CCM Case

[Gator05]

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Alright, here's a case from the other day.

Older woman with "normal" lungs and heart, undergoes Major Vascular Surgery including aorta. Complications ensue involving the gut. Portions of gut removed.

Patient on CVVH for renal failure. CI ~2.2 range, SvO2~60% and falling, EDVI 60, BP 90's/50's, lactates >3 and climbing. Pt made much more positive over several hours to the tune of >15 liters of mostly colloid, EDVI responds to 95. (Pt grossly edematous, low albumin and so replaced.) Dobutamine also started. SvO2 improves to 65, BP to 100's/60's, CI to 2.4. Lungs now quite wet on CXR, vent settings escalated for hypoxemia, CVVH to keep pt slightly negative.

SvO2, BP, CI begin to fall, vent settings escalated eventually to PIP almost 50, CPAP 15. Dobutamine escalated, pt started on milrinone. BP's 100/80's, CI 2.5, SvO2 62%, EDVI 90, and now falling. Lactates climbing.

Apologies for any and all missing details.

What would you do?

 

[militarymd]

sprinkle some dirt on the patient.

 

[militarymd]

then measure the bladder pressure.

 

[dhb]

Alright, here's a case from the other day.

Patient on CVVH for renal failure. CI ~2.2 range, SvO2~60% and falling, EDVI 60, BP 90's/50's, lactates >3 and climbing. Pt made much more positive over several hours to the tune of >15 liters of mostly colloid, EDVI responds to 95. (Pt grossly edematous, low albumin and so replaced.) Dobutamine also started. SvO2 improves to 65, BP to 100's/60's, CI to 2.4. Lungs now quite wet on CXR, vent settings escalated for hypoxemia, CVVH to keep pt slightly negative.

SvO2, BP, CI begin to fall, vent settings escalated eventually to PIP almost 50, CPAP 15. Dobutamine escalated, pt started on milrinone. BP's 100/80's, CI 2.5, SvO2 62%, EDVI 90, and now falling. Lactates climbing.
What would you do?

So obviously the patient is in shock and her lungs are stiff so where does it come from?
Are they sign of sepsis +- ARDS? if so treat with wide spect atb and appropriate ventilation
How's her heart? i would get an US to check for ventricular disfunction/mi/ tamponnade considering her edematous state + renal failure
would check her ions Ca, Mg etc.. can get washed out pretty fast on cvvh if not present in the bath.

 

[dhb]

oh yeah and the bladder pressure 😀

 

[Gator05]

Ions ok, bladder pressure ok, hct ok, no evidence of ARDS/sepsis although pt on lots of abx anyhow, echo results pending.

It gets more interesting. To prove a point that the high vent settings aren't contributing, someone disconnects pt for ~30 seconds. Except, sats remain ok, BP improves, by a lot, now 120/80's. Vent reconnected, pressures drop again.

 

[militarymd]

Ions ok, bladder pressure ok, hct ok, no evidence of ARDS/sepsis although pt on lots of abx anyhow, echo results pending.

It gets more interesting. To prove a point that the high vent settings aren't contributing, someone disconnects pt for ~30 seconds. Except, sats remain ok, BP improves, by a lot, now 120/80's. Vent reconnected, pressures drop again.

You're talking out of both sides of your mouth now....

You say CXR is shows wet lungs...and increasing vent settings for hypoxemia.....

Now you say that the patient can be left on ZEEP for 30 seconds without desaturation....

One story is not consistent with the other.

 

[Gator05]

Agreed, military, but this is as the case was posted to us. Now, 30 second disconnect, the pulse-ox is averaging over roughly the same time frame, so I can buy a short disconnect with sats remaining >90%, but I will say 30 seconds is pushing it.

This may be a good time to admit that I don't have a good explanation for what's going on. This case hasn't been resolved by the presenters. I would guess overresucitation leading to wet lungs leading to elevated vent settings leading to decreased venous return and thus low EDVI, low CI , which then repeats based on a low EDVI. Again, a guess, not an explanation.

Hence, the appeal to the experts.

 

[aredoubleyou]

echo results pending.
.

Hmmmm...lemme guess. Some kinda restrictive picture...High PEEP, preload dependant physiology, preload decreased...gets when intrathoracic pressures decrease. normal heart on CXR? JVP waves normal? Restrictive cardiomyopathy? Restrictive pericarditis? Tamponade?

 

[Pilot Doc]

Pneumothorax with vent pressures pushing it over to tension physiology?

 

[militarymd]

You're talking out of both sides of your mouth now....

You say CXR is shows wet lungs...and increasing vent settings for hypoxemia.....

Now you say that the patient can be left on ZEEP for 30 seconds without desaturation....

One story is not consistent with the other.

I stick with this.......The picture has not been painted accurately.

 

[SouthSideSteve]

sprinkle some dirt on the patient.

This is the correct answer. The fact that it was provided by an asian only further proves its legitimacy.

 

[Noyac]

Call in the family. Give them the dismal facts and hope they make the right decision.


I know you want to know how to treat this pt. I'd consider some vasopressin, inverse ratio ventilation with sedation and paralysis. Its been a long time since I have managed a ICU pt which may be obvious.

SvO2 is something that I put little faith in. How do you know if the value is low because of delivery or higher utilization? THe lactate helps.
But just as with high SvO2 how do you know if it is because of poor cellular utilization or higher delivery of O2?

Just some thoughts.

 

[Gator05]

I stick with this.......The picture has not been painted accurately.

CCM case was presented as it was to us. I've gone over it dozens of times, and agree this doesn't add up. I won't dispute details may be missing. This was so noted in the original post.

 

[militarymd]

CCM case was presented as it was to us. I've gone over it dozens of times, and agree this doesn't add up. I won't dispute details may be missing. This was so noted in the original post.

I would like to hear more when they give you more info.

 

[dhb]

someone disconnects pt for ~30 seconds. Except, sats remain ok, BP improves, by a lot, now 120/80's. Vent reconnected, pressures drop again.

So this shows the vent pressure is impeding venous return so she's iv depleted which is possible if you're kepping here negative with the cvvh and she can't transfer fluid from the extra-cellular to the intra-vascular compartment...

 

[aredoubleyou]

So this shows the vent pressure is impeding venous return so she's iv depleted ...

I agree, but I'm guessing she's got a bad ticker exacerbating the situation, preload dependant physiology for some reason (I'm sticking with my restrictive heart disease picture) - which is why the pressors arent doing much for her but decreasing her intrathoracic pressure does help. Or maybe she's just really dry now and autopeeping like mad. I aint all that bright, but trying inverse vent and decreasing CPAP seems to make sense to me.

 

[dhb]

I aint all that bright, but trying inverse vent and decreasing CPAP seems to make sense to me.

Especially if she can handle it sat wise...
So Gator any info on that pending echo result?

 

[aredoubleyou]

comeon dude - what happened? I have the patience of a 9 year old.

 

[jetproppilot]

comeon dude - what happened? I have the patience of a 9 year old.

 

[Gator05]

OK folks.

TTE comes back "normal". Yes, that's right, normal, albeit on milrinone.

Started patient on PGI to improve oxygenation, and boy did it ever, to the point where MAP and FiO2 was decreased.

Of course, PGI gets absorbed, and afterload dropped. Started up Vasopressin.

Things at this point looked really good, EDVI >100, SvO2 >80, SVI 40's, MAP>70 with CVVH to even.

Turns out HR was an issue. Multiple things tried to bring sustained HR of >110 (in a vascular patient 😕 😕 )under control, including lopressor and dilt and dig and esmolol. Eventually found high-dose lopressor worked, but brought BP down. EDVI dropped a bit too at this time, and BP picked up with some volume. Eventually tx to esmolol, which worked to bring HR <80's. Again, all the numbers looking good, right about the time the ST's started climbing.

Stay tuned...

 

[militarymd]

what's PGI?

 

[Noyac]

what's PGI?

prostaglandin something

 

[dhb]

prostaglandin something

...inhibitor?

 

[proman]

prostaglandin I, aka prostacyclin

 

[Gator05]

It's the poor-man's iNO. Placed in-line with the vent circuit sorta like a controlled neb. It works, but because it's systemically absorbed pretty darn well, it can end up working systemically too.

 

[militarymd]

It's the poor-man's iNO. Placed in-line with the vent circuit sorta like a controlled neb. It works, but because it's systemically absorbed pretty darn well, it can end up working systemically too.

So the patient was placed on pulmonary vasodilator for hypoxia....and experimental at that....

but the patient can tolerate ZEEP for 30 seconds?😕

 

[Gator05]

Alrighty, militarymd.

I'll bite; the pulse-ox observation must have been flawed. Following the last post, f/u ABG's noted consistently decreased PaO2's in the 60's range. Sounds like the 30 seconds was exagerated.

PGI may be experimental, but there are at least a handful of institutions using it as an iNO replacement for cost reasons. Uses include PH and hypoxia.

Incidentally, we noted >10tor increase in PaO2 within 1h of starting PGI. I don't have much experience (n=1), but studies below note less impressive improvements in PaO2. Perhaps the combination of phosphodiesterase inhibition and epoprostenol are super-additive?


Inhaled prostacyclin (PGI2) is an effective addition to the treatment of pulmonary hypertension and hypoxia in the operating room and intensive care unit.
Can J Anaesth. 2001 Oct;48(9):924-9


Inhaled prostacyclin is safe, effective, and affordable in patients with pulmonary hypertension, right heart dysfunction, and refractory hypoxemia after cardiothoracic surgery.
J Thorac Cardiovasc Surg. 2004 Apr;127(4):1058-67

 

[Noyac]

Iloprost (Ventavis) is a synthetic analogue of prostacyclin PGI2, which I think is what the other poster was referring to. It is the first inhaled prostacyclin therapy (not cheap - or a poor man's drug by any means!)

It dilates systemic & pulmonary arterial vascular beds. The advantage is there is little pulmonary rebound. It was just approved in 2003 or 2004 I think & not many hospitals have it on the formulary.

 

[Gator05]

Poor-man's anything is a joke when it comes to much of modern ICU care.

At our institution, it's considerably cheaper to avoid flicking the on switch of the iNO machine.

 

[Hockeyguy]

then measure the bladder pressure.

Mil do you completely paralyze folks for this? We do. But an ICU doc told me today it was unneccesary. Just curious on your take.

Mario

 

[militarymd]

Mil do you completely paralyze folks for this? We do. But an ICU doc told me today it was unneccesary. Just curious on your take.

Mario

Originally described by Kron...CT surgeon......

I actually don't remember if paralysis is required or not.

 

[Gator05]

Iloprost (Ventavis) is a synthetic analogue of prostacyclin PGI2, which I think is what the other poster was referring to. It is the first inhaled prostacyclin therapy (not cheap - or a poor man's drug by any means!)

It dilates systemic & pulmonary arterial vascular beds. The advantage is there is little pulmonary rebound. It was just approved in 2003 or 2004 I think & not many hospitals have it on the formulary.

Actually, the PGI2 we're using is epoprostenol. This is NOT the same formulation as iloprost, and IS considerably cheaper.

 

[Noyac]

Actually, the PGI2 we're using is epoprostenol. This is NOT the same formulation as iloprost, and IS considerably cheaper.

Point taken. 👍