CEREBRAL METABOLISM AND ISCHEMIA
The cerebral metabolic rate of O2 (CMRO2) is 3–3.8 mL/100 mg/min. Cerebral metabolism has two basic components: neuronal activity and cellular integrity. The brain depends on aerobic glucose metabolism; hence, large O2 demand consumes 20% of total body O2 to maintain neuronal activity for adenosine triphosphate (ATP) generation.
Cerebral ischemia occurs when metabolic demand exceeds tissue O2 supply. Ischemia can be either global or focal. Cerebral protection limits brain tissue injury. Maximizing O2 delivery and decreasing cerebral metabolism achieve protective goals. Clinical strategies for cerebral protection include physiologic and medical interventions.
Temperature control—Hypothermia decreases both the brain’s neuronal activity and cellular integrity. Profound hypothermia or deep hypothermic circulatory arrest (DHCA) at 15°C–18°C decreases cerebral metabolic and electrical requirements, with proven benefits for cardiac arrest lasting 30 minutes to 1 hour with adverse neurologic effects. Mild hypothermia at 33°C–35°C is also neuroprotective by decreasing the CMRO2 and attenuating inflammatory responses to an ischemic insult. Potential complications from induced hypothermia include coagulopathy and cardiac dysrhythmias.
Glycemic control—Hyperglycemia adversely affects neurologic outcomes during cerebral ischemia in the ICU setting, especially for prolonged hospitalizations.
Hemodilution—Whereas optimizing hemoglobin level maximizes O2-carrying capacity, hemodilution to decrease blood viscosity, thereby increasing O2 delivery, may provide cerebral protection.
Blood pressure control—Cerebral profusion pressure (CPP) = mean arterial pressure (MAP) − intracranial pressure (ICP). Maintaining MAP also maintains CPP. Critical CPP to avoid ischemic brain injury is greater than 50 mm Hg.
Avoidance of hypoxia and hypercapnia.
Anesthetic agents—Volatile and intravenous anesthetics can be used for cerebral protection by influencing brain neuronal activity and inducing an isoelectric EEG. Anesthetic agents are not protective against global insults. Barbiturates protect against focal ischemia by decreasing CMRO2. Propofol, etomidate, and inhalational agents (ie, isoflurane) similarly may protect against focal ischemia.
Steroids—Dexamethasone reduces brain tissue edema surrounding tumors. Otherwise, steroids are not neuroprotective following ischemic insult.
Ca2+ channel blockers—No impact on neurologic outcome after cerebral ischemia, but nimodipine decreases cerebral vasospasm after injury.
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Taghreed Alshaeri, MD and Marianne D. David, MD contributed to this chapter in the first edition and some material from that chapter has been retained here.