SMACC-Back – Myburgh on Catecholamines


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

Now on to the SMACC-Back…


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  1. says

    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?

  2. says

    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!

  3. rfdsdoc says

    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.

  4. DocXology says

    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.

    • K says

      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?

      • DocXology says

        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.

  5. Pablo says

    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 increase myocardial oxygen consumption in acute heart failure/mild cardiogenic shock is associated with higher mortality within the next 3-6 months. we use inotropes, we see the patients get better (perhaps not more better, but only better faster) on inotropes in the acute phase but they die more soon after hospital discharge when compared to similar patients who did not get inotropes. in severe sepsis, dobutamine stands greatly on the basis of the Rivers EGDT study. however, i suspect that the benefit achieved in that trial had more to do with the whole (early resuscitation using a standardized protocol aiming at metabolic goals), and less to do with any individual intervention used. time will tell.
    but perhaps it is time to start considering more strongly the use pure vasodilators in patients (acute heart failure or severe sepsis) with evidence of hypoperfusion who are able to maintain their own blood pressure after hypovolemia has been ruled out or corrected judiciously.
    i would love to hear your thoughts on this.

    • DocXology says

      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. Intropes, in this instance (like IABPs and EVADS) are just physiological support as a bridge to REAL treatment If you don’t have that the patient is no better off and as you mention probably worse off.

      I too find the dobutamine use in sepsis the Rivers Study perplexing. As mentioned by someone at a SMACC talk, Rivers essentially approached a broken system and cared it enough to do something. In centres with high-functioning EDs, his interventions would probably be have done anyway but I wouldn’t think dobutamine have had a primary place in the management.

      My approach to shock is simple – reverse the pathophysiology and treat the CAUSE. Hypovolaemia = volume/stop volume loss. Cardiogenic = intropes (but see warning above). Distributive = pressors/vasoconstrictors. Obstructive = remove the obstruction. I have never seen in any Oz ICU where the first line vasoactive drug for sepsis would be an ino-dilator. Scott talks about using dilatation (including GTN) to improve microcirculatory flow. This is an incorrect understanding of circulatory physiology and the disturbance in sepsis. Any vasodilator (as well as vasoconstrictor) is a blunt tool at best. Dilators in isolation will lower MAP and reducing driving pressure to the tissues. The special case of excessive after load affecting cardiac function is usually rare and would not be the first thing you target. Sepsis can be best considered as RE-distributive shock with impaired autoregulation in some vascular beds leading to blood shunted away from other tissues and vital organs. There is no drug that can specifically target regional circulation to correct this imbalance except to treat the underlying cause. Therefore any vasoactive drug or inotrope are only addressing gross haemodynamic parameters and currently we have insufficient tools to measure their true effects on regional circulation e.g. gastric pH etc.

      • says

        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 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.

        • DocXology says

          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 says

          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 and not flog it (LVAD or ECMO) should be considered at an earlier stage. IABP makes so much sense cause it is one of few interventions that works by decreasing the work of the heart. unfortunately the recent NEJM IABP paper did not show benefit.
          however, there are studies out there showing that using inotropes that increase myocardial oxygen consumption (thus, generating more myocardial ischemia) increase mortality in the short term.
          the point i am trying to make is that in acute heart failure and cardiogenic shock we should be concerned about preserving myocardial tissue as much, or even more, than end organ perfusion. straining the failing heart while trying to preserve end organs might lead to a patient with little heart left, and end organ perfusion (and death) will follow as a consequence anyway.
          when the heart is the main failing and hypoperfused organ driving hypoperfusion of other organs, should we focus on myocardial preservation and just tolerate some degree of end organ hypoperfusion?

          • says

            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.

  6. Pablo says

    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 inotropes when compared to vasodilators.
    FIRST trial showed nearly two fold increase in mortality at 6 months with the use of dobutamine.
    OPTIME-CHF study demonstrated increased risk of rehospitalization and death with the use of milrinone in patients with acute decompensated heart failure and ischemic cardiomyopathy.
    in cardiogenic shock:
    SOAP 2 showed increased mortality with the use of dopamine in patients with cardiogenic shock.
    it may not be evidence of the best level but it is the best evidence available and it is clearly pointing towards potential harm with the use of inotropes in patients with an acutely failing heart, shocked or not.
    problem is that we sometimes have no option but to use them, like in true cardiogenic shock.
    however, we should at least be aware that there is a tradeoff between short term improvement and other very important outcomes, and try to avoid them as much as posible.
    frequently ICU patients are started on inotropes with no other argument than “the patient has a bad heart” or “the cardiac output is low”. if the patient is perfusing well the cardiac output and heart function should be thought of as adequate, no matter what the number is.

    • DocXology says

      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.

    • says

      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.

      • DocXology says

        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)

        The ESCAPE trial patient characteristics were in this ballpark:

        Hemodynamic Measurement
        RAP 14
        Pulmonary capillary wedge pressure 25
        CO 1.9 L/min
        Systemic vascular resistance 2100 dynes ???? sec/cm5

        Only half needed inotropes.

        Milrinone, a PDE is similar to dobutamine in action i.e. an indicator with the additional benefit effect of lusitropy (improved diastolic relaxation).

  7. DocXology says

    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


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