Amplitude changes during ventricular fibrillation: A mechanistic insight

Jane Caldwell, Jane C. Caldwellf, Francis L. Burton, Stuart M. Cobbe, Godfrey L. Smith

    Research output: Contribution to journalArticlepeer-review

    Abstract

    Introduction: 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. Methods and Results: 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 60s of VF, perfusion was either maintained, global ischemia produced by low-flow (6 mL/min), or solution [K +] o 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 (LVvs. RV; 33 ±5 vs. 63 ±8%, p
    Original languageEnglish
    Article numberArticle 147
    JournalFrontiers in Physiology
    Volume3
    DOIs
    Publication statusPublished - 2012

    Keywords

    • ECG
    • Floating microelectrode
    • Ischemia
    • Optical mapping
    • Ventricular fibrillation

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