# CHF/COPD Exacerbation



## SugarSweetMedic (Nov 5, 2016)

New medic and just curious if anyone has an tips/tricks/advice for patients with CHF and COPD exacerbation. These types of patients are common in my response area and usually have prolonged transport times so just looking for outsider advice on management of these conditions.


----------



## TomB (Nov 5, 2016)

Differential diagnosis of shortness of breath is difficult, even for emergency physicians, and anyone who says otherwise is ignorant about the topic. Although it's true that these conditions can overlap, the mistake I see paramedics making most often is failure to recognize and treat acute decompensated heart failure, even when the patient has a cardiac history, presents with difficulty breathing, hypertension, low SpO2, and adventitious breath sounds. Don't become one of those paramedics who treats everything with nebulized albuterol, or says that breath sounds were clear when in fact they were absent due to low tidal volume and a poor quality stethoscope. These are some of the most difficult calls to manage in all of EMS. Call for help early, especially if you have to navigate stairs.



SugarSweetMedic said:


> New medic and just curious if anyone has an tips/tricks/advice for patients with CHF and COPD exacerbation. These types of patients are common in my response area and usually have prolonged transport times so just looking for outsider advice on management of these conditions.


----------



## Carlos Danger (Nov 5, 2016)

Like Tom said, these can be tricky. They say 90% of diagnosis is based on history, and (esp without imaging or labs), that's probably no truer anywhere than when it comes to breathers. 

Bipap is always your friend.


----------



## mttbdtd (Nov 5, 2016)

I am also a fairly new medic and I agree it is difficult to determine sometimes. I used to work in a system like you described. Aging population, lots of CHF/COPD patients, and long transports. One of the things that is a big caution is the quick application of Albuterol. As an EMT I've seen medics give it just routinely to the detriment of the patient. I have also arrived on scene to to first responders having given Albuterol and/or Duonebs to patients with a lot of CHF symptoms. The most recent being a patient that when I arrived was on a Duoneb but had productive cough with pink frothy sputum, dependent edema, diagnosed with CHF 2 weeks before, blah blah. Pretty much textbook picture of CHF. He had been placed on a Duoneb simply because he had wheezes. This did nothing but fill him up with fluid and worsen his symptoms. Removal of the neb and he tightened back up and his symptoms improved.


----------



## TXmed (Nov 5, 2016)

For CHFers, dont be afraid to use CPAP early. For COPDers CPAP is still useful but i will hit them with epi if theyre bad.


----------



## VFlutter (Nov 5, 2016)

Be familiar with the nuisances of CPAP vs BiPAP


----------



## VentMonkey (Nov 5, 2016)

SugarSweetMedic said:


> New medic and just curious if anyone has an tips/tricks/advice for patients with CHF and COPD exacerbation. These types of patients are common in my response area and usually have prolonged transport times so just looking for outsider advice on management of these conditions.


Like others have stated be familiar with both CPAP, and/ or BiPap. These devices are truly life-saving. If your service has RSI in their protocol/ formulary know the ins and outs, and risks vs. benefits to this procedure as well.

You stated you have prolonged transport times, which leads me to believe you have, or work in a rural setting. If your service provides ventilators on all of your ambulances _know and understand _it's capabilities to the best of your ability. Obviously, a good thorough assessment goes without saying. The adage I would use with interns was "the chicken or the egg" with these patients, meaning if said patient had a history of both, which one came on first, or which one seems to be presenting at the time of the call.

When you arrive are their breath sounds diminished because their so full or fluid? Are they dependently edematous? Are they audible wheezing (note there is such thing as "cardiac wheezes")? Again, it's looking at the overall clinical picture of the patient's presentation at the time of call, if that makes any sense. Are they so tachycardic, and or/ have an extensive cardiac/ age related history that a brochodilator such as Albuterol (ahem, Levalbuterol anyone??), and/ or Epi may be harmful? Sometimes all those patients would get from me is CPAP, and a lock.

If you have side streamed ETCO2, use it via the N/C while providing them PPV via CPAP/ BiPap. For a COPD, and/ or CHF patient who has clearly moved beyond CPAP, and is that air-hungry/ hypoxic, I would move on to aggressive airway management. Meaning again, if I had RSI capabilities available for me that day, they're being sedated and paralyzed. Once they're successfully intubated, they're getting another hit of a long-acting paralytic. My reasoning is because these patient's are often so fatigued that their respiratory muscles need the rest. 

Another interesting thing I would like to point out, and this pertains more so to the asthmatic/ COPD population, is the importance of a fluid bolus. Oftentimes I feel it's importance is overlooked, when in fact given that, again, they're so dehydrated from their increased WOB, it is of much benefit to them (think how much they can sweat from the WOB).

If said patient is an asthmatic/ COPD patient, you have an extended ETA to the ED, and it is also in your formulary, Magnesium Sulfate may also be worth a try. I have had some intermittent success in this patient category. Just know that hypermagnesemia can occur, however, you should have the antidote/ reversal to this as well (hint: it's in most paramedics medication scope).

If the patient appears more along the lines of a CHF exacerbation, hopefully you have SL NTG spray, but the pills, or even paste will do. Other than that, again, CPAP works wonders for the flash PE patient. A saline lock, and some fentanyl, and/ or versed may help with their anxiety, and/ or pain as well.

In the COPD/ asthma patient oftentimes it is better to start on the low end of the PEEP scale via CPAP/ BiPap, however, for the CHF exacerbation, you may require higher PEEP levels depending on the severity of their exacerbation at that given time (look up "alveolar recruitment"). There are often two simple groups for lung protective ventilator management: injury (ALI/ ARDS) approach, and obstructive approach (COPD/ asthma); here's one of many links on it as well...

http://lifeinthefastlane.com/ccc/protective-lung-ventilation/li

Also, something to keep in mind is that "the apple doesn't fall far from the tree". A lot of these patient's may have started off as a simple exacerbation of either/ or, but by the time they call 911 and you arrive, they've become severely septic, and/ or developed ARDS secondary to pneumonia brought about by anyone of their ailments (or both); this is just some food for thought.

As always, a solid clinician will be prepared way ahead of time, so perhaps try brushing up on these diseases and their pathologies if you haven't already. Airway management is the one of the things taught in paramedic school I think *all* paramedics should have a strong understanding of, and respect for, but cardiology is kind of important too I suppose...


----------



## NomadicMedic (Nov 5, 2016)

Please tell me that you're using end tidal capnography to at least _lean_ you in one direction or the other. Obstructive waveform morphology is a great indicator for the need of beta agonists.

A CHFer without an obstructive component will not present with an obstructive waveform, even if they have what you perceive as wheezes.

Add capnography to your tool box and use it to help guide you down the obstructive/non obstructive pathway.


----------



## VentMonkey (Nov 5, 2016)

DEmedic said:


> Please tell me that you're using and title capnography to at least lean you in one direction or the other. Obstructive waveform morphology is a great indicator for the need of beta agonists.
> 
> A CHFer without an obstructive component will not present with an obstructive waveform, even if they have what you perceive as wheezes.
> 
> Add capnography to your tool box and use it to help guide you down the obstructive/non obstructive pathway.


ETCO2 to me is another tool to guide someone in the direction of a rough estimate of the patients _exhaled ETCO2_, and is by no means something that would dictate my treatment modalities. Aside from the obvious extrinsic signs, and symptoms of impending respiratory failure, only a full ABG can diagnosis the patient as having respiratory failure, which obviously we cannot do in the field.

My reference to "cardiac wheezes" was meant to get the op to think on a broader scale so as _not_ to fall into the "they're wheezing so it must be solely pulmonary in nature" thought process. It was also in hopes that he would look up its pathology. 

I am glad you pointed this out for clarification though, so as uzzzh, thanks @DEmedic.


----------



## NomadicMedic (Nov 5, 2016)

Oksay, but wait... let me ask this; if you put nasal capnography on a breathing patient, do you agree that you can distinguish between  constructive and nonconstructive waveform morphology? The presence of bronchoconstriction in the waveform is not something that will show up with a straight CHFer. 

I certainly don't make treatment decisions based on ETCO2 alone, but I believe it's far more valuable than just a rough estimate the exhaled co2. 

I also believe having a member of our staff who was a senior trainer for Oridian got us far more tuned up on ETCO2 than the regular medic who used it for tube confirmation and to count a respiratory rate.


----------



## VentMonkey (Nov 5, 2016)

DEmedic said:


> if you put nasal capnography on a breathing patient, do you agree that you can distinguish between  constructive and nonconstructive waveform morphology?


Absolutely. And to further elaborate, I use it very frequently in our intubated patients to detect when they may be over-breathing the ventilator as well. 

If said patient is taking shorter, sharper breaths, chances are they are waking up, uncomfortable, or a combination of the two. It definitely has its place, and by no means is it just another gimmick, but to understand different waveforms, parameters for ETCO2 (e.g., permissive hyper, or hypocapnia) is something that the op (or any paramedic really) needs to A) take seriously, and B) take the time and initiative to learn about on their own.

ETCO2 really has many applications in the prehospital setting, and I agree, it's far beyond just being utilized for tube confirmation or to count a patient's respiratory rate (this is almost laughable, and kind of sad, IMO). I have even used it on peri-arrest patients that went from an ETCO2 of almost nil to 60 or more in a matter of seconds, as it can also be a strong clinical indicator of ROSC.

As a side note: a personal pet peeve of mine is when any paramedic, new or old, doesn't even take the time to adjust the monitor to obtain a _good reliable _SPO2 waveform pleth when assuming that the SPO2 of ~80% in screaming hypoxia. A classic "shark-fin" pattern alone in the presence of absent (silent chest) breath sounds with an asthmatic, and/ or COPD-er is for my feelers to go way up on index of suspicion for impending respiratory failure; a silent chest is bad! I realize most modern monitors default to a waveform pleth with SPO2, but if for whatever reason your (generalizing) service does not carry side streamed ETCO2, I strongly urge you (generalizing) to get into the habit of studying their waveform SPO2, and seeing the different types that there are, and moreover, the changes in the patterns with therapies provided, it's quite remarkable.

The point I think we're both trying to make is learn _how, why, and when_ to use these diagnostic tools, that is their purpose, and any paramedic worth their weight knows what it is each diagnostic tool offers, and how to use them (or not) their maximum capacities.


----------



## RRTMedic (Nov 6, 2016)

SugarSweetMedic said:


> New medic and just curious if anyone has an tips/tricks/advice for patients with CHF and COPD exacerbation. These types of patients are common in my response area and usually have prolonged transport times so just looking for outsider advice on management of these conditions.



*It's awesome that you care about your patient care enough to seek advice about this! Of course, it can be hard to differentiate between COPD/CHF exacerbation, especially if there is a documented history of both co-morbidities in the patient. 

First off, clinical presentation goes a long way. Look at your patient and get your general impression. 
What do you think when you see a...

COPD PATIENT: Pink Puffer? Blue Bloater? Wheezing? Emaciated due to the lack of proper nutrition? Diminished breath sounds? Wheezing? 

CHF PATIENT: Peripheral edema? Wheezing/Crackles? Hepatomegaly? Distended abdomen? Pitting edema? JVD? Hyper-/Hypotension? 

Don't forget, many later stage COPD patients have developed right sided heart failure due to the chronic respiratory condition resulting in pulmonary hypertension, leading to cor pulmonale... etc etc

THE BEST TOOL (in my opinion) for DIFFERENTIATING either condition/exacerbation is too observe waveform capnography. The "sharkfin" waveform is indicative of lower airway obstruction, leading one to consider emphysema/asthma as the culprit. This is the very nature of obstructive diseases--severe airway resistance resulting in prolonged expiratory times. If you patient is wheezy and shows evidence of CHF/RSHF, is the waveform square in nature? If so, bronchospasm is likely not to be causing the symptoms. 

As far as treatment goes---granted this is a severe exacerbation-- the same rules apply when it comes to airway management and ventilatory support. Non-invasive applied EARLY decreases hospital length of stay. My best advise would be to CPAP when in doubt. That is your first treatment (okay okay oxygen, duh). 

Next moving along to medications... this is where differentiating between the two helps out. 

COPD patients will benefit from bronchodilators (albuterol), antiinflammatory (solumedrol), smooth muscle relaxation (magnesium), and perhaps a fluid bolus for retained secretions and likely dehydration. I recommend hitting them HARD with the albuterol... as much as 10 mg albuterol in a single nebulizer. I have done it several times and rarely (per MD orders) are there side effects. Of course, stay in your local protocol, but I always give the max dose of albuterol I'm allowed. AND, I would say don't waste your time with Atrovent. There are plenty of studies that demonstrate albuterol to be just as effective and no changes in patient outcomes when compared to albuterol only verses Duonebs. 

On that note, I know I have heard many folks say that albuterol is contraindicated in CHF patients. Not so true, especially if the exacerbation is obstructive (COPD) in nature. Albuterol is generally INEFFECTIVE in CHF, but a short term treatment of albuterol is unlikely to "flood" a CHFer. If your CHF patient is dying because of the albuterol you gave, you probably didn't treat the actual problem (pulmonary edema).

CHF, or rather pulmonary edema, patients are a bit trickier to treat because they come in different shapes and sizes. Do they have right sided HF, left sided HF, kidney failure, fluid overload, diabetes, etc. AGAIN, early CPAP (or BiPAP) is essential to good outcomes. 

HYPERTENSIVE + Kidney Failure + Heart Failure = CPAP, Nitrates, Diuretics, Narcotics
HYPOTENSIVE + Cardiomyopathy (with pulm edema) = Dopamine, CPAP

If you take anything away from this.... DON'T BE AFRAID TO CPAP/BiPAP. These patients benefit GREATLY FROM NON INVASIVE. Can't tolerate it? Ketamine works great because it doesn't knock out the respiratory drive like verse, ativan, valium, narcotics, etc. I would just be cautious with ketamine because ketamine does increase blood pressure and heart rate (which can be beneficial in some situations).*


----------



## VentMonkey (Nov 6, 2016)

RRTMedic said:


> *It's awesome that you care about your patient care enough to seek advice about this! Of course, it can be hard to differentiate between COPD/CHF exacerbation, especially if there is a documented history of both co-morbidities in the patient.
> 
> First off, clinical presentation goes a long way. Look at your patient and get your general impression.
> What do you think when you see a...
> ...


*Very cool! Thanks for your input!!!.*


----------



## Tigger (Nov 6, 2016)

RRTMedic said:


> *On that note, I know I have heard many folks say that albuterol is contraindicated in CHF patients. Not so true, especially if the exacerbation is obstructive (COPD) in nature. Albuterol is generally INEFFECTIVE in CHF, but a short term treatment of albuterol is unlikely to "flood" a CHFer. If your CHF patient is dying because of the albuterol you gave, you probably didn't treat the actual problem (pulmonary edema).*


I am happy to see this. So many times I heard "don't give albuterol to CHF, you'll flash em!" During school I never really found evidence to support that but kept hearing it. Obviously we need to be treating the underlying problem, and if you keep giving nebs to a sick CHF patient they will probably deteriorate....because you're not doing anything to fix them.
*



			If you take anything away from this.... DON'T BE AFRAID TO CPAP/BiPAP. These patients benefit GREATLY FROM NON INVASIVE. Can't tolerate it? Ketamine works great because it doesn't knock out the respiratory drive like verse, ativan, valium, narcotics, etc. I would just be cautious with ketamine because ketamine does increase blood pressure and heart rate (which can be beneficial in some situations).
		
Click to expand...

*I wish we could use Ketamine for this instead of Versed, too bad the state would be rather angry. Apparently that is considered procedural sedation, not sure how using Versed makes it any better.


----------



## RRTMedic (Nov 6, 2016)

Tigger said:


> I am happy to see this. So many times I heard "don't give albuterol to CHF, you'll flash em!" During school I never really found evidence to support that but kept hearing it. Obviously we need to be treating the underlying problem, and if you keep giving nebs to a sick CHF patient they will probably deteriorate....because you're not doing anything to fix them.



Yeah I can't tell you how many times I've started continuous nebs to CHF patient's under a physician's order. It's not necessarily the worst thing to do, but most certainly not the most helpful. Some patients with CHF who take albuterol psychologically do better after a treatment, or at least state they feel like it's helping (whatever).



Tigger said:


> I wish we could use Ketamine for this instead of Versed, too bad the state would be rather angry. Apparently that is considered procedural sedation, not sure how using Versed makes it any better.



Yeah that's a fight we are having over in NC. Currently, our state office allows agencies to use ketamine only in conjunction with airway management. Seems really silly to me, esp since the standard of care for noninvasive sedation involves ketamine....even precedex for that matter!


----------



## Carlos Danger (Nov 7, 2016)

I was going to comment on the albuterol in CHF thing earlier, but didn't. Glad someone else brought it up.

As a beta agonist, albuterol can cause problems in folks with sick hearts, which of course CHF'ers have. Any increase in HR will increase myocardial oxygen demand while decreasing supply. Albuterol is also thought to increase PAP and which could theoretically contribute to worsening pulmonary hypertension and in turn, pulmonary edema. 

That said, it is probably a complete myth that albuterol causes "flash" pulmonary edema. It has actually been shown to stimulate clearance of fluid from the alveoli, and is probably safe to give to the patient with undifferentiated dyspnea. 

http://www.medscape.com/viewarticle/738536_3


----------



## SpecialK (Nov 7, 2016)

A sometimes overlooked fact is that you need to call pulmonary oedema from congestive heart failure_ "cardiogenic pulmonary oedema"_; there are other causes for pulmonary oedema, such as neurogenic or negative pressure, and just saying "pulmonary oedema" is a bit like saying the patient has "infection" when infact they have a UTI and you've made a diagnosis as such.

1.  Look for a cause - most commonly this is VT (or another tachydysrhythmia) or an MI
2.  Sit them up leaning forward with their legs lower than their body (for example over the side of a chair, bed or stretcher)
3.  The best treatment is GTN in 0.8 mg sprays (provided their BP is OK and they don't have an inferior STEMI)
4.  If they have STEMI take them directly to a cath lab, or if they'rre crook go to hospital fast.

I cant comment on slipstream ETCO2 or CPAP as I've never used them.

If I go to pop in the night who just slipped down off his 3 pillows and has a few crackles we fix up with GTN and oxygen then he is otherwise fine afterwards I'd lean towards leaving him at home; especicially if he has somebody who is there with him.


----------



## VentMonkey (Nov 7, 2016)

SpecialK said:


> A sometimes overlooked fact is that you need to call pulmonary oedema from congestive heart failure_ "cardiogenic pulmonary oedema"_; there are other causes for pulmonary oedema, such as neurogenic or negative pressure, and just saying "pulmonary oedema" is a bit like saying the patient has "infection" when infact they have a UTI and you've made a diagnosis as such.


This is a very good point.


----------



## Nova1300 (Nov 7, 2016)

Remi said:


> I was going to comment on the albuterol in CHF thing earlier, but didn't. Glad someone else brought it up.
> 
> As a beta agonist, albuterol can cause problems in folks with sick hearts, which of course CHF'ers have. Any increase in HR will increase myocardial oxygen demand while decreasing supply. Albuterol is also thought to increase PAP and which could theoretically contribute to worsening pulmonary hypertension and in turn, pulmonary edema.
> 
> ...




I always have to laugh a little about this albuterol in heart failure thing.   Remi is correct in that causing tachycardia in a patient with active myocardial ischemia is probably a bad idea.  It's also probably a bad idea if the pulmonary edema is due to a tight valvular lesion, like aortic stenosis.  

However, for run of the mill exacerbations of heart failure (e.g. chronic ischemic cardiomyopathy), most patients will be treated with some diuretics, afterload reduction, and inotropes - the vast majority of which are sympathomimetic beta agonists. Just like albuterol.  

My personal belief is that if you have a patient who carries a diagnosis of both chronic heart failure and copd (these frequently co-exist, as we all know) who have complaints of dyspnea, give the albuterol.


----------



## VentMonkey (Nov 7, 2016)

Nova1300 said:


> My personal belief is that if you have a patient who carries a diagnosis of both chronic heart failure and copd (these frequently co-exist, as we all know) who have complaints of dyspnea, give the albuterol.


To what degree would _you _sat?*

*merely curious, not seeking medical advice.


----------



## Nova1300 (Nov 7, 2016)

I think I should clarify a couple things after re-reading my post.  

If you have a patient who does not have a chronic HF diagnosis, and you believe to be in pulmonary edema from myocardial failure due to acute coronary syndrome (e.g. they are having the big one) I would probably avoid the tachycardia of beta agonists until revascularization, be it in the cath lab or the OR.  

Thing is, once those patients are revascularized, if they have knocked out a chunk of their myocardial muscle from infarct, they may very well have intermittent heart failure exacerbations due to sodium or volume overload.  These patients usually carry a heart failure diagnosis and will usually be taking the cocktail of beta blocker, ace-inhibitor, aspirin and statin, and often PRN or scheduled diuretics.  When these folks exacerbate, they don't typically have a new ischemic lesion.  Instead the heart has become volume overloaded or the afterload is too high and the weak heart just can handle the extra stress.  In these patients, I think it's probably very reasonable to use beta agonists because their hospital treatment will usually consists of IV beta agonists, in the form of inotropes, and some diuretics and afterload reduction.  

I think it is extremely reasonable that if a chronic copd patient who also has chronic heart failure has dyspnea, you give them beta agonists.


----------



## Nova1300 (Nov 7, 2016)

I'm not sure I clarified that much.  Does that make any more sense vent?  

Again, this is based solely on my own understanding of the failing circulation and not a bunch of research.


----------



## VentMonkey (Nov 7, 2016)

Nova1300 said:


> I think I should clarify a couple things after re-reading my post.
> 
> If you have a patient who does not have a chronic HF diagnosis, and you believe to be in pulmonary edema from myocardial failure due to acute coronary syndrome (e.g. they are having the big one) I would probably avoid the tachycardia of beta agonists until revascularization, be it in the cath lab or the OR.
> 
> ...


So let me ask this: 

In your experience, what is the likelihood of a beta agonist causing myocardial irritability in this patient population?

Most EM physicians seem somewhat liberal with them; thanks for the reply and clarification, BTW.


----------



## Nova1300 (Nov 7, 2016)

VentMonkey said:


> So let me ask this:
> 
> In your experience, what is the likelihood of a beta agonist causing myocardial irritability in this patient population?
> 
> Most EM physicians seem somewhat liberal with them; thanks for the reply and clarification, BTW.




Absolutely, you risk arrhythmia with any beta agonist, especially if the patient has a history of arrhythmia.  A physician may chose to avoid the pure beta agonists, and elect to use milrinone in these cases as the inotrope of choice.  

However, I'm still not sure that would stop me.  Especially if I was questioning whether I was treating COPD or CHF.  Inhaled albuterol usually doesn't have a tremendous systemic absorption, so I would pull the trigger and give it.  

Even in someone have acute heart failure from ACS where you are questioning CHF vs. COPD,  I think you are better off giving albuterol than blasting them with steroids.  I'm still very much of the belief that steroids in an infarcting heart is a bad, bad thing.


----------



## VentMonkey (Nov 7, 2016)

Nova1300 said:


> A physician may chose to avoid the pure beta agonists, and elect to use milrinone in these cases as the inotrope of choice...I'm still very much of the belief that steroids in an infarcting heart is a bad, bad thing.


Correct me if I am wrong, but the liberal use of steroids seems to be trending downward in the medical community.

As far as the milrinone goes, is there any specific reason you would select this as your inotrope of choice over dobutamine, or are we comparing oranges to oranges here?


----------



## Nova1300 (Nov 7, 2016)

VentMonkey said:


> Correct me if I am wrong, but the liberal use of steroids seems to be trending downward in the medical community.
> 
> As far as the milrinone goes, is there any specific reason you would select this as your inotrope of choice over dobutamine, or are we comparing oranges to oranges here?




I mostly say milrinone because it does not carry quite the risk of dysrhythmia which we see with the beta agonists.  And overall, I find it to be a relatively effective inotrope, though you may have to offset the dilator effects with a constrictor.  


I do still see a lot of steroid usage with COPD exacerbation.  Which is fine, I think steroids have their roll.  But I think if you are debating between heart failure and COPD, I would be more apt to give some albuterol than some solumedrol, especially if I thought the heart failure was due to an acute process like an infarct.


----------



## VentMonkey (Nov 7, 2016)

Nova1300 said:


> I mostly say milrinone because it does not carry quite the risk of dysrhythmia which we see with the beta agonists.  And overall, I find it to be a relatively effective inotrope, though you may have to offset the dilator effects with a constrictor.
> 
> 
> *I do still see a lot of steroid usage with COPD exacerbation*.  Which is fine, I think steroids have their roll.  But I think if you are debating between heart failure and COPD, I would be more apt to give some albuterol than some solumedrol, especially if I thought the heart failure was due to an acute process like an infarct.


Sorry, "I" should have clarified, I was implying it seems in the acute setting aside from say Solumedrol they aren't given quite as much.

I can still remember when Decadron was very much thought to have many advantages in different patient presentations, now not so much; this is more what I was trying to reference. Thanks again, Nova.


----------



## VFlutter (Nov 7, 2016)

VentMonkey said:


> As far as the milrinone goes, is there any specific reason you would select this as your inotrope of choice over dobutamine, or are we comparing oranges to oranges here?



It usually comes down to Physician preference and familiarity, Dobutrex is still the most popular Inotrope. Milirnone used to be used as a home infusion bridge to transplant before VADs become so prevalent. In my experience Mirinone is less arrhythmogenic than Dobutamine. Milirinone tends to have more vasodilatory effects (PD3 Inhibition) and is great with pulmonary HTN but can cause systemic hypotension. It is also sometimes more effective in patients in overt cardiogenic shock whom are already on tons of sympathomimetics when Dobutrex is not sufficient. It's like adding Vasopressin in refractory shock, the alternate mechanism of action sometimes gives better results.


----------



## VentMonkey (Nov 7, 2016)

Side note: sorry op, yet another thread has been hijacked. Though I must say, I am enjoying the direction most of these threads seem to be diverting.


----------

