Hypothermia After Cardiopulmonary Resuscitation

13 Hypothermia After Cardiopulmonary Resuscitation

A 61-year-old woman slumped down with rattling breathing and rapidly developing cyanosis. A bystander performed cardiopulmonary resuscitation, but the EMS arrived quickly and documented ventricular fibrillation. Several shocks were needed to restore circulation. The patient remained comatose and was intubated. External ice packs and iced saline was used during transportation, and after arrival to the intensive care unit, the patient was cooled to 33ûC using an external cooling device. An EEG showed suppressed activity but changed to epileptiform discharges during rewarming. Somatosensory-evoked potentials showed absent N₂₀ response on the right side. Serum neuron specific enolase is 55 ng/mL. The patient still requires substantial amount of vasopressors and inotropes for a failing heart. Neurologic examination two days after rewarming reveals no eye opening to pain, no motor response to pain, intact pupil responses to light, normal corneal reflexes, intact grimacing, and cough response to suctioning. The family wants to know what to expect, as does the cardiologist.

What do you do now?

Neurologists seem to be the arbiters of gloomy events in coronary care units, but that may change in the era of therapeutic hypothermia. The truth is that even when comatose patients are cooled immediately after cardiopulmonary resuscitation (CPR), the chance of survival is still about 50/50, and many patients die within a week from withdrawal of support. Hypothermia is now considered standard of care for patients with out-of-hospital arrest from ventricular fibrillation, and a protocol is shown in Table 13.1. Hypothermia protocols—as expected—vary considerably across centers, and this also applies to utilization. Selection of patients also varies with an increasing number of centers, including patients with asystole and in-hospital arrest. Yet, there is no evidence that therapeutic hypothermia is effective under these circumstances. More and more hospitals are set up to provide therapeutic hypothermia, but neurologists currently may see just about equal numbers of patients with or without hypothermia treatment.

Poor predictors of outcome at the time of resuscitation have been identified and the cardiac rhythm causing circulatory arrest is a major determinant of outcome. Outcome of patients with a “nonshockable” rhythm (asystole, pulseless electrical activity) is poor, but rapid defibrillation in other rhythms (ventricular fibrillation, ventricular tachycardia) may be successful, resulting in rapid awakening of the patient and even the probability of intact neurologic function.

TABLE 13.1. Hypothermia Protocol in Comatose Survivors after Cardiopulmonary Resuscitation

1.5 liter of refrigerated (4–6ûC) saline in 30–60 minutes

Operate cooling device to 33ûC

Monitor bladder temperature

Sedate patient before paralysis

Sedate with Midazolam 0.3 mg/kg/hr IV and Fentanyl 0.1 mcg/kg/hr IV

Paralyze (to prevent shivering) with Atracurium 0.2 mg/kg

Normalize serum magnesium and potassium values

Normalize serum glucose values

Monitor electrolytes, WBC, and platelets

Monitor EEG/video during rewarming and for 24 hours (if available)

The clinical picture of postcardiac resuscitation syndrome is concerning. Patients may have a major myocardial dysfunction (which may be reversible), a systemic ischemic-reperfusion syndrome with intravascular volume depletion, for a full-blown acute coronary syndrome requiring reperfusion strategies. More invasive treatments such as extracorporeal membrane oxygenation may be necessary in some cases. A profound kidney and liver injury may be present. The response to treatment of these complications plays an important role in planning the level of care.

The neurological examination is focused on motor response, presence of spontaneous eye movements, appearance of myoclonus or seizures and whether there has been brainstem injury resulting in changes in key brainstem reflexes. The immediate presence of localizing motor responses is the best evidence that the duration of ischemia to the brain has been brief. Long duration of circulatory arrest results in a more profound insult and may be apparent by the documentation of abnormal extensor or flexor response or no response to a noxious stimulus in the arms and legs. Motor response after CPR, however, has never been a very reliable predictor of outcome even before the wide application of induced hypothermia. Patients with withdrawal responses to pain may not wake up or may regain only minimal consciousness. Of even greater concern is myoclonic status epilepticus. Myoclonus involves the face, limbs, and axial muscles. These brief jerks are spontaneous and in the first hours after CPR may be unrelenting and forceful. It may make the patient move in the bed and cause considerable upset to family members.

Brainstem reflexes are typically normal because the brainstem is often spared from anoxic-ischemic injury. Absent brainstem reflexes may occur after prolonged periods of resuscitation or in resuscitation of trauma patients with substantial blood loss. Fixed and dilated pupils are more frequently associated with asystole than with ventricular fibrillation and that may simply be a reflection of more prolonged anoxic- ischemic brain injury. Fixed and dilated pupils throughout the resuscitation procedure usually indicate a poor chance of success. Successful cardiac resuscitation with good neurologic recovery more often occurs in patients with persistently contracted and reactive pupils from the onset.

TABLE 13.2 Poor Outcome Anticipated

0–24 hours	Myoclonus status epilepticus
24–72 hours	SSEP: absent cortical (N₂₀) responses
24–72 hours	Serum NSE > 33 ug/L*
> 72 hours	Absent pupil or corneal reflexesExtensor motor responsesAbsent motor responses*