Since we need to be more 'clinical' here's one case for you

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toughlife

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73 year old year with severe MR admitted for MVR and CABG redo evaluation. Past medical hx is remarkable for CAD with two recent MIs, DM, HTN, s/p CABG on 12/2001.

6 weeks ago pt presented to outside hospital with CP and found to have STEMI complicated with cardiogenic shock, respiratory failure and CHF and noted to have severe MR. She underwent placement of IABP on admission. One day PTA, LHC showed 80% stenosis of LIMA-LAD graft with placement of Taxus stent, codominant RCA with 100% occlusion, mild stenosis of the LCx, and left main trunk stenosis. 3+ MR and EF of 30%. Patient discharged.

LAte april patient presented to ED again c/o SOB and chest pressure for one week. Troponins noted to be at 0.59, BNP of 3630, and treated with Nitro, heparin, aspirin. She was admitted for MI and diuresed with lasix. Creatinine doubled from 1.2 to 2.1.

Echo: EF 30-35%, with 3+ MR and annular calcification, Trace AI and aortic sclerosis with mean gradient of 7mmhg.

One week post admission patient found unresponsive, bradycardic and hypotensive, requiring atropine but no CPR. Patient developed respiratory failure as a result and transferred to ICU. Also had IABP placed again and remained on it as attempts to weaning led to decreased urine output. At that time, patient also noted to have thrombocytopenia with platelets of 69 down from 302 on admission but prior to IABP placement. Heparin was d/c'd and switched to Argatroban. HIT panel sent but no results available.

Pt also c/o RUQ pain, LFTs showed AST: 757, ALT 985, Alk. 77. HIDA scan was suspicious for CBD obstruction and acute cholecystitis. RUQ u/s + for gallstones, no GB wall thickening. Repeat LFTs on 5/7 showed AST:69 and ALT: 508. Patient evaluated by CTS for possible redo-CABG/MVR but unable to due to inability to wean off IABP.

On arrival to our hospital, pt weaned off AIBP, Swan placed and CI noted to be 1.8 with PAPs 60/30, wedge= PAD and decreased UOP despite lasix gtt. Also c/p CP and put back on IABP. Patient placed on NTP and NTG for afterload reduction with no improvement in PA pressures. Patient now lethargic, creatinine increasing to 1.6. Also on Bivalirudin given ? of HIT.

Patient currently satting at 94% on 4L
EKG shows trifascicular block
Current Na= 130
Current platelets= 103

PMHx: s/p MI x2, HTN, questionable hx of CRI 2/2 to nephrosclerosis, PVD and DJD. No tobacco or ETOH use.



Patient evaluated by CTS and scheduled for OR for next day for MVR and redo-CABG.

Anesthesia called to preop patient.

What would be your plan for this patient?

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GETA with post op vent.
Next!
 
73 year old year with severe MR admitted for MVR and CABG redo evaluation. Past medical hx is remarkable for CAD with two recent MIs, DM, HTN, s/p CABG on 12/2001.

6 weeks ago pt presented with CP and found to have STEMI complicated with cardiogenic shock, respiratory failure and CHF and noted to have severe MR. She underwent placement of IABP on admission. One day PTA, LHC showed 80% stenosis of LIMA-LAD graft with placement of Taxus stent, codominant RCA with 100% occlusion, mild stenosis of the LCx, and left main trunk stenosis. 3+ MR and EF of 30%. Patient discharged.

LAte april patient presented to ED again c/o SOB and chest pressure for one week. Troponins noted to be at 0.59, BNP of 3630, and treated with Nitro, heparin, aspirin. She was admitted for MI and diuresed with lasix. Creatinine doubled from 1.2 to 2.1.

Echo: EF 30-35%, with 3+ MR and annular calcification, Trace AI and aortic sclerosis with mean gradient of 7mmhg.

One week post admission patient found unresponsive, bradycardic and hypotensive, requiring atropine but no CPR. Patient developed respiratory failure as a result and transferred to ICU. Also had IABP placed again and remained on it as attempts to weaning led to decreased urine output. At that time, patient also noted to have thrombocytopenia with platelets of 69 down from 302 on admission but prior to IABP placement. Heparin was d/c'd and switched to Argatroban. HIT panel sent but no results available.

Pt also c/o RUQ pain, LFTs showed AST: 757, ALT 985, Alk. 77. HIDA scan was suspicious for CBD obstruction and acute cholecystitis. RUQ u/s + for gallstones, no GB wall thickening. Repeat LFTs on 5/7 showed AST:69 and ALT: 508. Patient evaluated by CTS for possible redo-CABG/MVR but unable to due to inability to wean off IABP.

On arrival to our unit, pt weaned off AIBP, Swan placed and CI noted to be 1.8 with PAPs 60/30, wedge= PAD and decreased UOP despite lasix gtt. Also c/p CP and put back on IABP. Patient placed on NTP and NTG for afterload reduction with no improvement in PA pressures. Patient now lethargic, creatinine increasing to 1.6. Also on Bivalrudin given ? of HIT.

Patient currently satting at 94% on 4L

PMHx: s/p MI x2, HTN, questionable hx of CRI 2/2 to nephrosclerosis, PVD and DJD. No tobacco or ETOH use.

Current Na= 130
Current platelets= 103

Patient evaluated by CTS and scheduled for OR for next day for MVR and redo-CABG.

Anesthesia called to preop patient.

What would be your plan for this patient?

Nice case.

First thing to put in mind is that because of this patients critically ill preoperative status, his operative morbidity/mortality % is high.

This is almost a heroic effort.

Make sure prbcs/ffp/cryo/platelets are ready before starting. Have prbcs in the frig outside the room.

NTG + NTP for afterload reduction seems like overkill to me, especially with an IABP in place. I'd kill the NTP and minimize the NTG before induction, knowing whatever induction drugs given will contribute to lowering SVR. Even etomidate/opiods in this critically ill patient.

With high PA pressures, low EF, and concerns of keeping SVR low-normal range I think a phosphdiesterase inhibitor would've been a better choice than NTG + NTP.

Cardiac index of 1.8 is encouraging. Have seen much worse.

Keep in mind you're gonna hafta maintain high filling pressures and heart rate until the pump run. I'd run old-school thinking on blood administration here...if his HCT is below 30, I'd hang blood before starting. If its above 30, I'd have it ready for giving soon.

I'd start dopamine 2 ug/kg/min despite some studies questioning its renal efficacy.

Place another 9.0 cordis in the neck or subclav, plus a big peripheral IV, since his current central line has a SWAN in it. Cant give volume where the SWAN is living. Of course a radial A line, even though you've got balloon pump pressures.

Into the OR, monitors on, pre-O2, all the while giving incremental midazolam to the point of somnulence....if you can achieve near apnea with midazolam increments, this will benefit you in your induction, since amnesia is taken care of and you don't need a big bolus of anything, all the while with very little hemodynamic aberration. Usually.

Is he very, very sleepy now? Great. Give 6-10 mg etomidate followed by 10mg vecuronium or whatever muscle relaxant you prefer. Work in 100-250 ug fentanyl or 50-100ug sufentanil if pressures havent dropped alot..

Pressure starting to drop?

Intubate. That usually brings it back up.

Glycopyrrolate (.2-.4 mg) is a good drug to mildly-moderately increase heart rate if you need a faster rate. Of course if it drops very low pull out the atropine.

The main number I'd be watching in addition to BP and HR is the PAD. Its gonna be hard to maintain it at 30 post induction. Thats why I'd think liberal with blood administration. If he needs volume, give blood unless his HCT is normal, which I bet it isnt.

There you have it. Keeping his intravascular space full, and rich with hemoglobin, and his heart rate faster than normal, keeping filling pressures high, and SVR in the 600-800 range.

Assuming no catastrophes, you'll make it to the pump run.

30 minutes before coming off I'd start a phosphodiesterase inhibitor. Make sure the pump tech has maximized the HCT. Have platelets and FFP in the room and checked.

Give 1 gram CaCl as soon as the aortic clamp comes off.

Make sure everything is optimized before coming off bypass:

Temperature at least 36.0 C......temp 35.6? Wait a little longer.
NSR or equivalent at 90-100 rate. Unable to achieve? Pace at 100.
Systolic 90 or greater
HCT high twenties
Ventilating
SV02 optimized.


....................................then the fun starts.

Hard to say what happens next, after DCing bypass.
 
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My plan:

1)Betablock her
2) Remove all invasive monitors ie; Swan, A-line, etc.
3)No surgery at all.

See how she does.

These people never bothered to take care of themselves ad now we are supposed to perform miracles? Everyday we waste resources on these people. Why can't we allow them to expire in some sort of dignified way? Why do we continue to put on the full court press when everyone involved except the family members know it is futile?

The health care industry (I'm talking about the physicians involved in these cases) should come up with some sort of scoring system where if someone has a certain number of comorbidities that rank over a set number then they get medical management only and nothing invasive. No ICU admission, no operations unless it will relieve suffering or improve quality of life substantially. These are no win cases for anyone, not even the pts.
 
My plan:

1)Betablock her
2) Remove all invasive monitors ie; Swan, A-line, etc.
3)No surgery at all.

See how she does.

These people never bothered to take care of themselves ad now we are supposed to perform miracles? Everyday we waste resources on these people. Why can't we allow them to expire in some sort of dignified way? Why do we continue to put on the full court press when everyone involved except the family members know it is futile?

The health care industry (I'm talking about the physicians involved in these cases) should come up with some sort of scoring system where if someone has a certain number of comorbidities that rank over a set number then they get medical management only and nothing invasive. No ICU admission, no operations unless it will relieve suffering or improve quality of life substantially. These are no win cases for anyone, not even the pts.

I like your plan better, Noy.

Youre absolutely right.
 
It's going to be tough getting her off CPBP.
She has Left + Right heart failure, Pulm hypertension, impending renal failure, Hepatic ischemia most likely due to RV failure, and almost nonexistent conducting system.
Even if they improve her coronary perfusion and fix the mitral valve the damage is done.
On the other hand they will still want to operate on her despite all your concerns, so you take her to the OR and do all the good things that Jet mentioned, you will most likely need the IABP and pacer post op, and she will still die in a few months if she is lucky.
 
My plan:

1)Betablock her
2) Remove all invasive monitors ie; Swan, A-line, etc.
3)No surgery at all.

See how she does.

These people never bothered to take care of themselves ad now we are supposed to perform miracles? Everyday we waste resources on these people. Why can't we allow them to expire in some sort of dignified way? Why do we continue to put on the full court press when everyone involved except the family members know it is futile?

The health care industry (I'm talking about the physicians involved in these cases) should come up with some sort of scoring system where if someone has a certain number of comorbidities that rank over a set number then they get medical management only and nothing invasive. No ICU admission, no operations unless it will relieve suffering or improve quality of life substantially. These are no win cases for anyone, not even the pts.

Smartest post I have seen in a while. I can't believe CT surgery is even considering this - time to let it go.
 
Jet, I agree with the phosphdiesterase inh. in this case but I always found that epi worked better in conjunction with milrinone. Have you had the same experience? It has something to do with the cAMP intracellularly if I remember right. Someone correct me if I am wrong.

Where's SDN when we need her?:D
 
Jet, I agree with the phosphdiesterase inh. in this case but I always found that epi worked better in conjunction with milrinone. Have you had the same experience? It has something to do with the cAMP intracellularly if I remember right. Someone correct me if I am wrong.

Where's SDN when we need her?:D

yeah, they're synergistic, Noy. Have had the same experience.....but might wanna hold the epi until after the pump run (if you can) since it'll really increase SVR.
 
yeah, they're synergistic, Noy. Have had the same experience.....but might wanna hold the epi until after the pump run (if you can) since it'll really increase SVR.

And the dopamine will keep that rate up nicely as well.:thumbup:
 
patients like these are done everyday in the ORs at my training institution. I personally enjoy all the complicated stuff because it makes you really think about all the issues and, hopefully, will make me a good gaspasser once I am done.
 
Nice case.

First thing to put in mind is that because of this patients critically ill preoperative status, his operative morbidity/mortality % is high.

This is almost a heroic effort.

Make sure prbcs/ffp/cryo/platelets are ready before starting. Have prbcs in the frig outside the room.


NTG + NTP for afterload reduction seems like overkill to me, especially with an IABP in place. I'd kill the NTP and minimize the NTG before induction, knowing whatever induction drugs given will contribute to lowering SVR. Even etomidate/opiods in this critically ill patient.

I see your point but patient's SG parameters were still suboptimal with Ci in 2.1 or so range when only one afterload reducer was used and urine output reduced severely despite lasix.

With high PA pressures, low EF, and concerns of keeping SVR low-normal range I think a phosphdiesterase inhibitor would've been a better choice than NTG + NTP.

Ok so I thought about a sildenafil infusion but pharmacy said they don't have it on formulary :D B]

Cardiac index of 1.8 is encouraging. Have seen much worse.

Keep in mind you're gonna hafta maintain high filling pressures and heart rate until the pump run. I'd run old-school thinking on blood administration here...if his HCT is below 30, I'd hang blood before starting. If its above 30, I'd have it ready for giving soon.


I'd start dopamine 2 ug/kg/min despite some studies questioning its renal efficacy.
As far as knew , the renal vasodilatory effect of low-dose dopamine is effective in healthy subject but with little to no effect in critically ill patients.

Place another 9.0 cordis in the neck or subclav, plus a big peripheral IV, since his current central line has a SWAN in it. Cant give volume where the SWAN is living. Of course a radial A line, even though you've got balloon pump pressures.

Into the OR, monitors on, pre-O2, all the while giving incremental midazolam to the point of somnulence....if you can achieve near apnea with midazolam increments, this will benefit you in your induction, since amnesia is taken care of and you don't need a big bolus of anything, all the while with very little hemodynamic aberration. Usually.

Is he very, very sleepy now? Great. Give 6-10 mg etomidate followed by 10mg vecuronium or whatever muscle relaxant you prefer. Work in 100-250 ug fentanyl or 50-100ug sufentanil if pressures havent dropped alot..

Pressure starting to drop?

Intubate. That usually brings it back up.

Glycopyrrolate (.2-.4 mg) is a good drug to mildly-moderately increase heart rate if you need a faster rate. Of course if it drops very low pull out the atropine.

The main number I'd be watching in addition to BP and HR is the PAD. Its gonna be hard to maintain it at 30 post induction. Thats why I'd think liberal with blood administration. If he needs volume, give blood unless his HCT is normal, which I bet it isnt.

I agree and I initially thought increasing the IABP ratio would help to increase PA pressures since you would decrease its after load reduction effects. However, now that I understand it more, it would not make sense because you would be negating the positive effects IABP has on increasing O2 supply and decreasing myocardial oxygen demand. And in this patient that can easily mean another MI

There you have it. Keeping his intravascular space full, and rich with hemoglobin, and his heart rate faster than normal, keeping filling pressures high, and SVR in the 600-800 range.

Assuming no catastrophes, you'll make it to the pump run.

30 minutes before coming off I'd start a phosphodiesterase inhibitor. Make sure the pump tech has maximized the HCT. Have platelets and FFP in the room and checked.

Give 1 gram CaCl as soon as the aortic clamp comes off.

Make sure everything is optimized before coming off bypass:

Temperature at least 36.0 C......temp 35.6? Wait a little longer.
NSR or equivalent at 90-100 rate. Unable to achieve? Pace at 100.
Systolic 90 or greater
HCT high twenties
Ventilating
SV02 optimized.


....................................then the fun starts.

Hard to say what happens next, after DCing bypass.


Thanks for the input. I have many more cases and once I start my CA-1 year I'll be able to contribute more.
 
It's going to be tough getting her off CPBP.
She has Left + Right heart failure, Pulm hypertension, impending renal failure, Hepatic ischemia most likely due to RV failure, and almost nonexistent conducting system.
Even if they improve her coronary perfusion and fix the mitral valve the damage is done.
On the other hand they will still want to operate on her despite all your concerns, so you take her to the OR and do all the good things that Jet mentioned, you will most likely need the IABP and pacer post op, and she will still die in a few months if she is lucky.



well her elevated PAPs are largely due to her severe MR so replacing the valve could help that. Am I wrong? Also, in the ICU her NTG and NTP were not running at a max dose. We did try running them high and her wedge went down to 17.
 
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well her elevated PAPs are largely due to her severe MR so replacing the valve could help that. Am I wrong? Also, in the ICU her NTG and NTP were not running at a max dose. We did try running them high and her wedge went down to 17.

It depends on how long the MR has been present, because after a while, irreversible changes in the pulmonary circulation usually take place, and limit the benifit of replacing the valve.
The fact that her PAWP dropped with NTG + NTP is good but what happened to her BP when you did that? I suspect that her cardiac output dropped dramatically when you lowered her filling pressures.
 
It depends on how long the MR has been present, because after a while, irreversible changes in the pulmonary circulation usually take place, and limit the benifit of replacing the valve.
The fact that her PAWP dropped with NTG + NTP is good but what happened to her BP when you did that? I suspect that her cardiac output dropped dramatically when you lowered her filling pressures.

This patient had rheumatic heart disease when young. I think there was a decrease in her CO but I am not sure of its magnitude.
 
It's going to be tough getting her off CPBP.
She has Left + Right heart failure, Pulm hypertension, impending renal failure, Hepatic ischemia most likely due to RV failure, and almost nonexistent conducting system.
Even if they improve her coronary perfusion and fix the mitral valve the damage is done.
On the other hand they will still want to operate on her despite all your concerns, so you take her to the OR and do all the good things that Jet mentioned, you will most likely need the IABP and pacer post op, and she will still die in a few months if she is lucky.

Actually I was thinking that her elevation in LFTs was possibly due to shock liver during her earlier crash. The fact they are improving makes me think they were not chronically elevated and likely not due to hepatopulmonary syndrome.
 
Actually I was thinking that her elevation in LFTs was possibly due to shock liver during her earlier crash. The fact they are improving makes me think they were not chronically elevated and likely not due to hepatopulmonary syndrome.

This may also due to heart failure. You usually don't see those kind of number in HF though. I would agree that this looks more ischemic and is recovering (as a GI PA I can quickly dash out of the shadows). Usually the AST will recover first then ALT. Don't have a bili but assume there is no evidence of obstruction. First thing you learn in a specialty is blame the other specialties.

Interesting case. We see these frequently when we are called to do the PEG post op.

David Carpenter, PA-C
 
Actually I was thinking that her elevation in LFTs was possibly due to shock liver during her earlier crash. The fact they are improving makes me think they were not chronically elevated and likely not due to hepatopulmonary syndrome.

Man I hope they weren't planning this type of surgery on someone with hepatopulmonary syndrome. The treatment is lung transplant and can take 14 months to resolve. Not to mention the time waiting for a set of lungs. She doesn't have 14+ months in my book.
 
It depends on how long the MR has been present, because after a while, irreversible changes in the pulmonary circulation usually take place, and limit the benifit of replacing the valve.

Bingo.

Compound the fact that any heart that endures a pump run, albeit transiently in someone with pre-existing normal myocardial function (which this person did not have), exhibits physiology comparent to the pedi heart.

In other words, expect, immediately after separation from bypass, a non-compliant, stiff ventricle, where supra-normal filling pressures are needed.

Not always. But frequently.

Remember the physiolgy s hit: Heart rate X stroke volume = cardiac output.

Commonly, post bypass, dudes ventricle is pissed off and non compliant. Stiff. So not alotta volume can be pushed in. So your stroke volume is limited.

SO, in order to compensate, so you can maintain cardiac output, heart rate hassta be higher.

Just like a pedi heart.

So I treat post-bypass ventricles like a pedi heart until proven otherwise.

Looki'n for a rate of 100.

And if not, we're gonna make it 100.

With drugs or a pacer.
 
Bingo.

Compound the fact that any heart that endures a pump run, albeit transiently in someone with pre-existing normal myocardial function (which this person did not have), exhibits physiology comparent to the pedi heart.

In other words, expect, immediately after separation from bypass, a non-compliant, stiff ventricle, where supra-normal filling pressures are needed.

Not always. But frequently.

Remember the physiolgy s hit: Heart rate X stroke volume = cardiac output.

Commonly, post bypass, dudes ventricle is pissed off and non compliant. Stiff. So not alotta volume can be pushed in. So your stroke volume is limited.

SO, in order to compensate, so you can maintain cardiac output, heart rate hassta be higher.

Just like a pedi heart.

So I treat post-bypass ventricles like a pedi heart until proven otherwise.

Looki'n for a rate of 100.

And if not, we're gonna make it 100.

With drugs or a pacer.

From the post-op report
"The cross-clamp was removed. Heart was allowed to re-perfuse and de-aired for several minutes and then the patient was easily weaned from cardiopulmonary bypass. Her PA pressures were high and she required some inotropic support. The intraaortic balloon pump was resumed but she came off the pump quite easily. Good hemostasis was confirmed. The patient was decannulated and mediastinal and pleural chest tubes and epicardial pacing wires were placed and the patient was taken to the ICU in stable, but serious condition."

Saw patient in ICU and doing fine. :)
 
From the post-op report
"The cross-clamp was removed. Heart was allowed to re-perfuse and de-aired for several minutes and then the patient was easily weaned from cardiopulmonary bypass. Her PA pressures were high and she required some inotropic support. The intraaortic balloon pump was resumed but she came off the pump quite easily. Good hemostasis was confirmed. The patient was decannulated and mediastinal and pleural chest tubes and epicardial pacing wires were placed and the patient was taken to the ICU in stable, but serious condition."

Saw patient in ICU and doing fine. :)

Nice!

Thanks for the update.
 
From the post-op report
"The cross-clamp was removed. Heart was allowed to re-perfuse and de-aired for several minutes and then the patient was easily weaned from cardiopulmonary bypass. Her PA pressures were high and she required some inotropic support. The intraaortic balloon pump was resumed but she came off the pump quite easily. Good hemostasis was confirmed. The patient was decannulated and mediastinal and pleural chest tubes and epicardial pacing wires were placed and the patient was taken to the ICU in stable, but serious condition."

Saw patient in ICU and doing fine. :)
Is she off the IABP?
 
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