Why does pulmonary venous pressure rise after onset of LV dysfunction: a theoretical analysis.
One of the most important consequences of acute left ventricular dysfunction (LVD) is pulmonary edema resulting from a rise in pulmonary venous pressure (PVP). It is generally believed that the PVP rise is a direct hemodynamic consequence of LVD. While this paradigm seems plausible, especially if the LV is viewed as a sump pump, there is no specific evidence to support this simple explanation. A theoretical analysis was performed to assess the hemodynamic mechanisms responsible for the dramatic rise in PVP after acute LVD. The ventricles were modeled as time-varying elastances; pulmonary and systemic vascular systems were modeled as series of resistive and capacitive elements. In response to a 50% decrease in LV contractile strength [end-systolic elastance (Ees)], cardiac output (CO) and mean arterial pressure (MAP) dropped substantially, while PVP increased minimally from its baseline of 12 to approximately 15 mmHg. With LV Ees set at 50% of normal, the effects of sympathetic activation were tested. When heart rate and total peripheral resistance were increased, CO and MAP improved, yet PVP still did not rise. The only intervention that caused a substantial increase in PVP was to simulate the decrease in unstressed volume (VU) of the venous system known to occur with sympathetic activation. When VU was decreased by about 15-20% (comparable to experimentally observed shifts with acute heart failure), PVP increased above 25 mmHg. The effects of pericardial constraints were investigated, and the results suggest a major role of this organ in determining the overall hemodynamic response to acute LVD, sympathetic activation, and explaining the responses to therapy. Thus this analysis suggests that elevations of PVP do not occur simply as a direct hemodynamic consequence of acute LVD. Rather, changes in PVP may be dictated more by sympathetic control on venous capacity. If confirmed, recognition of this as a primary mechanism may prove important in directing development of new therapies and in understanding the mechanisms of disease progression in heart failure.
Burkhoff
D
D
Department of Medicine, Columbia Presbyterian Hospital, New York, New York 10032.
Tyberg
J V
JV
D000818:Animals; D001794:Blood Pressure; D002302:Cardiac Output; D006333:Heart Failure / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D008433:Mathematics; D008955:Models, Cardiovascular; D009131:Muscle, Smooth, Vascular / Q000502:physiology / Q000503:physiopathology; D009200:Myocardial Contraction; D011652:Pulmonary Circulation; D011667:Pulmonary Veins / Q000502:physiology / Q000503:physiopathology*; D014655:Vascular Resistance; D016277:Ventricular Function, Left