Hoit B D, Gabel M, Fowler N O
University of Cincinnati Medical Center, Division of Cardiology, Ohio 45267.
Circulation. 1990 Oct;82(4):1370-6. doi: 10.1161/01.cir.82.4.1370.
Echocardiographic and hemodynamic data were measured in closed-chest dogs during graded cardiac tamponade (pericardial pressure 5, 10, and 15 mm Hg) before and after production of diffuse ischemic left ventricular dysfunction. Left ventricular dysfunction was produced by intracoronary injection of nonradioactive microspheres (54 +/- 3.9 mm diameter). Changes in left atrial pressure with cardiac tamponade were influenced by coexisting left ventricular dysfunction. Left atrial pressure increased with tamponade and was equal to pericardial pressure before left ventricular dysfunction was produced. However, after left ventricular dysfunction was produced, left atrial pressure was significantly higher than pericardial pressure before tamponade, but it fell toward pericardial pressure when tamponade was produced. Pulsus paradoxus (greater than 10 mm Hg) was present in all animals with cardiac tamponade before left ventricular dysfunction but in only one animal afterward. During each level of tamponade, the inspiratory fall of aortic systolic pressure was greater before than with left ventricular dysfunction. The slope of the linear regression between pericardial pressure and millimeters of mercury of inspiratory fall in aortic systolic pressure was significantly greater before than with left ventricular dysfunction (0.74 +/- 0.12 versus 0.32 +/- 0.12, p less than 0.05). Left ventricular dysfunction caused a leftward and upward shift of the pericardial pressure-volume relation. As a result, right atrial and ventricular collapse occurred with significantly smaller volumes of pericardial fluid after than before left ventricular dysfunction. We conclude that pulsus paradoxus may be absent in cardiac tamponade with coexisting left ventricular dysfunction and unequal filling pressures. Echocardiographic signs of cardiac tamponade may occur with small effusions in the presence of left ventricular dysfunction.
在分级心脏压塞（心包压力为5、10和15 mmHg）期间，对开胸狗在产生弥漫性缺血性左心室功能障碍前后进行了超声心动图和血流动力学数据测量。通过冠状动脉内注射非放射性微球（直径54±3.9 mm）产生左心室功能障碍。心脏压塞时左心房压力的变化受并存的左心室功能障碍影响。在产生左心室功能障碍之前，随着压塞左心房压力升高且等于心包压力。然而，在产生左心室功能障碍之后，左心房压力显著高于压塞前的心包压力，但在产生压塞时其向心包压力下降。在左心室功能障碍之前，所有心脏压塞动物均出现奇脉（大于10 mmHg），但之后仅一只动物出现。在每个压塞水平，主动脉收缩压的吸气下降在左心室功能障碍之前比之后更大。心包压力与主动脉收缩压吸气下降毫米汞柱之间的线性回归斜率在左心室功能障碍之前比之后显著更大（0.74±0.12对0.32±0.12，p<0.05）。左心室功能障碍导致心包压力-容积关系向左上方移位。结果，与左心室功能障碍之前相比，心包积液量显著更小时就出现了右心房和心室塌陷。我们得出结论，在并存左心室功能障碍和充盈压力不等的心脏压塞中可能不存在奇脉。在存在左心室功能障碍时，少量积液可能出现心脏压塞的超声心动图征象。
