Beta-agonists/Beta Blockers- why and when? (25th Sept 2017) #LIVES2017


Brief summary: If the patient’s haemodynamics are stable, leave them alone! If they are in cardiogenic shock, consider inotropic support while getting them to the cath lab immediately (based on the new ESC guidelines…)

So why discuss beta blockade at all? Well, initial trials suggested a benefit of beta blockade during AMI (…), however later trials failed to show a benefit (…) leading to a downgrade of the original recommendation. There may still be a benefit in patients with established low EF who are having an MI, though.

Timing of beta blocker administration may also be an issue (the earlier the better, as suggested by

Patient in shock? Planning to use inotropes? It’s recommended to monitor the cardiac output, as well as other markers of organ perfusion.

Should we use catecholamines, inodilators, or both? This study suggests a benefit from combined inodilator/catecholamine therapy (…)

However adrenaline is associated with a WORSE outcome in cardiogenic shock ( increases troponin, creatinine and urea.

ESC guidelines recommend weaning vasopressors as soon as possible based on that data.

Patients can be risk stratified using biomarkers (ST2, BNP)…
Questions from the audience included choice of inotropes (combination agents recommended over catecholamines alone, based on above data) and whether there was still a role for PDE-III agents (milrinone, enoximone) and levosimendan.

Regarding the latter- there has been no mortality benefit so far, however they are better than using adrenaline alone.



Jean-Louis Vincent started off with a fantastic aide memoire on inotropic action:

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Inotropes have varying effects on the cardiovascular system- they are not all the same. They also have profound metabolic effects – such as the lactataemia seen with adrenaline…

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Their effects may be dose dependent, as seen with isoprenaline… and dobutamine…

Inotropes may help to recruit the microcirculation and reduce the inflammatory response in critical illness. According to JLV, inotrope induced myocardial infarction is rare in the ICU! If we are worried about tachycardia, ivabradine may have a role in obtunding that while allowing the other catecholaminergic effects to continue…

Individualised therapy seemed to be the take home message here.



There’s a link between hypoxia and inflammation… – by increasing oxygen delivery beta blockade may reduce the inflammatory response.

However beta adrenergic stimulation improves flow in sepsis… – so why is beta bl0ckade being talked about?

Well, there’s rat data showing that early beta blockade improves outcomes in sepsis… and then there is human data suggesting that prior treatment with beta blockers improves outcomes in septic shock…

Then came this- the Morelli paper showing improved mortality with esmolol in septic shock

So how does it work? It may reduce cardiac output but overall tissue perfusion seems preserved

So who would benefit? Daniel De Backer suggests:

-High contractility

-Low cardiac output state

-Non-fluid responders

-Diastolic dysfunction

– Individuals with systolic anterior motion of the mitral valve on echocardiography- De Backer reckons up to 30% of septic shock will have this!

(So basically do an echo to find out!)