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Original Research: CARDIOVASCULAR DISEASE |

Mechanisms of Periodic Breathing During Exercise in Patients With Chronic Heart Failure*

Piergiuseppe Agostoni, MD, PhD; Anna Apostolo, MD; Richard K. Albert, MD, FCCP
Author and Funding Information

*From Centro Cardiologico Monzino (Dr. Apostolo), IRCCS, Istituto di Cardiologia, Università di Milano, Milan, Italy; Department of Medicine (Dr. Agostoni), University of Washington, Seattle, WA; and Department of Medicine. Denver Health (Dr. Albert), and University of Colorado Health Sciences Center, Denver, CO.

Correspondence to: Piergiuseppe Agostoni, MD, PhD, Centro Cardiologico Monzino, IRCCS, Istituto di Cardiologia, Università di Milano, Via Parea 4, 20138 Milan, Italy; e-mail: piergiuseppe.agostoni@ccfm.it



Chest. 2008;133(1):197-203. doi:10.1378/chest.07-1439
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Background: Periodic breathing (PB) in heart failure (HF) is attributed to many factors, including low cardiac output delaying the time it takes pulmonary venous blood to reach the central and peripheral chemoreceptors, low lung volume, lung congestion, augmented chemoreceptor sensitivity, and the narrow difference between eupneic carbon dioxide tension and apneic/hypoventilatory threshold.

Methods and results: We measured expired gases, ventilation, amplitude, and duration of PB in 23 patients with PB during progressive exercise tests done with 0 mL, 250 mL, or 500 mL of added dead space. Periodicity of PB remained constant despite heart rate, oxygen consumption, and minute ventilation increasing. Within each PB cycle, starting from the beginning of exercise, the largest (peak) tidal volume approached maximum observed tidal volume, while the smallest (nadir) tidal volume increased as exercise power output increased. PB ceased when nadir tidal volume reached peak tidal volume. End-tidal carbon dioxide increased with added dead space, and PB ceased progressively earlier during the exercise done with increased dead space.

Conclusion: Circulatory delay does not contribute to the PB observed in exercising HF patients. The pattern of gradually increasing nadir tidal volume during exercise and the effect of dead space on both PB ceasing and end-tidal carbon dioxide suggest that low tidal volume and carbon dioxide apnea threshold are important contributors to PB that occurs during exercise in HF.

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