All posts by Matt Rowland


About Matt Rowland

Clinical Lecturer in ICM and Anaesthetics University of Oxford Oxford University Hospitals NHS Foundation Trust

Post-resuscitation care #LIVES2017

How we best manage patients after cardiac arrest is an area full of controversy. This session was designed to cover aspects of uncertainty surrounding this area with presentations from Alain Cariou on who should have early coronary angiography, Gavin Perkins on oxygenation and ventilation and Alain Combes on ECMO for refractory cardiogenic shock:

Three take home messages for me:

  1. Currently no indication for coronary reperfusion in non-STEMI. Need to consider on case-by-case basis locally and await evidence from multiple ongoing RCTs
  2. Need to pay close attention to O2 and CO2 in acute period post-arrest. Avoid hyperoxia and (most interestingly) avoid hyPOcapnia.
  3. ECMO-CPR shows promise in the management of cardiogenic shock post-arrest but needs large RCT data

Alain Cariou: Indications for early coronary reperfusion

Results from the PROCAT registry study from Paris is pretty clear that we should ideally perform early coronary angiogram in all survivors of cardiac arrest. However no RCT data to prove improved outcomes in those with non-STEMI so question still remains unclear

All patients with OHCA at his centre get immediate PCI – very different in UK due to lack of RCT data – hence reticence from cardiologists in UK

And whilst this seems wrong, it may not be such a difficult approach to justify given that a post-hoc analysis of TTM trial showed NO benefit from PCI for all-comers.

However, we may have some clear RCT data very soon…. The DISCO trial (great name) in Finland is a RCT randomised to immediate cath lab or ICU then decision. Similar trials in France (EMERGE) and US (PEARL) as well as trials in Germany/Holland are asking similar questions so we should soon have more data to guide our decision making in this period.

Still data from the PROCAT-II trial shows that there is a culprit lesion in 1/3 pts even without STE. We therefore need more data to help select those patients most at risk or identify better those likely to survive with preserved neurological function

So…can we predict neurological outcome better? CAHP score is one option he uses locally. Need more work on this though to help guide future management.

Great talk by Alain Cariou overall – was asked a question about in-hospital arrest? His answer is that it is a different population  and needs more research to be conducted.

Prof Gavin Perkins on Oxygenation and Ventilation post-ROSC

First question is what is the optimal level of oxygenation during/immediately after CPR? Nice review on this here

There is a growing awareness that like many things in ICM (e.g. fluids)  less may be more when it comes to oxygenation in the critically unwell. Data from animal trials suggest that outcomes are likely to be worse with higher FiO2 post-ROSC.

Arterial hyperoxia is also independently associated with higher in-hospital mortality compared to either hypoxia or normoxia

However, this is a difficult effect to isolate due to the fact that unmeasured confounders (e.g.severity of illness) can contribute in registry studies of FIO2 & outcome. For example, those patients who are more unwell tend to need higher FiO2

There is potentially a signal of increased heart damage too with higher oygenation although this was not reproduced in a larger 2017 trial. 

FiO2 1.0 assoc with higher biomarkers of brain injury e.g. enolase but in a small study

So pulling this together clinically – what shouldcurrent guidance in absence of large RCT


What about the role of CO2 post-arrest? 

Hypocapnia seems to be independently assoc with worse outcomes and hypercapnia protective – interesting result that goes against much of what we teach in managing brain injury on ICU – is cerebral vasodilation with slightly higher ICP better than lower CO2 and cerebral vasoconstriction.

Big take home for me: AVOID HYPEROXIA and HYPOCAPNIA post-arrest

Alain Combes on ECMO in cardiogenic shock

CPR duration is key still in determining outcomes – 

There has been a series of papers showing signal of improved outcome using ECMO-CPR approach – mainly from Japan where they have a very efficient resuscitation network

Data from a 2016 systematic review on ECMO-CPR showed a 27% survival compared to 15% with routine care. However, this survival benefit drops when you isolate those patients left with good neurlogical outcomes (18% v 7%).

So, what are Alain Combes’ local guidelines for E-CPR?


What is best strategy for E-CPR? E-CPR in specific settings in the management of refractory OHCA is feasible and can lead to a significant increase in neurological intact survivors.

Guess what though? Current evidence needs to be confirmed by a large RCT….. 😉 Luckily a few currently in the pipeline…


Overall a really enjoyable session and thanks to the ESICM and the speakers!









ESICM Regional Conference Athens 2017: Management of Shock – Others

Right then – last session on other techniques/approaches to managing shock…..

Mechanical assist devices – Alain Combes

Classical indications for mechanical assistance:


INTERMACS classification of indications for mechanical assist devices


LVADs should be for stable patients – not for acute cardiogenic shock


What about IABP? SHOCK-2 trial Lancet 2013 —> no difference between control/balloon

Indication downgraded from I —> III: no indication for routine use in cardiogenic shock

Should it now be in the “Museum of Medicine” — along with the iron lung and swan ganz? 😉


ESC/ – evidence now low

Tandem heart pVAFD

Not available in Europe – only US


Difficult transeptal cannulation – fair number of issues with this device to be fair

Impella miniature intraaortic pump

Available in Europe

Up to 4L/min (Impella 5.0)


  1. Cost – 10-15K euros for few days use
  2. Concerns about haemolysis

Recent study – IABP v Impella —-> No difference in mortality

HeartMate PHP


No data as of today for this pump

Major issues – only drain LV. Not of use in RV. New Impella for RV but cost ~20K euros



Worth remembering that it’s low cost compared to Impella (but still 8-9K Euros per patient….)

Accepted indications:

A: ST-elevation with profound cardiogenic shock?

Paper —-> ST-elevation with profound cardiogenic shock

Close to 50% survival and 68% weaning in survivors

B: End stage DCM?

C: Fulminant myocarditis?

Most surviving without need for complex heart surgery/transplant

D: After cardiac surgery?

Old data but benefit —->

E: Post cardiac transplant?

What are the trends/emerging indications?

1. Septic shock with severe LV failure

Small study (n=14) but very unwell – SOFA score 18 with LVEF 16 and mean lactate 10

2. Pulmonary embolism


3. Post-cardiac arrest

Post-resuscitation syndrome

Conflicting data on E-CPR —> benefit or no benefit

4. Combination – ECMO + Impella

Take home messages:



Cristalloids or colloids? Balanced or not? – Luciano Gattinoni

Why do we give fluids?


Review from 2013 in NEJM on resuscitation fluids —> here

So which fluid and what is the price to pay in terms of “health”?


Low pressure


Mechanics of fluid – no difference. Volume that creates a pressure

Issue is what price we pay by giving different fluids

CHEST trial – small differences in Cr. No standard deviations. Be careful interpreting data





Individualising haemodynamic targets – Bernd Saugel

Precision medicine popular term – as is personalised medicine



Personalised medicine approach can be applied to haemodynamic management of ICU patients


Does personalising BP in the operating room improve outcomes?

Seems not to be important at first glance —-> MAP > 65 as food as one based on percentage reduction from baseline

But BP does not mean perfusion —-> autoregulation


SSC recommends target of 65 BUT state ” when a better understanding of any pts condition obtained, BP target should be individualised”

Asfar et al NEJM 2014 – here

No difference in high v low target BP

BUT —-> Patients with chronic HT in the  low target group = increased RRT


What about SV/CO etc?

Pearse et al. Cardiac output guided management —> here

Maximisation of SV may not equate to optimisation


DO2 targeted?

Achievement of preoperative DO2 value associated with reduction in morbidity —> here

How to combine PERSONALISED treatment approached with PROTOCOLISED care?


What is the future?

Smaller sensors to record biosignals without heavy monitors/machines/cables



Take home messages:



ESICM Regional Conference Athens 2017: How to assess perfusion

First session this morning. Talks focusing on SvO2, ScvO2, PCO2 gap, lacate and measurement/assessment of peripheral perfusion

Again a fair amount of focus on the microcirculation…..

Massimo Antonelli – SvO2/ScvO2, PCO2 gap

“Shock is the clinical expression of circulatory failure that results in inadequate cellular O2 utilisation”
Vincent et al. NEJM 2013
Aim of treatment: restoring lost balance between O2 demand from peripheral tissue and O2 supply
What are the signs of tissue hypoperfusion?
Clinical indices
Mottled skin, altered mental status, diuresis <0.5ml/kh/hr, hypotension/tachycardia etc
Haem parameters:
Increased O2ER and anaerobic threshold —-> SvO2/ScvO2/Lactate
Inadequate DO2 —-> CO/Hb/PCO2 gap
Impaired peripheral perfusion with normal macro-haemodynamics —-> microcirculation e.g. sublingual
  • SvO2 = VO2 from the whole body, ScvO2 = VO2 from mostly brain and upper arms
  • Absolute values are not interchangeable but trends over time are the same
  • Sedation may influence both measurements
  • Septic patients may have abnormally high measurements
Rivers – early GDT —> suggested a benefit to targeting ScvO2 (amongst other variables….)
But ARISE/ProCESS/PROMISE ——> not replicated…although corrected ScvO2 higher in Arise/Process/Promise compared to Rivers – are we speaking about same populations when comparing studies?
What are the drawbacks of using ScvO2?
ScvO2 often high in septic pts ——> VO@ decreased in septic shock patients
Unclear the impact of microcirculatory impairment e.g. DeBacker ICM 2010
Venous admixture?
What about the elevated PCO2 gap (A-V)?
Nice review here by Vallet in ICM 2013 and in LITFL here
PCO2 gap is marker of inability of adequate venous flow
Elevated PCO2 gap means that:
  1. CO is not sufficient under conditions of suspected tissue hypoxia
  2. Microcirculatory flow is not high enough or adequately distributed to clear the CO2 excess even in the presence of a normal CO

“PCO2 gap should be considered as a marker of the ability of an adequate venous blood flow to remove the CO2 excess rather than as a marker of tissue hypoxia”

Mallet et al. Minerva Anesth 2015

Can we use it clinically?
Yes e.g. in tandem with lactate —->
Take home messages:
  1. DO2 is important when O2 consumption is dependent on it
  2. Very low SvO2/ScvO2 are markers of tissue hypoxia and should be corrected
  3. Sepsis alters normal DO2/VO2 relationship such that ScvO2 may not always be a good marker of tissue hypoxia
  4. CO2 gap may unmask those patients who are going to develop tissue hypoxia and should be considered a marker of low flow state

Interesting question from the floor:

Q: Should we be worried about patients post-CABG with low SvO2 (e.g. PAC-measured)?

A: Low SvO2 not always a marker patient is unwell e.g. when exercising, SvO2 can drop to 25%. So need to assess on case-by-case basis

Andrew Rhodes – Lactate as a marker of perfusion

Sepsis remains a huge problem – recent paper this year:

 Surviving Sepsis Campaign (SSC) targets:

  • CVP
  • MAP
  • UO
  • ScvO2
 BUT – ARISE/PROMISe/PROCESS —> can do it but doesn’t improve outcome (despite not being as sick/no signal of harm)
Lactate is a surrogate marker of inadequate tissue perfusion. But lots of causes of high lactate e.g.
Screen Shot 2017-06-16 at 14.28.08
Lactate and outcome?
  • Increased levels are associated with increased organ failure and mortality
  • Reduced clearance of lactate is associated with increased morbidity and mortality
Screen Shot 2017-06-16 at 14.11.14
Best lactate cutoff for predicting poor outcome was 1.5:
Mortality below 1.5 = 17%, above 1.5 > 60% —->
Similar in children —->
So — does measuring lactate improve pt outcomes?
Serial measurement is more useful than single measurement – sensitivity/specificity of single lacate level has been debated
 But problems…..
How can we use lactate to guide resuscitation?
RCT by Tim Jansen on lactate to guide resuscitation – especially nice protocol
(**But – no difference in lactate between control/intervention group after treatment…..**)
Effect replicated in RCT by Chinese group:
One protocol suggested by the speaker:
Screen Shot 2017-06-16 at 14.27.44
 SSC 2016: “We suggest guiding resus to normalise locate in patients with elevated locate levels as a marker of tissue perfusion” – weak recommendation, low quality of evidence
But what percentage reduction should we aim for and how should we do that? Still unclear…..
Take home messages:
  1. Lactate remains the best biomarker for risk assessment
  2. Low lactate clearance is a good predictor of mortality
  3. At the present time, lactate clearance alone has not been proven to be an adequate end point for resuscitation
  4. Further trials are needed to demonstrate the efficacy of lactate clearance as a primary endpoint in the resuscitation of severe sepsis or septic shock

Jacques Duranteau – Peripheral perfusion

Again – emphasis on the importance of the microcirculation


Need real-time measurement of peripheral perfusion

Screen Shot 2017-06-16 at 14.53.45

Mottling score predicts survival in septic shock —-> 

Subjective assessment of peripheral perfusion may be useful —->
Nurses can reliably assess microcirculation at the bedside with high sens/spec —>
Can use TTE to measure AKI – “resistive index” in kidney at bedside
Screen Shot 2017-06-16 at 14.48.32
Can also assess brain perfusion:
Screen Shot 2017-06-16 at 14.53.23

LIVES 2016: Neuromonitoring in acute brain injury

Interesting session on current and future neuromonitoring in acute brain injury – mainly focused on bedside monitoring but also some imaging

Excellent introductory slide from Giuseppe Citerio about options currently available for monitoring so have bumped it to the top:


Also worth looking at – nice review on neurological prognostication after cardiac arrest:

Automated infrared pupillometry – Mauro Oddo

Infrared video pupillometry: infrafred camera, processor and LED calibrated light source in simple handheld device

Two main options:

Neurolight Algi-scan (ID-MED France)


NPi-200 (Neuroptics, USA)


Only moderate inter-rater reliability in pupillary assessments using standard clinical approach i.e. torch and subjective assessment:

Good inter-rater reliability for pupillometry. Big difference between standard assessment v pupillometry:

Quantitative devices also much better at diagnosing pupillary asymmetry (L v R) and therefore highlighting deterioration quicker

In cardiac arrest, during CPR – possible to detect recovery of light reflex with pupillometry. Linked to survival v no reflex:

Awaiting larger cohort study post-arrest – 288 patients included and hoping to present next year at LIVES 2017

Also of potential benefit in acute TBI – predicting uncal herniation:

Non invasive assessment of brain oxygenation – Pierre Bouzat

Firstly NIRS – what exactly are we measuring and how?

Early discussion of limitations. Light scattering by tissues. A fair number of estimations so no actual value for cerebral oxygenation e.g. variation in diffusion path-length factor (DPF) between patients and injuries may affect values .

What anatomical and physiological factors affect NIRS?

  1. Hb
  2. Skull thickness
  3. Area of CSF layer

Caution using NIRS with subdural haemorrahge – may not be able to exclude that you are measuring oxygenation of clot

Extracranial contamination – significantly affect NIRS measurements of cerebral oxygen saturation:

NIRS in subarachnoid haemorrhage: no relationship between absolute rSO2 values and DCI

Tissue oxygen saturation monitoring using MRI – may be a future technique for prognostication:

Question: Could NIRS be more useful as a dynamic variable rather than static number? Overwhelming take home from talk was a lot of concern about use of NIRS outside operating room. Potentially of use post-cardiac arrest and in ECMO

Quantitative EEG: Ready for use by general intensivists? – Giuseppe Citerio

Continuous EEG gives us more information than we had before and as a consequence can potentially do things differently e.g. intervene earlier

Caution though: James Cash Penney – “Theory is splendid but until put into practice, it is valueless”

Options for ICU EEG:

  1. Spot EEG (one occasion)
  2. Continuous EEG
  3. Quantitative EEG

But substantial barriers to adopting routine clinical EEG services on intensive care:

  1. Lack of uniform terminology
  2. No consensus on clinical significance
  3. Infrastructure
  4. Need to simplify complex info so clinicians can quickly ID issues
  5. Personnel – to apply the EEG and interpret results

Important to fully engage neurophysiology services to set up critical care EEG

Also – role of mobile app technology to help adoption on ICU

Potential is huge though