Resuscitation · 2010
Effects of cerebral hypoperfusion on bispectral index: a randomised, controlled animal experiment during haemorrhagic shock.
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Cavus Erol, Meybohm Patrick, Doerges Volker, Hoecker Jan, Betz M, Hanss Robert, Steinfath Markus, Bein Berthold
Аннотация
BACKGROUND: The aim of this porcine haemorrhagic shock model was to investigate the changes of bispectral index (BIS) after slow and fast recovery of cerebral perfusion, and its correlation with plasma propofol concentrations.
METHODS: After Animal Investigational Committee approval, 16 pigs during propofol anaesthesia underwent a liver trauma with severe hypotension, and were randomly assigned to receive therapy for either slow recovery (fluid resuscitation; slow group; n=8) or fast recovery of cerebral perfusion (vasopressor combined with hypertonic-saline-starch; fast group; n=8), respectively. Cerebral perfusion pressure (CPP=MAP-ICP), cerebral tissue oxygenation index (TOI), BIS, and plasma concentrations of propofol and haemoglobin were measured at baseline (Pre-shock), haemodynamic decompensation (Shock), and 5 (Therapy) and 30 min (End) after therapy, respectively.
RESULTS: CPP, TOI, and BIS decreased significantly during shock (pre-shock vs. shock, fast: CPP: 65+/-14 vs. 15+/-4 mmHg; TOI: 64+/-6 vs. 47+/-7%; BIS 60+/-5 vs. 9+/-10; slow: CPP: 60+/-12 vs. 13+/-7 mmHg; TOI: 68+/-7 vs. 49+/-7%; BIS 63+/-5 vs. 13+/-12; P<0.05). In the fast group, CPP, TOI, and BIS increased after therapy compared to the slow group (Therapy, fast: CPP: 47+/-15 mmHg, TOI: 61+/-7%, BIS: 47+/-21; slow: CPP: 18+/-9 mmHg, TOI: 51+/-5%, BIS: 21+/-19; P<0.05). Propofol and haemoglobin concentrations were comparable between groups throughout the resuscitation phase.
CONCLUSIONS: In a haemorrhagic shock scenario, therapies with different impact on cerebral perfusion resulted in differing changes of BIS values, while plasma propofol and haemoglobin concentrations were comparable during the resuscitation phase; this suggests that BIS may also have reflected changes of cerebral perfusion.
METHODS: After Animal Investigational Committee approval, 16 pigs during propofol anaesthesia underwent a liver trauma with severe hypotension, and were randomly assigned to receive therapy for either slow recovery (fluid resuscitation; slow group; n=8) or fast recovery of cerebral perfusion (vasopressor combined with hypertonic-saline-starch; fast group; n=8), respectively. Cerebral perfusion pressure (CPP=MAP-ICP), cerebral tissue oxygenation index (TOI), BIS, and plasma concentrations of propofol and haemoglobin were measured at baseline (Pre-shock), haemodynamic decompensation (Shock), and 5 (Therapy) and 30 min (End) after therapy, respectively.
RESULTS: CPP, TOI, and BIS decreased significantly during shock (pre-shock vs. shock, fast: CPP: 65+/-14 vs. 15+/-4 mmHg; TOI: 64+/-6 vs. 47+/-7%; BIS 60+/-5 vs. 9+/-10; slow: CPP: 60+/-12 vs. 13+/-7 mmHg; TOI: 68+/-7 vs. 49+/-7%; BIS 63+/-5 vs. 13+/-12; P<0.05). In the fast group, CPP, TOI, and BIS increased after therapy compared to the slow group (Therapy, fast: CPP: 47+/-15 mmHg, TOI: 61+/-7%, BIS: 47+/-21; slow: CPP: 18+/-9 mmHg, TOI: 51+/-5%, BIS: 21+/-19; P<0.05). Propofol and haemoglobin concentrations were comparable between groups throughout the resuscitation phase.
CONCLUSIONS: In a haemorrhagic shock scenario, therapies with different impact on cerebral perfusion resulted in differing changes of BIS values, while plasma propofol and haemoglobin concentrations were comparable during the resuscitation phase; this suggests that BIS may also have reflected changes of cerebral perfusion.