Cheyne-Stokes Respiration

Dowell, Anthony R.

doi:10.1001/archinte.1971.00310160190015

Cited by 75 publications

(5 citation statements)

References 142 publications

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“…This has two important implications. On one hand, our findings widen the current knowledge of the PB phenomenon, because historically most studies have focused on its extreme manifestation of central apneas during sleep (7,14,27,35,42). On the other hand, they allow a more precise identification of the underlying physiopathological mechanisms, because they are not affected by the confounding effect of large system nonlinearities in ventilatory regulation and sleep-induced physiological changes (11,17).…”

Section: Discussionmentioning

confidence: 71%

“…Two main hypotheses have been proposed so far: the ''central'' hypothesis, which explains PB as the effect of a central vasomotor rhythm (2,44), and the ''instability'' hypothesis, which explains PB as a self-sustaining oscillation due to the loss of stability in the closed-loop chemical control of ventilation (3,18). Several investigators have observed that the cyclic rise and fall in ventilation, which characterizes PB (cycle length: 25-100 s), is accompanied by phase-linked oscillations of arterial blood gases, heart rate (HR), and arterial blood pressure (4,7,9,11,26,33,37), indicating that during PB a deep simultaneous involvement of the respiratory and cardiovascular systems does take place. Because of this peculiarity, PB constitutes a unique experimental model for investigating cardiorespiratory interactions at very low frequencies (VLF, Ͻ0.04 Hz) (28).…”

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confidence: 99%

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Cardiorespiratory interactions during periodic breathing in awake chronic heart failure patients

Pinna¹,

Maestri²,

Mortara

et al. 2000

American Journal of Physiology-Heart and Circulatory Physiology

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We applied spectral techniques to the analysis of cardiorespiratory signals [instantaneous lung volume (ILV), instantaneous tidal volume (ITV), arterial O(2) saturation (Sa(O(2))) at the ear, heart rate (HR), systolic (SAP), and diastolic (DAP) arterial pressure] during nonapneic periodic breathing (PB) in 29 awake chronic heart failure (CHF) patients and estimated the timing relationships between respiratory and slow cardiovascular (<0.04 Hz) oscillations. Our aim was 1) to elucidate major mechanisms involved in cardiorespiratory interactions during PB and 2) to test the hypothesis of a central vasomotor origin of PB. All cardiovascular signals were characterized by a dominant (>/=84% of total power) oscillation at the frequency of PB (mean +/- SE: 0.022 +/- 0.0008 Hz), highly coherent (>/=0.89), and delayed with respect to ITV (ITV-HR, 2.4 +/- 0.72 s; ITV-SAP, 6.7 +/- 0.65 s; ITV-DAP, 3.2 +/- 0.61 s; P < 0.01). Sa(O(2)) was highly coherent with (coherence function = 0.96 +/- 0. 009) and almost opposite in phase to ITV. These findings demonstrate the existence of a generalized cardiorespiratory rhythm led by the ventilatory oscillation and suggest that 1) the cyclic increase in inspiratory drive and cardiopulmonary reflexes and 2) mechanical effects of PB-induced changes in intrathoracic pressure are the more likely sources of the HR and blood pressure oscillations, respectively. The timing relationship between ITV and blood pressure signals excludes the possibility that PB represents the effect of a central vasomotor rhythm.

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Section: Discussionmentioning

confidence: 71%

mentioning

confidence: 99%

Cardiorespiratory interactions during periodic breathing in awake chronic heart failure patients

Pinna¹,

Maestri²,

Mortara

et al. 2000

American Journal of Physiology-Heart and Circulatory Physiology

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“…Cheyne-Stokes respiration (6,12). Often, the same patient may exhibit a continuum of different patterns of breathing, ranging from normal breathing (i.e., without cyclic modulation of ventilation) to mild PB up to cyclic periods of apnea.…”

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confidence: 99%

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

Pinna

Maestri

Mortara

et al. 2000

Journal of Applied Physiology

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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 degrees (95% confidence interval 198-212 degrees). 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.

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“…In contrast to the large quantity of literature about the effect of obstructive apnoea on sleep structure and cardiorespiratory physiology, there is a paucity of information about the effect of CSR on these variables in the sleeping heart failure patient. For example, the most widely cited article on Cheyne-Stokes respiration with 186 references does not even mention sleep [2].…”

Section: Sleep and Heart Failurementioning

confidence: 99%

Sleep and heart failure

Mh¹

1990

Eur Respir J

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Cheyne-Stokes Respiration

Cited by 75 publications

References 142 publications

Cardiorespiratory interactions during periodic breathing in awake chronic heart failure patients

Cardiorespiratory interactions during periodic breathing in awake chronic heart failure patients

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

Sleep and heart failure

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