Cardiac arrest (CA) is a major public health problem (1) because of its frequency (30000 to
50000 new cases of CA per year in France), a high mortality 80-90% and a relevant morbidity :
50% of survivors have cerebral sequela. Neurologic prognostication after CA is paramount. The
American Academy of Neurology identifies accurate predictors of poor neurologic outcome (2):
clinical examination findings such as no pupil response, no corneal reflexes, no motor
response to stimulation and early myoclonus status epilepticus; biologic parameters like high
neuron specific enolase (NSE) greater than 33 μg/L (3-4) and electrophysiologic results like
flat electroencephalogram (EEG) or with burst suppression and Somatosensory evoked potentials
(SEP) with no response to N20. Brain imaging may provide additional informations but not
recommended yet. However, these pronotic markers were developed before the introduction
therapeutic hypothermia (TH) (5-6). TH is now recommended after cardiac arrest by
international guidelines, based on demonstration of improved survival and neurological
recovery in comatose survivors of CA (7). TH and its associated use of sedative and paralytic
agent may delay neurologic recovery and affect the optimal timing of prognostic variables
Many classifications of electroencephalogram (EEG) (9-12) exist but no one is generally
accept and recommended and they were created before TH.
In a preliminary study based on a retrospective cohort of 64 patients in CA with initial TH,
we developped an electroencephalographic score to predict precocity the neurologic outcome
according to the Cerebral performance category (CPC) (13-14).
The purpose of this study is to evaluate a simple and objective electroencephalographic score
helpful to predict neurologic outcome after CA. Then, we would like to create a composite
score to have a multimodal prognostication.
Patients and methods After CA resuscitation, all patients underwent coronary angioplasty if
indicated and then were immediately admitted in emergency room of ICU. All patients were
intubated and mechanically ventilated. Sedation was performed with continuous infusion of
midazolam 0,15-0,2 mg/kg/h and sufentanil 0,15-0,2 μg/kg/h. All our patients were curarized
with cisatracurium 0,2-0,3 mg/kg/h to prevent shivering during TH and took anti-epileptic
medication phenobarbital 10-15 mg/ kg two times a day to prevent infra-clinic convulsive
Mild TH between 33 -34 °C was performed by active cooling with intravascular device
(CoolGard® - Zoll, Chelmsford, UK) for 24 hours. Mean arterial pressure was maintained
between [75-80] mmHg by titrated norepinephrine with or without inotropics (dobutamine,
epinephrine) according cardiac output monitored by echocardiography.
After 24 hours of hypothermia, warming was started at a rate of 0.2 ° C/hr; neuromuscular
blocking agents were arrested at 35.5°C and sedation at 36.5°C.
Neurological evaluation performed at 48 hours off sedation included a clinical evaluation
(Glasgow score, myoclonus status, response to orders, motor response to stimulation,
brain-stem reflexes). NSE was sampled between 48 and 72 H. EEGs were performed at Day-2,
Day-3 and Day-5 off sedation and SEP at Day-5 off sedation. All EEGs were interpreted by two
certified electroencephalographers blind from clinical neurologic outcome.
Survival and neurologic outcome according to CPC were assessed at ICU discharge and three