ECMO - beyond protective ventilation

Extracorporeal Life Support for

Adults

-a terse primer for the busy intensivist-

Bucuresti, Februarie 2017

Linking ECMO to ARDS

O2-CO2 diagram (ROF)

Alveolar gas equation (ROF)

Relaxation pressure-volume curves

for lung and chest wall (ROF)

WOB and contributions from elastic,

viscous and turbulent forces (Otis)

Alveolar stress distributions (J.

Mead)

Baby lung hypothesis

Initially an anatomical concept

Tidal Volume scaled to IBW

Esp is nearly normal (Esp=E×FRC)

OLV and RM

The baby lung is in fact a sponge lung

- proning changes the densities and

homogenizes the parenchyma

Body weight vs FRC/EELV scaling of

VT

Stress raisers are redefined

Transpulmonary approaches

Strain/Stress emphasis with regards

to PP, sighs, 48h-NMB, spont. (PAV,

APRV, NAVA) vs controlled MV

Inflammation(PET) may sometimes

pertai espe ially to the a y lu g dependent on VTroi/EELVroi

40’s- 0’s

0’s-2000’s

currently

The 40’s to 0’s

The 40’s to 0’s

Modified after Gattinoni

Peffective = Papplied = Pplateau-Ppl

The 40’s to 0’s

Modified after Gattinoni

Peffective = Papplied × (Vopen/Vclosed)2/3 = (Pplateau-Ppl)× (Vopen/Vclosed)2/3

The 40’s to 0’s

In uniformly expanded lungs, transpulmonary pressure is the distending

pressure

In nonuniformly expanded lungs, the effective distending pressure differs from

the transpulmonary pressure and in the appropriate sign to reduce the

nonuniformity

The principal functional risk that it entails is increase in capillary transmural

pressure in regions which become subjected to abnormally high outward-

acting stress

Mead J. et al, J. Applied Physiol,1970 May;28(5):596-608.

There might be no safe ventilation

The 40’s to 0’s

For a given alveolar ventilation optimal frequency will be lowered by

▲ the dead space, by ▲ the nonelastic resistance, or by ▼the elastic

resistance, i.e. by increasing the compliance.

It also appears that for a given dead space,compliance and resistance,

the optimal frequency will increase with increasing alveolar

ventilation.

It must be kept in mind that the above analysis assumes that

expiration is passive.

The 40’s to 0’s

Frutos-Vivar et al, Med Intensiva. 2013;37(9):605---617 .

The 40’s to 0’s

The only feasible means of expanding dependent portions of the lung is by

placement of the body in such a position that ventilation of the normally

dependent portions is facilitated. The prone position appears best suited

for this purpose and merits serious consideration.

Bryan AC, AJRCCM, Vol. 110, No. 6P2 | Dec 01, 1974.

What did the 40’s to 0’s tea h us?

Interfaces between non-uniformly expanded alveoli bring about

excessive stress

This same stress endangers capillary structure

WOB can be optimized with regards to RR and VT for the same MV

WOB can be optimized with regards to the risk of excessive stress

especially in non-uniform, diseased lungs by tweaking the MV

PP could be used to lessen stress as it might be able to educe an FRC

augmentation/ improved lung or V/Q homogeneity


The 0’s to 2000’s baby lung and OLV era

Mathe ati al odeli g to syste ati ally characterize P-V curves and objectively derive physiologically and li i ally useful para eters (Venegas, 1997)

The P-V curve is in fact a recruitment curve (Hickling 1998, Albaiceta 2008)

Setting open-PEEP is an expiratory phenomenon, pertaining to the deflation limb (PMC) (Hickling 2001, Suarez-Sipmann 2007)

Open up the lung and keep it open (Lachmann, 1992) – VALI/VILI and the derived biotrauma (Slutsky, 1998) concept are undeniable and PV finds

its place (ARDSnet, 2000)

PEEP was not systematically tailored to recruitability/lung inhomogeneity (ALVEOLI 2004, EXPRESS 2008, LOVS 2008) but subgroup analysis

favours high PEEP in severe ARDS (Briel et al, 2010)

Venegas J., J Appl Physiol (1985). 1998 Jan;84(1):389-95 . Albaiceta GM, Curr Opin Crit Care. 2008 Feb;14(1):80-6.

Da of the 0’s to 2000’s strain/stress beginnings

Santos R.,Anesth Analg 2016;122:1089–100

STEPRM provides a lower mean airway pressure with a higher EELV corresponding to each step – equivalent to lower stress, lower strain

STEPRM entails a milder hemodynamic impact as it gradually improves Elung (Lim 2004, Odenstedt 2005) – equivalent to a RV protective effect,

re i i g “utter’s approa h to ards the est PEEP (Sutter 1975)

STEPRM is capable of reducing the biotrauma (Santos 2016)

Sighs provide similar long term benefits as STEPRM, recently having been shown to elicit favorable effects with regards to strain and

heterogeneity (Mauri 2015)

RMs launched the sighs and the sighs then launched the variable ventilation – delineating the fractal behavior of the lung which entails a power-

law profile as well as avalanche dynamics in opening up (Brewster 2005, Suki 1998, Suki 1994, Barabasi 1996)


Noisy ventilation is to be understood as VT variability following a random law or a fractal auto-correlated pattern

Straightforward benefits comprise an increased EELV for the same PEEP (equivalent to improved strain should the VT remain the same) and an

improved V/Q

Noisy is the e at h: oisy e tilatio , oisy perfusio / ardiopul o ary ypass (Mutch 2000)

APRV a d PAV/PP“ a d NAVA are oisier tha P“/A“B or a y IMV ode


With GE permission . With GE permission .

Karason S et al, Acta Anaesthesiol

Scand, 2000; 44: 578-585

.

FRC/EELV - side stream paramagnetic O2 analyzer with a response time of 480 ms (

AS/3 –Datex Ohmeda Helsinki-Finland, Olegard 2005 and Weissman 2007, LUFU)

Good agreement with helium dilution or CT based techniques (Chiumello 2008)

Hampered by volume-dependence of RecV instead of grams-of-tissue

Shifting the paradigm from IBW scaling to a y lu g capacity scaling

Sizing the Ba y lu g – Mattingley 2011 (Vrel/TLC at 40cmH2O close to 0.45±0.11)

Sizing the Ba y lu g – Beiltler 2016 (VRM at 40cmH2O predicts stress)

V1, V2 = recruited volume

)1(

22

2

ETNETN

V

FRCbaseline

breaths

N

First modern automated approximation of strain analysis (Gonzalez-Lopez 2012),

although in this study a different approach to strain was used (VT/EELV)

EELV derived RecV predo i ately measures a slow fraction of inflation of already

aerated lung tissue and not recruitment of collapsed al eoli (Stahl & Stenqvist

2014). Thus, RecV may just represent a functional recruitment(stress relaxation).

Cdyn dynamics bears the same urse . Decremental best PEEP (Suarez-Sipmann

2007) may just as well represent functional recruitment.

Stress index (constant flow, pressure-time curve) is another functional, ursed

parameter

What did the 0’s to 2000’s tea h us?

VT needs to be tailored physiologically (to the baby lung)

Spontaneous and variable might benefit those with mild and moderate ARDS (Yoshida 2016) but asynchrony( i.e. reverse triggering) (Akoumianaki 2013) has to be

looked for sedulously

Gaining homogeneity through a 48h NMB (Papazian 2010) or/and PP (Guerin 2013) improves the strain/stress, serendipitously, where you would expect the highest

number of unstable alveoli (stress raisers) – severe ARDS

Overdistension and atelectasis coexist to a varying degree – one needs to compromise (Plataki & Hubmayr 2010)

Permissive atelectasis is a useful but risky concept (Page 2003, Fanelli 2009, Albaiaceta 2011), especially enticing when on ECMO

PEEP selection based on lung mechanics and/or absolute esophageal pressure is unrelated to recruitability and similar in mild, moderate and severe ARDS

(Chiumello 2013) (12-15cmH2O). A CT-SP based OLV PEEP was found to be 16cm H2O (Cressoni 2014) equally in recruiters and non-recruiters

Higher PEEP is a prerequisite in recruiters (Briel 2010)


Where Lately…i ARD“

ARDS may very well be preventable by means of a primary, secondary and tetiary strategy. Prevention is supported by chaos theory (i.e.

butterfly effect) (Yadav & Gajic 2016)

ARDS mimickers have been described as CRF – with much too often DAD – and have been ascribed a dismal prognosis, sometimes

benefiting from CS (Gibelin & Mekonto Dessap 2016)

Berlin based ARDS comprises only 56.4 % DAD which is a marker of higher hospital mortality (Kuo-Chin Kao 2015)

Latent Class Analysis (LCA) was used to differentiate and characterize two ARDS subphenotypes responding differently to fluid and PEEP

– Phenotype 2 has higher levels of inflammatory biomarkers ,a higher prevalence of shock, lower serum bicarbonate, and a higher

prevalence of sepsis, compared with Phenotype 1 (Calfee 2014-2016)

Toward Smarter Lumping and Smarter Splitting: Rethinking Strategies for Sepsis and Acute Respiratory Distress Syndrome Clinical Trial

Design (Prescott & Calfee 2016)

Functional instead of anatomical recruitment will suffice and Cdyn based strategies seem adequate (Santos 2015)

Inhomogeneity indexes using rapid response O2 analyzer such as LUFU (Weissman 2007) will be able in the future to guide MV at the

bedside similarly to ALPE, MIGET (Bikker & Gommers 2014)

Driving Pressure has been shown to be a rather useful bedside touchstone for the a y lu g (Amato 2015)

Transpulmonary approaches could be able to yield a transpulmonary DP (Chiumello 2016, Loring & Hubmayr 2016)

ACP scores have been described and MV is more hemodynamic as never before (Mekonto-Dessap & Vieillard Baron 2016)

Transpulmonary approaches

Chiumello, Intensive Care Med (2014) 40:1670–1678.

Talmor,Crit Care Med 2013;41:0–0.

(Δ PPL/ΔV) / (Δ PAO/ΔV) = ECW / E RS (static)

PPL = PAO × ECW/ERS

PL,EXP =Total PEEP - PPL at end expiration

PL,PLAT = PAO,PLAT - PPL at end inspiration

PL=PAO×EL/ERS

Directly measured end-expiratory

transpulmonary pressure: Airway pressure at PEEP – esophageal pressure at PEEP

Release-derived end-inspiratory

transpulmonary pressure:

(Airway pressure at endinspiration-

atmospheric pressure)-(esophageal

pressure at end-inspiration-esophageal

pressure at atmospheric pressure)

Release-derived end-expiratory

transpulmonary pressure: PEEP-(esophageal pressure at PEEP-

esophageal pressure at atmospheric

pressure)

Strain/Stress concepts

ΔPL=(Pawplateau-Pesplateau)-

(Patm-Pes at atm pressure)

Strain= ΔV/FRC=(ΔVT+ΔPEEP)/FRC

ΔPL=ΔV×EL=ΔV/FRC×FRC×EL=ΔV/

FRC×ELsp=Strain×ELsp

ELsp=13.5

Max Strain = 2

Max Stress=27cmH2O

ΔPL=ΔPaw×EL/(EL+ECW)

The strain/stress concept is only a GLOBAL refinement

Strain/Stress caveats

In the presence of intratidal recruitment, strain will be lower

Chiumello, AJRCCM, Vol 178. pp 346–355, 2008.

Strain/Stress implications

Scaling VT to IBW is inadequate


Strain/Stress implications

Plateau pressure based PV is inadequate


Statics and dynamics in strain analysis

Alveolar stability may be the key as Albaiceta had stated in 2011.

Maximizing recruitment and low VTs are the equivalent to Protti’s study.

This is in fact equivalent to a low DP. Protti, Crit Care Med 2013; 41:1046–1055

Strain and stress at the bedside

EL=ΔPEEP/ΔEELV the chest wall and abdomen gradually can accommodate

changes in lung volume Stenqvist,Acta Anaesthesiol Scand 2012

Strain and stress at the bedside

• EL= ΔPEEP/ΔEELV

• ELSP = EL × FRC

• Stress = Strain × ELSP

• Strain global = (VT+VPEEP)/FRC

Acta Anaesthesiologica Scandinavica 60 (2016) 69–78

Caveat: there is VT and/or VPEEP dependent recruitment which will alter the strain as they are not taken into

account. The actual strain will be lower. Using EELV instead of FRC will underestimate the strain. Gonzalez-

Lopez et al. found 0.27 using EELV in 2012.

Let us keep it simple - DP

For a lung stress of 24 and 26 cmH2O, the optimal cutoff value for the airway driving pressure were 15.0

cmH2O (ROC AUC 0.85, 95 % CI = 0.782–0.922); and 16.7 (ROC AUC 0.84, 95 % CI = 0.742–0.936).

Conclusions: Airway driving pressure can detect lung overstress with an acceptable accuracy. However, further

studies are needed to establish if these limits could be used for ventilator settings.

Chiumello et al. Critical Care (2016) 20:276

It’s all a out the e ergy i put

Gattinoni et al, Intensive Care Med (2016) 42:1567–1575

Dissipated Undissipated

Bei g glo al does ’t help lung inhomogeneities

Cressoni et al, AJRCCM, Vol 189, Iss 2, pp 149–158


HEALTHY MILD

MODERATE

SEVERE

PEEP

?


High regional lung strains may be present even when global lung strain is within acceptable limits.

Such localized metabolic activation is prevented by reducing and homogenizing regional tidal strain

with high PEEP and low VT.

Wellman et al,Crit Care Med 2014; 42:e491–e500


Dynamic [18F]fluoro-2-deoxyd-glucose

scans to quantify metabolic activation,

indicating local neutrophilic

inflammation.


Borges et al, Acta Anaesthesiologica Scandinavica (2016)


Synchrotron imaging was used

to measure lung aeration and

regional-specific ventilation (sV ̇ ).

LUNG PROTECTIVE VENTILATION

RV PROTECTIVE VENTILATION

LESS MECHANICAL POWER PRESERVE/INDUCE HOMOGENEITY

“OMETIME“ IT’“ NOT ENOUGH

THERE MIGHT BE NO SAFE VENTILATION

DISSOCIATE GAS EXCHANGE FROM MECHANICS

ECLS – ECMO/ECCO2R

LUNG PROTECTIVE VENTILATION

RV PROTECTIVE VENTILATION

LESS MECHANICAL POWER PRESERVE/INDUCE HOMOGENEITY

“OMETIME“ IT’“ NOT ENOUGH

THERE MIGHT BE NO SAFE VENTILATION

DISSOCIATE GAS EXCHANGE FROM MECHANICS

ECCO2R – SUPERNOVA TRIAL = OLV (EX) + UPV

Friday Night Ventilation

300 200 100

MILD MODERATE SEVERE

DP = Paw_pl-PEEPt = �

<20cmH20 <15cmH20 <12cmH20

INHOMOGENEITIES

� 6ml/kg IBW <6ml/kg IBW <4ml/kg IBW

� � + ≈ H >15cmH20

�

ECMO

ECCO2R

NMB 48h

Prone Position

Modified after Gattinoni L.

ECMO didactics

Introduction to ECMO History

Current Status

Risks and benefits

Membrane gas exchange physics and

physiology

Oxygen content, delivery and consumption

Shunt physiology

Types of ECMO

Future applications

Research

Physiology of the diseases treated with

ECMO Neonatal RF

Pneumonia

ARDS

Pulmonary embolism

Sepsis

Postoperative congenital heart disease

Heart transplantation

Cardiomyopathy and myocarditis

PreECMO procedures Notification of the ECMO Team

Cannulation procedures

Initiation of bypass

Responsibility of team members

Criteria for ECMO Patient selection

Selection criteria

PreECMO evaluation

Contraindications

Selection of ECLS support(VA,VV, VA-V)

Blood products and coagulation Blood products and interactions

Blood product management of the bleeding

patient

Coagulation cascade

Blood surface interactions

Heparin pharmacology

Activated clotting times

Anticoagulant monitoring studies

Protamine, Amicar and other drugs

Recombinant clotting factors

Disseminated intravascular coagulation

Mechanical emergencies and

complications on ECMO Circuit disruption

Raceway rupture

Cavitation

System failure

Air embolus

Inadvertent decannulation

Clots

Management of complex ECMO cases Surgery on ECMO

Transport on ECMO

Weaning from ECMO Technique s and complications

Pump and gas flow weaning techniques

ACT during weaning

Ventilator changes during weaning

Trial off

Decannulation from low flow

Decannulation Personnel needed

Medications required

Potential complications

Vessel ligation

Vessel reconstruction

Percutaneous approach

Post ECMO complications Platelet and electrolyte alterations

Short and long term development

outcome Institutional follow-up protocol

Literature review

Ethical and social issues Consent process

Parental and family support

Withdrawal of ECMO

Medical emergencies and complications

during ECMO Intracranial and other haemorrhages

Pneumothorax and pneumopericardium

Cardiac arrest

Arrhythmias

Hypotension and hypovolemia

Hypertension

Severe coagulopathy

Seizures

Hemothorax and hemopericardium

Uncontrolled bleeding

Renal failure

Daily circuit management on ECMO Aseptic techniques

Pump and gas flow

Pressure monitoring

Blood product infusion techniques

Circuit infusions

Management of anticoagulation

Circuit checks

Hemofiltration setup

ECMO equipment

Physiology of VA and VV ECMO Indications

Vessel cannulation

Physiology

Advantages and disadvantages

Cannulation and initiation of ECMO support

Daily patient management on ECMO Bedside care

Fluid, electrolytes and nutrition

Infection control

Respiratory support

Sedation and pain control

Hematology

Cardiac support

Pharmacological issues

Psychosocial

Abbreviation Definition Details

ECLS Extracorporeal life

support

All EC technologies and life support components including

oxygenation, CO2 removal, HD support; renal and liver

support may also be incorporated

ECMO

Extracorporeal

membrane

oxygenation

Older traditional term for EC life support that omits

reference to inherent additional life supports such as

haemodynamic support and CO2removal

VV ECLS

Veno-venous

extracorporeal life

support

Deoxygenated blood is drained from one or more major

vein and oxygenated blood returned to the RA; supports

respiratory function only and requires native heart

function to deliver oxygenated blood to the tissues

VA ECLS

Veno-arterial

extracorporeal life

support

Deoxygenated blood is drained from one or more major

vein and oxygenated blood pumped back into a major

artery, thus providing tissue perfusion in the absence of

adequate native heart function

ECPR

Extracorporeal

cardiopulmonary

resuscitation

Extracorporeal life support instituted during, and as an

adjunct to conventional CPR

VV-ECCO2R

Extracorporeal

membrane carbon

dioxide removal

Selective CO2 removal

AV-ECCO2R Arterio-venous

extracorporeal life

support

Pumpless ECLS, driving pressure is patie t’s arterio-

venous ΔP, supports CO2 removal

Gaffney et al,BMJ 2010;341:c5317)

Gaffney et al,BMJ 2010;341:c5317)

ECLS – most common conditions

ECLS – beginnings

Laffey & Kavanagh,Am J Respir Crit Care Med. 2017 Feb 1

1667 - Jean Baptiste Denis, physician to King Louis XIV experimented on cross-transfusing the blood of a human with that of a lamb, patient survived

1930 - John Gibbon MD and Mary Gibbon MD created a roller pump device for EC support as a response to the death of a patient suffering with PE

1953 - first use of the device by JG on 18 year old Cecilia Bavolek with ASD

1954 - cardiac surgeon C. Walton Lillehei operated via cross circulation with a bubble oxygenator he and Richard DeWall invented

1956 - Clowes invented membrane oxygenator

1957 - Kammermeyer invented the silicone rubber which was strong enough to withstand hydrostatic pressure and yet permeable to gas transfer

1972 - JD Hill first successful adult use of ECLS outside of the OR (posttraumatic ARDS, male, 24year old, aortic rupture)

1972 - Bartlett first to use ECLS on neonates (two year old boy, correction of TGV, cardiac failure)

1975 - Bartlett first to use ECLS for newborn with RF after meconium aspiration-Esperanza

1985 - first RCT o eo atal RF, Bartlett; play the i er ra do izatio ’

1989 - O’Rourke, ECL“ for eo ates ith PPH

1996 - UK Collaborative ECMO trial group – These preliminary results demonstrate the clinical effectiveness of a well-staffed and organised neonatal ECMO service. ECMO support should be actively considered for neonates with severe but potentially reversible respiratory failure

1979 - Zapol et al, RCT in VA ECMO for adult RF, 10% SR for both groups

1994 - Morris et al, RCT in VA ECCO2R for adult RF

2009 - Peek at al, CESAR trial, regionalized VV ECMO approach for adult RF

.

We recommend transferring of adult patients with severe but potentially reversible respiratory failure, whose

Murray score exceeds 3·0 or who have a pH of less than 7·20 on optimum conventional management, to a centre

with an ECMO-based management protocol to significantly improve survival without severe disability. This

strategy is also likely to be cost effective in settings with similar services to those in the UK.

ECLS – beginnings

ELSO registry January 2016

Let’s get i

ECMO is coming to your adult ICU

Barbaro et al, 2015

Let’s get read

ECMO is coming to your adult ICU

Let’s get read

ECMO is coming to your Adult ICU

ELSO Registry data

Let’s get read

ECMO configurations

ML is parallel to NL

ML is in series with

NL

Euler Liljestrand ▼

Lung alkalosis▲

RECIRCULATION

-

+

Resorbtion

atelectasis if

FiO2ML > FiO2NL

ECMO membrane

Cross current flow between gas and blood

Fi k’s La of Diffsion

Effective Diffusivity

=porosity

= constrictivity

τ= tortuosity

ECMO membrane

≈ hours weeks

Oxygenator overview

ECMO circuit

P1 = negative suction

pressure, see for

chattering/cavitation(

▼preload?)

P2 = positive ejection

pressure

P3 = pressure drop of

the oxygenator

ECMO gas transfers

O2content/dl = (Hb×SatO2×1.39)+(pO2×0.0031)

VO2ML = BF×(CoutO2×CinO2)

VO2NL = CO×(CaO2-CvmixO2)

VO2tot = VO2ML+VO2NL

VCO2NL = alvPCO2×RR×(VT-VD)=NLETCO2×MV

VCO2ML = MLETCO2×GF

DO2 depends on Hb and BF/CO/R

VCO2 depends on GF and is relatively

independent of BF

BF/CO > 60% => adequate oxygenation dis

soci

ati

on

Sch

mid

t et a

l

Inte

nsiv

e C

are

Me

d (2

01

3) 3

9:8

38–

84

6

VV ECMO recirculation

VO2ML = BF×(CoutO2×CinO2)


Gillon et al, Crit Care Med 2016; 44:e583–e586

VV ECMO – which shunt to begin with

VV ECMO – PaO2 as a function of R/BF -different BF-

Increasing R/BF will forestall oxygenation especially at low CO/BF

At high CO/BF, it does ’t atter a y ay

VV ECMO – SvmixO2 as a function of BF/CO -different VO2s-

SvmixO2 chiefly depends on SvO2(tissues), BF/CO and R when Hb is constant

At increasing VO2, for steady SvmixO2 one needs to increase the BF

Increasing Hb makes sense especially when not on ECMO

Full ECMO support should help the clinician resist unnecessary transfusion

VV ECMO – SvmixO2 as a function of Hb -different BF-

VV ECMO – PaO2 as a function of BF -different CO-

I reasi g the BF ill saturate the shu t a d e e tually the PaO2 ill soar, quite similar to the O2 dissociation curve

At the same BF, increasing the CO will bring about an increase in DO2 and

consequently PvO2 will rise. The same holds true if CO is stable and BF will

vary

VV ECMO – PvO2 as a function of BF -different CO-

VV ECMO – PaO2 as a function of BF -different shunts-

Increasing shunts(severity of lung injury) will mandate higher BF(BF/CO) to

achieve the same PaO2

VV ECMO – PaO2 as a function of BF -different FiO2NL-

I reasi g the BF ill e e tually saturate the urre t shu t a d the PaO2 will then soar, similar to the ODC. The higher the FiO2NL, the quicker it will

soar.

Increasing FiO2NL creates the chance of O2 toxicity.

VV ECMO – PaO2 as a function of BF -different FiO2ML-

I reasi g the BF ill e e tually saturate the urre t shu t a d the PaO2 will then soar, similar to the ODC. The higher the FiO2ML, the quicker it

will soar.

I reasi g FiO2ML ay ot e ise as it’s ee sho to eli it resorbtion

atelectasis when FiO2ML > FiO2NL .

Cannulae - definitions

Access cannulae – drain blood from the venous system into the ECMO circuit

Single-stage cannulae

Multi – stage cannulae

Return cannulae – deliver blood back to the patient

Single stage

Distal perfusion cannula – deliver blood antegradely into the FA

Double lumen cannulae

Cannula length

Long cannulae (55cm) – e ous

Short cannulae (15-25cm) – arterial . Return blood in both VA ECMO and VV ECMO

(fem-jug) and to access blood in high flow VV or in VAV. They have side ports to connect

to distal perfusion cannulae.

Multi-stage access cannula

Return cannula

Distal perfusion cannula

Double lumen cannula

Doufle, Crit Care. 2015; 19: 326

ECMO MODES

VV ECMO VA ECMO

Femoro-femoral

High-flow

Femoro-jugular

Dual lumen(Avalon)

Standard fem-fem

Emergency fem-fem

High-flow

Central

VPA ECMO

Femoro-femoral VV

Cavo-atrial flow direction

Access cannula(multistage) within hepatic IVC, 21-25 F

Return cannula(single stage) within RA, 21-25 F

Δd=10-15cm

Limited maximum flow rates, bed bound

High-flow VV

Starts with bi-femoral approach

An additional short access (arterial) cannula is

inserted in the RJV with the tip in the SVC, at a

safe distance from the RA cannula in order to

prevent visible recirculation

Bi-cavo-atrial flow direction

Allows high flows, easy to start off CRRT but

increases rate of complications

Fem-jug VV

Access cannula tip at the inferior cavo-atrial

junction, 21-25 F multistage

Return cannula is short (arterial), tip in the very low

SVC, 19-23 F single-stage


Allows high flows, easy to start off CRRT

Bed bound

Single cannula VV

Single cannula, two lumens, RJV

Two access stages (SVC & IVC), return port towards

TV

Bi-Cavo-atrial flow direction

Allows ambulation but technical difficulties at

insertion, large cannula (27-31 F), awkward to

implement CRRT

Fem-fem VA


Access cannula(multistage) within hepatic IVC, close to

RA, 21-25 F

Return cannula(single stage) within the common FA, 17-

21 F, lying in the common IA/lower aorta

Backflow cannula is mandatory, inserted in the common

FA and directed into the superficial FA

May need conversion to V-A-V if lung injury coxists with

preserved cardiac function

Emergency Fem-fem VA


Access cannula(multistage) within hepatic IVC, close to

RA, 19-21 F

Return cannula(single stage) within the common FA, 15

F, lying in the common IA/lower aorta

Ba kflo a ula is a dator , BUT it’s i serted o l after ECMO is established

Same disadvantage as the previous plus possible

inability to support CRRT

Much easier to initiate due to smaller cannulae

High-flow VA

Access cannula tip at the inferior cavo-atrial

junction, 21-25 F multistage

Return cannula is short (arterial), tip in the very low

SVC, 19-23 F single-stage


Allows high flows, easy to start off CRRT

Bed bound

ECMO START-UP TOOLKIT

Patient Selection -VV ECMO-

1. In hypoxic respiratory failure due to any cause (primary or secondary) ECLS should be considered when the risk

of mortality is 50% or greater, and is indicated when the risk of mortality is 80% or greater.

a. 50% mortality risk is associated with a PaO2/FiO2 < 150 on FiO2 > 90% and/or Murray score 2-3.

b. 80% mortality risk is associated with a PaO2/FiO2 < 100 on FiO2> 90% and/or Murray score 3-4 despite

optimal care for 6 hours or more.

2. CO2 retention on mechanical ventilation despite high Pplat (>30 cm H2O)

3. Severe air leak syndromes ELSO 2013

Ca 't make my own decisions

Or make any with pre isio

Absolute contraindications to all forms of ECMO 1. Progressive and non-recoverable heart disease (and not

suitable for transplant)

2. Progressive and non-recoverable respiratory disease

(irrespective of transplant status)

3. Chronic severe pulmonary hypertension

4. Advanced malignancy

5. Graft versus host disease

6. Unwitnessed cardiac arrest

7. Cachexia due to an underlying progressive chronic

disease

Specific absolute contraindications to veno-venous

ECMO 1. Severe (medically unsupportable) heart

failure/cardiogenic shock

2. Severe chronic pulmonary hypertension and right

ventricular failure (mean pulmonary artery

pressure approaching systemic blood pressure)

3. Cardiac arrest (ongoing)

Relative contraindications to all forms of ECMO 1. Age>70

2. Duration of conventional mechanical ventilation >7

days, with high inspiratory pressures

(Pplat>30cmH20), high FiO2 (FiO2 >0.8)

3. Trauma with multiple bleeding sites

4. Severe immunosuppression (transplant recipients >30

days, advanced HIV, recent diagnosis of

haematological malignancy, bone marrow transplant

recipients)

5. Intracranial bleeding

6. CPR duration >30 min without documented

neurological recovery

7. Severe multiple organ failure

8. CNS injury

9. BMI <18 or >40

Adapted after

Guy’s a d “t Tho as’ NH“ Fou datio Trust

Hemodynamics – mercurial behaviour?

In our cohort, an increase in pH was the only ECMO-related effect that

correlated with the reduction in pressor requirements we observed.

Improved PVR/RV function

(ACP score▼)

Improved ino-vasopressor

responsiveness

COMPREHENSIVE TTE/TOE before assignment

to rule out severe RV/LV failure

The ACP score -predicting VV ECMO dependent hemodynamic benefit-

Pneumonia as cause of ARDS

Driving pressure > 18 cmH2O

PaO2/FiO2ratio < 150 mmHg

PaCO2 > 48 mmHg

1

1

1

1

> 2

Comprehensive echo exam is

mandatory

Mekontso Dessap et al

Intensive Care Med (2016) 42:862–870

ACP defined as a dilated Rv in ME4CV

[end-diastolic RV/left ventricle (LV) area

ratio [0.6] + septal dyskinesia in the

transgastric short-axis view of the heart

Having a plan might be of help

We recommend transferring of adult patients with severe but potentially reversible respiratory failure, whose

Murray score exceeds 3·0 or who have a pH of less than 7·20 on optimum conventional management, to a centre

with an ECMO-based management protocol to significantly improve survival without severe disability. This

strategy is also likely to be cost effective in settings with similar services to those in the UK. CESAR TRIAL

Optimise ventilator settings

Slow recruitment manoeuvre, Cdyn-

PEEP/EELV-PEEP(Engstrom)/FiO2-

table based/Express-trial/Gattinoni

VT<6ml/kg/IBW, Pplat<30, DP<15

I:E ratio 1:1

RR 20-30

Optimise IAP (<20)

Consider PP, NMB

Optimise hemodynamics

ITBVI 850-1000ml/m2

EVLWI<15

PMSA approach (Parkin)

TTE/TOE screening

Flow monitoring (lactate, ScVO2,

diuresis, CRT, mottled skin score)

Keep alb > 30g/L

Hb>7-8g/dl

+

Negative fluid balance –

deresucitation

Assess FR, then fill

IF PaO2/FiO2<80-100 OR pH<7.2(RA) OR not able to achieve PV AND <7days of MV

Assess Murray score, if >3 OR ph<7.2

CT chest + RM

Significant LR

APRV

Phigh 24-28

Plow 0

I:E 10:1

HFOV

RM, bias flow 40

Initial f 6Hz

CDP<30 cmH2o

Significant ΔD-V

PP

Minimal LR OR

recruitable BUT barotrauma present

ECMO

FiO2 > 0.5

PEEP > 10

ECCO2R

pH<7.2

AND

FiO2<0.5

At 24-48h

APRV

PaO2/FiO2<80 OR

pH < 7.2 (RA) OR

Phigh>30

HFOV

PaO2/FiO2<80 OR ΔPaO2/FiO2<38% OR

pH < 7.2 (RA) OR

CDP >30

Prone position

PaO2/FiO2<80 OR

pH < 7.2 (RA) OR

Phigh>30

ECMO/ECCO2R

Patient Selection -VA ECMO-

Potentially reversible, severe, refractory cardiogenic shock in patients who have

failed alternative therapy.

DECATECHOLAMINIZATION Singer & Matthay, Crit Care. 2011;15:225

Selective V1A(ie

Selepressin) (He X et al) Clonidine

&Dexmedetomidine

Beta-blockers (Morelli

et al) Ivabradine (MODIFY)

Levosimendan

(LEOPARD)

Omecamtiv Mecarbil ?

Specific physiological indications (after 1-12

hours of commencement of inotropic support)

1. persisting lactate >3mmol/L

2. persisting cardiac index <2L/min/m2

3. evidence of end organ dysfunction

4. trans-thoracic echocardiography with left

ventricular ejection fraction <30% and aortic

velocity time integral (Ao VTI) <8cm.

Causes of cardiogenic shock

1. Viral cardiomyopathy

2. Cardiac toxic drug overdose

3. Septic cardiomyopathy

4. Peripartum cardiomyopathy

5. Massive pulmonary embolism

To be considered patients should:

1. Have no significant chronic medical co-morbidities

2. Be aged 60 years old or less

3. Be deemed to have a potentially reversible

aetiology

4. Be within 24 hours of the onset of cardiogenic shock

5. Not to be excluded from cardiac transplantation

Contraindications to VA-ECMO

1. Symptomatic chronic cardiac failure (NYHA 3 or 4)

2. Progressive chronic respiratory failure

3. Advanced malignancy

4. End-stage renal failure requiring dialysis

5. Advanced HIV

6. Significant immunocompromise from any cause

7. Child-Pugh B or C chronic hepatic failure

8. Any other significant medical co-morbidity

Contraindications to VA-ECMO

9. Age >60 years old

10. Severe peripheral arterial disease, severe aortic

valve regurgitation or aortic dissection precluding

cannulation

11. Any condition precluding heparinisation, including

active haemorrhage, intracerebral haemorrhage or

allergy

12. CPR >45 minutes (estimated time to cannulation)

13. Out of hospital cardiac arrest

Patient Selection -MODS precludes ECMO success-

Respiratory failure with septic shock & >3 of:

1. Lactate > 10

2. Norepinephrine > 1.5mcg/kg/min

3. Severe myocardial dysfunction

4. Advanced microcirculatory failure

Cardiogenic shock & > 3 of:

1. Lactate > 15

2. Advanced microcirculatory failure

3. AST/ALT > 2000 or/and INR > 4.5

4. Anuria > 4h

ECMO Guideline, Alfred Hospital, Melbourne

Mo za’s flo hart, “a galli et al, ECMO-

Extracorporeal life support in adults, 123-124

B. Riou, Réanimation 28 (2009) 182–186

Ca 't make my own decisions

Or make any with pre isio

To su arize…

Eddy Fan et al,Intensive Care Med (2016)

42:712–724

Basic tips and tricks

1. VV ECMO – bifemoral vein approach is preferred especially in

retrieval/emergency situations

2. Cannulation SHOULD be US-guided

3. Fluoroscopy SHOULD be used to document position except for peri-

arrest/arrest situations

4. US may be used instead of fluoroscopy

5. Once wires are in place, give 50UI/Kg of heparin systemically

6. Before starting ECMO, check ACT > 200sec

7. Establish baseline anticoagulation 10UI/Kg/H, APTT 1.5-2

8. Single dose Teicoplanin 400mg and Gentamicin 5mg/kg at line

insertion. Atb are not otherwise specifically prescribed.

9. VV ECMO – target BF/CO > 60%

10. VA ECMO – target 70-80% of COpred, aim for PP>10-20mmHg, SR

11. VAV – aim 1L venous flow using gate clamp

12. VA ECMO - Flow meters on the combined arterial return and the

aortic return to assess backflow cannula flow

13. VA ECMO – monitor using NIRS/pulse oximeter bilaterally

14. Assess for Harlequin syndrome

15. Never stop gas flow when on VA

Circuit flow 50-80 mL/kg/min

Sweep gas flow 50-80 mL/kg/min

Fractional inspired oxygen (sweep gas) 100%

► reduce accordingly when on VA

► reduce so that ML FiO2 ≈ NL FiO2

Inlet pressure (centrifugal pump) > -100 mmHg

Oxygen saturation (return cannula) 100%

Oxygen saturation (drainage cannula) > 65%

Arterial oxygen saturation VA > 95%; VV: 85%-92%

Mixed venous oxygen saturation > 65%

Arterial carbon dioxide tension 35-45 mmHg

pH 7.35-7.45

Mean arterial pressure 65-95 mmHg

Hematocrit 30%-40%

Activated clotting time 1.5-2.0 times normal

Activated partial thromboplastin time 1.5-2.0 times normal

Platelet count > 100,000/mm3 or >100,000 if bleeding occurs


Initial Settings and Goals After the

Institution of ECMO

Adapted after Sidebotham et al, Journal of

Cardiothoracic and Vascular Anesthesia, Vol

24, No 1 (February), 2010:

Arterial blood gases 3-4 hourly

Pre - and post - oxygenator blood gases daily

Activated coagulation time 1-2 hourly

Complete blood count 6 hourly

Coagulation tests 6 hourly

D dimer & AT3 daily

Thromboelastograph 12 hourly

Blood chemistry, renal function, and liver

function 12 hourly

Plasma free hemoglobin (<0.1) 12 hourly

Blood cultures from the circuit daily

Triglycerides daily

CK, Troponin, NT ProBNP/BNP (BNP t1/2 is

shorter) if VA ECMO daily


Schedule of Initial Point of Care Testing



24, No 1 (February), 2010:

Comprehensive cardiac

echo TTE/TOE daily

pre/post ECMO

Comprehensive lung US

daily

Douflé et al. Critical Care (2015)


100% FiO2 test (Cilley) – VV daily

Cdyn trends – VV daily

SRM to challenge the baby lung – VV ?

Transmembrane pressure gradients/R – VV/VA daily

Pre and post oxygenator blood gas – VV/VA daily

Sedation management – no fentanyl/midazolam

(Shekar K, Crit Care 2012), choose propofol and

alfentanil

Inotropic support to preserve PP 10-20mmHg – VA

Daily echo + AoVTI – VA

Cerebral oximetry ± lower/upper limbs bilaterally – VA

Right radial/brachial ± anywhere but the cannulated

femoral artery – VA

VV ECMO – refractory hO2

Strategies to i rease the lood’s o ge o te t:

i.increase of ECMO flow;

ii.increase of blood oxygen-carrying capacity

Strategies to reduce recirculation

Strategies to reduce oxygen consumption:

i.sedation and neuromuscular blockade

ii.therapeutic hypothermia

Manipulation of CO and intrapulmonary shunt:

i.β-blockers infusion

ii.prone positioning

Switch to VA ECMO or a hybrid configuration(VAV)

Adapted after Montisci, ASAIO Journal

2015; 61:227–236:

VV ECMO – refractory hO2

Levy B,Intensive Care Med (2015) 41:508–510:

VV/VA ECMO – clot formation

Pump head (centrifugal)

►Rising plasma free hemoglobin

►Change in sound of pump

Oxygenator

►Increasing pressure gradient across the oxygenator

►Fall in postoxygenator PO2

►Increase in sweep gas needed to maintain PaCO2

Tubing/bridge

►Visible fibrin strands or thrombus

Nonspecific markers of blood clot formation

►Increasing D-dimers or fibrin degradation products

►Increased bleeding



24, No 1 (February), 2010:

VV ECMO – recirculation

At higher circuit flows, recirculation

decreases effective circuit blood flow

Abrams et al, ASAIO

Journal 2015; 61:115–121

VV ECMO – recirculation

ELSO Guidelines, 2015

Increasing the distance between the cannulae

Use a bicaval, dual lumen cannula

Use a high flow configuration – it will cause less negative pressure => less recirculation

Sangalli et al, ECMO-Extracorporeal life

support in adults, 123-124



Constant improvement over the days



One patient lived



Patie t a gai s VO through his o NL hilst patie t’s NL de ours O o i g from the ML.



One patient lived



Trends from a progressive reduction in sweep flow

VA ECMO fem-fem – specifics

VA ECMO fem-fem – specifics (1st)

Optimise ventilation

Increase ECMO flow to push the mixing cloud

Switch to V-A-V configuration or even VV if cardiac function has improved

Switch to central VA (right subclavian or true central)

Christopher Lotz et al. Circulation.

2014;130:1095-1104

HARLEQUIN

Brain ischaemia

Cardiac ischaemia

VA ECMO fem-fem – specifics (2nd)

Increase ECMO BF to reduce pulmonary BF in the setting of a good RH but you may risk

an even more increased LVEDP

Get an IABP at once if not already initiated (A. Combes 2016, Reanimation)

Do an atrial septostomy

Switch to central VA (right subclavian or true central)

Christopher Lotz et al. Circulation.

2014;130:1095-1104

Start Levosimendan

Not so decatecholaminizing after

all, is t’t it?

After septostomy

VA ECMO fem-fem – specifics (3rd)

Backflow cannula is mandatory if not in periarrest context

Post decannulation period is also critical as it can elicit a reperfusion compartment

syndrome

Ventilation strategies

Permissive atelectasis is tricky

As the lung was conceived to contain air

I many patients the lung may proceed to total

consolidation before recovery occurs, but this might be

avoided by maintaining some inflation pressure as high

pressures are decreased, and by supplying nitrogen to

prevent adsorption atele tasis ELSO 2016


Decreasing ΔP/Pplateau/Pinsp/RR decreased meanPaw gravitational atelectasis

FiO2ML > FiO2NL � � �� (VV)

VCO2ML ↓RQNL PAO2 ↓ if PiO2 and PaCO2 are the same

Sighs are part of our normal physiology

When on VA, beware of pulmonary tissue alkalosis; PV still aplies

a Assuming airway resistance of

10cmH2O/l/s

Gattinoni L, Curr Opin Crit Care 2017 &i

Critical Care (2016) 20:130

Weaning strategies -VV ECMO-

If CXR/ LUNG ultrasound improves, Cdyn/ TV/ Cilley test improve, consider weaning

Decrease flow in steps to 1L/min at sweep FiO2 100% OR decrease flow to 2L/min then

decrease sweep FiO2 to maintain SaO2 > 95%

When SaO2 stable on these settings, on VV, trial off by clamping sweep on vent rest

settings PSV or CPAP 20 cm H2O. If SaO2 >95and PaCO2 <50 x 60 mins, come off OR

further observe on minimum PS

If PaCO2 >50 stay on at low flow, go to selective CO2 clearance mode

Venous duplex 24-48 hours following the removal of cannulae to assess for DVT

after ELSO Guidelines 2016

Weaning strategies -VA ECMO-

Daily comprehensive echo (LUNG + CARDIAC) exam is mandatory

Never stop the sweep gas flow!

As the BF is reduced in steps (0.5l) to 25%, perform repeated echos – observe AoVTI

(>12cm), RV-LV interaction, LV/ RV distension

Minimum low flow is 1l/min for 30 min max OR clamp circuit and allow recirculation

for trial period of 30 minutes to 4 hours AND flush cannulae with heparinized saline

continuously

Anticoagulation is paramount during weaning sessions (consider APTT 2-2.5)

Consider paired central venous and arterial blood gases to assess tissue perfusion

Consider Levosimendan if not already administered (Affronti, ASAIO Journal 2013;

59:554–557)

Venous/arterial duplex 24-48 hours following the removal of cannulae to assess for

DVT

after ELSO Guidelines 2016


LVOT_VTI > 10cm

LVEF > 20-25%

TDSa > 6cm/s

ECMO flow 1-1.5l/min

LVOT_VTI > 12cm

LVEF > 20-25%

TDSa > 6cm/s

Aissaoui ,Réanimation 2015

EC

MO

flo

w 1

-1.5

l/m

in


ΔRVEDV > 0

AND

ΔLVEDV < 0

As ECMO flow is weaned

ECMO - beyond protective ventilation

Health & Medicine

Transcript of ECMO - beyond protective ventilation