Respiratory

PaCO₂ is the single most potent physiologic determinant of CBF (Figure 132-3) and CBV. At a PaCO₂ between 20 and 80 mm Hg, CBF decreases 1 mL/100 g brain weight/min and CBV decreases 0.05 mL/100 g brain weight for each 1-mm Hg decrease in PaCO₂. Decreasing PaCO₂ to 25 to 28 mm Hg should provide near-maximal reductions in ICP, lasting up to 24 h, without adversely affecting acid-base or electrolyte status or decreasing cerebral O₂ delivery (i.e., resulting from combined cerebral vasoconstriction and leftward shift in the oxyhemoglobin dissociation curve). Accordingly, in the setting of severe traumatic brain injury, the Brain Trauma Foundation states that aggressive hyperventilation (i.e., PaCO₂ ≤ 25 mm Hg) is not recommended, as further reductions in PaCO₂ may result in iatrogenic brain injury.

Hypoxia (PaO₂ <50 mm Hg) will increase CBF and ICP. Application of positive end-expiratory pressure may decrease venous effluent from the cranium and exacerbate intracranial hypertension.

Coughing against a closed glottis (i.e., Valsalva maneuver) will increase ICP. Intravenously administered lidocaine, esmolol, or opioids can be used to attenuate the ICP response to direct laryngoscopy, tracheal intubation, or coughing.

Cardiovascular

Mean arterial pressure (MAP) is a determinant of cerebral perfusion pressure (CPP) (i.e., CPP = MAP – ICP). The blood-brain barrier and autoregulation may be disrupted at the site of cerebral ischemic, traumatic, hemorrhagic, or osmolar insults. In these regions, it is correct to assume that CBF is passively dependent on CPP. Before the dura is opened, it is prudent to treat all hypertensive episodes by deepening the level of anesthesia, administering antihypertensive drugs that lack the ability to dilate cerebral vessels—and thus elevate ICP—(e.g., esmolol, labetalol, metoprolol), or both deepen the level of anesthesia and administer antihypertensive drugs. With respect to CPP, the critical threshold for ischemia is approximately 50 to 60 mm Hg. However, routine use of vasopressors and intravenously administered fluids to maintain the CPP greater than 70 mm Hg is not advised. Taking this information together, one can infer that maintaining the CPP near 60 to 70 mm Hg is advisable in the setting of traumatic brain injury.

Intravenous fluid administration should not be spared at the expense of hemodynamic stability. Osmolar, not oncotic, pressure is the primary determinant of fluid shifts within the brain. Therefore, maintaining intravascular isovolemia with a near-isoosmolar solution (e.g., normal saline, lactated Ringer’s solution) is safe and beneficial to end-organ preservation. Hypoosmolar glucose-containing fluids (e.g., D₅W) have the ability to (1) increase cerebral edema, (2) increase ICP, and (3) induce hyperglycemia, which exacerbates ischemic neurologic injury.

Renal

Both osmotic (e.g., mannitol 0.25-1.0 g/kg) and loop diuretics are effective in reducing the parenchymal fluid compartment and decrease CSF formation. Mannitol administration in patients with intracranial hypertension is not associated with a transient increase in ICP.

Metabolic

Cerebral metabolism decreases approximately 6% to 7% per 1 of temperature reduction. Mild hypothermia (i.e., temperature reductions of 1°C – 6°C) has been reported to improve neurologic outcome following focal or global brain ischemia in laboratory studies. Conversely, fever may worsen postischemic neurologic outcome. Proposed mechanisms for temperature modulation of postischemic neurologic outcome include alterations in cerebral metabolism, blood-brain barrier stability, membrane depolarization, ion homeostasis (e.g., calcium), neurotransmitter release (e.g., glutamate or aspartate), enzyme function (e.g., phospholipase, xanthine oxidase, or nitric oxide synthase), and free radical production or scavenging. Despite convincing laboratory data, large clinical trials have produced mixed results.

Musculoskeletal

The use of a nondepolarizing neuromuscular blocking agent without histamine-releasing properties (e.g., rocuronium, vecuronium, cisatracurium) is ideal for facilitating tracheal intubation and maintaining muscle paralysis. In the pathologic brain, pancuronium and gallamine can induce systemic and intracranial hypertension. Succinylcholine may increase ICP, possibly by increasing muscle afferent activity, but the clinical relevance is debatable.

Specific anesthetic agents

In general, all inhalation anesthetic agents are vasodilators that, with normocapnia, will increase CBF, CBV, and ICP. The vasodilator potency of isoflurane, sevoflurane, and desflurane is similar. Cerebral vasodilation is overcome by hyperventilating patients.

All intravenously administered anesthetic agents except ketamine cause some degree of reduction in cerebral metabolism, CBF, and ICP (provided ventilation is not depressed). Todd and colleagues were unable to demonstrate a significantly different outcome (incidence of new neurologic deficits, total hospital stay, or hospital cost) in neurosurgical patients anesthetized with a combination of propofol and fentanyl, isoflurane and N₂O, or fentanyl and N₂O.

Postoperative

Rapid and smooth emergence enables the neurosurgeon to evaluate the patient’s neurologic status before discharge from the operative suite.