Conversion pathways of primary defects by annealing in proton-irradiated n-type 4H-SiC

TL;DR

This study investigates defect evolution in proton-irradiated n-type 4H-SiC during annealing, revealing mechanisms of defect transformation, recombination, and their impact on electrical properties using spectroscopy techniques.

Contribution

It provides a comprehensive model of defect interconversion in irradiated 4H-SiC, highlighting the role of specific defect complexes and their temperature-dependent behavior.

Findings

CAV pairs dissociate into separate defects at high temperatures.

VSi and VC are mainly annealed via recombination with self-interstitials.

Removal of free carriers is due to compensating defects, not passivation.

Abstract

The development of defect populations after proton irradiation of n-type 4H-SiC and subsequent annealing experiments is studied by means of deep level transient (DLTS) and photoluminescence (PL) spectroscopy. A comprehensive model is suggested describing the evolution and interconversion of irradiation-induced point defects during annealing below 1000{\deg}C. The model proposes the EH4 and EH5 traps frequently found by DLTS to originate from the (+/0) charge transition level belonging to different configurations of the carbon antisite-carbon vacancy (CAV) complex. Furthermore, we show that the transformation channel between the silicon vacancy (VSi) and CAV is effectively blocked under n-type conditions, but becomes available in samples where the Fermi level has moved towards the center of the band gap due to irradiation-induced donor compensation. The annealing of VSi and the carbon vacancy (VC) is shown to be dominated by recombination with residual self-interstitials at temperatures of up to 400{\deg}C. Going to higher temperatures, a decay of the CAV pair density is reported which is closely correlated to a renewed increase of VC concentration. A conceivable explanation for this process is the dissociation of the CAV pair into separate carbon anitisites and VC defects. Lastly, the presented data supports the claim that the removal of free carriers in irradiated SiC is due to introduced compensating defects and not passivation of shallow nitrogen donors.