Cite this post as:
Scott Weingart, MD FCCM. SMACC-Back – Myburgh on Catecholamines. EMCrit Blog. Published on June 26, 2013. Accessed on March 19th 2025. Available at [https://emcrit.org/emcrit/myburgh-on-catecholamines/ ].
Financial Disclosures:
The course director, Dr. Scott D. Weingart MD FCCM, reports no relevant financial relationships with ineligible companies. This episode’s speaker(s) report no relevant financial relationships with ineligible companies unless listed above.
CME Review
Original Release: June 26, 2013
Date of Most Recent Review: Jul 1, 2024
Termination Date: Jul 1, 2027
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Hi Scott Firstly – I think we need a U.N. resolution on the gland that lives just north of the kidney (supra-renal). The only solution…. Second point. The idea that out vasopressors main action is in increasing the squeeze on the venous side – hence increasing return, preload etc is an appealing one. Makes sense. My question is how this effects our thinking around fluid loading in sepsis – if sepsis is in some ways a form of distributive shock, and relative hypovolemia – then by using pressors early – i.e.. in conjuction with iV fluid boluses then are we… Read more »
Hey buddy, Exactly! 3 studies published on this in the past year. Will review them all in the vasopressors show.
Only Scott could SMACC back Myburgh. In style. Great idea mate and hope they keep coming. Indeed epi (upon) nephros (the kidney) is the ancient Greek name for the adrenal. Don’t fancy Australia’s chances in another battle of the Pacific, but one-on-one with Myburgh? that’s a different story. Looking forward to the vasopressor episode now. Will you cover vasopressin? Recent debate about vasopressin use in the context of cerebral vasospasm post aSAH. Does vasopressin really worsen cerebral vasospasm like some animal studies suggest? One context is induced hypertension for vasospasm, when high dose catecholamines sometimes cause SAM and drop cardiac… Read more »
thanks Scott
okay no more heckling!
I checked..apparently this is true of lidocaine vs lignocaine too. Oh dear..;-)
About the dobutamine..I see your point. But that French study of epi ( see we can compromise) vs norepi + dobutamine showed no great advantages btw groups…that convinced me.. at least for sepsis.
In primary cardiac conditions where inotropy is the main outcome , fair enough, dobutamine seems reasonable. and for retrieval, can be started via PIV too.
Love me some epi, messes with lactate clearance for resus goal though.
The main role or dobutamine as I see it as mainly to reduce preload (venous side of circulation) whilst maintaining or increasing inotropy. Its affects on MAP can be variable due to its arterial side dilatory effects and I have found it can increase CO at the expense of MAP. Without a driving arterial pressure, you are just further compromising microcirculatory flow. Clinically the most logical indication is in mild cardiogenic shock where you need to relieve the pulmonary oedema whist maintaining MAP through inotropy. However sometimes another inotrope with some alpha activity needs to be combined to prevent uncontrolled… Read more »
Sure, but one of the reasons that dobutamine is improving CO at the expense of MAP is because of that very fact. Afterload is being reduced, in addition to its effects on inotropy and chronotropy. Not necessarily a bad thing is it? I don’t care about BP as much as I do about CO and end-organ perfusion, within reason of course. What do you think about that?
I most care about end-organ perfusion which is neither the same as cardiac output or BP. But beyond measures such as mentation, urine output and big toe temperature our tools for assessing this are not that sophisticated. And let’s not forget that coronary perfusion is dependent on arterial pressure.
hi scott. great blog and podcasts. in the smacc back podcast you mentioned the attractiveness of dobutamine in patients with normal BP in which you just want to hit the heart with a little bit more inotropism (+/- vasodilation). patients in acute heart failure/mild cardiogenic shock and normotensive severe sepsis patients came to my mind with your example. however, we must keep in mind that dobutamine (and dopamine, and milrinone) used in acute heart failure/mild cardiogenic shock improves CO at the expense of increased myocardial oxygen consumption which in turn will favour more myocardial ischemia/necrosis. The use of inotropes that… Read more »
In answer to Pablo: I would only consider an ino-dilator like dobutamine for cardiogenic shock if there was evidence of all of the following – poor cardiac output/inadequate tissue perfusion, high filling pressures and pulmonary congestion. This is essentially a Forrester Class IV shock which has a grave mortality rate of 55%. These patients usually need a ballon pump and have any treatable underlying lesion treated ASAP e.g. coronary revascularisation, surgical intervention. Studies on use of intropes in cardiogenic shock are muddied by the fact these patients have high baseline mortality rates – you are a flogging a dying heart.… Read more »
This can be a whole new podcast, but in short: I don’t use dobutamine for heart failure I do use dobutamine for cardiogenic shock, which for me, by definition implies poor tissue perfusion. You can find this in one of the earlier podcasts. The main roles for dobutamine are post-arrest cardiac stunning and sepsis-induced cardiomyopathy. In both of these cases, the MAP may be fine (either b/c the pt is maintaining or we have added vasopressors), but the heart is pumping poorly. If there is some evidence of poor perfusion (i.e. elevated lactate, cold extremities, poor urine output, etc.) then… Read more »
The problem with this discussion is that the haemodynamic changes of sepsis is quite variable and depends on severity. Vasoplegia leading to relative hypovalaemia is universal. There is also capillary leak from SIRS resulting in fluid shift out of the vascular space. Cardiac output can also be reduced. In effect septic shock can be multifactorial – distributive, hypovolaemic and cardiogenic. However, one cannot tailor the correct intevention if there is inadequate information on any of these parameters i.e. filling pressures, SVRI and cardiac index. After moderate fluid resuscitation, pressors such as noradrenaline generally are first line treatment to address low… Read more »
agreed that in septic shock dobutamine improves microcirculatory flow and that as part of a metabolic driven resuscitation protocol dobutamine helps improve mortality. however, in acute heart failure and cardiogenic shock we continue to prioritize end organ perfusion while our main priority should be myocardial preservation (the primarily affected and suffering organ), above restoration of end organ perfusion. particularly when both of these goals are not achievable by the same means (eg, inotropic support). if inotropism is required perhaps drugs that do not work by increasing myocardial oxygen consumption should be used (levosimendan) or other interventions that rest the heart… Read more »
Pablo, I’m not sure which studies you mean. Are we again mixing up heart failure and cardiogenic shock.
Of course IABP and ECMO would be swell; most places can’t get those options in the ED.
No point in tweaking the microcirculation if your macrocirculation is failing.
hi scott. i don’t think there is a mix up. same principle applies to both acute heart failure and cardiogenic shock. the use of inotropic catecholamines and PDE inhibitors definitely improve hemodynamics but may do so at the expense of increased morbidity and mortality. no study has shown benefit other than short term hemodynamic improvement (cardiac index, filling pressures) while several studies point towards increased adverse events including mortality with their use. in acute heart failure: ESCAPE trial showed two fold risk of death with the use of dobutamine or milrinone. ADHERE registry showed increased mortality with the use of… Read more »
Which doesn’t come as any surprise. Flogging a dying heart is just causing more damage – we finally learnt this when we started using beta blockers for chronic failure. Most of Intensive Care Medicine is about supporting physiology until definitive treatment works (e.g. PTCA, valve repair) or the patient heals themselves (e.g. myocarditis). Many of the interventions have risks themselves and need to be finely adjusted according to the situation.
Pablo,
As I have mentioned inotropes are inappropriate for heart failure. I believe all of your studies revolve around that condition. Heart failure is not cardiogenic shock as I have mentioned. Dopamine is not dobutamine and and soap2 did not show increased mortality with dopamine, it showed increased mortality with dopamine as compared to norepinephrine.
Just so we are just talking the same language, cardiogenic shock is just bad acute heart failure. This AHA article offers one haemodynamic definition: SBP <80 to 90 mm Hg or MAP 30 mm Hg lower than baseline) CI <1.8 L · min?1 · m?2 without support or 18 mm Hg or RVEDP >10 to 15 mm Hg) http://circ.ahajournals.org/content/117/5/686.full The ESCAPE trial patient characteristics were in this ballpark: Hemodynamic Measurement RAP 14 PAWP Pulmonary capillary wedge pressure 25 CO 1.9 L/min Systemic vascular resistance 2100 dynes ???? sec/cm5 Only half needed inotropes. http://www.columbiamedicine.org/education/r/CCU/Escape%20Trial.pdf Milrinone, a PDE is similar to dobutamine… Read more »
Sorry bits of my post were chopped off or modified
CS definition:
SBP < 80-90 mm Hg or MAP 30mmHg < baseline
CI 1.8L/min/m2 without support or 18mmHg
RVEDP > 10-15 mmHg
Escape trial mean characteristics:
RAP 14mmHg
PCWP 25 mmHg
CI 1.9 L/min/m2
CO 3.8 L/min
SVR 1500 dynes.sec/cm5
Milrinone is an ino-dilator