INTENSIVE CARE
Ventilatory support in the
intensive care unit
Xavier John Frawley
Sarah Ann Yong
Abstract
Mechanical ventilation is a crucial supportive intervention that allows
time to facilitate investigations and provide definitive treatment in crit-
ically unwell patients. This article focuses on the various modes of res-
piratory support available, and the mechanical ventilation strategies
used in specific disease processes. It also highlights the possible
complications associated with mechanical ventilation and the adjuncts
that can be used to aid oxygenation.
Keywords COVID-19; lung-protective ventilation; mechanical venti-
lation; non-invasive ventilation; patient-ventilator dyssynchrony;
weaning
Royal College of Anaesthetists CPD Skills Framework: ICM and Emergency
Management; airway resuscitation
Overview of mechanical ventilation
Mechanical ventilation is a crucial supportive treatment for critically
unwell patients in the intensive care unit (ICU). Invasive mechanical
ventilation is initiated to decrease the work of breathing and improve
gas exchange in patients with respiratory failure as well as ensure a
secure airway when airway compromise is a risk. It also allows time to
facilitate investigations and provide definitive treatment in critically
unwell patients (see Box 1).
Modern mechanical ventilation is the delivery of positive
pressure into the patient during inspiration and allowing passive
expiration to occur from the alveoli back to the central airways.
This mechanism is the opposite to physiological breathing,
where inspiration occurs via negative pressure, and thus there
are several important considerations and complications to factor
in when initiating mechanical ventilation.
A simplistic schematic of a mechanically ventilated lung can
be considered as a balloon on a tube connected to a ventilator,
with the tube being the ventilator tubing, the endotracheal tube
(ETT) and the major airways, and the balloon representing the
alveoli. For gas flow and ventilation to occur there must be a
pressure differential, created by the positive pressure generated
by the machine, which must also overcome the resistance of the
circuit. For effective ventilation the ideal ventilator would have
the following characteristics:
Xavier John Frawley MD BSc is a Registrar in Intensive Care at the
Alfred Hospital, Melbourne, Australia. Conflicts of interest: none.
Sarah Ann Yong MBBS(Hons) FCICM FRACP MClinEd is a Consultant in
Intensive Care at the Alfred Hospital, Melbourne, Australia. Conflicts
of interest: none.
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Learning objectives
After reading this article you should be able to:
C describe the basic modes of ventilation and the differences be-
tween them
C explain the various forms of patient-ventilator dyssynchrony
C describe the various complications associated with mechanical
ventilation
C describe common adjuncts to mechanical ventilation and their
rationale
 a leak-proof connection between ventilator and patient
 a signal to initiate inspiration synchronized with the
patient
 ability to regulate the amount of air provided during
inspirator to meet the patient’s need
 a signal to terminate inspiration synchronized with the
patient
 a regulated pressurized air/oxygen blender.
The ventilator mode is the first key setting, an in-depth dis-
cussion of ventilator modes will follow. Depending on the
ventilator mode, selected several parameters and variables are
set to determine gas exchange. These include:
 FiO 2 e Fraction of inspired oxygen of the inhaled gas
being delivered to the patient. In general, the lowest
FiO 2 necessary to meet the target SpO 2 (target SpO 2 92
e96% in the majority of patients, may be lower e.g. 88
e92% for chronic CO 2 retainers) should be used.
Prolonged exposure to high concentrations of oxygen
(FiO 2 >0.5) increases the risk of adverse consequences
of hyperoxia including absorption atelectasis, wors-
ening hypercapnia, airway and parenchymal injury.
However, there is no evidence that brief exposure to
high concentrations is harmful.
 Positive end-expiratory pressure (PEEP) is the airway
pressure at the end of expiration. On a ventilator, PEEP
is applied to prevent alveolar collapse that occurs at
the end of expiration. The effect of this is to increase
functional residual capacity which minimises shunt
and improves oxygenation. The ideal level of PEEP is
one that recruits the maximal number of alveoli, whilst
not causing over distension of the alveoli. A typical
initial applied PEEP is 5 cmH 2 O; however, this may be
titrated according to FiO 2 , underlying pathology,
patient-specific factors (e.g. compliance) or indication
for mechanical ventilation.
 Inspiratory pressure and pressure support e In pressure-
controlled and supported modes the inspiratory pressure
or pressure support respectively, must be set and adjusted
to achieve an adequate tidal volume. The tidal volume
delivered will vary depending on lung compliance, airway
resistance and resistance in the ventilator circuit. This
pressure is generally set as either a pressure above PEEP,
or an upper ‘high’ pressure. In general, plateau airway
pressures should be below 25e30 cmH2O to minimize the
risk of barotrauma.
1 Ó 2022 Published by Elsevier Ltd.
 INTENSIVE CARE
Indications for mechanical ventilation
C Airway protection
C Treat or prevent airway obstruction
C Respiratory failure (hypoxic or hypercapnic)
C Decrease work of breathing (patient fatigue/exhaustion)
C To facilitate procedures, investigation or transport
C Minimize oxygen consumption and optimize oxygen delivery
C Prevent secondary brain injury
Box 1
 Respiratory rate is generally set between 12 and 16
breaths/minute, which is in keeping with normal physio-
logical parameters. Some patients may require a lower
respiratory rate (e.g. asthma) whereas others may require
a higher respiratory rate (e.g. acute respiratory distress
syndrome (ARDS); see below for detail). The respiratory
rate determines the time each respiratory cycle takes.
 Tidal volume is the amount of gas delivered to the patient
with each breath. In volume control ventilation tidal vol-
ume is set, whereas in pressure controlled and sponta-
neous modes of ventilation the tidal volume will vary from
breath to breath. Appropriate tidal volume is essential in
minimizing the risk of ventilator associated lung injury and
whilst historically high tidal volumes were used, it is now
widely accepted that lung-protective ventilation with vol-
umes of 4e8 ml/kg of predicted body weight is the stan-
dard of care for critically ill patients. This ventilation
practice stems from the landmark ARDSNet ARMA trial
which found significant reduction in duration of mechan-
ical ventilation and hospital mortality using lower tidal
volume ventilation,1 with these results being extrapolated
to all patients in ICU.
 Inspiratory time to expiratory time (I:E) ratio e The res-
piratory cycle can be split into inspiratory time and expi-
ratory time with the I:E ratio being the ratio of the two. This
is usually set at 1:2 to reflect the normal physiological ratio
and therefore optimize patient-ventilator synchrony.
Increasing this ratio (i.e. 1:1) may result in greater
oxygenation, however this comes at the expense of a shorter
expiration time which may result in hypercapnia and gas
trapping. For patients with airway obstruction (e.g. asthma)
it may be beneficial to decrease this ratio to allow maximum
time for passive expiration and minimize gas trapping.
 Mode of triggering is the method by which the ventilator
senses when to initiate inspiration. An appropriately sensi-
tive trigger is important for patient-ventilator synchrony.
Breaths can be triggered by either the patient or the venti-
lator. In a mandatory mode of ventilation where the patient
is not triggering any breaths, a breath will be triggered at
regular time intervals determined by the respiratory rate. In
modes where the patient is triggering the breath, a change in
air flow, airway pressure or electrical activity of the dia-
phragm can be used to initiate (trigger) the inspiratory cycle
from the ventilator.
 Flow e When a patient initiates a breath, they disrupt
the continuous flow established in the circuit. A typical
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value is 2 litres/minute. This is generally a more sensi-
tive and commonly used trigger as it requires less res-
piratory effort to trigger.
 Pressure e The effort from a patient attempting to
initiate a breath decreases the pressure in the circuit,
detected by a demand valve, and once this reaches a
predetermined level it triggers a breath. A typical value is
1 to 2 cmH2O.
 Electrical activity of the diaphragm e Neurally
adjusted ventilatory assist (NAVA) is where inspiration
is triggered by electrical activity of the diaphragm that is
detected by a specialized nasogastric tube with a sensor.
Modes of ventilation
High-flow nasal prongs (HFNP)
The use of HFNP as a method of oxygen delivery has grown in
popularity in recent times, offering improved patient comfort and
oxygenation. The HFNP device delivers high-flow humidified
oxygen which can have a flow rate of up to 60 litres/minute in
adults and an FiO2 between 21% and 100%.
Benefits of HFNP include improved patient tolerance due to
soft and flexible nasal prongs, effective warming and humidifi-
cation of secretions, reduced inspiratory effort and less entrain-
ment of room air (and hence more accurate delivery of O2), both
due to the higher flow rates achieved. There is also the benefit of
a small amount of PEEP being delivered via HFNP, between
approximately 2 cmH2O up and 7 cmH2O, depending on whether
the patient’s mouth is open or closed. Finally, washout of
nasopharyngeal dead space from the delivery of oxygen at high
flows can improve ventilation efficiency and oxygen delivery by
allowing a greater proportion of minute ventilation to participate
in alveolar gas exchange.
The appropriate role of HFNP in the management of hypoxia
is not yet widely agreed upon and supported by evidence.
However, HFNP was widely used in patients with severe
coronavirus disease (COVID-19) where it significantly decreased
the need for intubation when compared to conventional low-flow
oxygen.2
Non-invasive ventilation (NIV)
NIV refers to the delivery of positive pressure ventilation through
a non-invasive interface (e.g. face mask, nasal mask or hood) to
the patient’s own physiological airway. NIV can be used for
ventilatory support for awake patients with both acute and
chronic respiratory failure as well as a useful tool in preventing
re-intubation in patients at high risk of extubation failure.
The main contraindications to NIV are listed in Box 2. If the
patient is suitable for a trial of NIV the main modes that are used
are continuous positive airway pressure (CPAP) and bilevel
positive airway pressure (BPAP, also commonly referred to by a
trade name BiPAP).
 CPAP delivers a constant amount of positive pressure
throughout spontaneous ventilation without adjustment
during inspiration or expiration. It improves oxygenation
through recruitment of alveoli which increases the func-
tional residual capacity of the lungs.
 BPAP delivers different pressure support during inspira-
tion and expiration. The inspiratory positive airway
2 Ó 2022 Published by Elsevier Ltd.
 INTENSIVE CARE
Contraindications for NIV
C Need for emergent intubation (e.g. cardiac/respiratory arrest)
C Inability to protect the airway
C Maxillofacial surgery
C Facial trauma (especially base of skull fracture which can result in
pneumocephalus)
C Untreated pneumothorax
C Significant airway obstruction
C Significant haemodynamic instability
C Patient refusal/discomfort/intolerance
C Intractable vomiting
Box 2
pressure (IPAP) is delivered above a fixed expiratory
positive airway pressure (EPAP). In this way IPAP is
responsible for providing ventilation where EPAP (similar
to PEEP) recruits collapsed alveoli.
Conditions that respond well to NIV include:
 Acute cardiogenic pulmonary oedema (APO) e NIV, in
the form of CPAP, is thought to benefit patients in APO via
a mechanism of preload reduction, prevention of end-
expiratory alveolar collapse and decreased left ventricular
afterload. Meta-analyses have demonstrated that NIV
reduced the need for intubation, improved clinical markers
of respiratory failure and improved mortality.3
 Acute exacerbations of chronic obstructive pulmonary
disease (AECOPD) e NIV, in the form of BPAP is most
beneficial for patients with an AECOPD with hypercapnic
respiratory acidosis. The mechanism by which this occurs
is through improved respiratory mechanics and gas ex-
change, resulting in improved alveolar ventilation overall.
A 2017 systematic review found that bilevel NIV is bene-
ficial as a first line treatment (along with standard care) for
reducing mortality and the need for intubation.4
 COVID-19 e NIV is an acceptable option for respiratory
support in the early management of patients with COVID-
19 who have mild to moderate respiratory failure5
Invasive mechanical ventilation
The ventilation mode used is often dictated by clinical and
institutional familiarity or preference, with each having its own
advantages and disadvantages. Notably, there is minimal
evidence to recommend one mode over another, with no statis-
tically significant difference demonstrated in mortality, oxygen-
ation, or in work of breathing between volume control and
pressure control across numerous trials.
Volume-controlled ventilation (VCV)
In volume-controlled ventilation (also referred to as volume-
limited ventilation), the operator sets a target tidal volume and
minimum respiratory rate (along with FiO2, I:E ratio and PEEP),
and the ventilator delivers a variable pressure to ensure this tidal
volume target is met. The patient is therefore guaranteed a
minimum minute ventilation. Consequently, high peak pressures
may result from poor lung compliance, increased airway resis-
tance, high tidal volume targets or a short inspiratory time.
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Breaths can be initiated by either the patient or the ventilator.
If a patient does not initiate breaths to meet the minimum set
respiratory rate, then the ventilator will initiate enough breaths
to make up the difference. For patient triggered breaths the
ventilator will ensure the set tidal volume is delivered.
Pressure-controlled ventilation (PCV)
In pressure-controlled ventilation (also referred to as pressure-
limited ventilation), the operator sets the inspiratory pressure
(rather than tidal volume as in VCV) and respiratory rate (along
with FiO2, I:E ratio and PEEP). Typically, the pressure is titrated
to achieve a targeted tidal volume. Application of constant
pressure results in higher initial flow through the circuit which
falls to PEEP level by the end of inspiration.
The main disadvantage of PCV is the variability in tidal vol-
ume. If there is a decrease in compliance or increase in airway
resistance, the tidal volume and minute ventilation will fall. As
with VCV, breaths can be initiated by either the patient or the
ventilator (see Figure 1).
Synchronized intermittent mandatory ventilation (SIMV)
In SIMV, a set number of ventilator breaths are synchronized with
patient spontaneous breathing, such that the ventilator will delay
its machine-given breath if detecting patient effort, thus avoiding
delivering a breath while the patient is exhaling. These ventilator
breaths are usually volume-controlled, guaranteeing a minimum
minute ventilation. Patients can take additional breaths, which are
augmented with pressure support (PS), set by the operator. This
mode generally allows for better patient-ventilator synchrony.
Pressure support ventilation (PSV)
Pressure support ventilation is a spontaneous mode of ventilation
where the operator selects the inspiratory pressure (pressure
support) along with the PEEP and FiO2. This inspiratory pressure is
delivered in addition to the patient’s respiratory effort on each
breath. As the patient has control over the respiratory rate and
inspiratory flow, the tidal volume and minute ventilation will vary.
As this mode relies on patient-initiated breathing it is not
suitable for patients who require high levels of respiratory
Different forms of patient-ventilator dyssynchrony
a b
Flow/(l/min) Flow/(l/min)
Paw/(cmH2O)
Paw/(cmH2O)
Peos/(cmH2O)
Peos/(cmH2O)
c d
Flow/(l/min) Flow/(l/min)
Paw/(cmH2O) Paw/(cmH2O)
Pdi/(H2O)
Peos/(cmH2O)
Figure 1 Pressure versus volume control ventilation.
3 Ó 2022 Published by Elsevier Ltd.
 INTENSIVE CARE
support or those who are unable to initiate breaths (i.e. paralysed
or heavily sedated). It is also an unsafe mode for patients where
it is important to control the alveolar pressures (e.g. ARDS) and
can result in lung injury in these patients. If a patient does not
initiate a breath no support is given, although most ventilators
will automatically switch into a back-up mandatory mode of
ventilation after a set period of apnoea, e.g. 10e15 seconds.
Tube compensation
Some ventilators include a mode known as automatic tube
compensation. This is a type of PSV mode that calculates the
amount of pressure support needed to overcome the ventilator
circuit and ETT and varies the pressure support delivered breath
to breath to account for this.
Ventilation strategies
It is important to keep in mind that mechanical ventilation is not
a treatment for any disease, it is a supportive therapy that allows
time for definitive treatment and physiological recovery to occur.
However, there are certain strategies that can be employed for
certain disease pathologies.
Two important manoeuvres that can be performed on a stable
mechanically ventilated patient that give important information
that can help guide the ventilation strategy are inspiratory and
expiratory holds. These are ideally measured in the sedated and
paralysed patient ventilated in a mandatory mode.
 An inspiratory hold manoeuvre is used to determine lung
compliance (the measure of the change in volume of the
lung for a given pressure) and resistance in a respiratory
system. The inspiratory hold gives a plateau pressure of
the lungs which allows compliance to be calculated (VT/
[Pplat-PEEP]), a normal value in a mechanically ventilated
patient is in the range 50e100 ml/cm H2O. In restrictive
lung disease such as pulmonary fibrosis, there is a
decrease in compliance. In obstructive lung disease such as
emphysema there is increased compliance, peak airway
pressures can be high due to increased airway resistance
however plateau pressures are usually low to normal.
 An expiratory hold is achieved by a circuit occlusion for 3
e5 seconds at the end of expiration, allowing alveolar
pressure to equilibrate with airway pressure. This
manoeuvre is used to measure a patient’s intrinsic PEEP
(also referred to as autoPEEP). Intrinsic PEEP is important
to monitor during mechanical ventilation, as it can lead to
a number of sequelae including reduced cardiac output
and potential hypotension (due to raised intrathoracic
pressure), alveolar overdistension (and hence barotrauma
and ventilator-induced lung injury (VILI)) and hypoxaemia
(due to increased V/Q mismatch).
Disease-specific ventilation strategies
ARDS e See article on ARDS on pages 000e000 of this edition.
ARDS is a syndrome of inflammatory lung injury leading to
decreased lung compliance, loss of aerated lung tissue and acute
hypoxia. It is a diagnosis of exclusion, and is not a specific dis-
ease in itself, but rather is associated with a heterogeneous mix
of aetiologies. The severity of ARDS is characterized by PF ratio
(PaO2/FiO2 on a minimum of 5 cmH2O of PEEP), mild being a
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ratio of 200e300, moderate 100e200 and severe a ratio of less
than 100.6 Worsening PF ratio has been shown to correlate with
increased mortality.
Much of the ventilatory management of ARDS (and ventila-
tion principles generally) is based on the result of the landmark
ARMA Trial. The principles of ventilating a patient with ARDS
are lung-protective ventilation with low tidal volumes and safe
plateau (Pplat) and driving pressures, and an open lung strategy
with sufficient PEEP. Specifically, this strategy involves ventila-
tion in a controlled mode with tidal volumes of 4e8 ml/kg (based
on predicted body weight), whilst aiming for a plateau pressure
less than 30 cmH2O and a driving pressure (Pplat - PEEP) less
than 14. A degree of permissive hypercapnoea (such that pH
remains >7.2) is tolerated to minimize overdistention and risk of
VILI. Higher PEEP minimizes alveolar de-recruitment and should
be optimized in ARDS; one strategy includes the ARDSnet tables
which up-titrates PEEP in the setting of increased FiO2.
COVID-19: many of the strategies for managing ventilation with
COVID-19 are similar to ARDS, particularly protective lung
ventilation, however research suggests that these patients often
require prolonged periods of mechanical ventilation which brings
in additional challenges. In many cases these patients fail tradi-
tional low tidal volume ventilation and require adjunctive treat-
ment such as prone positioning, inhaled pulmonary vasodilators,
prolonged periods of neuromuscular blockade and at times, pe-
riods of extracorporeal membrane oxygenation.
Airflow obstruction: Ventilation of patients with obstructive
lung diseases such as asthma or chronic obstructive pulmonary
disease (COPD) presents a unique set of challenges. Complica-
tions of dynamic hyperinflation and barotrauma can precipitate
cardiovascular collapse, and thus ventilation strategies need to
reflect these challenges.
Airways obstruction and gas trapping can lead to dynamic
hyperinflation, where increasing levels of intrinsic PEEP leads to
raised intrathoracic pressure, reduced venous return and cardiac
output and potential haemodynamic collapse. Gas trapping can
be identified a number of ways via the ventilator: persistent end-
expiratory flow, presence of intrinsic PEEP (measured by expi-
ratory hold manoeuvre), an obstructive expiratory curve wave-
form (such as a deep concave curve in lower airways
obstruction) or, most accurately, measuring percentage volume
expired within the first 1 second of expiration (normal >80%,
<80% suggests obstruction). In patients with airflow obstruction
if the respiratory rate is too high there may not be sufficient
expiratory time to complete exhalation before the initiation of the
next breath, which leads to increasing gas trapping at the end of
expiration. To minimize the risk of dynamic hyperinflation, the
expiration time can be prolonged which maximizes passive
expiration. The respiratory rate and/or tidal volume can also be
reduced to minimize minute ventilation as well as treating any
underlying bronchospasm.
Similarly, intrinsic PEEP can also cause alveolar over-
distension, leading to pulmonary barotrauma, VILI and also
hypoxaemia if V/Q mismatch increases from compression of
pulmonary vasculature. Barotrauma and VILI are discussed in
further detail below.
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 INTENSIVE CARE

In asthma the major problem is high large airway resistance
(despite relatively normal lung compliance), resulting in high
airway pressures and risk of dynamic hyperinflation from gas
trapping. If traditional ventilator settings are applied, much of the
inspiratory pressure from the ventilator will be dissipated across
the airways rather than the alveoli. Rather than peak airway
pressure alone, alveoli pressure is the important value in regards
to potential damage. For this reason, plateau pressure is a more
relevant value to monitor (measured by an inspiratory hold
manoeuvre). Patients requiring mechanical ventilation for exac-
erbation of asthma have increased hospital mortality compared
with those who do not require invasive ventilation.7
The principles of ventilating COPD patients are similar to that
of asthma although the degree of bronchospasm (and thus
airway resistance) is usually less. These patients tend to have
additional comorbidities and are often intubated because of
worsening respiratory muscle fatigue causing progressive respi-
ratory failure and can therefore be difficult to wean from venti-
lation. Mechanical ventilation for acute respiratory failure in
patients with COPD is associated with high ICU mortality.8
Patient-ventilator dyssynchrony
Patient-ventilator dyssynchrony (PVD) is a common complica-
tion of mechanical ventilation that arises when the patient’s
respiratory demands are not met by the ventilation provided.
Dyssynchrony can occur from problems with timing of inspira-
tion, duration of inspiration, mismatch of flow between demand
and supply and the timing of switching to expiration. This

Examples of patient–ventilator dyssynchrony

Pressure

Flow

Volume

b
Pressure trigger
Pressure

Flow trigger
Flow

Volume

Pressure

Flow

Volume

Examples of different forms of dyssynchrony. (a) Wasted effort where ventilator is in a

mandatory mode and patient is trying to trigger. (b) Wasted effort where trigger is too high.
(c) Auto-triggering.

Figure 2

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 INTENSIVE CARE
mismatch between patient and ventilator causes an increase in
the patient’s work of breathing, inefficient oxygenation and
ventilation. This can lead to lung injury from excessive tidal
volumes and eccentric diaphragmatic contractions. Minimizing
PVD is critically important, as it increases the duration of me-
chanical ventilation and is associated with higher ICU mortality
and higher overall hospital mortality9 (see Figure 2).
The main causes of dyssynchrony are:
 Wasted patient effort can occur under several circum-
stances: 1) Ventilator is in a mandatory mode and the patient
wants to trigger but cannot. Patient effort is wasted when the
patient strains to inhale against a closed inspiratory valve
(that does not trigger a breath), strains to exhale against a
closed expiratory valve (when the patient is trying to
terminate a breath), or when they are trying to inhale more
gas (midway through a mandatory breath) than the venti-
lator is willing to deliver. To mitigate this, either change to a
patient-triggered mode of ventilation (such as PSV) or
establishing a deeper level of sedation. 2) Wasted effort
when the trigger is set too high in a spontaneous mode and
the ventilator does not provide a breath when the patient
demands it. The solution is to lower the trigger setting or
sedate the patient to allow ventilation in a mandatory mode.
3) Wasted effort due to excessive intrinsic PEEP, which the
patient is unable to overcome, thus making it harder to
trigger a breath. This occurs in states of significant airflow
limitation such as severe asthma or COPD. The solution is to
apply extrinsic PEEP to a value of 80% of intrinsic PEEP,
minimizing the pressure gradient between the patient and
circuit and reducing work of breathing. This needs ongoing
monitoring to avoid exacerbating gas trapping and high
inspiratory pressures due to excessive extrinsic PEEP.
 Auto-triggering occurs where non-respiratory effort trig-
gers a ventilator-initiated breath (e.g. cardiac oscillations,
hiccups, circuit leak). Increasing the trigger to a higher
setting usually fixes this.
 Double triggering is a form of dyssynchrony where the
ventilator is not meeting the patient’s need in terms of tidal
volume, so the patient inspires again as the ventilator is
wanting to cycle to expiration. Two forms of double trig-
gering are flow starvation and volume starvation, both
typically occurring in volume control ventilation. Solutions
include switching to a pressure control mode, increasing
respiratory rate or increasing sedation to obtain more
control of the patient’s ventilation.
 Reverse triggering is a form of dyssynchrony whereby the
mandatory ventilator breath causes the patient’s respiratory
muscles to contract, triggering patient inspiration or a
‘double breath’. Thus, the patient’s respiratory rate appears
to track the ventilator set rate. This is a result of the head
reflex, a lung stretch trigger, occurring in an obtunded pa-
tient. Management usually involves reducing sedation to
allow change to a spontaneous ventilation mode.
Complications
Whilst mechanical ventilation is often a life-saving intervention,
it is associated with several significant yet potentially prevent-
able complications.
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Ventilator induced lung injury
VILI is a major complication of mechanical ventilation and can
be caused by barotrauma (high lung inflating pressure), volu-
trauma (alveolar overdistension), atelectrauma (high shear
forces that open and close recruitable atelectatic lung units) and
biotrauma (activation of adverse inflammatory responses sec-
ondary to mechanical injury to the lungs). The clinical presen-
tation of VILI is similar to that of ARDS, with worsening
hypoxaemia and increasing tachypnoea and tachycardia.
There is no established, ideal ventilation strategy which re-
duces the incidence of VILI. Lung-protective ventilation, dis-
cussed earlier, is considered the cornerstone of minimizing the
risk of VILI. PEEP is also important in reducing damage caused
by atelectrauma. In the case of severe lung damage adjunct
therapy, discussed later, may be required.
Ventilator-associated pneumonia (VAP)
VAP is a common ICU complication that is a subset of hospital
acquired pneumonia, developing in patients who have been
intubated and ventilated for greater than 48 hours. VAP is
suspected in patients with new or progressive pulmonary in-
filtrates on chest imaging plus clinical features of infection
such as fever, purulent sputum or leukocytosis. The diagnosis
is confirmed when lower respiratory tract microbiological
sampling identifies a pathogen, with the appropriate accom-
panying clinical context.
The proposed mechanisms for the development of VAP include
microaspiration of oropharyngeal secretions and contamination of
endogenous flora, in the context of a critically unwell host with
diminished defences. VAP has an attributable mortality of 13%,
which is primarily caused by increasing the length of ICU stay.10
Numerous measures to prevent VAP have been recommended,
including minimizing aspiration (head of bed elevation, subglottic
drainage), decontamination of the oropharynx and digestive tract,
maintaining ventilator circuits, minimizing sedation, imple-
mentation of weaning protocols and importantly, early discon-
tinuation of mechanical ventilation.
Ventilator-induced diaphragmatic dysfunction (VIDD)
Diaphragmatic atrophy and contractile dysfunction occurs
rapidly with mechanical ventilation, within as little as 18 hours
post-initiation. Underlying pathophysiologic mechanisms include
oxidative stress, activation of proteolytic pathways, decreased
protein synthesis and mitochondrial dysfunction within the dia-
phragm. VIDD is associated with prolonged mechanical ventila-
tion, difficulty weaning, increased ICU length of stay and higher
risk of complications.11 Prevention and management of VIDD
complication remains a challenge, with no single intervention
associated with improved clinically significant outcomes.
Haemodynamic instability
There are several mechanisms through which positive pressure
ventilation can lead to reduced cardiac output and haemody-
namic instability. Firstly, positive pressure ventilation increases
intrathoracic pressure, resulting in decreased venous return; this
effect is also accentuated by PEEP (intrinsic or extrinsic) or
hypovolaemia. Secondly, alveolar inflation compresses pulmo-
nary vasculature, increasing pulmonary vascular resistance and
reducing right ventricular output. Increased pulmonary vascular
6 Ó 2022 Published by Elsevier Ltd.
 INTENSIVE CARE
resistance can also shift the interventricular septum to the left,
which impairs left ventricular diastolic filling, leading to reduced
left ventricular output.
In contrast, positive pressure ventilation may be beneficial for
the left ventricle (LV), as the increased intrathoracic pressure
results in decreased LV transmural pressure and therefore
decreased LV afterload, leading to improved LV wall stress, ox-
ygen consumption and overall LV function. The degree to which
these haemodynamic effects occur varies depending on chest
wall and lung compliance, where transmission of airway pres-
sure is greatest when there is low chest wall compliance (e.g.
fibrothorax) or high lung compliance (e.g. emphysema). It is also
important to note that to initiate mechanical ventilation the pa-
tient is often paralysed and sedated to facilitate intubation and
this can compound hypotension via systemic vasodilation.
Liberation from mechanical ventilation
Although invasive ventilation is an essential medical interven-
tion in the context of critical illness, it comes with various serious
complications, and as such liberating a patient from the venti-
lator as early as possible is crucial. This process involves
assessment for readiness, weaning and extubation.
Readiness testing should be considered once the under-
lying indication for mechanical ventilation has improved
enough for the patient to sustain spontaneous ventilation.
Box 3 outlines general assessment criteria to determine
readiness for extubation.
Following this, the specific practices of weaning from ventila-
tion varies between clinicians and facilities. In general, any patient
who has been intubated and ventilated for a period greater than 24
hours should undergo a daily spontaneous breathing trial. This
involves a period of at least 30 minutes on ‘minimal ventilator
settings’, minimal PEEP and pressure support, sufficient to over-
come the work of breathing associated with the circuit.
Weaning failure means failure to pass a spontaneous breath-
ing trial or requiring reintubation with 48 hours of extubation.
Although the majority of patients are able to be weaned off
mechanical ventilation, some patients require a prolonged period
of ventilation and may fail spontaneous breathing trials, which
has been associated with increased mortality.
Some characteristics that are predictive of weaning difficulty or
failure to wean are advanced age, prolonged mechanical ventila-
tion, COPD, high minute ventilation and a positive fluid balance.
A tracheostomy might be required in patients who have failed
extubation or for whom weaning is expected to be or is pro-
longed. There is no clear evidence to support timing of trache-
ostomy, however they are generally inserted between 1 week and
3 weeks post-intubation.
Adjuncts to mechanical ventilation
Paralysis
Short-term neuromuscular blockade may be beneficial,
particularly in patients with severe ARDS. This allows strict
control of ventilation parameters, hence reducing ventilator
dyssynchrony and associated lung damage from injurious
breathing patterns. A French multicentre trial demonstrated
that early neuromuscular blockade in patients with severe
ARDS showed a significant reduction in mortality rates and
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Assessment criteria for extubation
The criteria and decision to extubate is complex, multifactorial and
must be tailored to each individual patient. Some factors to consider
include:
C Disease resolution: Improvement or resolution of underlying pro-
cess requiring intubation, to allow for unassisted spontaneous
breathing
C Airway: Patent upper airway. Absence of significant airway oedema
(e.g. presence of cuff leak when cuff is deflated)
C Breathing: Adequate oxygenation with minimal ventilatory support
(SaO2 >92 with low PEEP and FiO2  0.4). Adequate CO2 clearance
without excessive respiratory effort. Low sputum load with
adequate cough
C Circulatory: Haemodynamic stability, with absent or low vaso-
pressor requirement and stable cardiac rhythm
C Disability: Intact neuromuscular function (e.g. can raise head off
the pillow), ability to follow commands, absence of significant
delirium. Adequate pain control
C Electrolytes and fluid: Absence of significant acidosis, electrolyte
disturbance or fluid overload
C Other factors to consider include airway grade, predicted difficulty
of reintubation, lack of planned procedures as well as staffing
considerations should reintubation be required.
Box 3
more ventilator-free days, whilst not increasing ICU-acquired
muscle weakness.12 However, a more recent multi-centre
randomized control trial suggested no benefit from neuro-
muscular blocking agents.13
Patients who are paralysed (or heavily sedated) must be in a
mandatory ventilator mode to ensure adequate ventilation. Pro-
longed periods of neuromuscular blockade and paralysis should
be avoided where possible as this can lead to weakness and
difficulty liberating a patient from the ventilator.
Nitric oxide
Inhaled nitric oxide (iNO) can improve oxygenation by
improving ventilation-perfusion mismatch. This is achieved
by causing pulmonary vasodilation in capillaries supplied by
ventilated alveoli. As it is delivered via inhalation. The cap-
illaries that receive the most iNO are those that are being
ventilated and thus blood flow for gas exchange is improved
to these regions of the lungs.
Although it can be an effective rescue therapy in refractory
hypoxia for some patients, there were no survival benefits in
trials.14 It is however, an effective treatment for pulmonary
hypertension and should be considered in this patient
population.
Prone positioning
Prone positioning optimizes both lung recruitment and ventilation
perfusion mismatch, as lung perfusion is more equally distributed
in the prone position. Collapse due to gravity and compression
from the abdominal compartments is less for the affected lung
segments in the prone position than it is in the supine position.
7 Ó 2022 Published by Elsevier Ltd.
 INTENSIVE CARE
The physiological improvements of prone positioning are
more pronounced in patients with ARDS where there is a
reduction in mortality rates if applied for a minimum of 12
hours/day.15 As a result, it has seen widespread use throughout
the COVID-19 pandemic in patients who are not thriving with
traditional ventilation settings. It is important to factor in that
there are significant complications associated with prolonged
proning including pressure injuries, ETT displacement or
obstruction and ophthalmic complications.
Extracorporeal membrane oxygenation (ECMO)
ECMO is a therapy derived from cardiopulmonary bypass that fa-
cilitates gas exchange via an external membrane oxygenator which
oxygenates the blood and removes CO2. It has become a mainstay
of treatment in specialized centres for the management of re-
fractory cardiac failure (veno-arterial ECMO) or respiratory failure
(veno-venous ECMO). Instituting ECMO can allow for extreme
protective ventilation of lungs using volumes and pressures that
would not normally be sufficient to allow adequate gas exchange.
Although the use of ECMO for severe ARDS patients has
increased in recent years, its use remains somewhat contro-
versial. In a recent trial, early initiation of ECMO did not
result in a statistically significant reduction in 60-day mor-
tality compared to standard care, however, standard care (i.e.
the control group) included rescue ECMO for refractory hyp-
oxia and is thus difficult to draw definitive conclusions.16 For
an Australian patient cohort with refractory respiratory failure
secondary to severe H1N1, ECMO was associated with lower
mortality rates.17
Conclusion
Ventilation, both mechanical and non-invasive, is an essential sup-
portive therapy for respiratory failure in the critically ill patient. There
is no universal mode of ventilation that is ideal for all patients, nor one
that is associated with superior clinical outcomes. Attention to
ventilation strategy in the context of specific patient populations is
important. Ongoing monitoring of ventilator waveforms and pres-
sures, suitability for weaning and development of complications is
essential. Adjunct therapies are available for refractory respiratory
failure in the mechanically ventilated patient. A 2007; 334: 779.
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Please cite this article as: Frawley XJ, Yong SA, Ventilatory support in the intensive care unit, Anaesthesia and intensive care medicine, https://
Descargado para Anonymous User (n/a) en Cayetano Heredia Pervuvian University de ClinicalKey.es por Elsevier en octubre 07, 2022. Para uso
doi.org/10.1016/j.mpaic.2022.08.001
personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2022. Elsevier Inc. Todos los derechos reservados.
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