Forst H, Racenberg J, Messmer K
Institut für Anaesthesiologie, Ludwig-Maximilians-Universität München, Klinikum Grosshadern.
Anaesthesist. 1988 Jun;37(6):356-65.
Impaired right ventricular (RV) performance due to increased RV afterload in patients with sepsis or acute respiratory failure has been attributed to relative hypoperfusion and myocardial ischemia of the stressed free RV wall. There is evidence from experiments, however, that the normal RV is able to respond to a pressure load with adequate increases in myocardial blood flow. Whether or not ischemia of the free wall contributes to RV failure and whether restoration of RV perfusion can improve RV performance remains to be elucidated. The aim of this study was to compare local RV contractility to parameters of global RV contractility prior to and after induction of ischemia to its free wall.
Studies were performed in a total of 16 open-chest dogs using sonomicrometry to determine local contractility (velocity and percentage of fiber shortening) in the RV inflow tract (n = 8) prior to, 5, and 30 min after acute ligation of the right coronary artery (RCA). Parameters of global RV contractility (dP/dtmax, Vmax) were derived from intraventricular pressure measurements (tip-manometer). Regional myocardial blood flow (n = 6) was determined by the radioactive microsphere technique. Furthermore, the septal-lateral diameters of the RV (n = 8) and left ventricle (LV, n = 5), as well as the anterior-posterior diameter (n = 4) of the LV were measured simultaneously by use of sonomicrometers (Fig. 1); ventricular pressure-diameter diagrams were constructed in order to assess the dynamic geometry of the heart.
Acute ligation of the RCA resulted in a reduction of myocardial blood flow (-39% to -72%), predominantly in the RV inflow tract (Table 1). The segment length of the RV free wall and diameter of the RV increased following RCA ligation (Fig. 3a) whereas the septal-lateral diameter of the LV decreased concomitantly. The LV anterior-posterior diameter remained unaffected (Table 2, Fig. 3b). While local RV contractility (percent shortening and velocity of fiber shortening) deteriorated (-40% and -32%, respectively), the parameters of global RV contractility (dP/dtmax, Vmax) remained unchanged (Fig. 4a). Heart rate, mean arterial pressure, RV systolic pressure, and LV filling pressure remained unchanged (Fig. 4b), whereas RV filling pressure increased (+52%) and cardiac output was reduced (-13%).(ABSTRACT TRUNCATED AT 400 WORDS)
脓毒症或急性呼吸衰竭患者因右心室(RV)后负荷增加导致右心室功能受损,这归因于受压的右心室游离壁相对灌注不足和心肌缺血。然而,实验证据表明,正常的右心室能够通过适当增加心肌血流量来应对压力负荷。游离壁缺血是否导致右心室衰竭以及恢复右心室灌注是否能改善右心室功能仍有待阐明。本研究的目的是比较右心室游离壁缺血诱导前后局部右心室收缩力与整体右心室收缩力参数。
对总共16只开胸犬进行研究,使用超声微测法在右冠状动脉(RCA)急性结扎前、结扎后5分钟和30分钟测定右心室流入道(n = 8)的局部收缩力(纤维缩短速度和百分比)。整体右心室收缩力参数(dP/dtmax、Vmax)由心室内压力测量(顶端压力计)得出。通过放射性微球技术测定局部心肌血流量(n = 6)。此外,使用超声微测仪同时测量右心室(n = 8)和左心室(LV,n = 5)的室间隔 - 侧壁直径以及左心室的前后径(n = 4)(图1);构建心室压力 - 直径图以评估心脏的动态几何形状。
RCA急性结扎导致心肌血流量减少(-39%至-72%),主要发生在右心室流入道(表1)。RCA结扎后右心室游离壁节段长度和右心室直径增加(图3a),而左心室的室间隔 - 侧壁直径随之减小。左心室前后径保持不变(表2,图3b)。虽然局部右心室收缩力(缩短百分比和纤维缩短速度)恶化(分别降低40%和32%),但整体右心室收缩力参数(dP/dtmax、Vmax)保持不变(图4a)。心率、平均动脉压(MAP)、右心室收缩压和左心室充盈压保持不变(图4b),而右心室充盈压升高(+52%),心输出量降低(-13%)。(摘要截断于400字)