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UBC Theses and Dissertations

The effect of negative intrathoracic pressure on heart-lung interaction in the presence of elevated lung volume and increased right ventricular preload and afterload Cheyne, William Spencer


While the hemodynamic effects of spontaneous respiration are normally considered minimal, large increases in negative intrathoracic pressure (ITP) are known to impair left ventricular (LV) function. Increased negative ITP is a hallmark of obstructive respiratory disease, and is often accompanied by elevations in lung volume and changes to the pulmonary vasculature, both of which have adverse effects on LV function through both series and direct ventricular interaction (DVI). While the hemodynamic effects of these stressors in isolation are generally well established, the interaction of these mechanisms, and their summative effect on LV function, has not been investigated. This study examined the hemodynamic effects of increased negative ITP, dynamic lung hyperinflation (DH), increased pulmonary vascular resistance (PVR) and increased preload (VL) alone and in combination in healthy, spontaneously breathing humans using echocardiography to evaluate LV volumes and geometry. Reducing ITP on inspiration to -20 cmH₂O significantly decreased LV SV by 7% (p<0.001), due to a reduced LV end-diastolic volume (LVEDV). DVI was implicated in this reduction, as evidenced by a significant increase in the radius of septal curvature (RSC) (p=0.002), indicating leftward septal shift. DH alone also decreased LV SV by 12% (p=0.001) and, in combination with increased negative ITP, caused a greater reduction in LVEDV than either condition in isolation (p=0.001). This LV under-filling was exacerbated by increased PVR, resulting in a 14% decrease in LV SV (p=0.001), which appears to be partially mediated by DVI, as indicated by significant increases in RSC (p=0.001). Under these conditions, when preload was increased by acute VL, we observed a paradoxical further decrease in LVEDV (-16%, p<0.001) and thus LV SV (-21%, p<0.001). Together with the observed increase in RSC (p=0.001), this is strong evidence for the role of DVI in impairing LV filling under these conditions. In conclusion, large increases in lung volume have a considerable deleterious effect on cardiac function. Moreover, at high volumes, DH may play a larger role than the associated increases in negative ITP in influencing hemodynamics. These findings have important implications for better understanding altered cardiopulmonary interaction in obstructive respiratory disease.

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