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Clinical Investigations: NPPV |

Effects of Nasal Continuous Positive Airway Pressure on Oxygen Body Stores in Patients With Cheyne-Stokes Respiration and Congestive Heart Failure*

Samuel L. Krachman, DO, FCCP; Joseph Crocetti, DO; Thomas J. Berger, BA, RPSGT, PA-C; Wissam Chatila, MD, FCCP; Howard J. Eisen, MD; Gilbert E. D’Alonzo, DO, FCCP
Author and Funding Information

*From the Sleep Disorders Center (Dr. Krachman and Mr. Berger), Division of Pulmonary and Critical Care (Drs. Crocetti, Chatila, and D’Alonzo), and Division of Cardiology (Dr. Eisen), Temple University School of Medicine, Philadelphia, PA.

Correspondence to: Samuel L. Krachman, DO, FCCP, Temple University School of Medicine, Division of Pulmonary and Critical Care, 767 Parkinson Pavilion, Broad and Tioga Sts, Philadelphia, PA 19140



Chest. 2003;123(1):59-66. doi:10.1378/chest.123.1.59
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Study objectives: The mechanism(s) by which nasal continuous positive airway pressure (CPAP) is effective in the treatment of Cheyne-Stokes respiration (CSR) in patients with congestive heart failure (CHF) remains uncertain, and may involve an increase in total oxygen body stores (dampening), changes in central and peripheral controller gain, and/or improvement in cardiac function. The purpose of this study was to evaluate the effects of nasal CPAP on total oxygen stores, as measured by the rate of fall of arterial oxyhemoglobin saturation (dSao2/dt), to determine if dampening may play a role in the attenuation of CSR in patients with CHF.

Design: Prospective controlled trial.

Setting: University hospital.

Patients: Nine male patients (mean ± SD age, 59 ± 8 years) with CHF and a mean left ventricular ejection fraction (LVEF) of 16 ± 4%.

Interventions and measurements: All patients had known CSR, as identified on a baseline polysomnographic study. Patients then underwent repeat polysomnography while receiving nasal CPAP (9 ± 0.3 cm H2O). The polysomnography consisted of recording of breathing pattern, pulse oximetry, and EEG. dSao2/dt was measured as the slope of a line drawn adjacent to the falling linear portion of the arterial oxygen saturation (Sao2) curve associated with a central apnea. All patients underwent echocardiography and right-heart catheterization within 1 month of the study to measure LVEF and cardiac hemodynamics, respectively.

Results: There was a significant decrease in the apnea-hypopnea index (AHI) with nasal CPAP, from 44 ± 27 events per hour at baseline to 15 ± 24 events per hour with nasal CPAP (p = 0.004). When compared to baseline, dSao2/dt significantly decreased with nasal CPAP from 0.42 ± 0.15% to 0.20 ± 0.07%/s (p < 0.001). The postapneic Sao2, when compared to baseline, significantly increased with nasal CPAP, from 87 ± 5% to 91 ± 4% (p < 0.05). The preapneic Sao2 did not significantly change, from a baseline of 96 ± 2% to 96 ± 3% with nasal CPAP (p = 0.8). When compared to baseline, the apnea duration and heart rate did not change with nasal CPAP. While there was a significant correlation noted between baseline postapneic Sao2 and dSao2/dt (r = 0.8, p = 0.02), no correlation was seen between baseline preapneic Sao2 and dSao2/dt (r = 0.1, p = 0.7). A significant correlation was noted between baseline dSao2/dt and the AHI (r = 0.7, p = 0.02). With CPAP, there was a significant correlation noted between dSao2/dt and the AHI (R = 0.7, p = 0.04), but no correlation was noted between dSao2/dt and postapneic Sao2 (R = 0.1, p = 0.8).

Conclusion: Nasal CPAP significantly decreases dSao2/dt and thus increases total body oxygen stores in patients with CSR and CHF. By increasing oxygen body stores, dampening may be one of the mechanisms responsible for the attenuation of CSR seen with nasal CPAP.

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