Yannopoulos Demetris, Zviman Menekhem, Castro Valeria, Kolandaivelu Aravindan, Ranjan Ravi, Wilson Robert F, Halperin Henry R
Cardiology Division, University of Minnesota, Mayo Mail Code 508, 420 Delaware St SE, Minneapolis, MN 55455, USA.
Circulation. 2009 Oct 6;120(14):1426-35. doi: 10.1161/CIRCULATIONAHA.109.848424. Epub 2009 Sep 21.
We investigated the effects of intra-cardiopulmonary resuscitation (CPR) hypothermia with and without volume loading on return to spontaneous circulation and infarction size in an ischemic model of cardiac arrest.
Using a distal left anterior descending artery occlusion model of cardiac arrest followed by resuscitation with a total of 120 minutes of occlusion and 90 minutes of reperfusion, we randomized 46 pigs into 5 groups and used myocardial staining to define area at risk and myocardial necrosis. Group A had no intervention. Immediately after return of spontaneous circulation, group B received surface cooling with cooling blankets and ice. Group C received intra-CPR 680+/-23 mL of 28 degrees C 0.9% normal saline via a central venous catheter. Group D received intra-CPR 673+/-26 mL of 4 degrees C normal saline followed by surface cooling after return of spontaneous circulation. Group E received intra-CPR and hypothermia after return of spontaneous circulation with an endovascular therapeutic hypothermia system placed in the right atrium and set at a target of 32 degrees C. Intra-CPR volume loading with room temperature (group C) or iced saline (group D) significantly (P<0.05) decreased coronary perfusion pressure (group C, 12.8+/-4.78 mm Hg; group D, 14.6+/-9.9 mm Hg) compared with groups A, B, and E (20.6+/-8.2, 20.1+/-7.8, and 21.3+/-12.4 mm Hg). Return of spontaneous circulation was significantly improved in group E (9 of 9) compared with groups A plus B and C (10 of 18 and 1 of 8). The percent infarction to the area at risk was significantly reduced with intra-CPR hypothermia in groups D (24.3+/-4.2%) and E (4+/-3.4%) compared with groups A (72+/-5.1%) and B (67.3+/-4.2%).
Intra-CPR hypothermia significantly reduces myocardial infarction size. Elimination of volume loading further improves outcomes.
我们在心脏骤停缺血模型中研究了心肺复苏期间低温以及低温联合容量负荷对自主循环恢复和梗死面积的影响。
采用左前降支远端闭塞心脏骤停模型,随后进行复苏,共闭塞120分钟,再灌注90分钟。我们将46头猪随机分为5组,并用心肌染色来确定危险区域和心肌坏死情况。A组未进行干预。自主循环恢复后,B组立即使用降温毯和冰块进行体表降温。C组通过中心静脉导管在心肺复苏期间输注680±23毫升28℃的0.9%生理盐水。D组在心肺复苏期间输注673±26毫升4℃生理盐水,自主循环恢复后进行体表降温。E组在自主循环恢复后通过置于右心房的血管内治疗性低温系统进行心肺复苏期间低温治疗,目标温度设定为32℃。与A、B、E组(分别为20.6±8.2、20.1±7.8和21.3±12.4毫米汞柱)相比,心肺复苏期间输注室温生理盐水(C组)或冰盐水(D组)显著(P<0.05)降低了冠状动脉灌注压(C组为12.8±4.78毫米汞柱;D组为14.6±9.9毫米汞柱)。与A加B组和C组(分别为18头中的10头和8头中的1头)相比,E组(9头中的9头)的自主循环恢复情况显著改善。与A组(72±5.1%)和B组(67.3±4.2%)相比,D组(24.3±4.2%)和E组(4±3.4%)在心肺复苏期间低温治疗后梗死面积占危险区域面积的百分比显著降低。
心肺复苏期间低温显著减小心肌梗死面积。消除容量负荷可进一步改善预后。