Critical Care Medicine-Neurologic Disorders>>>>>Increased Intracranial Pressure
Question 3#

An 18-year-old male is brought in to the emergency department after a motor vehicle crash. He was on a motorcycle and was found 30 feet away from his vehicle in unconscious state without a helmet. He has noted trauma to his left forearm, active bleeding from the left posterior portion of his scalp. He was intubated in the field with EMS. On arrival he is tachycardic (heart rate 120s), blood pressure 110/62. He was recently paralyzed for intubation and does not have twitches present on train of four testing. A head CT is completed which demonstrates a large left-sided subdural hematoma with 6 mm midline shift. In the interval, as neurosurgery team is taking the patient to the OR, hyperventilation is started to decrease cerebral edema.

How does hyperventilation decrease intracranial pressure?

a. Change in CSF pH results in constriction of vascular smooth muscle
b. Change in intracranial blood pH results in constriction of vascular smooth muscle
c. Change in CSF pH results in electrical quiescence of neurons, decreased metabolic demand, and decreased cerebral blood flow
d. Change in pCO2 sensed by carotid body chemoreceptors results in vasoconstriction
e. A drop in pCO2 leads to a large osmotic gradient and worsening interstitial edema

Correct Answer is D


Correct Answer: D

The intracranial pressure is influenced by pCO2 . A rise in pCO2 will result in brain blood vessel dilatation and then increase in the cerebral blood volume. In contrast, when the pCO2 drops, the blood vessel diameter decreases and results in decreased cerebral blood volume. Although hypocarbic strategy promotes transient decrease in ICP and considered one of the effective intracranial hypertension temporizing measures, hyperventilation carries a serious risk of significant reduction in cerebral blood flow (CBF) and cerebral ischemia. In addition, studies showed prolonged hypocapnia can lead to rebound ICP. For this reason the Brain Trauma Foundation changed recently their 2017 guidelines about hyperventilation and stated that “prolonged prophylactic hyperventilation with partial pressure of carbon dioxide in arterial blood (PaCO2 ) of 25 mm Hg or less is not recommended” (Level IIB).

The change in cerebral blood flow is independent of the pH as there is no change with metabolic acidosis and alkalosis. There is rapid CO2 equilibration between the arterial blood and CSF, and the change in pH of the CSF acts directly in the vasculature resulting in relaxation or contraction. 


  1. Souter MJ, Lam AM. Neurocritical Care. In: Miller RD, Erickssno LI, Fleisher L, Wiener-Kroonish JP, et al. eds. Miller’s Anesthesia. 7th ed. Philadephia PA: Churchill Livingstone;2009:2899-2921.
  2. Sato M, Pawlik G, Heiss WD. Comparative studies of regional CNS blood flow autogregulation and responses to CO2 in the cat. Effexts of altering aterial blood pressure and PaCO2 on rCBF of cerebrum, cerebellum and spinal cord. Stroke. 1984;15:91-97.
  3. Schieve JF, Wilson WP. The changes in cerebral vascular resistance of man in experimental alkalosis and acidosis. J Clin Invest. 1953;32:33.
  4. Muizelaar JP, Marmarou A, Ward JD, et al. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randompized clinical trial. J Neurosurg. 1991;75:731-739.
  5. Kinoshita K. Traumatic brain injury: pathophysiology for neurocritical care. J Intensive Care. 2016;v4;29.
  6. Yoon SH, Zuccarello M, Rapoport RM. pCO2 and pH regulation of cerebral blood flow. Front Physiol. 2012;3:265.
  7. Carney N, Totten AM, O’Reilly C, et al. Guidelines for the management of severe traumatic brain injury, fourth edition. Neurosurgery. 2017;80:6-15.