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Direct cerebral perfusion and cooling in experimental cardiac arrest.
Critical Care and Resuscitation : Journal of the Australasian Academy of Critical Care Medicine 2016 December
BACKGROUND: Cerebral protection is a key priority during cardiac arrest (CA). However, current approaches are suboptimal.
OBJECTIVE: To test whether direct perfusion and cooling of the anterior cerebral circulation by means of cerebral vessel cannulation and extracorporeal membrane oxygenation (ECMO) increases cerebral oxygenation and induces cerebral hypothermia during CA.
METHODS: We performed proof-of-concept animal experiments in sheep. We cannulated the carotid artery (for antegrade perfusion) or the jugular vein (for retrograde perfusion) for direct perfusion and cooling, and the jugular vein on the opposite side for drainage. We connected these cannulae to an ECMO circuit. We induced CA and, after 10 minutes, and during open-chest cardiac massage, we provided ECMO-based perfusion and cooling. We measured cerebral tissue oxygen saturation (SctO2 ) by near infrared spectroscopy (NIRS) and cerebral temperature by means of invasively inserted tissue temperature probes.
RESULTS: In the antegrade perfusion experiments (n = 2), CA markedly decreased the SctO2 to below 40% over 10 minutes, despite open-chest cardiac massage. ECMO-based cerebral perfusion and cooling increased SctO2 levels to 60% and lowered cerebral temperature to 25°C within about 3 minutes. With retrograde perfusion (n = 2), ECMObased cerebral perfusion and cooling was less effective; ECMO increased SctO2 levels slowly and to a much lesser extent and similarly decreased cerebral temperature slowly and to a lesser extent.
CONCLUSIONS: During experimental CA, cerebral perfusion and cooling are possible by means of an ECMO circuit connected to the anterior cerebral circulation. Antegrade perfusion appears to be superior. Further investigations of the antegrade perfusion technique appear justified.
OBJECTIVE: To test whether direct perfusion and cooling of the anterior cerebral circulation by means of cerebral vessel cannulation and extracorporeal membrane oxygenation (ECMO) increases cerebral oxygenation and induces cerebral hypothermia during CA.
METHODS: We performed proof-of-concept animal experiments in sheep. We cannulated the carotid artery (for antegrade perfusion) or the jugular vein (for retrograde perfusion) for direct perfusion and cooling, and the jugular vein on the opposite side for drainage. We connected these cannulae to an ECMO circuit. We induced CA and, after 10 minutes, and during open-chest cardiac massage, we provided ECMO-based perfusion and cooling. We measured cerebral tissue oxygen saturation (SctO2 ) by near infrared spectroscopy (NIRS) and cerebral temperature by means of invasively inserted tissue temperature probes.
RESULTS: In the antegrade perfusion experiments (n = 2), CA markedly decreased the SctO2 to below 40% over 10 minutes, despite open-chest cardiac massage. ECMO-based cerebral perfusion and cooling increased SctO2 levels to 60% and lowered cerebral temperature to 25°C within about 3 minutes. With retrograde perfusion (n = 2), ECMObased cerebral perfusion and cooling was less effective; ECMO increased SctO2 levels slowly and to a much lesser extent and similarly decreased cerebral temperature slowly and to a lesser extent.
CONCLUSIONS: During experimental CA, cerebral perfusion and cooling are possible by means of an ECMO circuit connected to the anterior cerebral circulation. Antegrade perfusion appears to be superior. Further investigations of the antegrade perfusion technique appear justified.
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