP rose above
60 mm Hg, the emergency physician
focused on intubating him using
etomidate and rocuronium, while using
bag-valve-mask ventilation during
periods of apnea to prevent respiratory
acidosis. Lung-protective ventilator
settings were used with a respiratory
rate that was equivalent to the man’s
preintubation respiratory rate.
A bolus dose of fentanyl was
administered followed by a dose of
propofol to provide sedation while the
patient remained chemically paralyzed.
Aware that this approach might cause
hypotension, the clinician continued
volume resuscitation and provided
a titrated dose of norepinephrine
while working on a central line. A
fentanyl infusion was also started.
After adequate time had passed for
the rocuronium to metabolize, the
patient was weaned off the propofol
but continued on the fentanyl drip. He
was then taken to the ICU for further
management.
13. Shehabi Y, Bellomo R, Reade MC, et al. Early intensive
care sedation predicts long-term mortality in ventilated
critically ill patients. Am J Respir Crit Care Med. 2012
Oct;186(8):724-731.
14. Barr J, Fraser GL, Puntillo K, et al. Clinical practice
guidelines for the management of pain, agitation, and
delirium in adult patients in the intensive care unit.
Crit Care Med. 2013 Jan;41(1):263-306.
15. Bonomo JB, Butler AS, Lindsell CJ, Venkat A.
Inadequate provision of postintubation anxiolysis
and analgesia in the ED. Am J Emerg Med. 2008
May;26(4):469-472.
16. Kendrick DB, Monroe KW, Bernard DW, Tofil NM.
Sedation after intubation using etomidate and a long-
acting neuromuscular blocker. Pediatr Emerg Care.
2009 Jun;25(6):393-396.
17. Roberts DJ, Haroon B, Hall RI. Sedation for critically
ill or injured adults in the intensive care unit: a shifting
paradigm. Drugs. 2012 Oct;72(14):1881-1916.
18. Reade MC, Eastwood GM, Bellomo R, et al. Effect
of dexmedetomidine added to standard care on
ventilator-free time in patients with agitated delirium:
a randomized clinical trial. JAMA. 2016 Apr;315(14):
1460-1468.
19. Oddo M, Crippa IA, Mehta S, et al. Optimizing
sedation in patients with acute brain injury. Crit Care.
2016 May;20(1):128.
20. Rayner SG, Weinert CR, Peng H, Jepsen S, Broccard
AF, Study Institution. Dexmedetomidine as adjunct
treatment for severe alcohol withdrawal in the ICU.
Ann Intensive Care. 2012 May;2(1):12.
21. Benson M, Junger A, Fuchs C, Quinzio L, Böttger S,
Hempelmann G. Use of an anesthesia information
management system (AIMS) to evaluate the physiologic
 effects of hypnotic agents used to induce anesthesia. Leatherman J. Mechanical Ventilation for Severe Asthma.
J Clin Monit Comput. 2000;16(3):183-190. Chest. 2015 Jun;147(6):1671-1680.
22. Heffner AC, Swords DS, Neale MN, Jones AE. Levitan, Richard. Timing Resuscitation Sequence Intubation
Incidence and factors associated with cardiac arrest for Critically Ill Patients. ACEPNow, ACEP/Wiley. August
complicating emergency airway management. 2015.
Resuscitation. 2013 Nov;84(11):1500-1504. Mosier JM, Hypes C, Joshi R, Whitmore S, Parthasarathy S,
23. Ribezzo S, Spina E, Di Bartolomeo S, Sanson Cairns CB. Ventilator strategies and rescue therapies
G. Noninvasive techniques for blood pressure for the management of acute respiratory failure in the
measurement are not a reliable alternative to direct emergency department. Ann Emerg Med. 2015 Nov;
measurement: a randomized crossover trial in ICU. 66(5):529-541
ScientificWorldJournal. 2014 Jan;2014:353628. Reade MC, Finfer S. Sedation and delirium in the intensive
24. Lakhal K, Ehrmann S, Benzekri-Lefèvre D, et al. care unit. N Engl J Med. 2014 Jan;370(5):444-454.
Brachial cuff measurements of blood pressure
during passive leg raising for fluid responsiveness
prediction. Ann Fr Anesth Reanim. 2012;31(5):e67-e72.
25. Boyd JH, Sirounis D, Maizel J, Slama M.
Echocardiography as a guide for fluid management.
Crit Care. 2016 Sep;20:274.
26. Lee CW, Kory PD, Arntfield RT. Development of a fluid
resuscitation protocol using inferior vena cava and lung
ultrasound. J Crit Care. 2016 Feb;31(1):96-100.
27. Fastle RK, Roback MG. Pediatric rapid sequence
intubation: incidence of reflex bradycardia and effects
of pretreatment with atropine. Pediatr Emerg Care.
2004 Oct;20(10):651-655.
28. Lin CC, Chen KF, Shih CP, Seak CJ, Hsu KH. The
prognostic factors of hypotension after rapid sequence
intubation. Am J Emerg Med. 2008 Oct;26(8):845-851.
29. Smischney NJ, Demirci O, Diedrich DA, et al. Incidence
of and risk factors for post-intubation hypotension in
the critically ill. Med Sci Monit. 2016;22:346-355.
30. Angus DC, Barnato AE, Bell D, et al. A systematic
review and meta-analysis of early goal-directed therapy
for septic shock: the ARISE, ProCESS and ProMISe
Investigators. Intensive Care Med. 2015 Sep;41(9):
1549-1560.
31. De Backer D, Biston P, Devriendt J, et al. Comparison
of dopamine and norepinephrine in the treatment of
shock. N Engl J Med. 2010 Mar;362(9):779-789.
32. Smischney NJ, Demirci O, Ricter BD, et al. Vasopressor
use as a surrogate for post-intubation hemodynamic
instability is associated with in-hospital and 90-day
mortality: a retrospective cohort study. BMC Res Notes.
2015;8:445.
33. Panchal AR, Satyanarayan A, Bahadir JD, Hays D,
Mosier J. Efficacy of bolus-dose phenylephrine for
peri-intubation hypotension. J Emerg Med. 2015
Oct;49(4):488-494.
34. Delgado T, Wolfe B, Davis G, Ansari S. Safety of
peripheral administration of phenylephrine in a
neurologic intensive care unit: a pilot study. J Crit Care.
2016 Aug;34:107-110.
35. Russell JA, Walley KR, Singer J, et al. Vasopressin versus
norepinephrine infusion in patients with septic shock.
N Engl J Med. 2008 Feb;358(9):877-887.
36. Levitan RM. Timing resuscitation sequence intubation
for critically ill patients. ACEPNow. https://www.
acepnow.com/article/timing-resuscitation-sequence-
intubation-for-critically-ill-patients. Published August
13, 2015.
37. Kim WY, Kwak MK, Ko BS, et al. Factors associated
with the occurrence of cardiac arrest after emergency
tracheal intubation in the emergency department.
PLoS One. 2014 Nov;9(11):e112779.
38. Leibowitz AB. Tracheal intubation in the intensive care
unit: extremely hazardous even in the best of hands.
Crit Care Med. 2006 Sep;34(9):2497-2498.
39. Aziz SG, Patel BB, Ie SR, Rubio ER. The lung point sign,
not pathognomonic of a pneumothorax. Ultrasound Q.
2016 Sep;32(3):277-279.
40. Sim SS, Lien WC, Chou HC, et al. Ultrasonographic
lung sliding sign in confirming proper endotracheal
intubation during emergency intubation. Resuscitation.
2012 Mar;83(3):307-312.
41. Grap MJ, Munro CL, Unoki T, Hamilton VA, Ward KR.
Ventilator-associated pneumonia: the potential critical
role of emergency medicine in prevention. J Emerg
Med. 2012 Mar;42(3):353-362.
42. Klompas M, Branson R, Eichenwald EC, et al. Strategies
to prevent ventilator-associated pneumonia in acute
care hospitals: 2014 update. Infect Control Hosp
Epidemiol. 2014 Aug;35(8):915-936.
43. Dezfulian C, Shojania K, Collard HR, Kim HM, Matthay
MA, Saint S. Subglottic secretion drainage for
preventing ventilator-associated pneumonia: a meta-
analysis. Am J Med. 2005 Jan;118(1):11-18.

ADDITIONAL READING
Angus DC, Barnato AE, Bell D, et al. A systematic review
and meta-analysis of early goal-directed therapy
for septic shock: the ARISE, ProCESS and ProMISe
Investigators. Intensive Care Med. 2015 Sep;41(9):
1549-1560.
Bonomo JB, Butler AS, Lindsell CJ, Venkat A. Inadequate
provision of postintubation anxiolysis and analgesia in
the ED. Am J Emerg Med. 2008 May;26(4):469-472.

June 2020 n Volume 34 Number 6 27

 Mechanical
Engineering
Ventilator Management

LESSON 17

By Andrew T. Schaub, DO; Christopher Peluso, DO; and

Matthew J. Stull, MD
Dr. Schaub is an attending emergency physician and clinical instructor at
MetroHealth/Case Western Reserve University in Cleveland, Ohio. Dr. Peluso is
a wilderness medicine fellow and an attending physician in the Department of
Emergency Medicine at Wake Forest University School of Medicine in Winston-
Salem, North Carolina. Dr. Stull is the assistant emergency medicine residency
director and an assistant professor in the Departments of Emergency Medicine and
Anesthesiology at University Hospitals-Cleveland Medical Center and Case Western
Reserve University in Cleveland, Ohio.
Reviewed by George Sternbach, MD, FACEP

OBJECTIVES
On completion of this lesson, you should be able to:
1. Devise a strategy for ventilator settings based on the
initial indication for intubation.
2. Describe the complications of inappropriate ventilator
settings in the emergency department.
3. Apply appropriate ventilator settings in response to
dynamic patient conditions.
4. Understand how initial emergency department ventilator
settings impact patient outcomes.
5. Recognize adjuncts to ventilator management to enhance
ventilator care for critically ill patients.
CRITICAL DECISIONS
n What initial ventilator strategies are most
appropriate after emergent intubation?
n How should intubated patients be monitored in
the emergency department?
n What strategies are available for patients who fail
to adequately ventilate?
n What strategies are available for patients who fail
to adequately oxygenate?

FROM THE EM MODEL

19.0 Procedures and Skills Integral to the Practice
of Emergency Medicine
19.1 Airway Techniques
19.1.6 Ventilatory Monitoring

Emergency physicians have the opportunity to intervene early to prevent downstream mortality and morbidity in
patients who must be mechanically ventilated, approximately 20.6% of whom die before leaving the hospital.1,2 As
the prevalence of critical care admissions and prolonged boarding continues to rise across the United States, it becomes
increasingly important to design effective, dynamic ventilator strategies to meet the unique and often-changing requirements
of each patient.

September 2020 n Volume 34 Number 9 3

 CASE PRESENTATIONS
■ CASE ONE
A 66-year-old woman with
COPD, morbid obesity, and tobacco
use presents via ambulance in
severe respiratory distress. Prior
to arrival, EMS established an IV
and administered three rounds of
nebulized albuterol and 125 mg IV
methylprednisolone. On arrival,
she is placed on bilevel positive-
airway pressure (BiPAP) with
pressure support of 10/5 cm H 2 O.
Her initial vital signs are blood
pressure 134/88, heart rate 122,
respiratory rate 38, temperature
36.8°C (98.2°F), and SpO 2 94% on
2  L/min supplemental oxygen via
nasal cannula.
Two grams of IV magnesium
sulfate and three rounds of nebulized
ipratropium bromide and albuterol
sulfate are administered. Laboratory
tests, including a CBC and ABG
measurement, are administered;
a chest x-ray is unremarkable
aside from hyperinflated lungs.
The patient is continued on BiPAP
CRITICAL DECISION
What initial ventilator strategies
are most appropriate after
emergent intubation?
There are four indications for
emergent intubation based on varying
pathophysiologies: airway protection
(eg, safety of procedures, depressed
mental status, severe agitation, expected
clinical course, transport), hypercapnia,
hypoxia, and excessive respiratory
load (eg, excessive work of breathing,
uncompensated acidosis, or shock).3
Ventilator strategies should be tailored
to each of these indications to maximize
supportive measures, return patients to a
physiologically neutral state, and provide
expedited extubation if possible.
Airway Protection
The approach to ventilator
management in the setting of airway
protection is relatively straightforward,
4 Critical Decisions in Emergency Medicine
with increasing inspiratory pressure
support to 20/5 cm H 2 O. Despite these
interventions, she does not improve —
as evidenced by worsening hypercapnia
with a PaCO 2 of 115 and increasing
somnolence. Subsequently, she is
intubated via rapid-sequence intubation
(RSI) and placed on mechanical
ventilation. The ICU is full, so the
patient will be boarded for multiple
hours prior to transfer.
■ CASE TWO
A 19-year-old man with no medical
history presents in respiratory distress.
He has had multiple sick contacts over
the last 5 days and flu-like symptoms
that have progressed over the last
48 hours. On arrival, he appears
diaphoretic and is in obvious distress,
with audible expiratory wheezes,
rhonchi midway up the thorax, and
bilateral intercostal and subcostal
retractions. His initial vital signs
are blood pressure 82/40, heart rate
138, respiratory rate 51, temperature
39.1°C (102.4°F), and SpO2 84% on
a nonrebreather mask at 15 L/min.
as the goal of mechanical support is to
temporarily match physiologic conditions
as closely as possible (Figure 1).
When selecting an ideal ventilator
mode for patients in acute respiratory
failure, both pressure-controlled (PC)
and volume-controlled (VC) settings
have been used. A recent meta-analysis
of 34 small studies comparing PC and
VC modes found no difference in the
work of breathing, oxygenation/gas
exchange, compliance, hemodynamic
stability, ICU mortality, and length of
stay.4
VC settings are easier to use
when implementing lung-protective
strategies, avoid the risk of ventilator-
associated lung injuries (VALIs), and
give clinicians total control over tidal
volume (VT), minute ventilation, and
minute volume. Additionally, assist-
controlled (AC) settings with a volume-
regulated strategy improve the work of
breathing and terminate inspiration at a
Supplemental oxygen is continued;
an IV is established; and a 30-mL/kg
normal saline fluid bolus and broad-
spectrum antibiotics, including
vancomycin and piperacillin-
tazobactam, are initiated.
Laboratory tests were initiated,
including a CBC with differential,
blood cultures, and lactate and ABG
measurements. A portable chest
x-ray reveals bilateral diffuse patchy
infiltrates with air bronchograms
that are worse at the bases. The
patient’s hypotension improves
over the next 5 minutes after the
administration of fluid, but he
remains hypoxic despite receiving
supplemental oxygen.
He is intubated via RSI, and an
endotracheal tube is placed. Despite
maximal FiO2 , the patient’s oxygen
saturation remains in the mid-80s.
The decision is made to transfer him
to the nearest ICU, but critical care
transport is approximately 90 minutes
away due to suboptimal weather
conditions.
set peak pressure, further reducing the
chances of VALI. However, VC keeps
pressure as the dependent variable in
flux, which is historically considered
a risk factor for injury if the airway
pressure is elevated in a system with
less compliance, increased resistance,
or acute active expiration, such as
excessive coughing.5
When intubating for the purpose
of airway protection, VC ventilation
settings are frequently appropriate, as a
predetermined volume is administered
over a given time period based on
the patient’s respiratory rate and
VT, regardless of fluctuating airway
pressures. Although this strategy
is appropriate for patients without
active pulmonary disease, emergency
physicians must be cognizant of
fluctuating airway pressures and act
accordingly, as the plateau pressure can
change without a simultaneous change
in static VT.
 The most suitable care for patients
who require airway protection and
have no pre-existing lung or cardiac
pathologies is an overall lung-protective
strategy involving a VT of 6 to 8 mL/
kg based on ideal body weight (IBW),
a respiratory rate of 12 to 16 breaths/
minute, PEEP of 5 cm H2O, and titration
of FiO2 to a goal SpO2 of 92% to 99%,
while avoiding excessive oxygenation
(Table 1).
Hyperventilation is one important
caveat regarding ventilator management
in patients with traumatic head injuries
and resultant mental status depression.
Lung-protective mechanical ventilation
strategies with a VT of 6 to 8 mL/kg
and goal normocapnia have been shown
to provide the best results, including a
reduction in direct injuries to the lung
and improved neurologic outcomes.6
Limited antiquated evidence suggests
that hyperventilation may reduce
intracranial pressure.6
However, current brain injury
guidelines discourage the prophylactic
or prolonged use of hyperventilation
and endorse its temporary use only
in the presence of acute neurologic
deterioration, assuming an intervention
to correct the underlying cause (eg,
mass lesion evacuation) is planned.
Thus, most patients with traumatic
brain injuries should be kept within the
normocapnic range using the ventilator
settings previously described.7,8
Hypercapnia
Hypercapnia — which often results
from decreased central drive, reduced
strength, increased respiratory load
from poor compliance or narrow
airways, or some combination
thereof — causes CO2 retention and
a subsequent loss of effective gas
TABLE 1. Indications and Initial Ventilator Settings for the Mechanically Ventilated Patient
Indication
for Emergent Ventilator Mode
Intubation
Airway protection Volume control
Hypercapnia Volume control
Hypoxemia Pressure control
or volume control
exchange. Expiratory flow limitations
are the principal physiologic alterations
in most obstructive lung processes,
including COPD. Airflow obstruction,
low elastic recoil, high ventilatory
demand, and short expiratory time
all result in air trapping.9 Therefore,
ventilator settings in patients with
obstructive processes are tailored
to minimize hyperinflation, rest
compromised respiratory muscles, and
allow adequate expiration.
Ventilation is measured, from a
physiologic perspective, by calculating
the minute ventilation, which is defined
as the respiratory rate multiplied by the
VT. Hypercapnia stems from disease
processes in which the respiratory rate
and VT are ineffective at adequately
removing CO2. Therefore, when
considering initial ventilator strategies
for hypercapnia, VC ventilator modes
are suitable.9,10
VT should be tailored based on the
patient’s IBW in a manner similar to
airway-protective strategies, aiming for
6 to 8 mL/kg. This approach allows
for adequate volume administration
while avoiding high airway pressures,
thereby decreasing the likelihood of
lung injuries, alveoli rupture, or a
pneumothorax.
Respiratory rate should ideally be
initiated at 16 to 20 breaths/minute
in order to approximate near-normal
physiologic conditions, allow time for
exhalation, and reduce breath stacking.11
The inspiratory-to-expiratory time
(I:E) ratio (ie, the relative time spent
in inspiration compared to expiration)
should be kept near 1:3, or even
extended to 1:4 or 1:5, to allow for
maximal expiratory time and further
help with CO2 elimination.
Respiratory Rate
VT
(breaths/min)
6-8 mL/kg 12-16
6-8 mL/kg 16-20 (with I:E ratio 1:3)
6-8 mL/kg 12-16
Using a technique known as
“permissive hypercapnia,” combined
VT and respiratory-rate strategies
for obstructive processes that cause
hypercapnia should aim to normalize
pH levels greater than 7.2, not PaCO2,
to avoid further lung injury.9
When attempting to normalize
PaCO2, excessive respiratory rates and
VTs can worsen existing lung damage.
Like any technique, there are caveats
to permissive hypercapnia. Absolute
contraindications include pregnancy,
pulmonary hypertension, salicylate
and tricyclic antidepressant toxicities,
and increased intracranial pressure,
in which case a PaCO2 level near 35
has been shown to improve patient
outcomes.12,13
Oxygen titration in nonhypoxemic
mechanically ventilated patients should
be initiated early to avoid inadvertent
oxygen toxicity. Due to the theoretical
free radical damage that high levels of
oxygen can produce, an initial FiO2 of
100% is reasonable, with rapid titration
of FiO2 to target an oxygen saturation
between 92% and 99% with a goal of
less than 60% FiO2.
If possible, positive end expiratory
pressure (PEEP) should be kept at or
below 5 cm H2O to avoid barotrauma,
particularly in patients with COPD
or other obstructive processes; in
such cases, higher PEEP can worsen
outcomes and prolong ventilator-
dependence.11,14
One potentially important caveat
to consider regarding ventilator
management in those with obstructive
pathologies is noted in the difference
between COPD and fixed-airway
obstruction. Applying PEEP during the
ventilatory support of a patient with
PEEP
FiO2
(cm H2O)
5 Titrate to goal SpO2 >92%
≤5 Titrate to goal SpO2 >92%
8-10 Titrate as necessary
(in conjunction with PEEP) with a
goal SpO2 >92% and PaO2 >75
September 2020 n Volume 34 Number 9 5
 TABLE 2. Titration Strategy for PEEP and FiO2 in Hypoxemia (ARDSnet)
FiO2 0.3 0.4 0.4
PEEP 5 5 8 8
FiO2 0.3 0.3 0.3
PEEP 5 8 10
fixed airflow obstruction, including
severe asthma and bronchospasm, may
produce potentially dangerous increases
in lung volume, airway pressure,
and intrathoracic pressure, causing
circulatory compromise.11
This occurs because a larger drop
in intrathoracic pressure is necessary
to trigger subsequent breaths. Thus,
emergency physicians should be aware
that the routine use of significant PEEP
during ventilatory support of a patient
with acute fixed-airway obstruction
remains controversial and is not
recommended.
Hypoxia
Hypoxemic respiratory failure,
defined as a PaO2 less than 60 mmHg
(8 kPa) or SpO2 less than 90%, is a
common reason for assisted mechanical
ventilation in the emergency setting.15,16
Initial ventilator management for
hypoxemic respiratory failure has
evolved extensively in recent years.
The literature has generated a shift
toward the use of early lung-protective
ventilator strategies for ARDS and is
considered safe and effective for nearly
all ventilated patients.14
This approach has consequently
reduced mortality, decreased the
worsening of ARDS, and decreased
lung injuries from both pressure
and volume consequence during the
duration of a patient’s ventilator
requirement.14,17-19
Given the advantages and
disadvantages for both VC and PC
ventilator settings, either mode can
be used when managing hypoxemic
patients, depending on the emergency
physician’s experience and comfort
level.
Achieving the best outcomes
in intubated hypoxemic patients in
6 Critical Decisions in Emergency Medicine
Lower PEEP/Higher FiO2
0.5 0.5 0.6 0.7 0.7 0.7 0.8 0.9 0.9 0.9 1.0
10 10 10 12 14 14 14 16 18 18-24
Higher PEEP/Lower FiO2
0.3 0.3 0.4 0.4 0.5 0.5 0.5-0.8 0.8 0.9 0.9 1.0
12 14 14 16 16 18 20 22 22 22 24
the emergency department requires prolonged states of hyperoxia,
adequate sedation, proper monitoring, especially in cases of ARDS and other
and specific attention to PEEP and space-occupying diagnoses.17,20
FiO2 titration, as these variables Starting at 100% FiO2 and
are responsible for oxygenation in titrating to the most effective lower
hypoxemic respiratory failure. The dose is an acceptable initial treatment
goal should be to achieve an adequate strategy as long as the physician
increase in mean airway pressure intends to reduce FiO2 in a timely
to aid in alveoli recruitment while manner. Titration in cases of ARDS,
simultaneously avoiding excessive for instance, can be done using the
pressure increases that result in VALI. ARDSnet PEEP tables (Table 2). The
Emergency physicians should use more effective strategy — which also
caution when titrating FiO2 alone, as allows the FiO2 to be decreased in a
this will ultimately result in ineffective timelier manner — is to increasingly
increases in PaO2 and SpO2. This up-titrate the PEEP while reducing
problem is due to preferential shunting the FiO2 to target an SpO2 of more
after the prolonged use of FiO2 than 92%. An effective PEEP titration
exceeding 50% to 60%. Moreover, strategy enables the patient to
free radical damage can occur during maintain alveolar patency, thereby
FIGURE 1. Stepwise Approach to Hypoxemic Ventilator Management
VOLUME-CONTROLLED SETTING
• VT 6-8 mL/kg IBW
• PEEP 5-8 cm H2 O
• FiO2 100% with goal <60%
Increase PEEP as needed while
maintaining plateau pressure
<30 cm H2 O. Consider using
ARDSnet tables if appropriate.
Increase FiO2
Goal to maintain <60%
Consider prone or Consider paralysis (rocuronium,
“good lung down” positioning vecuronium, cisatracurium)
• Consider a reversal of the I:E ratio
• Consider a consultation for ECMO
 FIGURE 2. Ventilator Airway Pressure Graph
Peak Inspiratory
PRESSURE
Pressure (Goal <30)
AIRWAY
PEEP
Inspiration Expiration
preserving adequate gas exchange and
alveolar perfusion. Thus, PEEP should
be factored in early when considering
an increase in FiO2, especially those
exceeding 50% to 60%.
In cases of hypoxemic respiratory
failure without an alveolar fluid-
occupying state and otherwise normal
lung parenchyma (eg, intracardiac
shunt), a physiologic respiratory rate is
appropriate (ie, 12-16 breaths/min).
PEEP settings targeting 8 to 10 mmHg
in patients with normal lung function
are appropriate. Protective lung
volumes of 6 to 8 mL/kg of IBW
remain, as this method has been shown
to reduce the progression to ARDS
and subsequent VALI.16 Theoretically,
an FiO2 greater than 60% should be
unnecessary in these instances.
If higher FiO2 values are needed,
immediately evaluate for a new lung-
occupying process, acutely worsening
intra- or extracardiac shunt, or
worsening ventilation/perfusion
mismatch.
CRITICAL DECISION
How should intubated patients
be monitored in the emergency
department?
Once a patient has been placed on
mechanical ventilation, the emergency
Plateau Pressure
(Goal <30)
Driving
Pressure
Inspiration Inspiratory Expiration
Hold
TIME
physician’s job has arguably just
begun. Initial ventilator strategies
based on the indication for intubation
can often address the underlying
cause of respiratory failure. However,
these situations can be highly dynamic
and require close monitoring. Without
instituting standard protocols for
assessing every patient intubated in
the emergency department, the risk of
morbidity and mortality is significant.
Monitoring the intubated patient
takes place in three parts:
1. Confirmation of endotracheal
positioning
2. Assessment of initial ventilator
settings
3. Ongoing monitoring
Tube Placement
The proper position of the
endotracheal tube must always be
confirmed; in fact, many experts
suggest that this confirmation is the
final procedural aspect of successful
endotracheal intubation. Waveform
end-tidal carbon dioxide (EtCO2)
monitoring is the ideal way to confirm
that an endotracheal tube is in the
trachea.21 Although many emergency
departments use colorimetric EtCO2,
care must be taken; there are multiple
reports of false-positives when using
this method.
AutoPEEP
}
Expiratory Hold
To increase the specificity of
colorimetric EtCO2, endotracheal
intubation should only be confirmed
after 5 to 6 breaths are given.
(Color changes may initially arise in
esophageal intubations from the CO2
that can accumulate in the stomach.)
Although waveform capnography can
confirm successful tracheal intubation,
a postintubation chest x-ray is still
warranted to verify that the tube is
placed at an appropriate depth above the
carina (ideally ~2 cm).
An endotracheal tube that is too
high (above the level of the clavicles)
risks accidental displacement, but tube
positioning that is too low will result in
a mainstem intubation and collapse of
the opposite lung. Emergency physicians
should also order medications to
promote adequate postintubation
analgesia and sedation. Once the tube
placement is confirmed, lifting the head
of the bed to 30 degrees can significantly
decrease the risk of aspiration and
further reduce morbidity.22
Ventilator Settings
Next, several simple maneuvers are
required to assess whether the initial
ventilator settings are appropriate for
the patient. Ideally, a lung-protective
VT of 6 to 8 mL/kg is set based on the
patient’s IBW. When specific volumes
September 2020 n Volume 34 Number 9 7
 are set on the ventilator, the airway
pressures differ from breath-to-
breath depending on many variables,
including the compliance of the
lung and resistance of the airways.
Barotrauma, which results when
airway pressures exceed 30 mmHg,
has been shown to increase mortality
in the ARDSnet trial.17
Assessing peak inspiratory
pressures (PIP) on the initial ventilator
settings to ensure that they are less
than 30 mmHg may prevent significant
downstream lung injuries. If the PIP is
above 30 mmHg, measure the plateau
pressure by completing an inspiratory
hold on the ventilator for roughly
1 second to allow the pressure to
equilibrate between the small airways
and alveoli.
Plateau pressure is the best
approximation of the pressure that
the alveoli are truly experiencing
on a breath-to-breath basis. If the
plateau pressure is above 30 mmHg,
barotrauma is likely, which can
contribute to mortality and morbidity.
Emergency physicians should note
that plateau pressure values must
be monitored regularly (every 30-60
minutes, or with any high-pressure
ventilator alarms), especially in the
early phase of the AC/VC ventilation
mode (Figure 2).
There are two broad categories
that can cause high PIP. The first,
increased airway resistance, leads to
increased PIPs but normal plateau
pressures during the inspiratory hold.
Airway-resistance issues can be caused
by an obstructed endotracheal tube,
dyssynchrony with the ventilator,
mucous plugs, or bronchospasm.
These potential causes should be
assessed. Alternatively, if both the PIP
and plateau pressure are elevated, the
problem likely stems from decreased
compliance of the lung.
Causes of decreased lung
compliance are plentiful and include
infiltrative processes like edema,
ARDS, pneumothorax, and obesity.
Plateau pressure can be reduced by
decreasing the VT (to as low as 4 mL/
kg), increasing sedation, considering
chemical paralysis, or switching to a
8 Critical Decisions in Emergency Medicine
PC ventilation mode. To prevent lung If VBG will be used to monitor
injury, the PIP (and plateau pressure, the impact of ventilator settings,
as needed) should be assessed after any carefully titrate the settings to produce
changes to the ventilator settings. an SpO2 of 92% to 99%.23 Evolving
evidence demonstrates the negative
Continued Monitoring
impact of hyperoxia on a variety of
After the patient’s initial ventilator
disease states ranging from traumatic
settings are deemed appropriate, it
brain injuries to cardiac arrest, so
is vital to continue monitoring the
it is important to avoid an SpO2 of
patient closely. Quantitative waveform
100% when treating any ventilated
capnography should be continued
patient.24-26
beyond the initial confirmation of
endotracheal tube placement because it CRITICAL DECISION
can be an excellent window into what is
What strategies are available
happening to the patient.
for patients who fail to
The flow of expired CO2 can
adequately ventilate?
be used to diagnose any number of
pathologies, including altered cardiac Troubleshooting acute
output, increased airway resistance, hypercapnic respiratory failure is a
and decreased lung compliance. task all emergency physicians must
Thus, not only is EtCO2 effective for be comfortable performing. When a
continually monitoring appropriate patient’s CO2 level remains elevated
placement of the endotracheal tube, despite the use of suitable ventilator
but it can also be a dynamic tool for settings, the respiratory rate is the
assessing hemodynamic and ventilatory first parameter to adjust, as it has
variables when caring for critically ill the greatest impact on gas exchange
patients in respiratory failure. and results in less alveoli damage and
A mechanically ventilated barotrauma than initially modifying
patient’s response to the ventilator VT.
settings should be evaluated within Hypercapnic respiratory failure
approximately 30 minutes. This and obstructive lung disorders
response is ideally assessed with an involve dynamic hyperinflation, a
ABG measurement, which can provide process in which a new breath often
a comprehensive snapshot of the begins before the lung has reached
patient’s oxygenation, ventilation, the static equilibrium volume.9 This
and basic metabolic parameters, such dynamic results in increasingly
as the pH value. However, multiple larger lung volumes and subsequent
studies have demonstrated that venous intrathoracic pressures, which worsens
blood gases (VBG) can approximate hemodynamic compromise and can
ABG values if oxygenation is not a cause difficulties when managing the
concern. initial hypercapnia.
n Titrate the FiO2 and PEEP using the ARDSnet PEEP table with a goal SpO2 of
92% to 99% to avoid both hypoxia and hyperoxia, as both negatively impact
critically ill patients.
n Use quantitative waveform EtCO2 to confirm endotracheal intubation.
Consider this approach for multiple physiologic conditions that affect
mechanically ventilated patients.
n When dealing with refractory hypercapnia, hypoxia, or significant ventilator
dyssynchrony, it is important to optimize analgesia and sedation. Consider the
use of neuromuscular blockade to achieve the goals of mechanical ventilation.
 particularly in situations associated
TABLE 3. The DOPES Mnemonic for Hypoxic Ventilator Troubleshooting with upper-airway obstruction.11
Heliox has been shown to reduce
D Displacement of the tube
dynamic hyperinflation by 15%,
O Obstruction of the tube (kinks and mucus plugs) placing the respiratory muscles at a
P Pneumothorax better mechanical advantage.27 The
drug has also been shown to decrease
E Equipment failure
intrathoracic pressures and may be an
S Stacked breaths (may require disconnecting with manual assist attractive option for COPD patients
exhalation) with dynamic hyperinflation who are
failing to appropriately ventilate.
Calibrating the respiratory rate is patient’s presenting complaints and The correction of electrolyte
the safest and most reliable option for identifying the underlying issue. deficiencies, including hypokalemia
improving CO2 retention. Emergency Additional strategies for and hypophosphatemia, can help
physicians should only consider raising maintaining adequate ventilation may improve neuromuscular strength.
a patient’s VT after the respiratory include pain control with fentanyl The resulting mechanism improves
rate has been optimized to avoid the (analgosedation); the administration ventilation through enhanced
significant risk of barotrauma and of dexmedetomidine for delirium, respiratory muscle recruitment.28
worsening the already-poor elastic when applicable; and increased Neuromuscular-blockade
recoil present in most obstructive sedation with medications such as agents — particularly long-acting
processes. Notably, the end goal of midazolam or propofol. formularies like rocuronium and
modifying a patient’s respiratory rate Ventilator dyssynchrony may also cisatracurium — have been shown
and VT is a pH greater than 7.2 (not result from air hunger, inappropriate to provide additional benefits when
normocapnia), as defining normal pH low-minute ventilation or PEEP, or establishing ventilator synchrony
has been shown to improve outcomes.9 “breath stacking.” Therefore, a solid and optimal minute ventilation.29
Multiple strategies aimed at understanding of ventilator mechanics Status asthmaticus can pose particular
treating hypercapnia involve VC is paramount for attaining an challenges because these patients
support with a fixed flow-rate pattern. effective solution. Interventions may are routinely difficult to ventilate
Asynchrony between mandatory include increasing the flow rate, the despite appropriate settings. Such
and spontaneous patient-initiated inspiratory time, or PEEP (assuming
cases routinely warrant deep sedation
breaths is a major disadvantage that it is a safe option based on the
immediately after RSI in addition to
can lead to inadequate ventilation. indications for intubation).
neuromuscular blockade with a long-
This asynchrony can originate from Helium-oxygen (Heliox) is
acting paralytic.29
agitation, otherwise known as another adjunctive therapy that has
Finally, the use of veno-
“bucking the vent,” and can indicate proven beneficial for the management
venous extracorporeal membrane
a primary pathologic state like pain, of inadequately ventilated patients.
oxygenation (VV-ECMO) for
anxiety, hypoglycemia, intracranial Because airway turbulence is
hemorrhage, or alcohol withdrawal, dependent on density, Heliox’s lower the management of refractory
among others. The management of density decreases airway resistance hypercapnic respiratory failure has
these situations should focus on the and improves the work of breathing, gained renewed interest.30 Indications
for VV-ECMO, which can be
found in the Extracorporeal Life
Support Organization guidelines,
include failure to oxygenate, severe
CO2 retention or the inability to
maintain acceptable CO2 levels
at safe airway pressures (plateau
n Neglecting to use lung-protective ventilation (6-8 mL/kg of IBW), a mistake
pressure <30 cm H2O), and severe
that can increase the morbidity and mortality of ventilated patients.
air-leak syndromes.31 Emergency
n Relying on FiO 2 alone to promote oxygenation for hypoxic, ventilated
physicians should consider an early
patients. Instead, titrate PEEP to help decrease the FiO 2 and prevent
further lung damage. surgical consultation regarding the
potential use of ECMO or a transfer
n Being unaware of high peak and plateau pressures (>30 mmHg) in
ventilated patients, an oversight that can lead to ongoing lung damage and to a facility that is well versed in
other significant complications. this potentially life-saving adjunctive
therapy.

September 2020 n Volume 34 Number 9 9

 CRITICAL DECISION
What strategies are available for
patients who fail to adequately
oxygenate?
Refractory or persistent hypoxemia
is a common phenomenon following
intubation. Given that more than
80% of ARDS patients will require
intubation, identifying and treating
refractory hypoxemia earlier is
more beneficial.18 The principles of
the early recognition and treatment
of a persistently poor oxygenation
state should be balanced with well-
established data concerning hyperoxia
in critically ill patients.
Detriments owed to hyperoxia
include but are not limited to fewer
ventilator-free days, increased episodes
of shock, liver failure, bacteremia,
and increased hospital mortality.24-26
As such, emergency physicians
should ensure that the corrections
for a refractory hypoxic state are not
overcorrections that actually permit
persistent hyperoxia.
When identifying a state of
refractory hypoxia, the physician
should first ensure adequate settings
and avoid obvious pulmonary-
circuit malfunctions, either via the
machinery or by changing the patient’s
physiology. The DOPES mnemonic is
one screening tool that can facilitate
an efficient bedside analysis (Table 3).
Notably, extra care should be taken to
choose ventilator settings that do not
encourage breath stacking (ie, auto-
PEEP), a complication that can lead
to cardiovascular collapse, worsened
respiratory status, and eventual arrest
if not recognized quickly. If breath
stacking does occur, disconnect the
endotracheal tube from the circuit,
allow full exhalation, and down-titrate
the VT if needed until an adequate
plateau pressure (<30 cm H2O) is
achieved.
Traditionally, hypoxemia on an
ABG measurement is defined as a PaO2
less than 80 mmHg; a normal expected
value is between 80 and 100 mmHg.
Noting that PaO2 rises with elevations
in FiO2, the PaO2/FiO2 ratio can be
calculated (with abnormal being
10 Critical Decisions in Emergency Medicine
<300 mmHg) and represents part of the
diagnostic criteria for ARDS.
FiO2 and PEEP
In VC mode, increases in FiO2 and
PEEP are the only two factors affecting
adequate oxygenation and the eventual
resolution of refractory hypoxemia.
Depending on the diagnosis, FiO2 and
PEEP should be titrated together when
managing patients with ARDS (using
the ARDSnet table) or independently
with otherwise normal or close-to-
normal lung parenchyma. In ARDS,
PEEP has the ability to improve the
PaO2/FiO2 ratio by recruiting alveoli.
Its use has also been shown to prevent
further refractory hypoxemia and
decrease the use of other rescue
therapies.
In those with acute lung injuries or
unilateral disease, more judicious use is
advised to avoid the overdistention of
normal, functional lung parenchyma.
If no response to PEEP titration is seen
over the course of a 30-minute trial,
continued titration can be attempted;
however, alternate avenues should
be considered early in the patient’s
course.18
Neuromuscular Blockade
Neuromuscular blockade is a
useful tool for mechanically supported
patients, especially those with refractory
hypoxemia because it allows external
control of the patient’s respiratory
cycling. The early use of neuromuscular
blockade may improve oxygenation,
90-day mortality, and total days off of
mechanical ventilation in hospitalized
patients with ARDS.32-33 Although a
more recent trial has called the overall
benefit of paralysis into question,
this approach can certainly enhance
oxygenation in hypoxic patients.34
Patient Positioning
Prone positioning has shown
benefit for the treatment of early
ARDS, with decreased progression
to ECMO, improved PaO2/FiO2, and
improved 28- and 90-day mortality
rates.35 Supine positioning causes direct
compression of lung tissue in the most
posterior aspects of the lungs, which
also receive the highest proportion
of perfusion when a person is lying
down. Consequently, ventilation of
the affected dorsal regions is also
diminished. Prone positioning is
believed to reverses these trends via the
gravitational effects of recruiting lung
units and by enhancing ventilation and
perfusion matching.
Although prone positioning
is uncommon in the emergency
department, it may be an effective
option for persistently hypoxemic
patients, particularly in light of
increasing wait times for ICU beds
nationwide. If prone positioning
remains too substantial of a physical
or logistical burden, a strategy that
positions the best-aerated lung down is
another viable option. The “good lung
down” technique enables improvement
in the distal aeration and recruitment
of the lung-occupying additional dead
space (ie, the more injured lung).
Other Strategies
Lung-recruitment maneuvers
(eg, sighing and short-duration PEEP
trials) are subject to recruitment
variability and must be done under close
observation, especially during the initial
implementation phase.18,30 Alternative
ventilator strategies, including high-
frequency oscillator ventilation;
pulmonary vasodilators; VV-ECMO;
and inverse ratio ventilation, in which
inspiratory time is increased at the
expense of a decrease in expiratory time,
can also be attempted.
These methods are largely found
in ICU care and are not always easily
executed in the emergency setting;
nevertheless, recognition of these
adjuvant therapies remains an important
aspect to improved patient care.
Summary
Few interventions in the emergency
setting have such an immediate and
dramatic impact on the mortality and
downstream morbidity of critically ill
patients as endotracheal intubation
and mechanical ventilation. The
indications for ventilatory support can
initially guide a patient’s ventilator
settings, but acute respiratory failure
remains a dynamic disease process
that requires the close monitoring
 CASE RESOLUTIONS
■ CASE ONE
After undergoing endotracheal
intubation, the elderly woman
was connected to the mechanical
ventilator on VC mode with the
following settings based on her IBW
of 65 kg: VT 455 mL, respiratory
rate 14, PEEP 5 mmHg, and FiO 2
80%. The endotracheal tube
placement was confirmed with an
EtCO 2 of 35 mmHg after 5 to 6
breaths on the ventilator, and a
chest x-ray showed the distal tip to
be 1.5 cm above the carina. Sedation
was initiated with propofol.
Fifteen minutes after the initial
ventilator settings were placed, an
ABG measurement revealed a pH
of 7.14, PaCO2 of 90 mmHg, and a
PaO2 of 182 mmHg. The respiratory
rate on the ventilator was increased
to 20 breaths/minute, and the
FiO2 was titrated to 40% to avoid
hyperoxia. A repeat ABG test 30
minutes after these changes revealed
a pH of 7.40, PaCO2 of 55 mmHg,
and PaO2 of 94 mmHg. Twenty
minutes later, the ventilator alarm
indicated high peak pressures. An
inspiratory hold was performed,
which revealed an elevated plateau
of multiple physiologic parameters
to ensure appropriate oxygenation
and ventilation. The careful
monitoring of abnormalities in patient
hemodynamics, ventilator waveforms,
and blood gas values improves the
quality of care and facilitates the early
initiation of adjunctive therapy when
other oxygenation and ventilation
strategies fail.
A stepwise approach to ensuring
ideal ventilator settings, including
confirmation of the endotracheal tube
position, enables the early identification
of persistently hypercapnic or hypoxic
patients, thereby allowing clinicians
to effectively implement changes to
the clinical course. Understanding the
basics of respiratory mechanics and
having a keen eye for fluctuations in
pressure of 35 cm H 2O, and the patient
was suctioned without improvement.
A chest x-ray showed no pneumo­
thorax. The patient was disconnected
from the ventilator for 5 seconds and
reconnected; this improved her peak
pressures, indicating critical breath
stacking. Subsequently, the I:E ratio
was prolonged and no further alarm
incidents were noted. She was admitted
to the ICU and successfully extubated
the following day. She was discharged
from the hospital 5 days later with
normal work of breathing.
■ CASE TWO
After successful intubation, the
young man was connected to the
ventilator on VC mode with the
following settings based on his IBW
of 75 kg: VT 525 mL, respiratory rate
14 breaths/minute, PEEP 8 mmHg,
and FiO2 100%. A propofol infusion
was initiated for sedation. His SpO2
remained 87% after intubation, and
a subsequent ABG measurement
15 minutes later revealed a PaO2
of 45 mmHg, indicating persistent
hypoxemia. His PEEP was titrated up
to 12 mmHg and gradually increased
over the next 90 minutes to 24 mmHg
respiratory support can help optimize
the ventilator management provided in
even the most tenuous of situations.
REFERENCES
1. Stefan MS, Shieh MS, Pekow PS, et al. Epidemiology
and outcomes of acute respiratory failure in the
United States, 2001 – 2009: a national survey. J Hosp
Med. 2013 Feb;8(2):76-82.
2. Cardoso LTQ, Grion CMC, Matsuo T, et al. Impact
of delayed admission to intensive care units on
mortality of critically ill patients: a cohort study.  12. Flomenbaum NE. Salicylates. In: Nelson LS, Lewin
Crit Care. 2011;15(1):R28.
3. Graham CA. Emergency department airway
management in the UK. J R Soc Med. 2005
Mar;98(3):107-110.
4. Rittayami N, Katsios DM, Beloncle F, Friedrich JO,
Mancebo J, Brochard L. Pressure controlled vs volume
controlled ventilation in acute respiratory failure.
A physiology based narrative and systemic review.
CHEST. 2015 Aug;148(2):340-355.
5. Campbell RS, Davis BR. Pressure-controlled versus
volume-controlled ventilation: does it matter? Respir
Care. 2002 Apr;47(4):416-424.
6. Marion DW, Firlik A, McLaughlin MR. Hyperventilation
therapy for severe traumatic brain injury. New Horiz.
1995 Aug;3(3):439-447.
7. Maung AA, Kaplan LJ. Mechanical ventilation after
injury. J Intensive Care Med. 2014;29:128-137.
8. Brain Trauma Foundation, American Association of
Neurological Surgeons, Joint Section on Neurotrauma
based on the ARDSnet table. A repeat
chest x-ray showed no signs of a
pneumothorax.
Despite these interventions,
the patient’s ABG level marginally
improved to show a PaO2 of 55 mmHg
and an SpO2 of 89%. His respiratory
mechanics were monitored, and his
PIP was found to be greater than
30 mmHg with a plateau pressure
of 41 mmHg, indicating severe
ARDS based on his chest x-ray and
severe hypoxemia. Consequently,
neuromuscular blockade was
introduced with a bolus dose of
rocuronium.
An ABG measurement showed
some improvement in the patient's
oxygenation status, so the decision
was made to transfer him to an
ECMO-capable tertiary facility. He
remained hypoxic upon admission
and was put in the prone position to
help with lung recruitment. He was
ultimately placed on VV-ECMO and
successfully decannulated 10 days
later. He was later discharged from
the hospital to an acute rehabilitation
facility, where he required respiratory
support with 2 L oxygen via nasal
cannula.
and Critical Care. Guidelines for the management
of severe head injury. J Neurotrauma. 1996 Nov;13:
641-734.
9. Ward NS, Dushay KM. Clinical concise review:
mechanical ventilation of patients with chronic
obstructive pulmonary disease. Crit Care Med. 2008
May;36(5):1614-1619.
10. Rose L. Clinical application of ventilator modes:
ventilatory strategies for lung protection. Aust Crit
Care. 2010 May;23(2):71-80.
11. Ahmed SM, Athar M. Mechanical ventilation in
patients with chronic obstructive pulmonary
disease and bronchial asthma. Indian J Anaesthesia.
2015 Sep;59(9):589-598.
NA, Howland MA, Hoffman RS, Goldfrank LR,
Flomenbaum NE, eds. Goldfrank’s Toxicologic
Emergencies. 9th ed. McGraw-Hill; 2011:508-520.
13. Chonghaile NM, Higgins B, Laffey JG. Permissive
hypercapnia: role in protective lung ventilatory
strategies. Curr Opin Crit Care. 2005 Feb;11(1):
56-62.
14. Neto AS, Cardoso SO, Manetta JA, et al.
Association between use of lung protective
ventilation with lower tidal volumes and clinical
outcomes among patients without acute respiratory
distress syndrome: a meta-analysis. JAMA. 2012
Oct 24;308(16):1651-1659.
15. Nee PA, Al-Jubouri MA, Gray AJ, O’Donnell
C, Strong D. Critical care in the emergency
department: acute respiratory failure. Emerg Med J.
2011 Feb;28:94-97.
16. Sutherasan Y, Vargas M, Pelosi P. Protective
mechanical ventilation in the non-injured lung:
September 2020 n Volume 34 Number 9 11
 review and meta-analysis. Crit Care. 2014 Mar
18;18(2):211.
17. Acute Respiratory Distress Syndrome Network;
Brower RG, Matthay MA, Morris A, Schoenfeld
D, Thompson BT, Wheeler A. Ventilation with
lower tidal volumes as compared with traditional
tidal volumes for acute lung injury and the acute
respiratory distress syndrome. ARDS Net. N Engl J
Med. 2000 May 4;342(18):1301-1308.
18. Esan A, Hess DR, Raoof S, George L, Sessler CN.
Severe hypoxemic respiratory failure: part 1 --
ventilatory strategies. CHEST. 2010 May;137(5):
1203-1216.
19. Needham DM, Colantuoni E, Mendez-Tellez PA, et al.
Lung protective mechanical ventilation and two year
survival in patients with acute lung injury: prospective
cohort study. BMJ. 2012 Feb 27;344:e2124.
20. West JB, Luks AM, eds. West’s Respiratory
Physiology: The Essentials. 10th ed. Wolters Kluwer;
2016.
21. Silvestri S, Ladde JG, Brown JF, et al. Endotracheal
tube placement confirmation: 100% sensitivity and
specificity with sustained four-phase capnographic
waveforms in a cadaveric experimental model.
Resuscitation. 2017 Jun;115:192-198.
22. Muscadere J, Dodek P, Keenan S, Fowler R, Cook
D, Heyland D; VAP Guidelines Committee and the
Canadian Critical Care Trials Group. Comprehensive
evidence-based clinical practice guidelines for
ventilator-associated pneumonia: prevention. J Crit
Care. 2008 Mar;23(1):126-137.
23. Zeserson E, Goodgame B, Hess JD, et al.
Correlation of venous blood gas and pulse oximetry
with arterial blood gas in the undifferentiated
critically ill patient. J Intensive Care Med. 2018
Mar;33(3):176-181.
24. de Jonge E, Peelen L, Keijzers PJ, et al. Association
between administered oxygen, arterial partial
oxygen pressure and mortality in mechanically
ventilated intensive care unit patients. Critical Care.
2008 Dec 10;12(6):R156.
25. Helmerhorst HJF, Arts DL, Schultz MJ, et al. Metrics
of arterial hyperoxia and associated outcomes in
critical care. Crit Care Med. 2017 Feb;45(2):187-195.
26. Vincent JL, Taccone FS, He X. Harmful effects
of hyperoxia in postcardiac arrest, sepsis,
traumatic brain injury, or stroke: the importance of
individualized oxygen therapy in critically ill patients.
Can Respir J. 2017 Jan 26;2017:2834956.
27. Swidwa DM, Montenegro HD, Goldman MD, Lutchen
KR, Saidel GM. Helium-oxygen breathing in severe
chronic obstructive pulmonary disease. CHEST. 1985
Jul;87(6):790-795.
28. Ackerman GL, Arruda, JL. Acid-base and electrolyte
imbalance in respiratory failure. Med Clin North Am.
1983 May;67(3):645-656.
29. Wright BJ. Lung-protective ventilation strategies and
adjunctive treatments for the emergency medicine
patient with acute respiratory failure. Emerg Med Clin
North Am. 2014 Nov;32(4):871-887.
30. Peek GJ, Mugford M, Tiruvoipati R, et al; CESAR trial
collaboration. Efficacy and economic assessment of
conventional ventilatory support versus extracorporeal
membrane oxygenation for severe adult respiratory
failure (CESAR): a multicentre randomised controlled
trial. Lancet. 2009 Oct 17;374(9698):1351-1363.
31. Extracorporeal Life Support Organization (ELSO).
General Guidelines for all ECLS Cases. ELSO.
Published August 2017. https://www.elso.org/
Portals/0/ELSO%20Guidelines%20General%20All%20
ECLS%20Version%201_4.pdf
32. Papazian L, Forel JM, Gacouin A, et al; ACURASYS
Study Investigators. Neuromuscular blockers in
early acute respiratory distress syndrome. N Engl J
Med. 2010 Sep;363(12):1107-1116.
33. Mosier JM, Hypes C, Joshi R, Whitmore,
Parthasarathy S, Cairns CB. Ventilator strategies
and rescue therapies for management of acute
respiratory failure in the emergency department.
Ann Emerg Med. 2015 Nov;66(5):529-541.
34. The National Heart, Lung, and Blood Institute PETAL
Clinical Trial Network. Early neuromuscular blockade
in the acute respiratory distress syndrome. N Engl J
Med. 2019 May 23;380(21):1997-2008.
35. Guérin C, Reignier J, Richard JC, et al; for the
PROSEVA Study Group. Prone positioning in severe
acute respiratory distress syndrome. N Engl J Med.
2013 Jun 6;368(23):2159-2168.

12 Critical Decisions in Emergency Medicine

 Clearing
the Air
Avoiding Postintubation
Complications

LESSON 13

By Matthew R. Dettmer, MD
Dr. Dettmer is an emergency and critical care physician at the Cleveland Clinic in
Cleveland, OH.
Reviewed by Sharon E. Mace, MD, FACEP

OBJECTIVES
On completion of this lesson, you should be able to: CRITICAL DECISIONS
1. Explain the physiological changes triggered by induction
n Which patients are at risk for postintubation
and intubation.
2. Name the main factors that raise a patient’s risk of hypotension?
postintubation complications. n How can the risk of postintubation hypotension be
3. Discuss the pros and cons of various induction agents and reduced?
preoxygenation techniques.
n How can postintubation hypoxemia be limited?
4. Describe the best tactics for intubating patients with COPD
and metabolic acidosis. n When and how should patients with metabolic
5. Recognize and respond appropriately to lung pressure acidosis be intubated?
buildup in a ventilated patient. n How should patients with obstructive lung disease
be intubated and monitored?
FROM THE EM MODEL
19.0 Procedures and Skills Integral to the Practice
of Emergency Medicine
19.1 Airway Techniques
19.1.1 Intubation

Endotracheal intubation is a common procedure both inside and outside the emergency department; however, many
patients who require emergency intubation are already critically ill, placing them at heightened risk for life-threatening
complications. Although postintubation complications can never be prevented completely, identifying the highest-risk
patients and understanding the most appropriate tactics for intubation can reduce the likelihood of deleterious effects.

July 2021 n Volume 35 Number 7 3

 CASE PRESENTATIONS
■ CASE ONE
A 62-year-old man presents
via ambulance with shortness of
breath. He is in significant distress
and unable to answer questions, but
his medical records reveal a history
of hypertension, diabetes mellitus,
and congestive heart failure with
reduced systolic function. His most
recent ejection fraction was 45%.
The patient’s wife says that he ran
out of his medications several weeks
ago and has had increasing difficulty
breathing since then. His vital
signs are blood pressure 180/110,
heart rate 122, respiratory rate 32,
temperature 37.6ºC (99.7ºF), and
SpO 2 82% on 6 L nasal cannula.
The patient is diaphoretic
and in severe respiratory distress,
but his neurological function
appears normal. A physical exam
reveals tachycardia with a regular
rhythm, diffuse crackles on lung
auscultation, and pitting edema in
both lower extremities. The patient
is placed on noninvasive positive
pressure ventilation, started on a
nitroglycerine infusion, and given
intravenous diuretics. Despite these
interventions, he remains tachypneic
Introduction
Airway management is a fundamental
skill for emergency physicians.
Intubations are typically successful when
they occur in controlled settings, such
as in preparation for a planned surgery,
but emergency endotracheal intubation
carries a higher risk of poor outcomes
in the period immediately following
the procedure. Patients who require
emergency airway management are often
already in severe physiological distress,
heightening the risk of postintubation
complications such as hypotension,
hypoxemia, and cardiac arrest.1 To treat
these patients, emergency physicians must
understand the potentially deleterious
physiological effects of endotracheal
intubation and master the techniques that
can help mitigate these effects in patients
who are critically ill.
4 Critical Decisions in Emergency Medicine
with a respiratory rate of 30 and
SpO 2 of 93% on FiO 2 of 0.6, and he is
beginning to appear fatigued and less
responsive.
■ CASE TWO
A 38-year-old woman with no
significant medical history presents
with fever and lethargy. The patient’s
wife explains that the patient has
experienced 2 days of worsening nausea
and vomiting that did not improve with
antiemetics prescribed by her primary
care doctor. The patient’s vital signs are
blood pressure 92/50, heart rate 132,
respiratory rate 44, temperature 39.1ºC
(102.4ºF), and SpO2 90% on 2 L nasal
cannula. On physical examination, she
appears fatigued and demonstrates high
work of breathing. She is tachycardic
with a regular rhythm and has clear
lungs on auscultation. Her abdomen
is soft but tender to the touch in the
suprapubic area. A point-of-care
lactate is 4.7 mmol/L, and urinalysis
is negative for pregnancy but shows
evidence of UTI.
The patient is given intravenous
antibiotics and 3 L of crystalloid fluids,
but she remains tachycardic with a
blood pressure of 103/57 and heart rate
CRITICAL DECISION
Which patients are at risk for
postintubation hypotension?
Life-threatening hypotension is
relatively common after emergent
intubation, complicating between
15% and 28% of procedures.2,3
Unsurprisingly, preintubation
hypotension is a strong predictor of
postintubation hypotension; however,
certain patients with normal blood
pressure are also at high risk of
postintubation hypotension and may
therefore benefit from additional
resuscitation.3-5 A single-center
FIGURE 1. Calculate Shock Index
Heart Rate
Systolic Blood Pressure
of 130. A second lactate test shows
no change since the initial exam. The
patient becomes increasingly drowsy
and seems to be struggling harder to
breathe.
■ CASE THREE
A 52-year-old man with a history
of COPD, multiple hospitalizations,
and three previous intubations presents
in severe respiratory distress. He is
diaphoretic and breathing 30 times
per minute. His vital signs are blood
pressure 162/92, heart rate 124, and
temperature 37.8ºC (100ºF). A lung
exam reveals diffuse wheezing with
a prolonged expiratory phase. A
venous blood gas obtained on arrival
shows a pH of 7.15 and PCO2 of 80,
indicating acute respiratory acidosis.
The patient is placed on noninvasive
positive pressure ventilation with an
inspiratory pressure of 12 cm H 2 O and
expiratory pressure of 5 cm H 2 O. He is
given intravenous methylprednisolone
and placed on continuous inhaled
bronchodilators. After 30 minutes,
a repeat blood gas shows worsening
respiratory acidosis, with a pH of 7.12
and PCO2 of 85. On reassessment, the
patient appears increasingly lethargic.
retrospective cohort study found that
in hemodynamically stable patients
who underwent emergency intubation,
patients with a shock index of >0.8
before the procedure were at the greatest
risk for postintubation hypotension.6
Shock index is calculated by dividing
heart rate by systolic blood pressure
(Figure 1). Additional risk factors
include baseline hemodynamic
compromise and right ventricular
dysfunction.
CRITICAL DECISION
How can the risk of
postintuba­tion hypotension
be reduced?
To understand potential
interventions to prevent hypotension,
it is important to first understand the
physiological changes that occur with

FIGURE 2. Preoxygenation with NIPPV
PHOTO COURTESY OF JAMES HEILMAN, MD – CC BY-SA 4.0
mechanical ventilation. Any anesthetic
agent used for rapid-sequence induction
will decrease overall sympathetic
tone, which may cause rapid arterial
vasodilation. Positive-pressure
ventilation also decreases venous return
and cardiac output, lowering blood
pressure further.
Of all the anesthetics typically used
for rapid-sequence induction, propofol
may be the most likely to worsen
hypotension, especially for patients
who are already in shock.7 As long
as there is no cardiogenic pulmonary
edema, using empiric fluid loading
and administering vasopressors early
to patients with a high shock index
may also help mitigate postintubation
hypotension.
A recent survey asked physicians
how they would manage patients
who need intubation for a variety of
reasons, including trauma, pneumonia,
and congestive heart failure.8 The
vast majority said they would provide
intravenous crystalloid resuscitation
before intubating the patient. By contrast,
only 4.9% of providers surveyed
would routinely use vasopressors in
these scenarios. In light of the data
reviewed above, using vasopressors
more consistently may be a way to make
emergency intubations safer.
CRITICAL DECISION
How can postintubation
hypoxemia be limited?
According to a retrospective
analysis of more than 3,000 patients
who underwent emergent intubation,
hypoxemia was a factor in 90% of cases
of cardiac arrest immediately following
the procedure.9 Apnea during rapid-
sequence induction places a patient at
high risk for hypoxemia, especially if
the airway is anatomically challenging
and requires multiple attempts to
intubate. The traditional approach for
limiting hypoxemia during intubation is
preoxygenation. This process provides
the patient with a high FiO2 in an effort
to dilute the nitrogen content of gas
in the alveoli and provide a reservoir
of oxygen-rich gas that can continue
to participate in gas exchange during
apneic periods. Preoxygenation has
historically been administered with a
nasal cannula or nonrebreather mask
(NRB); however, alternative approaches
using newer modes of preoxygenation
may benefit the critically ill patient.
Noninvasive positive pressure
ventilation (NIPPV) is known to be useful
for a variety of disease processes, and a
growing body of evidence suggests that
it is also a safe and beneficial method for
preoxygenation in patients who require
intubation (Figure 2).10 In a study of 53
consecutive ICU patients who underwent
preoxygenation with either NRBs or
NIPPV before intubation, only 1 patient
in the NIPPV cohort experienced
postintubation oxygen desaturation to
below 92% compared to 8 patients in the
NRB cohort.11 There were no differences
in episodes of regurgitation or aspiration
between the two groups. It is unclear
why NIPPV led to better outcomes than
NRBs, but it may be because NIPPV
is more effective at aerating atelectatic
alveoli. Preoxygenation with NIPPV may
especially benefit patients with morbid
obesity, for whom diaphragmatic pressure
on lung units can contribute to alveolar
collapse.
For patients with high oxygen
requirements but minimal deficits
in ventilation, humidified high-flow
nasal cannulas are another option
for respiratory support.12 In a before-
and-after study of ICU patients who
underwent intubation, high-flow nasal
cannulas were associated with fewer
instances of severe hypoxemia than
NRBs.13 A high-flow nasal cannula
can also be kept in position during
laryngoscopy, allowing oxygenation to
continue during apneic periods. This
offers another advantage over traditional
preoxygenation techniques.14
CRITICAL DECISION
When and how should
patients with metabolic
acidosis be intubated?
Acidosis, especially lactic acidosis, is
a marker of poor prognosis for patients
in shock states and can complicate the
physiology of emergency intubation.15,16
The body often compensates for severe
metabolic acidosis by maintaining a
high minute ventilation, which manifests
clinically as a high respiratory rate and
high work of breathing. In these cases,
initial resuscitation attempts are focused
on reversing early organ hypoperfusion
and mitigating acidosis in order to
decrease the work of breathing; however,
this is not always successful within the
first few hours of a patient’s course, and
the risk of cardiac arrest from acidemia
grows higher as the patient’s ventilatory
July 2021 n Volume 35 Number 7 5

FIGURE 3. Recognizing Intrinsic PEEP
Flow Time
Inspiration
Flow (L/min)
Expiration
abilities begin to wane. The savvy
emergency physician will recognize that
acidosis that persists despite adequate
resuscitation is a reason to intubate.
For patients with severe metabolic
acidosis, the aim during intubation
should be to minimize the amount of
time ventilation is interrupted. Foregoing
neuromuscular blocking agents to
avoid paralysis may allow the patient
to maintain some degree of respiratory
compensation during the procedure,
but the added challenge of intubating
a nonparalyzed patient may outweigh
this benefit. To minimize apnea, an
experienced physician should be the
one to attempt the intubation. After
intubation, the ventilator should be set to
a respiratory rate that approximates the
patient’s preintubation respiratory rate in
order to compensate for the acidosis.
The use of sodium bicarbonate to
treat acidemia has been suggested in
the past, but it is a practice that begs
reassessment. Theoretically, bicarbonate
treats acidemia when bicarbonate anions
bind with hydrogen ions and form
carbon dioxide and water. In order for
this strategy to effectively increase pH,
the patient must be able to adequately
ventilate and load this additional carbon
dioxide. As patients undergo induction
and reduced ventilation, this ability to
appropriately breathe off the excess
carbon dioxide is compromised, limiting
any theoretical improvement in pH
from the bicarbonate. Furthermore, the
additional carbon dioxide can easily
cross cell membranes and decrease
intracellular pH, causing cellular injury.
6 Critical Decisions in Emergency Medicine
Normal
Patient
Time (sec)
Trapping
intrinsic
PEEP
This principle has been demonstrated
in autopsy studies of rats following
bicarbonate administration.17
CRITICAL DECISION
How should patients with
obstructive lung disease be
intubated and monitored?
Patients with severe obstructive lung
disease lose their ability to ventilate as
a result of obstructed outflow through
small airways. Traditional therapies
include β2 agonists, anticholinergic agents,
and corticosteroids, which are aimed
at reversing bronchoconstriction and
inflammation. When these therapies fail,
however, patients may need mechanical
ventilation. In these cases, using ketamine
as an induction agent not only anesthetizes
patients for intubation but also provides
β agonism and bronchodilation that may
improve their ability to ventilate.18
Following intubation, the physician
must remain aware of positive end-
expiratory pressure (PEEP). When the
small airways are obstructed, expiratory
n In hemodynamically stable patients, a shock index (heart rate ÷ systolic
blood pressure) of >0.8 before intubation is an excellent predictor of
postintubation hypotension.
n For patients with severe hypoxemia and morbid obesity, consider preoxygen­
ating with noninvasive positive pressure ventilation before intubating.
n A high-flow nasal cannula is useful for preoxygenation and can remain in
place to provide oxygen during apneic periods of induction and intubation.
flow is impaired more than inspiratory flow,
and as a result, air from the previous breath
may remain in the alveoli when a new
breath is inspired. With each respiratory
cycle, the volume of air trapped in the
alveoli grows, creating increasing pressure
in the lungs at the end of expiration.
This buildup of pressure is referred to
as intrinsic PEEP, auto-PEEP, or breath
stacking, and it can have several harmful
effects on the patient.19,20 The inability to
adequately ventilate can contribute to and
exacerbate respiratory acidosis. If intrinsic
PEEP continues to climb, it puts the patient
at risk of barotrauma and pneumothorax.
At the bedside, intrinsic PEEP can be
detected by looking at the flow-vs-time
waveform displayed on the ventilator
(Figure 3). If the expiratory flow rate
does not return to zero (or the level
of applied PEEP set on the ventilator)
before rising again with a new breath,
this suggests some degree of air trapping
that contributes to intrinsic PEEP. To
quantify the degree of intrinsic PEEP, it is
useful to perform an end-expiratory pause
maneuver on the ventilator and note the
airway pressure reading during the pause.
This measurement minus any applied
PEEP represents intrinsic PEEP.
If significant air-trapping and carbon
dioxide retention are detected, the best
way to improve ventilation may be to
decrease the respiratory rate on the
ventilator. Lowering the respiratory rate
while keeping the inspiratory time fixed
provides more expiratory time in each
breath cycle, allowing for the complete
exhalation of each volume of air before
the initiation of the next breath.
Summary
Intubation and initial ventilator
management in the emergency department
 CASE RESOLUTIONS
■ CASE ONE
Physicians decided to intubate this
patient when less-invasive techniques
failed to reverse his hypoxemic
respiratory failure. Because hypoxemia
put him at high risk for further
desaturation during intubation, FiO2
through noninvasive positive pressure
ventilation was increased to 1.0 to
maximize preoxygenation. The patient
was also placed on high-flow oxygen
through a nasal cannula at 40 L/min
and FiO2 of 1.0. These interventions
raised the patient’s SpO2 to 98%. The
nasal cannula was left in place to take
advantage of passive oxygenation
while the patient underwent rapid-
sequence induction using etomidate
for anesthesia and rocuronium for
neuromuscular blocking. The patient’s
SpO2 decreased to 93% as the tube
was placed, but the intubation was
successful, and mechanical ventilation
slowly brought his oxygen level back
to normal.
are often complicated by the fact that
patients are already critically ill, placing
them at high risk for postintubation
complications. While it is impossible
to prevent these complications entirely,
understanding the pathophysiology
involved can inform basic interventions
that may limit harmful effects and improve
patient outcomes.
REFERENCES
1. Morris C, Perris A, Klein J, Mahoney P. Anaesthesia in
haemodynamically compromised emergency patients:
does ketamine represent the best choice of induction
agent? Anaesthesia. 2009 May;64(5):532-539.
2. Franklin C, Samuel J, Hu TC. Life-threatening
hypotension associated with emergency intubation and
the initiation of mechanical ventilation. Am J Emerg
n Failing to recognize that any medication used for induction can decrease
sympathetic tone and thereby precipitate hypotension.
n Administering sodium bicarbonate in an attempt to treat acidemia before
intubation.
n Increasing, rather than decreasing, the respiratory rate on the ventilator for
patients who are demonstrating intrinsic PEEP and limited expiratory flow.
■ CASE TWO
The woman’s high lactate, work
of breathing, and progressive fatigue
all pointed toward lactic acidosis and
impending respiratory failure. Her
low blood pressure and shock index
of 1.3 indicated a high probability of
postintubation hypotension, so she was
started on norepinephrine 5 mcg/min
IV, which improved her blood pressure
to 123/85. After rapid-sequence
induction, she was intubated quickly
by an attending physician, who focused
on minimizing apnea time to avoid
worsening the patient’s acidosis. The
ventilator was set to a respiratory
rate of 30 breaths/min to maintain
appropriate compensation for the
acidosis. Intubation dropped the patient’s
blood pressure to 90/52, but after an
hour of additional fluid resuscitation,
she was weaned off vasopressors and
remained hemodynamically stable. A
postintubation blood gas showed a pH
of 7.37 and a PCO2 of 24.
Med. 1994 Jul;12(4):425-428
3. Lin CC, Chen KF, Shih CP, Seak CJ, Hsu KH. The
prognostic factors of hypotension after rapid sequence
intubation. Am J Emerg Med. 2008 Oct;26(8):845-851.
4. Heffner AC, Swords DS, Neale MN, Jones AE. Incidence
and factors associated with cardiac arrest complicating
emergency airway management. Resuscitation. 2013
Nov;84(11):1500-1504.
5. Kim WY, Kwak MK, Ko BS, et al. Factors associated
with the occurrence of cardiac arrest after emergency
tracheal intubation in the emergency department. PLoS
One. 2014 Nov 17;9(11): e112779.
6. Heffner AC, Swords DS, Nussbaum ML, Kline JA, Jones
AE. Predictors of the complication of postintubation
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7. Johnson KB, Egan TD, Kern SE, et al. The influence of
hemorrhagic shock on propofol: a pharmacokinetic and
pharmacodynamic analysis. Anesthesiology. 2003 Aug;
99(2):409-420.
8. Green RS, Fergusson DA, Turgeon AF, et al.
Resuscitation prior to emergency endotracheal
intubation: results of a national survey. West J Emerg
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9. Mort TC. The incidence and risk factors for cardiac
■ CASE THREE
Despite noninvasive ventilation and
other appropriate therapies for acute
exacerbation of COPD, this patient’s
condition was deteriorating. Physicians
decided to intubate the patient and
opted to anesthetize him with ketamine
for the best chance of improving his
ventilation before the procedure. The
patient’s ventilator was initially set to
a respiratory rate of 20 breaths/min
with a tidal volume of 500 mL and an
applied PEEP of 5 cm H 2O. After 30
minutes, the peak pressure and plateau
pressure measured by the ventilator had
both increased markedly. By inspecting
the flow-vs-time waveform on the
ventilator, physicians determined that
the patient’s expiratory flow was being
interrupted each new breath, resulting in
a buildup of intrinsic PEEP. Decreasing
the ventilator respiratory rate to 12
breaths/min improved both the intrinsic
PEEP and the plateau pressure.
arrest during emergency tracheal intubation: a
justification for incorporating the ASA Guidelines in the
remote location. J Clin Anesth. 2004 Nov;16(7):508-516.
10. Nava S, Hill N. Non-invasive ventilation in acute
respiratory failure. Lancet. 2009 Jul 18;374(9685):250-259.
11. Baillard C, Fosse JP, Sebbane M, et al. Noninvasive
ventilation improves preoxygenation before intubation
of hypoxic patients. Am J Respir Crit Care Med. 2006
Jul 15;174(2):171-177
12. Frat JP, Thille AW, Mercat A, et al. High-flow oxygen
through nasal cannula in acute hypoxemic respiratory
failure. N Engl J Med. 2015 Jun 4;372(23):2185-2196.
13. Miguel-Montanes R, Hajage D, Messika J, et al. Use
of high-flow nasal cannula oxygen therapy to prevent
desaturation during tracheal intubation of intensive
care patients with mild-to-moderate hypoxemia. Crit
Care Med. 2015 Mar;43(3):574-583.
14. Jaber S, Monnin M, Girard M, et al. Apnoeic
oxygenation via high-flow nasal cannula oxygen
combined with non-invasive ventilation preoxygenation
for intubation in hypoxaemic patients in the intensive
care unit: the single-centre, blinded, randomized
controlled OPTINIV trial. Intensive Care Med. 2016
Dec;42(12):1877-1887.
15. Blow O, Magliore L, Claridge JA, Butler K, Young JS.
The golden hour and the silver day: detection and
correction of occult hypoperfusion within 24 hours
improves outcome from major trauma. J Trauma. 1999
Nov;47(5):964-969.
16. Fuller BM, Dellinger RP. Lactate as a hemodynamic
marker in the critically ill. Curr Opin Crit Care. 2012
Jun;18(3):267-272
17. Shapiro JI, Whalen M, Kucera R, Kindig N, Filley G,
Chan L. Brain pH responses to sodium bicarbonate and
Carbicarb during systemic acidosis. Am J Physiol. 1989
May;256(5 Pt 2):H1316-H1321.
18. Jabre P, Combes X, Lapostolle F, et al. Etomidate versus
ketamine for rapid sequence intubation in acutely ill
patients: a multicentre randomised controlled trial.
Lancet. 2009 Jul 25;374(9686):293-300.
19. Oddo M, Feihl F, Schaller MD, Perret C. Management of
mechanical ventilation in acute severe asthma: practical
aspects. Intensive Care Med. 2006 Apr; 32(4):501-510.
20. Ward NS, Dushay KM. Clinical concise review:
mechanical ventilation of patients with chronic
obstructive pulmonary disease. Crit Care Med. 2008
May;36(5):1614-1619.
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