A Frequency-Domain Framework for Cardiovascular Power Distribution

preprint OA: closed CC-BY-4.0
📄 Open PDF Full text JSON View at publisher

Abstract

Traditional cardiovascular models emphasize time-domain dynamics of blood flow and pressure, such as cardiac output and mean arterial pressure. However, the pulsatile nature of blood flow contains rich frequency content that interacts uniquely with organ-specific vascular properties. Drawing on wireless power transfer principles from electrical engineering, we propose a frequency-domain framework where the heart functions as a multi-frequency power source, generating a complex pressure waveform with multiple harmonics, and organs act as frequency-tuned loads, selectively absorbing power at their characteristic vascular resonance frequencies. This model introduces a frequency-division multiplexing analogy for cardiovascular power distribution, offering insights into physiological regulation, disease mechanisms, and therapeutic strategies. We present the theoretical foundation, mathematical models, physiological evidence, and potential clinical applications, supported by preliminary simulation results.
Full text 1,102 characters · extracted from oa-doi-fallback · click to expand
Abstract Traditional cardiovascular models emphasize time-domain dynamics of blood flow and pressure, such as cardiac output and mean arterial pressure. However, the pulsatile nature of blood flow contains rich frequency content that interacts uniquely with organ-specific vascular properties. Drawing on wireless power transfer principles from electrical engineering, we propose a frequency-domain framework where the heart functions as a multi-frequency power source, generating a complex pressure waveform with multiple harmonics, and organs act as frequency-tuned loads, selectively absorbing power at their characteristic vascular resonance frequencies. This model introduces a frequency-division multiplexing analogy for cardiovascular power distribution, offering insights into physiological regulation, disease mechanisms, and therapeutic strategies. We present the theoretical foundation, mathematical models, physiological evidence, and potential clinical applications, supported by preliminary simulation results. Competing Interest Statement The authors have declared no competing interest.

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

Ask this paper AI returns verbatim quotes from the full text · source: oa-doi-fallback

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Citation neighborhood (no data yet)

We don't have any in-corpus citations linked to this paper yet. This is a recent paper (2025) — citers typically take a year or two to land, and the OpenAlex reference graph may still be filling in.

Source provenance

europepmc
last seen: 2026-05-20T01:45:00.602351+00:00
unpaywall
last seen: 2026-06-02T02:00:03.124865+00:00
License: CC-BY-4.0