Suction Due to Left Ventricular Assist: Implications for Device Control and Management
ABSTRACT Left ventricular assist device (LVAD) overpumping is associated with hemolysis, thrombus release, and tissue damage at the pump inlet. However, the impact of LVAD suction on pulmonary circulatory function remains unknown. We investigated LVAD suction as induced by pulmonary artery banding and overpumping in experimental animals and in a computer model. In six sheep, a rotary LVAD was implanted. Before inducing suction, partial support (40-60% of cardiac output) was established and characterized by measuring pressures and flows. In the animals, pulmonary artery occlusion (PAOC) elicited LVAD suction (left ventricular pressure was from -10 to -20 mm Hg) within 5-10 heartbeats. During suction, aortic pressure dropped to 50% and LVAD flow decreased significantly. After releasing the occlusion (20 s), the collapsed state persisted for another 20 s. A similar trend was obtained by simulating PAOC in the computer model. Additional simulations showed that pulmonary vascular resistance (PVR), volume status, and right ventricular (RV) contractility are exponentially related to the persistence of collapse after a suction event. Even modest increases in predisposing factors (elevated PVR, RV dysfunction, hypovolemia) caused sustained hemodynamic collapse lasting in excess of 15 min. Both in selected animals and the computer model, comparable suction-induced collapse was obtained by increasing LVAD speed by about 33%. Attempted compensation by simply decreasing speed was not effective, but temporarily shutting down the LVAD caused rapid reversal of collapse. In conclusion, rotary LVAD suction causes unfavorable conditions for effective unloading. The use of pump interventions appears a promising tool to detect suction and to avoid the associated hemodynamic depression.
- SourceAvailable from: eprints.qut.edu.au
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- "Robert F Salamonsen is with the Department of Epidemiology and Preventative Medicine, Monash University, Melbourne, Australia. required to avoid hazardous events including ventricular suction, which results in reduced forward flow of blood, hence inducing ischaemia on the heart as well as distal organs, haemolysis, release of ventricular thrombus leading to stroke, tissue damage at VAD inlet and even subsequent right ventricular dysfunction   . The addition of an active physiological control system is required to automatically match LVAD flow with venous return, thus ensuring appropriate cardiac output at all times whilst avoiding ventricular suction. "
ABSTRACT: A physiological control system was developed for a rotary left ventricular assist device (LVAD) in which the target pump flow rate (LVADQ) was set as a function of left atrial pressure (LAP), mimicking the Frank-Starling mechanism. The control strategy was implemented using linear PID control and was evaluated in a pulsatile mock circulation loop using a prototyped centrifugal pump by varying pulmonary vascular resistance to alter venous return. The control strategy automatically varied pump speed (2460 to 1740 to 2700 RPM) in response to a decrease and subsequent increase in venous return. In contrast, a fixed-speed pump caused a simulated ventricular suction event during low venous return and higher ventricular volumes during high venous return. The preload sensitivity was increased from 0.011 L/min/mmHg in fixed speed mode to 0.47L/min/mmHg, a value similar to that of the native healthy heart. The sensitivity varied automatically to maintain the LAP and LVADQ within a predefined zone. This control strategy requires the implantation of a pressure sensor in the left atrium and a flow sensor around the outflow cannula of the LVAD. However, appropriate pressure sensor technology is not yet commercially available and so an alternative measure of preload such as pulsatility of pump signals should be investigated.Conference proceedings: ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Conference 08/2011; 2011:1335-8. DOI:10.1109/IEMBS.2011.6090314
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- "We do not exclude other alternatives that may have caused this apart from the Starling mechanism, such as the dependencies of PVR on the pulmonary blood volume, which was decreased with increasing pump speeds. Compared to most models that use a linear ESPVR for the ventricles , , we have adopted a curvilinear ESPVR as proposed by Kass et al. . This is supported by the published data , which show that the end systolic points of LV PV loops obtained with different pump speeds do not fall on the same straight line as those obtained without pump assist . "
ABSTRACT: A lumped parameter model of human cardiovascular-implantable rotary blood pump (iRBP) interaction has been developed based on experimental data recorded in two healthy pigs with the iRBP in situ. The model includes descriptions of the left and right heart, direct ventricular interaction through the septum and pericardium, the systemic and pulmonary circulations, as well as the iRBP. A subset of parameters was optimized in a least squares sense to faithfully reproduce the experimental measurements (pressures, flows and pump variables). Our fitted model compares favorably with our experimental measurements at a range of pump operating points. Furthermore, we have also suggested the importance of various model features, such as the curvilinearity of the end systolic pressure-volume relationship, the Starling resistance, the suction resistance, the effect of respiration, as well as the influence of the pump inflow and outflow cannulae. Alterations of model parameters were done to investigate the circulatory response to rotary blood pump assistance under heart failure conditions. The present model provides a valuable tool for experiment designs, as well as a platform to aid in the development and evaluation of robust physiological pump control algorithms.IEEE transactions on bio-medical engineering 09/2009; 57(2):254-66. DOI:10.1109/TBME.2009.2031629 · 2.35 Impact Factor
- Artificial Organs 03/2008; 32(3):240-258. DOI:10.1111/j.1525-1594.2007.00536.x · 2.05 Impact Factor