intraop hypotension

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stonemd

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60yo , previous stroke without residual for sitting shoulder arthroscopy
on ACE inhibitor and clonidine
preop interscalene block
in or preop bilat cerebral sat on room air supine 40%
after induction BP to 60/30 Csat 20%
treated with phenylephrine, ephedrine bolus with transient rise in BP, Csat to 30%
FiO2 to 1, ETCO2 to 43, head position checked, bolus IVF, reduce volatile agent
Csat still 30%
what next??

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Is this a true story? If so, there are more details you could provide. What were the pre-induction vitals? Any pre-op labs? Any chance your block was spinal or intravascular? Did patient take home meds prior to case? What meds did you give for induction? Anaphylaxis possible? You monitor cerebral sats regularly for these cases?

I'd give epinephrine or vasopressin if the hypotension was refractory.
 
Low initial Csat, what was the pre induction BP?

Pre load: depending on initial BP, maybe lab work if available (urine Na, osmols) pt may not have been optimal in terms of fluid status. Pt is also in the sitting position, which pools some ~500cc of blood into the pelvis, decreasing pre load. I am not sure if this pt has a hx of vasovagal syncope or if this would even be a consideration under GA, but with pressors on board, maybe not an issue. Does the pt have on compression stockings? Propofol for induction? History of CHF?
Physical exam to assess potential for pneumothorax. At this point I think starting some fluid boluses would be helpful.

cardiac: EF normal? Any cardiac hx? With history of CVA, maybe previous hx of MI and heart cant keep up with vasodilation of induction. Pt anticoagulated properly (PE) ECG show any abnormalities? Is the patient bradycardic?? If so, Hypotension, brady, coronary vasodilation = Bezold-Jarisch reflex. Keep the ephedrine bolus, add fluids and atropine.

Afterload: With continued hypotension after phenyl/ephedrine, something seems to be overriding the vascular ability to vasoconstrict enough to increase pressure, either by preventing vasoconstriction or limiting its effectiveness. What was the pressure s/p interscalene block? Potentially some carotid body damage or local anesthetic toxicity (d/t interscalene block), inhibiting the response to hypotension. Pressors work at the local level, so it would seem pressors could override this response, unless the carotid body damage/toxicity responds to the increase in pressure with more vasodilation. Or Bezold-Jarisch reflex as mentioned above.

After going through this process, I would say acutely, fluids, ephedrine and atropine (if brady) to get out of the woods. CXR to assess for PTX if surgery is post poned.

take with a grain of salt = student.
 
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We don't have Csat in our facilities, but isn't 40% on RA on the low side already? Without more details it's hard to know exactly what's going on - however - I would have returned them to a supine position immediately (you didn't mention that you did or didn't). Beach chair-position shoulders are among the more dangerous procedures we do IMHO. If you're reading 60/30 with a cuff pressure while sitting up, your pressure at the Circle of Willis is substantially less than that, so it's not surprising the Csat sucks. Put them supine, try vasopressin (my new favorite go-to pressor after an impressive anaphylaxis case recently), go from there.
 
Can anyone post a link about the CSAT machine? I have never heard of it. Maybe it goes by another acronym?
 
Is this a true story? yes
What were the pre-induction vitals? yes, 120/80, HR 70
Any pre-op labs? no
Any chance your block was spinal or intravascular? no, US guided, I do 500/yr
Did patient take home meds prior to case? yes
What meds did you give for induction? propofol sux
Anaphylaxis possible? doubtful, no tahcycardia, wheezing, hives, swelling
You monitor cerebral sats regularly for these cases? yes for sitting cases, use bilat if hx cerebrovascular dz


urine Na, osmols ASC so nope
Is the patient bradycardic?? no HR changes
What was the pressure s/p interscalene block? minimal change
PTX, no US guided by experienced anethesiologist
take with a grain of salt = student, very nice assessment

40% on RA on the low side already? YES most often 70-85%
supine position immediately, I didnt
try vasopressin

Sorry Csat is my abreviation for cerebral saturation
we use the Invos Covidien oximeter
http://www.covidien.com/rms/products/brain-monitoring/bis-complete-2-channel-monitor

So I used epinephrine, initially bolus 25mcg x 2 IV then infusion of 5mcg/min
BP and Csat returned to preop levels
patient awoke in PACU pain free and baseline neuro status


How would you use vasopressin, bolus? infusion, alone or in combo with other agents?
 
How would you use vasopressin, bolus? infusion, alone or in combo with other agents?

To me it sounds most like a combination of his ACEi giving you some refractory hypotension combined with the sitting position pooling all your volume in the lower extremities.

Personally, I really don't like doing cases like this with patients having taken their ACEi for just that reason.

In the situations where I do find myself doing the case, I usually draw up 20 units of vasopressin in a 100mL bag (0.2 units/ml final concentration). I then bolus a few cc at a time, repeat as needed and titrate to effect. Do that while aggressively replacing any volume deficits. I wouldn't start an infusion unless I was really struggling.
 
Because of AceI, fluid and vasopressin bolus of 0.2U to assess for response.
 
I agree that this is most likely ACEi effect. I find vasopressin is about as useful as neo but when used together they are fairLy good. But I would have done exactly what you did. Epi.

I probably would have put and amp of epi and an amp of neo in a 100 or 250cc bag and just ran an infusion.

With that being said, I've never really had to give epi for a shoulder case but if necessary I wouldn't hesitate.

Epi is the king.
 
most likely ACEi effect responsive to vasopressin, BUT...subarachnoid injection can happen with an ISB no matter how many you have done especially when not using a blunt touhey needle which most people dont
 
Epinephrine or Vasopressin are excellent choices here. Phenylephrine may not restore the Cerebral Oximetry back to baseline as you can get cutaneous vasoconstriction which will interfere with the Cerebral Oximeter.
 
Br J Anaesth. 2011 Aug;107(2):209-17. doi: 10.1093/bja/aer150. Epub 2011 Jun 3.
Effect of phenylephrine and ephedrine bolus treatment on cerebral oxygenation in anaesthetized patients.
Meng L1, Cannesson M, Alexander BS, Yu Z, Kain ZN, Cerussi AE, Tromberg BJ, Mantulin WW.
Author information

Abstract
BACKGROUND:
How phenylephrine and ephedrine treatments affect global and regional haemodynamics is of major clinical relevance. Cerebral tissue oxygen saturation (Sct(O2) )-guided management may improve postoperative outcome. The physiological variables responsible for Sct(O2) changes induced by phenylephrine and ephedrine bolus treatment in anaesthetized patients need to be defined.

METHODS:
A randomized two-treatment cross-over trial was conducted: one bolus dose of phenylephrine (100-200 µg) and one bolus dose of ephedrine (5-20 mg) were given to 29 ASA I-III patients anaesthetized with propofol and remifentanil. , mean arterial pressure (MAP), cardiac output (CO), and other physiological variables were recorded before and after treatments. The associations of changes were analysed using linear-mixed models.

RESULTS:
The CO decreased significantly after phenylephrine treatment [▵CO = -2.1 (1.4) litre min(-1), P<0.001], but was preserved after ephedrine treatment [▵CO = 0.5 (1.4) litre min(-1), P>0.05]. The was significantly decreased after phenylephrine treatment [▵ = -3.2 (3.0)%, P<0.01] but preserved after ephedrine treatment [▵ = 0.04 (1.9)%, P>0.05]. CO was identified to have the most significant association with (P<0.001). After taking CO into consideration, the other physiological variables, including MAP, were not significantly associated with (P>0.05).

CONCLUSIONS:
Associated with changes in CO, decreased after phenylephrine treatment, but remained unchanged after ephedrine treatment. The significant correlation between CO and implies a cause-effect relationship between global and regional haemodynamics.
 
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No CXR

No decrease in O2 sat or increase In Airway pressure. I really think my chance of pneumo is vanishingly low with ultrasound after doing >1000 of ISBs. I inject just above and below C5 nerve root at C6 vertebral level and add a superficial coz plexus block.

If I suspect a pneumothorax I would do an ultrasound exam for comet tails and lung sliding / sky-ocean-beach. Faster and perhaps more sensitive than CXR.
 
Effect of phenylephrine and ephedrine bolus treatment on cerebral oxygenation

Maybe phenylephrine should be contraindicated in sitting procedures. That would be a major change for a lot of people.
 
We have an orthopod who does all his shoulders lateral and I love him for that.
 
We have a bunch. Only 2 prefer arthroscopy sitting. But all the hemi, totals and humeral fx get done sitting. Of course In non arthroscopy we can keep the BP higher without the problem s they have seeing thru scopes when more bleeding occurs.
 
I know your problem was after induction and it was most likely an issue with theACE inhib. But remember that you have a good block on board. The patient only needs enough anesthesia to tolerate the tube or LMA plus amnesia. I go with spontaneous respiration in these cases with a mac around 0.6.
 
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No CXR

No decrease in O2 sat or increase In Airway pressure. I really think my chance of pneumo is vanishingly low with ultrasound after doing >1000 of ISBs. I inject just above and below C5 nerve root at C6 vertebral level and add a superficial coz plexus block.

If I suspect a pneumothorax I would do an ultrasound exam for comet tails and lung sliding / sky-ocean-beach. Faster and perhaps more sensitive than CXR.


I agree with you. These days I use U/S and NS to confirm the Brachial Plexus, e.g. C6 nerve root , then back off about 0.5 mm from the nerve root prior to injection. My block success is still 100% (ISB) with this technique and there is solid literature to support it. The idea behind the technique is to maintain efficacy while decreasing any potential complications.


Regional Anesthesia & Pain Medicine:
January/February 2014 - Volume 39 - Issue 1 - p 56–60
doi: 10.1097/AAP.0000000000000034
Daring Discourse
The Maximum Effective Needle-to-Nerve Distance for Ultrasound-Guided Interscalene Block: An Exploratory Study
Albrecht, Eric MD, DESA*; Kirkham, Kyle R. MD, FRCPC*; Taffé, Patrick PhD†; Endersby, Ryan V.W. MD, FRCPC*; Chan, Vincent W.S. MD, FRCPC*; Tse, Cyrus BSc*; Brull, Richard MD, FRCPC*
 
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subarachnoid injection can happen with an ISB no matter how many you have done especially when not using a blunt touhey needle which most people dont

I went to u Iowa ages ago takin each course on arrow stim caths and lab with anesthetized pigs. Boezaart recommended the safest block was with the biggest dullest. needle you could use!!
 
subarachnoid injection can happen with an ISB no matter how many you have done especially when not using a blunt touhey needle which most people dont

I went to u Iowa ages ago takin each course on arrow stim caths and lab with anesthetized pigs. Boezaart recommended the safest block was with the biggest dullest. needle you could use!!


Alternatively, you can stop penetrating the brachial plexus sheath which is entirely unnecessary; as I have posted above the injection can (should?) occur 0.5-1mm AWAY from the nerve root essentially eliminating the risk of a SAB injection.
 
[QUOTE="BLADEMDA, 0.5-1mm AWAY from the nerve root essentially eliminating the risk of a SAB injection.[/QUOTE]

Interesting that we used to use US to get the needle as close as possible to the nerve
And now can use it to get the needle as far as can still be effective away from the nerve.

Old habits do die hard tho
 
Cerebral sats in 40s are very rare. I use it as a surrogate for SvO2 and cardiac output. Every heart patient of mine gets them, and I only see numbers like that (<60) in some heart transplants and LVAD patients. Inotropes, transfusion, hypoventilation. Vasopressin may be better than phenylephrine in cerebral vasculature.
 
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