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A 62-year-old man with a medical history of hypertension was in a heated argument with his son when he suddenly complained of dizziness and collapsed to the floor. The son called 911, and paramedics arrived on the scene in 8 minutes. The patient was pulseless, and cardiopulmonary resuscitation (CPR) was initiated. He was found to have ventricular fibrillation (VF). A 200-joule biphasic shock was delivered without success. Chest compressions were continued and intravenous (IV) vasopressin, 40 units, was given. After 2 minutes of chest compressions, another 200-joule biphasic shock was delivered, with conversion to a wide-complex rhythm at 120 bpm. The blood pressure (BP) was 120/70 mm Hg. Amiodarone, 300 mg, was given IV. Estimated time from collapse to return of spontaneous circulation (ROSC) was 15 minutes. He was intubated at this point and then transported to the emergency department (ED) of a local hospital.

On arrival at the ED, the patient was in a narrow-complex sinus rhythm at 89 bpm, and his BP was 149/85 mm Hg (without vasopressors) and temperature was 36°C. Oxygen saturation was 100% on a fraction of inspired oxygen (fio2) of 0.5. His electrocardiogram (ECG) did not reveal any ST segment depressions or elevations, T-wave changes, or bundle branch blocks. The corrected QT (QTc) interval was normal. Initial laboratory values were remarkable for a negative troponin I (TnI). An echocardiogram revealed concentric left ventricular hypertrophy with high ejection fraction and no regional wall motion abnormalities. The chest radiograph was clear. A computerized tomographic (CT) scan of the head was unremarkable.

The patient’s initial neurologic examination showed no response to verbal stimulation and no eye opening to noxious stimulation. He had reactive pupils, trace corneal reflexes, weakly present horizontal oculocephalic reflexes, no gag reflex, and a weak cough reflex. Upon noxious stimulation, he had extensor posturing of the arms and triple flexion in legs. The Glasgow Coma Scale (GCS) score was 4.

Does this neurologic examination exclude the possibility of a good outcome?

Prognostication after cardiac arrest (CA) can be a challenging and complex task. Many patients and their surrogates would consider limiting care if there is no hope for meaningful neurologic recovery. Therefore, it is important for medical providers to be aware of the prognostic possibilities at all stages of care so that accurate information can be provided to family and informed decisions can be made. Ideally, variables used for prognostication should accurately predict with high specificity which patients have a universally poor prognosis. In other words, we want to make sure that close to 100% of those labeled as having a poor prognosis do in fact have no chance of meaningful recovery.

Unfortunately, most elements of the neurologic examination immediately after CA lack sufficient predictive value to provide accurate outcome prediction.1-3 Prognostication based solely on a clinical examination within hours after CA is not recommended.

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