Abstract 9918: Respiration Increases Ventricular Filling at Rest and Exercise via Pulmonary Compliance: A Clinical and Computational Modeling Study
Introduction: Due to the absence of a sub-pulmonary ventricle, the Fontan circulation is sensitive to respiration-induced changes in intrathoracic pressure. However, the importance of a ‘respiratory pump’ in creating forward flow remains controversial. We aim to investigate the effects and mechanisms of respiration on ventricular filling at rest and exercise using clinical data and computational modeling.
Hypothesis: We assess the hypotheses that (1) changes in intrathoracic pressure due to respiration would aid ventricular filling and output and (2) this effect would be maintained or enhanced during incremental exercise.
Methods: Ten Fontan patients (6 male, 20±4 years) underwent ungated cardiac magnetic resonance imaging at rest and during supine bicycle exercise (3 incremental intensities) to evaluate systemic ventricular volumes. Patient-specific computational simulations using a lumped-parameter network model of Fontan exercise elucidated resting and exercise physiology in details for each patient at each metabolic state tested.
Results: Compared to expiration, inspiration increased EDVi (98±16 to 103±15 mL/m2;P=0.001), SVi (55±9 to 59±9 mL/m2;P=0.001) and cardiac index (3.9±0.7 to 4.2±0.8 L/min/m2;P=0.002), but did not affect ESVi (P=0.096). Respiratory-dependent SVi did not change significantly during incremental exercise (3±2% to 5±3%; P=0.084). Computational modeling showed highest caval vein flow return during end-inspiration, and peak SV during expiration, exposing a phased time-delay mechanism at work. Removal of respiration in simulations corresponded to decreases in cardiac index of 0.39±0.037 L/min/m2.
Conclusions: Inspiration increased ventricular filling at rest and exercise by similar amounts. A phased time-delay between highest caval vein flow and highest SV suggests an indirect mechanism where respiration aids ventricular filling via pulmonary compliance.
Author Disclosures: E. Kung: None. A. Van De Bruaene: None. G. Claessen: None. A. La Gerche: None. A. Marsden: None. P. De Meester: None. S. Devroe: None. J. Bogaert: None. P. Claus: None. H. Heidbuchel: None. W. Budts: None. M. Gewillig: None.
- © 2015 by American Heart Association, Inc.