High-resolution spatial analysis of slow wave initiation and conduction in porcine gastric dysrhythmia

Abstract

Background: The significance of gastric dysrhythmias remains uncertain. Progress requires a better understanding of dysrhythmic behaviors, including the slow wave patterns that accompany or promote them. The aim of this study was to use high-resolution spatiotemporal mapping to characterize and quantify the initiation and conduction of porcine gastric dysrhythmias.

Methods: High-resolution mapping was performed on healthy fasted weaner pigs under general anesthesia. Recordings were made from the gastric serosa using flexible arrays (160-192 electrodes; 7.6mm spacing). Dysrhythmias were observed to occur in 14 of 97 individual recordings (from 8 of 16 pigs), and these events were characterized, quantified and classified using isochronal mapping and animation.

Key results: All observed dysrhythmias originated in the corpus and fundus. The range of dysrhythmias included incomplete conduction block (n=3 pigs; 3.9±0.5cpm; normal range: 3.2±0.2cpm) complete conduction block (n=3; 3.7±0.4cpm), escape rhythm (n=5; 2.0±0.3cpm), competing ectopic pacemakers (n=5, 3.7±0.1cpm) and functional re-entry (n=3, 4.1±0.4cpm). Incomplete conduction block was observed to self-perpetuate due to retrograde propagation of wave fragments. Functional re-entry occurred in the corpus around a line of unidirectional block. 'Double potentials' were observed in electrograms at sites of re-entry and at wave collisions.

Conclusions & inferences: Intraoperative multi-electrode mapping of fasted weaner healthy pigs detected dysrhythmias in 15% of recordings (from 50% of animals), including patterns not previously reported. The techniques and findings described here offer new opportunities to understand the nature of human gastric dysrhythmias.

Figure 1

Incomplete conduction block and wavelet rotation. A. Position diagram showing the PCB array over the greater curvature of the distal antrum and corpus (12 × 16 electrodes; inter-electrode spacing 7.6 mm; area 96 cm²). B. Electrogram sequence from eight electrodes positioned as shown in C, over 150 s. The dashed line shows onset of retrograde propagation in the displayed electrograms. C. Spatiotemporal maps relating to mapped area shown by the red rectangle in A, and the wavefronts a-d shown in B. The isochronal interval is 1 s. A normal wavefront (a) was followed by an incomplete conduction block (b), inducing a wavelet that rotated and subsequently activated the region distal the block. A self-sustaining cycle was then established, whereby the subsequent antegrade propagating collided with the retrograde propagating wavelet, inducing further incomplete blocks and wavelet rotations (c). After an initial unstable period of approximately 50 s, a relatively stable pattern was established (d) that continued for the remainder of the 150 s period, as shown in the electrograms in (B). (See also: animation Figure1.avi (supplementary material) of the same data. In the animation, successive wavefronts are colored red and blue to aid visualisation.)

Figure 2

Complete conduction block and escape. A. Position diagram showing the PCB array on the porcine fundus and upper corpus (12 × 16 electrodes; inter-electrode spacing 7.6 mm, 96 cm²). B. Electrogram sequence for 10 electrodes from the positions shown in C, over 250 s. The initial slow wave frequency was high at 4.3 ± 0.1 cpm. C. Spatiotemporal maps from the position indicated by the red rectangle in A and for the wavefronts a - j in B. The isochronal interval is 1 s. Cycles of normal activity are shown in a,c,d and e. Cycles b,f, and h show complete conduction block with a marked reduction in the activated area. In map g, an escape event occurred within a part of the field that was not activated in cycle f (local activation delay of 36 s). Similarly, map i shows retrograde propagation from an escape event arising distal to the mapped area, in a region not activated in cycle h, which collides with the antegrade wavefront (the dashed line indicates wavefront collision). In map (j), the retrograde activity is shown to entrain the entire mapped region, and this pattern was sustained for the remainder of the recording at frequency 3.7 ± 0.2 cpm. (See also: animation Figure2.avi (supplementary material) of the same data. In the animation, the normal antegrade wavefronts are colored blue and the ecoptic events are coloured red.)

Figure 3

Functional re-entry with double potentials. A. Position diagram showing the PCB array on the greater curvature of the fundus and corpus (12x16 electrodes; inter-electrode spacing 7.6 mm, 96 cm²). B. Electrogram sequence for 8 electrodes from the positions shown in D(a). Electrogram 1 is repeated below electrogram 8 to demonstrate continuity in propagation during the re-entrant cycle. C. Electrograms from another set of 5 electrodes from the positions shown in D(b), demonstrating double potentials. The two deflections corresponded to the antegrade and retrograde arms of re-entry occurring on opposite sides of the block line (line and dashed line). D. Spatiotemporal maps from the position indicated by the red rectangle A, and corresponding to the overlapping time periods (a-d) indicated in B. The isochronal interval is 1 s. Stable re-entry (4.1 ± 0.2 cpm) occurred around a line of functional block for several cycles, and competed with continuing antegrade wavefronts entering the top of the mapped field, causing collisions or merging. The re-entry spontaneously terminated 62 s into the recording, with reversion to normal antegrade activity. (See also: animation Figure3.avi (supplementary material) of the same data. In the animation, the normal antegrade wavefronts are colored blue and the re-entrant activities are coloured red.)

Figure 4

Multiple competing ectopic wavefronts. A. Position diagram showing the PCB array on the anterior serosal surface (8 × 20 electrodes; inter-electrode distance 7.6 mm; 77 cm²). B,C. Electrograms corresponding to 100 s of recordings from the 6 electrodes shown in D(a) and the subsequent 200 s from the 8 electrodes shown in D(g). D. Spatiotemporal maps for wave sequences a-j from B and C. The isochronal interval is 2 s. Sporadic, high-frequency (3.5 to 4.1 cpm) wavefront initiation from 1–3 ectopic pacemaker sites caused abnormal and irregular activity, including retrograde propagation (e.g., maps d,e), wavefront collisions (a-g and i), merging wavefronts (a-g and i) and conduction blocks (d-g). Map h also shows a single escape activity, which followed a quiescent interval of 26 s. See also: animation Figure4.avi (supplementary material) of time period 0–120s from the same data.

Figure 5

Stable colliding wavefronts from competing ectopic events. A. Position diagram showing the PCB array on the upper anterior serosa (8 × 20 electrodes; inter-electrode distance 7.6 mm: area 77 cm²). B. Electrograms corresponding to the 8 electrodes positioned as shown in C. Spatiotemporal maps showing four cycles of wave collision. The isochronal interval is 2 s. The two panels (–2) in each box (a-d) show alternate activation of the mapped field from the two distinct initiation sites. Each wave collides with the refractory tail of the previous event, causing a repeating pattern of abnormal propagation. Double potentials are evident in electrodes 4–5, corresponding to the boundary zone between the two colliding wavefronts, suggesting a irregular and heterogeneous area of tissue activation occurred in this region. (See also: animation Figure5.avi (supplementary material) of the same data. In the animation, the wavefronts emerging from the two distinct pacemaker sites are colored separately.)