Thanks for this segment - although I feel there are some major problems.
The pathophysiology of cardiogenic shock (CGS) was not sufficiently discussed. There is indeed significant data which informs us that CGS is not the classic low CO, high PCWP, high SVR state we once thought. CGS is associated with a systemic inflammatory response related to neurohormonal factors, cytokine release, and endogenous NO and can often be associated with low SVR. These interesting and complex physiologic concepts are discussed in an open access article by Judith Hochman in Circulation:
Because of this SIRS/vasodilatory component of CGS, Dr.Bucher's suggestion that high dose dobutamine as a first line agent is inherently risky. His description of dobutamine as a pressor that has inotropy is inaccurate. By way of its B2 agonism it causes systemic vasodilation and absolutely precipitously drops blood pressure in clinical practice. This is a very rational and very real fear clinicians should have. This agent should be considered an ino-dilator. The worse a patient looks, the MORE concerned one should be about starting high dose dobutamine!
Dysrhythmias (even afib) are very poorly tolerated in patients with cardiogenic shock. We learned in the SOAP-II trial (https://www.nejm.org/doi/full/10.1056/nejmoa0907118) that dopamine vs norepi was associated with higher mortality in patients with cardiogenic shock, and was associated with greater dysrhythmias. Although dobutamine is a different agent, it is widely considered to be equally arrythmogenic, especially at the doses recommended by the author. Norepi was the agent of choice for patients with a component of CGS in SOAP-II.
Epinephrine is has similar problems to dobutamine in terms of arrythmia potential and increases lactate which confounds a useful biochemical indicator of response to therapy.
I would suggest that based on available clinical data and understanding of CGS physiology the first line agent in CGS is Norepinephrine (an ino-pressor, by way of alpha>beta agonism). Get norepi on board first. This will restore/mobilize effective circulatory volume, restore SVR, and also start augmenting CO, while minimizing the risk of possibly fatal dysrhthmias and precipitous hypotension. Then, assess the patient. Do a TTE, check the mixed venous O2, assess their clinical perfusion. If needed, add dobutamine judiciously - we often use these agents together. In the cardiac ICU my colleagues and I often start at approximately 2.5 mcg/kg/min and gently titrate up if needed. We very rarely exceed 10mcg/kg/min and would have major concerns starting above this dose.
Hi Joseph. Thanks so much for your comments, I really appreciate it.
I think you make a good point about the use of dobutamine and the vasodilation. My anecdotal experience has been clinical improvement in blood pressure - but you are correct in that I underestimate the risk of hypotension in these patients.
I do think that there should be in intropic agent added first - I am very hesitant to add more vasoconstriction on the failing heart without any other agents. What are your opinions/experiences on the use of milrinone in these patients?
Absolutely - I think the combination of NE/DBT is where we are going to end up in these patients, but particularly in the immediate post arrest situation when we often don't even have an arterial line, starting inodilators as single agents is risky. If using an inotrope as part of my therapy, I generally prefer dobutamine to milrinone due to its on/off titratability and immediate effect. Some of my CVICU colleagues are very comfortable giving loading doses of milrinone in a highly monitored ICU setting, conversely others will frankly describe experiences of fatal consequences after a milrinone load. If we load milrinone and don't like the consequences, we are stuck with them for hours due to the prolonged half life. So - I rarely if ever use milrinone in the ED.
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Kenn G. - May 4, 2018 8:44 AM
Epinephrine dose should be 10-20 mcg/min and NOT mcg/kg/min as listed in the show notes (correctly noted on the podcast)
Joshua B. - May 4, 2018 9:47 AM
Thanks for finding that!
Mel H. - May 4, 2018 8:46 AM
Thanks Kenn G. you are correct we will get that dealt with.
James C. - May 23, 2018 6:09 AM
Just saying, the above picture is great and I will forever picture pressors this way.
Joseph B. - May 30, 2018 6:40 PM
Thanks for this segment - although I feel there are some major problems.
The pathophysiology of cardiogenic shock (CGS) was not sufficiently discussed. There is indeed significant data which informs us that CGS is not the classic low CO, high PCWP, high SVR state we once thought. CGS is associated with a systemic inflammatory response related to neurohormonal factors, cytokine release, and endogenous NO and can often be associated with low SVR. These interesting and complex physiologic concepts are discussed in an open access article by Judith Hochman in Circulation:
http://circ.ahajournals.org/content/107/24/2998.long
Because of this SIRS/vasodilatory component of CGS, Dr.Bucher's suggestion that high dose dobutamine as a first line agent is inherently risky. His description of dobutamine as a pressor that has inotropy is inaccurate. By way of its B2 agonism it causes systemic vasodilation and absolutely precipitously drops blood pressure in clinical practice. This is a very rational and very real fear clinicians should have. This agent should be considered an ino-dilator. The worse a patient looks, the MORE concerned one should be about starting high dose dobutamine!
Dysrhythmias (even afib) are very poorly tolerated in patients with cardiogenic shock. We learned in the SOAP-II trial (https://www.nejm.org/doi/full/10.1056/nejmoa0907118) that dopamine vs norepi was associated with higher mortality in patients with cardiogenic shock, and was associated with greater dysrhythmias. Although dobutamine is a different agent, it is widely considered to be equally arrythmogenic, especially at the doses recommended by the author. Norepi was the agent of choice for patients with a component of CGS in SOAP-II.
Epinephrine is has similar problems to dobutamine in terms of arrythmia potential and increases lactate which confounds a useful biochemical indicator of response to therapy.
I would suggest that based on available clinical data and understanding of CGS physiology the first line agent in CGS is Norepinephrine (an ino-pressor, by way of alpha>beta agonism). Get norepi on board first. This will restore/mobilize effective circulatory volume, restore SVR, and also start augmenting CO, while minimizing the risk of possibly fatal dysrhthmias and precipitous hypotension. Then, assess the patient. Do a TTE, check the mixed venous O2, assess their clinical perfusion. If needed, add dobutamine judiciously - we often use these agents together. In the cardiac ICU my colleagues and I often start at approximately 2.5 mcg/kg/min and gently titrate up if needed. We very rarely exceed 10mcg/kg/min and would have major concerns starting above this dose.
Joshua B. - June 19, 2018 7:43 AM
Hi Joseph. Thanks so much for your comments, I really appreciate it.
I think you make a good point about the use of dobutamine and the vasodilation. My anecdotal experience has been clinical improvement in blood pressure - but you are correct in that I underestimate the risk of hypotension in these patients.
I do think that there should be in intropic agent added first - I am very hesitant to add more vasoconstriction on the failing heart without any other agents. What are your opinions/experiences on the use of milrinone in these patients?
Joseph B. - June 23, 2018 11:50 AM
Absolutely - I think the combination of NE/DBT is where we are going to end up in these patients, but particularly in the immediate post arrest situation when we often don't even have an arterial line, starting inodilators as single agents is risky. If using an inotrope as part of my therapy, I generally prefer dobutamine to milrinone due to its on/off titratability and immediate effect. Some of my CVICU colleagues are very comfortable giving loading doses of milrinone in a highly monitored ICU setting, conversely others will frankly describe experiences of fatal consequences after a milrinone load. If we load milrinone and don't like the consequences, we are stuck with them for hours due to the prolonged half life. So - I rarely if ever use milrinone in the ED.