You are bagging too fast! You are bagging too slow! You aren’t bagging enough! Oh, that’s too much!
Weird. All of this sounds rather familiar. We all have heard it, but how often do we apply the appropriate ventilations for the head-injured patient?
ICP within the skull
I remember hearing on many accounts that hyperventilation is great for head injuries. I also heard the contrary. This back and forth was extremely confusing to me. Both sides of the argument hold some merit.
To start, the criticality of a closed head injury is proportionate to the level of intracranial pressure (ICP) that’s being applied by the body’s own physiology.
The cranium (skull) is an enclosed container that’s incapable of expanding, because the sutures of the skull solidify in early adolescence. Because the skull is incapable of expanding, any bleeding that’s inside of it has nowhere to go, and the ICP increases. The more pressure the less blood that’s supplied to the cerebral arterioles, because the vessels are being compressed shut.
The body’s response to this increased ICP is to increase blood pressure and pulse: The body perfuses the brain better, but it also pushes more and more blood into the intracranial space at an even higher pressure—thus, the problem worsens because of the body’s natural response.
Walking a tightrope
Moving toward the end of life from the injury itself, we meet up with herniation. Now, Hernie isn’t a good buddy. He shows up when the pressure that’s inside of the noggin’ is getting to the point when it’s starting to squeeze the brain/brainstem out of the foramen magnum (hole of the skull where the spinal cord exits).
The herniation will be noticeable when you start to see the three following signs: bradycardia (slowed heart rate < 50 bpm), hypertension (high blood pressure > 180 mm Hg systolic) and erratic respiratory rhythm (Cheyne-Stokes respirations). Known as the Cushing’s Triad, these three signs indicate that a cerebral herniation is at/nearing irreversible damage unless immediate surgical treatment (by a surgical team) is provided.
When does hyperventilation come into play? When a patient is hyperventilated, the individual becomes hypocarbic (low carbon dioxide). This response causes vasoconstriction, which can be good but also bad.
Starting hyperventilatory treatment when Cushing’s signs appear starts to occlude the cerebral arteries, which decreases the amount of blood in the brain, the swelling and the herniation. It all sounds really good, and it is.
However, what if you start hyperventilating too soon? If you start to cause vasoconstriction prior to herniation, you could cause further tissue necrosis (tissue death) by occluding cerebral arteries that aren’t involved.
Furthermore, hyperventilation and hypocarbia are global reactions throughout the entire body, not isolated to the brain. If you force hyperventilation, you also could see narrowing of the coronary arteries, which causes myocardial infarctions (heart attack), among other examples of hyperventilation-induced vascular stenosis.
The other issue that you face is that of mechanical ventilation. When you “force” air into a patient’s lungs, whether it be with a bag-valve mask or a ventilator, you have a high probability of injuring the lung tissue, which would cause ventilation-induced microaspirations, pneumonia or lung contusions.
Timing is everything
When it comes to treating head injuries with hyperventilation, you must be mindful as to when to start to use it. Too soon can be detrimental to not only neurologic function but other systems in the body as well.
If you start hyperventilating patients when signs of herniation start to show—I mean you, Hernie—start hyperventilating shooting, looking for positive changes in vitals. Maybe even throw in some elevated head positioning to keep all of that fluid out of the brain bucket.
