SLEEP 2011 Abstract Supplement
SLEEP 2011 Abstract Supplement
SLEEP 2011 Abstract Supplement
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B. Clinical Sleep Science I. Sleep Disorders – Breathing<br />
able, non-invasive, and low-cost, this algorithm has the potential for<br />
SDB screening in both hospital and home care environments.<br />
0381<br />
FEASIBILITY OF DETECTION OF PERIODIC BREATHING<br />
USING RESPIRATORY SINUS ARRHYTHMIA PATTERNS<br />
FROM <strong>SLEEP</strong> TIME AMBULATORY ECG RECORDINGS<br />
Stein PK 1 , Redline S 2<br />
1<br />
Cardiovascular Division, Washington University School of Medicine,<br />
St. Louis, MO, USA, 2 Department of Medicine and Division of Sleep<br />
Medicine, Harvard Medical School, Boston, MA, USA<br />
Introduction: Respiratory sinus arrhythmia (RSA), the response of<br />
the heart rate to autonomic changes during respiration, clearly tracks<br />
respiratory rate. RSA is especially prominent when subjects are supine.<br />
Periodic respiration is associated with a waxing and waning of the respiratory<br />
rate that should, in theory, be reflected in RSA and visible from a<br />
plot of instantaneous heart rate vs. time (HR tachogram).<br />
Methods: HR tachograms from the ECG channel of recordings from<br />
older adults in the Sleep Heart Health Study were examined. ECGs had<br />
been extracted and scanned to research standards on a MARS PC Holter<br />
system. (GE Medical Systems, Milwaukee, WI). N=23 participants were<br />
selected as having been identified by the technician as having periodic<br />
breathing (PERGP) and also as having a central sleep apnea (>1/hr).<br />
These were matched by age and gender with participants without periodic<br />
breathing or central sleep apnea (NOGP). The presence of periodic<br />
breathing was blindly scored from HR tachograms. Participants were<br />
categorized as definite, possible or no periodic breathing based on the<br />
presence of RSA patterns suggesting cycles of increasing and decreasing<br />
respiratory rates. When discrepancies between SHHS and visual scoring<br />
occurred, the respiratory channels of the PSG were examined.<br />
Results: Results: There were 38 interpretable recordings (9F,31M, age<br />
78 SD 4 yrs). Of the 20 usable recordings in the NOGP, 3 were categorized<br />
as definite, 3 as possible and 14 as no periodic breathing. After<br />
examination of the PSGs, one of the 3 categorized as definite periodic<br />
breathing did have it, one had missing respiratory data at the time of the<br />
periodic RSA on ECG and one had respiration that was periodic in amplitude<br />
but not frequency. Of the 3 scored as possible, one had periodic<br />
amplitude but not frequency patterns, one had an abnormal heart rate<br />
pattern and one did not have any periodic breathing. N=16 of 18 usable<br />
recordings in the PERGP were categorized as having definite periodic<br />
breathing, one as possible and one as no. After examination of the PSGs,<br />
it was determined that the PER subject classified as no, had the wrong<br />
ECG file and the PSG ECG file for that person was not available.<br />
Conclusion: Significant periodic respiration is clearly identifiable from<br />
RSA patterns on heart rate tachograms, suggesting that screening for this<br />
breathing pattern could be included in the information available from<br />
routine ambulatory ECG recordings.<br />
Support (If Any): 2RO1HL062181-09<br />
0382<br />
DELAYED CIRCADIAN PHASE AND THE TIMING OF THE<br />
POLYSOMNOGRAM TO DIAGNOSE OBSTRUCTIVE <strong>SLEEP</strong><br />
APNEA<br />
Ubaissi H, Jain V, Gutierrez G, Shan K<br />
Pulmonary, Critical Care and Sleep Medicine, George Washington<br />
University, Washington, DC, USA<br />
Introduction: False negative polysomnograms could adversely affect<br />
the diagnosis and management of patients with obstructive sleep apnea<br />
(OSA). We hypothesize that false negative polysomnograms could occur<br />
from discordance between the patient’s circadian phase and the routine<br />
sleep laboratory schedule.<br />
Methods: Prospective study of seven patients with delayed circadian<br />
phase and high clinical suspicion for OSA. Patients were included if the<br />
first diagnostic polysomnogram, done according to the sleep laboratory<br />
timing, was negative for OSA. These patients subsequently underwent<br />
a second polysomnogram performed in accordance with the patient’s<br />
circadian phase. We evaluated differences between the two polysomnograms<br />
with respect to apnea hypopnea index (AHI), total sleep time<br />
(TST) and time spent in REM sleep. Data were analyzed with paired t<br />
test, P < 0.05 was considered statistically significant. Mean ± SD.<br />
Results: There were statistically significant increases in all endpoints<br />
between the first and second polysomnograms. AHI and time spent in<br />
REM increased for all seven patients, while TST increased in six patients.<br />
AHI increased from 4.4 ± 1.7 events/hour to 14.3 ± 5.4 events/<br />
hour (P