Initiation of Mechanical

Ven t il ati o n i n P ati en t s

with Decompensated Respiratory
F a i l u re
Eric D. Signoff, MDa,*, Jason Y. Adams, b
MD, MS ,
Brooks T. Kuhn, MD, MASb

KEYWORDS
 Mechanical ventilation  Endotracheal intubation  COPD
 Acute respiratory distress syndrome  Heart failure  Ventilator weaning

HOSPITAL MEDICINE CLINICS CHECKLIST

1. Few absolute criteria for endotracheal intubation exist. Instead, knowledge of

the driving disease and trajectory should guide clinicians to intubate at the
safest time possible.
2. Hospitalists can play important roles in the management of patients in the peri-
intubation period by being prepared for the effects of endotracheal intubation
and the induction medications required, initiation of positive pressure ventila-
tion, and subsequent sedation.
3. Mechanical ventilation is a tool to support severe respiratory failure, but comes
with inherent risks, collectively termed ventilator-induced lung injury.
4. Initial ventilator settings vary by the disease that is being treated, but a strategy
of low tidal volume ventilation is recommended in most patients.
5. Patients should be assessed for readiness to extubate shortly after intubation
using a variety of predictive tools (eg, rapid shallow breathing index, sponta-
neous breathing trials), improvement of the reason for respiratory failure, and
ability to prevent aspiration.

No Disclosures.
a
Section of Hospital Medicine, Department of Internal Medicine, UC Davis Medical Center,
4150 V Street, Suite 3400, Sacramento, CA 95817, USA; b Division of Pulmonary, Critical Care,
and Sleep Medicine, Department of Internal Medicine, UC Davis Medical Center, 4150 V Street,
Suite 3400, Sacramento, CA 95817, USA
* Corresponding author.
E-mail address: esignoff@ucdavis.edu

Hosp Med Clin 6 (2017) 503–516

http://dx.doi.org/10.1016/j.ehmc.2017.05.006
2211-5943/17/Published by Elsevier Inc.
504 Signoff et al

INTRODUCTION

What is the role of the Hospitalist in the management of invasive mechanical

ventilation?
The hospitalist is a relatively new position with constantly expanding scope in the care
of hospitalized patients. Traditional boundaries limiting hospitalists to pre–intensive
care unit (ICU) and post-ICU management are fading because of a shortfall of inten-
sivists in the United States.1,2 As hospitalists become more involved in the care of crit-
ically ill patients, skill in the management of invasive mechanical ventilation (MV) is
increasingly valuable.
Acute respiratory failure (ARF) is the most common cause of admission to the ICU
in the United States, most commonly due to acute exacerbations of chronic obstruc-
tive pulmonary disease (AE-COPD), congestive heart failure, acute respiratory
distress syndrome (ARDS), sepsis, and pneumonia.1–3 Hospitalists regularly manage
the same diseases on the floor, while covering the ICU, and after ICU transfer. ARF is
inherently unstable, requiring frequent assessment, intervention, and reassessment.
Hospitalists possess the knowledge and skills to manage these diseases and meet
the dynamic needs of these patients. In fact, as many as 75% of MV patients in com-
munity settings are managed by hospitalists.4,5 Knowledge of the risks and benefits
of endotracheal intubation and MV is important to adeptly care for critically ill
patients.

ASSESSMENT

When should noninvasive positive pressure ventilation or high-flow nasal cannula be

considered as alternatives to endotracheal intubation?
Although potentially life-saving, endotracheal intubation and MV each carry serious
risks. Endotracheal intubation can lead to hemodynamic compromise, predominantly
from sedative medications and subsequent positive pressure ventilation. Direct me-
chanical injury of the mouth, teeth, vocal cords, or rarely, the cervical spine (typically
in patients with severe rheumatoid arthritis or Down syndrome) can occur from the
laryngoscope, stylet, or tube, or from manipulation of the neck.6,7 Nontraumatic com-
plications can occur as well, such as bronchospasm, aspiration of gastric contents,
elevated intracranial pressure, and tachyarrhythmia.7 Ventilator-induced lung injury
(VILI), barotrauma (pneumothorax, pneumomediastinum), atelectrauma (damage to
alveoli from repeated opening and closing), and volutrauma (alveolar damage from
excessive tidal volumes), are common and potentially life-threatening complications
of MV (Table 1).8 Prolonged endotracheal intubation itself is associated with nosoco-
mial pneumonia, upper airway injury, longer ICU stays, and increased sedation
requirements.7,9
Noninvasive positive pressure ventilation (NIPPV), encompassing bilevel and
continuous positive airway pressure (BiPAP and CPAP, respectively), has a clear
role for preventing the need for MV in several disease states. In AE-COPD, NIPPV
has been shown to improve mortality, decrease the need for invasive MV, and
decrease respiratory rate and dyspnea.10,11 In cardiogenic pulmonary edema, NIPPV
has been associated with a decreased need for intubation and lower mortality. The
literature is unclear as to whether BiPAP offers any advantages over CPAP, but the au-
thors suggest initiation of BiPAP over CPAP except in cases with known patient intol-
erance or high concern over gastric insufflation with air and subsequent aspiration.12
 Initiation of Mechanical Ventilation 505

Table 1
Ventilator-induced lung injury

Ventilator-Induced
Injury Cause Clinical Implications Tips to Avoid
Barotrauma Alveolar or bronchial Pneumothorax,  LTVV
rupture leading to pneumomediastinum,  Avoid dynamic
air leak subcutaneous hyperinflation (allow
emphysema exhalation before
initiation of next
breath)
Volutrauma Alveolar edema, Diffuse alveolar damage  Early initiation and
inflammation, (indistinguishable maintenance of LTVV
surfactant from ARDS)  Maintain
dysfunction from patient-ventilator
overdistension synchrony
of alveoli
Atelectrauma Damage from Diffuse alveolar damage  Open lung strategy
repeated collapse (indistinguishable (PEEP)
and reexpansion from ARDS)  LTVV
of alveoli  Minimize respiratory
rate as physiologically
tolerated
Oxygen toxicity Oxygen free-radical Alveolar damage, cilia  Target FiO2 <0.6 to
formation leading inhibition maintain tolerable
to cellular injury oxygen delivery
 Use PEEP to aid
oxygenation

Data from Marini JJ. Dynamic hyperinflation and auto-positive end-expiratory pressure: lessons
learned over 30 years. Am J Respir Crit Care Med 2011;184(7):756–62; and Santamaria JD, Tobin
AE, Reid DA. Do we practise low tidal-volume ventilation in the intensive care unit? A 14-year
audit. Crit Care Resusc 2015;17(2):108–12.

In patients with ARF secondary to ARDS, opinion may be shifting away from NIPPV
toward the use of high-flow nasal cannula. Frat and colleagues13 recently published a
trial comparing NIPPV to high-flow and standard oxygen delivery systems, demon-
strating an absolute decrease in endotracheal intubation of w25% and decrease
in mortality of w14% for high-flow nasal cannula. NIPPV allows unregulated tidal
volumes and is limited by leak in the amount of positive end expiratory pressure
(PEEP) it can deliver, which may partially explain these findings. However, a recent
study demonstrated a reduction in intubation rates and 90-day mortality in patients
with ARDS when NIPPV delivery was through a helmet as opposed to a mask.14
Although this modality is not available currently, it demonstrates that NIPPV for
ARDS may still have a future.
NIPPV and high-flow nasal cannula should be used with caution as a bridge to defin-
itive therapy. Providers should have a low threshold for initiation of invasive MV
if noninvasive modalities are unlikely to adequately support the patient before their
underlying failure can resolve.

When should endotracheal intubation and mechanical ventilation be considered?

Endotracheal intubation should be considered if a patient fails to “protect their airway”

(ie, unable to prevent aspiration of oral secretions or gastric contents); the patient is
506 Signoff et al

unable to meet their oxygenation or ventilation needs; or the expected trajectory sug-
gests impending respiratory failure.
Altered level of consciousness, whether from CO2 narcosis, drugs, or a neurologic
insult, leads to impaired gag and cough reflexes, which can lead to aspiration of oral
and gastric contents into the lower airway. Evaluation of the gag reflex is often pre-
formed to assess a patient’s ability to protect his or her airway, but may be an unre-
liable metric. Up to 37% of healthy individuals can have an absent gag reflex.15
Even if a gag reflex is intact, vocal cord paralysis or incomplete glottis closure can
lead to aspiration of oral contents. It is the authors’ recommendation to perform a
gag reflex assessment, but to place it in the context of the patient’s global level of
arousal, and the cause and expected course of the derangement. An easily reversible
cause such as narcotic overdose may be amenable to short-term noninvasive tempo-
rizing measures while rapidly working to correct the cause of the depressed senso-
rium, whereas altered level of consciousness from an acute stroke would warrant a
lower threshold to intubate because of the expectation of a protracted course.
There are no consensus vital sign, laboratory value, or physical examination criteria
to indicate initiation of invasive MV. Absolute, single data point thresholds to prompt
endotracheal intubation, such as oxygen saturation, arterial blood gas, and blood
pressure, are of little use, especially in patients with chronic respiratory disease. A
common and dangerous example is a patient with developing ARDS who has a
high minute ventilation due to increased dead space and work of breathing. A pulse
oximetry reading of 90% while receiving 4 L/min of supplemental oxygen via nasal
cannula should be interpreted as a sign of respiratory failure. Alternatively, the same
oxygen saturation in a patient with severe COPD may represent their baseline level
of oxygenation. Physical examination signs of impending respiratory failure (eg,
increased respiratory rate, use of accessory muscles of breathing, and paradoxic thor-
acoabdominal movements during inspiration) may be more predictive of respiratory
failure. Oxygen saturation and arterial partial pressure of oxygen should always be
interpreted in the context of a patient’s work of breathing and the amount of noninva-
sive support he or she is receiving, and one should have a lower threshold to intubate
patients with deterioration who are already receiving high levels of noninvasive
support.
Last, the expected clinical course should factor into the decision to intubate. As
mentioned above, quickly reversible causes (eg, narcotic overdose) or diseases
amenable to non-invasive management (ie, COPD and cardiogenic pulmonary edema)
may warrant avoiding MV.16,17 Other diseases such as ARDS typically have a longer
course until resolution, such that NIPPV should not be used to delay intubation
when failure appears imminent.

INTUBATION

What is the role of the hospitalist during the periendotracheal intubation period?

Endotracheal intubation is performed by a wide variety of health care providers,

including hospitalists in some settings. Although much attention is rightly paid
to the act of endotracheal intubation, medical management of the patient in the
peri-intubation period is equally important. Hospitalists should anticipate common
problems through understanding the underlying acute pathophysiology and a pa-
tient’s chronic comorbidities. Awareness of common medication effects and antici-
pating problems (eg, hemodynamic instability) before they occur is essential.
Hospitalists must anticipate postintubation sedation/analgesia requirements, because
 Initiation of Mechanical Ventilation 507

the duration of effect of induction medication is short (and often shorter than that of the
paralytic). This effect is particularly apparent in patients with underlying liver impair-
ment receiving rocuronium, in which clearance can be impaired. Table 2 describes
common medications used in endotracheal intubation and both their expected and
adverse effects.
The choice of induction medications should depend on the acute disease state.
Factors that influence this decision include concern for elevated intracranial pressure,
recent intubation (especially if with etomidate), bronchospasm, intravascular volume
status, renal/hepatic function, and hyperkalemia.18 Because intubating providers
are often not afforded the time for a thorough chart review, concise communication
of information from hospitalist to the intubating provider is key to appropriate selection
of induction medications.
Cardiac preload is decreased during initiation of MV secondary to positive pressure
ventilation and decreased sympathetic tone from induction medications. Decreased
preload is a benefit for patients with decompensated congestive heart failure, but
for patients with normal cardiac function, especially those in hypovolemic or distribu-
tive shock, the decrease in preload may lead to immediate and severe hypotension.
Hospitalists should anticipate hypotension during and after intubation and be ready
to administer resuscitative volume and/or vasopressors. The authors’ practice is to
have resuscitative fluids with a pressure bag accessing a large-bore intravenous
line, as well as immediate access to push-dose vasopressors (epinephrine or phenyl-
ephrine) to prevent hemodynamic collapse.
After endotracheal intubation, the Society of Critical Care Medicine guidelines
recommend choosing non-benzodiazepines such as propofol or dexmedetomidine.19
Analgesics such as fentanyl should be used primarily for the treatment of pain and not
sedation, or to decrease respiratory drive in patients with severe air hunger. Hospital-
ists should order sedation and analgesia before intubation to ensure that these med-
ications are available to start immediately following intubation and before induction
medications wear off. These guidelines also recommend titration of sedative medica-
tions to “light” rather than “deep” sedation to decrease ICU stay and improve
outcomes, unless contraindicated (eg, patient with ARDS may require deep sedation
to achieve low tidal volume ventilation [LTVV] goals).19

What factors should be considered when choosing the initial settings and mode of
mechanical ventilation?
Mounting evidence supports the use of LTVV (tidal volumes of 6–8 mL per kilogram of
predicted body weight) for all patients receiving invasive MV.20 There is no compelling
evidence to support any specific mode of tidal volume delivery over another. Plateau
pressure should be maintained less than 30 cm H2O to reduce the risk of barotrauma
(eg, pneumothorax) and prevent excessive alveolar distention. The fraction of inspired
oxygen (FiO2) should initially be set at 1.0, but rapidly decreased to nontoxic levels of
oxygen. For most patients, FiO2 titration can be guided by peripheral oxygen saturation
to avoid the delay of waiting for arterial blood gas–derived partial pressure of oxygen.
PEEP should be applied initially at 5 cm H2O and increased approximately every 15 mi-
nutes as needed using the ARDSnet PEEP-FiO2 titration tables.21 After intubation, res-
piratory rate and minute ventilation should be rapidly adjusted to achieve disease-
specific minute ventilation goals (Table 3), while avoiding breath stacking (incomplete
exhalation before initiation of the next breath resulting in hyperinflation). An initial rate
set to achieve a minute ventilation of 8 to 10 L/min will generally prevent extremes of
hypoventilation and hyperventilation in most patients. Frequent testing of arterial
 508
Table 2
Commonly used medications to facilitate endotracheal intubation

Signoff et al
Pretreatment Medication Mechanism Onset/Duration Advantage Adverse Effects
Fentanyl Rapid-acting synthetic opioid 1 min/30 min  Decreased hypertensive  Hypotension
response to intubation  Thoracic and abdominal
 Blunts sympathetic muscular rigidity (rare)
response to intubation
Sufentanil Rapid-acting synthetic opioid More rapid onset and  Rapid onset, short  Hypotension
shorter duration than duration
fentanyl
Midazolam GABA-A receptor agonist 2 min/3–5 min  Amnestic  Hypotension
Lidocaine Class IB antidysrhythmic with 1–2 min/10-20 min  Inhibits cough/gag reflex  Hypotension
local anesthetic properties  Theoretic benefit if intra-
cranial pressure (ICP) is of
concern

Induction Medication Mechanism Onset/Duration Advantage Adverse Effects

Etomidate GABA-2 receptor agonist of 30 s/3–5 min  Relatively minimal effect on  Repeated use can lead
reticular activating system blood pressure to adrenal insufficiency
 Decreases ICP
Propofol GABA-A receptor agonist/ <1 min/3–10 min  Decreases ICP  Cardiovascular
Na1 channel antagonist  Amnestic depression
 Hypotension
Ketamine NMDA receptor antagonist 30 s/5–10 min  Minimal hemodynamic  Increases ICP
effect  Hallucinations
 Bronchodilation

Neuromuscular Blockade Mechanism Onset/Duration Advantage Adverse Effects

Succinylcholine Depolarizing neuromuscular 30 s/4–6 min  Fast onset, fast clearance  Hyperkalemia
blocker  Malignant
hyperthermia
 Arrhythmia
Rocuronium Non-depolarizing 1 min/30–60 min  Decreases potassium  Prolonged duration of
neuromuscular blocker release from cells action when hepatic
(compared with impairment
succinylcholine)

Data from Refs.18,19

 Initiation of Mechanical Ventilation 509

Table 3
Mechanical ventilation goals for the management of common causes of acute respiratory
failure

Ventilation (Tidal Volume &

Disease Oxygenation (PEEP & FiO2) Respiratory Rate)
Heart  PEEP offers hemodynamic and  Maintain normal pH and CO2
failure oxygenation benefits through LTVV if tolerated
COPD/  PEEP can offer oxygenation and  LTVV if tolerated
asthma ventilation benefits in obstructive lung  Fastest respiratory rate that allows
disease near-complete exhalation (avoid
 Tolerate oxygen saturation 90%–94% breath stacking asynchrony)
ARDS  ARDSnet PEEP tables (use PEEP to avoid  LTVV (6–8 mL/kg PBW)
toxic FiO2 >0.6)  Permissive hypercapnia (tolerate
pH >7.2) if needed

Abbreviation: PBW, predicted body weight.

Data from Refs.4,17,22,25,26

blood gases may be necessary in selected patient subgroups such as moderate-

severe ARDS, severe obstructive lung disease, and patients with increased intracra-
nial pressure.

Heart Failure
MV can be used for more than administration of supplemental oxygen in decompen-
sated heart failure. PEEP has numerous beneficial effects in heart failure:
 Decreased preload through reducing venous return
 Decreased hypoxemic pulmonary vasoconstriction
 Decreased extravascular lung water thus improving pulmonary edema
 Improved cardiac oxygen delivery
 Decreased afterload through increased intrathoracic pressure and decreased
transmural pressure.16,22
The net effects of optimized MV settings in the acute setting are improved cardiac
output and decreased myocardial oxygen consumption.23 These effects of MV should
also be considered during the weaning phase. Heart failure is the most common cause
of failed extubation in all patients, not just those intubated for this indication.16 With-
drawal of even small amounts of PEEP and mechanical support upon extubation can
result in substantial increases in work of breathing, afterload, and preload that may
result in unanticipated extubation failure. Pharmacologic optimization of preload
with diuretics or ultrafiltration, afterload with short-acting vasodilators such as intrave-
nous hydralazine or nitroprusside, and augmentation of contractility with inotropic
medications may be necessary to liberate selected patients from MV. In some cases,
spontaneous breathing trials (SBTs) with supplemental oxygen supplied via a T-piece
attached to the end of the endotracheal tube may help to identify patients that require
additional hemodynamic optimization before or during extubation.

Asthma/Chronic Obstructive Pulmonary Disease

Patients with acute exacerbations of COPD and asthma usually require ventilatory
support because of high work of breathing, and worsening hypercarbia and/or hyp-
oxemia are late findings that may represent failed recognition of impending respi-
ratory failure earlier in a patient’s clinical course. Therefore, the goal of MV
should be to provide adequate ventilation support and offloading of the respiratory
510 Signoff et al

muscles. In patients without expiratory flow limitation, increasing respiratory rate is

the preferred method (compared with increasing tidal volume) to increase minute
ventilation. In obstructive lung disease, exhalation is prolonged such that prema-
ture initiation of a breath before complete exhalation can lead to dynamic hyperin-
flation (a phenomenon referred to as breath stacking), which in turn leads to an
increase in physiologic dead space and decreased effective alveolar ventilation.24
The respiratory rate should be adjusted to the highest rate that allows for near-
complete exhalation.
The goal of ventilation should not be a physiologically “normal” blood gas. Many pa-
tients with COPD have chronic respiratory acidosis; therefore, the goal should be to
treat the acute acidosis and not overcompensate for the chronic acidosis. PEEP
can be useful in COPD (typically between 8 and 12 cm H2O) to improve hyperinflation
by increasing expiratory flow rates and decrease the work of breathing by offsetting
intrinsic PEEP.25 In asthma, PEEP >5 cm H2O may not be as beneficial because of mu-
cous plugging and airway edema. When titrating PEEP, plateau pressures should be
maintained less than 30 cm H2O.24
Acute Respiratory Distress Syndrome
The goal of MV in ARDS is to provide adequate oxygenation with the least injurious
ventilator settings possible. LTVV targeting 6 mL/kg of predicted body weight, along
with a plateau pressure less than 30 cm H2O, has been proven to decrease mortality,
although adoption into practice has been poor.21,26 Patients with ARDS frequently
have high respiratory drive; therefore, many patients do not tolerate tidal volume
restriction without substantial patient-ventilator asynchrony (PVA). To prevent VILI in
patients with ARDS, it is important to not acquiesce to the patient’s drive for larger tidal
volumes, especially in the first hours to days of acute illness when the lungs are likely
more susceptible to VILI. To achieve target tidal volumes, deep sedation and even
neuromuscular blockade may be required.27
After restricting tidal volume, respiratory acidosis often results despite optimizing
the respiratory rate. “Permissive hypercapnia” refers to the strategy of accepting mod-
erate acidosis if it is hemodynamically tolerated (usually with a pH > w7.20).28 Using
PEEP for an “open lung strategy” to prevent atelectrauma—damage from repetitive
opening and closing of the alveoli—is recommended.29 Although high FiO2 may be
required for severe ARDS, use of the ARDSnet PEEP-FiO2 titration tables may help
to limit oxygen toxicity from unnecessarily high FiO2, ideally keeping the FiO2 less
than 0.6.30

MONITORING

What are the common pitfalls in the early management of mechanical ventilation?
Hospitalists should be aware of several early pitfalls to avoid the need for rescue later
in the hospital course. Hospitalists should identify the cause of the failure to set appro-
priate goals. For example, recent data have documented low rates of ARDS recogni-
tion even among intensivists, with only one-third of providers recognizing ARDS the
first day diagnostic criteria were met, and only 60% ever recognizing the condition
when present.31 Not surprisingly, studies have documented remarkably low rates of
adherence LTVV in patients with ARDS, even in patients with severe disease.26,31,32
Given the life-saving benefits of LTVV in patients with ARDS, clinicians should thus
maintain high suspicion for the diagnosis of ARDS and a low threshold for the use
of LTVV.20,33–35
 Initiation of Mechanical Ventilation 511

The easiest and most common intervention to improve hypoxemia for an intubated
patient is to increase the FiO2. Although this may be appropriate for mild to moderate
hypoxemia, oxygen free-radical formation can occur when the FiO2 increases beyond
w0.60. Hyperoxia, use of excessive FiO2, has been shown to have insidious, delete-
rious effects in multiple clinical scenarios: heart failure/myocardial ischemia,36–38
and post–cardiac arrest.30,39 Many physicians in clinical practice aim for physiologi-
cally normal targets, but Panwar and colleagues30 recently showed that lower targets
(oxygen saturation targets of 88%–92%) are tolerable in the short term. Aside from the
benefits of avoiding free radical damage, targeting lower oxygen saturation w88% to
92% aids the clinician in detecting worsening hypoxemia. This range represents the
upper inflection point of the oxygen-hemoglobin dissociation curve where worsening
gas exchange will immediately lead to lower oxygen saturation, resulting in immediate
recognition of deterioration at the bedside. For patients with oxygen saturations
greater than 96%, deteriorating alveolar gas exchange will have a minimal effect of
the oxygen saturation, potentially delaying identification and intervention.
In contrast to increasing the FiO2, titration of PEEP is often overlooked as a modality
to improve oxygenation through increasing functional residual capacity and thus sur-
face area and time available for gas exchange. ARDSnet tables for PEEP-FiO2 titration
prescribe recommended pressures for a given FiO2 and are an easy, online-accessible
tool to guide the optimization of these parameters.21
PVA, colloquially referred to as “bucking the vent,” occurs in nonparalyzed patients
requiring MV when patient respiratory demands are not met by ventilator support.40
This paradigm falsely suggests inadequate ventilator support as the cause, but it is
important to recognize that titrating support to patient demand may lead to injurious
ventilator settings. The clinician must find compromise in this complicated and
dynamic relationship.

What are the common complications of mechanical ventilation?

VILI refers to several deleterious effects of MV: barotrauma (pneumothorax, pneumo-
mediastinum), atelectrauma (alveolar damage from repetitive opening and closing of
the alveoli), and volutrauma (alveolar damage from excessive tidal volumes).8 VILI is
best prevented with LTVV and an open lung strategy, using PEEP to prevent atelec-
trauma (see Table 1).29 Barotrauma is often dramatic and rapidly evident, whereas
the effects of volutrauma and atelectrauma are more indolent, causing lung injury
that may be challenging to separate from the natural evolution of ARDS. Therefore,
early initiation of LTVV is recommended for patients with ARDS or at risk for ARDS,
such as those with the following conditions:
 Sepsis/septic shock
 Pneumonia
 Trauma
 Aspiration
 Pancreatitis
 Inhalational injury
 Massive blood product transfusion
 Cardiac or acute abdominal surgery8
ICU-acquired weakness describes muscular and/or neurologic injury resulting from
critical illness. Use of corticosteroids and immobility are the most important modifiable
risk factors.41 ICU-acquired weakness can manifest as myopathy/polyneuropathy,
with global weakness and difficultly liberating from the ventilator. Neuromuscular
512 Signoff et al

weakness develops in more than 25% of patients intubated for a week or more. Symp-
toms last weeks to months, but can persist indefinitely.41 Data supporting early mobi-
lization are mixed, but adverse effects are low, and so the authors recommend
initiation as early as the patient can safely tolerate.41

LIBERATION

How do you wean patients from the ventilator using spontaneous breathing trials and
the rapid shallow breathing index?
For many patients, the process of liberating from the ventilator begins immediately af-
ter intubation; however, unstable patients with ongoing severe shock or patients
requiring high levels of MV support should not have SBTs performed because this
may lead to clinical deterioration. SBTs, 30- to 120-minute trials on “minimal” venti-
lator support to assess readiness to wean from the ventilator, are recommended
daily.42 What constitutes “minimal” support is a topic of debate, because no support
(ie, T-piece trial), minimal PEEP (ie, CPAP), and PEEP with inhalation assistance to
overcome the resistance of the endotracheal tube are all used in practice.43,44 Even
small amounts of mechanical ventilator support and low levels of PEEP can offset
up to 30% of the work of breathing.45 A recent consensus statement by the American
College of Chest Physicians/American Thoracic Society recommends the use of inspi-
ratory support rather than T-piece for SBTs in patients admitted greater than
24 hours.42 This recommendation is based upon a large, but heterogeneous group
of studies that demonstrate shorter ICU length of stay associated with inspiratory sup-
port SBTs, but without a change in the overall time on MV.
During an SBT, failure is identified by worsening hypoxemia, tachypnea, tachy-
cardia, hypotension, or respiratory distress (defined as accessory muscle use, para-
doxic abdominal muscle use, diaphoresis, or dyspnea). Passing an SBT suggests
readiness to wean MV, but does not guarantee successful extubation, and 10% to
20% of patients who pass an SBT will require repeat endotracheal intubation.46
The rapid shallow breathing index (RSBI), the ratio of tidal volume in liters to the res-
piratory rate, is also used to assess readiness for extubation, typically as a complement
to an SBT. In the original report, an RSBI of less than 105 conferred a 78% chance of
successful extubation.47 A subsequent meta-analysis demonstrated only slight added
value of an RSBI less than 105 if the SBT is passed. The benefit of the RSBI is predicting
extubation failure as the likelihood ratio for failure is 2.3 if the RSBI is greater than 105.48
Before extubation, patients should have intact cough and gag reflexes to assure the
ability to prevent aspiration after extubation.49 The underlying reason for the patient’s
respiratory failure should be treated, and improving hemodynamic stability on
decreasing or no vasoactive medications should be present. Diuresis should be
considered before extubation in patients, especially those with underlying heart failure
or ARDS.47,50,51 Cabello and colleagues52 found heart failure to be the cause of failed
extubation in 42% of patients. Wiedemann and colleagues50 found that a fluid-
conservative management strategy focused on diuresis in hemodynamically stable
patients with ARDS resulted in 2.5 fewer days of MV compared with patients managed
with a more traditional, fluid-liberal strategy.

What options are available for support after extubation?

Although clinicians should not delay extubation to avoid the numerous potential com-
plications associated with extubation failure, patients who fail extubation (require
 Initiation of Mechanical Ventilation 513

unplanned NIPPV or reintubation) are at higher risk for prolonged hospital stay and
increased mortality.53 Certain high-risk patients, defined as those with heart failure,
COPD, age greater than 65 years old, resting hypercapnia, and those with high
severity of illness scores, benefit from immediate postextubation ventilation
support.16,42–46
Preemptive use of NIPPV in patients at increased risk of extubation failure who
otherwise appear ready to liberate does not carry the aforementioned risks of failure
and portends improved outcome when compared with simple oxygen supplementa-
tion methods. The two main options for postextubation respiratory support are
high-flow nasal cannula (HFNC) and NIPPV. Traditionally, NIPPV is considered for pa-
tients with COPD and heart failure, and although most data supporting efficacy come
from studies of BiPAP, CPAP may also play a role especially in patients that experi-
ence discomfort from pressure support delivered through a mask. A recent publication
by Hernández and colleagues54 showed less respiratory failure and reintubation in
patients receiving HFNC compared with venturi mask after extubation. HFNC may
be a good option for patients intolerant of, or with contraindications to, NIPPV.

REFERENCES

1. Stefan MS, Shieh M-S, Pekow PS, et al. Epidemiology and outcomes of acute res-
piratory failure in the United States, 2001 to 2009: a national survey. J Hosp Med
2013;8(2):76–82.
2. Sethi JM, Siegel MD. Mechanical ventilation in chronic obstructive lung disease.
Clin Chest Med 2000;21(4):799–818.
3. Wunsch H, Wagner J, Herlim M, et al. ICU occupancy and mechanical ventilator
use in the United States. Crit Care Med 2013;41(12):2712–9.
4. Heisler M. Hospitalists and intensivists: partners in caring for the critically ill–the
time has come. J Hosp Med 2010;5(1):1–3.
5. Angus DC, Kelley MA, Schmitz RJ, et al, Committee on Manpower for Pulmonary
and Critical Care Societies (COMPACCS). Caring for the critically ill patient. cur-
rent and projected workforce requirements for care of the critically ill and patients
with pulmonary disease: can we meet the requirements of an aging population?
JAMA 2000;284(21):2762.
6. Jöhr M, Salathé M. Unsuspected cervical fractures. Anesthesiology 1989;70(5):
869–70.
7. Loh KS, Irish JC. Traumatic complications of intubation and other airway manage-
ment procedures. Anesthesiol Clin North America 2002;20(4):953–69.
8. Slutsky AS, Ranieri VM. Ventilator-induced lung injury. N Engl J Med 2013;
369(22):2126–36.
9. Meng L, Wang C, Li J, et al. Early vs late tracheostomy in critically ill patients: a
systematic review and meta-analysis. Clin Respir J 2015;10(6):684–92.
10. Lightowler JV. Non-invasive positive pressure ventilation to treat respiratory failure
resulting from exacerbations of chronic obstructive pulmonary disease: cochrane
systematic review and meta-analysis. BMJ 2003;326(7382):185.
11. MacIntyre N, Huang YC. Acute exacerbations and respiratory failure in chronic
obstructive pulmonary disease. Proc Am Thorac Soc 2008;5(4):530–5.
12. Masip J, Roque M, Sánchez B, et al. Noninvasive ventilation in acute cardiogenic
pulmonary edema. JAMA 2005;294(24):3124.
13. Frat J-P, Thille AW, Mercat A, et al. High-flow oxygen through nasal cannula in
acute hypoxemic respiratory failure. N Engl J Med 2015;372(23):2185–96.
514 Signoff et al

14. Patel BK, Wolfe KS, Pohlman AS, et al. Effect of noninvasive ventilation delivered
by helmet vs face mask on the rate of endotracheal intubation in patients with
acute respiratory distress syndrome. JAMA 2016;315(22):2435–41.
15. Bleach NR. The gag reflex and aspiration: a retrospective analysis of 120 patients
assessed by videofluoroscopy. Clin Otolaryngol 1993;18(4):303–7.
16. Kuhn BT, Bradley LA, Dempsey TM, et al. Management of mechanical ventilation
in decompensated heart failure. J Cardiovasc Dev Dis 2016;3(4):33.
17. Vital FM, Ladeira MT, Atallah AN. Non-invasive positive pressure ventilation
(CPAP or bilevel NPPV) for cardiogenic pulmonary oedema. Cochrane Database
Syst Rev 2013;(5):CD005351.
18. Thompson Bastin M, Baker S, Weant K. Effects of etomidate on adrenal suppres-
sion: a review of intubated septic patients. Hosp Pharm 2014;49(2):177–83.
19. Barr J, Fraser GL, Puntillo K, et al. Clinical practice guidelines for the manage-
ment of pain, agitation, and delirium in adult patients in the intensive care unit.
Crit Care Med 2013;41(1):263–306.
20. Lipes J, Bojmehrani A, Lellouche F. Low tidal volume ventilation in patients without
acute respiratory distress syndrome: a paradigm shift in mechanical ventilation.
Crit Care Res Pract 2012;2012(5):1–12.
21. Brower RG, Matthay MA, Morris A, The Acute Respiratory Distress Syndrome
Network. Ventilation with lower tidal volumes as compared with traditional tidal
volumes for acute lung injury and the acute respiratory distress syndrome.
N Engl J Med 2000;342(18):1301–8.
22. Wiesen J, Ornstein M, Tonelli AR, et al. State of the evidence: mechanical venti-
lation with PEEP in patients with cardiogenic shock. Heart 2013;99(24):1812–7.
23. Ricard J-D, Roux D. Invasive ventilation and acute heart failure syndrome. In:
Mebazaa A, editor. Acute heart failure. London: Springer; 2008. p. 486–93.
24. Leatherman J. Mechanical ventilation for severe asthma. Chest 2015;147(6):
1671–80.
25. Marini JJ. Dynamic hyperinflation and auto-positive end-expiratory pressure: les-
sons learned over 30 years. Am J Respir Crit Care Med 2011;184(7):756–62.
26. Santamaria JD, Tobin AE, Reid DA. Do we practise low tidal-volume ventilation in the
intensive care unit? A 14-year audit. Crit Care Resusc 2015;17(2):108–12. Available
at: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom5pubmed&id5
26017128&retmode5ref&cmd5prlinks.
27. Papazian L, Forel JM, Gacouin A, et al. Neuromuscular blockers in early acute
respiratory distress syndrome. N Engl J Med 2010;363(12):1107–16.
28. Laffey JG, O’Croinin D, McLoughlin P, et al. Permissive hypercapnia–role in pro-
tective lung ventilatory strategies. Intensive Care Med 2004;30(3):347–56.
29. Kacmarek RM, Villar J, Sulemanji D, et al. Open lung approach for the acute res-
piratory distress syndrome: a pilot, randomized controlled trial. Crit Care Med
2016;44(1):32–42.
30. Panwar R, Hardie M, Bellomo R, et al. Conservative versus liberal oxygenation
targets for mechanically ventilated patients. A pilot multicenter randomized
controlled trial. Am J Respir Crit Care Med 2016;193(1):43–51.
31. Bellani G, Laffey JG, Pham T, et al. Epidemiology, patterns of care, and mortality
for patients with acute respiratory distress syndrome in intensive care units in 50
countries. JAMA 2016;315(8):788–800.
32. Weiss CH, Baker DW, Weiner S, et al. Low tidal volume ventilation use in acute
respiratory distress syndrome. Crit Care Med 2016;44(8):1515–22.
33. Futier E, Constantin J-M, Paugam-Burtz C, et al. A trial of intraoperative low-tidal-
volume ventilation in abdominal surgery. N Engl J Med 2013;369(5):428–37.
 Initiation of Mechanical Ventilation 515

34. Neto AS, Simonis FD, Barbas CSV, et al. Lung-protective ventilation with low tidal
volumes and the occurrence of pulmonary complications in patients without
acute respiratory distress syndrome: a systematic review and individual patient
data analysis. Crit Care Med 2015;43(10):2155–63.
35. Needham DM, Yang T, Dinglas VD, et al. Timing of low tidal volume ventilation
and intensive care unit mortality in acute respiratory distress syndrome. A pro-
spective cohort study. Am J Respir Crit Care Med 2015;191(2):177–85.
36. Mak S, Azevedo ER, Liu PP, et al. Effect of hyperoxia on left ventricular function and
filling pressures in patients with and without congestive heart failure. Chest 2001;
120(2):467–73. Available at: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?
dbfrom5pubmed&id511502645&retmode5ref&cmd5prlinks.
37. Haque WA, Boehmer J, Clemson BS, et al. Hemodynamic effects of supple-
mental oxygen administration in congestive heart failure. J Am Coll Cardiol
1996;27(2):353–7.
38. Nakamura K, Murakami M, Miura D, et al. Beta-blockers and oxidative stress in
patients with heart failure. Pharmaceuticals (Basel) 2011;4(8):1088–100.
39. Ball J, Ranzani OT. Hyperoxia following cardiac arrest. Intensive Care Med 2015;
41(3):534–6.
40. Zorowitz RD. ICU-acquired weakness: a rehabilitation perspective of diagnosis,
treatment, and functional management. Chest 2016;150(4):966–71.
41. Taito S, Shime N, Ota K, et al. Early mobilization of mechanically ventilated pa-
tients in the intensive care unit. J Intensive Care 2016;4(1):50.
42. Ouellette DR, Patel S, Girard TD, et al. Liberation from mechanical ventilation in
critically ill adults: an official American College of Chest Physicians/American
Thoracic Society clinical practice guideline. Chest 2017;151(1):166–80.
43. Pellegrini JAS, Moraes RB, Maccari JG, et al. Spontaneous breathing trials with
t-piece or pressure support ventilation. Respir Care 2016;61(12):1693–703.
44. Teixeira SN, Osaku EF, Costa CRL de M, et al. Comparison of proportional assist
ventilation plus, T-tube ventilation, and pressure support ventilation as sponta-
neous breathing trials for extubation: a randomized study. Respir Care 2015;
60(11):1527–35.
45. Tobin MJ. Extubation and the myth of “minimal ventilator settings”. Am J Respir
Crit Care Med 2012;185(4):349–50.
46. Thille AW, Richard J-CM, Brochard L. The decision to extubate in the intensive
care unit. Am J Respir Crit Care Med 2013;187(12):1294–302.
47. Yang KL, Tobin MJ. A prospective study of indexes predicting the outcome of tri-
als of weaning from mechanical ventilation. N Engl J Med 1991;324(21):1445–50.
48. Meade M, Guyatt G, Cook D, et al. Predicting success in weaning from mechan-
ical ventilation. Chest 2001;120(6):400S–24S.
49. Salam A, Tilluckdharry L, Amoateng-Adjepong Y, et al. Neurologic status, cough,
secretions and extubation outcomes. Intensive Care Med 2004;30(7):1334–9.
50. National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome
(ARDS) Clinical Trials Network, Wiedemann HP, Wheeler AP, Bernard GR, et al.
Comparison of two fluid-management strategies in acute lung injury. N Engl J
Med 2006;354(24):2564–75.
51. Mekontso-Dessap A, Roche-Campo F, Kouatchet A, et al. Natriuretic peptide-
driven fluid management during ventilator weaning: a randomized controlled trial.
Am J Respir Crit Care Med 2012;186(12):1256–63.
52. Cabello B, Thille AW, Roche-Campo F, et al. Physiological comparison of three
spontaneous breathing trials in difficult-to-wean patients. Intensive Care Med
2010;36(7):1171–9.
516 Signoff et al

53. Ferrer M, Valencia M, Nicolas JM, et al. Early noninvasive ventilation averts extu-
bation failure in patients at risk: a randomized trial. Am J Respir Crit Care Med
2006;173(2):164–70.
54. Hernández G, Roca O, Colinas L. High-flow nasal cannula support therapy: new
insights and improving performance. Crit Care 2017;21(1):1354.