The induction of reentry in cardiac tissue. The missing link: How electric fields alter transmembrane potential.

Chaos (Woodbury, N.Y.) · 1998 · Mixed · Low evidence

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MixedLow evidencePaper 4049

Study snapshot

PublicationChaos (Woodbury, N.Y.) · 1998

Study typereview

Reported directionMixed

Evidence ratingLow

Abstract

This review examines the initiation of reentry in cardiac muscle by strong electric shocks. Specifically, it concentrates on the mechanisms by which electric shocks change the transmembrane potential of the cardiac membrane and create the physiological substrate required by the critical point theory for the initiation of rotors. The mechanisms examined include (1) direct polarization of the tissue by the stimulating current, as described by the one-dimensional cable model and its two- and three-dimensional extensions, (2) the presence of virtual anodes and cathodes, as described by the bidomain model with unequal anisotropy ratios of the intra- and extracellular spaces, (3) polarization of the tissue due to changing orientation of cardiac fibers, and (4) polarization of individual cells or groups of cells by the electric field ("sawtooth potential"). The importance of these mechanisms in the initiation of reentry is examined in two case studies: the induction of rotors using successive stimulation with a unipolar electrode, and the induction of rotors using cross-field stimulation. These cases reveal that the mechanism by which a unipolar stimulation induces arrhythmias can be explained in the framework of the bidomain model with unequal anisotropy ratios. In contrast, none of the examined mechanisms provide an adequate explanation for the induction of rotors by cross-field stimulation. Hence, this study emphasizes the need for further experimental and theoretical work directed toward explaining the mechanism of field stimulation. (c) 1998 American Institute of Physics.

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AI evidence extraction

Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.

Study typereview

Effect directionmixed

PopulationNot supplied

Sample sizeNot supplied

ExposureNot supplied

Evidence strengthLowConfidence: 74% · Peer reviewed: yes

Main findings

The review discusses multiple mechanisms by which strong electric shocks can alter cardiac transmembrane potential and potentially create conditions for reentry/rotor initiation. Case studies suggest unipolar stimulation–induced arrhythmias can be explained within a bidomain model with unequal anisotropy ratios, whereas the reviewed mechanisms do not adequately explain rotor induction by cross-field stimulation.

Outcomes measured

Changes in cardiac transmembrane potential due to electric shocks
Initiation of reentry/rotors (arrhythmia induction)
Mechanistic explanations (cable model, bidomain model, virtual electrodes, fiber orientation effects, sawtooth potential)

Limitations

Narrative review; no primary experimental sample size reported in abstract
For cross-field stimulation, reviewed mechanisms are stated to be inadequate, indicating incomplete mechanistic explanation

View raw extracted JSON

{
  "study_type": "review",
  "exposure": {
    "band": null,
    "source": "strong electric shocks / electric field stimulation (cardiac tissue)",
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": null
  },
  "population": null,
  "sample_size": null,
  "outcomes": [
    "Changes in cardiac transmembrane potential due to electric shocks",
    "Initiation of reentry/rotors (arrhythmia induction)",
    "Mechanistic explanations (cable model, bidomain model, virtual electrodes, fiber orientation effects, sawtooth potential)"
  ],
  "main_findings": "The review discusses multiple mechanisms by which strong electric shocks can alter cardiac transmembrane potential and potentially create conditions for reentry/rotor initiation. Case studies suggest unipolar stimulation–induced arrhythmias can be explained within a bidomain model with unequal anisotropy ratios, whereas the reviewed mechanisms do not adequately explain rotor induction by cross-field stimulation.",
  "effect_direction": "mixed",
  "limitations": [
    "Narrative review; no primary experimental sample size reported in abstract",
    "For cross-field stimulation, reviewed mechanisms are stated to be inadequate, indicating incomplete mechanistic explanation"
  ],
  "evidence_strength": "low",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "cardiac tissue",
    "electric shocks",
    "electric fields",
    "transmembrane potential",
    "reentry",
    "rotors",
    "arrhythmia",
    "bidomain model",
    "virtual anodes",
    "virtual cathodes",
    "anisotropy",
    "cross-field stimulation",
    "unipolar stimulation"
  ],
  "suggested_hubs": []
}

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AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.

Identifiers and source

DOI: 10.1063/1.166298
PubMed: 12779722

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