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Clinical Investigations: SLEEP AND BREATHING |

Hemodynamic Effects of Simulated Obstructive Apneas in Humans With and Without Heart Failure*

T. Douglas Bradley, MD; Michael J. Hall, MB; Shin-ichi Ando, MD, PhD; John S. Floras, MD, DPhil
Author and Funding Information

Affiliations: *From the Departments of Medicine of the Toronto General Hospital and the Centre for Cardiovascular Research, University of Toronto, Toronto, Ontario, Canada. ,  Dr. Hall (deceased) was a recipient of a Medical Research Council of Canada/Canadian Lung Association Fellowship. Dr. Ando was a recipient of a Canadian Hypertension Society/Merck Frosst Canada Fellowship and of support from the George R. Gardiner Foundation (Toronto, Canada). Dr. Floras is a Career Scientist of the Heart and Stroke Foundation of Ontario, and Dr. Bradley holds a Senior Scientist Award from the Canadian Institutes of Health Research.

Correspondence to: T. Douglas Bradley, MD, NU 9–112, The Toronto General Hospital, University Health Network, 200 Elizabeth Street, Toronto, Ontario M5G 2C4, Canada; e-mail: douglas.bradley@utoronto.ca



Chest. 2001;119(6):1827-1835. doi:10.1378/chest.119.6.1827
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Study objectives: To determine whether generation of negative intrathoracic pressure during apnea would cause more pronounced and sustained reductions in cardiac output in patients with congestive heart failure (CHF) than in healthy subjects.

Design: Physiologic intervention study.

Setting: Cardiorespiratory physiology laboratory.

Participants: Nine patients with CHF and nine healthy control subjects matched for age and sex.

Interventions: Patients with CHF and healthy subjects generated − 30 cm H2O of intrathoracic pressure during 15-s Mueller maneuvers (MMs) to simulate the acute hemodynamic effects and aftereffects of obstructive apneas.

Results: In both groups, MMs caused an immediate rise in left ventricular transmural pressure during systole (LVPtmsys)[ p < 0.05], but in CHF patients, this immediate increase was followed by a significant drop in LVPtmsys (p < 0.05), associated with significantly greater reductions in systolic BP and cardiac index than in healthy subjects (− 25 ± 3 mm Hg vs − 11 ± 2 mm Hg[ p < 0.05] and − 0.53 ± 0.11 L/min/m2 vs− 0.15 ± 0.11 L/min/m2 [p < 0.05], respectively). Healthy subjects recovered promptly, but in CHF patients, these adverse hemodynamic effects were sustained following release of the MM.

Conclusions: CHF patients experience more pronounced and sustained reductions in BP and cardiac output both during and following the MM than do healthy subjects. These findings suggest the potential for adverse hemodynamic effects and aftereffects of negative intrathoracic pressure generation during obstructive sleep apnea in patients with CHF.

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