Category Archives: Respiratory

ESICM LIVES 2017 NEXT Day – ECMO #LIVES2017

ECMO Course

Session 1 – Antonio Pesenti, Refractory Hypoxaemia Therapuetic Strategies

Before deciding on support, first need to know what targets. One might be PaO2? If you climb up a mountain it’s low? Is this important – not according to Grocott in NEJM 2009 where low levels were compensated for by higher Hb.

Rx hypoxia broadly divided as follows

  1. Treat cause – antibiotics, thrombolysis, etc, etc
  2. Increase FiO2
  3. Reduced atelectasis – PEEP
  4. Increase pulmonary blood flow
  5. Reduce venous admixture – ECMO

Reabsorption atelectasis complicates high FiO2 administration.

PEEP prevents collapse = recruitment manoeuvres are needed to open collapsed lung. Indeed main difference between traditional IPPV & HFOV/APRV is high airway pressure – theory being more recruitment AND retention.

Don’t forget effects of heart + shunt upon O2 but iNO doesn’t work.

The benefits of proning extend beyond its effects on PaO2 – failure to improve this variable does not mean you should stop doing it.

Longer term, hypoxemia is a risk factor for long-term neuropsychological impairment but HYPEROXIA IS BAD.

 

Session 2 – Jan Bakker, Haemodynamic effects upon ECMO

Very variable! Limited prospective scores – ENCOURAGE might be useful for VA, or clearing fluid balance on day three but in essence little evidence.

When considering you need to ask:

  • What other support have you got?
  • What configuration are you using?

Peripheral VA-ECMO can significantly increase after load – first consider dilators, then increase forward flow whilst remember to treat acidodsis/anaemia. If that doesn’t work, add an IABP.

With VV-ECMO, RV afterload will fall with PVR effect because of beneficial effects upon CO2/PAO2.

 

Session 3 – Weaning from ECMO Giacomo Grasselli

No science to this – lack of definite criteria, indications from guidelines and local protocol and personal experience

Four scenarios

  1. wean ECMO, then vent
  2. Emergency discontinuation, e.g. bleed
  3. First wean vent, then ECMO
  4. Withdraw

Weaning from VV is weaning gas flow – you don/t need to reduce flow

Weaning GF increases muscle effort and needs vent support 

ELSO guidelines

You need haemodynamic stability as well as respiratory improvement. Measure oxygen delivery – the target is tissue oxygenation NOT PaO2.

How long do you keep the gas off? – Karolinska say 4 hours

Some authors propose leaving cannulae in place for put to 48 hours flushed with heparinised solution – practice VARIABLE

How to decannulate VV?

  • Stop/reduce heparin
  • Put purse string around insertion cannula
  • Clamp lines
  • Stop pump
  • Remove pipe allowing small amount of leakage to red air embolism
  • Manual compression 20 min for venous and 30 min for arterial.
  • Close monitoring distal perfusion for arterial and consider  vascular ultrasound in both as high incidence of clot or injury

 

Keynote – Michael QUINTEL, 50 years of ECMO

ECLS first developed by John Gibbon and Mali in 1936 in response to sudden death young patient with PE and first used in ORD for ASD repair May 1953

First trials negative – but badly done – so perhaps can be better interpreted as even if you do ECMO badly, you don’t kill everyone…

CESAR trial goo.gl/T6tdEL

First oxygenators bubble before developed hollow fibre oxygenator

The development of heparin-coated circuits allowing limiting APTT was one the major steps in reducing morbidity and mortality

Single centres such as Michigan have led the way – now more adult/paed, less neonates

Then H1N1 prompted exploration http://ja.ma/2xp301Q

H1N1 make worldwide excessive use of the technology but there is no new real data.

Reasonable data about risk/benefit ratio does not exist. Cerebral micro emboli are universal. 85% get DVT.

Is informed consent even possible?

 

Pro: Is ECMO always an Option? Steffen Weber-Carstens

UK evidence summarised by @CochraneUK in 2015

Similar International Consensus Position Paper by Coombes and colleagues on what defines an ECMO centre

Triage essentially as duration IPPV significant risk factor of deaths.

Con: Giacomo Bellani 

In one series, 87% of referrals had at least one relative contraindication

25% of patients in CESAR didn’t get it

EOLIA trial has not reported and is ongoing – we are in the infancy of what we know

16% rates of head bleed

20% nosocomial infection

Why use more resources when you can achieve the same thing with less? LungSafe shows we still don’t get optimium PEEP, NMBA, fluid balance and supportive care in ARDS.

 

EuAsia 2017 Day 2: Spontaneous breathing and ARDS

Role of NIV (M Antonelli)

Mechanism of VILI: role of transpulmonary pressure (PL)

PL = Paw (ventilator) – Ppl (muscle)

Low Vt is almost impossible to obtain during NIV

The problem with ARDS trials….

  • Different disorders lead to ARDS
  • Different pts respond differently

Recognition of ARDS by clinicians is poor especially mild ARDS

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References

Fifty Years of Research in ARDS. Spontaneous Breathing During Mechanical Ventilation – Risks, Mechanisms &Amp; Management

Neuromuscular Blockers in Early Acute Respiratory Distress Syndrome

The LUNG SAFE study: a presentation of the prevalence of ARDS according to the Berlin Definition! 

 

HFOT (CY Lim)

Physiological effects

  • Warmth and humidity in upper airways
  • Reduction in inspiratory resistance
  • Positive pressure in nasopharynx
  • Washout of nasopharyngeal dead space

HFNC for ARDS

  • Hypoxia
    • increase end-expiratory volume
    • help homogenise distribution of ventilation
  • High dead space fraction
    • increase tidal volume
    • decrease Vd/Vt

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References

High-Flow Oxygen through Nasal Cannula in Acute Hypoxemic Respiratory Failure

Oxygen delivery through high-flow nasal cannulae increase end-expiratory lung volume and reduce respiratory rate in post-cardiac surgical patients

Nasal highflow improves ventilation in patients with COPD 

 

The dark side of spontaneous breathing in ARDS (T Yashida)

Harm of spontaneous breathing

  • Better oxygenation with paralysis
  • Less inflammation
  • Less work of breathing after paralysis
  • Improve mortality with early paralysis (in severe ARDS)

Pt may have a PS 5 and PEEP of 5 but with strong effort, can generate Vt of 12ml/kg –> barotrauma

The beneficial effects of spontaneous breathing is seen only in mild ARDS

Mechanism of harm

  • Large Vt and Pl
    • The negative pressure of SV can lead to high Pl
  • Pendelluft
    • Injured lung do not have homogenous ventilation
    • Worsening inflammation
  • Worsening capillary leak
  • Asynchrony

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References

Spontaneous Effort Causes Occult Pendelluft during Mechanical Ventilation

Fifty Years of Research in ARDS. Spontaneous Breathing During Mechanical Ventilation – Risks, Mechanisms & Management

EuAsia 2017 – Day 1: Respiratory failure and organ interaction

Respiratory failure and organ interaction

Lung failure (S Jabar)

Classical mechanism of damage – volutrauma, barotrauma, biotrauma, atelectatrauma

Low pressure and low volume ventilation but… –> reduces alveolar ventilation

You need to recruit before increasing PEEP

Low TV and high PEEP has a preventative role in the development of ARDS

All ICU patients are at risk of developing ARDS

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References:

Happy 50th birthday ARDS

What’s new in ARDS: can we prevent it?

8 year trends on ARDS

Berlin definition ARDS

 

Pump failure (A Pesenti)

Sick muscle and/or too much work for muscle (they need to work less or to rest)

Measuring auto PEEP – measure pressure at end expiration

2017-04-06 08.25.03

References:

Respiratory Muscle Contribution to Lactic Acidosis in Low Cardiac Output

The role of PEEP in patients with chronic obstructive pulmonary disease during assisted ventilation 

Changes of Respiratory Mechanics in COPD Patients from Stable State to Acute Exacerbations with Respiratory Failure.

 

Diaphragmatic dysfunction (CY Lim)

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References:

Diaphragm dysfunction assessed by ultrasonography: influence on weaning from mechanical ventilation.

Ultrasonography evaluation during the weaning process: the heart, the diaphragm, the pleura and the lung

Diaphragm dysfunction on admission to the intensive care unit. Prevalence, risk factors, and prognostic impact-a prospective study.

Patterns of diaphragm function in critically ill patients receiving prolonged mechanical ventilation: a prospective longitudinal study

Diaphragmatic dysfunction and respiratory illness (Review)

Evolution of Diaphragm Thickness during Mechanical Ventilation. Impact of Inspiratory Effort.

Mechanical Ventilation and Diaphragmatic Atrophy in Critically Ill Patients: An Ultrasound Study. 

Effect of theophylline on ventilator-induced diaphragmatic dysfunction

 

Heart Lung Interaction (M Cecconi)

Fluid responsiveness doesn’t mean the pt needs fluids

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The Changes in Pulse Pressure Variation or Stroke Volume Variation After a Tidal Volume Challenge Reliably Predict Fluid Responsiveness During Low Tidal Volume Ventilation* 

Respiratory variation in inferior vena cava diameter: surrogate of central venous pressure or parameter of fluid responsiveness? Let the physiology reply

Predicting volume responsiveness by using the end-expiratory occlusion in mechanically ventilated intensive care unit patients. 

What role does the right heart play?

 

Lungs don’t interact just with the heart (K Zirpe)

Lung open to environment

2017-04-06 09.40.03

References:

Mechanical Ventilation as a Mediator of Multisystem Organ Failure in ARDS

Cardio-pulmonary-renal interaction

Brain-lung crosstalk: Implications for neurocritical care patients

Pulmonary-intestinal cross-talk in mucosal inflammatory disease

 

Respiratory Monitoring to Guide Treatment

…or “You don’t know what you don’t know”

A bit of a personal piece for me. And I think the title says it all. Unless you have all of the information, then it’s hard to have all of the answers. And this is very true for ventilation. We all know that ventilation can cause as much harm as it tries to cause good in some patients, but also in some parts of some patients. But who are those patients, and are we causing a little bit of harm in all of them (that could be avoided)?

Oesophageal Pressure Monitoring

Laurent Brochard makes a compelling case for measuring this.

9780007505142And after a short talk I get it. We make many assumptions about what’s going on at the pleural and alveolar level when we drive ventilation. But we don’t really know and now perhaps we can. And when you look at the respiratory mechanics you of course see that, like all science, and to use the words of Ben Goldacre, “I Think You’ll Find It’s a Bit More Complicated Than That”.

It seems that true ventilator-patient interaction might be more accessible when you measure oesophageal pressure, and potentially the opportunity for true tailored or individualised patient therapy, a recurring theme at this year’s ESICM.

Oesophageal pressure monitoring might be the ‘missing measurement’. And it’s not just for ARDS either. In his review, and in the interview I had the pleasure of having with him this morning, Brochard explains that during the spontaneous phase of breathing on the ventilator (weaning) there might be more information to had by measuring the oesophageal pressure.

Good information, good decisions

This all needs to be integrated into patient care, and added to the clinical picture, just as an ultrasonographer like me, who also uses a stethoscope, I won’t be hanging up the latter just yet, or making decisions about my patients just because of something I am shown on a screen.

The future of oesophageal pressure monitoring is interesting, and the ESICM’s PLUG Section are working towards refining this new old technology and hopefully giving us the thing that quickly prizes money from people’s hands, some outcome improvements.