Department of Anesthesiology, Centre hospitalier de l'Université de Montréal, Hôpital St-Luc, Montreal, QC, Canada.
Transplantation. 2010 Apr 27;89(8):920-7. doi: 10.1097/TP.0b013e3181d7c40c.
A regimen of fluid restriction, phlebotomy, vasopressors, and strict, protocol-guided product replacement has been associated with low blood product use during orthotopic liver transplantation. However, the physiologic basis of this strategy remains unclear. We hypothesized that a reduction of intravascular volume by phlebotomy would cause a decrease in portal venous pressure (PVP), which would be sustained during subsequent phenylephrine infusion, possibly explaining reduced bleeding. Because phenylephrine may increase central venous pressure (CVP), we questioned the validity of CVP as a correlate of cardiac filling in this context and compared it with other pulmonary artery catheter and transesophageal echocardiography-derived parameters. In particular, because optimal views for echocardiographic estimation of preload and stroke volume are not always applicable during liver transplantation, we evaluated the use of transmitral flow (TMF) early peak (E) velocity as a surrogate.
In study 1, the changes in directly measured PVP and CVP were recorded before and after phlebotomy and phenylephrine infusion in 10 patients near the end of the dissection phase of liver transplantation. In study 2, transesophageal echocardiography-derived TMF velocity in early diastole was measured in 20 patients, and the changes were compared with changes in CVP, pulmonary artery pressure (PAP), pulmonary capillary wedge pressure (PCWP), cardiac output (CO), and calculated systemic vascular resistance (SVR) at the following times: postinduction, postphlebotomy, preclamping of the inferior vena cava, during clamping, and postunclamping.
Phlebotomy decreased PVP along with CO, PAP, PCWP, CVP, and TMF E velocity. Phenylephrine given after phlebotomy increased CVP, SVR, and arterial blood pressure but had no significant effect on CO, PAP, PCWP, or PVP. The change in TMF E velocity correlated well with the change in CO (Pearson correlation coefficient 95% confidence interval 0.738-0.917, P< or =0.015) but less well with the change in PAP (0.554-0.762, P< or =0.012) and PCWP (0.576-0.692, P< or =0.008). TMF E velocity did not correlate significantly with CVP or calculated SVR.
Phlebotomy during the dissection phase of liver transplantation decreased PVP, which was unaffected when phenylephrine infusion was used to restore systemic arterial pressure. This may contribute to a decrease in operative blood loss. CVP often increased in response to phenylephrine infusion and did not seem to reflect cardiac filling. The changes in TMF E velocity correlated well with the changes in CO, PAP, and PCWP during liver transplantation but not with the changes in CVP.
在原位肝移植期间,采用液体限制、放血、血管加压素和严格的、基于方案的产品替代的方案与血液制品的低用量有关。然而,这种策略的生理基础仍不清楚。我们假设,放血会导致门静脉压(PVP)降低,在随后的苯肾上腺素输注期间,PVP 将保持降低,这可能解释了出血减少的原因。由于苯肾上腺素可能增加中心静脉压(CVP),我们质疑 CVP 在这种情况下作为心脏充盈的相关性,并将其与其他肺动脉导管和经食管超声心动图衍生参数进行了比较。特别是,由于在肝移植期间并非总是可以获得用于超声心动图估计前负荷和心排量的最佳视图,因此我们评估了使用二尖瓣血流(TMF)早期峰值(E)速度作为替代。
在研究 1 中,在肝移植解剖阶段结束时,在 10 名患者中记录了放血前后直接测量的 PVP 和 CVP 的变化,并在随后给予苯肾上腺素输注。在研究 2 中,在 20 名患者中测量了经食管超声心动图衍生的 TMF 早期舒张期速度,并在以下时间比较了 CVP、肺动脉压(PAP)、肺毛细血管楔压(PCWP)、心排量(CO)和计算的全身血管阻力(SVR)的变化:诱导后、放血后、下腔静脉夹闭前、夹闭时和夹闭后。
放血导致 PVP 降低,同时 CO、PAP、PCWP、CVP 和 TMF E 速度降低。苯肾上腺素在放血后给予时增加了 CVP、SVR 和动脉血压,但对 CO、PAP、PCWP 或 PVP 没有显著影响。TMF E 速度的变化与 CO 的变化密切相关(Pearson 相关系数 95%置信区间 0.738-0.917,P<0.015),但与 PAP 的变化(0.554-0.762,P<0.012)和 PCWP 的变化(0.576-0.692,P<0.008)相关性较差。TMF E 速度与 CVP 或计算的 SVR 无显著相关性。
肝移植解剖阶段的放血降低了 PVP,当使用苯肾上腺素输注来恢复全身动脉血压时,PVP 没有受到影响。这可能有助于减少手术出血。苯肾上腺素输注后 CVP 通常会升高,似乎并不能反映心脏充盈。TMF E 速度的变化与肝移植期间 CO、PAP 和 PCWP 的变化密切相关,但与 CVP 的变化无关。