Periodic Breathing Promotes Circulatory Oscillations at Rest and during Exercise in Patients with Heart Failure

Abstract

Instability of breathing control in HF patients is manifest as periodic breathing (PB) and characterized by regular and marked oscillations of minute ventilation (VE) and tidal volume (VT) in a crescendo-decrescendo pattern. PB has been associated with decreased exercise capacity and adverse prognosis. Previous studies suggest circulatory oscillations may accompany oscillation of VE though this has not been well characterized. Augmented intrathoracic pressure changes during periods of increased VE may promote phasic increases of venous return and pulmonary blood flow. Hypothesis: In HF patients with PB, the predicted (by modified alveolar gas equation) decline of end-tidal carbon dioxide (PetCO2) associated with increased VE is offset by increased circulatory CO2 delivery to the lungs. Methods: 50 consecutive patients with HF and PB were identified by cardiopulmonary exercise. Exercise PB was defined as >25% variation of amplitude (peak VE-nadir VE/mean VE) persisting >60% exercise duration. Breath by breath gas exchange measurements obtained at rest and during exercise included oxygen uptake (VO2), CO2 production (VCO2), ventilatory equivalent for CO2 (VE/VCO2), PetCO2, VE, and VT. Predicted PetCO2 was estimated by the modified alveolar gas equation: VE = (.863∗VCO2)/PaCO2∗(1-VD/VT), where PetCO2 was substituted for arterial CO2 tension (PaCO2). Ventilatory dead space (VD) was presumed to be constant. Results: (Table) During peak periods of VE at rest, 50% max and max work the measured decline of PetCO2 was less than predicted (Pred PetCO2) from measured VE and due to proportionately greater increase of VCO2.Tabled 1Rest (n=50)50% max (n=50)Max (n=50)NadirPeakNadirPeakNadirPeakMean (60 secs)VT(L)0.51.00.61.41.41.81.6VE(L/min)7.4019.615.534.243.167.056VCO2(ml/min)141481375881110216481425VEVCO257424540404240PetCO2(mmHg)32313331312930Pred PetCO232203318312430 Open table in a new tab Conclusion: In HF patients with PB, the decline of PetCO2 observed during periods of increased VE is less than predicted by the modified alveolar gas equation and likely attributable to phasic augmentation of circulatory CO2 delivery to the lungs. Cardiopulmonary interaction in HF patients with PB includes phasic increases of pulmonary blood flow which promotes modulation and stabilization of PaCO2.