How would you do this induction?

[sevoflurane]

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These threads are great.

Love these threads. Wish we had more of them.

 

[Arch Guillotti]

That said, she won't be an easy spinal and my real world answer is give her 2 units of FFP over 2 hours then proceed with the case under Isobaric SAB. I would do a single shot technique. An arterial line sounds like a good idea in the holding area or prior to the SAB.

What is the utility of giving FFP when the INR is 1.5? The INR of FFP is supposed to be around 1.5 so I don't really think you are accomplishing anything except exposing her to some unnecessary risks.

I might just do an isobaric bupi single shot spinal and call it a day😱. Clean pass with 22 guage quincke with an arterial line beforehand. I would have a great IV or two but skip the CVC and PA cath.

good case BTW and count me in the group that loves to use a little vasopressin every now and then. I would place an ETT (definitely not an LMA) but that just me. Some sort of block to minimize discomfort afterwards and also minimize opiod use.

 

[Ignatius J]

I think that hypoventilation/hypoxia (i.e. need for nasal trumpet/jaw thrust/etc, even LMA with spontaneous ventilation) could kill this pt with severe pulm htn and poor LV function. This chick sounds like she's right on the tipping point and any nudge up on her pulmonary pressures could cease all forward flow. If I couldn't do a regional technique, I'd go ETT/controlled ventilation/slow controlled wakeup in the OR vs ICU with little/no elevation of CO2. Pulmonary htn is one of the few disease processes that really tightens my sphincter, and if you don't respect it it will bite you in the ass someday.

I see your point, but to me, the fact that general anesthesia can really create V/Q mismatch and be a direct antagonist in optimizing oxygenation makes me want to avoid general anesthesia. That and the fact that the inhalational agents just have way to many cardiovascular effects.

If you use remifentantil the right way, you can keep the patient arousable enough to not worry about apnea. Worst case-scenario you do a jaw thrust and consider going to GA as the patient keeps going apneic. But I think it's worth trying a regional approach with minimal sedation first.

I did a hip on a guy with 20% EF with an epidural the other week. It worked great. Bolused it up and gave him 5cc of 2% lidocaine through the epidural every 45 minutes to an hour.

I'm just not comfortable putting this patient to sleep. My whole plan revolves around minimizing cardiovascular insults and keeping them spontaneously breathing.

Good discussion. There is more than one way to skin a cat.

 

[nap$ter]

nice thread. tough spot.

epi is an under-utilized drug. this lady's pHTN is largely due to her valvular dysfxn, and her RV is failing at baseline. she needs to be fastish, fullish, and forwardish. i mighta started an epi gtt with induction and used those 5-10ug bolusses you had ready instead of phenylephrine.

otherwise would have done the same.

 

[cincincyreds]

Why fast, full, and forward here with pulmonary hypertension. Also, why is vasopressin useful here? Always enjoy learning new things.

 

[Mman]

It's doubtful her lumbar fusion was L2-S1. Most likely she had a 1 or 2 level lumbar fusion 20 years ago meaning a spinal is still an option.

That said, she won't be an easy spinal and my real world answer is give her 2 units of FFP over 2 hours then proceed with the case under Isobaric SAB. I would do a single shot technique. An arterial line sounds like a good idea in the holding area or prior to the SAB.

Of course, I'd make sure the family and surgeon know there is a significant chance (?50%) the patient won't survive the perioperative course. They need to be prepared for that outcome. This would follow along with my suggestion that the patient is too sick for General anesthesia and needs a Spinal after getting the FFP.

Would my outcome be any different? Would she survive the operation then die on POD 1 or POD 2? I just prefer that they don't die in the operating room if at all possible.

I'd rather do the spinal with an INR of 1.5 than potentially worsen her CHF or pulmonary function by transfusing multiple units of FFP. There's no need. The risk of spinal hematoma is so tiny as it is.

 

[nap$ter]

Why fast, full, and forward here with pulmonary hypertension. Also, why is vasopressin useful here? Always enjoy learning new things.

"ish". MR and wide open TR in the setting of pHTN. promote forward cardiac output. inotropy and a bit of chronotropy would serve this lady well.

i assume vasopressin has been mentioned given its touted selectivity for the systemic vasculature over the pulmonary vasculature. however, i wouldn't give this lady any pressor without inotropy in the setting of decreased cardiac output.

 

[sevoflurane]

"ish". MR and wide open TR in the setting of pHTN. promote forward cardiac output. inotropy and a bit of chronotropy would serve this lady well.

i assume vasopressin has been mentioned given its touted selectivity for the systemic vasculature over the pulmonary vasculature. however, i wouldn't give this lady any pressor without inotropy in the setting of decreased cardiac output.

Yep. IMO, in this patient particular patient, you may wish to give vaso with something like milronone or dobutamine. A little too much hastle for me when I can use Norepi and get contractility and avoidence of likely tachycardia/O2 demand in an ICM low EF patient. Don't want to tip the scale too much.

Otherwise, vaso is a great drug to use when getting in a pickle. I've seen the ACE-I hypotension post induction/resistant to pressors a handful of times. These patients have always been very responsive to vasopressin.

 

[epidural man]

Here's the (actual) case:

93 year-old lady comes in with a broken hip and is booked for a TFN. She has an ICM, echo last month showed an EF of 15-20% (yes, really) with PASP estimated at 90 mmHg. Large RV, 2-3+ MR and wide open TR. Labs show an INR of 1.5, Cr of 1.9, normal platelets and moderate anemia (9 / 28). PSH includes a lumber fusion 20 years ago. Hospice was discussed with patient and family and refused. They desire to proceed...

Your move, doctor!

1. No question...spinal.

2. If I can't get it - FI cath with very mild sedation.

3. Send that CRNA home that gave the versed. Tell them to go study or something. 1mg to a 93 y/o? Holy crap.

 

[narcusprince]

So, I brought your case up today at the "mecca" of cardiac surgery with some of our senior cardiac staff. It was a consensus regarding the induction. Placing an LMA would be dangerous in this patient they were not concerned about positive pressure ventilation inhibiting preload and or adding to the pulmonary hypertension. For induction, the consensus was pre-induction aline(as discussed), Induction drugs Succinycholine and Etomidate and a little bit of fentanyl and secure the airway ASAP. No one thought that placing a pre-induction central would be of any use unless you wanted to run vasopressors throughout induction. Post- induction a central line would be very helpful. As far as vasopressors of choice Phenylephrine is a horrible choice int his scenario because this patient has severe MR and what determines forward flow in MR lower after load and if you increase the after load with wide open MR you basically ejecting blood back into the pulmonary side with each heartbeat. What you need is more forward flow IE epinephrine and probably Norepinephrine remember it has B-1 as we'll as alpha 1 effects. Back to this patients EF of 15% with 3+ MR how much flow is really going forward? This case is a real Kobayashi-Maru (100 bucks to whomever gets this reference). Midazolam in the prep area by your CRNA just awarded herself an earlier day home.

 

[ssmallz]

So, I brought your case up today at the "mecca" of cardiac surgery with some of our senior cardiac staff. It was a consensus regarding the induction. Placing an LMA would be dangerous in this patient they were not concerned about positive pressure ventilation inhibiting preload and or adding to the pulmonary hypertension. For induction, the consensus was pre-induction aline(as discussed), Induction drugs Succinycholine and Etomidate and a little bit of fentanyl and secure the airway ASAP. No one thought that placing a pre-induction central would be of any use unless you wanted to run vasopressors throughout induction. Post- induction a central line would be very helpful. As far as vasopressors of choice Phenylephrine is a horrible choice int his scenario because this patient has severe MR and what determines forward flow in MR lower after load and if you increase the after load with wide open MR you basically ejecting blood back into the pulmonary side with each heartbeat. What you need is more forward flow IE epinephrine and probably Norepinephrine remember it has B-1 as we'll as alpha 1 effects. Back to this patients EF of 15% with 3+ MR how much flow is really going forward? This case is a real Kobayashi-Maru (100 bucks to whomever gets this reference). Midazolam in the prep area by your CRNA just awarded herself an earlier day home.

I agree that you don't need a central line for induction but once you start inducing, place the tube, and start PPV, this pts BP is gonna go down the toilette. Do you really wanna be farting around w/a central at this point? Under optimal conditions it's gonna take 10 minutes to place from positioning to flushing. If we agree that we expect to run a pressor through your CVC during the case, why wait until the pt is crashing before we place the line? Just place it awake when the pt is still stable that way when the pt crumps you can just start your drip ASAP.

The other point that needs to be made is that a lot of us don't work in academic institutions where there is someone to take care of the pt while you place the line. This is another pro for placing it preinduction

 

[pseudoknot]

This case is a real Kobayashi-Maru (100 bucks to whomever gets this reference).

Only one man ever beat it, but he cheated.

 

[pgg]

This case is a real Kobayashi-Maru (100 bucks to whomever gets this reference).

In a world with Google and Wikipedia, you're going to go broke quick placing bets like that. 😀

 

[Idiopathic]

i kind of feel like when you talk about epi and forward flow, to some degree you are relying on the right heart to help out the left heart and vice versa, but this lady also had WIDE OPEN TR...probably what she needed was more volume then she could tolerate, just to help offset the regurgitant flow. i assume any dramatic increase in inotropy and afterload would lead to increased pulmonary HTN and consequently, as her pulmonary pressure crept up, she would have a greater component of regurgitant flow than forward flow. i think neo is in general a poor choice for someone with severe cardiomyopathy (i also think vasopressin is a terrible choice). in a perfect world milrinone and epi infusions and inhaled flolan is the way i would go but thats hindsight.

sorry the case went this way for you, we all learn from these things. thanks for sharing.

edit:btw, i think she had a 95% chance of dying on induction regardless of what you did, given the picture painted.

 

[sevoflurane]

Placing an LMA would be dangerous in this patient they were not concerned about positive pressure ventilation inhibiting preload and or adding to the pulmonary hypertension.

I respectfully disagree. Placing an LMA is not dangerous. If it's delivering good TV's/effectively ventilating the patient and you are monitoring ETCO2 why would it be dangerous? If anything, you are not paralyzing/reversing and adding PPV post induction in a likely hypovolemic patient with a big RV and low EF. Remember, surgical time = 15 minutes. She's an easy AW; you can have PVC down the trachea in seconds.
There is no right answer as there are positives and negatives to both approaches. But to call an LMA dangerous is not correct IMO.

Just my 2 cents.

 

[amyl]

agree w ETT (being an anesthesiologist i am a control freak and want to manipulate ventilation as i see fit 🙂, preop aline, etomidate not propofol, long talk w family and a syringe of vaso... we also do 20 in 20 and yes, its saved the day for me a time or two as well. would also want central line as i want all vasopressor options on the table ;-) i favor TEE over swan to make sure shes fluid optomized so i can walk the line between low EF and regurgitant AV valves... feel like placement of TEE is justified in this case tho i am sure some of the pp guys will say thats overkill.
gosh its going to be a hard transition from my beloved CCF to private practice 🙂

good case, many thanks for posting

 

[Idiopathic]

I respectfully disagree. Placing an LMA is not dangerous. If it's delivering good TV's/effectively ventilating the patient and you are monitoring ETCO2 why would it be dangerous? If anything, you are not paralyzing/reversing and adding PPV post induction in a likely hypovolemic patient with a big RV and low EF. Remember, surgical time = 15 minutes. She's an easy AW; you can have PVC down the trachea in seconds.
There is no right answer as there are positives and negatives to both approaches. But to call an LMA dangerous is not correct IMO.

Just my 2 cents.

ill respectfully disagree with you, a general under LMA with spontaneous ventilation mandates a small amount of hypercarbia, as we saw in this patient, that could perhaps be fatal (i believe she got hypotensive over hypercarbic, but I believe either could do it). i would induce, take over ventilation and secure the airway quickly.

 

[sevoflurane]

ill respectfully disagree with you, a general under LMA with spontaneous ventilation mandates a small amount of hypercarbia, as we saw in this patient, that could perhaps be fatal (i believe she got hypotensive over hypercarbic, but I believe either could do it). i would induce, take over ventilation and secure the airway quickly.

Not SV. Gentle induction + LMA with say 10 of PS and a backup rate. LMA does not mandate hypercarbia IMO.

 

[sevoflurane]

I understand you guys who want to secure the AW with an ETT from the get go.

 

[lgher]

as a side note: in a patient who took their AM ACE inhibitor with refractory post induction hypotension, how much Vasopressin have you required to conteract their hypotension, and how long has this hypotension persisted? based on past experience....

I recall a recent 80 something year old who I was up to about 10 U of vasopressin about 1 hour post induction before her BP settled (maybe she was the type of old lady who was gonna need a pressor infusion to keep a reasonable BP regardless of whether she was on an ACE I or not?)

 

[Mman]

So, I brought your case up today at the "mecca" of cardiac surgery with some of our senior cardiac staff. It was a consensus regarding the induction. Placing an LMA would be dangerous in this patient they were not concerned about positive pressure ventilation inhibiting preload and or adding to the pulmonary hypertension.

If you ask people who do hearts all day every day, they will never choose an LMA in any patient because they never use them. If you are a hammer, everything is a nail.

An LMA can be safely used, but it requires skill and close monitoring. I see no problem with the patient generating her own breaths with a little positive pressure assistance to ensure adequate ventilation. Heck, you cold breathe her down with sevo and just slip it in between breaths and let her keep chugging right along.



But yes, there is no right answer. It's a bad situation.

 

[jwk]

agree w ETT (being an anesthesiologist i am a control freak and want to manipulate ventilation as i see fit 🙂, preop aline, etomidate not propofol, long talk w family and a syringe of vaso... we also do 20 in 20 and yes, its saved the day for me a time or two as well. would also want central line as i want all vasopressor options on the table ;-) i favor TEE over swan to make sure shes fluid optomized so i can walk the line between low EF and regurgitant AV valves... feel like placement of TEE is justified in this case tho i am sure some of the pp guys will say thats overkill.
gosh its going to be a hard transition from my beloved CCF to private practice 🙂

good case, many thanks for posting

ill respectfully disagree with you, a general under LMA with spontaneous ventilation mandates a small amount of hypercarbia, as we saw in this patient, that could perhaps be fatal (i believe she got hypotensive over hypercarbic, but I believe either could do it). i would induce, take over ventilation and secure the airway quickly.

If you ask people who do hearts all day every day, they will never choose an LMA in any patient because they never use them. If you are a hammer, everything is a nail.

An LMA can be safely used, but it requires skill and close monitoring. I see no problem with the patient generating her own breaths with a little positive pressure assistance to ensure adequate ventilation. Heck, you cold breathe her down with sevo and just slip it in between breaths and let her keep chugging right along.

But yes, there is no right answer. It's a bad situation.

It really is striking to see how differently these cases would be done in private practice vs academia. Honestly though - these truly are bread-and-butter cases in private practice that we see every day. They just don't get us that excited or worried. Old people with busted hips almost always have a half dozen significant comorbidities. None of them are "ASA I o/w healthy 90 y/o female". We're simply not going to put a bunch of invasive monitors into these patients. TEE? Not a chance. CVP/Swan? Not even in the thought process unless they have poor peripheral access.

The FI blocks are an interesting idea - I've never seen one done, but we've only been going block-crazy for about a year, so it wouldn't surprise me to see that coming before long.

 

[Arch Guillotti]

It really is striking to see how differently these cases would be done in private practice vs academia. Honestly though - these truly are bread-and-butter cases in private practice that we see every day. They just don't get us that excited or worried. Old people with busted hips almost always have a half dozen significant comorbidities. None of them are "ASA I o/w healthy 90 y/o female". We're simply not going to put a bunch of invasive monitors into these patients. TEE? Not a chance. CVP/Swan? Not even in the thought process unless they have poor peripheral access.

I don't care how slick the surgeons are and your group may be the greatest thing since sliced bread, but my opinion is that a decrepit patient with a PA pressure of 90 mm Hg is not a slam-dunk any day of the week.

I see plenty of sick old gomers with busted hips. I don't see a PASP of 90 very often though.

The EF doesn't bother me much and I wouldn't put a PA cath/CVP/TEE in this patient either.

 

[ssmallz]

I don't care how slick the surgeons are and your group may be the greatest thing since sliced bread, but my opinion is that a decrepit patient with a PA pressure of 90 mm Hg is not a slam-dunk any day of the week.

I see plenty of sick old gomers with busted hips. I don't see a PASP of 90 very often though.

The EF doesn't bother me much and I wouldn't put a PA cath/CVP/TEE in this patient either.

I really think a CVC is absolutely necessary in the case b/c of this pts MR, TR, and pHTN. Given the pts echo and age, you know you're going to need to run a pressor and neo is probably the worst option for this pt. If we need to run norepi, dobutamine, milranone, epi, or some combination you really should run it though a central line. I've stated the reasons I feel it should be placed preop but I understand why others are advocating for it post induction.

As for a PA cath, it would be nice to use to monitor your drips effects on the PA pressures and that's what I would use it for but given the outcome data on PACs I can understand why a lot of people wouldn't want use it. FWIW, when I have a pt w/pHTN and I don't expect to run a drip I wouldn't opt for a PAC

 

[Arch Guillotti]

We are going to have to agree to disagree on this one although I might change my mind after laying eyes on the patient.

I think an arterial line is a necessity preinduction.

I will take a large bore free flowing PIV though for the case, particularly if it is placed in the EJ.

This pulm htn is no joke and can be a killer though.

I really think a CVC is absolutely necessary in the case b/c of this pts MR, TR, and pHTN. Given the pts echo and age, you know you're going to need to run a pressor and neo is probably the worst option for this pt. If we need to run norepi, dobutamine, milranone, epi, or some combination you really should run it though a central line. I've stated the reasons I feel it should be placed preop but I understand why others are advocating for it post induction.

As for a PA cath, it would be nice to use to monitor your drips effects on the PA pressures and that's what I would use it for but given the outcome data on PACs I can understand why a lot of people wouldn't want use it. FWIW, when I have a pt w/pHTN and I don't expect to run a drip I wouldn't opt for a PAC

 

[nap$ter]

I don't care how slick the surgeons are and your group may be the greatest thing since sliced bread, but my opinion is that a decrepit patient with a PA pressure of 90 mm Hg is not a slam-dunk any day of the week.

I see plenty of sick old gomers with busted hips. I don't see a PASP of 90 very often though.

The EF doesn't bother me much and I wouldn't put a PA cath/CVP/TEE in this patient either.

yeah. that. c the leaky valves and big ol' RV.

no offense, jwk, but if you or your group apply your cooky-cutter LOL (lil'ol'lady) recipe to this gal (and i gotta call the utter BS of you calling this lady your bread and butter), she's gonna die.

oh yeah, that's what happened.

 

[Mman]

question for people that want to put a PA cath in these patients. How long are you going to try to get it to float? I ask because in somebody with that high of a PA pressure and wide open TR, it might be a tad tricky to get it to float forward.

If you would want a PA cath, at what point would you give up?

 

[narcusprince]

Correct me if I am wrong. This patient has 3-4+ MR now with a dilated ventricle with poor EF 15%. Her Pulmonary hypertension is a result of her MR which in turn is why she more than likely has elevated RV pressures which leads me to believe thats why she has wide open tricuspid regurgitation. Also her RV is probably dilated too worsening the regurgitation around the tricuspid valve. Everything is at a tipping point EF drops pulmonary pressures rise RV pressures increase and CVP goes up. With all the valves in regurgitant failure CVP pressures are all i need to know that the patient is in RV failure we know she is in LV failure and the treatment for a poor EF is epi/dobutamine and levophed. I think the only way to help her poor RV and TR is forward flow. So a PA catheter is not going to tell me much more, also the time to float the damn thing with wide open TR the nail will be in place.

 

[ssmallz]

question for people that want to put a PA cath in these patients. How long are you going to try to get it to float? I ask because in somebody with that high of a PA pressure and wide open TR, it might be a tad tricky to get it to float forward.

If you would want a PA cath, at what point would you give up?

I would give a solid attempt or 2 but wouldn't persist if it doesn't go easy. I want it mainly to titrate my drips for pulmonary pressures and making sure my interventions are optimizing the PA pressures. The numbers are helpful but that doesn't necessarily mean a better outcome which is why I wouldn't persist if things didn't go smoothly.

 

[proman]

Correct me if I am wrong. This patient has 3-4+ MR now with a dilated ventricle with poor EF 15%. Her Pulmonary hypertension is a result of her MR which in turn is why she more than likely has elevated RV pressures which leads me to believe thats why she has wide open tricuspid regurgitation. Also her RV is probably dilated too worsening the regurgitation around the tricuspid valve. Everything is at a tipping point EF drops pulmonary pressures rise RV pressures increase and CVP goes up. With all the valves in regurgitant failure CVP pressures are all i need to know that the patient is in RV failure we know she is in LV failure and the treatment for a poor EF is epi/dobutamine and levophed. I think the only way to help her poor RV and TR is forward flow. So a PA catheter is not going to tell me much more, also the time to float the damn thing with wide open TR the nail will be in place.

I'm not sure how this patient turned into someone with life-threatening MR. Here's the original post:

93 year-old lady comes in with a broken hip and is booked for a TFN. She has an ICM, echo last month showed an EF of 15-20% (yes, really) with PASP estimated at 90 mmHg. Large RV, 2-3+ MR and wide open TR.

Grading of MR is still subjective, 2-3+ MR is not usually associated with pulmonary hypertension. While severe MR is a sometimes a cause of secondary pulmonary hypertension, I don't think it's the leading cause in this patient. She certainly could have intrinsic lung disease, decreased ventricular compliance, or even primary pHTN. While her RV is reported to be dilated, it's able to generate extremely high RV systolic pressures. This is a sign that the RV isn't about to fail (unless we make it fail with hypoxia, ischemia or hypercarbia). When you see an estimated PASP by echo, it's based on the simplified Bernoulli equation of the maximum velocity of the TR jet. Without a right heart cath, we really have no idea what her true PA pressures are. People seem to be focusing way too much on the low EF or the MR or even the pulmonary hypertension. The single most important thing is her baseline functional status. The induction should be based on one that protects the right heart by maintaining perfusion pressure (the arterial line), avoid hypoxia and hypercarbia (secure the airway ASAP and control ventilation). Liberal phenylephrine to stay out of trouble and epi if you get into trouble.

One last point: in TR the CVP is absolutely worthless (it's mostly worthless otherwise). Maybe you could use the trend, but even that is of questionable value. What would be a huge mistake is to assume that a rising CVP is indicative of a LV failure. I guarantee that this 93 year old sick heart has significant impaired relaxation and measured venous or PA pressures will not necessarily reflect LVEDP.

 

[Arch Guillotti]

The induction should be based on one that protects the right heart by maintaining perfusion pressure (the arterial line), avoid hypoxia and hypercarbia (secure the airway ASAP and control ventilation). Liberal phenylephrine to stay out of trouble and epi if you get into trouble.

I think this is very well put and sums up the approach to this old bird; whatever your technique.

 

[dhb]

I would give a solid attempt or 2 but wouldn't persist if it doesn't go easy. I want it mainly to titrate my drips for pulmonary pressures and making sure my interventions are optimizing the PA pressures. The numbers are helpful but that doesn't necessarily mean a better outcome which is why I wouldn't persist if things didn't go smoothly.

Sorry ssmall but this patient is dead and everybody knows it, what you don't want to be is the straw that is going to break the dead camel's back.
A-line yes but a Swan for what should be a < 30 min procedure is just asking for trouble. You can send her into a-fib, rupture her RV or AP + you won't be 100% focused on the patient while you're doing the procedure. As the OP said she tanked in the blink of a eye.
Keep her alive for 30min and let her go on someone else's watch

 

[ssmallz]

Sorry ssmall but this patient is dead and everybody knows it, what you don't want to be is the straw that is going to break the dead camel's back.
A-line yes but a Swan for what should be a < 30 min procedure is just asking for trouble. You can send her into a-fib, rupture her RV or AP + you won't be 100% focused on the patient while you're doing the procedure. As the OP said she tanked in the blink of a eye.
Keep her alive for 30min and let her go on someone else's watch

I'm advocating for doing this stuff prior to induction. Once you induce this pt the most important thing is gettin her outta the OR and into the ICU asap b/c like you said she's dead anyway so anymore time spent under anesthesia than is absolutely necessary is bad. Under optimal conditions I'd want it but I would certainly proceed w/out it. I want it because I expect to be titrating drips and I'm certainly concerned enough about their effect on the PA pressures and it's effects on the RV to warrant monitoring.

 

[sketchy9]

Here's the (actual) case:

93 year-old lady comes in with a broken hip and is booked for a TFN. She has an ICM, echo last month showed an EF of 15-20% (yes, really) with PASP estimated at 90 mmHg. Large RV, 2-3+ MR and wide open TR. Labs show an INR of 1.5, Cr of 1.9, normal platelets and moderate anemia (9 / 28). PSH includes a lumber fusion 20 years ago. Hospice was discussed with patient and family and refused. They desire to proceed...

Your move, doctor!

Wow, a lot of cavalier attitudes here. First off, the LVEF of 15-20% in the setting of mod-severe MR means means her actual forward flow is a lot worse than that. Most of the 20% is going back into the LA. I can't stress enough how concerning the PASP pressure is to me. I'm not sure what her systemic pressure was, but if we assume that the PA pressure is 3/4 systolic that means she is at high risk for RV ischemia and subsequent RV failure. The RV is notoriously resistant to inotropes, so once it starts to go down that's it. The RV must be protected, almost at all costs.

There are several ways to approach this patient. This is not a true "emergency", in the sense it needs to go NOW. Given the patient has severe pulmonary HTN in the setting of ischemc cardiomyopathy, I would opt for the following: she gets admitted to the ICU pre-op and swanned, and subsequently "optimized". That means several things. First, it means seeing what her true PA pressure is, and second, likely means some diuresis to minimize her PA pressure. It may also mean iNO, depends on how she repsonds to diuresis. Also, an IABP should be considered, especially considering she has known CAD (ICM). That will improve both forward flow from the LV by decreasing afterload, as well as improving perfusion to both ventricles. That might take 24-36h, but so be it.

For induction, she needs an art line awake and central access for pressor/infusion administration (both of which should have been done pre-op in the ICU). I would induce with etomidate & roc and intubate. Pressors I would have available are epi and vasopressin and I would have iNO available as well. I would avoid agents that have alpha effects such as phenylephrine and even levo. The rationale is that the pulmonary vascular circulation has alpha receptors but minimal to no V1 receptors-- hence why vaso is a good choice in order to avoid further increases in PVR.

I would plan to keep her intubated post-op unless she can show me a good reason why she should be extubated. In general with severe pulm HTN you want to avoid prolonged intubation, but I think in a geriatric patient who will be sensitive to all sedatives, it is better to have her fully awake before extubation, and that might require a few hours. Also, it will allow reliable iNO delivery if necessary. Now, it may be the case that she's wide awake at the end of surgery and her agitation on the tube will increase her PAP. Fine, in that case it's reasonabe to extubate if she meets other criteria.

As a disclaimer, I work in a large tertiary (quarternary?) academic hospital in the second largest city in the U.S., and I'm a cardiac anesthesiologist. That probably means my ideas are more invasive and labor- and time-intensive than what most level 1- and 2-centers would do. Fair enough. In the so-called real world, there may not be time, motivation, and money to properly optimize a patient like this. All I can tell you is what I would consider to be appropriate care for this patient and would give her the best chance of surviving both the operation and the post-op course. If I saw this patient on my schedule, I wouldn't think twice about implementing the plan I've laid out. I've seen enough M&M with these types of patients to be very cautious.

-R

 

[dhb]

All I can tell you is what I would consider to be appropriate care for this patient and would give her the best chance of surviving both the operation and the post-op course.

No the best chance of surviving the peri-operative period is not to do the case.
What you say is fine but a bit expensive for someone who is not going to make it out of the hospital.

 

[cincincyreds]

Wow, a lot of cavalier attitudes here. First off, the LVEF of 15-20% in the setting of mod-severe MR means means her actual forward flow is a lot worse than that. Most of the 20% is going back into the LA. I can't stress enough how concerning the PASP pressure is to me. I'm not sure what her systemic pressure was, but if we assume that the PA pressure is 3/4 systolic that means she is at high risk for RV ischemia and subsequent RV failure. The RV is notoriously resistant to inotropes, so once it starts to go down that's it. The RV must be protected, almost at all costs.

There are several ways to approach this patient. This is not a true "emergency", in the sense it needs to go NOW. Given the patient has severe pulmonary HTN in the setting of ischemc cardiomyopathy, I would opt for the following: she gets admitted to the ICU pre-op and swanned, and subsequently "optimized". That means several things. First, it means seeing what her true PA pressure is, and second, likely means some diuresis to minimize her PA pressure. It may also mean iNO, depends on how she repsonds to diuresis. Also, an IABP should be considered, especially considering she has known CAD (ICM). That will improve both forward flow from the LV by decreasing afterload, as well as improving perfusion to both ventricles. That might take 24-36h, but so be it.

For induction, she needs an art line awake and central access for pressor/infusion administration (both of which should have been done pre-op in the ICU). I would induce with etomidate & roc and intubate. Pressors I would have available are epi and vasopressin and I would have iNO available as well. I would avoid agents that have alpha effects such as phenylephrine and even levo. The rationale is that the pulmonary vascular circulation has alpha receptors but minimal to no V1 receptors-- hence why vaso is a good choice in order to avoid further increases in PVR.

I would plan to keep her intubated post-op unless she can show me a good reason why she should be extubated. In general with severe pulm HTN you want to avoid prolonged intubation, but I think in a geriatric patient who will be sensitive to all sedatives, it is better to have her fully awake before extubation, and that might require a few hours. Also, it will allow reliable iNO delivery if necessary. Now, it may be the case that she's wide awake at the end of surgery and her agitation on the tube will increase her PAP. Fine, in that case it's reasonabe to extubate if she meets other criteria.

As a disclaimer, I work in a large tertiary (quarternary?) academic hospital in the second largest city in the U.S., and I'm a cardiac anesthesiologist. That probably means my ideas are more invasive and labor- and time-intensive than what most level 1- and 2-centers would do. Fair enough. In the so-called real world, there may not be time, motivation, and money to properly optimize a patient like this. All I can tell you is what I would consider to be appropriate care for this patient and would give her the best chance of surviving both the operation and the post-op course. If I saw this patient on my schedule, I wouldn't think twice about implementing the plan I've laid out. I've seen enough M&M with these types of patients to be very cautious.

-R

Thanks for the response. In my private practice, I was paged while I was on the opposite side of the hospital finishing up an epidural on ob to start a similar case like this. The only difference was the patient also had a pfo on top of the poor lv fuction, pulmonary HTN, and severe MR. The patient was already in the room when I was reviewing the preop while the orthopaedic surgeon had his arms crossed in a pissed off mood waiting for me to arrive. Since I am not a cardiac anesthesiologist and realized the badness of this situation, I asked the floor runner if they could page from home one of the cardiac anesthesiologist to do this case since I felt uncomfortable with this. The orthopod was really infuriated since he had no idea what the issue was here, and I was not interested in killing this patient that evening. I haven't placed a SGC in a few years now as I do mainly ambulatory anesthesia, but I did realize a SGC was perfect for this kind of situation. Anyway, the cardiac anesthesiologist refused to come in. They found some clown in my group to do this case as he is that guy who does anything. I was since relieved to go home. I found out later at the m and m they couldn't get in a preinduction a line but decided to proceed with the case with a NIBP inducing with propofol, lidocaine, fentanyl, and rocuronium. Again, not really an emergency. To keep the pressure up, they were running a wide open phenylephrine drip until the patients right arm where they were trying to get an a line in turned black. When the case was finished, they took the patient to the ICU where they died 3 hours later.

I just kept my mouth shut at the m and m session. The orthopaedic surgeon didn't even show up cause he could have cared less.

 

[Bertelman]

Thanks for the response. In my private practice, I was paged while I was on the opposite side of the hospital finishing up an epidural on ob to start a similar case like this. The only difference was the patient also had a pfo on top of the poor lv fuction, pulmonary HTN, and severe MR. The patient was already in the room when I was reviewing the preop while the orthopaedic surgeon had his arms crossed in a pissed off mood waiting for me to arrive. Since I am not a cardiac anesthesiologist and realized the badness of this situation, I asked the floor runner if they could page from home one of the cardiac anesthesiologist to do this case since I felt uncomfortable with this. The orthopod was really infuriated since he had no idea what the issue was here, and I was not interested in killing this patient that evening. I haven't placed a SGC in a few years now as I do mainly ambulatory anesthesia, but I did realize a SGC was perfect for this kind of situation. Anyway, the cardiac anesthesiologist refused to come in. They found some clown in my group to do this case as he is that guy who does anything. I was since relieved to go home. I found out later at the m and m they couldn't get in a preinduction a line but decided to proceed with the case with a NIBP inducing with propofol, lidocaine, fentanyl, and rocuronium. Again, not really an emergency. To keep the pressure up, they were running a wide open phenylephrine drip until the patients right arm where they were trying to get an a line in turned black. When the case was finished, they took the patient to the ICU where they died 3 hours later.

I just kept my mouth shut at the m and m session. The orthopaedic surgeon didn't even show up cause he could have cared less.

That sends a chill down my spine.

 

[Foodie]

That sends a chill down my spine.

That makes two of us.

This case is making me strongly consider either a CT or CCM fellowship to keep up my SGC skills (and to get TEE cert) before I join the real world.

Thanks to everyone for sharing your experiences and thoughts.

Now I need a drink.

 

[Arch Guillotti]

What you say is fine but a bit expensive for someone who is not going to make it out of the hospital.

I don't think that this is necessarily true.

 

[Arch Guillotti]

Are you still with the same group? Sounds like a terrible set-up.

First you get the dump in the OR without notice.

Then the CT guy dumps on you.

Then one of your partners takes a dump on you. He (along with anyone else who happened to get involved) should have stood by you 100%. To me, this is inexcusable. Members and partners need to stay cohesive in these type of situations.

Thanks for the response. In my private practice, I was paged while I was on the opposite side of the hospital finishing up an epidural on ob to start a similar case like this. The only difference was the patient also had a pfo on top of the poor lv fuction, pulmonary HTN, and severe MR. The patient was already in the room when I was reviewing the preop while the orthopaedic surgeon had his arms crossed in a pissed off mood waiting for me to arrive. Since I am not a cardiac anesthesiologist and realized the badness of this situation, I asked the floor runner if they could page from home one of the cardiac anesthesiologist to do this case since I felt uncomfortable with this. The orthopod was really infuriated since he had no idea what the issue was here, and I was not interested in killing this patient that evening. I haven't placed a SGC in a few years now as I do mainly ambulatory anesthesia, but I did realize a SGC was perfect for this kind of situation. Anyway, the cardiac anesthesiologist refused to come in. They found some clown in my group to do this case as he is that guy who does anything. I was since relieved to go home. I found out later at the m and m they couldn't get in a preinduction a line but decided to proceed with the case with a NIBP inducing with propofol, lidocaine, fentanyl, and rocuronium. Again, not really an emergency. To keep the pressure up, they were running a wide open phenylephrine drip until the patients right arm where they were trying to get an a line in turned black. When the case was finished, they took the patient to the ICU where they died 3 hours later.

I just kept my mouth shut at the m and m session. The orthopaedic surgeon didn't even show up cause he could have cared less.

 

[dhb]

I don't think that this is necessarily true.

Never say never but unless you want to hold her hand 24/7 and pray she doesn't catch an infection she's toast.

 

[Mman]

Wow, a lot of cavalier attitudes here. First off, the LVEF of 15-20% in the setting of mod-severe MR means means her actual forward flow is a lot worse than that. Most of the 20% is going back into the LA. I can't stress enough how concerning the PASP pressure is to me. I'm not sure what her systemic pressure was, but if we assume that the PA pressure is 3/4 systolic that means she is at high risk for RV ischemia and subsequent RV failure. The RV is notoriously resistant to inotropes, so once it starts to go down that's it. The RV must be protected, almost at all costs.

There are several ways to approach this patient. This is not a true "emergency", in the sense it needs to go NOW. Given the patient has severe pulmonary HTN in the setting of ischemc cardiomyopathy, I would opt for the following: she gets admitted to the ICU pre-op and swanned, and subsequently "optimized". That means several things. First, it means seeing what her true PA pressure is, and second, likely means some diuresis to minimize her PA pressure. It may also mean iNO, depends on how she repsonds to diuresis. Also, an IABP should be considered, especially considering she has known CAD (ICM). That will improve both forward flow from the LV by decreasing afterload, as well as improving perfusion to both ventricles. That might take 24-36h, but so be it.

For induction, she needs an art line awake and central access for pressor/infusion administration (both of which should have been done pre-op in the ICU). I would induce with etomidate & roc and intubate. Pressors I would have available are epi and vasopressin and I would have iNO available as well. I would avoid agents that have alpha effects such as phenylephrine and even levo. The rationale is that the pulmonary vascular circulation has alpha receptors but minimal to no V1 receptors-- hence why vaso is a good choice in order to avoid further increases in PVR.

I would plan to keep her intubated post-op unless she can show me a good reason why she should be extubated. In general with severe pulm HTN you want to avoid prolonged intubation, but I think in a geriatric patient who will be sensitive to all sedatives, it is better to have her fully awake before extubation, and that might require a few hours. Also, it will allow reliable iNO delivery if necessary. Now, it may be the case that she's wide awake at the end of surgery and her agitation on the tube will increase her PAP. Fine, in that case it's reasonabe to extubate if she meets other criteria.

As a disclaimer, I work in a large tertiary (quarternary?) academic hospital in the second largest city in the U.S., and I'm a cardiac anesthesiologist. That probably means my ideas are more invasive and labor- and time-intensive than what most level 1- and 2-centers would do. Fair enough. In the so-called real world, there may not be time, motivation, and money to properly optimize a patient like this. All I can tell you is what I would consider to be appropriate care for this patient and would give her the best chance of surviving both the operation and the post-op course. If I saw this patient on my schedule, I wouldn't think twice about implementing the plan I've laid out. I've seen enough M&M with these types of patients to be very cautious.

-R

the best part of this plan is the possibility that the family changes their mind about surgery after they see her with the balloon pump and intubated on nitric in the unit preop and you tell them that it will probably be worse postop.

edit: can you even use a IABP intraop in this patient with the combination of positioning and possibility of moving the leg around during the case?

 

[ssmallz]

That makes two of us.

This case is making me strongly consider either a CT or CCM fellowship to keep up my SGC skills (and to get TEE cert) before I join the real world.

Thanks to everyone for sharing your experiences and thoughts.

Now I need a drink.

There's no need to do a cc or cv fellowship to learn how to take care of sick patients. If you're at a good residency you should learn how to treat and optimize all types of sick path and do the cases.

FWIW, I think these types of cases are way tougher than CV cases. In CV cases the surgeon knows how sick the pt is, you have a perfusionist on standby if things go south, and you've got plenty of IV access and monitoring. When dealing with these cases it's on you to figure out what the appropriate monitoring is and convince a surgeon with little knowlege (care) for the acute pathology that you need time to place an a line and central line/PAC on a case that we normally do with a PIV and LMA. Learning to stand your ground in the face of ignorance can be the toughest par of our job.

 

[BLADEMDA]

Wow, a lot of cavalier attitudes here. First off, the LVEF of 15-20% in the setting of mod-severe MR means means her actual forward flow is a lot worse than that. Most of the 20% is going back into the LA. I can't stress enough how concerning the PASP pressure is to me. I'm not sure what her systemic pressure was, but if we assume that the PA pressure is 3/4 systolic that means she is at high risk for RV ischemia and subsequent RV failure. The RV is notoriously resistant to inotropes, so once it starts to go down that's it. The RV must be protected, almost at all costs.

There are several ways to approach this patient. This is not a true "emergency", in the sense it needs to go NOW. Given the patient has severe pulmonary HTN in the setting of ischemc cardiomyopathy, I would opt for the following: she gets admitted to the ICU pre-op and swanned, and subsequently "optimized". That means several things. First, it means seeing what her true PA pressure is, and second, likely means some diuresis to minimize her PA pressure. It may also mean iNO, depends on how she repsonds to diuresis. Also, an IABP should be considered, especially considering she has known CAD (ICM). That will improve both forward flow from the LV by decreasing afterload, as well as improving perfusion to both ventricles. That might take 24-36h, but so be it.

For induction, she needs an art line awake and central access for pressor/infusion administration (both of which should have been done pre-op in the ICU). I would induce with etomidate & roc and intubate. Pressors I would have available are epi and vasopressin and I would have iNO available as well. I would avoid agents that have alpha effects such as phenylephrine and even levo. The rationale is that the pulmonary vascular circulation has alpha receptors but minimal to no V1 receptors-- hence why vaso is a good choice in order to avoid further increases in PVR.

I would plan to keep her intubated post-op unless she can show me a good reason why she should be extubated. In general with severe pulm HTN you want to avoid prolonged intubation, but I think in a geriatric patient who will be sensitive to all sedatives, it is better to have her fully awake before extubation, and that might require a few hours. Also, it will allow reliable iNO delivery if necessary. Now, it may be the case that she's wide awake at the end of surgery and her agitation on the tube will increase her PAP. Fine, in that case it's reasonabe to extubate if she meets other criteria.

As a disclaimer, I work in a large tertiary (quarternary?) academic hospital in the second largest city in the U.S., and I'm a cardiac anesthesiologist. That probably means my ideas are more invasive and labor- and time-intensive than what most level 1- and 2-centers would do. Fair enough. In the so-called real world, there may not be time, motivation, and money to properly optimize a patient like this. All I can tell you is what I would consider to be appropriate care for this patient and would give her the best chance of surviving both the operation and the post-op course. If I saw this patient on my schedule, I wouldn't think twice about implementing the plan I've laid out. I've seen enough M&M with these types of patients to be very cautious.

-R

Now we know why health care is so expensive in this country. Obama and the Brits have it right when it comes to this patient. A frank discussion about the risks/benefits and likely death post op. I'd give 2 units FFP with Lasix preop over 2-3 hours. Minimal to no sedation, arterial line and SAB.

What you consider "appropriate care" is why this country is going broke and Obama has created the review panels in his healthcare law.

No amount of "optimization" guarantees any better outcome in this patient. What is does guarantee is this operation will cost up to $100,000 in medical care withhout any justification. Death is a part of life. It is something we must learn to all face at some point; I've lost several relatives and it's painful. I had the option of spending $200K or more of taxpayer money on a famly member. I chose Hospice and a humane death instead.

I respect and understand your post; you are doing what you were trained to do. But, experience and time coupled with the harsh reality of Medicare funding cuts will alter your approach.

 

[dhb]

Death is a part of life.

👍 exactly and her time is up... sad but true

 

[BLADEMDA]

Regional anesthesia has been used successfully for cesarean delivery in patients with PPH, and it may allow for limiting central respiratory depressant drugs given with general anesthesia that might postoperatively lead to hypercarbia and increased pulmonary vascular pressures (7). The adverse platelet aggregation effects of epoprostenol and the potential of spinal hematoma with central neuroaxial block were a concern in this case. The alternative of peripheral nerve block was difficult given the surgeon's wish to expose both groins for possible skin harvesting.
An additional concern with spinal anesthesia was hypotension due to sympathetic nervous system blockade. In patients with severe pulmonary hypertension, a reduction in systemic blood pressure and coronary perfusion pressure can precipitate acute cardiovascular decompensation resulting in cardiac arrest (8). IV administration of catecholamines to treat hypotension during spinal anesthesia could potentially increase pulmonary vascular resistance precipitating acute cor pulmonale. Because of the latter concern, we chose to infuse vasopressin preemptively to limit hypotension.

 

[BLADEMDA]

The Internet Journal of Anesthesiology ISSN: 1092-406X



Succesful Use Of Continuous Spinal Anesthesia Technique For Femoro-Popliteal By-Pass In A Patient With Congestive Heart Failure And Pulmonary Hypertension

 

[BLADEMDA]

In addition to this, it is widely believed that regional anesthesia has benefit for patients with severe pulmonary disease. Harald et al. reported that, even high thoracic regional anesthesia is well tolerated in patients with severe pulmonary disease, although FEV1 and vital capacity may be slightly decreased [11].

 

[BLADEMDA]

Regional techniques, including peripheral nerve blockade and neuraxial blockade (epidural,

spinal anesthesia) have been successfully utilized in patients with severe pulmonary

hypertension. Among the benefits are avoidance of the stimulation of direct laryngoscopy

and endotracheal intubation. Even with adequate IV hypnotics, opioids and neuromuscular

blockade, it is difficult to avoid increases in sympathetic nervous system activity with direct

laryngoscopy. These increases could lead to increases in PVR and potential acute right heart

failure. Additionally, during a general anesthetic, with the variable stimulation during the

operative procedure, the anesthesiologist is continually managing the balance between

excessive sympathetic outflow, increased PVR and potential acute right heart failure on one

hand and excessive depth of anesthesia, low cardiac output, low coronary perfusion and

cardiovascular collapse on the other hand. (Hohn L et al., 1999) The healthy patient

tolerates these variations well, but the patient with severe PH has limited reserve to tolerate

acute increases in PVR or decreased coronary perfusion. A peripheral nerve block technique

can limit anesthesia to the specific location of the surgery and avoid the need for the

stimulation of intubation and reduced likelihood of sympathectomy and low blood pressure

as one would achieve with general anesthesia. An important distinction is that a

sympathectomy is still possible when utilizing a regional anesthesia technique such as

epidural or spinal anesthesia. This may lead to arterial and venous dilation and reduced

preload and cardiac output compromising coronary perfusion.

 

[BLADEMDA]

Hypotension should be treated according to causes. Phenylephrine and norepinephrine

have been used to treat persistent systemic hypotension. Norepinephrine has the

advantage of being both a vasoconstrictor and positive inotropic agent. In hypotension,

dobutamine and vasopressin have also been advocated for treatment of hypotension

[Pearl, 2005; Subramaniam & Yared 2007].