Electrical impedance measurements have been made from the human trunk over the frequency range 9.6 kHz to 614 kHz. Measurements have been made from 12 normal subjects and the amplitude of the impedance changes associated with the cardiac and respiratory cycles have been recorded. It was found that the real part of the impedance fell to 64.0% of its low frequency value over the measured range of frequencies and that the changes associated with respiration fell in a similar manner. However, the cardiac related changes fell more rapidly with increasing frequency to 28.2% of the low frequency value. The origin of the measured changes is discussed with a view to understanding why the cardiac related changes fall more rapidly. It is not possible to relate in any simple way the frequency dispersion of a single component to that of the whole trunk. However, the results are consistent with the lungs being the major origin of both the cardiac and respiratory related components. The origin of the cardiac related impedance changes could be the pulsatile volume changes in the pulmonary tree. These could be shunted by nonpulsatile lung tissue that has decreasing impedance at high frequency and thus decreases the relative magnitude of the cardiac related changes. This hypothesis needs to be tested using localized measurements from the thorax and 3-D modeling of the trunk.

Hypoglycemia produces electrocardiographic QTc lengthening, a predictor of arrhythmia risk and sudden death. This results from both sympatho-adrenal activation and a lowered serum potassium. It has been suggested that cardiac autonomic neuropathy (CAN) might indicate those who are at particular risk. We tested this hypothesis in 28 adults with type 1 diabetes and 8 nondiabetic control subjects. After standard tests of autonomic function and baroreflex sensitivity (BRS) measurement, diabetic participants were divided into three groups: 1) CAN؊ with normal BRS (BRS؉; n ‫؍‬ 10), 2) CAN؊ with impaired BRS (BRS؊; n ‫؍‬ 9), and 3) CAN؉ (n ‫؍‬ 9). QTc was then measured during controlled hypoglycemia (2.5 mmol/l) using a hyperinsulinemic clamp. Mean (؎SE) QTc lengthened from 377 ؎ 9 ms (baseline) to a maximum during hypoglycemia of 439 ؎ 13 ms in BRS؉ subjects and from 378 ؎ 5 to 439 ؎ 10 ms in control subjects. Peak QTc tended to be lower in CAN؉ (baseline, 383 ؎ 6; maximum, 408 ؎ 10) and BRS؊ groups (baseline, 380 ؎ 8; maximum, 421 ؎ 11; F ‫؍‬ 1.7, P ‫؍‬ 0.18). Peak epinephrine concentrations (nmol/l) were 3.1 ؎ 0.8 (BRS؉), 2.6 ؎ 0.5 (BRS؊), 1.4 ؎ 0.3 (CAN؉), and 5.7 ؎ 0.8 (control subjects). These data do not indicate that those with CAN are at particular risk for abnormal cardiac repolarization during hypoglycemia. Indeed, they suggest that such patients may be relatively protected, perhaps as a result of attenuated sympatho-adrenal responses. Diabetes 53: [1535][1536][1537][1538][1539][1540][1541][1542] 2004

EIT images have been recorded from the upper thorax of 10 normal subjects and from two patients with pulmonary emboli. The Sheffield Mk2 system was used to obtain the EIT images during quiet tidal breathing and the images were then analysed to extract the cardiac and respiratory related components. In the 10 normal subjects the mean measured change in resistivity during tidal breathing was 9% (SD 3%) with no significant difference in four lung regions. The mean changes during the cardiac cycle were different in the four regions, ranging from -0.9% to -2.6%. The two patients showed very different cardiac related changes from those found in the normals in the posterior lung regions. The sign of the changes was positive, whereas it was negative in the normals. The changes in the anterior lung regions were within the range found in our normal group.

Two studies concerning multi-frequency impedance measurements are presented. The first uses tetrapolar measurements made on the thorax and the second electrical impedance tomography images, also made from the thorax. The way in which the impedance and the changes in impedance with ventilation depend upon frequency are investigated using Cole-Cole modelling and also a physiological model of lung tissue. There is an excellent fit to the Cole-Cole model, and the results show that it should be possible to identify tissue on the basis of the impedance spectrum and the spectrum of the changes in impedance during breathing.