Lateral Sleeping Position Reduces Severity of Central Sleep Apnea / CheyneStokes Respiration
Irene Szollosi BSc1,2; Teanau Roebuck BAppl Sc1; Bruce Thompson PhD1; Matthew T Naughton MD1,2
Department of Allergy Immunology and Respiratory Medicine, Alfred Hospital, Melbourne, Australia; 2Department of Medicine, Monash University,
Melbourne, Australia
1
wave sleep, 15.9 ± 6.4 events per hour vs 5.4 ± 2.9 events per hour [p <
.01]; rapid eye movement sleep, 38.0 ± 7.3 events per hour vs 11.0 ± 3.0
events per hour [p < .001]). Lateral position attenuated apnea and hypopnea associated desaturation (supine 4.7% ± 0.3%, lateral 3.0% ± 0.4%;
p < .001) with no difference in event duration (supine 25.7 ± 2.8 seconds,
lateral 26.9 ± 3.4 seconds; p = .921). Mixed apneas were longer than central (29.1 ± 2.1 seconds and 19.3 ± 1.1 seconds; p < .001) and produced
greater desaturation (6.1% ± 0.5% and 4.5% ± 0.5%, p = .003). Lateral
position decreased desaturation independent of apnea type (supine 5.4%
± 0.5%, lateral 3.9% ± 0.4%; p = .003).
Conclusions: Lateral position attenuates severity of CSA-CSR. This effect is independent of postural effects on the upper airway and is likely
to be due to changes in pulmonary oxygen stores. Further studies are
required to investigate mechanisms involved.
Keywords: Central sleep apnea, body position, ventilatory control
Citation: Szollosi I; Roebuck T; Thompson B et al. Lateral Sleeping Position Reduces Severity of Central Sleep Apnea / Cheyne-Stokes Respiration. SLEEP 2006;29(8):1045-1051.
Introduction: The influence of sleeping position on obstructive sleep
apnea severity is well established. However, in central sleep apnea with
Cheyne Stokes respiration (CSA-CSR) in which respiratory-control instability plays a major pathophysiologic role, the effect of position is less
clear.
Study Objectives: To examine the influence of position on CSA-CSR severity as well as central and mixed apnea frequency.
Methods: Polysomnograms with digitized video surveillance of 20 consecutive patients with heart failure and CSA-CSR were analyzed for total
apnea-hypopnea index, mean event duration, and mean oxygen desaturation according to sleep stage and position. Position effects on mixed and
central apnea index, mean apnea duration, and mean desaturation were
also examined in non-rapid eye movement sleep.
Results: Data are presented as mean ± SEM unless otherwise indicated.
Group age was 59.9 ± 2.3 years, and total apnea-hypopnea index was
26.4 ± 3.0 events per hour. Compared with supine position, lateral position reduced the apnea-hypopnea index in all sleep stages (Stage 1, 54.7
± 4.2 events per hour vs 27.2 ± 4.1 events per hour [p < .001]; Stage 2,
43.3 ± 6.1 events per hour vs 14.4 ± 3.6 events per hour [p < .001]; slow-
ment of cardiovascular disease,7 occurring in 2% to 4% of the
general adult population.8 Upper-airway instability during sleep
and an inadequate capacity of upper-airway musculature to maintain airway patency is thought to be the main pathophysiologic
event, with respiratory-control instability (loop gain) playing a
potential role in some patients.9,10
It has been established that OSAHS severity as measured by
the apnea-hypopnea index (AHI) is increased in the supine position.11 Even in nonpositional OSAHS, the duration of respiratory events and the consequent hypoxemia is more marked in the
supine position.12 This effect is attributed to gravitational effects
on the upper airway13 leading to increased upper-airway collapsibility while supine. In support of this, Penzel et al confirmed that
body position has a significant impact on the pharyngeal critical closing pressure, an objective measure of upper-airway collapsibility.14 In addition, the optimal continuous positive airway
pressure required to treat OSAHS has been demonstrated to be
approximately 2 cmH2O higher in the supine position compared
with the lateral.15
The impact of position in CSA-CSR is less clear. Recently, it
has been reported that patients with heart failure have a preference for the lateral sleeping position16 and, furthermore, that the
right lateral decubitus position is preferred over the left lateral decubitus position.17 In addition, Sahlin et al have shown that central
AHI is increased during supine sleep compared with nonsupine
sleep.18 However, previous investigators have also observed that
upper-airway instability is common during CSA-CSR, with many
patients exhibiting mixed apneas in which pharyngeal occlusion
prevents the immediate resumption of airflow when ventilatory
effort returns.19,20 It remains unclear whether upper-airway col-
INTRODUCTION
SLEEP-RELATED BREATHING DISTURBANCES OCCUR
IN UP TO 50% OF PATIENTS WITH HEART FAILURE, WITH
40% EXHIBITING CENTRAL SLEEP APNEA and CheyneStokes respiration (CSA-CSR) and a further 10% of patients exhibiting obstructive sleep apnea hypopnea syndrome (OSAHS).1
CSA-CSR is attributed to respiratory-control instability in which
periodic hyperventilation drives PaCO2 below the apneic threshold, such that central drive and efferent output to the respiratory
pump muscles are transiently reduced or absent. Proposed mechanisms for hyperventilation include stimulation of pulmonary vagal afferents secondary to pulmonary congestion2 and heightened
sympathetic activation.3,4 Increased chemosensitivity of the central and peripheral chemoreceptors and the underlying increase
in circulation time associated with heart failure5,6 predisposes to
ventilatory instability that manifests as CSA-CSR.
OSAHS is a known independent risk factor for the develop-
Disclosure Statement
This was not an industry supported study. Dr. Naughton is on the medical
advisory board of ResMed Inc. Ms. Szollosi, Roebuck, and Dr. Thompson
have indicated no financial conflicts of interest.
Submitted for publication November 16, 2005
Accepted for publication March 21, 2006
Address correspondence to: Matthew T. Naughton, Alfred Hospital, PO Box
315, Prahran, Victoria, 3181, Australia; Tel: +61 3 9276 3770; Fax: +61 3
9276 3601; E-mail: m.naughton@alfred.org.au
SLEEP, Vol. 29, No. 8, 2006
1045
Influence of Position on CSA-CSR Severity—Szollosi et al
Figure 1—Representative polygraph from 1 subject, showing classification of central, mixed, and obstructive apneas while supine.
CSA-CSR. Measurements included electroencephalogram (C4A1, C3-A2, O2-A1, O1-A2), EOG, submental electromyogram,
electrocardiogram, oronasal flow measured with thermistor and
nasal pressure cannula (Pro-Tech Services, Mukilteo,WA), ribcage and abdominal effort measured by piezoelectric sensors,
calibrated body position sensor, SpO2 with 2-second averaging
time (Oxypleth, Novametrix, Wallingford, CT), esophageal pressure manometry (Millar Instruments, Houston,TX), and snoring
sound. All signals were stored onto a computerized polysomnographic data acquisition and analysis system (Compumedics Eseries, Abbottsford, Australia).
In order for lateral position to be confirmed, patients had to
have 1 shoulder elevated visually on the digitized video and the
position sensor reading either left or right position; supine sleep
required both shoulders to be in contact with the bed on video
and confirmed with position sensor. Sleep stages were manually
scored as previously described.21 Apneas were scored in the absence of oronasal flow in both the thermistor and nasal cannula
signals—obstructive if continued effort persisted in the ribcage
and abdominal bands or esophageal pressure, central in the absence of ventilatory effort, and mixed if there was an absence of
oronasal flow when ventilatory effort resumed. Hypopneas were
scored on the basis of a 50% or greater reduction in oronasal flow
associated with a 2% desaturation and/or arousal—obstructive in
the event of paradoxical motion in the effort bands or increasing
esophageal pressure amplitude and central if ribcage and abdominal effort remained in phase22 or esophageal pressure swings decreased. Examples of central, mixed, and obstructive apneas are
shown in Figure 1. CSA-CSR was defined as an AHI greater than
5 events per hour, with fewer than 25% of events being obstruc-
lapse favored by the supine position is important in the initiation
or propagation of CSA-CSR.
Our primary aims were to assess the effect of position on the
severity of CSA-CSR, as measured by AHI, respiratory-event duration, and hypoxemia associated with events, while controlling
for sleep-stage effects. Secondary aims were to examine whether
mixed apneas during CSA-CSR were more severe than central
apneas in terms of duration and desaturation. Finally, we wished
to examine whether the increase in respiratory-control instability observed in the supine position is associated with an increase
in mixed-apnea frequency, reflecting an increased contribution of
upper-airway collapse to the development of ventilatory instability.
METHODS
Consecutive patients aged 18 to 80 years with stable congestive heart failure, as defined by a past episode of acute cardiogenic pulmonary edema, no hospital admission for more than 3
months, left ventricular ejection fraction less than 45%, and New
York Heart Association class 2 or worse despite optimal medical
management, who were referred to our institution’s heart failure
program were assessed. Exclusion criteria included pregnancy
and significant pulmonary, renal, or neurologic disease. All patients provided written informed consent, and data were collected
prospectively.
Twenty consecutive patients with continuous digital video
surveillance during polysomnography with predominantly CSACSR and who spent at least 30 minutes sleeping in the supine and
lateral positions were analyzed for the effects of position on CSACSR severity. Patients were not selected on the basis of positional
SLEEP, Vol. 29, No. 8, 2006
1046
Influence of Position on CSA-CSR Severity—Szollosi et al
AHI (events/h)
Table 1—Subject Characteristics
Age, y
Sex
Men
Women
CHF etiology
IHD
DCM
HOCM
ECG Rhythm
SR
AF
Paced
NYHA
II
III
IV
Echo FS, %
LVEF, %
BMI, kg/m2
ESS
AHI, events/h
Total
Central
Mixed
Obstructive
TST, h
SpO2, %
Mean
Min
PtcCO2, mm Hg
Max
Mean
Min
Sleep Stage (%TST)
1
2
SWS
REM
Position (%TST)
Supine
Left
Right
70
59.9 (2.3)
60
18
2
*
50
*
40
13
6
1
30
10
5
5
0
#
20
10
1
2
SWS
REM
* p < .001, # p < .01
10
5
5
18.2 (2.1)
26.5 (2.2)
26.5 (0.8)
7.4 (0.8)
Figure 2—Apnea-hypopnea index (AHI) by sleep stage and sleeping
position inclusive of all central and mixed events. Right and left positions combined into a single lateral position. SWS refers to slow wave
sleep; REM, rapid eye movement sleep. Note significant reduction in
AHI with lateral compared to supine positon in all sleep stages.
gen desaturation, mean minimum saturation, and mean baseline
SpO2 were calculated (excluding obstructive events) for each
subject in each combination of sleep stage and position. The
baseline SpO2 was calculated as the sum of the minimum saturation and the desaturation associated with each respiratory event
and, thus, reflects the oxygen saturation in each sleep stage and
position, excluding the dips in saturation occurring with respiratory events. Mixed and central apnea contribution to the apnea
index was examined in the supine and lateral positions with the
left and right positions combined during non-rapid eye movement
(NREM) sleep. Apnea index, mean duration, and mean desaturation associated with central and mixed apneas was calculated for
each subject in the supine and lateral positions.
Preliminary analysis revealed no differences between right and
left positions for any of the outcome variables of interest, consistent with previous observations.17 As such, data from the right
and left positions were combined into a single lateral position for
analysis. AHI and ArI were not normally distributed; therefore,
we used a negative binomial regression model to analyze the
number of events per time in each sleep stage and body position.
All other outcome variables for the group (i.e., mean event duration, desaturation, and minimum and baseline saturation) were
normally distributed with equal variances across groups; therefore, we used linear regression to assess the influence of sleep
stage and position. Similarly, the apnea index was analyzed using negative binomial regression to assess the influence of apnea
type and position on the number of events per time; linear regression was used to assess influence of apnea type and position on
mean duration and mean desaturation associated with events. All
analyses were performed with robust standard errors adjusted for
clustering by subject using Stata9 (StataCorp LP, College Station,
TX). Data presented as mean ± SEM.
26.4 (3.0)
21.1 (2.7)
3.2 (1.6)
2.1 (0.4)
5.0 (0.3)
96.5 (0.3)
86.6 (1.3)
48.3 (1.4)
43.6 (1.5)
38.9 (1.6)
16.2 (1.9)
51.3 (1.8)
14.2 (1.7)
18.2 (1.9)
39.1 (5.0)
23.5 (5.2)
37.5 (6.7)
Data presented as mean (SEM). CHF refers to congestive heart failure; ECG electrocardiogram; IHD ischemic heart disease; DCM, dilated cardiomyopathy; HOCM, hypertrophic obstructive cardiomyopathy; SR, sinus rhythm; AF, atrial fibrillation and flutter; NHYA,
New York Heart Association classification; FS, fractional shortening
measured by echocardiography; LVEF, left ventricular ejection fraction measured gated blood pool scan; BMI, body mass index; ESS,
Epworth Sleepiness Scale score; AHI, apnea-hypopnea index; TST,
total sleep time; SWS, slow-wave sleep; REM, rapid eye movement
sleep).
tive in nature. Arousals were scored according to American Sleep
Disorders Association criteria.23 Sleep-stage, respiratory-event,
and arousal information was exported for manual analysis.
RESULTS
The group of patients studied were typical of a heart failure
population with a mean age of 59.9 ± 2.3 years, male predominance, sinus rhythm in approximately 50% and atrial fibrillation or
pacemaker in approximately 50%, mean left ventricular ejection
fraction (via 99Tc equilibrium radionuclide angiography) 26.5% ±
Statistical Analyses
To determine the influence of position on CSA-CSR severity,
all obstructive events were removed from further analysis. AHI,
Arousal Index (ArI), mean respiratory event duration, mean oxySLEEP, Vol. 29, No. 8, 2006
supine
lateral
*
1047
Influence of Position on CSA-CSR Severity—Szollosi et al
��
DESATURATION
%
1*
2*
SWS
.09]).
The mean duration of events for all subjects was 26.2 ± 2.0
seconds (supine 25.7 ± 2.8 seconds and lateral 26.9 ± 3.4 seconds) and was not significantly influenced by either sleep stage
or sleeping position.
The desaturation and minimum saturation were significantly
influenced by position in Stage 1 and Stage 2 sleep, during which
29% and 51% of events occurred, respectively (Figure 3). The
lateral position was associated with decreased apnea-hypopnea–
related hypoxemia during Stage 1 and Stage 2 sleep. The differences were not statistically significant in SWS and REM sleep,
probably due to the relatively small numbers of events occurring
in these sleep stages (20% of all events). There was no significant influence of sleep stage or position on baseline SpO2 (supine
96.8% ± 0.3% and lateral 97.4% ± 0.1 %).
The supine position was associated with a significantly greater
total apnea index compared with the lateral position (19.0 ± 4.9/
hour and 7.0 ± 2.9/hour; p < .001). This increase in the supine apnea index was driven by significant increases in both central and
mixed events; however, the proportion of central versus mixed
events remained similar in both positions (supine 71:29 and lateral 69:31, p = NS).
During NREM sleep, mixed apneas were of longer duration
than central apneas (29.1 ± 2.1 and 19.3 ± 1.1 seconds; p < .001)
and resulted in greater desaturation (6.1% ± 0.5% and 4.5% ±
0.5%; p = .003) and lower minimum SpO2 (91.5% ± 0.6% and
92.9% ± 0.6%; p = .039). Similar to the apnea-hypopnea results,
there was no influence of position on apnea duration; however,
the supine position was associated with significantly greater desaturations independent of apnea type (supine 5.4% ± 0.5% and
lateral 3.9% ± 0.4%, p = .003).
REM
0
supine
lateral
1
2
3
4
5
6
7
�� MINIMUM SpO2
%
98
96
94
92
90
88
86
84
1*
2*
SWS
REM
* p < .001
Figure 3—Influence of body position on (a) oxygen desaturation and
(b) minimum oxygen saturation associated with respiratory events.
SWS refers to slow wave sleep; REM, rapid eye movement sleep.
Note significantly greater desaturation and lower minimum SpO2 in
the supine compared with lateral position in Stage 1 and Stage 2 sleep,
where the majority of events occurred.
2.2%, and fractional shortening (via transthoracic echocardiography) 18.2% ± 2.1%. The overall AHI was 26.4 ± 3.0 events per
hour; central, mixed and obstructive AHI were 21.1±2.7, 3.2±1.6,
and 2.1±0.4 events per hour, respectively (Table 1). Six of 20 patients tolerated the esophageal pressure manometer.
A total of 2326 central and mixed events during 5996 minutes
of sleep were analyzed from polygraphs of 20 patients. Mean time
spent sleeping supine was 118.7 ± 17.4 minutes, left lateral was
65.4 ± 17.3 minutes, and right lateral was 115.7 ± 21.6 minutes.
The AHI was significantly influenced by both sleep stage and position (Figure 2). AHI showed a progressive decrease from Stage
1 to Stage 2 to slow-wave sleep (SWS) (all p < .005); respiratory events persisted during rapid eye movement (REM) sleep,
with greater frequency than during SWS (p < .05) but with lower
frequency than during Stage 1 sleep (p < .001). Position had a
significant influence on AHI, independent of sleep-stage effects.
The lateral position was associated with significant reduction in
AHI compared with supine in all sleep stages (Stage 1, 54.7 ± 4.2
events per hour vs 27.2 ± 4.1 events per hour [p < .001]; Stage 2,
43.3 ± 6.1 events per hour vs 14.4 ± 3.6 events per hour [p < .001];
SWS, 15.9 ± 6.4 events per hour vs 5.4 ± 2.9 events per hour [p
< .01]; REM, 38.0 ± 7.3 events per hour vs 11.0 ± 3.0 events
per hour [p < .001]). Similarly, the ArI decreased from Stage 1
to Stage 2 and SWS with a small rise in REM; however, the decrease in ArI observed in the lateral position reached statistical
significance only during Stage 2 sleep (Stage 1, 46.3 ± 4.9 events
per hour vs 41.3 ± 5.7 events per hour [p = .55]; Stage 2, 28.2 ±
5.8 events per hour vs 12.6 ± 2.1 events per hour [p < .01]; SWS,
5.7 ± 2.5 events per hour vs 2.8 ± 0.7 events per hour [p = .24];
REM, 12.1 ± 3.4 events per hour vs 9.7 ± 2.5 events per hour [p =
SLEEP, Vol. 29, No. 8, 2006
DISCUSSION
There are 2 important novel observations that have emerged
from this detailed study of CSA-CSR in patients with heart failure. First, compared with the supine position, the lateral position
is associated with reduced apnea-hypopnea–related hypoxemia
despite respiratory events of similar duration in addition to a more
than 50% reduction in AHI. Second, mixed apneas were of longer
duration and produced greater desaturation than central apneas;
however, the ratio of mixed to central apneas was unchanged by
the move from supine to lateral position (~30:70 ratio). These
novel findings would suggest that the effect of posture on respiratory-control instability during sleep is more likely to be due to supine reductions in pulmonary oxygen stores rather than increases
in upper-airway instability in this patient group.
Our findings support 2 recently published articles in which
the importance of sleeping posture in patients with heart failure
was highlighted. We have confirmed the findings of Sahlin et al,
who reported a higher central AHI in the supine compared with
nonsupine position (41 and 26 events per hour) in a group of 20
patients.18 Similarly, Leung and coworkers reported a voluntary
predisposition to sleep in the right lateral decubitus position compared to the left lateral decubitus position in 75 patients with heart
failure. Of note, Leung reported the AHI and mean and minimum
SpO2 values to be similar in the left and right lateral positions.17
As well as confirming these previous findings, the present study
extends upon these previous observations. Importantly, we have
shown that the severity of CSA-CSR, as assessed by the magni1048
Influence of Position on CSA-CSR Severity—Szollosi et al
tude of hypoxemia but not of event duration, is also reduced in
the lateral position. This observation offers valuable insights into
the pathogenesis of CSA-CSR, namely that the supine increase in
CSA-CSR occurs in the presence of reduced oxygen stores.
The pathogenesis of CSA-CSR has been explained by instability in the metabolic control of ventilation. Recently, this hypothesis has also been applied to explain the pathogenesis of OSAHS,
with some studies reporting that patients with OSAHS also have
an underlying instability in ventilatory control.9,10 In terms of control theory, a negative feedback loop, such as the metabolic control of ventilation, will exhibit unstable behavior if the loop gain
of the system exceeds 1. If the loop gain is less than 1, any disturbance causing changes in blood gases will be dampened out, and
ventilation will return to a stable pattern. Simplistically, there are
3 factors that can contribute to increasing loop gain and the development of oscillatory behavior in ventilatory control, namely, increased circulation time, increased sensitivity of chemoreceptors
(controller gain), and decreases in lung volume (plant gain).24,25
The limited evidence for each of these 3 factors is discussed in
the context of transverse postural changes. Although this study
was not designed to identify which of these mechanisms may be
influenced by postural changes during sleep, our results provide
indirect evidence that the increase in supine AHI in this patient
group occurred in the presence of decreased oxygen stores/lung
volumes, as reflected by the greater degree of hypoxemia occurring with events of similar duration in the supine position.
The influence of transverse gravitational effects on hemodynamics in humans are few and, to date, have only been conducted
during wakefulness. Pump et al reported that, in healthy subjects,
the left lateral posture increases left atrial diameter, facilitates
venous return, and decreases mean systemic arterial pressure;
however, the right lateral posture was not examined.26 The importance of posture on sleep-disordered breathing is also highlighted
by observations that both central and obstructive apneas are decreased during microgravity conditions.13 Postural hemodynamic
changes during sleep may therefore be important in the setting of
heart failure. Increased venous return in the lateral position may
contribute to maintaining increased cardiac output, decreasing
circulation time, and thus favoring ventilatory stability.
Postural changes in lung volume in the transverse plane are
also not well documented. In a study by Hurewitz et al, which
assessed regional ventilation in obese and nonobese controls,
the lateral decubitus position was associated with an increase in
functional residual capacity of approximately 560 mL, compared
with the supine position in the control subjects.27 However, the
numbers were small (n = 3) and generalizations thus difficult to
make. Patients with heart failure are known to have decreased
lung volumes due to pulmonary congestion with or without enlargement of the heart within the thorax.28 Recently, it has also
been observed that, during CSA-CSR, fluctuations in end-expiratory lung volume occur with changes in tidal volume.29 Decreases
in lung volume, and therefore oxygen stores, favors the development of CSA-CSR as the ability of the lungs to buffer changes
in blood gases is reduced, leading to an increase in plant gain. A
small reduction of lung volume that may occur from the lateral
to supine position may therefore be an important mechanism that
would explain the supine increase in AHI that we and others have
observed. Given that we found a greater degree of hypoxemia resulting from respiratory events in the supine position, without any
differences in the duration of events, lung-volume changes are
SLEEP, Vol. 29, No. 8, 2006
likely to be involved in explaining positional changes in ventilatory stability. Further indirect evidence to support the importance of lung-volume changes come from studies investigating
the efficacy of continuous positive airway pressure (CPAP) and
supplemental oxygen in the treatment of CSA-CSR secondary to
heart failure. Application of CPAP has been equally effective in
reducing AHI and ArI, as compared with the administration of
supplemental oxygen.30,31 CPAP is known to increase lung volumes,32 and both forms of treatment acutely reduce hypoxemia
through increasing total body oxygen stores,33 thus favoring the
development of ventilatory stability. Furthermore, CPAP as well
as supplemental oxygen have been shown to improve left ventricular ejection fraction after a 3-month treatment period.4,34 Thus,
the importance of reductions in lung volume and its effect on reducing oxygen stores may be underestimated in the pathogenesis
of CSA-CSR.
At present, there have been no studies that have investigated
the influence of transverse postural changes in chemoreceptor
sensitivity; thus we cannot rule out this mechanism as playing
a role in explaining the increase in AHI observed in the supine
position. However, this is unlikely given that supine to upright
changes in chemoreceptor sensitivity to CO2 have not been observed in normal subjects.35,36
Previous investigators have reported that upper-airway collapse is common during CSA-CSR19,20 and that the tendency for
upper-airway collapse is enhanced in the supine position in patients with OSAHS.14 This observation, together with evidence
that upper-airway collapse is common during CSA-CSR, may
make it plausible that an obstructive component during CSACSR may be important in explaining the increased frequency of
respiratory events in the supine position. It has also been reported
that fluctuations in state changes, such as those that occur as a
consequence of the arousal response, illicit changes in chemoreceptor sensitivity and that involvement of the peripheral chemoreceptors amplifies the state-related changes in ventilation.37 During sleep, chemoreceptor sensitivity is blunted to both hypoxic
and hypercapnic stimuli.38,39 The arousal response or the wakefulness drive is thus associated with an increase in chemoreceptor
sensitivity. It is possible that as the supine position favors upper-airway collapse, it would lead to longer apneas and a greater
degree of oxygen desaturation. The resultant increase in hypoxic
drive, together with an increased sensitivity of chemoreceptors
associated with the arousal response, may be associated with an
exaggerated ventilatory response and be an important mechanism
that promotes respiratory instability.
To address this question, we have examined the prevalence of
upper-airway collapse that resulted in mixed apneas during CSACSR in both supine and lateral positions during NREM sleep.
We have limited this part of the analysis to include only apneas
because the subclassification of hypopneas into central and mixed
is difficult, even with the presence of esophageal pressure measurement in a subgroup of our patients. Mixed apneas were found
to be longer in duration and resulted in a greater degree of hypoxemia than did central apneas. For both duration and desaturation,
this effect was independent of position; however, desaturation
associated with mixed and central apneas was further increased
in the supine position. Importantly, the proportion of central and
mixed apneas was similar in both positions; therefore, we believe
that mechanisms other than upper-airway collapse are responsible
for the increased ventilatory instability that we have found in the
1049
Influence of Position on CSA-CSR Severity—Szollosi et al
supine position. Our findings give indirect support that lung-volume reductions may be more important than previously thought
in the pathophysiology of CSA-CSR. It is likely that changes in
lung volume occur in association with postural changes in the
transverse plane; however, we cannot rule out that changes in
cardiac chamber dimensions, cardiac filling, cardiac output, or
other hemodynamic variables affecting circulation time, as well
as changes in chemoreceptor sensitivity, may also contribute to
ventilatory instability in the supine position. It is also possible that
active or passive collapse of the upper airway may be occurring
during central apneas.
In summary, this study has shown that the lateral position is
associated with a greater than 50% reduction in the AHI and the
apnea index independent of sleep-stage effects. These reductions
are of similar magnitude to those observed with application of
CPAP.4 Although event duration is not influenced by position,
hypoxemia is attenuated in the lateral position, suggesting that
postural changes in lung volume may be responsible for postural
changes in ventilatory instability. Thus, changes in loop gain rather than upper-airway collapse are likely to cause the increase in
AHI observed in the supine position in patients with heart failure
and CSA-CSR.
Because the prevalence of CSA-CSR is common in patients
with heart failure, avoiding the supine position during sleep may
be important in altering the expression of ventilatory instability in
this patient group. This may have profound effects on sleep quality by promoting consolidation of sleep architecture and by reducing hypoxic damage, sympathetic nervous system activation, and
consequent cardiovascular morbidity. However, further studies
are required to identify precise mechanisms involved and whether
a simple therapeutic intervention such as avoidance of the supine
position during sleep can contribute to improvements in quality
of life and survival. Finally, this study highlights that AHI during
CSA-CSR, as in obstructive sleep apnea, is highly dependent on
body position and sleep stage. The weak correlation between AHI
and morbidity in many studies40 may in part be explained by the
shifting expression of ventilatory instability caused by positional
influences.
8.
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10.
11.
12.
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14.
15.
16.
17.
18.
19.
20.
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