Today, we have a new CV-EMCrit episode: Inotropes Part I with Editor of CV-EMCrit, Trina Augustin.
What Heart Rate to Shoot For?
90-110 in most patients
may go higher if compensating for RHF or extremely low EF
The Inotropes
Dobutamine, the ChronoInotrope
Hits B1, B2 and at higher doses, alpha
Not as much vasodilation as milrinone, but a lot of chronotropy and the possibility of arrhythmia induction
Our Dose Recs
1-5 mcg/kg/min (can go up to 10, but you start risking excessive chronotropy)
Milrinone, the InoDilator
Phosphodiesterase-3 (PDE-3) inhibitor that increases cAMP levels in cardiac myocytes by inhibiting cAMP breakdown by the PDE-3 enzyme leading to increased availability of Ca
Inotropy, lusitropy, but not as much chronotropy. Also comes with vasodilation (arterial, venous, and pulmonary arterial)
Our Dose Recs
0.125 – 0.25 mcg/kg/min (max out at 0.37 mcg/kg/min)
45 minutes to really see clinical effects
DO NOT GIVE THE BOLUS
titrate every 45-60 minutes
2.5 hr clinical half life, but at least doubled with renal failure and in a pt on RRT can be 20 hours
can consider in a patient who is strongly beta-blocked
Inotropic Epinephrine, Dual-faced: the pure Inotrope/Inopressor
Dose range for intrope use
0.01-0.08 mcg/kg/min (for a 70 kg pt, this is 1-5 mcg/min)
Hits B1, B2, and at higher doses, Alpha
Digoxin, Original-G
Trina uses this in AF with RVR in patients with reduced EF
30-45 min before you see clinical effects after a bolus
Delayed clearance with renal dysfunction
125-250 mcg bolus, may repeat x 1, two hours after 1st dose
after those 2 boluses, you really need levels
Levosimendan, New Toy?
A calcium sensitizer that we do not discuss as neither of us have access to the drug
Calcium, “God's” Inotrope
we discuss this in part 2
Dopamine, Fool's Inotrope
Just don't do it, just don't…
Studies Mentioned…
DOREMI Study
Dobutamine vs. milrinone as inotropes in cardiogenic shock [10.1056/NEJMoa2026845]
CAT STUDY
Epi vs. Norepi in ICU Pts [10.1007/s00134-008-1219-0]
Optima CC
Epi vs. Norepi in Cardiogenic Shock post-MI [10.1016/j.jacc.2018.04.051]
Dobutamine increases heart rate more than epinephrine in patients recovering from aortocoronary bypass surgery
Dobutamine vs. epi (study uses ng but when you convert 0.01-0.03 mcg/kg/min) [10.1016/1053-0770(92)90095-O]
Additional New Information
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Great episode!
I’m Pedro Mansur, a second year emergency medicine resident in Brazil.
For part 2, I got a question about the use of dobutamine in AR and MR.
Recently read about valvular emergencies from two papers: https://doi.org/10.1016/j.jacadv.2024.101402
https://doi.org/10.1093/ehjacc/zuac086
And also listened to Sara Crager on ICUedu podcast.
The papers do not mention dobutamine.
And on the other side, Sara favors the use with great arguments.
What do you do about it in your practice?
It’s interesting that the way you use these agents in cardiogenic shock should really be tailored to patient specific physiology. In the most practical terms (and I believe you touched on this in the episode), in the ED, in absence of invasive hemodynamic monitoring (which I think would be exceedingly rare), we at the bedside, are going to be titrating these inotropes based on a clinical findings that suggest increased CO (ie) skin findings, mentation, urine output etc? Or are our physician colleagues preforming serial ultrasound exams to judge improvement in contractility?
this discussion prompted me to re-listen to the other 2 episodes you did with Dr Agustin on acute valvular emergencies (which turned out to be super worthwhile)..just wanted to comment on what a solid addition she is to your team 🙂
Loved the episode. As someone in a non-academic center it’s good to hear discussions between people who are not part of your group to double check that your current take on things jibes with those outside of your particular bubble. As a pediatric ICU doc (about 90 miles north of Dr. Augustin) in addition to the physiology I just love that Dr. Augustin discussed these medications in mcg/kg/min.
Awesome podcast!!!! Long awaited 🙂 Thanks!
Can you talk a bit about Angiotensin-II?
we talk about that in the specific EMCrit episode on AngioII
Great episode. I’m wondering people’s thoughts on acute RV failure leading to cardiac arrest or peri-arrest situations and the role of pulmonary vasodilators in this situation. In the CVICU endotracheal milrinone is described in the anesthesia literature which I believe has saved some patients in a pinch for me. Is anyone else doing this? In the same vein, Dr. Farkas has described nebulized nitroglycerin in detail in the IBCC but in the peri-arrest situation or full arrest situation where RV failure is seen in POCUS has anyone ever given nitroglycerin straight down the endotracheal tube if a nebulizer is not… Read more »
see the episode I did with Sara Crager on this exact topic
Great post! I haven’t much experience with milrinone, but I do have experience with levosimendan, which is a calcium sensitizer. By your description of milrinone, I find it to be similar to levosimendan: Inodilator, little chronotropic effect and halflife like plutonium. I do sometimes use it when I figure the patient needs inotropy and I’m not afraid of vasodilatation. I never use it in hyperacute settings. Some of the cardiologists use it for intermittent infusions for chronic heart failure. With regards to monitoring, a ED placed central line with blood gas analysis gives you an saturation in vena cava superior.… Read more »
thanks for that Erlend, can’t wait to get my hands on it
This podcast was very timely for me. I have been wanting to ask a couple of questions as it pertains to some nuance of vasopressors in general. This may be covered in the “Part 2: Conditions”, but I wanted to ask it if not. During various shock and/or low flow states in which much of the endogenous catecholamines have been depleted, what is the actual mechanism of action that makes one Inotrope and/or Vasopressor work better than another? I am willing to do the leg work to research if you can point me in the right direction for reliable resources.… Read more »
Thanks for the podcast!
I feel the majority of the time my hypotensive patients are undifferentiated and I reach for norepinephrine. Once I grab the ultrasound and find out it may predominantly be heart failure leading to their presentation I typically then add dobutamine if needed. Or would you try coming off the levophed while hanging low dose Epi or the dobutamine?
I’m a fan of switching to epinephrine and keeping the dobutamine if the vasodilation it causes isn’t profound and forcing you up to heroic doses of epinephrine. Some people respond well to just epinephrine, but sometimes the extra kick of dobutamine gets the cardiac output where it needs to be. I’ve never really found a good way to tell which patient responds to which mixture other than trying a drip or drips and measuring the cardiac output, mixed venous, cap refill, urine output, mentation for the next 2 hours afterwards.
Great episode here. I’ve been an ED nurse for 15 years and worked in a variety of environments. I taught ACLS for a few years and did spend a year in ICU (was not for me). I left a level II trauma center to work in a rural freestanding ED with minimal resources. We definitely get sicker patients than my previous freestanding, and more frequently …but not working in a facility with Cath lab, it’s easy to lose skills if one doesn’t continue to expose themselves to educational material. It’s also so so easy to fall into the ‘tasking’ mentality… Read more »
Such a usefull and great episode!! Basic question, but can you start dobutamine peripherally in the ED while waiting to get central access? Thanks for such quality content.
Yes you can… BUT in case of extravasation its going to cause damage, so you have to be careful… but it’s the same thing with norepi… if you use norepi while you wait for the central line in your shop you can do the same with dobutamine.
extrav injury from dobutamine is definitely possible due to the alpha effects of one of the enantiomers, but it is quite rare.
Yea but since it has a pH round 4 its generally considered that it needs a central line and potentially a bad thing if it extravasate… but as I said… in most situation that risk (if you take minimal precautions) is negligible to the benefit if the patient need the drug (the seme logic as norepi though a periferal IV)… so you definetly can (and some times must) you just need to be careful and document accordingly.
Epi gtt 50mcg/min in cardiac arrest after 2 or 3 1 mg boluses in the field or in the ED vs more 1 mg boluses of epi
Great I would love to hear in the second part some comments on methilene blue and ivabradine, we had a couple of cases in which what started as cardiogenic shock (secondari to an MI)developed profound vasoplegia and was rescued with MB, this is well described in the cardithoracic ICU for post operative vasoplegia but this is maybe diferent I would like to hear if you use it and HOW, also en a couple of cases with cardiogenic shock and a lot of tachicardia (more than we wanted at least) and multiple vasopressors we used ivabradine to slow the heart rate… Read more »
Do you feel that the increase in lactate resultant from an epinephrine infusion actually results in any truly clinically significant acidosis? And could this type b lactate from excess pyruvate actually be independent of any physiological acidosis? Of course the teaching is that lactate contributes to AGMAs; are there any physiologists who might challenge this?… If we have decided that “lactic acidosis” is a misnomer then when do we care, if at all, about a type b lactate level? At what point, if any, does a type b lactate result in a true metabolic acidosis? Someone help pull me out… Read more »
I know there are factions that try to pretend that you can have an elevated lactate without a resultant acidosis, but that is impossible–all of physical chemistry would break down. I think the more important take-home is that acidosis is not bad. In fact everything works better in the face of a mild acidosis. So the lactate from epi is usually a net benefit to heart function and compensation.
Thank you very much for the thoughtful response! In regards to the benefit of a mild acidosis, is this related to a rightward shift of the oxyhemoglobin dissociation curve, and thus increased unloading of O2 to tissues, or is it something else? I understand that lactate is fuel for the heart and brain. If a mild acidosis is physiologically beneficial, but a more severe acidosis has a negative inotropic effect, is there a relative pH range where you would say negative inotropic effects may take hold? I think its reasonable to not be concerned about a pH above ~7.2 in… Read more »