Gonzalez M S, Basnight M A, Appleton C P
Department of Internal Medicine, Veterans Affairs Medical Center, Tucson, Arizona 85723.
J Am Coll Cardiol. 1991 Jan;17(1):239-48. doi: 10.1016/0735-1097(91)90733-p.
Pericardial effusion is associated with an abnormal increase in respiratory variation in mitral flow velocity. However, the relation of the changes in flow velocity to pericardial pressure, hemodynamics and two-dimensional echocardiographic findings is not established. Therefore, 11 sedated dogs with extensive hemodynamic instrumentation were studied with two-dimensional and Doppler echocardiography during four stages of progressively larger pericardial effusion. During all stages of effusion, respiratory variation in peak mitral flow velocity in early diastole and left ventricular isovolumetric relaxation time was increased compared with baseline (p less than 0.05). This increase was seen at the earliest stage of effusion (mean pericardial pressure 4.2 +/- 1.4 versus -0.8 +/- 0.9 mm Hg at baseline, p less than 0.05), and preceded the appearance of unequivocal diastolic right heart collapse in every dog. Maximal respiratory variation coincided with the appearance of right atrial collapse (mean pericardial pressure 7.1 +/- 2.4 mm Hg; mean inspiratory decrease in aortic pressure 9.5 +/- 2.6 mm Hg; mean aortic pressure 88.2 +/- 15.2 versus 102.2 +/- 11.2 mm Hg at baseline, p less than 0.05; and cardiac output 3.8 +/- 1.2 versus 5.5 +/- 1.3 liters/min at baseline, p less than 0.05), but did not increase at stages associated with more severe hemodynamic compromise. In addition, the respiratory changes in peak mitral flow velocity in early diastole were associated with simultaneous changes in the diastolic transmitral pressure gradient. It is concluded that in this model of acute pericardial effusion 1) increased respiratory variation in early diastolic mitral flow velocity, peak mitral flow velocity in early diastole and left ventricular isovolumetric relaxation time occurs almost immediately as pericardial pressure increases and persists at all stages of increasing pericardial effusion; 2) the abnormal respiratory variation occurs before equalization of intracardiac pressures and before the onset of unequivocal right heart collapse; 3) the respiratory variation occurs as a result of changes in the diastolic transmitral pressure gradient; and 4) the magnitude of the respiratory change is not necessarily predictive of pericardial pressure or severity of hemodynamic compromise, especially at the more severe stages of pericardial effusion.
心包积液与二尖瓣血流速度呼吸变化异常增加有关。然而,血流速度变化与心包压力、血流动力学及二维超声心动图表现之间的关系尚未明确。因此,对11只使用镇静剂且配备广泛血流动力学监测设备的犬进行研究,在逐渐增加心包积液的四个阶段采用二维和多普勒超声心动图检查。在积液的所有阶段,舒张早期二尖瓣血流峰值速度和左心室等容舒张时间的呼吸变化均较基线水平增加(p<0.05)。这种增加在积液最早阶段即可出现(平均心包压力4.2±1.4 mmHg,而基线时为-0.8±0.9 mmHg,p<0.05),且在每只犬出现明确的舒张期右心塌陷之前就已出现。最大呼吸变化与右心房塌陷的出现同时发生(平均心包压力7.1±2.4 mmHg;平均吸气时主动脉压力下降9.5±2.6 mmHg;平均主动脉压力88.2±15.2 mmHg,而基线时为102.2±11.2 mmHg,p<0.05;心输出量3.8±1.2 L/min,而基线时为5.5±1.3 L/min,p<0.05),但在与更严重血流动力学损害相关的阶段并未增加。此外,舒张早期二尖瓣血流峰值速度的呼吸变化与舒张期跨二尖瓣压力阶差的同时变化有关。得出结论:在这个急性心包积液模型中,1)随着心包压力升高,舒张早期二尖瓣血流速度、舒张早期二尖瓣血流峰值速度和左心室等容舒张时间的呼吸变化几乎立即增加,并在心包积液增加的所有阶段持续存在;2)异常呼吸变化发生于心腔内压力平衡之前以及明确的右心塌陷出现之前;3)呼吸变化是由舒张期跨二尖瓣压力阶差的变化引起的;4)呼吸变化的幅度不一定能预测心包压力或血流动力学损害的严重程度,尤其是在心包积液较严重阶段。