Doppler ultrasound, ultrasound M-mode analysis, fetal electrocardiography, and fetal magnetocardiography are methods by which the fetal heart can be monitored non-invasively. In this paper, they are evaluated and compared. Customarily, it is solely the fetal heart rate, which is monitored using the Doppler ultrasound technique since it is both simple to use and cheap. However, this method inherently produces an averaged heart rate and therefore cannot give the beat-to-beat variability. Fetal electrocardiography has similar advantages, but in addition offers the potential for monitoring beat-to-beat variability and performing electrocardiogram morphological analysis. Its disadvantage is that its reliability is only 60%, although it is the only technique that offers truly long-term ambulatory monitoring. Ultrasound M-mode analysis allows a estimation of atrial and ventricular coordination, as well as an estimation of PR intervals. Bradycardias, supraventricular tachycardias, extra systoles are readily diagnosed using this method although timing will be inaccurate. Fetal magnetocardiograms can be detected reliably and used for accurate beat-to-beat measurements and morphological analysis. Consequently, they can be used for the classification of arrhythmias and the diagnosis of a long QT syndrome and some congenital heart diseases.

In order to relate the structure of cardiac tissue to its passive electrical conductivity, we created a geometrical model of cardiac tissue on a cellular scale that encompassed myocytes, capillaries, and the interstitial space that surrounds them. A special mesh generator was developed for this model to create realistically shaped myocytes and interstitial space with a controlled degree of variation included in each model. In order to derive the effective conductivities, we used a finite element model to compute the currents flowing through the intracellular and extracellular space due to an externally applied electrical field. The product of these computations were the effective conductivity tensors for the intracellular and extracellular spaces. The simulations of bi-domain conductivities for healthy tissue resulted in an effective intracellular conductivity of 0.16S/m (longitudinal) and 0.005 S/m (transverse) and an effective extracellular conductivity of 0.21S/m (longitudinal) and 0.06 S/m (transverse). The latter values are within the range of measured values reported in literature. Furthermore, we anticipate that this method can be used to simulate pathological conditions for which measured data is far more sparse.

ST depression at the epicardium appears over a lateral boundary between healthy and ischemic tissue.

We quantify and provide biophysical explanations for some aspects of the relationship between the bidomain conductivities and ST-segment epicardial potentials that result from subendocardial ischemia. We performed computer simulations of ischemia with a realistic whole heart model. The model included a patch of subendocardial ischemic tissue of variable transmural thickness with reduced action potential amplitude. We also varied both intracellular and extracellular conductivities of the heart and the conductivity of ventricular blood in the simulations. At medium or high thicknesses of transmural ischemia (i.e., at least 40% thickness through the heart wall), a consistent pattern of two minima of the epicardial potential over opposite sides of the boundary between healthy and ischemic tissue appeared on the epicardium over a wide range of conductivity values. The magnitude of the net epicardial potential difference, the epicardial maximum minus the epicardial minimum, was strongly correlated to the intracellular to extracellular conductivity ratios both along and across fibers. Anisotropy of the ischemic source region was critical in predicting epicardial potentials, whereas anisotropy of the heart away from the ischemic region had a less significant impact on epicardial potentials. Subendocardial ischemia that extends through at least 40% of the heart wall is manifest on the epicardium by at least one area of ST-segment depression located over a boundary between ischemic and healthy tissue. The magnitude of the depression is a function of the bidomain conductivity values.

Background-ICD implants in children and patients with congenital heart disease are complicated by body size and anatomy. A variety of creative implant techniques have been utilized empirically in these groups on an ad hoc basis.