Volume 31, Issue 5 pp. 369-376

Left Ventricular Pressure–Volume Loop Analysis During Continuous Cardiac Assist in Acute Animal Trials

Francesco Moscato

Francesco Moscato

Department of Biomedical Engineering and Physics;

Department of Mechanical Engineering, University of Calabria, Arcavacata di Rende (CS), Italy

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Michael Vollkron

Michael Vollkron

Department of Cardiothoracic Surgery and Ludwig Boltzmann Institute for Cardiosurgical Research;

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Helga Bergmeister

Helga Bergmeister

Department of Biomedical Research, Medical University of Vienna, Vienna, Austria;

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Georg Wieselthaler

Georg Wieselthaler

Department of Cardiothoracic Surgery and Ludwig Boltzmann Institute for Cardiosurgical Research;

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Edward Leonard

Edward Leonard

Department of Chemical Engineering, Columbia University, New York, NY, USA; and

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Heinrich Schima

Corresponding Author

Heinrich Schima

Department of Biomedical Engineering and Physics;

Department of Cardiothoracic Surgery and Ludwig Boltzmann Institute for Cardiosurgical Research;

Dr. Heinrich Schima, Center for Biomedical Engineering and Physics, AKH—4L, Waehringer Guertel 18-20, A-1090 Vienna, Austria. E-mail: [email protected]Search for more papers by this author
First published: 26 April 2007
Citations: 31

Presented in part at the 14th Congress of the International Society for Rotary Blood Pumps held August 31–September 2, 2006 in Leuven, Belgium.

Abstract

Abstract: For better understanding of the interaction between left ventricle and continuous cardiac assist, the effect of different working conditions and support levels on left ventricular pressure–volume (PV) loop was investigated in acute animal experiments. A MicroMed-DeBakey ventricular assist device (MicroMed Cardiovascular Inc., Houston, TX, USA) was implanted in seven healthy sheep (102 ± 20 kg). Measurements of hemodynamic variables were taken with clamped graft, on minimum, medium, and maximum support, and in pump-off condition (backflow). Each pump condition was studied for different heart rates, central venous pressures, and under pharmacologically altered contractility. End-systolic and end-diastolic volume normalized by the body surface area (BSA) (end systolic volume index [ESVI] and end diastolic volume index [EDVI]) showed significant correlation both within each sheep and in the pooled data. The linear regression for the pooled data was ESVI = 0.845 × EDVI − 15.21, R2 = 0.924, P < 0.0001, n = 200. EDVI and stroke volume (SV) normalized by BSA (stroke volume index [SVI]) also showed a lower but significant correlation: SVI =  0.155 × EDVI + 15.21, R2 = 0.291, P < 0.0001, n = 200. An increase of preload due to infusion caused, in the clamped graft condition, an increase in end diastolic volume of 22%, no significant increase in SV, a decrease both of systemic vascular resistance of 30% and ventricular contractility (maximum elastance [Emax] and peak rate of rise of ventricular pressure [dP/dtmax] decreasing 38 and 21%, respectively). PV loop analysis in continuous cardiac assist reveals that the ESVI and the EDVI are strongly correlated and that ESVI varies considerably with preload. SVI becomes slightly dependent on EDVI, which may be due to autoregulatory mechanisms.

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