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StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

Mechanical Ventilation
Sean M. Hickey; Al O. Giwa.

Author Information and Affiliations

Last Update: January 26, 2023.

Continuing Education Activity

Mechanical ventilation (MV) works by applying a positive pressure breath and is
dependent on the compliance and resistance of the airway system. Although
mechanical ventilation can be a complex and seemingly elusive topic,
expectations are that healthcare professionals who deal with critically ill patients
have a basic familiarity with the management of a patient on a ventilator.
Providers must also recognize how applying mechanical ventilation affects
patient physiology and response to disease states. The focus of this activity will be
on managing the intubated patient in the first few hours of care on mechanical
ventilation and will review the basics of mechanical ventilation and highlight
ventilator strategies when managing a patient by an interprofessional team.

Objectives:

Explain the basics of mechanical ventilator management.

Describe the different ventilator strategies utilized for different disease

processes.

Outline major complications of mechanical ventilation.

Summarize the advantages of a patient receiving mechanical ventilation.

Access free multiple choice questions on this topic.

Introduction
Mechanical ventilation is necessary to sustain life in acute settings; hence, its
management is essential for clinicians and other healthcare providers to
understand and apply it safely. This knowledge must be built on a solid
understanding of the basic principles of human physiology and airway
mechanics. This article will focus on the management of the intubated patient
in the first few hours of care on mechanical ventilation. It will review the basics
of invasive mechanical ventilation, the common modes of ventilation, initial
settings, and supportive care for intubated patients will be discussed in this
review. Noninvasive ventilation (NIV) will be addressed separately.[1]

The primary indications for invasive mechanical ventilation can be divided into
the following categories:

1. Airway disease of compromise.[2]

 Airway protection in a patient who is obtunded or has a dynamic
airway, e.g., from trauma or oropharyngeal infection.

Airways obstruction is either proximal ( eg angioedema) or distal

(asthmatic bronchospasm or acute exacerbation of chronic obstructive
pulmonary disease).

2. Hypoventilation due to impaired drive, pump failure, or inability to

exchange gases resulting in hypercapnic respiratory failure. The etiology
can be divided into the following subcategories:

Impaired central drive (e.g., drug overdose)[3]

Respiratory muscle weakness (e.g., muscular dystrophy and myositis)

[4]

Peripheral nervous system defects (e.g., Guillain-Barré syndrome or

myasthenic crisis)[5]

Restrictive ventilatory defects (e.g., chest wall trauma or disease or

massive pneumothorax or effusion)

3. Hypoxemic respiratory failure can be due to the inability to exchange

oxygen or delivery to the peripheral tissues due to one of the following
reasons:

Alveolar filling defects (e.g., pneumonia, acute respiratory distress

syndrome (ARDS), or pulmonary edema)

Pulmonary vascular defects leading to ventilation-perfusion (VQ)

mismatch (massive pulmonary embolism or air emboli)

Diffusion defects (advanced pulmonary fibrosis)

4. Increased ventilatory demand due to severe sepsis, shock, or severe

metabolic acidosis[6]

Function
Mechanical ventilation (MV) works by applying a positive pressure breath and is
dependent on the compliance and resistance of the airway system. During
spontaneous inspiration, the lung expands as transpulmonary pressure (P) is
produced mainly by a negative pleural pressure generated by the inspiratory
muscles. In contrast, during controlled mechanical ventilation, a positive airway
pressure drives gas into the lungs, resulting in a positive P. [7] The tidal volume
(VT) is the amount of air that moves in or out of the lungs with each respiratory
cycle.[8] Physiologically VT is dependent on the height and gender of the person
and ranges between 8-10 mL/kg ideal body weight.[2]

MV can be delivered in different modes, including mandatory mode or assisted

mode. In the assisted mode the inspiratory effort generated by the patient triggers
the MV to deliver the breath while the P is the product of negative pleural
pressure and positive alveolar pressure combination. The most common modes
of MV include:
 Volume-limited assist control ventilation (VAC)

Pressure-limited assist control ventilation (PAC)

Synchronized intermittent mandatory ventilation with pressure support

ventilation (SIMV-PSV)

Pressure support ventilation (PS) is usually not used alone; instead, it is

commonly used during weaning from MV. Other types of modes of MV include
controlled mechanical ventilation (CMV; volume-limited or pressure-limited),
intermittent mandatory ventilation (IMV), and airway pressure release
ventilation (APRV) or Bilevel MV are less commonly used as initial settings.[9]

Generally, breath delivery can be divided into either volume-limited or pressure-

limited types. Depending on respiratory compliance, airway resistance, and the
type or mode of MV, the breath's VT and airway pressure will change. For
example, in cases of using volume assist control VAC mode, VT is set to a fixed
amount; therefore, the static airway pressure (or plateau pressure at end
inspiration) will depend on lung compliance. On the other hand, when pressure
assists control PAC mode is used, the driving pressure is set and fixed; hence VT is
variable from breath to breath and dependent on lung compliance (i.e., when the
lung compliance is high, VT is high, and when lung compliance is low, VT is low).

There are four stages of mechanical ventilation. There is the trigger phase, the
inspiratory phase, the cycling phase, and the expiratory phase. The trigger phase
is the initiation of an inhalation which is triggered by an effort from the patient
or by set parameters by the mechanical ventilator. The inhalation of air into the
patient defines the inspiratory phase. The cycling phase is the brief moment
when inhalation has ceased but before exhalation has begun. The expiratory
phase is the passive exhalation of air from the patient.

Setting MV

Mode selection: It is recommended to use commonly used MV modes listed above

for initiation of MV. The selection of MV mode should be individualized to achieve
safety via optimization of ventilation-perfusion matching and pressure-volume
relationship of the lungs. [10] In addition,patient-ventilator synchrony and
comfort are important factors for the mode selection.

VAC mode: When VAC mode is chosen, the following parameters have to be set
on the ventilator:

Tidal volume: VT is usually selected based on ideal or predicted body weight

(PBW), not actual weight. In conditions such as ARDS that require a
protective lung strategy, the VT is set at a low range of 4 to 8 mL/kg PBW.[11]

Respiratory rate (RR): RR is typically set at 12 to 16 breaths/minute, and

higher RR ( up to 35 breaths/minute) is selected to achieve adequate minute
ventilation, such as during protective lung strategy in ARDS to avoid severe
hypercapnia or to offset severe acidosis.[12]

Inspiratory flow rate (IFR): IFR is usually set at 40 to 60 L/minute to target an

inspiratory: expiratory ratio of 1:2 or 1:3. Higher IFR is usually
 recommended (up to 90 L/min) in cases of severe distal airway obstruction
such as acute COPD exacerbation or severe asthma exacerbation which will
allow longer expiratory time to empty the lung and hence target I:E ratio of
more than 1:3.[10]

Fraction of inspired oxygen (FI02): FI02 should be set to the lowest level to
achieve pulse oximetry (SP02) of 90% to 96%, as hyperoxemia has been
shown to increase mortality in critically ill patients.[13][14]

Positive end-expiratory pressure (PEEP): PEEP is used to increase the

functional residual capacity and stent open collapsable alveoli, thus
reducing atelectatic trauma.[2] The level of PEEP is usually set at 5 cmH2O
and titrated based on the underlying condition and oxygenation needs. For
example, in ARDS, there is a specific level of PEEP titrated according to
respiratory system mechanics or the ARDSNetwork table.[15]

Trigger sensitivity: The triggers are two types flow-trigger and pressure-
trigger. For pressure-trigger, it is usually set at -2 cmH2O but should be
avoided in cases where auto-PEEP is suspected, and instead, flow-trigger
should be used and set at a 2 L/min threshold.

PAC mode: When PAC mode is selected, the following parameters have to be set
on the ventilator:

Inspiratory Pressure (Pi): Pi level is usually selected (10 to 20 cmH2) to

achieve adequate tidal volume based on the patient's underlying condition,
as discussed above.

Inspiratory time (Ti): Ti is typically set to 1 second and adjusted to achieve

an I:E ratio of 1:2 to 1:3.

PEEP and FiO2 are selected similarly to VAC mode. However, the Pi adds
additional pressure to the peak airway pressure and may further increase
the risk of barotrauma.

SIMV/PSV mode: When SIMV/PSV mode is selected, the initial settings include
the following:

Pressure support (PS): The PS typically starts with 5 to 15 cm H2O for

spontaneous breaths taken by the patient above the set rate. The PS can
be adjusted as needed to maintain certain Minute ventilation.

Tidal volume: VT is set similarly to VAC mode at levels to achieve targeted

minute ventilation without causing ventilator-associated lung injury (4 to 8
mL/kg PBW) for the non-spontaneous breaths.

Airway Pressure Release Ventilation Mode

APRV is a form of continuous positive airway pressure (CPAP) characterized by a

timed pressure release while allowing for spontaneous breathing.[16] (See Figure
1) APRV functions by providing continuous pressure to keep the lungs open with
a timed release to lower set pressure.[17][18] The continuous pressure phase of
APRV transmits pressure to the chest wall, which allows for the recruitment of
both proximal and distal alveoli. The prolonged continuous pressure phase with
the short release phase avoids the continuous cycles of recruitment-
derecruitment in pressure/volume control vent settings.[19] This helps to avoid
atelectrauma, barotrauma, and resulting ventilator-induced lung injury.[19] (See
Figure 2) The timed release allows for a passive exhalation and improved
clearance of CO2. Since APRV relies upon spontaneous ventilation, it requires less
sedation than conventional modalities, thus mitigating adverse events due to
sedation. Spontaneous breathing has the benefit of increasing end-expiratory
lung volume, decreasing atelectasis, and improving ventilation to dependent lung
regions.[19] Spontaneous breathing further improves the hemodynamic profile
by decreasing intrathoracic pressure, thus improving preload and cardiac
output.

Setting up APRV requires adjusting four main variables, P-high, P-low, T-high, and
T-low.[17][18] P-high is the continuous pressure set, while P-low is the pressure
release part of the cycle. T-high is how long the continuous pressure is set to last,
while T-low is the release phase duration. The patient should initially be set on
AC/VC immediately post-intubation until the paralysis wears off. Then, an
inspiratory hold should be performed to determine the plateau pressure. This
plateau pressure becomes the P-high and should generally be around 27 to 29 cm
H2O, though obese patients may require higher pressure. The P-low is generally
set to 0. However, there is generally intrinsic PEEP, as full exhalation does not
occur. The T-high is generally set to 4 to 6 seconds, while the T-low is set to 0.2 to
0.8 seconds in restrictive lung disease and .8-1.5 seconds in obstructive lung
disease. To properly set the T-low, you should examine the Flow-Time Waveform
on the ventilator. The T-low should be set to approximately 75% of the Peak
Expiratory Flow Rate (PEFR).[19][17] (See Figure 3) The T-low needs to be
continuously readjusted to 75% of the PEFR as lung recruits over time. FI02
should be titrated downwards once the patient is on APRV and comfortable.

Spontaneous breathing is paramount in APRV; thus, a small amount of pressure

support or automatic tube compensation should be added to account for the
endotracheal tube's intrinsic resistance.[17] Hypoxemia can be corrected by
increasing the P-high and T-high.[17] Hypoxemia can also be corrected by
shortening the T-low. Permissive hypercapnia is allowed in APRV. However,
hypercapnia can be corrected if needed by decreasing sedation and/or increasing
P-high and T-high. It can further be corrected by increasing the T-low. However,
increasing the T-low can be problematic as APRV relies upon intrinsic PEEP
(iPEEP) to keep the lungs open during P-low. If the T-low increases, the iPEEP will
decrease, thus risking the derecruitment of alveoli.

Issues of Concern
Ventilator-associated lung injury (VALI): Lung injury related to ventilator use is
common when the setting is not selected based on PBW, particularly in cases of
stiff lungs such as ARDS that require lung protective strategy using low tidal
volume and targeted airway pressures to prevent lung injuries.[20]
Ventilator-associated events (VAE): VAE is defined as "deterioration in respiratory
status after a period of stability or improvement on the ventilator, with evidence
of infection or inflammation, and laboratory evidence of respiratory infection."
[21] Risk factors for VAE include sedation (such as with benzodiazepines or
propofol), fluid overload, high tidal-volume ventilation, and high inspiratory
driving pressures.[22] Potential strategies to prevent VAEs include ventilator
bundles by minimizing sedation, daily spontaneous awakening and breathing
trials, encouraging early mobilization, conservative fluid, transfusion strategies,
and lung protective strategies. Recent studies have tested some of these
interventions on patients' outcomes, such as the utilization of ventilator bundles.
[23][24]

Hemodynamic changes: When placing a patient on mechanical ventilation, there

is a change in their natural negative pressure ventilation to one of positive
pressure ventilation; this will affect the heart-lung physiology and can alter the
patient's hemodynamic status. The addition of positive pressure ventilation
increases intrathoracic pressure. The increase in intrathoracic pressure will lead
to a decrease in right ventricular preload and left ventricular preload and
afterload. It will also increase the right ventricular afterload.[25] While these
effects could have a minimal change on a healthy person's hemodynamics, they
can cause profound alterations in the hemodynamics of a critically ill patient. For
example, a patient with acute pulmonary edema will benefit from the reduced
preload, while someone in septic shock will not.

Clinical Significance
Three clinical strategies may be chosen to assist in ventilator management.

Lung Protective Strategy

This strategy should be used for any patient with the potential to develop acute
lung injury (ALI) or whose disease state risks progression to acute respiratory
distress syndrome (ARDS). This low tidal volume strategy was developed after the
landmark ARDSnet trials, specifically, the ARMA study, which showed low tidal
volume ventilation in patients with ARDS improved mortality.[26] This method is
used to avoid barotrauma, volume trauma, and atelectatic trauma. Pneumonia,
severe aspiration, pancreatitis, and sepsis are examples of patients with the acute
potential to develop ALI and should be managed with the lung protective
strategy.

Tidal volume should be initially set at 6 ml/kg based on ideal body weight.[27][26]
[28][29] As patients develop ALI and progress into ARDS, their lungs become
progressively recruited and develop shunts, which leads to decreased functional
lung volume.[30] A low tidal volume strategy offsets the decreased functional
lung volume. Tidal volume should not be adjusted based on minute ventilation
goals. The respiratory rate is adjusted based on minute ventilation goals and the
patient's acid-base status. An initial rate of 16 breaths/minute is appropriate for
most patients to achieve normocapnia.[31] A blood gas should be sent
approximately 30 minutes after initiation of mechanical ventilation, and RR
should be adjusted based on the acid-base status and PaCO2 of the patient. If the
PaCO2 is significantly greater than 40 mmHg, then the RR should be increased. If
the PaCO2 is significantly lower than 40, then the RR should be decreased. It is
important to remember that the ETCO2 is not a reliable indicator of PaCO2 as the
ETCO2 can be affected by the physiological shunt, dead space, and decreased
cardiac output. The inspiratory flow rate should be set at 60L/minute. It can
increase if the patient appears to be trying to inhale more during the initiation of
inspiration.[30]

Immediately after intubation, an attempt should be made to reduce the FI02 to

40% to avoid hyperoxemia.[13] From there, adjustments of the FI02 and PEEP are
simultaneously controlled in the lung-protective strategy. Difficulty in
oxygenation in ALI is due to de-recruited alveoli and physiological shunt. To
counteract this, you should increase the FIO2 and PEEP together. The oxygenation
goal of 88%-95% should follow the ARDSnet protocol.[28]

Table 1. ARDSnet PEEP/FIO2 Protocol

Upon connecting a patient to mechanical ventilation, it is essential to frequently

reassess its effects on the patient, especially the alveoli.[28] This assessment is
done by examining the plateau pressure and driving pressure. The plateau
pressure is the pressure applied to small airways and alveoli. The plateau
pressure should be under 30 to prevent volume trauma, which is an injury to the
lung secondary to overdistension of the alveoli. To obtain the plateau pressure,
one must perform an inspiratory pause. Most ventilators have a button to
calculate it. The driving pressure is the tidal volume ratio to the lung's
compliance, providing an approximation of the "functional" amount of lung that
hasn't been de-recruited or shunted.[32] The driving pressure can be calculated
simply by subtracting the amount of PEEP from the plateau pressure.[32] The
driving pressure should remain below 14. If plateau and driving pressures start
to exceed these limits, then decrease TV to 4ml/kg. The respiratory rate can be
increased to compensate for the decrease in minute ventilation, though
permissive hypercapnia might be necessary. Permissive hypercapnia is a
"ventilation strategy to allow for an unphysiologically high partial pressure of
carbon dioxide (PCO2) to permit lung-protective ventilation with low tidal
volumes."[33] Recruitment maneuvers have been found to increase mortality in
moderate to severe ARDS and should not be routinely used.[34]

Obstructive Strategy

Generally, patients with obstructive lung disease (OLD), such as asthma and
COPD, are often treated with non-invasive ventilation. However, they sometimes
require intubation and placement on mechanical ventilation. Obstructive lung
disease is characterized by narrowed airways and the collapse of the small
airways on expiration. [2] This condition leads to increased airflow resistance and
decreases the expiratory flow, resulting in more time required to exhale the tidal
volume fully. If inhalation begins before the full tidal volume has been exhaled,
some residual air is left inside the chest. The intrathoracic pressure increases as
more and more air is trapped inside the alveoli. This pressure is called auto-PEEP,
which must be overcome during inhalation. As the amount of air trapped inside
the chest increases, you have to flatten off the diaphragm and expand the lungs,
decreasing compliance, which is called dynamic hyperinflation. s auto-PEEP and
dynamic hyperinflation progress, there is an increased work of breathing,
decreased efficiency of inhalation, and potential for hemodynamic instability due
to the high intrathoracic pressure. Given these unique circumstances in OLD, the
ventilator strategy must offset these pathologically increased intrathoracic
pressures. Furthermore, to reverse the obstructive process, ventilatory
management must be combined with maximal medical therapy, such as in-line
nebulizers.

The most important thing to accomplish when managing the ventilator for an
obstructive patient is to increase the expiratory phase, allowing for more time to
exhale, which will reduce auto-PEEP and dynamic hyperinflation.[2][30][31] It is
important to recall that most patients will require deep sedation to not over-
breathe the ventilator and inspire too often. The tidal volume should be set at 8
ml/kg, while the respiratory rate should start at ten breaths per minute.[30] These
settings will allow for ample time for a full expiration and hence decreased auto-
PEEP, which tends to employ the above-described permissive hypercapnia
strategy by focussing on lowered tidal volumes and oxygenation over elevated
PaCO2. The inspiratory flow rate should be set at 60 L/minute. FI02 should be set
at 40% after the initiation of ventilation. s obstructive lung disease is typically a
problem with ventilation and not oxygenation; the FIO2 should not be increased.
Minimal PEEP should be employed, with some studies advocating for a PEEP of
zero while some advocate for a small amount of PEEP to help overcome auto-
PEEP.

The ventilator waveform requires careful assessment. If the waveform does not
reach zero by the beginning of the new breath, then the RR must be decreased, or
else hyperinflation and auto-PEEP will rise. If an obstructive patient suddenly
desaturates or drops their blood pressure, they should be disconnected from the
vent to allow for a full exhalation with a clinician pushing on their chest to
facilitate exhalation. After this, a full workup specifically ruling out
pneumothorax due to volume trauma should be undertaken.[31] If plateau
pressures are chronically high, then pneumothorax must also be ruled out.

Intermediate Strategy

The PReVENT trial showed no difference in an intermediate tidal volume strategy

(10 ml/kg) versus a low tidal volume strategy (6 ml/kg) in patients without ARDS.
[35] If the patient is being placed on mechanical ventilation and has no
obstructive physiology or risk of developing acute lung injury, an intermediate
tidal volume strategy using 8 to 10 ml/kg could be employed. Generally, as this
patient would not have oxygenation or ventilation difficulties, minimal ventilator
settings could be employed. Starting with a tidal volume of 8ml/kg, RR of 16, IFR
of 60 L/minute, FIO2 of 40%, and PEEP of 5, with titration as needed, is a
reasonable starting point.

Other Issues
Ventilator bundles play a vital role in preventing ventilator-associated events.
Some of these measures include minimizing sedation, daily spontaneous
breathing trials, early mobilization, conservative fluid and transfusion strategies,
and lung protective strategies.

Sedation: Before initiating mechanical ventilation, one should also consider what
medications to provide for post-intubation pain control and sedation. An
"analgesia first" sedation strategy is recommended, with the most commonly used
agent being fentanyl due to its forgiving, i.e., minimally hypotension-inducing
hemodynamic properties.[36][37] If the patient is still agitated while getting an
analgesia sedation regimen, additional agents, such as propofol, can be added
depending on the patient's hemodynamics and clinical needs. A chest x-ray and
blood gas should be obtained to determine proper endotracheal placement and to
assess minute ventilation. Many centers are now utilizing ultrasound to confirm
endotracheal tube (ETT) placement; however, its use has not become the standard
of care. Plateau pressures should be checked frequently to assess alveolar
integrity.

Head of the bed elevation: All patients on mechanical ventilation should have
the head of the bed elevated to at least 30 degrees. According to a 2016 Cochrane
review on ventilator-associated pneumonia (VAP), "a semi-recumbent (30º to 60º)
position reduced clinically suspected VAP by 25.7% when compared to a 0° to 10°
supine position" however, they acknowledge that the data is severely limited.[38]

Airway maintenance: If the patient suddenly desaturates, then the DOPES

mnemonic should be followed to determine the causes of the problem. DOPES
stands for displacement, obstruction of the ETT or airways,
pneumothorax/pulmonary embolism/pulmonary edema, equipment failure, and
stacked breaths. The patient should immediately be disconnected from the
ventilator and switched to a bag valve mask. The person bagging should ventilate
calmly and allow for a full exhalation. Following this, a systematic approach
should be followed. Does the patient still have a good waveform on their ETCO2?
If not, then the ET tube may have become dislodged. Does the patient bag easily
or with difficulty? If bagging is difficult, this will inform you of some obstructive
problems, such as an obstructed ET tube, pneumothorax, or bronchospasm. If the
patient bags easily and SpO2 rises rapidly, it points to equipment failure. While
this is under evaluation, another provider should assess the patient with an
ultrasound of the lungs and heart, and a chest X-ray should be obtained ASAP.
Pulmonary embolism should be a consideration if no other cause of the
desaturation is found.

Venous thromboembolism prophylaxis: Invasive mechanical ventilation is an

independent risk factor for increased odds of venous thromboembolism in the
intensive care unit.[39] Hence adding prophylactic measures are essential to
prevent additional morbidities.

Gastrointestinal prophylaxis: Gastrointestinal bleeding occurs in approximately

5 % of critically ill patients not receiving prophylaxis.[40] In a multicenter study,
invasive mechanical ventilation was one of two independent risk factors for GI
bleeding (odds ratio for bleeding, 15.6; 95% CI, 3.0 to 80.1).[41] Therefore the use
of an acid suppression strategy for patients on mechanical ventilation has been
recommended.[42] proton pump inhibitors (PPIs) are the most effective agents in
preventing clinically important gastrointestinal bleeding, but they may increase
the risk of pneumonia. It is, however, unnecessary to continue acid suppression
after discharge from the ICU.[43]

Enhancing Healthcare Team Outcomes

Managing a patient on mechanical ventilation requires an interprofessional team
involving clinicians, nurses, and respiratory therapists. Good communication
among team members is paramount. Respiratory therapists are crucial in
managing ventilated patients, and their expertise should be utilized extensively.
[44] Finally, only one dedicated professional should be in charge of the ventilator,
and vent changes should not be made without communication with others in
charge of the patient. [Level 3]

Review Questions

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Comment on this article.

Figure

Figure 1. APRV Pressure cycles with superimposed

Spontaneous Breathing Airway pressure release
ventilation is a form of continuous positive airway
pressure (CPAP). The Phigh is equivalent to a CPAP
level; Thigh is the duration of Phigh. The CPAP
phase (more...)

Figure

Figure 2. Tidal Volume during APRV vs

Conventional Ventilation Ventilation during airway
pressure release ventilation is augmented by
release volumes and is associated with decreasing
airway pressure and lung distension. Conversely,
tidal volumes during (more...)

Figure

Figure 3: Depiction of a Peak Expiratory Flow Curve

A patient with a lung that initially has low
compliance has a steeper expiratory flow curve
(30°) and will require a short release phase (TLow)
(0.3 s in this example) to terminate the expiratory
(more...)

References
1. Gong Y, Sankari A. StatPearls [Internet]. StatPearls Publishing; Treasure Island
(FL): Dec 11, 2022. Noninvasive Ventilation. [PubMed: 35201716]
2. Pham T, Brochard LJ, Slutsky AS. Mechanical Ventilation: State of the Art.
Mayo Clin Proc. 2017 Sep;92(9):1382-1400. [PubMed: 28870355]
3. Farkas A, Lynch MJ, Westover R, Giles J, Siripong N, Nalatwad A, Pizon AF,
Martin-Gill C. Pulmonary Complications of Opioid Overdose Treated With
Naloxone. Ann Emerg Med. 2020 Jan;75(1):39-48. [PubMed: 31182316]
4. Jablonski R, Bhorade S, Strek ME, Dematte J. Recognition and Management of
Myositis-Associated Rapidly Progressive Interstitial Lung Disease. Chest. 2020
Jul;158(1):252-263. [PubMed: 32059958]
5. Neumann B, Angstwurm K, Mergenthaler P, Kohler S, Schönenberger S, Bösel
J, Neumann U, Vidal A, Huttner HB, Gerner ST, Thieme A, Steinbrecher A,
Dunkel J, Roth C, Schneider H, Schimmel E, Fuhrer H, Fahrendorf C, Alberty A,
Zinke J, Meisel A, Dohmen C, Stetefeld HR., German Myasthenic Crisis Study
Group. Myasthenic crisis demanding mechanical ventilation: A multicenter
analysis of 250 cases. Neurology. 2020 Jan 21;94(3):e299-e313. [PubMed:
31801833]
6. Jung B, Martinez M, Claessens YE, Darmon M, Klouche K, Lautrette A, Levraut
J, Maury E, Oberlin M, Terzi N, Viglino D, Yordanov Y, Claret PG, Bigé N.,
Société de Réanimation de Langue Française (SRLF). Société Française de
Médecine d’Urgence (SFMU). Diagnosis and management of metabolic
acidosis: guidelines from a French expert panel. Ann Intensive Care. 2019 Aug
15;9(1):92. [PMC free article: PMC6695455] [PubMed: 31418093]
7. Cronin JN, Camporota L, Formenti F. Mechanical ventilation in COVID-19: A
physiological perspective. Exp Physiol. 2022 Jul;107(7):683-693. [PMC free
article: PMC8667647] [PubMed: 34541721]
8. Hallett S, Toro F, Ashurst JV. StatPearls [Internet]. StatPearls Publishing;
Treasure Island (FL): May 1, 2023. Physiology, Tidal Volume. [PubMed:
29494108]
9. Spiegel R, Hockstein M. Airway Pressure Release Ventilation: A Field Guide for
the Emergency Physician. Emerg Med Clin North Am. 2022 Aug;40(3):489-501.
[PubMed: 35953213]
10. Mireles-Cabodevila E, Hatipoğlu U, Chatburn RL. A rational framework for
selecting modes of ventilation. Respir Care. 2013 Feb;58(2):348-66. [PubMed:
22710796]
11. Chang HC, Ho CH, Kung SC, Chen WL, Wang CM, Cheng KC, Liu WL, Hsu HS.
Maintenance of low driving pressure in patients with early acute respiratory
distress syndrome significantly affects outcomes. Respir Res. 2021 Dec
15;22(1):313. [PMC free article: PMC8672606] [PubMed: 34911557]
12. Laffey JG, O'Croinin D, McLoughlin P, Kavanagh BP. Permissive hypercapnia--
role in protective lung ventilatory strategies. Intensive Care Med. 2004
Mar;30(3):347-56. [PubMed: 14722644]
13. Girardis M, Busani S, Damiani E, Donati A, Rinaldi L, Marudi A, Morelli A,
Antonelli M, Singer M. Effect of Conservative vs Conventional Oxygen
Therapy on Mortality Among Patients in an Intensive Care Unit: The Oxygen-
ICU Randomized Clinical Trial. JAMA. 2016 Oct 18;316(15):1583-1589.
[PubMed: 27706466]
14. Palmer E, Post B, Klapaukh R, Marra G, MacCallum NS, Brealey D, Ercole A,
Jones A, Ashworth S, Watkinson P, Beale R, Brett SJ, Young JD, Black C, Rashan
A, Martin D, Singer M, Harris S. The Association between Supraphysiologic
Arterial Oxygen Levels and Mortality in Critically Ill Patients. A Multicenter
Observational Cohort Study. Am J Respir Crit Care Med. 2019 Dec 01;200(11):1373-
1380. [PMC free article: PMC6884048] [PubMed: 31513754]
15. Krebs J, Pelosi P, Rocco PRM, Hagmann M, Luecke T. Positive end-expiratory
pressure titrated according to respiratory system mechanics or to
ARDSNetwork table did not guarantee positive end-expiratory
transpulmonary pressure in acute respiratory distress syndrome. J Crit Care.
2018 Dec;48:433-442. [PubMed: 30336419]
16. Fredericks AS, Bunker MP, Gliga LA, Ebeling CG, Ringqvist JR, Heravi H,
Manley J, Valladares J, Romito BT. Airway Pressure Release Ventilation: A
Review of the Evidence, Theoretical Benefits, and Alternative Titration
Strategies. Clin Med Insights Circ Respir Pulm Med.
2020;14:1179548420903297. [PMC free article: PMC7003159] [PubMed:
32076372]
17. Habashi NM. Other approaches to open-lung ventilation: airway pressure
release ventilation. Crit Care Med. 2005 Mar;33(3 Suppl):S228-40. [PubMed:
15753733]
18. Zhou Y, Jin X, Lv Y, Wang P, Yang Y, Liang G, Wang B, Kang Y. Early
application of airway pressure release ventilation may reduce the duration
of mechanical ventilation in acute respiratory distress syndrome. Intensive
Care Med. 2017 Nov;43(11):1648-1659. [PMC free article: PMC5633625]
[PubMed: 28936695]
19. Kollisch-Singule M, Andrews P, Satalin J, Gatto LA, Nieman GF, Habashi NM.
The time-controlled adaptive ventilation protocol: mechanistic approach to
reducing ventilator-induced lung injury. Eur Respir Rev. 2019 Jun 30;28(152)
[PMC free article: PMC9488504] [PubMed: 30996041]
20. Fuller BM, Mohr NM, Ablordeppey E, Roman O, Mittauer D, Yan Y, Kollef MH,
Carpenter CR, Roberts BW. The Practice Change and Clinical Impact of Lung-
Protective Ventilation Initiated in the Emergency Department: A Secondary
Analysis of Individual Patient-Level Data From Prior Clinical Trials and
Cohort Studies. Crit Care Med. 2023 Feb 01;51(2):279-290. [PubMed: 36374044]
21. Weinberger J, Cocoros N, Klompas M. Ventilator-Associated Events:
Epidemiology, Risk Factors, and Prevention. Infect Dis Clin North Am. 2021
Dec;35(4):871-899. [PubMed: 34752224]
22. Klompas M. Ventilator-Associated Events: What They Are and What They Are
Not. Respir Care. 2019 Aug;64(8):953-961. [PubMed: 31346070]
23. Qi W, Murphy TE, Doyle MM, Ferrante LE. Association Between Daily Average
of Mobility Achieved During Physical Therapy Sessions and Hospital-
Acquired or Ventilator-Associated Pneumonia among Critically Ill Patients. J
Intensive Care Med. 2023 May;38(5):418-424. [PMC free article:
PMC10065937] [PubMed: 36278257]
24. Hassan EA, Elsaman SEA. Relationship between ventilator bundle
compliance and the occurrence of ventilator-associated events: a prospective
cohort study. BMC Nurs. 2022 Aug 01;21(1):207. [PMC free article:
PMC9341085] [PubMed: 35915444]
25. Grübler MR, Wigger O, Berger D, Blöchlinger S. Basic concepts of heart-lung
interactions during mechanical ventilation. Swiss Med Wkly.
2017;147:w14491. [PubMed: 28944931]
26. 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. N Engl J Med. 2000 May
04;342(18):1301-8. [PubMed: 10793162]
27. Sutherasan Y, Vargas M, Pelosi P. Protective mechanical ventilation in the
non-injured lung: review and meta-analysis. Crit Care. 2014 Mar 18;18(2):211.
[PMC free article: PMC4056601] [PubMed: 24762100]
28. Brower RG, Lanken PN, MacIntyre N, Matthay MA, Morris A, Ancukiewicz M,
Schoenfeld D, Thompson BT., National Heart, Lung, and Blood Institute ARDS
Clinical Trials Network. Higher versus lower positive end-expiratory
pressures in patients with the acute respiratory distress syndrome. N Engl J
Med. 2004 Jul 22;351(4):327-36. [PubMed: 15269312]
29. Needham DM, Colantuoni E, Mendez-Tellez PA, Dinglas VD, Sevransky JE,
Dennison Himmelfarb CR, Desai SV, Shanholtz C, Brower RG, Pronovost PJ.
Lung protective mechanical ventilation and two year survival in patients
with acute lung injury: prospective cohort study. BMJ. 2012 Apr 05;344:e2124.
[PMC free article: PMC3320566] [PubMed: 22491953]
30. Weingart SD. Managing Initial Mechanical Ventilation in the Emergency
Department. Ann Emerg Med. 2016 Nov;68(5):614-617. [PubMed: 27289336]
31. 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):529-41. [PubMed: 26014437]
32. Amato MB, Meade MO, Slutsky AS, Brochard L, Costa EL, Schoenfeld DA,
Stewart TE, Briel M, Talmor D, Mercat A, Richard JC, Carvalho CR, Brower RG.
Driving pressure and survival in the acute respiratory distress syndrome. N
Engl J Med. 2015 Feb 19;372(8):747-55. [PubMed: 25693014]
33. Fuchs H, Rossmann N, Schmid MB, Hoenig M, Thome U, Mayer B, Klotz D,
Hummler HD. Permissive hypercapnia for severe acute respiratory distress
syndrome in immunocompromised children: A single center experience.
PLoS One. 2017;12(6):e0179974. [PMC free article: PMC5478142] [PubMed:
28632754]
34. Writing Group for the Alveolar Recruitment for Acute Respiratory Distress
Syndrome Trial (ART) Investigators. Cavalcanti AB, Suzumura ÉA, Laranjeira
LN, Paisani DM, Damiani LP, Guimarães HP, Romano ER, Regenga MM,
Taniguchi LNT, Teixeira C, Pinheiro de Oliveira R, Machado FR, Diaz-Quijano
FA, Filho MSA, Maia IS, Caser EB, Filho WO, Borges MC, Martins PA, Matsui M,
Ospina-Tascón GA, Giancursi TS, Giraldo-Ramirez ND, Vieira SRR, Assef
MDGPL, Hasan MS, Szczeklik W, Rios F, Amato MBP, Berwanger O, Ribeiro de
Carvalho CR. Effect of Lung Recruitment and Titrated Positive End-
Expiratory Pressure (PEEP) vs Low PEEP on Mortality in Patients With Acute
Respiratory Distress Syndrome: A Randomized Clinical Trial. JAMA. 2017 Oct
10;318(14):1335-1345. [PMC free article: PMC5710484] [PubMed: 28973363]
35. Writing Group for the PReVENT Investigators. Simonis FD, Serpa Neto A,
Binnekade JM, Braber A, Bruin KCM, Determann RM, Goekoop GJ, Heidt J,
Horn J, Innemee G, de Jonge E, Juffermans NP, Spronk PE, Steuten LM,
Tuinman PR, de Wilde RBP, Vriends M, Gama de Abreu M, Pelosi P, Schultz
MJ. Effect of a Low vs Intermediate Tidal Volume Strategy on Ventilator-Free Days
in Intensive Care Unit Patients Without ARDS: A Randomized Clinical Trial. JAMA.
2018 Nov 13;320(18):1872-1880. [PMC free article: PMC6248136] [PubMed:
30357256]
36. Barr J, Fraser GL, Puntillo K, Ely EW, Gélinas C, Dasta JF, Davidson JE, Devlin
JW, Kress JP, Joffe AM, Coursin DB, Herr DL, Tung A, Robinson BR, Fontaine
DK, Ramsay MA, Riker RR, Sessler CN, Pun B, Skrobik Y, Jaeschke R.,
American College of Critical Care Medicine. 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. [PubMed:
23269131]
37. Devlin JW, Skrobik Y, Gélinas C, Needham DM, Slooter AJC, Pandharipande
PP, Watson PL, Weinhouse GL, Nunnally ME, Rochwerg B, Balas MC, van den
Boogaard M, Bosma KJ, Brummel NE, Chanques G, Denehy L, Drouot X,
Fraser GL, Harris JE, Joffe AM, Kho ME, Kress JP, Lanphere JA, McKinley S,
Neufeld KJ, Pisani MA, Payen JF, Pun BT, Puntillo KA, Riker RR, Robinson
BRH, Shehabi Y, Szumita PM, Winkelman C, Centofanti JE, Price C, Nikayin S,
Misak CJ, Flood PD, Kiedrowski K, Alhazzani W. Clinical Practice Guidelines
for the Prevention and Management of Pain, Agitation/Sedation, Delirium,
Immobility, and Sleep Disruption in Adult Patients in the ICU. Crit Care Med.
2018 Sep;46(9):e825-e873. [PubMed: 30113379]
38. Wang L, Li X, Yang Z, Tang X, Yuan Q, Deng L, Sun X. Semi-recumbent
position versus supine position for the prevention of ventilator-associated
pneumonia in adults requiring mechanical ventilation. Cochrane Database
Syst Rev. 2016 Jan 08;2016(1):CD009946. [PMC free article: PMC7016937]
[PubMed: 26743945]
39. Tran A, Fernando SM, Rochwerg B, Cook DJ, Crowther MA, Fowler RA,
Alhazzani W, Siegal DM, Castellucci LA, Zarychanski R, English SW,
Kyeremanteng K, Carrier M. Prognostic Factors Associated With
Development of Venous Thromboembolism in Critically Ill Patients-A
Systematic Review and Meta-Analysis. Crit Care Med. 2022 Apr 01;50(4):e370-
e381. [PubMed: 34636806]
40. Krag M, Perner A, Wetterslev J, Wise MP, Borthwick M, Bendel S, McArthur C,
Cook D, Nielsen N, Pelosi P, Keus F, Guttormsen AB, Moller AD, Møller MH.,
SUP-ICU co-authors. Prevalence and outcome of gastrointestinal bleeding and
use of acid suppressants in acutely ill adult intensive care patients. Intensive
Care Med. 2015 May;41(5):833-45. [PubMed: 25860444]
41. Cook DJ, Fuller HD, Guyatt GH, Marshall JC, Leasa D, Hall R, Winton TL,
Rutledge F, Todd TJ, Roy P. Risk factors for gastrointestinal bleeding in
critically ill patients. Canadian Critical Care Trials Group. N Engl J Med. 1994
Feb 10;330(6):377-81. [PubMed: 8284001]
42. Alhazzani W, Alshamsi F, Belley-Cote E, Heels-Ansdell D, Brignardello-
Petersen R, Alquraini M, Perner A, Møller MH, Krag M, Almenawer S,
Rochwerg B, Dionne J, Jaeschke R, Alshahrani M, Deane A, Perri D, Thebane
L, Al-Omari A, Finfer S, Cook D, Guyatt G. Efficacy and safety of stress ulcer
prophylaxis in critically ill patients: a network meta-analysis of randomized
trials. Intensive Care Med. 2018 Jan;44(1):1-11. [PMC free article:
PMC5770505] [PubMed: 29199388]
43. Cook D, Guyatt G. Prophylaxis against Upper Gastrointestinal Bleeding in
Hospitalized Patients. N Engl J Med. 2018 Jun 28;378(26):2506-2516. [PubMed:
29949497]
44. Kollef MH. Evaluating the Value of the Respiratory Therapist: Where Is the
Evidence? Focus on the Barnes-Jewish Hospital Experience. Respir Care. 2017
Dec;62(12):1602-1610. [PubMed: 29162728]
Disclosure: Sean Hickey declares no relevant financial relationships with ineligible companies.

Disclosure: Al Giwa declares no relevant financial relationships with ineligible companies.

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