SAH and Hyperventilation

[18G]

I had a SAH patient today that we transferred 40mins to a regional medical center. Patient was intubated and on the vent on arrival. I inquired about target EtCO2 prior to transferring and RRT stated CO2 from ABG was 32 with current vent settings (VT 500, RR 16, PEEP 2.5, PS 10, FiO2 50%). RRT also advised ED doc did not want hyperventilation. We didn't have a vent so we bagged the patient 40mins to receiving facility. This patient had unequal pupils with pinpoint on right and no no real movement on the left on initial ED arrival as reported. Patient was hypertensive initially at 200's/100 which decreased to 140's/70's after I started the fosphenytoin. Patient was also bradycardic in 50's. Pt. was on propofol and fosphenytoin infusions.

From the time we had patient on our monitor, EtCO2 showed hypocapnia at 22-24mmHg. Patient was breathing on his own and we continued with vent rate of 16. I had the nurse decrease ventilatory rate slightly and EtCO2 remained same. Strict attention was given to ensure proper rate was being delivered throughout the transfer so it wasn't because we were bagging too fast.

On arrival at the ICU I informed the doc what the EtCO2 was and that we tried to maintain it on low end of normal and he said that "if the patient is breathing fast on their own and inducing hypocapnia, we let them do that". I'm kinda confused.

So my question is this.... what is the difference if we induce hypocapnia or if the patient induces hypocapnia? Isn't it still bad? I realize that head bleeds/TBI can cause hyperventilation. Should these patient types receive paralytics so we can fully control the resp rate and CO2?

Any insight is appreciated.

 

[Veneficus]

http://ajrccm.atsjournals.org/content/171/2/96

This may help.

Miller's also has a bunch on it. Way too much to type, sorry.

 

[18G]

I appreciate the post but that doesn't really address my question. Is permitting a patient as I described to have an EtCO2 of 22-25 okay if it's the patient's resp rate that is causing it? I have always held on to the practice of EtCO2 no lower than 30 for hyperventilation. Literature says CO2 <25 causes cerebral ischemia.

 

[18G]

I just came across this research paper today. Although a small sample it does backup what I was thinking to be true.

http://jnnp.bmj.com/content/81/7/793.abstract

 

[jwk]

I just came across this research paper today. Although a small sample it does backup what I was thinking to be true.

http://jnnp.bmj.com/content/81/7/793.abstract

Interesting article. I think it answers your question for the most part - hyperventilation, particularly to the extent you described, is harmful.

I think this patient was hyperventilated too much, even in the ER. You don't give a weight for the patient, but I think the initial ventilator settings are pretty high at an 8 liter minute volume, especially if you're already getting PaCO2 reading in the low 30's.

If this patient is breathing spontaneously, and you're measuring an EtCO2, there's really no need for you to be squeezing the bag at all, except for perhaps an assisted resp here and there to help prevent atelectasis. If you're reading an EtCO2 of 22-24, hand bagging will just depress your EtCO2 even further. What is the "proper rate" you describe? What do you mean by having the nurse decrease the respiratory rate? Decrease it to what? Are you trying to mimic the ventilator settings when bagging the patient? That's pointless. You have an EtCO2 right in front of you to guide you.

So to answer the second part of your question, yes, if you can, I think these patients should definitely receive some sort of paralytic agent so you can control their ventilation. And lastly - a critical care transport of this sort really needs a vent, although I'm totally unaware of your practice situation and location, so I'll be the first to admit that's not always possible - but it certainly would be the preference.

 

[18G]

Interesting article. I think it answers your question for the most part - hyperventilation, particularly to the extent you described, is harmful.

I think this patient was hyperventilated too much, even in the ER. You don't give a weight for the patient, but I think the initial ventilator settings are pretty high at an 8 liter minute volume, especially if you're already getting PaCO2 reading in the low 30's.

If this patient is breathing spontaneously, and you're measuring an EtCO2, there's really no need for you to be squeezing the bag at all, except for perhaps an assisted resp here and there to help prevent atelectasis. If you're reading an EtCO2 of 22-24, hand bagging will just depress your EtCO2 even further. What is the "proper rate" you describe? What do you mean by having the nurse decrease the respiratory rate? Decrease it to what? Are you trying to mimic the ventilator settings when bagging the patient? That's pointless. You have an EtCO2 right in front of you to guide you.

So to answer the second part of your question, yes, if you can, I think these patients should definitely receive some sort of paralytic agent so you can control their ventilation. And lastly - a critical care transport of this sort really needs a vent, although I'm totally unaware of your practice situation and location, so I'll be the first to admit that's not always possible - but it certainly would be the preference.

Thanks for your feedback!

The patient was fairly big... I think his weight was 120kg. We started out with a RR per the vent setting at 16. After seeing what the EtCO2 was I had the nurse ventilate at 10 and still no change.

I had the thought of mainly allowing the patient to breathe on his own to see what the EtCO2 would do but with pt. being intubated and on propofol I guess I shyed away from that approach. And now that I think about it, the ABG the patient had with the vent was probably right after he was put on the vent and the pt. received vecuronium as part of the RSI.

I hear ya with the "should have had a vent". I have had the conversation with my supervisor and we have just gotten in two additional transport ventilators which hopefully will go in service soon.

You made some good points and looking back I learned from this call.

 

[medicdan]

Forgive me for intervening outside my SOP, but isn't this all an indication of Cushing's reflex (hypertension/wide pulse pressure, irregular or slow breathing and bradycardia) following TBI (with unequal or abnormal pupils)?

Isn't the idea (at least initially) to assist ventilation/hyperventilate (up to 20
bpm), which would bring the CO2 down/induce hypocapnia, which would decrease ICP?

If CPP=MAP - ICP, then decreasing ICP should increase the CPP, right?

Is my logic wrong here? Does this not work long-term? Why would the patient be spontaneously hyperventilating?

 

[jwk]

Forgive me for intervening outside my SOP, but isn't this all an indication of Cushing's reflex (hypertension/wide pulse pressure, irregular or slow breathing and bradycardia) following TBI (with unequal or abnormal pupils)?

Isn't the idea (at least initially) to assist ventilation/hyperventilate (up to 20
bpm), which would bring the CO2 down/induce hypocapnia, which would decrease ICP?

If CPP=MAP - ICP, then decreasing ICP should increase the CPP, right?

Is my logic wrong here? Does this not work long-term? Why would the patient be spontaneously hyperventilating?

Hyperventilation does decrease ICP, but it also causes cerebral vasoconstriction which decreases cerebral blood flow.

 

[18G]

I have heard back briefly from my medical director who has said that he checked with one of the intensivist who advised he shoots for no lower than 30mmHg in these patient types which is what I have always been taught and read to be the goal.

Still waiting to hear further.

 

[46Young]

Hyperventilation does decrease ICP, but it also causes cerebral vasoconstriction which decreases cerebral blood flow.

A lot of this stuff regarding ETCO2, hyperventilation, etc. in the setting of herniation is largely voodoo medicine, IMO. For example, ITLS says for the TBI w/ signs of herniation to titrate SBP to 110-120, and to titrate ETCO2 to 30-35 mmHg. Studies haven't proven one way or the other if this helps or harme the pt.

As an aside, hyperventilating the pt raises intrathoracic pressure, which impedes venuous return. A downward trending ETCO2 also suggests impending shock as well.

 

[medicdan]

Hyperventilation does decrease ICP, but it also causes cerebral vasoconstriction which decreases cerebral blood flow.

Thanks for the quick reply. That makes sense. Unfortunately, that's what's in my protocols. Is this just another example of EMS being behind the evidence based times?

Sent from my DROID2 using Tapatalk 2

 

[18G]

A lot of this stuff regarding ETCO2, hyperventilation, etc. in the setting of herniation is largely voodoo medicine, IMO. For example, ITLS says for the TBI w/ signs of herniation to titrate SBP to 110-120, and to titrate ETCO2 to 30-35 mmHg. Studies haven't proven one way or the other if this helps or harme the pt.

There are studies that show hyperventilation to be harmful which is where the target of 30 comes from. And maintaining BP of 110 maintains a MAP sufficient to maintain cerebral blood flow which overcomes increased ICP.

 

[jwk]

A lot of this stuff regarding ETCO2, hyperventilation, etc. in the setting of herniation is largely voodoo medicine, IMO. For example, ITLS says for the TBI w/ signs of herniation to titrate SBP to 110-120, and to titrate ETCO2 to 30-35 mmHg. Studies haven't proven one way or the other if this helps or harme the pt.

As an aside, hyperventilating the pt raises intrathoracic pressure, which impedes venuous return. A downward trending ETCO2 also suggests impending shock as well.

It might be voodoo to you, but since I do a significant amount of anesthesia for neurosurgery, this is something I deal with every day in the OR.

An EtCO2 of 30-35 is mild hyperventilation. That's generally where we run a lot of our patients, not just the head cases. In the past, we would indeed run EtCO2s in the low 20's, thinking if a little hyperventilation was good for decreasing ICP, then a lot must be better. Way back when, we just didn't have the physiologic understanding we have now. A little hyperventilation can decrease ICP and not cause cere

We will occasionally use more significant hyperventilation, but the difference is that when we do, we're actually looking at the exposed brain after a bone flap has been removed. Sometimes the ICP is so high, the brain wants to push out through the hole that was just made. At that point, we have to try just about anyting to keep the brain from herniating, including big-time hyperventilation.

A downward trend on EtCO2 is not indicative of shock with a normal blood pressure - it's indicative of hyperventilation.