Caldwell Jane C, Burton Francis L, Cobbe Stuart M, Smith Godfrey L
Institute of Cardiovascular and Medical Sciences, University of Glasgow Glasgow, UK.
Front Physiol. 2012 May 23;3:147. doi: 10.3389/fphys.2012.00147. eCollection 2012.
Clinically in ventricular fibrillation (VF), ECG amplitude, and frequency decrease as ischemia progresses and predict defibrillation success. In vitro ECG amplitude declines without ischemia, independent of VF frequencies. This study examines the contribution of cellular electrical activity and global organization to ECG amplitude changes during VF.
Rabbit hearts were Langendorff-perfused (40 mL/min, Tyrode's solution) and loaded with RH237. During VF, ECG, and epicardial optical action potentials were recorded (photodiode array; 256 sites, 15 mm × 15 mm). After 60 s of VF, perfusion was either maintained, global ischemia produced by low-flow (6 mL/min), or solution K(+) raised to 8 mM. Peak-to-peak amplitude was determined for all signals. During VF, in control, ECG amplitude decreased to a steady-state (∼57% baseline), whereas in low-flow steady-state was not reached with the amplitude continuing to fall to 33% of baseline by 600 s. Optically, LV amplitude declined more than RV, reaching significance in control (LV vs. RV; 33 ± 5 vs. 63 ± 8%, p < 0.01). During VF in 8 mM K(+), amplitude changes were more complex; ECG amplitude increased with time (105 ± 13%), whilst LV amplitude decreased (60 ± 15%, p < 0.001). Microelectrode studies showed amplitude reduction in control and 8 mM K(+) (to ∼79 and ∼93% baseline, respectively). Evaluation of electrical coordination by cross-correlation of optical signals showed as VF progressed coordination reduced in control (baseline 0.36 ± 0.02 to 0.28 ± 0.003, p < 0.01), maintained in low-flow (0.41 ± 0.03 to 0.37 ± 0.005, p = NS) and increased in 8 mM K(+) (0.36 ± 0.02 to 0.53 ± 0.08, p < 0.05).
ECG amplitude decline in VF is due to a combination of decreased systolic activation at the cellular level and increased desynchronization of inter-cellular electrical activity.
在临床上，心室颤动（VF）时，随着缺血进展，心电图（ECG）幅度和频率降低，且可预测除颤成功率。在体外，ECG幅度在无缺血情况下下降，与VF频率无关。本研究探讨细胞电活动和整体组织结构对VF期间ECG幅度变化的作用。
兔心采用Langendorff灌注（40毫升/分钟，台氏液）并加载RH237。在VF期间，记录ECG和心外膜光学动作电位（光电二极管阵列；256个位点，15毫米×15毫米）。VF持续60秒后，要么维持灌注，要么通过低流量（6毫升/分钟）造成整体缺血，或将细胞外钾离子浓度[K⁺]ₒ提高到8毫摩尔。测定所有信号的峰峰值幅度。在VF期间，对照组中，ECG幅度降至稳态（约为基线的57%），而在低流量组中未达到稳态，到600秒时幅度持续降至基线的33%。从光学角度看，左心室（LV）幅度下降幅度大于右心室（RV），在对照组中具有显著性差异（LV对RV；33±5%对63±8%，p<0.01）。在8毫摩尔[K⁺]ₒ的VF期间，幅度变化更为复杂；ECG幅度随时间增加（105±13%），而LV幅度下降（60±15%，p<0.001）。微电极研究显示对照组和8毫摩尔[K⁺]ₒ时幅度降低（分别降至基线的约79%和约93%）。通过光学信号互相关评估电协调性显示，随着VF进展，对照组电协调性降低（基线0.36±0.02降至0.28±0.003，p<0.01），低流量组维持（0.41±0.03降至0.37±0.005，p=无显著性差异），8毫摩尔[K⁺]ₒ时增加（0.36±0.02升至0.53±0.08，p<0.05）。
VF时ECG幅度下降是由于细胞水平收缩期激活减少和细胞间电活动去同步化增加共同所致。
