Direct and series transmission of left atrial pressure perturbations to the pulmonary artery: a study using wave-intensity analysis

2004 ◽  
Vol 286 (1) ◽  
pp. H267-H275 ◽  
Author(s):  
Ellen H. Hollander ◽  
Gary M. Dobson ◽  
Jiun-Jr Wang ◽  
Kim H. Parker ◽  
John V. Tyberg

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) = 5–9 mmHg], high volume (HiV; LVEDP = 16–19 mmHg), and HiV with the pericardium removed. Wave-intensity analysis demonstrated that, except during late systole, balloon inflation created forward-going 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 ± 3 ms (HiV) and 103 ± 5 ms (LoV; P < 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.

2016 ◽  
Vol 310 (5) ◽  
pp. H619-H627 ◽  
Author(s):  
Christopher J. Broyd ◽  
Sukhjinder Nijjer ◽  
Sayan Sen ◽  
Ricardo Petraco ◽  
Siana Jones ◽  
...  

Wave intensity analysis (WIA) has found particular applicability in the coronary circulation where it can quantify traveling waves that accelerate and decelerate blood flow. The most important wave for the regulation of flow is the backward-traveling decompression wave (BDW). Coronary WIA has hitherto always been calculated from invasive measures of pressure and flow. However, recently it has become feasible to obtain estimates of these waveforms noninvasively. In this study we set out to assess the agreement between invasive and noninvasive coronary WIA at rest and measure the effect of exercise. Twenty-two patients (mean age 60) with unobstructed coronaries underwent invasive WIA in the left anterior descending artery (LAD). Immediately afterwards, noninvasive LAD flow and pressure were recorded and WIA calculated from pulsed-wave Doppler coronary flow velocity and central blood pressure waveforms measured using a cuff-based technique. Nine of these patients underwent noninvasive coronary WIA assessment during exercise. A pattern of six waves were observed in both modalities. The BDW was similar between invasive and noninvasive measures [peak: 14.9 ± 7.8 vs. −13.8 ± 7.1 × 104 W·m−2·s−2, concordance correlation coefficient (CCC): 0.73, P < 0.01; cumulative: −64.4 ± 32.8 vs. −59.4 ± 34.2 × 102 W·m−2·s−1, CCC: 0.66, P < 0.01], but smaller waves were underestimated noninvasively. Increased left ventricular mass correlated with a decreased noninvasive BDW fraction ( r = −0.48, P = 0.02). Exercise increased the BDW: at maximum exercise peak BDW was −47.0 ± 29.5 × 104 W·m−2·s−2 ( P < 0.01 vs. rest) and cumulative BDW −19.2 ± 12.6 × 103 W·m−2·s−1 ( P < 0.01 vs. rest). The BDW can be measured noninvasively with acceptable reliably potentially simplifying assessments and increasing the applicability of coronary WIA.


2007 ◽  
Vol 292 (3) ◽  
pp. H1533-H1540 ◽  
Author(s):  
Tracy N. Hobson ◽  
Jacqueline A. Flewitt ◽  
Israel Belenkie ◽  
John V. Tyberg

The left atrium (LA) acts as a booster pump during late diastole, generating the Doppler transmitral A wave and contributing incrementally to left ventricular (LV) filling. However, after volume loading and in certain disease states, LA contraction fills the LV less effectively, and retrograde flow (i.e., the Doppler Ar wave) into the pulmonary veins increases. The purpose of this study was to provide an energetic analysis of LA contraction to clarify the mechanisms responsible for changes in forward and backward flow. Wave intensity analysis was performed at the mitral valve and a pulmonary vein orifice. As operative LV stiffness increased with progressive volume loading, the reflection coefficient (i.e., energy of reflected wave/energy of incident wave) also increased. This reflected wave decelerated the forward movement of blood through the mitral valve and was transmitted through the LA, accelerating retrograde blood flow in the pulmonary veins. Although total LA work increased with volume loading, the forward hydraulic work decreased and backward hydraulic work increased. Thus wave reflection due to increased LV stiffness accounts for the decrease in the A wave and the increase in the Ar wave measured by Doppler.


2016 ◽  
Vol 218 (4) ◽  
pp. 239-249 ◽  
Author(s):  
J. Su ◽  
O. Hilberg ◽  
L. Howard ◽  
U. Simonsen ◽  
A. D. Hughes

2015 ◽  
Vol 308 (12) ◽  
pp. H1603-H1611 ◽  
Author(s):  
Michael A. Quail ◽  
Daniel S. Knight ◽  
Jennifer A. Steeden ◽  
Liesbeth Taelman ◽  
Shahin Moledina ◽  
...  

Pulmonary wave reflections are a potential hemodynamic biomarker for pulmonary hypertension (PH) and can be analyzed using wave intensity analysis (WIA). In this study we used pulmonary vessel area and flow obtained using cardiac magnetic resonance (CMR) to implement WIA noninvasively. We hypothesized that this method could detect differences in reflections in PH patients compared with healthy controls and could also differentiate certain PH subtypes. Twenty patients with PH (35% CTEPH and 75% female) and 10 healthy controls (60% female) were recruited. Right and left pulmonary artery (LPA and RPA) flow and area curves were acquired using self-gated golden-angle, spiral, phase-contrast CMR with a 10.5-ms temporal resolution. These data were used to perform WIA on patients and controls. The presence of a proximal clot in CTEPH patients was determined from contemporaneous computed tomography/angiographic data. A backwards-traveling compression wave (BCW) was present in both LPA and RPA of all PH patients but was absent in all controls ( P = 6e−8). The area under the BCW was associated with a sensitivity of 100% [95% confidence interval (CI) 63–100%] and specificity of 91% (95% CI 75–98%) for the presence of a clot in the proximal PAs of patients with CTEPH. In conclusion, WIA metrics were significantly different between patients and controls; in particular, the presence of an early BCW was specifically associated with PH. The magnitude of the area under the BCW showed discriminatory capacity for the presence of proximal PA clot in patients with CTEPH. We believe that these results demonstrate that WIA could be used in the noninvasive assessment of PH.


2008 ◽  
Vol 294 (5) ◽  
pp. R1554-R1562 ◽  
Author(s):  
Joseph J. Smolich ◽  
Jonathan P. Mynard ◽  
Daniel J. Penny

The physiological basis of a characteristically low blood flow to the fetal lungs is incompletely understood. To determine the potential role of pulmonary vascular interaction in this phenomenon, simultaneous wave intensity analysis (WIA) was performed in the pulmonary trunk (PT) and left pulmonary artery (LPA) of 10 anesthetized late-gestation fetal sheep instrumented with PT and LPA micromanometer catheters to measure pressure (P) and transit-time flow probes to obtain blood velocity ( U). Studies were performed at rest and during brief complete occlusion of the ductus arteriosus to augment pulmonary vasoconstriction ( n = 4) or main pulmonary artery to abolish wave transmission from the lungs ( n = 3). Wave intensity (d IW) was calculated as the product of the P and U rates of change. Forward and backward components of d IW were determined after calculation of wave speed. PT and LPA WIA displayed an early systolic forward compression wave (FCWis) increasing P and U, and a late systolic forward expansion wave decreasing P and U. However, a marked midsystolic fall in LPA U to near-zero was related to an extremely prominent midsystolic backward compression wave (BCWms) that arose ∼5 cm distal to the LPA, was threefold larger than the PT BCWms ( P < 0.001), of similar size to FCWis at rest ( P > 0.6), larger than FCWis following ductal occlusion ( P < 0.05) and abolished after main pulmonary artery occlusion. These findings suggest that the absence of pulmonary arterial midsystolic forward flow which accompanies a low fetal lung blood flow is due to a BCWms generated in part by cyclical vasoconstriction within the pulmonary microcirculation.


2017 ◽  
Vol 2017 (1) ◽  
Author(s):  
C J Broyd ◽  
J E Davies ◽  
J E Escaned ◽  
A Hughes ◽  
K Parker

Wave intensity analysis (WIA) is a technique developed from the field of gas dynamics that is now being applied to assess cardiovascular physiology. It allows quantification of the forces acting to alter flow and pressure within a fluid system, and as such it is highly insightful in ascribing cause to dynamic blood pressure or velocity changes.When co-incident waves arrive at the same spatial location they exert either counteracting or summative effects on flow and pressure. WIA however allows waves of different origins to be measured uninfluenced by other simultaneously arriving waves. It therefore has found particular applicability within the coronary circulation where both proximal (aortic) and distal (myocardial) ends of the coronary artery can markedly influence blood flow. Using these concepts, a repeating pattern of 6 waves has been consistently identified within the coronary arteries, 3 originating proximally and 3 distally. Each has been associated with a particular part of the cardiac cycle. The most clinically relevant wave to date is the backward decompression wave, which causes the marked increase in coronary flow velocity observed at the start of the diastole. It has been proposed that this wave is generated by the elastic re-expansion of the intra-myocardial blood vessels that are compressed during systolic contraction. Particularly by quantifying this wave, WIA has been used to provide mechanistic and prognostic insight into a number of conditions including aortic stenosis, left ventricular hypertrophy, coronary artery disease and heart failure. It has proven itself to be highly sensitive and as such a number of novel research directions are encouraged where further insights would be beneficial. 


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