Evolution of activation patterns during long-duration ventricular fibrillation in pigs

Abstract

Quantitative analysis has demonstrated five temporal stages of activation during the first 10 min of ventricular fibrillation (VF) in dogs. To determine whether these stages exist in another species, we applied the same analysis to the first 10 min of VF recorded in vivo from two 504-electrode arrays, one each on left anterior and posterior ventricular epicardium in six anesthetized pigs. The following descriptors were continuously quantified: 1) number of wavefronts, 2) wavefront fractionations, 3) wavefront collisions, 4) repeatability, 5) multiplicity index, 6) wavefront conduction velocity, 7) activation rate, 8) mean area activated by the wavefronts, 9) negative peak rate of voltage change, 10) incidence of breakthrough/foci, 11) incidence of block, and 12) incidence of reentry. Cluster analysis of these descriptors divided VF into four stages (stages i-iv). The values of most descriptors increased during stage i (1-22 s after VF induction), changed quickly to values indicating greater organization during stage ii (23-39 s), decreased steadily during stage iii (40-187 s), and remained relatively unchanged during stage iv (188-600 s). The epicardium still activated during stage iv instead of becoming silent as in dogs. In conclusion, during the first 10 min, VF activation can be divided into four stages in pigs instead of five stages as in dogs. Following a 16-s period during the first minute of VF when activation became more organized, all parameters exhibited progressive decreased organization. Further studies are warranted to determine whether these changes, particularly the increased organization of stage ii, have clinical consequences, such as alteration in defibrillation efficacy.

Fig. 1.

Diagrams of the heart indicating the location of the mapping electrodes on the anterior left ventricular (LV) surface (A) and the posterior LV surface (B). Black dots represent the individual plaque recording electrodes. Directions of the x- and y-components of the conduction velocity vectors of the ventricular fibrillation (VF) wavefronts are indicated. PDA, posterior descending artery; LAD, left anterior descending artery; LVA, left ventricular apex.

Fig. 2.

Snapshots of activation during stages i-ii (A) and iii-iv (B) of VF in 1 pig. Each colored pixel is an electrode site at which the rate of voltage change (dV/dt) is less than or equal to −0.3V/s sometime during the 15-ms interval represented by each frame. The numbers show the time from the beginning of each VF stage. Different-colored pixels indicate distinct isolated wavefronts. Examples of wavefront fractionation (A: stage i, anterior, 195–210 ms) and collision (A: stage i, anterior, 165–180 ms) are indicated by arrows. Recordings from the same electrode are shown below the activation maps for each stage. Wavefront during stage i on posterior surface propagated in one direction for four cycles immediately after VF induction and then degenerated into chaotic pattern (not shown).

Fig. 3.

Evolution of the number of epicardial wavefronts during the first 600 s of VF for the anterior LV in pig (red), the posterior LV in pig (green), and the anterior LV in dog (black). Data in this and Figs. 4–9 are means from 6 pigs and 6 dogs. Short vertical lines demarcate the times of transition from one stage to the next for the 4 stages in pigs and the 5 stages in dogs. A short stage of increased organization is present (stage ii in pigs and stage iii in dogs) in which the number of wavefronts is briefly decreased. For this and Figs. 4–10, please see the text for additional description.

Fig. 4.

Evolution of wavefront fractionation (A) and collision (B) during VF.

Fig. 5.

Evolution of multiplicity (A) and repeatability (B) during VF.

Fig. 6.

Mean conduction velocity (A) and mean activation rate (B) during VF.

Fig. 7.

Evolution of the area swept out by each wavefront (A) and the peak negative dV/dt (B) during VF.

Fig. 8.

Evolution of wavefront breakthrough or foci on the epicardium (A) and block incidence (B) during VF.

Fig. 9.

Incidence of wavefront families that formed reentrant pathways during VF.

Fig. 10.

Decomposition of the weighted velocity vectors into x- and y-components over the anterior (A) and posterior (B) LV with x-velocity parallel to the atrioventricular groove and y-velocity from apex to base.