This work presents a modular approach to the development of strain sensors for large deformations. The proposed method separates the extension and signal transduction mechanisms using a soft, elastomeric transmission and a high-sensitivity microelectromechanical system (MEMS) transducer. By separating the transmission and transduction, they can be optimized independently for application-specific mechanical and electrical performance. This work investigates the potential of this approach for human health monitoring as an implantable cardiac strain sensor for measuring global longitudinal strain (GLS). The durability of the sensor was evaluated by conducting cyclic loading tests over one million cycles, and the results showed negligible drift. To account for hysteresis and frequency-dependent effects, a lumped-parameter model was developed to represent the viscoelastic behavior of the sensor. Multiple model orders were considered and compared using validation and test data sets that mimic physiologically relevant dynamics. Results support the choice of a second-order model, which reduces error by 73% compared to a linear calibration. In addition, we evaluated the suitability of this sensor for the proposed application by demonstrating its ability to operate on compliant, curved surfaces. The effects of friction and boundary conditions are also empirically assessed and discussed.

pulmonary circulation, remains a major clinical burden bearing high morbidity and mortality, particularly in the perioperative setting. [1] Specifically, procedures including valve repairs, implantation of LVAD devices or cardiopulmonary bypass bear a high risk of refractory RV failure due to sudden altered hemodynamic demand on the ventricle, which requires fast adaptation. [2,3] The development of suitable mechanical circulatory solutions to provide adequate perioperative support to the RV is an active area of research. Two primary clinical requirements drive this system design challenge: 1) Solutions should be designed to avoid contact with blood and 2) Solutions should be designed toward the elimination of pneumatic drivelines. The ideal solution should provide temporary perioperative support, with the potential for long-term implantation.Despite ongoing research and development efforts toward artificial cardiac assist devices, often heart transplantation remains the sole definitive treatment option for patients suffering from severe heart failure. [4] Mechanical alternatives to transplantation have been the focus of decades of research, with ventricular assist devices (VADs) and vascular pulsation devices emerging as key clinical strategies to provide mechanical cardiac support. Vascular pulsatile support has been widely investigated and clinically adopted to provide Right ventricular (RV) failure remains a significant clinical burden particularly during the perioperative period surrounding major cardiac surgeries, such as implantation of left ventricular assist devices (LVADs), bypass procedures or valvular surgeries. Device solutions designed to support the function of the RV do not keep up with the pace of development of left-sided solutions, leaving the RV vulnerable to acute failure in the challenging hemodynamic environments of the perioperative setting. This work describes the design of a biomimetic, soft, conformable sleeve that can be prophylactically implanted on the pulmonary artery to support RV ventricular function during major cardiac surgeries, through afterload reduction and augmentation of flow. Leveraging electrohydraulic principles, a technology is proposed that is non-blood contacting and obviates the necessity for drivelines by virtue of being electrically powered. In addition, the integration of an adjacent is demonstrate, continuous pressure sensing module to support physiologically adaptive control schemes based on a real-time biological signal. In vitro experiments conducted in a pulsatile flowloop replicating physiological flow and pressure conditions show a reduction of mean pulmonary arterial pressure of 8 mmHg (25% reduction), a reduction in peak systolic arterial pressure of up to 10 mmHg (20% reduction), and a concomitant 19% increase in diastolic pulmonary flow. Computational simulations further predict substantial augmentation of cardiac output as a result of reduced RV ventricular stress and RV dilatation.