In-situ investigation of the interaction between hydrogen and stacking faults in a bulk austenitic steel

The interaction between hydrogen (H) atoms and various microstructural defects remains a key to understand the H-induced damage and the subsequent premature failure of high-strength metallic materials. Previous studies on this subject are mainly focused on the in-situ probing of dislocations in a th...

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Veröffentlicht in:Acta materialia 2024-01, Vol.262, p.119441, Article 119441
Hauptverfasser: Shi, Hao, Nandy, Supriya, Cheng, Huijie, Sun, Binhan, Ponge, Dirk
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Sprache:eng
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Zusammenfassung:The interaction between hydrogen (H) atoms and various microstructural defects remains a key to understand the H-induced damage and the subsequent premature failure of high-strength metallic materials. Previous studies on this subject are mainly focused on the in-situ probing of dislocations in a thin foil placed in an environmental transmission electron microscopy (TEM) cell. Here, a three-point bending test coupled with electron channeling contrast imaging (ECCI) has been applied to investigate the interaction of H with stacking faults (SFs) in a bulk high Mn austenitic steel. The expansion of some SFs, in terms of one partial dislocation movement within a partial dislocation pair, was observed on the H pre-charged sample when kept at a constant loading (i.e., a continuous H migration and likely build-up close to the pre-prepared notch tip). A temporal-resolved cross-correlation EBSD (CC-EBSD) measurement shows that the migration of H towards the notch tip region has a minor effect on the internal stress evolution. However, the local shear modulus (μ) and stacking fault energy (γSF) can be reduced by a local H segregation. Further theoretical calculation of SF ribbon width indicates that the reduction of μ by H results in the shrinkage of SF, while the H-induced reduction of γSF results in SF expansion at a lower resolved shear stress. The observed expansion of SF ribbons can be interrupted by a combined reduction of both μ and γSF due to H. [Display omitted]
ISSN:1359-6454
1873-2453
DOI:10.1016/j.actamat.2023.119441