Periodic breathing in heart failure patients: testing the hypothesis of instability of the chemoreflex loop
Departments of 1 Biomedical Engineering, 2 Cardiology, and 3 Pneumology, Fondazione S. Maugeri, Clinica del Lavoro e della Riabilitazione, IRCCS, Istituto Scientifico di Montescano, 27040 Montescano (PV), Italy; and 4 Cardiovascular Medicine, John Radcliffe Hospital, Oxford OX39DU, United Kingdo...
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Published in | Journal of applied physiology (1985) Vol. 89; no. 6; pp. 2147 - 2157 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Bethesda, MD
Am Physiological Soc
01.12.2000
American Physiological Society |
Subjects | |
Online Access | Get full text |
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Summary: | Departments of 1 Biomedical Engineering,
2 Cardiology, and 3 Pneumology, Fondazione S. Maugeri,
Clinica del Lavoro e della Riabilitazione, IRCCS, Istituto Scientifico
di Montescano, 27040 Montescano (PV), Italy; and
4 Cardiovascular Medicine, John Radcliffe Hospital, Oxford
OX39DU, United Kingdom
In this study, we applied
time- and frequency-domain signal processing techniques to the analysis
of respiratory and arterial O 2 saturation
(Sa O 2 ) oscillations during nonapneic periodic
breathing (PB) in 37 supine awake chronic heart failure patients.
O 2 was administered to eight of them at 3 l/min.
Instantaneous tidal volume and instantaneous minute ventilation (IMV)
signals were obtained from the lung volume signal. The main objectives
were to verify 1 ) whether the timing relationship between
IMV and Sa O 2 was consistent with modeling predictions
derived from the instability hypothesis of PB and 2 ) whether
O 2 administration, by decreasing loop gain and increasing
O 2 stores, would have increased system stability reducing
or abolishing the ventilatory oscillation. PB was centered around 0.021 Hz, whereas respiratory rate was centered around 0.33 Hz and was almost
stable between hyperventilation and hypopnea. The average phase shift
between IMV and Sa O 2 at the PB frequency was 205°
(95% confidence interval 198-212°). In 12 of 37 patients in
whom we measured the pure circulatory delay, the predicted lung-to-ear
delay was 28.8 ± 5.2 s and the corresponding observed delay
was 30.9 ± 8.8 s ( P = 0.13). In seven of
eight patients, O 2 administration abolished PB (in the
eighth patient, Sa O 2
did not increase). These results show a remarkable consistency between
theoretical expectations derived from the instability hypothesis and
experimental observations and clearly indicate that a condition of loss
of stability in the chemical feedback control of ventilation might play
a determinant role in the genesis of PB in awake chronic heart failure patients.
respiratory control; spectral analysis; ventilatory oscillations; O 2 administration; chemoreceptors |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 8750-7587 1522-1601 |
DOI: | 10.1152/jappl.2000.89.6.2147 |