Brugada syndrome has many theorised pathologies. Three of the most prevalent are genetic abnormalities in depolarisation, repolarisation, or a combination of both. It is one of the leading causes of ventricular fibrillation, which may be refractory to defibrillation shocks. Pharmaceutical intervention is recommended for shock-refractory cardiac arrest, however the efficacy of resuscitative drugs appears different in patients with Brugada syndrome. Amiodarone monotherapy has been clinically observed to be relatively ineffective in Brugada syndrome patients, however sequential amiodarone-lidocaine administration has a high termination rate. The effects of resuscitative drug protocols were explored in the three pathological mechanisms of Brugada syndrome in computational models to elucidate the differences in ventricular fibrillation termination dynamics between normal and Brugada syndrome cardiac arrest at the single cell level. Acute IV bolus of amiodarone, lidocaine, and sequential amiodarone-lidocaine were simulated by altering ion channel conductances according to literature and clinical observations. A dynamic restitution protocol was applied to achieve the fastest stable pacing rate before loss of action potential dome. Each drug protocol was then applied and the model paced for a further 100 beats at different cycle lengths to find the new fastest stable pacing rate. Changes in phase 1 notching and action potential duration were compared between the control and Brugada models for different drug protocols. Acute amiodarone monotherapy acts similarly in Brugada cells compared to control, opposing clinical observations and implying that tissue-level effects are vital to capture the full termination dynamics. Sequential amiodarone-lidocaine administration had opposite effects in Brugada cells, increasing action potential duration opposed to the reduction seen in the control. Lowest stable pacing rate decreased for control but increased for Brugada models. The termination mechanism remains unclear in the single-cell model, implying tissue level effects are critical for the differences observed between control and Brugada syndrome patient resuscitation.