Pulmonary Vascular Input Impedance Research Articles

Pediatric Artificial Lung: A Low-Resistance Pumpless Artificial Lung Alleviates an Acute Lamb Model of Increased Right Ventricle Afterload.

Lung disease in children often results in pulmonary hypertension and right heart failure. The availability of a pediatric artificial lung (PAL) would open new approaches to the management of these conditions by bridging to recovery in acute disease or transplantation in chronic disease. This study investigates the efficacy of a novel PAL in alleviating an animal model of pulmonary hypertension and increased right ventricle afterload. Five juvenile lambs (20-30 kg) underwent PAL implantation in a pulmonary artery to left atrium configuration. Induction of disease involved temporary, reversible occlusion of the right main pulmonary artery. Hemodynamics, pulmonary vascular input impedance, and right ventricle efficiency were measured under 1) baseline, 2) disease, and 3) disease + PAL conditions. The disease model altered hemodynamics variables in a manner consistent with pulmonary hypertension. Subsequent PAL attachment improved pulmonary artery pressure (p = 0.018), cardiac output (p = 0.050), pulmonary vascular input impedance (Z.0 p = 0.028; Z.1 p = 0.058), and right ventricle efficiency (p = 0.001). The PAL averaged resistance of 2.3 ± 0.8 mm Hg/L/min and blood flow of 1.3 ± 0.6 L/min. This novel low-resistance PAL can alleviate pulmonary hypertension in an acute animal model and demonstrates potential for use as a bridge to lung recovery or transplantation in pediatric patients with significant pulmonary hypertension refractory to medical therapies.

Measurement uncertainty in pulmonary vascular input impedance and characteristic impedance estimated from pulsed-wave Doppler ultrasound and pressure: clinical studies on 57 pediatric patients

Pulmonary vascular input impedance better characterizes right ventricular (RV) afterload and disease outcomes in pulmonary hypertension compared to the standard clinical diagnostic, pulmonary vascular resistance (PVR). Early efforts to measure impedance were not routine, involving open-chest measurement. Recently, the use of pulsed-wave (PW) Doppler-measured velocity to non-invasively estimate instantaneous flow has made impedance measurement more practical. One critical concern remains with clinical use: the measurement uncertainty, especially since previous studies only incorporated random error. This study utilized data from a large pediatric patient population to comprehensively examine the systematic and random error contributions to the total impedance uncertainty and determined the least error prone methodology to compute impedance from among four different methods. We found that the systematic error contributes greatly to the total uncertainty and that one of the four methods had significantly smaller propagated uncertainty; however, even when this best method is used, the uncertainty can be large for input impedance at high harmonics and for the characteristic impedance modulus. Finally, we found that uncertainty in impedance between normotensive and hypertensive patient groups displays no significant difference. It is concluded that clinical impedance measurement would be most improved by advancements in instrumentation, and the best computation method is proposed for future clinical use of the input impedance.

Relationship between the changes in pulmonary vascular input impedance and the site of action of vasoactive agents in the excised canine lung lobe preparation and model circuit

Relationship between the changes in pulmonary vascular input impedance and the site of action of vasoactive agents in the excised canine lung lobe preparation and model circuit

Pulmonary vascular input impedance is a combined measure of pulmonary vascular resistance and stiffness and predicts clinical outcomes better than pulmonary vascular resistance alone in pediatric patients with pulmonary hypertension

Pulmonary vascular resistance (PVR) is the current standard for evaluating reactivity in children with pulmonary arterial hypertension (PAH). However, PVR measures only the mean component of right ventricular afterload and neglects pulsatile effects. We recently developed and validated a method to measure pulmonary vascular input impedance, which revealed excellent correlation between the zero harmonic impedance value and PVR and suggested a correlation between higher-harmonic impedance values and pulmonary vascular stiffness. Here we show that input impedance can be measured routinely and easily in the catheterization laboratory, that impedance provides PVR and pulmonary vascular stiffness from a single measurement, and that impedance is a better predictor of disease outcomes compared with PVR. Pressure and velocity waveforms within the main pulmonary artery were measured during right heart catheterization of patients with normal pulmonary artery hemodynamics (n = 14) and those with PAH undergoing reactivity evaluation (49 subjects, 95 conditions). A correction factor needed to transform velocity into flow was obtained by calibrating against cardiac output. Input impedance was obtained off-line by dividing Fourier-transformed pressure and flow waveforms. Exceptional correlation was found between the indexed zero harmonic of impedance and indexed PVR (y = 1.095x + 1.381, R2 = 0.9620). In addition, the modulus sum of the first 2 harmonics of impedance was found to best correlate with indexed pulse pressure over stroke volume (y = 13.39x - 0.8058, R2 = 0.7962). Among a subset of patients with PAH (n = 25), cumulative logistic regression between outcomes to total indexed impedance was better (R(L)2 = 0.4012) than between outcomes and indexed PVR (R(L)2 = 0.3131). Input impedance can be consistently and easily obtained from pulse-wave Doppler and a single catheter pressure measurement, provides comprehensive characterization of the main components of RV afterload, and better predicts patient outcomes compared with PVR alone.

Pulmonary Hemodynamic Consequences of ECG-Synchronized Ventilation

The pulmonary hemodynamic consequences of ECG-synchronized jet ventilation were studied in an acute closed chest swine model ( n = 11). Eight jet timing protocols were compared to conventional mechanical ventilation. Hearts were paced atrially at 120 beats per minute, and analog measurements of pulmonary arterial flow and pulmonary arterial, tracheal, pleural, left atrial, and femoral arterial pressure were digitized in real time at 200 Hz. Fourier analysis of pulmonary artery pressure and flow waveforms was employed to calculate mean and oscillatory right ventricular hydraulic power and pulmonary vascular input impedance. Measurements were taken at 0, 5, and 10 cm H 2O of positive end-expiratory pressure (PEEP) during conventional respiration and synchronized ventilation modes. No difference was found in mean pulmonary pressure and flow between conventional and synchronized ventilation at any level of PEEP, regardless of the timing of the jet pulse relative to the cardiac cycle. A significant difference in mean tracheal pressure between conventional and jet ventilation could be found only in the absence of PEEP (3.8 ± 0.5 vs 2.5 ± 0.3 mm Hg, P < 0.05). In the absence of PEEP, total hydraulic power was significantly less with respect to conventional ventilation when the jet pulse trailed the QRS complex by 90 and 135°. A significant decrease in the ratio of oscillatory-to-mean power versus conventional respiration was found when jet ventilation lagged the QRS by 135° (0.115 ± 0.015 vs 0.147 ± 0.013). These differences did not persist when PEEP was added. Moreover, no significant difference in hemodynamic variables was found when the various jet timing protocols were compared to each other. These data affirm the dominant role of mean tracheal pressure as the major variable modifying pulmonary hemodynamics but suggest that, at normal airway pressure, pulmonary hemodynamics may be modestly affected by synchronization of ventilation with the cardiac cycle.

Pulmonary vascular impedance in microembolic pulmonary hypertension: Effects of synchronous high-frequency jet ventilation

Increased intrathoracic pressure (ITP) during conventional mechanical ventilation may interfere with the adaptation of right ventricular function to pulmonary hypertension. We studied the effects of synchronous cardiac cycle-specific high frequency jet ventilation (HFJV) in 10 anesthetized dogs before and after embolization of the pulmonary artery with 150–200 μm glass beads. The delivery of the jet was synchronized with early systole, late systole, early diastole and late diastole of the cardiac cycle. Right and left ventricular pressures (Prv and Plv) and pulmonary arterial pressures (Ppa) were measured by transducer-tipped catheters and pulmonary blood flow by an ultrasonic flow probe. Right ventricular end-systolic and end-diastolic volumes (rvESV and rvEDV) were estimated from the thermodilution curve obtained with a Swan-Ganz catheter equipped with a fast response thermistor. Pulmonary hypertension caused significant increases in heart rate (89 ± 7 to 152 ± 8 beats/min), rvEDV (80 ± 7 to 131 ± 23 ml), diastolic transmural Prv (2 ± 1 to 5 ± 1 mm Hg), and rv peak dP/dt (652 ± 151 to 1035 ± 160 mm Hg/s). The spectrum of pulmonary vascular input impedance was displaced towards higher frequencies, input resistance was increased and characteristic impedance decreased. The latter change contributed to a relative disease in the pulsatile component of right ventricular power output. Cardiac outpur remained unchanged (2.1 ± 0.2 to 1.9 ± 0.1 L/min, P NS). Non of these measurements was affected by the timing of the increase in ITP to specific instants in the cardiac cycle compared to apneic periods at any level of pulmonary hypertension. We conclude that in acute microembolic pulmonary hypertension 1° a decrease in characteristic impedance contributes to the adaptation of right ventricular function to increased afterload and 2° synchronous cardiac cylce-specific HFJV has no detectable hemodynamic effect.

Changes in the pulmonary vascular input impedance in patients with atrial septal defect after surgical correction.

In order to evaluate whether there is pulmonary vascular disease in patients with atrial septal defect (ASD), we used the pulmonary vascular input impedance to estimate the stiffness of the pulmonary vessels with before and after surgical intervention. Ten control subjects and 11 patients with ASD (9 operable and 2 inoperable) were examined. In preoperative patients the decreased total pulmonary resistance (Rin) and pulmonary vascular resistance appeared to open new parallel vascular channels with increased blood flow. Further, there were no significant differences in the pulmonary vascular input impedance spectrum and phase, and characteristic impedance among control subjects, preoperative and postoperative patients. Although distensibility of the pulmonary vascular wall in operable patients was similar to that in control subjects, an excessive elevation in Rin and input impedance modulus was observed in inoperable patients. The results demonstrate that the normal input impedance spectrum and phase in patients with ASD is predictive of a good prognosis after successful surgical correction.

Pulmonary vascular input impedance in the newborn and infant pig.

The input impedance of the main pulmonary artery in 26 pigs aged from 1 h to 2 weeks has been calculated from measurements of pressure and flow. From these data we have derived estimates of the hydraulic power output of the right heart. The impedance spectra were similar in form to those in many other studies and were consistent with the presence of a single reflection site within the lung. The frequency of the (single) minimum decreased steadily with increasing age as did the corresponding zero crossing point on the phase curve. From estimates of propagation velocity the position of this "reflection site" was found to coincide with the position of the lung periphery in each age group. An overall fall in characteristic impedance with increasing age was found to be due to the increasing diameter of the pulmonary artery rather than to changes in its elasticity. The total power output/body weight of the right heart fell from 10.4 to 4.8 mW X kg-1 from birth to 4 weeks of age. During this period the ratio of pulsatile to steady power fell from 0.5 to 0.31. We conclude that this fall is related to a reduction in the effective reflection of pressure and flow waves within the lung due to increasing attenuation and possibly to a reduction in the magnitude of the lumped reflection coefficient itself.

Effects of Oxygen Breathing on Pulmonary Vascular Input Impedance in Patients with Pulmonary Hypertension

The effect of oxygen breathing on the stiffness of the large pulmonary artery has not been elucidated. We analyzed the proximal pulmonary arterial impedance with a multisensor catheter in ten patients with pulmonary arterial hypertension (PAH), eight patients with pulmonary venous hypertension, and six control subjects. The stiffness of the vessel was quantified by the characteristic impedance (Zo) and compared with the plasma norepinephrine level. Ten minutes of high-oxygen breathing decreased the Zo (from 78 +/- 18 to 57 +/- 14 dynes.sec.cm-5, p less than 0.01) and pulmonary arterial resistance in all the cases with PAH. In this group, norepinephrine also decreased (from 381 +/- 89 to 319 +/- 77 pg/ml, p less than 0.01) following the correction of hypoxemia. Yet, those parameters did not change in the other two groups. These results indicate that in patients with PAH, oxygen breathing can reduce the stiffness of the main pulmonary artery because of the sympatholytic effect.

The Influence of Pulmonary Blood Flow Rate on Vascular Input Impedance and Hydraulic Power in the Sympathetically and Noradrenaline Stimulated Cat Lung

This study was designed to evaluate the influence of sympathetic nerve stimulation (SN) and alpha-adrenergic receptor stimulation (alphaS) on the pulmonary vascular input impedance and hydraulic power output of the right heart during variations of cardiac output (CO). An open chest cat preparation was used and pulsatile pressure and flow in the pulmonary artery were measured by high frequency response transducers. Calculations showed that vascular resistance (VR) was inversely dependent on CO, but input impedance of the unstimulated lung was not influenced by CO variations. NS or alphaS increased VR and input impedance significantly, and the relation pulsatile hydraulic power/total hydraulic power (Wp/Wt) increased 40%, indicating that such stimulation has larger relative influence on impedance than on resistance. The reduction of arterial compliance during NS (maximal stimulus) was calculated to be 60%, independent of CO. Input impedance during NS or alphaS was reduced by CO elevations, probably because the concomitant distension of the arterial bed reduced arterial resistance and inertance. The ratio Wp/CO, which expresses the fraction of pulsatile hydraulic power lost per ml mean arterial flow, was found to be flow dependent both in control and stimulated conditions: Wp/CO was positively correlated to CO in control condition and weakly negatively correlated to CO during stimulation. At high CO the arterial vessels could be stimulated and stiffened without much extra load on the right heart.

Measurement of ascending aortic flow patterns in man.

ArticleMeasurement of ascending aortic flow patterns in man.J B Uther, K L Peterson, R Shabetai, and E BraunwaldJ B Uther, K L Peterson, R Shabetai, and E BraunwaldPublished Online:01 Apr 1973https://doi.org/10.1152/jappl.1973.34.4.513MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByAn immersogeometric variational framework for fluid–structure interaction: Application to bioprosthetic heart valvesComputer Methods in Applied Mechanics and Engineering, Vol. 284Fluid–structure interaction analysis of bioprosthetic heart valves: significance of arterial wall deformation6 August 2014 | Computational Mechanics, Vol. 54, No. 4Evaluation of blood flow velocity waveform in common carotid artery using multi-branched arterial segment model of human arteriesBiomedical Signal Processing and Control, Vol. 8, No. 6In vivo validation of a transit-time ultrasonic volume flow meterJournal of Pharmacological and Toxicological Methods, Vol. 31, No. 3Effects of exercise and nitroprusside on left ventricular ejection dynamics in idiopathic dilated cardiomyopathyThe American Journal of Cardiology, Vol. 59, No. 6Blood flow and blood velocity measurementin vivo by electromagnetic inductionMedical & Biological Engineering & Computing, Vol. 22, No. 3Effects of Oxygen Breathing on Pulmonary Vascular Input Impedance in Patients with Pulmonary HypertensionChest, Vol. 83, No. 3Blood flow and blood velocity measurement in vivo by electromagnetic induction2 July 2016 | Transactions of the Institute of Measurement and Control, Vol. 4, No. 2Use of catheter-tip velocity--pressure transducer to evaluate left ventricular function in man: effects of intravenous propranolol.Circulation, Vol. 61, No. 5Evaluation of a new catheter-mounted electromagnetic velocity sensor during cardiac catheterizationCatheterization and Cardiovascular Diagnosis, Vol. 6, No. 1Instantaneous blood flow responses to positive end-expiratory pressure with spontaneous ventilation.Circulation, Vol. 59, No. 6Input impedance of the systemic circulation in man.Circulation Research, Vol. 40, No. 5Comparison of Isovolumic and Ejection Phase Indices of Myocardial Performance in ManCirculation, Vol. 49, No. 6 More from this issue > Volume 34Issue 4April 1973Pages 513-8 https://doi.org/10.1152/jappl.1973.34.4.513PubMed4698610History Published online 1 April 1973 Published in print 1 April 1973 Metrics

Pulmonary vascular response to exercise in the dog.

The effects of exercise on the pulmonary circulation were studied in seven experiments on five dogs. Pulsatile pulmonary arterial flow and pressure and left arterial pressure were measured by chronically implanted transducers; pulmonary vascular input impedance, resistance, and hydraulic power were computed. The average effects of running on a treadmill at 6.5 mph, as compared with the resting state, were an increase in cardiac output from 2.59 liters/ min to 5.30 liters/ min, a rise in mean pulmonary arterial pressure from 18 mm Hg to 28 mm Hg, and no consistent change in mean left arterial pressure. Pulmonary vascular resistance fell from 482 dyne sec cm at rest to 372 dyne sec cm -5 during exercise. Characteristic input impedance rose from 147 dyne sec cm-- at rest to 199 dyne sec cm -5 during exercise, and the oscillations of the impedance modulus with frequency decreased in magnitude. These changes were consistent with passive distention of the pulmonary vessels, decreasing the compliance of the large arteries and improving the impedance match between proximal and distal vessels.

Pulse wave velocity in the main pulmonary artery of the dog.

Apparent phase velocities in the main pulmonary artery were calculated from simultaneous measurements of pressure at two sites in 11 anesthetized, open-chest dogs, at heart rates ranging from 24 to 240 beat/min. The distribution of apparent phase velocity with harmonic frequency was similar to that reported previously for input impedance and frequency. Phase velocity in the absence of reflections, estimated by averaging apparent phase velocities at frequencies from 9 to 23 cycle/sec, averaged 275 cm/sec in the control state and 417 cm/sec during the infusion of 5-hydroxytryptamine (serotonin). The elastic modulus of the pulmonary arterial wall implied by these velocities was calculated to be approximately 1.2 x 10 6 dyne/cm 2 in the controls and 2.7 x 10 6 dyne/cm 2 during serotonin. These results are consistent with previous observations on normal pulmonary vascular input impedance in the dog under these conditions, and with the relationships predicted by the Womersley equations, and suggest that the effects of serotonin on the input impedance spectrum are due in part to an increase in pulse wave velocity.

Hydraulic power associated with pulmonary blood flow and its relation to heart rate.

Pulmonary vascular input impedance and hydraulic power were measured at various heart rates in 29 anesthetized and 5 unanesthetized dogs. Hydraulic power at the pulmonary veno-atrial junction was measured in 5 dogs. The pulmonary vascular impedance spectrum in the unanesthetized dogs did not differ significantly from that in the anesthetized dogs. Average pulmonary arterial power in the anesthetized dogs was 157 milliwatts (mw), of which 108 mw was associated with mean pressure and flow, and 49 mw with the pulsations around these means. Seventy-eight per cent of this input power was dissipated in passage through the pulmonary bed. Kinetic energy accounted for 7% of the total input power. Because of a steep fall in impedance between zero and 3 cycles/sec, and a rate-dependent change in the harmonic structure of flow pulsations, there was an inverse relationship between heart rate and the input power for a given mean flow, up to 180 beats/min. Pulmonary vascular dimensions and elasticity, which determine impedance, thus embody a mechanism whereby tachycardia can increase pulmonary blood flow by as much as 35% with an increase in pulmonary arterial input power of less than 5%, without the intervention of vasomotor activity.