Updates in respiratory critical care 1/11/17 – #FOAMED #FOAMcc

These are the notes Dr David Popple (ITU Consultant), took during the Updates in Respiratory Critical Care Meeting at the RCOA back in November. I merely took them, expanded them and added links etc. Thanks to him for providing these. Update in renal replacement coming too. So…onward, what’s new then?

Identifying and managing ventilator asynchrony

  • Approx 1/3 of ICU pts affected.
  • If the patient is asynchronous, adjust the vent rather than sedation.
  • If >10% breaths are asynchronous, this increases duration of ventilation, mortality and number of tracheostomies.

Types of asynchrony:

  • Support
    • Too much ASB causing periodic breathing
    • Too little ASB causing over-work
  • Timing
    • Trigger asynchrony – most commonly due to iPEEP (pt can’t exceed this to trigger), trigger may be set too high…compounded by neuromuscular weakness.
    • Treat by reducing trigger, reduce ASB (reduces insp. time and increases exp. time, hence reducing iPEEP), reduce sedation, increase PEEP to meet iPEEP.
    • Double triggering with a large inspiratory effort is a sign of pt still inspiring when vent has moved to exp phase.
  • Auto triggering
    • When trigger on vent is too sensitive
  • Flow asynchrony – flow mismatch. i.e. inadequate PS which increases WOB.
    • Treat by increasing PS.
  • Cycling asynchrony
    • Inspiration cycles ‘off’ when flow reduced to 25% of max during expiration.
    • Can adjust this to when flow = 10% exp. flow etc.
    • Early flow change on the graph is often a marker of premature exp. triggering

See also:

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Weaning from mechanical ventilation

  • Around 10% of patients will experience difficulty in weaning and will spend on average >28 days on vent.
  • 25% of them will need home NIV!

Approach to patient looking for cause

  1. Is it CNS (trigger)?
    • Do neuro exam +/- imaging
  2. Is it neuromuscular (transmission)
    • do neuro exam +/- imaging and Nerve Conduction Studies (hyper-reflexia and muscle wasting is most often MND)
  3. Is it Respiratory
  4. Is it cardiac (pump)
  • Muscle weakness occurs early and fast.
  • Diaphragm wastes 2x as frequently as periph muscles.
  • Both muscle and diaphragm wasting predict poor outcome.
  • Wasting is worse in MOF than single organ failure.
  • Pts with poor premorbid condition (i.e. LVF/COPD), take much longer to rehabilitate
  • Sometimes, especially in elderly with chronic disease, need to stop wean and rehabilitate, then weaning tends to happen on its own.
  • Physio’s are the key!
    • We should focus more on number of sitting to standing / distance walked per day, rather than arbitrary weaning 1cmH2O/day!

See also:

The ICS 2007 Weaning Guidelines

See this weaning review here.

Also this from the BJAScreen Shot 2017-12-15 at 12.05.45


Hypercapnoeic respiratory failure

  • High CO2 in ARDS is associated with higher mortality, higher CVS failure, higher renal failure rate.
  • No RCTs have examined this.
  • Noted from observational studies with attempts to control for confounding variables

 Approach to hypercapnoea on PCV:

  1. Do insp hold to determine plateau pressure and adjust vent pressure to achieve VT around this pressure, (as per Dixiegraph below)
  2. Do Exp hold to determine iPEEP (total PEEP) with vent set to zero end exp. pressure
  3. Try adding vent PEEP and reassess iPEEP to see if it remains the same or improves.
    • Keep vent PEEP at it’s highest level possible so as not to increase total PEEP. (Improves V/Q matching and CO2 removal).
  4. Adjust RR so there is zero flow at end of expiration.
    • Avoid increasing frequency to the point where it encroaches on higher flow section of flow time loop!
  5. Adjust Ti to achieve sub max VT.

Driving pressure 2

Is it ARDS?

See our section here on big papers in ARDS.


  • Pts often labelled as ARDS, when the likelihood is that it’s severe pneumonia.
  • Be suspicious when there is single organ failure, a prodromal illness and haemoptysis

Interstitial Lung Disease

  • Difficult with this in the background, as minimal infection on top will give a picture of ALI.

Other points

  • Diffuse alveolar haemorrhage often do better on ECMO
  • Look at eosinophils – normally low in critically ill.
  • Acute eosinophilic pneumonia often present with normal eosinophils and all symptoms and signs of CAP.
  • Can be precipitated by smoking.
  • Later eosinophils go up and need pulsed methyl-pred / other immunosuppression.
  • Early liaison with Rheumatology/resp.


  • New guidance published 2017
  • Found very poor care for NIV pts nationally.
  • Most pts on NIV in UK very frail (Rockwood frailty index)
  • Should be started when pH 7.3-7.35
  • Should not be used in all pts
    • 54% pts deemed inappropriate.
    • Associated mortality 35%

 FOB in the critically ill

  • Little new except increasing use of DNAse for clearing thick airway secretions (no evidence in adult ICU, but there may be in paeds post cardiac surgery).
  • Need to have endobronchial blockers on standby, in case of pulm. haemorrhage from bronchoscopy in high risk bleed cases.

Lung Ultrasound

  • Little new
  • If B lines/lung sliding seen – no pneumo
  • To diagnose a pneumo, need absence of sliding and to see lung point (point below which you see lung sliding and above none).
  • Don’t view as diagnostic tool, but clinical aid like stethoscope.

See our Section here

Submassive PE – Thrombolysis is the treatment of choice?

  • Mostly same as new guidelines
  • General move to use ½ dose thrombolysis for anything less than very near death PE.
  • Suggested use PESI to risk stratify – if high risk mod PE, should come to ICU.
  • Then can observe whilst anticoagulating and thrombolyse early if deteriorates.
  • Suggested use of UFH in this group, as able to stop this to thrombolyse, but not very logical as time to reverse anticoag effect 4-6 hours and T1/2 of Alteplase is 4-5 mins, so not reversed by time thrombolysis finished.
  • Also, often pts subtherapeutically anticoag with UFH, so not getting benefit and probably more likely to deteriorate and need tPA!
  • Therefore reserve UFH for AKI/liver dysfunction.
  • Not much support for thrombolysis in submassive PEs, as numbers needed to harm (major or intracranial bleed) worse than NNT.
  • Use of catheter guided thrombolysis not proven yet.
    • Reserved for centres with experience and adequate interventional radiology cover to support it and saved for cases with high bleeding risk. Not for Us at NGH!
    • Newer options for I.R. include ultrasonic clot disruption and hydrodistruction. Not yet studied properly.
    • New study starting to look at ½ dose rtPA for PEs to look more at this.

See also:


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What we said about it all

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Notes by: Dr David Popple (ITU Consultant)

Edited by: Dr Jonny Wilkinson

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