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Idiopathic

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80 ish year old male, reasonably healthy, leg sparing hemipelvectomy for ischial sarcoma. hx of sick sinus syndrome with implantable backup pacer, currently in sinus brady at 52 with 1st degree AV block, RBB, LAFB. All labs and vitals okay.

standard induction, radial aline, RIJ MAC, 16g 18g. first 6 hours are pristine, lost about 2500cc, transfused 6 units PRBC 6000 crystalloid, good UOP, vitals are rock solid.

after the pelvis is resected, surgeons are cleaning up the field and I get a page from the res:"phenylephrine not working for BP" go in find out shes given a stick of neo or so and tried ephedrine, HR is now 90 and BP is 80, i get hespan and hang it, ABG from 20 minutes ago is 7.32/48/250 Hct 33, Ca 4.1. I give a gram of Ca and adjust resp rate. BP trending down to a nadir of 32/24 (cuff is 40/24). No reaming, no cement, no implant, no meds...nothing new for the last hour. HR is actually down to 60s but still sinus and no change in morphology. ETCO2 stable and no change in pulmonary mechanics.

Thoughts?
 
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Interesting. Didn't know you could do leg sparing. I have done a few of those and they all lost a few blood volumes.

My knee jerk reaction would be to hang some blood until I'm convinced it's not hypovolemia. I'm sure there is a bunch of emboli going on...

Why was the Ca 4? Too high to be ionized, too low to be plasma Ca.
 
its ionized we use mg/dL so low end of normal is 4.5

i asked for more blood but last crit 33 and bleeding essentially done
 
80 ish year old male, reasonably healthy, leg sparing hemipelvectomy for ischial sarcoma. hx of sick sinus syndrome with implantable backup pacer, currently in sinus brady at 52 with 1st degree AV block, RBB, LAFB. All labs and vitals okay.

standard induction, radial aline, RIJ MAC, 16g 18g. first 6 hours are pristine, lost about 2500cc, transfused 6 units PRBC 6000 crystalloid, good UOP, vitals are rock solid.

after the pelvis is resected, surgeons are cleaning up the field and I get a page from the res:"phenylephrine not working for BP" go in find out shes given a stick of neo or so and tried ephedrine, HR is now 90 and BP is 80, i get hespan and hang it, ABG from 20 minutes ago is 7.32/48/250 Hct 33, Ca 4.1. I give a gram of Ca and adjust resp rate. BP trending down to a nadir of 32/24 (cuff is 40/24). No reaming, no cement, no implant, no meds...nothing new for the last hour. HR is actually down to 60s but still sinus and no change in morphology. ETCO2 stable and no change in pulmonary mechanics.

Thoughts?

Pump failure? Secondary to ischemia? Fat embolism?

epi, draw labs. Float a PA catheter or TEE.
 
so, everything else looked fine (HR, ETCO2, pulse ox). I gave 200mcg of epi (40mcg, 60 mcg, 100mcg) and 2 units vasopressin. BP SLOWLY recovered to 120s but sagged from then on out. Required 10 units VP (which I hate to give) and next gas came back with HCT of 23 (from 33) although lactate and base deficit within range.

At conclusion of case, decided not to extubate although patient did not tolerate tube, was ready from every perspective, except BP 50-60s systolic and followed commands. Proceeded to pull tube and transport to ICU with pressures 60-70 systolic for volume resuscitation. Its weird having a patient with a systolic bp of 55 talk to you coherently.

My thoughts are fat embolism leading to vasodilation uncovering BIG volume deficit that I never really recovered from, but he couldnt mount an appropriate HR response...do you think that hurt me or is this not a big issue (i.e. his HR went down as his hypotension got worse but it didnt get junctional or trend towards junctional, etc).

I probably should have put in a probe but the positioning was problematic and my experience is somewhat limited. I guess the answer would have been there but oh well.

Tough case for my 3rd clinical day as attending

p.s. one of my colleagues mentioned severe vagal response from pain leading to this event in a likely autonomically compromised 80 year old. I thought that unlikely but possible
 
Could just be volume. Respiratory variation on aline/ pulse ox? I'm assuming you would have seen an arrythmia (dudes set up for 3rd degree heart block 2/2 ischaemia). Possible cardiogenic shock, also very possible low svr state (fat emboli as you said), sepsis, etc. Sick sinus might not be able to compensate (HR wise). In unresponsive hypotension also think of steroids (hx?).

As a side note, why was the backup rate below 52 for someone w a sick sinus?

The vagal stuff dont make as much sense with a pacer in place.

I think a central line would have been a good idea from the get go, fluid management in an 80 yr old with a bad ticker can get tricky. He's got a relative contraindication for a PAC, so dont even go there.
 
Sounds similar to what you can see on reperfusion after TKAs. Did you check DIC labs like platelets, coags and fibrinogen?

You had a MAC, so putting in a PA catheter would have been easy (the pacer would have protected you). I wouldn't have extubated, especially without having a good grip on what was going on.

BTW I thought that the concern with PA-C and bundle branch blocks was mostly with the patients with LBBB, knocking out the right bundle. The left anterior and posterior fasicles are pretty far away from where the PA-C would go.
 
I'll stick to my knee jerk reaction.

Pt was volume depleted.
 
just a couple random thoughts:

did the surgeons manipulate or do anthing that could have been compressing the IVC knocking out preload? follow up to that....was the contralateral leg swollen?

could the surgeons have knocked out some sympathetic ganglia in the pelvic region which may explain the bradycardia?


all of this in the setting of hypovolemia....
 
BTW I thought that the concern with PA-C and bundle branch blocks was mostly with the patients with LBBB, knocking out the right bundle. The left anterior and posterior fasicles are pretty far away from where the PA-C would go.

True that. My bad.

Still wouldnt have put one in preop.
 
Was your patient taking an ACE inhibitor or an ARB pre-op?
If the answer is yes then you don't have to look any further.

I would doubt that would be the problem just now showing up 7+ hours into the case. ACE inhibitor hypotension usually causes a problem just after induction.
 
I would doubt that would be the problem just now showing up 7+ hours into the case. ACE inhibitor hypotension usually causes a problem just after induction.

Actually it can happen later during the case especially when you add hypovolemia, hypocalcemia and most likely big doses of narcotics.
 
Was your patient taking an ACE inhibitor or an ARB pre-op?
If the answer is yes then you don't have to look any further.

No and no reason to be adrenally insufficient either. I explored everything else mentioned in this thread at the time, all negative. My first thought was that they had a clamp on the iliac vessels that they took off but really there was a nothing else.

I have no idea what's up with the pacer except to say that it was interrogated and functioning well and never spiked during the entire case. Thanks for all the discussion, patient doing well today but still on a few mics of norepinephrine.
 
Required 10 units VP (which I hate to give) and next gas came back with HCT of 23 (from 33) although lactate and base deficit within range.

I also hate to give VP. Seen significant coronary vasospasm once right after giving it. Kidneys hate it as does splanchnic circ. I like epi before vaso as you did.

Looks like you may have lost a couple units acutely... 33-23 hct, although I don't know how often you were checking HCT's. Prolly upset his heart function, which may explain his HR fluctuations. So likely dealing with at least 2 issues. With a MAC, 16g and 14g you should have no problem fixing the volume status unless you are worried about CHF. I would be very hesitant of extubating with BP's in the 50's. Once you remove the catecholamine producing ETT, you may end up with BP's that are lower.

I've done 3-4 of these and enjoyed them. Staying ahead with hct/FFP/Platelets is key. I would place a TEE over PAC in this case although I wouldn't have a problem with a PAC if TEE was not available.

Good case Idiopathic. 👍
 
I also hate to give VP. Seen significant coronary vasospasm once right after giving it.
Kidneys hate it as does splanchnic circ. I like epi before vaso as you did.

How much vasopressin are you giving? I have never given more than 2 or 3 units then I go back to the other pressors and have never seen any remote complication from it. I agree with the epi as well. If you need BP then give epi.

I have always found vasopressin to be a good intermediate vasopressor. I use it as a synergistic agent.

Sevo, you probably have more opportunities to use vasopressin than I do so I will punt to your experience but I am curious as to how much you are using.
 
I have never had any problem with vasopressin; although almost always I only give a small amount like Noy (other than the ICU players that come down on a vasopressin drip).

I like using 1 unit boluses at a time.
 
I also hate to give VP. Seen significant coronary vasospasm once right after giving it. Kidneys hate it as does splanchnic circ. I like epi before vaso as you did.

How are you seeing the vasospasm? Ischemia or regional wall motion changes after a bolus? What do you mean about the kidneys hating it? I think it's hard to separate the effects of AVP from the consequence of a physiology that makes us give it.
 
I use very little and in specific circumstances. I actually put vasopressin in with the other big guns, epi and norepi. When bolusing I use it .5-1 unit at a time. Even .5 units can give you a robust increase in B.P. I rarely need more than 1-4 units unless I'm dealing with cardiac arrest. If perfusion asks for it I give them 2u in 20cc syringe. They sometimes used it more than I think they should. That's just me though.

I use it almost exclusively in low SVR states:

  • Vasoplegic Shock
  • Septic Shock/Neurogenic shock/Vasodilatory shock
  • Refractory hypotension 2nd to ARB/ACE inhibition
  • High Epidural/Spinal (N=0, but if it happens I would use it if Neo isn't doing the trick)

Exceptions to low SVR states:

  • Uncontrollable Hemorragic Shock (keep in as much as you can while you fill the tank)- I don't use it in patients who have had a significant drop in Hct over hours.
  • Refractory cardiac arrest

In general, if someone is hypovolemic, has refractory hypotension (refractory to neo or ephedrine), and needs a pressor while you administer crystalloids/products, vasopressin will not be at the top of my list. SVR would be high in these people, so I like to choose something that has some Alpha + Beta. If they are tachy I like norepi. If they are not, epi.

As a CA-3, I was bouncing around from heart room to heart room trying to get my hands on as many TEE cases as possible. One of the rooms I popped into was a 85 y/o patient with refractory hypotension. TEE probe in place, then came 2 Units of Vasopressin (likely too much for this guy). Either way, I immediately saw worsening RWMA/LV function. It was like night and day. Corrected the situation with NTG and EPI. Significant improvement. Temporal relationship could not be denied.

I have a healthy respect for vasopressin. It is a great drug, but as most big guns, they have equal potential to fix or hurt someone if not used correctly.

S/E of Vasopressin out of the Handbook of Anesthesia:

Vasoconstriction of coronary, splanchnic, muscular and cutaneous vascular beds.
May cause oliguria, H20 intoxication, pulmonary edema, myocardial ischemia, arrhythmias, abdominal cramps, anaphylaxis, contraction of smooth muscle, gall bladder, urinary bladder and uterus, vertigo, nausea and tremors.

Another experience:

2 months into PP I was on call and got called by surgery to do an ex-lap for lower GI bleed. Long story short, GI had tried their best to control bleeding and ended up putting the patient on Vasopressin after multiple attemps to control the bleeding via scope. Saw him in pre-op. Dude was white as a ghost, shaky, stomach cramps, hypertensive with a hgb of 7.0 (after receiving 6 units on the floor that day). I looked at his gtt's and found vaso going at 0.6U/min.
Back to the OR, opened him up. Bowels looked like shait. They were only getting a trickle of heme traversing them. I turned off the vaso. Within 20 minutes his skin had normal color and his bowels beautifully pinked up. Next lactate was 2.5 from 6.
I know that .6u/m is higher than recommended, but the experience showed me the dramatic effects of Vasopressin. I respect it tremendously.

Skeletal muscle breakdown has been linked to oliguria and worsening renal failure with vasopressin:
http://www.ncbi.nlm.nih.gov/pubmed/6610943

Interesting editorial:
http://www.anesthesia-analgesia.com/content/102/6/1908.2.full
http://www.anesthesia-analgesia.org/content/101/3/830.full?sid=70b305b9-e48d-4775-81a8-4282f5ca867c

Myocardial Ischemia:
http://circ.ahajournals.org/cgi/content/short/83/6/2111
http://www.anesthesia-analgesia.org...html?sid=253a7e73-9f63-4a05-b5dc-4adea2481328

Vasopressin remains a potent tool in the anesthesia arsenal, but I use it with extreme exclusivity.

Noy, to answer your question:

In general if they fit my criteria (low SVR or otherwise), I bolus .5-2U over a 30min interval. I may repeat this once more. If I don't get an adequate result, they go on a drip usually in conjunction with other exogenous catecholamines.
 
As a CA-3, I was bouncing around from heart room to heart room trying to get my hands on as many TEE cases as possible. One of the rooms I popped into was a 85 y/o patient with refractory hypotension. TEE probe in place, then came 2 Units of Vasopressin (likely too much for this guy). Either way, I immediately saw worsening RWMA/LV function. It was like night and day. Corrected the situation with NTG and EPI. Significant improvement. Temporal relationship could not be denied.

I hope you are not citing this as evidence of coronary spasm.
 
Urge, you can call it whatever you like. Myocardial ischemia if you will. The patient got Vaso, literally saw it coming in via TEE, and immediately the patient was in worse trouble than he had been in. His situation got remarkably better with NTG and EPI. Culprit = Vasopressin. No doubt. Black and White. That case is burned into my brain as if it was yesterday.
 
Culprit = Guy at head of the table. No doubt. Black and White.

Fixed that for you.

His situation got remarkably better with NTG and EPI.

Why did you bold NTG? You gave them both at the same time but somehow are able to determine it was the ntg that helped, not the epi?

You got to be kidding.
 
Urge, you can call it whatever you like. Myocardial ischemia if you will. The patient got Vaso, literally saw it coming in via TEE, and immediately the patient was in worse trouble than he had been in. His situation got remarkably better with NTG and EPI. Culprit = Vasopressin. No doubt. Black and White. That case is burned into my brain as if it was yesterday.

The temporal relationship seems undeniable.

Urge can add some here, but I think what he is wondering is if the worsening function was due to coronary spasm or the likely abrupt increase in afterload caused by the vasopressin.
 
You state you have a central line, that there are significant fluid shifts (as anticipated), yet provide no info re CVP other than the poor man's CVP (good UOP). Am I missing something? Using Vigileo, Lidco or something similar? Maybe I just read this thread too quickly on my little iPhone.
Great post Sevo.
Tuck
 
Fixed that for you.



Why did you bold NTG? You gave them both at the same time but somehow are able to determine it was the ntg that helped, not the epi?

You got to be kidding.

Hey man. I'm not here to argue. I'm here sharing my experience and hoping others can learn from it.

Now, I sincerely hope you are not offended as this is not my intention.

Certainly they both helped, but the ST changes went away with the NTG and EPI. 😀

There were 2 CT trained anesthesiolgists in the room who agreed on the diagnosis. One co-authored the book "A Practical approach to Cardiac Anesthesia". Sometimes it is hard to determine exactly who the culprit is, but I'm certainly going to listen when an expert in the field has something to say. Vasopressin did not help his B.P. It made it worse. Sudden increase in afterload is an explanation given the information I have shared. We did not think this was the cause. My 2 cents dude.
 
Urge, you can call it whatever you like. Myocardial ischemia if you will. The patient got Vaso, literally saw it coming in via TEE, and immediately the patient was in worse trouble than he had been in. His situation got remarkably better with NTG and EPI. Culprit = Vasopressin. No doubt. Black and White. That case is burned into my brain as if it was yesterday.

Is it possible that this happened because your Vasopressin caused a sudden increase in after-load that the sick heart could not handle?
And if that's the case this is really not an effect specific to Vaso but you probably would have gotten the same result with any other medication that increases SVR.
 
Is it possible that this happened because your Vasopressin caused a sudden increase in after-load that the sick heart could not handle?
And if that's the case this is really not an effect specific to Vaso but you probably would have gotten the same result with any other medication that increases SVR.

Yes. Very possible. The working diagnosis was vasoplegic shock, hence AVP. Pressure was in the 50's when I got in the room despite other vasopressor infusions. AVP was then delivered in higher dose than normal to attempt and bring his BP up to acceptable levels. I'm not convinced an increase in afterload made things worse when an increase in preload/afterload was exactly what this guy needed. He ended up getting methylene blue. But that is another topic all together.
 
Yes. Very possible. The working diagnosis was vasoplegic shock, hence AVP. Pressure was in the 50's when I got in the room despite other vasopressor infusions. AVP was then delivered in higher dose than normal to attempt and bring his BP up to acceptable levels. I'm not convinced an increase in afterload made things worse when an increase in preload/afterload was exactly what this guy needed. He ended up getting methylene blue. But that is another topic all together.

Methylene blue is a good rescue medication as long as you can live with loosing your SPO2 accuracy for a while.
 
Coronary vasospasm has been well described in animal studies. I think it's plausible. I also think that Plankton's explanation (afterload) is just as plausible depending on where the wall motion changes happened. Interestingly enough, in an dog model of low cardiac output syndrome, vasopressin increased coronary artery blood flow assessed by ultrasound probe.

I would not give methylene blue in patients with CAD (though a case series has described it in refractory vasoplegia post CPB). It's a great last ditch pressor for shock states like sepsis but it inhibits guanylate cyclase and nitric oxide production. I'd keep it for when there are no other options.
 
👍

I would not give methylene blue in patients with CAD (though a case series has described it in refractory vasoplegia post CPB). It's a great last ditch pressor for shock states like sepsis but it inhibits guanylate cyclase and nitric oxide production. I'd keep it for when there are no other options.
 
Skeletal muscle breakdown has been linked to oliguria and worsening renal failure with vasopressin:
http://www.ncbi.nlm.nih.gov/pubmed/6610943

Agree that it shouldn't be a first line pressor but those case reports are interesting. Published in 1984, they received vasopressin 20 unit bolus then 0.4unit/min. That's kind of an outrageous dose. Plus, at that time the importance of volume resuscitation wasn't really appreciated. The 2 cases received blood and had good hematocrits but may have still been volume depleted.
 
Yes. High doses for sure.

Correct me if I'm wrong but aren't doses for esophageal varices and LGIB something in the order of .2 - .8 U/m.? For 12-48 hrs.?
Even if you are lucky enough to get interventional radiology, I believe their intra-arterial doses are pretty high as well.
 
so, everything else looked fine (HR, ETCO2, pulse ox). I gave 200mcg of epi (40mcg, 60 mcg, 100mcg) and 2 units vasopressin. BP SLOWLY recovered to 120s but sagged from then on out. Required 10 units VP (which I hate to give) and next gas came back with HCT of 23 (from 33) although lactate and base deficit within range.

At conclusion of case, decided not to extubate although patient did not tolerate tube, was ready from every perspective, except BP 50-60s systolic and followed commands. Proceeded to pull tube and transport to ICU with pressures 60-70 systolic for volume resuscitation. Its weird having a patient with a systolic bp of 55 talk to you coherently.

My thoughts are fat embolism leading to vasodilation uncovering BIG volume deficit that I never really recovered from, but he couldnt mount an appropriate HR response...do you think that hurt me or is this not a big issue (i.e. his HR went down as his hypotension got worse but it didnt get junctional or trend towards junctional, etc).

I probably should have put in a probe but the positioning was problematic and my experience is somewhat limited. I guess the answer would have been there but oh well.

Tough case for my 3rd clinical day as attending

p.s. one of my colleagues mentioned severe vagal response from pain leading to this event in a likely autonomically compromised 80 year old. I thought that unlikely but possible

My thoughts:

WE'VE BECOME TOO DEPENDENT ON MONITORS/NUMBERS.

You are describing abysmal numbers, yet a patient with PVC IN THEIR MOUTH, CLAWING AT SAID PVC.

Dude, you gotta patient

WIDE AND AWAKE

COHERENT

you did the right thing:

you used CLINICAL SENSE

which isnt taught alot current day.

Lemme ask you a question....answer honestly pls...

when you saw those scary LOW blood pressure numbers from the machine....

DIDJA FEEL FOR A RADIAL PULSE?

DIDJA FEEL FOR A CAROTID PULSE?

Can't tell you how many times I've seen scary MACHINE NUMBERS but then felt for

A RADIAL

A CAROTID

and

AT LEAST

known we're still in business.

Heres another BIG TIP:

Keep looking at the ETC02.

If theres still a wave,

YOU'RE STILL GOOD.

If ETCO2 evaporates,

YOU ARE F U K KED.

Chest compressions are imminent. 😱
 
I would not give methylene blue in patients with CAD (though a case series has described it in refractory vasoplegia post CPB). It's a great last ditch pressor for shock states like sepsis but it inhibits guanylate cyclase and nitric oxide production. I'd keep it for when there are no other options.

We actually routinely give it pre-pump for patients deemed to be at risk for vasoplegic syndrome. Don't recall all of the criteria, but certainly the folks on ACEI.

Run an infusion for about 30 min once we've settled in. Can't quote the dose, either. It's been about a year since I've hung in those rooms.
 
jet im with you, i got a lot of **** for extubating that patient with sbp in the 50s but would do it again in the situation (awake, fighting the tube)

also, i agree with you on the assessment...as i said, ETCO2/SpO2 stayed it baseline so i was more perplexed than anything. However, had i not been there when it happened (i.e. gotten called to the room after it happened) i predict a different ending to the story. I got my big drugs in quicker than my brand new CA1 would have and warded off the impending disaster.

at least thats how i see it.
 
ive also watched a patient get ST changes after VP was given, get called to the room (SRNA thought it was hypotensive demand) and seen it given again and watched the scenario unfold: hypotension into the 40s, ST elevation, bradycardia and drop in ETCO2 --> in other words, impending doom.

i gave 100mcg NTG and followed with a few ccs neo. did the trick. so thats my experience with what i presume to be VP induced coronary vasospasm. anecdotal yes but something that i watch for,
 
hey sevo,
I am sure that was a while ago, but how much NTG and Epi did you use?
 
Don't remember as I wasn't administering medications. I had my hand on the probe while this was going on. Probably 40-80mcgs NTG along with 30-50mcgs of Epi maybe more. + infusions of both.
 
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