Dear Editor, We report the case of a comatose survivor from cardiac arrest (CA) in whom cerebral oximetry helped insure adequate brain perfusion. A 64-year old man was admitted to our Department of Intensive Care after out-of-hospital CA secondary to ventricular fibrillation. Urgent coronary angiography did not reveal any significant lesion. Cardiac output (CO) (PiCCO, PULSION Medical Systems AG, Munich, Germany) was 3.9 L/min, stroke volume variation (SVV) 10 %, superior vena cava oxygen saturation (SvcO2) 69 % and lactate 4.2 mEq/L (Table 1). Bilateral transcranial doppler (TCD, Philips S4-2 probe, USA) of the middle cerebral arteries (MCA) and cerebral oxygen saturation (StO2) by frontal oximetry (Fore-sight, Casmed, Branford, CT—normal values [65 %) were within normal ranges (Table 1). The patient was cooled with blankets to achieve therapeutic hypothermia (TH). Blood temperature progressively decreased to 33 C within 70 min at which time CO was 2.2 L/min, SVV 9 % and SvcO2 68 %. Transesophageal echocardiography (TEE) showed global biventricular hypokinesia and a left ventricular ejection fraction of 25 %; however, arterial lactate level had decreased to 2.4 mEq/L and urine output exceeded 1 ml/kg/h. Although PaCO2 was constant between 34 and 36 mmHg, TCD showed a slight reduction in mean MCA velocities (MCAV) and increase in pulsatility index (PI) (Table 1) from baseline values; StO2 was only 55 and 57 % on the left and right sides, respectively. Increasing mean arterial pressure (MAP) to 80 mmHg with norepinephrine had no impact on brain oxygenation. Initiation of a dobutamine infusion (5 lg/kg/min) resulted in an increase in CO to 3.7 L/min and SvcO2 to 76 %, without significant changes in MAP; PI, mean MCA velocities, and StO2 values increased (Table 1, Fig. 1). Dobutamine was maintained for 48 h, until the patient recovered consciousness. He was discharged after 16 days with only moderate amnesia. Brain damage remains the most important cause of disability and death among CA survivors. Despite restoration of an adequate systemic blood pressure, complex pathological phenomena lead to reduced cerebral blood flow (CBF) and inadequate oxygen supply, which contribute to secondary brain injury [1]. During TH, a reduction in global metabolism and blood flow is expected, however systemic hemodynamic variables cannot predict cerebral oxygen delivery and cerebral hypoperfusion may persist; moreover, hypocapnia is frequent during TH, and can induce cerebral vasoconstriction and further decrease cerebral perfusion [2]. In this setting, monitoring of CBF and oxygenation is of paramount importance. The TCD provides information on CBF autoregulation during dynamic interventions, even after CA [3]; we found that dobutamine administration raised MCAV while reducing PI, which suggested an increase in blood flow. However, TCD is not useful for estimating brain oxygenation. The adequacy of cerebral hemispheric oxygenation can be estimated by the venous hemoglobin saturation measured in the internal jugular vein, but this requires