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Effects of Left Heart Loading on the...

Wright, Stephen P.

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Effects of Left Heart Loading on the Right Ventricular-Pulmonary Arterial Circulatory Unit.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Effects of Left Heart Loading on the Right Ventricular-Pulmonary Arterial Circulatory Unit./
Author:	Wright, Stephen P.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2018,
Description:	213 p.
Notes:	Source: Dissertations Abstracts International, Volume: 80-06, Section: B.
Contained By:	Dissertations Abstracts International80-06B.
Subject:	Medicine. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10936212
ISBN:	9780438683792

Effects of Left Heart Loading on the Right Ventricular-Pulmonary Arterial Circulatory Unit.
Wright, Stephen P.

Effects of Left Heart Loading on the Right Ventricular-Pulmonary Arterial Circulatory Unit. - Ann Arbor : ProQuest Dissertations & Theses, 2018 - 213 p.

Source: Dissertations Abstracts International, Volume: 80-06, Section: B.

Thesis (Ph.D.)--University of Toronto (Canada), 2018.

This item must not be sold to any third party vendors.

The right ventricle (RV) and pulmonary vasculature (PV) form a circulatory unit which is sensitive to downstream left atrial (LA) function. Exercise may significantly stress the RV-PV circulatory unit, even in healthy individuals. This thesis aimed to characterize normal hemodynamic mechanisms through which RV-PV circulatory unit function is influenced in-series by LA function during exercise. Healthy males and females >45 years old were recruited. Right heart catheterization was used to measure cardiac output, RV and PV pressures, and pulmonary artery wedge pressure (PAWP). Echocardiography was used to measure LA volumes. Participants were studied at rest and during 7-10 minute stages of Light- and Moderate-intensity cycle-ergometry. Project one described the PAWP and PV pressure response as exercise was initiated, sustained, and escalated in intensity. PAWP was 11 ± 3 mmHg at rest, increased to 22 ± 5 mmHg at early-Light exercise (p<0.01), then declined to 17 ± 5 mmHg with sustained-Light exercise. Project two examined the relationships of PV resistance, compliance, and their product RC-time, to PAWP. RC-time reflects the time constant for diastolic pressure decay, and provides an index of resistive relative to pulsatile RV afterload. RC-time decreased with Light exercise (0.39 ± 0.08 to 0.25 ± 0.08, p<0.001) without further change with Moderate exercise, and decreases in RC-time were correlated with increases in PAWP (r 2 = 0.26, p<0.001). Project three examined whether RV to PV systolic pressure gradients develop with exercise, and explored potential correlates. Mean gradients developed with Light exercise (8 [7-9] mmHg) and increased with Moderate exercise (12 [9-14] mmHg, p<0.001); their magnitude was correlated with cardiac output (r2 = 0.70, p<0.001). Project four constructed LA pressure-volume relations to assess LA compliance and the contribution of the LA to effective RV afterload. LA compliance was 9.4 ± 4.0 mL/mmHg at rest and unchanged with exercise. LA function was closely related to phasic PV pressures, but was not related to increases in pulsatile RV afterload. These analyses indicate that increasing LA pressure, decreasing PV compliance, and a widening RV to PV pressure gradient sequentially contribute to augmented pulsatile RV afterload during exercise in healthy adults.

ISBN: 9780438683792Subjects--Topical Terms:

641104
Medicine.

Effects of Left Heart Loading on the Right Ventricular-Pulmonary Arterial Circulatory Unit.
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520 $a The right ventricle (RV) and pulmonary vasculature (PV) form a circulatory unit which is sensitive to downstream left atrial (LA) function. Exercise may significantly stress the RV-PV circulatory unit, even in healthy individuals. This thesis aimed to characterize normal hemodynamic mechanisms through which RV-PV circulatory unit function is influenced in-series by LA function during exercise. Healthy males and females >45 years old were recruited. Right heart catheterization was used to measure cardiac output, RV and PV pressures, and pulmonary artery wedge pressure (PAWP). Echocardiography was used to measure LA volumes. Participants were studied at rest and during 7-10 minute stages of Light- and Moderate-intensity cycle-ergometry. Project one described the PAWP and PV pressure response as exercise was initiated, sustained, and escalated in intensity. PAWP was 11 ± 3 mmHg at rest, increased to 22 ± 5 mmHg at early-Light exercise (p<0.01), then declined to 17 ± 5 mmHg with sustained-Light exercise. Project two examined the relationships of PV resistance, compliance, and their product RC-time, to PAWP. RC-time reflects the time constant for diastolic pressure decay, and provides an index of resistive relative to pulsatile RV afterload. RC-time decreased with Light exercise (0.39 ± 0.08 to 0.25 ± 0.08, p<0.001) without further change with Moderate exercise, and decreases in RC-time were correlated with increases in PAWP (r 2 = 0.26, p<0.001). Project three examined whether RV to PV systolic pressure gradients develop with exercise, and explored potential correlates. Mean gradients developed with Light exercise (8 [7-9] mmHg) and increased with Moderate exercise (12 [9-14] mmHg, p<0.001); their magnitude was correlated with cardiac output (r2 = 0.70, p<0.001). Project four constructed LA pressure-volume relations to assess LA compliance and the contribution of the LA to effective RV afterload. LA compliance was 9.4 ± 4.0 mL/mmHg at rest and unchanged with exercise. LA function was closely related to phasic PV pressures, but was not related to increases in pulsatile RV afterload. These analyses indicate that increasing LA pressure, decreasing PV compliance, and a widening RV to PV pressure gradient sequentially contribute to augmented pulsatile RV afterload during exercise in healthy adults.
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