Simultaneous pulmonary trunk and pulmonary arterial wave intensity analysis in fetal lambs: evidence for cyclical, midsystolic pulmonary vasoconstriction

2008 ◽  
Vol 294 (5) ◽  
pp. R1554-R1562 ◽  
Author(s):  
Joseph J. Smolich ◽  
Jonathan P. Mynard ◽  
Daniel J. Penny
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Compression Wave ◽  
Main Pulmonary Artery ◽  
Pulmonary Trunk ◽  
Wave Intensity ◽  
Intensity Analysis ◽  
Wave Intensity Analysis ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Arterial

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.

scholarly journals A review of wave mechanics in the pulmonary artery with an emphasis on wave intensity analysis

2016 ◽  
Vol 218 (4) ◽  
pp. 239-249 ◽  
Author(s):  
J. Su ◽  
O. Hilberg ◽  
L. Howard ◽  
U. Simonsen ◽  
A. D. Hughes
Keyword(s):  
Pulmonary Artery ◽  
Wave Intensity ◽  
Intensity Analysis ◽  
Wave Intensity Analysis ◽  
Wave Mechanics

scholarly journals Noninvasive pulmonary artery wave intensity analysis in pulmonary hypertension

2015 ◽  
Vol 308 (12) ◽  
pp. H1603-H1611 ◽  
Author(s):  
Michael A. Quail ◽  
Daniel S. Knight ◽  
Jennifer A. Steeden ◽  
Liesbeth Taelman ◽  
Shahin Moledina ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Left Pulmonary Artery ◽  
Wave Intensity ◽  
Healthy Controls ◽  
Intensity Analysis ◽  
Wave Intensity Analysis ◽  
Pulmonary Vessel ◽  
Golden Angle ◽  
Angiographic Data

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.

Aortic wave intensity analysis of ventricular-vascular interaction during incremental dobutamine infusion in adult sheep

2008 ◽  
Vol 294 (1) ◽  
pp. H481-H489 ◽  
Author(s):  
Daniel J. Penny ◽  
Jonathan P. Mynard ◽  
Joseph J. Smolich
Keyword(s):  
Compression Wave ◽  
Fold Increase ◽  
Detailed Examination ◽  
Wave Intensity ◽  
Expansion Wave ◽  
Dobutamine Infusion ◽  
Intensity Analysis ◽  
Wave Intensity Analysis ◽  
Aortic Blood ◽  
Aortic Blood Pressure

This study undertook a detailed examination of the ventricular-vascular interaction of the predominant β-adrenergic agonist dobutamine using wave intensity analysis. Eight anesthetized open-chest ewes were instrumented with an aortic micromanometer to measure central aortic blood pressure (P) and an ultrasonic flow probe to obtain ascending aortic blood velocity ( U). Hemodynamics were recorded during incremental dobutamine infusion (0.5, 1, 2.5, 5, 7.5, and 10 μg·kg−1·min−1). Wave intensity (d IW) was calculated as the product of the rates of change of P and U with customized software using ensemble-averaged signals. Forward and backward components of d IW, P, and U were determined after calculation of wave speed. As well as the typical initial forward compression wave (FCW), midsystolic backward compression wave (BCW), and late-systolic forward expansion wave (FEWes), two minor and previously unheralded waves were also detectable in the wave intensity profile at baseline. The first was an early systolic backward expansion wave (BEW), which reduced P but increased peak U. The second was a mid-systolic forward expansion wave (FEWms), which reduced P and U. During dobutamine infusion FCW d IW increased 18-fold ( P < 0.001), but BCW d IW rose 12-fold ( P < 0.001) while FEWes d IW fell by 70% ( P < 0.001). However, the latter changes were accompanied by a 44-fold increase in BEW d IW ( P = 0.005) that augmented the initial aortic forward flow and a >100-fold rise in FEWms d IW ( P < 0.001) that produced earlier and enhanced aortic blood deceleration. These findings provide new insights into the ventricular-vascular interaction of dobutamine.

4.6 WAVE INTENSITY ANALYSIS IN THE PULMONARY ARTERY

2014 ◽  
Vol 8 (4) ◽  
pp. 127 ◽  
Author(s):  
J. Su ◽  
C. Manisty ◽  
K. Parker ◽  
A. Hughes
Keyword(s):  
Pulmonary Artery ◽  
Wave Intensity ◽  
Intensity Analysis ◽  
Wave Intensity Analysis

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
Keyword(s):  
Pulmonary Artery ◽  
Left Ventricular ◽  
Wave Intensity ◽  
Pulmonary Vasculature ◽  
Pressure Waves ◽  
Intensity Analysis ◽  
Wave Intensity Analysis ◽  
Compression Waves ◽  
In Series ◽  
Late Systole

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.

Pulmonary artery wave intensity analysis following lung resection

2017 ◽  
Vol 31 ◽  
pp. S5-S6
Author(s):  
Adam Glass ◽  
P McCall ◽  
A Arthur ◽  
J Kinsella ◽  
B Shelley
Keyword(s):  
Pulmonary Artery ◽  
Lung Resection ◽  
Wave Intensity ◽  
Intensity Analysis ◽  
Wave Intensity Analysis

Interactions between the right ventricle and pulmonary vasculature in the fetus

1999 ◽  
Vol 87 (5) ◽  
pp. 1637-1643 ◽  
Author(s):  
Daniel A. Grant ◽  
Ellen Hollander ◽  
Elizabeth M. Skuza ◽  
Jean-Claude Fauchère
Keyword(s):  
Blood Flow ◽  
Right Ventricle ◽  
Traveling Wave ◽  
Ductus Arteriosus ◽  
Pulmonary Trunk ◽  
Pulmonary Vasculature ◽  
Intensity Analysis ◽  
Wave Intensity Analysis ◽  
Blood Flows ◽  
The Right

A midsystolic plateau differentiates the pattern of fetal pulmonary trunk blood flow from aortic flow. To determine whether this plateau arises from interactions between the left (LV) and right ventricle (RV) via the ductus arteriosus or from interactions between the RV and the lung vasculature, we measured blood flows and pressures in the pulmonary trunk and aorta of eight anesthetized (ketamine and α-chloralose) fetal lambs. Wave-intensity analysis revealed waves of energy traveling forward, away from the LV and the RV early in systole. During midsystole, a wave of energy traveling back toward the RV decreased blood flow velocity from the RV and produced the plateau in blood flow. Calculations revealed that this backward-traveling wave originated as a forward-traveling wave generated by the RV that was reflected from the lung vasculature back toward the heart and not as a forward-traveling wave generated by the LV that crossed the ductus arteriosus. Elimination of this backward-traveling wave and its associated effect on RV flow may be an important component of the increase in RV output that accompanies birth.

Pulmonary arterial distension does not cause pulmonary vasoconstriction

1986 ◽  
Vol 61 (2) ◽  
pp. 741-745 ◽  
Author(s):  
T. C. Lloyd
Keyword(s):  
Pulmonary Artery ◽  
Perfusion Pressure ◽  
Pressor Response ◽  
Main Pulmonary Artery ◽  
Pulmonary Vasoconstriction ◽  
Balloon Distension ◽  
Pressor Responses ◽  
Alveolar Hypoxia ◽  
Pulmonary Arterial ◽  
Arterial Branch

Distension of the main pulmonary artery or its major branches with an intraluminal balloon has been reported to cause pulmonary vasoconstriction by an unknown mechanism. This study was an attempt to confirm the pressor response and explore its cause. Several balloon distension methods were tried and discarded because they caused unintentional obstruction. Ultimately, I inflated a balloon placed retrogradely and confined to the left main pulmonary artery of six anesthetized open-chest dogs after ligating left lobar arterial branches. Blood flow and systemic gas composition were controlled by interposing an external pump oxygenator between the left ventricle and aorta. Pressures in the aorta, main pulmonary artery, and left atrium were recorded. Alveolar hypoxia was used as an independent test of pulmonary vasoreactivity. Although hypoxic pressor responses occurred, challenges with arterial distension did not change lung perfusion pressure. Silicone rubber casts were made of the arteries of six dogs used in pilot experiments. These revealed the limited lengths in which distenders can be placed without unintentional encroachment on flow. I could not support the conclusion that arterial distension causes vasoconstriction and am suspicious that the perfusion pressure increases reported by others may have been caused by undetected obstruction of a major arterial branch.

Angiographic evidence of backward compression wave: systolic compression of septal perforators in a child with hypertrophic cardiomyopathy

2020 ◽  
pp. 1-2
Author(s):  
Rupesh Natarajan ◽  
Rebecca Ameduri ◽  
Massimo Griselli ◽  
Varun Aggarwal
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Coronary Arteries ◽  
Compression Wave ◽  
Poor Prognosis ◽  
Wave Intensity ◽  
Compressive Deformation ◽  
Intensity Analysis ◽  
Wave Intensity Analysis ◽  
Angiographic Evidence

Abstract Intracoronary wave intensity analysis in hypertrophic cardiomyopathy has shown a large backward compression wave due to compressive deformation of the intramyocardial coronary arteries in systole. The authors describe the angiographic evidence of this backward compression wave, which has not been described in this physiological context and can be a marker of poor prognosis.

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