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812 PART 6: Neurologic Disorders

(at least every other day) of endotracheal secretions, urine, and blood. can be safely performed to a P CO 2 of 30 mm Hg, and perhaps to less than
The long half-life of pentobarbital (approximately 24 hours) leads to 25 mm Hg in selected patients without consequent cerebral ischemia.
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slow recovery, even when abruptly stopped. Shivering is common during Furthermore, it has been shown that hyperoxia can transiently improve
the recovery period from barbiturate anesthesia and may require treat- oxygen delivery to the brain during hyperventilation. 148
ment with opiates or short-acting sedatives (eg, propofol). In addition, The potential benefits of hyperventilation must be balanced against
chaotic EEG patterns are common and are often misinterpreted as status the potential deleterious consequences, including but not limited
epilepticus. to diminished cardiac filling pressures with resultant hypotension,
In place of barbiturates, propofol and other sedatives have been decreased myocardial oxygen supply with an increase in myocardial
used to induce sedation and coma and have been shown to be safe and demand, elevation in mean airway pressure leading to accentuation of
effective (see Table 86-14). In addition to neural suppression caused intracranial hypertension, electrolyte disturbances (eg, alkalosis, hypo-
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by activation of the γ-aminobutyric acid A receptor and inhibition kalemia, and hyperchloremia), and cardiac arrhythmias. 149
of N-methyl-d-aspartate receptor, propofol may have a direct neuro- Once other ICP-lowering strategies control ICP and CPP adequately,
protective effect. For example, a combination of 5 to 50 µg/kg/min hyperventilation should be lifted. Gradual withdrawal of hyperventila-
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propofol with fentanyl (100 µg/h) allows serial neurological examina- tion is necessary to avoid rebound elevations in ICP as the P CO 2 is nor-
tions due to their short half-lives. Potential adverse reactions from malized. We recommend increasing P CO 2 by <2 to 3 mm Hg per hour in
propofol and other interventions in managing elevated ICP are listed patients with brittle ICP elevations. Inadvertent fluctuations in the P CO 2
in Table 86-15. levels due to variable ventilation is a common problem during patient
transport. We recommend using transport ventilators for patients with
Mechanical Ventilation and Hyperventilation: Hyperventilation induces intracranial hypertension to minimize variation in P CO 2 .
rapid and effective ICP reduction through vasoconstriction induced Prophylactic hyperventilation should be avoided. A prospective,
by hypocapnia-associated CSF alkalosis, which eventually decreases randomized clinical study found that comatose patients who received
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cerebral blood flow. 144,145 The duration of ICP reduction in response prophylactic hyperventilation had significantly worse outcomes than
to hypocapnia is variable, but in general the ICP returns to baseline patients with normocapnia. 150
within minutes to hours after commencing hyperventilation due to nor- Tris (hydroxymethyl) aminomethane (THAM) is a buffer used to
malization of CSF alkalosis through compensatory adjustments in the correct acidotic states, and is used at times to assist in the manage-
bicarbonate buffering systems in the brain and vascular smooth muscle. ment of patients with intracranial hypertension. The advantage of
Due to its transient efficacy and risk for resultant ischemia, hyperventi- THAM is that it alkalinizes without changing plasma sodium or P CO 2 .
lation should only be utilized as a short-term emergency measure until THAM may have a role in limiting rebound ICP elevation during the
more definitive methods of lowering ICP are implemented. withdrawal of hyperventilation, or prolonging the benefit of hyperven-
When hyperventilation is required for urgent management, it can be tilation in some patients. It is administered intravenously at a dose
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accomplished with an ambu mask or mechanical ventilation. Providing of 1 mL/kg per hour. Some of the complications associated with its use
a 7 to 10 mL/kg tidal volume at a rate of 14 to 20 breaths per minute include local skin irritation and necrosis, hypoglycemia, and respira-
usually achieves substantial reduction in the partial pressure of carbon tory depression.
is variable depending on baseline blood
dioxide (P CO 2 ). The ideal P CO 2
pH, the clinical situation and the individual patient’s response. Excessive Corticosteroid Therapy: Corticosteroids are mainly indicated for vaso-
hyperventilation can cause cerebral ischemia through prolonged cerebral genic edema from brain tumors, for example, in patients who underwent
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vasoconstriction, a phenomenon suggested by several studies in traumatic tumor irradiation or surgical manipulation. Steroids decrease tight-
brain-injured patients. However, in patients with severe traumatic brain junction permeability stabilizing the blood-brain barrier. 153,154 Since
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injury, positron emission tomography demonstrated that hyperventilation AQP4 plays a key role in the pathogenesis of CNS edema, it is logical

TABLE 86-14 Drug Effects of Anesthetic Agents and Sedatives on Cerebral Physiology
Agent Cerebral Metabolic Rate Cerebral Blood Flow CSF Production CSF Absorption Cerebral Blood Volume Increased Intracranial Pressure
Barbiturates −4 −3 + +1 −2 −3
Benzodiazepines −2 ? + +1 −1 −1
Desflurane −3 +1 +1 −1 ? +2
Dexmedetomidine −1 −2 ? ? ? −1
Enflurane −2 +2 +1 −1 +2 +2
Etomidate −3 −2 + +1 −2 −2
Fentanyl −1 +1 + ? −1 +1
Halothane −2 +3 −1 −1 +2 +2
Isoflurane −3 +1 ± +1 +2 +1
Ketamine ± +2 ± −1 +2 +2
Lidocaine −2 −2 ? ? −2 −2
Nitrous oxide −1 +1 ± + + +1
Opioids ± + ± +1 ± ±
Propofol −3 −4 ? ? −2 −2
Sevoflurane −3 +1 ? ? ? +2
(+, +1, +2, +3), increase; (−, −1,−2,−3,−4), decrease; ±, little or no change; ?, unknown; CSF, cerebrospinal fluid; CO , carbon dioxide; ICP, intracranial pressure.
2
The effect of commonly used anesthetics and sedatives on ICP.

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