Hyperventilation in Severe Traumatic Brain Injury

ALS AXE

ALS AXE

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Have any of you ever though about hyperventilation during a transport of a critical trauma PT w/ a known traumatic brain injury? Have you seen it decrease ICP s/s? My longest transport time is not longer than 10 minutes max here in Sacramento, so I have never had the time to think about hyperventilation.

Thanks kyle.
 
This used to be done years ago on the hypothesis hyperventilation would decrease PaCO2, increase cerebral vasoconstriction, lower cerebral blood flow, and thus lower ICP. All it ended up doing was making severe TBI even more severe.

We can do nothing about the primary brain injury which has occurred, but what we can have a huge impact on in the prevention of secondary brain injury; so essentially ensuring good blood pressure, normoxaemia, and if the pt is intubated, normal ETCO2.
 
It does work to a point, and is indicated for short-term management when signs of herniation are present.
 
ALS AXEMAN said:
Have any of you ever though about hyperventilation during a transport of a critical trauma PT w/ a known traumatic brain injury? Have you seen it decrease ICP s/s? My longest transport time is not longer than 10 minutes max here in Sacramento, so I have never had the time to think about hyperventilation.

Thanks kyle.
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This is a very select group of patients and takes a fair amount of insight into TBI's to fully comprehend when and why you would hyperventilate a TBI/ bleed.

I will let the more knowledgeable folk on the forum chime in with their two cents. I await their replies, and input.
 
VentMonkey said:
This is a very select group of patients and takes a fair amount of insight into TBI's to fully comprehend when and why you would hyperventilate a TBI/ bleed.

I will let the more knowledgeable folk on the forum chime in with their two cents. I await their replies, and input.
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Also, research is your friend as well. Don't be afraid to seek out answers on your own via goggle, journals, abstracts, podcasts, etc.
 
ALS AXEMAN said:
Have any of you ever though about hyperventilation during a transport of a critical trauma PT w/ a known traumatic brain injury? Have you seen it decrease ICP s/s? My longest transport time is not longer than 10 minutes max here in Sacramento, so I have never had the time to think about hyperventilation.

Thanks kyle.
Click to expand...
I'm also in Sacramento. Your longest transport could be > 10 minutes if the hospitals have to go on round-robin divert.... but I digress. As others have said, hyperventilation of the TBI patient used to be the standard but all that really did was make the injury worse. It leads to cerebral artery vasoconstriction which causes further hypoxia of the brain. Yes it does limit the rise in ICP but you're sacrificing brain to do it. If you have ETCO2 (and your monitors should) you ventilate to keep SPO2 > 94% and ETCO2 in a normal range of 35-45. Once you've met those goals, don't be surprised if you're ventilating much SLOWER than you think you should.

In the Sacramento Region, I doubt you'll ever really need to hyperventilate unless there's clear signs of herniation present and even then at that point you're looking at a tissue donor...

Oh, and if you head out to some of the more rural-ish stations, like Metro Fire Station 59, your transports could easily be >20 minutes routinely.
 
In class I never really understood the reason behind it. Increased ICP=less perfusion. Vasoconstriction=less perfusion.....soooooo, how exactly would it be any better? I haven't yet looked to see if there are any studies that compare the outcomes of the two, but always seemed like a damned if you do, damned if you don't situation. The one major head trauma pt I had I doubt would have had any significant change from an adjustment in ventilation rate.
 
StCEMT said:
In class I never really understood the reason behind it. Increased ICP=less perfusion. Vasoconstriction=less perfusion.....soooooo, how exactly would it be any better? I haven't yet looked to see if there are any studies that compare the outcomes of the two, but always seemed like a damned if you do, damned if you don't situation. The one major head trauma pt I had I doubt would have had any significant change from an adjustment in ventilation rate.
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Look up "permissive hypocapnia". This is what is encouraged at our service for closed head injury/ ICH pts requiring vent management at our service.

Hope yhis helps...
 
VentMonkey said:
Look up "permissive hypocapnia". This is what is encouraged at our service for closed head injury/ ICH pts requiring vent management at our service.

Hope yhis helps...
Click to expand...
I understand the theory of how it is supposed to work by intentionally shooting for a low EtCO2. Up until it gets to the part of its desired effect of decreasing ICP to try to reduce damage to the brain. To decrease the ICP by vasoconstriction, you are reducing perfusion...which also happens when ICP rises and pressure restricts blood flow...So we are essentially causing the same problem through a different method, which solves what?
 
StCEMT said:
I understand the theory of how it is supposed to work by intentionally shooting for a low EtCO2. Up until it gets to the part of its desired effect of decreasing ICP to try to reduce damage to the brain. To decrease the ICP by vasoconstriction, you are reducing perfusion...which also happens when ICP rises and pressure restricts blood flow...So we are essentially causing the same problem through a different method, which solves what?
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You're forgetting what the body does to overcome the blood flow restriction. BP skyrockets, HR drops in an attempt to maintain a CPP while trying to limit the increase in ICP. However, when you see that, herniation of the brain through the Foramen Magnum isn't that far off.
 
Thank you, Akulahawk.

You articulate your point much better than I.
What he said is the body's protective mechanism which can lead to hypoxia.

This is why hypoxia and hypotension are catastrophic to this patient population.
 
VentMonkey said:
Thank you, Akulahawk.

You articulate your point much better than I.
What he said is the body's protective mechanism which can lead to hypoxia.

This is why hypoxia and hypotension are catastrophic to this patient population.
Click to expand...
This body's protective mechanism is in place to prevent hypoxia of the brain tissue. If we routinely hyperventilate, we end up constricting cerebral arteries, which does lead to lower ICP and tissue level hypoxia. If the body is allowed to become hypoxic that's a double whammy against brain tissue survival. If the body becomes hypotensive, that's a triple whammy against brain tissue survival if you're already doing hyperventilation.

In a sense, you want to allow the body's protective mechanism to do its job so you simply keep a "decent" SpO2 and normal CO2 level and boogie safely to a facility that can handle complex neurosurgical cases. The brain is going to lose tissue. You just don't want to be the cause of any "extra" tissue damage that could have been avoided. Once you get to such a facility, hopefully the neurosurgeons will be able to further limit the damage before herniation begins.
 
I knew a nurse could explain better than me.
My wife always does, too...:(
 
StCEMT said:
I understand the theory of how it is supposed to work by intentionally shooting for a low EtCO2. Up until it gets to the part of its desired effect of decreasing ICP to try to reduce damage to the brain. To decrease the ICP by vasoconstriction, you are reducing perfusion...which also happens when ICP rises and pressure restricts blood flow...So we are essentially causing the same problem through a different method, which solves what?
Click to expand...

It is a fine line that is difficult to walk without any objective way to measure cerebral perfusion. This is probably why it's never been shown to work when done prehospital.
 
Hmm true. Guess I also forget we cap how far we go with hyperventilation, while the body will continue to compensate by increasing pressures.
 
The other obstacle for prehospital use of hyperventilation is V/Q mismatch. The ETCO2 will always have a gradient due to circuit and sampling tube dead space. This gradient is worsened by any anatomical mismatch as well. And patients with severe brain injury and intracranial hypertension have plenty of reasons to have VQ mismatch. So, the actual ETCO2 value on the monitor is frequently quite different than the measured PaCO2. Leaves you flying blind when trying to titrate in the field.

That is why in-hospital, arterial PaCO2 is measured instead of using EtCO2 to titrate hyperventilation.
 
Maintain proper MAP and Spo2...always...These 2 simple things will do wonders in improving the outcome of TBI. If you work a TBI keep your eyes locked on these 2 numbers as much as you can...use them to help drive your treatment...focus on these.

In addition to the initial trauma, edema and herniation...there is a neurotoxic cascade happening during TBI...Cell rupture released TNFa and other nasties which trigger domino effect cell death. The injured brain truly is a complex neurochemical nightmare...
 
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