Impedance cardiography: Pulsatile blood flow and the biophysical and electrodynamic basis for the stroke volume equations

Impedance cardiography (ICG) is a branch of bioimpedance primarily concerned with the determination of left ventricular stroke volume (SV). As implemented, using the transthoracic approach, the technique involves applying a current field longitudinally across a segment of thorax by means of a constant magnitude, high frequency, low amplitude alternating current (AC). By Ohm’s Law, the voltage difference measured within the current field is proportional to the electrical impedance Z (Ω). Without ventilatory or cardiac activity, Z is known as the transthoracic, static base impedance Z0. Upon ventricular ejection, a characteristic time dependent cardiac-synchronous pulsatile impedance change is obtained, ΔZ(t), which, when placed electrically in parallel with Z0, constitutes the time-variable total transthoracic impedance Z(t). ΔZ(t) represents a dual-element composite waveform, which comprises both the radially-oriented volumetric expansion of and axially-directed forward blood flow within both great thoracic arteries. In its majority, however, ΔZ(t) is known to primarily emanate from the ascending aorta. Conceptually, commonly implemented methods assume a volumetric origin for the peak systolic upslope of ΔZ(t), (i.e. dZ/dtmax), with the presumed units of Ω·s–1. A recently introduced method assumes the rapid ejection of forward flowing blood in earliest systole causes significant changes in the velocity-induced blood resistivity variation (Δρb(t), Ωcm·s–1), and it is the peak rate of change of the blood resistivity variation dρb(t)/dtmax (Ωcm·s–2) that is the origin of dZ/dtmax. As a consequence of dZ/dtmax peaking in the time domain of peak aortic blood acceleration, dv/dtmax (cm·s–2), it is suggested that dZ/dtmax is an ohmic mean acceleration analog (Ω·s–2) and not a mean flow or velocity surrogate as generally assumed. As conceptualized, the normalized value, dZ/dtmax/Z0, is a dimensionless ohmic mean acceleration equivalent (s–2), and more precisely, the electrodynamic equivalent of peak aortic reduced average blood acceleration (PARABA, d<v>/dtmax/R, s–2). As necessary for stroke volume calculation, dZ/dtmax/Z0 must undergo square root transformation to yield an ohmic mean flow velocity equivalent. To compute SV, the square root of the dimensionless ohmic mean acceleration equivalent ([dZ/dtmax/Z0]0.5, s–1) is multiplied by a volume of electrically participating thoracic tissue (VEPT, mL) and left ventricular ejection time (TLVE, s). To find the bulk volume of the thoracic contents (i.e. VEPT), established methods implement exponential functions of measured thoracic length (L(cm)n) or height-based thoracic length equivalents (0.01×%H(cm)n). The new method conceptualizes VEPT as the intrathoracic blood volume (ITBV, mL), which is approximated through allometric equivalents of body mass (aMb). In contrast to the classical two-element parallel conduction model, the new method comprises a three-compartment model, which incorporates excess extra-vascular lung water (EVLW) as a component of both Z0 and VEPT. To fully appreciate the evolution and analytical justification for impedance-derived SV equations, a review of the basics of pulsatile blood flow is in order.

Impact of physiological variables and genetic background on myocardial frequency-resistivity relations in the intact beating murine heart

Conductance measurements for generation of an instantaneous left ventricular (LV) volume signal in the mouse are limited, because the volume signal is a combination of blood and LV muscle, and only the blood signal is desired. We have developed a conductance system that operates at two simultaneous frequencies to identify and remove the myocardial contribution to the instantaneous volume signal. This system is based on the observation that myocardial resistivity varies with frequency, whereas blood resistivity does not. For calculation of LV blood volume with the dual-frequency conductance system in mice, in vivo murine myocardial resistivity was measured and combined with an analytic approach. The goals of the present study were to identify and minimize the sources of error in the measurement of myocardial resistivity to enhance the accuracy of the dual-frequency conductance system. We extended these findings to a gene-altered mouse model to determine the impact of measured myocardial resistivity on the calculation of LV pressure-volume relations. We examined the impact of temperature, timing of the measurement during the cardiac cycle, breeding strain, anisotropy, and intrameasurement and interanimal variability on the measurement of intact murine myocardial resistivity. Applying this knowledge to diabetic and nondiabetic 11- and 20- to 24-wk-old mice, we demonstrated differences in myocardial resistivity at low frequencies, enhancement of LV systolic function at 11 wk and LV dilation at 20–24 wk, and histological and electron-microscopic studies demonstrating greater glycogen deposition in the diabetic mice. This study demonstrated the accurate technique of measuring myocardial resistivity and its impact on the determination of LV pressure-volume relations in gene-altered mice.

A self-calibrating telemetry system for measurement of ventricular pressure-volume relations in conscious, freely moving rats

Using Bluetooth wireless technology, we developed an implantable telemetry system for measurement of the left ventricular pressure-volume relation in conscious, freely moving rats. The telemetry system consisted of a pressure-conductance catheter (1.8-Fr) connected to a small (14-g) fully implantable signal transmitter. To make the system fully telemetric, calibrations such as blood resistivity and parallel conductance were also conducted telemetrically. To estimate blood resistivity, we used four electrodes arranged 0.2 mm apart on the pressure-conductance catheter. To estimate parallel conductance, we used a dual-frequency method. We examined the accuracy of calibrations, stroke volume (SV) measurements, and the reproducibility of the telemetry. The blood resistivity estimated telemetrically agreed with that measured using an ex vivo cuvette method ( y = 1.09 x − 11.9, r2 = 0.88, n = 10). Parallel conductance estimated by the dual-frequency (2 and 20 kHz) method correlated well with that measured by a conventional saline injection method ( y = 1.59 x − 1.77, r2 = 0.87, n = 13). The telemetric SV closely correlated with the flowmetric SV during inferior vena cava occlusions ( y = 0.96 x + 7.5, r2 = 0.96, n = 4). In six conscious rats, differences between the repeated telemetries on different days (3 days apart on average) were reasonably small: 13% for end-diastolic volume, 20% for end-systolic volume, 28% for end-diastolic pressure, and 6% for end-systolic pressure. We conclude that the developed telemetry system enables us to estimate the pressure-volume relation with reasonable accuracy and reproducibility in conscious, untethered rats.