Thoughts on case?

[pharmer]

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Doing an MVR today on otherwise healthy 42 yo WM who had endocarditis from a tooth abscess (or so thought) that resulted in mod MR but pretty significant anemia (starting Hgb 8.9). Pre-op w/u showed good ventricular fxn on echo with EF65% no other significant valvular pathology, left heart cath did not reveal any significant CAD, very mild Pulm HTN with PA low 30s/20 with PCWP ~14. Pre-op CXR was clear, no pulm congestion/edema etc. In CV holding area patient was laying flat, denied SOA laying flat but with ambulation of 2 flights of stairs he said he would feel fatigued but not necessarily SOA, no chest pain (anemia most likely cause as opposed to his mod MR). Induction goes fine, sternotomy fine, cannula's in place cruising along smoothly and probably a few minutes away from going on pump (our CTS guys are pretty slow) and all of a sudden my PIP shoot up from 25 or so with TV of 600s to 40's with TVs of 60-80 , systolic pressures tank to 40-60s and PAp shoot up to 60s/40s and we have to crash onto pump. My thoughts were tension PTX or acute exacerbation of the MR (blown pap muscle?) although did not necessarily notice giant V-waves on PAC tracing (in all honesty to quite have time to appreciate). No tension PTX found but the right lung pleaural space was very full and surgeon tapped and pulled off 1L of clear yellow/amber fluid. This was likely the cause but why would this suddenly develop? Again pre-op CXR was clear (not sure how many days before the surgery the CXR was done though). I would love to hear people's thoughts.

 

[Bertelman]

Doing an MVR today on otherwise healthy 42 yo WM who had endocarditis from a tooth abscess (or so thought) that resulted in mod MR but pretty significant anemia (starting Hgb 8.9). Pre-op w/u showed good ventricular fxn on echo with EF65% no other significant valvular pathology, left heart cath did not reveal any significant CAD, very mild Pulm HTN with PA low 30s/20 with PCWP ~14. Pre-op CXR was clear, no pulm congestion/edema etc. In CV holding area patient was laying flat, denied SOA laying flat but with ambulation of 2 flights of stairs he said he would feel fatigued but not necessarily SOA, no chest pain (anemia most likely cause as opposed to his mod MR). Induction goes fine, sternotomy fine, cannula's in place cruising along smoothly and probably a few minutes away from going on pump (our CTS guys are pretty slow) and all of a sudden my PIP shoot up from 25 or so with TV of 600s to 40's with TVs of 60-80 , systolic pressures tank to 40-60s and PAp shoot up to 60s/40s and we have to crash onto pump. My thoughts were tension PTX or acute exacerbation of the MR (blown pap muscle?) although did not necessarily notice giant V-waves on PAC tracing (in all honesty to quite have time to appreciate). No tension PTX found but the right lung pleaural space was very full and surgeon tapped and pulled off 1L of clear yellow/amber fluid. This was likely the cause but why would this suddenly develop? Again pre-op CXR was clear (not sure how many days before the surgery the CXR was done though). I would love to hear people's thoughts.

The serous pleural effusion did not pop up that morning. I'm wondering if you maybe mainstemmed the tube into the Rt, where you uncovered the effusion.

Or perhaps the endocarditis involved the Rt heart, and this was an embolic event.

 

[pharmer]

The serous pleural effusion did not pop up that morning. I'm wondering if you maybe mainstemmed the tube into the Rt, where you uncovered the effusion.

Or perhaps the endocarditis involved the Rt heart, and this was an embolic event.

Had breath sounds on both sides so less likely mainstemmed but still possible as I just listened over the anterior aspect of the chest (? resonance from right side to the left). Meant to get FOB to check placement but got sidetracked with other tasks and didn't. When we came off pump patient's airway pressures were still slightly elevated mid-upper 30's with TV in 600's. Also thought about this being embolic event as well, ST depression went from baseline of -0.4 to -1.5 when pressures were tanking but pushed 100mcg of epi with improved pressures and ST normalization in II and V5, also coming off pump TEE did not show any wall montion abnormalities (wish we would have had echo in place during case prior to going on pump when all this was happening).

Just realized you likely meant PE in regards to embolic event...possible.

 

[Bertelman]

Confused as to why you would embark on an MVR for endo without TEE.

 

[sevoflurane]

I dont think 1liter of pleural fluid is going to affect your pa pressures and particularly TV's (600-->60-80 Tv's) to that degree. I've seen a lot bigger pleural effusions with much better TV's. Compliance usually improves significantly immediately after.

Drug reaction? Bronchospasm/hypotension?

 

[sevoflurane]

If it was a drug rx, that 100mcgs of epi u pushed prolly helped the bronchospasm. I have seen bronco spasm that is so severe I get little to no ETCO2 and TV's.

 

[Idiopathic]

almost has to be anaphylaxis/drug rx

 

[Bertelman]

Agree. Heparin maybe? Was cannulating

 

[pharmer]

We don't routinely place TEE for our pump cases except for valve repair and in this case it is done by cardiology (Im not certified in TEE) specifically to check the integrity of the valve. Bronchospasm is a possible thought, still had ETCO2 and did not appreciated any wheezing when bagging by hand but then again not a whole lot of air movement was taking place. Im not sure what the allergic reaction would have been to as I had not introduced anything new really since induction, ?Amicar but I give this pretty quickly after induction and lines are placed, ?Vec, Heparin.

 

[Idiopathic]

We don't routinely place TEE for our pump cases except for valve repair and in this case it is done by cardiology (Im not certified in TEE) specifically to check the integrity of the valve. Bronchospasm is a possible thought, still had ETCO2 and did not appreciated any wheezing when bagging by hand but then again not a whole lot of air movement was taking place. Im not sure what the allergic reaction would have been to as I had not introduced anything new really since induction, ?Amicar but I give this pretty quickly after induction and lines are placed, ?Vec, Heparin.

2 likely causes, especially if you didnt redose heparin

 

[HalO'Thane]

This seemed to occur almost in sync with the placement of the arterial and venous cannulae. Any chance this could have been a cpb circuit/cannula induced emboli; either air or particulate? Without a TEE it would be really hard to tell.

 

[Idiopathic]

i dont know if i would expect the severity of bronchospasm that was seen with that scenario, if the cause were embolic, but it has to be considered.

 

[urge]

Surgeon probably introduced a lot of air into the venous circulation while cannulating and the lungs didn't like it.

 

[HalO'Thane]

i dont know if i would expect the severity of bronchospasm that was seen with that scenario, if the cause were embolic, but it has to be considered.

You can get pretty severe bronchospam and unilateral pulmonary edema after a PE. There are quite a few papers on this subject. Anecdotaly, I've seen a few cases of PE on awake patients during my SICU rotations. Often their primary presentation is severe bronchospasm that can mimic an asthma/COPD exacerbation.

 

[sevoflurane]

This might be a good case for the med studs out there to review v/q mismatch.

So is this perfusion w/o ventilation? or vent w/o perfusion? or both?

So far we have:

Air embolism and drug rx./anaphylaxis.

Not being critical here, but if the TEE probe was in you should be able tell pretty easily if it was an air embolism with outflow obstuction causing hypotension.

I am not going to go into specifics on this thread... but one my biggest cases this year was a massive Co2 embolism. Catastrophic. TEE was in lickidy split and the diagnosis was secured in less than 3 minutes of the onset symptoms (non-cardiac case). CT surgeon was called and CPB was implemented shortly after.

 

[Idiopathic]

You can get pretty severe bronchospam and unilateral pulmonary edema after a PE. There are quite a few papers on this subject. Anecdotaly, I've seen a few cases of PE on awake patients during my SICU rotations. Often their primary presentation is severe bronchospasm that can mimic an asthma/COPD exacerbation.

thanks i looked up some case reports of this and retract my earlier statement. i still think its a drug rx but embolism seems just as likely.

 

[lushmd]

Knowing what sort of support the patient required post bypass may provide some insight as to the etiology of the pre-bypass instability. OP, care to share this information?

 

[RT2MD]

This might be a good case for the med studs out there to review v/q mismatch.

So is this perfusion w/o ventilation? or vent w/o perfusion? or both?

So far we have:

Air embolism and drug rx./anaphylaxis.

Not being critical here, but if the TEE probe was in you should be able tell pretty easily if it was an air embolism with outflow obstuction causing hypotension.

I am not going to go into specifics on this thread... but one my biggest cases this year was a massive Co2 embolism. Catastrophic. TEE was in lickidy split and the diagnosis was secured in less than 3 minutes of the onset symptoms (non-cardiac case). CT surgeon was called and CPB was implemented shortly after.

I'll attempt... If there was a PE, then it would be ventilation without perfusion... Unless there was superimposed bronchospasm. I actually hadn't heard about the link between bronchospasm and PE. If there was bronchospasm then it would be a ventilation problem as well. If it was a drug rxn, then the primary problem would be perfusion without ventilation, but wouldn't the vasodilation also cause some problems with perfusion? It would seem like the distribution of the west zones would be disrupted from a perfusion standpoint as well... Not to mention decreased cardiac output due to decreased preload.

 

[sevoflurane]

I'll attempt... If there was a PE, then it would be ventilation without perfusion... Unless there was superimposed bronchospasm. I actually hadn't heard about the link between bronchospasm and PE. If there was bronchospasm then it would be a ventilation problem as well. If it was a drug rxn, then the primary problem would be perfusion without ventilation, but wouldn't the vasodilation also cause some problems with perfusion? It would seem like the distribution of the west zones would be disrupted from a perfusion standpoint as well... Not to mention decreased cardiac output due to decreased preload.

Forgot about this thread, sorry 'bout the late response RT2MD:

Here is a little review for the med studs and those getting ready to take in-training exams or boards etc. Everything below is fair game on these tests:

So lets' define v/q. V= ventilation, Q= perfusion.
Normal v/q mismatch ratio in an adult is about .8

Now regarding PE's:

In it's purest form, a pulmonary emboli is a DEAD SPACE lesion and not a shunt.

So what is DEAD SPACE?

Ventilation without perfusion. 2 types:

1. Anatomic dead space = does not participate in gas exchange ie trachea
2. Alveolar dead space = is at the alveolar level and does not participate in gas exchange due to POOR PERFUSION as in a PE, cardiogenic shock, peep (too much peep will compress surrounding vascular structures) or west zone 1 if you are looking at differences in V/Q matching in the upright lungs. etc.

Together anatomic dead space and alveolar dead space is referred to as physiologic dead space.

The equation for Dead space is: (PaCo2-ETCo2/PaCo2)

So what is a SHUNT?

It's the opposite of dead space... Shunt is perfusion without ventilation. In other words blood gets to the left side of the heart without getting oxygenated... it is beeing shunted past the alveoli and therefore bypasses gas exchange.

Is shunt normal? The answer to this is yes. Bronchial, pleural and thebasian veins dump directly into the LEFT side of the heart and therefore do not participate in gas exchange. This is referred to as physiologic shunt = 5% of CO. Above this, you need to find a reason.

So what are some examples of shunt?

Atelectasis, airway obstruction, bronchospasm, PTX, main stem intubation and....... PULMONARY EDEMA!

So back to out question...

Is a PE a dead space or shunt problem?

In it's purest form it's ventilation without perfusion = Dead space. HOWEVER, a big enough PE can cause bronchospasm and micro/macroscopic alveolar edema and if bad enough profound pulmonary edema... all of which are SHUNTS. So in reality, massive PE's cause both Dead Space (primarily) and a Shunt (secondarily) lesion.

Just like to add that big PE's can be difficult to treat. Dead space of that nature will not respond very effectively to raising the partial pressure of O2 as those alveoli are not being perfused due to lack of blood flow to that area (no gas exchange). Big PE's can be very tough to treat, sometimes requiring CPB as a way to provide some means of gas exchange/oxygenation and a conduit to fix the problem (big air embolus, saddle embolus, etc). Last one of these I did, we went onto bypass with sats in the 30% range on 100% O2 = No es bueno.

An acutely ischemic heart is impressive to see.... as is its ability to rapidly pink up once you fix the problem.

I hope this helped some of you rock stars out there... sorry ‘bout the late response.

 

[sevoflurane]

and just cuz I like pictures...

Kind of fun to read through:

http://www.omicsonline.org/2155-6148/2155-6148-2-169.php

 

[drmwvr]

no pfo, I see.

 

[RT2MD]

Forgot about this thread, sorry 'bout the late response RT2MD:

.....

I hope this helped some of you rock stars out there... sorry ‘bout the late response.

Thanks for the reply, for some reason I didn't get an email about a reply on this thread, so I was late as well! 😎 Anyway, thanks again for the contribution!