Periodic breathing in heart failure patients: Testing the hypothesis of instability of the chemoreflex loop

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Abstract

In this study, we applied time- and frequency-domain signal processing techniques to the analysis of respiratory and arterial O2 saturation (Sa(O2)) oscillations during nonapneic periodic breathing (PB) in 37 supine awake chronic heart failure patients. O2 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(O2) was consistent with modeling predictions derived from the instability hypothesis of PB and 2) whether O2 administration, by decreasing loop gain and increasing O2 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(O2) 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, O2 administration abolished PB (in the eighth patient, Sa(O2) 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.

Original languageEnglish
Pages (from-to)2147-2157
Number of pages11
JournalJournal of Applied Physiology
Volume89
Issue number6
Publication statusPublished - 2000

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Respiration
Heart Failure
Ventilation
Lung
Hyperventilation
Tidal Volume
Respiratory Rate
Ear
Confidence Intervals

Keywords

  • Chemoreceptors
  • O administration
  • Respiratory control
  • Spectral analysis
  • Ventilatory oscillations

ASJC Scopus subject areas

  • Endocrinology
  • Physiology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

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title = "Periodic breathing in heart failure patients: Testing the hypothesis of instability of the chemoreflex loop",
abstract = "In this study, we applied time- and frequency-domain signal processing techniques to the analysis of respiratory and arterial O2 saturation (Sa(O2)) oscillations during nonapneic periodic breathing (PB) in 37 supine awake chronic heart failure patients. O2 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(O2) was consistent with modeling predictions derived from the instability hypothesis of PB and 2) whether O2 administration, by decreasing loop gain and increasing O2 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(O2) 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, O2 administration abolished PB (in the eighth patient, Sa(O2) 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.",
keywords = "Chemoreceptors, O administration, Respiratory control, Spectral analysis, Ventilatory oscillations",
author = "Pinna, {G. D.} and R. Maestri and A. Mortara and {La Rovere}, {M. T.} and F. Fanfulla and P. Sleight",
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TY - JOUR

T1 - Periodic breathing in heart failure patients

T2 - Testing the hypothesis of instability of the chemoreflex loop

AU - Pinna, G. D.

AU - Maestri, R.

AU - Mortara, A.

AU - La Rovere, M. T.

AU - Fanfulla, F.

AU - Sleight, P.

PY - 2000

Y1 - 2000

N2 - In this study, we applied time- and frequency-domain signal processing techniques to the analysis of respiratory and arterial O2 saturation (Sa(O2)) oscillations during nonapneic periodic breathing (PB) in 37 supine awake chronic heart failure patients. O2 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(O2) was consistent with modeling predictions derived from the instability hypothesis of PB and 2) whether O2 administration, by decreasing loop gain and increasing O2 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(O2) 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, O2 administration abolished PB (in the eighth patient, Sa(O2) 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.

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