INVITED REVIEW SERIES:
NEW FRONTIERS IN SLEEP-DISORDERED BREATHING
SERIES EDITORS: MATTHEW NAUGHTON, PETER A. CISTULLI AND PHILIP DE CHAZAL
Advances in non-invasive positive airway pressure technology
AMANDA J. PIPER1,2
1
Department of Respiratory and Sleep Medicine, Royal Prince Alfred Hospital, Sydney, NSW, Australia; 2Faculty of Medicine
and Health, University of Sydney, Sydney, New South Wales, Australia
ABSTRACT
Non-invasive ventilation (NIV) has become the standard
of care for patients with a range of respiratory and sleep
breathing disorders. Technological advances have
enabled the development of several newer modes of
automatically adapting NIV suitable for patients with
more complex breathing abnormalities that may be dif-
ficult to manage effectively with more traditional posi-
tive airway pressure therapy. These modes allow for
more stable ventilation when fluctuating ventilation
requirements occur such as in positional upper airway
obstruction or state-related variations in respiratory
mechanics and drive. Adaptive servoventilation (ASV) is
designed for patients with periodic breathing and cen-
tral apnoeas in whom carbon dioxide levels are normal
to low, with the goal of therapy to dampen and stabilize
ventilation. In contrast, volume-assured pressure sup-
port is used in diagnostic groups characterized by hypo-
ventilation, where targeting an effective level of
ventilation irrespective of sleep stage or body position is
required. These newer modes have the potential to sim-
plify and optimize ventilation, although at present there
is no evidence that they are clinically superior to stan-
dard home ventilation techniques. The complexity and
differences in algorithms and features of various device
brands, along with a limited evidence base documenting
longer term outcomes, complicate decisions around
which patient phenotypes are best suited to these newer
modes. In-built sensor and data storage capabilities of
newer home ventilation devices provide the opportunity
for earlier recognition of issues with ventilation and to
guide corrective action. Further work is needed to
determine how this impacts longer term clinical
outcomes.
Key words: adaptive servoventilation, bilevel ventilation, cen-
tral sleep apnoea, nocturnal hypoventilation, volume-assured
pressure support.
Correspondence: Amanda J. Piper, Department of
Respiratory and Sleep Medicine, Royal Prince Alfred Hospital,
Missenden Road, Camperdown, Sydney, NSW 2050, Australia.
Email: amanda.piper@sydney.edu.au
Received 16 October 2018; invited to revise 5 February 2019;
revised 28 April 2019; accepted 10 June 2019
© 2019 Asian Pacific Society of Respirology
INTRODUCTION
Non-invasive ventilation (NIV) has become the key-
stone in managing hypercapnic respiratory failure, and
is arguably one of the most important clinical advance-
ments in respiratory medicine over the past three
decades. Initially, therapy was delivered using a volume
mode of ventilation, where tidal volume is set by the
clinician, resulting in variable airway pressures
reflecting airway resistance and respiratory system
compliance. The efficacy of this approach was clearly
shown in patients with chronic neuromuscular and
chest wall disorders1–3 as well as in those with acute
respiratory failure secondary to lung disease.4,5 In 1990,
Sanders and Kern6 introduced bilevel positive airway
pressure (BPAP) therapy as a means of independently
adjusting inspiratory positive airway pressure (IPAP)
and expiratory positive airway pressure (EPAP) for
treating obstructive sleep apnoea (OSA). By providing
overall airway lower pressures, the authors felt this
could improve comfort and hence compliance with
therapy. However, it quickly became apparent that
BPAP, a form of pressure-preset ventilation, was
equally effective as volume-preset ventilation in provid-
ing ventilatory support for patients with both acute and
chronic hypercapnic respiratory failure.7–9 The advan-
tages of BPAP over volume-preset ventilation including
greater comfort and better leak tolerance has led to this
form of ventilation becoming the primary method of
non-invasive ventilatory support currently used in
acute settings10 as well as being extensively prescribed
in home ventilation programmes.11
In the past few years, significant improvements in sen-
sor and microprocessor technology have been incorpo-
rated into BPAP devices. In conjunction with the
introduction of newer algorithms, these devices now
come with an ever expanding choice of ventilation
modes, many of which are able to self-adjust in response
to changes in various respiratory variables such as flow,
tidal volume and respiratory rate. Fluctuations in venti-
latory requirements can arise due to positional or state-
related alterations in upper airway calibre, ventilatory
drive or respiratory mechanics. In general, these modes
can be divided into two broad categories: those designed
for patients with central events where CO2 is normal or
low—adaptive servoventilation (ASV), and modes for
managing hypoventilation syndromes (volume-assured
Respirology (2019)
doi: 10.1111/resp.13631
2 AJ Piper
pressure support or Va-BPAP). Different brands of
machine use proprietary algorithms for these newer
modes, and it is beyond the scope of this article to pro-
vide specific details on how these devices operate. This
review covers the evidence for the clinical use and effi-
cacy of these newer modes of ventilation, highlighting
which clinical populations could benefit (Table 1).
Advances in device software for recording and monitor-
ing of ventilatory data and the role this may play in clini-
cal management will also be covered.
ADAPTIVE SERVOVENTILATION
This mode of ventilation, sometimes referred to as anti-
cyclical ventilation, was designed to manage patients
with predominantly central or mixed apnoeas where
significant respiratory variability is present, but PaCO2
is in the low to normal range. The target population for
this mode of ventilation are patients with Cheyne–
Stokes breathing, opioid-inducing breathing or those
with treatment-emergent (TE) central sleep apnoea
(CSA). ASV provides automatically adjusting pressure
support so that during periods of central apnoea or
hypopnoea, inspiratory support is increased on a
breath-by-breath basis which then reduces during
periods of hyperventilation or stable breathing (Fig. 1).
Depending on the brand of device, either peak flow or
minute ventilation is monitored by the device, with
adjustment of the output (pressure support and back-
up rate) to mirror the patient’s spontaneous respiratory
efforts in order to maintain a more stable breathing
pattern.12 Although a fixed EPAP can be set, newer
devices now incorporate an autotitrating EPAP setting
to maintain upper airway patency.
Treatment-emergent CSA
Previously known as complex sleep apnoea, TE-CSA
refers to patients presenting with what appears to be
classic OSA who then develop central apnoeas and
periodic breathing on continuous positive airway pres-
sure (CPAP). As these central events may resolve spon-
taneously over time in some with ongoing CPAP use,13
there has been some debate around the best manage-
ment approach for such individuals. Although some
have documented the successful use of BPAP in
patients with TE-CSA,14,15 there is a high risk of increas-
ing the frequency of periodic breathing compared to
CPAP due to the generation of large tidal volumes dur-
ing hyperpnoeic periods, lowering PaCO2 and worsen-
ing central apnoeas.16 ASV can overcome some of the
shortcomings of BPAP. Morgenthaler et al.17 random-
ized 66 subjects with TE-CSA to either CPAP or ASV for
3 months. In the intention-to-treat analysis, 90% of
those allocated to ASV achieved an apnoea–hypopnoea
index (AHI) < 10 compared to 64% of the CPAP group,
confirming previous work showing ASV is more reliable
than CPAP in reducing sleep-disordered breathing
(SDB) in TE-CSA.14 Of interest, both modes of therapy
produced similar symptomatic changes.17 At present, it
is unclear whether any longer term clinical advantages
are derived from using more expensive ASV devices in
this population. However, recent retrospective analyses
© 2019 Asian Pacific Society of Respirology
of a large telemonitoring positive airway pressure
(PAP) database showed that TE or persistent CSA dur-
ing CPAP was associated with reduced adherence to
therapy,18 which was improved by switching to ASV.19
Opioid-induced central apnoea
Altered respiratory control and SDB are highly preva-
lent in patients using chronic opioid medications,
resulting in a spectrum of abnormal respiratory events
including CSA, hypoventilation, slowing of respiratory
rate and ataxic breathing.20–22 Although CPAP effec-
tively treats any obstructive events that are frequently
present, central apnoeas are generally unresponsive
and may even worsen.23,24 In contrast, most studies
have shown that ASV is more effective than other ther-
apies, including CPAP and BPAP, in reducing central
events,24,25 although this finding is not universal.23,26
Long-term use of ASV has been reported in two stud-
ies, confirming sustained control of SDB and good
adherence to therapy.24,27 However, there is a lack of
data concerning the impact of PAP including ASV on
clinical outcomes such as quality of life or mortality.
Cheyne–Stokes breathing
CSA and Cheyne–Stokes respiration (CSR) are common
in patients with heart failure28 and may be seen follow-
ing ischaemic or haemorrhagic stroke, although the
prevalence is significantly less than that seen in heart
failure.29,30 Sleep fragmentation arising from arousals
following apnoeic events likely contribute to fatigue
and sleepiness reported by patients. Furthermore,
repetitive apnoeas and arousals induce an increase in
sympathetic nerve activity, which is associated with
adverse physiological effects and poorer prognosis in
patients with chronic heart failure (CHF).31 A post hoc
analysis of the Canadian Continuous Positive Airway
Pressure for Patients with Central Sleep Apnea and
Heart Failure (CANPAP) trial found a significant reduc-
tion in AHI in around 60% of patients with CSA-CSR
treated with CPAP, with significant improvements in
left ventricular ejection fraction (LVEF) and transplant-
free survival compared with the control group and
those in whom CPAP did not reduce to <15/h.32 The
belief that continued abnormal nocturnal breathing in
this population is detrimental longer term has led to
the use and evaluation of other forms of PAP therapy
for CPAP non-responders.
Fixed pressure BPAP-spontaneous timed (ST) can
stabilize nocturnal breathing in some patients with
CSA-CSR,33,34 but it can be difficult to titrate settings
appropriately. The introduction of ASV provided an
alternative and potentially more effective approach to
therapy. A number of observational studies and small
randomized trials emerged demonstrating the superior-
ity of ASV over both CPAP and fixed BPAP therapy in
reducing AHI,33,35–38 improving quality of life35,36 and
exercise capacity,38 and increasing LVEF.35,36,38 In 2012,
the American Academy of Sleep Medicine released
guidelines recommending the use of ASV for the treat-
ment of CSA related to heart failure targeted to normal-
ize the AHI.39
Respirology (2019)
Advances in non-invasive PAP technology 3

Table 1 Newer modes of ventilation with potential clinical uses

Mode Clinical use Comments

ASV Designed for patients with significant respiratory
instability resulting in predominately central and
mixed apnoeas with PaCO2 in normal or low
range
TE-CSA, opioid-induced SDB, idiopathic CSA or
stroke
Has been used in the treatment of CSA arising
from chronic opioid-induced SDB and TE
Although previously used for CSA in CHF, recent
evidence for an increase in risk of death in
patients those with an ejection fraction ≤45%
Va pressure Provides variable inspiratory support to maintain a
support target level of ventilation, despite changes in
lung or chest wall compliance or alterations in
airway resistance
Use reported in OHS, COPD and neuromuscular
disorders with hypoventilation
Can be added to ST or PC modes of BPAP
Observational and small, short-term randomized
trials have demonstrated similar outcomes to
fixed pressure BPAP when both modes set to
deliver similar target tidal volumes
Autotitrating Automatic adjustment of EPAP to prevent upper
EPAP airway obstruction
Can be added to ASV, Va or fixed pressure support
modes of BPAP, depending on the device used
Useful for patients with obesity or suspected
concomitant OSA particularly where substantial
sleep state or positional variation in upper
airway behaviour is present
Generally shown to be more effective than CPAP
or BPAP in reducing central events and
stabilizing breathing during sleep
In patients with TE and opioid-induced central
apnoea, data are lacking regarding longer term
benefits of ASV over other forms of PAP in
terms of quality of life and survival
In patients with CHF and predominantly CSA with
an ejection fraction ≤45%, ASV is not
recommended due to the significant risk of
harm. CPAP may be used in those who are
shown to respond to it
Not shown to provide better ventilation or
outcomes than fixed level BPAP
May improve acclimation and tolerance to BPAP
by reducing pressure during wakefulness
May improve access to therapy and reduce delay
in commencing treatment by reducing need for
in-laboratory titration settings
Manual adjustment to settings still required to
optimize therapy
Excessive non-intentional leak and/or residual
upper airway obstruction may produce less
efficient ventilation than expected
Bench testing demonstrates variable response to
events such as leak type (inspiratory/expiratory
and intermittent/continuous) and circuit
configuration between various Va-BPAP devices
Shown to be non-inferior to PSG-directed
manually titrated EPAP in single night
randomized trials
No longer term data regarding outcomes
compared to fixed level BPAP or EPAP
To data, only investigated in patients already
established on NIV
Offers the potential to reduce the need for
in-laboratory titration, thereby improving access
to BPAP therapy

ASV, adaptive servoventilation; BPAP, bilevel PAP; CHF, chronic heart failure; CPAP, continuous PAP; CSA, central sleep apnoea;
EPAP, expiratory PAP; NIV, non-invasive ventilation; OHS, obesity hypoventilation syndrome; OSA, obstructive sleep apnoea; PaCO2,
Partial pressure of arterial carbon dioxide; PAP, positive airway pressure; PC, pressure controlled; PSG, polysomnogram; SDB,
sleep-disordered breathing; ST, spontaneous timed; TE, treatment emergent; Va, volume-assured.

The SERVE-HF trial was designed and undertaken to
confirm the findings of these small, short-term investi-
gations.40 Over 1300 patients with heart failure and
reduced ejection fraction (LVEF ≤ 45%) were recruited
and randomized to either ASV or optimal medical ther-
apy over a median follow-up of 31 months. The pri-
mary end point was a composite of death from any
cause, a life-saving cardiovascular intervention or an
unplanned hospitalization for worsening CHF. On an
intention-to-treat basis, there was no difference
between groups with respect to this primary end point
(hazard ratio: 1.13, 95% CI: 0.97–1.31, P = 0.10). Unex-
pectedly, however, all-cause death and cardiovascular
death were significantly increased in those allocated to
ASV, with no benefits across a broad range of func-
tional measures including quality of life and symptoms.
This is despite ASV effectively treating CSA. A follow-
up ‘on-therapy’ analysis confirmed an increased risk of
death in ASV-treated patients but showed no increase
in risk with increasing therapy usage.41 The mecha-
nisms underlying these findings have not yet been fully
explained, but do not appear to be related to adverse
cardiac remodelling or worsening heart failure.42 These
findings stimulated much discussion among clinicians
and resulted in changes to guidelines around the man-
agement of CSA, advising against the use of ASV in

Respirology (2019) © 2019 Asian Pacific Society of Respirology

4 AJ Piper
adults with heart failure and moderate or severe CSA
with an ejection fraction ≤45%.43 While most clinical
and much research activity with ASV in patients with
heart failure and reduced ejection fraction was ceased
following the release of the SERVE-HF results,44–46 the
Effect of ASV on Survival and Hospital Admissions in
HF (ADVENT-HF) study47 continued patient recruit-
ment following review by the trial’s data and safety
monitoring committee. This trial is evaluating a newer
generation ASV device incorporating autotitrating EPAP
and a different pressure support algorithm to the
SERVE-HF study in patients with reduced ejection frac-
tion and either CSA or OSA. The ADVENT-HF trial is
also examining a much broader population of patients
with heart failure and the results should provide
greater insights into what role, if any, ASV may play in
patients with heart failure and reduced ejection fraction
across the spectrum of SDB.
In contrast to heart failure, the use of ventilatory sup-
port for CSA in patients following stroke has been
sparsely addressed, with most studies reporting the use
of CPAP for OSA.48 One study described BPAP use in
64 of 356 consecutive patients admitted to a tertiary hos-
pital stroke service with acute cerebral ischaemia.49 Ther-
apy was commenced on the first day of admission as part
of standard of care in patients with a history of OSA,
suspected OSA or persisting proximal arterial occlusions
with neurological worsening during sleep. No objective
measures of the type or severity of any SDB were under-
taken. BPAP was set with an IPAP of 10 cm H2O and
titrated upward to achieve a tidal volume of 5–7 mL/kg,
while EPAP remained at 5 cm H2O. Four patients were
intolerant of therapy, with seven experiencing an adverse
event, mainly facial skin breakdown. No difference in in-
hospital mortality was seen between BPAP users and
non-users, but among survivors, neurological improve-
ment during hospitalization tended to be greater in the
BPAP group. However, whether this translated into better
functional outcomes is unknown as no post-discharge
follow-up was reported.
In a retrospective analysis, Brill et al. reported the
outcome of ASV treatment for persistent CSA in
15 post-acute ischaemic stroke patients without con-
comitant CHF.45 Therapy commenced a median of
11 months following the cerebrovascular event, with
© 2019 Asian Pacific Society of Respirology
Figure 1 A 5-min epoch
showing patient flow and
mask pressure during ASV in
a patient with CSA/CSR. Dur-
ing apnoeic phases, the
device progressively increases
IPAP and then reduces the
degree of pressure assistance
during hyperpnoea. Breaths
are machine-triggered during
the apnoeic phase and patient-
triggered during hyperpnoea.
ASV, adaptive servoventilation;
CSA, central sleep apnoea;
CSR, Cheyne–Stokes respira-
tion; IPAP, inspiratory posi-
tive airway pressure.
11 initially treated with CPAP and 2 with BPAP. Vari-
able pressure support was set between 3 and
9 cm H2O, and EPAP at 5 cm H2O with an automatic
back-up rate. ASV successfully reduced AHI from
47  24 to <10 events/h at both 3 and 6 months. While
this study demonstrated the feasibility and potential
effectiveness of ASV in this population, data regarding
the impact of therapy or lack of it on recurrent cardio-
vascular events, cognitive function and survival remain
unknown.
Clinical implications
While patients may be classified as having predomi-
nantly CSA, most present with more complex SDB
which includes obstructive events and variability in
breathing pattern. To further complicate the matter,
the predominant type of breathing abnormality can
vary across the night due to body position and sleep
stage, as well as change over time with alterations in
medications, weight or fluid status. It is not surprising
then that any PAP therapy using static pressures and
back-up rates titrated over a single night may fail to
fully correct the diverse and dynamic sleep breathing
abnormalities that can occur in these populations. The
algorithms and features of ASV devices are theoretically
well suited to providing appropriate and stable ventila-
tory support under such dynamic conditions. However,
beyond reducing AHI during sleep and potentially
improving adherence to therapy is some patients, there
is a paucity of data from randomized trials showing
clear clinical benefits with ASV use such as improved
quality of life, reduced incident cardiovascular events
or improved survival.
Failure of ASV to control sleep breathing events in
some studies could be related to the use of older tech-
nology especially the use of fixed EPAP.23,40 The incor-
poration of autoadjusting EPAP and back-up rate in
newer generation ASV devices not only simplifies ther-
apy titration, but also potentially optimizes therapy.50,51
Although fully automated ASV therapy provides the
potential to commence therapy earlier without the
need for a polysomnogram (PSG)-guided titration
night, clinicians need to be mindful that algorithm and
device performance may vary from that expected in the
Respirology (2019)
Advances in non-invasive PAP technology
real-world situation. This highlights the need for close
and independent monitoring of the individual’s
response to therapy. Furthermore, good quality, long-
term studies are also needed to determine the impact
of correcting central events on relevant patient and
clinical outcomes.
VOLUME-ASSURED PRESSURE
SUPPORT
This is a hybrid mode of ventilation, incorporating fea-
tures of both volume and pressure ventilation. The cli-
nician sets a target tidal volume or alveolar ventilation
along with an IPAP/pressure support range which per-
mits the device to deliver a variable level of inspiratory
assistance in order to maintain tidal volume or alveolar
ventilation close to the target value. Va pressure sup-
port offers an alternative approach to initiating, titrat-
ing and maintaining effective ventilation in individuals
with hypoventilation syndromes. The ability of the
device to augment ventilation sufficiently even in the
presence of changing airway resistance or lung compli-
ance is touted as one of the advantages of this mode of
ventilation (Fig. 2). Other theoretical benefits could be
a reduction in pressure support during wakefulness,
improved comfort and potentially compliance with
treatment.
Clinical studies
Most studies around the use of Va-BPAP have been con-
ducted in patients with obesity hypoventilation syndrome
or COPD presenting with chronic respiratory failure.52–57
However, Va-BPAP has also been successfully used in
congenital central hypoventilation syndrome58 and
restrictive chest wall disorders.59–61 Early studies reported
better control of nocturnal CO2 with volume assurance
compared to fixed pressure BPAP,53,57 although this was
often achieved at the expense of poorer sleep quality.53
Figure 2 While fixed
pressure-preset modes of
ventilation provide consistent
breath-to-breath airway pres-
sure, the delivered tidal vol-
ume can vary substantially
due to changes in sleep stage
or body position. This 10-min
epoch illustrates a reduction
in patient airflow and tidal
volume in the absence of leak.
Note the patient is being pas-
sively ventilated with total
respiratory rate and machine
BUR equivalent. BUR, back-up
rate; VT, Tidal Volume.
Respirology (2019)
5
However, when titration protocols for fixed pressure
BPAP-ST and Va-BPAP modes were set to achieve similar
target tidal volumes, clinical differences were no longer
apparent.59 In a group of 46 super-obese individuals with
obesity hypoventilation syndrome, Murphy et al. reported
similar control of nocturnal gas exchange with both
modes of ventilation and consequently equivalent
3-month outcomes in awake gas exchange, quality of life
and compliance with therapy.54 Mean IPAP delivered
with Va-BPAP in this study was 22  5 cm H2O com-
pared with 23  4 cm H2O for those on fixed pressure
BPAP. Likewise, Oscroft et al. found no difference in gas
exchange or clinical outcomes after 3 months of therapy
with either Va-BPAP or fixed pressure BPAP in 40 patients
with stable hypercapnic COPD.56
Use of high-pressure or high-intensity NIV has received
a significant amount of attention recently with publication
of two large, randomized trials showing reduced
readmissions62 and improved survival63 in patients with
COPD and chronic hypercapnia. This approach, while
effective, requires several days of patient acclimation,
monitoring and pressure adjustment,63 which may not be
feasible in many health systems. In a randomized cross-
over trial comparing Va-BPAP and BPAP-ST in
ventilation-naïve patients with nocturnal hypoventilation,
Va-BPAP was equally effective in improving nocturnal gas
exchange and sleep quality as overnight manual titration
by an expert group.64 The use of higher nocturnal inspira-
tory pressures without adversely affecting sleep quality55
along with less time to acclimate to these higher pres-
sures56 highlight the potential role of Va-BPAP in initiat-
ing and optimizing nocturnal ventilatory support
(Figs 3–4).
Few studies have reported the use of Va-BPAP in the
acute setting. A small prospective case–control study
compared Va-BPAP in 11 COPD patients with hyper-
capnic encephalopathy with 11 similar patients treated
with BPAP-ST alone.65 Improvements in PaCO2, respi-
ratory rate and level of consciousness improved more
rapidly in patients receiving volume assurance. However,
© 2019 Asian Pacific Society of Respirology
6 AJ Piper

Figure 3 Recording of
volume-assured BPAP during
non-REM sleep in a patient
with COPD. The device has
been set to deliver a target
tidal volume of 550 mL, with
IPAP range of 16–25 cm H2O,
EPAP fixed at 6 cm H2O and a
back-up rate of 15 bpm. Dur-
ing the first part of this 5-min
epoch, tidal volume is below
the set target and IPAP is pro-
gressively increasing. Once
the target is met or exceeded,
the IPAP again ramps down to
the minimum value. BPAP,
bilevel positive airway pres-
sure; EPAP, expiratory posi-
tive airway pressure; IPAP,
inspiratory positive airway
pressure; REM, rapid eye
movement; VT, Tidal Volume.

this was achieved using significantly higher IPAP levels
with Va-BPAP (initial maximum IPAP of 19.8  2.2 vs
12.3  0.9 cm H2O). Furthermore, no difference in dura-
tion of NIV use or length of hospital stay was observed.
A more recent randomized study compared the out-
comes of BPAP-Spontaneous and AVAPS-Spontaneous
modes in patients with acute or acute-on-chronic hyper-
capnic respiratory failure who were admitted to an inten-
sive care unit (ICU).66 Both modes were set to deliver a
tidal volume of 8 mL/kg of ideal body weight, although
mean peak inspiratory pressure was higher with Va-
BPAP (22.2  5.1 vs 17.5  3.5 cm H2O). Despite this, no
difference between groups was seen in the course of CO2
improvement, duration of NIV or length of hospital stay.
These findings echo those of another randomized trial
comparing BPAP-ST to Va-BPAP-ST performed on gen-
eral respiratory wards in patients with acute hypercapnic
respiratory failure.67 Reductions in PaCO2 after 2 and 6 h
of therapy, need for intubation and in-hospital mortality
did not differ between therapy modes.
Clinical considerations
Current evidence does not suggest any superiority of
Va-BPAP over BPAP in treating either acute or chronic
hypercapnic respiratory failure. Nevertheless, there are
some practical advantages of using Va-BPAP to imple-
ment and maintain therapy particularly where monitor-
ing resources or skilled staff are scarce, or where rapid
changes in sleep breathing are likely to occur. Impor-
tantly, no safety concerns have been raised with the
widespread use of this ventilatory mode.
In general, tidal volumes of 6–10 mL/kg of ideal
body weight have been used, with targets adjusted to

Figure 4 Recording of
volume-assured BPAP during
REM sleep in the same patient
as shown in Figure 3. The
device is consistently deliver-
ing an IPAP of 16 cm H2O to
achieve the set target tidal
volume in this sleep stage. A
potential benefit of this mode
over fixed BPAP is the ability
to adjust inspiratory support
to maintain ventilation despite
changes in lung or chest wall
compliance that can arise
from changes in sleep stage
or body position. BPAP,
bilevel positive airway pres-
sure; EPAP, expiratory posi-
tive airway pressure; IPAP,
inspiratory positive airway
pressure; REM, rapid eye
movement; VT, Tidal volume.

© 2019 Asian Pacific Society of Respirology Respirology (2019)

Advances in non-invasive PAP technology
Figure 5 A 5-min recording
of data downloaded from in-
built ventilator software dur-
ing volume-assured ventila-
tory support illustrating the
impact of persistent upper air-
way obstruction on ventila-
tion. Higher EPAP or the use
of autotitrating EPAP would
be appropriate in this case.
EPAP, expiratory positive air-
way pressure; VT, Tidal
Volume.
accommodate patient comfort and degree of hyper-
capnia.52,54,68,69 The EPAP is usually set at 4–5 cm H2O
if upper airway collapse is not thought to be an
issue,52,64 or around the minimum CPAP level
required to prevent obstruction.54,69 Autotitrating
EPAP simplifies decisions about this setting (see
below). A back-up rate of 2–4 breaths below the
patient’s awake spontaneous rate is usually used54,64,70,
or can be set a few breaths above the patient’s sponta-
neous sleep breathing rate if more passive ventilation
is the goal.63,71
However, clinicians cannot simply assume that these
Va algorithms will optimize ventilation. Non-
intentional leak and upper airway obstruction will pro-
duce poorer than expected performance of the ventila-
tor (Fig. 5). In bench tests, unintentional leaks
significantly affected ventilator performance, reducing
pressure support and altering the delivered tidal vol-
ume by as much as 40%.72 Circuit configuration and
type of intentional leak port can also influence the
accuracy of the delivered tidal volumes.73 Conse-
quently, close monitoring and review of the efficacy of
ventilation remain key aspects of NIV with Va-BPAP
devices.
Clinical follow-up of patients on home ventilation
has ranged from simple awake blood gases to full PSG
with transcutaneous carbon dioxide monitoring.11 With
recent technological advancements, remote monitoring
of a range of respiratory parameters recorded by the
built-in ventilator software is now possible. This infor-
mation can be stored on datacards within the device
for later downloading and review, or uploaded to the
cloud for more immediate access by prescribers or
home care providers, including remote alteration in
some ventilator settings. While these data can be valu-
able in identifying problems with ventilation such as
insufficient use, hypoventilation, leak and upper airway
obstruction,74 the validity of many of the signals pro-
vided by home ventilator software has yet to be
confirmed.74–76 For example, recent work suggests data
downloaded to the datacard frequently underestimates
tidal volume relative to the target tidal volume, which
could trigger unnecessary clinician intervention.77
Respirology (2019)
7
Furthermore, different factors influenced the size of
this difference depending on the brand of device
used.77 Nevertheless, these data can improve the clini-
cian’s ability to recognize potential problems early and
intervene.78 Incorporation of additional signals into the
ventilator such as oximetry in conjunction with
machine-derived signals such as airflow and leak can
provide valuable information to guide the optimization
of therapy, with potentially significant clinical impact.79
Automatic EPAP
Some NIV modes now incorporate automatically
adjusting EPAP (AutoEPAP) to maintain upper airway
patency during BPAP or Va-BPAP therapy. By provid-
ing the lowest optimal level of EPAP needed for any
sleep stage or body position, overall airway pressure
may be lower without compromising tidal volume or
unnecessarily increasing leak. Theoretically, this could
improve comfort and acceptance of therapy, produc-
ing better long-term outcomes. However, there is a
paucity of data confirming the efficacy of this mode.
McArdle et al. recently evaluated AutoEPAP in combi-
nation with Va-BPAP in 25 patients with chronic hypo-
ventilation and co-morbid OSA.80 Patients were stable
and established on BPAP (S or ST modes). Randomiza-
tion was to either AutoEPAP or fixed EPAP Va-BPAP on
two separate nights. No difference in mean AHI or other
PSG-derived sleep and breathing variables was seen
between modes with self-reported sleep quality also simi-
lar. However, there were some individual patient differ-
ences in response to the two modes, and while the
authors were unable to identify specific predictors for
this, post hoc analysis suggested leaks in the AutoEPAP
mode might influence control of OSA.80 A subsequent,
multicentre randomized study of 38 patients with chronic
respiratory failure and AHI > 5 h previously established
on BPAP (either fixed and Va modes) has likewise found
the use of AutoEPAP to be non-inferior to manually
titrated EPAP in controlling upper airway obstruction dur-
ing a single night of Va-BPAP therapy.81 Longer term
studies evaluating the impact on adherence and clinical
© 2019 Asian Pacific Society of Respirology
8 AJ Piper
outcomes are needed, as well as studies of BPAP-naïve
patients.81
In a retrospective, cohort-matched trial, Gursel et al.
evaluated the addition of AutoEPAP to Va-BPAP in a
heterogeneous group of hypercapnic patients admitted
to ICU.82 The target tidal volume set for both groups
was similar (501  42 mL for Va-BPAP-AutoEPAP vs
497  37 mL for Va-BPAP). A significant difference in
the reduction in PaCO2 in the first 6 h was seen
favouring Va-BPAP-AutoEPAP (7  7 vs 2  5 mm Hg),
with PaCO2 falling greater than 5 mm Hg in 93% of
those with added AutoEPAP compared to 60% of those
using volume assurance alone. A similar proportion of
patients in both groups experienced a 10% fall in CO2
levels over the treatment period, although this occurred
more rapidly in those with added AutoEPAP. Mean
inspiratory pressures were similar, but maximum EPAP
and actual delivered tidal volumes were higher in the
Va-BPAP-AutoEPAP group.
Clinical implications
The use of AutoEPAP in conjunction with BPAP may be
particularly applicable to the acute setting. Frequently,
patients require ventilatory support on a near-continuous
basis initially, with potentially differing EPAP require-
ments during wakefulness compared to sleep. Clinicians
may not be aware or do not have the time to continu-
ously adjust EPAP to optimize airway patency with
changing sleep–wake states. In either the acute or chronic
setting, autotitrating EPAP may be of greatest benefit in
obese patient and those with concomitant OSA.
Overall, the use of Va-BPAP with AutoEPAP offers
the possibility of simplifying the set up of BPAP, poten-
tially reducing the need for an in-laboratory titration to
commence therapy or to review the efficiency of venti-
lation in those already established on treatment. By
providing a more immediate response to issues affect-
ing the efficacy of ventilatory support such as upper
airway obstruction or hypoventilation, autotitrating
BPAP therapy modes may enhance adherence to ther-
apy, reduce costs and improve clinical outcomes.68,83
Longer term studies are required to determine if these
potential advantages will translate into relevant clinical
benefits.
CONCLUSIONS
Clinicians managing patients with SDB or nocturnal
hypoventilation now have a broader range of ventila-
tory modes using varying algorithms and ancillary fea-
tures to choose from. While this provides the
opportunity to select a mode of therapy which best fits
the ventilatory needs of the patient, it also requires a
clear understanding of the principles and indications of
the chosen mode. Automatically adjusting modes of
ventilation have the potential to both simplify and opti-
mize therapy in patients with a wide range of complex
sleep breathing abnormalities. However, it must also
be acknowledged that robust evidence demonstrating
these newer modes of ventilation provide any greater
clinical benefits than fixed pressure modes is lacking,
© 2019 Asian Pacific Society of Respirology
and in some clinical situations or patients, outcomes
may prove worse.
Advancements in technology are also broadening
our options for continuous long-term monitoring of a
patient’s response to and acceptance of therapy. While
these developments are a very welcome addition to our
clinical toolkit,78 they do not replace informed clinical
judgment and considered manual intervention.
The Author: A.J.P. is a physiotherapist responsible for managing
the acute and home ventilation services provided by the Depart-
ment of Respiratory and Sleep Medicine at Royal Prince Alfred
Hospital. Her research interests include the assessment and man-
agement of nocturnal hypoventilation syndromes with a particular
focus on obesity hypoventilation and neuromuscular disorders.
Abbreviations: ADVENT-HF trial, Adaptive Servo-ventilation for
Therapy of Central and Obstructive Sleep Apnea in Heart
Failure; AHI, apnoea–hypopnoea index; ASV, adaptive
servoventilation; AutoEPAP, automatically adjusting EPAP;
BPAP, bilevel PAP; CHF, chronic heart failure; COPD, chronic
obstructive pulmonary disease; CPAP, continuous PAP; CSA,
central sleep apnoea; CSR, Cheyne–Stokes respiration; EPAP,
expiratory PAP; ICU, intensive care unit; IPAP, inspiratory PAP;
LVEF, left ventricular ejection fraction; NIV, non-invasive
ventilation; OSA, obstructive sleep apnoea; PaCO2, Partial
pressure of arterial carbon dioxide; PAP, positive airway
pressure; PSG, polysomnogram; REM, rapid eye movement;
SDB, sleep-disordered breathing; SERVE-HF trial, Treatment of
Predominant Central Sleep Apnoea by Adaptive Servo
Ventilation in Patients With Heart Failure Trial; ST, spontaneous
timed; TE, treatment emergent; Va, volume-assured; VT, Tidal
volume.
REFERENCES
1 Ellis ER, Bye PTP, Bruderer JW, Sullivan CE. Treatment of respira-
tory failure during sleep in patients with neuromuscular disease.
Am. Rev. Respir. Dis. 1987; 135: 148–52.
2 Ellis ER, Grunstein RR, Chan S, Bye PT, Sullivan CE. Noninvasive
ventilatory support during sleep improves respiratory failure in
kyphoscoliosis. Chest 1988; 94: 811–5.
3 Piper A, Sullivan C. Effects of short-term NIPPV in the treatment of
patients with severe obstructive sleep apnea and hypercapnia.
Chest 1994; 105: 434–40.
4 Bott J, Carroll MP, Conway JH, Keilty SE, Ward EM, Brown AM,
Paul EA, Elliott MW, Godfrey RC, Wedzicha JA et al. Randomised
controlled trial of nasal ventilation in acute ventilatory failure due
to chronic obstructive airways disease. Lancet 1993; 341: 1555–7.
5 Piper AJ, Parker S, Torzillo PJ, Sullivan CE, Bye PT. Nocturnal nasal
IPPV stabilizes patients with cystic fibrosis and hypercapnic respi-
ratory failure. Chest 1992; 102: 846–50.
6 Sanders MH, Kern N. Obstructive sleep apnea treated by indepen-
dently adjusted inspiratory and expiratory positive airway pres-
sures via nasal mask. Physiologic and clinical implications. Chest
1990; 98: 317–24.
7 Meduri GU, Conoscenti CC, Menashe P, Nair S. Noninvasive face
mask ventilation in patients with acute respiratory failure. Chest
1989; 95: 865–70.
8 Meecham Jones DJ, Wedzicha JA. Comparison of pressure and vol-
ume preset nasal ventilator systems in stable chronic respiratory
failure. Eur. Respir. J. 1993; 6: 1060–4.
9 Restrick LJ, Fox NC, Braid G, Ward EM, Paul EA, Wedzicha JA.
Comparison of nasal pressure support ventilation with nasal inter-
mittent positive pressure ventilation in patients with nocturnal
hypoventilation. Eur. Respir. J. 1993; 6: 364–70.
Respirology (2019)
Advances in non-invasive PAP technology
10 Lindenauer PK, Stefan MS, Shieh MS, Pekow PS, Rothberg MB,
Hill NS. Outcomes associated with invasive and noninvasive ventila-
tion among patients hospitalized with exacerbations of chronic
obstructive pulmonary disease. JAMA Intern. Med. 2014; 174: 1982–93.
11 Garner DJ, Berlowitz DJ, Douglas J, Harkness N, Howard M,
McArdle N, Naughton MT, Neill A, Piper A, Yeo A et al. Home
mechanical ventilation in Australia and New Zealand. Eur.
Respir. J. 2013; 41: 39–45.
12 Selim B, Ramar K. Advanced positive airway pressure modes:
adaptive servo ventilation and volume assured pressure support.
Expert Rev. Med. Devices 2016; 13: 839–51.
13 Cassel W, Canisius S, Becker HF, Leistner S, Ploch T, Jerrentrup A,
Vogelmeier C, Koehler U, Heitmann J. A prospective polys-
omnographic study on the evolution of complex sleep apnoea.
Eur. Respir. J. 2011; 38: 329–37.
14 Allam JS, Olson EJ, Gay PC, Morgenthaler TI. Efficacy of adaptive
servoventilation in treatment of complex and central sleep apnea
syndromes. Chest 2007; 132: 1839–46.
15 Morgenthaler TI, Gay PC, Gordon N, Brown LK. Adaptive ser-
voventilation versus noninvasive positive pressure ventilation for
central, mixed, and complex sleep apnea syndromes. Sleep 2007;
30: 468–75.
16 Johnson KG, Johnson DC. Bilevel positive airway pressure worsens
central apneas during sleep. Chest 2005; 128: 2141–50.
17 Morgenthaler TI, Kuzniar TJ, Wolfe LF, Willes L, McLain WC 3rd,
Goldberg R. The complex sleep apnea resolution study: a prospective
randomized controlled trial of continuous positive airway pressure
versus adaptive servoventilation therapy. Sleep 2014; 37: 927–34.
18 Liu D, Armitstead J, Benjafield A, Shao S, Malhotra A, Cistulli PA,
Pepin JL, Woehrle H. Trajectories of emergent central sleep apnea
during CPAP therapy. Chest 2017; 152: 751–60.
19 Pepin JD, Woehrle H, Liu D, Shao S, Armitstead JP, Cistulli PA,
Benjafield AV, Malhotra A. Adherence to positive airway therapy
after switching from CPAP to ASV: a big data analysis. J. Clin. Sleep
Med. 2018; 14: 57–63.
20 Cao M, Javaheri S. Effects of chronic opioid use on sleep and wake.
Sleep Med. Clin. 2018; 13: 271–81.
21 Farney RJ, Walker JM, Cloward TV, Rhondeau S. Sleep-disordered
breathing associated with long-term opioid therapy. Chest 2003;
123: 632–9.
22 Wang D, Teichtahl H, Drummer O, Goodman C, Cherry G,
Cunnington D, Kronborg I. Central sleep apnea in stable metha-
done maintenance treatment patients. Chest 2005; 128: 1348–56.
23 Farney RJ, Walker JM, Boyle KM, Cloward TV, Shilling KC. Adap-
tive servoventilation (ASV) in patients with sleep disordered
breathing associated with chronic opioid medications for non-
malignant pain. J. Clin. Sleep Med. 2008; 4: 311–9.
24 Javaheri S, Harris N, Howard J, Chung E. Adaptive servoventilation
for treatment of opioid-associated central sleep apnea. J. Clin.
Sleep Med. 2014; 10: 637–43.
25 Cao M, Cardell CY, Willes L, Mendoza J, Benjafield A, Kushida C.
A novel adaptive servoventilation (ASVAuto) for the treatment of
central sleep apnea associated with chronic use of opioids. J. Clin.
Sleep Med. 2014; 10: 855–61.
26 Ramar K, Ramar P, Morgenthaler TI. Adaptive servoventilation in
patients with central or complex sleep apnea related to chronic opioid
use and congestive heart failure. J. Clin. Sleep Med. 2012; 8: 569–76.
27 Shapiro CM, Chung SA, Wylie PE, Hossain NK, Holle RH,
Rosenberg RP, Muehlbach MJ, Doekel RC, Pegram GV, Jasko JG.
Home-use servo-ventilation therapy in chronic pain patients with
central sleep apnea: initial and 3-month follow-up. Sleep Breath.
2015; 19: 1285–92.
28 Lanfranchi PA, Somers VK, Braghiroli A, Corra U, Eleuteri E,
Giannuzzi P. Central sleep apnea in left ventricular dysfunction: prev-
alence and implications for arrhythmic risk. Circulation 2003; 107:
727–32.
29 Bravata DM, McClain V, Austin C, Ferguson J, Burrus N, Miech EJ,
Matthias MS, Chumbler N, Ofner S, Foresman B et al. Diagnosing
and managing sleep apnea in patients with chronic
Respirology (2019)
9
cerebrovascular disease: a randomized trial of a home-based strat-
egy. Sleep Breath. 2017; 21: 713–25.
30 Parra O, Arboix A, Montserrat JM, Quinto L, Bechich S, Garcia-
Eroles L. Sleep-related breathing disorders: impact on mortality of
cerebrovascular disease. Eur. Respir. J. 2004; 24: 267–72.
31 Naughton MT, Benard DC, Liu PP, Rutherford R, Rankin F,
Bradley TD. Effects of nasal CPAP on sympathetic activity in
patients with heart failure and central sleep apnea. Am. J. Respir.
Crit. Care Med. 1995; 152: 473–9.
32 Arzt M, Floras JS, Logan AG, Kimoff RJ, Series F, Morrison D,
Ferguson K, Belenkie I, Pfeifer M, Fleetham J et al. Suppression of
central sleep apnea by continuous positive airway pressure and
transplant-free survival in heart failure: a post hoc analysis of the
Canadian Continuous Positive Airway Pressure for Patients with
Central Sleep Apnea and Heart Failure Trial (CANPAP). Circulation
2007; 115: 3173–80.
33 Teschler H, Dohring J, Wang YM, Berthon-Jones M. Adaptive pres-
sure support servo-ventilation: a novel treatment for Cheyne-
Stokes respiration in heart failure. Am. J. Respir. Crit. Care Med.
2001; 164: 614–9.
34 Willson GN, Wilcox I, Piper AJ, Flynn WE, Norman M,
Grunstein RR, Sullivan CE. Noninvasive pressure preset ventilation
for the treatment of Cheyne-Stokes respiration during sleep. Eur.
Respir. J. 2001; 17: 1250–7.
35 Kasai T, Kasagi S, Maeno K-I, Dohi T, Kawana F, Kato M, Naito R,
Ishiwata S, Ohno M, Yamaguchi T et al. Adaptive servo-ventilation
in cardiac function and neurohormonal status in patients with
heart failure and central sleep apnea nonresponsive to continuous
positive airway pressure. JACC Heart Failure 2013; 1: 58–63.
36 Philippe C, Stoica-Herman M, Drouot X, Raffestin B, Escourrou P,
Hittinger L, Michel PL, Rouault S, d’Ortho MP. Compliance with and
effectiveness of adaptive servoventilation versus continuous positive
airway pressure in the treatment of Cheyne-Stokes respiration in
heart failure over a six month period. Heart 2006; 92: 337–42.
37 Randerath WJ, Nothofer G, Priegnitz C, Anduleit N, Treml M,
Kehl V, Galetke W. Long-term auto-servoventilation or constant
positive pressure in heart failure and coexisting central with
obstructive sleep apnea. Chest 2012; 142: 440–7.
38 Wu X, Fu C, Zhang S, Liu Z, Li S, Jiang L. Adaptive servoventilation
improves cardiac dysfunction and prognosis in heart failure
patients with sleep-disordered breathing: a meta-analysis. Clin.
Respir. J. 2017; 11: 547–57.
39 Aurora RN, Chowdhuri S, Ramar K, Bista SR, Casey KR, Lamm CI,
Kristo DA, Mallea JM, Rowley JA, Zak RS et al. The treatment of
central sleep apnea syndromes in adults: practice parameters with
an evidence-based literature review and meta-analyses. Sleep 2012;
35: 17–40.
40 Cowie MR, Woehrle H, Wegscheider K, Angermann C,
d’Ortho MP, Erdmann E, Levy P, Simonds AK, Somers VK,
Zannad F et al. Adaptive servo-ventilation for central sleep apnea
in systolic heart failure. N. Engl. J. Med. 2015; 373: 1095–105.
41 Woehrle H, Cowie MR, Eulenburg C, Suling A, Angermann C,
d’Ortho MP, Erdmann E, Levy P, Simonds AK, Somers VK et al.
Adaptive servo ventilation for central sleep apnoea in heart failure:
SERVE-HF on-treatment analysis. Eur. Respir. J. 2017; 50: 1601692.
42 Cowie MR, Woehrle H, Wegscheider K, Vettorazzi E, Lezius S,
Koenig W, Weidemann F, Smith G, Angermann C, d’Ortho MP
et al. Adaptive servo-ventilation for central sleep apnoea in systolic
heart failure: results of the major substudy of SERVE-HF. Eur.
J. Heart Fail. 2018; 20: 536–44.
43 Aurora RN, Bista SR, Casey KR, Chowdhuri S, Kristo DA,
Mallea JM, Ramar K, Rowley JA, Zak RS, Heald JL. Updated adap-
tive servo-ventilation recommendations for the 2012 AASM guide-
line: "the treatment of central sleep apnea syndromes in adults:
practice parameters with an evidence-based literature review and
meta-analyses". J. Clin. Sleep Med. 2016; 12: 757–61.
44 Ayas NT, Patil SP, Stanchina M, Malhotra A. Treatment of central
sleep apnea with adaptive servoventilation in chronic heart failure.
Am. J. Respir. Crit. Care Med. 2015; 192: 132–3.
© 2019 Asian Pacific Society of Respirology
10
45 Brill AK, Rosti R, Hefti JP, Bassetti C, Gugger M, Ott SR. Adaptive
servo-ventilation as treatment of persistent central sleep apnea in
post-acute ischemic stroke patients. Sleep Med. 2014; 15: 1309–13.
46 O’Connor CM, Whellan DJ, Fiuzat M, Punjabi NM, Tasissa G,
Anstrom KJ, Benjafield AV, Woehrle H, Blase AB, Lindenfeld J
et al. Cardiovascular outcomes with minute ventilation-targeted
adaptive servo-ventilation therapy in heart failure: the CAT-HF
Trial. J. Am. Coll. Cardiol. 2017; 69: 1577–87.
47 Lyons OD, Floras JS, Logan AG, Beanlands R, Cantolla JD,
Fitzpatrick M, Fleetham J, John Kimoff R, Leung RS, Lorenzi
Filho G et al. Design of the effect of adaptive servo-ventilation on
survival and cardiovascular hospital admissions in patients with
heart failure and sleep apnoea: the ADVENT-HF trial. Eur. J. Heart
Failure. 2017; 19: 579–87.
48 Parra O, Sanchez-Armengol A, Capote F, Bonnin M, Arboix A,
Campos-Rodriguez F, Perez-Ronchel J, Duran-Cantolla J,
Martinez-Null C, de la Pena M et al. Efficacy of continuous positive
airway pressure treatment on 5-year survival in patients with
ischaemic stroke and obstructive sleep apnea: a randomized con-
trolled trial. J. Sleep Res. 2015; 24: 47–53.
49 Tsivgoulis G, Zhang Y, Alexandrov AW, Harrigan MR, Sisson A,
Zhao L, Brethour M, Cava L, Balucani C, Barlinn K et al. Safety
and tolerability of early noninvasive ventilatory correction using
bilevel positive airway pressure in acute ischemic stroke. Stroke
2011; 42: 1030–4.
50 Javaheri S, Goetting MG, Khayat R, Wylie PE, Goodwin JL,
Parthasarathy S. The performance of two automatic servo-
ventilation devices in the treatment of central sleep apnea. Sleep
2011; 34: 1693–8.
51 Javaheri S, Winslow D, McCullough P, Wylie P, Kryger MH. The
use of a fully automated automatic adaptive servoventilation algo-
rithm in the acute and long-term treatment of central sleep apnea.
Chest 2015; 148: 1454–61.
52 Crisafulli E, Manni G, Kidonias M, Trianni L, Clini EM. Subjective
sleep quality during average volume assured pressure support
(AVAPS) ventilation in patients with hypercapnic COPD: a physio-
logical pilot study. Lung 2009; 187: 299–305.
53 Janssens JP, Metzger M, Sforza E. Impact of volume targeting on
efficacy of bi-level non-invasive ventilation and sleep in obesity-
hypoventilation. Respir. Med. 2009; 103: 165–72.
54 Murphy PB, Davidson C, Hind MD, Simonds A, Williams AJ,
Hopkinson NS, Moxham J, Polkey M, Hart N. Volume targeted ver-
sus pressure support non-invasive ventilation in patients with
super obesity and chronic respiratory failure: a randomised con-
trolled trial. Thorax 2012; 67: 727–34.
55 Nilius G, Katamadze N, Domanski U, Schroeder M, Franke KJ.
Non-invasive ventilation with intelligent volume-assured pressure
support versus pressure-controlled ventilation: effects on the respi-
ratory event rate and sleep quality in COPD with chronic hyper-
capnia. Int. J. Chron. Obstruct. Pulmon. Dis. 2017; 12: 1039–45.
56 Oscroft NS, Chadwick R, Davies MG, Quinnell TG, Smith IE. Volume
assured versus pressure preset non-invasive ventilation for compen-
sated ventilatory failure in COPD. Respir. Med. 2014; 108: 1508–15.
57 Storre JH, Seuthe B, Fiechter R, Milioglou S, Dreher M, Sorichter S,
Windisch W. Average volume-assured pressure support in obesity
hypoventilation: a randomized crossover trial. Chest 2006; 130:
815–21.
58 Khayat A, Medin D, Syed F, Moraes TJ, Bin-Hasan S, Narang I, Al-
Saleh S, Amin R. Intelligent volume-assured pressured support
(iVAPS) for the treatment of congenital central hypoventilation
syndrome. Sleep Breath. 2017; 21: 513–9.
59 Crescimanno G, Marrone O, Vianello A. Efficacy and comfort of
volume-guaranteed pressure support in patients with chronic ven-
tilatory failure of neuromuscular origin. Respirology 2011; 16:
672–9.
60 Nicholson TT, Smith SB, Siddique T, Sufit R, Ajroud-Driss S,
Coleman JM III, Wolfe LF. Respiratory pattern and tidal volumes
differ for pressure support and volume-assured pressure support
in amyotrophic lateral sclerosis. Ann. Am. Thorac. Soc. 2017; 14:
1139–46.
© 2019 Asian Pacific Society of Respirology
AJ Piper
61 Piesiak P, Brzecka A, Kosacka M, Jankowska R. Efficacy of noninva-
sive volume targeted ventilation in patients with chronic respira-
tory failure due to kyphoscoliosis. Adv. Exp. Med. Biol. 2015;
838: 53–8.
62 Murphy PB, Rehal S, Arbane G, Bourke S, Calverley PMA,
Crook AM, Dowson L, Duffy N, Gibson GJ, Hughes PD et al. Effect
of home noninvasive ventilation with oxygen therapy vs oxygen
therapy alone on hospital readmission or death after an acute
COPD exacerbation: a randomized clinical trial. JAMA 2017; 317:
2177–86.
63 Kohnlein T, Windisch W, Kohler D, Drabik A, Geiseler J, Hartl S,
Karg O, Laier-Groeneveld G, Nava S, Schonhofer B et al. Non-
invasive positive pressure ventilation for the treatment of severe
stable chronic obstructive pulmonary disease: a prospective, multi-
centre, randomised, controlled clinical trial. Lancet Respir. Med.
2014; 2: 698–705.
64 Kelly JL, Jaye J, Pickersgill RE, Chatwin M, Morrell MJ,
Simonds AK. Randomized trial of ’intelligent’ autotitrating ventila-
tion versus standard pressure support non-invasive ventilation:
impact on adherence and physiological outcomes. Respirology
2014; 19: 596–603.
65 Briones Claudett KH, Briones Claudett M, Chung Sang Wong M,
Nuques Martinez A, Soto Espinoza R, Montalvo M, Esquinas
Rodriguez A, Gonzalez Diaz G, Grunauer Andrade M. Noninvasive
mechanical ventilation with average volume assured pressure sup-
port (AVAPS) in patients with chronic obstructive pulmonary dis-
ease and hypercapnic encephalopathy. BMC Pulm. Med. 2013;
13: 12.
66 Turk M, Aydogdu M, Gursel G. Effects of modes, obesity, and body
position on non-invasive positive pressure ventilation success in
the intensive care unit: a randomized controlled study. Turk.
Thorac. J. 2018; 19: 28–35.
67 Cao Z, Luo Z, Hou A, Nie Q, Xie B, An X, Wan Z, Ye X, Xu Y,
Chen X et al. Volume-targeted versus pressure-limited noninvasive
ventilation in subjects with acute hypercapnic respiratory failure: a
multicenter randomized controlled trial. Respir. Care 2016; 61:
1440–50.
68 Murphy PB, Arbane G, Ramsay M, Suh E-S, Mandal S, Jayaram D,
Leaver S, Polkey MI, Hart N. Safety and efficacy of auto-titrating
noninvasive ventilation in COPD and obstructive sleep apnoea
overlap syndrome. Eur. Respir. J. 2015; 46: 548–51.
69 Selim BJ, Wolfe L, Coleman JM 3rd, Dewan NA. Initiation of non-
invasive ventilation for sleep related hypoventilation disorders:
advanced modes and devices. Chest 2018; 153: 251–65.
70 Berry R, Chediak A, Brown L, Finder J, Gozal D, Iber C, Kushida C,
Morgenthaler T, Rowley J, Davidson-Ward S. Best clinical practices
for the sleep center adjustment of noninvasive positive pressure
ventilation (NPPV) in stable chronic alveolar hypoventilation syn-
dromes. J. Clin. Sleep Med. 2010; 6: 491–509.
71 Windisch W, Storre JH. Target volume settings for home mechani-
cal ventilation: great progress or just a gadget? Thorax 2012; 67:
663–5.
72 Luján M, Sogo A, Grimau C, Pomares X, Blanch L, Monsó E. Influ-
ence of dynamic leaks in volume-targeted pressure support nonin-
vasive ventilation: a bench study. Respir. Care 2015; 60: 191–200.
73 Khirani S, Louis B, Leroux K, Delord V, Fauroux B, Lofaso F.
Harms of unintentional leaks during volume targeted pressure
support ventilation. Respir. Med. 2013; 107: 1021–9.
74 Rabec C, Georges M, Kabeya NK, Baudouin N, Massin F, Reybet-
Degat O, Camus P. Evaluating noninvasive ventilation using a
monitoring system coupled to a ventilator: a bench-to-bedside
study. Eur. Respir. J. 2009; 34: 902–13.
75 Contal O, Vignaux L, Combescure C, Pepin J, Jolliet P, Janssens J.
Monitoring of noninvasive ventilation by built-in software of home
bilevel ventilators: a bench study. Chest 2012; 141: 469–76.
76 Janssens JP, Borel JC, Pepin JL. Nocturnal monitoring of home
non-invasive ventilation: the contribution of simple tools such as
pulse oximetry, capnography, built-in ventilator software and
autonomic markers of sleep fragmentation. Thorax 2011; 66:
438–45.
Respirology (2019)
Advances in non-invasive PAP technology
77 Stagnara A, Baboi L, Nesme P, Subtil F, Louis B, Guerin C. Reli-
ability of tidal volume in average volume assured pressure support
mode. Respir. Care 2018; 63: 1139–46.
78 Mansell SK, Cutts S, Hackney I, Wood MJ, Hawksworth K,
Creer DD, Kilbride C, Mandal S. Using domiciliary non-invasive
ventilator data downloads to inform clinical decision-making to
optimise ventilation delivery and patient compliance. BMJ Open
Respir. Res. 2018; 5: e000238.
79 Gonzalez-Bermejo J, Morelot-Panzini C, Arnol N, Meininger V,
Kraoua S, Salachas F, Similowski T. Prognostic value of efficiently
correcting nocturnal desaturations after one month of non-
invasive ventilation in amyotrophic lateral sclerosis: a retrospective
monocentre observational cohort study. Amyotroph. Lateral Scler.
Frontotemporal Degener. 2013; 14: 373–9.
80 McArdle N, Rea C, King S, Maddison K, Ramanan D,
Ketheeswaran S, Erikli L, Baker V, Armitstead J, Richards G et al.
Treating chronic hypoventilation with automatic adjustable versus
fixed EPAP intelligent volume-assured positive airway pressure
Respirology (2019)
11
support (iVAPS): a randomized controlled trial. Sleep 2017; 40:
zsx136.
81 Orr JE, Coleman J, Criner GJ, Sundar KM, Tsai SC, Benjafield AV,
Crocker ME, Willes L, Malhotra A, Owens RL et al. Automatic
EPAP intelligent volume-assured pressure support is effective in
patients with chronic respiratory failure: a randomized trial.
Respirology 2019; xxx: xxxx. https://doi.org/10.1111/resp.13546.
82 Gursel G, Zerman A, Basarik B, Gonderen K, Aydogdu M,
Memmedova S. Noninvasive auto-titrating ventilation (AVAPS-AE)
versus average volume-assured pressure support (AVAPS) ventila-
tion in hypercapnic respiratory failure patients. Intern. Emerg.
Med. 2018; 13: 359–65.
83 Mandal S, Arbane G, Murphy P, Elliott MW, Janssens JP, Pepin JL,
Muir JF, Cuvelier A, Polkey M, Parkin D et al. Medium-term cost-
effectiveness of an automated non-invasive ventilation outpatient
set-up versus a standard fixed level non-invasive ventilation inpa-
tient set-up in obese patients with chronic respiratory failure: a
protocol description. BMJ Open 2015; 5: e007082.
© 2019 Asian Pacific Society of Respirology