COPD is associated with dynamic lung hyperinflation (DH), increased pulmonary vascular resistance (PVR) and large increases in negative intrathoracic pressure (nITP). The individual and interactive effect of these stressors on left ventricular (LV) filling, emptying and geometry, and the role of direct ventricular interaction (DVI) in mediating these interactions have not been fully elucidated. Twenty healthy subjects were exposed to the following stressors alone and in combination: 1) inspiratory resistive loading of -20 cmH2O (nITP), 2) expiratory resistive loading to cause dynamic hyperinflation (DH), and 3) normobaric-hypoxia to increase PVR (hPVR). LV volumes and geometry were assessed using tri-plane echocardiography. nITP reduced LV stroke volume (LVSV) by 7±7% (p<0.001) through a 4±5% reduction in LV end-diastolic volume (LVEDV) (p=0.002), while DH reduced LVSV by 12±13% (p=0.001) due to a 9±10% reduction in LVEDV (p<0.001). nITP in combination with DH (nITP+DH) caused larger reductions in LVSV (16±16%, p<0.001) and LVEDV (12±10%, p<0.001) than nITP alone (p<0.05). The addition of hPVR to nITP+DH did not further reduce LV volumes. Significant septal flattening (indicating DVI) occurred in all conditions, with a significantly greater leftward septal shift occurring with nITP+DH than either condition alone (p<0.05). In summary, the interaction of nITP and DH reduces LV filling through DVI. However, DH may be more detrimental to LV hemodynamics than nITP, likely due to mediastinal constraint of the heart amplifying DVI.
- Dynamic hyperinflation
- Direct ventricular interaction
- Intrathoracic pressure
- Copyright © 2016, American Journal of Physiology-Heart and Circulatory Physiology