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Clinical Investigation:
C. Schmidt, G. Theilmeier, H. Van Aken, P. Korsmeier, S. P. Wirtz, E. Berendes, A. Hoffmeier, and A. Meissner
Comparison of electrical velocimetry and transoesophageal Doppler echocardiography for measuring stroke volume and cardiac output{dagger}
Br. J. Anaesth. 2005; 0: aei224v1 [Abstract] [PDF]
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[Read E-letter] Is this new, and clinically useful?
Gordon B Drummond   (19 November 2005)

Is this new, and clinically useful? 19 November 2005
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Gordon B Drummond,
Senior Lecturer
Department of Anaesthesia, Critical Care, and Pain Medicine, Edinburgh University

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Re: Is this new, and clinically useful?

The study conducted by Schmidt and co-workers 1 represents another step in the genesis of equations adapted to manipulate thoracic impedance changes to estimate mean aortic blood flow. With this measure of flow, stroke volume can be calculated by also measuring cardiac ejection time, and hence cardiac output calculated if one of a number of scaling factors is incorporated. Good accounts of the development of these “fudge factors” are provided by previous authors, describing how the factors attempt to fit the body size, shape, and composition to the electrical signal.2;3 One of these modifications was that of Bernstein4 who went on to “tweak” the maximum impedance change by using a square root to improve the relationship with cardiac output measured by thermodilution.5

The description given of the details of the apparently new method used by the authors is confusing. They state that the signal is transformed from the ohmic equivalent of mean flow acceleration into an equivalent of mean aortic blood flow velocity. Put more simply, this could be stated: a signal indicating the acceleration of blood is transformed into a signal that indicates blood velocity. In mathematical terms, this is the transformation of an acceleration (rate of change of velocity) in to a velocity. This is an integration: not what the stated equation shows.

There is no doubt that the signal is a complex one: for example Wtorek stated “main contributions to (the impedance) signal come from ventricles, atria, aorta, and lungs. The relations between these components have been found to be dependent nonlinearly on spatial conductivity distribution. As a result, reliable and reproducible measurements of stroke volume (SV) using ICG are impossible.”6, a view that was supported by others: “the effect of ventricular contraction is opposite to that of the other changes in systole: the expansion of major vessels, decrease in blood resistivity due to increased blood flow velocity, and decrease in lung resistivity due to increased blood perfusion. Ventricular contraction, the only factor that tends to increase systolic impedance, has a larger effect than any of the other factors.”7 Subsequent work by Wtorek suggests that flowing blood may change its resistance8 but this of itself cannot be used to explain the impedance cardiograph signal. It is thus highly misleading to describe this phenomenon as the basis for the measurements made by Schmidt and colleagues.

In their paper they state: “this new method is based on the properties of pulsatile blood flow and the alignment of erythrocytes from a random orientation prior to aortic valve opening….towards an orientation with their disc-shaped bodies parallel to the axial blood flow ~60 ms after the opening of the aortic valve. The parallel alignment of the erythrocytes produces a change in the resisitivity of blood in the aorta, which is equivalent to the mean aortic blood flow acceleration”. Sadly this crucial and surprising statement is substantiated by citing an US patent, which is not readily available, at least not without paying a fee. The patent in question (US patent 6,511,438 B2) bears the names of Bernstein and Osypka. Bernstein has published widely on the impedance method, predominantly on modifications of the equation, as noted above, and Osypka less so.9-11 However I am surprised that Schmidt and his co- workers consider that this patent is a sufficiently substantial support for this claim. Cynics might suspect that this new explanation of the well -know phenomena of thoracic impedance changes, might perhaps be a way of obtaining a fresh patent. I feel that the real “improvement” in fitting the well-known impedance derivative is more likely to stem from the new (ish) fudge factor of the exponent of “less than 1”. Schmidt and colleagues should provide a more thorough explanation of exactly how the “basic equation has been modified profoundly” as they claim: it’s not very different from those used before, apart from the exponent. I fail to understand how the method is thus “likely to provide more accurate information”, as they claim.

In fact, I would hesitate to make clinical decisions using a method where if a patients cardiac output were 3 litre/min. the reading from my monitor might be anything from 2 and 4.4 litre/min. Is this a commonly “clinically acceptable accuracy”? Finally, the authors should test for any trend in the comparison they made: their plot in figure 3B of their paper suggests that when cardiac output is small, the impedance measurement is too small.

G.B.Drummond Edinburgh UK g.b.drummond@ed.ac.uk References

(1) Schmidt C, Theilmeier G, Van Aken H, Korsmeier P, Wirtz SP, Berendes E et al. Comparison of electrical velocimetry and transoesophageal Doppler echocardiography for measuring stroke volume and cardiac output. British Journal of Anaesthesia 2005; 95, 603-10.

(2) Van de Water JM, Miller TW, Vogel RL, Mount BE, Dalton ML. Impedance cardiography - The next vital sign technology? Chest 2003; 123, 2028-33.

(3) Critchley LAH. Impedance cardiography - The impact of new technology. Anaesthesia 1998; 53, 677-84.

(4) Bernstein DP. A New Stroke Volume Equation for Thoracic Electrical Bioimpedance - Theory and Rationale. Critical Care Medicine 1986; 14, 904-9.

(5) Bernstein DP, Lemmens HJM. Stroke volume equation for impedance cardiography. Medical & Biological Engineering & Computing 2005; 43, 443-50.

(6) Wtorek J. Relations between components of impedance cardiogram analyzed by means of finite element model and sensitivity theorem. Annals of Biomedical Engineering 2000; 28, 1352-61.

(7) Wang YQ, Haynor DR, Kim Y. A finite-element study of the effects of electrode position on the measured impedance change in impedance cardiography. Ieee Transactions on Biomedical Engineering 2001; 48, 1390- 401.

(8) Wtorek J, Polinski A. The contribution of blood-flow-induced conductivity changes to measured impedance. Ieee Transactions on Biomedical Engineering 2005; 52, 41-9.

(9) Gersing E, Osypka M. Eit Using Magnitude and Phase in An Extended Frequency-Range. Physiological Measurement 1994; 15, A21-A28.

(10) Osypka M, Gersing E. Tissue Impedance Spectra and the Appropriate Frequencies for Eit. Physiological Measurement 1995; 16, A49- A55.

(11) Gersing E, Hofmann B, Osypka M. Influence of changing peripheral geometry on electrical impedance tomography measurements. Medical & Biological Engineering & Computing 1996; 34, 359-61.

Conflict of Interest:

None declared