Arterial Blood Pressure Response to
Transient Arousals From NREM Sleep in
Nonapneic Snorers With Sleep
Fragmentation*
Frederic Lofaso, MD; Francoise Goldenberg, MD; Marie Pia d'Ortho, MD;
Andre Coste, MD; and Alain Harf, MD
Study objectives: To assess the hemodynamic effects of graded arousals during nonrapid eye
(NREM) sleep in patients with partial upper airway obstruction during sleep without
obstructive sleep apnea/hypopnea, overnight beat-to-beat BP was recorded in six patients.
Setting: At the end of each nonapneic obstructive event, EEG responses were graded as follows:
grade 2, grade 1, and grade 0 were defined as increased high-frequency EEG lasting > 15 s, 3 to
15 s, and no EEG arousals according to the American Sleep Disorders Association, respectively.
Measurements and results: The following were observed during grade 0, 1, and 2 EEG patterns
(mean±SD): systolic pressure increased by 7.1±1.5, 11.7±1.9, and 14.2±3.4 (p<0.005), respec¬
tively; diastolic pressure increased by 4.6±0.6, 6.7±1.7, and 9.4±3.0 (p<0.005), respectively;
heart rate increased by 2.9±0.4, 3.9±2.2, and 8.6±4.6 (p<0.005), respectively.
Conclusions: We conclude that nonapneic-nonhypopneic obstructive events are followed by
arterial systemic pressure increases whose magnitude varies with the grade of the arousal.
movement
(CHEST 1998; 113:985-91)
Key words: arousal; blood pressure; snoring; upper airway resistance
Abbreviations: ASDA=American Sleep Disorders Association; NREM=no rapid eye movement; OSAS=obstructive
sleep apnea syndrome; REM rapid eye movement
=
long been recognized that the obstructive
sleep apnea syndrome (OSAS) is associated with
acute increases in arterial BP at the termination of
respiratory events.1 This phenomenon has been as¬
cribed to hypoxemia,2'3 to the hemodynamic effects
of intrathoracic pressure changes,46 to interruptions
in respiration,7-9 and to disruption of sleep.10-14 For
others, the magnitude of the increase in arterial BP
does not vary with the grade of the arousal.15
Recent reports have demonstrated that an abnor¬
mal amount of breathing effort due to partial upper
airway obstruction, even in the absence of sleep
apnea or oxygen desaturation, can disrupt sleep
architecture by causing arousals.1617 The purpose of
this study was to examine whether the termination of
nonapneic-nonhypopneic obstructive events coin¬
cides with an abrupt increase in arterial BP similar to
T t has
-*-
*From the Service de
Physiologie-Explorations Fonctionnelles,
Institut National de la Sante et de la Recherche
Hopital Henri Mondor, Creteil, France.
Medieale,
Manuscript received January 28, 1997; revision accepted October
requests: F. Lofaso, MD, Service de Physiologie-ExploReprint
rations
Henri
94010
7, 1997.
France
Fonctionnelles, Hopital
Mondor,
Creteil,
that seen in OSAS, despite the absence of oxygen
desaturation and interruption of ventilation. In addi¬
tion, the relationship between the magnitude of the
arterial BP increase and the change in the EEG
pattern was examined. We recorded acute increases
in systemic arterial BP at the time of the abrupt
reduction in upper airway obstruction, and found
that this BP rise was primarily due to sleep disrup¬
tion.
Materials
and
Methods
Patients
Six men were studied. Mean age was 45 ± 11 years (range, 33 to
65 years). Mean body mass index was 27±3 kg/m2. All six subjects
had heavy snoring confirmed by a roommate or bed partner and
daytime sleepiness with an Epworth sleepiness scale18 >10.
Patients were included in the study after a home polysomnog¬
raphy study, including EEG (C4-Al9 C3-A2), electro-oculography,
chin electromyography, electromyography of the tibialis anterior
muscle of both legs, oronasal airflow recordings, rib cage move¬
ment recordings (Multi-Parameter Analysis recorder 2/Medilog
9200; Oxford Medical Instruments; Abingdon, England), and
arterial pulse oximetry (Nellcor BS; Nellcor Inc; Hayward Calif).
CHEST/ 113/4 /APRIL, 1998
Downloaded From: http://journal.publications.chestnet.org/ on 10/01/2016
985
To be eligible for the study, subjects had to have an at-home
polysomnography study that met the following criteria: apneaindex <5/h of sleep (apnea was defined as cessation of
hypopnea
airflow lasting ^10 s and hypopnea
2:50% fall in oronasal
airflow for 10 s or a fall in oronasal airflow with an oxygen
desaturation ^3% of the preceding baseline level); and arousal
index >10/h of sleep (arousals were detected on the basis of an
abrupt shift in EEG frequency, including alpha and/or frequen¬
cies >16 Hz but not spindles, and were scored according to
standard criteria19). To relate clinical complaints and sleep
fragmentation to an upper airway obstruction without obstructive
sleep apnea/hypopnea, a sleep polygraphic investigation, includ¬
ing respiratory effort evaluation, was performed as recommend¬
ed.20 The study was approved by the Research Ethics Committee
of our institution, and each subject gave consent in accordance
committee's
as a
with the
requirements.
The clinical trial consisted of a repeat polysomnography study,
including EEG (C4-Al5 C3-A2), electro-oculography, chin elec¬
tromyography, thoracic and abdominal movement recording, and
arterial pulse oximetry (Nellcor BS, Nellcor Inc.). During the
study night, oronasal airflow was quantified using a tight-fitting
facial mask and a No. 2 pneumotachograph (Fleisch; Lausanne,
Switzerland) connected to a differential pressure transducer
MP45 ±5
cm
H20; Northridge, Calif).
frequencies
>16
Hz, except
spindles; grade 0b, low-frequency
EEG changes (K-complexes and/or delta wave burst) without any
increase in EEG frequency except spindles; grade 0c, no increase
in cortical high frequency and no occurrence of K-complexes or
Clinical Trial
(Validyne
and after the end of respiratory events were looked for. Arousal
was performed by one of us (F.G.), who was
aware of the time at which respiratory events were terminated,
but was not aware of the changes in respiratory effort and in BP
at the time ofthe respiratory event. EEG changes were graded as
follows: grade 2, shift in EEG frequency lasting >15 s and
including alpha activity and/or frequencies >16 Hz, according to
the standard criteria of awakening;22 grade 1, shift in EEG
frequency lasting from 3 to 15 s and including alpha activity
and/or frequencies >16 Hz, except spindles, according to stan¬
dard criteria of arousal;19 grade 0, no EEG changes or minor
EEG changes, usually not classified as arousals in the American
Sleep Disorders Association (ASDA) criteria.19 Grade 0 EEG
changes were further classified as follows: grade 0a, shift in EEG
frequency lasting <3 s and including alpha activity and/or
scoring analysis
In
addition,
respiratory effort was monitored by measuring esophageal pres¬
sure (Gaeltec; Dunvegan, Isle of Skye, UK), and BP and heart
rate were monitored by recording digital arterial beat-to-beat
systolic/diastolic pressure at the third finger ofthe left hand using
an infrared plethysmographic volume clamp method (Finapres;
Ohmeda; Maurepas, France). As previously proposed,1112 the left
hand was taped to the epigastric area to avoid artifactual BP
modifications caused by changes in hydrostatic pressure associ¬
ated with hand movement. All signals were recorded using a
14-channel paper recorder (Electroencephalograph; Nihon Kohden;
Japan) digitized at 128 Hz and sampled using an analogic/
Tokyo,
numeric system (MP100; Biopac System; Goleta, Calif) for
subsequent analysis.
Data Analysis
nonapneic-nonhypopneic obstructive event was defined as
the occurrence, in the absence of hypopnea (airflow drop <50%
of the preceding baseline during 10 s or airflow drop with
desaturation <3% of the preceding baseline level), of a progres¬
sive
in the
of the
flow
A
change
shape
inspiratory contour charac¬
terized by increasing limitation21 and of a concomitant increase in
the esophageal pressure swing, with termination of the vent as
abrupt normalization of both the inspiratory flow contour and the
esophageal
pressure swing. Esophageal pressure swings were
calculated as the difference between the maximal expiratory
value and the minimal inspiratory value. Esophageal pressure
swing decrease was quantified as the decrease in esophageal
pressure swing at the termination ofthe respiratory event, ie, the
difference between esophageal swings immediately before and
after the termination of the respiratory event. BP parameters and
heart rate were analyzed over two 10-s periods before and after
the termination of the respiratory event. BP parameters were
taken into account only during the expiratory phase of the
breathing cycle. They corresponded to at least three data points
for each 10-s period.
Sleep staging was performed according to standard criteria.22
Only respiratory events from nonrapid eye movement (NREM)
sleep periods were used. EEG changes during the 10 s before
delta wave bursts.
Statistical Analysis
For each patient and each type of EEG change, the changes in
arterial pressure and in
esophageal pressure at the end of the
nonapneic-nonhypopneic respiratory events were averaged and
Friedman's two-way analysis of variance was performed. Where
appropriate (p value <0.05), pairwise comparisons were per¬
formed using a Wilcoxon matched paired test. The level of
significance was set at 5%.
Results
Epworth sleepiness
scale18 and main sleep and
respiratory parameters during the polysomnography
with arterial BP measurement are presented in
Table 1. A mean (±SD) of 167 (±145) nonapneicevents were observed per
nonhypopneic respiratory
patient during NREM sleep. Distribution of EEG
patterns during these nonapneic-nonhypopneic re¬
spiratory events is presented in Table 2.
Systolic and diastolic BPs and heart rate rose after
the end of the respiratory events, reaching a peak
within 10 s after event termination (Fig 1).
BP and heart rate changes in response to different
grades of EEG modifications are shown in panels A
(top) and B (center) of Figure 2, respectively. The
were observed during grade 0, 1, and 2
following
EEG patterns (mean±SD): systolic pressure in¬
creased by 7.1 + 1.5, 11.7+1.9, and 14.2+3.4
(p<0.005), respectively; diastolic pressure increased
by 4.6+0.6, 6.7±1.7, and 9.4+3.0 (p<0.005), re¬
spectively; heart rate increased by 2.9±0.4, 3.9±2.2,
and 8.6±4.6 (p<0.005), respectively.
No differences were observed across the three
grade 0 subclasses (0a, 0b, and 0c). Systolic and
diastolic BP increases were significantly higher for
grade 2 and grade 1 than for grade 0. The heart rate
increase was significantly higher for grade 2 than for
grade 0.
Clinical
Downloaded From: http://journal.publications.chestnet.org/ on 10/01/2016
Investigations
Table
Respiratory Data During Polysomnography With Arterial BP
1.Epworth Sleepiness Score and Sleep andMeasurements*
Epworth
Sleepiness
Patient
A
B
C
D
E
F
min
%TST
%TST
%TST
80
112
146
163
160
102
93
72
84
77
65
58
0
17
16
13
25
19
/
59
11
¦0
10
10
17
22
54
12
14
23
Scale
mm
19
21
11
12
11
12
426
398
279
362
360
182
*TST.total sleep time; WASO=wake after sleep onset;
swing decreases in response
Esophageal pressure
different grades of arousals are shown in panel C
(bottom) of Figure 2. No differences in esophageal
pressure swing changes were observed across grades.
The mean fall in arterial oxygen saturation was
<0.3% for each grade of arousal, with no significant
differences across grades.
Discussion
airway obstruction without
exhibit increased
sleep apnea/hypopnea
NREM
during
sleep, often withof
respiratory
EEG pattern changes. We found that termination
these nonapneic-nonhypopneic obstructive events
was consistently followed by a rise in BP, and that
the magnitude of this rise increased with the inten¬
sity of EEG arousal, although significant but smaller
in
of
efforts
rises
were
detectable
EEG arousal.
In this study,
as
the absence
REM,
apparent
previously proposed,1113 BP was
analyzed by infrared plethysmography. Because this
noninvasive indirect method may overestimate BP,12
we measured only arterial BP changes. However,
increased arteriolar vasoconstriction at the periphery
could increase systolic BP measured at the finger by
a phenomenon of reflectance ofthe pressure wave at
the resistance vessels causing amplification and rise
systolic BP. However, diastolic BP is virtually
by this phenomenon.11 We found that
magnitude of diastolic pressure increases also varied
with the grade of arousal. This indicates that the BP
rises that we observed cannot be due solely to this
artifact of pulse wave amplification.
Although we analyzed both rapid eye movement
(REM) and NREM data, the amount of data was too
small to allow comparisons of the different grades of
arousal during REM sleep. Only two patients expe¬
rienced nonapneic-nonhypopneic obstructive events
both with and without awakening/arousal during
REM sleep. This is due in part to the fact that
apneas/hypopneas were predominant in REM sleep,
whereas nonapneic-nonhypopneic obstructive events
were observed less frequently.
The age range in our six patients was quite large,
but only one patient was >50 years (patient E, 65
he was the patient who had the
years). Interestingly,
lowest arterial BP response to the different levels of
arousal. During grade 2, 1, and 0 EEG patterns,
by only 10, 9, and 4 mm
systolic pressure increased
This
result
corroborates the study
Hg, respectively.
of Hajduczok et al23 that demonstrated that sympa¬
thetic activity is impaired with senescence.
The cardiovascular consequences of OSAS include
a rise in systemic BP after each episode of apnea.1
These postapneic BP elevations contribute signifiin
unaffected
Table 2.EEG Patterns at the End of Nonapnoeic-Nonhypopnoeic
Patients
A
B
C
D
E
F
Mean
SD
Nonapneic-Nonhypopneic
Grade 2,
421
137
250
59
73
59
167
145
16
12
8
12
26
2
13
8
Respiratoiy Events
Hour of Sleep
AHI=apnoea-hypopnoea index; UAR=upper airway resistance.
to
Patients with upper
Nonapneic-Nonhypopneic
Respiratory Events per
Hour of Sleep
Stages 3+4,
WASO,
obstructive
AHI, Events per
Stages 1+2,
TST,
Respiratory Events During NREM Sleep
Grade 0,
Grade 1,
Total Grade 0
% %
66
48
81
27
53
72
57
23
18
40
11
61
21
26
30
18
Grade 0a
Grade 0b
Grade Oc
12
24
7
49
16
23
21
15
3
14
3
13
2
1
6
6
CHEST/113/4/APRIL, 1998
Downloaded From: http://journal.publications.chestnet.org/ on 10/01/2016
987
Arousal grade 1
^*^r^W^^
*¦'.»i' j
(L/sec)
Peso
(cmH20)
.ji'ifw.4.k><.
.0.5
0
-20
s:: siis^^
(mmHg) 100
grade Oh
m^fc^^
(L/sec)
+0;.5
.0U5
Peso
°
Flow
(cmHiO) .20
Pressure
(mmHg) 100
If^tyj^^
Flow
+0.5
(L/sec)
Peso
_05
°
(cmH20)
.20
,.
Arterial J40
Pressure
(mmHg) 100
polysomnographic
recordings obtained in a patient, showing BP changes in
arousals due to nonapneic-nonhypopneic respiratory events. The
grades of EEGchin
EEG, electro-oculogram (EOG),
electromyogram (EMG), air flow (Flow) pneumotachograph
recording, esophageal pressure (Peso) recording, and arterial BP recordings are shown.
Figure 1. Continuous
response
to various
cantly to the nocturnal hypertension and perhaps
also to the diurnal hypertension seen in patients with
obstructive sleep apnea. A recent study demon¬
strated that acute increases in systemic arterial BP
also occur after each respiratory event in the patients
with upper airway obstruction without obstructive
sleep apnea/hypopnea.24 We found that the magni¬
tude of these BP increases is related to the intensity
of EEG arousal.
Both arterial hypoxemia23 and arousal from
sleep10-14 have been suggested as the main causes of
988
Downloaded From: http://journal.publications.chestnet.org/ on 10/01/2016
the nocturnal hemodynamic oscillations seen in pa¬
tients with OSAS, although Rees et al15 found no
between the rise in BP and the occur¬
relationship
rence of EEG change. To evaluate the respective
contributions of hypoxia and arousal, investigators
have used a variety of approaches to isolate these two
factors from each other. To maintain arterial oxygen
saturation >90% at the end of apneas, Ringler et al10
and Ali et al12 provided supplementary oxygen to
OSAS
patients undergoing polysomnography. They
found that oxygen supplementation did not alter the
Clinical
Investigations
20
H"
X
ISA
10
is
©
o
0
12
s
n-1-r
nr
J
5
10
also induced arousals by auditory stimulation in
normal subjects. In their study, the magnitude ofthe
BP increase was proportional to the degree of
arousal, as defined by the duration of the increase in
high-frequency EEG activity. In our study, in pa¬
tients with upper airway obstruction without ob¬
structive sleep apnea/hypopnea, we also found that
the magnitude of the BP rise was closely related to
the degree of arousal. These data corroborate the
findings from the studies on OSAS, providing addi¬
tional evidence that arousals related to obstructive
respiratory events may be accompanied by signifi¬
cant BP rises even in the absence of oxygen desatu¬
ration.
Other factors than arousal
have been
hypoxia for
suggested possibly being responsible the BP
elevation in OSAS. These factors include reinflation
of the lung, which may change cardiovascular per¬
formance via a number of mechanisms,7-9 and ter¬
mination of deep negative pleural pressure dips
generated
by frustrated inspiratory efforts during
obstructive apnea.25 These factors may also be in¬
volved in patients with upper airway obstruction
without obstructive sleep apnea/hypopnea, either in
combination with arousals or
since
or
as
SA
5
10
m
s
7.5
«8 «
2.5
W
i-1-r
2
Figure 2.
Systolic
0a
10
Ob
Grade of Arousal From Sleep
pressure
(squares)
0c
and diastolic pressure
The left-sided panels show the values observed during
2, 1, and 0 arousals. In the right-sided panels, grade 0
grade
arousals are divided into three subgroups (see "Materials and
Methods" for definition). No differences were observed across
diastolic BP increases were
grade 0 subtypes. for
Systolic and
2 and grade 1 than for grade 0.
significantly
higher
grade
Heart rate increases were significantly higher for grade 2 than for
0. No differences in esophageal pressure swing changes
grade
were observed across grades. Values are means± SEM.
events.
BP increase after apnea termination. In
et
al10 induced
during nonapneic-nonhypopneic
respiratory events
only 100 mL. It can be postulated that such a
small increase in end-inspiratory thoracic volume at
the end of a respiratory event will result in insignif¬
icant inflation-associated cardiovascular responses. A
second factor may be intrathoracic pressure changes,
which are known to influence BP. BP decreases from
expiration to inspiration, and when pleural pressure
becomes more negative during inspiration, such as in
with
was
(diamonds) changes (top, A), heart rate changes (center, B), and
esophageal
pressure swing decrease (bottom, C) in response to
various grades of arousal at the end of nonapneic respiratory
Ringler
we ob¬
alone,
served some increase in BP in the absence of
arousals (EEG pattern scored as grades 0). In a
discussion of the lung volume changes in patients
with upper airway obstruction without obstructive
sleep apnea/hypopnea, Stoohs and Guilleminault26
pointed out that the mean decrease in tidal volume
addition,
nonrespiratory (auditory)
arousals in OSAS patients treated by nasal positive
airway pressure and observed that the BP increase
after auditory arousal was similar to the BP increase
after obstructive apnea. Similarly, Ali et al11 demon¬
strated that arousals induced by periodic leg move¬
ments induce an increase of BP in the same order as
the rises seen after obstructive apneas. Davies et al13
asthma, inspiratory arterial pressure
patients
decreases further.5 Because part of the increase in
BP occurring at the end of respiratory events may be
ascribable to a reduction in the inspiratory decline of
arterial BP, we decided to avoid this possible me¬
chanical effect by measuring arterial BP during
expiration. However, because mean intrathoracic
pressure is more negative during an obstructive
respiratory event, left ventricular ejection may de¬
following increases in left ventricular afterload4 and in venous return,6 which increase enddiastolic volume of this cardiac chamber: this
increase of end-diastolic volume of right ventricle
can also decrease the left ventricular diastolic com¬
therefore the left ventricular preload
pliance and
the
mechanisms
of the ventricular interdethrough
crease
CHEST/ 113/4 /APRIL, 1998
Downloaded From: http://journal.publications.chestnet.org/ on 10/01/2016
pendence.27 Thus, a return to normal intrathoracic
pressure after the end of the obstructive respiratory
event may increase BP by raising left ventricular
ejection. Such a phenomenon may explain the in¬
crease in BP that occurred in our study after the end
of nonapneic-nonhypopneic respiratory events, even
in the absence of visible EEG changes. However, the
putative role of a decrease in intrathoracic pressure
in decreasing left ventricular ejection under condi¬
tions appropriate to sleep apnea syndrome has not
yet been confirmed by experimental studies.27 In
addition, in our study, although esophageal pressure
did become more negative during these respiratory
events, the mean esophageal pressure swing increase
was <10 cm H20, a value much lower than in the
sleep apnea syndrome.
Since none of these previous hypotheses is satis¬
an increase in BP (during
factory,Ocwe suggest thatoccur
as a result of brainstem
grade arousals) may
activation caused by the respiratory event and suffi¬
response
produceThisan autonomic has
ciently marked toarousal.
been
but not cortical
hypothesis
who
Davies
et
observed
al,13
suggested previously by
that auditory stimuli could also induce BP increases
(with magnitudes similar to those in our study during
0 arousals) without causing EEG arousal.
grade
A recent study investigated a subpopulation of
patients with upper airway obstruction without ob¬
structive sleep apnea/hypopnea and without detect¬
able EEG arousals.20 In our study, one third of
respiratory events were
nonapneic-nonhypopneic
not associated with arousals according to AS DA
criteria (grades 0), but were associated with abrupt
these
events with¬
BP increases.
out
respiratory
Among
arousal, many (80%) were associated with EEG
changes, which were usually of low frequency (grade
Ob: K-complexes and/or delta wave bursts). Since it
has been demonstrated that a minimal EEG event,
such as a K complex, may induce an increase of the
sympathetic
discharge,28 we checked whether these
events with minimal EEG changes (grades 0a and
Ob) were associated with larger arterial BP elevations
than events with no EEG changes (grade 0c). We
found
no
differences, suggesting that use of arous-
ability criteria that are more sensitive than AS DA
criteria does not provide any additional clinical in¬
formation on the cardiovascular consequences of
upper airway obstruction without obstructive sleep
apnea/hypopnea.
conclusion, we found that, similar to OSAS
patients, snorers with upper airway obstruction with¬
In
sleep apnea/hypopnea exhibited
transient systemic BP elevations at termina¬
abrupt
tion of respiratory events. In addition, the magnitude
of the transient BP increases during NREM sleep
varied with the grade of the arousal associated with
out
obstructive
990
Downloaded From: http://journal.publications.chestnet.org/ on 10/01/2016
the
nonapneic-nonhypopneic respiratory
event.
However, BP increases were also seen in the absence
of detectable EEG arousal. Because the other factors
generally believed to produce postapneic BP eleva¬
tion in OSAS are absent or insignificant in patients
with upper airway obstruction without obstructive
sleep
apnea/hypopnea, we believe that arousal is the
main cause of the systemic BP increases seen after
termination of nonapneic-nonhypopneic obstructive
events. In addition, given that BP increases also oc¬
curred without apparent EEG arousal, beat-to-beat BP
evaluation may be a more sensitive means of identifying
nonapneic-nonhypopneic respiratory events than con¬
ventional evaluation of EEG changes.
ACKNOWLEDGMENT: We are grateful to Djibril Bokar Thire,
Nathalie Gadenne, Denise Henry, and Richard Morales for their
skillful technical assistance.
1
2
References
Coccagna G, Montovani M, Brignani F,
et
al. Continuous
recording of the pulmonary and systemic arterial pressure
during sleep in syndromes of hypersomnia with periodic
breathing. Bull Eur Physiopathol Respir 1972; 8:1159-72
Shepard
JJ. Gas exchange and hemodynamics during sleep.
Clin
Med
North Am 1985; 69:1243-64
3 O'Donnell C, Ayuse T, King E, et al.
Air-way obstruction
during sleep increases blood pressure without arousal. J Appl
Physiol 1996; 80:773-81
4 Buda AJ, Pinsky MR, Ingels NB, et al. Effect of intrathoracic
pressure on left ventricular performance. N Engl J Med 1979;
301:453-59
5 Jardin F, Bourdarias JP. Influence of abnormal breathing
conditions on right ventricular function. Intensive Care Med
1991; 17:129-35
6 Lloyd T. Effect of inspiration on inferior vena caval blood
flow in dogs. J Appl Physiol 1983; 55:1701-08
7 Howell J, Permutt S, Proctor D, et al. Effect of inflation of
the lung on different parts on pulmonary vascular bed. J Appl
Physiol 1961; 16:71-76
8 Marini JJ, Culver BH, Butler J. Mechanical effects of lung
distension with positive pressure on cardiac function. Am Rev
Respir Dis 1981; 124:382-86
9 Kaufman M, Iwamoto G, Ashton J, et al. Response to inflation
of vagal afferents with endings in the lungs of dogs. Circ Res
1982; 51:525-31
10 Ringler J, Basner R, Shannon R, et al. Hypoxemia alone does
not explain blood pressure elevations after obstructive apneas.
J Appl Physiol 1990; 69:2143-48
11 Ali NJ, Davies RJ, Fleetham JA, et al. Periodic movements of
the legs during sleep associated with rises in systemic blood
pressure. Sleep 1991; 14:163-65
12 Ali N, Davies R, Fleetham
continuous
on
J,
et
al. The
acute
effects of
positive airway pressure on oxygen administration
blood pressure
during
obstructive
1992; 101:1526-32
13 Davies R, Belt P, Roberts S,
sleep
apnea. Chest
et al. Arterial blood pressure
responses to graded transient arousal from sleep in normal
humans. J Appl Physiol 1993; 74:1123-30
14 Ringler J, Garpestad E, Basner R, et al. Systemic blood
pressure elevation after airway occlusion during NREM
sleep. Am J Crit Care Med 1994; 150:1062-66
15 Rees K, Spence D, Earis J, et al. Arousal responses from
Clinical
Investigations
16
apneic events during non-rapid-eye-movement sleep. Am J
Respir Crit Care Med 1995; 152:1016-21
Guilleminault C, Stoohs R, Duncan S. Snoring (I): daytime
23
sleepiness in heavy snorers. Chest 1991; 99:40-48
17 Guilleminault C, Stoohs R, Clerk A, et al. A cause of excessive
daytime sleepiness: the upper airway resistance syndrome.
Chest 1993; 104:781-87
18 Murray W. A new method for measuring daytime sleepiness:
the Epworth sleepiness scale. Sleep 1991; 14:540-45
19 American Sleep Disorders Association. EEG arousals: scoring
rules and examples. Sleep 1992; 15:174-84
20 Guilleminault C, Stoohs R, Clerk A, et al. Excessive daytime
24
25
26
somnolence in women with abnormal respiratory effort dur¬
Respir Physiol 1991; 85:151-67
27 Scharf S. The effect of decreased intrathoracic pressure on
ventricular function. J Sleep Res 1995; 4S:53-58
28 Somers V, Dyken M, Mark A, et al. Sympathetic-nerve
ing sleep. Sleep 1993;
16:sl37-38
21 Liistro G, Stanescu C, Veriter C, et al. Pattern of snoring in
obstructive
sleep apnea patients an in heavy snorers. Sleep
1991; 14:517-25
22 Rechtschaffen A, Kales A. A manual of standardized
AMERICAN
activity during sleep in normal subjects. N Engl J Med 1993;
328:303-07
termi¬
COLLEGE
nology, techniques and scoring system for sleep stages of
human subjects. Washington, DC: National Institutes of
Health 1968; publication No. 204
Hajduczok G, Chapleau MW, Johnson SL, et al. Increase in
sympathetic activity with age: I. Role of impairment of arterial
baroreflexes. Am J Physiol 1991; 260:H1113-20
Guilleminault C, Stoohs R, Shiomi T, et al. Upper airway
resistance syndrome, nocturnal blood pressure monitoring,
and borderline hypertension. Chest 1996; 109:901-08
Parish JM, Shepard JW Jr. Cardiovascular effects of sleep
disorders. Chest 1990; 97:1220-26
Stoohs R, Guilleminault C. Snoring during NREM sleep:
respiratory timing, esophageal pressure and EEG arousal.
OF
BCHE ST
CONTINUING MEDICAL EDUCATION
PHYSICIANS
SleepforMedicine
the Chest Physician
May 20-23, 1998
Chicago, Illinois
FOR INFORMATION CALL 800*343*2227 OR 847*498*1400
CHEST/113/4/APRIL, 1998
Downloaded From: http://journal.publications.chestnet.org/ on 10/01/2016
991