Reversal of Central Sleep Apnea With Oxygen

Franklin, Karl A.; Sahlin, Carin; Lundgren, R; Eriksson, Peter

doi:10.1378/chest.111.1.163

Cited by 170 publications

(112 citation statements)

References 29 publications

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“…It must be stressed that most studies were interested in abolishing the dips in SaO 2 rather than understanding how such dips contribute to the genesis of Cheyne-Stokes respiration. [53][54][55][56][57] All studies were consistent in showing small but significant reductions in the total amount of Cheyne-Stokes respiration. For instance, Hanly showed that low flow O 2 administered to patients with CHF reduced the duration of Cheyne-Stokes respiration-CSA mainly during stage 1 sleep, with no significant change during stage 2, slow wave, or rapid eye movement (REM) sleep.…”

Section: Hypoxiasupporting

confidence: 54%

“…23,67,68,79,84,85 Oxygen administration has been shown to cause a modest reduction in the severity of Cheyne-Stokes respiration, to reduce overnight urinary norepinephrine levels, and cause an increase in peak O 2 consumption during graded exercise over periods of 1 to 4 weeks. [53][54][55][56][57] Finally, theophylline has been shown to reduce the severity of CheyneStokes over 5 days, but has not been shown to improve cardiac function, neurohumoral activity, or quality of life. 86 Pepperell et al have recently shown in a prospective randomized trial that 1 month of nocturnal-assist servoventilation was able to reduce daytime sleepiness in conjunction with improvements in plasma brain natriuretic peptide and urinary metadrenaline excretion in patients with CHF and Cheyne-Stokes.…”

Section: Consequences Of Cheyne-stokes Respirationmentioning

confidence: 99%

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Cheyne-Stokes Respiration in Patients With Congestive Heart Failure: Causes and Consequences

Lorenzi-Filho¹,

Genta

Figueiredo

et al. 2005

Clinics

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Cheyne-Stokes respiration is a form of periodic breathing in which central apneas and hypopneas alternate with periods of hyperventilation, producing a waxing and waning pattern of tidal volume. This review focuses on the causes and consequences of Cheyne-Stokes respiration in patients with congestive heart failure, in whom the prevalence is strikingly high and ranges from 30% to 50%. Several factors have been implicated in the genesis of Cheyne-Stokes respiration, including low cardiac output and recurrent hypoxia. The key pathophysiological mechanism triggering Cheyne-Stokes respiration is hyperventilation and low arterial CO 2 (PaCO 2 ) that when below the apneic threshold triggers a central apnea. Hyperventilation is associated with pulmonary congestion, and Cheyne-Stokes respiration is more prone to occur during sleep, when the respiratory system is mainly dependent on chemical control. It is associated with recurrent dips in oxygen saturation and arousals from sleep, with oscillations in blood pressure and heart rate, sympathetic activation and increased risk of ventricular tachycardia. Cheyne-Stokes respiration is an independent marker of poor prognosis and may participate in a vicious cycle, further stressing the failing heart.

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Section: Hypoxiasupporting

confidence: 54%

Section: Consequences Of Cheyne-stokes Respirationmentioning

confidence: 99%

Cheyne-Stokes Respiration in Patients With Congestive Heart Failure: Causes and Consequences

Lorenzi-Filho¹,

Genta

Figueiredo

et al. 2005

Clinics

View full text Add to dashboard Cite

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“…Hyperoxia has been demonstrated to stabilize the breathing pattern in humans with central sleep apnea associated with high altitude (3) and, to some extent, congestive heart failure (22,25,27). The present study identified several mechanisms for this therapeutic effect, including decreased influence of the peripheral chemoreceptor, widened ⌬PCO 2 , lengthened duration of hypocapnia required to produce apnea, and reduced susceptibility to posthyperventilation apnea.…”

Section: Discussionmentioning

confidence: 58%

Influence of arterial O₂ on the susceptibility to posthyperventilation apnea during sleep

Xie¹,

Skatrud²,

Puleo³

et al. 2006

Journal of Applied Physiology

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Xie, Ailiang, James B. Skatrud, Dominic S. Puleo, and Jerome A. Dempsey. Influence of arterial O2 on the susceptibility to posthyperventilation apnea during sleep. J Appl Physiol 100: 171-177, 2006. First published September 22, 2005 doi:10.1152/japplphysiol.00440.2005.-To investigate the contribution of the peripheral chemoreceptors to the susceptibility to posthyperventilation apnea, we evaluated the time course and magnitude of hypocapnia required to produce apnea at different levels of peripheral chemoreceptor activation produced by exposure to three levels of inspired PO 2. We measured the apneic threshold and the apnea latency in nine normal sleeping subjects in response to augmented breaths during normoxia (room air), hypoxia (arterial O 2 saturation ϭ 78 -80%), and hyperoxia (inspired O2 fraction ϭ 50 -52%). Pressure support mechanical ventilation in the assist mode was employed to introduce a single or multiple numbers of consecutive, sighlike breaths to cause apnea. The apnea latency was measured from the end inspiration of the first augmented breath to the onset of apnea. It was 12.2 Ϯ 1.1 s during normoxia, which was similar to the lung-to-ear circulation delay of 11.7 s in these subjects. Hypoxia shortened the apnea latency (6.3 Ϯ 0.8 s; P Ͻ 0.05), whereas hyperoxia prolonged it (71.5 Ϯ 13.8 s; P Ͻ 0.01). The apneic threshold end-tidal PCO 2 (PETCO 2 ) was defined as the PETCO 2 at the onset of apnea. During hypoxia, the apneic threshold PET CO 2 was higher (38.9 Ϯ 1.7 Torr; P Ͻ 0.01) compared with normoxia (35.8 Ϯ 1.1; Torr); during hyperoxia, it was lower (33.0 Ϯ 0.8 Torr; P Ͻ 0.05). Furthermore, the difference between the eupneic PET CO 2 and apneic threshold PET CO 2 was smaller during hypoxia (3.0 Ϯ 1.0 Torr P Ͻ 001) and greater during hyperoxia (10.6 Ϯ 0.8 Torr; P Ͻ 0.05) compared with normoxia (8.0 Ϯ 0.6 Torr). Correspondingly, the hypocapnic ventilatory response to CO 2 below the eupneic PETCO 2 was increased by hypoxia (3.44 Ϯ 0.63 l ⅐ min Ϫ1 ⅐ Torr Ϫ1 ; P Ͻ 0.05) and decreased by hyperoxia (0.63 Ϯ 0.04 l ⅐ min Ϫ1 ⅐ Torr Ϫ1 ; P Ͻ 0.05) compared with normoxia (0.79 Ϯ 0.05 l ⅐ min Ϫ1 ⅐ Torr Ϫ1 ). These findings indicate that posthyperventilation apnea is initiated by the peripheral chemoreceptors and that the varying susceptibility to apnea during hypoxia vs. hyperoxia is influenced by the relative activity of these receptors. apnea threshold THE RELATIVE CONTRIBUTION of peripheral vs. central chemoreception in initiating the posthyperventilation apneas remains an unresolved question. The importance of peripheral chemoreception in mediating the rapid ventilatory response to hypocapnia has been supported using animal models. Carotid body denervation either eliminated or prolonged the time course for the development of apnea after the administration of augmented breaths (6, 39). However, carotid body denervation profoundly alters central chemoreception as indicated by the substantial CO 2 retention after denervation. Our laboratory has previously demonstrated the complex effect of hypoxia in t...

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“…Nocturnal supplemental O 2 has been shown to abolish apnea-related hypoxia, to alleviate CSA, to decrease nocturnal norepinephrine levels over periods of 1 night to 1 month, 291,358,359 and to increase maximum O 2 uptake during a graded exercise test. 360 However, when administered for 1 month, O 2 had no impact on cardiac function or quality of life.…”

Section: Treatment Options In Csamentioning

confidence: 99%