The pulmonary arterial branching pattern suggests that the early systolic forward-going compression wave (FCW) might be reflected as a backward-going expansion wave (BEW). Accordingly, in 11 open-chest anesthetized dogs we measured proximal pulmonary arterial pressure and flow (velocity) and evaluated wave reflection using wave-intensity analysis under low-volume, high-volume, high-volume + 20 cmH2O positive end-expiratory pressure (PEEP), and hypoxic conditions. We defined the reflection coefficient R as the ratio of the energy of the reflected wave (BEW [-]; backward-going compression wave, BCW [+]) to that of the incident wave (FCW [+]). We found that R = -0.07 +/- 0.02 under low-volume conditions, which increased in absolute magnitude to -0.20 +/- 0.04 (P < 0.01) under high-volume conditions. The addition of PEEP increased R further to -0.26 +/- 0.02 (P < 0.01). All of these BEWs were reflected from a site ~3 cm downstream. During hypoxia, the BEW was maintained and a BCW appeared (R = +0.09 +/- 0.03) from a closed-end site ~9 cm downstream. The normal pulmonary arterial circulation in the open-chest dog is characterized by negative wave reflection tending to facilitate right ventricular ejection; this reflection increases with increasing blood volume and PEEP.

Patients exposed to a surgical safety checklist experience better postoperative outcomes, but this could simply reflect wider quality of care in hospitals where checklist use is routine.

PHT patients have reduced RV strain patterns and more dyssynchronous ventricles compared with controls, which was relatable to clinical outcomes. AS best correlated with RVEF and provides prognostic information independent of other variables.

Endografting in the proximal descending aorta cause unfavorable changes in the ascending aortic input impedance and an increase in the PWV through the grafted segment, consistent with an increase in the modulus of elasticity. The grafts produce a negative Gamma at the distal end, an uncommon occurrence in the systemic circulation. Whether this change is of sufficient magnitude to result in post-graft dilation is unknown.

. Direct and series transmission of left atrial pressure perturbations to the pulmonary artery: a study using wave-intensity analysis. Am J Physiol Heart Circ Physiol 286: H267-H275, 2004. First published September 25, 2003 10.1152/ ajpheart.00505.2002-Pressure waves are thought to travel from the left atrium (LA) to the pulmonary artery (PA) only retrogradely, via the vasculature. In seven anesthetized open-chest dogs, a balloon was placed in the LA, which was rapidly inflated and deflated during diastole, early systole, and late systole. High-fidelity pressures were measured within and around the heart. Measurements were made at low volume [LoV; left ventricular end-diastolic pressure (LVEDP) ϭ 5-9 mmHg], high volume (HiV; LVEDP ϭ 16-19 mmHg), and HiV with the pericardium removed. Wave-intensity analysis demonstrated that, except during late systole, balloon inflation created forwardgoing PA compression waves that were transmitted directly through the heart without measurable delay; backward PA compression waves were transmitted in-series through the pulmonary vasculature and arrived after delays of 90 Ϯ 3 ms (HiV) and 103 Ϯ 5 ms (LoV; P Ͻ 0.05). Direct transmission was greater during diastole, and both direct and series transmission increased with volume loading. Pressure waves from the LA arrive in the PA by two distinct routes: rapidly and directly through the heart and delayed and in-series through the pulmonary vasculature. lung; arteries; hemodynamics; wave transmission WAVE TRANSMISSION through the heart is poorly understood. Among the clinical syndromes in which wave transmission could be an important, unappreciated factor are the stiff left atrium (LA) syndrome (6, 15) and the Bernheim syndrome (1,5,24). To study the transmission of waves generated in the LA, we created a system where a backward-going wave, originating from the LA, could be detected in the proximal pulmonary artery (PA; backward and forward are defined with respect to PA flow.) To create such a wave in a controlled fashion, we used an LA counterpulsation balloon. Pressure and velocity waveforms in the proximal PA were analyzed to evaluate the effects of LA pressure (P LA ) perturbations.Most commonly, pulsatile arterial phenomena have been characterized using Fourier analysis where the observed waveforms are decomposed into sinusoidal wave trains, and the results are expressed as amplitude and phase as a function of frequency (16,17). This frequency-domain analysis has provided much information. However, wave-intensity analysis where the observed waveforms are decomposed into a succession of infinitesimal wave fronts that are described by their amplitude and time (13,19) allows the interaction of forwardand backward-going waves and their relation to primary hemodynamic parameters (pressure, flow, etc.) to be studied directly. This method utilizes changes in pressure and velocity to evaluate the direction, intensity, and type of waves and has been used recently to study the systemic (18), pulmonary (8,11,22), and coronary circulations...

In order to explore a new approach to the analysis of diastolic dysfunction, we adapted wave-intensity analysis (WIA), a time-domain analysis that provides information regarding both upstream and downstream events, to left ventricular (LV) filling. WIA considers the pressure and flow waves as summations of successive wavelets, characterised by the direction they travel and by the sign of the pressure gradient associated with them. Wave intensity is the product, dPdU, calculated from the incremental differences in LV pressure (dP) and mitral velocity (dU) and, during the diastolic filling interval, yields up to five dPdU peaks. Peak 1 is caused by backward-travelling expansion waves that accelerate the blood while LV pressure falls, and may be related to "diastolic suction". Peak 2 is caused by forward-travelling compression waves which occur if acceleration continues after LV pressure begins to increase. Peak 3 is caused by backward compression waves and is associated with rising LV pressure and deceleration. Peak 4 is caused by forward compression waves and is associated with the increasing LV pressure and acceleration caused by atrial contraction. Peak 5 is caused by backward compression waves and is associated with increasing pressure and deceleration. These preliminary observations suggest that WIA can be useful in describing the mechanics of LV filling and, after much further work has been accomplished, it might prove useful in the detection and characterization of diastolic dysfunction.

Endovascular stents are commonly used to manage arterial diseases such as Aortic Abdominal Aneurysm (AAA), aortic dissection and coarctation. The radial force the stent applies to the vessel must be large enough to resist stent migration, but not so large that the mechanical stimulus initiates adverse vessel remodeling. We employed two approaches to characterize the radial force of Gianturco stents: first, by applying an external pressure to the stent and, second, by measuring the force exerted by the stent when deployed. From the second approach, we determined the force exerted at various area reductions that correspond to clinically relevant diameter oversizings. In this study, stent stiffness was determined from the force-area reduction curves. Comparing similar stents of various diameters revealed that smaller diameter stent had greater radial force and stiffness than larger diameter stents. Comparing similar stents of various lengths revealed that stents with longer lengths (and greater number of wires) has greater force and stiffness. Overlapping two stents increased the force and stiffness to values greater than the sum of those parameters for the individual stents. These data may have important clinical implications for understanding the effect of oversized and overlapped stents on vessel mechanics.

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