Effects of changes in abdominal pressure on left ventricular performance and regional blood flow

Many clinical conditions are associated with an increase in abdominal pressure. While the effects on venous return have been studied in the past, little attention has been given to the effect of abdominal pressure on left-sided hemodynamic events. The effects of acute changes in abdominal pressure (P(ab)) on left ventricular (LV) hemodynamics and outflow distribution were evaluated in ten open-chest dogs, which had undergone right heart bypass to eliminate the influence of changes om P(ab) on systemic venous return. Pressures were measured in the left atrium (P(la)), aorta (P(ao), and stomach (P(ab)). Electromagnetic flow probes were positioned around the ascending aorta (Q̇(aa)), descending aorta (Q̇(da)) and the innominate or subclavian artery (Q̇(in)) to reflect total cardiac output and the respective regional caudad and cephalad blood flows. Compressing the abdomen to increase acutely P(ab) (9.2 ± 0.6 torr) also significantly increased P(ao)) (7.8 ± 1.2 torr), P(la) (1.7 ± 0.4 torr), and Q̇(in) (15.2 ± 4.5%), while Q̇(aa) (-9.5 ± 2.0%) and Q̇(da) (-26.3 ± 7.0%) significantly decreased. Opposite findings were obtained immediately after release of abdominal compression. Thus, an acute increase in P(ab) with a constant pulmonary artery inflow increased the after-load imposed on the left ventricle and redistributed LV output, with a reduction in flow to the abdomen. Part of the fall in Q̇(aa) and increase in P(la) could be attributed to passive elevation of the diaphragm by the increase in P(ab), i.e., heart-lung-diaphragm interdependence. We conclude that acute changes in P(ab) may significantly effect left-sided hemodynamic events through changes in LV afterload, regional distribution of cardiac output, and diaphragmatic position. These findings have important clinical implications for understanding hemodynamic events under numerous conditions associated with changes in P(ab).