Licker Marc, Ellenberger Christoph, Sierra Jorge, Christenson Jan, Diaper John, Morel Denis
Department of Anesthesiology, Pharmacology and Surgical Intensive Care, University Hospital of Geneva.
Crit Care Med. 2005 Mar;33(3):591-7. doi: 10.1097/01.ccm.0000156446.03285.e0.
Preoperative acute normovolemic hemodilution induces an increase in circulatory output that is thought to be limited in patients with cardiac diseases. Using multiple-plane transesophageal echocardiography, we investigated the mechanisms of cardiovascular adaptation during acute normovolemic hemodilution in patients with severe coronary artery disease.
Prospective case-control study.
Operating theater in a university hospital.
Consecutive patients treated with beta-blockers, scheduled to undergo coronary artery bypass (n = 50).
After anesthesia induction, blood withdrawal and isovolemic exchange with iso-oncotic starch (1:1.15 ratio) to achieve a hematocrit value of 28%.
In addition to heart rate and intravascular pressures, echocardiographic recordings were obtained before and after acute normovolemic hemodilution to assess cardiac preload, afterload, and contractility. In a control group, not subjected to acute normovolemic hemodilution, hemodynamic variables remained stable during a 20-min anesthesia period. Following acute normovolemic hemodilution, increases in cardiac stroke volume (+28 +/- 4%; mean +/- sd) were correlated with increases in central venous pressure (+2.0 +/- 1.3 mm Hg; R = .56) and in left ventricular end-diastolic area (+18 +/- 5%, R = .39). The unchanged left ventricular end-systolic wall stress and preload-adjusted maximal power indicated that neither left ventricular afterload nor contractility was affected by acute normovolemic hemodilution. Diastolic left ventricular filling abnormalities (15 of 22 cases) improved in 11 patients and were stable in the remaining four patients. Despite reduction in systemic oxygen delivery (-20.5 +/- 7%, p < .05), there was no evidence for myocardial ischemia (electrocardiogram, left ventricular wall motion abnormalities).
In anesthetized patients with coronary artery disease, moderate acute normovolemic hemodilution did not compromise left ventricular systolic and diastolic function. Lowering blood viscosity resulted in increased stroke volume that was mainly related to increased venous return and higher cardiac preload.
术前急性等容性血液稀释可使循环输出量增加，而这一增加在心脏病患者中被认为是有限的。我们使用多平面经食管超声心动图，研究了严重冠状动脉疾病患者急性等容性血液稀释期间心血管适应的机制。
前瞻性病例对照研究。
大学医院手术室。
连续接受β受体阻滞剂治疗、计划进行冠状动脉搭桥术的患者（n = 50）。
麻醉诱导后，采血并用等渗淀粉进行等容置换（比例为1:1.15），使血细胞比容值达到28%。
除心率和血管内压力外，在急性等容性血液稀释前后进行超声心动图记录，以评估心脏前负荷、后负荷和收缩力。在未进行急性等容性血液稀释的对照组中，血流动力学变量在20分钟的麻醉期内保持稳定。急性等容性血液稀释后，心搏量增加（+28±4%；平均值±标准差）与中心静脉压升高（+2.0±1.3 mmHg；R = 0.56）及左心室舒张末期面积增加（+18±5%，R = 0.39）相关。左心室收缩末期壁应力和前负荷调整后的最大功率未改变，表明急性等容性血液稀释既未影响左心室后负荷，也未影响收缩力。22例患者中有15例存在舒张期左心室充盈异常，其中11例有所改善，其余4例保持稳定。尽管全身氧输送减少（-20.5±7%，p < 0.05），但未发现心肌缺血的证据（心电图、左心室壁运动异常）。
在麻醉的冠状动脉疾病患者中，适度的急性等容性血液稀释并未损害左心室的收缩和舒张功能。降低血液粘度导致心搏量增加，这主要与静脉回心血量增加和心脏前负荷升高有关。
