MODELING AND ANALYSIS OF INTERACTIONS BETWEEN A PULSATILE PNEUMATIC VENTRICULAR ASSIST DEVICE AND THE LEFT VENTRICLE

The use of a ventricular assist device (VAD) is a promising option for the treatment of end-stage heart failure. In many cases VADs provide not only temporary support, but contribute to the recovery of the native ventricle. Many studies have reported incidences where the native ventricle has recovered function, leading to device explantation and eliminating the need for heart transplantation. Despite strong interest in the subject for many years, the determinants of the recovery process are poorly understood and number of patients successfully weaned from chronic support remains low.A mathematical model was developed to gain an understanding of the complex mechanical interactions between a pneumatic, pulsatile VAD and the left ventricle. The VAD model was verified in-vitro using a mock circulatory loop. Over a wide range of experimental conditions, it correctly described observed dynamic behaviors and was accurate in predicting both VAD stroke volume and fill-to-empty rate within 6% error. This validated VAD model was coupled to a simple, lumped parameter cardiovascular model. The coupled model qualitatively reproduced the temporal patterns of various hemodynamic variables observed in clinical data. A concept of VAD characteristic frequency (fc) was developed to facilitate the analysis of VAD-ventricle synchrony. Characteristic frequency, defined as VAD rate in the absence of ventricular contraction, was essentially independent of cardiovascular parameters. For a given set of VAD parameters, synchrony was found to occur over a range of native heart rates. While the lower bound was determined by fc alone, the upper bound was a function of various cardiovascular parameters (e.g., left ventricular contractility, EMAX and systemic vascular resistance, SVR). In the case of synchronous behavior, the VAD and native heart have matched rates and counter-pulse, resulting in reduced ventricular loading. A decrease in EMAX or an increase in SVR increases asynchrony, resulting in frequent occurrences of co-pulsed beats (i.e., high ventricular loading). In conclusion, we found that VAD-ventricle synchrony is determined by a complex interaction between VAD and cardiovascular parameters. Our model-based analysis of VAD-ventricle interaction may be useful for optimizing the VAD operation, characterizing native ventricular contractility, and better understanding of the recovery process