Interruption of the tricuspid regurgitant jet: A possible consequence of reflected waves.

Reflected pressure waves can impact central aortic pressure, and can cause notching of the pulmonic valve Doppler signal. However, reflected waves in the venous system usually do not achieve a high enough velocity to alter Doppler flow patterns. Herein we report a case of systolic notching of the tricuspid regurgitant signal that likely resulted from reflected venous waves.

Genesis of the characteristic pulmonary venous pressure waveform as described by the reservoir-wave model.

Conventional haemodynamic analysis of pulmonary venous and left atrial (LA) pressure waveforms yields substantial forward and backward waves throughout the cardiac cycle; the reservoir wave model provides an alternative analysis with minimal waves during diastole. Pressure and flow in a single pulmonary vein (PV) and the main pulmonary artery (PA) were measured in anaesthetized dogs and the effects of hypoxia and nitric oxide, volume loading, and positive-end expiratory pressure (PEEP) were observed. The reservoir wave model was used to determine the reservoir contribution to PV pressure and flow. Subtracting reservoir pressure and flow resulted in 'excess' quantities which were treated as wave-related.Wave intensity analysis of excess pressure and flow quantified the contributions of waves originating upstream (from the PA) and downstream (from the LA and/or left ventricle (LV)).Major features of the characteristic PV waveform are caused by sequential LA and LV contraction and relaxation creating backward compression (i.e.pressure-increasing) waves followed by decompression (i.e. pressure-decreasing) waves. Mitral valve opening is linked to a backwards decompression wave (i.e. diastolic suction). During late systole and early diastole, forward waves originating in the PA are significant. These waves were attenuated less with volume loading and delayed with PEEP. The reservoir wave model shows that the forward and backward waves are negligible during LV diastasis and that the changes in pressure and flow can be accounted for by the discharge of upstream reservoirs. In sharp contrast, conventional analysis posits forward and backward waves such that much of the energy of the forward wave is opposed by the backward wave.

Wave reflections in the pulmonary arteries analysed with the reservoir-wave model.

Conventional haemodynamic analysis of pressure and flow in the pulmonary circulation yields incident and reflected waves throughout the cardiac cycle, even during diastole. The reservoir-wave model provides an alternative haemodynamic analysis consistent with minimal wave activity during diastole. Pressure and flow in the main pulmonary artery were measured in anaesthetized dogs and the effects of hypoxia and nitric oxide, volume loading and positive end-expiratory pressure were observed. The reservoir-wave model was used to determine the reservoir contribution to pressure and flow and once subtracted, resulted in 'excess' quantities, which were treated as wave-related. Wave intensity analysis quantified the contributions of waves originating upstream (forward-going waves) and downstream (backward-going waves). In the pulmonary artery, negative reflections of incident waves created by the right ventricle were observed. Overall, the distance from the pulmonary artery valve to this reflection site was calculated to be 5.7 ± 0.2 cm. During 100% O2 ventilation, the strength of these reflections increased 10% with volume loading and decreased 4% with 10 cmH2O positive end-expiratory pressure. In the pulmonary arterial circulation, negative reflections arise from the junction of lobar arteries from the left and right pulmonary arteries. This mechanism serves to reduce peak systolic pressure, while increasing blood flow.

Classical electrical and hydraulic Windkessel models validate physiological calculations of Windkessel (reservoir) pressure.

Our "reservoir-wave approach" to arterial hemodynamics holds that measured arterial pressure should be considered to be the sum of a volume-related pressure (i.e., reservoir pressure, P(reservoir)) and a wave-related pressure (P(excess)). Because some have questioned whether P(reservoir) (and, by extension, P(excess)) is a real component of measured physiological pressure, it was important to demonstrate that P(reservoir) is implicit in Westerhof's classical electrical and hydraulic models of the 3-element Windkessel. To test the validity of our P(reservoir) determinations, we studied a freeware simulation of the electrical model and a benchtop recreation of the hydraulic model, respectively, measuring the voltage and the pressure distal to the proximal resistance. These measurements were then compared with P(reservoir), as calculated from physiological data. Thus, the first objective of this study was to demonstrate that respective voltage and pressure changes could be measured that were similar to calculated physiological values of P(reservoir). The second objective was to confirm previous predictions with respect to the specific effects of systematically altering proximal resistance, distal resistance, and capacitance. The results of this study validate P(reservoir) and, thus, the reservoir-wave approach.

Wave Intensity Analysis of Right Ventricular Function during Pulsed Operation of Rotary Left Ventricular Assist Devices.

Changing the speed of left ventricular assist devices (LVADs) cyclically may be useful to restore aortic pulsatility; however, the effects of this pulsation on right ventricular (RV) function are unknown. This study investigates the effects of direct ventricular interaction by quantifying the amount of wave energy created by RV contraction when axial and centrifugal LVADs are used to assist the left ventricle. In 4 anesthetized pigs, pressure and flow were measured in the main pulmonary artery and wave intensity analysis was used to identify and quantify the energy of waves created by the RV. The axial pump depressed the intensity of waves created by RV contraction compared with the centrifugal pump. In both pump designs, there were only minor and variable differences between the continuous and pulsed operation on RV function. The axial pump causes the RV to contract with less energy compared with a centrifugal design. Diminishing the ability of the RV to produce less energy translates to less pressure and flow produced, which may lead to LVAD-induced RV failure. The effects of pulsed LVAD operation on the RV appear to be minimal during acute observation of healthy hearts. Further study is necessary to uncover the effects of other modes of speed modulation with healthy and unhealthy hearts to determine if pulsed operation will benefit patients by reducing LVAD complications.

Quantification of Pulsed Operation of Rotary Left Ventricular Assist Devices with Wave Intensity Analysis.

The current generation of left ventricular assist devices (LVADs) provides continuous flow and has the capacity to reduce aortic pulsatility, which may be related to a range of complications associated with these devices. Pulsed LVAD operation using speed modulation presents a mechanism to restore aortic pulsatility and potentially mitigate complications. We sought to investigate the interaction of axial and centrifugal LVADs with the LV and quantify the effects of continuous and pulsed LVAD operations on LV generated wave patterns under different physiologic conditions using wave intensity analysis (WIA) method. The axial LVAD created greater wave intensity associated with LV relaxation. In both LVADs, there were only minor and variable differences between the continuous and pulsed operations. The response to physiologic stress was preserved with LVAD implantation as wave intensity increased marginally with volume loading and significantly with infusion of norepinephrine. Our findings and a new approach of investigating aortic wave patterns based on WIA are expected to provide useful clinical insights to determine the ideal operation of LVADs.

Alternative Approaches to the Assessment of the Systemic Circulation and Left Ventricular Performance: A Proof-of-Concept Study.

BACKGROUND: The purpose of this article is to examine the systemic circulation and left ventricular (LV) performance by alternative, nonconventional approaches: systemic vascular conductance (G SV ) and the head-capacity relation (ie, the relation between LV pressure and cardiac output), respectively; in so doing, we aspired to present a novel and improved interpretation of integrated cardiovascular function. METHODS: In 16 open-chest, anaesthetized pigs, we measured LV pressure (P LV ), central aortic pressure (P Ao ), and central venous pressure (P CV ) and aortic flow (Q Ao ). We calculated heart rate (HR), stroke volume, cardiac index (CI = cardiac output/body weight), mean PLV ( P ¯ LV ) , and the average arteriovenous pressure difference ( Δ P = P ¯ Ao - P ¯ CV ); G SV  = CI/( P ¯ Ao - P ¯ CV ). We studied the effects of changing loading conditions with the administration of phenylephrine (Δ P ¯ Ao ≥ +25 mm Hg), isoproterenol (ΔHR ∼+25%), sodium nitroprusside (Δ P ¯ Ao ≥ -25 mm Hg), and proximal aortic constriction (to maximize developed P LV and minimize Q Ao ). RESULTS: Sodium nitroprusside and isoproterenol increased G SV compared with phenylephrine and constriction. A maximum head-capacity curve was derived from pooled data using nonlinear regression on the maximum P ¯ LV values in Q Ao bins 12.5 mL/min/kg wide. The head-capacity relation and the plots of conductance were combined using CI as a common axis, which illustrated that CI is the output of the heart and the input of the circulation. CONCLUSIONS: Thus, at a given CI, G SV determines the driving pressure and, thereby, P Ao . We also demonstrated how decreases in G SV compensate for arterial hypotension by restoring the arteriovenous pressure difference and arterial pressure.

CONTEXTE: Le présent article examine l'efficacité de la circulation générale et la fonction ventriculaire gauche à l'aide de paramètres de rechange non conventionnels, soit la conductance vasculaire systémique (G VS ) pour l'une et la relation pression-volume (c.-à-d. la relation entre la pression ventriculaire gauche et le débit cardiaque) pour l'autre, dans le but de présenter une interprétation nouvelle et améliorée de la fonction cardiovasculaire intégrée. MÉTHODOLOGIE: Chez 16 porcs anesthésiés, nous avons mesuré à thorax ouvert la pression ventriculaire gauche (P VG ), la pression aortique centrale (P AC ), la pression veineuse centrale (P VC ) et le flux aortique (Q A ). Nous avons établi la fréquence cardiaque (FC), le volume d'éjection systolique, l'index cardiaque (IC; rapport entre le débit cardiaque et le poids corporel), la P VG moyenne ( P ¯ VG ) et la différence de pression artérioveineuse moyenne ( Δ P = P ¯ A C − P ¯ V C ); G VS  = IC/( P ¯ AC − P ¯ VC ). Nous avons aussi étudié les effets d'une modification des conditions de charge cardiaque provoquée par l'administration de phényléphrine (Δ P ¯ AC ≥ + 25 mmHg), d'isoprotérénol (ΔFC d'environ + 25 %) ou de nitroprussiate de sodium (Δ P ¯ AC ≥ − 25 mmHg) et par la constriction de l'aorte proximale (pour maximiser la P VG développée et réduire le plus possible le Q A ). RÉSULTATS: Le nitroprussiate de sodium et l'isoprotérénol ont augmenté la G VS comparativement à la phényléphrine et à la constriction. Une courbe de la relation pression-volume maximale a été dérivée à partir des données groupées, au moyen d'une régression non linéaire sur les valeurs maximales de la P ¯ VG réparties dans des classes de Q A de 12,5 ml/min/kg d'amplitude. La courbe de la relation pression-volume et le tracé de la conductance ont été superposés en utilisant l'IC comme axe commun, ce qui a permis de constater que l'IC correspond au débit cardiaque et au volume entrant dans la circulation. CONCLUSIONS: Pour un IC donné, la G VS détermine la pression motrice et donc, la P AC . Nous avons aussi démontré comment une diminution de la G VS compense l'hypotension artérielle en rétablissant la différence de pression artérioveineuse et la pression artérielle.

Electrical power to run ventricular assist devices using the Free-range Resonant Electrical Energy Delivery system.

BACKGROUND: Models of power delivery within an intact organism have been limited to ionizing radiation and, to some extent, sound and magnetic waves for diagnostic purposes. Traditional electrical power delivery within the intact human body relies on implanted batteries that limit the amount and duration of delivered power. The efficiency of current battery technology limits the substantial demands required, such as continuous operation of an implantable artificial heart pump within a human body. METHODS: The fully implantable, miniaturized, Free-range Resonant Electrical Energy Delivery (FREE-D) system, compatible with any type of ventricular assist device (VAD), has been tested in a swine model (HVAD) for up to 3 hours. Key features of the system, the use of high-quality factor (Q) resonators together with an automatic tuning scheme, were tested over an extended operating range. Temperature changes of implanted components were measured to address safety and regulatory concerns of the FREE-D system in terms of specific absorption rate (SAR). RESULTS: Dynamic power delivery using the adaptive tuning technique kept the system operating at maximum efficiency, dramatically increasing the wireless power transfer within a 1-meter diameter. Temperature rise in the FREE-D system never exceeded the maximum allowable temperature deviation of 2°C (but remained below body temperature) for an implanted device within the trunk of the body at 10 cm (25% efficiency) and 50 cm (20% efficiency), with no failure episodes. CONCLUSIONS: The large operating range of FREE-D system extends the use of VAD for nearly all patients without being affected by the depth of the implanted pump. Our in-vivo results with the FREE-D system may offer a new perspective on quality of life for patients supported by implanted device.

The reservoir-wave approach to characterize pulmonary vascular-right ventricular interactions in humans.

Using the reservoir-wave approach (RWA) we previously characterized pulmonary vasculature mechanics in a normal canine model. We found reflected backward-traveling waves that decrease pressure and increase flow in the proximal pulmonary artery (PA). These waves decrease right ventricular (RV) afterload and facilitate RV ejection. With pathological alterations to the pulmonary vasculature, these waves may change and impact RV performance. Our objective in this study was to characterize PA wave reflection and the alterations in RV performance in cardiac patients, using the RWA. PA pressure, Doppler-flow velocity, and pulmonary arterial wedge pressure were measured in 11 patients with exertional dyspnea. The RWA was employed to analyze PA pressure and flow; wave intensity analysis characterized PA waves. Wave-related pressure was partitioned into two components: pressures due to forward-traveling and to backward-traveling waves. RV performance was assessed by examining the work done in raising reservoir pressure and that associated with the wave components of systolic PA pressure. Wave-related work, the mostly nonrecoverable energy expended by the RV to eject blood, tended to vary directly with mean PA pressure. Where PA pressures were lower, there were pressure-decreasing/flow-increasing backward waves that aided RV ejection. Where PA pressures were higher, there were pressure-increasing/flow-decreasing backward waves that impeded RV ejection. Pressure-increasing/flow-decreasing backward waves were responsible for systolic notches in the Doppler flow velocity profiles in patients with the highest PA pressure. Pulmonary hypertension is characterized by reflected waves that impede RV ejection and an increase in wave-related work. The RWA may facilitate the development of therapeutic strategies.

The case for the reservoir-wave approach.

The Reservoir-Wave Approach is an alternative, time-domain approach to arterial hemodynamics that is based on the assertion that measured pressure and flow can be resolved into their volume-related (i.e., reservoir) and wave-related (i.e., excess) components. The change in reservoir pressure is assumed to be proportional to the difference between measured inflow and calculated outflow. Wave intensity analysis of the excess components yields a pattern of aortic wave propagation and reflection in the dog that is novel and physiologically plausible: waves are reflected positively from a site in the femoral circulation and negatively from a site below the diaphragm, where the total "daughter-vessel" cross-sectional area exceeds the "mother-vessel" area. With vasodilatation, the negative reflection is augmented and with vasoconstriction, it is virtually eliminated. On the other hand, conventional hemodynamic analysis has been shown to yield a paradoxical "forward-going backward wave" and the impedance minimum, previously assumed to be an indicator of the source of wave reflection according to quarter-wave-length theory, has been shown to be due to the reservoir component. Clinical studies employing the Reservoir-Wave Approach should be undertaken to verify experimental observations and, perhaps, to gain new diagnostic and therapeutic insights.

Alterations in aortic wave reflection with vasodilation and vasoconstriction in anaesthetized dogs.

BACKGROUND: Using the reservoir-wave approach, we studied wave propagation, reflection, and re-reflection in the canine aorta with administrations of sodium nitroprusside (NP) and methoxamine (Mtx). METHODS: In 8 anaesthetized dogs, excess pressures were calculated from pressure and flow measurements at 4 locations along the aorta; wave intensity analysis was employed to identify wavefronts and the type of waves. RESULTS: NP (intravenous; 14 µg/min) decreased mean aortic pressure from 80 ± 3 mm Hg to 48 ± 1 mm Hg; Mtx (intravenous; 10 µg/min) increased mean pressure from 80 ± 3 mm Hg to 104 ± 4 mm Hg. NP increased negative reflection near the kidneys (reflection coefficient: -0.33 vs -0.18; P < 0.01) and produced new negatively reflecting sites just beyond the arch and in the proximal femoral arteries, consistent with a vasodilating effects of nitrates on conducting arteries. Mtx negated negative reflection from near the kidneys (-0.02 vs -0.17; P < 0.01) and increased positive femoral reflection (0.38 vs 0.26; P < 0.01). The large reflected compression wave was re-reflected from the closed aortic valve to produce a prominent increase in middiastolic pressure in the distal aorta. CONCLUSIONS: The reservoir-wave approach explains decreasing diastolic pressure without positing waves that travel at near-infinite velocities and reveals the pressure changes that are uniquely due to wave motion.

Partitioning pulmonary vascular resistance using the reservoir-wave model.

The conventional determination of pulmonary vascular resistance does not indicate which vascular segments contribute to the total resistance of the pulmonary circulation. Using measurements of pressure and flow, the reservoir-wave model can be used to partition total pulmonary vascular resistance into arterial, microcirculation, and venous components. Changes to these resistance components are investigated during hypoxia and inhaled nitric oxide, volume loading, and positive end-expiratory pressure. The reservoir-wave model defines the pressure of a volume-related reservoir and the asymptotic pressure. The mean values of arterial and venous reservoir pressures and arterial and venous asymptotic pressures define a series of resistances between the main pulmonary artery and the pulmonary veins: the resistance of large and small arteries, the microcirculation, and veins. In 11 anaesthetized, open-chest dogs, pressure and flow were measured in the main pulmonary artery and a single pulmonary vein. Volume loading reduced each vascular resistance component, whereas positive end-expiratory pressure only increased microcirculation resistance. Hypoxia increased the resistance of small arteries and veins, whereas nitric oxide only decreased small-artery resistance significantly. The reservoir-wave model provides a novel method to deconstruct total pulmonary vascular resistance. The results are consistent with the expected physiological responses of the pulmonary circulation and provide additional information regarding which segments of the pulmonary circulation react to hypoxia and nitric oxide.