Online Medical Education on Emergency Department (ED) Critical Care, Trauma, and Resuscitation
One of the best lectures from SMACC 2013 was Dr. John Myburgh on Catecholamines.
Here is the Video Version of the Lecture:
Or you can listen to the audio on the SMACC Feed or in Itunes
Podcast: Play in new window | Download (4.6MB) | Embed
Subscribe: Apple Podcasts | Android | Google Play | RSS | More
Scott Weingart. SMACC-Back – Myburgh on Catecholamines. EMCrit Blog. Published on June 26, 2013. Accessed on April 26th 2018. Available at [https://emcrit.org/racc/myburgh-on-catecholamines/ ].
Unless otherwise noted at the top of the post, the speaker(s) and related parties have no relevant financial disclosures.
Already an EMCrit CME Subscriber?
Click Here to Get CME Credit for the Episode
.
If you enjoyed this post, you will almost certainly enjoy our others. Subscribe to our email list to keep informed on all of the Resuscitation and Critical Care goodness.
This Post was by the EMCrit Crew, published 5 years ago. We never spam; we hate spammers! Spammers probably work for the Joint Commission.
Comment Here
24 Comments on "SMACC-Back – Myburgh on Catecholamines"
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 going to be acieving the same physiological end-points – improve preload and hence C.O?
So can we then give less fluid if we are reversing the “relative hypovolemia” and correcting distribution problems?
This would be appealing as we know (and Prof. Myburg) reminded us about the evils of too much fluid and the downstream effects on the patient later in their ICU stay.
Any evidence to support this concept in practice?
Casey
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 output, and vasopressin can help – would be interested to here your take on that!
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 dilatation.
Evidence is that Adrenaline + GTN can achieve similar haemodynamic effects and it is easier to titrate preload reduction.
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.
This can be a whole new podcast, but in short:
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 dobutamine makes sense.
DocX-not sure I said any of that. And if there is any drug that improves the microcirc in sepsis, it actually is dobutamine (albeit the evidence is not at the robust stage yet, but better than the other stuff out there.) You can search for Peter Spronk’s work on the subject. In the meantime I guess I’ll bone up on my circulatory physiology, b/c I am obviously lacking in this area.
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 SVRI +/- filling pressures. If there is still evidence of poor perfusion resulting from depressed cardiac function then an inotrope such as dobutamine would be indicated. However, it wouldn’t be first line because it doesn’t address the initial derangement associated with sepsis and may actually worsen its impact on the circulation (i.e. further vasodilation)
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.
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 in action i.e. an indicator with the additional benefit effect of lusitropy (improved diastolic relaxation).
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
[…] my approach (listen to the lecture and then to Scott Weingart defending dobutamine here <http://emcrit.org/wee/myburgh-on-catecholamines/> at emcrit.org and decide for […]
[…] Go to EMCRIT, subscrtibe to his podcast, and join in the discussion that Scott has ignited! […]
[…] Go to EMCRIT, subscrtibe to his podcast, and join in the discussion that Scott has ignited! […]
[…] and John Myburgh on Catecholamines from SMACC […]