Sherman S V, Wall M H, Kennedy D J, Brooker R F, Butterworth J
Department of Anesthesiology, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-109, USA.
Anesth Analg. 2001 May;92(5):1117-22. doi: 10.1097/00000539-200105000-00007.
There are few quantitative data on the extent or mechanism of pulmonary artery catheter (PAC)-induced valvular dysfunction. We hypothesized that PACs cause or worsen tricuspid and pulmonic valvular regurgitation, and tested this hypothesis by using transesophageal echocardiography. In 54 anesthetized adult patients, we measured color Doppler jet areas of tricuspid regurgitation (TR) in two planes (midesophageal [ME] 4-chamber and right ventricular inflow-outflow views) and pulmonic insufficiency (PI) in one plane (ME aortic valve long-axis view), both before and after we advanced a PAC into the pulmonary artery. Regurgitant jet areas and hemodynamic measurements were compared by using paired t-test. There were no significant changes in blood pressure or heart rate after passage of the PAC. After PAC placement, the mean PI jet area was not significantly increased. The mean TR jet area increased significantly in the right ventricular inflow-outflow view (+0.37 +/- 0.11 cm(2)) (P = 0.0014), but did not increase at the ME 4-chamber view. Seventeen percent of patients had an increase in TR jet area > or =1 cm(2); 8% of patients had an increase in PI jet area >/=1 cm(2).
In patients without pulmonic or tricuspid valvular pathology, placement of a pulmonary artery catheter (PAC) worsened tricuspid regurgitation, which is consistently visualized in the right ventricular inflow-outflow view, and often not seen in the midesophageal 4-chamber view. This is consistent with malcoaptation of the anterior and posterior leaflets. PAC-induced pulmonic insufficiency was rarely detected in the midesophageal aortic valve long-axis view. We conclude that a PAC is very unlikely to be the sole cause of severe tricuspid regurgitation or pulmonic insufficiency.
关于肺动脉导管(PAC)引起的瓣膜功能障碍的程度或机制,定量数据很少。我们假设PAC会导致或加重三尖瓣和肺动脉瓣反流,并通过经食管超声心动图来验证这一假设。在54例成年麻醉患者中,我们在将PAC推进肺动脉之前和之后,在两个平面(食管中段[ME]四腔心和右心室流入流出视图)测量三尖瓣反流(TR)的彩色多普勒射流面积,并在一个平面(ME主动脉瓣长轴视图)测量肺动脉瓣关闭不全(PI)的射流面积。通过配对t检验比较反流射流面积和血流动力学测量值。PAC通过后血压和心率无显著变化。放置PAC后,平均PI射流面积没有显著增加。在右心室流入流出视图中,平均TR射流面积显著增加(+0.37±0.11 cm²)(P = 0.0014),但在ME四腔心视图中没有增加。17%的患者TR射流面积增加≥1 cm²;8%的患者PI射流面积增加≥1 cm²。
在没有肺动脉或三尖瓣病变的患者中,放置肺动脉导管(PAC)会加重三尖瓣反流,这在右心室流入流出视图中始终可见,而在食管中段四腔心视图中通常不可见。这与前后叶瓣叶对合不良一致。在食管中段主动脉瓣长轴视图中很少检测到PAC引起的肺动脉瓣关闭不全。我们得出结论,PAC极不可能是严重三尖瓣反流或肺动脉瓣关闭不全的唯一原因。