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I'm just trying to understand the different bases of treatment. In my studies I've learned that you hyperoxygenate in s/s of cerebral herniation syndrome, and you hyperventilate in s/s of cushings triad. And now I have a textbook saying hyperventilation is a thing in the past but ITLS says the exact opposite. What I'm looking for is the difference between hyperventilate and hyperoxygenate, and when to use either one. Can someone please clear my confusion?

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Hyperoxygenate is administering significantly greater amounts of Oxygen and increasing the blood Oxygen levels higher than normal. Hyperventilate is to move air in and out of the lungs at a greater than normal rate. For example, you can hyperventilate your self on room air but not hyperoxygenate. You can also hyperoxygenate a patient but not hyperventilate.

*Ventilation is the movement of gas in and out of the lungs. (Minute ventilation is the product of respiratory rate and tidal volume and generally measured by looking at the PaCO2)

*Oxygenation is the amount of Oxygen in the blood. (Measured by the content of arterial Oxygen equation but generally the PaO2 is a reasonable reflection of Oxygenation)

Many people, including health care providers, confuse these two concepts.

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Posted

I'm just trying to understand the different bases of treatment. In my studies I've learned that you hyperoxygenate in s/s of cerebral herniation syndrome, and you hyperventilate in s/s of cushings triad. And now I have a textbook saying hyperventilation is a thing in the past but ITLS says the exact opposite. What I'm looking for is the difference between hyperventilate and hyperoxygenate, and when to use either one. Can someone please clear my confusion?

* Your textbook is probably referring to routine hyperventilation in all patients with signs and symptoms of a closed head injury. This has not been the standard of care for about 20 years.

* Cushing's triad is a set of signs of a closed head injury, not a clinical entity in itself.

* Hyperventilation is still recommended in suspected herniation, the signs of which include Cushing's traid, aniscoria, and posturing.

The physiologic basis behind hyperventilation as a treatment is that it causes vasoconstriction of cerebral vesses, which decreases cerebral blood flow. This will decrease the rate of extravasation of fluid through an injured vessel. This was thought to have minimal consequences and was used routinely.

The down-side to hyperventilation is that in the absence of herniation, it's better to allow the cerebral circulation to do what it does best. Artificially restricting cerebral blood flow in patients without herniation has been demonstrated to worsen outcomes. Instead the focus should be on maintaining an appropriate MAP, minimising stimulation and unnecessary instrumentation, preventing hypoglycemia, maintaining normoxia and eucapnia, and preventing recurrent seizure activity.

[Also worth noting, that the effect of hyperventilation is quite transient.]

* In addition, careful hyperventilation to a PETCO2 of 30 mmHg should be distinguished from autoPEEPing the patient to a BP of 0/0, and it should be recognised that PETCO2 has some limitations as an estimate of PaCO2.

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