Category Archives: LIVES 2017 – VIENNA

Effect of Systematic Intensive Care Unit Triage on Long-term Mortality Among Critically Ill Elderly Patients in France

Hot Topics Session

It is well recognised that critically ill elderly patient have a higher mortality and therefore the beneficial effect of intensive care unit (ICU) admission variable ICU use among this population have let to significant difference in uptake.

Guidet and colleagues performed a cluster, randomised trial of admission versus standard care in 3036 elderly patients aged 75 years and above. In their multicentre randomised trail, suitable patients were allocated to routine or non-routine admission as per the following:


Outcome Measures

  • Primarily 6 months
  • Secondarily ICU admission rate, in-hospital death, functional status and quality of life.





  • Disappointingly there was no difference seen in any of the outcome measures, even after adjustment for differences in illness severity and patients admitted to ICU had an INCREASED risk of death at six months despite an increase ICU admission rates.
  • Functional status and physical quality of life at six months did not differ significantly.


What does this mean?

  • As our ICU population changes it may be that a systematic approach which admits all elderly patients has no effect upon outcome.
  • Further international trials are needed before we know whether this is applicable to other populations.

New Technology in Ventilation 25th September 2017 #LIVES2017

In respiratory failure, there is regional variability in oxygenation (and perfusion)- imaging can be used to monitor this. Point of care ultrasound for instance…

Electrical Impedance tomography can monitor regional changes as well

Oesophageal manometry can help us monitor transpulmonary pressure… – however is only used in about 1% of ARDS patients according to the LUNG-SAFE study…

Respiratory muscle functioning can be done using the NAVA device… – this may end up being key to keeping intrapleural driving pressure low (Amato)

Mechanical power can be roughly calculated at the bedside as a product of driving pressure and respiratory rate- this may become our key targeted variable in future (Amato)…

However both driving pressure and mechanical power remain static measures of lung mechanics. In future we’ll need dynamic bedside tools.

Ventilator dissynchrony remains a problem and contributes to mortality….


And of course there’s ECMO. Some patients still require ventilation while on ECMO and the reasons for this will vary- for some it will be gas exchange, for others it will be muscular (Camporotta).

There remain several unanswered questions in the ECMO population- how to wean, who needs (and doesn’t need) mechanical ventilation… hopefully answers will come.


The future may well be closed-loop ventilation, such as that seen with the Hamilton ventilators in their ASV mode.…




The ICU Airway- 25th September 2017 #LIVES2017


10-20% of the ICU population will be difficult to intubate- and this can lead to significant morbidity and mortality, as the excellent UK NAP4 audit showed NAP4: Executive summary | The Royal College of Anaesthetists

3% of patients will have an intubation related cardiac arrest…

It’s been suggested that we treat every ICU patient as a difficult intubation. Assess the airway beforehand- the MACHOCA score has been recommended The MACOCHA score is feasible to predict intubation failure of … – NCBI

Tips to optimise intubation?

Should we use VL first line? Maybe- but MACMAN says no…

And what about high flow oxygen as apnoeic oxygenation? Maybe or maybe not?…

Or combine HFNC with non-invasive ventilation for the ultimate oxygenator?…


So some controversies remain- hopefully with more data to come we can make ICU intubation safer.

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:

Screen Shot 2017-09-30 at 22.30.52

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…

Screen Shot 2017-09-30 at 22.32.03

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!)