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A 62-year-old man with past 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 five cycles of chest compressions and breaths, a 360-joule (maximum for this unit) 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, his BP was 149/85 mm Hg (without pressors) with a temperature of 36°C. Spo2 100% on a Fio2 of 0.5. His electrocardiogram (ECG) did not reveal any ST-T changes, or bundle branch blocks. The QTc was normal and there were no Brugada-type changes. Initial labs were remarkable only 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.
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Does this neurologic examination exclude the possibility of a good outcome?
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Many patients and their surrogates would consider limiting care if there is no hope for 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 produce few or no instances of “false positives.” 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 recovery.
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Unfortunately, most elements of the neurologic examination immediately after cardiac arrest (CA) lack sufficient predictive value to provide accurate outcome prediction.1-3 Prognostication based solely on a “poor examination” in the hours after CA is inadvisable.
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What happens to the brain when deprived of blood and/or oxygen?
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