Professional Documents
Culture Documents
40 (2007) 713–743
The term ‘‘polysomnography’’ (PSG) has Greek and Roman roots, and
refers to the recording of multiple sleep-related signals. It employs various
methods to simultaneously and continuously record neurophysiological,
cardiopulmonary, and other physiological parameters over the course of
several hours, usually during an entire night (overnight polysomnography).
PSG provides information on the physiological changes occurring in many
different organ systems in relation to sleep stages and wakefulness. It allows
qualitative and quantitative documentation of abnormalities of sleep and
wakefulness, sleep-wake transition, and of physiological function of other
organ systems that are influenced by sleep. Many of these, such as sleep
apnea, may not be present during wakefulness.
Four types of sleep studies are available, depending upon the number of
physiological variables recorded [1]:
Level I. Standard PSG with a minimum of seven parameters measured,
including electroencephalogram (EEG), electro-oculogram (EOG),
chin electromyogram (EMG), and EKG, as well as monitors for air-
flow, respiratory effort, and oxygen saturation. A technician is in con-
stant attendance.
Level II. Comprehensive portable PSG studies are essentially the same,
except that a heart rate monitor can replace the ECG and a technician
is not in constant attendance.
* Corresponding author. North Florida South Georgia VAHS Sleep Disorders Center,
#111A, Malcom Randall Veterans Administration Medical Center, 1601 Archer Road,
Gainesville, FL 32608.
E-mail address: rahul.kakkar@medicine.ufl.edu (R.K. Kakkar).
Fig. 1. The EEG electrodes are placed using the conventional 10–20 system. For sleep recording
and staging, the current standards require monitoring of at least central (C3, C4) and occipital
(O1, O2) derivations. Additional EEG electrodes can be placed depending on the need. The new
AASM standards to be published in spring 2007 will require frontal derivations to be recorded
as well. (Courtesy of Compumedics USA, El Paso, Texas; with permission.)
INTERPRETATION OF THE ADULT POLYSOMNOGRAM 715
Fig. 2. Placement of EOG electrodes. See text for details. (Courtesy of Compumedics USA,
El Paso, Texas; with permission.)
saturation and body position [2]. EKG is recorded routinely during all PSG
studies. Video monitoring during a PSG, although not required, is extremely
valuable, both from a diagnostic as well as medico-legal perspective.
Additional variables can be recorded according to patient age, standards
of the sleep laboratory, and indication for performing the study. Examples
Fig. 3. Placement of submental EMG electrodes. A third electrode is often used and placed
under the chin. (Courtesy of Compumedics USA, El Paso, Texas; with permission.)
716 KAKKAR & HILL
Important considerations
Polysomnography is considered to be the ‘‘gold standard’’ for diagnosing
SDB and other sleep disorders. A gold standard should have 100% sensitivity
and specificity [5]; however, like most other diagnostic tests, PSG is not ideal,
but rather the best available method to diagnose SDB. Furthermore,
breathing disturbances may vary from night to night within certain limits
[6,7]. Some sleep disorders such as nocturnal laryngospasm, sleep-related
epilepsy, or parasomnias that occur episodically may be missed in a one-night
recording [8].
A PSG should always be interpreted in light of a patient’s clinical history.
The physician’s orders should be reviewed to determine the reason for
obtaining the PSG and for the type of study requested. The interpreting
physician should ascertain that the PSG was performed as requested. If
a split-night study (diagnostic and PAP titration in the same night) was
ordered but the patient has difficulty sleeping, demonstrates only mild ob-
structive sleep apnea (OSA), or does not tolerate the PAP trial, it is helpful
to write a brief explanation as to why PSG was not performed as requested.
This helps the referring physician to decide whether to order another study
with PAP trial, or to refer the patient for alternative therapies.
It is pertinent to review the referring physician’s notes and the prestudy
questionnaire before interpreting PSG. The referring physician’s notes
provide information on comorbid conditions that may increase the likeli-
hood of prevalence of certain sleep disorders. For example, heart failure
with ejection fraction of less than 40% increases the risk of having
Cheyne-Stokes breathing, hypothyroidism increases the likelihood of having
OSA, and Parkinson’s disease is associated with higher incidence of RBD.
The physician’s notes are also helpful in explaining certain findings on
the PSG, such as cardiac arrhythmias or abnormal oxygen saturation at
baseline.
Generally, each patient is given a pre-study questionnaire to fill out
before performing the PSG. This questionnaire provides sleep history in
greater detail than is usually available otherwise. The questionnaire is
intended to obtain information on patient’s sleep-wake schedule and various
sleep symptoms such as snoring, excessive daytime sleepiness, witnessed
apneas, irresistible urge to move legs, dream enactment, teeth grinding,
cataplexy, and so forth. The patient’s usual bedtime and rise time are taken
into account when commenting on sleep latency and efficiency (see below).
Some degree of insomnia can be expected in the unfamiliar environment of
the sleep laboratory, especially on the first night (first-night effect) [9].
718 KAKKAR & HILL
Video recording
The authors routinely perform video recording on all patients coming to
our sleep laboratories, and a written consent for this is obtained from every
patient. Video recording should begin from the time of starting the hookup,
and should continue until the study is completed. It provides objective
assessment of seizures, sleep-related movement disorders, and parasomnias.
It can also be used to confirm the patient’s position in case of doubt. It may
sometimes be possible to see mouth opening and paradoxical respiratory
movements on the video. Video also provides added security to the
patient and the laboratory personnel from inappropriate interaction or
allegations of such an interaction. The video files typically consume a large
amount of storage space. DVD and tape drives are the currently preferred
methods of storing video data.
Fig. 4. EKG artifact (solid arrows). Note the presence of prominent EKG artifact in the EEG
(C3, C4, O1, and O2) and EOG (ROC, LOC) channels. It persisted despite re-referencing the
derivations to average (AVG) of all electrodes.
Sleep staging
Until recently sleep staging was based on the original Rechtschaffen and
Kales’ criteria devised more than 30 years ago. The AASM task force has
recommended implementation of new criteria for sleep staging, which will
replace the current staging system [2]. Sleep is now scored in the following
stages; stage awake (W), NREM stages 1, 2, 3 ( N1, N2 and N3 respectively)
and stage REM (R) sleep. EEG, EOG and chin EMG are required to score
INTERPRETATION OF THE ADULT POLYSOMNOGRAM 721
Fig. 5. Value of different display ranges. (A) Displaying the trends in 10-second range increases
the resolution of EEG waveforms. Alpha waves are clearly recognized in the EEG (C3, C4, O1,
and O2) tracings. Frequency is determined by counting the ‘‘peaks’’ in one-second interval. (B)
Displaying the data in a compressed format (display range 480 seconds) accentuates the classi-
cal pattern of Cheyne-Stokes breathing.
Fig. 6. The arrow points towards alpha waves (30-second montage; vertical grid lines are
1 second apart). Note that they are most prominent in occipital leads.
Fig. 7. Beta waves (black arrows) recorded during a documented period of wakefulness during
the PSG (see technician notations on top and bottom of (A). (A) 30-second and (B) 10-second
display periods showing difference between beta and alpha (white arrows) rhythms.
INTERPRETATION OF THE ADULT POLYSOMNOGRAM 723
prominent during stage awake and eyes open. They are of low amplitude
and disappear during sleep. The frequency for theta waves ranges from
4–8 Hz (Fig. 8) and for delta waves it is less than 4 Hz (Fig. 9). Theta
frequency is the most prevalent frequency seen during a polysomnography.
In addition to these four frequencies, four morphologic waveforms are
important. Vertex waves are sharp negative waves (in EEG terminology,
a negative wave causes an upward deflection) (Fig. 10). They first appear
in stage N1 sleep and are most abundant during stage N2 sleep. K-complex
is a biphasic wave with an initial upward (negative) deflection followed by
a slower downward (positive) deflection (see Fig. 8). Sleep spindles are
so-named because of their characteristic shape. They have a frequency of
12 to 14 Hz and duration of 0.5 to 1.5 seconds (Fig. 11). K-complexes
and sleep spindles are characteristic of stage 2 sleep. Sawtooth waves also
have a characteristic appearance (Fig. 12). They have low amplitude and
are in the theta frequency.
Staging of sleep is performed in 30-second epochs, and is more of
a pattern recognition exercise. An epoch is assigned a sleep stage according
to the predominant stage present in that epoch. Stage awake with open eyes
is characterized by presence of low amplitude beta rhythm. Stage awake
with eyes closed is characterized by prominent alpha waves (see Fig. 6).
As the patient becomes drowsy, slow lateral eye movements (SEM) are often
seen while alpha activity is still prominent (Fig. 13). Stage N1 sleep is the
most difficult of all stages to recognize because it is not defined by the pres-
ence of any particular waveform, but rather by the disappearance of alpha
Fig. 8. Theta waves (black arrow) and K-complexes (white arrows) in a patient in stage 2 sleep
(30-second montage; vertical grid lines are 1 second apart).
724 KAKKAR & HILL
Fig. 9. The solid arrows point towards the delta waves (30-second montage; vertical grid lines
are 1 second apart). For sleep staging, the duration should be at least 0.5 sec (frequency 2 Hz or
less) and amplitude should be more than 75 mV. The reference marker for voltage is displayed
in lower right hand corner (broken arrow).
waves and the onset of a mixed frequency, low amplitude pattern. Other
clues to the presence of stage N1 sleep are the appearance of SEM, a decrease
in EMG tone, and the appearance of vertex waves (although they are not
required to identify stage N1 sleep). Appearance of K-complexes and sleep
Fig. 10. Vertex waves, shown by the solid arrow, in a series (30-second montage; vertical grid
lines are 1 second apart). Note that they do not have a component of positive (downward)
deflection and are much narrower than K-complexes. They appear in stage 1 sleep, but are most
prominent during stage 2 sleep.
INTERPRETATION OF THE ADULT POLYSOMNOGRAM 725
Fig. 11. Sleep spindles, shown by the solid arrow, (10-second montage; vertical grid lines are
1 second apart). Note the characteristic shape, frequency and duration.
Fig. 12. Sawtooth waves (solid arrow). Note characteristic appearance. They are in theta
frequency and are most prominent during REM sleep.
726 KAKKAR & HILL
Fig. 13. Stage 1 sleep. Note the onset of low amplitude, mixed frequency waveforms in EEG
channels and slow eye movements (SEM) in EOG channels.
Fig. 14. REM. Notice sharp deflections in EOG channels and compare them with SEM shown
in Fig. 13. Normal ‘‘phasic’’ bursts in leg EMG during REM sleep are also present (arrows).
Fig. 15. Hypnogram. (Courtesy of Compumedics USA, El Paso, Texas; with permission.)
728 KAKKAR & HILL
Fig. 17. Bruxism. 29-year-old female with subvalvular stenosis was noted to have several
episodes of prolonged 1–2 Hz disturbance in EEG and chin EMG. Prominent gritting sounds
were heard on video replay.
Fig. 18. Nasal pressure cannulae. (Courtesy of Compumedics USA, El Paso, Texas; with
permission.)
Fig. 19. Nasal pressure tracing (marked NPRES) shows significant decrease in amplitude,
characteristic flattening, and reflection of snoring during a hypopnea while there is little change
in the thermistor signal (marked AIRFLOW).
734 KAKKAR & HILL
Fig. 20. An example of exaggerated mouth breathing. Increased signal at mouth transition
from additional sensor at mouth. Note the nasal pressure signal does not disappear. (Courtesy
of Compumedics USA, El Paso, Texas; with permission.)
Fig. 21. Obstructive apnea with paradoxical breathing. Note the out-of-phase movements in
chest and abdominal effort during the obstructive sleep apnea, which returns to in-phase
movements at the termination of the event.
INTERPRETATION OF THE ADULT POLYSOMNOGRAM 735
Fig. 23. Cheyne-Stokes breathing. Note characteristic crescendo decrescendo pattern in breath-
ing effort, paralleling the airflow.
INTERPRETATION OF THE ADULT POLYSOMNOGRAM 737
however, some patients may show worsening CSA and oxygen desaturation
with continuous positive airway pressure (CPAP) or bi-level PAP titration.
This is called complex sleep apnea [33]. Several treatment options are avail-
able for the treatment of complex sleep apnea.
Continuous pulse oximetry is used to assess baseline oxygen saturation
and degree of hypoxemia during PSG recording. The authors prefer not
to use supplemental oxygen during diagnostic or PAP titration studies as
long as severe hypoxemia (!80%) is not present. Supplemental oxygen
may make recognition of hypopneas difficult [34]. Many patients on noctur-
nal oxygen therapy for mild nocturnal hypoxemia often do not require
supplemental oxygen with PAP therapy. This is because PAP increases
the functional residual capacity (FRC), which is critical in determining
oxygenation in an individual. True oxygen desaturation with respiratory
events is associated with a smooth drop in the pulse oximetry tracing and
recovery to baseline upon termination of the event (see Figs. 19 and 21).
Respiratory events may cause an arousal resulting in abrupt movements
of limbs. Such movements may make recognition of the pulse wave difficult,
and result in an artifactual lowering of pulse oximetry. Abrupt drops and
recovery in pulse oximetry signal are usually indicative of artifacts and
should be ignored. A drop in oxygen saturation to zero is always artifactual
(Fig. 24). Some of the manufacturers offer real time display of pulse pleth-
ysmography signal. This is particularly helpful in differentiating true oxygen
Fig. 24. Excessive leak during PAP titration causing ‘‘hypopnea.’’ Note a leak greater than
60 L/min (1 L/sec). Associated arousal caused artifactually low reading of oxygen saturation
at 0%.
738 KAKKAR & HILL
desaturation from an artifact, because the latter does not have the charac-
teristic waveform of a peripheral arterial pulse.
Snoring is recorded from a snore microphone, and the signal is
displayed as a continuous waveform. Technician notes are the most useful
way of assessing the severity of snoring. Snoring signal is also prominently
reflected in chin EMG, in nasal pressure tracing (see Fig. 22), and
occasionally in the thermistor tracing. Crescendo snores associated with
progressively increasing effort are indicative of upper airway obstruction.
It should be noted that crescendo snoring could also be seen in Cheyne-
Stokes breathing; however, an associated decrescendo component is
characteristic.
During a PAP titration study, the airflow signal is detected by the
device itself and is displayed as ‘‘C-flow.’’ One should look for the effective
pressure to eliminate apnea, hypopneas, hypoxemia, and snoring. Some
laboratories attempt to eliminate flow limitation also during PAP titration.
Persistent arousals with seemingly adequate titration are either caused by
underlying mild airway obstruction or by excessive pressure. Under such
circumstances, the technicians generally increase or decrease the pressure
according to their judgment, and compare the results on different pres-
sures. Occurrence of excessive air leak during PAP titration is a challenging
situation. Most modern PSG and PAP systems continuously display
breath-to-breath measurement of leak. Some leak (intentional leak) is
needed for the effective operation of PAP machines. Excessive leak is de-
fined as the degree of leak that compromises effectiveness of PAP therapy
(see Fig. 24). Different manufacturers have different guidelines for their
equipment, but a leak in excess of 0.4 liters per second is usually consid-
ered excessive. Leak can also be suspected by looking at the PAP wave-
form, which may show a sudden dip at the beginning of expiration.
Presence of snoring-like artifact during the expiration is also indicative
of air leak rather than upper airway obstruction. Excessive air leak can
be caused either by problems with the mask seal or by mouth opening;
however, true differentiation between the two may be difficult while look-
ing at the PSG data. The technician’s notes are quite valuable in making
this determination. Mask leaks are more common with full-face mask than
with nasal interfaces. When choosing a therapeutic pressure, the clinician
should ensure that it is effective in both supine position and during
REM sleep. Other factors in choosing a therapeutic pressure are the degree
of consolidated sleep obtained at that pressure, patient’s tolerance, degree
of air leak, and the length of time it was tested. The authors prefer to
choose the lowest effective pressure, provided it was tested for an adequate
length of time. If bilevel PAP was used, the technician should document
the reason for using it. If no therapeutic pressure could be determined, a re-
peat PAP titration should be requested. If supplemental oxygen was used,
one should ensure that it was indeed effective and necessary for treatment
of hypoxemia.
INTERPRETATION OF THE ADULT POLYSOMNOGRAM 739
Electrocardiography
Patients who have SDB often exhibit cardiac arrhythmias at night
(Figs. 25, 26). Most laboratories monitor one EKG lead to determine heart
rate and to detect cardiac arrhythmias. The authors routinely record two
EKG leads. The extra EKG electrode provides a backup in case one
electrode becomes loose during the course of the study. The most common
arrhythmias noticed in patients who have OSA are sinus bradycardia, sinus
arrest, and sinus tachycardia. Periods of bradycardia intervening with nor-
mal heart rate or tachycardia are also sometimes noted in patients who have
OSA. The bradycardia is a result of massive vagal discharge that occurs with
breathing against a closed upper airway [35]. Termination of sleep apnea
invariably results in a surge in catecholamine levels, which results in tachy-
cardia and a rise in blood pressure [36]. It should be noted that atrial
fibrillation is especially common in OSA. Presence of atrial fibrillation is
one of the strongest independent predictors of the presence of OSA [37].
The medical director of the sleep laboratory should be alerted about any
dangerous arrhythmias.
Fig. 25. Atrial flutter appearing with an obstructive sleep apnea. The patient did not have any
previous history of cardiac arrhythmias and was noted to have three prolonged episodes of
atrial flutter during this PSG, which returned to normal sinus rhythm spontaneously.
740 KAKKAR & HILL
physiological parameters that were recorded, the equipment used for record-
ing, and pertinent numerical data in tabular form. Any additional monitor-
ing, such as extra EEG or EMG derivations recorded during the study,
should also be mentioned. The tabular data should contain information
on recording time, TIB, TST, SPT, SE, SL, RL, sleep stage distribution,
percentage of time spent in supine position, total AHI, supine AHI, AHI
during REM sleep, the nature of respiratory events (obstructive or central),
whether baseline hypoxemia was present, degree of hypoxemia, heart rate,
and the PLM index. Some laboratories also report arousal index. There
are many other indices reported on the automatically generated PSG
reports. Most of the data in these reports are redundant and confusing,
and the clinical utility of many of these indices is unclear.
The descriptive part of the report should be brief, with emphasis on
important findings while avoiding unnecessary repetition of numerical
data. One should develop an overall impression of the study as opposed
to just the numerical interpretation, especially when reporting severity of
sleep apnea and prescribing an effective PAP setting. Long apneas may ar-
tificially lower the AHI, whereas many patients have severely disrupted
sleep or significant oxygen desaturation with respiratory events of short
duration. Lack of REM sleep or lack of sleep in the supine position may
underestimate the severity of sleep apnea, and a note should be made to re-
flect this. The AHI reflected on the PAP table may be misleading because it
does not characterize sleep consolidation, patient discomfort, or air leak.
Further, if only a short time is spent on a given pressure, it may artifactually
lower or elevate the AHI because of sampling error. On should always
INTERPRETATION OF THE ADULT POLYSOMNOGRAM 741
Summary
PSG interpretation is a time-consuming process that requires close
attention to the patient’s history, medications, technician notes, pre- and
poststudy sleep questionnaires, and overall impression of the raw data. It
is a unique opportunity to correlate clinical and electrophysiological data,
however, and is a good investment of time toward improving patient
outcomes and avoidance of unnecessary testing. The adage, ‘‘Your
eyes see what your brain knows’’ holds particularly true for interpreting
a PSG.
Appendix
How likely are you to doze off or fall asleep in the following situations, in
contrast to feeling just tired? This refers to your usual way of life in recent
times. Even if you have not done some of these things recently, try to work
out how they would have affected you.
Use the following scale to choose the most appropriate number for each
situation:
0 ¼ no chance of dozing
1 ¼ slight chance of dozing
2 ¼ moderate chance of dozing
3 ¼ high chance of dozing
Table 1
Epworth sleepiness scale
Situation Chance of dozing
Sitting and reading
Watching TV
Sitting inactive in a public place (eg, a theater or a meeting)
As a passenger in a car for an hour without a break
Lying down to rest in the afternoon when circumstances permit
Sitting and talking to someone
Sitting quietly after a lunch without alcohol
In a car, while stopped for a few minutes in traffic
Score: 0–10, normal range; 10–12, borderline; 12–24, abnormal.
742 KAKKAR & HILL
References
[1] ASDA Standards of Practice. Portable recording in the assessment of sleep. Sleep 1994;17:
378–92.
[2] Iber C, Ancoli-Israel S, Chesson A and Quan SF for the American Academy of Sleep Med-
icine. The AASM Manual for the Scoring of Sleep and Associated Events- Rules, Terminol-
ogy and Technical specifications. 1st edition. Westchester Illinois: American Academy of
Sleep Medicine; 2007.
[3] McEvoy RD, Sharp DJ, Thornton AT. The effects of posture on obstructive sleep apnea. Am
Rev Respir Dis 1986;133:662–6.
[4] Oksenberg A, Khamaysi I, Silverberg DS, et al. Association of body position with severity of
apneic events in patients with severe nonpositional obstructive sleep apnea. Chest 2000;118:
1018–24.
[5] Sackett DL, Haynes RB, Tugwell P, et al. Clinical epidemiology: a basic science for clinical
medicine. 2nd edition. Boston: Lippincott Williams & Wilkins; 1991.
[6] Chediak AD, Acevedo-Crespo J, Seiden DJ, et al. Nightly variability in the indices of sleep-
disordered breathing in men being evaluated for impotence with consecutive night polysom-
nograms. Sleep 1996;19:589–92.
[7] Witting RM, Romaker A, Zorick FJ, et al. Night-to-night consistency of apneas during
sleep. Am Rev Respir Dis 1984;129:244–6.
[8] Hirshkowitz M, Moore CA, Hamilton CR III, et al. Polysomnography of adults and elderly:
sleep architecture, respiration, and leg movement. J Clin Neurophysiol 1992;9:52–62.
[9] Agnew HW Jr, Webb WB, Williams RL. The first night effect: an EEG study of sleep.
Psychophysiology 1966;2:263–6.
[10] Johns MW. A new method for measuring daytime sleepiness: the Epworth Sleepiness Scale.
Sleep 1991;14:540–5.
[11] Johns MW. Daytime sleepiness, snoring, and obstructive sleep apnea. The Epworth Sleepi-
ness Scale. Chest 1993;103:30–6.
[12] Chervin RD, Aldrich MS, Pickett R, et al. Comparison of the results of the Epworth Sleep-
iness Scale and the Multiple Sleep Latency Test. J Psychosom Res 1997;42:145–55.
[13] Penzel T, Conradt R. Computer based sleep recording and analysis. Sleep Med Rev 2000;4:
131–48.
[14] American Sleep Disorders Association. EEG arousal: scoring rules and examples. Sleep
1992;15:173–84.
[15] Reynolds CF III, Hoch CC, Buysse DJ, et al. Sleep in late-life recurrent depression: changes
during early continuation therapy. Neuropsychopharmacology 1991;5:85–96.
[16] Benca RM, Obermeyer WH, Thisted RA, et al. Sleep and psychiatric disorders: a meta-anal-
ysis. Arch Gen Psychiatry 1992;49:651–68.
[17] Nofzinger EA, Reynolds CF III, Thase ME, et al. REM sleep enhancement by bupropion in
depressed men. Am J Psychiatry 1995;152:274–6.
[18] Olivier LB, Luc S, Guy H, et al. Shorter REM latency associated with more sleep cycles of
a shorter duration in healthy humans. Psychiatry Res 2001;104:75–83.
[19] Kryger MH, Roth T, Dement WC, editors. Principles and practice of sleep medicine.
3rd edition; 2000. p. 20.
[20] Ohayon MM, Carskadon MA, Guilleminault C, et al. Metaanalysis of quantitative sleep pa-
rameters from childhood to old age in healthy individuals: developing normative sleep values
across the human lifespan. Sleep 2004;27:1255–73.
[21] Yoder EA, Klann K, Strohl KP. Inspired oxygen concentrations during positive pressure
therapy. Sleep Breath 2004;8:1–5.
[22] American Sleep Disorders Association. Recording and scoring leg movements. The Atlas
Task Force. Sleep 1993;16:748–59.
[23] Zucconi M, Ferri R, Allen Baier PC, et al. The official World Association of Sleep Medicine
(WASM) standards for recording and scoring periodic leg movements in sleep (PLMS) and
INTERPRETATION OF THE ADULT POLYSOMNOGRAM 743
wakefulness (PLMW) developed in collaboration with a task force from the International
Restless Legs Syndrome Study Group (IRLSSG). Sleep Med 2006;7:175–83.
[24] Jobert M, Jahnig P, Schulz H. Effect of two antidepressant drugs on REM sleep and EMG
activity during sleep. Neuropsychobiology 1999;39:101–9.
[25] Winkelman JW, James L. Serotonergic antidepressants are associated with REM sleep with-
out atonia. Sleep 2004;15(27):317–21.
[26] De Backer WA, Verbraecken J, Willemen M, et al. Central apnea index decreases after pro-
longed treatment with acetazolamide. Am J Respir Crit Care Med 1995;151:87–91.
[27] Sleep-related breathing disorders in adults: recommendations for syndrome definition and
measurement techniques in clinical research. The report of an American Academy of Sleep
Medicine task force. Sleep 1999;22(5):667–89.
[28] Morgenthaler TI, Kapen S, Lee-Chiong T, et al. Practice parameters for the medical therapy
of obstructive sleep apnea. Sleep 2006;29:1031–5.
[29] Redline S, Kapur VK, Sanders MH, et al. Effects of varying approaches for identifying
respiratory disturbances on sleep apnea assessment. Am J Respir Crit Care Med 2000;161:
369–74.
[30] Redline S, Bonekat W, Gottlieb D, et al. Variation in the apnea hypopnea index (AHI)
according to hypopnea definition. Am J Respir Crit Care Med 1997;155:A128.
[31] Guilleminault C, Black JE, Palombini L, et al. A clinical investigation of obstructive sleep
apnea syndrome (OSAS) and upper airway resistance syndrome (UARS) patients. Sleep
Med 2000;1:51–6.
[32] Loube DI, Andrada TF. Comparison of respiratory polysomnographic parameters in
matched cohorts of upper airway resistance and obstructive sleep apnea syndrome patients.
Chest 1999;115:1519–24.
[33] Gilmartin GS, Dalyb RW, Thomas RJ. Recognition and management of complex sleep-
disordered breathing. Curr Opin Pulm Med 2005;11:485–93.
[34] Mayos M, Hernandez Plaza L, Farre A, et al. [The effect of nocturnal oxygen therapy in
patients with sleep apnea syndrome and chronic airflow limitation]. Arch Bronconeumol
2001;37:65–8 [Spanish].
[35] Zwillich C, Devlin T, White D, et al. Bradycardia during sleep apnea: characteristics and
mechanism. J Clin Invest 1982;69:1286–92.
[36] Launois SH, Averill N, Abraham JH, et al. Cardiovascular responses to nonrespiratory and
respiratory arousals in a porcine model. J Appl Physiol 2001;90:114–20.
[37] Gami AS, Pressman G, Caples SM, et al. Association of atrial fibrillation and obstructive
sleep apnea. Circulation 2004;110:364–7.