利用压力—容量环评价非停跳冠状动脉搭桥术术中右心室功能的变化
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摘要
目目的心室压力-容量环(pressure-volume loop, P-V环)是评估心功能变化的非负荷依赖性的方法,不仅适用于左心室,同样也适用于右心室。本研究旨在:一方面,探讨通过容量性肺动脉导管(pulmonary artery catheter,PAC)获取右心室心动周期内几个特殊时刻的压力、容量数据,并据此绘制右心室P-V环的方法和临床可行性;另一方面,通过右心室收缩末弹性(end-systolic elastance, Ees)和舒张末僵硬度(end-diastolic stiffness, EED),评估非停跳冠状动脉搭桥术(off-pump coronary artery bypass surgery, OPCAB)术中右心室收缩和舒张功能的变化。
方法择期行OPCAB术的三支病变冠心病患者28例(男19例,女9例),年龄(67.3±6.5)岁,术前左室射血分数为(61.4±10.7)%,心功能NYHA分级为Ⅰ～Ⅲ,各系统无严重并发症。麻醉诱导后经右侧颈内静脉放置容量性PAC,连接普通监护仪和Vigilance监测系统。数据记录时点包括:T1,切皮前麻醉稳定时(术前水平);T2,心脏前壁血管搭桥、心肌固定器放置后5min;T3,心脏侧壁血管远端搭桥、心肌固定器放置后5min;T4,心脏后壁血管远端搭桥、心肌固定器放置后5min;T5,关胸后(术毕)。每个时点共收集三组数据:⑴记录右心血流动力学参数;⑵计算右室Ees和EED:Ees为右室收缩期末压力/容量之比;EED为右室舒张期末压力/容量之比;⑶将心动周期内几个主要时刻(舒张期末、等容收缩期末、射血峰压期、收缩期末、等容舒张期末)的压力、容量数据输入计算机,绘制右室P-V环。
结果根据舒张期末、等容收缩期末、射血峰压期、收缩期末、等容舒张期末等5个时刻的压力、容量数据,可以绘制出右室P-V环,P-V环大致呈三角形。OPCAB术中不同时点P-V环明显向左侧移动,特别是舒张末时点向左上方移动,提示右室被动舒张功能受损。不同时点Ees的变化未达统计学差异(P>0.05),但T4、T5时升高。与T1相比,EED在T2～T4明显升高(P<0.05),T5虽然有所恢复,但并未恢复到T1水平(P<0.05)。与T1比较,RVEF值在T4明显下降(P<0.05)。RVEDVI呈降低趋势,T3、T4、T5下降明显(P<0.05)。SVI与RVEDVI变化相似,但与T1比较,T4时SVI下降程度(18%)大于RVEDVI(10%)。与T1比较,术中PVRI明显降低(P<0.05),但T2～T4却是逐渐升高的趋势,T5又下降(P<0.05)。与T1相比,T2～T4的RAP明显升高(P<0.05),T5又恢复到T1水平。各时点间PAWP没有明显变化(P<0.05),MAP在T3和T4明显下降。
结结论利用容量性PAC可以获得右心室心动周期内几个特殊时刻的压力、容量数据,根据这些数据可以生成右室P-V环,并计算Ees和EED,据此可以评价右心室心肌收缩性和被动舒张能力的变化。结果表明,OPCAB术中心脏后壁血管搭桥时,右心室收缩功能(RVEF下降)的降低不代表心肌收缩性(Ees)下降,而是每搏量和前负荷下降,以及后负荷相对升高的结果,至术毕收缩功能恢复。术中右室舒张功能降低,表现为室壁僵硬度(EED)增加,顺应性下降,且至术毕未能恢复。
Objective Right ventricular function plays an important role in the hemodynamic derangement during off-pump coronary artery bypass (OPCAB) surgery. Pressure-volume loops have been shown to provide load-independent information of cardiac function. Therefore, the aim of this study is to investigate the feasibility of construction of right ventricular pressure-volume loops with pressure and volume data measured by a volumetric pulmonary artery catheter (PAC) and to evaluate right ventricular systolic and diastolic function by end-systolic elastance (Ees) and end-diastolic stiffness (EED) in OPCAB surgery.
Methods Twenty-eight patients who underwent OPCAB surgery were included. After anesthesia induction, a volumetric PAC was placed via the right internal jugular vein. Data were recorded at: anesthesia steady-state before skin incision (T1); 5min after stabilizer device placed for anastomosis of the heart’s anterior wall (T2), lateral wall (T3), posterior wall (T4), respectively; after sternal closure (T5). Three sets of data were collected at each time point: firstly, hemodynamic variables were measured; secondly, right ventricular end-systolic elastance (Ees) was estimated by end-systolic pressure divided by end-systolic volume, and end-diastolic stiffness (EED) was estimated by end-diastolic pressure divided by end-diastolic volume; thirdly, right ventricular pressure-volume loops were constructed with pressure and volume data measured from end-diastole point, end-isovolumic systole point, peak-ejection point, end-systole point and end-isovolumic diastole point.
Results Right ventricular pressure-volume loops were constructed successfully with pressure/volume data measured from several specific time-points by a volumic PAC, and they generally shifted to the left during OPCAB surgery. Especially, shift upward and to the left in end-diastole point indicated that right ventricular passive relaxation properties were impaired compared with that at T1. The change of Ees was not statistically significant during operation (P>0.05), whereas EED increased throughout the OPCAB surgery (P<0.05). Decrease in right ventricular ejection fraction, stroke volume index and end-diastolic volume index occurred (P<0.05) at T4 compared with values at T1. Pulmonary vascular resistance index at T4 increased relatively compared with that at T2 and T3. Right atrial pressure increased only during coronary anastomoses (P<0.05)
Conclusion Right ventricular pressure-volume loops can be constructed and Ees and EED can be estimated using a volumetric PAC. Right ventricular systolic dysfunction occurred during anastomoses on the heart’s posterior wall not due to impaired contractility but as a result of reduced stroke volume and preload and a relative increase in afterload. Right ventricular diastolic function was impaired throughout OPCAB surgery.
方法择期行OPCAB术的三支病变冠心病患者28例(男19例,女9例),年龄(67.3±6.5)岁,术前左室射血分数为(61.4±10.7)%,心功能NYHA分级为Ⅰ～Ⅲ,各系统无严重并发症。麻醉诱导后经右侧颈内静脉放置容量性PAC,连接普通监护仪和Vigilance监测系统。数据记录时点包括:T1,切皮前麻醉稳定时(术前水平);T2,心脏前壁血管搭桥、心肌固定器放置后5min;T3,心脏侧壁血管远端搭桥、心肌固定器放置后5min;T4,心脏后壁血管远端搭桥、心肌固定器放置后5min;T5,关胸后(术毕)。每个时点共收集三组数据:⑴记录右心血流动力学参数;⑵计算右室Ees和EED:Ees为右室收缩期末压力/容量之比;EED为右室舒张期末压力/容量之比;⑶将心动周期内几个主要时刻(舒张期末、等容收缩期末、射血峰压期、收缩期末、等容舒张期末)的压力、容量数据输入计算机,绘制右室P-V环。
结果根据舒张期末、等容收缩期末、射血峰压期、收缩期末、等容舒张期末等5个时刻的压力、容量数据,可以绘制出右室P-V环,P-V环大致呈三角形。OPCAB术中不同时点P-V环明显向左侧移动,特别是舒张末时点向左上方移动,提示右室被动舒张功能受损。不同时点Ees的变化未达统计学差异(P>0.05),但T4、T5时升高。与T1相比,EED在T2～T4明显升高(P<0.05),T5虽然有所恢复,但并未恢复到T1水平(P<0.05)。与T1比较,RVEF值在T4明显下降(P<0.05)。RVEDVI呈降低趋势,T3、T4、T5下降明显(P<0.05)。SVI与RVEDVI变化相似,但与T1比较,T4时SVI下降程度(18%)大于RVEDVI(10%)。与T1比较,术中PVRI明显降低(P<0.05),但T2～T4却是逐渐升高的趋势,T5又下降(P<0.05)。与T1相比,T2～T4的RAP明显升高(P<0.05),T5又恢复到T1水平。各时点间PAWP没有明显变化(P<0.05),MAP在T3和T4明显下降。
结结论利用容量性PAC可以获得右心室心动周期内几个特殊时刻的压力、容量数据,根据这些数据可以生成右室P-V环,并计算Ees和EED,据此可以评价右心室心肌收缩性和被动舒张能力的变化。结果表明,OPCAB术中心脏后壁血管搭桥时,右心室收缩功能(RVEF下降)的降低不代表心肌收缩性(Ees)下降,而是每搏量和前负荷下降,以及后负荷相对升高的结果,至术毕收缩功能恢复。术中右室舒张功能降低,表现为室壁僵硬度(EED)增加,顺应性下降,且至术毕未能恢复。
Objective Right ventricular function plays an important role in the hemodynamic derangement during off-pump coronary artery bypass (OPCAB) surgery. Pressure-volume loops have been shown to provide load-independent information of cardiac function. Therefore, the aim of this study is to investigate the feasibility of construction of right ventricular pressure-volume loops with pressure and volume data measured by a volumetric pulmonary artery catheter (PAC) and to evaluate right ventricular systolic and diastolic function by end-systolic elastance (Ees) and end-diastolic stiffness (EED) in OPCAB surgery.
Methods Twenty-eight patients who underwent OPCAB surgery were included. After anesthesia induction, a volumetric PAC was placed via the right internal jugular vein. Data were recorded at: anesthesia steady-state before skin incision (T1); 5min after stabilizer device placed for anastomosis of the heart’s anterior wall (T2), lateral wall (T3), posterior wall (T4), respectively; after sternal closure (T5). Three sets of data were collected at each time point: firstly, hemodynamic variables were measured; secondly, right ventricular end-systolic elastance (Ees) was estimated by end-systolic pressure divided by end-systolic volume, and end-diastolic stiffness (EED) was estimated by end-diastolic pressure divided by end-diastolic volume; thirdly, right ventricular pressure-volume loops were constructed with pressure and volume data measured from end-diastole point, end-isovolumic systole point, peak-ejection point, end-systole point and end-isovolumic diastole point.
Results Right ventricular pressure-volume loops were constructed successfully with pressure/volume data measured from several specific time-points by a volumic PAC, and they generally shifted to the left during OPCAB surgery. Especially, shift upward and to the left in end-diastole point indicated that right ventricular passive relaxation properties were impaired compared with that at T1. The change of Ees was not statistically significant during operation (P>0.05), whereas EED increased throughout the OPCAB surgery (P<0.05). Decrease in right ventricular ejection fraction, stroke volume index and end-diastolic volume index occurred (P<0.05) at T4 compared with values at T1. Pulmonary vascular resistance index at T4 increased relatively compared with that at T2 and T3. Right atrial pressure increased only during coronary anastomoses (P<0.05)
Conclusion Right ventricular pressure-volume loops can be constructed and Ees and EED can be estimated using a volumetric PAC. Right ventricular systolic dysfunction occurred during anastomoses on the heart’s posterior wall not due to impaired contractility but as a result of reduced stroke volume and preload and a relative increase in afterload. Right ventricular diastolic function was impaired throughout OPCAB surgery.
引文
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1. Suga H, Sagawa K, Shoukas AA. Load Independence of the Instantaneous Pressure-Volume Ratio of the Canine Left Ventricle and Effects of Epinephrine and Heart Rate on the Ratio. Circ Res 1973; 32(3): 314-322.
2. Suga H, Sagawa K. Instantaneous Pressure-Volume Relationships and Their Ratio in the Excised, Supported Canine Left Ventricle. Circ Res 1974; 35(1): 117-126.
3. Klotz S, Hay I, Dickstein ML, Yi GH, Wang J, Maurer MS, Kass DA, Burkhoff D. Single-beat estimation of end-diastolic pressure-volume relationship: a novel method with potential for noninvasive application. Am J Physiol Heart Circ Physiol 2006; 291(1): H403-H412.
4. Katz AM. Influence of altered inotropy and lusitropy on ventricular pressure-volume loops. J AM Coll Cardiol 1988; 11(2): 438-445.
5. Stekelenburg-de vos S, Steendijk P, Ursem NT, Wladimiroff JW, Delfos R, Poelmann RE. Systolic and diastolic ventricular function assessed by pressure-volume loops in the stage 21 venous clipped chick embryo. Pediatr Res 2005; 57(1): 16-21.
6. Asanoi H, Sasayama S, Kameyama T. Ventriculoarterial coupling in normal and failing heart in humans. Circ Res 1989; 65(2): 483-493.
7. Acosta F, Sansano T, Palenciano CG, Falcon L, Domenech P, Robles R, Bueno FS, Ramirez P, Parrilla P. Effects of dobutamine on right ventricular function andpulmonary circulation in pulmonary hypertension during liver transplantation. Transplant Proc 2005; 37(9): 3869-3870.
8. Steendijk P, Tulner SA, Bax JJ, Oemrawsingh PV, Bleeker GB, van Erven L, Putter H, Verwey HF, van der Wall EE, Schalij MJ. Hemodynamic effects of long-term cardiac resynchronization therapy: analysis by pressure-volume loops. Circulation 2006; 113(10): 1295-1304.
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17. Steendijk P, Tulner SA, Bax JJ, Oemrawsingh PV, Bleeker GB, van Erven L, Putter H, Verwey HF, van der Wall EE, Schalij MJ. Response to Letter Regarding Article,“Hemodynamic Effects of Long-Term Cardiac Resynchronization Therapy: Analysis by Pressure-Volume Loops”. Circulation 2006; 114(9): e372.
18. Steendijk P, Baan J Jr, Van der Velde ET, Baan J. Effects of critical coronary stenosis on global systolic left ventricular function quantified by pressure-volume relations during dobutamine stress in the canine heart. J Am Coll Cardiol 1998; 32(3): 816–826.
19. Sunagawa K, Maughan WL, Sagawa K. Optimal arterial resistance for the maximal stroke work studied in isolated canine left ventricle. Circ Res 1985; 56(4): 586-595.
20. Sunagawa K, Maughan WL, Burkhoff D, Sagawa K. Left ventricular interaction with arterial load studied in isolated canine ventricle. Am J Physiol 1983; 245(5 Pt 1): H773-H780.
21. Knaapen P, Allaart CP, de Cock CC, Bronzwaer JG. Letter by Knaapen et al regarding article, "hemodynamic effects of long-term cardiac resynchronization therapy: analysis by pressure-volume loops". Circulation 2006; 114(9): e371.
1. Biswas S, Clements F, Diodato L, Hughes GC, Landolfo K. Changes in systolic and diastolic function during multivessel off-pump coronary bypass grafting. Eur J Cardiothorac Surg 2001; 20: 913-917.
2. Mathison M, Edgerton JR, Horswell JL, Akin JJ, Mack MJ. Analysis of hemodynamic changes during beating heart surgical procedures. Ann Thorac Surg 2000; 70: 1355-1360.
3. Kwak YL, Oh YJ, Jung SM, Yoo KJ, Lee JH, Hong YW. Change in right ventricular function during off-pump coronary artery bypass graft surgery. Eur J Cardiothorac Surg 2004; 25: 572-577.
4. Steendijk P. Right ventricular function and failure: Methods, models, and mechanisms. Crit Care Med 2004; 32: 1087-1089.
5. Tulner SA, Klautz RJ, Van Rijk-Zwikker GL, Engbers FH, Bax JJ, Baan J, et al. Perioperative assessment of left ventricular function by pressure-volume loops using the conductance catheter method. Anesth Analg 2003; 97: 950-957.
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10. Kass DA, Maughan WL, Guo ZM, Kono A, Sunagawa K, Sagawa K. Comparative influence of load versus inotropic states on indexes of ventricular contractility: Experimental and theoretical analysis based on pressure-volumerelationships. Circulation 1987; 76:1422-1436.
11. Stekelenburg-de Vos S, Steendijk P, Ursem NT, Wladimiroff JW, Delfos R, Poelmann RE. Systolic and diastolic ventricular function assessed by pressure-volume loops in the stage 21 venous clipped chick embryo. Pediatr Res 2005; 57: 16-21.
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13. de Vroomen M, Cardozo RH, Steendijk P, van Bel F, Baan J. Improved contractile performance of right ventricle in response to increased RV afterload in newborn lamb. Am J Physiol Heart Circ Physiol 2000; 278:H100–H105.
14. Brookes CI, White PA, Bishop AJ, Oldershaw PJ, Redington AN, Moat NE. Validation of a new intraoperative technique to evaluate load-independent indices of right ventricular performance in patients undergoing cardiac operations. J Thorac Cardiovasc Surg 1998; 116:468-476.
15. Leeuwenburgh BP, Steendijk P, Helbing WA, Baan J. Indexes of diastolic RV function: Load dependence and changes after chronic RV pressure overload in lambs. Am J Physiol Heart Circ Physiol 2002; 282: H1350-H1358.
16. Klotz S, Hay I, Dickstein ML, Yi GH, Wang J, Maurer MS, et al. Single-beat estimation of end-diastolic pressure-volume relationship: a novel method with potential for noninvasive application. Am J Physiol Heart Circ Physiol 2006, 291: H403-H412.
17. Chen CH, Fetics B, Nevo E, Rochitte CE, Chiou KR, Ding PA, et al. Noninvasive single-beat determination of left ventricular end-systolic elastance in humans. J Am Coll Cardiol 2001; 38:2028–2034.
18. Steendijk P, Baan J Jr, Van der Velde ET, Baan J. Effects of critical coronarystenosis on global systolic left ventricular function quantified by pressure-volume relations during dobutamine stress in the canine heart. J Am Coll Cardiol 1998; 32:816–826.
19. Steendijk P, Tulner SA, Bax JJ, Oemrawsingh PV, Bleeker GB, van Erven L, et al. Hemodynamic effects of long-term cardiac resynchronization therapy: analysis by pressure-volume loops. Circulation 2006; 113:1295-1304.
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23. Asanoi H, Sasayama S, Kameyama T. Ventriculoarterial coupling in normal and failing heart in humans. Circ Res 1989, 65: 483-493.
24. Maughan WL, Shoukas AA, Sagawa K, Weisfeldt ML. Instantaneous pressure-volume relationship of the canine right ventricle. Circ Res 1979; 44: 309-315.
25. Chassot PG, Van der Linden P, Zaugg M, Mueller XM, Spahn DR. Off-pump coronary artery bypass surgery: physiology and anaesthetic management. Br J Anaesth 2004; 92: 400-413.
26. Knaapen P, Germans T, Knuuti J, Paulus WJ, Dijkmans PA, Allaart CP, et al. Myocardial Energetics and Efficiency: Current Status of the Noninvasive Approach. Circulation 2007; 115:918-927.
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29. De Simone R, Wolf I, Mottl-Link S, B?ttiger BW, Rauch H, Meinzer HP, et al. Intraoperative assessment of right ventricular volume and function. Eur J Cardiothorac Surg 2005; 27:988-993.
2. De Simone R, Wolf I, Mottl-Link S, B?ttiger BW, Rauch H, Meinzer HP, Hagl S. Intraoperative assessment of right ventricular volume and function. Eur J Cardiothorac Surg 2005; 27 (6): 988-993.
3. Steendijk P. Right ventricular function and failure: Methods, models, and mechanisms. Crit Care Med 2004; 32(4): 1087-1089.
4. Mathison M, Edgerton JR, Horswell JL, Akin JJ, Mack MJ. Analysis of hemodynamic changes during beating heart surgical procedures. Ann Thorac Surg 2000; 70(4): 1355-1360.
5. Porat E, Sharony R, Ivry S, Ozaki S, Meyns BP, Flameng WJ, Uretzky G. Hemodynamic changes and right heart support during vertical displacement of the beating heart. Ann Thorac Surg 2000; 69(4): 1188-1191.
6. Kwak YL, Oh YJ, Jung SM, Yoo KJ, Lee JH, Hong YW. Change in right ventricular function during off-pump coronary artery bypass graft surgery. Eur J Cardiothorac Surg 2004; 25(4): 572-577.
7. Tulner SA, Klautz RJ, Rijk-Zwikker GL, Engbers FH, Bax JJ, Baan J, van der Wall EE, Dion RA, Steendijk P. Perioperative assessment of left ventricular function by pressure-volume loops using the conductance catheter method. Anesth Analg 2003; 97(4): 950-957.
8. Kass DA, Maughan WL, Guo ZM, Kono A, Sunagawa K, Sagawa K. Comparative influence of load versus inotropic states on indexes of ventricular contractility: Experimental and theoretical analysis based on pressure-volume relationships. Circulation 1987; 76(6): 1422–1436.
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4. Katz AM. Influence of altered inotropy and lusitropy on ventricular pressure-volume loops. J AM Coll Cardiol 1988; 11(2): 438-445.
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