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

Abstract

Introduction: Tissue 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.

Methods: Retrospective analysis including patients suffering from acute brain injury and monitored with brain oxygen pressure (PbtO₂) catheter, in whom inotropic agents were administered according to the decision of the treating physician's decision; PbtO₂ values were collected before, 1 and 2 h after the initiation of therapy from the patient data monitoring system. PbtO₂ "responders" were patients with a relative increase in PbtO₂ from baseline values of at least 20%.

Results: A 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], PbtO₂ 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 PbtO₂ "responders," in particular if low PbtO₂ was observed at baseline. A PbtO₂ of 17 mmHg at baseline had a sensibility of 84% and a specificity of 91% to predict a PbtO₂ responder. A significant direct correlation between changes in PbtO₂ 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 PbtO₂ and cerebral perfusion pressure [r = -0.389 (95% CI -0.681 to -0.010), p = 0.05] were observed.

Conclusions: In 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.

Keywords: acute brain injury; brain oxygenation; cerebral blood flow; hemodynamics; inotropic agents.

Figure 1

Brain tissue oxygenation (PbtO₂) values at baseline (before initiation of inotropes—T0), at 1 (T1) and 2 (T2) hours after the introduction of inotropic continuous infusion in the overall population (A) and in responders and non-responders (B). P-value was calculated by Friedmann test.

Figure 2

Receiver Operator Curve (ROC) of baseline brain oxygen pressure (PbtO₂) to predict a significant PbtO₂ increased after therapy.