Defining pulsatility during continuous-flow ventricular assist device support

• Published in: The Journal of heart and lung transplantation Vol. 32; no. 6; pp. 581 - 587
• Main Authors: Soucy, Kevin G., PhD, Koenig, Steven C., PhD, Giridharan, Guruprasad A., PhD, Sobieski, Michael A., RN, CCP, Slaughter, Mark S., MD
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01-06-2013
• Subjects: Blood Flow Velocity - physiology; Blood Pressure - physiology; continuous-flow; energy equivalent pressure; Heart Failure - physiopathology; Heart Failure - therapy; Heart-Assist Devices; Hemodynamics - physiology; Humans; Models, Cardiovascular; pulsatile-flow; Surgery; surplus hemodynamic energy; vascular pulsatility; ventricular assist device; ventricular assist device; continuous-flow; pulsatile-flow; surplus hemodynamic energy; vascular pulsatility; energy equivalent pressure
• ISSN: 1053-2498; 1557-3117
• DOI: 10.1016/j.healun.2013.02.010

Continuous-flow ventricular assist devices (CVADs) have gained widespread use as an effective clinical therapy for patients with advanced-stage heart failure. Axial and centrifugal CVADs have been successfully used as bridge-to-transplant and destination therapy. CVADs are smaller, more reliable, and less complex than the first-generation pulsatile-flow ventricular assist devices. Despite their recent clinical success, arteriovenous malformations, gastrointestinal bleeding, hemorrhagic strokes, aortic valve insufficiency, and valve fusion have been reported in heart failure patients supported by CVADs. It has been hypothesized that diminished arterial pressure and flow pulsatility delivered by CVAD may be a contributing factor to these adverse events. Subsequently, the clinical significance of vascular pulsatility continues to be highly debated. Studies comparing pulsatile-flow and continuous-flow support have presented conflicting findings, largely due to variations in device operation, support duration, and the criteria used to quantify pulsatility. Traditional measurements of pulse pressure and pulsatility index are less effective at quantifying pulsatility for mechanically derived flows, particularly with the growing trend of CVAD speed modulation to achieve various pulsatile flow patterns. Kinetic measurements of energy equivalent pressure and surplus hemodynamic energy can better quantify pulsatile energies, yet technologic and conceptual challenges are impeding their clinical adaption. A review of methods for quantifying vascular pulsatility and their application as a research tool for investigating physiologic responses to CVAD support are presented.