Moments from call

[ranvier]

Pt rushed to OR for worsening shock on multiple pressors. I remove the clonidine patch on his shoulder. He did well after three liters of blood removed from his abdomen. "It was a home medication."

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[sethco]

Had a number of CABG patients in the past couple months where I have found a NTG patch/paste on while I was putting on monitors...Half of these patients were on NTG drips that were stopped couple hours prior to surgery

Also, had a massive transfusion protocol patient brought down from the ICU with NTG paste still on and on Levophed 0.8 (!!!!) mcg/kg/min. No arterial line and trying to run a rapid infuser through a PICC. WTF!!!!!

 

[WholeLottaGame7]

Had a number of CABG patients in the past couple months where I have found a NTG patch/paste on while I was putting on monitors...Half of these patients were on NTG drips that were stopped couple hours prior to surgery

Also, had a massive transfusion protocol patient brought down from the ICU with NTG paste still on and on Levophed 0.8 (!!!!) mcg/kg/min. No arterial line and trying to run a rapid infuser through a PICC. WTF!!!!!

Never understood the CCU. Half the heart transplants I did, I would pick up a patient with an EF of 10% w/ an IABP and on dobutamine/etc: one 20g PIV. No a-line, no central line, not even backup IV access...

 

[criticalelement]

they dont get paid for a lines

 

[vector2]

Never understood the CCU. Half the heart transplants I did, I would pick up a patient with an EF of 10% w/ an IABP and on dobutamine/etc: one 20g PIV. No a-line, no central line, not even backup IV access...

I'm pretty sure every type A dissection I've had in residency has come from the ICU or ER with a 20g IV, maxed out on esmolol and cardene, no a-line or central line, and the NIPB set to cycle every 15 minutes.

 

[nimbus]

Had a number of CABG patients in the past couple months where I have found a NTG patch/paste on while I was putting on monitors...Half of these patients were on NTG drips that were stopped couple hours prior to surgery

Also, had a massive transfusion protocol patient brought down from the ICU with NTG paste still on and on Levophed 0.8 (!!!!) mcg/kg/min. No arterial line and trying to run a rapid infuser through a PICC. WTF!!!!!

Never understood the CCU. Half the heart transplants I did, I would pick up a patient with an EF of 10% w/ an IABP and on dobutamine/etc: one 20g PIV. No a-line, no central line, not even backup IV access...

I'm pretty sure every type A dissection I've had in residency has come from the ICU or ER with a 20g IV, maxed out on esmolol and cardene, no a-line or central line, and the NIPB set to cycle every 15 minutes.

So it's everywhere. Mind boggling. Then I get calls from the intensivist asking if their intern can do/practice lines on my patients. I'm thinking to myself, "What about all YOUR patients that need lines??!!" So many missed opportunities.

 

[deleted171991]

Never understood the CCU. Half the heart transplants I did, I would pick up a patient with an EF of 10% w/ an IABP and on dobutamine/etc: one 20g PIV. No a-line, no central line, not even backup IV access...

That makes 3 out of 3 crappy CCUs I know about.

I honestly think most cardiologists should not be allowed to practice cardiac intensive care.

 

[deleted171991]

they dont get paid for a lines

It's not about money. Those are not elective outpatients that could just go find another doctor. When one takes the damn job, one takes the entire package, and that includes all the stuff one is not paid for but would do for one's own mother.

 

[PainDrain]

The ridiculous care I have seen in "ICUs" by "intensivists" amazes me. GI bleeds with a single 22 in the AC and their arms have pipes running up them. Vented patients breathing at 20+ a min and TV of 800 with CO2 in the teens. Never bothering to draw an ABG. Multiple pressors running through peripheral IVs for days with no A-line in place and no consideration of placing a CVC.

 

[Stank811]

Do a CC fellowship and rotate through units run by different departments or even better rotate through a non academic hospital where the intensivist are only consulted for vent management or if it is time for palliative care. There is a lot of M and M that is occurring in such settings.

 

[G-Man82]

Sounds like the community ICUs I cover remotely where asking for an arterial line or central line leads to a picture of some Hospitalist repeatedly stabbing the poor patients neck or wrists. One those ICU nurses also kept dialing up on the norepi overnight from 0.1 all the way to 0.9 mcg/kg/min using a 20g and a NIBP set to q15 mins. They didn't bother to call me or the in-house Hospitalist. That's just the level of care that exists out there. It's very shameful.

I get type A dissections all the time in my ICU preop. They get an arterial line and some large bore peripherals. I leave the central line for the OR unless they're unstable, and then I put it in myself. But if a type A needs a cordis in the ICU, then it's likely their days are numbered.


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[deleted171991]

The ridiculous care I have seen in "ICUs" by "intensivists" amazes me. GI bleeds with a single 22 in the AC and their arms have pipes running up them. Vented patients breathing at 20+ a min and TV of 800 with CO2 in the teens. Never bothering to draw an ABG. Multiple pressors running through peripheral IVs for days with no A-line in place and no consideration of placing a CVC.

Don't get me started on some internist "intensivists" from community hospitals.

 

[criticalelement]

It's not about money. Those are not elective outpatients that could just go find another doctor. When one takes the damn job, one takes the entire package, and that includes all the stuff one is not paid for but would do for one's mother.

Why do you think you dont see any swans anymore... Is it because it does not convey info? or nobody gets paid for swans anymore... That used to be an 800 dollar procedure.

Icu docs in private practice used to make a ton of money billing patients.

 

[deleted171991]

You don't see Swans because they don't improve outcomes.

 

[Planktonmd]

Never understood the CCU. Half the heart transplants I did, I would pick up a patient with an EF of 10% w/ an IABP and on dobutamine/etc: one 20g PIV. No a-line, no central line, not even backup IV access...

Cardiologists don't bother with silly things like central lines and arterial lines, they are usually busy saving lives and talking directly to God!

 

[G-Man82]

Cardiologists don't bother with silly things like central lines and arterial lines, they are usually busy saving lives and talking directly to God!

Or telling us to avoid hypoxia, tachycardia, and to do a spinal to get their critical AS patient through their elective hernia repair.


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[urge]

The cardiologists I work with do the same. No aline or central line on a guy getting high dose cathecolamines. However, I'm not under the impression that they get into trouble for this.

I think is because their patients are not as unstable as ours. No 3rd spacing, no sudden hypertension from emergence of anesthesia... Our patients are usually miserable from all the pain and tubes coming out of everywhere. Theirs are usually happy to be alive. If one of our patients goes into respiratory insufficiency they get reintubated, theirs get a BiPAP, and so forth. It's a different animal.

 

[GravelRider]

The cardiologists I work with do the same. No aline or central line on a guy gettinghigh dose cathecolamines. However, I'm not under the impression that they get into trouble for this.

I think is because their patients are not as unstable as ours. No 3rd spacing, no sudden hypertension from emergence of anesthesia... Our patients are usually miserable from all the pain and tubes coming out of everywhere. Theirs are usually happy to be alive. If one of our patients goes int ok respiratory insufficiency they get reintubated, theirs get a BiPAP, and so forth. It's a different animal.

I'm not so sure about that. Some of those patients are very unstable. I can think many situations in which those cardiac patients are just as unstable as ours..or even more so. It's more of a local culture thing. Where I trained for IM, cardiology was very aggressive with those kinds of things. They floated swans all the time for the heart failure patients. These were the kinds of patients that went home on milrinone. As the residents taking care of those patients, we used to fight to place A-lines and central lines for them.

 

[Robotic Wis-Hipple]

My personal favorite is systolic caps/floors with only a NIBP.

The last dissection I got showed up as a transfer, on a transport defib monitor with only EKG connected/being monitored and a single 20g. I asked what current pressure was and they literally couldn't tell me, hadn't checked one since pickup.

 

[deleted171991]

My favorite is when they kill patients with inotropes. They get a low EF patient in shock, and instead of putting her on norepi, they put her on milrinone. The next thing is that the patient gets seriously tachycardic, which they let go on for a few days, until the patient infarcts for good and dies. I have seen this happen a couple of times, and still nothing registers up there about the fact that a too high O2 demand increases mortality.

 

[bigdan]

Just came off a week-long ICU bender. 100+ hours, two big saves (if I do say so myself!) and one sad loss...

When I started working in this unit (cardiac only - mixed medical and surgical cardiac), a cardiologist commented to me "Wow - you sure do love putting in a-lines". I told him I love knowing an accurate blood pressure.

Regarding how sick medical cardiac patients get, and with the disclaimer that I am an inexperienced new attending, the single sickest patient I have ever seen was a fulminant viral myocarditis. Entered the ED, walkie-talkie with "a little shortness of breath" at 0400, cath'ed at 1300 (LV-gram EF: 30%), in my ICU at 1400, where a STAT TTE showed LVEF of 10%, and pronounced dead at 1500. Early 40s. Absolutely horrific experience. Everything went south, and quicker than I'd ever imagine. The whole f'in computer screen was red numbers, and her legs mottled literally in front of my eyes. They'd called from the cath lab to tell me the patient has "clean coronaries and 'what looks like a little heart failure'"!!! Now that you mention it - she arrived with just a 20g...

 

[Planktonmd]

My favorite is when they kill patients with inotropes. They get a low EF patient in shock, and instead of putting her on norepi, they put her on milrinone. The next thing is that the patient gets seriously tachycardic, which they let go on for a few days, until the patient infarcts for good and dies. I have seen this happen a couple of times, and still nothing registers up there about the fact that a too high O2 demand increases mortality.

You are talking about a patient with low EF who is in hypovolemic or septic shock I am assuming?

 

[Planktonmd]

Just came off a week-long ICU bender. 100+ hours, two big saves (if I do say so myself!) and one sad loss...

When I started working in this unit (cardiac only - mixed medical and surgical cardiac), a cardiologist commented to me "Wow - you sure do love putting in a-lines". I told him I love knowing an accurate blood pressure.

Regarding how sick medical cardiac patients get, and with the disclaimer that I am an inexperienced new attending, the single sickest patient I have ever seen was a fulminant viral myocarditis. Entered the ED, walkie-talkie with "a little shortness of breath" at 0400, cath'ed at 1300 (LV-gram EF: 30%), in my ICU at 1400, where a STAT TTE showed LVEF of 10%, and pronounced dead at 1500. Early 40s. Absolutely horrific experience. Everything went south, and quicker than I'd ever imagine. The whole f'in computer screen was red numbers, and her legs mottled literally in front of my eyes. They'd called from the cath lab to tell me the patient has "clean coronaries and 'what looks like a little heart failure'"!!! Now that you mention it - she arrived with just a 20g...

So... do you think whatever happened in the cath lab might have contributed to this very quick decline???

 

[deleted171991]

You are talking about a patient with low EF who is in hypovolemic or septic shock I am assuming?

Cardiogenic. In both septic and cardiogenic shock, norepi should be the first choice, not inotropes (which can be titrated in later, if there is proof that they help). Even phenylephrine (just enough to better perfuse those coronaries) can be better than revving up the heart to a rate of 130. One doesn't fix anything if, while increasing the SV and systemic MAP, one puts the heart in subclinical demand ischemia.

 

[GravelRider]

Just came off a week-long ICU bender. 100+ hours, two big saves (if I do say so myself!) and one sad loss...

When I started working in this unit (cardiac only - mixed medical and surgical cardiac), a cardiologist commented to me "Wow - you sure do love putting in a-lines". I told him I love knowing an accurate blood pressure.

Regarding how sick medical cardiac patients get, and with the disclaimer that I am an inexperienced new attending, the single sickest patient I have ever seen was a fulminant viral myocarditis. Entered the ED, walkie-talkie with "a little shortness of breath" at 0400, cath'ed at 1300 (LV-gram EF: 30%), in my ICU at 1400, where a STAT TTE showed LVEF of 10%, and pronounced dead at 1500. Early 40s. Absolutely horrific experience. Everything went south, and quicker than I'd ever imagine. The whole f'in computer screen was red numbers, and her legs mottled literally in front of my eyes. They'd called from the cath lab to tell me the patient has "clean coronaries and 'what looks like a little heart failure'"!!! Now that you mention it - she arrived with just a 20g...

Saw a patient like that during IM residency...giant cell myocarditis in a young guy. RVAD/LVAD plus CVVH as he awaited a transplant. He walked out a month or two later. Myocarditis like that is very difficult to diagnose and the patients crash hard and fast.

The problem with cardiologists in the icu is that they always think "heart first," and will often overlook other diagnoses like sepsis. It's not uncommon for there to be demand ischemia with myocardial damage and a troponin bump with a reduction in EF in sepsis, which can confuse the picture. Norepi should almost always be the "go to" pressor in acute hypotension in the icu until things are sorted out (with obvious exceptions).

 

[urge]

Cardiogenic. In both septic and cardiogenic shock, norepi should be the first choice, not inotropes (which can be titrated in later, if there is proof that they help). Even phenylephrine (just enough to better perfuse those coronaries) can be better than revving up the heart to a rate of 130. One doesn't fix anything if, while increasing the SV and systemic MAP, one puts the heart in subclinical demand ischemia.

How do reconcile this management with the traditional afterload reduction treatment for heart failure?

 

[psychbender]

Just came off a week-long ICU bender. 100+ hours, two big saves (if I do say so myself!) and one sad loss...

When I started working in this unit (cardiac only - mixed medical and surgical cardiac), a cardiologist commented to me "Wow - you sure do love putting in a-lines". I told him I love knowing an accurate blood pressure.

Regarding how sick medical cardiac patients get, and with the disclaimer that I am an inexperienced new attending, the single sickest patient I have ever seen was a fulminant viral myocarditis. Entered the ED, walkie-talkie with "a little shortness of breath" at 0400, cath'ed at 1300 (LV-gram EF: 30%), in my ICU at 1400, where a STAT TTE showed LVEF of 10%, and pronounced dead at 1500. Early 40s. Absolutely horrific experience. Everything went south, and quicker than I'd ever imagine. The whole f'in computer screen was red numbers, and her legs mottled literally in front of my eyes. They'd called from the cath lab to tell me the patient has "clean coronaries and 'what looks like a little heart failure'"!!! Now that you mention it - she arrived with just a 20g...

This reminds me of two similar stories from residency, both from different regionally-recognized "big" names for cardiac. The first was a 30-something with viral myocarditis coming down from the CCU to be put on ECMO. Her biggest complaint as I saw her when she arrived to the OR was that the nurses wouldn't let her have the ginger ale that her mom brought. She coded immediately after I put an a-line in (came down with just the obligatory 20-g AC PIV), and twice more before her chest was opened. Her function recovered enough that she was decannulated ten days later.

At the other center, there was a 40-something with critical AS and heart failure that was admitted the night before, and was urgently going for AVR. I went down to the CCU to see him, and he's tubed, on 2mg/hr versed and 50mcg/hr fentanyl through another 20g PIV, pulse-ox disconnected because the nurse said, "the numbers didn't make sense, and it was an odd-waveform," and the NIBP showing 70/38 from an hour ago (the nurse again said, something to the effect of "yeah, I don't think that's real, so I turned it off"). I rushed him to the OR, my attending thought my art line was venous (nope, PO2 40s), and his pressure really was in the ****ter. Good times.

 

[deleted171991]

Saw a patient like that during IM residency...giant cell myocarditis in a young guy. RVAD/LVAD plus CVVH as he awaited a transplant. He walked out a month or two later. Myocarditis like that is very difficult to diagnose and the patients crash hard and fast.

The problem with cardiologists in the icu is that they always think "heart first," and will often overlook other diagnoses like sepsis. It's not uncommon for there to be demand ischemia with myocardial damage and a troponin bump with a reduction in EF in sepsis, which can confuse the picture. Norepi should almost always be the "go to" pressor in acute hypotension in the icu until things are sorted out (with obvious exceptions).

I am sorry, but most of them don't "think". They are like midlevels, cookbook medicine. Were they thinking, they would consider cardiac work and demand-supply balance. That's usually how they kill their patients: they rev up that poor heart till it burns out.

 

[deleted171991]

How do reconcile this management with the traditional afterload reduction treatment for heart failure?

Cardiogenic shock is beyond decompensated heart failure. Even in acute decompensated HF, inotropes are not the goto drugs anymore.

That is exactly the problem, that cardiologists are somewhere in the last decade or behind when about treating (almost) shock. Letting them manage cardiac intensive care is like letting surgeons manage the SICU: a lot of midlevel medicine, no offense. Most of them don't get proper training for this during residency and fellowship, respectively.

A good intensivist (or anesthesiologist) doesn't treat a disease, but a pathophysiologic state, which by definition is in flux, and may even be different between two patients with the same diagnosis. It is intensive care, something that requires continuous evaluation and adjustments, something that most internists and surgeons are not trained/willing to do.

 

[GravelRider]

How do reconcile this management with the traditional afterload reduction treatment for heart failure?

In acute cardiogenic shock you need to maintain coronary perfusion. Reducing afterload too much may worsen coronary perfusion. IABP is a good option here. This is a bit different than the chronic decompensated heart failure where you unload the ventricle by diuresing and afterload reduction.

 

[Planktonmd]

Cardiogenic. In both septic and cardiogenic shock, norepi should be the first choice, not inotropes (which can be titrated in later, if there is proof that they help). Even phenylephrine (just enough to better perfuse those coronaries) can be better than revving up the heart to a rate of 130. One doesn't fix anything if, while increasing the SV and systemic MAP, one puts the heart in subclinical demand ischemia.

This applies to Dobutamine more than Milrinone, but yes adding a medication that causes peripheral vascular constriction could help decrease the reflex tachycardia caused by the vasodilation of Milrinone.
But wouldn't you want to do both simultaneously? a positive inotrope and a vasoconstrictor?

 

[deleted171991]

This applies to Dobutamine more than Milrinone, but yes adding a medication that causes peripheral vascular constriction could help decrease the reflex tachycardia caused by the vasodilation of Milrinone.
But wouldn't you want to do both simultaneously? a positive inotrope and a vasoconstrictor?

You might, but you start with the pressor, and keep in mind that the inotrope (while fixing the numbers) will squeeze your heart like a diuretic the kidney. We don't give diuretics in AKI, do we? So we should watch the inotrope and the heart like a hawk.

The idea is that the inotrope should be an adjunct, not the first line. I want to optimize that Starling curve, not overwhelm the heart. As with most stuff in critical care, it ends up with a little bit of this and a little bit of that; using medications at doses where one takes advantage of their therapeutical effects with minimal side effects.

It just drives me crazy to see patients on milrinone-only with heart rates of 130-150 for days.

 

[urge]

Cardiogenic shock is beyond decompensated heart failure. Even in acute decompensated HF, inotropes are not the goto drugs anymore.

That is exactly the problem, that cardiologists are somewhere in the last decade or behind when about treating (almost) shock. Letting them manage cardiac intensive care is like letting surgeons manage the SICU: a lot of midlevel medicine, no offense. Most of them don't get proper training for this during residency and fellowship, respectively.

A good intensivist (or anesthesiologist) doesn't treat a disease, but a pathophysiologic state, which by definition is in flux, and may even be different between two patients with the same diagnosis. It is intensive care, something that requires continuous evaluation and adjustments, something that most internists and surgeons are not trained/willing to do.

Do you have any good review on the matter?

I have always liked to run BPs on the higher side but some of the people I work with freak out and switch everything around in the name of afterload reduction. But so far I have not been able to tell them they are doing it wrong.

 

[deleted171991]

Do you have any good reviewon the matter?

Yeah. It's called Marik's Evidence-Based Critical Care. (Regardless how many books and articles I read, I end up agreeing with this guy in 90% of the cases.)

I'll try to find a good review article, but it might take a while.

I have always liked to run BPs on the higher side but some of the people I work with freak out and switch everything around in the name of afterload reduction. But so far I have not been able to tell them they are doing it wrong.

Afterload should be low-normal, not low, because that's how one gets low MAP (and, more importantly, low DBP, meaning poor coronary and peripheral capillary perfusion). If I decrease the SVR, I need to rev up the CO (including HR) to maintain the same MAP, which is exactly what cardiologists tend to do, putting the heart in subclinical demand ischemia for days, until it crashes. They are trained to watch the numbers, not the physiology.

 

[ranvier]

Had a number of CABG patients in the past couple months where I have found a NTG patch/paste on while I was putting on monitors...Half of these patients were on NTG drips that were stopped couple hours prior to surgery

Also, had a massive transfusion protocol patient brought down from the ICU with NTG paste still on and on Levophed 0.8 (!!!!) mcg/kg/min. No arterial line and trying to run a rapid infuser through a PICC. WTF!!!!!

I've done a handful of flaps/extremity debridements from extravasation of vasopressors.

Multiple pressors without arterial line....agree wtf.

Milrinone hangs around so long I tend to try dobutamine or even inhaled nitric first for right sided support.

I know my guy got better from finding and fixing the bleeder (and transfusion in the OR) but what happened to knowing everything and every inch on your critically ill patient. Not knowing or finding a patch that has pretty profound hemodynamic consequences is very poor form.

 

[Planktonmd]

Do you have any good review on the matter?

I have always liked to run BPs on the higher side but some of the people I work with freak out and switch everything around in the name of afterload reduction. But so far I have not been able to tell them they are doing it wrong.

Just wait, sooner or later Blade will find this little discussion and you will have all the reviews and articles you want, both in favor and against your argument with a few completely irrelevant on top too!

 

[deleted171991]

Here's the beginning (I am on an iPad, so it's tough to copy-paste more): http://onlinelibrary.wiley.com/doi/10.1016/S1388-9842(02)00178-2/pdf

Milrinone is worse than placebo for ischemic CHF (i.e. increases mortality), and not much better for non-ischemic.

One would expect people to know this 10+ years after the RCT, and yet I regularly see cardiac patients revved up on milrinone, without any pressor.

 

[urge]

Here's the beginning (I am on an iPad, so it's tough to copy-paste more): http://onlinelibrary.wiley.com/doi/10.1016/S1388-9842(02)00178-2/pdf

Milrinone is worse than placebo for ischemic CHF (i.e. increases mortality), and not much better for non-ischemic.

One would expect people to know this 10+ years after the RCT, and yet I regularly see cardiac patients revved up on milrinone, without any pressor.

I'm aware of that study. I would have a hard time trying to convince someone to treat a post op patient with low EF just with norepi based on it. I can bring a low EF pt just on norepi with good BP, urinating, and low lactates but the intensivists will start an inotrope and aim for a low bp the moment they hear the EF is low. Not what I would do but I have not seen any convincing data in this regard.

 

[OB1🤙]

Norepi is my go-to first line pressor for pretty much everything.

People forget that it's a positive inotrope as well.

Agree 1000% with the comments regarding overuse of inotropes like milrinone above.

 

[deleted171991]

It would be funny if it weren't sad: http://journal.publications.chestnet.org/data/Journals/CHEST/21722/1129.pdf

 

[deleted171991]

I'm aware of that study. I would have a hard time trying to convince someone to treat a post op patient with low EF just with norepi based on it. I can bring a low EF pt just on norepi with good BP, urinating, and low lactates but the intensivists will start an inotrope and aim for a low bp the moment they hear the EF is low. Not what I would do but I have not seen any convincing data in this regard.

It's still an open debate whether inotrope (and/or pressor) use increases mortality. From what I have personally seen, it does, as long as we allow the cardiac supply/demand ratio to get out of control. Norepi is a better first drug. People tend to forget that these medications are just for bridging, until we fix the root cause of the problem, or insert a mechanical assist device. Hence we should focus on all vital organs, including the heart, when we resuscitate/temporize.

A heart rate above 110-120 for days in an elderly patient is bad, especially in a sick heart, regardless how nice the other numbers look, regardless what the latest stupid algorithm says. Same goes for exaggerating the increase in contractility, despite the obvious increase in oxygen consumption and signs of demand ischemia. Or exaggerating the increase in afterload and MAP, just to get nice numbers, while the LV is failing.

 

[GravelRider]

I'm aware of that study. I would have a hard time trying to convince someone to treat a post op patient with low EF just with norepi based on it. I can bring a low EF pt just on norepi with good BP, urinating, and low lactates but the intensivists will start an inotrope and aim for a low bp the moment they hear the EF is low. Not what I would do but I have not seen any convincing data in this regard.

I don't understand the goal of low BP even in decompensated heart failure or cardiogenic shock. So are they also aiming to stop the patient from urinating and increasing the lactate? Afterload reduction is one way to decrease myocardial oxygen demand, but you don't start an ACE in a patient who is hypotensive and in decompensated failure. Decreasing blood flow through the coronaries is also bad for myocardial oxygen demand.

 

[Planktonmd]

It's still an open debate whether inotrope (and/or pressor) use increases mortality. From what I have personally seen, it does, as long as we allow the cardiac supply/demand ratio to get out of control. People tend to forget that these medications are just for bridging, until we fix the root cause of the problem, or insert a mechanical assist device. Hence we should focus on all vital organs, including the heart, when we resuscitate.

A heart rate above 110-120 for days in an elderly patient is bad, especially in a sick heart, regardless how nice the other numbers look, regardless what the latest stupid algorithm says. Same goes for exaggerating the increase in contractility, despite the obvious increase in oxygen consumption and signs of demand ischemia. Or exaggerating the increase in afterload and MAP, just to get nice numbers, while the LV is failing.

The question is: if an inotrope does not cause tachycardia or if the tachycardia is somehow suppressed does it really improve the cardiac output in a clinically meaningful way?
I mean is the whole class of inotropes useless?

 

[Planktonmd]

I don't understand the goal of low BP even in decompensated heart failure or cardiogenic shock. So are they also aiming to stop the patient from urinating and increasing the lactate? Afterload reduction is one way to decrease myocardial oxygen demand, but you don't start an ACE in a patient who is hypotensive and in decompensated failure. Decreasing blood flow through the coronaries is also bad for myocardial oxygen demand.

If the heart is forced to produce higher systolic pressure or to contract against high SVR, it is also more demand on the myocardium, and it could cause ischemia just as tachycardia would.
So you don't induce hypotension, but you also don't aim too high in your BP expectations.

 

[GravelRider]

If the heart is forced to produce higher systolic pressure or to contract against high SVR, it is also more demand on the myocardium, and it could cause ischemia just as tachycardia would.
So you don't induce hypotension, but you also don't aim too high in your BP expectations.

Agreed.

 

[GravelRider]

The question is: if an inotrope does not cause tachycardia or if the tachycardia is somehow suppressed does it really improve the cardiac output in a clinically meaningful way?
I mean is the whole class of inotropes useless?

Absolutely not. Inotropes are often necessary. However, they are usually not first line or "go to" agents. I can't think of any situation where I would start milrinone as a lone agent for acute hypotension.

 

[Robotic Wis-Hipple]

If the heart is forced to produce higher systolic pressure or to contract against high SVR, it is also more demand on the myocardium, and it could cause ischemia just as tachycardia would.
So you don't induce hypotension, but you also don't aim too high in your BP expectations.

Iirc myocardial O2 consumption is affected by HR>afterload/wall tension. So sure, increasing afterload increases myocardial O2 consumption, but it does so less than HR does while also increasing myocardial O2 delivery. And NE does provide positive inotropy in addition to increasing SVR, which makes sense then as to why it is the favored first line agent.

And outside of perhaps acute R heart failure secondary to pulmonary hypertension I don't see milrinone used first line ever.

 

[vector2]

I would say 80% of decompensating LV failure pts I've taken down for an LVAD have been on dobutamine and a maxed out lasix drip. We turn that sh~t off, start 0.04 norepi and maybe 0.02 epi and things are magically better in 5 minutes.

 

[dhb]

ICU call:
Nurse: "I took a venous pH it's 7.33 do you want me to do something?"
Me: you are $hitting me?!
Nurse: "ok, oh and nurse 2 has something to ask"
Nurse 2 : "Oh btw my patient has been convulsing for about 10min..?"
Me: "WTF!?"

I kidd you not

 

[Planktonmd]

Maybe it's time to revisit our strategies for treating cardiogenic shock!
I think the issue is that we need to focus more on tissue perfusion and less on improving cardiac contractility?