Routine private practice laminectomy

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

Planktonmd

Full Member
Moderator Emeritus
Lifetime Donor
15+ Year Member
Joined
Nov 2, 2006
Messages
7,243
Reaction score
3,056
70 Y/O in holding area for laminectomy L1-L5 with placement of hradware.
Surgeon is not the fastest guy and tends to lose blood.
PMH:
MI 10 years ago, followed by angioplasty with drug eluting stents and on plavix.
Plavix stopped 6 days ago.
EF on recent Echo= 30%
Cardiologist told patient that he is "borderline" for placement of AICD but told him he is OK to undergo planned surgery.
Hgb = 12g/dl.
Current medications: Atacacnd, Loprerssor, Norvasc, aspirine (all taken this morning), Plavix (stopped 6 days ago)
Unable to asses exercise tolerance due to back pain.
Chemical stress test last week was negative for ischemia but showed multifocal PVC's and unsustained V tach.
Pt anxious to get his back fixed.
What is the plan?

Members don't see this ad.
 
70 Y/O in holding area for laminectomy L1-L5 with placement of hradware.
Surgeon is not the fastest guy and tends to lose blood.
PMH:
MI 10 years ago, followed by angioplasty with drug eluting stents and on plavix.
Plavix stopped 6 days ago.
EF on recent Echo= 30%
Cardiologist told patient that he is "borderline" for placement of AICD but told him he is OK to undergo planned surgery.
Hgb = 12g/dl.
Current medications: Atacacnd, Loprerssor, Norvasc, aspirine (all taken this morning), Plavix (stopped 6 days ago)
Unable to asses exercise tolerance due to back pain.
Chemical stress test last week was negative for ischemia but showed multifocal PVC's and unsustained V tach.
Pt anxious to get his back fixed.
What is the plan?

Lemme see, 70 y.o. who is "borderline" for AICD. First, since the test was already done, I think that I would want to know how close to his max HR was actually achieved on the chemical stress test. Then, I would want to know why Dr. cardiologist said that he was borderline for an AICD (is this relating to the non-sustained V-Tac?) I doubt it.... So I'm gonna bypass your reply of the "cardiologist has died since his evaluation" and go ahead and give you my plan & concerns: GETA + a-line (since your surgeon sucks). Have defib pads on this guy. As for his stent, keep'em on ASA. Heart already medically optimized.
 
70 Y/O in holding area for laminectomy L1-L5 with placement of hradware.
Surgeon is not the fastest guy and tends to lose blood.
PMH:
MI 10 years ago, followed by angioplasty with drug eluting stents and on plavix.
Plavix stopped 6 days ago.
EF on recent Echo= 30%
Cardiologist told patient that he is "borderline" for placement of AICD but told him he is OK to undergo planned surgery.
Hgb = 12g/dl.
Current medications: Atacacnd, Loprerssor, Norvasc, aspirine (all taken this morning), Plavix (stopped 6 days ago)
Unable to asses exercise tolerance due to back pain.
Chemical stress test last week was negative for ischemia but showed multifocal PVC's and unsustained V tach.
Pt anxious to get his back fixed.
What is the plan?

preop: main concern - anything else to be done?
if there is no CHF, cardiac status is as good as it is going to get. Due to increased risk of cardiac death (EF<35%) 2/2 arrhythmia patient should have defib/pacing pads placed. patient should have taken his beta blocker morning of surgery.
intermediate risk surgery in patient with what appears to be well controlled

intraop: main concerns - maintain supply/control demands. likely to require fluid/blood factor resuscitation with risk of CHF.
GA with pre-induction a line. induction/intubation taking care to minimize tachycardia/hypotension/HTN. would place central line, as well, so that, if needed, vasoactive drugs can be given closer to central circulation. a large bore IV should be available for fluid resuscitation. maintain temperature.

patient may need to remain intubated if has airway or pulmonary edema.

postop:
aggressive control of HR and pain. vigilance for MI.

http://circ.ahajournals.org/cgi/reprint/CIRCULATIONAHA.107.185700
see page 1981
 
Members don't see this ad :)
What is the plan?

How about some vital signs and a physical exam? Is the guy as well optimized as it sounds or is he in decompensated failure? I have no idea what this guy looks like clinically.

A potassium, a creatinine, and an EKG might be nice as well.
 
How about some vital signs and a physical exam? Is the guy as well optimized as it sounds or is he in decompensated failure? I have no idea what this guy looks like clinically.

A potassium, a creatinine, and an EKG might be nice as well.

Sure,
BP in holding is 120/70, HR= 70, SPO2 = 99% on room air
Patient is in no acute distress, states that he is ready for his back to be fixed because he misses golfing.
EKG shows NSR,interestingly R waves do not rise in any of the precordial leads! PR normal, QT normal.
Chest auscultation reveals some rales in the bases, S1 S2 and no murmurs or gallop.
Creatinine 0.5, K= 3.7 rest of electrolytes normal.
No jugular distension.
No palpable hepetomegaly.
 
Sure,
BP in holding is 120/70, HR= 70, SPO2 = 99% on room air
Patient is in no acute distress, states that he is ready for his back to be fixed because he misses golfing.
EKG shows NSR,interestingly R waves do not rise in any of the precordial leads! PR normal, QT normal.
Chest auscultation reveals some rales in the bases, S1 S2 and no murmurs or gallop.
Creatinine 0.5, K= 3.7 rest of electrolytes normal.
No jugular distension.
No palpable hepetomegaly.

So he does 18 holes of Golf daily--skip all cardiac anything and get this guy's back fixed:laugh:
 
How about some vital signs and a physical exam? Is the guy as well optimized as it sounds or is he in decompensated failure? I have no idea what this guy looks like clinically.

A potassium, a creatinine, and an EKG might be nice as well.

May I ask 'bout why do you want a baseline EKG when a pharmacologic stress test has been already done and is available for you to review...? Just askin'...
 
prop roc tube next. (variation on line stolen from zippy) would have usual neo and ephedrine ready, really I see guys like this ALL the time. Probably don't need an a-line but good peripheral access since you said your surgeon is crappy.
 
Then, I would want to know why Dr. cardiologist said that he was borderline for an AICD (is this relating to the non-sustained V-Tac?) I doubt it....

I can't remember the name of the study but there was a New England Journal article showing improved mortality when AICD's are placed in patients with low EF's (<35%?) That's why he's borderline.
 
May I ask 'bout why do you want a baseline EKG when a pharmacologic stress test has been already done and is available for you to review...? Just askin'...

Because if/when he infarcts intraoperatively or postoperatively, or develops CP, you're not gonna have a pharmacologic stress test to compare to. You're gonna have your baseline EKG as your reference.
 
So, everyone seems to agree that we should proceed with the surgery.
And so far it seems that most people will place an A line and a couple of IV's.
How about a CVP? or a PA catheter?
 
Members don't see this ad :)
I agree with Plank.

Zoll pads on
This patient is at risk for sudden cardiac death and has been judged "borderline" for AICD placement. This patient gets a set of Zoll pads put on before I even think about bringing him back to the OR.

Awake A-line
The four indications for a-line placement are: tight control, anticipated wide hemodynamic swings, inability to obtain non-invasive blood pressure (obesity usually) and frequent blood gas analysis. For this patient, the indications are mainly tight control and possibly wide hemodynamic swings with this potentially sloppy surgeon. For induction, my main concern is tight control, so I would want the a-line in before the patient goes off to sleep.

Intoducer with PAC
This patient has an EF of 30% and is about to undergo a pretty long operation with a potential for significant blood loss and is also going to be in the prone position. I would want a PAC to manage hemodynamics and fluid replacements. If this guy's heart starts to crap out, I would want to know the cardiac output, SVR and stroke volume so I could optimize fluids and possibly vasopressors. However, I think one could make the argument that by just placing a CVP, one could follow the CVP trend and optimize fluids/hemodynamics that way without subjecting the patient to the risks of a PAC. Regardless, I think a CVP, preferably an introducer, needs to be placed in this patient.

Other Special Risks
This patient needs to be informed of the special risks of being placed in the prone position - mainly post-op visual defects. This patient in particular is at risk because of his predisposition to hypotension by virtue of his cardiac status. This patient also needs to be advised about the potential for massive blood product administration. Finally, this patient and his family needs to be counseled on the possibility of post-op ventilation so there are no surprises when you bring him to the unit sucking plastic.
 
I can't remember the name of the study but there was a New England Journal article showing improved mortality when AICD's are placed in patients with low EF's (<35%?) That's why he's borderline.

Plenty of people with EF of 35% who do just fine without AICD's. I wondered why he needed it--was it something else? An underlying, frequent dysrhythmia for example?...
 
Because if/when he infarcts intraoperatively or postoperatively, or develops CP, you're not gonna have a pharmacologic stress test to compare to. You're gonna have your baseline EKG as your reference.

Why is he gonna infarct intra-op: you are gonna stress him beyond 80% of his max heart rate? He had no ischemia on his stress test.... Will the surgery stress him greater than the negative stress test? Will he be that mis-managed intra-op/post op? I suppose you can stress anyone to death by going above and beyond what a pharm stress does, but that would be horrible anesthesia care, no? Point I'm making is: EKG is a snap shot of a resting myocardium--really of little help as a point of "reference," when compared to a pharm stress test that was negative when the patient was at at least 80% of max HR (a much more useful, dynamic test than an EKG).
 
Plenty of people with EF of 35% who do just fine without AICD's. I wondered why he needed it--was it something else? An underlying, frequent dysrhythmia for example?...

And if he came to the OR with an ICD, I think most of us would have it turned off anyway and put Zoll pads on. Some have called for a CVP or a PAC. I don't know what the data show about CVP in the prone position, but I saw some limited data from a large center on CVP in the lateral position, and it was pretty inconsistent. That on top of the overwhelming data that CVP even supine is probably as good as a coin flip for volume status anyway.
 
Very Interesting points everyone- I personally would put large central line
/cordos but a line with vigileo monitor over PAC. Been using this for some time now, recent anesthesia articles supporting it with better abd surgery outcomes when used to maintain good fluid control. I know not available everywhere, but I find it very useful since you get CO, etc, and guide fluid by SVV (principle of fluid management in intubTED PT'S with respiratory variation). Just my two sense, but Ive been happy with it, especially since recent data questions Swean Ganz interpretation and safety.
Thanks:thumbup:
 
Why not an awake A line? I do all my A lines awake before the patient goes to the OR.

I don't think it's needed for induction in this patient. Our hatchet-wielding surgeon hasn't caused any bleeding yet and it's an elective case in an NPO patient. There's no reason a slow, careful induction of this patient can't be hemodynamically stable without an a-line.

You're right though, an awake a-line in skilled hands is no big deal. If the first couple attempts failed, or if a CA-1 was placing it, there's something to be said for doing it after he was asleep, just to be kind.
 
Awake a-line - no need to be a cowboy if we're gonna place an a-line anyway, I'm skilled enough to do it awake w/out causing too much pain

I'd run a sufent or remi drip during the case in addition to the gas b/c of the stable hemodynamic profile

Induction - Gentle induction, start the drip, Propofol/Etomidate, Roc, tube

Maintanance - Drip/VA, check Hct every 2 hrs or so. More if we have a lot of blood loss. Agressive transfusion with blood b/c of his cardiac history. I wouldn't let the crit drift much below 28

Extubation - Depends on airway and case. Assuming airway is easy b/c plank hasn't said anything about it, I would plan to extubate on the table unless there was a lot of blood loss and subsequent transfusion.
 
So, proceeded with case as follows:
A line and 2 big peripheral IV's, Propofol + Roc + Sufenta for induction.
Then anesthesia was maintained with Propofol infusion and Sufenta boluses.
We allowed the patient to regain 4 twitches for motor EP monitoring.
BP starts drifting from base line of 125/70 to 80/40 and not responding to Ephedrine or phenylephrine.
HR remains 55 BPM even after giving Ephedrine.
No ST changes on monitor.
ETCo2 is OK, Patient making 50cc/hr urine.
So far blood loss is 200cc and we are 1 hour through the surgery.
What's going on?
 
So, proceeded with case as follows:
A line and 2 big peripheral IV's, Propofol + Roc + Sufenta for induction.
Then anesthesia was maintained with Propofol infusion and Sufenta boluses.
We allowed the patient to regain 4 twitches for motor EP monitoring.
BP starts drifting from base line of 125/70 to 80/40 and not responding to Ephedrine or phenylephrine.
HR remains 55 BPM even after giving Ephedrine.
No ST changes on monitor.
ETCo2 is OK, Patient making 50cc/hr urine.
So far blood loss is 200cc and we are 1 hour through the surgery.
What's going on?

First, I would make sure that I wasn't injecting drugs through an infiltrated IV. Once I confirmed that the drugs were actually reaching the patient, I would be concerned about refractory hypotension due to the angiotensin II receptor blocker (atacand). I would draw up some vasopressin and administer it through the central line I placed after induction.
 
So, proceeded with case as follows:
A line and 2 big peripheral IV's, Propofol + Roc + Sufenta for induction.
Then anesthesia was maintained with Propofol infusion and Sufenta boluses.
We allowed the patient to regain 4 twitches for motor EP monitoring.
BP starts drifting from base line of 125/70 to 80/40 and not responding to Ephedrine or phenylephrine.
HR remains 55 BPM even after giving Ephedrine.
No ST changes on monitor.
ETCo2 is OK, Patient making 50cc/hr urine.
So far blood loss is 200cc and we are 1 hour through the surgery.
What's going on?

Yeah, try a little Vaso (1unit/ml) boluses.... and tell the butcher to limit his blood loss....
 
Great!
You suspect hypotension triggered by the ARB but you also think that maybe you should try first to improve the cardiac output with some Dopamine, you start at 10mcg/k/min and titrate up to 20mcg/k/min
with that the sys pressure goes from 80 to 60!
The heart rate increases from 55 to 60 :)
What happened?

Then you decide that Dopamine is probably a bad idea, you stop it and sure enough the pressure goes back to 80!

You give a vasopressin bolus and start an infusion and this barely brings the pressure to 90 even with a neo drip fully open, 5 liters of fluids, and 2 units of PRBC!
The surgery still has 3 hours to go.
Another funny thing is that the CRNA is running only Propofol 50mcg/K/min and with that the BIS monitor still in the low 30's.
The only other anesthetic is 20mcg of Sufenta that the CRNA had already given.
What are your concerns?
 
What are your concerns?

CO is low, BP is low, CPP is low --> BIS is low. Not a good sign.

Pt probably needs external pacing. Or a stronger inotropic agent, however, I would try pacing first.
 
Great!
You suspect hypotension triggered by the ARB but you also think that maybe you should try first to improve the cardiac output with some Dopamine, you start at 10mcg/k/min and titrate up to 20mcg/k/min
with that the sys pressure goes from 80 to 60!
The heart rate increases from 55 to 60 :)
What happened?

Then you decide that Dopamine is probably a bad idea, you stop it and sure enough the pressure goes back to 80!

You give a vasopressin bolus and start an infusion and this barely brings the pressure to 90 even with a neo drip fully open, 5 liters of fluids, and 2 units of PRBC!
The surgery still has 3 hours to go.
Another funny thing is that the CRNA is running only Propofol 50mcg/K/min and with that the BIS monitor still in the low 30's.
The only other anesthetic is 20mcg of Sufenta that the CRNA had already given.
What are your concerns?

So is the patient in florid CHF now? Lots of fluids given, all for the 200 cc of EBL thus far?!... You've got sucky perfusion all over the place, noggin' included with that pressure.... So once the HR increased, the pressure dropped on Dopamine? Does he have SAM? Florid CHF from all of the fluids? Is he really THAT brady cause he's over B-blocked? Starting paramaters looked alot better than this and--supposedly--your CRNA gave a whiff of anesthesia: the pump was not THAT bad and the EBL of 200 was not THAT bad. What did you guys do to the patient?:eek::laugh: Either iatrogenic florid CHF from fluid overload, or something funky within the heart.... You are on a high enough vasocontrictor dose with minimal responses...tells me that maybe the pump is not ejecting....
 
Great!
You suspect hypotension triggered by the ARB but you also think that maybe you should try first to improve the cardiac output with some Dopamine, you start at 10mcg/k/min and titrate up to 20mcg/k/min
with that the sys pressure goes from 80 to 60!
The heart rate increases from 55 to 60 :)
What happened?

Then you decide that Dopamine is probably a bad idea, you stop it and sure enough the pressure goes back to 80!

You give a vasopressin bolus and start an infusion and this barely brings the pressure to 90 even with a neo drip fully open, 5 liters of fluids, and 2 units of PRBC!
The surgery still has 3 hours to go.
Another funny thing is that the CRNA is running only Propofol 50mcg/K/min and with that the BIS monitor still in the low 30's.
The only other anesthetic is 20mcg of Sufenta that the CRNA had already given.
What are your concerns?

who the fug asked for dopamine? did i miss something?
 
Wouldn't a CVP be helpful guiding your fluid management in a patient with low EF who is going to have a 5 hours surgery with expected significant bleeding?

Why not an awake A line? I do all my A lines awake before the patient goes to the OR.

A CVP would be helpful, but I don't think it is necessary for this case as long as you have some good peripherals.

There is nothing wrong with an awake aline. I wouldn't hesitate to put this guy to sleep without an aline though.
 
So is the patient in florid CHF now? Lots of fluids given, all for the 200 cc of EBL thus far?!... You've got sucky perfusion all over the place, noggin' included with that pressure.... So once the HR increased, the pressure dropped on Dopamine? Does he have SAM? Florid CHF from all of the fluids? Is he really THAT brady cause he's over B-blocked? Starting paramaters looked alot better than this and--supposedly--your CRNA gave a whiff of anesthesia: the pump was not THAT bad and the EBL of 200 was not THAT bad. What did you guys do to the patient?:eek::laugh: Either iatrogenic florid CHF from fluid overload, or something funky within the heart.... You are on a high enough vasocontrictor dose with minimal responses...tells me that maybe the pump is not ejecting....

Although the BP dropped after dopamine there was no other sign of CHF, the SPO2 is 100%, the PIP did not change, and the blood gas remained benign except a base excess of -3.
We are unable to get the systolic pressure above 90 even with Vasopressine and Neo drips going.
Calcium chloride didn't help either.
Turned off Propofol (just to eliminate another cause of myocardial depression) and maintained anesthesia with little sevo only, this caused the BIS to start rising which I thought was reassuring (the brain still works) :D
Anyone would have tried another inotrope?
How concerned would you be about the patient waking up blind after a case like this?

The question now do we continue with the surgery or ask them to wrap it up?
 
His heart needs a kick. Took BB in am so Dobutamine in this pt is B2>B1 with resulting vasodilation.

I would try to jump start downstream and try some milrinone. Wish I had the PA now!
 
Patient may be in right ventricular failure, if you can get a a TEE probe in him it could show that, try dobutamine and some agent to decrese his afterload perhaps.
 
Although the BP dropped after dopamine there was no other sign of CHF, the SPO2 is 100%, the PIP did not change, and the blood gas remained benign except a base excess of -3.
We are unable to get the systolic pressure above 90 even with Vasopressine and Neo drips going.
Calcium chloride didn't help either.
Turned off Propofol (just to eliminate another cause of myocardial depression) and maintained anesthesia with little sevo only, this caused the BIS to start rising which I thought was reassuring (the brain still works) :D
Anyone would have tried another inotrope?
How concerned would you be about the patient waking up blind after a case like this?

The question now do we continue with the surgery or ask them to wrap it up?


Still preplexed here: his pressure went down with increased HR, no? You claim that there was no heart failure going on.... was his right heart failing? If it is right sided issues, from pulm htn for example, then consider milrinone and continue with the vaso...If on the other hand he has no RHF signs, then maybe you should continue down the differential of LHF and consider small doses of epi (if you are not concerned about SAM, etc..)...I suppose that a swan may have definitely helped here!:idea:
 
This is one of those scenarios where you're left without some monitors you'd like to have, and have to made an educated clinical guess as to whether this is a pump or SVR problem. Preload shouldn't be an issue given the volume given and EBL.

You'd love to have a TEE in this spot, you'd love to go back in time and put in a cordis + PAC, and I'd love to drop into some lines in Alaska with Noyac, but wishful thinking will have to remain just that. I would look over the recent echo to see if there was any significant TR or other evidence of right-sided pathophysiology. Assuming there isn't...

Clouding the picture here are the blockade of the beta and angiotensin systems. Preop HR was 70, so the degree of beta blockade doesn't seem inappropriate. One thing I would do is stop giving more narcotic- I'd prefer HR to be closer to 65-70 here, and the sufent isn't helping that. Anesthetized patients don't experience pain.

We don't have clinical evidence of heart failure, we have a recent negative stress test, and there are no EKG changes. So we'll assume for the time being that the heart is not ischemic, and we suspect this may be an SVR issue in the setting of a ARB + CCB + anesthetic. You've made some headway with vaso and neo. I'd give some consideration to changing the neo to the bigger gun of norepi if I truly believed the issue here was SVR and wanted to continue the case. But then you'd need a central line, and you don't have one.

My decision to continue or cancel would depend on where they were in the case, how convinced I was that ischemia/pump failure was not the issue, and whether I could get the perfusion pressure to a satisfactory level without resorting to flipping and starting a central line.

As it stands, your ABG shows that you aren't in the midst of gross systemic hypoperfusion, and by backing off the anesthesia, you've had some improvement. I'd most likely stay the course given the current data. As mentioned, I'd stop giving narcotic. You've already started gas so your MEPs are shot anyway, so I'd just titrate gas to the BIS and give a splash of midaz if I got nervous about the MAC. Continue neo/vaso. Adding milrinone could be worth a shot for some extra inotropy, but again, we're giving a lot of stuff through this PIV as it is.

If the pressures stayed low or the base deficit got worse, I'd have them wrap it up.
 
Is Dopamine the wrong choice here?
If so why?

yeah. dopamine is not advised in pts prone (pun intended) to tachyarrythmia for its propensity to exacerbate such rhythms. bad choice in this guy.

vasopressin would be my first choice as a second pressor to augment neo in a pt on an ARB; I routinely hang it when i know i have a spine patient on and ARB or ACEI. second choice might be levophed +/- milrinone.

but - this case should not continue to its finale as is. if this guy looks this poorly on neo and vaso after fluids with only 200mL EBL, something else is going on and you should tell surg dude to close shop and get outta dodge, or figure out what's wrong and fix it before proceeding. guy isn't gonna tolerate any other blood loss.

i assume that before you maxed the neo and vasopressin and gave 5L! of fluid for an EBL of 200mL you did some troubleshootin of your BP measurement and aline, ie the waveform isn't damped, you can draw back, you've checked NIBP's on a cuppla limbs. it seems your low BP is one variable out of context with the rest of your data. palpate some pulses.

if the BP is truly that smarmy on that much support, get someone (not me) good enough to throw in a TEE probe prone and get some more data. or, close up shop and wake him up.
 
has vasopressin been shown to be particularly the best pressor for ARB/ACEI related hypotension in the OR?
 
Still preplexed here: his pressure went down with increased HR, no? You claim that there was no heart failure going on.... was his right heart failing? If it is right sided issues, from pulm htn for example, then consider milrinone and continue with the vaso...If on the other hand he has no RHF signs, then maybe you should continue down the differential of LHF and consider small doses of epi (if you are not concerned about SAM, etc..)...I suppose that a swan may have definitely helped here!:idea:
Great reasoning, except that there was really no heart rate increase with Dopamine (went from 55 to 60).
 
Dopamine is an easily available positive inotrope and I wanted to give the heart a little push before increasing the afterload further since we really were just guessing at that point.
The point about tachyarrhythmias is well taken though. Milrinone would have probably been a smarter choice.
The funny thing is that Dopamine did not increase the heart rate and lowered the blood pressure!
As for checking the monitors and making sure the A line is working, this was done.
As for the volume of crystaloids given, you have to remember that when you are working with CRNA's you are not in the room all the time, I wouldn't have given that much but it was done and my job is to deal with it!


yeah. dopamine is not advised in pts prone (pun intended) to tachyarrythmia for its propensity to exacerbate such rhythms. bad choice in this guy.

vasopressin would be my first choice as a second pressor to augment neo in a pt on an ARB; I routinely hang it when i know i have a spine patient on and ARB or ACEI. second choice might be levophed +/- milrinone.

but - this case should not continue to its finale as is. if this guy looks this poorly on neo and vaso after fluids with only 200mL EBL, something else is going on and you should tell surg dude to close shop and get outta dodge, or figure out what's wrong and fix it before proceeding. guy isn't gonna tolerate any other blood loss.

i assume that before you maxed the neo and vasopressin and gave 5L! of fluid for an EBL of 200mL you did some troubleshootin of your BP measurement and aline, ie the waveform isn't damped, you can draw back, you've checked NIBP's on a cuppla limbs. it seems your low BP is one variable out of context with the rest of your data. palpate some pulses.

if the BP is truly that smarmy on that much support, get someone (not me) good enough to throw in a TEE probe prone and get some more data. or, close up shop and wake him up.
 
Excellent post!
This is exactly how I saw it, patient is hypotensive, but clinically the picture did not look too bad.
I had to focus on the idea that the patient took a Beta bolcker, An ARB and a calcium channel blocker THIS MORNING.
The combination of these drugs with Sufnta is the main issue here.
I can't reverse the effects of the antihypertensive medications but I can reverse Sufentanyl, should I do it?


This is one of those scenarios where you're left without some monitors you'd like to have, and have to made an educated clinical guess as to whether this is a pump or SVR problem. Preload shouldn't be an issue given the volume given and EBL.

You'd love to have a TEE in this spot, you'd love to go back in time and put in a cordis + PAC, and I'd love to drop into some lines in Alaska with Noyac, but wishful thinking will have to remain just that. I would look over the recent echo to see if there was any significant TR or other evidence of right-sided pathophysiology. Assuming there isn't...

Clouding the picture here are the blockade of the beta and angiotensin systems. Preop HR was 70, so the degree of beta blockade doesn't seem inappropriate. One thing I would do is stop giving more narcotic- I'd prefer HR to be closer to 65-70 here, and the sufent isn't helping that. Anesthetized patients don't experience pain.

We don't have clinical evidence of heart failure, we have a recent negative stress test, and there are no EKG changes. So we'll assume for the time being that the heart is not ischemic, and we suspect this may be an SVR issue in the setting of a ARB + CCB + anesthetic. You've made some headway with vaso and neo. I'd give some consideration to changing the neo to the bigger gun of norepi if I truly believed the issue here was SVR and wanted to continue the case. But then you'd need a central line, and you don't have one.

My decision to continue or cancel would depend on where they were in the case, how convinced I was that ischemia/pump failure was not the issue, and whether I could get the perfusion pressure to a satisfactory level without resorting to flipping and starting a central line.

As it stands, your ABG shows that you aren't in the midst of gross systemic hypoperfusion, and by backing off the anesthesia, you've had some improvement. I'd most likely stay the course given the current data. As mentioned, I'd stop giving narcotic. You've already started gas so your MEPs are shot anyway, so I'd just titrate gas to the BIS and give a splash of midaz if I got nervous about the MAC. Continue neo/vaso. Adding milrinone could be worth a shot for some extra inotropy, but again, we're giving a lot of stuff through this PIV as it is.

If the pressures stayed low or the base deficit got worse, I'd have them wrap it up.
 
Excellent post!
This is exactly how I saw it, patient is hypotensive, but clinically the picture did not look too bad.
I had to focus on the idea that the patient took a Beta bolcker, An ARB and a calcium channel blocker THIS MORNING.
The combination of these drugs with Sufnta is the main issue here.
I can't reverse the effects of the antihypertensive medications but I can reverse Sufentanyl, should I do it?


Monday morning quarterback here. We use a lot of remi for our backs. In this case, I think it would have been a better choice for obvious reasons. Still shaking my head about giving a patient with a mediocre EF 5L of crystals.
 
DA at 10mcg/kg/min theoretically predominantly beta effects...pt is on a beta blocker, hence more of beta2 response dropping his afterload, hence bp...

is the underlying issue some type of a neurogenic shock secondary to a surgical move...
 
just another reason why most of world works without mid level providers..... best of luck with the pt, though
 
MAP-CVP=COxSVR=HR*SV*SVR=preload*afterload*contractility*HR*SVR

your preload is fine s/p 5 Liters, if anything you may be overdistended and falling off the Starling curve.

-however - patient may have converted from sinus into a-fib (rate controlled cause he's already b-blocked) and lost his atrial kick. i would take a close look at the underlying rhythm.

afterload - will use SVR as a proxy may still be low (will leave wall tension out for now). i think if you truly wanted to control the SVR, norepi would be my choice. if pressure doesn't come up after a bit of NE, i would be satisfied that SVR is not the issue in this case.

contractility may be an issue if patient is hypocalcemic (which he is not) or ischemic which may be silent without ekg change. nothing to be done for this. already on asa, beta blocked, on oxygen. and you're not going to give NTG due to hypotension.


HR - may be an issue. maybe a touch of glyco/a bit of narcan (40mcg boluses q3 min until effect) could do the trick here (brady secondary to opioid?).
pacing may help, but, with external pads all you can do is essentially VVI, so while you increase the HR you may decrease preload from eliminating a timely atrial contraction.
 
Here is what happened:
Told the surgeon that I am going to give a muscle relaxant so they are going to have to live with absent motor evoked potentials for a while.
Gave 20 mg of Rocuronium to avoid patient movement if anesthesia got lighter, increased Sevo a little, then gave 100mcg of Naloxone.
2 minutes later the BP started to rise and we were able to get off the vasopressin and the neo.
Rest of case went smoothly.
Postop patient did great.
IMHO this was simply the combination of effects of beta blocker + ARB + calcium channel blocker + Sufenta.
The Dopamine caused hypotension because (as someone mentioned) we got an unopposed beta 2 effect.
I learned that vasopressin is not always the solution in these cases.
I also learned to have a lower threshold to place cenral access in these patients.
 
Here is what happened:
Told the surgeon that I am going to give a muscle relaxant so they are going to have to live with absent motor evoked potentials for a while.
Gave 20 mg of Rocuronium to avoid patient movement if anesthesia got lighter, increased Sevo a little, then gave 100mcg of Naloxone.
2 minutes later the BP started to rise and we were able to get off the vasopressin and the neo.
Rest of case went smoothly.
Postop patient did great.
IMHO this was simply the combination of effects of beta blocker + ARB + calcium channel blocker + Sufenta.
The Dopamine caused hypotension because (as someone mentioned) we got an unopposed beta 2 effect.
I learned that vasopressin is not always the solution in these cases.
I also learned to have a lower threshold to place cenral access in these patients.

I woulda squirted a little epi there, no big harm in small doses....but that's just me.
 
Here is what happened:
Told the surgeon that I am going to give a muscle relaxant so they are going to have to live with absent motor evoked potentials for a while.
Gave 20 mg of Rocuronium to avoid patient movement if anesthesia got lighter, increased Sevo a little, then gave 100mcg of Naloxone.
2 minutes later the BP started to rise and we were able to get off the vasopressin and the neo.
Rest of case went smoothly.
Postop patient did great.
IMHO this was simply the combination of effects of beta blocker + ARB + calcium channel blocker + Sufenta.
The Dopamine caused hypotension because (as someone mentioned) we got an unopposed beta 2 effect.
I learned that vasopressin is not always the solution in these cases.
I also learned to have a lower threshold to place cenral access in these patients.

How much Sufenta was given? did it match the 5L of cristalloid?
 
I can't remember the name of the study but there was a New England Journal article showing improved mortality when AICD's are placed in patients with low EF's (<35%?) That's why he's borderline.

MADIT-II study randomized approximately 1200 post-infarction patients with an ejection fraction of </=30% to ICD or conventional therapy. In the ICD group, they found a 30% decrease in the risk of total mortality.
 
Top