Fig. 1: Timing of physiology throughout the dying process until circulatory arrest with pathology correlates.
From: Characterizing the physiology of circulatory arrest in humans
a, WLST was undertaken by extubation with heterogeneous timing until PEA and EA. SBP of <60 mm Hg (white dots) denotes when blood-based brain biomarkers were acquired in each study patient (M, male; F, female). The last recorded breath (green diamonds) was recorded to the minute in each study patient with a bedside assessment. Study patients who underwent donation after circulatory death are denoted with an asterisk. b, Study patients showed heterogeneity in whether the MCAv or PCAv ceased first. c, In all study patients, intracranial blood flow velocities (MCAv or PCAv) ceased before PEA and EA. The last intracranial vessel that stopped giving a velocity signal was used for each study patient so that both anterior and posterior circulations had cessation of flow for comparison to PEA and EA. d, After death determination, the time until autopsy was recorded. e–g, Macrovascular (e and f), microvascular (g) and neural (h) injury in the brain, as determined from autopsies, are probably contributing factors to the heterogeneity of the dying process: examples of macroscopic postmortem brain evaluations include a lethal tumor-associated acute brainstem hemorrhage (e) and a thrombotic occlusion of the left-middle cerebral artery in the circle of Willis and not the other major cerebral arteries (f). The inset shows the left-middle cerebral artery at higher magnification (f). Notable arteriolosclerosis (that is, small vessel disease) were frequent chronic changes identified in this cohort (N = 15; 47%) (g). Scale bar, 50 µm (g). Summary data are presented as medians with IQRs. EA, electrical asystole; HIBI, hypoxic-ischemic brain injury; ICH, intracerebral hemorrhage; MAID, medical assistance in dying; PEA, pulseless electrical activity; SAH, subarachnoid hemorrhage; TBI, traumatic brain injury.
