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Effects of sleep posture on upper airway stability in patients with obstructive sleep apnea

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  • Flinders University and Flinders Medical Centre
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Effects of sleep posture on upper airway stability in patients with obstructive sleep apnea

Abstract and Figures

Changes in sleep posture have been shown to improve obstructive sleep apnea (OSA). To investigate the mechanisms by which this occurs we assessed upper airway stability in eight patients with severe OSA in three postures (supine, elevated to 30 degrees, and lateral). We used a specially adapted nasal continuous positive airway pressure (nCPAP) mask to measure upper airway closing pressure (UACP) and upper airway opening pressure (UAOP) during non-REM sleep. Statistical comparisons were made between postures using ANOVA for repeated measures. Elevation resulted in a less collapsible airway compared with both the supine and lateral positions (mean UACP: 30 degrees elevation -4.0 +/- 3.2 compared with supine 0.3 +/- 2.4 cm H2O, p < 0.05 and; lateral -1.1 +/- 2.2 cm H2O, p < 0.05). Supine UACP and lateral UACP were not significantly different. Elevation or lateral positioning produced a 50% reduction in mean UAOP (supine 10.4 +/- 3.5 cm H2O compared with 30 degrees elevation 5.3 +/- 2.1, p < 0.05; and lateral 5.5 +/- 2.1 cm H2O, p < 0.05). We conclude that in severely affected OSA patients upper body elevation, and to a lesser extent lateral positioning, significantly improve upper airway stability during sleep, and may allow therapeutic levels of nCPAP to be substantially reduced.
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Effects
of
Sleep Posture
on
Upper Airway Stability
in Patients with Obstrudive Sleep Apnea
ALISTER
McKENZIE NEILL,
SUSAN
MICHELLE ANGUS, DIMITAR
SAJKOV,
and RONALD DOUGLAS McEVOY
Sleep Disorders Unit, Repatriation General Hospital, Adelaide, Australia
Changes in sleep posture have
been
shown to improve obstructive sleep
apnea
(OSA).To investigate
the
mechanisms by which this occurs we assessed
upper
airway stability in
eight
patients with severe
OSAin
three
postures (supine, elevated to 30
0
,
and
lateral). We used a specially
adapted
nasal con-
tinuous positive airway pressure (nCPAP) mask to
measure
upper
airway closing pressure (UACP)
and
upper
airway
opening
pressure (UAOP)during non-REMsleep. Statistical comparisons were
made
be-
tween
postures using
ANOVA
for
repeated
measures. Elevation resulted in a less collapsible airway
compared
with both
the
supine
and
lateral positions
(mean
UACP:
30
0
elevation
-4.0
± 3.2 compared
with supine
0.3 ±
2.4
cm H20, p <
0.05
and; lateral
-1.1
±
2.2
cm H20, p <
0.05).
Supine
UACP
and
lateral
UACP
were
not
significantly different. Elevation or lateral positioning
produced
a
50%
reduc-
tion in mean
UAOP
(supine
10.4
± 3.5 cm H20
compared
with
30
0
elevation
5.3
± 2.1, P <0.05;
and
lateral
5.5
± 2.1 cm H20, p <
0.05).
We conclude
that
in severely affected OSA patients
upper
body
elevation,
and
to a lesser
extent
lateral positioning, significantly improve
upper
airwaystability during
sleep,
and
may allow
therapeutic
levels of nCPAPto be substantially reduced. Neill AM,
Angus
SM,
SaJkov D, McEvoy RD. Effects
of
sleep
posture
on
upper
airway
stability
In
patients
with
ob-
structive
sleep
apnea.
AM J RESPIR CRIT CARE MED
1997;155:199-204.
Sleep posture is known to influence the frequency of sleep-dis-
ordered breathing inabout
60070
of patients with obstructive sleep
apnea syndrome (OSAS)(1-3). Improvements in sleep-disordered
breathing have been demonstrated in the lateral compared with
the supine posture (1-3) and shown to be more pronounced in
non-rapid eye movement (non-REM) sleep (3) and in the non-
obese patient
(1). We previously found that upper body eleva-
tion of 30° to 60° also reduced the frequency
of
sleep-disordered
breathing eventsin OSAS patients with the greatest improvements
occurring in the most obese (2).
The mechanisms by which these postural changes improve
sleep-disordered breathing remain poorly understood.
It
has been
proposed that in the lateral posture there is a reduced tendency
for the tongue to relapse posteriorly making collapse of the phar-
ynx lesslikely(1).A similar mechanism may operate while sleep-
ingwith upper body elevation, although this postural change also
increases lung volume (4) which itself has been shown to be as-
sociated with increased upper airway size (5-7)
and
reduced up-
per airway resistance (8, 9).
The effects
of
posture on upper airway size have been inves-
tigated in awake normal subjects and patients with OSAS using
lateralcephalometry
(10),
an acoustic reflection technique
(11-14),
(Receivedin original form January 22, 1996 and in revised form May 1, 1996)
Supported by the National Health and Medical
Research
Council and the Depart-
ment
of Veterans' Affairs (Australia).
Correspondence and requests for reprints should be addressed to Dr. Alister
Neill, Departmentof Respiratory Medicine, Repatriation General Hospital, Daw
Park, South Australia
5041,
Australia.
Am
J Respir Crit
Care
Med Vol
155.
pp
199-204,
1997
and
computed tomographic (CT) scanning (15). An increase in
upper airway size has been demonstrated moving from the su-
pine to sitting position
(11-14)
but no significant change in size
in moving from the supine to the lateral position (12, 14, 15).
It
is not known whether these changes apply in sleep
and
at best
they would account for only some of the previously reported ef-
fects
of
posture on sleep-disordered breathing.
Tobetter understand the effects of posture on sleep-disordered
breathing wemeasured upper airwaystability in sleeping, severely
affected OSAS patients in three different sleep postures (supine,
lateral, and 30° elevation) using two different measures
of
up-
per airway stability:
(1) upper airway closing pressure (UACP)
by the method
of
Issa
and
Sullivan (16), and (2) upper airway
opening pressure (UAOP) defined as the minimal level
of
nasal
continuous positive airway pressure (nCPAP) required to prevent
apneas and hypopneas. We hypothesized that a small degree of
upper body elevation or lateral positioning during sleep would
producea more stable airway compared with the supine posture.
Of
additional practical interest was the extent to which sleeping
with a small degree
of
upper body elevation, or in the lateral
decubitus position would allow the therapeutic nCPAP to be re-
duced in severely affected OSAS patients.
METHODS
Patient
Selection
Eight obese patients with severe OSAS (body mass index [BMI] >30
kg/rrr', respiratory disturbance index [RDI]
>40/h) wererecruited from
our clinic population. All patients had had a previous diagnostic sleep
study and nCPAP titration study and were established on treatment at
home at therapeutic pressure
of
~
9 cm H
2
0 . Nasal CPAP therapy was
discontinued for one night before the study in an attempt to approxi-
200
AMERICAN JOURNALOF
RESPIRATORY
AND CRITICAL
CARE
MEDICINE
VOl155
1997
mate the untreated state before making measurements
of
upper airway
opening and closing pressures (17). Patients were instructed to refrain
from taking alcohol or sedative medication on the evening prior to the
study. Clinical data,
pulmonary
function tests,
and
routine hematology
and
biochemistry tests were collected from all patients to exclude other
significant medical conditions (e.g.,chronic obstructivepulmonary dis-
ease, diabetes, renal failure). Written informed consent was obtained
in all cases
and
the study was approved by
our
institution's research and
ethics committee.
Measurements
All physiologic signals were recorded on a computer(Sleepwatch; Com-
pumedics, Melbourne, Australia)
and
displayed on a high-resolution
20-inch monitor (NEC multisync 6FG, Tokyo, Japan). Standard poly-
somnographic recordings were made
of
electroencephalogram (EEG),
electro-oculogram (EOG), and submental electromyogram (EMG) (digital
sampling speeds: 125Hz for
EEG,
EOG, EMG). A two-lead electrocar-
diogram (ECG), pulse oximetry (Criticare 504 Systems Inc., Waukesha,
WI), thoracic and abdominal movements (inductance plethysmography)
were also recorded (digital sampling speed 50 Hz). The pressure in a
specially designed mask (as described subsequently)was measuredcon-
tinuously and displayed simultaneously on a laptopcomputer using data
acquisition software (Windaq, version 1.15, 1992-1994; Datac Instru-
ments, Inc., Akron,
OH)
and
on the Sleepwatch, Compumedics system.
Diaphragmatic
EMG
was recorded using a pair
of
silver chloride sur-
faceelectrodes, placed in the anterior axillary line in an intercostal space
adjacent to the costal margin. The position
of
the patient in bed, and
leg movements were also recorded.
Experimental
Protocol
On the study night each patient was fitted with a modified nCPAP mask
similar to
that
described by Issa
and
Sullivan (16). A nCPAP mask
(ResMed, Sydney, Australia) was fitted with a rigid plastic tube (inter-
nal diameter [ID] 23 mm) for delivery
of
a bias flow
of
roomair at vary-
ing levels
of
positive pressure (3.8 to 20.0 em H
2
0, Sullivan III nasal
CPAP pump; ResMed, Sydney,Australia). Small
paired holes weredrilled
into the walls
of
the
tube
allowing two Foley urinary balloon catheters
to be positioned across the direction
of
bias airflow in the inlet
and
out-
let ports respectively. These catheters were joined by a T-piece
and
at-
tached to a long piece
of
thin plastic tubing
that
extended outside the
patient's room
and
was attached to a 60-ml air-filled syringe. The sy-
ringe was used to inflate the balloons thereby causing rapid, complete
airway obstruction. Release
of
the syringe plunger allowed deflation of
the balloons
and
restoration
of
airflow. Another smaller catheter was
positioned in the mask to measure airway pressure. Before turning the
lights out the
mouth
was sealed with tape, to prevent air leaks
that
might
invalidate pressure measurements.
The patient was placed in one
of
three randomly allocated positions
(supine, lateral, or 30° elevation) and allowed to fall asleep. Once the
patient was in non-REM sleep (stage II, III, or IV) for a minimum
of
5 min and direct video monitoring confirmed
that
the patient had main-
tained this sleep posture, we made replicate measurements
of
UAOP
and
UACP.
Upper
Airway
Opening
Pressure
We defined UAOP as the minimal level
of
nCPAP
that
abolished ob-
structive apneas
and
hypopneas, and prevented falls in Sa02
of>
2070
from baseline.
It
was determined by slowly increasing nCPAP from a
levelat which cyclicdisordered breathing was clearly evident until com-
plete airway opening was achieved according to the above criteria. The
pressure wasthen lowered until spontaneous apneas
and
hypopneas were
again seen
and
the procedure to determine UAOP repeated three times.
The UAOP was measured from the polysomnographic record by aver-
aging the airway pressure values at 0.5-s intervals for five consecutive
breaths after the UAOP was reached. The mean
of
three UAOP deter-
minations was calculated for each posture.
Upper
Airway
Closing
Pressure
With the patient at opening pressure, in non-REM sleep (stage II, III,
or IV), rapid complete airway occlusion was achieved by inflation of
the nasal mask balloons. Inspiratory efforts against the totally occluded
airway produced a characteristic pattern
of
airway pressure change in
all patients. Typically, after 1 to 3 breaths the smooth decrease in mask
pressure seen during early inspiration was noted to abruptly cease at
a critical level and thereafter plateau despite continuing respiratory ef-
fort (Figure 1).This sudden plateauing
of
pressure has previously been
shown to indicate closure
of
the upperairway between the nose
and
tho-
rax (16). With subsequent breathsduringthe period
of
nasal occlusion,
airway pressure repeatedly plateaued at the same critical value despite
progressive augmentation
of
respiratory effort (reflected by increased
thoracoabdominal movement
and
inspiratory diaphragmatic
EMG
ac-
tivity). In approximately
20070
of
occlusion tests the airway pressure did
not
increase during expiration with subsequent respiratory cycles but
remained at the plateau level. This different pattern has been observed
previously (16)
and
indicatescontinued closure
of
the upperairway dur-
ing the nasal occlusion test. Airway occlusion was maintained until an
arousal (EEG
alpha
waveswith increase in submental EMG) occurred,
or until 5 to 6 breaths demonstrating upper airway closure.
The
UACP
was definedas the mean
of
the minimum pressures generated in the last
two breaths before an arousal occurred, or the balloons were deflated
(whichever came first).
The
criteria for selection
of
a nasal occlusion test for analysis were:
(l)
the demonstration
of
a clear plateau
of
nasal mask pressure in the
presence
of
(2) increasing respiratory effort (i.e.,progressive augmenta-
tion
of
the respiratory bands
and/or
increasing activity
of
the diaphrag-
matic EMG), and (3)uninterrupted non-REMsleep (stages II-IV). Mul-
tiple occlusion tests were attempted (range 5 to 10)in each patient and
the mean UACP calculated for each sleep posture from successful trials.
Sleep
Staging
Sleep stage was scored manually according to the method
of
Rescht-
shaffen and Kales (18) and recorded for the 3 min before,
and
during
each opening pressure determination or nasal occlusion test.
Statistical Analysis
Analysis
of
variance (ANOVA) for repeated measures with Neuman-
Keuls multiplecomparison test was used to compare mean opening
and
closing pressures between sleeping postures in non-REM sleep (stages
II-IV). Student's
t test wasused to compareopening pressures in a speci-
fied sleep posture according to sleep stage (stage II versus
III/IV).
SIIQ Z
EEG
Pmask 15I
(an
H2O)
-15
Thoracic
Abdoninal
EMGdiaph
Timebase =45 seconds I page
Figure 1. Polysomnographic record showing a typical nasal occlu-
sion test. The nasal airway was occluded by balloon inflation for the
period between the arrows
during
stage II sleep in a
patient
with
OSAS.During this occlusion, mask pressure became negative early
during
eachinspiratory effort
but
then reachedaplateau despitecon-
tinuing
inspiratory effort. The
minimum
pressure in the mask
with
each successivebreath
during
the occlusion
did
not
become more
negative despite augmenting respiratory efforts reflected by the in-
creasing amplitude of thoracoabdominal movementsand inspiratory
diaphragmatic EMGactivity. From this
itcan
be inferred
thatthe
col-
lapsible portion
ofthe
upper
airway
closed
during
inspiration. UACP
was the mean of the
minimum
pressure generated in the last
two
breaths
prior
to arousal.
Neill, Angus, Sajkov, et
01.:
Sleep Posture
and
Upper Airway Stability
201
TABLE
1
DEMOGRAPHIC
CHARACTERISTICS
OF
THE
EIGHT
PATIENTS
STUDIED
Patient
Age
sex
8MI
AHI Prescribed nCPAP
Treatment
No.
(yr)
Male/female
(kg/m
2
)
(/h)
(em H2O)
(wk)
1
50
Male 32 75
9.5 24
2 24
Male 37 75 12.0
20
3 53
Male
36
66 9.0 20
4
50
Male 35
70 14.0 56
5 48
Male 30
73
10.0
1
6
29
Male 35
97
16.0
52
7 34
Male
50
119
20.0 6
8 38
Male
30
57 10.0 10
Mean 40.8 35.5
79.0 12.6 23.6
SO 11.0 6.4
19.8 3.9 20.3
Definition of abbreviations: 8MI = body mass index; AHI = apnea + hyponea per hour of sleep.
* Treatment duration
prior
to study.
RESULTS
Individual patientdetails are shown in Table 1.The patients were
all male, ranging in age from 24 to 53 yr,
and
obese with severe
obstructivesleep apnea(apneaplus hypopneaindex lAHI)
>60)
All
but
two
of
the
patients
had
been treated for more
than
2 mo
with nCPAP
and
all required a moderately high therapeutic pres-
sure (9 em H
20
or greater).
Influence of Posture on Upper Airway Closing Pressure
Weperformed repeated nasal occlusion tests in all eight patients
during
non-REM
sleep for each
of
the
three postures. In two
patients
the
criteria for an adequate nasal occlusion test were
not satisfied for
one
of
the sleep positions. The
data
from the
other (successful) sleep posture measurements in these patients
are shown in Figure 2
but
they were
not
included in the statisti-
cal analysis. In
the
remaining six patients we found the
UACP
at 30
0
elevation (mean ± SO:
-4.0
± 3.2 em H
20)
was signifi-
cantlylower
than
in the supine (mean ± SO: 0.3 ± 2.4 em H
20)
or lateral (mean ± SO: -1.1 ± 2.2em H
20)
positions. No statisti-
cally significant difference was found in UACP between the su-
pine
and
the lateral position. The statistically significant dif-
ferences remained when we compared mean
data
obtained
exclusively in stages
III/IV
non-REM sleep (n = 4). We
had
in-
sufficient
data
to determine whether sleep stage in a particular
posture affected UACP.
Influence of Posture on
Upper
Airway
Opening
Pressure
The
upper airway opening pressure for each patient in each
of
the three postures is shown in Figure 3. In one patientin the lateral
position
and
four patients in the elevated position, the airway
was open at the minimal pressure
that
could be achieved using
our
modified nCPAPcircuit (viz.,3.8em H
20).
In these instances
3.8 em H
20
was recorded as the UAOP, although in reality it
may well have been less.
The
mean UAOP for
the
eight patients
studied was significantly lower at 30
0
elevation (mean ± SO:
5.3
± 2.1em H
20)
and
in the lateral position (mean ± SD: 5.5 ±
UpperAirway Closing Pressure
Upper Airway Opening Pressure
Lateral
Elevation 30
0
p<0.05
r------------------------------------i
p < 0.05
-----------------··--·-----1
Supine
20
18
- 16
o
£ 14
5 12
- 10
!
i 8
fI)
! 6
0-
4
2
o
lateral
Elevation 30°
ns
I----~-----~--~--------------------l
~<O.05
r-- -
----------1
r__
----.Il~~·05
I
Supine
8
6
6' 4
N
:t: 2
E
~
0
~
-2
::s
~
-4
~
0-
-6
-8-
-10
Figure 2. Upper airway closing pressure in cm H20 for each subject
(n
= 8) inthreesleep postures. Data were obtained in
non-REM
sleep
stages
II-IV. The mean value for all patients according to sleep pos-
ture isshown by
the
bar. Elevationto 30° resulted in a less collapsi-
ble airway compared with both the supine
and
lateral positions.
Figure 3. Upper airway opening pressure in cm H20 for each sub-
ject (n
= 8) in three sleep postures. Data were obtained in
non-REM
sleep
s~ges
II-IV.
The mean value for allpatients according to sleep
posture
ISshown bythe bar. Elevationor lateral positioning produced
a 50% reduction in mean
UAOP.
202 AMERICAN JOURNAL OF
RESPIRATORY
AND
CRITICAL CARE
MEDICINE
VOL 155
1997
UpperAirway Opening Pressure
per airway closure. Closing pressurewas determined by repeated
trials
of
a variable stepwise
drop
in
nCPAP
for 1 to 2 breaths.
These investigators reported closing pressure estimates ranging
from - 2 to 7 em H
20
with the great majority
of
values being
slightly positive (i.e., 1 to 2 em H
20).
Our
results for UACP in
the supine posture were close to atmospheric pressure (mean
±
SD: 0.3 ± 2.4 cm H
20),
thatis, slightly higher thanthose reported
by Issa
and
Sullivan using the same technique
but
slightly lower
than
the closing pressure estimated by either extrapolation from
upperairway pressureversus flow curves or during direct visual-
ization
of
the
airway. Nasal occlusion over multiple breathsmay
result in increasing chemical drive
and
recruitment
of
pharyn-
geal dilator muscles. This has been
proposed
previously as the
reason for
the
lower values
of
UACP reported by Issa
and
Sul-
livan (16)
compared
with the more recent studies using extrapo-
lation to zero airflow (19) or direct visualization
of
the airway
(20). Issa
and
Sullivan, however, noted
that
UACP did not ap-
pear to change with increasing airway closure time; an observa-
tion
with which we concur (see, for example, Figure 1). There-
fore, the reasons for the different closing pressureestimates from
these different techniques remain unclear at this time.
The reason for the difference between
our
estimation
of
a
slightly positive supine UACP
and
the
negative values reported
by Issa
and
Sullivan most probably relates to different patient
selection:
our
patients weremore obese,
and
required higher levels
of
therapeutic nCPAP. The patients studiedby Issa
and
Sullivan
had
a mean
body
weight
of
115.8
±
6.0070
of
ideal (range 77 to
159%), whereas
our
patients' body weight, expressed in the same
way,was 162
± 30%
of
ideal (range 132to 230%). Wepostulate
that
our
patients would have
had
anatomically smaller and there-
fore more collapsible pharyngeal airways.
In the present study upper body elevation significantly reduced
upper
airway collapsibilityin sleep toward values more typically
seen in supine sleeping nonapneic snorers (19). However, mov-
ing to the lateral position appeared
not
to change upper airway
collapsibility. This latter result differs from the only previous
study
that
has examined the effects
of
posturalchangeon UACP
during sleep in patients with OSAS (16). Issa
and
Sullivan found
a significant reduction in upper airway collapsibility (as mea-
sured by UACP) in the lateral compared with the supine posture
in three patients. Withsuch a small
number
of
subjects
and
with-
out
the
anthropomorphic
details
of
their three patients, it is dif-
ficult to
make
meaningful comparisons. However, the patient
group from which they were selected was considerably less obese
than
the patients in
our
study. Supine to lateral position change
may cause quite different changes in
upper
airway stability in
lean versus obese OSAS patients. Cartwright (1)found a signifi-
cant
reduction in sleep-disordered breathing in 30 patients with
OSAS in
the
lateral compared with supine posture,
but
the im-
provement was virtually confinedto those patients with near nor-
mal weight.
Post
hoc review
of
the diagnostic sleep studies
of
our
eight obesepatients revealed no evidence
of
a supine to lateral
improvement in sleep-disordered breathing in the six in whom
sufficient posture
data
were available (two patients spent most
of
the night sleeping supine).
Our
study did
not
address the mechanisms by which postural
change in sleeping OSAS patients improved (upper body eleva-
tionversus supine) or did
not
improve (lateral versus supine) up-
per airway collapsibility. However, results from several recent
studies examining
the
effects
of
postural.change on upper air-
way caliber in awake OSAS patients
and
normal subjects may
provide some insight.
Martin
and
coworkers (14) recently com-
pared
the
effect
of
posture(sitting, supine,
and
lateral) on upper
airway caliber in
40 awake normal subjects, 70 snorers,
and
110
patients with OSAS by acoustic reflection. They found
that
both
mean
and
minimal pharyngeal cross-sectional area decreased
from sitting to lying down (supine or lateral) in patients with
n=4
StageII StageIII,IV
Lateral
n=4
StageII StageIII,IV
Elevation 30°
....
n=5
Stage n Stage III,IV
Supine
..p < 0.05
Figure 4. Upper airway
opening
pressure in cm H20 according to
sleep
stage
in three sleep postures. Mean UAOPwas lower in stage
III/IV
compared with stage IIsleep in
the
elevated position,
and
there
was a similar nonsignificant
trend
in
the
other
postures.
2.1 em H
20),
compared with
the
supine position (mean ± SD:
10.4
± 3.5 em H
20).
No statistically significant difference was
found
between the mean UAOP at 30° elevation
and
the lateral
posture.
Influence of Sleep Stage on Upper Airway Opening Pressure
Data
in
both
non-REM stage II
and
non-REM stages
III/IV
were
available in four subjects at 30° elevation
and
in the lateral posi-
tion, and in five subjects in
the
supine position. There was a trend
(Figure 4) in all sleep positions for opening pressure to be higher
in
non-REM
stage II sleep
than
in non-REM stages
III/IV
but
this reached statistical significance only in the upperbodyelevated
posture.
DISCUSSION
In this study
of
obese patients with severe OSAS, we have shown
that
the
upper
airway became less collapsible (reduced UACP)
and
was more easily opened (reduced UAOP) with
upper
body
elevation compared with the supinesleep position. Lateral postur-
ing did
not
reduce upper airway collapsibility
but
did increase
the
ease with which the airway could be fully opened.
Both
up-
per
body
elevation
and
the
lateral posture resulted in at least a
50% reduction in the therapeutic
nCPAP
comparedwith
the
su-
pine position.
Upper Airway Closing Pressure
Abnormal
upper
airway collapsibility is
thought
to be an im-
portant
factor in the pathophysiology
of
OSAS (16, 19). Using
the
same technique as in
our
study, Issa
and
Sullivan previously
found
UACP in patients with OSAS, sleeping in
the
supine pos-
ture, to be - 3.1
± 0.4 em H
20
in stages I/I1 sleep
and
- 4.2 ±
0.2 em H
20
in stages
III/IV
sleep (16). In a study by Gleadhill
and
colleagues
upper
airway closing pressure (Pcrit) was deter-
mined during sleep by relating changes in maximal inspiratory
airflowto varying levels
of
nCPAP
by least squares linear regres-
sion (19);Pcrit representing
the
extrapolated pressure at zero air-
flow.Upper airway closing pressure in adultsupine sleeping OSAS
patients was found by this
method
to be 2.5 ± 1.5 cm H
20.
In
another
studyby Morrison
and
coworkers (20),
both
site
of
nar-
rowing
and
UACPweredeterminedsupine, in 41sleeping OSAS
patients by direct endoscopic visualization
of
end-expiratory up-
Neill, Angus, Sajkov, et
01.:
Sleep Posture
and
Upper
Airway Stability
OSAS, snorers,
and
normal control subjects
but
did not show
any significant changes in upper airway size between the supine
and lateral posture. Similarly, Pevernagie
and
colleagues using
fast cine CT found no significant change in the cross-sectional
area
of
the pharynx from supine to lateral in a subgroup of awake
obese patients with severe (position nondependent) OSAS (15).
While it is acknowledged
that
these
data
were obtained during
wakefulness
and
not sleep, they are consistent with
our
findings
and suggest
that
the different effects
of
upper body elevation
and lateral positioning on UACP may relate to their different
effects on upper airway caliber. Thus, it seems possible
that
the
mechanism by which upper body elevation improves UACP
and
sleep-disordered breathing is byincreasing upper airway dimen-
sions.
Perhaps the most likely mechanism by which upper body ele-
vation could lead to an increase in upper airway size and stabil-
ity is a posture-related increase in lung volume (4). An increase
in lung volume has been shown in experimental animals to de-
crease upper airway resistance (8). In these experiments dener-
vation excluded reflex upper airway dilatation as a mechanism,
and
therefore it has been postulated to be due to a mechanical
coupling
of
the thorax
and
upper airway such that with increas-
ing lung volume caudal movement
of
the larynx results in sec-
ondary stiffening
and
dilatation of the pharynx.
Upper Airway-Opening Pressure
Wefound
that
the pressure required to produce full airway open-
ing wasreduced byapproximately
50070
at 30° upper body eleva-
tion compared with the supine position.
It
is possible
that
this
reduction in airway opening pressure was greater given that in
4of 8 patients the airway wasfully open at 3.8em H
20
(the lower
pressure limit imposed by our circuit). These results are consis-
tent with the hypothesis that upper body elevation results in a
more stable (2), less collapsible and larger pharyngeal airway
(11-14). Wealso found that patients required significantly lower
positive pressure to produce full airway opening in the lateral
compared with the supine position, although as indicated ear-
lierwedid not find that this postural change reduced airway clos-
ing pressure. Wehave no direct experimental evidence to explain
this apparent discrepancy. However, these two indices
of
upper
airway stability measure different aspects
of
upper airway me-
chanics in sleep. Upper body elevation appears to increase up-
per airway size
(11-14) (possibly via downward traction on the
larynx [8]) which would tend to shift the upper airway pres-
sure/volume curve to the left, thereby reducing both the UACP
and the pressure required to open the airway (UAOP). Lateral
positioning does not appear to improve upper airway size (12,
14, 15) but it may render the upper airway more distensible (i,e.,
more compliant) perhaps by shifting the gravitational vector on
the relativelymore mobile components
of
the airway,e.g.,tongue
and soft palate.
If
this were the case, the upper airway in the
lateral position might continue to closeat or closeto atmospheric
pressure (as was observed supine) but UAOP would be reduced.
Effect of Sleep Stage on Airway Stability
One previous study has suggested that UACP is lower (i,e., air-
wayis more stable) in slow wavesleep compared with stages
1111
non-REM sleep (16). In
our
study the majority
of
all successful
nasal occlusion tests were obtained in slow wavesleep
(67070
su-
pine,
67070
upper body elevation,
and
75% lateral). There were
insufficient
data
to statistically compare UACP between non-
REM stagesII and III/IV. Becausethere was no systematicdiffer-
ence in the distribution
of
measurements with respect to sleep
stage between the three postures, weconsidered it reasonable to
combine all non-REM UACP
data
for statistical comparisons.
Sufficient
data
were obtained to enable a statistical analysis
of
203
the effects
of
sleep stage on UAOP. There was a trend toward
higher opening pressures in non-REM stage II compared with
stages
IIIIIV
for all sleep postures suggesting a less compliant
upper airway in lighter stages
of
non-REM sleep.
Potential Clinical Importance of
the
Findings
The results
of
our study are
of
potential clinical importance to
obese patients with severe obstructive sleep apnea, particularly
thosehaving difficulty tolerating nCPAP or requiring high ther-
apeutic pressures. The magnitude
of
the change in UACP with
upper body elevation is similar to
that
previously shown by
Schwartz and colleagues to be associated with a clinically sig-
nificant improvement in sleep-disordered breathing in OSAS pa-
tients following weightloss (21)or successfuluvulopalatopharyn-
goplasty
(UPPP)
(22). These researchers have
data
that
suggest
that
a reduction in UACP (or Pcrit)
of
approximately 5 em H
20
(as shown in
our
patients at 30° elevation) might be expected
to abolish obstructive hypopneas or convert obstructive apneas
into hypopneas
(19).
Indeed, in a previous study wedemonstrated
such an effect as obese OSAS patients wereprogressivelyelevated
to 60° during sleep (2). Wehave also encountered some extremely
obese patients in whom the maximal pressure available from a
conventional nCPAP circuit (approximately 20 em H
20)
is in-
sufficient to maintain airway patencyin supine sleep.In this study
we have shown that upper body elevation or lateral positioning
will allow a substantial reduction (approximately 50%) in the
therapeutic level
of
nCPAP in non-REM sleep. Weconsider
that
in the acute management
of
severeobstructive sleep
apnea
(e.g.,
accompanied by cardiorespiratory failure) these postural inter-
ventions are likely to be
of
substantial clinical benefit.
Of
the
two postural interventions studied, 30° upperbody elevation pro-
duced the greater improvement in upper airway stability
and
was
relatively easy to maintain. Furtherstudies are required to deter-
mine whether this treatment strategy is useful in the long-term
management
of
patients with OSAS and whether
our
findings
also apply in REM sleep.
Acknowledgment: The writers thank Mr. Robin Woolford (Departmentof Bio-
medical Engineering, Repatriation General Hospital, Daw Park,South Austra-
lia) for designing and manufacturing the modified nCPAPmask and the pneu-
matic solenoid-driven balloon occlusion system. They also acknowledge the
excellenttechnical assistance
of
Ms. Ivanka Mykytyn and Sleep Disorders
Unit
staff.
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... Sleeping on the back is thought to increase the possibility and frequency of upper airway collapse (Isono, Tanaka, Nishino, 2002;Cartwright, 1984). There is a higher pressure needed to maintain an open airway (Neill, Angus, Sajkov, McEvoy, 1997) and more depressed oxygen desaturation (Oksenberg, Khamaysi, Silverberg, Tarasiuk, 2000). In 1991 'positional dependency' was identified as a possible factor in patients with obstructive sleep apnea (OSA) and 'positional therapy' was introduced by having individuals sleep in a lateral position which reduced their apnea-hypopnea index (AHI) approximately by half (Cartwright, Ristanovic, Diaz, Caldarelli, Alder, 1991) The incidence of positional obstructive sleep apnea (POSA) reported in the literature ranges from 50% to 67% among individuals who have been diagnosed with OSA (Teerapraipruk, Chirakalwasan, Simon, Hirunwiwatkul, Jaimchariyatam, Desudchit, Charakon, Wanlapakorn, 2011;Richard, Kox, den Herder, Laman, van Tinteren, de Vries, 2006;Mador, Kufel, Magalang, Rajesh, Watwe, Grant, 2005;Oksenberg, Silverberg, Arons, Radwan, 1997;Cartwright, 1984.) ...
... It has been reported that sleep in an angle-adjustable chair, such as a recliner, improved the sleep quality through the sleep at a higher angle of posture or the neck [20][21][22]. In particular, it has been proven that some sleep disorders could be medically improved in patients with sleep apnea [22][23][24][25] and nocturnal gastroesophageal reflux through sleep in a recliner [26]. In this paper, we propose an additional way to further improve the quality of sleep with providing a rocking motion to the recliner. ...
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... 69,70 In particular, the soft palate of the upper airway is highly susceptible to collapse in the supine position after the administration of anesthetics, sedatives, and opioids. 71 Rostral fluid shifts may further worsen airway obstruction due to edema. 72 Lateral positioning of the patient can structurally improve the maintenance of the passive pharyngeal airway in OSA. ...
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... [26] Patients should cease exposure to airway irritants like tobacco smoke and partake in activities that encourage patency of the airway like sleeping in inclined or lateral positions and playing wind instruments. [26][27][28][29] CPAP devices are considered the gold standard of OSA therapy. They function by creating consistent air pressures in airways to keep them patent during sleep. ...
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Chapter
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Previous investigators have demonstrated variable responses to uvulopalatopharyngoplasty (UPP) in patients with obstructive sleep apnea. We hypothesized that this variability is due to either (1) differences in baseline pharyngeal collapsibility preoperatively or (2) differences in magnitude of the decrease in pharyngeal collapsibility resulting from surgery. To determine the relationship between changes in collapsibility and the response to UPP surgery, we measured the upper airway critical pressure (Pcrit) before and after UPP in 13 patients with obstructive sleep apnea. During non-REM sleep, maximal inspiratory airflow (VImax) was quantitated by varying the level of nasal pressure (PN), and Pcrit was determined by the level of PN below which VImax ceased. A positive response to UPP was defined by a greater than or equal to 50% fall in non-REM disordered breathing rate (DBR). In the entire group, UPP resulted in significant decreases in DBR from 71.1 +/- 22.4 to 44.7 +/- 38.4 episodes/h (p = 0.025) and in Pcrit from 0.2 +/- 2.4 to -3.1 +/- 5.4 cm H2O (p = 0.016). Moreover, the percent change in DBR was correlated significantly with the change in Pcrit (p = 0.001). Subgroup analysis of responders and nonresponders demonstrated that significant differences in Pcrit were confined to the responders. Specifically, responders demonstrated a significant fall in Pcrit from -0.8 +/- 3.0 to -7.3 +/- 4.9 cm H2O (p = 0.01), whereas no significant change in Pcrit was detected in the nonresponders (1.1 +/- 1.6 versus 0.6 +/- 2.0 cm H2O. No clinical, polysomnographic, or physiologic predictors of a favorable response were found preoperatively.(ABSTRACT TRUNCATED AT 250 WORDS)
Article
A retrospective analysis of positional data from 100 male patients with obstructive sleep apnea (OSA) was conducted to determine whether or not 1) the degree of positional dependency was similar in rapid eye movement (REM) compared to non-REM (NREM) sleep, 2) positional dependency correlated with effective levels of nasal continuous positive airway pressure (CPAP) and 3) patients with positional OSA preferentially avoided sleeping in the supine position. The apnea-hypopnea index (AHI) was scored separately for sleep state (NREM and REM) and for posture [off back (AHI-O) and on back (AHI-B)]. The ratio of AHI-O/AHI-B was used to define positional OSA as AHI-O/AHI-B less than or equal to 0.50 (P group) and nonpositional OSA as 0.50 less than AHI-O/AHI-B (NP group). A group of 31 patients who had sufficient sleep time in NREM and REM sleep in both sleep postures was selected. In this group 9 out of 22 subjects who showed positional dependency during NREM sleep became nonpositional during REM sleep (0.05 less than p less than 0.10). The mean effective nasal CPAP level was slightly, but significantly, lower in the P group than in the NP group (8.0 versus 9.1 cm H2O; p less than 0.05). In addition, a correlation between AHI and effective nasal CPAP levels was found (r = 0.491; p = 0.0001). The P group had less supine sleep time (SST) than the NP group (32% versus 45% of total sleep; p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
The effect of posture on upper airway dimensions was assessed for two reasons. First, some patients with untreated sleep apnea/hypopnea syndrome (SAHS) report they sleep better sitting upright. Second, to allow comparison of the differing techniques used to determine the site of maximal airway narrowing in awake patients with SAHS, as some are carried out in the erect and others in the supine posture. Lateral cephalometry was therefore carried out in 33 nonsnoring normal subjects and in 29 patients with obstructive SAHS (mean apneas plus hypopneas, 46 per hour; range, 17 to 103). In both normal subjects and patients, uvular width was increased (p less than 0.05) in the supine posture, and this was associated with significant narrowing of the retropalatal airway in the patients with SAHS (erect, 5.0 +/- SD 2.6 mm; supine, 3.6 +/- 2.8 mm; p less than 0.01). In both normal subjects and patients, the retroglossal hypopharynx widened (p less than 0.05) in the supine posture (e.g., in patients with SAHS, posterior airway space was: erect, 11.5 +/- 4.5 mm; supine, 13.4 +/- 4.8 mm; p = 0.003). In the supine posture there was anterior movement of the hyoid and neck flexion in both groups. However, a study of the effect of neck flexion in the erect posture showed that neck flexion produced no changes in airway caliber. Thus, posture is an important determinant of upper airway dimensions.
During sleep, mild reduction in inspiratory airflow is associated with snoring, whereas obstructive hypopneas and apneas are associated with more marked reductions in airflow. We determined whether the degree of inspiratory airflow reduction was associated with differences in the collapsibility of the upper airway during sleep. Upper airway collapsibility was defined by the critical pressure (Pcrit) derived from the relationship between maximal inspiratory airflow and nasal pressure. In 10 asymptomatic snorers, six patients with obstructive hypopneas, and 10 patients with obstructive apneas, during nonrapid eye movement sleep, Pcrit ranged from -6.5 +/- 2.7 cm H2O to -1.6 +/- 1.4 and 2.5 +/- 1.5 cm H2O, respectively (mean +/- SD, p less than 0.001). Moreover, higher levels of Pcrit were associated with lower levels of maximal inspiratory airflow during tidal breathing during sleep (p less than 0.005). We conclude that differences in upper airway collapsibility distinguish among groups of normal subjects who snore and patients with periodic hypopneas and apneas. Moreover, the findings suggest that small differences in collapsibility (Pcrit) along a continuum are associated with reduced airflow and altered changes in pattern of breathing.
Article
The total upper airway resistances are modified during active changes in lung volume. We studied nine normal subjects to assess the influence of passive thoracopulmonary inflation and deflation on nasal and pharyngeal resistances. With the subjects lying in an iron lung, lung volumes were changed by application of an extrathoracic pressure (Pet) from 0 to 20 (+Pet) or -20 cmH2O (-Pet) in 5-cmH2O steps. Upper airway pressures were measured with two low-bias flow catheters, one at the tip of the epiglottis and the other in the posterior nasopharynx. Breath-by-breath resistance measurements were made at an inspiratory flow rate of 300 ml/s at each Pet step. Total upper airway, nasal, and pharyngeal resistances increased with +Pet [i.e., nasal resistance = 139.6 +/- 14.4% (SE) of base-line and pharyngeal resistances = 189.7 +/- 21.1% at 10 cmH2O of +Pet]. During -Pet there were no significant changes in nasal resistance, whereas pharyngeal resistance decreased significantly (pharyngeal resistance = 73.4 +/- 7.4% at -10 cmH2O). We conclude that upper airway resistance, particularly the pharyngeal resistance, is influenced by passive changes in lung volumes, especially pulmonary deflation.
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Patency of the upper airway (UA) is usually considered to be maintained by the activity of muscles in the head and neck. These include cervical muscles that provide caudal traction on the UA. The thorax also applies caudal traction to the UA. To observe whether this thoracic traction can also improve UA patency, we measured resistance of the UA (RUA) during breathing in the presence and absence of UA muscle activity. Fifteen anesthetized dogs breathed through tracheostomy tubes. RUA was calculated from the pressure drop of a constant flow through the isolated UA. RUA decreased 31 +/- 5% (SEM) during inspiration. After hyperventilating seven of these dogs to apnea, we maximally stimulated the phrenic nerves to produce paced diaphragmatic breathing. Despite absence of UA muscle activity, RUA fell 51 +/- 11% during inspiration. Graded changes were produced by reduced stimulation. In six other dogs we denervated all UA muscles. RUA still fell 25 +/- 7% with inspiration in these spontaneously breathing animals. When all caudal ventrolateral cervical structures mechanically linking the thorax to the UA were severed, RUA increased and respiratory fluctuations ceased. These findings indicate that tonic and phasic forces generated by the thorax can improve UA patency. Inspiratory increases in UA patency cannot be attributed solely to activity of UA muscles.