WHY DOES PULMONARY VENOUS-PRESSURE RISE AFTER ONSET OF LV DYSFUNCTION - A THEORETICAL-ANALYSIS

被引:103
作者
BURKHOFF, D
TYBERG, JV
机构
[1] UNIV CALGARY, HLTH SCI CTR, DEPT INTERNAL MED, CALGARY T2N 4N1, AB, CANADA
[2] UNIV CALGARY, HLTH SCI CTR, DEPT MED PHYSIOL, CALGARY T2N 4N1, AB, CANADA
来源
AMERICAN JOURNAL OF PHYSIOLOGY | 1993年 / 265卷 / 05期
关键词
VENOUS SYSTEM; SYMPATHETIC NERVOUS SYSTEM; PERICARDIUM; CARDIOVASCULAR MODEL;
D O I
10.1152/ajpheart.1993.265.5.H1819
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
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 (E(es))], 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 E(es) 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 (V(U)) 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.
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页码:H1819 / H1828
页数:10
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