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Clinical Investigations: SLEEP/CPAP |

Cardiogenic Oscillations on the Airflow Signal During Continuous Positive Airway Pressure as a Marker of Central Apnea*

Indu Ayappa, PhD; Robert G. Norman, MS, RRT; David M. Rapoport, MD, FCCP
Author and Funding Information

*From the Division of Pulmonary and Critical Care Medicine, New York University Medical Center, New York, NY. Supported by National Institutes of Health-National Heart, Lung, and Blood Institute grants HL53931 and RR00096, and by grants from Mallinckrodt Nellcor Puritan Bennett and the Foundation for Research in Sleep Disorders.

Correspondence to: David M. Rapoport, MD, FCCP, Department of Medicine, New York University Medical Center, 550 First Avenue, New York, NY 10016; e-mail: rapopd01@mcgc16.med.nyu.edu



Chest. 1999;116(3):660-666. doi:10.1378/chest.116.3.660
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Therapeutic decisions in patients with sleep apnea (eg, adjustment of continuous positive airway pressure[ CPAP]) depend on differentiating central from obstructive apnea. Obstructive apnea is defined by cessation of airflow in the presence of continued respiratory effort, which is conventionally inferred from chest wall movement or intrathoracic pressure swings. Cardiogenic oscillations in the airflow have been observed during some central apneas, but there is controversy over whether they correlate with airway patency. The present study investigates whether these oscillations are markers of the absence of respiratory effort (central apnea) without regard to airway patency.

Methods: We examined 648 apneas in 52 patients undergoing nocturnal polysomnograms and CPAP titrations. Airflow was measured using the output of the CPAP generator, and apneas were identified from reduction of airflow to< 10% for > 10 s. We used only the presence or complete absence of thoracoabdominal motion to classify apneas: obstructive apnea when motion was present (297 apneas); and central apnea if motion was totally absent (351 apneas). Central apneas most often occurred at sleep onset or followed arousal with a big breath. Using only the flow signal, all apneas were examined for the presence of cardiogenic oscillation by an observer blinded to other signals and apnea types.

Results: No obstructive apnea showed definite cardiogenic oscillations. In four cases, there was a suggestion of oscillation that was not regular enough to be called cardiac. Sixty percent of central apneas showed clear, regular oscillations at cardiac frequency. Cardiogenic oscillations also were seen intermittently during quiet exhalation in apnea-free periods.

Conclusion: The presence of cardiogenic oscillations on the CPAP flow signal is a specific indicator of central apnea and may have a role in self-titrating CPAP algorithms. We speculate that transmission of these cardiac-induced oscillations may relate to the relaxation of thoracic muscles during central apnea and is impeded by high muscle tone during obstructive apnea.

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