Impedance In Dogs Research Articles

Editorial: Cardiac electronic remodeling and susceptibility to arrhythmias: an introduction and brief historical overview.

Editorial: Cardiac electronic remodeling and susceptibility to arrhythmias: an introduction and brief historical overview.

Muscular arterial impedance in dogs with chronic degenerative mitral valve disease

Systemic vascular impedance represents the retrograde strength of the blood flow to the left ventricle, thus it is one of the main compounds of afterload. Mitral regurgitation is markedly sensitive to afterload alterations. The purpose of this study was to evaluate muscular arterial impedance in dogs with chronic degenerative mitral valve disease (CDMVD) by use of duplex Doppler ultrasonography (DDU), since its technique there was not used before to determine impedance index in dogs with CDMVD. For this purpose, ten healthy dogs and ten dogs with CDMVD were used. Some parameters related to blood flow impedance in the common femoral artery were measured by DDU: pulsatility index (PI), resistance index (RI), high-resistance index (HRI), and acceleration velocity (AC) and deceleration velocity (DC) of the systolic peak. The results showed that RI and HRI were significantly higher in animals with CDMVD than in healthy animals. These findings showed that DDU provides quantitative data related to vascular impedance. Broader studies may therefore provide new aspects related to physiopathology and therapy in CDMVD patients.

Effect of hypoxia on respiratory system impedance in dogs.

The effects of hypoxia on lung and airway mechanics remain controversial, possibly because of the confounding effects of competing reflexes caused by systemic hypoxemia. We compared the effects of systemic hypoxemia with those of unilateral alveolar hypoxia (with systemic normoxemia) on unilateral respiratory system impedance (Z) in intact, anesthetized dogs. Independent lung ventilation was obtained with a Kottmeier endobronchial tube. Individual left and right respiratory system Z was measured during sinusoidal forcing with 45 ml of volume at frequencies of 0.2-2.1 Hz during control [100% inspired O2 fraction (FIO2)], systemic hypoxemia (10% FIO2), and unilateral alveolar hypoxia (0% FIO2 to left lung, 100% FIO2 to right lung). During systemic hypoxemia, there was a mean Z magnitude increase of 18%. This change was entirely attributable to a decrease in the imaginary component of Z; there was no change in the real component of Z. Administration of atropine (0.2 mg/kg) did not block the increase in Z with systemic hypoxemia. In contrast, there was no change in Z in the lung subjected to unilateral alveolar hypoxia. We conclude that alveolar hypoxia has no direct effect on lung mechanical properties in intact dogs. In contrast, systemic hypoxemia does increase lung impedance, apparently through a noncholinergic mechanism.

Propofol Alters Left Ventricular Afterload as Evaluated by Aortic Input Impedance in Dogs

Systemic vascular resistance incompletely describes left ventricular afterload because of the phasic nature of arterial pressure and blood flow. Aortic input impedance is an experimental description of left ventricular afterload that incorporates the frequency- dependent characteristics and viscoelastic properties of the arterial system. The effects of propofol on aortic input impedance were examined using three variables derived from the three-element Windkessel model: characteristic aortic impedance, total arterial compliance, and total arterial resistance. Eight dogs were chronically instrumented for measurement of aortic pressure, left ventricular pressure, +dP/dt, subendocardial segment length, and aortic blood flow. Systemic hemodynamics and aortic blood pressure and flow waveforms were recorded in the conscious state and after a bolus of 5 mg x kg(-1) propofol and infusion for 15 min at 25, 50 and 100 mg x kg(-1) x h(-1). Aortic input impedance spectra were generated using power spectral analysis of aortic pressure and flow waveforms corrected for the phase responses of the pressure and flow transducers. Characteristic aortic impedance, total arterial resistance, and total arterial compliance were calculated from the aortic input impedance spectrum and the aortic pressure waveform. Parameters describing the net site and magnitude or arterial wave reflection were determined from aortic impedance. Propofol decreased total arterial resistance (3.05 +/- 0.20 during control to 2.29 +/- 0.18 dynes x s x cm(-5) x 10(3) at the high dose) and increased total arterial compliance (0.53 +/- 0.04 during control to 1.15 +/- 0.17 ml x mmHg(-1) at the high dose) in a dose- related manner. Propofol increased characteristic aortic impedance (1.49 +/- 0.15 during control to 2.20 +/- 0.20 dynes x s x cm(-5) x 10(2) at the high dose). The net site and the magnitude of arterial wave reflection were unchanged by the propofol. In chronically instrumented dogs, propofol decreased total arterial resistance, a property of arteriolar resistance vessels, consistent with the known actions of this drug on systemic vascular resistance. Propofol also increased total arterial compliance and characteristic aortic impedance, indicating that this anesthetic affects the mechanical properties of the aorta. Propofol had no effect on arterial wave reflection patterns. The results indicate that propofol reduces left ventricular afterload via decreases in peripheral resistance and increases in arterial compliance.

Measurement of total respiratory impedance in dogs by the forced oscillation technique.

The resistance (Rrs) and reactance (Xrs) of the total respiratory system were determined at various frequencies in 14 healthy conscious beagle dogs. A pseudorandom noise pressure wave was produced at the nostrils of the animals by means of a loudspeaker adapted to the nose by a tightly fitting mask. A Fourier analysis of the pressure and flow signals yielded mean Rrs and Xrs, over 16 s, at frequencies from 2 to 26 Hz. The influence of the posture of the dog, the position of its head, the linearity of the respiratory system, the reproducibility of the method and the effects of upper and lower airway obstructions were studied. In sitting and standing healthy dogs with the head in the extended position, Rrs values increased progressively with frequency from 5.4 +/- 0.4 (SEM) cmH2O L-1s at 6 Hz up to 8.8 +/- 0.7 cmH2O L-1s at 26 Hz, the mean resonant frequency being 6.1 +/- 0.5 Hz. No significant differences were observed between measurements performed with the head in the normal or the extended position. In a recumbent posture, all Rrs values were increased but Rrs was still dependent on the frequency in the same way (7.1 +/- 0.7 cmH2O L-1s at 6Hz up to 10.0 +/- 0.5 cmH2O L-1s at 26 Hz). Tracheal compression also induced higher Rrs values without changes in the frequency dependence or in the resonant frequency. In anaesthetized dogs, airway obstruction was induced by inhalation of histamine (4 mg/ml for 5 min; the Rrs values tended to decrease with increasing frequency, and the resonant frequency was markedly increased.

Effects of tidal volume and methacholine on low-frequency total respiratory impedance in dogs

The frequency dependence of respiratory impedance (Zrs) from 0.125 to 4 Hz (Hantos et al., J. Appl. Physiol. 60: 123-132, 1986) may reflect inhomogeneous parallel time constants or the inherent viscoelastic properties of the respiratory tissues. However, studies on the lung alone or chest wall alone indicate that their impedance features are also dependent on the tidal volumes (VT) of the forced oscillations. The goals of this study were 1) to identify how total Zrs at lower frequencies measured with random noise (RN) compared with that measure with larger VT, 2) to identify how Zrs measured with RN is affected by bronchoconstriction, and 3) to identify the impact of using linear models for analyzing such data. We measured Zrs in six healthy dogs by use of a RN technique from 0.125 to 4 Hz or with a ventilator from 0.125 to 0.75 Hz with VT from 50 to 250 ml. Then methacholine was administered and the RN was repeated. Two linear models were fit to each separate set of data. Both models assume uniform airways leading to viscoelastic tissues. For healthy dogs, the respiratory resistance (Rrs) decreased with frequency, with most of the decrease occurring from 0.125 to 0.375 Hz. Significant VT dependence of Rrs was seen only at these lower frequencies, with Rrs higher as VT decreased. The respiratory compliance (Crs) was dependent on VT in a similar fashion at all frequencies, with Crs decreasing as VT decreased. Both linear models fit the data well at all VT, but the viscoelastic parameters of each model were very sensitive to VT. After methacholine, the minimum Rrs increased as did the total drop with frequency. Nevertheless the same models fit the data well, and both the airways and tissue parameters were altered after methacholine. We conclude that inferences based only on low-frequency Zrs data are problematic because of the effects of VT on such data (and subsequent linear modeling of it) and the apparent inability of such data to differentiate parallel inhomogeneities from normal viscoelastic properties of the respiratory tissues.

Modeling of low-frequency pulmonary impedance in dogs

The mechanical impedance of the lungs (ZL) was measured in open-chest dogs with small-amplitude pseudorandom volume oscillations between 0.125 and 5 Hz, at mean transpulmonary pressures (Ptp) of 0.2, 0.4, and 0.8 kPa. At the lowest frequencies, the pulmonary resistance showed a marked negative frequency dependence and mirrored the changes in the reactance with altered Ptp. The ZL data were evaluated on the basis of two models, each containing the same airway compartment with a resistance and an inertance. The tissue impedance (Zti) in model 1 was represented with two compliances and a resistance (L. E. Mount. J. Physiol. Lond. 127: 157-167, 1955), whereas in model 2 a two-parameter formulation implying rate-independent dissipated work and frequency-dependent elastance (J. Hildebrandt. J. Appl. Physiol. 28: 365-372, 1970) was employed. The estimation of model parameters showed that model 2 was superior to model 1 in both fitting performance and parameter insensitivity to weighting in the fitting criterion. The model 2 coefficients of damping and elastance, characterizing the real and imaginary parts of Zti, respectively, depended on the lung distension and were closely correlated. Although ZL exhibited a slight dependence on the peak-to-peak volume excursion, at a given oscillatory volume no inconsistency with linear tissue viscoelasticity was detected.

Respiratory system, lung, and chest wall impedances in anesthetized dogs.

We measured impedances of the respiratory system (Zrs) and lung (ZL) in anesthetized and paralyzed dogs at frequencies between 4 and 64 Hz. Zrs was measured at functional residual capacity (FRC) and with mean transpulmonary pressures (Ptp) of 12 and 30 cmH2O; ZL was measured with the chest wall open at FRC and Ptp = 12 cmH2O. From these data we derived chest wall impedances at FRC and 12 cmH2O. Effective resistances of the respiratory system, lung, and chest wall were all frequency dependent. At frequencies below 22 Hz frequency dependence of respiratory system resistance was due to the frequency dependence of the chest wall, whereas at higher frequencies it was due to frequency dependence of the lung. Analysis of the impedance data between 4 and 32 Hz provided estimates of resistance, inertance, and compliance of the lung, chest wall, and respiratory system. At FRC, 41% of the respiratory system resistance was due to the lung and 59% was associated with the chest wall. Nearly all of the respiratory inertance (98%) was due to the lung. Lung compliance was approximately twice that of the chest wall, the former accounting for approximately one-third of respiratory elasticity. As lung volume was increased, respiratory resistance and compliance decreased; inertance also decreased, although this change was not significant.

Pulmonary impedance in dogs measured by forced random noise with a retrograde catheter.

Retrograde catheter and forced random noise techniques were combined to study the distribution of resistance and compliance in dogs following the inhalation of aerosols containing 2.5 and 5.0 mg/ml of histamine. Mean base-line peripheral resistance was 0.367 cmH2O . l-1 . s, agreeing with previous estimates. After correction for the endotracheal tube, the mean central airway resistance was 0.040 cmH2O . l-1 . s, considerably lower than previous estimates. This discrepancy was attributed to an overcorrection for the endotracheal tube resistance. The lower histamine dose caused a substantial increase in peripheral resistance, a relatively small increase in central resistance, and substantial decreases in total and peripheral compliance. After the higher histamine dose, changes in peripheral resistance and both compliances were similar to those obtained with the lower dose; however, the increase in central resistance was much larger than at the lower dose. The difference between total and peripheral compliance yielded estimates of airway compliance of 0.00306 l/cmH2O before and 0.00104 l/cmH2O after 2.5 mg/ml of histamine.

Frequency dependence and partitioning of respiratory impedance in dogs.

Total pulmonary resistance (Rt) and reactance (Xt) from 1 to 30 Hz were determined by time series analysis in open-chest vagotomized dogs. Rt and Xt were partitioned by retrograde catheter into central airway resistance (Rc) and reactance (Xc) and peripheral resistance (Rp) and reactance (Xp). Rt, Rc, or Rp did not change with transpulmonary pressure (Pst) from 5 to 15 cmH2O, although Rc tended to decrease and Rp to increase. Vagal stimulation (Vs) and intravenous histamine (H) increased all resistances (R) at all lung volumes (V) and produced an inverse relationship between R and V. The increases in Rt produced by H and Vs were not significantly different at any volume, but H predominantly increased Rp and Vs predominantly increased Rc. In the control (vagotomized) dogs at Pst of 5 cmH2O, Rp/Rt was 0.41 +/- 0.03 (SE). Rp/Rt was significantly increased by H but not by Vs. Control Rt decreased slightly from 5 to 10 Hz and increased from 15 to 30 Hz. The increase of Rt at higher frequencies caused by the frequency dependence of Rc was not changed by H but was augmented by Vs. The slope of Xt and Xc vs. frequency was increased by Vs but not by H. The frequency dependence of Rt and Xt above 10 Hz appears to be caused by inertial losses proximal to the 2-mm airways. Thus central and peripheral bronchoconstriction caused by Vs and H, respectively, could be differentiated by increased frequency dependence of Rt and Xt above 15 Hz.