ruptured aaa's

[nap$ter]

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how many of you place PA caths or TEE intraop for your ruptured aaa's?

i've had a couple recently where before and after unclamping we weren't all that sure how much of the hypotension was from hypovolemia/evil humors or from cardiac ischemia.

we have a pretty smooth system at our hospital - ruptured aaa's bypass the ed and come straight down to the OR. we usually have a crash room set up with belmont, hotline, pressure lines, etc. in the 5 minutes before the patient arrives transfusion support brings the fridge with MTP products uncrossmatched.

the patient stays awake while vascular accesses the femoral and slides a balloon above the aaa. while they're doing this we place an aline and big bore iv's or usually an IJ cordis (if they're not already in). after they ensure proximal control with the balloon we induce and they open for graft repair.

i had a patient recently who before unclamping even became hypotensive, and we did the usual things - volume, blood, calcium, bicarb, vasopressors. his QRS also widened every time his pressure dropped below 100. we ended up pounding the fluids and vasopressors to keep his pressure up, but toward the end of the case he went into massive pulmonary edema with liters of pink frothy stuff from the ett. he had new LBBB at the end of the case (which disappeared in the days following as his troponin peaked). postop echo was normal.

in retrospect I wish we had floated a swan or placed a TEE probe in the time available after they opened before they started clamping and unclamping. i think we woulda gone with more inotropy if that info had been available.

I'm considering making it a standard part of my game plan to float a swan if there is a cordis or place the TEE (if no cordis) in every aaa patient.

what do y'all think/do?

 

[Idiopathic]

how many of you place PA caths or TEE intraop for your ruptured aaa's?

i've had a couple recently where before and after unclamping we weren't all that sure how much of the hypotension was from hypovolemia/evil humors or from cardiac ischemia.

we have a pretty smooth system at our hospital - ruptured aaa's bypass the ed and come straight down to the OR. we usually have a crash room set up with belmont, hotline, pressure lines, etc. in the 5 minutes before the patient arrives transfusion support brings the fridge with MTP products uncrossmatched.

the patient stays awake while vascular accesses the femoral and slides a balloon above the aaa. while they're doing this we place an aline and big bore iv's or usually an IJ cordis (if they're not already in). after they ensure proximal control with the balloon we induce and they open for graft repair.

i had a patient recently who before unclamping even became hypotensive, and we did the usual things - volume, blood, calcium, bicarb, vasopressors. his QRS also widened every time his pressure dropped below 100. we ended up pounding the fluids and vasopressors to keep his pressure up, but toward the end of the case he went into massive pulmonary edema with liters of pink frothy stuff from the ett. he had new LBBB at the end of the case (which disappeared in the days following as his troponin peaked). postop echo was normal.

in retrospect I wish we had floated a swan or placed a TEE probe in the time available after they opened before they started clamping and unclamping. i think we woulda gone with more inotropy if that info had been available.

I'm considering making it a standard part of my game plan to float a swan if there is a cordis or place the TEE (if no cordis) in every aaa patient.

what do y'all think/do?

i dont think you need PAC or TEE to make that diagnosis. im not sure that adding inotropes is the way to go, as its seems like the heart is ischemic 2/2 huge afterload, and you would just be making it work harder, increasing O2 demand. its counterintuitive maybe but offloading the heart could have been more appropriate there. adjuncts could have helped you decide the course, but i still think you could be misled by full heart, decreased EF etc. maybe im off base, i usually decide case by case but honestly these patients are crashed in the OR for the most part after access and induction.

 

[Arch Guillotti]

This is a classic AAA thread from a few years ago. Post #57 by zip is great.

I would not put in a TEE or PA cath beforehand.

Maybe a TEE probe later to help your assessment.

Depending on the peripheral access, I may not even put in a central line.

 

[nap$ter]

i dont think you need PAC or TEE to make that diagnosis. im not sure that adding inotropes is the way to go, as its seems like the heart is ischemic 2/2 huge afterload, and you would just be making it work harder, increasing O2 demand. its counterintuitive maybe but offloading the heart could have been more appropriate there. adjuncts could have helped you decide the course, but i still think you could be misled by full heart, decreased EF etc. maybe im off base, i usually decide case by case but honestly these patients are crashed in the OR for the most part after access and induction.

i omitted a key bit of info. the patient crumped a bit after they opened the abdomen - even with the balloon up. there was 2-3L of blood in the belly, and they lost another liter or so while deflating the balloon/ placing the external clamp. so once the clamp was on we played catch-up with volume (crit of 23 from 38), but the pt didn't respond as readily as we expected, and with the widened QRS we didn't know how much of the hypotension was from ischemia, and how much was from hypovolemia.

i get the academic point about afterload, but i think most would be loathe to reduce afterload in a hypotensive ruptured aaa patient - especially without a tee or some sort of CO monitor (and given the fact that there is no way to reduce afterload without affecting preload).

hence my question - the picture can be confusing in these patients - they all have coronary disease and so potential for ischemia, they all bleed/have bled, and they all get clamped/unclamped and have potential for vasoplegia. so at any given time you have potential for the eternal conundrum - is the hypotension from problems with the preload, afterload, or contractility?

i also don't place a cordis unless they have crappy veins - a cuppla 14's or 16's (or you can change that pink one in the AC from the ER to a RIC) is fine, and cvp is not so useful.

but, half of these patients have elevated troponins post-op. the mortality/morbidity rate is pretty crappy - crappy disease.

i just wonder if more info from a PA cath or swan might change the population outcome.

 

[dhb]

I agree that sometimes it can get confusing at that point i would drop a TEE probe which would give you more info imho than a swan.

 

[gaspasser2004]

I understand the concept of internal combustion, but would be hard pressed to identify all the car parts if you popped the hood. Yet, I am totally capable of driving a car.

I know in concept how the internet works, the difference between ROM and RAM. I can't fix a crashed computer, but I can surf the internet and post on SDN.

My house has a furnace and air conditioner. I know the air conditioning unit is outside and the furnace is in the basement. I also know that there are vents connecting all the systems. What I can really do best is turning the thermostat down or up.

I understand the concepts of TEE, ejection fraction, regional wall motion abnormalities, etc. However, I haven't done a cardiac fellowship or gained the necessary experience to obtain superior proficiency. Today, I would need someone else to fully interpret TEE findings. In the future, technology will hopefully give us a TEE probe that any anesthesiologist can insert (maybe it will be smaller like a oropharyngeal suction catheter) and results that are easy to interpret (either computer or algorithm aided).

 

[proman]

There's technology that streams a TEE across the web in real-time. That may allow future specialty backup in cases like this. With the development of the basic PTEexam by the NBE and the recent emphasis of real echo questions by the ABA, it's clear that residencies will have to start preparing trainees to do a basic (noncardiac, nonvalvular) exam.

 

[Idiopathic]

i omitted a key bit of info. the patient crumped a bit after they opened the abdomen - even with the balloon up. there was 2-3L of blood in the belly, and they lost another liter or so while deflating the balloon/ placing the external clamp. so once the clamp was on we played catch-up with volume (crit of 23 from 38), but the pt didn't respond as readily as we expected, and with the widened QRS we didn't know how much of the hypotension was from ischemia, and how much was from hypovolemia.

i get the academic point about afterload, but i think most would be loathe to reduce afterload in a hypotensive ruptured aaa patient - especially without a tee or some sort of CO monitor (and given the fact that there is no way to reduce afterload without affecting preload).

hence my question - the picture can be confusing in these patients - they all have coronary disease and so potential for ischemia, they all bleed/have bled, and they all get clamped/unclamped and have potential for vasoplegia. so at any given time you have potential for the eternal conundrum - is the hypotension from problems with the preload, afterload, or contractility?

i also don't place a cordis unless they have crappy veins - a cuppla 14's or 16's (or you can change that pink one in the AC from the ER to a RIC) is fine, and cvp is not so useful.

but, half of these patients have elevated troponins post-op. the mortality/morbidity rate is pretty crappy - crappy disease.

i just wonder if more info from a PA cath or swan might change the population outcome.

so yould feel comfortable doing an open ruptured AAA with a "cuppla 16s"? im sorry if you are getting your aorta urgently/emergently cross clamped in my operating room you get central access, end of story. i dont think its insane and i dont think the risk outweighs the rewards of a secure route for high-volume resuscitation and caustic med administration. just me, i guess. i dont think you are doing these patients any favors by not sticking the neck. plus, all your discussion above speaks towards heightened sense of concern, sicker patients, worse outcomes, yada yada.

i guess my other point is that in the setting of huge afterload and very aggressive resuscitation (to the point of pulmonary edema), it suggests that the pump is failing and sure you can push that pump harder but you are seeing ischemic changes as well, so i could make the case that working the LV harder is not the answer and offloading the heart might be (i.e. reducing preload, not afterload).

 

[nap$ter]

so yould feel comfortable doing an open ruptured AAA with a "cuppla 16s"? im sorry if you are getting your aorta urgently/emergently cross clamped in my operating room you get central access, end of story. i dont think its insane and i dont think the risk outweighs the rewards of a secure route for high-volume resuscitation and caustic med administration. just me, i guess. i dont think you are doing these patients any favors by not sticking the neck. plus, all your discussion above speaks towards heightened sense of concern, sicker patients, worse outcomes, yada yada.

i guess my other point is that in the setting of huge afterload and very aggressive resuscitation (to the point of pulmonary edema), it suggests that the pump is failing and sure you can push that pump harder but you are seeing ischemic changes as well, so i could make the case that working the LV harder is not the answer and offloading the heart might be (i.e. reducing preload, not afterload).

did i say comfortable? no - i take as much access as i can get. i agree - you need the equivalent of a cordis at least. minimum of 2 16's, the more the better. if i can get 2 14's or a 14 and a 16, i wouldn't put in a cordis. if i have just 2 16's, i'm not going to be comfortable but i won't delay the case for a cordis. maybe add an 18 or change a 16 for a RIC. i agree - a cordis is optimal.

i'm a bit confused - you say afterload is the problem, but then you suggest lowering preload. i guess it's semantics, because we don't have a drug selective for either. you said before that you would not place a TEE or swan - so i have 2 questions.

1 - you made the case for reducing afterload/preload - but would you actually try it in a hypotensive ruptured aaa pt with ekg changes, with no monitoring of CO or R heart function?

2 - if the answer is yes - what would you use?

 

[Idiopathic]

did i say comfortable? no - i take as much access as i can get. i agree - you need the equivalent of a cordis at least. minimum of 2 16's, the more the better. if i can get 2 14's or a 14 and a 16, i wouldn't put in a cordis. if i have just 2 16's, i'm not going to be comfortable but i won't delay the case for a cordis. maybe add an 18 or change a 16 for a RIC. i agree - a cordis is optimal.

i'm a bit confused - you say afterload is the problem, but then you suggest lowering preload. i guess it's semantics, because we don't have a drug selective for either. you said before that you would not place a TEE or swan - so i have 2 questions.

1 - you made the case for reducing afterload/preload - but would you actually try it in a hypotensive ruptured aaa pt with ekg changes, with no monitoring of CO or R heart function?

2 - if the answer is yes - what would you use?

1. yes, because the diastolic pressure is likely high and that component of the coronary perfusion is adequate, i.e. you have the afterload to maintain CPP. it sounds like you guys kept up with resuscitation, even though you are hemodiluted (the pulmonary edema seals it). what is hurting you is wall tension and the fact that you are already ischemic with slight drops in bp suggests to me that the ischemia could easily be the cause of the bp, rather than the other way around. if you really think that you had a widened QRS every time the SBP<100 then you have to find a way to unload the heart. im not sure that working it harder (inotropes) is the way to go, since it will probably worsen the O2-demand and hence the ischemia. ballsy, i know, but you probably started the case with 2 16's so you already know ballsy 😉

2. nitroglycerin

TEE makes the decision quick and easy and in this case id probably elect to place one.

by the way 2 16s may be close to a cordis for VOLUME administration, but not necessarily for rapid administration of vasoactive agents or electrolytes, and you wont get a Belmont/Level1 going full speed through them either.

 

[jwk]

by the way 2 16s may be close to a cordis for VOLUME administration, but not necessarily for rapid administration of vasoactive agents or electrolytes, and you wont get a Belmont/Level1 going full speed through them either.

Actually, two 16's is nowhere close to the flow capability of a 9Fr introducer. From Poiseuille's Law, we know that flow is proportional to the 4th power of the radius. So a catheter with a radius of 1mm has 16 times the flow capability of a catheter with a radius of 0.5mm.

A 16ga catheter has an internal radius of about 0.597mm.

A 9Fr introducer has an internal radius of about 1.25mm or so, more than twice the diameter. That means it would take more than sixteen 16ga catheters to equal the flow of a single 9Fr introducer.

 

[pgg]

Actually, two 16's is nowhere close to the flow capability of a 9Fr introducer. From Poiseuille's Law, we know that flow is proportional to the 4th power of the radius. So a catheter with a radius of 1mm has 16 times the flow capability of a catheter with a radius of 0.5mm.

A 16ga catheter has an internal radius of about 0.597mm.

A 9Fr introducer has an internal radius of about 1.25mm or so, more than twice the diameter. That means it would take more than sixteen 16ga catheters to equal the flow of a single 9Fr introducer.

What's the internal radius of IV tubing? (I'm not trying to be a smartass or facetious.)

 

[fakin' the funk]

Actually, two 16's is nowhere close to the flow capability of a 9Fr introducer. From Poiseuille's Law, we know that flow is proportional to the 4th power of the radius. So a catheter with a radius of 1mm has 16 times the flow capability of a catheter with a radius of 0.5mm.

A 16ga catheter has an internal radius of about 0.597mm.

A 9Fr introducer has an internal radius of about 1.25mm or so, more than twice the diameter. That means it would take more than sixteen 16ga catheters to equal the flow of a single 9Fr introducer.

You make valid points, but unless you are pressurizing your infusate (as in through a Level 1 or Belmont) the rate of infusion could be pretty similar between 2 16g's and a 9fr PSI, since it's just the gravity of the fluid column driving the fluid into the patient, definitely at a "submaximal" rate.

 

[nap$ter]

Actually, two 16's is nowhere close to the flow capability of a 9Fr introducer. From Poiseuille's Law, we know that flow is proportional to the 4th power of the radius. So a catheter with a radius of 1mm has 16 times the flow capability of a catheter with a radius of 0.5mm.

A 16ga catheter has an internal radius of about 0.597mm.

A 9Fr introducer has an internal radius of about 1.25mm or so, more than twice the diameter. That means it would take more than sixteen 16ga catheters to equal the flow of a single 9Fr introducer.

this is incorrect, i think. poiseuille's law is only part of the picture.

in practice, 2 16's actually produce about the same flow as an 8.5F. idiopathic is right.

A Comparison of Flow Rates and Warming Capabilities of the Level 1 and Rapid Infusion System with Various-Size Intravenous Catheters

 

[RabbMD]

Radius is not the only variable there either. The length of the catheter also affects flow. If the cordis was say for times longer tban the two 16s then you must adjust the flow accordingly.

 

[Bertelman]

...but you probably started the case with 2 16's so you already know ballsy 😉

That's a great sig

 

[sevoflurane]

Radius is not the only variable there either. The length of the catheter also affects flow. If the cordis was say for times longer tban the two 16s then you must adjust the flow accordingly.

Absolutely. Related to the diameter and inversely related to length. That is why a triple lumen with a couple of 16gauges will never equate to a couple of well placed 16g in the AC. Those puppies are pretty darn good... good enough for just about any case that does not require CVP/Swan.

 

[jennyboo]

how many of you place PA caths or TEE intraop for your ruptured aaa's?

I'm a little late to this discussion, but here goes. I am assuming a non-contained rupture with a rapidly hypotensive patient (sounds like the case you are describing may be a contained rupture given the patient was stable enough to be awake during femoral arterial access & ballooning, so that is a different animal).

1) Get a few other hands on deck if available (harder to do by yourself at night but 3 anesthetists are often better than 1) to help with the following steps (see below)

2) Get as big a large bore peripheral IV as possible, preferably a couple of them, 14 better than 16

3) Get an a-line in addition to standard monitors

4) Do not hold up induction for CVC placement in an unstable patient who needs rapid control of bleeding, i.e. aortic cross-clamp

5) Hemodynamically stable induction of your choice

6) CVC placement "in parallel" with other processes such as drapes, positioning etc -- always an introducer (Cordis or MAC), never a standard triple or quad lumen. Depending on circumstances, a signout to the ICU may be required that this is a dirty line that will need to be replaced with a sterile one.

7) Transfuse, transfuse, transfuse -- 1:1 FFP to PRBC ratio with a unit of platelets here and there, and CaCl for the hypoglycemia.

8) Go easy on the crystalloids to avoid making the patient puffy and worsening coagulopathy. There's no study I know of that demonstrates colloid to have any outcome advantage over crystalloid.

Additional points:

- The emergent ruptured AAA is mostly a volume case and in most cases you don't need a PAC or TEE to figure out whether you have made an adequate resuscitation. You have CVP, urine output, pressor requirements and labs (CBC, coags, pH, cvO2/mvO2, lactate) to guide you.

- A PAC or TEE may be helpful in the situation you describe -- when the patient crumps hemodynamically and you don't know why.

- With an introducer already in place, if I think a PAC would be helpful I would throw one in. I would make a TEE decision the same way if I were trained to use the TEE.

- Nobody has ever demonstrated that PAC improves outcome in any way whatsoever. (But, as well all know, it may still be useful.)

 

[nap$ter]

I'm a little late to this discussion, but here goes. I am assuming a non-contained rupture with a rapidly hypotensive patient (sounds like the case you are describing may be a contained rupture given the patient was stable enough to be awake during femoral arterial access & ballooning, so that is a different animal).

1) Get a few other hands on deck if available (harder to do by yourself at night but 3 anesthetists are often better than 1) to help with the following steps (see below)

2) Get as big a large bore peripheral IV as possible, preferably a couple of them, 14 better than 16

3) Get an a-line in addition to standard monitors

4) Do not hold up induction for CVC placement in an unstable patient who needs rapid control of bleeding, i.e. aortic cross-clamp

5) Hemodynamically stable induction of your choice

6) CVC placement "in parallel" with other processes such as drapes, positioning etc -- always an introducer (Cordis or MAC), never a standard triple or quad lumen. Depending on circumstances, a signout to the ICU may be required that this is a dirty line that will need to be replaced with a sterile one.

7) Transfuse, transfuse, transfuse -- 1:1 FFP to PRBC ratio with a unit of platelets here and there, and CaCl for the hypoglycemia.

8) Go easy on the crystalloids to avoid making the patient puffy and worsening coagulopathy. There's no study I know of that demonstrates colloid to have any outcome advantage over crystalloid.

Additional points:

- The emergent ruptured AAA is mostly a volume case and in most cases you don't need a PAC or TEE to figure out whether you have made an adequate resuscitation. You have CVP, urine output, pressor requirements and labs (CBC, coags, pH, cvO2/mvO2, lactate) to guide you.

- A PAC or TEE may be helpful in the situation you describe -- when the patient crumps hemodynamically and you don't know why.

- With an introducer already in place, if I think a PAC would be helpful I would throw one in. I would make a TEE decision the same way if I were trained to use the TEE.

- Nobody has ever demonstrated that PAC improves outcome in any way whatsoever. (But, as well all know, it may still be useful.)

you shouldn't have CVP unless you've been silly enough to put a triple lumen slic through your cordis (and hopefully you are using the cordis for belmont infusion and not transducing a CVP... i guess you could stop the belmont periodically and check isolated measures). multiple studies have shown the uselessness of CVP - both absolute value and trends.

you may not have urine output, either, if the clamp or the balloon is at or above the renals.

you will have aline systolic pressure variation - but this has not been validated in patients undergoing aaa repair - clamping and unclamping.

you will have the labs you mentioned - but these are perfusion labs and nonspecific for differentiating between preload, afterload, and contractility issues.

all that being said, the problem in a ruptured aaa is almost always volume, i agree.

but, the more i think about it, the lower my threshold to place a TEE probe or PA cath...

 

[proman]

8) Go easy on the crystalloids to avoid making the patient puffy and worsening coagulopathy. There's no study I know of that demonstrates colloid to have any outcome advantage over crystalloid.

Blood is a pretty awesome colloid.

But realistically, there's no way I can "throw a PA" or "throw a TEE" in 5 minutes. Do you guys have a room with all this set up and ready to go? I sure don't. What I can do is place a dirty IJ or subclavian introducer in a few minutes. Peripherals if you can. Forget the PA-C, that's not going to help. Echo in after the surgeons have started.

In these cases, the question is, "am I going to wait until X is done", for both echo and PA-C the answer is no.

 

[Planktonmd]

A real ruptured AAA is very similar to a major trauma case with the main problem being hypovolemia.
So, everything we do from the moment we see the patient should focus on one thing: give volume fast!
What you accept as IV access before you allow them to make incision depends entirely on how rapidly the patient is deteriorating, so some times you might have to let them start with only one large bore IV because the patient is about to arrest and the only way to save his life is to clamp the aorta as fast as possible, while in less dire circumstances you might want to obtain more IV access or central access before you start.
An A line is good to have but you don't always have that time luxury especially if you are alone in the middle of the night.
The use of a PA catheter or TEE could be helpful in rare occasions after the initial resuscitation but I don't think it should be done routinely on every ruptured AAA.