Autonomously self-healing dielectric elastomer actuators from thermoplastic polydimethylsiloxane elastomer

Abstract

Dielectric elastomer actuators (DEAs) are usually operated at high voltage to induce sufficient electric pressure between two compliant electrodes sandwiching the dielectric elastomer. However, a harsh environment (e.g. humid environment combined with high voltage) often induces electrical breakdown (EB) of the DEAs, which results in pinhole formation or even tearing of the device, followed by macroscopic failure. Therefore, it is ideal for DEAs to be self-healing to extend robustness and lifetime, such as observed for biological muscles, which can be healed from injuries by inherent biological processes. Herein, we prepared a soft (Young’s modulus: 187 kPa) polydimethylsiloxane (PDMS) thermoplastic elastomer (TPE) to demonstrate an autonomous self-healing ability. The system exploits hydrogen bonding (H-bonding) in two types of transient cross-linkers: urea group serves as a sacrificial bond under loading and ureidopyrimidone (UPy) serves as a strong, load-carrying crosslinker. The PDMS TPE shows a crossover of the elastic moduli at 119 °C and highly frequency dependent elastic modulus. The DEA is prepared with compliant, corrugated silver electrodes on both sides of a corrugated PDMS TPE film. A maximum actuation strain (6.8 % in longitudinal direction) is achieved at 18.8 V μm-1. A further increase in potential does not increase the actuation strain, but EBs are observed on the electrodes and the actuation is maintained without any detrimental effects to the film despite the previous breakdown. The EBs do not form permanent pinholes, nor do they cause tearing of films. Instead, only the removal of the silver electrode is observed, which is the so-called self-clearing effect commonly observed for metallic electrodes. In combination with the self-clearing effect, the heat generated by the EBs allows the PDMS TPE to soften. The polymer molecules are then capable of flowing into the voids that were created at the initiation of the EBs. As a result, further propagation of the EB is hindered, and instead, an instantaneous and autonomous self-healing of the DEA is observed.