Pulmonary Arterial Input Impedance Research Articles

The natural matching of harmonic responses in the pulmonary circulation.

Key points The right ventricle of the mammal heart is highly sensitive to the afterload imposed by a combination of the pulmonary circulation and the retrograde contribution of the left heart.Right ventricular afterload can be analysed in terms of pulmonary artery input impedance, which we were able to decompose as the result of the harmonic frequency responses of the pulmonary vessels and the left heart attached in series.Using spectral methods, we found a natural matching between the pulmonary vasculature and the left chambers of the heart. This coupling implies that the upstream transmission of the left heart frequency‐response has favourable effects on the pulmonary tree.This physiological mechanism protects the right ventricle against acute changes in preload, and its impairment may be a relevant contribution to right ventricle dysfunction in pulmonary hypertension. The right ventricle (RV) of the mammal heart is highly sensitive to the afterload imposed by the pulmonary circulation, and the left heart (LH) retrogradely contributes significantly to this vascular load. Transmission‐line theory anticipates that the degree of matching between the frequency responses of the pulmonary vasculature and the LH should modulate the global right haemodynamic burden. We measured simultaneous high‐fidelity flow (pulmonary artery) and pressure (pulmonary artery and left atrium) in 18 healthy minipigs under acute haemodynamic interventions. From these data, we decomposed the impedance spectra of the total right‐circulation system into the impedance of the pulmonary vessels and the harmonic response of the LH. For frequencies above the first harmonic, total impedance was below the pulmonary impedance during all phases (P < 0.001; pooled phases), demonstrating a favourable effect of the LH harmonic response on RV pulsatile load: the LH harmonic response was responsible for a 20% reduction of pulse pulmonary artery pressure (P < 0.001 vs. a theoretical purely‐resistive response) and a 15% increase of pulmonary compliance (P = 0.009). This effect on compliance was highest during acute volume overload. In the normal right circulation, the longitudinal impedance of the pulmonary vasculature is matched to the harmonic response of the LH in a way that efficiently reduces the pulmonary pulsatile vascular load. This source of interaction between the right and left circulations of mammals protects the RV against excessive afterload during acute volume transients and its disruption may be an important contributor to pulmonary hypertension.

Pulmonary arterial input impedance reflects the mechanical properties of pulmonary arterial remodeling in rats with pulmonary hypertension

AimsAlthough pulmonary arterial remolding in pulmonary hypertension (PH) changes the mechanical properties of the pulmonary artery, most clinical studies have focused on static mechanical properties (resistance), and dynamic mechanical properties (compliance) have not attracted much attention. As arterial compliance plays a significant role in determining afterload of the right ventricle, we evaluated how PH changes the dynamic mechanical properties of the pulmonary artery using high-resolution, wideband input impedance (ZPA). We then examined how changes in ZPA account for arterial remodeling. Clarification of the relationship between arterial remodeling and ZPA could help evaluate arterial remodeling according to hemodynamics. Main methodsPH was induced in Sprague–Dawley rats with an injection of Sugen5416 (20 mg/kg) and 3-week exposure to hypoxia (10% oxygen) (SuHx). ZPA was evaluated from pulmonary artery pressure and flow under irregular pacing. Pulmonary histology was examined at baseline and 1, 3, and 8 weeks (n = 7, each) after Sugen5416 injection. Key findingsSuHx progressively increased pulmonary arterial pressure. ZPA findings indicated that SuHx progressively increased resistance (baseline: 9.3 ± 3.6, SuHx1W: 20.7 ± 7.9, SuHx3W: 48.8 ± 6.9, SuHx8W: 62.9 ± 17.8 mm Hg/mL/s, p < 0.01) and decreased compliance (baseline: 11.9 ± 2.1, SuHx1W: 5.3 ± 1.7, SuHx3W: 2.1 ± 0.7, SuHx8W: 1.9 ± 0.6 × 10−3 mL/mm Hg, p < 0.01). The time constant did not significantly change. The progressive reduction in compliance was closely associated with wall thickening of small pulmonary arteries. SignificanceThe finding that changes in resistance were reciprocally associated with those in compliance indicates that resistant and compliant vessels are anatomically inseparable. The analysis of ZPA might help evaluate arterial remodeling in PH according to hemodynamics.

Noninvasive determination of the pulmonary artery input impedance

A reliable noninvasive method for the estimation of pulmonary function in healthy and diseased subjects should be of great importance in the prognosis, diagnosis, and treatment of pulmonary hypertension. Here we propose such a method, which is based on the parameter identification of the five-element Windkessel model of pulmonary circulation. The method requires the following input variables: the heart rate, the stroke volume, the Doppler echocardiographic measurements of the tricuspid regurgitation and the pulmonary valve velocity profiles, and estimations of the right atrium and the pulmonary vein pressure. The stroke volume is calculated as a product of the left ventricle outflow tract area and the velocity-time integral measured at the same place. The model parameter identification procedure is based on minimization of the root mean square error between the pulmonary artery root pressure calculated from the aforementioned Doppler velocity profiles (from the Bernoulli equation applied during the ejection phase) and the pressure from the Windkessel model during the same period. The output from the model contains the calculated pulmonary artery input impedance (i.e. the model parameters: pulmonary vascular resistance, pulmonary artery proximal and distal compliances, inertance, and characteristic impedance) and the pulmonary artery pressure profile during the whole heart period. Our method is applied to a subject with pulmonary hypertension. The right heart Swan-Ganz catheterization has been performed in this subject. The results obtained by using this method show that the five-element Windkessel model reconstructs the main features of the pulmonary artery input impedance very well: its modulus shows the minimum where the phase angle changes its sign. The pulmonary vascular resistance, the systolic, diastolic and mean pulmonary artery pressures obtained from the method are in good agreement with the values obtained invasively from the catheterization. Sensitivity analysis shows that the mean pulmonary pressure is fairly insensitive to slight overestimation/ underestimation of all input parameters, except for the right atrium pressure. The absolute error in the mean pulmonary artery pressure is nearly the same as the error in the right atrium pressure. Since the proposed method offers a deeper insight into the pulmonary circulation than the catheterization itself because it provides the proximal and distal compliance, the inertance and the characteristic impedance, it seems that it can serve in clinical practice as a good substitute for catheterization.

Abstract 17109: Input Impedance Analysis of Pulmonary Hypertension Models Indicates That Monocrotaline and Sugen/hypoxia Induce Mechanically Different Vascular Remodeling

Introduction: Although complex pulmonary arterial remolding characterizes pulmonary hypertension (PH), the vascular mechanics has been evaluated by the static pressure-flow relationship (resistance, R) ignoring dynamic mechanical properties (compliance, C). We therefore evaluated pulmonary arterial input impedance (Z) capable of identifying not only resistance but also compliance in monocrotaline (MCT) and Sugen/Hypoxia (SuHx) PH models. Methods: In 6 weeks Sprague-Dawley rats, we induced PH by the subcutaneous injection of MCT (60 mg/kg) or Sugen5416 (20 mg/kg) with 3 weeks hypoxia. In anesthetized PH rats, we measured pulmonary artery flow (PAF) and pressure (PAP) at 1000 Hz for 107.52 seconds under irregular pacing. We Fourier transformed both PAF and PAP to derive ensembled power spectra and crosspower spectra and taking their ratio yielded Z. We fitted the 2-element Windkessel model to Z and estimated R and C. Results: MCT and SuHx significantly increased mean PAP (Control: 19.4±2.0, MCT: 31.3±4.0, SuHx: 39.4±6.5 mmHg, p &lt;0.01) and shifted Z upward indicating the increased R (Control: 17.8±3.3, MCT: 71.4±16.3, SuHx: 81.8±18.4 mmHg/ml/sec, p &lt;0.01). MCT and SuHx both decreased C (Control: 2.6±0.4, MCT: 1.5±0.6, SuHx: 0.9±0.2 х10 -3 ml/mmHg, p &lt;0.01). However, the time constant was higher in MCT than in SuHx (Control: 90.7±8.6, MCT: 130.0±21.5, SuHx: 92.6±2.0 msec, p &lt;0.05) (Figure). MCT predominantly remodeled resistance vessels while SuHx remodeled both resistance and compliance vessels. Conclusions: We conclude that the impedance analysis is capable of characterizing how remodeling affects vascular mechanical properties, which are not identifiable if we analyze resistance alone. Hence the impedance analysis is applicable in patients, it may serve as a new tool in functionally analyzing vascular remodeling in PH patients.

Determinants of right ventricular afterload (2013 Grover Conference series).

Right ventricular (RV) afterload consists of both resistive and capacitive (pulsatile) components. Total afterload can be measured directly with pulmonary artery input impedance spectra or estimated, either with lumped-parameter modeling or by pressure-volume analysis. However, the inverse, hyperbolic relationship between resistance and compliance in the lung would suggest that the pulsatile components are a predictable and constant proportion of the resistive load in most situations, meaning that total RV load can be estimated from mean resistive load alone. Exceptions include elevations in left atrial pressures and, to a lesser extent, chronic thromboembolic disease. The pulsatile components may also play a more significant role at normal or near-normal pulmonary artery pressures. Measures of coupling between RV afterload and RV contractility may provide important information not apparent by other clinical and hemodynamic measures. Future research should be aimed at development of noninvasive measures of coupling.

Findings in the Pulmonary Vascular Bed in the Remote Phase After Kawasaki Disease

Kawasaki disease (KD) is a form of systemic vasculitis that causes chronic changes in arterial walls, including pulmonary arteries. The aim of this study was to test the hypothesis that pulmonary arterial wall properties and hemodynamics are abnormal after the resolution of KD. Pulmonary arterial input impedance was measured during cardiac catheterization (4.8 ± 4.5 years after disease onset) in 47 consecutive patients (mean age 7.8 ± 5.7 years) with KD and coronary artery lesions (CALs) in the acute phase and 42 control patients (mean age 6.7 ± 4.6 years). Patients with KD were subdivided into 2 groups: 28 with persistent CALs and 19 with regressed CALs. There were no significant differences in characteristic impedance and peripheral vascular resistance between patients with KD and controls. Compared with controls, patients with persistent CALs had significantly lower pulmonary arterial compliance, suggesting increased wall stiffness of the peripheral pulmonary vascular bed (p <0.05, analysis of variance). Patients with persistent CALs also exhibited increased wave reflection compared with other groups (p <0.05, analysis of variance). In conclusion, unlike patients with regressed CALs, patients with persistent CALs have abnormal mechanical properties and hemodynamics of the pulmonary artery after KD. Together with previous reports of abnormal properties of coronary and systemic arteries, these data suggest that KD vasculitis causes chronic changes in arterial wall properties in the entire arterial system to varying degrees and extent. The fate of these abnormalities in the pulmonary bed and other arterial systems and their potential adverse effects must be monitored in long-term follow-up.

Pulmonary arterial input impedance in patients with chronic pulmonary diseases

To evaluate pulmonary vascular lesions, input impedance of pulmonary arterial system was determined in 52 patients with chronic pulmonary diseases (CPD) by using a multisensor catheter. Mean values of impedance parameters in 14 subjects with normal mean arterial pressure (less than 15 mmHg) were 31 +/- 3 dyne.sec.cm-5 in characteristic impedence (Zo), 3.5 +/- 0.3 Hz in the frequency at which the first minimum of the impedance modulus occurs (fmin) and 0.85 +/- 0.3 in Zx oscillation (Zxos). In patients with CPD, Zo increased with an elevation of pulmonary arterial pressure (p less than 0.01) and fmin shifted to the right with that (p less than 0.05). These results show that stiffness of the proximal arteries in CPD is increased. In patients of interstitial fibrosis with pulmonary arterial hypertension, Zo was not significantly increased, but fmin shifted to the right. Pulse wave velocity correlated with fmin, but did not correlate with Zo. In conclusion, these results suggest that analysis of pulmonary arterial input impedance with a multisensor catheter provides useful information for patients with pulmonary hypertension.

Extraction of Pulmonary Vascular Compliance, Pulmonary Vascular Resistance, and Right Ventricular Work From Single-Pressure and Doppler Flow Measurements in Children With Pulmonary Hypertension: a New Method for Evaluating Reactivity

Current evaluation of pulmonary hypertension (PH) in children involves measurement of pulmonary vascular resistance (PVR); however, PVR neglects important pulsatile components. Pulmonary artery (PA) input impedance and ventricular power (VP) include mean and pulsatile effects and have shown promise as alternative measures of vascular function. Here we report the utility of pulsed-wave (PW) Doppler-measured instantaneous flow and pressure measurements for estimation of input impedance and VP and use this method to develop a novel parameter: reactivity in compliance. An in vitro model of the general pulmonary vasculature was used to obtain impedance and VP, measured by PW Doppler and a reference flow meter. The method was then tested in a preliminary clinical study in subjects with normal PA hemodynamics (n=4) and patients with PH undergoing reactivity evaluation (8 patients; 23 data points). In vitro results showed good agreement between the impedance spectra computed from both flow-measurement methods. Excellent correlation was seen in vitro between actual resistance and the zero-frequency (Z(o)) impedance value (r2=0.984). Excellent agreement was also found between Z(o) and PVR in the clinical measurements (y=1.075x+0.73; r=0.993). Furthermore, total VP and VP/cardiac output increased significantly with hypertension (128.73 to 365.91 mW and 2.42 to 6.69 mW x mL(-1) x s(-1), respectively). The first-harmonic value of impedance (Z1) was used as a measure of compliance reactivity; older patients exhibited markedly less compliance reactivity than did younger patients. Input impedance and VP calculated from Doppler measurements and a single-catheter pressure measurement provide comprehensive characterization of PH and reactivity.

Pulmonary vascular effects of dobutamine in experimental pulmonary hypertension.

To characterize the dose-related effects of dobutamine on pulmonary vascular tone and associated changes in right ventricular afterload in canine microembolic lung injury . Prospective, interventional study. University laboratory. Ten anesthetized and ventilated dogs. Right heart catheterization for the measurement of pulmonary vascular resistance by multipoint mean pulmonary artery pressure (Ppa)/cardiac output (Q) plots, partitioning of pulmonary vascular resistance by the occlusion method, and determination of pulmonary arterial input impedance from spectral analysis of Ppa and Q waves, in ten anesthetized and ventilated dogs, before and after induction of acute microembolic lung injury, and without or with 5, 10, 15, and 20 microg.kg(-1).min(-1) dobutamine. Microembolic pulmonary hypertension was associated with a shift of Ppa/Q plots to higher pressures, a slight decrease in the arterial component of pulmonary vascular resistance, a decrease in characteristic impedance, and an increase in the pulsatile component of right ventricular hydraulic load. At baseline, dobutamine had no effect on Ppa/Q plots at 5 and 10 microg.kg(-1).min(-1) but increased Ppa at 15 and 20 microg.kg(-1).min(-1). In microembolic pulmonary hypertension, the only effect of dobutamine on Ppa/Q plots was a decrease in Ppa at 20 microg.kg(-1).min(-1). Dobutamine had no effect on the partitioning of pulmonary vascular resistance or on pulmonary arterial input impedance spectrum. Dobutamine at doses up to 10 microg.kg(-1).min(-1) has no flow-independent effect on the normal or the acutely hypertensive pulmonary circulation. Higher doses may be constricting or dilating depending on preexisting tone.

Modulation of pulmonary arterial input impedance during transition from inspiration to expiration.

We investigated whether respiration influences pulmonary arterial input impedance during transition from inspiration to expiration in five anesthetized, spontaneously breathing dogs. Impedance (Z) was separately assessed for heart beats occurring in inspiration, in expiration, and during the transition from inspiration to expiration (transitional beat). Transitional beats were scored by the ratio between the fraction of beat falling in expiration and the total beat duration [expiratory fraction (Efr)] to quantify their position within the transition. In transitional beats, input resistance linearly increased with Efr; Z modulus at the heart-rate frequency (fHR) decreased up to -50% for Efr = 50%. Z phase at fHR was greater than in inspiration for Efr <40% and lower for Efr >50%. Unlike blood flow velocity, mean value and first harmonic of pulmonary arterial pressure were correlated to Efr and paralleled the changes of input resistance and Z at fHR. This indicates that respiration influences Z through modifications in arterial pressure. The evidence of important respiratory influences on Z function may help the pathophysiological interpretation of dysfunctions of the right heart pumping action, such as the so-called cor pulmonale.

Does spontaneous respiration alter pulmonary artery input impedance?

The aim of this study was to determine whether spontaneous respiration influences pulmonary artery input impedance, a question that has received little attention in the literature. Impedance values were assessed during three different phases of the respiratory cycle, namely inspiration, expiration and postexpiration (i.e. the null respiratory flow period between expiration and the next inspiration) in five anaesthetized spontaneously breathing dogs. Firstly, impedance values during postexpiration were taken as the reference baseline, and compared with values obtained during inspiration and expiration. Then, differences between values in inspiration and in expiration were tested, taking impedance during inspiration as the baseline. Differences with respect to postexpiration were found for three parameters of input impedance: input resistance, characteristic impedance, and the frequency at the first zero-crossing of the impedance phase from negative to positive values (f(cross)). Input resistance was significantly lower in inspiration (85% of the baseline), characteristic impedance was significantly greater in inspiration and in expiration (112 and 119% respectively), and f(cross) was significantly lower in expiration (89%). By contrast, only input resistance differed significantly when inspiration was compared to expiration. Therefore, spontaneous respiration was shown to influence input impedance significantly. The observed changes in characteristic impedance and f(cross) might be explained by a stiffening of the pulmonary artery wall, due to neural and/or mechanical factors, during inspiration and expiration.

Role of arterial design on pulse wave reflection in a fractal pulmonary network.

A novel interpretation of pulmonary arterial input impedance was evaluated for the lung as a fractal vascular network. We hypothesized that local sources of reflection introduce trends of global reflection into the input impedance spectra. These trends are related to the network topology, geometry, and design according to Rb = Rdx, where Rb is the branching ratio, Rd is the diameter ratio, and x is the fractal dimension quantifying design. Simulations using values of Rd and x, which were derived morphometrically, confirmed two patterns of global reflection: a continuous trend attributed to a single effective site of reflection caused by frequency-dependent sources of impedance contrast and a discrete trend arising from a longitudinal distribution of frequency-independent sources of reflection. The continuous trend depended only on the network parameter Rd, whereas the discrete trend depended on Rd and x. Our results indicate that the impedance-matching properties of a deterministic pulmonary fractal network encode arterial geometry and topology via function and that typical values of Rd and x for the pulmonary circulation facilitate shear stress amplification in its peripheral vessels. Thus, inasmuch as shear forces may be involved in the endothelial mechanisms for pathological, or physiological, vascular remodeling, broadband input impedance analysis may reveal interactions between network organization and vascular function.

Time-varying pulmonary arterial input impedance via wavelet decomposition.

Wavelet decomposition is proposed as a novel approach for determining pulmonary arterial input impedance throughout the breathing cycle. The canine pulmonary arterial input impedance was evaluated throughout the ventilatory cycle at 5, 10, and 15 cmH2O of positive end-expiratory pressure. The impedance spectrum was obtained by Fourier transformation of wavelets generated by decomposing the pulmonary arterial pressure and flow waveforms. With wavelet decomposition, each heart beat is viewed individually as a transient pulse rather than as an interval within a continuous function of pressure and flow. The advantage of using this approach is the ability to obtain stable estimates of input impedance spectra with high-frequency resolution over the entire frequency range with only a limited data set of pressure and flow decomposed to wavelets as short as singular extrapolated cardiac cycles. This method was used to define the changes of input impedance that occur during the ventilatory cycle. Results show that the impedance spectrum undergoes notable changes during the breathing cycle and demonstrate the utility of the proposed method.

Vascular impedance analysis in dog lung with detailed morphometric and elasticity data

On the basis of experimentally measured morphometric and elasticity data and model-derived mean pressure-flow conditions, we attempt a theoretical modeling of pulsatile flow in the whole lung. In the model we use the "elastic tube" for arteries and veins, and the vascular impedance in arteries and veins follows Womersley's theory and electric analogue. We employ the "sheet-flow" theory to describe the flow in the capillaries and to obtain the microvascular impedance matrix. The characteristic impedance of each order along the vascular tree, the input impedance at the capillary entrance and exit, and the pulmonary arterial input impedance at the main pulmonary artery are computed under certain physiological conditions. Using the pulsatile flow model, we investigate the effects of arterial vascular obstruction on pulmonary vascular impedance. The model-derived data are compared with the available experimental results in the literature.

Beat-by-beat changes of viscoelastic and inertial properties of the pulmonary arteries.

We tested the hypothesis that pulmonary arterial input impedance varies during the ventilatory cycle due to alterations not only of the viscoelastic components of the pulmonary vasculature but also due to changes of the inertial components. A four-element lumped-parameter model was used to fit the pulmonary arterial pressure-flow recordings in the time domain in 10 anesthetized dogs. The four elements consisted of a resistor (R) that represents input resistance, a second resistor (R1) and a capacitor (C1) that represent the viscoelastic properties of the pulmonary vasculature, and an inductor (L1) that represents inertial properties of blood within the pulmonary vasculature. The parameters were evaluated at each heartbeat throughout the ventilatory cycle at three levels of positive end-expiratory pressure. All four parameters varied significantly during the ventilatory cycle. R, C1, L1, and R1 varied by up to 97, 33, 13, and 17%, respectively. Changes in parameter values were most apparent at the start of expiration when the most rapid changes of lung volume occur. This pattern of the results is consistent with the hypothesis that the time variation of pulmonary arterial impedance is due to dynamic shifts of blood volume between the extra-alveolar and alveolar arteries.

Effect of compliance on a time-domain estimate of the characteristic impedance of the pulmonary artery during acute pulmonary hypertension

In 11 pigs under general endotracheal anaesthesia, the time-domain method of determining the pulmonary arterial input impedance was compared with the frequency-domain equivalent under normal conditions as well as acute pulmonary hypertension induced by glass microspheres. The time-domain methods of determining the pulmonary arterial compliance C and pulmonary vascular bed resistance Rp compared favourably with the frequency-domain equivalents (r = 0.774, n = 60, p < 0.001 and r = 0.906, n = 60, p < 0.001, respectively), even at mean pulmonary artery pressures (MPAP) of 35 mmHg and above. A consistent and ever-increasing difference between characteristic impedance Zo(omega), estimated by averaging input impedance modulus values over a selected frequency range, and its time domain equivalent Ro with increasing MPAP was shown to be the cause of the poor fit between the measured and remodelled pulmonary blood flow. By analysing a time-domain estimate of the pulmonary characteristic impedance Ro(C, Rp, t), it was demonstrated that the characteristic impedance was dependent on C. Ro is therefore not an accurate representation of the characteristic impedance, especially under conditions of acute pulmonary hypertension. Ro(C, Rp, t) should therefore be calculated instead.

Right ventricular dynamics during left ventricular assistance in closed-chest dogs

To determine the effects of left ventricular assist device (LVAD) support on global right ventricular (RV) systolic mechanics, 8 closed-chest, conscious, sedated dogs were studied after placement of an LVAD (left ventricle to femoral artery bypass) and implantation of 27 tantalum markers into the left ventricular and RV walls for computation of biventricular volumes and geometry. Biplane cinefluoroscopic marker images and hemodynamic parameters were recorded during transient vena caval occlusion at various levels of LVAD support. Right ventricular contractility was assessed using end-systolic elastance and preload recruitable stroke work, and the myocardial (pump) efficiency of converting mechanical energy to external work (stroke work/total pressure-volume area) was calculated. With full LVAD support, RV end-diastolic volume increased from 60 ± 15 to 62 ± 17 mL ( p < 0.002), pulmonary artery input impedance decreased from 940 ± 636 to 587 ± 347 dyne · s/cm 5 ( p < 0.007), and measurement of RV and left ventricular septal-free wall dimensions demonstrated a significant leftward septal shift ( p < 0.0005). Global RV end-systolic elastance and preload recruitable stroke work decreased from 2.4 ± 1.0 to 1.7 ± 0.7 mm Hg/mL ( p < 0.004) and 14.1 ± 3.3 to 12.1 ± 3.9 mm Hg ( p < 0.02), respectively; however, RV power output and myocardial efficiency did not change significantly ( p > 0.74 and p > 0.33, respectively). Therefore, during LVAD support, global RV contractility is impaired with leftward septal shifting, but RV myocardiol efficiency and power output are maintained through a decrease in RV afterload and an increase in RV preload.

Pulmonary artery hemodynamics in primary pulmonary hypertension

Objectives. The present investigation compared and contrasted steady and pulsatile pulmonary hemodynamics at rest and during exercise in patients with primary pulmonary hypertension and normal control subjects.Background. A complete description of the relation between pressure and flow in the pulmonary circulation includes both steady and pulsatile hemodynamic behavior. Patients with primary pulmonary hypertension provide a unique opportunity to study the effects of primary alterations in pulmonary vasculature on pulmonary artery vascular hydraulic load.Methods. Catheter tip pressure and velocity recordings from the main pulmonary artery in 8 patients with primary pulmonary hypertension and 10 control subjects were used to derive the pulmonary artery input impedance spectrum and the extent of pulse wave reflection at rest and during exercise.Results. As expected, in patients with primary pulmonary hypertension, mean pulmonary artery pressure (50 ± 10 mm Hg) and pulmonary vascular resistance (880 ± 446 dynes·s·cm−5) were markedly elevated at rest and remained so during exercise (mean pressure 71 ± 15 mm Hg, mean resistance 750 ± 530 dynes·s·cm−5). Pulmonary artery characteristic impedance was elevated at rest and did not change with exercise (rest 55 ± 25 dynes·s·cm−5; exercise 66 ± 33 dynes·s·cm−5). Measures of arterial wave reflection indicated that the extent of wave reflection in the pulmonary bed in those with primary pulmonary hypertension is large at rest (reflection coefficient 0.89 ± 0.09) and that the composite reflected wave arrived during the midportion of right ventricular ejection. Although the extent of wave reflection decreased with exercise (reflection coefficient 0.81 ± 0.10, p < 0.05), the magnitude and timing of these reflections remained adverse. Furthermore, in patients with primary pulmonary hypertension, the stroke volume response to exercise was strongly related to rest levels of pulmonary artery diastolic pressure, pulmonary vascular resistance and the reflection factor, whereas no such relation was found in the control subjects.Conclusions. In addition to the expected abnormalities in steady measures of pulmonary artery hemodynamics at rest in patients with primary pulmonary hypertension, rest and exercise measures of oscillatory behavior (characteristic impedance and pulse wave reflection) are perturbed. Measures of steady and pulsatile behavior, particularly wave reflection, appear to have an important role in the exercise response of these patients.

Effects of Pulmonary Vascular Obstruction on Right Ventricular Afterload

We compared the effects of three forms of vascular obstruction: positive end-expiratory pressure (PEEP), ensnarement of the left main pulmonary artery (SN), and pulmonary thromboembolism (EMB) on right ventricular afterload. We measured right ventricular and pulmonary arterial pressures and flow in open-chested dogs under anesthesia (n = 8). Pulmonary artery input impedance (Zin) was calculated by Fourier analysis of the pressure and flow waves. Characteristic impedance (Zc) and pulmonary arterial compliance (Ca) were estimated from Zin with a lumped parameter model. Although PEEP, SN, and EMB all increased mean pulmonary arterial pressure, PEEP, had negligible effect on Zc and Ca, whereas SN increased Zc but decreased Ca (+24% and -49%, respectively), and EMB decreased both Zc and Ca (-33% and -39%, respectively). These changes of Zc affect wave reflection and alter the energy transmission ratio, which is the ratio of hydraulic power output in the measured and forward waves (Wm/Wf). Under control conditions, Wm/Wf was 62% and was not affected significantly by SN (59%) or by PEEP (46%), but it fell significantly to 30% after EMB. Simulation of these experiments in a mathematical model suggested that the increase of Zc with SN was due to an active neurohumoral effect; all other responses were consistent with passive mechanical effects. In additional experiments, we tested the effects of meclofenamate (n = 6) and ketanserin (n = 6) and of atropine and vagotomy (n = 5) on the response to SN and EMB. The serotonin antagonist, ketanserin, blunted the increase of Zc to SN, but none of the interventions significantly affected the response of Zc or Ca to EMB.(ABSTRACT TRUNCATED AT 250 WORDS)

Characterization of pulmonary arterial input impedance with lumped parameter models

Page H587: B. J. B. Grant and L. J. Paradowski. “Characterization of pulmonary arterial input impedance with lumped parameter models.” Equations 5 and 6 should appear as the following. (See PDF)