VenovenousECMO physiology f extracorporeal life support where an external artificial circuit carries venous blood

A form of extracorporeal life support where an external artificial circuit carries venous blood from the patient to a gas exchange device (oxygenator) where blood becomes enriched with oxygen and has carbon dioxide removed. This blood then re-enters the patient circulation.

2. •A form of extracorporeal life support wh
ere an external artificial circuit carries ve
nous blood from the patient to a gas exc
hange device (oxygenator) where blood
becomes enriched with oxygen and has
carbon dioxide removed. This blood then
re-enters the patient circulation.

4. •Oxygen Consumption(VO2)is controlled by
tissue metabolism, hence decreased at rest,
paralysis, and hypothermia.
•VO2is increased by increases in muscular
activity, infection, hyperthermiaand increased
levels of catecholamineand thyroid hormones.

5. O2Delivery –DO2
=5/1 = DO2/VO2Ratio
Cardiac index = 3L/min/m²
Sata= 100%
CaO2= 200cc/dl
VO2 120cc/min/m²
CO
Ca
600cc
120cc
Cv
Satv = 80%
Sata= 100%
VO2 120cc
Metabolism
Fuel + O2

6. •Oxygen Delivery(DO2) is the product of cardiac
output(CO)times arterial oxygen content(Ca)
•Oxygen Consumption(VO2)is the amount of oxygen
consumed across the lungs(identical –systemic
metabolism)
•O2delivery should be 4-5timesthe amount of O2
consumption.
•Venous blood saturation measures the ratio
between DO2 and VO2

7. •Defined as : VO2or calculations based on
VO2(Volumes of oxygen consumed multiplied by
5cal/L estimates the energy expenditure
expressed in calories)
•The value of oxygen consumption in normal
resting humans is 3-5cc/Kg/min in adults.
•VO2can increase up to ten times with exercise,
but under catecholamine and sepsisit increases
to between 50 to 60%

8. •DO2is the amount of oxygen delivered to peripheral
tissue each minute or the product of arterial oxygen
content times CO.
•O2delivery is controlled by CO, Hbconcentration, Hb
saturation, and dissolved oxygen, in that order.
•The normal value of DO2is four to five times VO2
regardless of patient size.
•O2content of arterial blood(20cc O2/dl), is the same for
all patient ages.
•O2delivery is thus determined by CO

9. •O2content is rarely measured; accustomed to
describe blood oxygen as PaO2or Hb saturation.
•O2content is of utmost importance in the
physiologic management of critically ill patients.
•So let us look at the relationship in the following
figure.

10. 50 75 90 99 100
SAT
PO2
O2
content

11. Cardiorespiratory hemeostasis is the tendency to
maintain systemic oxygen delivery;
•In anemia the CO will increase until DO2 is normalized.
•In Hypoxia the CO increases, and in chronic hypoxia red
cell mass increases under the influence of erythropoietin
until systemic oxygen delivery is again normalized.
We should recognize and support these
mechanisms in the critically ill patient.

12. Example : The best treatment for a ventilated
patient who is:
•Hypoxic
•Anemic
•Tachycardic
•Hypotensive
•Hypermetabolic
Is Red Blood Cell Transfusion(rather than inotropic
support)

13. •Factors influence oxygen content:
•CaO2= (Hb) x (art Sat) x (1.36) + (0.0031 x paO2) oxygen content
•Hemoglobin example:
CaO2=(12x 1.0 x 1.36)+ (0.0031 x 100)= 16.63%
CaO2=(10.8x 1.0 x 1.36) + (0.0031 x 100)= 15%
•A 10% change in Hb causes a 10% change in oxygen content

14. •The amount of CO2produced during systemic metabolism each
minute(VCO2) is approximately equal to the amount of oxygen
consumed.
•The ratio of CO2production to oxygen consumption is known as
respiratory quotient, depending on energy substrate it varies from
0.7 for fat to 0.8 for protein to 1.0 for carbohydrate.
•Under normal conditions the rate and depth of breathing are
controlled to maintain the arterial PCO2at 40mmHg.
•Even a slight increase in metabolic produced CO2will result in
proportionate increase in alveolar ventilation.
•Unlike systemic O2delivery, CO2excretion is not affected by
hemoglobin or blood flow but is sensitive to changes in ventilation.

15. •For this reason , and because CO2excretion is
much more efficientthan oxygenation in the Lung,
CO2removal can be maintained at normal levels
during severe lung dysfunction.

17. •Robert H Bartlett, MD
–Director of the Extracorporeal Life Support Program
–The University of Michigan Extracorporeal Life Supp
ort Team
•Largest ECMO experience in the world (>1,000
cases prior to 2000)
•1985 Prospective Randomised Trial in
Neonatal Respiratory Failure,
Pediatrics 1985,76(4)479-87
–1 patient in conventional arm (died)
–11 patients in the study arm (all survived)

20. Conventional ventilation or ECMO for Severe Adult Respiratory failure
Lancet 2009, 374:1351-63
Single ECMO centre at Glenfield Hospital, UK
Survival without severe disability (confined to bed, or una
ble to dress/wash oneself)by 6 months
•ECMO: 57 in 90 patients (63%)
•Conventional ventilation: 41 in 90 patients (47%)
•Relative risk reduction in favour of ECMO
•0.69 (0.05–0.97; P = 0.03)
•NNT to save one life without severe disability is 6

22. The Australia and New Zealand Extracorporeal Membrane Oxygenation (ANZ ECMO) Influenza Investigators
JAMA.2009;302(17):1888-1895. Published online October 12, 2009(doi:10.1001/jama.2009.1535)
During winter 2009 (1 June 2009 to 31 August 2009), Australia
& New Zealand ICUs
68(34%) required ECMO out of 133 patients with IPPV
For patients given ECMO
•48/68 (71%) survivedICU
•32/68 (47%) survived hospital
•16/68 (24%) still in hospital
•6/68 (9%) still in ICU
•14/68 (21%) died
9% of VV ECMO convertedto VA ECMO due to worsening meta
bolic and Hemodynamic status(concomitant septic shock)

23. VS

24. Return limb
positive pressure
(70to 300mmHg)
Positive pressure
(100 to500mmHg)
Drainage limb
Negative pressure
(-20to-100mmHg)

25. Bad lung
Good Heart
Good lung
Bad heart
Bad lung
Bad heart
V-V 0 X X
V-A peripheral X 0 0
V-A Central (not required) 0 0
V-V ECMO V-A ECMO

26. Arterial Cannulation
•Femoral artery
VA-ECMO for CPR
•Simple and rapid to establish
•Temporary for retrieval
•Limb ischemia
Upper-body Hypoxemia

28. Disadvantages: NO
•Normal lung blood flow
•Oxygenated lung blood
•Pulsatile Blood Pressure
•Oxygenated blood delivered to root of aorta (except central)
Advantages
•Cardiac support also
•No local recirculation through oxygenator at high flows
•No reversed gas exchange in lung
•Power to create high oxygen tensions in blood
28

30. Advantages
•Normal lung blood flow
•Oxygenated lung blood
•Pulsatile Blood Pressure
•Oxygenated blood delivered to root of aorta
•Must be used when native cardiac output is high
Disadvantages
•No Cardiac support
•Local recirculation through oxygenator at high flows
•Reversed gas exchange in lung if FiO2 low
•Limited power to create high oxygen tensions in blood
30

31. •Single drainage cannula
•Efficient CO2 removal
•Weak effect on Oxygenation
•Use for respiratory indications
when severe hypoxia is not a
problem
31

32. •Twodrainage cannulae
•Effectivenessof high flow limited by
recirculationfrom return to drainage
cannulae
•Oxygenationlimited by effective flo
w (total-recirculated) (but not a probl
em for CO2)
•Usedin lung conditions with severe
hypoxia

33. •Cannulate 1vein
•Minimal recirculation
•Don’t guidewire pass tricuspid
valve or hepatic vein.

34. V-V Double lumenV-V Two-site
Cannulacomplication 21% 12%
Survival rate 66% 51%
Neurologicproblem 1.8% 1.5%
Renalproblem 16% 14%
Blood hemolysis 7.8% 12%
The totalcomplication rate was found to be similar in both
groups

36. •Recirculation: Oxygenated blood pass into the
ECMO drainage cannulae
Deoxygenated
Blood
Large Central
Vein
Oxygenated
Blood
RA
Pulmonary
Circulation
Arterial
Oxygenation

37. Common target for SaO2: 86%~92%
ECMO circuit flow -70% of cardiac output
(even if lungs are not contributed)
SaO2 : 86% ↑, flows 3.0-6.0L/min
Example
•CO : 5L/min , ECMO : 3.5L/min (SvO2:70%)
•ECMO circuit(3.5L/min)----SO2=100%
•Native venous return(1.5L/min)----SO2=70%
•Pulmonary artery blood = 91%

38. •Positions of the drainage
•Return cannulae
•ECMO flow
•Intravascular volume
•Cardiac output
•Patient position

39. High
Preoxygenator
SO2(75%)
Low
SaO2(85%)
Recirculation
Low
Preoxygenator
SO2(60%)
Low
SaO2(85%)
CO-abnormal
(ECMO flow high/Low)
Preoxygenator
PO2
Postoxygentor
PO2
High separation -No recirculation

40. •“Systemic venous oxygen saturation” is confusing
•Pulmonary arterial blood =
systemic venous return +
oxygenated blood from return cannulae
•Preoxygnator SO2> Systemic venous SO2 because
some recirculation

41. •Potentially reversible and life-threatening respirator
y failure unresponsive to optimum conventional ven
tilation and therapy.
•Severe respiratory failure was defined in the CESA
R trial as:
•Murray score≥3; or
Uncompensated hypercapnia with pH ≤7.20
41

42. Parameter / Score 0 1 2 3 4
PaO
2/FiO
2
(On 100%Oxygen)
≥300mmHg
≥40kPa
225-299
30-40
175-224
23-30
100-174
13-23
<100
<13
CXR normal 1 point per quadrant infiltrated
PEEP(cmH
2O) ≤5 6-8 9-11 12-14 ≥15
Compliance
(ml/cmH
2O)
≥80 60-79 40-59 20-39 ≤19
42

43. •Advanced malignancy or any fatal diagnosis
•Unwitnessed cardiac arrest
•Progressive and non-recoverable respiratory disease
•Severe pulmonary hypertension and right ventricular failure
(mean PAP approaching systemic pressure)
•Severe cardiac failure: consideration should be given to veno-arterial
(VA)-ECMO
•Immunosuppression
–Transplant recipients beyond 30 days
–Advanced HIV defined by secondary malignancy, prior hepatic or renal failure (cir
rhosis or serum creatinine >250μmol/L), or requiring salvage anti-retroviral treat
ment
–Recent diagnosis of hematological malignancy
–Bone marrow transplant recipients
•Body size <20kg or >120kg
43

44. •Preexisting conditions which affect the quality of life
•Age >80 year-old
•CPR duration >60 minutes
•Multiple organ failure
•Central nervous system injury
•Contraindication to anticoagulation (no citrate)
•Patient who had been on high pressure
(peak pressure >30cmH
20) or high FiO
2(>0.8) ventilation for >7days
44

45. Consumable /Equipment Qty Remarks
1.
Maquet PLS set with:
Quadrox PLS Oxygenator
Rotaflow Centrifugal pump
1 From vendor
2.NS (1L bag) 1 For priming of circuit
3.ECMO machine + Clean tube clamps 1+4 Inform CCU
5.
Venous cannula +
Percutaneous Insertion Kit
1+1 size with cannulating physician
6.
Arterial cannula +
Percutaneous Insertion Kit
1+1 size with cannulating physician
45

46. •Check for leakage of the heat exchanger by flushing it with water
before priming the oxygenator.
•The circuit is primed with normal saline (1L bag) under sterile co
nditions.
–Make sure no bubbles in the circuit tubing, oxygenator and Rotaflow
–If concomitant CVVH is required, leave behind one of the 3-waystopcock
s on the venous line for connection to the dialysis machine.
•The fluid in the circuit is warmed by the heat exchanger before it
is attached to the patient.
–For HSI patients, keep >37
o
C
46

47. Vascular access in VV-ECMO
47
•Two-cannula Technique
–Drained cann:
IVC tip 5-10cm below the RA-IVC
junction(25-29F,50cm>).
–Returned cann:
RA-SVC junction(17-19F,20cm).
RA(21-25F,50cm>)
•Single-cannula Technique
–Avalon : 27 or 31F,
•Three-cannula Technique
–Femorofemoral cann
–2
nd
RIJV 19-21F,20cm

48. •If the desired blood flow cannot be achieved with a single access ca
nnula, insert a second access cannula.
•Decide on 2 cannulation sites for blood drainage and return.
–Jugular vein cannulation is contraindicated in unilateral internal jugular vein thr
ombosis.
–Cannulation into the subclavian vein for ECMO is not preformed.
•Xray, fluro or echocardiogram can be used to guide cannula position
ing.
–The access and return cannulae should be placed at some distance apart to m
inimize access recirculation.
48

49. 49

50. •PMP(poly-methypentene)
–Plasma leak
–Thrombus formation
–Hemolysis
•The mechanism of failure
–Deposition of fibrous network of RBC
–Deposition of Platelet onto the membrane
•Company
QuadroxPLS
MedosHilite7000LT
EurosetsECMO

51. •Begin extracorporeal blood flow at 50ml/kg/min for adults.
•Titrate blood flow to maintain systemic arterial oxygen saturation while on low v
entilator settings.
A systemic arterial saturation around 80% will be adequate for systemic oxygen deli
very if the hematocrit is over 40% and cardiac function is good.
The absence of persistent metabolic acidosis is indicative of an adequate systemic
oxygen delivery.
In-line venous saturation monitor may not reflect the true venous saturation in the p
resence of circuit recirculation.
•If oxygenation cannot be maintained with persistent metabolic acidosis, the follo
wings can be considered:
Increase extracorporeal blood flow
In access insufficiency, increase intravascular volume, or insert a second access ca
nnula.
Blood transfusion to maintain a hematocrit level between 40-45%
Increase ventilator FiO2 and ventilatory support
In cardiac failure, increase cardiac output using volume, inotropes, or conversion to
VA-ECMO for cardiac support.
51

52. •Use 100% oxygen as sweep gas.
•Begin with a sweep gas flow rate of 6L/min. After the extr
acorporeal blood flow has been adjusted, set the sweep g
as to extracorporeal blood flow ratio to 1:1
–A higher PaCO
2is beneficial to subsequent weaning
•Titrate sweep gas flow rate according to carbon dioxide p
artial pressure: Increase sweep gas flow rate to increase
carbon dioxide clearance
52

53. •Bolus heparin 50-100 units/kg after successful cannulation
followed by continuous infusion.
•Continuous heparin infusion at 10-15units/kg/hour.
–Titrate dose to maintainAPTT of 50-60s.
–A higher APTT level should be targeted for extracorporeal blood f
low in the range of 0.5 to 2.5L/min.
•Monitor APTT every 6 hours.
•Some center may choose to monitor TEG(Thromboelastog
raphanalyzer)
53

54. •ECMO blood flow: 50-80 ml/kg/min(3.0-6.0L/min)
•Gas flow:50-80 ml/kg/min
•FiO
2(sweep gas): 1.0
•Arterial oxygen saturation: 85-95%
•PaCO
2: 4.7–6.0kPa(35-45mmHg)
•pH: 7.35–7.45
•Mean arterial pressure: >65mmHg
•Hemoglobin: 10g/dl >
•APTT: 50-60s
•Platelet count: >100,000

55. •Goals
–Maximize lung rest
–Minimize further lung injury
1.Volutrauma
•Low tidal volume 4-6ml/kg or less
•Keeppip<30cmH
2O
•Low respiratory rate 8-10/min
2.Atelectotrauma
•Higher PEEP 10-20cmH
2O
3.Reduce oxygen toxicity
•FiO
2>0.3 and <0.4

56. •should be thoroughly sedated at the time of cannulation
and for the first 12 to 24 hours
–facilitate successful cannulation
–avoid air embolism in the presence of spontaneous breathing
–minimize metabolic rate
–enhance comfort.
•Once the patient is stable on VV-ECMO,
sedation should be minimized
56

57. •Hemolysis
–Intravascular hemolysis can result from Access insufficiency:
•Insufficient venous return
•Obstructedaccess cannula
•Access cannulatoo small
•Clots within the circuit
•Inappropriate pump speed
•Bleeding
–Apply direct pressure to accessible sites.
–In case of bleeding at the cannulation site, rule out decannulation.
•Circuit rupture
–Cleaning circuit (polycarbonate components) with alcohol predisposes to fract
ure and should be avoided
57

58. •Pump failure
–Causes:
•Pump head disengagement from accidental contact or incorrect placement
•Motor failure
•Battery failure in the absence of AC power
•Air in circuit
–To prevent air embolism, it is necessary to maintain the pressure at the blood si
de higher than that at the gas side:
•Keep the oxygenator below the level of the patient.
•Clotting in circuit
–Clots larger than 5mm or enlarging clots on the return side of the circuit should
be removed.
•Decannulation
–Accidental removal of either or both cannulae.
58

60. •For CRRT circuit, the blood drainage side is conventionally lab
eled as arterial, and the blood return side as venous. This is in
opposite to that of the ECMO circuit.
•The return line of the CRRT circuit is connected to the luer lock
connector on the arterial cannula or a distal connector placed b
etween the oxygenator and return cannula on the ECMO circui
t via a 3-way tap.
•If CRRT machine with adjustable access pressure alarm or its
equivalentis used, the access line of the CRRT circuit is conne
cted to a proximal connector between the oxygenator and retur
n cannula on the ECMO circuit via a 3-way tap.
60

61. •Increase ventilator support to a setting acceptable off VV-ECMO.
•Turn off the sweep gas but continue pump rate to maintain extraco
rporeal blood flow.
•Monitor systemic arterial oxygen saturation and pCO
2. If paramete
rs remain adequate after one hour of ventilation at an acceptable s
etting with the sweep gas turned off, the patient is ready to come o
ff VV-ECMO.
•Stop heparin infusion once the decision has been made to come o
ff VV-ECMO. The circuit can be removed after 4 hours
61

62. •Turn off pump and clamp lines on both the access and ret
urn sides.
•Remove the cannulae. Apply direct pressure manually or
with a C-clamp
•Long time direct decannulation site compression.
62

63. 1. Peek GJ, MugfordM, TiruvoipatiR, et al: Efficacy and economic assessment of conventional ventilatorysupport
versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR): A multicentre randomised
controlled trial Lancet 374:1351-1363, 2009
2. ECLS Registry Report International Summary. Ann Arbor, MI: Extracorporeal Life Support Organisation; 20113. Noah
MA, Peek GJ, Finney SJ, et al: Referral to an extracorporeal membrane oxygenation center and mortality among
patients with severe 2009 influenza A(H1N1). JAMA 306:1659-1668, 2011
4. Davies A, Jones D, Bailey M, et al: Extracorporeal membrane oxygenation for 2009 influenza A(H1N1) acute
respiratory distress syndrome. JAMA 302:1888-1895, 2009
5. Patroniti N, Zangrillo A, Pappalardo F, et al: The Italian ECMO network experience during the 2009 influenza
A(H1N1) pandemic: Preparation for severe respiratory emergency outbreaks. Intensive Care Med 37:1447-1457, 2011
6. Smith IJ, SidebothamDA, McGeorgeAD, et al: The use of ECMO during resection of tracheal papillomatosis.
Anesthesiology 110:427-429, 2009
7. Collar RM, Taylor JC, HogikyanND, et al: Awake extracorporeal membrane oxygenation for management of critical
distal tracheal obstruction. OtolaryngolHead Neck Surg142:618-620, 2010
8. ZapolWM, Snider MT, Hill JD, et al: Extracorporeal membrane oxygenation in severe acute respiratory failure. A
randomized prospective study. JAMA 242:2193-2196, 1979
9. Buckley E, SidebothamD, McGeorgeA, et al: Extracorporeal membrane oxygenation for cardiorespiratoryfailure in
four patients with pandemic H1N1 2009 influenza virus and secondary bacterial infection. Br J Anaesth 104:326-329,
2010
10. SidebothamD, McGeorgeA, McGuinnessS, et al: Extracorporeal membrane oxygenation for treating severe cardiac
and respiratory failure in adults: Part 2-technical considerations. J CardiothoracVascAnesth24:164-172, 2010
11. Locker GJ, LosertH, SchellongowskiP, et al: Bedside exclusion of clinically significant recirculation volume during
venovenousECMO using conventional blood gas analyses. J ClinAnesth15:441-445, 2003