Propofol: myocardial depressant

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urge

urge

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Yes or no?

60 yo with 15% ef coming for whatever MAC case. What would be your approach? Avoid propofol?
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Perhaps just versed. Propofol does cause some myocardial depression, but I also be cautious about treating a propofol-induced drop in SVR. Too much alpha agonist activity (from say, phenylephrine) is gonna be bad for this heart.
 
It's how you use the drug that matters most.
 
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GasEmDee said:
Perhaps just versed. Propofol does cause some myocardial depression, but I also be cautious about treating a propofol-induced drop in SVR. Too much alpha agonist activity (from say, phenylephrine) is gonna be bad for this heart.
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I was going to ask if midazolam and ketamine would be a useful combo? I've seen ketamine used for procedural sedation some (a lot of docs seem to be (for want of a better word) "afraid" of the psychosis, so I haven't seen it used a lot) but with the benzo on board it should keep them stoned through the psychosis. I just don't know much about procedural sedation, but the ketamine shouldn't have the negative effects on SVR or the myocardium. Now the increase in rate may give pause, but if someone is teetering on the edge that they couldn't handle a little tachycardia, should they be on the table?
 
I def. would not avoid propofol. It is the smoothest induction/Mac drug out there. Great synergism when mixed with other agents.
 
Don't have to avoid propofol…have used it many of times on patients with similar EFs for all types of MAC. Go slower and allow the propofol to work before titrating up quickly. I usually do not use propofol with anything else except local in most situations. Doesn't hurt to have an oh sh** stick of dwindle epi available if you need it. I have used etomidate for cardioversion when the patients arrhythmia is still perfusing and the patient already has an EF of 10% and their blood pressure is 70/40 and it works well but tend to avoid etomidate in most situations bc the unknowns associations with its effects on steroid metabolism and outcomes. Usually can do it safely with propofol.
 
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Yes it may be a myocardial depressant but it's also going to drop your afterload which will decrease the work the heart has to do.
 
A lot of smart answers in this thread. This a typical oral boards question, by the way.
 
Physio Doc 2 Be said:
I was going to ask if midazolam and ketamine would be a useful combo? I've seen ketamine used for procedural sedation some (a lot of docs seem to be (for want of a better word) "afraid" of the psychosis, so I haven't seen it used a lot) but with the benzo on board it should keep them stoned through the psychosis. I just don't know much about procedural sedation, but the ketamine shouldn't have the negative effects on SVR or the myocardium. Now the increase in rate may give pause, but if someone is teetering on the edge that they couldn't handle a little tachycardia, should they be on the table?
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The psychosis is only with large doses of ketamine. In someone like this you would not need to give more than 10-20mg of Special K depending on the length of the case and the amount of discomfort. I personally believe that ketamine is one of the best drugs in our armamentarium. You can do so much with so little. I used it all day today in endo. Healthy folks and sickos. All of them loved it. And the propofol as well.
Propofol is definitely a myocardial depressant but as Sevo stated, it depends how you use it. Obviously, someone with an EF of 15% needs very little. The problem is that most people forget how long it takes for someone with this sort of EF to circulate the drugs and they get impatient. Then they are burned.
 
Let's say the pt is getting hypotensive. How do you treat? Fluid? Phenylephr? Epi? Ephedrine? Vaso?

Anybody considered precedex?
 
urge said:
No tachy. Same as the pt started.
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A gentle bump of fluids and a little bit of phenylephrine while the fluids are running. I am admittedly worried about the negative outcomes for both interventions. Too much fluid and alveoli turn into swimming pools and too much increase in SVR and I drop CO and/or increase myocardial O2 demand on a heart that might not take kindly to as much and already has a supply problem. I picked fluids and neosynephrine because I am anticipating the vasodilator effect of propofol to be the biggest problem.

Edit - I'm assuming this patient got propofol in the development of this hypotension.
 
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Precedex takes time and people respond differently. It also can cause bradycardia. IMO less titratable and more time consuming. I would not use it as a sole anesthetic for EGD/colonoscopy/etc.

+2 on low dose ketamine. Little bit goes a long ways and decreases your prop dosage substantially.
 
Ketamine releases endogenous catecholamines... Good thing when adding a myocardial depressant.
 
urge said:
Let's say the pt is getting hypotensive. How do you treat? Fluid? Phenylephr? Epi? Ephedrine? Vaso?

Anybody considered precedex?
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I'm an epi guy. Small doses. 10mcg at a time. Love that ****.
There is no harm in giving a little epi.

Oh and I never would have considered precedex. Maybe a few years ago but not any longer.
 
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urge said:
Let's say the pt is getting hypotensive. How do you treat? Fluid? Phenylephr? Epi? Ephedrine? Vaso?

Anybody considered precedex?
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A bit of fluid to make up the NPO deficit, and something with beta 1 agonism (not a pure alpha agonist like epi.) While i know SVR is the primary issue, I just don't know how much neo is needed. With an EF of 10-15% its easy to overdo it. Like Noyac, I like small doses of epi in this case. Start with 10mcg bolus and see.
 
Noyac said:
Oh and I never would have considered precedex. Maybe a few years ago but not any longer.
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Why no precedex? Same concerns as Sevo's?

Precedex takes time and people respond differently. It also can cause bradycardia. IMO less titratable and more time consuming.
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urge said:
Why no precedex? Same concerns as Sevo's?
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It just doesn't add anything of value here. Precedex is a good adjunct at times when your looking to get fancy, expensive and to do something different. Otherwise, it's just another expensive drug with more work (having to mix it and wait for it to work) and looking for a good indication. Personally, I have not been that impressed with it. I see people waking kids up,with it, using it for awake FOB, for MAC's, etc. But none of these uses has proven better than our cheaper easier faster drug like propofol, ketamine, versed, etc.

Oh and what Sevo said.
 
GasEmDee said:
A bit of fluid to make up the NPO deficit, and something with beta 1 agonism (not a pure alpha agonist like epi.) While i know SVR is the primary issue, I just don't know how much neo is needed. With an EF of 10-15% its easy to overdo it. Like Noyac, I like small doses of epi in this case. Start with 10mcg bolus and see.
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When did EPI become a "pure alpha agonist"?
 
Noyac said:
It just doesn't add anything of value here. Precedex is a good adjunct at times when your looking to get fancy, expensive and to do something different. Otherwise, it's just another expensive drug with more work (having to mix it and wait for it to work) and looking for a good indication. Personally, I have not been that impressed with it. I see people waking kids up,with it, using it for awake FOB, for MAC's, etc. But none of these uses has proven better than our cheaper easier faster drug like propofol, ketamine, versed, etc.

Oh and what Sevo said.
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I agree with you...
Over the years I have tried hard to find an indication for Precedex where I could justify the extra effort but could not find one.
 
I frequently use epi in low (10 mcg) doses for hypotension in patients with low EF who need that positive inotropic boost. They seem to respond much more predictably than to phenylephrine or ephedrine where i end up requiring escalating doses.

Only thing I use Precedex for is super long angiography on sick vasculopaths by our slow vascular surgeons. They request no pressors, take hours and hours, and since the angio doesn't hurt the Precedex keeps them asleep but not hypotensive.


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Wouldn't beta agonist be detrimental to the patient considering beta blockers are the mainstay of heart protection?
 
No, because we are talking about interventions to restore hemodynamic stability. You do what you have to do.

In this case, the patient might benefit more from a combined beta+alpha agonist than a pure-alpha one - which might depress inotropism even more, and send the heart into a death spiral. Same goes for a pure-beta approach, which could exagerate ischemia.

P.S. That's just my personal logic, and it may be wrong.
 
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I love ketamine, but dont forget ketamine has a dIrect negative inotropic effect on the myocardium....usually, but not always, overshadowed by central sympathetic stimulation (which may be blunted in say a critically Ill patient)

http://www.ncbi.nlm.nih.gov/pubmed/9209606
 
I see a few people saying they use EPI 10mcg for boluses. which is fine , but you can get a very good response with just 1.6mcg. 10 can be a bit much in the wrong patient, so trainees should go slow and titrate in the smaller doses just until you get the experience needed to know when to go a little bigger.
 
To the original question, the slight, reasonably predictable myocardial depression that will result from the small bit of propofol it will take for this patient is far superior to the large, unpredictable swings in sympathetic outflow that you are likely to get with other agents. I'll take propofol for $200.

Agree with ketamine as a useful adjunct.

Has anyone noticed recent variability with Epi potency? In my experience, 10mcg of Epi gives a very predictable result. Recently the required doses have been all over the place from 5-40mcg or so. I'm thinking it may be a storage issue, but perhaps someone else has noticed this. (And yes I checked the expiration dates)

-pod
 
urge said:
Wouldn't beta agonist be detrimental to the patient considering beta blockers are the mainstay of heart protection?
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Don't forget the often overlooked lusitropic effect of epi. It's great in the exact scenario you are talking about. In fact when I was in training there was a cardiologist who used to run simultaneously esmolol infusion and low-dose isoproteronol in patients who came in in fulminant CHF when I was on my ICU rotation. People thought he was crazy. He couldn't support it with the literature in that combination. But I'll be damned if it didn't seem to work. And work well.
 
BuzzPhreed said:
Don't forget the often overlooked lusitropic effect of epi. It's great in the exact scenario you are talking about. In fact when I was in training there was a cardiologist who used to run simultaneously esmolol infusion and low-dose isoproteronol in patients who came in in fulminant CHF when I was on my ICU rotation. People thought he was crazy. He couldn't support it with the literature in that combination. But I'll be damned if it didn't seem to work. And work well.
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Wonder why he didn't have any data? Maybe because it is crazy? Guess he was looking for beta 2 agonism. Might as well just give them a few puffs of Xopenex.
 
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urge said:
Wonder why he didn't have any data? Maybe because it is crazy? Guess he was looking for beta 2 agonism. Might as well just give them a few puffs of Xopenex.
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In the cases where they had a Swan in their numbers got better. Just saying.
 
urge said:
Wouldn't beta agonist be detrimental to the patient considering beta blockers are the mainstay of heart protection?
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what is it exactly that you are concerned about?
Is it the up regulation of the beta receptors or the blockage that you are eluding to? What if they skipped their morning beta blocker dose?
Because like you, I can see a few issues that could be trouble.
 
Noyac said:
what is it exactly that you are concerned about?
Is it the up regulation of the beta receptors or the blockage that you are eluding to? What if they skipped their morning beta blocker dose?
Because like you, I can see a few issues that could be trouble.
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Both. Mostly, increasing demand on a sick heart.
 
L-U-S-I-T-R-O-P-Y.

Especially important when there is underlying and severe diastolic dysfunction.
 
BuzzPhreed said:
L-U-S-I-T-R-O-P-Y.

Especially important when there is underlying and severe diastolic dysfunction.
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Wouldn't you want more lusitropy all the time? If it is that important, why are beta blockers beneficial on heart failure?
 
Ketafol (ketamine 2mg/mL propofol)
 
I think some people are a little confused on the benefit of small dose beta blockers in the chronic treatment of heart failure where beta blockers have shown decreased mortality (probably because of decreased fatal arrhythmias) and the completely different issue of acutely induced or exacerbated heart failure caused by a myocardial depressant.
In the second scenario where the acute exacerbation of heart failure is caused by a medication, it is absolutely acceptable to give a positive inotrop, and these patients are rarely fully beta blocked because they never really tolerate a full dose of beta blockers, so the risk of unopposed alpha effect is not that significant.
 
periopdoc said:
To the original question, the slight, reasonably predictable myocardial depression that will result from the small bit of propofol it will take for this patient is far superior to the large, unpredictable swings in sympathetic outflow that you are likely to get with other agents. I'll take propofol for $200.

Agree with ketamine as a useful adjunct.

Has anyone noticed recent variability with Epi potency? In my experience, 10mcg of Epi gives a very predictable result. Recently the required doses have been all over the place from 5-40mcg or so. I'm thinking it may be a storage issue, but perhaps someone else has noticed this. (And yes I checked the expiration dates)

-pod
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POD,

Throughout my years I have also found Vasopressin (low dose) to be an excellent choice in this situation if low dose Epi (5-10 ug) doesn't give you the desired results. Vasopressin (1-2 units) is a great way to treat hypotension in this subgroup of patients as well.
 
periopdoc said:
To the original question, the slight, reasonably predictable myocardial depression that will result from the small bit of propofol it will take for this patient is far superior to the large, unpredictable swings in sympathetic outflow that you are likely to get with other agents. I'll take propofol for $200.

Agree with ketamine as a useful adjunct.

Has anyone noticed recent variability with Epi potency? In my experience, 10mcg of Epi gives a very predictable result. Recently the required doses have been all over the place from 5-40mcg or so. I'm thinking it may be a storage issue, but perhaps someone else has noticed this. (And yes I checked the expiration dates)

-pod
Click to expand...
I have recently noticed variability in the potency of every medication we use... especially muscle relaxants and local anesthetics... it is related to the frequent shortages and the continuous change of manufacturers.
 
urge said:
Wouldn't you want more lusitropy all the time? If it is that important, why are beta blockers beneficial on heart failure?
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Because the long-term increase of circulating catecholamine levels, in chronic CHF, is toxic on the myocardial cells.
 
Acute CHF benefits from increased contractility and relaxation. It's no secret that dobutamine is the mainstay even in very low cardiac output states for this very reason.

Carvedilol is an interesting drug that basically pushed the AHA into using beta blockers in heart failure which was very controversial at the time and maybe still is. Again the key is diastolic dysfunction and the premise was not only long term myocardial remodeling but also slowing the heart down to allow for greater filling.

The incorrect and indiscriminate use of beta blockers at least in my humble opinion, especially in a patient who is having acute low output MI, is a good way to put someone in a pine box. I'm sure most of us who've been doing this more than a few years have seen that scenario at least once.
 
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