Effect of inotropic agents on oxygenation and cerebral perfusion in acute brain injury

IntroductionTissue hypoxia and insufficient energy delivery is one of the mechanisms behind the occurrence of several complications in acute brain injured patients. Several interventions can improve cerebral oxygenation; however, the effects of inotropic agents remain poorly characterized. MethodsRetrospective analysis including patients suffering from acute brain injury and monitored with brain oxygen pressure (PbtO(2)) catheter, in whom inotropic agents were administered according to the decision of the treating physician's decision; PbtO(2) values were collected before, 1 and 2 h after the initiation of therapy from the patient data monitoring system. PbtO(2) "responders" were patients with a relative increase in PbtO(2) from baseline values of at least 20%. ResultsA total of 35 patients were included in this study. Most of them (31/35, 89%) suffered from non-traumatic subarachnoid hemorrhage (SAH). Compared with baseline values [20 (14-24) mmHg], PbtO(2) did not significantly increase over time [19 (15-25) mmHg at 1 h and 19 (17-25) mmHg at 2 h, respectively; p = 0.052]. A total of 12/35 (34%) patients were PbtO(2) "responders," in particular if low PbtO(2) was observed at baseline. A PbtO(2) of 17 mmHg at baseline had a sensibility of 84% and a specificity of 91% to predict a PbtO(2) responder. A significant direct correlation between changes in PbtO(2) and cardiac output [r = 0.496 (95% CI 0.122 to 0.746), p = 0.01; n = 25] and a significant negative correlation between changes in PbtO(2) and cerebral perfusion pressure [r = -0.389 (95% CI -0.681 to -0.010), p = 0.05] were observed. ConclusionsIn this study, inotropic administration significantly increased brain oxygenation in one third of brain injured patients, especially when tissue hypoxia was present at baseline. Future studies should highlight the role of inotropic agents in the management of tissue hypoxia in this setting.