Cerebral blood ow direct measurement is difcult to obtain in clinical setting. It is usually invasive and expensive and requires moving the patients outside the intensive care unit. Transcranial Doppler (TCD) is a noninvasive, non-expensive bedside technique that can pro­vide serial assessment of cerebral perfusion with­out interfering with clinical care. Although it does not assess cerebral perfusion directly, as explained elsewhere in this textbook, it can be used to assess modications in cerebral blood ow and cerebral autoregulation, in addition to inferring functional status of cerebral microcirculation.

compression [36]. However, despite being a reli­able tool to estimate systemic circulation in this setting [37], EtCO2 does not give any information on target organ perfusion, in particular the brain. Lewis etal. investigated the use of TCD to assess cerebral circulation during CPR on animal model [38] and human subjects [39] and concluded that TCD can provide real-time information about cerebral perfusion. During CPR, cerebral perfu­sion is produced during chest compressions and maximum systolic velocity in intracranial arteries reects cerebral perfusion during each compres­sion. Data showed that optimal cerebral blood ow is maintained for no longer than 3min during CPR on human subjects, despite the rescuer not complaining of any fatigue [39]. Successfully resuscitated patients showed recovery of cerebral blood ow immediately before return of sponta­neous circulation was noted, while patients with­out ROSC showed progressive deterioration in cerebral blood ow velocities over time during CPR, until absence of net forward blood ow was seen [39]. Similarly, de Wilde et al. observed return of spontaneous cerebral blood ow before arterial pressure was recorded on invasive moni­toring in a male patient who suffered from cardiac arrest during ICU stay [40]. Carmona-Jimenez etal. compared intracranial blood ow velocities during manual and mechanical chest compression by LUCAS® device in four patients affected by nontraumatic, witnessed cardiac arrest. They found mean maximum ow velocity during man­ual chest compression to be 31.6 ± 8.32 cm/s compared to 50.6±27.1cm/s during mechanical chest compression, thus supporting the hypothe­sis that mechanical chest compressions are more effective than manual compressions in maintain­ing adequate brain perfusion [41]. Blumestein etal. reported a case of incidental use of TCD dur­ing cardiopulmonary resuscitation in a female patient undergoing minimally invasive transcath­eter aortic valve implantation under general anes­thesia. The authors expanded intravascular volume and increased depth of chest compression in order to obtain continuously positive diastolic blood ow. The authors were also able to evaluate the effect of different therapeutic interventions to ameliorate cerebral blood ow, among which

administration of sodium bicarbonate seemed to be most effective. The patient eventually recov­ered with no neurological decits [42]. However, artifacts are frequent and may interfere with inter­pretation of signal. Lewis etal. reported insonation of both middle cerebral artery through temporal window and ophthalmic artery to be unsuccessful or to result in damped or to be concealed by arti­fact signal. However, insonation of the internal carotid artery by transorbital approach was suc­cessful and resulted in a good-quality and stable signal.

and severe endothelial dysfunction. Alvarez­Fernandez et al. summarized the evolution of mean blood ow velocity (FV) and pulsatility index (PI) on middle cerebral artery after recov­ery from cardiac arrest [58]. In general, PI between 0.6 and 1.1 is considered to be associ­ated with normal intracranial hemodynamics; PI below 0.6 may indicate hyperemia; PI between

protocols. Core temperature may have an inu­ence on cerebral blood ow and its regulation [68] and hypothermia showed some benets on CAR in the animal model of TBI [69]. However, clinical management differs from center to center and to date few studies have been published enrolling patients treated by targeted temperature management, showing opposite results [64, 70,

ies investigated the use of TCD during cardiopulmonary resuscitation. TCD was able to detect suboptimal cerebral blood ow during external cardiac massage as well as early recov­ery of cerebral perfusion, before any other sign of ROSC was noted, in a small cohort of human subjects [39], but any other consideration on the clinical use of TCD during resuscitation efforts is anecdotal [42]. A larger body of literature is available on the use of TCD in post-resuscitation care. TCD has been extensively applied to moni­tor the evolution of cerebral blood ow after resuscitation from cardiac arrest [33, 58–62]. With certain limitations, monitoring of cerebral autoregulation by TCD may be applicable in titrating MAP after cardiac arrest, so as to avoid hypo- or hyper-perfusion and limit secondary brain injury after cardiac arrest. Alteration of TCD parameters, such as indexes related to blood ow or vascular resistance in intracranial arteries after cardiac arrest, may also be of prognostic values [35, 45, 53, 54, 64, 72]. Unfortunately, comparisons of results of different studies are limited by differences in study protocols and a denite result on association between alterations in TCD parameters and outcome in patients resuscitated from cardiac arrest is still lacking. At the time being, despite its many potential appli­cations and despite being recommended as a part of multi-modality monitoring in the intensive care unit [74], more studies are needed to imple­ment TCD in cardiac arrest survivors as part of routine practice in hospital centers.