Cerebral oximetry during extracorporeal cardiopulmonary resuscitation

optimize brain perfusion in a patient receiving extracorporeal cardiopulmonary resuscitation (eCPR) after out-of-hospital cardiac arrest (OHCA). A 52-year-old woman (height of 165 cm and weight of 67 kg) had an OHCA secondary to acute myocardial infarction. Th e ambulance arrived on the scene 10 minutes after the call, and mechanical CPR (Lucas; Physio Control Inc., Brussels, Belgium) was initiated. She was fi nally transferred to our hospital with ongoing CPR 50 minutes after the initial call. Monitoring of frontal oxygenation (Foresight; Casmed, Branford, CT, USA; normal values of greater than 65%) was started, and tissue hemoglobin satura tion (StO2) values of around 30% were shown during CPR (Figure 1). A right radial artery catheter was inserted and an extracorporeal membrane oxygena tion (ECMO) veno-arterial device was placed in the femoral vessels within 30 minutes after admission. Just after initiation of ECMO (with blood fl ow of 3 L/minute, sweep gas fl ow of 10 L/minute, and fraction of inspired oxygen (FiO2) of 100%), the mean arterial pressure (MAP) was 67 mm Hg, temperature was 33°C, arterial partial oxygen pressure (PaO2) was 78 mm Hg, blood lactate was 10 mEq/L, and StO2 had increased to 47% bilaterally. After 4 minutes with persistently low StO2 values, we increased the ECMO blood fl ow to 3.5 L/minute, which resulted in increases in MAP to 73 mm Hg, PaO2 to 83 mm Hg, and StO2 to around 60%. Arterial lactate levels were still very high (9.5 mEq/L), and the patient had mottled skin. Th e ECMO blood fl ow was then increased to 4 L/minute, which resulted in increases in MAP to 83 mm Hg and StO2 to greater than 75% in both hemispheres. Despite recovery of spontaneous cardiac activity, the patient died from severe hypoxic-ischemic encephalopathy and multiple organ failure. Brain damage remains the most important cause of morbidity and mortality among survivors after cardiac arrest. However, it remains unclear how systemic hemodynamics should be adjusted to ensure adequate cerebral oxygenation. Cerebral oximetry has been used to optimize cerebral perfusion during conventional CPR [1], and very low cerebral saturation (<40%) may predict poor neurological outcomes at hospital discharge in patients with OHCA [2]. ECMO has been shown to be eff ective to resuscitate adult patients following refractory cardiac arrest with intact neurological outcomes in 15% to 30% of cases [3,4]. Nevertheless, only scarce data are available on the adequacy of cerebral oxygenation during eCPR, and most of them focus on pediatric patients. In one retrospective study, Wong and colleagues [5] described their experience with cerebral oximetry monitoring in 20 adult patients with ECMO; in this population, low cerebral saturation occurred in all patients and was corrected in 80% of them by various interventions to optimize brain perfusion, including increasing MAP or ECMO blood fl ow [5]. In our patient, cerebral saturation remained very low during CPR and only just exceeded © 2010 BioMed Central Ltd Cerebral oximetry during extracorporeal cardiopulmonary resuscitation