Patient 6 was a 71-year-old male pedestrian struck by a vehicle with reported field GCS = 14. The patient was intubated for airway compromise, and arrived at the trauma center with presentation GCS = 3T5. His primary survey revealed polytrauma with gross limb deformities and signs of craniofacial injury. A Focused Assessment with Sonography for Trauma examination was negative; CT of the head revealed diffuse traumatic SAH and a small falcine subdural hematoma. He was found to have coagulopathy by admission laboratory evaluation. After resuscitation and correction of coagulopathy, the patient was admitted to neurocritical care and an ICP monitor was placed. Repeat cranial imaging demonstrated worsening bifrontal contusions and an enlarging left temporal contusion. The patient's neurologic examination declined to GCS = 3T despite aggressive medical management for refractory ICP. A family discussion was held on day 2, at which time a DNR-CC order was activated. The patient was terminally extubated. The end-of-life recordings are shown in Figure C.
Patient 1 was a 52-year-old woman with aSAH. Until day 3, she had 13 SDs (2 spreading depressions and 11 isoelectric SDs) with a PTDDD of 487.9 minutes that occurred on day 3. On the same day, a computed tomography (CT) scan showed multiple infarcts in the territories of the right middle cerebral artery (MCA) and both posterior cerebral arteries. On the following day, a control scan revealed increasing lesions, 10mm midline shift, and beginning brain herniation. From the beginning, she required intravenous noradrenaline at a rate of 0.08 µg/kg/min to maintain adequate cerebral perfusion pressure (CPP) under sedation with propofol. Stress cardiomyopathy was ruled out using echocardiography, electrocardiography, and cardiac biomarkers. However, noradrenaline had to be further increased to 0.26 µg/kg/min on day 4 when she developed Staphylococcus aureus–caused pneumonia and midazolam was added to the sedative regimen to control progressive increase in ICP. Thiopental was added for the same reason 12 hours before she died on day 6. Thiopental resulted in cerebral isoelectricity, and intravenous noradrenaline had to be increased to a rate of 0.43 µg/kg/min. Eventually, a DNR-CC order was activated after family discussion and the patient was terminally extubated. Withdrawal of the life-sustaining treatment resulted in complete circulatory arrest after 17 minutes. Figure A shows the time course of the systemic arterial pressure including the circulatory arrest and subsequent terminal SD that started at electrode 4 and then spread to the other electrodes. For comparison, Figure C displays a typical terminal SD of a rodent brain after injection of air into the heart via the femoral vein (experimental setup in Fig D); circulatory arrest is followed by nonspreading depression and then terminal SD. The Supplementary Table provides the statistical data of 5 thiopental-anesthetized rats with previously healthy brains in which death resulted from sudden circulatory arrest by air injection into the femoral vein.