Pulmonary HTN and dobutamine drip?

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sevoflurane

sevoflurane

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How safe is it to be on a drip of dobutamine 4 mcg/kg,/min, 5 Mg. IV X 2 followed by 25 mg po of metoprolol followed by 100 mg of lasix po, in a patient with extensive scleroderma causing pulmonary fibrosis and SEVERE pulmonary htn, who presented 1 day ago with RHF (probably acute cor pulmonale) and ARF (cr. 3.6). This patient was sat. in the high 80's low 90's on 10L , was consistently running tachy around 100 bpm and pressures were around 80/50?

It seemes to me that fluid loading rather than unloading and a vasoconstrictor is a better method of the treatment in this scenerio of RHF (optimize frank-starling). What physiological reason would push you to choose dobutamine (beta -2/vasodialator) rather than another inotrope w/o vasodilatory properties, something like dopamine? Her lungs were completely clear. Maybe I'm missing something here. Is it to reduce pulmonary pressures at the expense of ventricular filling?

Also, how safe is Dobutamine in ARF. Do you have to adjust the dose? I presume it causes N/V like Digoxin does.

Patient felt out of breath, then N/V possibly even aspirated, 15 min. of ACLS for “asystole”. Anybody have any experience with this situation?
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Right heart failure secondary to the pulmonary sequelae you describe is a death sentence, where lung transplant is really the only long term option.

Perfusion in this patient's body is obviously low. It'd be interesting to see the patient's SVI (Military's favorite SWAN number). The goal is to improve overall perfusion, so maybe the attending wanted to use an inotrope without vasoconstrictive properties.

The problem with fluids in a patient like this is that because of the very low compliance in the ischemic myocardium, any volume increase can exacerbate ventricular failure.
An inotrope with vasoconstrictive properties can worsen already-compromised perfusion issues- sounds like renal perfusion is already compromised as reflected by the increased creatinine.
SO, when choosing an inotrope, you have to look at the whole picture..this isnt to say you can't use say epi in a poor-perfusion state...sometimes you need a big gun and are forced to use it, at least for a while.
Dobutamine is a great drug. The only problem is the tachycardia, as you know, which is a primary determinant of myocardial oxygen consumption.
Milrinone, a phosphodiesterase inhibitor, may be a better choice...the only problem is the patient's hypotension, which may be worsened by milrinone.
If the patient is intubated, pulmonary-delivered nitric oxide may help, but is a big deal to set up, is very expensive, and is not available everywhere.
 
"Heart failure" is a term that we, anesthesiologists, throw around very loosely, and most of the time we are using the term incorrectly. We tend to equate CHF with myocardial failure with inadequate O2 delivery....as is the case when separating from CPB.

However, the vast majority of patients with poor EFs who come into the hospital with a CHF exacerbation HAVE adequate cardiac output...ie they are not developing a metabolic acidosis from inadequate organ perfusion.

The patients come in with complaints related to total body sodium overload. That is why the majority of patients are treated with Lasix....treating total body sodium overload, and not an inotrope...which is a treatment for myocardial failure.

CHF or any type of Heart Failure is a syndrome of inappropriately high compensatory mechanisms (high stress state) that leads to sodium retention, which leads to the symptoms of heart failure.

In this particular case, right sided pump failure, with heart failure syndrome, the patient has total body sodium overload while the mechanics of right sided pump inefficiency leads to edema in places other than the lung. Blood isn't getting through the lung.....leading to hypoxia.

Volume loading won't help the situation....will actually worsen edema. These patients are very difficult to take care of....their volume overload needs to be treated while inotropes need to be used to improve pulmonary blood flow....They usually don't do well.
 
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jetproppilot said:
sevoflurane said:
Also, how safe is Dobutamine in ARF. Do you have to adjust the dose? I presume it causes N/V like Digoxin does.

QUOTE]
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I don't know the whole picture, but in the absence of some pre existing renal problem, the ARF is probably from decreased perfusion, so the inotrope may improve renal function by improving perfusion. Your dose is whatever dose improves perfusion without exacerbating already-existent myocardial ischemia.
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It is very common for CHF patients to have elevated creatine levels secondary to the high renin/AT activiation that is pathogonomic for the disease process.....but despite the elevated creatine which can progress to ATN and need to HD...treatment is still Lasix and ACE Inhibition unless there is hypotension or worsening metabolic acidosis.
 
militarymd said:
It is very common for CHF patients to have elevated creatine levels secondary to the high renin/AT activiation that is pathogonomic for the disease process.....but despite the elevated creatine which can progress to ATN and need to HD...treatment is still Lasix and ACE Inhibition unless there is hypotension or worsening metabolic acidosis.
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absolutely...hence the inotrope in this hypotensive patient.
 
sevoflurane said:
How safe is it to be on a drip of dobutamine 4 mcg/kg,/min, 5 Mg. IV X 2 followed by 25 mg po of metoprolol followed by 100 mg of lasix po, in a patient with extensive scleroderma causing pulmonary fibrosis and SEVERE pulmonary htn, who presented 1 day ago with RHF (probably acute cor pulmonale) and ARF (cr. 3.6). This patient was sat. in the high 80's low 90's on 10L , was consistently running tachy around 100 bpm and pressures were around 80/50?
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Why did you give a beta blocker to a patient who is in acute RHF and on dobutamine? The metoprolol will work against the dobutamine you're giving him, and beta blockers are contraindicated in cardiogenic shock anyway.

The pt was probably tachycardic for 2 reasons -- 1st is from the chronotropic effects of dobutamine, and 2nd because their stroke volume is probably so low that they need the tachycardia to keep up their cardiac output. Because of these two reasons, a beta blocker is not the treatment of choice if you are worried about their HR - if you treat them with a BB you would drop their HR as well as stroke volume and risk completely losing thier CO.

I'll echo what jetpro and x-mmd already said. Milrinone and dobutamine are the inotropes of choice in patients with decompensated RHF for the reasons they mentioned above. You would want to avoid agents with pressor effects unless absolutely forced to because the increased afterload would likely kill most of these patients (since their heart is doing all it can just to maintain a piss-poor cardiac output).

As a side note, I'm impressed you were able to bring the pt back. Codes on pts with severe pulm HTN are not pretty... it sounds like the biggest intervention you can make on this patient now is to have a serious code status discussion with him and his family.
 
The other thing is that the low O2 sats the patient is having is hurting their right heart function -- you need to try to get their sats up so that they're at least consistently above the low 90's. The pulmonary vasculature vasoconstricts in the setting of hypoxemia, which will therefore further increase the afterload on the right heart.
 
Milrinone and dobutamine are the inotropes of choice in patients with decompensated RHF for the reasons they mentioned above. You would want to avoid agents with pressor effects unless absolutely forced to because the increased afterload would likely kill most of these patients (since their heart is doing all it can just to maintain a piss-poor cardiac output).

Ditto: You will also need to do what ever necessary to decrease the PVR. That is increase O2 delivery, decrease CO2, treat pain,etc. If dobutamine does not do the trick, then epi works synergistically with milrinone.
 
I can see the use of dobutamine with many patients. Absolutely great drug. No questions. Specialy when her cardiac index was 1.1. I was just a little worried that systemic vasodialation would further compromise her already low blood pressure (80/50), would cause worsening of renal failure, cause an increase in HR on her already tachycardic state, and end up in a disasterous loop requirering more oxygen demand. Do the inotropic effects of dobutamine overshadow the vasodilatory effects on renal perfusion?
I was thinking along the lines of dopamine at doses where alpha activation would not be predominating (5-10 mcg/kg/min.). Why was she given a Beta blocker? The answer is I don't know. I never felt comfortable giving her a beta-blocker for rate control. I would have much preferred a cardizem drip. My superiors felt it necessary for some reason which I don't quite understand. She is in a better place now. This a.m. before returning to the floors I was going over the scenerio muliptle times in my head, trying to find what would have been the correct management to her medical issues. Fact is, she was endstage and as sweet as she was, this was bound to happen.
 
sad story for sure

you need to keep the systemic pressures higher than the pulm pressures... so giving a vasodilator will lead you down a very bad path (ie: CPR to bring systemic pressures up again).... Dobutamine/milrinone etc all cause systemic vasodilation. so this is what i would do: Levophed, then start milrinone without a loading dose (or at worst a 1/4th of normal loading dose), for god's sake stay away from Dobutamine, you can always add Nitric Oxide to help her pulm. HTN or adding a prostaglandin (but that will also drop your systemic pressures... In my experience Nitric only works every once in a while.

by the way there is no such thing as acute cor pulmonale - cor pulmonale is a chronic development... and i would absolutely tolerate a sat in the high 80s on 10L, HR=100 and 80/50 BP... unless the patient feels like **** i wouldn't do anything about it. pt needs to be on transplant list for lung or lung/heart.
 
Cor pulmonale is defined as an alteration in the structure and function of the right ventricle caused by a primary disorder of the respiratory system. Pulmonary hypertension is the common link between lung dysfunction and the heart in cor pulmonale. Right-sided ventricular disease caused by a primary abnormality of the left side of the heart or congenital heart disease is not considered cor pulmonale, but cor pulmonale can develop secondary to a wide variety of cardiopulmonary disease processes. Although cor pulmonale commonly has a chronic and slowly progressive course, acute onset or worsening cor pulmonale with life-threatening complications can occur.

A saddle embolus is an example of acute cor pulmonale. Big clot, pulmonary resistance goes through the roof and pulmonary circulation seizes to a grinding halt, right heart goes into immediate failure then death. This all happens within seconds. My lady had a case of rapidly progressing scleroderma. She had such thick skin, getting an A-line in her was nearly an impossible task.
 
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Tenesma said:
sad story for sure

you need to keep the systemic pressures higher than the pulm pressures... so giving a vasodilator will lead you down a very bad path (ie: CPR to bring systemic pressures up again).... Dobutamine/milrinone etc all cause systemic vasodilation. so this is what i would do: Levophed, then start milrinone without a loading dose (or at worst a 1/4th of normal loading dose), for god's sake stay away from Dobutamine, you can always add Nitric Oxide to help her pulm. HTN or adding a prostaglandin (but that will also drop your systemic pressures... In my experience Nitric only works every once in a while.

by the way there is no such thing as acute cor pulmonale - cor pulmonale is a chronic development... and i would absolutely tolerate a sat in the high 80s on 10L, HR=100 and 80/50 BP... unless the patient feels like **** i wouldn't do anything about it. pt needs to be on transplant list for lung or lung/heart.
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I strongly disagree. Norepinephrine will make your numbers look better temporarily because of its strong alpha adrenergic component, but will work against you concerning systemic perfusion.

Unless the patient is on deaths door, I'd strive to keep the SVR in the low normal range to ensure minimal load on the left ventricle, and work to optimize things on the right side comcominantly.
 
Do you guys think vasopressin and/ or steroids (for relative adrenal insufficiency) would have any role?
 
Annette said:
Do you guys think vasopressin and/ or steroids (for relative adrenal insufficiency) would have any role?
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Vasopressin and steroids are used for sepsis induced hypotension....at least that's what the literature supports....both becoming more and more used and published in the last 5 to 10 years.

Both have little indication in primary pulmonary hypertension with cardiovascular/pulmonary collapse.

I suppose when the patient fibs from hypoxia then you could use vasopressin per ACLS protocols.
 
Ditto: vasopressin is for septic shock. It helps to maintain messenteric perfusion. Not necassary in this case, until you are in a code situation. I used it twice last week (bad week) and it worked like charm in septic situations.
However, there are more and more uses for this drug coming about every year. I have also used it in really bad hearts but I still don't see any use in this situation since it will increase SVR and further prevent forward flow.
 
my mistake - i wasn't aware that the literature was referring to acute RV failure as acute cor pulmonale ...

in RV failure you need good normal to good SVR - when that SVR starts dropping then you are stuck in a vicious cycle...

when was the last time you guys took care of an acute RV failure (outside of a CABG coming off pump or after putting a new heart into somebody w/ pulm HTN?)????
 
Not infrequently up until last year when I stopped doing CCM.
 
militarymd said:
Vasopressin and steroids are used for sepsis induced hypotension....at least that's what the literature supports....both becoming more and more used and published in the last 5 to 10 years.

Both have little indication in primary pulmonary hypertension with cardiovascular/pulmonary collapse.

I suppose when the patient fibs from hypoxia then you could use vasopressin per ACLS protocols.
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Vasopressin at supraphysiologic levels ( > 0.04 U/min) essentially eliminates the benefit of maintaining mesenteric, renal, cerebral, and coronary perfusion and will lead to vasoconstriction of those vascular beds. Unfortunately, in all of the septic shock patients I have seen treated with Vasopressin, 0.05 U/min or greater has been required to reestablish reasonable pressures.
 
UTSouthwestern said:
Vasopressin at supraphysiologic levels ( > 0.04 U/min) essentially eliminates the benefit of maintaining mesenteric, renal, cerebral, and coronary perfusion and will lead to vasoconstriction of those vascular beds. Unfortunately, in all of the septic shock patients I have seen treated with Vasopressin, 0.05 U/min or greater has been required to reestablish reasonable pressures.
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Are you using it alone or as an adjunct to some other pressor?
 
Both. As an adjunct the levels can be kept closer to physiologic rates and I usually keep its rate fixed while going up or down on the complementary vasopressors/inotropes. The more severe hypotensive patients, tend to need higher doses of those complementary agents, which leads to the same problems with vasoconstriction of sensitive vascular beds.
 
In patients who have septic shock and are resistant to vasopressors, I will start vasopressin at 2.5 u/hour and not titrate it. The norepinephrine goes up and down.

If I start vasopressin, I usually start some kind of "stress dose" steroids also.
 
for those who don't know much about vasopressin.... it is a great drug... also because it works in acidotic patients - whereas the other pressors usually start losing their punch at 7.15 or lower... vasopressin doesn't care much about pH :)
 
What's the difference between dobutamine and milrinone? I'm an MS4 doing a CCM rotation, and today on rounds, there was some discussion about switching a patient's dobutamine to milrinone, b/c (what i understood) the dobutamine has a bigger vasodil effect. . .? I didn't really understand. . .

Anyway, in the end i double checked with my resident, and he said we're not switching it (i.e. we're leaving him on the dobutamine). . .still confused about why. . .

Some context--the pt is a 70 y.o male with sever mitral regurg, s/p massive hemorrhage from injured R subclavian during attempted mitral valve repair (procedure was aborted after intraop resuscitation and repair of the artery).
 
chicamedica said:
What's the difference between dobutamine and milrinone? I'm an MS4 doing a CCM rotation, and today on rounds, there was some discussion about switching a patient's dobutamine to milrinone, b/c (what i understood) the dobutamine has a bigger vasodil effect. . .? I didn't really understand. . .

Anyway, in the end i double checked with my resident, and he said we're not switching it (i.e. we're leaving him on the dobutamine). . .still confused about why. . .

Some context--the pt is a 70 y.o male with sever mitral regurg, s/p massive hemorrhage from injured R subclavian during attempted mitral valve repair (procedure was aborted after intraop resuscitation and repair of the artery).
Click to expand...

Dobutamine = synthetic catecholamine
Milrinone = PDE inhibitor (prevents inactivation of cAMP/cGMP)

From my experience, milrinone will cause a much larger drop in the SVR than dobutamine (and a greater increase in the patients CI). Maybe they decided on staying with the dobutamine for its positive chronotropic as well as inotropic effects with the severe MVR.
 
coccygodynia said:
Dobutamine = synthetic catecholamine
Milrinone = PDE inhibitor (prevents inactivation of cAMP/cGMP)

From my experience, milrinone will cause a much larger drop in the SVR than dobutamine (and a greater increase in the patients CI). Maybe they decided on staying with the dobutamine for its positive chronotropic as well as inotropic effects with the severe MVR.
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Milrinone + epi (low dose, 2-5ug/min range), if you are worried about low SVR, is superior to dobutamine in my humble opinion.
 
jetproppilot said:
Milrinone + epi (low dose, 2-5ug/min range), if you are worried about low SVR, is superior to dobutamine in my humble opinion.
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I completely agree.
 
jetproppilot said:
Milrinone + epi (low dose, 2-5ug/min range), if you are worried about low SVR, is superior to dobutamine in my humble opinion.
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Ditto Jet. Throw some CaCl in there and they are all synergistic. It goes back to that biochemistry thingy and cAMP.
 
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