Effective arterial elastance as index of arterial vascular load in humans

Raymond P. Kelly, Chih Tai Ting, Tsong Ming Yang, Chung Peng Liu, W. Lowell Maughan, Mau Song Chang, David A. Kass

Research output: Contribution to journalArticle

Abstract

Background. This study tested whether the simple ratio of ventricular end-systolic pressure to stroke volume, known as the effective arterial elastance (Ea), provides a valid measure of arterial load in humans with normal and aged hypertensive vasculatures. Methods and Results. Ventricular pressure-volume and invasive aortic pressure and flow were simultaneously determined in 10 subjects (four young normotensive and six older hypertensive). Measurements were obtained at rest, during mechanically reduced preload, and after pharmacological interventions. Two measures of arterial load were compared: One was derived from aortic input impedance and arterial compliance data using an algebraic expression based on a three-element Windkessel model of the arterial system [Ea(Z)], and the other was more simply measured as the ratio of ventricular end-systolic pressure to stroke volume [Ea(PV)]. Although derived from completely different data sources and despite the simplifying assumptions of Ea(PV), both Ea(Z) and Ea(PV) were virtually identical over a broad range of altered conditions: Ea(PV)=0.97·Ea(Z)+0.17; n=33, r2=0.98, SEE=0.09, pa(PV) also correlated with mean arterial resistance, it exceeded resistance by as much as 25% in older hypertensive subjects (because of reduced compliance and wave reflections), which better indexed the arterial load effects on the ventricle. Simple methods to estimate Ea (PV) from routine arterial pressures were tested and validated. Conclusions. Ea(PV) provides a convenient, useful method to assess arterial load and its impact on the human ventricle. These results highlight effects of increased pulsatile load caused by aging or hypertension on the pressure-volume loop and indicate that this load and its effects on cardiac performance are often underestimated by mean arterial resistance but are better accounted for by Ea.

Original languageEnglish (US)
Pages (from-to)513-521
Number of pages9
JournalCirculation
Volume86
Issue number2
StatePublished - 1992

Fingerprint

Blood Vessels
Stroke Volume
Compliance
Arterial Pressure
Blood Pressure
Information Storage and Retrieval
Ventricular Pressure
Electric Impedance
Pharmacology
Hypertension
Pressure

Keywords

  • Afterload
  • Hypertension
  • Pressure-volume relations
  • Ventricle

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Kelly, R. P., Ting, C. T., Yang, T. M., Liu, C. P., Maughan, W. L., Chang, M. S., & Kass, D. A. (1992). Effective arterial elastance as index of arterial vascular load in humans. Circulation, 86(2), 513-521.

Effective arterial elastance as index of arterial vascular load in humans. / Kelly, Raymond P.; Ting, Chih Tai; Yang, Tsong Ming; Liu, Chung Peng; Maughan, W. Lowell; Chang, Mau Song; Kass, David A.

In: Circulation, Vol. 86, No. 2, 1992, p. 513-521.

Research output: Contribution to journalArticle

Kelly, RP, Ting, CT, Yang, TM, Liu, CP, Maughan, WL, Chang, MS & Kass, DA 1992, 'Effective arterial elastance as index of arterial vascular load in humans', Circulation, vol. 86, no. 2, pp. 513-521.
Kelly RP, Ting CT, Yang TM, Liu CP, Maughan WL, Chang MS et al. Effective arterial elastance as index of arterial vascular load in humans. Circulation. 1992;86(2):513-521.
Kelly, Raymond P. ; Ting, Chih Tai ; Yang, Tsong Ming ; Liu, Chung Peng ; Maughan, W. Lowell ; Chang, Mau Song ; Kass, David A. / Effective arterial elastance as index of arterial vascular load in humans. In: Circulation. 1992 ; Vol. 86, No. 2. pp. 513-521.
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abstract = "Background. This study tested whether the simple ratio of ventricular end-systolic pressure to stroke volume, known as the effective arterial elastance (Ea), provides a valid measure of arterial load in humans with normal and aged hypertensive vasculatures. Methods and Results. Ventricular pressure-volume and invasive aortic pressure and flow were simultaneously determined in 10 subjects (four young normotensive and six older hypertensive). Measurements were obtained at rest, during mechanically reduced preload, and after pharmacological interventions. Two measures of arterial load were compared: One was derived from aortic input impedance and arterial compliance data using an algebraic expression based on a three-element Windkessel model of the arterial system [Ea(Z)], and the other was more simply measured as the ratio of ventricular end-systolic pressure to stroke volume [Ea(PV)]. Although derived from completely different data sources and despite the simplifying assumptions of Ea(PV), both Ea(Z) and Ea(PV) were virtually identical over a broad range of altered conditions: Ea(PV)=0.97·Ea(Z)+0.17; n=33, r2=0.98, SEE=0.09, pa(PV) also correlated with mean arterial resistance, it exceeded resistance by as much as 25{\%} in older hypertensive subjects (because of reduced compliance and wave reflections), which better indexed the arterial load effects on the ventricle. Simple methods to estimate Ea (PV) from routine arterial pressures were tested and validated. Conclusions. Ea(PV) provides a convenient, useful method to assess arterial load and its impact on the human ventricle. These results highlight effects of increased pulsatile load caused by aging or hypertension on the pressure-volume loop and indicate that this load and its effects on cardiac performance are often underestimated by mean arterial resistance but are better accounted for by Ea.",
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AU - Ting, Chih Tai

AU - Yang, Tsong Ming

AU - Liu, Chung Peng

AU - Maughan, W. Lowell

AU - Chang, Mau Song

AU - Kass, David A.

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N2 - Background. This study tested whether the simple ratio of ventricular end-systolic pressure to stroke volume, known as the effective arterial elastance (Ea), provides a valid measure of arterial load in humans with normal and aged hypertensive vasculatures. Methods and Results. Ventricular pressure-volume and invasive aortic pressure and flow were simultaneously determined in 10 subjects (four young normotensive and six older hypertensive). Measurements were obtained at rest, during mechanically reduced preload, and after pharmacological interventions. Two measures of arterial load were compared: One was derived from aortic input impedance and arterial compliance data using an algebraic expression based on a three-element Windkessel model of the arterial system [Ea(Z)], and the other was more simply measured as the ratio of ventricular end-systolic pressure to stroke volume [Ea(PV)]. Although derived from completely different data sources and despite the simplifying assumptions of Ea(PV), both Ea(Z) and Ea(PV) were virtually identical over a broad range of altered conditions: Ea(PV)=0.97·Ea(Z)+0.17; n=33, r2=0.98, SEE=0.09, pa(PV) also correlated with mean arterial resistance, it exceeded resistance by as much as 25% in older hypertensive subjects (because of reduced compliance and wave reflections), which better indexed the arterial load effects on the ventricle. Simple methods to estimate Ea (PV) from routine arterial pressures were tested and validated. Conclusions. Ea(PV) provides a convenient, useful method to assess arterial load and its impact on the human ventricle. These results highlight effects of increased pulsatile load caused by aging or hypertension on the pressure-volume loop and indicate that this load and its effects on cardiac performance are often underestimated by mean arterial resistance but are better accounted for by Ea.

AB - Background. This study tested whether the simple ratio of ventricular end-systolic pressure to stroke volume, known as the effective arterial elastance (Ea), provides a valid measure of arterial load in humans with normal and aged hypertensive vasculatures. Methods and Results. Ventricular pressure-volume and invasive aortic pressure and flow were simultaneously determined in 10 subjects (four young normotensive and six older hypertensive). Measurements were obtained at rest, during mechanically reduced preload, and after pharmacological interventions. Two measures of arterial load were compared: One was derived from aortic input impedance and arterial compliance data using an algebraic expression based on a three-element Windkessel model of the arterial system [Ea(Z)], and the other was more simply measured as the ratio of ventricular end-systolic pressure to stroke volume [Ea(PV)]. Although derived from completely different data sources and despite the simplifying assumptions of Ea(PV), both Ea(Z) and Ea(PV) were virtually identical over a broad range of altered conditions: Ea(PV)=0.97·Ea(Z)+0.17; n=33, r2=0.98, SEE=0.09, pa(PV) also correlated with mean arterial resistance, it exceeded resistance by as much as 25% in older hypertensive subjects (because of reduced compliance and wave reflections), which better indexed the arterial load effects on the ventricle. Simple methods to estimate Ea (PV) from routine arterial pressures were tested and validated. Conclusions. Ea(PV) provides a convenient, useful method to assess arterial load and its impact on the human ventricle. These results highlight effects of increased pulsatile load caused by aging or hypertension on the pressure-volume loop and indicate that this load and its effects on cardiac performance are often underestimated by mean arterial resistance but are better accounted for by Ea.

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