Huang Jian, Rogers Jack M, Killingsworth Cheryl R, Singh Karan P, Smith William M, Ideker Raymond E
Cardiac Rhythm Management Laboratory, Volker Hall B140, 1670 University Blvd., Birmingham, AL 35294-0019, USA.
Am J Physiol Heart Circ Physiol. 2004 Mar;286(3):H1193-200. doi: 10.1152/ajpheart.00773.2003.
Although resuscitation for sudden cardiac arrest attempts are frequently not instituted for several minutes after the onset of ventricular fibrillation (VF), previous mapping studies have examined only the first 40 s of VF or have involved isolated perfused hearts that did not become ischemic during VF. We applied quantitative pattern analysis to mapping data throughout the first 10 min of VF acquired from a 21 x 24 unipolar electrode array located on the ventricular epicardium of six open-chest dogs. The following twelve descriptors were continuously quantified: 1) number of wavefronts, 2) incidence of reentry, 3) wavefront propagation velocity, 4) incidence of breakthrough/focus, 5) incidence of block, 6) mean area activated by the wavefronts, 7) wavefront fractionations, 8) wavefront collisions, 9) multiplicity index, 10) repeatability, 11) negative peak rate of voltage change, and 12) peak frequency of activation. Cluster analysis of these descriptors divided VF into five stages (stages i-v). The values of most descriptors (except block and breakthrough incidence) increased during stage i (1-11 s after VF induction) and maintained high values with rapid dynamic fluctuations during stage ii (12-62 s). Descriptors changed quickly to values indicating greater organization during stage iii (63-86 s), decreased steadily during stage iv (87-310 s), and approached zero during stage v (311-600 s). There was a high incidence of reentry just before, during, and after stage iii. In conclusion, during the first 10 min, VF can be divided into five stages according to the evolution of electrophysiological characteristics. All of the parameters show a rapid deterioration during VF, except for a temporary reversal approximately 1 min after induction when activation briefly became more organized. Thus a quantitative description of activation does not uniformly decrease as VF progresses, but undergo rapid changes and exhibit a brief interval of increased organization after approximately 1 min of VF. Further studies are warranted to determine whether these changes, particularly the increased organization of stage iii, have clinical consequences, such as an alteration in defibrillation efficacy.
尽管在心室颤动(VF)发作后的几分钟内常常不会立即进行心脏骤停复苏尝试,但以往的标测研究仅考察了VF发作后的前40秒,或者所涉及的是在VF期间未发生缺血的离体灌注心脏。我们将定量模式分析应用于从位于6只开胸犬心室心外膜的21×24单极电极阵列获取的VF发作最初10分钟内的标测数据。连续定量了以下12个描述符:1)波前数量,2)折返发生率,3)波前传播速度,4)突破/灶点发生率,5)阻滞发生率,6)波前激活的平均面积,7)波前碎裂,8)波前碰撞,9)多重性指数,10)重复性,11)电压变化的负峰值速率,以及12)激活的峰值频率。对这些描述符进行聚类分析将VF分为五个阶段(阶段i - v)。大多数描述符(除阻滞和突破发生率外)的值在阶段i(VF诱导后1 - 11秒)升高,并在阶段ii(12 - 62秒)保持高值且伴有快速的动态波动。描述符在阶段iii(63 - 86秒)迅速变为表明组织性增强的值,在阶段iv(87 - 310秒)稳步下降,并在阶段v(311 - 600秒)接近零。在阶段iii之前、期间和之后折返发生率都很高。总之,在最初10分钟内,VF可根据电生理特征的演变分为五个阶段。除了在诱导后约1分钟激活短暂变得更有组织时出现暂时逆转外,所有参数在VF期间都迅速恶化。因此,激活的定量描述并非随VF进展而均匀下降,而是经历快速变化,并在VF约1分钟后表现出短暂的组织性增强间隔。有必要进行进一步研究以确定这些变化,特别是阶段iii组织性增强是否具有临床后果,如除颤效果的改变。