Interscalene block and intravascular injection

[Matty44]

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So I was reading some posts on another website discussing the rationale for hyperventilation after recognizing intravascular injection of local during an IS block, and am just looking for some SDN wisdom on the topic. I agreed with most of what they were saying, but had some issues with two statements

1) Hyperventilation will decrease the amount of LA delivered to the brain.

Okay, I understand the rationale for this (i.e. vasoconstriction with dec. PaCO2) but if you inject 5cc of LA into the vertebral artery, by the time you recognize what you've done and started hyperventilating the pt, is there going to be any appreciable change in the amount of LA that reaches the brain? Seems to me the damage has been done at that point....

2) Hyperventilation will drive extracellular K+ into the cell causing it to hyperpolarize.

Rationale followed stating that in a hypokalemic state, the gradient for K+ movement out of the cell is increased, and therefore, hyperpolarizes the cell as more K+ move extracellularly. But the way I look at it is that if you hyperventilate and drive K+ inward, didn't you just "DEpolarize" the cell? Seems to me that hypokalemia from say, diuretics or vomiting, is different than hypokalemia from forcing intracellular movement of potassium...Am I missing something here?

Thanks in advance.

 

[Idiopathic]

thats one statement, but its also a true one, in that hyperventilation reduces cerebral blood flow for a short time.

 

[Matty44]

thats one statement, but its also a true one, in that hyperventilation reduces cerebral blood flow for a short time.

I understand that, but it seems to me that if you injected 5cc of local into the vertebral artery, that amount would reach the brain within a matter of seconds, no? So by the time you are able to grab the bag and start hyperventilating, wouldn't the LA already have reached tissues in the brain? I mean, it totally makes sense if you went intravascular with a FNB, because you have some time before it circulates and reaches that brain, but not interscalene.

 

[aredoubleyou]

I understand that, but it seems to me that if you injected 5cc of local into the vertebral artery, that amount would reach the brain within a matter of seconds, no? So by the time you are able to grab the bag and start hyperventilating, wouldn't the LA already have reached tissues in the brain? I mean, it totally makes sense if you went intravascular with a FNB, because you have some time before it circulates and reaches that brain, but not interscalene.

If you inject anything into the vetebral artery than all of it will go to the brain. If you inject it into a peripheral vein than, i think, you might theoretically, on the 5th sunday of every other leap year be able to make a SIGNIFICANT CLINICAL difference by hyperventilating the patient by diverting a greater proportion to other tissues for uptake. It can't hurt, tho. Ive read the hyperpolarization thing before, too, but at the same time I've never heard of a seizure being broke by hyperventilation.

Best way outside of aspirating to reduce the amount of drug delivered is perhaps epi. Of course its a marker, so by the time the hr increases, the deed is done to some degree.

 

[Matty44]

So am I thinking about something backwards regarding the hyperpolarization? Again, it seems to me that by driving K+ into the cell, you would be essentially depolarizing it, not hyperpolarizing it...what am I missing?

 

[Idiopathic]

I understand that, but it seems to me that if you injected 5cc of local into the vertebral artery, that amount would reach the brain within a matter of seconds, no? So by the time you are able to grab the bag and start hyperventilating, wouldn't the LA already have reached tissues in the brain? I mean, it totally makes sense if you went intravascular with a FNB, because you have some time before it circulates and reaches that brain, but not interscalene.

so think of what local anesthetics do, which is block sodium conduction and block DEPOLARIZATION; i think the rationale for hyperventilation-->increased K conductance and therefore making it easier to depolarize is one that may be valid.

i would wager that this debate is ONLY for peripherally injected local anesthetics (i.e. large volumes in the venous circulation or some in a peripheral artery - NOT one directly leading to the brain) so i wouldnt think it would apply to carotid/vert injections since those patients will seize before you can get the needle out

 

[Matty44]

Okay, thanks for the response. So you would say that hyperventilating won't do anything to stop a seizure due to hyperpolarization of nerve membranes? Cause I'm pretty positive that's what the other people were saying (even though I think they are wrong...)

 

[Matty44]

So I found this here http://www.uic.edu/classes/phar/phar403/ld2.htm "The onset of seizures may reflect selective depression of inhibitory cortical neurons by local anesthetics, leaving excitatory pathways unopposed." So would hyperventilation and subsequent K+ influx aid in depolarization of these depressed inhibitory neurons, thus helping to terminate a seizure? Just trying to wrap my head around all this...

 

[Idiopathic]

id argue that its unlikely you will terminate a seizure with these maneuvers but that you may prevent one in the right circumstance