Anaesthesia

Review Article and Intensive Care

Anaesthesia and Intensive Care
2021, Vol. 49(2) 86–97
Patient–ventilator dyssynchrony in the ! The Author(s) 2021
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Brandon Oto1 , Janet Annesi2 and Raymond J Foley3

Abstract
Patient–ventilator dyssynchrony or asynchrony occurs when, for any parameter of respiration, discordance exists
between the patient’s spontaneous effort and the ventilator’s provided support. If not recognised, it may promote
oversedation, prolong the duration of mechanical ventilation, create risk for lung injury, and generally confuse the clinical
picture. Seven forms of dyssynchrony are common: (a) ineffective triggering; (b) autotriggering; (c) inadequate flow; (d)
too much flow; (e) premature cycling; (f) delayed cycling; and (g) peak pressure apnoea. ‘Reverse triggering’ also occurs
and may mimic premature cycling. Correct diagnosis of these phenomena often permits management by simple venti-
lator optimisation rather than by less desirable measures.

Keywords
Synchrony, patient-ventilator synchrony, vent synchrony, vent dyssynchrony, waveform, bucking

Background
Mechanical ventilation of intubated patients is con-
trolled by a combination of patient and ventilator-
determined variables. Except in the case of a complete-
ly passive (i.e. deeply sedated, paralysed, or comatose)
patient, effective ventilation requires a close concor-
dance between the patient’s effort and the ventilator’s
contributions. Anomalies in this harmony—where var-
iables such as the patient’s intrinsic flow of inspiration
or desired inspiratory time do not match those offered
by the ventilator—produce the undesirable situation of
patient–ventilator dyssynchrony.
Does this phenomenon have a patient-relevant
impact? Outcome data are limited. Significant dyssyn-
chrony (or asynchrony, an equivalent term) results in
‘bucking’ of the ventilator and frank patient discom-
fort, but subtle dyssynchronies are often not obvious,
requiring a well-trained eye or even specialised studies
such as oesophageal manometry to detect. When pre-
sent, patient distress and agitation may result in
increased sedation requirements, which are associated
with increased delirium and intensive care unit (ICU)
length of stay.1 However, observational studies suggest
that even subtle dyssynchrony is associated with mor-
tality and an increased duration of mechanical ventila-
tion.2–4 This may be due to a variety of effects, as
diaphragmatic effort that is dissociated from effective
ventilator support can fatigue the respiratory muscles,
confound ventilator weaning, and even predispose to
lung injury by inducing regional alveolar stress.5 More
subjectively, inability by clinicians to understand
unusual patterns during mechanical ventilation lends
to it a general air of mystery, obscuring its fundamental
nature as a physical, deterministic, and controllable
process.
Basic concepts of mechanical ventilation
Failures of synchrony are most easily recognised and
categorised in the context of a systematic approach
towards ventilation as a whole.
1
Adult Critical Care, UConn Health, Farmington, USA
2
Respiratory Therapy Department, UConn Health, Farmington, USA
3
Division of Pulmonary, Critical Care, and Sleep Medicine, UConn
Health, Farmington, USA
Corresponding author:
Brandon Oto, Adult Critical Care, UConn Health, 265 Farmington Ave,
Farmington, CT 06030, USA.
Email: oto.brandon@gmail.com
Oto et al.
Most mechanical ventilation in the modern ICU is
performed using one of several basic modes. Although
nomenclature in mechanical ventilation has become
highly variable, several modes are both clinically com-
monplace and relatively standard in terminology. The
first, used for full ventilatory support, is assist control
ventilation with either a volume or pressure target
(denoted respectively as volume control ventilation
(VCV) or pressure control ventilation (PCV)). The
second is pressure support ventilation (PSV) and is
used when spontaneous patient effort is encouraged.
A variety of other modes now exist, such as synchron-
ised intermittent mandatory ventilation, pressure regu-
lated volume control, volume support, and more, but
for the purposes of this discussion are merely amal-
gams of existing principles. Several truly novel modal-
ities have also been introduced, usually proprietary to
specific ventilators (such as proportional assist ventila-
tion and neurally adjusted ventilatory assist), but have
not yet achieved widespread adoption. Many of the
same principles of invasive mechanical ventilation are
also applicable to non-invasive positive pressure venti-
lation, with appropriate modifications and some differ-
ences in nomenclature.
Disregarding idiosyncratic modes such as airway
pressure release ventilation (APRV) or oscillatory ven-
tilation, any mechanical breath is defined by three
parameters:
• The trigger: the variable that initiates inspiration.
• The target or limit (terms used interchangeably): the
variable that defines or controls the inspiratory
phase.
• The cycling parameter: the variable that ends inspi-
ration, after which passive expiration begins.
Similarly, four variables are at work within the ven-
tilator to fill these parameters: delivered inspiratory
volume, inspiratory pressure, inspiratory flow, and
inspiratory time, all of which are closely interrelated.
By combining these features, the standard modes can
be created (Table 1).
With this framework, it becomes more straightfor-
ward to understand synchrony, using the following
maxim:
Ventilatory dyssynchrony occurs when, for any param-
eter of respiration, discordance exists between the
patient’s spontaneous effort and the ventilator’s pro-
vided support.
An obvious corollary is that dyssynchrony occurs
most often in patients with a spontaneous respiratory
drive. Completely apnoeic patients, such as the deeply
sedated, are usually straightforward to ventilate,
87
because the ventilator can control the respiratory pat-
tern with little interference from the patient. This
maxim and its corollary hold true for nearly all dys-
synchronies, with a few rare exceptions such as reverse
triggering and ‘peak pressure apnoea’. Another conse-
quence is that modes of ventilation which directly con-
trol more variables of ventilation are generally at
higher risk of producing dyssynchrony than those
which allow more control by the patient; for example,
VCV is more likely to yield certain dyssynchronies
(such as flow dyssynchrony) than PCV, and PCV is
at higher risk than PSV.
The common types of dyssynchrony
Seven types of dyssynchrony are commonly encoun-
tered. As terminology is inconsistent, these are best
recognised by their features rather than by a universal
nomenclature.
Triggering dyssynchrony
These relate to breath initiation.
1. Failure to trigger: The patient is unable to trigger a
breath, or there is a delay between their effort and
the resulting breath.
2. Autotriggering: Undesired breaths are repeatedly
delivered due to a spurious trigger.
Flow dyssynchrony
These relate to the delivery of the breath, in which
mismatch typically involves flow.
3. Inadequate flow: Patient flow demand exceeds
ventilator-delivered flow, resulting in inadequate
support.
4. Flow overshoot: Ventilator-delivered flow exceeds the
patient’s flow demand.
Cycling dyssynchrony
These relate to the ending of the breath. Also known as
expiratory dyssynchrony.
5. Premature (early) cycling: The ventilator’s set inspi-
ratory time (“machine I-time”) is shorter than the
patient’s intrinsic inspiratory time (“neural I-
time”); the delivered breath therefore ends while
the patient still desires continued flow.
6. Delayed cycling: Machine I-time is longer than
neural I-time, resulting in a longer breath than the
patient desires.
88 Anaesthesia and Intensive Care 49(2)

Table 1. Common ventilator modes and parameters.

Assist control ventilation

Volume control ventilation Pressure control ventilation Pressure support ventilation

Trigger Time (vent-initiated breath) or Time (vent-initiated breath) or Negative flow/pressurea

Negative flow/pressurea Negative flow/pressurea
(patient-initiated breath) (patient-initiated breath)
Target/limit Inspiratory volume Inspiratory pressure Inspiratory pressure
Cycle Inspiratory timeb Inspiratory time Inspiratory flow decayc
a
Determining flow versus pressure triggering is usually clinician-configurable.
b
Ventilators in volume control ventilation (VCV) modes appear to cycle the breath after the inspiratory volume is reached, but in fact are usually cycling
after the inspiratory time predicted for the set volume and flow. As flow in VCV is fixed, this has the same result.
c
Pressure support ventilation cycling is most often defined by a fraction of the peak inspiratory flow; e.g. a breath ends when the flow decays to 25% (or
some user-defined value) of the highest flow reached during the breath. On other ventilators, this cycling value may instead be set as a non-relative
figure, such as 5 l/min.

Alarm dyssynchrony Failure to trigger

A final idiosyncratic dyssynchrony exists, which we will
denote:
7. Peak pressure apnoea: In VCV, a user-defined cap on
peak inspiratory pressure causes termination of
inspiratory flow before adequate tidal volumes can
be achieved.
A clinical approach to patient–ventilator
dyssynchrony
Let us consider these seven phenomena in turn. Most
can be readily identified by a combination of clinical
examination and inspection of the real-time ventilator
waveforms, particularly the scalars depicting pressure
and flow over time. All figures depicted here are
derived from VCV with a decelerating ramp of flow
(constant pressure), but in other modes the key features
are similar.
In many cases, the most important information
missing from the ventilator’s graphics is the patient’s
contribution to the circuit; that is, the negative pressure
introduced by spontaneous patient muscular effort
(usually denoted Pmus). While this can be extrapolated
to some extent, it cannot be directly measured without
specialised methods, the most useful of which is oeso-
phageal pressure monitoring. In this technique, a bal-
loon is introduced into the oesophagus, permitting
transduction via the compliant muscular walls of an
oesophageal pressure that approximates the pleural
pressure, which falls during spontaneous patient inspi-
ration (Figure 1). Relatively few centres utilise this
device in clinical practice, so its use is not discussed
here, but its potential utility in diagnosing dyssyn-
chrony is high, and other applications—such as titrat-
ing lung-protective ventilation in obese patients—may
present as well.
(also known as ineffective triggering, wasted effort)
Causes. A majority of triggering failures occur in the
setting of intrinsic positive end-expiratory pressure
(‘autoPEEP’). Any combination of factors that prolong
the inspiratory time constant (e.g. large tidal volumes),
prolong the expiratory time constant (bronchoconstric-
tion, fixed airway obstruction, high compliance), or
shorten the time available for the latter (rapid respira-
tory rate) will tend to promote the presence of
autoPEEP. Practically, the most common contributing
factor is chronic obstructive pulmonary disease
(COPD) and similar obstructive lung pathologies.3,4
The expiratory flow obstruction in these patients pro-
longs the expiratory time, causing mechanical
breaths—whether patient or ventilator-initiated—to
occur before complete exhalation of the prior breath.
The result is air trapping and unintended autoPEEP.
Patient triggering on modern ventilators occurs by
either a pressure or flow trigger. In the former, the
patient inspires until a threshold of negative pressure
is reached (e.g. –2 cmH2O), at which point mechanical
inspiration is triggered. In the latter, the triggering
threshold is instead set at a threshold of negative
flow, such as –2 l/min.
Flow triggering is enabled by a continuous flow-by
gas current (bias flow) through the ventilator circuit,
usually between 2 and 20 l/min. As the patient inspires,
they divert flow between the inspiratory and expiratory
branches of the circuit, and this differential is noted by
sensors. The relatively recent adoption of flow trigger-
ing—now the default on many ventilators—was hoped
to decrease the problem of ineffective triggering, and in
some cases it may do so, although the benefit seems
greatest for pressure support breaths.6,7 However,
even with flow triggering, the presence of intrinsic
PEEP still hampers the patient’s ability to trigger,
Oto et al.
because flow can only occur once alveolar pressure
becomes negative.
With a pressure trigger, on the other hand, the impli-
cations of autoPEEP are clear. If mechanical ventila-
tion is triggered at –2 cmH2O, at rest, this requires the
patient to produce a negative inspiratory force (NIF) of
only 2 cmH2O. However, if 5 cmH2O of autoPEEP is
present, that positive pressure must first be drawn
down to zero; the total required pressure gradient to
trigger a breath thus becomes –7 cmH2O. At higher
levels of autoPEEP, pressure triggering becomes very
difficult to achieve, particularly as a large end-
expiratory volume also places the diaphragm in a
flattened, less advantageous position for further inspi-
ration. As exhalation continues, one or more breath
attempts may fail to trigger until autoPEEP has dwin-
dled enough to permit successful triggering. (Switching
to PSV does not resolve this problem, because trigger-
ing in PSV is no different than patient-initiated trigger-
ing in assist control modes.) Attenuation of the
maximal NIF by weakness of the respiratory muscles
further exacerbates the problem, and in severe cases—
such as neuromuscular disease—may cause inability to
trigger even in the absence of autoPEEP.
Clinical implications. Ineffective triggering is a subtle and
often unnoticed phenomenon, and is likely underappre-
ciated. In most formal audits it is the most common
type of dyssynchrony found,2,4 although it may be less
ubiquitous in populations with a lower prevalence of
COPD, such as surgical ICU patients. In mild cases
(‘triggering delay’), a discomforting sensation of lag is
created as patients exert effort on the circuit without
immediately receiving a breath. In more severe cases,
inspiratory effort fails to trigger a breath altogether,
and dissociation is created between the patient’s intrin-
sic respiratory rate and the actual ventilatory rate.
Either situation increases respiratory effort, induces
unnecessary diaphragmatic fatigue, and may provoke
patient distress leading to increased sedation; the false-
ly low apparent ventilatory rate also presents an inac-
curate picture of the true rapid shallow breathing index
(RSBI). Whatever the mechanisms, ineffective trigger-
ing is associated with a reduced chance of liberation
from mechanical ventilation.3,4
Clinical signs. Patient examination (by inspection or pal-
pation with a hand on the chest and abdomen) may reveal
respiratory effort which is not followed by a ventilator
breath. This may manifest as flexing of the abdominal
muscles, retraction of the intercostal spaces, or paradox-
ical thoracoabdominal movement. Unfortunately, such
clinical findings are usually subtle and in many cases may
not be appreciable.
89
Figure 1. Simultaneous tracings of airway and oesophageal
pressures. Negative deflections of the latter (boxes) prove the
presence of muscular effort during each breath. (Source image
courtesy of Elias Baedorf-Kassis, personal files)
Waveform manifestations. Small perturbations are visible,
appearing negative in the pressure tracing, but positive
in the flow tracing (Figures 2 and 3). In minor cases,
these are actually followed by a breath, but only after
undesirable delay; in moderate cases, they intermittent-
ly fail to ‘‘trigger’’ a subsequent breath; in severe cases
they rarely or never trigger a breath, and all breaths are
triggered instead by a time trigger. They are therefore
similar in significance to P waves in the setting of heart
block.
Potential remedies.
• Reduce intrinsic PEEP: AutoPEEP is present in
many cases of ineffective triggering, and should be
managed by the usual methods: increase the expira-
tory time, decrease the inspiratory time, and
decrease the respiratory rate. One method of
decreasing inspiratory time (and hence increasing
available expiratory time) in VCV modes is by
increasing the inspiratory flow rate, which can be
modestly effective; however, this should be done
with caution, as higher flow rates may secondarily
increase the spontaneous respiratory rate, for rea-
sons that are not clear.8 Improving triggering by
reducing autoPEEP may also increase the effective
respiratory rate due to the higher number of success-
ful breaths, which may in turn tend to worsen
autoPEEP. In such cases the goal should be effective
triggering at a reasonable rate. Finally, the most
definitive method of reducing autoPEEP is by
addressing the underlying airway resistance, such
as treatment of obstructive disease by bronchodila-
tors and corticosteroids, or removal of an under-
sized, kinked, or obstructed endotracheal tube.
• Reduce inspiratory pressure: Ineffective triggering is
associated with higher levels of inspiratory pressure
(in PCV/PSV modes), perhaps due to increased
autoPEEP in the presence of larger tidal volumes.4
90
Pressure
Negative pressure deflections
(wasted effort)
0
Patient effort successfully
triggers breath once autoPEEP
drops towards zero
Positive flow reversals
fail to trigger breaths
while expiration is ongoing
0
Rapid initial expiratory flow
tapers to prolonged expiratory phase
Figure 2. Multiple failed efforts before finally triggering a suc-
cessful breath. Note the prolonged expiratory phase with
resulting intrinsic positive end-expiratory pressure (autoPEEP).
Reducing excessive amounts of support may
improve triggering.9
• Add extrinsic PEEP: If intrinsic PEEP is present and
cannot be eliminated, increasing the ventilator PEEP
can reduce the work of triggering assisted breaths,
because the patient will only need to draw down
inspiratory pressure to the level of extrinsic PEEP,
not to zero. If autoPEEP can be measured accurate-
ly with an end-expiratory pause manoeuvre,
machine PEEP can be set at approximately 75% of
the measured autoPEEP, a figure which should limit
the work of triggering without adding work of expi-
ration and hence worsening autoPEEP (extrinsic
PEEP will not alter expiratory flow until it exceeds
intrinsic PEEP).10
• Reduce trigger thresholds: Shrinking the pressure or
flow trigger towards zero will increase ease of trig-
gering (although patients will still need to generate
enough negative pressure to cross the baseline).
However, very sensitive triggers may result in auto-
triggering, the inverse problem, which will paradox-
ically increase the respiratory rate and may worsen
Anaesthesia and Intensive Care 49(2)
autoPEEP; titration should therefore be performed
with caution.
• Promote respiratory drive: Greater muscular
strength and respiratory drive will increase the prob-
ability of successful triggering, even in the presence
of obstacles such as autoPEEP. This can be promot-
ed by reduced sedative and opioid use, avoidance of
hyperventilation or overoxygenation, and scaled
breathing exercise for patients with diaphragmatic
weakness.
• Switch triggering type: If a pressure trigger is in use,
it can be switched to flow triggering (the trigger
threshold should then be adjusted to maximise
appropriate triggers and minimise autotriggering).
Novel trigger types making use of neurally adjusted
ventilatory assist or oesophageal pressure manome-
try may be particularly helpful, but are unavailable
in most centres.
Autotriggering
(also known as accidental triggering)
Causes. As discussed above, autotriggering is exacer-
bated by sensitive trigger settings and is particularly
common with flow triggering. In that context, and in
the absence of any intrinsic PEEP, small artefacts in the
circuit may easily stimulate breaths. The most common
sources are:
• Cardiac oscillations: Pressure waves transmitted
from robust cardiac contractions.11
• Fluid in the circuit: Particularly common with
actively humidified circuits, which experience con-
densation (‘rainout’); this collects at dependent
points of the circuit (often near the wye), and its
sloshing can produce pressure fluctuations.
• Air leaks: Active loss of gas from the circuit can
generate a continuous negative flow, causing repeat-
ed autotriggers.12
Clinical implications. Autotriggering can produce respira-
tory rates in excess of both patient comfort and respi-
ratory physiology. Respiratory alkalosis may result. As
tachypnoea can lead clinicians to infer patient distress,
autotriggering may also indirectly cause increased seda-
tion and failed breathing trials, all tending to prolong
the duration of mechanical ventilation. The false
appearance of spontaneous breathing may also confuse
the picture of brain death.13
Clinical signs. Autotriggering can be difficult to appreci-
ate. The main clinical feature is an unusually rapid
respiratory rate. Less specific although highly sensitive
is a respiratory rate in excess of the set ventilator rate,
Oto et al.
Figure 3. Pressure (top) and flow (bottom) scalars showing in
vivo examples of ineffective triggering. Here the wasted efforts
are mainly visible on the pressure tracing, and the effort that
finally does trigger is strong enough to result in flow starvation
for the ensuing breath (see Inadequate flow).
Pressure
High respiratory rate
(not explained by set rate
or patient triggering)
Baseline artifact
0 However, a finite amount of time is required to build
0
Baseline artifact
Figure 4. Autotriggering caused by a continuous artefact such
as cardiac oscillations.
despite the presence of neuromuscular blockade.
Inspection of the ventilator circuit may reveal depen-
dent fluid collections or an air leak.
Waveform manifestations. A jagged or irregular wave-
form may be noted, particularly on the pressure trac-
ing; in the case of cardiac oscillations, this may
correspond to the heart rate (Figures 4 and 5).
91
Potential remedies.
• Eliminate the source of artefact: Address leaks or
drain excess fluids (cardiac oscillations usually
cannot be eliminated).
• Reduce trigger sensitivity: Trigger threshold can be
increased gradually until the contributory artefact
no longer triggers breaths.
• Switch to a pressure trigger: If flow triggering is in
use, switching to a pressure trigger may be
attempted.
Inadequate flow
(also known as flow starvation, work shifting)
Causes. A spontaneous patient-initiated breath has a
natural flow rate associated with it. The ventilator,
however, will provide flow at a rate which is either
fixed—as in VCV—or variable and patient determined,
as in PCV or PSV. In the case of VCV, the set flow is
often set lower than the patient’s desired rate, resulting
in dyssynchrony.
In pressure modes, flow dyssynchrony is less
common, because the ventilator adjusts flow dynami-
cally to match patient effort, using flow as a free var-
iable to achieve the manually set inspiratory pressure.
airway pressure, and initial flow can be increased faster
or slower to reach the set pressure; because flow is itself
a rate of change, this ‘rate of rate’ is known as the rise
time (sometimes denoted ramp time, pressure slope,
pressurisation rate, inspiratory percentage, or other
names) and can be set too slow, creating flow
dyssynchrony.14,15
Clinical implications. Flow starvation generally occurs in
patients with a vigorous respiratory drive and strong
muscles of inspiration. For many clinicians, the picture
of a tachypnoeic patient with obvious distress and
bizarre ventilator waveforms will prompt an increase
in sedation, with all the associated harms. If such
patients can be made comfortable by ventilator adjust-
ments alone, they can be kept awake and transitioned
more rapidly towards extubation.
Significant flow deficit also denotes a failure of the
basic goals of mechanical ventilation (‘work shifting’),
because it indicates a failure to unload and rest the
patient’s respiratory muscles adequately, which may
increase oxygen consumption, challenge efforts at lib-
eration, and stimulate patient discomfort.15 It may pro-
mote lung injury from barotrauma, as strong,
unmatched negative pleural pressure establishes a
high transpulmonary pressure gradient, even in the set-
ting of a modest intra-alveolar pressure.
92
Figure 5. In vivo example of autotriggering from a continuous
artefact such as cardiac oscillations (boxes).
Clinical signs. In the setting of inadequate flow, patients
will successfully trigger spontaneous breaths, yet can
nevertheless be observed (on inspection and palpation)
to exert continuous respiratory effort, actively pulling
at the ventilator throughout inspiration. Paradoxical
motion of the chest and abdomen are common, and
patients are often tachypnoeic and uncomfortable in
appearance.
Waveform manifestations. The pressure scalar should be
carefully inspected (Figures 6 and 7). A normal wave-
form has the appearance of a flat or gently domed
structure. In the case of flow starvation, the patient is
attempting to inspire faster than the flow provided,
pulling the airway pressure more negatively. In mild
cases, the pressure curve becomes flattened and then
upwardly concave. In severe cases, that concavity
drops below the baseline, indicating a negative airway
pressure and outright flow starvation.
This concave waveform may easily be mistaken for
the scooped-out appearance that develops in passive
breaths when tidal volume exceeds lung compliance;
this has been described as a ‘stress index greater than
1’ and may be associated with volutrauma.16 However,
that phenomenon occurs during passive breaths,
whereas flow starvation occurs during active patient
effort. Although the concave appearance may be virtu-
ally identical in both, the distinction can be easily made
by either observing the patient for effort, or by noting
on the ventilator whether the breath was triggered by
the patient or by the passive time trigger.
Potential remedies.
• In volume control: Increase set inspiratory flow until
the pressure waveform flattens out. If unable to
match patient flow successfully (e.g. if effort is
Anaesthesia and Intensive Care 49(2)
Severe flow starvation;
pressure is actually
negative in inspiration
Inadequate flow;
pressure is "pulled"
down into concavity
Normal breath,
Pressure
good flow matching
Flow tracing is preserved
0
Figure 6. Three breaths with increasing flow mismatch. Note
these are all patient-triggered breaths (proved by the negative
deflection at the start of each inspiration), and hence this is not
an example of poor compliance (positive ‘stress index’). The flow
curve is unchanged, because inspiratory flow is fixed in volume
control ventilation (VCV), regardless of patient factors.
variable or very brisk), consider switching to a pres-
sure mode.17
• In pressure control or pressure support: Shorten rise
time.14
• If patient effort is pathological (i.e. resulting in
unnecessarily large tidal volumes and minute venti-
lation): Attempt to resolve the cause of increased
respiratory drive, such as managing pain and dis-
tress, controlling fever, etc. If this cannot be
achieved, increase sedation.
Too much flow
(also known as pressure overshoot, flow overshoot)
Causes. This phenomenon is relatively unusual, as
many clinicians are more likely to set flow rates too
low than too high. However, if flow on VCV has
been titrated up to prevent flow starvation, overcom-
pensation may sometimes occur. In pressure modes, the
Oto et al. 93

Early pressure spike

Pressure
0

Figure 7. In vivo example of inadequate flow; note concave

pressure curves (boxes).

same phenomenon can occur with excessively quick rise

times, particularly when inspiratory pressure is also set 0

very high.

Clinical implications. Excessive flow is not always patho-

logical, but several undesired consequences are possi-
ble. First, it may result in patient discomfort. Second, it
can affect cycling in PSV, in which the cycle-off param-
eter is typically defined by flow decay from the peak
inspiratory flow (i.e. the breath ends when flow drops
to a certain percentage of the peak flow, such as 25%).
If that peak flow is artificially high—even for a brief
‘spike’, as in the case of flow overshoot—it will config-
ure the cycle-off flow threshold too high as well. The
breath will therefore be artificially shortened, resulting
in premature cycling (see below) and inadequate tidal
volumes.
Finally, a high flow rate has an independent in vivo
effect of reducing neural inspiratory time and hence
increasing respiratory rates.8 This may result in inap-
propriate tachypnoea.
Clinical signs. Excessive flow may present with patient
discomfort or the appearance of gagging.
Waveform manifestations. An early ‘spike’ or peak may
be seen on the pressure scalar, as initial flow is deliv-
ered faster than respiratory compliance can accommo-
date it. The inspiratory duration may also be unusually
short in VCV or PSV modes (Figures 8 and 9).
Potential remedies.
• Volume control: Decrease set flow.
• Pressure control/Pressure support: Lengthen rise time.
Figure 8. Initial flow overshoot creates an early spike or peak
at the start of inspiratory pressure.
Premature cycling
(also known as short cycling, double triggering, breath
stacking)
Causes. Premature cycling occurs when the neural
(patient) I-time exceeds the machine I-time. In this phe-
nomenon, inspiratory time, volume, and flow interact
in important ways. In VCV, for instance, premature
cycling can be correctly conceived as an inappropriate-
ly short I-time, but it may be easier to understand as an
inappropriately small tidal volume; as machine I-time
in VCV is determined by the volume and set flow, these
amount to the same thing. Whatever the case, prema-
ture cycling in VCV is usually due to a patient seeking
larger tidal volumes, and often occurs when small vol-
umes are intentionally used for lung protection.
In PCV, premature cycling may have the same
cause; however, as machine I-time is manually set,
adjusting it is particularly straightforward.
94
Figure 9. In vivo example of severe flow overshoot. Although
the pressure curve would typically be square-waved in volume
control ventilation with a decelerating flow ramp, here the
dramatic pressure spikes (boxes) create a sloped waveform
instead.
In PSV, premature cycling may occur due to flow
overshoot (as noted above) or an inappropriately set
flow-cycle threshold.
Clinical implications. As with most dyssynchrony, prema-
ture cycling can result in patient discomfort and agita-
tion. However, a more important consequence is seen
when the patient’s effort to prolong the breath results
in ‘double triggering’, or stacking of mechanical
breaths. This creates an effective tidal volume and
inspiratory pressure far in excess of the set parame-
ters—as much as double the set volume—which may
predispose to lung injury.
Clinical signs. Premature cycling is usually associated
with strong patient effort, so patients will often be vis-
ibly roused and tachypnoeic.
Waveform manifestations. In minor cases, the patient’s
effort continues beyond the ventilator’s, but does not
trigger an additional breath (Figures 10 and 11). This
can be seen as a positive deflection on the flow scalar at
the start of expiration, as the patient continues to
inspire after the ventilator has initiated exhalation.
More subtly, the corresponding pressure scalar may
show a sudden, near-vertical drop-off in pressure,
rather than the more gentle downslope seen on regular
inspiratory termination.
In more significant cases during assist control ven-
tilation, the prolonged patient effort actually triggers
an additional ventilator breath, occurring shortly after
the last breath and long before full expiration has com-
pleted. This results in ‘breath stacking’ or ‘double trig-
gering’, with a characteristic appearance on the
pressure tracing. PSV is less susceptible to this, because
a second triggered breath is usually small.
Anaesthesia and Intensive Care 49(2)
Pressure
Very steep (near vertical)
downslope
Continued inspiratory
effort triggers a
second breath
before full
expiration
0
Positive deflection at
beginning of expiration
Figure 10. In the first breath, an upward flow deflection early in
expiration reveals that neural I-time (inspiratory time) exceeds
machine I-time. In the second breath, this continued effort is
substantial enough to trigger another full ventilator breath, which
stacks onto the first. Note that these are patient-triggered
breaths, and hence this is not an example of ‘reverse triggering’.
Potential remedies.
• Volume control: Increase machine I-time. Most
often, this requires increasing the tidal volume. In
principle, it can also be achieved by reducing inspi-
ratory flow; however, as premature cycling tends to
occur in patients with a strong respiratory drive, this
often results in flow starvation.
• Pressure control: Increase the set machine I-time.
• Pressure support: Decrease cycle threshold (e.g. 30%
to 20%), thus prolonging the period of inspiratory
support.
Reverse triggering: a special case of double triggering.
Although most instances of double triggering are the
result of premature cycling, one important subset has a
distinctly different cause. This recently recognised phe-
nomenon, dubbed ‘reverse triggering’ or ‘entrainment’,
occurs when an initial ventilator breath triggers a sub-
sequent patient-initiated breath.18 This occurs for
unclear reasons, but may be the result of reflex
Oto et al. 95

Uptick at the end of machine

inspiration, as patient exhalation
adds pressure

Pressure
Figure 11. In vivo examples of premature cycling. In the first
breath, continued inspiratory effort is visible at the start of
expiration (single line). In the second, this effort is sufficient to
trigger a stacked breath (double line). Note the prolonged 0

expiratory time that results due to the additional tidal volume.

stimulation of the diaphragm. Unlike premature

cycling, and indeed most other asynchronies—which
tend to occur in the setting of a potent respiratory
drive—reverse cycling occurs more often in deeply
sedated or comatose patients; it has even been
described in brain-dead individuals, in whom it can 0
potentially confuse the neurological exam.19 The stim-
ulated diaphragmatic effort may be minor (a small
waveform perturbation only), or may be sufficient to
trigger a breath, in which case double triggering will
occur.
Reverse triggering can most easily be identified by
noting whether the initial breath was patient triggered
(indicating that the stacked breath is the result of pre-
mature cycling) or ventilator triggered (suggesting
Figure 12. A small ‘horn’ is created at the end of the pressure
reverse triggering). In cases in which the nature of the
curve as the patient attempts to stop the breath by exhaling
second breath remains unclear, a lengthy manual expi- against it. Flow remains fixed due to the volume control venti-
ratory hold manoeuvre may be revealing, as withhold- lation (VCV) mode.
ing additional ventilator breaths may make the
presence or absence of spontaneous patient effort (via
negative pressure deflections) obvious.20 The most exhaling during ventilator insufflation, creating elevat-
effective strategy for managing it seems to be one ed peak pressures. It also may predispose to autoPEEP,
that encourages patient-triggered respirations, such as as an unnecessarily long I-time shortens the effective
transitioning to PSV, adjusting the set respiratory rate, time for expiration.
or perhaps most effectively, reducing the level of seda-
tion.18,21 Neuromuscular blockade is effective for
refractory cases that are resulting in harmful sequelae. Clinical signs. Patients may be seen actively to expire via
activation of the abdominal muscles.
Delayed cycling
Causes. Delayed cycling occurs when machine I-time Waveform manifestations. On the pressure curve, a posi-
exceeds neural I-time. Similar to premature cycling, it tive inflection is seen at the end of inspiration; this
may therefore be caused by some combination of exces- reflects the pressure spike caused by the patient
sive tidal volume (in VCV), overly long I-time (in actively exhaling to resist the machine breath22
PCV), or an incorrect cycle parameter (in PSV). It is (Figures 12 and 13).
particularly common when PSV (a flow-cycled mode) is
used in COPD, in which prolonged expiration causes
late attainment of the flow decay threshold, and breath Potential remedies.
termination is consequently delayed. • Volume control: Shorten machine I-time. This can
be achieved by either increasing the flow rate or
Clinical implications. In addition to patient discomfort, decreasing the tidal volume.
delayed cycling often results in patients actively • Pressure control: Shorten set machine I-time.
96
Figure 13. An in vivo example of delayed cycling. Circles
denote the end-inspiratory pressure spike. Flow curve is
unchanged. (Image courtesy of Alex Yartsev, personal files.)
• Pressure support: Increase the flow threshold for
cycling (e.g. 30% to 40%), thus shortening the
breath.23
Peak pressure apnoea
A seventh type of dyssynchrony does not fit into our
standard rubric, but has great potential to cause harm
if not immediately recognised.24 All modern ICU ven-
tilators have the ability to set a variety of alarms, one
of which is typically a ‘peak pressure alarm’ that
sounds when the airway pressure at the ventilator
outlet exceeds a set limit. This alerts staff to circuit
occlusions, mucus plugging, and other troublesome
issues (although also alarming from time to time due
to coughing and similar transient events).
However, on the majority of ventilators, this param-
eter functions not only as an alert, but also as a max-
imum. When the pressure reaches the set limit or a
figure close to it, inspiratory flow is automatically ter-
minated. The result is a curtailed breath: in mild cases,
the inspired volume is reduced, and in severe cases the
volume may become zero or nearly zero, resulting in
functional apnoea.
This phenomenon is often unrecognised and can be
extremely hazardous; although high pressure alarms
require troubleshooting, apnoea rarely improves the sit-
uation. Some patients, such as those with bronchocon-
striction, have perpetually elevated peak pressures but a
normal plateau pressure; others, such as the obese, have
elevated plateau pressures but a normal transpulmonary
pressure. In either case, elevated peak pressures must be
tolerated to permit adequate ventilation.
‘Peak pressure apnoea’ is primarily a phenomenon
of volume-targeted modes, as in pressure modes the
inspiratory pressure is set directly by the clinician.
Dual-control modes such as pressure regulated
volume control, in which pressure is titrated
Anaesthesia and Intensive Care 49(2)
automatically by the ventilator to achieve a set
volume goal, are also susceptible.
Diagnosis is straightforward: the combination of a
peak pressure that is repeatedly fixed at the set limit
(often defaulted to 40 cmH2O), along with consistently
low tidal volumes, is nearly pathognomonic for this
phenomenon. The diagnosis can be confirmed and res-
olution immediately achieved simply by increasing the
pressure limit, which will promptly result in an increase
of both inspiratory pressure and tidal volume. The
patient can then be evaluated to determine whether
the elevated peak pressure is clinically acceptable or
requires further manoeuvres to reduce it.
Conclusions
Patient–ventilator dyssynchrony is a common phenome-
non which is nevertheless poorly understood. In many
cases, subtle failures of synchrony are not noted, but
may result in diaphragmatic fatigue or occult lung
injury; in more frank cases, the standard clinician
response may be to increase sedation, which is a blunt
response and rarely the preferred solution. A keen under-
standing of the causes of dyssynchrony, and a practised
eye at examining ventilator waveforms, is often sufficient
to diagnose these problems and recommend a response
which focuses on simple ventilator optimisation.
Declaration of conflicting interests
The author(s) declared no potential conflicts of interest with
respect to the research, authorship, and/or publication of this
article.
Funding
The author(s) received no financial support for the research,
authorship, and/or publication of this article.
ORCID iDs
Brandon Oto https://orcid.org/0000-0002-1505-1113
Janet Annesi https://orcid.org/0000-0001-8861-7213
Raymond J. Foley https://orcid.org/0000-0001-6336-3683
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