dopamine distrust

[morri493]

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Hi all,
I have a question regarding Dopamine, particularly post-cardiac surgery. I am a new cardiac anesthesia attending in private practice. In residency and in fellowship, Dopamine was a drug that we just didn't really use. We were always told it s a "dirty drug," dose dependence on receptor stimulation just sounds awful compared to E and NE. The practice I have joined has some old school surgeons and ICU nurses that live and die by dopamine. When I've asked why they genuinely feel that it necessary post CPB. I've been trying to find EBM to disprove this, and have found some. Notable dopamine vs NE as a vasoconstrictor increasing mortality in cardiogenic shock, but I really haven't found much data supporting Dopamine vs epinephrine as an inotrope. Anecdotally, I see a lot more tachycardia with DA, which is obviously less than ideal in most cardiac surgical patients. Is dopamine something that actually has a actual role in modern medicine, that I seemed to have missed during training, or are there studies that support my view that DA does nothing that E or NE can do better? I wouldn't greatly appreciate any information on either side of the issue - I haven't been very successful in trying to find this data on my own. Thanks in advance for any input/opinions y'all can provide!

 

[dabears505]

5 o dope. That's what an old school guy I used to work with loved. His patients did well. He liked it too avoid using the pacer.

 

[coffeebythelake]

i don't use dopamine nor do i plan to use dopamine anytime in the future. i think there are plenty of other better choices out there with more evidence behind it. when the last 15 years have basically been disproving many of dopamine's supposed benefits, there ain't much else to say about it.

 

[abolt18]

Got an old school surgeon who is all about dopamine. He don't care. He's been doing this longer than many of us have been alive. He's an excellent surgeon who has easily the best outcomes of all our CT surgeons despite operating on horrendous patients that get rejected by all other CT surgeons in the state.

I don't think anyone wants to argue it...

 

[chessknt]

A lot of the distrust originates from this study. There is honestly not a lot of research on pressors but this was a study that in all comers showed dopamine is probably worse than norepinephrine. That doesn’t mean it is always the wrong choice but that you need to have a really good reason to use it instead.

Comparison of dopamine and norepinephrine in the treatment of shock - PubMed

Although there was no significant difference in the rate of death between patients with shock who were treated with dopamine as the first-line vasopressor agent and those who were treated with norepinephrine, the use of dopamine was associated with a greater number of adverse events...

pubmed.ncbi.nlm.nih.gov

 

[Hork Bajir]

I could see an argument for running low doses around induction or pre-CPB in patients with severe AI, esp if acute, to keep HR high and counteract the bradycardia from fentanyl (if that’s your thing). Can also use pacing swans, glyco, less narcotic… But dopamine is nice for this purpose in that it’s a relatively titratable way to maintain HR

 

[partydoc]

If you're a new attending, go with the flow. You don't need to be the new guy causing problems. And I can guarantee you this surgeon won't give two sh+ts about whatever you find as far as EBM goes.

 

[Blockit]

If you're a new attending, go with the flow. You don't need to be the new guy causing problems. And I can guarantee you this surgeon won't give two sh+ts about whatever you find as far as EBM goes.

This, a million times.
And being that the presence of your old-school cardiac surgeon allows the CEO to keep that profitable Cath Lab going, said cardiac surgeon will get anything that he wants, including the ability to take a dump on the operating room floor unmolested if he so chooses.

 

[icuanesthesiology]

The hatred of dopamine is greatly overexaggerated and I agree with the above poster about the paper that started it all. I have been doing cardiac surgical and MICU for about 10 years now. I have used everything from dopamine to levo to dobutamine to milrinone to neo to vaso. In general, it doesn't matter what we use as much as we think. If you look at the details of that paper, the patients are on 20mcg/kg/min of dopamine. When I have used it in a cardiac surgical ICU, we almost never go above 5, rarely above 8 as a temporizing measure, but at that time we add other agents, and importantly start looking for the cause of hypotension/shock.

For inotropic support, there are advantages to dopamine
epi almost always causes a metabolic acidosis which is a real PIA.
dobutamine is great at no more than 4 or so, but its beta 2 activity means you get limited BP support. often need to pair with neo or levo
milrinone sucks in the immediate post-op period. too much hypotension and t 1/2 is way too long. better started 24 hours after bypass when SIRS state is abating
norepi: obviously more of a pressor

of all those, which brings up BP, is an inotrope and doesn't cause a metabolic acidosis?...dopamine. the perfect drug.

And EBM never beats solid years of clinical experience. Don't be the new guy who rocks the boat because some guy published a paper 10 years ago utilizing dopamine at a dose that almost no one uses in a cardiac surgical ICU. you will be slaughtered by that old school surgeon. Go with the flow, listen to the old timers, be agreeable, and take some time to gain their trust, then you can start changing stuff.

 

[vector2]

The hatred of dopamine is greatly overexaggerated and I agree with the above poster about the paper that started it all. I have been doing cardiac surgical and MICU for about 10 years now. I have used everything from dopamine to levo to dobutamine to milrinone to neo to vaso. In general, it doesn't matter what we use as much as we think. If you look at the details of that paper, the patients are on 20mcg/kg/min of dopamine. When I have used it in a cardiac surgical ICU, we almost never go above 5, rarely above 8 as a temporizing measure, but at that time we add other agents, and importantly start looking for the cause of hypotension/shock.

For inotropic support, there are advantages to dopamine
epi almost always causes a metabolic acidosis which is a real PIA.
dobutamine is great at no more than 4 or so, but its beta 2 activity means you get limited BP support. often need to pair with neo or levo
milrinone sucks in the immediate post-op period. too much hypotension and t 1/2 is way too long. better started 24 hours after bypass when SIRS state is abating
norepi: obviously more of a pressor

of all those, which brings up BP, is an inotrope and doesn't cause a metabolic acidosis?...dopamine. the perfect drug.

And EBM never beats solid years of clinical experience. Don't be the new guy who rocks the boat because some guy published a paper 10 years ago utilizing dopamine at a dose that almost no one uses in a cardiac surgical ICU. you will be slaughtered by that old school surgeon. Go with the flow, listen to the old timers, be agreeable, and take some time to gain their trust, then you can start changing stuff.

Type B lactic acidosis from epinephrine in the CTICU is a non-issue. The acidosis is not caused by hypoperfusion, tissue hypoxia, and ischemia,. It's due to increased beta-mediated lipolysis, glycogenolysis, and glycolysis causing so much pyruvate to be made that the TCA cycle is overwhelmed. But eventually the lactate makes it through the Cori cycle at some point assuming a normally functioning liver and all is well. Ultimately, it's a surplus of fuel. Don't treat the number, treat the patient...

 

[Hork Bajir]

Type B lactic acidosis from epinephrine in the CTICU is a non-issue. The acidosis is not caused by hypoperfusion, tissue hypoxia, and ischemia,. It's due to increased beta-mediated lipolysis, glycogenolysis, and glycolysis causing so much pyruvate to be made that the TCA cycle is overwhelmed. But eventually the lactate makes it through the Cori cycle at some point assuming a normally functioning liver and all is well. Ultimately, it's a surplus of fuel. Don't treat the number, treat the patient...

View attachment 342898

All very true… But good luck with explaining that to a surgeon lol

 

[icuanesthesiology]

Type B lactic acidosis from epinephrine in the CTICU is a non-issue. The acidosis is not caused by hypoperfusion, tissue hypoxia, and ischemia,. It's due to increased beta-mediated glycolysis causing so much pyruvate to be made that the TCA cycle is overwhelmed. But eventually the lactate makes it through the Cori cycle at some point assuming a normally functioning liver and all is well. Ultimately, it's a surplus of fuel. Don't treat the number, treat the patient...

View attachment 342898

Have you ever met a CT surgeon who doesn't give an amp of bicarb for a base deficit (their favorite measurement of acid base status) of negative 2?!?...got to "treat" the surgeon as well. And I'm not sure that I completely agree with your assessment that the metabolic acidosis caused by epi is a is a non issue. Can you really say with a 100% degree of certainty that a metabolic acidosis which causes a decreased pH has absolutely no side effects? What if you have a COPD'er, for example, with an FEV1 of 40% of predicted, they are on epi, they have a metabolic acidosis, and now they now have to increase the RR in their weak and edematous lungs as compensation. How long is that going to last? Will that increase time to extubation? Throw in some poorly controlled sternotomy pain after extubation...Does that increased RR increase risk for reintubation? I'm not sure that I know the answer, but I do know that a metabolic acidosis will increase RR, so I ask again, why utilize an agent which causes a metabolic acidosis when you can use dopamine, an agent that doesn't cause a metabolic acidosis?
It seems rather confident and all knowing to state with a 100% degree of certainty that a metabolic acidosis caused by epi is 100% benign. In general, I never make such blanket, confident statements in medicine. The body is far too complex for that kind of confidence. My goal in medicine is to do as little as possible so that the body can do the bulk of the work. the body usually outsmarts me. If the body likes a normal pH, I want to avoid giving something that will take that pH off its norm...seems common sense to me.

Anyways, there is no the prospective randomized trial that looks at low to moderate dose dopamine compared to low to moderate dose epi in post-operative CABGs and valves and the effects on mortality, length of stay, afb, renal function, etc? It doesn't exist. Therefore, there is no gold standard "proof" that dopamine is really bad in the cardiac surgical ICU.

 

[vector2]

Have you ever met a CT surgeon who doesn't give an amp of bicarb for a base deficit (their favorite measurement of acid base status) of negative 2?!?...got to "treat" the surgeon as well.

I think we both agree that placating CT surgeons has very little to do with the evidence of benefit or harm for an intervention.

And I'm not sure that I completely agree with your assessment that the metabolic acidosis caused by epi is a is a non issue. Can you really say with a 100% degree of certainty that a metabolic acidosis which causes a decreased pH has absolutely no side effects?

It seems rather confident and all knowing to state with a 100% degree of certainty that a metabolic acidosis caused by epi is 100% benign. In general, I never make such blanket, confident statements in medicine. The body is far too complex for that kind of confidence. My goal in medicine is to do as little as possible so that the body can do the bulk of the work. the body usually outsmarts me. If the body likes a normal pH, I want to avoid giving something that will take that pH off its norm...seems common sense to me.

Can we really make any claims in medicine that have a 100% degree of certainty? Of course not. Even with a multi-center, randomized, controlled, double-blinded trial there is no 100% in medicine. I never used the words "100%" - you just assumed I did. I simply said it was a non-issue. And I'm not saying epi and acidosis is a non-issue because it's written in scripture or on a stone tablet. I thought it was relatively obvious to most here that when we give our opinion or our clinical recommendation about something, that recommendation is based upon our experience and our best understanding of the literature and evidence. Moreover, the buyer should beware.

What if you have a COPD'er, for example, with an FEV1 of 40% of predicted, they are on epi, they have a metabolic acidosis, and now they now have to increase the RR in their weak and edematous lungs as compensation. How long is that going to last? Will that increase time to extubation? Throw in some poorly controlled sternotomy pain after extubation...Does that increased RR increase risk for reintubation? I'm not sure that I know the answer, but I do know that a metabolic acidosis will increase RR, so I ask again, why utilize an agent which causes a metabolic acidosis when you can use dopamine, an agent that doesn't cause a metabolic acidosis?

Anyways, there is no the prospective randomized trial that looks at low to moderate dose dopamine compared to low to moderate dose epi in post-operative CABGs and valves and the effects on mortality, length of stay, afb, renal function, etc? It doesn't exist. Therefore, there is no gold standard "proof" that dopamine is really bad in the cardiac surgical ICU.

As you point out, when looking at meta-analyses it really doesn't appear that there are good outcome data one way or another when it comes to selection of inotropes post-CPB.. And specifically, in that meta-analysis they state "No studies were found regarding the effect of epinephrine on major clinical outcomes or survival."

And if take a moment and broaden out the pt population to those with septic shock and look at a comparison of epinephrine vs. dobutamine/norepinephrine, we'll see that not only was there no difference in mortality, but there was
"no evidence for a difference between the two therapeutic options in terms of delay in haemodynamic stabilisation, resolution of organ dysfunction, or adverse events." Now think about that for a second.....we are talking about a cohort of patients who are already acidotic, who already have hyperlactatemia, who already have capillary leak, and who are already in full-blown respiratory failure (95% vented in each cohort at randomization), and yet there was no difference when using epi- a catechol that has beta2 activity orders of magnitude higher than dobutamine. Even the authors were surprised at the lack of difference: "We expected a 20% absolute reduction in 28-day mortality with norepinephrine combined with dobutamine. Indeed, we thought that potentially deleterious regional haemodynamic and metabolic effects of epinephrine could have been associated with a substantial increase in mortality."

I also find using a COPD'er FEV 40% of predicted to be an odd choice for the hypothetical patient who epi would make fail at weaning from mechanical ventilation. Sure, there might be a mild reduction in the pH and an increased respiratory drive, but we're also talking about giving a beta2 agonist to a guy with obstructive lung disease. When we have a COPD'er or asthma patient who's crumping, what do we give them? High dose beta2 agonists, with nary a thought about the lactic acidosis. That's not to say that you still couldn't be right. If you cherry pick the exact patient who's on the knife's edge of vent weaning and then push their RR up just a bit, I suppose that could cause them to fail, but I think that sort of patient is exceedingly rare based both on my experience and some of the literature comparing inotropes/pressors vis a vis outcomes.

 

[DirtDocMD]

Dopamine-All the tachycardia of epi, with none of the BP support (Yeah, it’s SUPPOSED to go up, but it never seems to happen. It’s the closest thing to “wheel spinning” as you’ll see. The “rpm’s” go up, but the pressure goes nowhere.)

Hate using the stuff....

 

[Beeftenderloin]

Dopamine-All the tachycardia of epi, with none of the BP support

To this point, it’s an okay drug for chemical pacing while your waiting for the SA node to wake up post pump. That’s about it though.

 

[drmwvr]

Dopamine-All the tachycardia of epi, with none of the BP support (Yeah, it’s SUPPOSED to go up, but it never seems to happen. It’s the closest thing to “wheel spinning” as you’ll see. The “rpm’s” go up, but the pressure goes nowhere.)

Hate using the stuff....

you need more fluid😊

 

[icuanesthesiology]

I think we both agree that placating CT surgeons has very little to do with the evidence of benefit or harm for an intervention.



Can we really make any claims in medicine that have a 100% degree of certainty? Of course not. Even with a multi-center, randomized, controlled, double-blinded trial there is no 100% in medicine. I never used the words "100%" - you just assumed I did. I simply said it was a non-issue. And I'm not saying epi and acidosis is a non-issue because it's written in scripture or on a stone tablet. I thought it was relatively obvious to most here that when we give our opinion or our clinical recommendation about something, that recommendation is based upon our experience and our best understanding of the literature and evidence. Moreover, the buyer should beware.


As you point out, when looking at meta-analyses it really doesn't appear that there are good outcome data one way or another when it comes to selection of inotropes post-CPB.. And specifically, in that meta-analysis they state "No studies were found regarding the effect of epinephrine on major clinical outcomes or survival."

And if take a moment and broaden out the pt population to those with septic shock and look at a comparison of epinephrine vs. dobutamine/norepinephrine, we'll see that not only was there no difference in mortality, but there was
"no evidence for a difference between the two therapeutic options in terms of delay in haemodynamic stabilisation, resolution of organ dysfunction, or adverse events." Now think about that for a second.....we are talking about a cohort of patients who are already acidotic, who already have hyperlactatemia, who already have capillary leak, and who are already in full-blown respiratory failure (95% vented in each cohort at randomization), and yet there was no difference when using epi- a catechol that has beta2 activity orders of magnitude higher than dobutamine. Even the authors were surprised at the lack of difference: "We expected a 20% absolute reduction in 28-day mortality with norepinephrine combined with dobutamine. Indeed, we thought that potentially deleterious regional haemodynamic and metabolic effects of epinephrine could have been associated with a substantial increase in mortality."

I also find using a COPD'er FEV 40% of predicted to be an odd choice for the hypothetical patient who epi would make fail at weaning from mechanical ventilation. Sure, there might be a mild reduction in the pH and an increased respiratory drive, but we're also talking about giving a beta2 agonist to a guy with obstructive lung disease. When we have a COPD'er or asthma patient who's crumping, what do we give them? High dose beta2 agonists, with nary a thought about the lactic acidosis. That's not to say that you still couldn't be right. If you cherry pick the exact patient who's on the knife's edge of vent weaning and then push their RR up just a bit, I suppose that could cause them to fail, but I think that sort of patient is exceedingly rare based both on my experience and some of the literature comparing inotropes/pressors vis a vis outcomes.

All great points! I actually agree with all except the surgeon comment...prevention of harm by placating surgeons is actually my most important job! I say that only semi-sarcastically...

I actually work in solo private practice and somewhat miss these great debates on physiology, inotropic support, etc.
For full disclosure, I actually stopped using dopamine about 5 years ago. I got tired of all the weird looks, its just easier to utilize other agents. As for the debate about dopamine...just playing devils advocate.

My main point is the following: We put too much stock in EBM. This is not just about dopamine. It is an attitude about the practice of medicine. Most published studies are in perfectly selected patients who do not actually represent the daily grind of patients. Furthermore, the results are all just probabilities and p values. EBM certainly influences my practice, and I read religiously, but everyday, I am presented with a new problem to solve which has never been truly studied. Every patient is completely different from the next. While it is obvious from your posts you do not practice cookbook medicine, there are many who do. I worry it is the standard way we are training doctors nowadays. Guidelines and studies have now become autochecked order sets which a monkey can put in. Lactate elevation = always sepsis = always 30cc/kg of volume. Dopamine causes tachycardia = always and never ever ever ever use, never.

In my mind, the dislike of dopamine is emblematic of this dogmatic way of practicing medicine. I was "forced" to use it by an old school cardiac surgeon in my first job. It was a strikingly similar situation to the OP (may be the same place for all I know). When I finally opened my mind to dopamine (and a host of other things this guy taught), I began to realize that this old school cardiac surgeon was one of the best docs I have ever worked with. There may have been some hot **** Harvard academics somewhere who had "proved" the evils of dopamine, but this old school bad ass had lived in the trenches for 40 years. He had a lot of non EBM teachings which have overall made me a better doc. In other words, I learned to not be an arrogant just out of fellowship prick who knew everything. He taught me to look beyond the studies and guidelines and focus on what is always most important...the patient.

Anyways, I'll get off my soapbox. I enjoyed your well thought our post.

 

[Twiggidy]

If it’s not going to hurt the patient (HCOM, SAM) I just humor our “old school surgeon” and just turn it on. I start the good stuff if needed and just inform him.