gms | German Medical Science

33. Internationale Konferenz für Elektrokardiographie

Internationale Konferenz für Elektrokardiographie

Myocardial Oedema Estimated By Bioimpedance And Coronary Blood Flow Changes During Ischema

Meeting Abstract

Suche in Medline nach

  • corresponding author presenting/speaker I. Rätsep - Smartimplant., Tallinn, Estland
  • A. Kink - Smartimplant., Tallinn, Estland
  • M. Min - Tallinn Technical University, Tallinn, Estland
  • T. Parve - Tallinn Technical University, Tallinn, Estland

33rd International Congress on Electrocardiology. Cologne, 28.06.-01.07.2006. Düsseldorf, Köln: German Medical Science; 2007. Doc06ice072

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/ice2006/06ice072.shtml

Veröffentlicht: 8. Februar 2007

© 2007 Rätsep et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Question: In many clinical situations even otherwise healthy heart is a subject of low arterial pressure leading to coronary hypoperfusion and consequently to myocardial ischemia. Relationship between ischemic myocardial oedema and coronary perfusion is controversial. In our experimentwe will demonstrate how to estimate coronary blood flow (CBF) using electrical bioimpedance (EBI).

Method Used: Isolated human size animal heart is used in experimental setup where a retrograde perfusion via aortic root using animals own oxygenated blood is enabled. Ischemia is induced by low perfusion pressure. During measurements, the coronary perfusion pressure was kept constant (30 mmHg). CBF was dynamically regulated to keep perfusion pressure constant. The CBF depends on changes in heart vascular resistance during the experiment. Myocardial oedema was measured recording left ventricle EBI values (both, real and imaginary parts). For impedance measurements two pairs of cold electrodes were fixed to myocardial wall, and a 1kHz and 10ìA excitation current was applied to calculate the bioimpedance from the mV range voltage response.

Results: During a measurement period, an observed contractile function was seriously damaged until cardiac arrest. Typically, rapid spontaneous heart rate was initially supported and later fully replaced by external pacing. The resistive (real) part of myocardial impedance has an increasing trend which correlates left ventricle oedema, and the perfusion flow has a decreasing trend. In the Figure 1 [Fig. 1], a negatively acting feedback to oedema through the perfusion reduction to myocardial tissue is represented.

Conclusion: Ischemia induces myocardial oedema leading to gradual reduction in CBF. Decrease in CBF results further ischemia in a vicious circle manner. This study has revealed clear relatioship between CBF and oedema presenting a number of potential applications for the future. The bioimpedance method is sensitive to estimate myocardial swelling and CBF.