A 34-year-old man is treated in the intensive care unit after being involved in a motorcycle accident. He has multiple injuries, including severe traumatic brain injury. Head CT scan shows areas of contusion and swelling without subdural or epidural hematoma. On the second day of hospitalization, a ventriculostomy is placed for invasive intracranial pressure monitoring. On the third day, his pressure is high despite adequate sedation, elevation of the head of the bed, and removal of cerebrospinal fluid. Hyperventilation would decrease this patient's intracranial pressure by which of the following mechanisms?

Question

A 34-year-old man is treated in the intensive care unit after being involved in a motorcycle accident.  He has multiple injuries, including severe traumatic brain injury.  Head CT scan shows areas of contusion and swelling without subdural or epidural hematoma.  On the second day of hospitalization, a ventriculostomy is placed for invasive intracranial pressure monitoring.  On the third day, his pressure is high despite adequate sedation, elevation of the head of the bed, and removal of cerebrospinal fluid.  Hyperventilation would decrease this patient's intracranial pressure by which of the following mechanisms?

Quizplus · Accepted Answer

11ec25c8_d5d3_3b9d_bc81_b1d3b2c7253a_MD0003_00 Because the brain is an encased organ, relatively small changes in pressure can alter the intracranial pressure in important ways. The pressures in 3 distinct compartments of the brain - the brain parenchyma, the cerebrospinal fluid (CSF), and cerebral blood flow (CBF) - determine the overall intracranial pressure (ICP). Both brain parenchyma and CSF have relatively constant pressures except in certain circumstances, including space-occupying lesions and obstructions to CSF flow. CBF is influenced by systemic blood pressure and is held constant over a fairly wide range of pressures by cerebrovascular autoregulation. However, the partial pressures of O₂ and CO₂ also play an important role in regulating CBF. In conditions such as stroke or trauma, these systems are disrupted and interventions may be required to lower ICP. CBF is an important target for therapy, and paCO₂ is a potent regulator of CBF (much greater than paO₂). As levels of cerebral paCO₂ rise, so does blood flow. Lowering cerebral arterial paCO₂ through hyperventilation results in rapid vasoconstriction and a consequent decrease in ICP. Other interventions to lower ICP do so by lowering systemic pressures and reducing metabolic demand (sedation), or increasing venous outflow (head elevation), reducing brain parenchyma water content/volume (mannitol), or reducing the volume of CSF (therapeutic lumbar punctures). (Choice B) The CBF system is tightly regulated and mediated by cerebral vasodilation rather than capillary leak. (Choice C) Hyperventilation does not significantly affect the sympathetic output of the brain, which is mediated predominantly by pressures in the compartments (eg, brain, CSF, blood). (Choice D) Ventilatory rate has a much greater effect on arterial pCO₂ than on pO₂, which can be modified by changing the concentration of inhaled oxygen or the end-expiratory pressure in a mechanically ventilated patient. (Choice E) Increased venous outflow from the head is achieved by elevation of the head rather than hyperventilation. Educational objective: Short-term hyperventilation helps lower increased intracranial pressure by causing cerebral washout of CO₂, leading to vasoconstriction and decreased cerebral blood flow. References: Every breath you take: hyperventilation and intracranial pressure. (http://www.ncbi.nlm.nih.gov/pubmed/14964473)

A 34-Year-Old Man Is Treated in the Intensive Care Unit