All posts by segun olusanya

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

  1. IN ACUTE MYOCARDIAL INFARCTION- BETA STIMULANTS OR BETA BLOCKERS?

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 academic.oup.com/eurheartj/arti…)

So why discuss beta blockade at all? Well, initial trials suggested a benefit of beta blockade during AMI (circ.ahajournals.org/content/early/…), however later trials failed to show a benefit (acc.org/~/media/Clinic…) 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 ncbi.nlm.nih.gov/pubmed/27052688)

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 (journals.plos.org/plosone/articl…)

However adrenaline is associated with a WORSE outcome in cardiogenic shock (ncbi.nlm.nih.gov/pubmed/27374027)- 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) journals.lww.com/ccmjournal/Abs…
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.

 

2: BETA AGONISTS IN SEPTIC SHOCK

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 ncbi.nlm.nih.gov/pmc/articles/P… and dobutamine link.springer.com/article/10.100…

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.

 

3. BETA BLOCKERS IN SEPTIC SHOCK

There’s a link between hypoxia and inflammation nejm.org/doi/full/10.10… – by increasing oxygen delivery beta blockade may reduce the inflammatory response.

However beta adrenergic stimulation improves flow in sepsis ncbi.nlm.nih.gov/pmc/articles/P… – so why is beta bl0ckade being talked about?

Well, there’s rat data showing that early beta blockade improves outcomes in sepsis ncbi.nlm.nih.gov/m/pubmed/19829… and then there is human data suggesting that prior treatment with beta blockers improves outcomes in septic shock journals.lww.com/ccmjournal/Abs…

Then came this- the Morelli paper showing improved mortality with esmolol in septic shock ncbi.nlm.nih.gov/pubmed/24108526

So how does it work? It may reduce cardiac output but overall tissue perfusion seems preserved ncbi.nlm.nih.gov/pubmed/27411452

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!)

 

 

 

Preventing Lung injury in ARDS- Ranieri (Keynote 25th Sept 2017) #LIVES2017

Claudio Ranieri starts us off with a discussion and reminder about the importance of transpulmonary pressure- elegantly described in this excellent NEJM paper http://www.nejm.org/doi/full/10.1056/NEJMra1208707?af%3DR%26rss%3DcurrentIssue …

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Titrating ventilation to transpulmonary pressure may have a mortality benefit, as seen in this H1N1 series ncbi.nlm.nih.gov/m/pubmed/22323…

Spontaneous breathing isn’t always protective- extreme negative intrathoracic pressures can cause large increases in transpulmonary pressure ncbi.nlm.nih.gov/pubmed/10593817

Targeting low transpulmonary pressures isn’t just of benefit to those with ARDS- surgical patients (nejm.org/doi/full/10.10…) and organ donors (ncbi.nlm.nih.gov/pubmed/21156950) have both seen benefits from a lung protective approach.

There is some evidence that ventilator induced lung injury causes direct neurological damage (ncbi.nlm.nih.gov/pubmed/23962032)- could this be directly contributing to the delirium we see?

 

FURTHER READING

Try Jon-Emile Kenny’s excellent pulmonary physiology series here pulmccm.org/main/2017/unca…

 

Incorporating advanced echocardiography into clinical practice #LIVES2017

It was delightful listening to Paul Mayo deliver this excellent talk based on his clinical experience.

Critical care echocardiography is a different beast to the traditional “echo lab” approach favoured by cardiology. Our environment does not lend itself well to hour long studies per patient recording every measurement.

His unit adopts a flexible approach, deploying aspects of advanced echo as needed to answer specific clinical questions. Occasionally a full study will be performed. For quality control reasons, all their TOEs (TEEs) are full studies.

NYC is staffed by 10 attending and 6 “night owls”, all of whom are competent in general critical care ultrasound. 3 of the team are competent in advanced echo.

As an example of how they apply advanced skills, All shocked patients will get VTI to estimate stroke volume. Other measurements are used selectively such as:

  • E/e’ to estimate filling pressures
  • Bubble studies for hypoxemia
  • Quantitative studies of valve function
  • Precise measurements of RV function (PASP, PADP, PAMP, RV S’, PAT, TAPSE)
  • Regional wall motion abnormality assessments
  • serial echoes for dobutamine or nitric oxide trials

Images are saved, and relevant findings documented in notes (except TOEs which all get a ful, report). Interesting cases are discussed at a weekly meeting.

For those training in advanced CCE, Mayo recommends ALL views and ALL measurements are performed in a specific sequence, and images rejected if they are suboptimal. Not only does it upskill the user, it brings credibility to the field and reassures our cardiology and imaging colleagues.

These were certainly useful points that all of us in the critical care and imaging community should take note of.

 

Advanced Echo: Right Ventricular failure #LIVES2017

Prof Vieillard-Baron delivered this lecture and began by pointing out a great overall review on the topic https://t.co/5TZsRZIZ12

 

Causes:

1: pulmonary embolism – management strategies here https://t.co/Cwc7drmG5z

 

2: Acute myocardial infarction

3: Mechanical  ventilation – especially if a PFO is recanalised https://t.co/NwC6XPI91H

4: ARDS (https://t.co/pVj3GBSJnE)- here are some expert guidelines to manage haemodynamics https://t.co/VJjyQbbZnA

5: chronic RV failure- differentiate this from acute using RV wall thickness and the PASP (again, 5 minute sono has a wonderful example https://t.co/hmDtjSNZJ6)

If your RV is failing, Prof Vieillard-Baron recommends noradrenaline as it’s “magic for the RV”!