Microstructural origins of enhanced work hardening and ductility in laser powder-bed fusion 3D-printed AlCoCrFeNi2.1 eutectic high-entropy alloys

Limited tensile ductility usually restricts the practical applications of new classes of high-strength materials in many industrial fields. Therefore, in-depth understanding of the work hardening behavior and its underlying plastic deformation mechanism are critical for the newly developed high-entropy alloys (HEAs). In this work, a geometric atomistic model of face-centered cubic (FCC)/ordered body-centered cubic (BCC (B2)) interfaces and the evolution of dislocation substructures have been investigated to explore the microstructural origins of work hardening responses for two additively manufactured AlCoCrFeNi_2.1 eutectic high-entropy alloys (EHEAs) with the respective lamellar and cellular microstructures. Unlike the lamellar interphase interfaces with the most classical Kurdjumov-Sachs (KS) FCC-BCC relationship of ${\left\{111\right\}}_{\text{FCC}}\parallel {\left\{110\right\}}_{B2}{〈011〉}_{\text{FCC}}\parallel {〈111〉}_{B2}$, the Nishiyama-Wassermann (NW) relationship, namely ${\left\{111\right\}}_{\text{FCC}}\parallel {\left\{110\right\}}_{B2}{〈011〉}_{\text{FCC}}\parallel {〈001〉}_{B2}$, is observed to be dominant on the cellular interphase interfaces. Furthermore, our intermittent high-resolution transmission electron microscopy (HR-TEM) results directly show that the deformation of lamellar AlCoCrFeNi_2.1 alloy first proceeds with massive stacking faults (SFs) and then dislocation walls developed across phases interfaces, due to the effective dislocation transfer capability of lamellar boundaries. The large uniform elongation of the cellular AlCoCrFeNi_2.1 alloy is attributed to the stable and progressive strain-hardening mechanism that is stemmed from the activated multiple slip systems, deformation-induced SF networks, and the associated Lomer-Cottrell locks in the middle and later stages of plastic deformation. Moreover, the nano-bridging of FCC cells in the 3D-printed microstructure provides unique channels for dislocation movement, which offsets the “blocking effect” of cellular boundaries and thus suppresses the pre-mature fracture.