Age-dependent and 'pathologic' changes in ICG waveforms resulting from superposition of pre-ejection and ejection waves.

Impedance cardiography (ICG) is a popular bioimpedance application used for the non-invasive evaluation of the left ventricular stroke volume and contractility. It implies the correct determination of ejection start and end points and the amplitudes of certain peaks in a differentiated impedance cardiogram. An accurate identification of ejection onset by ICG is often problematic, especially in cardiologic patients, due to the peculiar character of the waveforms. A simple theoretical model was employed to test the consequences of the hypothesis that two major processes can contribute to the formation of an impedance systolic wave: (1) the pre-ejection changes in heart geometry and the surrounding vessels produced by ventricular contraction during the isovolumic phase, and (2) the expansion of aorta and adjacent arteries during the ejection per se. The former process initiates the pre-ejection wave while the latter triggers the ejection wave, both of which contribute to the impedance pulse waves associated with the heartbeats. A new two-bell model predicts a potential mechanism responsible for the abnormal shapes of ICG derivative dZ/dt due to the presence of the pre-ejection waves and explains the related errors in systolic time intervals and amplitude parameters derived from such ICG waveforms. It also advances an alternative viewpoint on the nature of the dZ/dt B-point notch. An appropriate decomposition method opens a promising way to avoid the masking effects of these waves and to correctly determine the onset of ejection as well as the corresponding peak amplitudes from the 'pathologically shaped' ICG signals.