TY - JOUR
T1 - Hypotension-induced changes in cerebral function during cardiac surgery
AU - Stockard, James J.
AU - Bickford, Reginald G.
AU - Myers, Robert R.
AU - Aung, Maung H.
AU - Dilley, Ralph B.
AU - Schauble, James F.
N1 - Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 1974
Y1 - 1974
N2 - In a series of 75 patients undergoing cardiac operations with the assistance of car-diopulmonary bypass (CPB), 15 patients were subjected to relatively large hypotensive stresses during CPB as measured by the depth and duration of the fall in cerebral perfusion pressure. Of these 15 patients, eight manifested cerebral dysfunction pos topera lively ranging from temporary exacerbation of pre-existing focal neurological deficits to irreversible coma. In each of these eight cases, EEG disturbances which first appeared at the time of hypotensive episodes during CPB persisted postoperatively and correlated with the nature and evolution of the clinical deficit. In two of the patients who did not regain consciousness postoperatively, neuropathological studies revealed bilateral laminar cortical necrosis, primarily involving cerebral cortex in one case and cerebellar cortex in the other, with accentuation in arterial border iones. Of seven other patients who suffered comparable exposures to hypotension during CPB, none evidenced cerebral dysfunction postoperatively. The most important determinants of this selective vulnerability to low extracorporeal perfusion pressure appeared to be the “reperfusion” pressure established after the hypotensive episode, postoperative blood pressure and cardiac output, and brain temperature at the time of the hypotension. Advanced age and history of cerebrovascular insufficiency were the greatest risk factors among patient variables.
AB - In a series of 75 patients undergoing cardiac operations with the assistance of car-diopulmonary bypass (CPB), 15 patients were subjected to relatively large hypotensive stresses during CPB as measured by the depth and duration of the fall in cerebral perfusion pressure. Of these 15 patients, eight manifested cerebral dysfunction pos topera lively ranging from temporary exacerbation of pre-existing focal neurological deficits to irreversible coma. In each of these eight cases, EEG disturbances which first appeared at the time of hypotensive episodes during CPB persisted postoperatively and correlated with the nature and evolution of the clinical deficit. In two of the patients who did not regain consciousness postoperatively, neuropathological studies revealed bilateral laminar cortical necrosis, primarily involving cerebral cortex in one case and cerebellar cortex in the other, with accentuation in arterial border iones. Of seven other patients who suffered comparable exposures to hypotension during CPB, none evidenced cerebral dysfunction postoperatively. The most important determinants of this selective vulnerability to low extracorporeal perfusion pressure appeared to be the “reperfusion” pressure established after the hypotensive episode, postoperative blood pressure and cardiac output, and brain temperature at the time of the hypotension. Advanced age and history of cerebrovascular insufficiency were the greatest risk factors among patient variables.
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U2 - 10.1161/01.STR.5.6.730
DO - 10.1161/01.STR.5.6.730
M3 - Article
C2 - 4432253
AN - SCOPUS:0016346595
VL - 5
SP - 730
EP - 746
JO - Stroke
JF - Stroke
SN - 0039-2499
IS - 6
ER -