triple A surgery

i am by no means an expert - there are those on this board who will (i am sure) give you an amazing answer - however

the pt sounds dry (initially w/ cvp of 3?!?) what "fluids" were given - hopefully hespan or another colloid....

the drop in h/h is too signifigant to be hemodilution

perhaps this pt was bleeding out.......that would explain your continual drops in bp - and perhaps your tachycardia

as the or sedation wears off - the 25mcg/kg/min is not that high of a dose.....it is probably enough to keep your pt asleep but it doesn't control pain - so you will have to judge from your pt's vs, breathing patterns, and perhaps movement when to start your pca - i found that generally 1 hour post op the pt starts requiring some type of pain control...

another question - if they felt the pt was dry enough to "fluid resus..." why the lasix - was it just to increase urine output?!? or was the pt in some sort of failure?

500 of hespan or my personal fav albumin goes along way - i would have held on the lasix for awhile to see if the urine output and cvp picked up....

as for the bp.... i am not yet too familiar w/ esmolol - but the low bp could be attributed to the volume deficit and/or bleeding....

most of the post ops that i have seen fluctuate from 60-220 were in pain....

sorry i don't have more - give me a few months to a year - and i am sure i can toss an answer to ya w/o a problem....

my novice thoughts-

1- treat the cause not the hr...if the pt has a rapidly decreasing h/h especially if you are taking care of the dilutional factor already (lasix)...dont know why esmolol would be in the picture here...why not another blocker?

2- keeping the pt intubated throughout the night might warrant throwing out the PC in the EA. Also, use an icu sedative other than Propofol since we have some hypotension. Depending on the agent used in the EA, if it was bupivicaine without opioid, start it at a basal rate....if it includes fentanyl watch how it effects your hypotension.

3- The patient is still dry, if they have AS, then they are too dry. I agree with Athomas...try some colloid.

4- I know a lot more happened in that 8 hour period than you wrote about. What were the MIVF? How many crystalloids/ colloids/blood products were given? UOP?

Sounds like a fun one. Let us know what happened.

Originally posted by ethelbsnrn

This is re: a s/p triple A patient last week in our unit. The anesthesia provider was a CRNA. Patient came out of the surgery intubated with just a cordis in place where all the IV drips were going. ...propofol, levophed. BP was unstable from SBP 60-220. He ordered Esmolol drip. HR- 101-112. HAd a clamped epidural cath, ordered to start epidural analgesia when patient starts to wake up and complains of pain. Patient was heavily sedated from OR, Propofol was 25 mcg/kg/min. He further ordered to keep the patient intubated through-out the night. Before he left he inserted a triple-lumen cath through the existing cordis. QUESTIONS:

1 - why do you think he ordered esmolol drip?hr- 112?even with low sbp.. (heard the surgeon saying," he is just a crna, not a doctor" re: this order)

2 - when the patient was heavily sedated, with propofol going - when is the best time to start the pcea pump?

3 - cvp - initially 3, went up to 6-9 after volume resuscitation. Still 30-60 cc/hr urine output. Lasix was given. ..cvp went down to 5-6. Do you think the patient was still dry?

4 - h & h - 14 & 42. after 8 hrs - was 7 & 30. Why the big drop ? Hemodilution ? thought the patient was on the dry side?

ahhhh.....can't stop figuring out this hemodynamics...

1. Esmolol doesn't really make any sense to me unless he was using it to help with the BP, but then the propofol would also affect BP. Esmolol and Propofol would then dramatically drop BP, and he'd then have to start the levophed. Basically chasing his own tail. Example: Pt's BP and HR begins to go up because of pain. Esmolol is started for BP. Then the pt starts to wake up, so CRNA increases or gives a bolus of propofol. Then BP tanks. CRNA starts levophed.

2. I'd say turn off the propofol and then start using the pump or even fentanyl, which won't affect BP so much.

3. Normal CVP is 2-6, so 3 is a little bit on the low side, and the pt could do with some volume. I'd go with NS bolus. With a CVP of 5-6, I don't think the pt would be dry, but a clinical assessment would definitely be in order.

4. Hct is RBC's per volume of blood, so if the pt was on the dry side, you'd have a higher hct. Sounds like the pt was bleeding s/p procedure. Did they do any coag studies, PT/PTT/INR? I'd go ahead and T&C for 2 units PRBC.

Thanks for the case. This is real interesting. Looking forward to hearing other people's viewpoints.

1) esmolol is a short acting beta-blocker (which the best choice of beta-blocker in this patient as it is short-acting and his behavior sounds so labile) and as such will not drop your blood pressure (significantly - UNLESS you are dry, in which case you will see a drop in BP.... Cardiac output in adults is a lot more preload dependent (or Stroke Volume dependent) then compared to Pedi where CO is more dependend on Heart Rate..... In somebody who is s/p AAA repair and there is concern with the proximal anastomosis site (ie: the native aorta is diseased and can tear easily), then it would be a good idea to have ideal BP and HR control.... What i don't understand is why he would want a HR 100-112 - first of all, those are very random numbers; second, you would want a lot lower Heart Rate probably between 50 and 70 for the first day or two...

2) propofol at 25mcg/kg/min is a joke of a sedating dose - i would start the epidural as soon as the patient demonstrates that he has motor function of his lower limbs (not earlier) - if you are unable to get a somewhat decent motor/neuro exam, then a narcotic drip with the propofol would be more appropriate... i wouldn't stop the propofol unless hypotension becomes a serious issue and/or patient is demonstrating cardiac ischemia.

3) CVP w/ a Urine output of 30-60cc/hr - this is not very much information - how do we know that the AAA wasn't juxta-renal or even supra-renal??? and even in circumstances of infra-renal clamping you can see hits to the kidneys... I wouldn't even focus that much on urine output unless it dropped below 30cc/hr - instead of giving lasix which is the wrong drug at this point, i would volume resuscitate the patient (NOT diurese) - usually hemodynamic instability (as you showed with his BP 60-220) is due to hypovolemia. One thing is for sure with AAA repairs, there is definite thirdspacing (whether it is a midline or retro-peritoneal approach) and these patients usually have HIGH volume requirements for the first 2 days or so. Plus it is erroneous to use CVP as an indicator for volume status - it measures Central Venous Pressure (since WHEN ??? has that been shown to be related to ventricular filling pressures - which is probably the most accurate way of assessing volume status (either by swan or by ECHO). at most you could argue that following CVP trends gives an idea in a monitored setting of changes in volume - but that is it!!!

4) the drop in H&H is difficult to interpret - does it correlate with increasing drops in BP? does it correlate with an increasingly distended/firm abdomen? does it correlate with loss of pulses in the distal lower extremities? in that case you have to worry about oozing/bleeding (which can happen with diseased aortas...) to suggest that the drop in H&H is due to hemodilution doesn't make much sense if you tell us that you were just using lasix to diurese the patient.... now i am suspecting that you didn't mention to us that the patient was being fluid resuscitated with large volumes of fluid - in which case hemodilution might be the right answer. however the drop is so significant that i would argue that the patient has been oozing... and i would also argue that post-operatively for AAA this patient needs a blood transfusion (which fixes the whole issue regarding colloid vs crystalloid) as the number ONE cause for peri-operative vascular death is cardiac in origin - and you wouldn't want to deprive a vasculopath in this setting of extra oxygen carrying capacity.

Tenesma:

What I learned about CVP was that CVP was an estimate of RVEDP. Because RVEDP is taken when the tricuspid valve is open, you get what can be assumed to be a open venous system, which can then be used to estimate ventricular pressures, which is then assumed to be related to volume in a normal heart. Obviously, there are a lot of assumptions in this and the result is something sort like a grey blob. I think if one has to resort to using CVP it would be best to use it in conjuction with stroke volume or, even better, stroke index, and like you said, watch the pattern rather than actual numbers.

As always, your post was greatly appreciated.

Diprivan/Vented:

while you are right that CVP is an estimate of RVEDP - it is in no way an estimate of left venticular pressures by any means. While you are also right that in a normal heart, not undergoing the stresses of anesthesia and/or surgery, in a healthy 25 year old, the CVP can be used as an indicator of volume in some instances... but that isn't the population we are dealing with.

CVP will be elevated in certain circumstances that have nothing to do with hypervolemia: metabolic acidosis, hypoxia or systemic hypertension which all three will increase pulmonary pressures and therefore retrograde increase the CVP, positive-pressure ventilation, deep breaths, straining, valsalva, right ventricular failure, or even worse biventricular failure, systemic vasoconstriction leading to higher right sided pressures and the list goes on and on... Even worse when the CVP is measured through a femoral line, those are famously inaccurate (primarily due to the stricture of the IVC between the diaphragm and the superior border of the liver which can be tightened even further in the setting of intra-abdominal events --- it isn't unusual for a femoral CVP to have a falsely elevated reading, and when you measure a CVP through a subclavian or a jugular vein you get a reading that is a good 10-20mmHg lower!!!

Now i can also list a whole bunch of stuff that will make a CVP look falsely lower than it should....

My point is that the CVP is useless - unless you are only planning on using it to follow trends - for example, during cardiac, when you are coming off the pump, you can follow trends to see how well your heart is doing at evacuating blood from the right side...

You are right that stroke volume is much more accurate in gauging intravascular volume status... but i disagree with the use of the stroke index... Using an index whether it is for SVR index, or Cardiac index or Stroke index is patently misleading....

i think it is far better to use a real measurable number and using clinical criteria - rather than polluting your numbers with "body surface area"... i think that is one of the most asinine additions to hemodynamic calculation/monitoring (initially used in studies when they tried to correlate canine/porcine hemodynamic studies with humans - in which case using differences in body surface area was useful in describing different patterns in horses, pigs, dogs and humans)... but between humans it isn't a good idea. Here is an example, two identical twins other wise healthy and both euvolemic with the exact same Cardiac Output... Now if one of those twins loses both limbs, his Cardiac Index would drop - however nothing has changed to his heart or his cardiac output... I really encourage those who are involved with hemodynamics to focus on the numbers that matter and can be directly measured, and avoid the use of numbers that are made more vague by multiple calculations ....

i'll step off my soapbox.... :)

Interesting stuff regarding indexed numbers Tenesma.

I think the majority of nurses were taught that indexed numbers were more accurate and thus our preoccupation for using them.

I think I'll agree with you for the most part on this point.

However, do you think it's a valid arguement to say that although a four foot 6 inch granny would have an adequate CO at 4L, a 7 foot tall basketball player would not?

Or do you think this is a falsehood and that all adult humans can be adequately perfused at a normal cardiac output of 4 - 8L?

i must say - i learn alot reading your posts!!

brenna's dad:

you bring up a good point... first those two examples represent 2 extremes, but i still feel that a Cardiac Output of 4-8l/min is fine regardless of size in adult patients (unless they are truely less than 4 feet tall...)... I think what matters more than their size is how they are doing clinically... A 7foot basketball player who has a Map of 45 and is having mental status changes with a CO=4 is more concerning than a 7foot basketball player who has a MAP of 70 and is perfectly healthy with a CO=4...

So i think that the numbers need to be looked at individually and based on clinical presentation....