主动脉瓣重度狭窄病人外科手术的麻醉处理

重度主动脉瓣狭窄（severe aortic stenosis，AS）病人手术的麻醉【摘要】目的：分析总结178例重度主动脉瓣狭窄病人外科手术的麻醉经验及住院期间转归。

方法：2000年1月至2006年12月，阜外心血管病医院实施的重度主动脉瓣狭窄（A V A<1.0cm2，主动脉瓣跨瓣压差>60mmHg）手术治疗病人共178例，其中主动脉瓣置换例，Ross手术例，主动脉瓣联合升主动脉置换（或成形）例，重度主动脉瓣狭窄合并冠心病手术治疗结果：全组无麻醉死亡，术中外科原因死亡1例，术后死亡2例结论：麻醉处理应注意，麻醉诱导期至CPB开始前避免低血压，围术期心肌保护，重视心脏复苏期灌注压维持及药物治疗，围术期一般不需大剂量正性肌力药、可应用β受体阻滞药,术后早期需维持较高的血压，积极治疗室性心律失常。

关键词【Abstract】重度主动脉瓣狭窄病人因长期左心室后负荷增高致左心室壁肥厚，围术期易发生心肌缺血，一旦发生室颤，复苏成功率低。

CPB术中恢复心肌灌注后常发生心脏复跳困难，是心血管外科手术病人麻醉处理难点之一。

本研究分析总结了178例重度主动脉瓣狭窄病人的麻醉处理经验及住院期间病人转归。

1.资料与方法年龄49±16岁，体重65±12Kg，CPB时间100±37 min，阻断时间76±31min，停跳液2102±826ml，灌注次数2.3±1次，术前主动脉瓣压差94±34mmHg，室间隔厚度14±2.7mm 术前左室舒张末内径49±7mm，EF64％±9％，术后主动脉瓣压差25±11mmHg, 术后左室舒张末内径46±7mm，EF60％±7％。

芬太尼诱导10.6±4.5ug/kg，总用量26±9ug/kg。

气管拔管时间13.4± 8 h ICU时间42±27 h住院时间11±5d。

2.结果3.讨论1)围术期β受体阻滞药的应用2)围术期心肌保护3)CPB中恢复心肌灌注后心脏的复苏a)开放前温氧合血灌注心脏b)β受体阻滞药c)可达龙＋肾上腺α受体激动剂d)4)术后循环维持及正性肌力药应用问题5)死亡病例讨论，由于左心室肥厚注意维持一定的血压，血容量，避免低血压导致心肌灌注不足，心肌缺血，室颤。

Calcific deposits in the bodies of aortic cusps cause stiffness,restrain normal movement, and prevent adequate valve opening (28).If the normal aortic valve opening area of 3–4 cm2 decreases to approximatelyone-fourth of that area, the stenosis becomes hemodynamically significant.Mild aortic stenosis is present with a valve area of1.5 cm2; moderate aortic stenosis, with a valve area between 1.0and 1.5 cm2;severe aortic stenosis, with a valve area of 1.0 cm2 or less; and critical aortic stenosis, with a valve area of 0.7 cm2 or less (6). Findings of our study indicate for the first time, to our knowledge, that planimetric measurements of the AVA by using retrospectively electrocardiographically gated16–detector row CT allow a classification of aortic stenosis that is similar to measurements achieved with established routine echocardiographic techniques. Multi–detector row CT furthermore provides morphologic information, such as cusp calcification and restriction of cusp movement,and allows the distinction between bicuspid and tricuspid aortic valves.Structural Valve Abnormalities and Surgical Valve Replacement Preoperative knowledge about aortic valve morphologic characteristics and extent of aortic valve calcification is desirable when one is planning surgical valve replacement (19). For example, the presence or absence of a bicuspid aortic valve poses a risk factor for postoperative complications after aortic valve and aortic root replacement (29). Similarly, extensive valve calcification is associated with a higher prevalence of surgical difficulties; placement and fixation of the valve prosthesis into the annulus, as well as insertion of the coronary arteries, after aortic root replacement are complicated by severe calcification (30). Furthermore, preoperative quantification of valve calcification in patients who are undergoing aortic valve replacement allows prediction of postoperative conduction defects (31). Our results were similar to the results of a previous study (18) with four–detector row CT, for we were able to accurately depict morphologic abnormalities of the aortic valve with similar results when we compared results achieved with CT and echocardiography. In addition, the use of 20reformations in 5% steps of the R-R interval enabled dynamic aortic valve imaging throughout the cardiac cycle and allowed a correct estimation of cusp motion restriction, which represents the major pathophysiologic contributor to aortic stenosis (32).Classification of Aortic StenosisDetermination of severity of aortic stenosis is crucial, and many laboratory tests are available; however, exact classification remains difficult because all methods have limitations peculiar to the techniques (1,5,6,11–13,33,34).Previously, direct planimetry of the AVA by using magnetic resonance(MR) imaging was demonstrated to be feasible, and results with that technique and results with echocardiography and ventriculography with a catheter (7,8) showed a good correlation. The results of our study are similar tothose reported with MR imaging and demonstrate that there is a significant correlation between planimetric AVA measurements with multi–detector row CT and the results obtained with TEE and TTE. Furthermore, the association between planimetry with CT and transvalvular pressure gradients was moderate and indicated a reduction of the AVA with increasing transvalvular pressure gradients.When we assessed the planimetrically measured orifice area, a potential flaw might have occurred in that with poor left ventricular systolic function and low stroke volume, the pressure necessary to open the cusps to the full extent may not have been generated and, hence,may have led to an underestimation of the AVA (7). On the other hand,researchers in a study (35) with TEE simultaneously compared the planimetric measurement of the AVA with the calculated AVA in patients with aortic stenosis and demonstrated that changes of transvalvular blood flow did not result in significant alterations of planimetric AVA measurements.Another limitation of planimetric AVA measurements could arise from the fact that the continuity equation is used to determine the effective area, whereas planimetry is used to measure the anatomic area; the latter is supposed to be larger than the former (12). This could explain the slight overestimation in regard to AVA measurements with CT and TEE compared with measurements with TTE, as also has been observed in our study; however, these differences were not significant.Aortic Valve Calcification and StenosisRecently, investigators in a large comprehensive study (19) examined the hemodynamic correlates, the diagnostic value, and the outcome implications of quantitative aortic valve calcification measurements in 100 patients with aortic stenosis and found this correlation to be curvilinear. These investigators concluded that the grade of aortic valve calcification and that of stenosis provide complementary information. Moreover, the valve calcification score was an independent predictor of survival and, thus, provided important outcome information (19).This finding supports the idea that valve calcification is associated with a 50% increase in the risk of death from cardiovascular disease,even in the absence of left ventricular outflow tract obstruction(36). One of the implications of our investigation for application in further imaging studies in patients with aortic stenosis is that the extent of aortic valve calcification should not be taken as a direct marker of the severity of aortic stenosis, as has been previously suggested (15–18), but that aortic valve calcification should be separately quantified in addition to severity of aortic stenosis.。