Right Heart Failure; severe volume overload, hypotension

[lunaire]

Hello everyone,

Looking to find some wisdom here about a case I recently had in the cardiac ICU..

Patient with ESRD, multivessel CAD (including a completely occluded RCA that cannot be revascularized - no distal target), s/p CABG x2, all to the left coronary distribution. Post bypass had right heart strain and failure, They basically had to do a hemodialysis in the OR to remove 'a few liters of fluids,' with improvement in right heart function.

Post op received in ICU on multiple inotropes - epi, dobutamine, milrinone, and norepi. Had elevated lactate, so was given some fluid boluses without response, then was given some blood, with some response (lactate started trending down, pressure still sucky on pressors/inotropes).

Then the liver started failing. No transaminitis, so I'm thinking liver congestion. Did a bedside focused TTE, right heart is big & dilated, low contractility. At this point, we were struggling with shock on 4 pressors, and decided to focus on improving hemodynamics and deferred fluid removal. CRRT was started, but at absolute zero, no fluids pulled at all.

Liver failure progressed, and the patient is now encephalopathic... Dunno if it's from fulminant hepatic failure or some other cause. Patient also had a swan that showed persistent low SVR, got diagnosed with septic shock (she also had leukocytosis, post-op, of course), and the NP just bombarded her with more fluids over the weekend, which had no good effect.

My question is how the hell do you manage these volume overloaded, cardiogenic shock patients? Would you keep the patient on high dose inotropes and pressors, and aggressively pull fluids? Would you just ride out the hypervolemia and just keep try to slowly wean down the pressor while keeping the patient hypervolemic?

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[deleted171991]

Hello everyone,

Looking to find some wisdom here about a case I recently had in the cardiac ICU..

Patient with ESRD, multivessel CAD (including a completely occluded RCA that cannot be revascularized - no distal target), s/p CABG x2, all to the left coronary distribution. Post bypass had right heart strain and failure, They basically had to do a hemodialysis in the OR to remove 'a few liters of fluids,' with improvement in right heart function.

Post op received in ICU on multiple inotropes - epi, dobutamine, milrinone, and norepi. Had elevated lactate, so was given some fluid boluses without response, then was given some blood, with some response (lactate started trending down, pressure still sucky on pressors/inotropes).

Then the liver started failing. No transaminitis, so I'm thinking liver congestion. Did a bedside focused TTE, right heart is big & dilated, low contractility. At this point, we were struggling with shock on 4 pressors, and decided to focus on improving hemodynamics and deferred fluid removal. CRRT was started, but at absolute zero, no fluids pulled at all.

Liver failure progressed, and the patient is now encephalopathic... Dunno if it's from fulminant hepatic failure or some other cause. Patient also had a swan that showed persistent low SVR, got diagnosed with septic shock (she also had leukocytosis, post-op, of course), and the NP just bombarded her with more fluids over the weekend, which had no good effect.

My question is how the hell do you manage these volume overloaded, cardiogenic shock patients? Would you keep the patient on high dose inotropes and pressors, and aggressively pull fluids? Would you just ride out the hypervolemia and just keep try to slowly wean down the pressor while keeping the patient hypervolemic?

This is a tough one. The way I see it:
- This is a patient with ESRD, well-functioning (now) left heart, with right heart failure.
- She did better once she had some fluid removed post bypass.
- Somebody misdiagnosed her as sepsis (epinephrine raises lactate, dobutamine and milrinone drop SVR), and loaded her with fluids (especially blood, OMG), despite the fact that she did better after fluid removal.
- Then she developed shock liver, unclear if related to her cardiac surgery, or post-bypass/postop cardiogenic shock. That will only sink the SVR ship even more.

There is an important question here, that has not been answered: What were/are her pulmonary artery pressures? If there is one thing the Swan is good at, it's diagnosis of changes in PVR (not SVR/PCWP and all the left-sided stuff that's so sensitive to a bunch of things). Coupled with a CVP and a cardiac output, and the knowledge that the left heart is not the culprit, it should have made for a much easier management post-op, even for a TTE-challenged person. Unless you have other proof for sepsis, this is cardiogenic shock (2/2 to RV failure) until proven otherwise. The question is whether she needs RVAD/ECMO etc. to survive, before she starts developing shock everything (not just liver).

Also, no offense, but this probably should not have been an APRN patient.

 

[lunaire]

Yeah, the PAC values would've been useful. Basically, PA mean in the 30s, systolic mean in the 60s with pressors/inotropes. CVP in the high teens. SVRI ~1500. Cardiac index always 2 to 2.6. Post CABG TEE intraop was hyperdynamic LV, moderate-severe RV systolic dysfunction, RA, RV dilation. Yeah, right heart failure is her big problem. She has leukocytosis and some skin breakdown, but no good reason to be septic.

I'm the ICU fellow. Unfortunately, this was one of the more straightforward case of the day, and the attending and myself was occupied dealing with more decompensated patients. It was a bad week, and this one kinda fell through the cracks.

 

[caligas]

nitric/flolan?

 

[bkell101]

what did the preop or prebypass TEE look like? specifically the right heart and the estimated PA pressures? what were the preop/pre bypass right heart pressures and PA pressures compared to post bypass? just wondering what caused the RV failure ....was this already there? was it an RV with minimal reserve and just enough insult during the intraop period to tip it over the edge?

seems like the fluid really hurt the struggling RV, maybe a TTE bedside plus the PA cath values prior to more fluid could have helped figure out what the problem was

any nitric to help the RV?

 

[deleted171991]

Yeah, the PAC values would've been useful. Basically, PA mean in the 30s, systolic mean in the 60s with pressors/inotropes. CVP in the high teens. SVRI ~1500. Cardiac index always 2 to 2.6. Post CABG TEE intraop was hyperdynamic LV, moderate-severe RV systolic dysfunction, RA, RV dilation. Yeah, right heart failure is her big problem. She has leukocytosis and some skin breakdown, but no good reason to be septic.

I'm the ICU fellow. Unfortunately, this was one of the more straightforward case of the day, and the attending and myself was occupied dealing with more decompensated patients. It was a bad week, and this one kinda fell through the cracks.

The leukocytosis is probably surgical, too.

If the nitric/flolan don't work, or are not available, or are not enough. I would start removing fluids by CRRT (or try some nitroglycerine gtt). The pulmonary pressures can be increased by hypervolemia, too, not just pulmonary vasoconstriction. The low SVR despite hypervolemia and peripheral vasoconstrictors might be just from the 2 inodilators, so I would try to wean those off, too, when the right heart picks up. I would do repeat TTEs and watch how the right heart behaves with diuresis and treatment.

 

[bkell101]

My question is how the hell do you manage these volume overloaded, cardiogenic shock patients? Would you keep the patient on high dose inotropes and pressors, and aggressively pull fluids? Would you just ride out the hypervolemia and just keep try to slowly wean down the pressor while keeping the patient hypervolemic?

cardiogenic is likely too broad....this seems like cardiogenic shock 2/2 isolated RV failure vs RV failure plus PA HTN ....which makes management much different than either global RV/LV failure or LV failure alone ...my impression is that it's very easy to overwhelm a weak muscle (RV) with too much volume

 

[RemyMcswain]

Wedge Pressure? What were the PA pressures pre-op?

Most likely RV failure from ischemia. Patient needs RV afterload reduction, inotropy, and decrease in wall stretch

I would add iNO, increase dobutamine and see if you can come off epi as this is increasing RV afterload. I would add Vasopressin for peripheral squeeze which should not increase pulmonary pressures.Patient also would benefit from lasix gtt or CRRT. Target a lower CVP. Patient is not going anywhere any time soon. Try targeting 1 L negative over next 12 hours.

Could consider an IABP as a means to increase Right coronary flow.

 

[Planktonmd]

Right heart failure will get worse if you try to decrease the preload and remove volume.
At this point you have right heart failure and volume overload so your only option is to give inotropes, sit tight, and pray that the heart will start to recover soon!

 

[deleted171991]

Right heart failure will get worse if you try to decrease the preload and remove volume.

Unless the right heart failure was induced by fluid overload in the first place.

Let me put it this way: The patient had a therapeutic trial post-bypass, got some fluid removed, and got better. Then she got fluids and blood, and got worse.

 

[RemyMcswain]

Right heart failure will get worse if you try to decrease the preload and remove volume.
At this point you have right heart failure and volume overload so your only option is to give inotropes, sit tight, and pray that the heart will start to recover soon!

I respectfully disagree. Its analogous to the patient with left sided systolic heart failure (HFrEF). If they are grossly overloaded, diuresis will increase cardiac output and raise blood pressure. This patient is on the failing portion of the starling curve and needs to have fluid taken off. In addition, the abnormal geometry of the heart 2/2 gross RV dilation is likely disrupting LV filling and LV squeeze.

 

[Stank811]

Slowly take fluid off. If you have indexes in the mid 2s and the rv can generate mean pressures in the 30s the patient should be able to turn around. If the patient revieved etomidate give them a stress dose steroid. Agree with getting rid of epi if possible and adding vassopressin if needed.

 

[lunaire]

what did the preop or prebypass TEE look like? specifically the right heart and the estimated PA pressures? what were the preop/pre bypass right heart pressures and PA pressures compared to post bypass? just wondering what caused the RV failure ....was this already there? was it an RV with minimal reserve and just enough insult during the intraop period to tip it over the edge?

seems like the fluid really hurt the struggling RV, maybe a TTE bedside plus the PA cath values prior to more fluid could have helped figure out what the problem was

any nitric to help the RV?

Wedge Pressure? What were the PA pressures pre-op?

Most likely RV failure from ischemia. Patient needs RV afterload reduction, inotropy, and decrease in wall stretch

I would add iNO, increase dobutamine and see if you can come off epi as this is increasing RV afterload. I would add Vasopressin for peripheral squeeze which should not increase pulmonary pressures.Patient also would benefit from lasix gtt or CRRT. Target a lower CVP. Patient is not going anywhere any time soon. Try targeting 1 L negative over next 12 hours.

Could consider an IABP as a means to increase Right coronary flow.

Patient has a complete RCA occlusion by left heart cath pre-bypass; they weren't able to get a distal target to fix this. Diffuse RCA disease. Very poor RV function pre-bypass, moderately poor RV function post. She's got some collaterals from the left coronary helping out. Mean PA pressure was high 20s, low 30s pre-bypass, but she was in right heart failure even then.

We never took a wedge; but the left heart had no MV or AV pathology, no LVH, normal function.. No reason to think it's left heart failure. We're trying epoprostenol inhaled; iNO is prohibitively expensive here, probs wouldn't get approved for this level of PAH.

The patient was badly hypervolemic on ICU admission, and got more hypervolemic after getting a septic protocol fluid resuscitation. I mean she gained 20kg weight in 4 days... and she's mostly NPO.

I guess the question boils down to this: If you agree that the patient needs to get fluids off, and given that she is in shock, on multiple pressors, would you titrate up the pressors to allow you to remove fluids via CRRT? Even to a high pressor dose, and for a few days? Would this lead to an overall better outcome than just keeping the patient on moderate dose inotropes and pressors, and pray the RV gets better?

 

[deleted171991]

20 kgs. And this has been going on for days. OMG.

In my book, the RV failure is due to fluid overload. It has about the same chance of going away on its own as a pulmonary edema in LV failure due to fluid overload.

We are taught that the RV is fluid responsive, but that does not mean that in can't get overwhelmed.

Septic "protocol" for fluids, especially in cardiac patient? OMG.

 

[lunaire]

Yeah, we tried very hard to get a net negative on POD 1 after watching that RV baloon up on TTE, got about a liter off... Handed the patient to the weekend team (CT surgery fellow in-house with NPs), and was rewarded with multiple rounds of fluid boluses and blood transfusion. Because fluids is good, and more fluids is better, right?

Trying to see if we can salvage this situation.

 

[deleted171991]

It was just yesterday I was trying to convince @Mman why having the wrong people do knee-jerk medicine in the ICU is such a bad idea. Where the wrong people almost always include surgeons.

 

[fakin' the funk]

Unclear how this patient got so severely volume overloaded in the first place, unless the patient was very close already but asymptomatic. I mean, there's TEE from minute 5 in the cardiac OR, and TTE/TEE as you see fit throughout this rocky postop phase.

With RV failure you certainly have to FIX the volume status, whether it be too high or too low. Echo, CVP, PA, CI, and PA pulse pressure/CVP are all metrics you can use to assess R heart filling status.
You also have to basically wail on the L heart and the systemic circulation. Bump CI and SVR with epi, norepi, vaso, stress dose steroids as mentioned.
If the RV is still failing all you have left is selective pulmonary vasodilators like the aforementioned NO or flolan. Failing that, and I'm talking out of my ass a bit here, RVAD, or V-A ECMO if you think the RV failure is transient.

 

[Planktonmd]

I respectfully disagree. Its analogous to the patient with left sided systolic heart failure (HFrEF). If they are grossly overloaded, diuresis will increase cardiac output and raise blood pressure. This patient is on the failing portion of the starling curve and needs to have fluid taken off. In addition, the abnormal geometry of the heart 2/2 gross RV dilation is likely disrupting LV filling and LV squeeze.

The patient is overloaded probably because he is in renal failure secondary to the cardiogenic shock. We should be focusing on improving systemic blood pressure by all means possible to avoid further kidney and liver damage, but most likely the patient will need dialysis very soon which will allow better control of the volume status.

 

[bkell101]

Unclear how this patient got so severely volume overloaded in the first place, unless the patient was very close already but asymptomatic. I mean, there's TEE from minute 5 in the cardiac OR, and TTE/TEE as you see fit throughout this rocky postop phase.

With RV failure you certainly have to FIX the volume status, whether it be too high or too low. Echo, CVP, PA, CI, and PA pulse pressure/CVP are all metrics you can use to assess R heart filling status.
You also have to basically wail on the L heart and the systemic circulation. Bump CI and SVR with epi, norepi, vaso, stress dose steroids as mentioned.
If the RV is still failing all you have left is selective pulmonary vasodilators like the aforementioned NO or flolan. Failing that, and I'm talking out of my ass a bit here, RVAD, or V-A ECMO if you think the RV failure is transient.

When do u go to impella?

 

[idiot07]

Right hear failure from poor protection (no plegia administered to the right side if rca occlude) /fluid overload. Concur on everything said above. We tend to use a combo of epi/milrinone (I think both are great drugs for right heart support for support) in our postop patients rather than dobutamine, but different strokes for different folks. PVR should be reduced with milrinone, the inhaled agent du jour of your institution, vasopressin to reduce the alpha agonist load, and keeping the patient a little alkalotic. The volume status should be optomized with CVVH as needed. This patient clearly needs volume removed, and I think a short term increase in pressors to do this would benefit the patient immensely. Is there any tricuspid reguritation by the way? This can falsely elevate the CI on your swan and you should use mixed venous to titrate your therapy. Keeping the systemic afterload a little higher (Map~70) supports the RV by helping maintain the LV/RV geometrical relationship. Consequently, an IABP may actually hurt you, but it probably won't do much either way. I think with these guys you should throw the boat at them with everything listed above, and then peel back, rather than adding one thing at a time, becuase they can go off the cliff quick.

With regard to mechanical support, it's hard to say without knowing exact pressors hemodynamics etc, but I think you're approaching that threshold, particularly if you're bumping your lfts and have signs of right sided congestion. You can look at the cvp and rv pulse pressure to get an idea of things. For instance, a patient with a cvp of 17, but a rvsp of 50, probably has pretty good rv function to be able to generate a systolic pressure of 50 and has a good chance of responding to medcial therapy. The same patient with a cvp of 18-20 and a rvsp of 25 is much more worrisome as they have an rv that can't generate any pressure. Your options would be ecmo or an rvad depending on the lungs, the lv, and your surgeon. The impella is mainly for left sided support. There is a right sided an impella that was just approved, but not may hospitals have this.

 

[bkell101]

In retrospect...

Predicting rv failure is an interesting topic. PAPi score has been looked at in various circumstances. Anybody using this metric?

Just thinking if this could have been anticipated and if anything more could have been done during the case or prior to leaving the operating room. I guess Hard to know without seeing the sequence of echo's and pa cath data.

 

[OB1🤙]

I'll write more later but the first thing I'd do to this patient would be a trial of a nitro gtt.

There almost no more Jedi maneuver in the ct ICU than making someone's blood pressure go up with nitro. This might be a case for it.

No guarantee it'll work, but if RV volume overload is the issue here, is what I'd do first.

 

[Stank811]

TR will underestimate CI. Small dose NTG is not a bad idea to help with your micro vascular perfusion. Still would just use CRRT to pull volume of slowly and if you really have CI in the mid 2s and sco2 greater than 60 your liver should recover from its shock soon.

 

[Mman]

It was just yesterday I was trying to convince @Mman why having the wrong people do knee-jerk medicine in the ICU is such a bad idea. Where the wrong people almost always include surgeons.

I think you are confused. I've never suggested anything about knee jerk medicine. I merely pointed out that the vast majority of critical care decisions are not complicated. It's pretty straight forward and the semantics of open vs closed ICU is meaningless in most cases.

 

[vector2]

Ditch the dobutamine. Epi, vaso, milrinone, low dose nitro, and eat the cost of the iNO. Crrt running net negative and do some daily or bid TEE in the unit until Rv looks better and hepatic flow reversal is abolished.

 

[fakin' the funk]

For the milrinone fans out there: you're using it in this ESRD'er? As part of Plan A?

 

[vector2]

For the milrinone fans out there: you're using it in this ESRD'er? As part of Plan A?

If on HD, dose 0.2mcg/kg/min. If Cvvvhdf, dose normally. For this pt, yes, plan A.

 

[Hoya11]

it can be interesting to talk about how to manage this tough case, but this is exactly the reason i am not into cardiac, how often do you do ESRD patients for cabg? just give them a morphine drip and see you later, I cant imagine they do well long-term post op, why revacularize the heart and go through all this time and energy when the kidney/dialysis complications will kill them soon anyhow?

 

[lunaire]

it can be interesting to talk about how to manage this tough case, but this is exactly the reason i am not into cardiac, how often do you do ESRD patients for cabg? just give them a morphine drip and see you later, I cant imagine they do well long-term post op, why revacularize the heart and go through all this time and energy when the kidney/dialysis complications will kill them soon anyhow?

Coz the patient went into VF preop, was brought back, and wanted the surgery despite the risk. She is young and has 2 kids. If nothing was done, her prognosis was maybe days to weeks to mortality. If this worked, would be back to her ESRD prognosis of a few years to a decade or so... If it failed, back to days to weeks to mortality.

My hospital is actually one of those that has the right sided impella, just did that on another patient with good outcome. We get barely alive patients like this pretty regularly.

This patient, though: the Cardiac surgeons snuck in some hydroxycobalamin when we weren't looking, and that dramatically improved hemodynamics. She's down to dobutamine & milrinone plus inhaled epoprostenol. SVRI looks great. Overall consensus here is to take the hit on the liver while just throwing everything we got to reboot the cardiovascular system. Gotta love the multidisciplinary ICU approach.

 

[bkell101]

B12? did they think it was vasoplegia related? i saw a poster on that at the SCA this year

 

[lunaire]

Patient had mixed shock picture. Definitely cardiogenic from the low CI despite inotropes; this is most likely right heart failure given normal left side EF, hypervolemia, and lack of PAH. She also had low SVRI, despite on epi/norepi pressing on. Maybe vasoplegia from the CPB, maybe a little sepsis, maybe a touch of liver failure...

B12 basically induces vasoconstriction, extremely well... It will raise the pressure in most clinical scenario... Just like phenylephrine would raise the pressure in a patient with severe cardiogenic shock that's clinically cold and clammy.. Doesn't mean that it's the best drug, or even a good choice. There's almost no data on this treatment. It did fix the low SVR for now. Hopefully it lasts.

 

[fakin' the funk]

how often do you do ESRD patients for cabg? just give them a morphine drip and see you later

So a patient with 3v CAD and stable ESRD on HD, you want to palliate this person? Not sure you'd feel the same way if it was, say, your family member. You do know that it's cardiovascular disease that most commonly kills these patients, not "kidney/dialysis" complications?

 

[bkell101]

Patient had mixed shock picture. Definitely cardiogenic from the low CI despite inotropes; this is most likely right heart failure given normal left side EF, hypervolemia, and lack of PAH. She also had low SVRI, despite on epi/norepi pressing on. Maybe vasoplegia from the CPB, maybe a little sepsis, maybe a touch of liver failure...

B12 basically induces vasoconstriction, extremely well... It will raise the pressure in most clinical scenario... Just like phenylephrine would raise the pressure in a patient with severe cardiogenic shock that's clinically cold and clammy.. Doesn't mean that it's the best drug, or even a good choice. There's almost no data on this treatment. It did fix the low SVR for now. Hopefully it lasts.

That's cool, the case I saw was vasoplegia post bypass after methylene blue and all else failed. Wonder if you guys are the same institution

 

[dhb]

So a patient with 3v CAD and stable ESRD on HD, you want to palliate this person? Not sure you'd feel the same way if it was, say, your family member. You do know that it's cardiovascular disease that most commonly kills these patients, not "kidney/dialysis" complications?

Depending on age i'd say this patient was candidate for death. Retrospectively looking at all the patients i've taken care of in the icu i can say with confidence that there's very little meaningful care being done.

 

[OB1🤙]

Vasoplegia and right heart failure are (obviously) very different causes of major badness.

To throw the warning out there, if right heart failure is on your radar is a likely factor, the treatments for vasoplegia are likely to be disastrous.

I admit I'm not familiar with b12 in this scenario, but things like methylene blue will jack up your PVR just as they will your SVR, and will piss the right heart off.

It's hard to comment on a patient like this without seeing the whole picture.

And I want a right sided impella to use at my shop. Bad.

 

[2win]

Hello everyone,

Looking to find some wisdom here about a case I recently had in the cardiac ICU..

Patient with ESRD, multivessel CAD (including a completely occluded RCA that cannot be revascularized - no distal target), s/p CABG x2, all to the left coronary distribution. Post bypass had right heart strain and failure, They basically had to do a hemodialysis in the OR to remove 'a few liters of fluids,' with improvement in right heart function.

Post op received in ICU on multiple inotropes - epi, dobutamine, milrinone, and norepi. Had elevated lactate, so was given some fluid boluses without response, then was given some blood, with some response (lactate started trending down, pressure still sucky on pressors/inotropes).

Then the liver started failing. No transaminitis, so I'm thinking liver congestion. Did a bedside focused TTE, right heart is big & dilated, low contractility. At this point, we were struggling with shock on 4 pressors, and decided to focus on improving hemodynamics and deferred fluid removal. CRRT was started, but at absolute zero, no fluids pulled at all.

Liver failure progressed, and the patient is now encephalopathic... Dunno if it's from fulminant hepatic failure or some other cause. Patient also had a swan that showed persistent low SVR, got diagnosed with septic shock (she also had leukocytosis, post-op, of course), and the NP just bombarded her with more fluids over the weekend, which had no good effect.

My question is how the hell do you manage these volume overloaded, cardiogenic shock patients? Would you keep the patient on high dose inotropes and pressors, and aggressively pull fluids? Would you just ride out the hypervolemia and just keep try to slowly wean down the pressor while keeping the patient hypervolemic?

Welcome to the ICU world!
No RCA - right ventricle is dead...
Obtain contractility with inotropes - pendulum effect for the septum.
Fluid balance tricky - dry better.
Lactate going up - no reason to give fluids. PERFUSION!
I never got the dogma - lactate fluids - id the preload is OK.
Get rid of dobutamine - although make sense for splanhnic perfusion .
The NO is better than flolan.
No studies though.
How old is she?
Low svr good for the heart.
Keep it like that.
IABP for the left heart.
Right heart failure - better without positive pressure ventilation.
If it is worth it - ECMO to allow for recovery.
This is my world - transplant ....
2win

 

[Hoya11]

So a patient with 3v CAD and stable ESRD on HD, you want to palliate this person? Not sure you'd feel the same way if it was, say, your family member. You do know that it's cardiovascular disease that most commonly kills these patients, not "kidney/dialysis" complications?

dialysis patients live for ~5yrs, less if very old. its a temporary solution. there may be some value in doing the case especially if the person is with it and is saying they want it done (which lets be real is rarely the case). but i am still amazed at the effort and technology developed and used for these sick patients with such low yield in terms of quality years of life gained vs resources spent.

 

[Hoya11]

.

 

[fakin' the funk]

dialysis patients live for ~5yrs, less if very old.

I'm sorry, but your views are callous and inaccurate, and likely the result of recall bias.

From kidney.org:
"Average life expectancy on dialysis is 5-10 years, however, many patients have lived well on dialysis for 20 or even 30 years."

I'm not just arguing numbers here. There is a world outside of the immediate perioperative setting, one that we (anesthesiologists) never get to see because of our limited timeframe of patient care. Don't be so quick to say someone should be "on a morphine drip" merely because they're in suboptimal health.

 

[Mman]

I'm sorry, but your views are callous and inaccurate, and likely the result of recall bias.

From kidney.org:
"Average life expectancy on dialysis is 5-10 years, however, many patients have lived well on dialysis for 20 or even 30 years."

I'm not just arguing numbers here. There is a world outside of the immediate perioperative setting, one that we (anesthesiologists) never get to see because of our limited timeframe of patient care. Don't be so quick to say someone should be "on a morphine drip" merely because they're in suboptimal health.

If the average is 5-10 years, his comment that they live about 5 years isn't far off.

 

[Planktonmd]

The thing is if you are an ESRD patient on HD and have a crappy heart to start with that got worse after lengthy open heart surgery to the point you are now in refractory cardiogenic shock, I can say with reasonable confidence that your life expectancy falls a bit under the 5 years average!

 

[bkell101]

Welcome to the ICU world!
No RCA - right ventricle is dead...
Obtain contractility with inotropes - pendulum effect for the septum.
Fluid balance tricky - dry better.
Lactate going up - no reason to give fluids. PERFUSION!
I never got the dogma - lactate fluids - id the preload is OK.
Get rid of dobutamine - although make sense for splanhnic perfusion .
The NO is better than flolan.
No studies though.
How old is she?
Low svr good for the heart.
Keep it like that.
IABP for the left heart.
Right heart failure - better without positive pressure ventilation.
If it is worth it - ECMO to allow for recovery.
This is my world - transplant ....
2win

Does positive pressure ventilation increase rv after load?

 

[Scotty_G]

yes