Critical AS case

[vector2]

70 yo M, blue collar worker (active at baseline), no reported PMH, never seen a doctor. Walks into the ED with 3 day hx of dyspnea and 2-3 weeks of new lower extremity edema. Also has a URI. HR 101, BP 97/55, satting 96 on RA. Super high BNP, negative trop. Admitted for new HF. CT chest shows incidental 5.0 cm ascending aorta and also small pleural effusions.

Here are some TTE instead of TEE images for a change.

What else do you need to know? Any other workup? What specific inferences can be made from the mitral inflow, atria size, and strain pattern? What are our treatment options?

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[T-burglar]

Good case. Looks like restrictive cardiomyopathy with a high LVEDP . May or may not be altering the AI PHT and the transvalvular gradients (but in terms of valve lesion severity, with these numbers, doesn’t matter). despite the burned out cardiomyopathy, the LV seems to be producing a decent stroke volume with that gradient, but I’d still like to see the quantified cardiac output for procedural planning . The transvalvular flow rate isn’t as important since we know it’s severe AS.

The LV shape doesn’t look globular so I’d like to see a diameter and volume to know if it’s dilated. A volume overload cardiomyopathy should be dilated , but this looks like it could be a primary restrictive CM on top of a valve lesion. A consideration for other causes of RCM would be a good idea, may need to be treated separately from the valve.

CT TAVR protocol, LHC. Decide if AVR/Ascending/CABG or TAVR/PCI and ascending some other time . Right heart cath - Whether to treat the CHF volume overload first or just do the TAVR. I’m of the opinion that CHF doesn’t need to be treated before a TAVR

 

[PpfSuxTube]

Ill delete it for now...

 

[Beeftenderloin]

That aortic valve has got to go. Just a matter of when, how, and what else. Difficult to say if mitral inflow is from restrictive infiltrative cardiomyopathy vs grade 3 diastolic dysfunction from LV pumping against a brick wall for years. AS is often found concomitantly with cardiac amyloid, supporting this etiology. The worsening strain pattern in the septum relative to elsewhere speaks toward restrictive cardiomyopathy as well. Mitral inflow respiratory variation can help sus out some of that, but ultimately this diagnosis isn’t made with echo, just suggested by it. If infiltrative cardiomyopathy, prognosis is poor and patient could end up needing a transplant vs DT VAD vs palliative. But those are considerations for later. Assuming patient is amenable to intervention: As above he needs a TAVR CT, LHC, but also a cardiac MRI vs myocardial biopsy to sort out the etiology of restriction. And some GENTLE diuresis while they finish their work-up as they’re clearly in decompensated failure. Once all that data is collected this is the type of guy that would get discussed at our multidisciplinary valve conference.

These 2 options seem clear to me.

Clean/PCI-able coronaries +/- infiltrative CMO > TAVR, leave ascending alone.

Surgical coronary disease, no infiltrative CMO > SAVR, CABG, ascending

If he has surgical coronaries with infiltrative CMO he needs to be discussed by people smarter than me.

Edit: Mostly because I don’t know if he’s going to live long enough with an infiltrative cardiomyopathy to realize the mortality benefit of surgical revascularization +/- ascending. This scenario requires input from people who follow these types of patients longitudinally.

 

[dchz]

Clean/PCI-able coronaries +/- infiltrative CMO > TAVR, leave ascending alone.

You're really leaving a 5.0 cm ascending because he has amyloid or some other infiltrative cardiomyopathy?

I have to admit that I don't know the correct answer to this. But laplace/grant wahl says it's worth questioning....

Edit: I forgot the prognosis for amyloid was so poor after cardiac involvement. All the previously quoted posts is valid (assuming the low ef is due to amyloid and not the aortic valve/coronaries).

 

[vector2]

CT TAVR protocol, LHC.. Right heart cath

Anatomy is amenable to TAVR. Isolated ascending aneurysm. No arch or descending aneurysm.

LHC: Clean coronaries. IC (non structural guy) tried to cross AV multiple times with multiple wires to do a pullback gradient and direct LVEDP but was unable to do it.

RHC (when he was still 2-3L volume overloaded):

Systemic pressure: 90/52 mmHg

Findings:
RA: 8 mmHg
RV: 90/8 mmHg
PA: 90/34 mmHg
PCWP: 34 mmHg
CO by TD: 5.2 L/min (CI by TD: 2.8 L/min/m2)
CO by assumed Fick: 3.9 L/min (CI by assumed Fick: 2.2 L/min/m2)

Sats:
RA: 59%
PA: 56%
Ao: 91%

 

[Nexus5]

Diuretics for days and days then tavr.

 

[T-burglar]

Diuresis to get him out of CHF first

Option 1. transfemoral TAVR, followed by ascending aorta at a later date. if the CM is related to the valve, he might recover a little strength and tolerate CPB better. If there’s a primary restrictive CM he may not get much better, but it probably won’t get any worse.

Option 2. Straight to AVR / ascending. His echo looks worse than his history and symptoms and His measured cardiac output isn’t that bad lol. He might do relatively ok.

 

[vector2]

Good replies so far. Definitely highlights the importance of cardiac anesthesiologists having broad echo knowledge even when it comes to disease processes you don't necessarily see every day. In fact, the non-echo boarded OSH cardiologist who read his first TTE didn't even comment on the biatrial enlargement and restrictive mitral inflow being suggestive of RICM/amyloid, so it's not inconceivable that cases like these go to surgery sometimes without a thorough workup being done.

Anyway, cardiac MRI done. No LGE or other signs of infiltration. Quant LVEF is 39%. RVEF mildly moderately reduced (forgot the number). CI>2.2. He has diuresed 2L and had a 1L pleural effusion drained. BPs now are 85-90 awake and 80-85 sleeping. On 1-2L N/C. PAs appear to have come down on repeat echo. Mostly asymptomatic from a cardiopulmonary standpoint when he's just chilling on the floor.

Surgeon wants to do bentall.

For med studs/residents/fellows first:

1. Which pre-op pathologies pose the highest risk for perioperative/peri-induction arrest during cardiac surgery?

e:1.5 What is your interpretation of the right heart cath hemodynamics? What kind of pulmonary hypertension in this? What implications does this have for management in addition to the HFrEF and AS?

2. What is your pre-op and induction game plan for this pt?

 

[Drägerman]

Good replies so far. Definitely highlights the importance of cardiac anesthesiologists having broad echo knowledge even when it comes to disease processes you don't necessarily see every day. In fact, the non-echo boarded OSH cardiologist who read his first TTE didn't even comment on the biatrial enlargement and restrictive mitral inflow being suggestive of RICM/amyloid, so it's not inconceivable that cases like these go to surgery sometimes without a thorough workup being done.

Anyway, cardiac MRI done. No LGE or other signs of infiltration. Quant LVEF is 39%. RVEF mildly moderately reduced (forgot the number). CI>2.2. He has diuresed 2L and had a 1L pleural effusion drained. BPs now are 85-90 awake and 80-85 sleeping. On 1-2L N/C. PAs appear to have come down on repeat echo. Mostly asymptomatic from a cardiopulmonary standpoint when he's just chilling on the floor.

Surgeon wants to do bentall.

For med studs/residents/fellows first:

1. Which pre-op pathologies pose the highest risk for perioperative/peri-induction arrest during cardiac surgery?

2. What is your pre-op and induction game plan for this pt?

Thanks again for doing these. I would be worried about the severe AS. On induction, I would want to keep the heart rate reasonable and afterload high (phenylephrine?) in order to maintain coronary perfusion.

Edit: student response attempt

 

[abolt18]

My biggest concern for induction is the systemic pulmonary pressures. Second is the critical AS. Slow, gentle, controlled induction is crucial. Very gentle positive pressure ventilation after intubation. Avoid hypoxia, hypercapnia, and a drop in SVR.

Bentall or Wheat procedure is ideal to correct described pathologies. Clip the LAA while you're in there. Going to need some help coming off bypass I'd suspect. Maybe a little pulmonary edema as well. He'll likely not be a "fast-track" patient.

 

[Beeftenderloin]

Anatomy is amenable to TAVR. Isolated ascending aneurysm. No arch or descending aneurysm.

LHC: Clean coronaries. IC (non structural guy) tried to cross AV multiple times with multiple wires to do a pullback gradient and direct LVEDP but was unable to do it.

RHC (when he was still 2-3L volume overloaded):

Systemic pressure: 90/52 mmHg

Findings:
RA: 8 mmHg
RV: 90/8 mmHg
PA: 90/34 mmHg
PCWP: 34 mmHg
CO by TD: 5.2 L/min (CI by TD: 2.8 L/min/m2)
CO by assumed Fick: 3.9 L/min (CI by assumed Fick: 2.2 L/min/m2)

Sats:
RA: 59%
PA: 56%
Ao: 91%

Did they bother with a pulmonary vasodilator challenge for those systemic PAs in cath lab? Or were they just assuming group 2 so unlikely to respond?

 

[vector2]

Did they bother with a pulmonary vasodilator challenge for those systemic PAs in cath lab? Or were they just assuming group 2 so unlikely to respond?

They didn't for a few reasons. One is they thought group 2. Two, I don't think cardiologist has much experience with nitroprusside or other vasodilator challenges in cathlab. Three, the guys bp was like 90-100 during the cath and the odds that the IC has ever used i-flolan or iNO are even lower than him having used IV SNP.

 

[EYY]

Good replies so far. Definitely highlights the importance of cardiac anesthesiologists having broad echo knowledge even when it comes to disease processes you don't necessarily see every day. In fact, the non-echo boarded OSH cardiologist who read his first TTE didn't even comment on the biatrial enlargement and restrictive mitral inflow being suggestive of RICM/amyloid, so it's not inconceivable that cases like these go to surgery sometimes without a thorough workup being done.

Anyway, cardiac MRI done. No LGE or other signs of infiltration. Quant LVEF is 39%. RVEF mildly moderately reduced (forgot the number). CI>2.2. He has diuresed 2L and had a 1L pleural effusion drained. BPs now are 85-90 awake and 80-85 sleeping. On 1-2L N/C. PAs appear to have come down on repeat echo. Mostly asymptomatic from a cardiopulmonary standpoint when he's just chilling on the floor.

Surgeon wants to do bentall.

For med studs/residents/fellows first:

1. Which pre-op pathologies pose the highest risk for perioperative/peri-induction arrest during cardiac surgery?

e:1.5 What is your interpretation of the right heart cath hemodynamics? What kind of pulmonary hypertension in this? What implications does this have for management in addition to the HFrEF and AS?

2. What is your pre-op and induction game plan for this pt?

1. My guess would be severe RV systolic dysfunction, but critical AS is probably up there too.
2. based on the history, likely this is mostly postcapillary pHTN, although calculated PVR from the RHC is a little high, so perhaps there is a mixed component here, so there is a chance your PA pressures remain a little high after AVR, RV might need some support, and there might be a role for flolan / iNO if needed.
3. preinduction arterial line, consider awake lines / PAC, avoid hypoxia / hypercapnia when manipulating airway. Induce with etomidate. maintain afterload with phenylephrine, pads on pt preinduction incase there is arrhythmias.

 

[T-burglar]

Why phenylephrine and not norepinephrine

 

[greatnt249]

Good replies so far. Definitely highlights the importance of cardiac anesthesiologists having broad echo knowledge even when it comes to disease processes you don't necessarily see every day. In fact, the non-echo boarded OSH cardiologist who read his first TTE didn't even comment on the biatrial enlargement and restrictive mitral inflow being suggestive of RICM/amyloid, so it's not inconceivable that cases like these go to surgery sometimes without a thorough workup being done.

Anyway, cardiac MRI done. No LGE or other signs of infiltration. Quant LVEF is 39%. RVEF mildly moderately reduced (forgot the number). CI>2.2. He has diuresed 2L and had a 1L pleural effusion drained. BPs now are 85-90 awake and 80-85 sleeping. On 1-2L N/C. PAs appear to have come down on repeat echo. Mostly asymptomatic from a cardiopulmonary standpoint when he's just chilling on the floor.

I'll admit I'm a bit skeptical of the LVEF of 39% on MRI after looking at the echo pictures you posted, unless the heart looks better on other views that you didn't post.

 

[Beeftenderloin]

I'll admit I'm a bit skeptical of the LVEF of 39% on MRI after looking at the echo pictures you posted, unless the heart looks better on other views that you didn't post.

MRI is the current gold standard for measuring EF. They probably got some volume off between echo and MRI. Plus echo derived EF is well documented as being typically a little lower than MRI.

With echo there’s a lot of estimation/assumptions made about cavity dimension, even with Simpson’s method on good quality images.

 

[greatnt249]

MRI is the current gold standard for measuring EF. They probably got some volume off between echo and MRI. Plus echo derived EF is well documented as being typically a little lower than MRI.

With echo there’s a lot of estimation/assumptions made about cavity dimension, even with Simpson’s method on good quality images.

I'm aware of MRI being the standard; I'm also aware of cardiologists not being careful with precisely looking at the measurements they spit out when they have a significant number of studies to read in a given day. My point was that unless significant medical optimization had occurred between when the echo was done and the MRI was done, I wouldn't be walking away with the warm and fuzzies because the MRI said the LVEF was 39% when it looks roughly in the mid-20s based on the echo pictures.

 

[Beeftenderloin]

I'm aware of MRI being the standard; I'm also aware of cardiologists not being careful with precisely looking at the measurements they spit out when they have a significant number of studies to read in a given day. My point was that unless significant medical optimization had occurred between when the echo was done and the MRI was done, I wouldn't be walking away with the warm and fuzzies because the MRI said the LVEF was 39% when it looks roughly in the mid-20s based on the echo pictures.

Your incredulity is reasonable. I also find myself disagreeing with cardiologist interpretation of cardiac imaging from time to time. But I don’t know how anyone could comfortably call the EF anything specific other than “low”, based on the echo images provided. We’re shown approximately 5/17 segments. If all I had was the above data set and a gun to my head I would say LVEF likely at least moderately decreased on this limited exam. Not a whole lot more than that (about LVEF specifically). And frankly LVEF isn’t even top 3 in terms of my periop concerns for this guy given he’s able to generate an adequate CO/CI, even in a decompensated state.

Edit: Several echo clips did not load on my phone initially. Ignore the part about segments and limited data set. More than enough images to get a general sense of this guys probably severely reduced LV function. I still only say probably because aside from TG SAX we don’t have any good views of the LAD distribution which could be doing work.

Even if you disagree with cardiologist read, you have to at least agree it has to have improved some amount between echo and MRI (or gotten worse if timing reversed). For an imaging cardiologist to be that far off when the imaging modality has been proven to be superior would be impressively bad.

Stand by what I said about leaning far more on CI/CO than EF, especially in light of patients history.

 

[T-burglar]

We all have to remember as well that imaging is not the end all be all of cardiopulmonary function. We have a tendency to look at a quivering LV and say “this patient must be all kinds of jacked up” , but remember he was pretty active until very recently . As stated above, his measured cardiac output isn’t that bad despite the somewhat striking imaging , and that’s in line with his clinical presentation.

 

[Robotic Wis-Hipple]

Good case.

Dudes’ LV is gonna be fine (perioperatively), he’s able to generate a Vmax over 5m/s and a Peak of >125mmHg. RV support with PVR modulation is where you get this dude through it or slip on the banana peel.

 

[pgg]

Good case.

Dudes’ LV is gonna be fine (perioperatively), he’s able to generate a Vmax over 5m/s and a Peak of >125mmHg. RV support with PVR modulation is where you get this dude through it or slip on the banana peel.

Sure the thick LV is big and strong and can generate high pressures, but that very thickness is one of the things that makes it vulnerable to ischemia and dysrhythmmias. We know from the diastolic dysfunction that it's already ATP starved, the LVEDP pressures aren't helping coronary perfusion, and that's not going to get better for a while, if ever. The LV isn't my chief concern but I wouldn't blow it off as fine either ...

 

[Robotic Wis-Hipple]

Sure the thick LV is big and strong and can generate high pressures, but that very thickness is one of the things that makes it vulnerable to ischemia and dysrhythmmias. We know from the diastolic dysfunction that it's already ATP starved, the LVEDP pressures aren't helping coronary perfusion, and that's not going to get better for a while, if ever. The LV isn't my chief concern but I wouldn't blow it off as fine either ...

Sure. It’s heart surgery, none of us are thinking there’s no way to get the LV into trouble. But in this dude all the ways you get into LV failure you’d have been in acute RV failure first with the exception of dysrhythmias as you prudently state.

We’ve all seen sicker LVs in the setting of aortic stenosis. The systemic PAs and RV are far more likely to be the cause of a bad day in this particular case.

 

[lunaire]

This dude has no emergent need for surgery that I see. Keep PA cath in, medical optimization in cardiac ICU, diurese, maybe start milrinone. See what happens when LVEDP is upper range of normal.

Slow induction - midaz/fent heavy, with etomidate & paralize. rapid sequence. Keep an eye on BP and PA cath parameters. Low PEEP. Have the surgeon in the room for induction; induction to incision time should be minimal given pt already lined up in ICU.

Mechanical device support could be used at any time periop if indicated. Patient could have a decent postop prognosis assuming he survives the immediate periop timeline. Mechanical device bridge to recovery is reasonable.

 

[Arch Guillotti]

Slow induction....rapid sequence.

lol wut

 

[Robotic Wis-Hipple]

This dude has no emergent need for surgery that I see. Keep PA cath in, medical optimization in cardiac ICU, diurese, maybe start milrinone. See what happens when LVEDP is upper range of normal.

Slow induction - midaz/fent heavy, with etomidate & paralize. rapid sequence. Keep an eye on BP and PA cath parameters. Low PEEP. Have the surgeon in the room for induction; induction to incision time should be minimal given pt already lined up in ICU.

Mechanical device support could be used at any time periop if indicated. Patient could have a decent postop prognosis assuming he survives the immediate periop timeline. Mechanical device bridge to recovery is reasonable.

Are you an Intensivist?

 

[vector2]

This dude has no emergent need for surgery that I see. Keep PA cath in, medical optimization in cardiac ICU, diurese, maybe start milrinone. See what happens when LVEDP is upper range of normal.

Slow induction - midaz/fent heavy, with etomidate & paralize. rapid sequence. Keep an eye on BP and PA cath parameters. Low PEEP. Have the surgeon in the room for induction; induction to incision time should be minimal given pt already lined up in ICU.

Mechanical device support could be used at any time periop if indicated. Patient could have a decent postop prognosis assuming he survives the immediate periop timeline. Mechanical device bridge to recovery is reasonable.

I agree with keeping the swan in if you know he's going to surgery imminently within a day or so, but barring that, 1. What ICU admission criteria does this guy have? 2. What is your rationale for pre-op inotropes like milrinone?

He's on room air. He's got a perfusing blood pressure on no vasoactive agents. His MVO2 is low but it's chronic so I'm sure his tissue extraction is compensating. He's got no worrisome syncope, angina, arrhythmias, or trop leak. He's got good baseline functional capacity (all things considered) and is able to ambulate slowly + do his ADLs...

 

[PpfSuxTube]

This dude has no emergent need for surgery that I see. Keep PA cath in, medical optimization in cardiac ICU, diurese, maybe start milrinone. See what happens when LVEDP is upper range of normal.

Slow induction - midaz/fent heavy, with etomidate & paralize. rapid sequence. Keep an eye on BP and PA cath parameters. Low PEEP. Have the surgeon in the room for induction; induction to incision time should be minimal given pt already lined up in ICU.

Mechanical device support could be used at any time periop if indicated. Patient could have a decent postop prognosis assuming he survives the immediate periop timeline. Mechanical device bridge to recovery is reasonable.

What? Do you want to go to jail? Milrinone??

 

[T-burglar]

This dude has no emergent need for surgery that I see. Keep PA cath in, medical optimization in cardiac ICU, diurese, maybe start milrinone. See what happens when LVEDP is upper range of normal.

Slow induction - midaz/fent heavy, with etomidate & paralize. rapid sequence. Keep an eye on BP and PA cath parameters. Low PEEP. Have the surgeon in the room for induction; induction to incision time should be minimal given pt already lined up in ICU.

Mechanical device support could be used at any time periop if indicated. Patient could have a decent postop prognosis assuming he survives the immediate periop timeline. Mechanical device bridge to recovery is reasonable.

Lmao

I like this post. Why the low peep lol?

Is that after or before we put in an LVAD for bridge to recovery

 

[lunaire]

lol wut

LOL, poor choice of words, lower dose hypnotics, wait a bit longer for effect, then rapid sequence dose paralytics without mask ventilation.

Are you an Intensivist?

Yes

I agree with keeping the swan in if you know he's going to surgery imminently within a day or so, but barring that, 1. What ICU admission criteria does this guy have? 2. What is your rationale for pre-op inotropes like milrinone?

He's on room air. He's got a perfusing blood pressure on no vasoactive agents. His MVO2 is low but it's chronic so I'm sure his tissue extraction is compensating. He's got no worrisome syncope, angina, arrhythmias, or trop leak. He's got good baseline functional capacity (all things considered) and is able to ambulate slowly + do his ADLs...

Perhaps I am anticipating the future too much. The intent of the milrinone is altering the PA pressure and low normal cardiac index, if patient is still symptomatic, or worsening after adequate diuresis. ICU criteria is simply to maintain PA cath and close monitoring. You can be more aggressive with medical management with ICU monitoring. This patient does appear to be in a window of opportunity to get whatever repair he needs done. Some optimization can give you a smoother intraop/postop course, but if that window is closing, you want to detect that early, and get the procedure done somewhat urgently.

What? Do you want to go to jail? Milrinone??

As mentioned above, for PA pressure modulation. We assume type 2 PAH, but that's an assumption. In my experience, you can pair milrinone with vaso/norepi and get somewhat selective PA vasodilation, if you're concerned about the AS.

Lmao

I like this post. Why the low peep lol?

Is that after or before we put in an LVAD for bridge to recovery

You don't need high PEEP for a non-hypoxic, severe PAH patient, right? By low PEEP, I mean PEEP of 5-6.

I wasn't thinking LVAD; more of RP impella, protek duo, or VA ECMO. Bridge to recovery can also mean use of temporary mechanical devices.


I take care of these patients postop. I know most cardiac anesthesiologist here can get this patient through the bentall alive, but a fraction of these people will go into RV failure, and/or renal failure postop. Fluid overloaded at baseline plus these postop complication will mean poor response to medical management, and likely dialysis need/prolonged intubation. Preop medical optimization help to reduce this risk.

 

[PpfSuxTube]

Forget it man, youre lost.
You would kill this guy on induction.

Preop medical optimization, my ass. Rcri = 1, recommend anesthesia reduce fluid intraop.

Milrinone, rapid sequence. Holy smokes

His only hope is none of your optimization

 

[GassYous]

LOL, poor choice of words, lower dose hypnotics, wait a bit longer for effect, then rapid sequence dose paralytics without mask ventilation.


Yes


Perhaps I am anticipating the future too much. The intent of the milrinone is altering the PA pressure and low normal cardiac index, if patient is still symptomatic, or worsening after adequate diuresis. ICU criteria is simply to maintain PA cath and close monitoring. You can be more aggressive with medical management with ICU monitoring. This patient does appear to be in a window of opportunity to get whatever repair he needs done. Some optimization can give you a smoother intraop/postop course, but if that window is closing, you want to detect that early, and get the procedure done somewhat urgently.


As mentioned above, for PA pressure modulation. We assume type 2 PAH, but that's an assumption. In my experience, you can pair milrinone with vaso/norepi and get somewhat selective PA vasodilation, if you're concerned about the AS.


You don't need high PEEP for a non-hypoxic, severe PAH patient, right? By low PEEP, I mean PEEP of 5-6.

I wasn't thinking LVAD; more of RP impella, protek duo, or VA ECMO. Bridge to recovery can also mean use of temporary mechanical devices.


I take care of these patients postop. I know most cardiac anesthesiologist here can get this patient through the bentall alive, but a fraction of these people will go into RV failure, and/or renal failure postop. Fluid overloaded at baseline plus these postop complication will mean poor response to medical management, and likely dialysis need/prolonged intubation. Preop medical optimization help to reduce this risk.

That's not what an rsi is
Do you routinely push paralytics in divided doses or something?

 

[Robotic Wis-Hipple]

That's not what an rsi is
Do you routinely push paralytics in divided doses or something?

To be fair I don’t think that’s what he’s saying. I think he’s saying he wouldn’t give a slug of induction agent or mask ventilate.

 

[PpfSuxTube]

If you cant articulate well an anesthetic induction for a complex patient on an internet forum and you prescribe an inodilator for a patient with critical AS with CI over 2, what hope do you have in real life when your clear actions, thought and speech in the next 60 seconds determines life or death?

An impella rp? For a right heart that moves like that and can generate those pressures? Yeah the rv may crump but its not the primary problem. A percival valve can be in in under an hour pump time

 

[vector2]

Here's some clips from the case. I'll post some comments later

Pre:

Post:

Fun fact, the post-CPB clips are on a teeny tiny baby dose of inotropic support. Food for thought about what the word "contractility" truly means vis a vis being an intrinsic property of the myocardium.

 

[BlueRug]

What? Do you want to go to jail? Milrinone??

Oh god I can’t stop laughing. This might be the best reply I’ve ever read

 

[anaesthetic]

This dude has no emergent need for surgery that I see. Keep PA cath in, medical optimization in cardiac ICU, diurese, maybe start milrinone. See what happens when LVEDP is upper range of normal.

Slow induction - midaz/fent heavy, with etomidate & paralize. rapid sequence. Keep an eye on BP and PA cath parameters. Low PEEP. Have the surgeon in the room for induction; induction to incision time should be minimal given pt already lined up in ICU.

Mechanical device support could be used at any time periop if indicated. Patient could have a decent postop prognosis assuming he survives the immediate periop timeline. Mechanical device bridge to recovery is reasonable.

What? Do you want to go to jail? Milrinone??

Oh god I can’t stop laughing. This might be the best reply I’ve ever read

I kind of get where he's coming from. Optimize, maybe start some meds, do the case as follows:

Rapidly slow sequential induction. Have the surgeon put in ECMO cannulas as the patient's being slowly rapidly induced. Have the LVAD, Impella, and Protek Duo reps in the room for induction. Recommend that the patient's upper chest be left open as they're closing the lower chest. Turn in my badge and pager after the case and fast track myself to HR.

 

[NumTacos]

I kind of get where he's coming from. Optimize, maybe start some meds, do the case as follows:

Rapidly slow sequential induction. Have the surgeon put in ECMO cannulas as the patient's being slowly rapidly induced. Have the LVAD, Impella, and Protek Duo reps in the room for induction. Recommend that the patient's upper chest be left open as they're closing the lower chest. Turn in my badge and pager after the case and fast track myself to HR.

 

[NumTacos]

If you cant articulate well an anesthetic induction for a complex patient on an internet forum and you prescribe an inodilator for a patient with critical AS with CI over 2, what hope do you have in real life when your clear actions, thought and speech in the next 60 seconds determines life or death?

An impella rp? For a right heart that moves like that and can generate those pressures? Yeah the rv may crump but its not the primary problem. A percival valve can be in in under an hour pump time

Honestly, I am not sure he is going to understand anything you said.

 

[Beeftenderloin]

Here's some clips from the case. I'll post some comments later

Pre:

Post:

Fun fact, the post-CPB clips are on a teeny tiny baby dose of inotropic support. Food for thought about what the word "contractility" truly means vis a vis being an intrinsic property of the myocardium.

That’s a happy looking heart. What a great case, and great outcome for this patient (at least echocardiographically). One of my surgeon’s is totally obsessed with the pre and post intervention LVEF we put in our report. They’d get a kick out of this one.

 

[dchz]

That’s a happy looking heart. What a great case, and great outcome for this patient (at least echocardiographically). One of my surgeon’s is totally obsessed with the pre and post intervention LVEF we put in our report. They’d get a kick out of this one.

The single most important thing I do is to make sure the post EF is at least 5% more than the pre op EF.

 

[Radetzky]

Good case. I was surprised that that LV the way it looked on the preop echo was able to generate such a high gradient, but I guess it’s just a good reminder how much EF is influenced by loading conditions