Special cerebral resuscitation measures

Numerous drug treatments have been investigated in studies with short-term mechanism-oriented animal models, including outcome models of incomplete forebrain ischemia in rats, global brain ischemia in monkeys, and (clinically most relevant) cardiac arrest in dogs without a breakthrough effect. Intravenous barbiturate loading can lower increased intracranial pressure after traumatic brain injury and mitigate focal brain ischemia, but is risky after cardiac arrest. Calcium entry blockers (lidoflazine, nimodipine), given early after cardiac arrest or global brain ischemic anoxia and reperfusion, reduce brain damage in dogs and monkeys, and in subgroups of patients in randomized clinical trials. However, their use is controversial since they give no breakthrough effect and can produce postarrest hypotension or rearrest. Targeted agents for the prevention of calcium accumulation in neurons might become available in the future. After a normothermic cardiac arrest of duration 10 to 12 min in dogs, only measures promoting cerebral blood flow and mild hypothermia have reproducibly and significantly improved cerebral outcome.

In over 50 per cent of cases of sudden death outside hospital, standard external cardiopulmonary resuscitation with advanced life support has failed to achieve restoration of spontaneous circulation. In such cases, restoration of spontaneous circulation and promotion of cerebral blood flow, during and after reperfusion from prolonged cardiac arrest, might be achieved with open-chest cardiopulmonary resuscitation or (portable) emergency (closed-chest) cardiopulmonary bypass and a combination of early postcardiac arrest induced hypertension, mild hemodilution, and PaCO2 control. Cerebral blood flow promotion can be achieved by creating the above-mentioned initial hypertensive bout followed by controlled mild hypertension for a few hours, mild hemodilution with colloid plasma substitute to a hematocrit of about 30 per cent, and PaCO2 control. After admission to the intensive care unit (ICU), these measures to promote cerebral blood flow could be titrated against mixed cerebral venous PO2 (superior jugular bulb) to achieve values of at least 30 mmHg. This variable would reflect normal average global cerebral oxygen delivery.

Since its introduction in the 1950s, therapeutic hypothermia has been used for cerebral protection/preservation in cardiac and neurological surgery, but not for resuscitation after normothermic cardiac arrest. The beneficial mechanism of hypothermia during and/or after ischemic or traumatic vital organ insults is multifactorial. The lower the temperature, the better is cerebral protection/preservation, but mild hypothermia (34-36 °C) seems to be more effective for post-cardiac arrest resuscitation than moderate (28-32 °C) or deep (15-25 °C) hypothermia. For hypothermia to be therapeutic, shivering must be prevented. Deep hypothermia causes cardiac arrest and requires cardiopulmonary bypass. Moderate hypothermia is compatible with spontaneous circulation but can cause management problems and arrhythmias, particularly when induced in unstable patients after cardiac arrest. Therefore resuscitative hypothermia was dormant for 30 years. In the late 1980s, the results obtained by us in dogs and by others in rats documented that even mild hypothermia had beneficial effects during or after ischemia. A series of cardiac arrest outcome studies in dogs demonstrated the protective and resuscitative effects of mild hypothermia, which is safe ( SafaE.. .1.9.9.6.).

Mild hypothermia should be induced as soon as possible during and after reperfusion, ideally starting during attempts to restore spontaneous circulation in the field, and be sustained for at least 12 h. Implementation of hypothermia requires monitoring of brain temperature as the tympanic membrane or nasopharyngeal temperature, and core temperature as the esophageal, central venous, pulmonary artery, or urinary bladder temperature. Mild hypothermia can be induced in many different ways. Methods available range from the slowest (head-neck-trunk surface cooling which could be started at the scene with cold packs) through intermediate (e.g. additional nasopharyngeal cold irrigation and gastric and intravenous cold loads) to rapid invasive brain cooling. The last of these requires a trained physician and includes intraperitoneal instillation of cold Ringer's solution, blood cooling with cardiopulmonary bypass or other measures, or intracarotid injection of cold Ringer's solution. Although achieving a tympanic membrane temperature of about 35 °C within 15 min of restoration of spontaneous circulation seems desirable, recent data from studies of rats and gerbils suggest that even mild cooling delayed several hours after reperfusion can be beneficial if sustained for 12 or 24 h.

Complete recovery after cardiac arrest (no-flow) of duration about 10 min is clinically important because the average 8-min response time of mobile ICU ambulance services cannot be reduced further. The most promising protocol so far for cerebral resuscitation has been demonstrated using a reproducible cardiac arrest outcome model in dogs (Safaretal 1996); after 11 min of normothermic cardiac arrest, a combination of cerebral blood flow promotion and mild hypothermia (from 15 min to 12

h of reperfusion) achieved complete functional and near-complete histological cerebral recovery. Benefit from either treatment alone has been reported in several animal studies. A clinically feasible protocol based on this latest dog study is ready for clinical feasibility and side-effect trials inside and outside hospitals. Mild to moderate resuscitation hypothermia has also improved outcome after focal brain ischemia or severe hemorrhagic shock in rats and after brain trauma in rats, dogs, and humans.

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