Post-cardiac arrest syndrome is a complex condition increasingly present in our cardiac intensive care units (ICU). Intensive care cardiologists must assess neurological prognosis and address conditions like status epilepticus, which can further deteriorate outcomes. This necessitates a multiparametric approach involving neurological examination, laboratory tests, radiological and neurophysiological studies. Electroencephalogram (EEG) is crucial for detecting epileptiform brain activity. International guidelines recommend performinf EEG after 48 hours from admission, which may delay non convulsive status epilepticus (NCSE) diagnosis. In our unit, we have recently introduced bispectral index (BIS) monitoring for post-cardiac arrest comatose patients. BIS analyzes with a set of electrodes applied on the forehead the EEG signal, displaying a simplified EEG trace, a spectroscopic representation of brain activity, and a sedation depth index. We hypothesize that BIS monitoring can aid in early NCSE detection and treatment in comatose, sedated patients. A 43-year-old male was admitted to our cardiac ICU after an out-of-hospital cardiac arrest. The patient, with a known history of supraventricular extrasystoles, was found gasping by cohabitants. After 15 minutes of ineffective bystander CPR, the advanced rescue team arrived and detected fine-wave ventricular fibrillation. Return of spontaneous circulation was achieved after five resuscitation cycles according to ACLS protocol. Upon admission, the patient was comatose with a Glasgow Coma Scale (GCS) score of 3 but corneal and pupillary reflexes were present. BIS during sedation showed prevalent cerebral activity in the 4 Hz frequency band, indicating deep coma. BIS simplified EEG trace showed pointed abnormalities suggestive of NCSE, which was confirmed by a prompt standard EEG. PESS were also performed, revealing bilateral absence of the N20 complex. BIS monitoring detected persistent epileptiform abnormalities in the following days of hospitalization, with low-frequency prevalent cerebral activity, despite initiation and adjustments in antiepileptic therapy. These findings were confirmed with serial standard EEGs. Within the first three days, the multiparametric evaluation of the neurological prognosis was completed. The brain MRI revealed signs of diffuse anoxic damage and the NSE were particularly high. Given the unfavorable neurological prognosis, an attitude of therapeutic desistance was agreed upon.