Beat-to-beat noninvasive stroke volume from arterial pressure and Doppler ultrasound

Lieshout, Johannes J. van; Toska, Karin; Lieshout, Erik Jan van; Eriksen, Morten; Walløe, Lars; Wesseling, Karel H.

doi:10.1007/s00421-003-0901-8

Cited by 119 publications

(106 citation statements)

References 36 publications

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“…The Modelflow system for stroke volume estimation has been validated by several clinical or physiological studies in healthy individuals (5,19,45,48). Since the Modelflow aortic age calculation is based on an inverse function of the Modelflow stroke volume calculation, this finding is consistent with these previous studies.…”

Section: Modelflow Aortic Age Vs Chronological Agesupporting

confidence: 82%

“…However, the present finding that the Modelflow aortic age differed only slightly during LBNP supports the reliability of this index under moderate orthostatic stress. Moreover, the fact that the validity of the Modelflow method to estimate stroke volume has been confirmed by numerous studies (5,19,22,24,48,49), including during open-heart cardiac surgery, which involves huge hemodynamic changes beyond normal physiological conditions, also supports the reliability of the Modelflow aortic age under various physiological conditions.…”

Section: Study Limitationsmentioning

confidence: 72%

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Biological aortic age derived from the arterial pressure waveform

Shibata

Levine

2011

Journal of Applied Physiology

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Shibata S, Levine BD. Biological aortic age derived from the arterial pressure waveform. J Appl Physiol 110: 981-987, 2011. First published February 3, 2011 doi:10.1152/japplphysiol.01261.2010.-Indexes for arterial stiffness are, by their nature, influenced by the ambient blood pressure due to the curvilinear nature of arterial compliance. We developed a new concept of the "Modelflow aortic age," which is, theoretically, not influenced by the ambient blood pressure and provides an easily understood context (biological vs. chronological age) for measures of arterial stiffness. The purpose of the present study was to validate this pressure-independent index for aortic stiffness in humans. Twelve sedentary elderly (65-77 yr), 11 Masters athletes (65-73 yr), and 12 sedentary young individuals (20 -42 yr) were studied. Modelflow aortic ages were comparable with chronological ages in both sedentary groups, indicating that healthy sedentary individuals have age-appropriate aortas. In contrast, Masters athletes showed younger Modelflow aortic ages than their chronological ages. The coefficient of variation of sedentary subjects was three times smaller with the Modelflow aortic age (21%) than with other indexes, such as static systemic arterial stiffness (61%), central pulse wave velocity (61%), or carotid ␤-stiffness index (58%). The typical error was very small and two times smaller in the Modelflow aortic age (Ͻ7%) than in static systemic arterial stiffness (Ͼ13%) during cardiac unloading by lower body negative pressure. The Modelflow aortic age can more precisely and reliably estimate aortic stiffening with aging and modifiers, such as life-long exercise training compared with the pressure-dependent index of static systemic arterial stiffness, and provides a physiologically relevant and clinically compelling context for such measurements. arterial stiffness; aging; Modelflow ARTERIOSCLEROSIS WITH AGING leads to large-vessel arterial stiffening in humans. This process is characterized primarily by the development of fibrosis and degeneration of elastin, which result in structural changes in the arterial wall (28, 29). Indeed, work by Langewouters et al. (30, 31) and Wesseling et al. (49) showed that structural properties of the thoracic and abdominal aortas are altered linearly with age in humans and are clinically relevant. Large arterial stiffness is an independent predictor of mortality and morbidity from cardiovascular disease in the elderly population (3,4,7,11,33,37,39,44,50).Central aortic stiffness can be evaluated by several methods, such as pulse-wave velocity (PWV) of the central aorta, systemic arterial compliance (ratio of stroke volume to pulse pressure), or aortic impedance (dynamic relationship between aortic flow and pressure) (34, 41). However, all of these approaches are, by their nature, influenced by the ambient blood pressure due to the curvilinear nature of arterial compliance (arterial pressure-area relationship) (38). For example, higher blood pressures shift the operational point of the ar...

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Section: Modelflow Aortic Age Vs Chronological Agesupporting

confidence: 82%

Section: Study Limitationsmentioning

confidence: 72%

Biological aortic age derived from the arterial pressure waveform

Shibata

Levine

2011

Journal of Applied Physiology

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“…HR, SV, CO, and MAP were determined with a finometer (Finapres Medical Systems, Amsterdam, The Netherlands) positioned at heart level. SV was calculated from beat-by-beat pressure waveforms assessed by photoplethysmography using the Modelflow method (Beatscope, version 1.1; Finapres Medical Systems), which in combination with HR has been documented to accurately estimate CO during a variety of experimental protocols (1,4,5,34,39). In the subset of six subjects, intravascular systolic and diastolic arterial and mean venous pressures (MVP) were determined from in-line pressure transducers (Baxter, Deerfield, IL) placed at the level of the catheters.…”

Section: Measurementsmentioning

confidence: 99%

Impact of body position on central and peripheral hemodynamic contributions to movement-induced hyperemia: implications for rehabilitative medicine

Trinity

McDaniel

Venturelli

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…HR, SV, and CO were determined with a finometer (Finapres Medical Systems, Amsterdam, the Netherlands). SV was calculated from beat-by-beat pressure waveforms assessed by photoplethysmography using the Modelflow method (Beatscope version 1.1; Finapres Medical Systems), which, in combination with HR, has been documented to accurately estimate CO during a variety of experimental protocols (4,8,9,39,42). Intravascular systolic and diastolic arterial and mean venous pressures (MVP) were determined from in-line pressure transducers (Baxter, Deerfield, IL) placed at the level of the catheters.…”

Section: Measurements Hcvr Testmentioning

confidence: 99%

Limb movement-induced hyperemia has a central hemodynamic component: evidence from a neural blockade study

Trinity

Amann²,

McDaniel

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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Limb movement-induced hyperemia has a central hemodynamic component: evidence from a neural blockade study. Am J Physiol Heart Circ Physiol 299: H1693-H1700, 2010. First published August 27, 2010; doi:10.1152/ajpheart.00482.2010.-The purpose of this investigation was to partially remove feedback from type III/IV skeletal muscle afferents and determine how this feedback influences the central and peripheral hemodynamic responses to passive leg movement. Heart rate (HR), stroke volume (SV), cardiac output (CO), mean arterial pressure, leg vascular conductance (LVC), and leg blood flow (LBF) were measured during 2 min of passive knee extension in eight young men before and after intrathecal fentanyl injection. Passive movement increased HR by 14 beats/min from baseline to maximal response during control (CON) (65 Ϯ 4 to 79 Ϯ 5 beats/min, P Ͻ 0.05), whereas HR did not significantly increase with the fentanyl block (BLK). LBF and LVC increased in both conditions; however, these increases were attenuated and delayed during BLK [%change from baseline to maximum, LBF: CON 295 Ϯ 109 vs. BLK 210 Ϯ 86%, (P Ͻ 0.05); LVC: CON 322 Ϯ 40% vs. BLK 231 Ϯ 32%, (P Ͻ 0.04)]. In CON, HR, SV, CO, and LVC increased contributing to the hyperemic response. However, under BLK conditions, statistically insignificant increases in HR and SV combined to yield a small, but significant, increase in CO and an attenuated hyperemic response. Therefore, partially blocking skeletal muscle afferent feedback blunts the central hemodynamic response due to passive limb movement, which then results in an attenuated and delayed movement-induced hyperemia. In combination, these findings provide evidence that limb movement-induced hyperemia has a significant central hemodynamic component induced by peripheral nerve activation. afferent nerve fiber; blood flow; hemodynamics CENTRAL AND PERIPHERAL HEMODYNAMIC factors contribute to the hyperemic response at the onset of exercise. These factors include the muscle pump (24, 38) mechanically induced vasodilation (6,19,41), mechanical deformation of arterioles (37), flow-mediated vasodilation (22, 34), and cardioacceleration (26, 30 -33, 43) due to stimulation of afferent mechanosensitive and metabosensitive fibers in the working muscles (25,36). Isolating the relative importance of these numerous mechanisms is difficult and requires a systematic approach to understand the nature of any single mechanism.One approach to study the movement-induced central and peripheral hemodynamic responses to the onset of exercise is to perform passive movement, thereby minimizing the metabolic contribution of voluntary exercise. Recently, our group (26, 43) and others (30,31,33) have highlighted the role of cardioacceleration in the hyperemic responses to passive movement. Wray et al. (43) reported that passive knee extension resulted in significant tachycardia and increased leg blood flow (LBF) during the first 5 s of movement. However, in this study, stroke volume (SV) was not measured, and cardiac output (CO) was assumed to r...

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Beat-to-beat noninvasive stroke volume from arterial pressure and Doppler ultrasound

Cited by 119 publications

References 36 publications

Biological aortic age derived from the arterial pressure waveform

Biological aortic age derived from the arterial pressure waveform

Impact of body position on central and peripheral hemodynamic contributions to movement-induced hyperemia: implications for rehabilitative medicine

Limb movement-induced hyperemia has a central hemodynamic component: evidence from a neural blockade study

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