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Elevated ICP: Hyperventilation
Last updated: 03/04/2015
Intracranial pressure (ICP) is determined by the volume of brain parenchyma (80%), blood (12%), and CSF (8%) within a rigid cranial vault. Normal ICP ranges from 5-15mmHg. Because the cranial compartment is enclosed by a rigid skull, it has a limited ability to accommodate additional volume. When intracranial contents increase in volume (e.g., secondary to tumor, blood, swelling, hydrocephalus), initially, circulating blood and CSF are displaced to offset the extra volume and ICP remains unchanged. However, beyond a certain threshold, if intracranial contents continue to increase in volume, then ICP will quickly increase as there is diminished compliance in the fixed intracranial vault. This dynamic is critical in surgical patients with already decreased intracranial compliance from space occupying lesions, who may be extremely sensitive to ICP changes associated with anesthetic effects (e.g., cerebral vasodilation from inhalation anesthetics or vasodilation from periods of hypoventilation/hypercapnia).
Hyperventilation is one known method of rapidly lowering ICP. Cerebral blood flow is largely dependent on PaCO2. Hyperventilation causes decreased PaCO2 which subsequently leads to arterial vasoconstriction thus lowering cerebral blood flow (CBF), cerebral blood volume, and ICP. This effect is mediated my pH changes in the extracellular fluid which cause cerebral vasoconstriction or vasodilation depending on the pH. There is approximately a 2% decrease in CBF for every 1 mmHg decrease in PaCO2 levels. Although the effects of hyperventilation are almost immediate, these effects on CBF diminish over 6-24 hours as the brain adapts by changing bicarbonate levels in the extracellular fluid to normalize the pH. Additionally, if prolonged hyperventilation is suddenly discontinued and normocapnia is restored too quickly, there is a resultant rebound increase in CBF and thus ICP which can be deleterious.
Hyperventilation is commonly used to facilitate intracranial surgery because it is thought to quickly provide brain “relaxation” in the surgical field. One multicenter randomized trial found that hyperventilation to moderate hypocapnia (PaCO2= 25 ± 2mmHg) was effective at reducing ICP and decreasing the brain bulk in the surgical field during craniotomy (Gelb et al., 2008). On the other hand, hyperventilation can also have adverse effects. Hyperventilation to PaCO2 levels below 20mmHg has been shown to induce cerebral ischemia. Cerebral ischemia with extreme hyperventilation is likely mediated by severe vasoconstriction of cerebral vessels and alkalosis induced leftward shift of the oxyhemoglobin curve, thus decreasing oxygen delivery to brain tissue. For this reason, hyperventilation to moderate levels (PaCO2 = 25-35) is generally considered a short term temporizing measure to decrease ICP, or to reduce brain bulk during neurosurgery, and overly aggressive hyperventilation (PaCO2 <25mmHg) should be avoided.
References
- Adrian W Gelb, Rosemary A Craen, G S Umamaheswara Rao, K R Madhusudan Reddy, Joseph Megyesi, Bibek Mohanty, Hari H Dash, Kai C Choi, Mathew T V Chan Does hyperventilation improve operating condition during supratentorial craniotomy? A multicenter randomized crossover trial. Anesth. Analg.: 2008, 106(2);585-94 Link
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