Neurologic recovery after cardiac arrest occurs in only a small number of patients. One of the biggest challenges in the intensive care unit (ICU) is prognosticating outcomes in comatose patients and optimizing treatment decisions when a patient survives a cardiac arrest. The physical examination can help greatly in predicting death or poor outcome in comatose survivors of cardiac arrest.

When a cardiac arrest occurs, there is cessation of flow to the brain and other organs. The oxygen stores of the brain last for only approximately 20 seconds after arrest and the glucose and adenosine triphosphate (ATP) stores in the brain last less than 5 minutes. Neuronal death occurs after arrest and, depending on the extent, can result in a coma. During effective cardiopulmonary resuscitation, flow is restored, but it is almost always abnormal (e.g., a low flow state). With a shorter duration of arrest and resuscitation, the damage due to ischemic injury and hypoperfusion is expected to be less. When spontaneous circulation is restored, there is a brief period of cerebral hyperemia, followed by vasospasm and prolonged hypoperfusion.

The overall rate of a poor outcome in patients surviving a cardiac arrest who are comatose is approximately 77%. Poor outcomes were defined as severe cerebral disability, coma, vegetative state, or death (Glasgow-Pittsburgh Cerebral Performance Categories 3 through 5). Clinical exam findings can assist in determining the prognosis of comatose survivors of cardiac arrest. Decisions to withdraw care should not be made on the basis of these findings alone, but this information is often useful in helping the family make decisions about further care. The physical exam findings that were found to be most helpful in predicting poor outcome were related to motor and brain-stem function. The precision of the neurologic exam in predicting outcomes was found to be only moderately to substantially helpful. The positive likelihood ratios (LR) of various physical exam findings in predicting poor outcome are listed in Table 205.1.